NMS Surgery [6th Edition] 9781496319173

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NMS

Na tio na l Me d ic a l Se rie s fo r Ind e p e nd e nt Stud y

Surgery

NMS

Na tio na l Me d ic a l Se rie s fo r Ind e p e nd e nt Stud y

Surgery Sixth Ed itio n

Bruce E. Jarrell, MD Professor Department of Surgery University of Maryland School of Medicine Baltimore, Maryland

Stephen M. Kavic, MD Associate Professor Department of Surgery Program Director Residency in General Surgery University of Maryland School of Medicine Baltimore, Maryland

Acquisitions Editor: ari Broderick Product Development Editor: Amy Weintraub Editorial Assistant: Joshua Haf ner Marketing Manager: Joy Fisher-Williams Production Project Manager: Priscilla Crater Design Coordinator: erry Mallon Manufacturing Coordinator: Margie Orzech Prepress Vendor: Absolute Service, Inc. Sixth Edition Copyright © 2016 Wolters Kluwer Copyright © 2008, © 2000, Lippincott Williams & Wilkins, a Wolters Kluwer business All rights reserved. T is book is protected by copyright. No part o this book may be reproduced or transmitted in any orm or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any in ormation storage and retrieval system without written permission rom the copyright owner, except or brie quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part o their o cial duties as U.S. government employees are not covered by the abovementioned copyright. o request permission, please contact Wolters Kluwer at wo Commerce Square, 2001 Market Street, Philadelphia, PA 19103, via email at [email protected], or via our website at lww.com (products and services). 987654321 Printed in China Library of Congress Cataloging-in-Publication Data NMS surgery / [edited by] Bruce E. Jarrell, Stephen M. Kavic. — Sixth edition. p. ; cm. — (National medical series or independent study) National medical series surgery Includes index. ISBN 978-1-60831-584-0 I. Jarrell, Bruce E., editor. II. Kavic, Stephen M. (Stephen Michael), editor. III. itle: National medical series surgery. IV. Series: National medical series or independent study. [DNLM: 1. Surgical Procedures, Operative—Examination Questions. 2. Surgical Procedures, Operative—Outlines. 3. General Surgery— methods—Examination Questions. 4. General Surgery—methods—Outlines. WO 18.2] RD37.2 617.0076—dc23 2015010501 T is work is provided “as is,” and the publisher disclaims any and all warranties, express or implied, including any warranties as to accuracy, comprehensiveness, or currency o the content o this work. T is work is no substitute or individual patient assessment based on healthcare pro essionals’ examination o each patient and consideration o , among other things, age, weight, gender, current or prior medical conditions, medication history, laboratory data, and other actors unique to the patient. T e publisher does not provide medical advice or guidance and this work is merely a re erence tool. Healthcare pro essionals, and not the publisher, are solely responsible or the use o this work including all medical judgments and or any resulting diagnosis and treatments. Given continuous, rapid advances in medical science and health in ormation, independent pro essional veri cation o medical diagnoses, indications, appropriate pharmaceutical selections and dosages, and treatment options should be made and healthcare pro essionals should consult a variety o sources. When prescribing medication, healthcare pro essionals are advised to consult the product in ormation sheet (the manu acturer’s package insert) accompanying each drug to veri y, among other things, conditions o use, warnings, and side ef ects and identi y any changes in dosage schedule or contraindications, particularly i the medication to be administered is new, in requently used, or has a narrow therapeutic range. o the maximum extent permitted under applicable law, no responsibility is assumed by the publisher or any injury and/or damage to persons or property, as a matter o products liability, negligence law or otherwise, or rom any re erence to or use by any person o this work. LWW.com

We b o th tha nk the m a ny m e nto rs who ha ve a d vis e d us e a c h thro ug ho ut o ur c a re e rs . We a re fo re ve r ind e b te d to the m . I wis h to tha nk m y wife , Le s lie , a nd m y wo nd e rful c hild re n fo r a ll o f the ir s up p o rt d uring m y c a re e r, a nd fo r the ir und e rs ta nd ing d uring the writing o f the m a ny e d itio ns o f NMS Surg e ry – BEJ De d ic a te d to m y lo ving wife J e nnife r a nd to m y lo ve ly d a ug hte r Em ily – SMK

Foreword It is with tremendous pride that I introduce the sixth edition o NMS Surgery. T is work has occupied a central role in the education o a generation o medical students. T e outline ormat makes it a superb re erence or those learning the basics o surgery and a thorough review or those who already practice our art. T e current edition has special signi cance to the University o Maryland School o Medicine. Dr. Jarrell is the Chie Academic and Research O cer and Dean o the Graduate School. He also was my predecessor as Chair o the Department o Surgery. Dr. Kavic is the current program director o our surgery residency. T e chapter authors and contributors include a virtual directory o our trainees and aculty. It is a privilege to be associated with these esteemed educators. I am continually impressed by the talents o the surgeons and surgeons-in-training at the University o Maryland. T at quality is re ected in the ollowing chapters. I know that you will enjoy this edition as much as I take pride in it. Ste p h e n T. Ba rtle tt, MD P e te r An g e los Dis tin g u is h e d P rofe s s or of Su rg e ry Ch a ir De p a rtm e n t of Su rg e ry Su rg e on -in -Ch ie f Un ive rs ity of Ma ryla n d Me d ic a l Sys te m Un ive rs ity of Ma ryla n d Sc h ool of Me d ic in e Ba ltim ore , Ma ryla n d

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Pre ace Welcome to the sixth edition o NMS Surgery. T is book aims to build on the legacy o the previous ve editions. We have retained much o the organization and ormat rom the last versions. At the same time, we have strived to make this volume more readable. It is an increasing challenge to limit content in the ace o rapidly expanding surgical knowledge. As in previous editions, the text is not meant to be all-inclusive but rather serves as an introduction or the student o surgery. All o the chapters have been thoroughly reviewed, rewritten, and updated to re ect the current state o the art in surgery. T ere are dramatic dif erences in the ormat o this volume. Perhaps most importantly, each section now begins with “Chapter Cuts and Caveats,” which are some o the most important principles worthy o the reader’s attention. Within each chapter, we have added “Quick Cuts,” which are highlights that have been brought out separately rom the text. In addition, we have added a new section at the end, “Grade A Cuts,” which are pairings that highlight associations in surgical thinking. For the tremendous work put into this edition, we are indebted to the authors. T eir high-quality and requently punctual contributions have made our jobs as editors pleasant. We are also grate ul to the editorial team at Wolters Kluwer or their guidance and support throughout the process. T e sixth edition o NMS Surgery is written primarily or students and residents in general surgery, but practicing surgeons as well as physicians in other specialties will no doubt nd it a use ul re erence. We hope that all readers will nd that the book represents a declaration o the state o surgical art in 2015. —Bru c e E. J a rre ll, MD —Ste p h e n M. Ka vic , MD

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Contributors Willia m R. Ale x, MD, FACS Cardiothoracic Surgery Riverside, Cali ornia H. Ric ha rd Ale xa nd e r, MD, FACS Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland And re a C. Ba ffo rd , MD, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland Em ily Be lla va nc e , MD, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland Hug o Bo na tti, MD, FACS General and Minimally Invasive Surgery Easton, Maryland Che rif Bo utro s , MB, CHB, MSc , FACS Associate Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland J o na tha n Bro m b e rg , MB, P hD, FACS Pro essor o Surgery Chie Division o ransplantation University o Maryland School o Medicine Baltimore, Maryland Bra nd o n Bruns , MD, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland La ura S. Buc ha na n, MD, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland

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Whitne y Burro ws , MD, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland Clint D. Ca p p ie llo , MD Resident in Surgery University o Maryland Medical Center Baltimore, Maryland Ke nne th M. Cra nd a ll, MD Resident in Neurosurgery University o Maryland Medical Center Baltimore, Maryland Ro b e rt S. Cra wfo rd , MD, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland P e te r E. Da rwin, MD Pro essor o Medicine University o Maryland School o Medicine Baltimore, Maryland J o s e J . Dia z, MD, FACS Pro essor o Surgery Chie Division o Acute Care Surgery University o Maryland School o Medicine Baltimore, Maryland Ga rim a Do s i, MD Fellow in Vascular Surgery University o Maryland Medical Center Baltimore, Maryland Ric ha rd N. Ed ie , MD, FACS Cardiothoracic Surgery Philadelphia, Pennsylvania Ste ve n Fe ig e nb e rg , MD Pro essor o Radiation Oncology University o Maryland School o Medicine Baltimore, Maryland

Contributors

J e s s ic a Fe lto n, MD Resident in Surgery University o Maryland Medical Center Baltimore, Maryland J a m e s S. Ga m m ie , MD, FACS Pro essor o Surgery Chie , Division o Cardiac Surgery University o Maryland School o Medicine Baltimore, Maryland J inny Ha , MD Resident in Surgery University o Maryland Medical Center Baltimore, Maryland Na ta s ha Ha ns ra j, MD Resident in Surgery University o Maryland Medical Center Baltimore, Maryland And re a He b e rt, MD Resident in Otolaryngology University o Maryland Medical Center Baltimore, Maryland Trip p Ho lto n, MD, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland

Ste p he n M. Ka vic , MD, FACS Associate Pro essor o Surgery Program Director Residency in General Surgery University o Maryland School o Medicine Baltimore, Maryland Ed win Ke nd ric k, MD Fellow in Vascular Surgery University o Maryland Medical Center Baltimore, Maryland Sus a n B. Ke s m o d e l, MD, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland Ma rk D. Klig m a n, MD, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland And re w Kra m e r, MD, FACS Associate Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland Na ta lia Kub ic ki, MD Resident in Surgery University o Maryland Medical Center Baltimore, Maryland

He le n G. Hui-Cho u, MD Fellow in Plastic Surgery University o Maryland Johns Hopkins University Baltimore, Maryland

Ka the rine G. La m o nd , MD, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland

Aja y J a in, MD, FACS Associate Pro essor o Surgery State University o New York Upstate Medical University Syracuse, New York

Ma tthe w Lis s a ue r, MD, FACS, FCCM Associate Pro essor o Surgery Rutgers Robert Wood Johnson Medical School New Brunswick, New Jersey

Ste ve n B. J o hns o n, MD, FACS, FCCM Pro essor and Chairman Department o Surgery University o Arizona Phoenix, Arizona

Da nie l E. Ma ns o ur, MD Resident in Surgery University o Maryland Medical Center Baltimore, Maryland

J e s s ic a J o ine s , MA, MGC Instructor o Medicine University o Maryland School o Medicine Baltimore, Maryland

Da nie l Me d ina , MD, P hD Resident in Surgery University o Maryland Medical Center Baltimore, Maryland

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x

Contributors

Ma yur Na ra ya n, MD, MP H, MBA, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland

Cha rle s A. Sa ns ur, MD Assistant Pro essor o Neurosurgery University o Maryland School o Medicine Baltimore, Maryland

Silke Nie d e rha us , MD, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland

Ra ja b ra ta Sa rka r, MD, FACS Pro essor o Surgery Chie Division o Vascular Surgery University o Maryland School o Medicine Baltimore, Maryland

J o hn A. Ols o n J r, MD, P hD Pro essor o Surgery Chie Division o General Surgery and Surgical Oncology University o Maryland School o Medicine Baltimore, Maryland Na ta lie A. O’Ne ill, MD Resident in Surgery University o Maryland Medical Center Baltimore, Maryland D. Bruc e P a na s uk, MD, FACS Chie o Surgery Wilmington VA Medical Center Wilmington, Delaware J o na tha n P. P e a rl, MD, FACS Assistant Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland Srine va s K. Re d d y, MD, FACS Surgical Oncology and Hepatobiliary Surgery Minneapolis, Minnesota Da nie l Re znic e k, MD Resident in Urologic Surgery University o Maryland Medical Center Baltimore, Maryland Erne s t L. Ro s a to , MD, FACS Pro essor o Surgery Director Division o General Surgery T omas Jef erson University Philadelphia, Pennsylvania Fra nc is E. Ro s a to J r, MD, FACS General and Minimally Invasive Surgery Pennington, New Jersey

J o s e p h R. Sc a le a , MD ransplant Surgery Fellow University o Wisconsin Madison, Wisconsin Tho m a s Sc a le a , MD, FACS Pro essor o Surgery Physician-in-Chie R Adams Cowley Shock rauma Center University o Maryland School o Medicine Baltimore, Maryland Ma x Se a to n, MD Resident in Surgery University o Maryland Medical Center Baltimore, Maryland De vind e r Sing h, MD, FACS Associate Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland Ale xis D. Sm ith, MD Resident in Surgery University o Maryland Medical Center Baltimore, Maryland Ro b e rt Ste rling , MD Assistant Pro essor o Surgery Johns Hopkins University School o Medicine Baltimore, Maryland Eric Stra uc h, MD, FACS Associate Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland Olive r Ta nno us , MD Resident in Orthopedic Surgery University o Maryland Medical Center Baltimore, Maryland

Contributors

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J ulia Te rhune , MD Resident in Surgery University o Maryland Medical Center Baltimore, Maryland

Ro na ld J . We ig e l, MD, P hD, MBA, FACS Pro essor and Chair o Surgery University o Iowa Iowa City, Iowa

Do ug la s J . Turne r, MD, FACS Associate Pro essor o Surgery University o Maryland School o Medicine Baltimore, Maryland

Niluka A. Wic kra m a ra tne , MD Resident in Surgery Virginia Commonwealth University Richmond, Virginia

Ke li Turne r, MD Resident in Surgery University o Maryland Medical Center Baltimore, Maryland

J e ffre y S. Wo lf, MD Associate Pro essor o Otolaryngology—Head and Neck Surgery University o Maryland School o Medicine Baltimore, Maryland

A. Cla ire Wa tkins , MD Resident in Cardiothoracic Surgery University o Maryland Medical Center Baltimore, Maryland

Contents Preface vii Acknowledgments Contributors viii

P a rt I: Intro d uc tio n 1

P rinc ip le s o f Surg ic a l P hys io lo g y . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Ste ve n B. J o hns o n a nd Ma tthe w Lis s a ue r Fluid and Electrolytes 3 Acid–Base Disturbances 11 Coagulation 13 Packed Red Blood Cell rans usion T erapy 16 Nutrition and the Surgical Patient 17 T e Intensive Care Unit 22 Shock 27

2

Es s e ntia ls o f Ge ne ra l Surg e ry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Na ta s ha Ha ns ra j a nd Do ug la s J . Turne r Wounds 30 Surgical ubes and Drains 33 Hernias 35 Postoperative Complications 39 Surgical In ections 40 Gastrointestinal Fistula 41

3

Me d ic a l Ris k Fa c to rs in Surg ic a l P a tie nts . . . . . . . . . . . . . . 43 Sus a n B. Ke s m o d e l, Na ta lia Kub ic ki, a nd Ma yur Na ra ya n General Aspects or Evaluation and Management o the Surgical Patient 43 Evaluation o the Surgical Patient with Cardiac Disease 46 Evaluation o the Surgical Patient with Lung Disease 51 Evaluation o the Surgical Patient with Renal Disease 53 Evaluation o the Surgical Patient with Liver Disease 55

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Contents

4

xiii

Life -thre a te ning Dis o rd e rs : Ac ute Ab d o m ina l Surg ic a l Em e rg e nc ie s . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58 La ura S. Buc ha na n a nd J o s e J . Dia z Acute Abdomen 58 Obstruction 63 Hemorrhage 65 Study Questions or Part I 67 Answers and Explanations 73

P a rt II: Tho ra c ic Dis o rd e rs 5

P rinc ip le s o f Tho ra c ic Surg e ry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78 J inny Ha a nd Whitne y Burro ws General Principles o T oracic Surgery 78 Chest Wall Disorders 83 Pleural and Pleural Space Disorders 83 Pulmonary In ections 85 Solitary Pulmonary Nodules (Coin Lesions) 85 Bronchogenic Carcinoma 85 Bronchial Adenomas 88 Metastatic umor 89 racheal Disorders 89 Mediastinal Lesions 90 T oracic rauma 90

6

He a rt . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93 A. Cla ire Wa tkins , D. Bruc e P a na s uk, Willia m R. Ale x, Ric ha rd N. Ed ie , a nd J a m e s S. Ga m m ie Acquired Heart Disease 93 Congenital Heart Disease 102 Study Questions or Part II 108 Answers and Explanations 113

P a rt III: Va s c ula r Dis o rd e rs 7

Arte ria l Dis e a s e

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 118

Ga rim a Do s i a nd Ro b e rt S. Cra wfo rd General Principles 118 Lower Extremity Arterial Occlusive Disease 118 Aortoiliac Occlusive Disease (AIOD) 120 Femoropopliteal Occlusive Disease 122 In rageniculate ibial Disease 123 Acute Arterial Insu ciency 124 Amputations 125 Extracranial Cerebrovascular Disease 125

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Contents

Aortic Dissection 127 Arterial Aneurysms 128 Mesenteric Vascular Disease 130 Renal Artery Stenosis 132 Miscellaneous 133

8

Ve no us a nd Lym p ha tic Dis e a s e . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135 Ed win Ke nd ric k a nd Ra ja b ra ta Sa rka r Acute Deep Venous T rombosis 135 Acute Pulmonary Embolism 138 Chronic Venous Disorders: Varicose Veins and Chronic Venous Insu ciency 140 Super cial Venous T rombophlebitis 142 Lymphedema 142 Study Questions or Part III 144 Answers and Explanations 148

P a rt IV: Ga s tro inte s tina l Dis o rd e rs 9

Es o p ha g us

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153

J o na tha n P. P e a rl Introduction 153 Esophageal Motility Disorders 154 Esophageal Strictures 158 Esophageal umors 158 Esophageal Per oration 160 Mallory-Weiss Syndrome 160

10

Sto m a c h a nd Duo d e num

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161

Che rif Bo utro s , Erne s t L. Ro s a to , a nd Fra nc is E. Ro s a to J r. Stomach 161 Peptic Ulcer Disease 163 Gastric Cancer 168 Postgastrectomy Syndromes 170 Benign Stomach Lesions 171 Gastritis 171

11

Sm a ll Inte s tine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173 Ka the rine G. La m o nd Introduction 173 Diseases 175

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Co lo n, Re c tum , a nd Anus

xv

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 180

J ulia Te rhune a nd And re a C. Ba ffo rd Introduction 180 Evaluation 182 Bowel Preparation 184 Benign and Malignant Colorectal umors 184 Diverticular Disease 189 Angiodysplasia 192 In ammatory Bowel Disease 192 Pseudomembranous Colitis (Antibiotic-Associated Colitis) 196 Ischemic Colitis 196 Volvulus 197 Anorectal Dys unction 198 Benign Anorectal Disease 199 Perianal and Anal Canal Neoplasms 202

13

Live r, Ga llb la d d e r, a nd Bilia ry Tre e

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 204

Da nie l Me d ina a nd Srine va s K. Re d d y General Aspects 204 Hepatic umors 207 Hepatic Abscesses and Cysts 209 Gallbladder Pathology 212 Biliary ree Pathology 213

14

P a nc re a s . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215 H. Ric ha rd Ale xa nd e r, P e te r E. Da rwin, a nd Ro na ld J . We ig e l Anatomy and Physiology 215 Pancreatitis 217 Pancreatic Malignancies 225

15

Sp le e n

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 230

Da nie l E. Ma ns o ur, Ma yur Na ra ya n, a nd Aja y J a in Introduction 230 Pathology 231 echnical Aspects o Splenectomy 234 Complications a er Splenectomy 235 Study Questions or Part IV 237 Answers and Explanations 248

P a rt V: Bre a s t a nd End o c rine Dis o rd e rs 16

Bre a s t . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 256 Em ily Be lla va nc e , Ste ve n Fe ig e nb e rg , a nd J e s s ic a J o ine s Introduction 256 Breast Evaluation 256 Benign Breast Disease 259 Malignant Diseases 260

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17

Contents

Thyro id , P a ra thyro id , Ad re na l Gla nd s , a nd Thym us . . . . . . . . . . . . . . . . . 266 J o hn A. Ols o n J r. T yroid Gland 266 Abnormalities o T yroid Descent 268 T yroid Dys unction Requiring Surgery 269 Parathyroid Glands 276 Adrenal Gland 279 umors o the Endocrine Pancreas 285 Multiple Endocrine Neoplasia 287 T ymus Gland 289 Study Questions or Part V 290 Answers and Explanations 294

P a rt VI: Sp e c ia l Sub je c ts 18

He a d a nd Ne c k Surg e ry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 299 And re a He b e rt a nd J e ffre y S. Wo lf Components o the Head and Neck Exam 299 Benign Lesions o the Head and Neck 300 Neck Abscesses 300 Congenital Masses 302 Acquired Lesions 305 Head and Neck In ections 308 Malignant Lesions o the Head and Neck 308 Neck Cancer 311 Nasal Cavity and Paranasal Sinus Cancer 312 Nasopharynx Cancer 313 Oral Cavity Cancer 314 Oropharynx Cancer 315 Hypopharynx and Cervical Esophagus Cancer 316 Larynx Cancer 317 Skin Cancer 318 Head and Neck Lymphoma 319 Unusual umors 320 Parotid Gland 320 Evaluation and Management o Parotid Masses 322 Parotid Neoplasms 322 Parotid rauma 323 In ammatory Disorders 324

19

Ba ria tric Surg e ry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 326 Ma rk D. Klig m a n Background 325 Surgical reatment o Obesity 326 Postoperative Mortality and Complications 329

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Minim a l Ac c e s s Surg e ry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335 Da nie l Me d ina , Hug o Bo na tti, a nd Ste p he n M. Ka vic History 335 General Principles 335 Selected Laparoscopic Procedures 338 Robotic echnology 343

21

Surg ic a l Onc o lo g y . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 344 Ke li Turne r, Na ta lie A. O’Ne ill, a nd Ste p he n M. Ka vic Cancer 344 Cancer Etiology and Epidemiology 344 Screening and Diagnosis 346 Diagnostic Procedures 347 Staging 348 Surgical reatment 348 Multidisciplinary reatment 350 Research and raining 351

22

Tra um a a nd Burns . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 352 Bra nd o n Bruns a nd Tho m a s Sc a le a rauma 352 Speci c Injuries 354 Burns 359

23

Org a n Tra ns p la nta tio n . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 362 J o s e p h R. Sc a le a , Ma x Se a to n, Silke Nie d e rha us , a nd J o na tha n Bro m b e rg Overview 362 Organ-Speci c Considerations 368

24

P e d ia tric Surg e ry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376 Clint D. Ca p p ie llo , Ale xis D. Sm ith, a nd Eric Stra uc h Introduction 376 Congenital Hernias 376 Abdominal Wall De ects 379 Esophageal Atresia and racheoesophageal Mal ormations 381 Intestinal Malrotation 383 Intestinal Atresia 385 Hirschsprung Disease 387 Disorders o In ancy 390 Solid umors 395 Study Questions or Part VI 397 Answers and Explanations 405

xviii Contents

P a rt VII: Surg ic a l Sub s p e c ia ltie s 25

Uro lo g ic Surg e ry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 412 J e s s ic a Fe lto n, Da nie l Re znic e k, a nd And re w Kra m e r Urologic Emergencies 412 Urinary ract Stones 414 Benign Prostatic Disorders 415 Genitourinary Malignancies 417 Male Erectile Dys unction 423 Voiding Dys unction 424 Urologic rauma 427

26

P la s tic a nd Re c o ns truc tive Surg e ry

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 430

Niluka A. Wic kra m a ra tne , He le n G. Hui-Cho u, De vind e r Sing h, a nd Trip p Ho lto n Overview 430 Reconstructive Plastic Surgery 430 Wound Healing and Diseases o Skin and So issue 442 Cranio acial Surgery 444 Hand Surgery 445 Aesthetic Plastic Surgery 446 Innovations and Devices in Plastic Surgery 449

27

Ne uro s urg e ry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 450 Ke nne th M. Cra nd a ll a nd Cha rle s A. Sa ns ur Anatomy 450 Pathophysiology 451 Evaluating the Neurosurgical Patient 453 Head Injury 454 Spinal Cord Injury 457 Central Nervous System umors 462 Congenital Nervous System Lesions 466 Functional Neurosurgery 466 Degenerative Spine Disease 467 Spine umors 470 Peripheral Nerves 470

28

Ortho p e d ic s . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 472 Olive r Ta nno us a nd Ro b e rt Ste rling Orthopedic Emergencies 472 Orthopedic Urgencies 475 rauma 478 Arthritis 486 In ections 488 umors 489 Adult Orthopedics 491 Study Questions or Part VII 494 Answers and Explanations 499

Ap p e n d ix A Gra d e “A” Cu ts 503 In d e x 509

Intr du t n Chapter Cuts and Caveats

Part I

CHAP TER 1 P rinc ip le s o Surg ic a l P hys io lo g y: Management s k pat ents requ res resus tat n, w th the g al rest rat n per us n. Qu kly and a urately f nd ng the s ur e the l n al deter rat n and f x ng that pr blem s ru al; therw se, the resus tat n w ll ult mately a l t all w adequate xygen del very. Sh k s the state phys l g de mpensat n result ng n nadequate t ssue per us n ( xygen demand utstr ps xygen supply). Ult mately, n ne rmula best determ nes p st perat ve u d and ele tr lyte management. H gh nsens ble l sses (b th evap rat ve l sses and leakage nt the th rd spa e) ur dur ng and a er surg al pr edures that nv lve pen b dy av t es; that are nvas ve and pen many t ssue planes; that are pr l nged; that are ass ated w th seps s, n ammat ry nd t ns, and s hem a rgans; that result n hyp tens n; and that are d ne n emergent sett ngs. Hyperkalem a must be treated aggress vely t av d l e-threaten ng arrhythm as. T e best emergent treatment s IV b arb nate and IV nsul n and glu se, wh h m ves p tass um ntra ellularly and l wers serum levels. IV al um s als use ul by a e t ng the thresh ld r a t n p tent al and de reas ng ard a membrane ex tab l ty. Adequate xygenat n s assessed by m re than bl d pressure and pulse. It s als m n t red by assess ng markers t ssue per us n (ur ne utput and renal un t n), xygenat n ( hest x-ray and lung aus ultat n r s gns pulm nary edema, bl d xygenat n, and ther measures), serum ele tr lyte levels, pH, arrhythm as, mentat n, external s gns hydrat n state, hemat r t, and the pat ent’s verall appearan e. When evaluat ng a pat ent wh s l n ally deter rat ng, always pr r t ze the evaluat n d agn ses n y ur d erent al that w ll lead t the astest and greatest deter rat n. New anem a n a p st perat ve pat ent s surg al bleed ng unt l pr ven therw se. Pa ked RBC trans us n pr v des ex ellent phys l g supp rt but has s de e e ts n lud ng allerg rea t ns and the p tent al r n e t us transm ss n—treat blood like a drug! Cler al err r s the m st mm n ause r trans us n rea t n. Enteral nutr t n s pre erred n m st pat ents. T e r sk entral ven us atheters utwe ghs nutr t nal benef ts r sh rt-term supplementat n nutr t nal supp rt s needed r less than 1 week. L w album n levels rrelate w th m rtal ty. Pat ents w th nadequate xygenat n r n reased w rk breath ng sh uld have vent lat ry supp rt: When in doubt, intubate.

CHAP TER 2 Es s e ntia ls o Ge ne ra l Surg e ry: F r w und n e t ns: Abs ess must be dra ned, ne r t t ssue must be debr ded, rep tus suggests a ne r t z ng gas- rm ng n e t n demand ng that the w und be pened, re gn b d es ( n lud ng tubes r dra ns) must be rem ved, and enter leak must be ntr lled.

System ant b t s are n t the pr mary treatment r w und n e t ns. Per perat ve ant b t s g ven t pat ents w th lean- ntam nated w unds (wh h are usually l sed pr mar ly) redu e the n den e w und n e t ns and the subsequent r sk hern a. Any nd t n that nter eres w th the ur phases w und heal ng (hem stas s, n ammat n, pr l erat n, and rem del ng) w ll mpa r the rate heal ng and the f nal w und strength. B th l al and system a t rs have an e e t. L al a t rs: W unds sh uld be ree bleed ng, hemat ma, gr ss ntam nat n, and ne r t t ssue; w und edges sh uld be ree tens n; and l al t ssue sh uld be healthy and well vas ular zed. System a t rs that mpa r w und heal ng: metab l sm, p r nutr t nal state, z n and v tam ns A and C def en y, presen e n e t n, hyp x a, l w- w states, sm k ng, p rly ntr lled d abetes, bes ty, llagen vas ular d seases, and renal and l ver a lure Med at ns: system glu rt ds, s me hem therapeut and mmun suppress ve drugs, and ang genes s nh b t rs P st perat ve evers may result r m the 5 W’s: w und, water, w nd, walk ng, and w nder drugs. Surg al s te n e t ns are a maj r s ur e m rb d ty and are m st mm nly due t sk n ra (espe ally Staphylococcus). N nheal ng GI f stulas may result r m FRIEND ( re gn b dy, rad at n, n ammat n, ep thel al zat n, ne plas a, d stal bstru t n) and en resp nd t n n perat ve management.

CHAP TER 3 Me d ic a l Ris k Fa c to rs in Surg ic a l P a tie nts : Assessment med al r sk r nvas ve surg al pr edures n ludes a th r ugh h st ry, phys al, and lab rat ry exam nat n. Pat ents w th ard a nd t ns are at n reased r sk r ard a mpl at ns ll w ng n n ard a surgery, and standard zed lass f at n systems help strat y r sk. Fun t nal apa ty m re than 4 ME s pred ts a l w r sk p st perat ve ard a events. Ele t ve surgery sh uld be p stp ned at least 4 weeks ll w ng acute ard a events r revas ular zat n. All pat ents sh uld be assessed r the degree r sk r ven us thr mb emb l events, and pr phylax s w th hepar n s appr pr ate r m st surg al pat ents.

CHAP TER 4 Li e -Thre a te ning Dis o rd e rs : Ac ute Ab d o m ina l Surg ic a l Em e rg e nc ie s : When evaluat ng a pat ent r a ute abd m nal pa n, f rst determ ne whether the pat ent has a surg al abd men n exam nat n, judged by a d stressed pat ent w th pa n that s severe and general zed and ass ated w th reb und r guard ng. Cl n al judgment s supplemented by rad graph stud es, su h as extralum nal per t neal ree a r, and lab rat ry stud es, su h as f nd ngs supp rt ve s hem a, n ammat n, a ute hem rrhage nt the per t neal av ty, r n e t n. I the judgment a surg al abd men s made, mmed ate ntervent n a er resus tat n s nd ated. GI hem rrhage ne ess tates l al z ng the bleed ng and rmulat ng a plan t ntr l t be re surgery. Ident y ng the s ur e bleed ng n the perat ng r m by evaluat ng the external sur a e the GI tra t s very d ult. manage a s gn f ant GI hem rrhage, balan ng three pr blems s multane usly be mes ne essary: v lume resus tat n, agulat n de e t rre t n, and dent f at n and ntr l the s te hem rrhage. rans us n bl d and bl d pr du ts may be r t al n manag ng all three pr blems. rans us n bey nd several un ts results n n reased m rb d ty and m rtal ty be ause bl d and ts pr du ts have many p tent al s de e e ts, su h as trans us n rea t ns w th anaphylax s and hem lys s, n e t us agent transm ss n, and mmune suppress n, am ng thers. L at n an nd ate mm n path l gy: RUQ suggests the b l ary tree; RLQ, the append x; and LLQ, the s gm d l n.

2

Chapter 1

Pr n ples Surg al Phys l gy Steven B. Johnson and Matthew Lissauer

FLUID AND ELECTROLYTES No rm a l Bo d y Co m p o s itio n I. Bo d y wa te r: Water a unts r 50%–70% b dy we ght (the h gher per entage n y ung pe ple, th n pe ple, and man—the l wer per entage n lder pe ple, bese pe ple, and w men). B dy water s d v ded nt var us ntra ellular and extra ellular mpartments (F g. 1-1). A. w -th rds rule: T s s a s mple meth d appr x mat ng mpartment v lume be ause the var at n am ng pat ents and w th n the same pat ent. tal b dy water mpr ses sl ghtly less than tw -th rds b dy we ght. B. Plasma v lume: Us ng the ab ve rule, 5% b dy we ght s plasma v lume (e.g., 3.5 L r a 70-kg male). Plasma s 60% the bl d v lume ( the hemat r t s 40%); there re, the 70-kg male has 5 L bl d. II. Ele c trolyte c om pos ition: Ele tr lytes determ ne the am unt water that ex sts n any ne spa e at any t me, and the r n entrat ns and mp s t ns d er between ntra ellular and extra ellular spa es due t n pumps (pr n pally Na /K A Pase), as sh wn n able 1-1. Change n sm t pressure n ne mpartment auses water t red str bute r m the ther mpartments t rega n equ l br um. A. Intracellular (pr nc pal sm t c cat n s p tass um): has h gher n entrat n sm t and n t (pr te n) part les than the extra ellular mpartment, thus all w ng water t w nt the ell, reat ng turg d ty B. Extracellular (pr nc pal sm t c cat n s s d um): Interst t al and plasma mp s t n s nearly but n t qu te dent al.

Quic k Cut The compartments are important becaus e calculating f uid los s es , blood los s es , and amount o res us citation needed is key to ens uring patients ’ s urvival.

Quic k Cut Two-thirds rule: Total body water (slightly less than) two-thirds total body weight.

Quic k Cut O total body water, two thirds is intracellular and one third extracellular (three ourths inters titial and one ourth intravas cular).

Quic k Cut Water ollows electrolytes acros s cell membranes to equilibrate os molality.

Wa te r a nd Ele c tro lyte Ma inte na nc e I. Wa te r: Requ red am unt depends n the pers n’s we ght, age, gender, and llness. A. Water calculat n meth ds 1. Am unt b dy water excreted a. M st water l st r m the b dy s thr ugh ur ne pr du t n; generally, 0.5 mL/kg/hr s the m n mum needed t ex rete the da ly s lute l ad.

Quic k Cut Adequate urine output is ½ mL/kg/hr, or about 250 mL/8 hr in adults .

3

4

Chapter 1

Flu d and Ele tr lytes

Tota l body wa te r: 60% of tota l body we ight

Intra ce llula r: 40% of tota l body we ight (2/3 of the tota l body wa te r)

Extra ce llula r: 20% of tota l body we ight (1/3 of the tota l body wa te r)

Inte rs titia l: 15% tota l body we ight (3/4 of the e xtra ce llula r fluid)

P la s ma : 5% tota l body we ight (1/4 of the e xtra ce llula r fluid)

Fig ure 1-1: Water compartments .

Ta b le 1-1: Ele c tro lyte Co m p o s itio n o Va rio us Wa te r Co m p a rtm e nts Ele c tro lyte s

Intra c e llula r Co m p a rtm e nt

Extra c e llula r Co m p a rtm e nt

Anio ns 10 mEq/L

142 mEq/L

140 mEq/L

4 mEq/L

4 mEq/L

103 mEq/L

Bicarbonate (HCO3 )

10 mEq/L

28 mEq/L

Phosphate (PO4 3 )

75 mEq/L

4 mEq/L

Sul ate (SO4 2 )

2 mEq/L

1 mEq/L

Calcium (Ca

1 mEq/L

5 mEq/L

18 mEq/L

2 mEq/L

Sodium (Na ) Potassium (K ) Chloride (Cl )

)

Magnesium (Mg Org a nic a c id s Va rio us p ro te ins

)

— 40 mEq/L

5 mEq/L 1 mEq/L

Chapter 1

Pr n ples

Surg al Phys l gy

5

b. T e next h ghest da ly water l ss s nsens ble l ss ( .e., sweat, resp rat n, st l), wh h s est mated as 600–900 mL/24 hr. c. M n mal water ma ntenan e r a 70-kg man: (70 kg 0.5 mL/kg/hr 24 h urs) 750 mL/24 hr 1,590 mL/24 hr. (Aga n, th s s the m n mum and d es n t take nt a unt any ex ess l ss su h as ever, wh h w ll n rease the nsens ble l ss.) 2. B dy we ght: T s meth d s en used r ped atr pat ents be ause the r b dy we ghts vary w dely; est mat ns are 100 mL/kg/day r 4 mL/kg/hr r the f rst 10 kg b dy Quic k Cut we ght, 50 mL/kg/day r 2 mL/kg/hr r the se nd 10 kg Remember the b dy we ght, and 20 mL/kg/day r 1 mL/kg/hr r ea h shortcut or estimating f uid maintenance: The rst 20 kg add t nal k l gram b dy we ght. o weight 60 mL/hr and then 3. G ven am unt water per k l gram b dy we ght: T e 1 mL/kg/hr above that, so a value used r th s meth d s generally 35–40 mL/kg/day, 60-kg person 100 mL/hr. adjusted h gher r l wer based n age ( lder adults en requ re nly 15 mL/kg/24-hr ma ntenan e due t h gher at/ l wer mus le mass). Quic k Cut B. Evaluat ng ma ntenance rates: Pat ents n t nly have d erent Becaus e water ma ntenan e needs, but repla ng water r rem v ng ex ess requirements vary. Fever, water may als be n ern (see I C 1). S mple meth ds n environmental temperature, the noncritically ll p pulat n t m n t r adequa y ud and res piratory rate can increas e ins ens ible los s adm n strat n n lude the ll w ng: and increas e maintenance 1. Ur ne utput var at ns: I ur ne utput s h gh requirements . ( .e., 1 mL/kg/hr), then less water may be requ red; ur ne utput s l w, m re water may be requ red, r urther assessment may be ne essary. Quic k Cut 2. achycard a: an be a s gn dehydrat n r l w Older adults may not ntravas ular v lume produce as much urine as the C. Adjust ng f u d rates and type r nd v dual pat ents: F rst, young and can be pus hed into al ulate the pat ent’s ma ntenan e rate, then adjust the am unt conges tive heart ailure (CHF). up r d wn based n the need r resus tat n, r repla ement gastr ntest nal (GI) l sses, and the type based n type l sses ( able 1-2). 1. Injury, llness, and surgery: Can result n u d l sses due t bl d l ss, th rd spa ng, nsens ble l sses r m d arrhea, ever, et . Pr v d ng m re than al ulated ma ntenan e u d t repla e l sses (e.g., 1.5 r 2 ma ntenan e) s ne essary, and rate adequa y an be judged r m the ab ve r ter a. 2. Hyperv lem a and d ures s: Pat ents wh requ re d ures s already are verl aded w th lu d, and ntraven us (IV) lu ds sh uld be w thheld; h wever, ele tr lyte r nutr t nal aspe ts lu d adm n strat n may requ re water as a arr er r ther substan es dur ng d ures s.

Ta b le 1-2: Ele c tro lyte Co m p o s itio n o Ga s tro inte s tina l Se c re tio ns Org a n

Vo lum e /d a y

Na (m Eq /L)

K (m Eq /L)

Cl (m Eq /L)

HCO 3 (m Eq /L)

1–5 L

20–150

10–20

120–140

Nil

0.1–2 L

100–120

10–20

110

10–20

Ileum

1–3 L

80–140

5–10

60–90

30–50

Colon

0.1–2 L

100–120

10–30

90

30–50

Gallbladder

0.5–1 L

140

5

100

25

Pancreas

0.5–1 L

140

5

Stomach Duodenum

30 (higher when not stimulated)

115 (lower when not stimulated)

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Chapter 1

Flu d and Ele tr lytes

II. So d ium : N rmally, pe ple take 150–200 mEq s d um da ly, mu h wh h s ex reted n the ur ne. A. I the b dy needs t nserve s d um, t an redu e renal ex ret n t less than 1 mEq/day. B. Da ly h me stas s s eas ly ma nta ned w th 1–2 mEq/kg/day. III. P o ta s s ium : T e n rmal da ly ntake p tass um s 40–120 mEq/day, w th ab ut 10%–15% ex reted n ur ne; an am unt 0.5–1 mEq/kg/day s appr pr ate t ma nta n h me stas s.

Quic k Cut D5 ½ NS with 20 mEq/L potas s ium is a nearper ect maintenance f uid.

Quic k Cut

IV. Ma inte na nc e IV: able 1-3 g ves ele tr lyte n entrat ns several IV u ds. Us ng the prev us est mates r a 70-kg male, the we ght rmula r IV u d w uld equal 110 mL/hr. A. M n mal s d um ma ntenan e w uld requ re 70–140 mEq/day, and m n mal p tass um requ rements w uld be 35–70 mEq/day. B. I 0.5% n rmal sal ne (NS) has 77 mEq/L s d um and 20 mEq/L p tass um are added, then us ng 0.5% NS w th 20 mEq/L p tass um hl r de at 110 mL/hr w uld equal ab ut 2.6 L u d, 200 mEq s d um, and 52 mEq p tass um . . . pretty l se!

Wa te r a nd Ele c tro lyte De f c its a nd Exc e s s e s I. Wa te r A. Hyp v lem a 1. S gns acute v lume l ss: n lude ta hy ard a, hyp tens n, and de reased ur ne utput 2. S gns gradual v lume l ss: n lude l ss sk n turg r, th rst, alterat ns n b dy temperature, and hanges n mental status 3. Replac ng water de c ts: A ute def ts sh uld be repla ed a utely; hr n def ts sh uld be repla ed m re sl wly, w th hal the def t repla ed ver the f rst 8 h urs and the rest n 24–48 h urs. B. Hyperv lem a: well t lerated n healthy pat ents, wh w ll just ur nate the ex ess 1. S gns acute hyperv lem a: a ute sh rtness breath, ta hy ard a 2. S gns chr n c hyperv lem a: per pheral edema, pulm nary edema II. So d ium : l se relat nsh p t v lume status A. Hyp natrem a (Na 130 mEq/L): F gure 1-2 1. Causes a. Hyper sm lar: hypergly em a, mann t l n us n, r presen e ther sm t ally a t ve part les that draw n water

Remember, bas ed on a patient’s s peci c need, maintenance f uids can be altered to optimize blood chemis try.

Quic k Cut In the cas e o hypernatremia with hypovolemia, do not allow the s odium concentration to drop more than 0.5–1 mEq/hr.

Quic k Cut Complications o acute CHF can aris e in acutely hypervolemic patients with poor cardiac unction.

Quic k Cut Diures is may be needed in s ome chronically hypervolemic patients to reduce volume.

Quic k Cut For a hyponatremia workup, rs t check the s erum os molar value then, i needed, volume s tatus .

Ta b le 1-3: Ele c tro lyte Co nc e ntra tio n in Va rio us Intra ve no us Fluid s Na (m Eq /L)

K (m Eq /L)

Mg (m Eq /L)

Normal saline (0.9% NaCl)

154

0

0

½ normal saline (0.5% NaCl)

77

0

Hypertonic saline (3% saline)

513

Lactated Ringer’s Plasmalyte*

Fluid

Cl (m Eq /L)

La c ta te (m Eq /L)

Os m o la rity (m Os m /L)

0

154

0

308

0

0

77

0

154

0

0

0

513

0

1027

130

4

0

2.7

98

28

525

140

5

3

0

98

0

294

*Plasmalyte also contains 27 mEq/L acetate and 23 mEq/L gluconate.

Ca (m Eq /L)

Chapter 1

Pr n ples

Surg al Phys l gy

7

Hypona tre mia

Hypovole mic

Hypo-os motic

Normo-os motic

Euvole mic

Hype rvole mic

Hype ros motic

Fig ure 1-2: Hyponatremia.

b. N rm - sm lar (pseud hyp natrem a): Quic k Cut Hypertr gly er dem a, hyperl p dem a, and hyperpr te nem a; Do not give NaCl large, m n mally sm t m le ules displace water and or hyponatremia unles s nter ere w th the lab measurement s d um. hypovolemia is pres ent. c. Hyp - sm lar (1) Hyp v lem c: renal l sses, renal tubular a d s s, erebral salt wast ng, GI l sses, “tea and t ast Quic k Cut syndr me,” trans utane us l sses (burns, trauma) In hypovolemic (2) Hyperv lem c: T e path l gy s en related t hypo-os molar hyponatremia, l w ard a utput (the k dneys see less bl d w, total body s odium is als o us ually low, whereas in and ree water s nserved) r hyp album nem hypervolemic hypo-os molar (e.g., rrh s s) r ther edemat us states where hyponatremia, total body salt (ren n-ang tens n system) and ree water s odium is us ually high. (ant d uret h rm ne [ADH]) ann t be ex reted by the k dneys (e.g., renal a lure, CHF, nephr t syndr me). Quic k Cut (3) Euv lem c: uld be e ther the states ment ned ADH s ecretion earl er, r (m re requently n the per perat ve can be s timulated by the pat ent) syndr me nappr pr ate ant d uret c s tres s res pons e to trauma h rm ne (SIADH) secret n, r thers and s urgery, caus ing ree water retention and, in turn, (e.g., glu rt d def en y, hyp thyr d sm, water euvolemic hypo-os molar nt x at n [psy h gen p lyd ps a]) hyponatremia. 2. Sympt ms a. Acute hyp natrem a: ass ated w th a ute erebral edema, se zures, and ma b. Chr n c hyp natrem a: Well t lerated t Na n entrat ns 110 mEq/L; sympt ms generally n lude n us n/de reased mental status, rr tab l ty, and de reased deep tend n re exes. 3. D agn s s and categ r zat n: Cl n al exam and lab determ nat n sm lar state are en en ugh r d agn s s, but, n d ubt (espe ally w th hyp - sm lar hyp natrem a), he k ur ne sm lar ty and s d um n entrat n. a. Hyp v lem c, hyp - sm lar hyp natrem a: ur ne Na greater than 20 mEq/L renal l sses, less than 10 mEq/L extrarenal l sses b. Hyperv lem c, hyp - sm lar hyp natrem a: ur ne Na greater than 20 mEq/L renal a lure; Na less than 10 mEq/L rrh s s, heart a lure c. Euv lem c, hyp - sm lar hyp natrem a: ur ne sm lar ty usually h gh; ur ne Na usually greater than 20 mEq/L ex ept n water nt x at n

8

Chapter 1

Flu d and Ele tr lytes

4.

reatment ( m n mally sympt mat c) Quic k Cut a. Hyper sm lar: C rre t hypergly em a r s ur e ther With acutely a t vely sm t part les. s ymptomatic hypo-os molar b. N rm - sm lar: reat the underly ng d sease pr ess. hyponatremia, give hypertonic c. Hyp - sm lar or is otonic s aline. (1) Hyp v lem c: reat w th s t n u d n us n t rest re u d and s d um def ts. (2) Hyperv lem c: reat underly ng med al ause Quic k Cut f rst, then usually salt and ree water restr t ns are I the s odium appr pr ate. de cit is s evere with hypoos molar, hypovolemic (3) Euv lem c: F rst determ ne the true ause s ne hyponatremia, hypertonic the prev usly ment ned states; SIADH s the ause, s odium replacement can be ree water restr t n usually s en ugh (d not repla e cons idered. salt n s lut n, wh h an parad x ally l wer serum s d um, as the k dney ex retes s d um and nserves water). Quic k Cut B. Hypernatrem a (Na 150 mEq/L) Giving hypertonic 1. Categ r es s odium to patients with a. Hyp v lem a: Hypernatrem a alm st always represents a SIADH can make them wors e. ree water def t; t tal b dy s d um may be l w. The patient will excrete the s odium via the kidneys and b. Hyperv lem a: Iatr gen n us n t mu h s d um hold on to the water. an lead t hyperv lem hypernatrem a, but th s s rare. 2. Sympt ms: Can n lude th se v lume deplet n (e.g., ta hy ard a, hyp tens n) as well as ther s gns dehydrat n (e.g., dry mu us membranes, de reased sk n turg r); lethargy, n us n, and ma result r m water sh s r m the ntra ellular mpartment n the entral nerv us system (CNS). 3. D agn s s/et l gy (usually s mple): h gh serum s d um w th bv us ree water l sses; n surg al pat ents, u d l sses may be: a. Extrarenal: nsens ble l sses due t ever, me han al vent lat n, burns, d arrhea, r measured l sses r m the GI tra t b. Renal: ex ess ve ree water ex ret n (1) Osm t d ures s r m hypergly em a r mann t l adm n strat n (2) H gh- utput d lute ur ne r m the p lyur phase a ute tubular ne r s s (A N) 4. reatment a. Hyp v lem a: Need t repla e v lume; al ulate ree water def t f rst: (1) Water de c t 0.6 b dy we ght (kg) (serum Na /140 1) (2) Repla e hal the def t n the f rst 8 h urs and the rema nder n the next 16 h urs. (3) I the hyp v lem state s severe ( .e., sh k), n t al resus tat n an be s t n u ds; the def t s less severe, r n e per us n s adequate and the def t reversed, sw t h t dextr se 5% n water (D5W) t mplete the ree water repla ement. b. Hyperv lem a (1) I the pat ent’s t tal b dy water s n reased, f rst Quic k Cut de rease the am unt s d um adm n stered. Giving uros emide (2) I s d um ntake (e.g., ant b t s, t tal parenteral to hypernatremic patients nutr t n [ PN]) ann t be de reased, ree water an can rais e the s odium concentration, even in be n used t l wer the serum s d um level, but th s hypervolemic s tates . Us e d es n t de rease the t tal b dy s d um r water ree water to equilibrate the ntent. s odium concentration prior to (3) D uret s an be used, but s d um an r se. diures is . (4) Als ns der natr ures s III. P o ta s s ium A. Hyp kalem a (K 3.5 mEq/L): Severe hyp kalem a s def ned as a serum p tass um level 3.0 mEq/L r less; n s me pat ents ( ard a ), a K h gher than 4.0 s des rable. 1. Sympt ms: In lude leus and weakness, and pr und deplet n results n ard a dysrhythm as. Ele tr ard gram (ECG) hanges an be me man est bel w a K 3.0 mEq/L and n lude, n n reas ng rder sever ty, -wave atten ng r nvers n, depressed S segments, devel pment

Chapter 1

Pr n ples

Surg al Phys l gy

9

U waves, pr l nged Q nterval, and f nally ventr ular Quic k Cut ta hy ard a. More important than 2. D agn s s/et l gy (s mple and based n bl d chem stry): diagnos ing hypokalemia is rarely und n healthy humans w th a n rmal d et and unders tanding the caus e. n rmal k dneys; auses all n ne ur ateg r es: a. Renal: d uret s, v m t ng (renal ex ret n K t preserve Na ), renal tubular a d s s b. Extrarenal: d arrhea, burns c. Intracellular sh : nsul n, alkal t state d. Med cal d sease: hyperald ster n sm, Cush ng syndr me 3. reatment Quic k Cut a. I sympt ms are severe, adm n ster p tass um IV as Remember, s erum needed t redu e sympt ms. K concentration is not an b. I sympt ms are m ld, n use 20 mEq/hr max mum n the indication o total body s tores unm n t red pat ent and 40 mEq/hr n the m n t red pat ent. o potas s ium. I the s erum c. Adm n strat n r m re hr n nd t ns an be v a the K is repleted but total body s tores are low, s erum K will enteral r ute. drop again quickly as K B. Hyperkalem a (K 6 mEq/L) s hi ts into cells . 1. Sympt ms: Rare but n lude d arrhea, ramp ng, nerv usness, weakness, and a d paralys s; m re en, ard a dysrhythm as are man est be re ther sympt ms Quic k Cut be me severe, and ECG hanges n lude peaked waves A general rule o and w dened QRS and an eventually degenerate nt thumb is that every 10 mEq ventr ular f br llat n. o IV K s hould rais e s erum 2. D agn s s/et l gy (numer us): am ng the m re mm n concentration by 0.1 mEq/L. are as ll ws: a. Renal a lure: w th nappr pr ate nsumpt n and adm n strat n K b. Extracellular sh : rhabd my lys s, mass ve t ssue ne r s s, metab l a d s s, hypergly em a c. Med cal d sease: Add s n d sease, et . 3. reatment a. Acutely sympt mat c pat ent Quic k Cut (1) IV calc um stab l zes ard a my yte membranes and Acutely, the goal an prevent dysrhythm as (1 g Ca glu nate IV s a is to s tabilize the cardiac standard d se). membrane and to lower (2) Gluc se/ nsul n adm n strat n an be used t sh s erum potas s ium in the K ntra ellularly a utely and qu kly (1 ampule D50 hypokalemic patient. Once the patient is s tabilized, w th 10 un ts regular nsul n s en en ugh). maneuvers to remove K (3) B carb nate adm n strat n w ll als sh K permanently rom the body ntra ellularly. s hould be ins tituted. b. rem ve K and t l wer b dy st res permanently: (1) I n-ex hange res n: used e ther by m uth r re tally and b nds K n the l n, a l tat ng ex ret n (2) Fur sem de: nly use k dneys are able t ex rete and l sely m n t r ther ele tr lytes and u d balan e (3) D alys s IV. Chlo rid e A. Hyp chl rem a (Cl 90 mEq/L) 1. Sympt ms: usually ass ated w th dehydrat n r hyp kalem a due t v m t ng r ther GI l ss 2. D agn s s/et l gy a. St ma h hydr hl r a d (HCl) s l st r m v m t ng, lead ng t l w hl r de and a bu ldup b arb nate, aus ng a metab l c alkal s s. b. It s en ass ated w th parad x c ac dur a. N rmally, the k dneys w uld ex rete b arb nate t redu e pH; h wever, as the dehydrat n w rsens, the k dneys’ dr ve t reta n s d um pred m nates, and the k dney ex retes b th K and H t nserve s d um.

10

Chapter 1

Flu d and Ele tr lytes

3.

reatment: Repla e the hl r de and v lume def t w th s d um hl r de s lut ns and repla e K as needed. B. Hyperchl rem a (Cl 110 mEq/L) 1. Cause: T e m st mm n ause n surg al pat ents s the adm n strat n large am unts hl r de n IV s lut ns Quic k Cut (the hl r de ntent n n rmal sal ne [154 mEq/L] s Remember that NS has 154 mEq Cl . Generating s gn f antly h gher than that n plasma [90–110 mEq/L]). a hyperchloremic metabolic 2. D agn s s/et l gy (easy—check the bl d chem stry): acidos is is eas y i too much Ex ess hl r de de reases the str ng n d eren e, thereby s aline is us ed. aus ng m re water t d ss ate and m re H ns t be present, lead ng t metab l a d s s. 3. reatment: De rease the am unt hl r de be ng n used; l k r all s ur es (IV ant b t s) n add t n t IV u ds ( s t n sal ne needs t be adm n stered r ther reas ns, ns der s d um b arb nate r s d um a etate t redu e hl r de l ad [e.g., ½ NS w th 1.5 amps NaHCO3 /L has 152 mEq/L Na , nly 77 mEq/L hl r de, and 75 mEq/L b arb nate]). V. Ca lc ium A. Hyp calcem a (Ca 8 mg/dL) Quic k Cut 1. Sympt ms: In lude neur mus ular rr tab l ty w th per ral Clas s ic s igns and extrem ty numbness that may pr gress t arp pedal o hypocalcemia include spasm and tetany; premature ventr ular ntra t ns an be Trous s eau and Chvos tek s igns (carpopedal s pas m and redu ed w th treatment hyp al em a as pr l ngat n cheek twitch). the Q nterval s n ted n these pat ents. 2. D agn s s/et l gy (numer us) a. Surg cal pat ents: Suppress n n rmal parathyr d un t n r m the rem val aden mat us r hyperplast glands s m st mm n, ll wed by a dental damage the parathyr ds dur ng thyr d surgery. b. Cr t cally ll pat ents: la tate, trate r m bl d trans us ns, and numer us med nes c. Other: v tam n D def en y, hr n renal a lure, ntest nal malabs rpt n, ex ess d etary r therapeut (laxat ve) magnes um, mer ury exp sure, helat n therapy 3. reatment a. Asympt mat c utpat ents: Can be supplemented rally— nvest gate p ss ble med al auses (see prev us d s uss n). b. Sympt mat c pat ents: M n t r and treat. (1) I sympt ms are m ld, large d ses ral al um are en adequate (espe ally n the p stparathyr de t my pat ent). (2) Severely sympt mat pat ents sh uld be repleted w th IV al um unt l sympt ms res lve and an appr pr ate ral reg men s t lerated. B. Hypercalcem a (Ca 10.5 mg/dL) 1. Sympt ms: Fat gue, n us n, nausea, v m t ng, d arrhea, dehydrat n, and an rex a are mm n; when related t hyperparathyr d sm, renal al ul and ul er d sease are m re mm n. 2. D agn s s/et l gy (numer us) a. End cr ne: pr mary hyperparathyr d sm (m st mm n), thyr t x s s b. Mal gnancy: m st mm n (up t 20%–30% an er pat ents), en r m ste lyt r parathyr d h rm ne–related pr te n (P HrP)–se ret ng les ns c. Granul mat us d sease: sar d s s, tuber ul s s d. Med cat ns: ex ess al um ngest n, v tam n D t x ty, th az de d uret s e. Other: renal d sease, m lk alkal syndr me, am l al hyp al ur hyp al em a 3. reatment a. F rst-l ne therapy: Aggress ve s t n resus tat n, lead ng t d ures s and al um ex ret n; unsu ess ul, Quic k Cut ur sem de an be added. Severe, s ymptomatic b. Med cal therapy: Med at ns t st p ste last a t v ty hypercalcemia is a medical are the ma nstream ( .e., b sph sph nates, al t n n, and emergency and requires ster ds are all used; pl a amy n s n l nger ava lable n immediate treatment. the Un ted States).

Chapter 1

Pr n ples

ACID–BASE DISTURBANCES Re g ula to ry Sys te m s I. Ca rb o n d io xid e : CO2 pr du t n an ex eed 15,000 mm l/ day r m metab l pr esses (e.g., lung ex ret n). I Pco 2 n reases, water d ss ates and HCO3 and H rm based n the Henders n-Hasselbalch equat n, thus de reas ng pH. T e reverse happens r l wer Pco 2 n entrat ns. E ther a l ss b arb nate r a ga n n pr t ns an ause a d s s. II. Stro ng io ns : I ns that mpletely d ss ate n water (e.g., Na , Cl , Ca , Mg , K ). In a pure salt s lut n, n n entrat ns are equal, and pH s neutral, whereas n plasma, at ns utnumber an ns. ma nta n ele tr al neutral ty, water d ss ates, H s ex reted, and HCO3 n entrat n n reases, reat ng a pH 7.4, n t 7.0. III. We a k a c id s : Weak a ds an ex st as negat vely harged m le ules r a ept H and ex st un harged. T ese bu er ng systems n lude pr te ns and ph sphates.

Surg al Phys l gy

11

Quic k Cut The human body requires a very narrow pH range o 7.35–7.45 to unction properly. Three main s ys tems in the body maintain the pH within normal parameters : carbon dioxide, s trong ions , and weak acids .

Quic k Cut The Henders onHas s elbalch equation: pH pK log [HCO 3 /(0.03 P CO 2 )].

Ac id o s is T e b dy’s pH de reases when the Pco 2 n reases, the n entrat n HCO3 n reases, the n entrat n str ng an ns n reases, r the Quic k Cut n entrat n weak a ds n reases. A pH less than 7.35 s ns dered Acidosis is a pHlowering proces s ; acidemia is path l g , but pat ents an mpensate r m the ll w ng d s rders a d– a low blood pH. base metab l sm r have a m xed p ture w th a pH n the n rmal range. I. Re s p ira to ry a c id o s is A. Causes 1. Decreased vent lat n leads t n reased CO2 n entrat n. Any ause depressed resp rat ns an ause th s path l gy. 2. Increased CO2 pr duct n. Ex ess enteral r parenteral arb hydrate adm n strat n an n rease the resp rat ry qu t ent and pr du t n CO 2. H sp tal zed pat ents may n t be able t mpensate. B. reatment: T e pr mary meth d r resp rat ry a d s s s t n rease alve lar vent lat n. In ases drug verd se, th s may be a mpl shed w th appr pr ate revers ng agents; h wever, m st alve lar hyp vent lat n requ res ntubat n w th me han al vent lat n t lear CO 2 and return the pH t n rmal values. II. Me ta bolic a c idos is results e ther r m HCO3 l ss r a umulat n Quic k Cut str ng an ns (measured r n nmeasured) r weak a ds. To determine the etiology o metabolic A. Causes acidos is , check the anion 1. Weak ac d accumulat n (an n gap): Et l gy n ludes l ss gap. I high, remember CUTE HCO3 t ma nta n ele tr neutral ty. DIMPLES: cyanide, uremia, a. A d a umulat n an ur be ause renal a lure and toluene, ethanol, diabetic the nab l ty the k dneys t lear a d by-pr du ts ketoacidos is , is oniazid, methanol, propylene glycol, metab l sm. lactic acidos is , ethylene b. Lact c ac d s s: A mm n ause s la t a d, wh h glycol, s alicylates . results r m nadequate t ssue per us n and anaer b metab l sm. c. D abet c ket ac d s s: A et a etate and beta-hydr xybutyrate are weak a ds. d. x ns (p lyethylene glyc l, methan l): Methan l s metab l zed t rmaldehyde and then rm a d. 2. Str ng an n accumulat n: n rmal an n gap a. Hyperchl rem c ac d s s: Ex ess hl r de ndu es water t d ss ate, H t a umulate, and pH t dr p. 3. L ss b carb nate: n rmal an n gap a. Ex ess renal ex ret n b arb nate b. D arrhea

12

Chapter 1

A d–Base D sturban es

B. reatment: T e pr mary treatment r metab l a d s s s rre t n the underly ng metab l pr blem/d sease and pr per u d and ele tr lyte management. B arb nate adm n strat n sh uld rarely be used unless pH s danger usly l w ( 7.2) and the underly ng de e t s be ng rre ted (ex ept n: I the pr mary de e t s ex ess l ss b arb nate [d arrhea, renal tubular a d s s], b arb nate therapy uld be ns dered).

Alka lo s is I. Re s p ira to ry a lka lo s is Quic k Cut A. Causes Some proces s es 1. Sp ntane usly breath ng pat ent: aused by alve lar (think of pulmonary embolus!) caus ing hypoxia vent lat n n rease and subsequent redu t n n CO2 levels or intrapulmonary s hunts (anx ety, pa n, sh k, seps s, t x substan es [sal ylate can lead to hypocarbia and p s n ng], r CNS dys un t n) alkalos is . 2. Mechan cally vent lated pat ent: Iatr gen vervent lat n s mm n. B. reatment: In ludes de reas ng m nute vent lat n and all w ng CO2 levels t return t n rmal. M st ases are sel -l m ted, h wever, as pat ents ann t keep ex ess ve vent lat ry dr ve r extended per ds. II. Me ta b o lic a lka lo s is : pH n reases t h gher than 7.45, and HCO3 s greater than 26 mEq/L. A. Causes 1. M st mm n n n atr gen ause metab l alkal s s s l ss gastr ntents (HCl and large v lumes water are l st). mpensate r dehydrat n, the k dney ex retes H t nserve Na (parad x cal ac dur a). T e n entrat n str ng an ns s redu ed, and water s less l kely t d ss ate, urther de reas ng H and n reas ng pH. 2. Other causes a. Drugs that l m t renal ex ret n HCO3 (e.g., ster ds Quic k Cut and d uret s) P a ra d o xic a l b. Overadm n strat n alkal (e.g., n ul er therapy), a etate a c id uria : The kidney n PN that s used t repla e ther an ns, and trate n exchanges H or Na , s o the trans used bl d that s nverted t CO2 and water and urine may be acidic but the patient alkalotic. then t HCO3 by the k dneys B. reatment: T e f rst step s t st p the l ss hl r de and t repla e the water and hl r de w th s t n s d um hl r de and p tass um supplementat n. F r ther auses, st pp ng the end ng agent s usually su ent.

Dia g no s ing Ac id –b a s e Dis o rd e rs Ba s e d o n the Blo o d Ga s (Ta b le 1-4) Ta b le 1-4: Ac id –b a s e Dis o rd e rs Dis o rd e r Respiratory acidosis

Respiratory alkalosis

Metabolic acidosis

P CO 2

pH

Exp e c te d Co m p e ns a tio n

7.35

1–4 mEq/L HCO3 or each 10 mm Hg P CO2 rise

Acute

↑

Normal

Compensated

↑

↑

Acute

↓

Normal

Compensated

↓

↓

Normal

↓

↓

↓

Normal

↑

↑

↑

Acute Compensated

Metabolic alkalosis

HCO 3

Acute Compensated

7.35–7.40 7.45

2–5 mEq/L HCO3 or each 10 mm Hg P CO2 drop

7.40–7.45 7.35

Expected P CO2 1.5(HCO3 ) 8

7.35–7.40 7.45 7.40–7.45

Expected P CO2 0.7(HCO3 ) 20

Chapter 1

Pr n ples

Surg al Phys l gy

13

COAGULATION He m o s ta s is Me c ha nis m P ha s e s I. P rim a ry he m o s ta s is A. Platelet adherence: T e f rst step n ntr ll ng hem rrhage s platelet adheren e t the njured vessel v a gly pr te n (Gp) re ept r Ib n njun t n w th v n W llebrand a t r. B. Platelet act vat n: A t vated platelets pr du e thr mb xane A2 and ther vas nstr t rs, wh h redu e bl d w thr ugh the njured vessel. Gp IIb/IIIa s expressed, wh h pr m tes platelet–platelet adhes n (f br n gen requ red) and platelet plug rmat n. II. Clo t o rm a tio n: ssue a t r exp sed due t vessel njury r n resp nse t n ammat n beg ns the cl tt ng cascade (trad t nally taught as hav ng an ntr ns and extr ns pathway; h wever, n v v , b th pathways a t n n ert). A. Extr ns c pathway: ssue a t r b nds a t r VII and a t vates Quic k Cut t (VIIa). VIIa subsequently a t vates a t r X. Xa then nverts The extrins ic s ys tem pr thr mb n t thr mb n. us ually begins the clotting B. Intr ns c pathway: In general, a t r XIIa a t vates XI, then cas cade. Components o the extrins ic s ys tem als o activate XIa a t vates IX. IX then nverges w th the extr ns pathway the intrins ic s ys tem. by a t vat ng a t r X. T s pathway an be n t ated e ther by exp sure t a negat vely harged sur a e (exp sed llagen r m a damaged vessel) r thr mb n tsel a t vates a t r IX. Quic k Cut C. B th pathways c nverge at act r X: Fa t r Xa then med ates The extrins ic nvers n pr thr mb n t thr mb n w th a t r Va as a a t r. pathway is ref ected in the T r mb n med ates f br n gen nvers n t f br n. F nally, a t r p ro thro m b in tim e (P T). XIIIa med ates r ss-l nk ng f br n. III. Re g ula tio n a nd f b rino lys is : T e agulat n system s a cascade, mean ng that ea h a t vated ntermed ate a t r s able t a t vate many the a t rs n subsequent steps. T r mb n tsel a ts as a p s t ve eedba k l p by a t vat ng a t r IX. T e f br n lyt system a ts t balan e the agulat n as ade and t rem ve l ts n e heal ng has started. A. ssue a t r pathway nh b t r ( FPI) may nh b t F–VIIa mplexes. 1. Pr te n C and pr te n S degrade a t rs V and VIII. 2. Ant thr mb n III nh b ts thr mb n-Xa mplexes. 3. F br n lys s: ssue-type plasm n gen a t vat r (t-PA) and ur k nase-type plasm n gen a t vat r (uPA) med ate nvers n plasm n gen t plasm n, wh h leaves f br n.

Co a g ulo p a thy

Quic k Cut I. His to ry: Lab stud es sh uld n t be r ut nely rdered pre perat vely The his tory is n a pat ent w th a negat ve h st ry, whereas n a p s t ve h st ry, the mos t important tool to stud es an be used t spe y the d agn s s. diagnos e a coagulopathy. A. Include any pat ent-perce ved c agul pathy: bru s ng, pete h a, easy bleed ng/n sebleeds, h st ry bleed ng r m ther pr edures (dental/surg al) B. Fam ly h st ry C. Med cal c nd t ns/r sk act rs: l ver d sease ( rrh s s), renal a lure (urem a)

II. P hys ic a l: ev den e

bru s ng r pete h a

III. La b o ra to ry e va lua tio n A. Platelet c unt: n rmal s 150,000–400,000/mL bl d B. Bleed ng t me: Measure platelet un t n. D s rders platelet un t n n lude urem a, drugs (asp r n, l p d grel, Gp II B/III A nh b t rs), v n W llebrand d sease, and l w platelet unt. C. Pr thr mb n t me: P measures the extr ns as ade. Be ause a t rs II (thr mb n), VII, and X are pr du ed by the l ver, P represents a g d measure v tam n K–dependent agulat n a t rs and s there re used t m n t r war ar n therapy. T e nternat nal n rmal zed rat (INR) s a n rmal zat n a t r t equate lab values between labs.

Quic k Cut Platelets higher than 100,000 are neces s ary or major s urgery. Keep higher than 50,000/mL or general hemos tas is . Counts les s than 10,000/mL put patients at ris k or s pontaneous bleeding.

14

Chapter 1

C agulat n

D. Act vated part al thr mb plast n t me (aP ): measures Quic k Cut the ntr ns as ade and s use ul r ll w ng pat ents n IV The TEG is rapidly un ra t nated hepar n therapy becoming the s tandard o E. T r mb n t me: ests the nvers n f br n gen t f br n care tes t to identi y bleeding v a thr mb n; t s elevated when f br n gen s depleted r dis orders in trauma patients n n un t n ng and n the presen e hepar n. and in the intens ive care unit (ICU). F. T r mb elast gram ( EG): measures h l st ally l t rmat n and breakd wn k net s G. Act vated cl tt ng t me (AC ): rap dly determ nes e e t h gh-d se hepar n; used n ard a surgery H. Ant - act r Xa act v ty: used t m n t r l w-m le ular-we ght hepar n a t v ty

Sp e c if c Hyp o c o a g ulo p a thic Sta te s I. Firs t, e ns ure b le e d ing is no t a s urg ic a l c o m p lic a tio n: D n t ne essar ly blame p st perat ve bleed ng n agul pathy unt l surg al bleed ng s ruled ut. II. Live r d is e a s e : In severe l ver d sease, hepat ytes ann t manu a ture l tt ng a t rs. P /INR s elevated. reatment n ludes repla ng a t rs w th resh r zen plasma (FFP). Chr n ally, v tam n K an mpr ve hepat synthet un t n. III. Re na l d is e a s e : Urem a auses platelet dys un t n. reatment an be w th DDAVP, wh h auses release v n W llebrand a t r r FFP. IV. Dis s e m ina te d intra va s c ula r c o a g ulo p a thy (DIC): M r vas ular agulat n due t n ammat n r m seps s, trauma, and ther severe nsults leads t a nsumpt n and def t a t rs, lead ng t agul pathy. T e ma nstay treatment n ludes treat ng the underly ng ause. Repla ement a t rs may exa erbate the nd t n; parad x ally, ant agulant therapy may be benef al. V. Co ns um p tio n/d ilutio n A. Due t severe trauma, seps s, maj r surgery, and the r attendant u d resus tat n; treatment nv lves rre t ng the underly ng ause and repla ng a t rs w th FFP. B. Hyp f br n gen states need ry pre p tate. C. Hyp therm a and ac d s s: nh b t pr per l tt ng me han sms VI. Me d ic a lly ind uc e d A. Asp r n: permanently b nds y l xygenase (COX), prevent ng platelet aggregat n B. Plav x: bl ks aden s ne d ph sphate (ADP)–med ated platelet aggregat n C. Gp IIb/IIIA nh b t rs: nh b t platelet aggregat n D. War ar n: bl ks v tam n K–dependent l ver synthes s a t rs II, VII, IX, and X E. Hepar n and hepar n ds: augment ant thr mb n-III un t n F. L w-m lecular-we ght hepar n: nh b ts a t r Xa G. D rect thr mb n nh b t rs: argatr ban, dab gatran Quic k Cut H. Fact r Xa nh b t rs: ap xaban Recombinant I. F br n lyt cs: t ssue plasm n gen a t vat r (tPA), ur k nase, et ., activated actor VII (r VIIa) is med ate f br n lys s approved or us e in treating VII. He m o p hilia hemophiliacs who have developed antibodies to A. Hem ph l a A: C ngen tal de en y a t r VIII; actors VIII and IX. Although treatment s a t r repla ement. FFP an be used n emergent not replacing the mis s ing s tuat ns. actors , s upraphys iologic B. Hem ph l a B: C ngen tal de en y a t r IX; treatment dos es o r VIIa caus e a s a t r repla ement. FFP an be used n emergent thrombin burs t and clot to orm, which has led to s tudy s tuat ns. o its e cacy to treat other VIII. vo n Wille b ra nd d is e a s e : T e m st mm n ngen tal coagulopathies , including agul pathy (1%–2% adults) s def en y v n W llebrand war arin therapy when quick revers al is needed a t r. reatment s ntranasal DDAVP n m ld ases, IV DDAVP (i.e., intracranial bleed) pr r t surg al pr edures, and ry pre p tate r FFP n and in s evere traumatic emergen es. coagulopathy. IX. Othe rs : aut mmune d seases, an er, snake ven m

Chapter 1

Pr n ples

Surg al Phys l gy

15

Sp e c if c Hyp e rc o a g ula b le Sta te s I. Surg ic a l p a tie nts : Surgery, trauma, and seps s ause pr n ammat ry states that lead t a hyper agulable state; there re, surg al pat ents are at r sk r deep ven us thr mb s s (DV ). Quic k Cut A. Maj r r sk a t rs n lude maj r abd m nal r pelv surgery; Always as s es s rth ped surgery, espe ally l wer extrem ty; trauma, your s urgical patients or espe ally sp ne, pelv s, and l wer extrem ty ra tures; pr l nged thromboembolic prophylaxis . Mos t hos pitals have protocols mm b l zat n; an er; sm k ng; bes ty; entral l ne pla ement; now that mus t be ollowed. and thers. B. Hepar n 5,000 un ts sub utane usly every 8 h urs r l wm le ular-we ght hepar n sub utane usly da ly r tw e da ly sh uld be used; n pat ents wh have ntra nd at ns t pr phylax s ( ntra ran al bleed), n er r vena ava f lters sh uld be ns dered. II. Co ng e nita l ris k a c to rs : Suspe t pat ents have mult ple DV r DV w th ut an ther kn wn r sk a t r; treatment s usually ant agulat n. A. Pr te n S de c ency B. Pr te n C de c ency C. Fact r V Le den mutat n D. Ant thr mb n III mutat ns E. Others

Quic k Cut There are more than 100 mutations known to caus e hypercoagulability.

PACKED RED BLOOD CELL TRANSFUSION THERAP Y Tra ns us io n Ris ks I. Fe b rile re a c tio ns /a lle rg ic : m o s t c o m m o n im m une re a c tio n A. Usually related t e ther yt k nes r d n r leuk yte r ther ntam nants r a m ld ant b dy resp nse and s usually sel -l m ted B. Can be prevented by leuk deplet n and pretrans us n ant pyret s

Quic k Cut The longer blood is s tored, the wors e it per orms . Over time, cells lys e, and 2,3-diphos phoglycerate (2,3-DPG) levels all, caus ing oxygen to bind more avidly.

II. Ele c tro lyte d is turb a nc e s A. Hyperkalem a: Lysed ells an ause hyperkalem a. B. Hyp calcem a: C trate n st red bl d an b nd al um. III. Co a g ulo p a thy: Pa ked red bl d ells (pRBCs) d n t nta n l tt ng a t rs r platelet. Largev lume trans us n w th ut these ther pr du ts an ause a agul pathy. IV. ABO inc o m p a tib ility A. Et l gy: ntravas ular mmune rea t n, lead ng t lump ng and lys s red ells w th m smat hed bl d B. S gns and sympt ms: hem gl b nur a, ever, h lls, agul pathy, renal a lure, and r ulat ry llapse V. De la ye d he m o lytic re a c tio n: usually takes 3–7 days t man est A. S gns and sympt ms: ever, mala se, hyperb l rub nem a, and de reas ng hemat r t, usually related t m n r ant b dy systems (e.g., Rh system) B. Usually but n t always preventable w th re p ent ant b dy s reen ng C. reatment: hydrat n and supp rt ve are

Quic k Cut ABO incompatibility prevention is key by ens uring correct patient identity and blood type to avoid cons equent preventable reactions.

VI. Dis e a s e tra n s m is s io n : Many v ruses are transm tted by bl d, wh h was n e a real r sk. W th m dern s reen ng meth ds (e.g., nu le a d te hn l gy), the r sk s the ret al and negl g ble. A. HIV: est mated t be 1:2,000,000 B. Hepat t s C: est mated t be 1:2,000,000 C. Hepat t s B: est mated t be 1:2,000,000

16

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Pa ked Red Bl

d Cell rans us n T erapy

D. Others: R sks less kn wn but have been des r bed. Human t-lymph tr p v rus (H LV) 1 and 2, West N le v rus, Creutz eldt-Jak b d sease; verall r sk v ral transm ss n may be as h gh as 1:50,000. VII. Im m uno s up p re s s io n: Negat ve ut mes n lude the ll w ng: A. M rb d ty: n reased n ect us c mpl cat ns, n lud ng vent lat r-ass ated pneum n a B. P ss ble n reases n cancer recurrence ll w ng p tent ally urat ve surgery C. Increased m rtal ty: n ICU pat ents

Tra ns us io n Ind ic a tio ns I. Ac ute c o ro na ry d is e a s e : Standard tr gger s 8 g/dL. II. Tra um a p a tie nts : Exsangu nat ng pat ents ( lass III sh k) sh uld be g ven bl d as resus tat n. A. T e r Hgb measurement may st ll be h gh a utely, but they are l s ng bl d and ts attendant xygen- arry ng apa ty. B. Bl d/FFP rat s are be ng urrently stud ed, but resus tat n w th 1:1 rat bl d/FFP w th platelets every urth r und and m n mal t n rystall d. III. ICU p a tie nts : I needed, d re t measurements xygen del very and xygen extra t n an help t gu de trans us n therapy t determ ne extra xygen- arry ng apa ty s needed. IV. Ge ne ra l (no n-ICU) p a tie nts : nly trans use sympt mat (e.g., ta hy ard a, ta hypnea, n us n, lethargy, and a d s s)

Tra ns us io n Alte rna tive s

Quic k Cut Blood is an immunos uppres s ant as s ociated with advers e outcomes in s urgical patients . Only us e when needed.

Quic k Cut P rio r tra ns us io n trig g e rs o a hemoglobin (Hgb) o 10 g/dL or hematocrit (hct) o 30% were arti cially s et. Transfusion decisions should be based on individual patient circumstances. In general, it is s a e to let the Hgb drop to 7 mg/dL and even lower in healthy, young individuals .

Quic k Cut Patients with acute coronary s yndromes may need higher Hgb levels , but this is debatable.

Quic k Cut

I. Ele c tive s urg e ry ( the t me bl d l ss s kn wn) An Hgb trans us ion A. Aut l g us banked bl d trigger o 7 is as s a e as 10 B. Ep et n alpha: an n rease h t pre perat vely t help av d and reduces complications . . . even in thos e with a his tory o trans us n; use ul n renal a lure pat ents and th se w th cardiac dis eas e. hr n anem a C. Aut trans us n: re y le bl d l st dur ng surgery D. Acute n rm v lem c hem d lut n 1. On e a pat ent s anesthet zed, bl d an be rem ved, st red, Quic k Cut Is otonic f uids and repla ed w th rystall d r ll d t ma nta n euv lem a. can be us ed to s upport 2. Bene ts intravas cular volume. a. Bl d l st dur ng surgery has a l wer h t; there re, ewer red ells are shed. b. T se that are shed an be repla ed w th resh (n t st red) Quic k Cut aut l g us bl d that was just rem ved. Quick prevention E. D rected d n r: R sk v rus transm ss n s l wer, but s m lar o urther blood los s is the r sks mmun m dulat n and ther rea t ns ex st. bes t therapy or unexpected F. Hem stat c agents: prevent bl d l ss n the f rst pla e blood los s . 1. FFP/cry prec p tate: r pat ents w th agul pathy 2. DDAVP: r platelet dys un t n, espe ally renal a lure 3. ranexam c ac d: nh b ts ser ne pr teases, n lud ng plasm n, and s there re ant f br n lyt ; n reas ngly used n trauma 4. Lys ne anal gs: -am n apr a d 5. p cal hem stat cs: f br n glue II. Ac ute une xp e c te d b lo o d lo s s A. Aut trans us n: may st ll be an pt n, read ly ava lable 1. Emergent a rt c rupture 2. rauma lapar t my 3. Hem th rax: Aut trans use bl d r m the hest tube. B. Prevent urther bl d l ss.

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NUTRITION AND THE SURGICAL PATIENT Ene rg y So urc e s : P ro te in, Gluc o s e , a nd Fa t I. P ro te in A. Requ res nvers n t glu se v a hepat glu ne genes s t be used as a al r uel s ur e B. Adequate ntake s mp rtant r mus le mass ma ntenan e and ther pr te n-dependent, n n–energy-pr du ng pr esses. II. Gluc o s e : an be st red as gly gen and used as a sh rt-term reserv r energy III. Fa t: Maj r ty energy s st red as at and t a lesser degree as pr te n (skeletal mus le).

Ca lo ric a nd P ro te in Re q uire m e nts I. Ca lo ric re q uire m e nts A. Basal metab l c rate (BMR): am unt energy used by an Quic k Cut unstressed, asted nd v dual at rest REE is 1.2 times B. Rest ng energy expend ture (REE): am unt energy used by the BMR or 25 kcal/kg/day. an unstressed, n n asted nd v dual at rest C. tal energy expend ture ( EE): a tual am unt energy an nd v dual uses Quic k Cut 1. EE an n rease s gn f antly ab ve REE by hypermetab l Fever increas es the nd t ns (e.g., surgery, trauma, seps s, and burns). TEE 10% or each increas e 2. EE an n reased by v luntary w rk (e.g., exer se), whereas in degree Cels ius ; trauma/ dur ng starvat n, the BMR de reases as the b dy adjusts t burns can double TEE. nserve b dy mass. Cal r requ rements an be determ ned by nd re t al r metry r the F ck equat n. II. P ro te in Re q uire m e nts A. N rmal 1. L w be ause ea h pr te n m le ule has a spe f purp se and s there re n t generally ava lable as an energy s ur e 2. Generally, da ly pr te n requ rements are nly 0.8–1.0 g/kg/day, wh h s s gn f antly less than the average Amer an eats da ly. B. Starvat n 1. T e b dy makes every attempt t nserve pr te n. Be ause gly gen st res are metab l zed w th n the f rst 24 h urs starvat n, an ther s ur e glu se must be und r the t ssues that ann t, r usually d n t, use ats ( .e., bra n ells, red and wh te bl d ells). Pr te ns are br ken d wn and nverted t glu se n the l ver by gluc ne genes s t supply the bra n and bl d ells w th glu se. 2. In unstressed starvat n, pr te n atab l sm an be prevented by ex gen us adm n strat n glu se. T e bra n adapts t use ket nes, wh h are pr du ed when at s metab l zed, and de reases the am unt pr te n that must be metab l zed as a glu se s ur e. A er all the ava lable at s metab l zed, pr te n s degraded at a h gh rate unt l the t tal b dy pr te n st res are ½ basel ne, at wh h t me death urs. C. Severe llness 1. T e b dy s n t able t nserve energy and pr te n st res as t d es dur ng unstressed starvat n. 2. T e h rm nal m l eu n reases the BMR, de reases the ab l ty t use ats and ket nes, and thereby n reases the dependen e n glu se as an energy s ur e. T s glu se an me nly r m pr te n that s be ng degraded. 3. As the degree llness r njury n reases, the catab l c rate n reases a rd ngly, lead ng t a rap d breakd wn pr te n st res and mult rgan dys un t n n t he ked. Dur ng the a ute phase severe llness r stressed starvat n, pr te n atab l sm s m n mally a e ted by ex gen us adm n strat n glu se. 4. Pr mary treatment: El m nate the underly ng ause the stress resp nse and pr v de en ugh al r es and pr te n t repla e metab l and atab l l sses. 5. As the llness beg ns t subs de, the h rm nal m l eu hanges, wh h leads t less retent n salt and water and a hange r m a atab l pr te n env r nment t an anab l c env r nment. T e n tr gen balan e s p s t ve, mean ng that less n tr gen s l st than s adm n stered t the pat ent. T s balan e represents pr te n that s be ng la d d wn and thus mpr vement the pat ent’s health.

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Nutritio n Sta tus Eva lua tio n I. Thin, c a c he c tic p a tie nt: Exh b ts h ll wed heeks, n b dy at, and very l ttle mus le and s bv usly n a p r nutr t nal state. Generally, pat ents wh have a utely l st 10% the r b dy we ght are ns dered maln ur shed and need nutr t nal supp rt. II. Ob e s e p a tie nt a nd we ll-d e ve lo p e d p a tie nts : may need as mu h nutr t nal supp rt as the pat ent n a p r nutr t nal state, depend ng n the underly ng d sease pr ess III. P re vio us ly we ll-no uris he d p a tie nt: Generally able t endure a maj r perat n and 5–10 days starvat n w th ut an n rease n m rb d ty r m rtal ty. I the per d starvat n extends bey nd 10 days, nutr t nal supp rt s ne essary. IV. P a tie nts with s e ve re illne s s : I unable t eat r m re than 10 days be ause surgery, ns der early nutr t nal supp rt. Be ause t takes several days t take e e t, beg nn ng su h supp rt there s any quest n nutr t nal def t s m re e e t ve than wa t ng unt l a severe def t urs.

The ra p y I. Go a ls : T e average h sp tal zed pat ent requ res 2,000 al da ly and 60 g pr te n. A. Energy: Determ ne al r requ rements t pr v de adequate energy substrates ( .e., arb hydrates, ats) and av d ex ess al r es n ne ur ways. 1. Ind rect cal r metry: Measures am unt xygen nhaled m nus am unt xygen exhaled t determ ne am unt xygen nsumed. Be ause xygen nsumpt n (VO2) measured n mL O2/m n s d re tly rrelated t k al/day (1 mL O2/m n 7 k al/day), measurement the am unt xygen nsumed an determ ne da ly al r requ rements. 2. F ck equat n: Am unt xygen nsumed, and there re k al requ red, s determ ned by mult ply ng the ard a utput by the arter ven us xygen ntent d eren e. 3. Harr s-Bened ct equat ns: Da ly al r requ rements are determ ned by al ulat ng REE r m gender-based equat ns us ng gender, he ght, we ght, and age var able and then mult ply ng by an est mated stress a t r. 4. Est mated REE (25 kcal/kg/day): mult pl ed by an est mated stress a t r B. Pr te n: Determ ne pr te n requ rements n ne ur ways. 1. N tr gen balance: T e maj r ty atab l zed pr te n s l st as ur nary urea n tr gen, w th 2–4 g n tr gen l st n st l. Pr te n grams d v ded by 6.25 equals n tr gen grams. Am unt n tr gen ntake m nus n tr gen utput sh uld be p s t ve adequate pr te n s g ven and the pat ent s n t t atab l . 2. V sceral pr te n measurement (e.g., album n, trans err n, prealbum n) a. Due t the l ng hal -l e album n, t sh uld nly be used t assess malnutr t n n utpat ent and ele t ve surgery pat ents. b. Prealbum n has a sh rter hal -l e and s m re re e t ve pr te n nutr t n n h sp tal zed pat ents. c. A C-rea t ve pr te n (CRP) sh uld be he ked be ause elevated levels n ammat n (trauma/seps s/burns) w ll alter v s eral pr te n pr du t n away r m prealbum n synthes s.

Quic k Cut The overall goal o nutritional support is to supply adequate energy in the orm o calories and adequate protein or building proteins in the body.

Quic k Cut A ratio o 150 cal:1 g o protein is optimal. Mineral and trace elements are included in most ormulas in adequate amounts to prevent de ciencies or toxicities.

Quic k Cut Fick equation: CO VO2/(C a C v), where CO cardiac output, C a oxygen concentration o arterial blood, and C v oxygen concentration o mixed venous blood. Ca C v is also known as the a rte riove nous oxyge n di e re nc e .

Quic k Cut Harris -Benedict gender-bas ed equations : Men: BMR 88.362 (13.397 weight in kg) (4.799 height in cm) (5.677 age in years ) Women: BMR 447.593 (9.247 weight in kg) (3.098 height in cm) (4.330 age in years )

Quic k Cut The protein requirement or most adults is 0.8 g/kg/day (or 56 g or the hypothetical 70-kg patient). During severe illness with a high catabolic rate, this requirement may increase to 2 g/kg/day o protein or greater.

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3. We ght ga n (p r meth d): Be ause m st pat ents need ng Quic k Cut nutr t nal supp rt n the h sp tal are stressed, they tend When determining t reta n water and be me edemat us. Als , they w ll be whether nutritional s upport atab l and l se lean b dy we ght desp te the n rease is adequate or hos pitalized the r a tual b dy we ght r m u d ga n. patients , obs erving the 4. Observe the verall c nd t n the pat ent (best verall patient’s overall condition is better than monitoring weight meth d): Obta n n tr gen balan es (max mum tw e gain alone. weekly), ll w v s eral pr te ns (prealbum n/CRP tw e weekly), and n rease pr te n adm n strat n (alth ugh there s n the ret al l m t t the max mum am unt pr te n that an be adm n stered, pr te n n ex ess the pat ent’s needs w ll result n a r se n bl d urea n tr gen [BUN]). II. En te ra l n u t ritio n : he pre erred r ute t pr v de nutr t n Quic k Cut s enterally t ma nta n gut mu sal ntegr ty and redu e Us e the gut or mpl at ns. he gut s mp rtant n r t ally ll pat ents; eeding whenever pos s ible. unused r even br e per ds, the mu sa beg ns t atr phy and l se ts barr er un t n, lead ng t ba ter al transl at n and w rsen ng system n lammat n. In add t n t transl at n, the atr ph ed mu sa s unable t d gest d when d s ult mately presented, wh h leads t urther delays n adequate nutr t n. A. F rmula c mp s t ns: When p ss ble, pat ents sh uld be ed by m uth; h wever, w th r t al llness, asp rat n r sk, depressed mental status, r nab l ty t take adequate al r es r pr te n rally, adm n strat n enteral eed ng rmulas s ne essary. T ese rmulas are des gned t pr v de adequate nutr t n and may be r ut ne r nes that are h ghly spe al zed t serve the needs un que pat ent p pulat ns. 1. Standard rmulas: su table r m st pat ents a. Pr v de a balan ed al r e/pr te n rat w th 50%–65% al r es r m arb hydrates, 10%–20% r m pr te ns, and the rest r m ats b. Cal r dens ty s 1.0–1.2 k al/mL; they n lude the essent al ats, m nerals, and tra e elements. 2. Elemental rmulas: am n a d r small pept de–based r ease d gest n and l wer res due n pat ents w th sh rt gut syndr me r d stal enter utane us f stulas 3. Cal r e-dense rmulas: nta n m re al r es per m ll l ter than standard rmulas (typ ally 1.5–2.0 k al/mL) r pat ents need ng u d restr t n r very h gh al r requ rements 4. Pr te n-dense rmulas: pr v de n reased pr te n (20%–25% al r es) r pat ents w th very h gh pr te n needs 5. Fat-based rmulas: pr v de m re al r es r m ats rather than glu se and attempt t redu e CO2 pr du t n by alter ng the resp rat ry qu t ent r pat ents w th mpr m sed m nute vent lat n (e.g., severe hr n bstru t ve pulm nary d sease [COPD] and a ute resp rat ry d stress syndr me [ARDS] pat ents) 6. Immun m dulat ng rmulas: Pr v de glutam ne and typ ally mega-3 atty a ds t enhan e mmun l g un t n; h wever, e a y s m xed. S me re mmend them r me han ally vent lated pat ents w th system n ammat ry resp nse syndr me (SIRS) r m seps s, trauma, burns, a ute lung njury (ALI), et . B. Adm n strat n r ute 1. Enteral nutr t n rmulas an be del vered by tubes pla ed nt the GI tra t d re tly (gastr st my, eed ng jejun st my) r v a the n se (nas gastr , nas du denal, r nas jejunal). 2. An abd m nal rad graph t determ ne pr per tube pla ement sh uld be bta ned pr r t start ng tube eed ngs n eed ng tubes pla ed rally r nasally at the beds de. 3. P stpyl r pla ement (jejun st my, nas du denal, nas jejunal) s ass ated w th earl er t leran e but s m re d ult, lead ng t p tent al delays n n t at n enteral nutr t n. 4. Early n t at n enteral nutr t n ( 48 h urs) s ass ated w th ewer mpl at ns and sh uld be used even n the mmed ate p st perat ve per d ll w ng abd m nal surgery r trauma.

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Chapter 1

Nutr t n and the Surg al Pat ent

C. Adm n strat n rate: Enteral nutr t n sh uld be started as nt nu us n us n. 1. A reas nable start ng p nt s ull strength at 20 mL/hr and n reased by 20 mL/hr every 6–12 h urs unt l the g al rate s bta ned r ex ess ve res duals are n ted. 2. T e g al rate s determ ned by the pat ent’s al r needs and the al r dens ty the rmula. 3. Gastr res dual v lumes tube eed ngs sh uld be he ked every 4 h urs r ex ess ve res dual v lumes ( 500 mL), even eed ngs are p stpyl r . a. I res dual v lumes are h gh, the n us n sh uld be st pped and then resumed a er 4 h urs. b. I res duals nt nue t be h gh, the ause ( leus, bstru t n) sh uld be s ught. D. C mpl cat ns 1. Gastr ntent asp rat n s the m st mm n mpl at n Quic k Cut enteral nutr t n but an be redu ed by m n t r ng res dual Although s tudies v lumes and ma nta n ng the head the bed up 30 degrees. conf ict, there appears to be 2. Bl at ng, mesenter s hem a (rare), and d arrhea may ur no bene t rom pos tpyloric w th tube eed ngs, but adjustments n mp s t n and rate eeding in terms o as piration, an m n m ze these ssues. pneumonia, or outcomes . 3. Inadequate nutr t nal supplementat n aused by requent eed ng essat n s n t un mm n unless n erted e rts are made t av d t. III. P a re nte ra l (IV) nutritio n: PN all ws the pr v s n adequate nutr t n when the GI tra t s usable due t malabs rpt n, bstru t n, f stulas, r anat m hanges. C mb ned enteral and parenteral adm n strat n s s met mes benef al. A. F rmula c mp s t n: PN s lut ns sh uld nta n mp nents nutr t nal requ rements be ause ther s ur es may n t be ava lable. 1. Carb hydrates: Pred m nantly as glu se s lut n; pr v de 50% t tal al r es and ause PN t have a h gh sm lal ty. Part al ( r per pheral) parenteral nutr t n (PPN) nta ns l wer n entrat n glu se and s n t s gn f antly hyper sm lar. 2. Am n ac d s lut n: pr v de 10% t tal al r es and mp rtantly pr v d ng essent al am n a ds r metab l sm, espe ally n hyper atab l pat ents 3. Fats: adm n stered e ther nt nu usly r nterm ttently as l p d emuls n and are ne essary t av d essent al atty a d def en y a. L p d emuls ns als pr v de the m st al r es n the smallest v lume ( at has the h ghest al r dens ty) and pr du e less CO2 (l west resp rat ry qu t ent), wh h may be mp rtant n pat ents w th v lume restr t ns r mpr m sed vent lat n. b. Adm n strat n l p d emuls ns an lead t hypertr gly er dem a; levels sh uld be r ut nely m n t red. 4. Electr lytes: n lude the m n valent at ns, s d um and p tass um; the d valent at ns, al um and magnes um; and the an ns, hl r de and a etate ( nverted t b arb nate n the l ver), wh h an be adjusted as needed 5. V tam ns and trace elements: Must be pr v ded t av d a qu red def en es; spe f ally, the ex gen us adm n strat n B v tam ns, v tam n E/selen um (l p d per x dat n and ree rad al s aveng ng), z n (w und heal ng, mmun ty), and hr m um ( nsul n sens t v ty) sh uld be ns dered n pat ents re e v ng PN. 6. Med cat ns: May be n rp rated nt PN; parenteral stress ul er pr phylax s med at ns and nsul n are the m st requently added. B. Adm n strat n r ute: usually v a a per utane usly pla ed Quic k Cut ven us l ne w th the t p l ated n the vena ava The high os molality C. Adm n strat n rate: PN s typ ally pr v ded nt nu usly at o TPN caus es phlebitis a rate that pr v des adequate al r es t meet the pat ent’s needs and s cleros is i in us ed and depends n al r dens ty and degree hypermetab l sm. into a peripheral vein (les s 1. C mm nly, pat ents are started at hal the g al rate r 12 h urs hyperos molar PPN can be delivered via a peripheral vein be re advan ng t the ull rate t av d severe hypergly em a. but typically does not meet 2. S me adv ate de reas ng the PN rate by hal r 6–12 h urs caloric needs ). pr r t st pp ng t av d hyp gly em a. 3. Cy l ng t all w pat ents t be d s nne ted r per ds t me dur ng the day an be a mpl shed but sh uld nly be pres r bed by exper en ed pers nnel and n sele ted pat ents.

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D. C mpl cat ns 1. In lude th se related t l ne pla ement (hem th rax, pneum th rax); n e t ns (l ne seps s, pneum n a, a al ul us h le yst t s); hypergly em a (ass ated w th n reased n e t n r sk and death); hepat dys un t n; and abn rmal t es n ele tr lytes, v tam ns, atty a ds, and tra e elements 2. PN s ass ated w th h gher m rb d ty and m rtal ty than enteral nutr t n usually due t n e t us and hepat mpl at ns. In pat ents unable t re e ve adequate enteral nutr t n, th s n reased r sk s unav dable.

THE INTENSIVE CARE UNIT Sp e c ia lize d Inte ns ive Ca re Unit Ca re a nd Mo nito ring

Quic k Cut The ICU is an attitude or an approach, not a place.

I. Inte ns ive p a tie nt c a re : T e a u ty a pat ent’s nd t n may requ re l se nurs ng and phys an bservat n and management, wh h an nly be pr v ded n an ICU sett ng, where ne nurse ares r nly ne r tw pat ents at a t me and phys ans are present at all t mes. II. Ma na g e m e nt s p e c if c to the ICU: pr v des r t ally ll pat ents w th spe f are and m n t r ng n t typ ally ava lable n Quic k Cut ther h sp tal un ts I you think you A. A rway c ntr l (end tracheal ntubat n): pla ement an might have to intubate a art f al a rway t prevent a rway bstru t n r t pr v de patient . . . do it! It is eas ier to me han al vent lat n extubate an intubated patient 1. Placement: Art f al a rways an be pla ed translaryngeally, than to res us citate rom res piratory arres t. e ther r tra heal r nas tra heal, r d re tly nt the tra hea by an n s n n the l wer anter r ne k (trache st my). 2. Cr c thyr d t my: per rm when ntubat n s requ red emergently and ann t be per rmed translaryngeally 3. Assessment r ntubat n: T e de s n t ntubate a pat ent by wh hever r ute s a r t al de s n w th ser us nsequen es per rmed t late. Assess early and repeat requently based n pat ent a u ty; t s n t s mple but sh uld n lude at least the ll w ng: a. Resp rat ry rate (RR): m st s mple t assess (1) T e n rmal RR s 12–16 breaths per m nute (bpm). (2) I a pat ent’s RR s greater than 40 bpm, ntubate. (3) I a pat ent s breath ng 30–40 bpm, n t ate therapy t get RR less than 30 bpm, r the pat ent w ll t re and g nt resp rat ry a lure (m st humans ann t susta n RRs 30 bpm r very l ng w th ut at gue). (4) L w RRs are alm st always aused by a neur l g d s rder (e.g., al h l, drugs, head njury), wh h w ll determ ne ntubat n s needed. b. Resp rat ry e rt: represents the w rk breath ng (1) Pat ents exert ng a s gn f ant e rt ( .e., us ng a ess ry resp rat ry mus les, hav ng d ulty speak ng n ull senten es, r bly exhal ng, r un m rtably nhal ng) typ ally need ntubat n. (2) I le t pr gress w th ut ntervent n, these pat ents be me verly t red w th pr gress ve hyp vent lat n and p tent al resp rat ry arrest. c. Hyp x a: an be an nd at n r ntubat n but Quic k Cut als manageable by n n nvas ve n reased xygen Patients with acute n entrat ns. Intubat n a l tates b th n reased arterial oxygen s aturations ract n nsp red xygen (F 2) and a rway pressure les s than 92% typically need pr v s n t redu e ntrapulm nary shunt and mpr ve s upplemental oxygen or xygenat n. intubation to improve their d. Impend ng a rway bstruct n: nd at n r ntubat n oxygenation s tatus . t prevent mplete bstru t n and l ss the a rway (1) Anat m (e.g., r m trauma, tum rs, edema, r v al rd abn rmal t es) and un t nal hanges (e.g., r m depressed neur l g status r m head trauma, drugs, anesthes a, r str ke) an nter ere w th a rway paten y.

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(2) W th n ern r mpend ng a rway bstru t n, Quic k Cut ntubate early r ntr lled passage the Except or occasional end tra heal tube. cases o chronically ventilated B. Vent lat r supp rt: M st mm n reas n t be adm tted t an ICU. patients, all patients requiring On e the de s n has been made t ntubate, next de de h w mechanical ventilation will be t manage the vent lat r pat ent. Vent lat r supp rt sh uld managed in an ICU. address vent lat n and xygenat n. M de vent lat n (see the ll w ng d s uss n) w ll alter h w these are a h eved; h wever, m re mm nly, m de n uen es pat ent t leran e Quic k Cut me han al vent lat n. For any patient receiving ventilatory s upport, 1. Vent lat n: determ nes CO2 el m nat n and depends n ventilator-as s ociated lung alve lar m nute vent lat n injury is an inherent ris k to a. Alve lar m nute vent lat n: t tal m nute vent lat n mechanical ventilation. dead spa e vent lat n b. tal m nute vent lat n: pr du t RR t dal v lume, expressed as L/m n. de rease Pco 2, als adjust RR and Quic k Cut t dal v lume w th n reases n m nute vent lat n. Increas e mean 2. Oxygenat n ( r Po 2): determ ned by the part al pressure airway pres s ure (increas e alve lar xygen and the ntrapulm nary shunt PEEP, s witch modes ) or a. In reas ng Fio 2 w ll n rease alve lar xygen, whereas improvements in oxygenation. n reas ng mean a rway pressure (e.g., by n reas ng Change minute ventilation or improvements in ventilation. p s t ve end-exp rat ry pressure [PEEP]) w ll de rease shunt and n rease Po 2. 3. M de vent lat n: Determ nes h w the vent lat r w ll pr v de a me han al breath t the pat ent and s based n pressure r v lume. (Many ther m des ex st than are d s ussed here, but these w ll su e n m st pat ents.) a. Synchr n zed nterm ttent mandat ry vent lat n (SIMV): pr v des a preset rate and t dal v lume (1) Sp ntane us breath ng by the pat ent pr v des add t nal m nute vent lat n (t dal v lume rate) dependent n the pat ent’s w rk breath ng apab l ty. (2) T e w rk breath ng s shared between the ma h ne’s m nute vent lat n and the pat ent’s sp ntane us m nute vent lat n. (3) Usual m de vent lat n when wean ng a pat ent: By turn ng d wn the vent lat r rate, the pat ent assumes m re w rk breath ng unt l the vent lat r s n l nger needed. (4) Pressure supp rt (see the ll w ng d s uss n) an be added t a l tate sp ntane us breaths. b. Ass st r v lume c ntr l (AC/VC): pr v des a preset rate and t dal v lume, and all add t nal pat ent breaths are ully ass sted by the vent lat r t the preset t dal v lume (1) M nute vent lat n be mes the result the preset t dal v lume (the preset vent lat r’s pat ent’s rates). (2) T s all ws the pat ent t re e ve ull vent lat ry supp rt w th ut expend ng extra energy n the w rk breath ng. c. Pressure supp rt (PS): Rather than pr v d ng a preset v lume r rate, th s m de pressur zes the vent lat r r u t t a preset level when the pat ent n t ates a breath and ma nta ns that level unt l the pat ent st ps nhal ng. T e pat ent s able t n t ate and term nate the resp rat ry y le n th s m de. (1) Insp red t dal v lume: determ ned by the am unt PS and the pat ent’s ntr ns w rk breath ng apa ty (2) In reas ng PS redu es the w rk breath ng r the same t dal v lume r all ws a larger t dal v lume r the same am unt w rk. (3) PS a l tates wean ng r m the vent lat r. (4) Usual start ng p nt: 5–10 mm Hg ab ve the basel ne pressure ( nt nu us p s t ve a rway pressure [CPAP]/PEEP) and an be used al ne r n mb nat n w th SIMV d. CPAP and PEEP: T ese m des are s m lar n that b th result n the vent lat r r u t be ng pressur zed t a spe f ed level ab ve atm spher at all t mes, dur ng nsp rat n and exp rat n. (1) T s pr mary means n reas ng xygenat n n reases mean a rway pressure and the number n ated alve l , wh h n reases lung sur a e area ava lable r gas ex hange and de reases ntrapulm nary shunt.

Chapter 1

4.

5.

6.

7.

Pr n ples

Surg al Phys l gy

23

(2) Usually, CPAP/PEEP 5 mm Hg ab ve atm spher pressure s used and s n reased as ne essary t mpr ve xygenat n. (3) Be ause these m des n rease ntrath ra pressure at h gher levels, they an de rease ven us return t the heart and there re CO. (4) PEEP s used w th SIMV and AC, whereas CPAP s used w th PS. Quic k Cut Rate: A er m de, the next parameter t set s rate (n rmal, Remember that 10–12 bpm). i the patient is s everely a. H gher rates may be ne essary t de rease the Pco 2 acidotic, he or s he may have h gher m nute vent lat n r l wer t dal v lumes are been compens ating with the requ red. res piratory s ys tem and may b. N rate s needed r PS. require a much higher RR. dal v lume: N rmal t dal v lume s 5 mL/kg, but vent lated pat ents are usually set at 6–8 mL/kg. a. H gher v lumes are needed t ver me dead spa e and t ensure alve lar f ll ng. b. W th de reas ng lung mpl an e (e.g., w th ARDS), smaller t dal v lumes 4–6 mL/kg have been sh wn t redu e m rtal ty. c. Adjust v lume as the pat ent’s nd t n requ res. d. O as nally, perm ss ve hyper apn a s benef al t av d bar trauma. R ut ne vent lat r supp rt start ng p nt: T e vent lat r sett ngs des r bed prev usly all w management m st vent lat ry pr blems. Depend ng n the pat ent’s nd t n, ther m des are ava lable t vent late pat ents, but these su e r r ut ne vent lat ry management. a. M de: SIMV; h wever, n w rk breath ng s des red, use the AC m de. b. Rate: 10–12 bpm c. dal v lume: 6–8 mL/kg (4–6 mL/kg the pat ent has ALI r ARDS) d. PS: 5–10 mm Hg (n t used n AC/VC) e. PEEP/CPAP: 5–10 mm Hg . Fio 2: 0.4 g. M d y sett ngs r the pat ent’s c nd t n: h gher Fio 2 and/ r h gher PEEP the pat ent s hyp x , l wer PEEP hyp tens ve, aster rate a d t , et . Extubat n: Vent lat r wean ng s the pr gress ve trans er the w rk breath ng r m the vent lat r t the stable pat ent. Quic k Cut Patients with a a. Muscle atr phy: Vent lat r pat ents are usually n a s igni cant acidos is with or atab l state, thus break ng d wn mus le pr te n r without compens ation s hould uel. Be ause pat ents n mplete vent lat r supp rt d not be extubated without n w rk breath ng, the r resp rat ry mus les rap dly care ul cons ideration o the atr phy. underlying caus e. b. Stable pat ent: Adjust the am unt vent lat ry supp rt t all w the pat ent t d s me w rk breath ng t keep the resp rat ry mus les nta t. As the pat ent’s nd t n mpr ves, the RR del vered by the vent lat r s de reased unt l the pat ent adequately assumes the w rk breath ng. c. Sp ntane us breath ng tr al (SB ): T s da ly test has been sh wn t sh rten me han al vent lat n durat n. T e pat ent wh passes the SB w th adequate parameters (des r bed bel w), s awake en ugh t ntr l a rway, and has a eptable a d–base balan e may be ready r extubat n. T e SB an be a l w am unt CPAP and pressure supp rt (5 mm Hg r ea h) r m re lass ally (and m re pred t ve su ess ul extubat n) be a w-by xygen tr al the vent lat r. (1) Rap d shall w breath ng ndex (RR bpm by t dal v lume n L) less than 100 (s me use a l wer number, r example, 60 r 80, r PS tr als) (2) V tal capac ty: greater than 15–20 mm Hg (3) Negat ve nsp rat ry rce greater than 20 m H 2O (4) Arter al bl d gases: T e pat ent must have a eptable bl d gases as well as sp r metry values. (a) Oxygen saturat n sh uld be h gher than 90% due t the l m tat ns pr v d ng h gh xygen n entrat ns v a a e mask. (b) Pco 2 sh uld be 35–45 mm Hg w th pH 7.35–7.45.

24

Chapter 1

T e Intens ve Care Un t

C. Hem dynam c and ther nvas ve m n t r ng: Ma nstays Quic k Cut n m dern ICUs are the arter al l ne r bl d pressure; the Monitoring with pulm nary artery atheter r COs, pulm nary artery wedge invas ive techniques s uch as pressures, and m xed ven us xygen saturat n; and the arterial lines , pulmonary artery ntra ran al atheter r ntra ran al pressure (ICP) m n t r ng. catheters , and ICP take place H wever, pulm nary artery atheters are n w used mu h less, w th only in the ICU. n n nvas ve te hn l g es su h CO measurement based n arter al l ne tra ngs and ard a per rman e based n e h ard graphy. 1. Arter al catheter: Usually pla ed n ne the a ess ble rad al arter es. I a rad al artery ann t be annulated, ther s tes are em ral, ax llary, and bra h al arter es. a. T e arter al l ne pr v des nt nu us bl d pressure m n t r ng and s a s mple, n npa n ul s ur e r bl d sampl ng. b. T ree pressure measurements bta ned: syst l , d ast l , and mean. (1) Syst l c: h ghest ard a y le pressure re rded (2) D ast l c: l west ard a y le pressure re rded (3) Mean: Measured by ntegrat ng the area under the urve the ard a pressure wave. T e mean pressure an be nd re tly determ ned as (BPsyst l 2 BPd ast l )/3 and represents the pressure ava lable t per use the rgans. 2. Pulm nary artery (Swan-Ganz) catheter: Fl w-d re ted atheter nserted nt a sub lav an r jugular ve n w th an n atable ball n n ts t p t at thr ugh the heart and nt the pulm nary artery. It has an pen ng (p rt) n the t p d stal t the ball n, an ther pen ng n ts s de at a p s t n that rests n the vena ava r r ght atr um, and a therm st r (a temperature-measur ng dev e) near the d stal p rt (F g. 1-3). Extra p rts may n use med at ns. a. Pulm nary cap llary wedge pressure (PCWP)/ cclus n pressure (PCOP): When the atheter s n p s t n n Quic k Cut a d stal pulm nary artery, the ball n s n ated and Swan-Ganz ludes antegrade bl d w, thereby all w ng the d stal catheters are only us ed in p rt t measure retr grade pressure r m the le atr um, s pecial circums tances , but an nd re t measure le ventr ular prel ad. By assess ng knowledge o them helps ventr ular prel ad, alterat ns n u d therapy an be in unders tanding noninvas ive meas urement o made t max m ze CO based n the Starl ng curve. cardiovas cular phys iology. b. T erm d lut n meth d l gy: T e atheter s able t determ ne CO by a urately measur ng hanges n bl d temperature (therm d lut n) a er ntr du t n a kn wn thermal hallenge. c. M xed ven us xygen saturat n (SvO2): an be assessed Quic k Cut by e ther asp rat ng bl d r m the d stal p rt r by us ng SvO 2 is one o x metry l ated n the d stal t p the bes t meas ures readily (1) SvO2 pr v des a means t determ ne the am unt available to determine i xygen be ng pumped by the heart (oxygen delivery) s hock is pres ent. s adequate r the am unt xygen the b dy needs (oxygen consumption). (2) N rmal SvO2: 70%; xygen nsumpt n s elevated r xygen del very s de reased, saturat n w ll be less than 70%. (3) I the SvO2 s pers stently l w (60% r less), xygen del very s nsu ent, and rgan dys un t n w ll ur. (4) Us ng s m lar te hn l gy, a less nvas ve but n t as a urate meth d r determ n ng SvO 2 an be bta ned r m the end a entral ven us atheter. d. System c vascular res stance (SVR)/pulm nary vascular Quic k Cut The basic in ormation res stance (PVR): By kn w ng the CO, the mean arter al that can be gathered rom pressure (MAP), and the entral ven us pressure (CVP), the pulmonary artery catheter SVR and PVR an be al ulated (MPAP, mean pulm nary includes le t atrial and le t artery pressure; 80, a nvers n a t r). ventricle preload pressures, (1) SVR [(MAP CVP)/CO] 80; n rmal: 800–1,200 CO, SvO2, SVR, and PVR. 5 dynes.se nd/ m

Chapter 1

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25

B IV s olution in pre s s ure ba g

P ulmona ry a rte ry

S upe rior ve na ca va

G Dis ta l

lume n of PA ca the te r

Monitor

A

G S te rile s le e ve of PA ca the te r

ECG PA

RA

S he a th with s ide port P roxima l lume n

Ca ble s

Dis ta l lume n ope ning Tra ns duce r, s topcock, flus h de vice

Ba lloon infla te d

C

P roxima l infus ion port

D

Dis ta l infus ion port

E The rmis tor conne ctor

F Ba lloon

F

E The rmis tor

lume n ope ning

infla tion va lve

Fig ure 1-3: Pulmonary artery (PA) catheter and pres s ure monitoring s ys tems . (A) Beds ide monitor that connects with cables to (B) the pres s ure monitoring s ys tems (includes IV s olution in a pres s ure bag, IV tubing, and two trans ducers with s topcocks and f us h devices ). This s ys tem connects to (C) the proximal in us ion port that opens in the right atria and is us ed to in us e f uids or med ications and monitor central venous pres s ures and (D) the d is tal in us ion p ort. This port op ens in the PA and is us ed to monitor PA p res s ures . (E) The thermis tor connector is attached to the beds ide cardiac monitor to obtain CO. (F ) An air- lled s yringe is attached to the balloon inf ation valve during catheter ins ertion and meas urement o PA wedge pres s ure. (G) PA catheter pos itioned in the pulmonary artery. Note the s terile s leeve over the PA catheter. The PA catheter is threaded through the s heath until it reaches the des ired p os ition in the PA. The s id e port on the s heath is us ed to in us e medications or f uid s . ECG, electrocardiogram; RA, right atrium. (From Farrell M, Demps ey J . Smeltzer and Bare’s Textbook of Medical-Surgical Nursing, 2nd ed. Philadelphia: Lipp incott Williams & Wilkins ; 2010.)

(2) PVR [(MPAP PCWP)/CO] 80; n rmal: 20–120 dynes se nd/ m 5 (3) L w SVR nd ates system n ammat n r ther d str but ve sh k states (e.g., seps s). (4) H gh SVR nd ates ther sh k states w th nadequate CO. e. Other: Add t nal data an be gleaned, wh h s bey nd th s b k’s s pe. As n ted, nearly all t an n w be bta ned n n nvas vely. (1) Pulm nary artery pressures: an be est mated by e h ard graphy (2) CO/SVR: an be measured w th a s mple A-l ne tra ng and the appr pr ate hardware and s ware

26

Chapter 1

T e Intens ve Care Un t

D. Vas act ve med cat ns and ant arrhythm c dr ps: In the Quic k Cut ICU, many pat ents are n vas a t ve med at ns t a e t the r Vasopressors such hem dynam parameters; m st the t me, th s s t n rease as norepinephrine, dobutamine, bl d pressure (vas nstr t rs) and m re mp rtantly CO and nitroprusside are usually ( n tr pes), but there are als t mes when these parameters need only administered in the ICU. t be de reased. 1. C mm n med cat ns: All are adm n stered v a nt nu us IV dr p. a. D pam ne: E e ts depend n n entrat n used. Quic k Cut (1) L w d se (1–3 g/kg/m n): pr mar ly a e ts Renal dos e d pam ne re ept rs n the k dneys and ntest ne, dopamine is s ometimes us ed lead ng t n reased bl d w in certain patient populations (2) Intermed ate d se (3–10 g/kg/m n): pr mar ly a beta(cardiac s urgery), but its re ept r ag n st, n reas ng ard a ntra t l ty w th us e as a natriuretic agent is mos tly his torical. result ng n rease n CO (3) H gh d se ( 10 g/kg/m n): Pr mar ly an alpha ag n st and vas nstr t r. Its l m t ng e e t s ta hy ard a but s use ul n sh k where b th ntra t l ty and a heart rate (HR) n rease are needed. b. D butam ne: pr mar ly a e ts b th the beta-1 and beta-2 re ept rs, n reas ng CO and vas d latat n, wh h an be benef al n ard gen sh k, where n reased CO and de reased SVR are s ught c. N rep nephr ne: Str ng alpha ag n st that pr mar ly Quic k Cut auses vas nstr t n w th m ld beta ag n st a t v ty that Norepinephrine n reases heart ntra t l ty. Started at 1–2 g/kg/m n, the is the rs t choice in s eptic d se s n reased n 1–2- g/kg/m n n rements unt l the s hock. des red e e t s rea hed. a hy ard a s ts maj r l m t ng e e t (but g d r sept sh k); therw se, there s really n upper l m t. d. Ep nephr ne: Pr mar ly an alpha ag n st w th s me beta ag n st e e t. It s use ul r vas nstr t n and n reas ng CO; t s d sed s m lar t n rep nephr ne but auses m re ta hy ard a. e. Phenylephr ne: Alpha ag n st that auses pure arter al Quic k Cut nstr t n but s n t very p tent. Dr ps are usually begun Phenylephrine at 50 g/m n and n reased n n rements 50 g/m n s hould not be us ed in cas es unt l a t tal d se 300 g/m n s rea hed, when a m re o hypotens ion as s ociated p tent vas nstr t r s needed. with low CO becaus e it 2. C mm n vas d lat rs: O as nally, pat ents have decreas es oxygen delivery. hypertens n and need the r bl d pressure l wered r the r SVR w ll be ex ess vely h gh and need vas d lat n. In ard gen sh k, l wer ng the a erl ad by de reas ng SVR Quic k Cut w ll n rease CO and get the pat ent ut sh k. Nitroprus s ide us ed a. N tr pruss de: Pr mar ly an arter al vas d lat r. T e in large dos es or a prolonged n t al d se s 0.3 g/kg/m n, w th a max mum d se period can caus e cyanide 3 g/kg/m n. It an result n re ex ta hy ard a, and ne pois oning and acidos is . ts metab l tes s yan de. b. N tr glycer n: pr mar ly a ven d lat r and a r nary artery d lat r that de reases ven us prel ad t de rease d ast l wall tens n and t all w better heart ntra t n t has been verstret hed (1) Als all ws better d ast l bl d w t the heart tsel and may n rease CO (2) Pr mar ly used n ases r nary s hem a (3) D s ng starts at 5 g/m n and n reases n 5–20- g/m n n rements unt l the des red e e t s bta ned. c. Labetal l: a ts a m xed alpha- and beta-bl ker n IV rm d. Esm l l: pure beta-bl ker e. N card p ne: p tent al um hannel bl ker

Chapter 1

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27

SHOCK De f nitio n Sh ck s the l n al syndr me result ng r m nadequate t ssue per us n t ma nta n n rmal ellular metab l sm. Essent ally, t s nadequate xygen del very t meet xygen demand. I. Oxyg e n d e live ry e q ua tio n: DO2 [1.39 Hgb (grams) Sao 2 (0.003 Pao 2)] CO. A. Pao 2 ntr butes very l ttle t xygen del very. B. Hgb Sao 2 represents the bl d’s xygen- arry ng apa ty. C. CO s determ ned by HR str ke v lume (SV), and SV s determ ned by ard a prel ad, ntra t l ty, and a erl ad. D. W th nadequate xygen del very: “f x” Hgb, Sao 2, HR, prel ad, c ntract l ty, and a erl ad.

Quic k Cut The s ix variables to adjus t to improve oxygen delivery are Hgb, Sa O 2 , HR, preload, contractility, and a terload.

II. Typ e s o s ho c k: Sh k an result r m p r xygen del very r Quic k Cut ( n rare ases) r m n reased demand; able 1-5 summar zes types Revers ing s hock as sh k based n analys s the pat ent’s hem dynam pr f le. early as pos s ible is critical or reducing organ ailure and A. Hyp v lem c sh ck: M st mm n type sh k, and complications in the ICU. hem rrhage s the m st mm n reas n r hyp v lem a. L ss plasma v lume (e.g., w th maj r burns, th rd spa ng, r GI l sses) an als result n hyp v lem a. De reased prel ad Quic k Cut de reases CO and xygen del very t ells. L ss red ell Although v lume redu es Hgb levels. hypotens ion occurs with 1. Cl n cal presentat n and m rtal ty: Depend n the hypovolemia, the important magn tude and durat n sh k. In reased la tate concept is los s o per us ion, pr du t n urs as n rmal aer b ellular metab l sm not decreas ed pres s ure. pr gresses t less energy e ent anaer b metab l sm ( ewer aden s ne tr ph sphate [A P] pr du ed), result ng n ellular damage and death. Quic k Cut 2. reatment (prel ad rest rat n): bl d and plasma v lume Bleeding a. Aggress ve v lume adm n strat n s needed, pre erably hypovolemic s hock patients thr ugh tw large-b re IV atheters. s hould get blood. b. St p ng ng bl d l ss and trans use bl d as needed. c. C ns der entral ven us a ess r m n t r ng and h ghw u d adm n strat n. Quic k Cut B. Card gen c sh ck: aused by my ard al s hem a, CHF, and Res us citate valvular d seases hemorrhage by trans us ing pRBCs and FFP in a 1. Bl d v lume rema ns n rmal r n reased, but l ss 1:1 ratio with platelets or c ntract l ty r ther mped ments t rward w results n every 4 units . . . minimize de reased per us n. crys talloid. 2. reatment: Rest re pump un t n e ther by n reas ng c ntract l ty r de reas ng a erl ad s the weak pump has an eas er t me generat ng w. N tr gly er ne an help reverse Quic k Cut ard a s hem a bl d pressure w ll t lerate t. Res toring pump C. Neur gen c sh ck: aused by vas vagal resp nse, unction in cardiogenic s hock erv th ra sp nal rd njury, r sp nal anesthes a may reduce blood pres s ure, but blood pres s ure is not the 1. L ss sympathet t ne lead ng t per pheral vas d latat n goal . . . per us ion is ! an result n p r per us n. 2. reatment: F rst n rease prel ad, then n rease a erl ad w th phenylephr ne r n rep nephr ne unresp ns ve. D. Sept c sh ck: x ns released by m r bes result n pr und hyper n ammat ry phys l g derangements, n lud ng th rd spa ng u ds (de reased prel ad), ard a dys un t n (p r c ntract l ty), and redu t n n SVR (de reased a erl ad). 1. Sept sh k results n pr gress ve mald str but ve hyp per us n: CO may be de reased, n rmal, r n reased, depend ng n the degree hyp v lem a and the sever ty the n ammat ry nsult. T e hyper n ammat ry resp nse s hara ter zed by n reased ellular metab l sm and

28

Chapter 1

Sh k

Ta b le 1-5: Typ e s o Sho c k Ba s e d o n He m o d yna m ic P ro f le Ana lys is

Typ e o Sho c k

He a rt Ra te

Blo o d P re s s ure Cha ng e s

Le t He a rt Filling P re s s ure s (CVP /PAOP )

Mixe d Ve no us Sys te m ic Oxyg e n Va s c ula r Ca rd ia c Outp ut/ Sa tura tio n Re s is ta nc e Ind e x (SvO 2 )

Hypovolemic

Elevated

First: none Second: narrow pulse pressure/ elevated diastolic Third: systolic hypotension

Low

High

Low

Low

Cardiogenic

Usually increased

Usually decreased

High*

High

Low

Low

Neurogenic

Normal or decreased

Decreased

Low

Low

Decreased (loss o cardiac compensation)

Low

Obstructive

Usually increased but could be decreased

Decreased

Usually high*

High

Low

Low

Elevated

Usually low

Normal or low

Low

Elevated or normal

Normal or low

Elevated

Low

Low, normal, or high Normal or High

Normal or high O ten high

Septic: Early: A ter f uid resuscitation (late):

*Right ventricular ailure can lead to increased central venous pressure (CVP), but decreased capillary wedge pressure, pulmonary embolus, and tension pneumothorax can also lead to high CVP but low or normal pulmonary artery occlusion pressure (PAOP) pressures. In tamponade, all lling pressures are elevated.

xygen demand. Cellular hyp per us n and anaer b metab l sm are ass ated w th rgan dys un t n and death. 2. reatment: n ludes ant b t s, ntr ll ng the n e t n s ur e, and revers ng sh k a. F rst use u ds t n rease CVP t 8–12 (prel ad). b. F ll w la tate/SvO 2 levels. (1) I they are deranged, trans use bl d t an Hgb 10. (2) Use n rep nephr ne t ma nta n MAP h gher than 65 mm Hg as a erl ad may be l w. (3) I la tate/SvO2 s st ll deranged, add d butam ne t n rease CO (c ntract l ty). E. Obstruct ve sh ck: T e hallmark s CO w th elevated CVP result ng n t ssue hyp per us n r m a phys al bstru t n (e.g., tens n pneum th rax, ard a tamp nade, mass ve pulm nary emb l sm, ven us a r emb l sm, and severe ard a valvular sten s s). 1. reatment: u d resus tat n (prel ad) ll wed by pr mpt res lut n the bstru t n, en thr ugh pr edural means a. ens n pneum th rax: An njured lung devel ps a ne-way valve that all ws a r nt but n t ut the pleural spa e. (1) rapped a r reates an n rease n pleural pressure, d spla ng the heart and med ast nal stru tures (e.g., vena ava, a rta) and mpress ng them t the ntralateral s de w th de reased ven us return t the heart. (2) A hest tube pla ed n the a e ted s de rel eves the pr blem. b. Card ac tamp nade: Bl d r u d a umulates ar und the heart n the per ard um. (1) T e result ng n reased pressure n the per ard al sa mpa rs ven us return nt the r ght atr um, de reas ng CO. (2) reatment: Dra n the per ard um t all w ven us return t n rease and CO t n rmal ze.

Chapter 1

Pr n ples

Surg al Phys l gy

29

c. Pulm nary emb l sm: Bl ks bl d w thr ugh the pulm nary artery, result ng n de reased CO and hyp x a. reatment ranges r m ant agulat n thr ugh perat ve pulm nary thr mbe t my. d. Abd m nal mpartment syndr me s n reased pressure n the abd men that mpresses the IVC and de reases prel ad. e. Me han al vent lat n w th ex ess ve PEEP (p s t ve end-exp rat ry pressure) may n rease ntrath ra pressure and lead t bstru t ve sh k. F. M scellane us sh ck: en d str but ve (redu ed a erl ad) n nature (e.g., anaphylax s, adrenal nsu en y) 1. Cyan de t x ty mpa rs xygen usage d re tly. 2. In s me pat ents (e.g., Jeh vah’s W tnesses, wh d n t a ept bl d trans us ns r rel g us reas ns), the Hgb level s s l w that t auses sh k and p r xygen del very. 3. Severe hyp x a r m resp rat ry a lure r ALI/ARDS an als lead t sh k ( xygen saturat n).

Chapter 2

Essentials o General Surgery Natasha Hansraj and Douglas J. Turner

WOUNDS Skin I. Cha ra c te ris tic s : Skin is the largest organ o the body and comprises three layers. A. Epidermis: composed o stratif ed squamous epithelial cells aiding in protection B. Dermis: connective tissue with papillary digitation into the epidermis composed o collagen f bers, hair ollicles, capillaries, and sweat glands C. Hypodermis (subcutaneous tissue): deepest layer; loose, at-containing vascular tissue II. Fa s c ia : connective tissue able to withstand tension

Wo und He a ling I. He a ling : comprises three stages A. Inf ammatory (days 1–10): in ux o polymorphonuclear leukocytes and macrophages, cytokine release, and epithelialization B. Proli erative (days 2–21): Fibroblasts appear, producing collagen and granulation tissue; neovascularization occurs to overcome ischemia. C. Remodeling (3 weeks–1 year): Collagen f bers remodel to increase strength but collagen amount remains the same. ype 1 collagen is predominant in wounds a er 3 weeks. II. Stre ngth o tis s ue : issue strength grows with healing and is there ore stronger with longer times rom the initial wound. At 20 days, strength is 20% o normal; 40 days, 40% o normal; and at 1 year, it is 70% o normal.

Wo und Cla s s if c a tio n I. Cle a n: unin ected operative site without crossing a mucosal barrier II. Cle a n c o nta m ina te d : Respiratory, gastrointestinal (GI), or genitourinary (GU) tract is entered in controlled conditions (e.g., appendix or biliary surgery). III. Co nta m ina te d : open accidental wounds or gross GI spillage IV. Dirty: old wounds with devitalized tissue, purulence, or per orated viscus

Wo und Re p a ir

Quic k Cut Wound clas s if cation is important becaus e it predicts the ris k o in ectious complications in the pos toperative wound.

Quic k Cut I. Purpos e : to restore injured tissue to its normal unction and integrity The mos t important II. Typ e s actor in healing is collagen A. Primary intention: All layers are sutured; used or clean cases depos ition providing tens ile s trength. causing minimal scarring (Fig. 2-1). 1. Advantage: most cosmetic 2. Disadvantage: Bacterial colonization can lead to wound in ection and breakdown.

30

Chapter 2

1

2

A

3

He a ling by prima ry inte ntion (wounds with a pproxima te d e dge s )

B

Essentials o General Surgery

1

2

3

4

31

He a ling by s e conda ry inte ntion (wounds with s e pa ra te d e dge s )

Fig ure 2-1: Wound healing by primary and s econdary intention. (Image modif ed rom Rubin E, Farber J L. Pathology, 4th ed. Philadelphia: Lippincott Williams & Wilkins ; 2005, with permis s ion.)

B. Secondary intention: Fascia is closed, leaving subcutaneous and skin layers open to heal spontaneously; used or contaminated wounds (see Fig. 2-1). 1. Mechanism: Healing results rom re-epithelialization rom wound edges and sweat glands along with granulation tissue. Myof broblasts aid in wound contracture. 2. Advantage: minimal risk o in ection 3. Disadvantage: requires dressing changes and leads to broad scars C. Delayed primary intention: Wounds are initially le open or repeated debridement. Once healthy granulation tissue is present without signs o in ection, wound de ect is closed by sutures or aps.

Wo und Clo s ure I. Stitc h: Sutures can be interrupted or continuous. Quic k Cut A. Interrupted closure: series o sutures tied individually a er In wound clos ure, passage through both sides o the wound atraumatic tis s ue handling, tis s ue evers ion, and early 1. Advantage: allows better alignment, especially in wounds s taple removal will minimize with irregular edges s carring. 2. Disadvantage: requires longer time or closure B. Continuous closure (running stitch): Stitches are placed one a er the other with the same suture and tied only at the end. Quic k Cut 1. Advantage: aster; provides equal tension rom bite to bite Interrupted clos ure 2. Disadvantage: can strangulate tissue and carries the risk o allows opening o individual complete unraveling o entire closure with suture racture portions o the wound or II. Ap p ro a c h: Sutures can be sewn in a simple or complex manner drainage o wound in ection. (Fig. 2-2). A. Simple suture: equidistant bites taken through the skin and subcutaneous tissue rom one side to the other B. Vertical mattress suture: Needle is placed in the skin in a ar– ar, reverse direction, near–near ashion. C. Horizontal mattress suture: Parallel bites are taken in a ar– ar, move along incision and reverse the direction, ar– ar ashion.

32

Chapter 2

Wounds

Fig ure 2-2: Suture techniques include interrupted, continuous , and mattres s s uturing.

Suture Cha ra c te ris tic s

Quic k Cut I. Suture s ize : Diameter o the suture. As the number o 0s Tis s ue s trength increases, diameter decreases (i.e., 5-0 [00000] is smaller than in a wound never reaches 4-0 [0000]). 100% o the s trength o intact tis s ue. II. Suture m a te ria l: divided into monof lament versus braided, absorbable versus nonabsorbable ( able 2-1) A. Mono lament: made o a single strand Quic k Cut 1. Advantage: Less drag through tissue causes less tissue The s maller the reaction. s uture s ize, the les s er the 2. Disadvantage: easily breaks; needs more knots to secure tens ile s trength. B. Braided: multif lament 1. Advantages: greater shear strength; so er, more exible, pliable; easily passes through tissue; and needs ewer knots 2. Disadvantage: can tear ragile tissue and be a nidus or in ection C. Absorbable suture: degrades over time because it is made o collagen, which is enzymatically digested, or synthetic polymers, which hydrolyze causing less tissue reaction (Fig. 2-3) 1. Advantages: Decreased risk o in ection because they are nonpermanent. Ideal or biliary and GU tracts, where oreign body would be a nidus or stone ormation and in ection. 2. Disadvantage: Patients with impaired healing or in ection increase rate o suture degradation. T ere ore, i the suture loses strength be ore the wound heals, dehiscence can result. D. Nonabsorbable suture: permanent oreign body that is encapsulated by f broblasts (see Fig. 2-3) 1. Uses: used in heart valves, hernias, and vascular anastomosis. T is suture is pre erred when healing may be slow or requires long-term rein orcement (hernia repair) or when the consequences o suture ailure are high (blood vessels and heart valves). 2. Disadvantage: nidus or in ection

Chapter 2

Essentials o General Surgery

33

Ta b le 2-1: Typ e s o Suture Ma te ria ls Suture s

Ma te ria l

Monof la m e nt vs . Bra ide d

Ha l -li e

Na tura l vs . Synthe tic

Co m m e nts a nd Typ ic a l Us e s

Ab s o rb a b le s uture s Gut (catgut)

Collagen rom intestine—bee serosa or sheep submucosa

Monof lament

7–10 days

Natural

Originally rom cats; packaged in alcohol, must be kept wet; rarely used

Chromic gut (chromic catgut)

Chromatetanned gut

Monof lament

2 weeks

Natural

Ties well; packaged in alcohol, must be kept wet; less used than in years past

Polyglactin-910 polyglycolic acid

Synthetic polymer

Braided

2–3 weeks

Synthetic

Bo we l, s ub c uta ne o us tissue, ascia

Polydioxanone polyglyconate

Synthetic polymer

Monof lament

4 weeks

Synthetic

Fascia, bowel, biliary, and urina ry tra c t

Poliglecaprone 25

Synthetic polymer

Monof lament

1–2 weeks

Synthetic

Subcuticular skin closure

Natural

Best handling, hemostasis

P e rm a ne nt s uture s Silk

Silk-organic protein, f broin

Braided

20 years

Polyester

Polyester

Braided

Permanent

Synthetic

Heart valves, ascia; known or potential or harboring in ection

Polypropylene

Polypropylene

Monof lament

Permanent

Synthetic

Cardiovascular, hernias, ascia

Nylon

Nylon

1. Monof lament 2. Braided

Permanent

Synthetic

1. Skin 2. Looks and handles like silk

Cotton, linen

Plant derived

Braided

Permanent

Natural

Obsolete due to extent o resulting tissue reaction

Stainless steel

316L stainless

Monof lament

Permanent, can racture a ter years

Synthetic

Sternum, hernias; di f cult to handle, sharp ends

ePTFE*

ePTFE

Porous monof lament

Permanent

Synthetic

Cardiovascular, hernias; has properties o both braided and monof lament

Staples

1. Skin-steel 2. Stapling devices— titanium

Monof lament

Permanent

Synthetic

Skin staples: aster than sutured closures. Stapling devices: used or bowel anastomoses; vascular closures, bronchial closures

*ePTFE, expanded polytetra uoroethylene.

SURGICAL TUBES AND DRAINS Dra ins

Quic k Cut Tubes and drains allow exit o exces s or abnormal body uids , but may clog. In this cas e, low drain output may not repres ent adequate drainage.

I. Typ e s A. Closed drains: Drain connects to the body cavity in closed system. 1. Gravity drains (e.g., Foley): ubes are attached to a reservoir at a lower height. 2. Underwater seal drainage system (e.g., chest tubes): prevents air and uid rom re-entering the body 3. Suction drain (e.g., Jackson-Pratt): Apply suction to evacuate larger volumes o remove dead space.

uid and

34

Chapter 2

Surgical ubes and Drains Abs orba ble

Monofila me nt

P la in a nd chromic gut us e d in pla ce s of infe ction but de gra de e a s ily S ynthe tic type la s ts longe r with le s s tis s ue re a ction.

Nona bs orba ble

Bra ide d

Mos t us e d s uture Minima l dra g a nd e a s y ha ndling Us e d for GI, vis ce ra l, a nd ge ne ra l clos ure (e .g., polygla ctin [Vicryl] a nd polyglycolic)

Us e d in fa s cia , GU, a nd GI s urge rie s (e .g., polydioxa none [P DS ])

Monofila me nt

Bra ide d

S tiffe r a nd ha rde r to us e Us e d in ca rdia c, fa s cia l, a nd he rnia s urge rie s

Le s s fa vore d a s high ris k of infe ction (e .g., s ilk a nd polye s te r)

S ta pling de vice s a ct a s pe rma ne nt monofila me nt; fire multiple rows of tita nium s ta ple s for GI, va s cula r, a nd re s pira tory tra ct No ris k of infe ction a nd a re nonre a ctive a nd pe rma ne nt (e .g., nylon a nd s ta inle s s s te e l)

Fig ure 2-3: Major s uture types by category.

B. Open drains (e.g., Penrose): Open at both ends to allow pus to drain. Quic k Cut C. Sump drains (e.g., nasogastric [NG] tubes): double-lumen Drains are not catheters allowing air and irrigation uid to enter through one s ubs titutes or hemos tas is . lumen while suction is applied to the other lumen II. Co m p lic a tio ns : Drains should be removed once their purpose has been met to minimize complications. A. Colonization: Microorganisms increase the risk o in ection. B. Corrosion: Rigid drains can corrode into nearby organs and vessels. C. Necrosis: Excessive suction can lead to necrosis. D. Retraction: Drains can retract into the body or can be sutured in place internally.

GI Tub e s I. Ga s tro s to m y tub e s : Inserted in the stomach through the skin or eeding purposes or prolonged gastric decompression. T e epithelialized tract orms a er several weeks in place, then closes in 6–24 hours once the tube is removed. II. Se ng s ta ke n-Bla ke m o re /Minne s o ta tub e s : NG tubes with in atable esophageal and gastric balloons to tamponade esophageal variceal bleed III. NG tub e s : can be used or relieving partial small bowel obstruction IV. J e juno s to m y tub e s : provide nutrition to those unable to tolerate gastric eeds V. Re c ta l tub e s : large-caliber tubes inserted through the anus into the rectum or decompression

Ca the te rs

Quic k Cut I. Ce ntra l ve no us c a the te rs : single-, double-, or triple-lumen Central venous tubes placed with their tips in the superior vena cava catheters are generally inserted A. Purpose: Administer uids, pressors, parental nutrition, or into the internal jugular, hemodialysis. subclavian, or emoral vein. B. Complications: in ection leading to bacteremia or pneumothorax 1. Central line–associated bloodstream in ections: 40,000 occur in the United States per year. 2. Minocycline or ri ampin: Central venous catheters coated with either o these agents have been demonstrated to lower bloodstream in ections without contributing to antibiotic resistance.

Chapter 2

Essentials o General Surgery

35

II. Pe riphe ra lly ins e rte d c e ntra l c a the te rs (PICCs ): placed through the antecubital vein into a central vein III. P o rt: similar to a central venous catheter with access under the skin; commonly used or chemotherapy IV. Cu e d c e ntra l ve no us c a the te rs (e .g ., Hic km a n): unnelled catheters used or long-term access or hemodialysis, chemotherapy, and parental nutrition. T e Dacron cu permits ingrowth o granulation tissue to secure the line and act as a mechanical barrier to in ection. V. P e rito ne a l d ia lys is c a the te rs : inserted into the peritoneal cavity or peritoneal dialysis

HERNIAS Ove rvie w I. De f nitio n: Abnormal protrusion o contents through a de ect into a separate body cavity. Most commonly, hernias are present on the abdominal wall. II. Inc id e nc e a nd e tio lo g y: In both men and women, 70% o hernias occur in the inguinal region. A. Congenital de ects: include indirect inguinal hernia B. Loss o tissue strength and elasticity: rom aging or repetitive stress, as in hiatal hernia C. Trauma (especially operative trauma): Normal tissue strength is altered surgically and can lead to the development o hernia. Quic k Cut D. Increased intra-abdominal pressure: contributes to hernia A wound in ection symptoms; may result rom the ollowing: greatly increas es the ris k o s ubs equent incis ional hernia. 1. Heavy li ing 2. Coughing, asthma, and chronic obstructive pulmonary disease (COPD) 3. Bladder outlet obstruction (e.g., benign prostatic hypertrophy) 4. Prior pregnancy 5. Ascites and abdominal distention 6. Obesity III. De s c rip tive te rm s A. Reducible: Hernia contents can be pushed back into their normal position. B. Incarcerated: Hernia contents cannot be reduced. C. Obstructing: Hernia contains bowel that is kinked and obstructs the GI tract. D. Strangulated: issue contained in the hernia is ischemic and will necrose due to blood supply compromise. E. Sliding: Wall o the hernia sac is partly ormed by a retroperitoneal structure, such as the colon or the bladder, rather than being ormed completely by peritoneum. F. Richter hernia: Only one side o the bowel wall is trapped in Quic k Cut the hernia (typically, the antimesenteric side). T e incarcerated A Richter hernia can portion o bowel can necrose and per orate in the absence o per orate without s igns and obstructive symptoms. s ymptoms o obs truction. IV. Co m p lic a tio ns : Hernias should be repaired electively to alleviate symptoms and to prevent the development o major complications. A. Intestinal obstruction B. Intestinal strangulation with bowel per oration

Ing uina l He rnia I. Ana to m y o the ing uina l re g io n: Figures 2-4 and 2-5 A. Internal inguinal ring: opening in the transversalis ascia lateral to the in erior epigastric vessels B. External inguinal ring: opening in the external oblique aponeurosis C. Inguinal canal: communication between the internal and external rings 1. Anterior wall: ormed by the external oblique aponeurosis 2. In erior wall: ormed by the inguinal ligament (Poupart ligament) 3. Roo (superior wall): made up o f bers o the internal oblique and transversus abdominis muscles, orming the conjoint tendon 4. Posterior wall (f oor): ormed by the transversalis ascia a. Hesselbach triangle: located within oor b. Triangle constituents: ormed laterally by the in erior epigastric artery, in eriorly by the inguinal ligament, and superomedially by the lateral border o the rectus sheath

36

Chapter 2

Hernias

Inguina l liga me nt Infe rior e piga s tric ve s s e ls Re ctus s he a th

He s s e lba ch tria ngle

S pe rma tic cord

Conjoint te ndon

Fe mora l s he a th

Fe mora l ve s s e ls

S he lving e dge of inguina l liga me nt P ubic ra mus

Fig ure 2-4: Inguinal anatomy.

5. Round ligament: traverses the inguinal canal in women 6. Spermatic cord structures: Pass through both rings in the inguinal canal and into the scrotum in men. Structures include the ollowing: a. Arteries: testicular and cremasteric b. Veins: pampini orm plexus c. Vas de erens d. Processus vaginalis: evagination o peritoneum that accompanies testicle descent through the abdominal wall Ante rior-s upe rior ilia c s pine Inguina l liga me nt Point of exit of indire ct he rnia Inte rna l ring Infe rior e piga s tric ve s s e ls Point of dire ct he rnia Inguina l ca na l Exte rna l ring

Fe mora l ve s s e ls

P ubis

Fos s a ova le

S pe rma tic cord S a phe nous ve in

Point of fe mora l he rnia

Fig ure 2-5: Sites o inguino emoral hernias .

P ubic ra mus a nd Coope r liga me nt

Chapter 2

e. Nerves: Ilioinguinal and genital branch o the genito emoral nerves are within the inguinal canal but are external to the cremasteric ascia.

Essentials o General Surgery

37

Quic k Cut A patent proces s us vaginalis is a congenital indirect inguinal hernia.

II. Typ e s A. Indirect inguinal hernias: passes rom the peritoneal cavity through the internal inguinal ring (i.e., lateral to the epigastric vessels) 1. Spermatic cord hydrocele: may occur i the processus vaginalis is incompletely obliterated 2. Incidence: Indirect inguinal hernias are the most common type o hernia and are 5 more common than direct hernias. a. Gender: 10 more common in men than in women. At least 5% o men develop an inguinal hernia. b. Age: may occur rom in ancy to old age but generally occur by the f h decade o li e 3. Pediatric inguinal hernia: Almost always indirect and has a high risk o incarceration. It is more common on the right (75%). B. Direct inguinal hernias: occurs through the oor o the inguinal Quic k Cut canal (i.e., through Hesselbach triangle; see Fig. 2-4) because o The in erior an acquired weakness in the tissue epigas tric ves s els are the 1. Site: Direct hernias occur medial to the epigastric vessels anatomic landmarks that and are direct protrusions o abdominal structures into the dis tinguis h indirect rom direct oor o the canal posterior to the spermatic cord. It is not inguinal hernias . contained in the cord as is an indirect hernia. 2. Sac: broadly based de ect; much less o en associated with strangulation than an indirect inguinal hernia 3. Cause: increases in occurrence with age and is related to physical activity C. Recurrent inguinal hernia: Usually recurs as a direct hernia. Most commonly, the de ect occurs in the most medial aspect o the repair o the oor o the inguinal canal. D. Pantaloon hernias: combinations o direct and indirect hernias in which the hernia sac passes both medially and laterally to the epigastric vessels E. Femoral hernias: occurs along the emoral sheath in the emoral canal (see Figs. 2-4 and 2-5) 1. Site: Hernia contents protrude posterior to the inguinal ligament, anterior to the pubic ramus periosteum (i.e., Cooper ligament), and medial to the emoral vein. T e hernia traverses the emoral canal and may also turn cephalad once it has exited the oramen ovale and can cross anteriorly to the inguinal ligament. 2. Sac: Narrow neck; 30%–40% o emoral hernias become incarcerated or strangulated. 3. Cause: more common in women than in men and are associated with emale gender, prior pregnancy, and prior inguinal hernia repair III. Dia g no s is : based on history and physical examination A. History: May include the appearance o a lump in the groin. T e mass may be intermittently present and may be pain ul. Its appearance is o en associated with activity. B. Physical examination: Done with the patient in both supine and standing positions; mass may be visible, and its size and visibility may depend on the patient’s position. T e mass may be tender or may be reducible with gentle pressure. C. Di erential diagnosis: includes hydrocele, varix (especially i thrombosed), lymphadenopathy, lipoma o the spermatic cord, undescended testicle, abscess, or tumor IV. Re p a ir: Surgery is the only curative procedure or inguinal hernias. Most patients develop symptoms, so routine repair is recommended or even minimally symptomatic patients. A. Indirect inguinal hernia: Repair involves returning hernia contents into the peritoneal cavity. 1. Division and/or ligation o the base o the hernia sac at the level o the peritoneal cavity: Sac is always anteromedial to the cord at the level o the internal ring. 2. In adults: o prevent recurrence, the internal inguinal ring must be tightened in addition to repair o any de ect o the oor o the inguinal canal. B. Direct inguinal hernia: Repair is based on rein orcement o the inguinal canal oor a er invaginating the hernia sac. C. Femoral hernia: Repair involves approaching the emoral sheath through the oor o the inguinal canal. T e space is usually closed by apposing the posterior re ection o the inguinal ligament to Cooper ligament (Cooper ligament repair).

38

Chapter 2

Hernias

D. Inguinal canal f oor: Repair can be done with many techniques. wo classic techniques used less commonly now are described f rst, and then two newer techniques are described. 1. Bassini repair: ransversalis ascia and conjoint tendon above are sutured to the re ection o the inguinal ligament (i.e., the shelving edge o Poupart ligament) below. a. In men: Spermatic cord is returned to its normal anatomic location between the rein orced inguinal canal oor and the external oblique aponeurosis. b. In women: Round ligament may be ligated and the internal ring closed. 2. Cooper ligament repair (McVay method): similar to the Bassini repair except that the transversalis ascia and conjoint Quic k Cut tendon are sutured to Cooper ligament Cooper ligament is a. Relaxing incision: Because Cooper ligament is more a portion o the perios teum o posterior than the inguinal ligament and subjects the the pubic ramus . repair to increased tension, this counterincision is o en made superiorly and allows the conjoint tendon to be sutured to Cooper ligament with less tension. b. Disadvantage: ension is the problem with this technique, causing both postoperative pain and early and late recurrences. 3. Shouldice repair: Uses the transversalis ascia, which is divided longitudinally and imbricated upon itsel in two layers. T e internal oblique muscle and conjoint tendon are then sutured to the re ection o the inguinal ligament in two layers. 4. Prosthetic mesh repairs (Lichtenstein repairs): have supplanted other techniques a. Procedure: involves repairing the inguinal oor by using mesh to close the space, suturing it (as in a Bassini repair) to the transversalis ascia and conjoint tendon above and to the re ection o the inguinal ligament below b. Open and laparoscopic techniques: Used to place Quic k Cut polypropylene mesh to rein orce the weakened transversalis Pros thetic mes h ascia. Open techniques also place mesh into the de ect. repairs can be accomplis hed 1. Indirect hernias: Cone-shaped polypropylene mesh by an open or a laparos copic may be placed adjacent to (anteromedial to) the approach. spermatic cord. 2. Direct hernias: Cone-shaped mesh is used to “plug” the transversalis ascia de ect. V. Re c urre nc e ra te s : Vary depending on the type o hernia; generally, inguinal hernias recur in less than 10% o cases. T is f gure is usually higher or hernias at other sites. VI. Sp e c ia l s itua tio ns A. Strangulation or necrosis o the incarcerated bowel: I the bowel returns to the peritoneal cavity spontaneously be ore visual examination, the abdomen is usually opened to resect any necrotic bowel. B. Recurrent hernias or hernias with large de ects: may require the insertion o prosthetic material such as polypropylene mesh to repair the abdominal wall de ect adequately C. Pediatrics: Simple high ligation o the hernia sac is used or hernias in this age group. No oor repair is needed. D. Truss: device that exerts external compression over the hernia de ect; used only when surgery cannot be sa ely per ormed or when the patient re uses surgery

Ab d o m ina l Wa ll He rnia s I. Um b ilic a l he rnia s : occur through the de ect where the umbilical structures passed through the abdominal wall A. Incidence: Occur 10 more o en in women than in men. T e Quic k Cut de ect is common in children but usually closes by age 2 years, In adults , umbilical and less than 5% persist into later childhood and adult li e. hernias are o ten as s ociated B. Repair: with small umbilical hernias, consists o a simple with increas ed intratransverse repair o the ascial de ect abdominal pres s ure as with as cites or pregnancy. II. Ep ig a s tric he rnia s (e p ip lo c e le s ): result rom a de ect in the linea alba above the umbilicus A. Incidence: Occur more commonly in men (3:1 ratio); 20% are multiple at the time o repair. B. Repair (simple suturing): associated with a recurrence rate as high as 10%

Chapter 2

Essentials o General Surgery

39

III. Ve ntra l he rnia s : occur in the abdominal wall in areas other than the inguinal region A. Incisional hernia: most common type o ventral hernia; results rom poor wound healing in a previous surgical incision and occurs in up to 20% o abdominal incisions 1. Common causes: include wound in ection, advanced age, obesity, general debilitation or malnutrition, improper surgical technique, or a postoperative increase in abdominal pressure (ascites or pulmonary complications) 2. Repair: Per ormed a er the patient has recovered rom the prior surgical trauma. Requires def nition o the adequate ascial edges surrounding the de ect, closure with nonabsorbable sutures, and use o prosthetic mesh (polypropylene or eP FE) when the de ect is too large to be closed primarily. B. Spigelian hernias: protrude through the abdominal wall along Quic k Cut the semilunar line (the lateral edge o the rectus muscle) at the Spigelian hernias are semicircular line o Douglas (below the umbilicus) lateral epigas tric hernias that C. Obturator hernias: occur in the pelvis through the obturator may be di f cult to diagnos e. oramen and can cause pain along the obturator nerve (midanterior thigh), re erred to as Howship-Romberg sign D. Lumbar hernias: occur on the ank and are seen in the superior (Gryn eltt) and in erior (Petit) triangles E. Perineal hernias: occur in the pelvic oor usually a er surgical procedures such as an abdominoperineal resection F. Peristomal hernias: develop adjacent to an intestinal ostomy

P OSTOP ERATIVE COMP LICATIONS P o s to p e ra tive Fe ve r I. “5 W’s ”: use ul mnemonic or common causes o postoperative ever Quic k Cut A. Wind: Pulmonary complications occur on postoperative days Remember the 1–3, usually as a result o incisional pain, shallow breathing, and 5 “W’s ” or pos toperative depressed cough rom narcotics. ever. 1. Atelectasis: Due to peripheral collapse o alveoli. reated with pulmonary toilet (i.e., deep breathing, early ambulation, and incentive spirometer) to recruit most o the alveoli. More severe cases may need bronchoscopy to remove a mucus plug. 2. Pneumonia: presents as ever, cough, leukocytosis, and pulmonary inf ltrate on chest x-ray B. Water: Urinary tract in ections occur on postoperative days 3–5 due to urinary catheterization; aided by early postoperative removal o catheters. C. Wound in ections: Usually cause ever postoperative days 3–7. More virulent orms (streptococcal or Clostridium in ections) cause necrotizing in ection earlier. D. Walk: Deep venous thrombosis (DV ) usually occurs in the lower extremities and can cause ever at any postoperative point. Immobilization and hypercoagulable state associated with surgery can increase the risk o thrombosis. Complications o DV can include pulmonary emboli with associated tachycardia, tachypnea, and hypoxemia. E. Wonder drugs: Any drug can cause “drug ever,” especially antibiotics, which are o en used empirically. II. Othe rs : Less common causes include anastomotic leak a er bowel surgery, sinusitis, pancreatitis, pseudomembranous colitis, postpericardiotomy syndrome (5–7 days postoperatively), and perirectal abscess.

Myo c a rd ia l In a rc tio n (MI) I. P e rio p e ra tive MI: o en non–S -segment elevation MI (NS EMI) II. Sym ptom s : presents as shortness o breath, chest pain, or arrhythmias III. Tre a tm e nt: Mortality rom perioperative MI is 30%; there ore, suspicion requires electrocardiography (ECG), troponins, telemetry, and early management.

Quic k Cut Arrhythmias , es pecially atrial f brillation, are common a ter s urgery due to changes in electrolytes or volume s tatus .

Fluid Sta tus I. Hyp o vo le m ia : common early a er surgery due to third-space uid sequestration II. Sym p to m s : presents as tachycardia, hypotension, and oliguria

40

Chapter 2

Surgical In ections

III. Tre a tm e nt: hydration IV. Ove rhyd ra tio n: On postoperative days 3–4, the body begins to mobilize this uid intravascularly with high renal output, causing congestive heart ailure, tachyarrhythmias, or pulmonary congestion with impaired oxygenation requiring urther diuresis.

SURGICAL INFECTIONS Surg ic a l Site In e c tio n I. De f nitio n: in ection present in any location along the surgical tract II. Co m m o n o rg a nis m s : Staphylococcus aureus most common in ection overall A. Escherichia coli: most common gram-negative rod B. Bacteroides fragilis: most common anaerobe III. Fe a ture s : ever on postoperative days 5–8 with local tenderness, cellulitis, drainage, and wound dehiscence IV. Tre a tm e nt: Superf cial in ections need incision and drainage; deeper wound in ections or necrosis need operative debridement and antibiotics. V. P ro p hyla c tic a ntib io tic s : Given preoperatively to combat Quic k Cut bacterial contamination o tissue during operative period. Follow Prophylactic these general rules. antibiotics are bes t given A. Signi cant risk or postoperative in ection exists. s hortly be ore incis ion in the B. Discontinue a er surgery (usually be ore 1 day). operating room. C. Antibiotics e ective against the pathogens most likely present. D. Bene ts should outweigh risks o allergy or superin ection.

Te ta nus Inje c tio n I. Ac tive im m uniza tio n: etanus toxoid injections provide protective titers in 30 days; given in in ancy with boosters every 10 years. II. P ro p hyla xis : any person with penetrating injury Quic k Cut A. Unknown tetanus status: must receive tetanus immunization All patients with B. I more than 5 years since last immunization: must receive a booster penetrating trauma s hould C. Contaminated wounds without immunization: require both have tetanus prophylaxis . tetanus toxoid and passive immunity with tetanus immune globulin (protective or 1 month) III. De vita lize d tis s ue : must be debrided IV. Antib io tic s : High doses o penicillin are administered prophylactically with extensive necrosis or suspected Clostridium tetani in ection.

Ab s c e s s e s I. Cuta ne o us a b s c e s s A. Furuncle (boil): cutaneous staphylococcal abscess associated with acne and skin disorders B. Carbuncle: spreads through the dermis into subcutaneous tissues; common with diabetes C. Hidradenitis suppurativa: In ections o the apocrine sweat glands in the groin and axilla that occur as chronic recurrent abscesses and are o en caused by staphylococci. reatment includes drainage, antibiotics, and excision o the involved area containing multiple abscesses or sinus tracts. II. Intra -a b d o m ina l a b s c e s s e s : Most common sites are the subphrenic and subhepatic spaces, pelvis, and periappendiceal and pericolonic areas. A. External: caused by penetrating trauma or surgical procedure B. Internal: caused by a per orated viscus (e.g., appendix) or bacterial seeding (e.g., tubo-ovarian abscess) C. Clinical eatures: ever, pain, leukocytosis, tachycardia, and sepsis D. Diagnosis: Needs high clinical suspicion. Computed tomography (C ) or ultrasound can conf rm diagnosis. E. Treatment: Mainstay is drainage. 1. Unilocular abscess: can be drained percutaneously 2. Multilocular abscess: Complex or necrotic debris may require surgical drainage.

Chapter 2

Essentials o General Surgery

41

Ce llulitis I. De f nition: in ammation o the dermal and subcutaneous tissue due to nonsuppurative bacterial invasion II. Clinic a l e a ture s : Produces erythema, edema, and tenderness. May invade the lymphatics, causing red tender streaks (lymphangitis). III. Tre a tm e nt: antibiotics, usually penicillin because Streptococcus is usually the causative organism

Ne c ro tizing Fa s c iitis I. De f nitio n: In ection introduced through a puncture wound or surgical incision that has a rapidly progressive measurable mortality rate. Pathologically, it invades through ascial planes, causing vascular thrombosis and tissue necrosis. II. Clinic a l e a ture s : Patient becomes toxic with ever and tachycardia. Quic k Cut Treat cellulitis with A. Overlying skin: may appear normal or may have hemorrhagic antibiotics and abs ces s bullae with edema and crepitus with drainage. I there is B. Discharge: oul smelling i present no res pons e to antibiotics , C. Tests: Plain x-ray or C scan reveals air in the so tissue. s us pect an underlying abs ces s . III. Ca us e : multiple organisms; microaerophilic beta-hemolytic streptococci, staphylococci, or aerobes and anaerobes IV. Tre a tm e nt: aggressive surgical debridement o all devitalized tissue and high-dose antibiotics

Clo s trid ium Myo s itis a nd Ga s Ga ng re ne I. Clos trid iu m p e rfrin g e n s : causative agent; anaerobic, gram-positive bacilli secreting alphalecithinase toxin II. Wo und c ha ra c te ris tic s : T e ollowing make wounds susceptible to this in ection: A. Extensive necrosis: creates a redox potential or the anaerobe B. Impaired blood f ow to the area: as in vascular thrombosis C. Gross contamination D. Immunocompromise: as in diabetes or patients on steroid therapy III. Clinic a l e a ture s : can occur as early as 6 hours a er injury A. Presentation: severe pain (out o proportion to exam), weakened pulse, diaphoresis, tenderness to touch, and crepitus B. Tests: Falling hematocrit and rising bilirubin rom hemolysis. Gram-positive bacilli with spores without white blood cells in drainage and air in so tissue on x-ray. III. Tre a tm e nt: Extensive debridement o tissue; delay is usually catastrophic.

GASTROINTESTINAL FISTULA I. De f nitio n: Abnormal communication between two or more hollow organs or between a hollow organ and the body sur ace. Named according to the sites they connect (e.g., enterocutaneous f stula connects the small bowel and skin). II. Ca us e s A. Congenital: as in tracheoesophageal f stula B. Operative: as in anastomotic breakdown C. Inf ammation: as in Crohn disease D. Malignancy: in which tumor destroys tissue (e.g., sigmoid cancer invades into the bladder) E. Radiation III. Eva lua tio n a nd m a na g e m e nt: Determine cause (e.g., diverticulitis or cancer) and volume o drainage (low output has higher rate o closure) and examine to determine location. A. Fluid and electrolyte disturbances: Correct electrolyte losses. 1. Stomach: Output is rich in H and Cl , causing hypokalemic metabolic alkalosis; replace with D5 ½ normal saline with K .

Quic k Cut To remember caus es or nonhealing f s tulae, us e the mnemonic FRIENDS: Foreign body, Radiation, In ammation, Epithelialization, Neoplas m, Dis tal obs truction, and Seps is /in ection.

Quic k Cut Upper GI tract f s tulas produce higher output than lower GI tract f s tulas .

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Chapter 2

Gastrointestinal Fistula

2. Pancreatic/biliary: High bicarbonate content; can cause dehydration and metabolic acidosis. Replace with lactated Ringer with HCO3 . 3. Small intestine: Drainage is rich in K and bicarbonate; replace with lactated Ringer with HCO3 . 4. Large intestines: Higher potassium loss. Replace with lactated Ringer with K . B. In ection/sepsis: Organ leak contaminates sterile spaces, causing abscess/peritonitis. 1. CT/magnetic resonance imaging (MRI): can determine undrained abscesses associated with the f stula i persistent ever 2. Healing: requires appropriate antibiotic and drainage C. Malnutrition: High caloric needs during in ection and either loss o nutrition or poor absorption require early advent o total parental nutrition ( PN). D. Inhibit organ secretion: Use H 2 blockers or the stomach and octreotide with the pancreas. E. Skin care: Output can cause skin excoriation; drains, collection bags, or surgical diversion are necessary to protect the skin. F. Nonoperative management: Bowel rest, PN, and minimizing drainage can allow f stula to heal in 1–2 months. G. Operative repair: I nonhealing, then operative repair can be Quic k Cut per ormed in a nonseptic, well-nourished patient. GI f s tulas may 1. Fistulogram: First, determine anatomy and exclude distal res ult rom trauma or s urgery, obstruction with contrast by mouth, rectum, or into the in ammation, malignancy, f stula. or radiation. The main 2. Resection: With current management, the f stula tract and complications rom thes e f s tulas are in ectious and a ected bowel are resected with anastomosis to restore bowel nutritional. continuity. 3. Mortality: Current management has lowered the mortality rate to 5%–15%. H. Sepsis prevention: Enteric and colonic f stulas are complications a er trauma, surgery, diverticulitis, cancer, in ammatory bowel disease, and radiation warranting a mortality rate o 6%–33% mostly due to sepsis. Initial management depends on hydration, nutritional support, and octreotide to decrease output and drainage o abscesses, with repair o 25%–75% o f stulas at 3 months.

Chapter 3

Medical Risk Factors in Surgical Patients Susan B. Kesmodel, Natalia Kubicki, and Mayur Narayan

GENERAL ASP ECTS FOR EVALUATION AND MANAGEMENT OF THE SURGICAL PATIENT As s e s s m e nt o Me d ic a l Co m o rb id itie s a nd Ris k Fa c to rs I. P re o p e ra tive e va lua tio n: f rst step in ensuring success ul surgical outcomes A. Short-term risk: perioperative period including intraoperative and up to 48 hours postoperative B. Long-term risk: up to 30 days postoperative

Quic k Cut In mos t cas es when patients are undergoing elective, noncardiac procedures , minimal preoperative tes ting is neces s ary.

II. Co m p re he ns ive his to ry a nd p hys ic a l e xa m : to identi y existing medical problems and other risk actors that may impact surgical outcomes A. Medical history: Focus on underlying medical conditions, prior di culties with anesthesia, and the ollowing: 1. Medications: current prescriptions, over-the-counter, alternative medications and supplements, and allergies to medications 2. Physiologic parameters: including volume and nutritional status, and presence o in ection 3. Substance abuse: history o tobacco, excessive alcohol use, and drug use 4. Familial disorders: bleeding disorders or problems with anesthesia B. Physical exam: include evaluation o the ollowing: 1. Cardiac unction: heart rate, irregular heart rhythm, heart murmur, lower extremity (LE) edema, jugular venous distention 2. Pulmonary unction: accessory muscle use, cyanosis, chest wall de ormity, abnormalities on auscultation 3. Volume status/renal unction: blood pressure (BP), skin turgor, mucous membrane moistness, presence o dialysis access, edema 4. Hepatic unction: jaundice, ascites, hepatomegaly, muscle wasting, spider angiomata, telangiectasias 5. Nutritional status: body mass index, temporal wasting 6. Coagulation disorders: petechiae, ecchymoses, thromboses

43

44

Chapter 3

General Aspects or Evaluation and Management o the Surgical Patient

P re o p e ra tive Te s ting I. Re c o m m e nd a tio ns o r p re o p e ra tive te s ting : Ultimately it is the surgeon who must decide on the extent o testing based on the preoperative assessment o the patient and the expected risks o the surgery. Guidelines are listed in able 3-1. A. Elective surgery: Routine preoperative testing should be per ormed selectively in these patients based on history; although elderly patients have a higher incidence o abnormal laboratory values, routine testing based on age alone may not impact outcome. B. Emergency surgery: Goal o testing is to identi y pre-existing medical conditions and acute organ dys unction that may impact surgical outcome so that these problems can be monitored during the perioperative period. Most patients will have laboratory and noninvasive testing that includes a complete blood count (CBC), comprehensive medical panel, coagulation prof le, electrocardiogram (ECG), and chest x-ray. C. ype o surgery: Also in uences extent o preoperative testing; patients undergoing more complicated surgical procedures, where greater uid shi s and blood loss are expected, will require a more comprehensive assessment. Severity o surgical procedures stratif ed by the risk o cardiac complications is shown in able 3-2.

Quic k Cut Routine preoperative tes ting or elective s urgery is not as s ociated with a decreas e in s urgical complications . Only American Society o Anes thes iologis ts (ASA) clas s if cation and type o s urgical procedure were independent predictors o pos toperative complications .

Quic k Cut Operative morbidity and mortality is increas ed in patients undergoing emergency s urgery. I time permits , electrolyte abnormalities , hypovolemia, acid–bas e dis orders , and coagulopathy s hould be corrected preoperatively.

Ta b le 3-1: Ge ne ra l Guid e line s o r P re o p e ra tive Te s ting in the Surg ic a l P a tie nt Complete blood count

• History o chronic kidney disease, liver disease, cardiovascular disease, hematologic disorders, and malignancy • History o anemia or bleeding disorders • Patients undergoing cardiovascular surgery or other high-risk surgical procedures • Patients undergoing intermediate-risk surgical procedures with comorbid conditions • History o malignancy • Pregnant patients • Extremes o age

Basic metabolic panel (electrolytes, creatinine, glucose)

• • • •

History o chronic kidney disease, liver disease, endocrine disorders, and diabetes Use o medications associated with electrolyte abnormalities Patients undergoing cardiovascular or other high-risk surgery Patients undergoing intermediate or high-risk surgical procedures with comorbid conditions

Coagulation parameters

• • • •

History o chronic kidney disease, liver disease, cardiovascular disease, and pulmonary disease History o a bleeding disorder Patients taking anticoagulants Patients undergoing high-risk surgical procedures

Liver unction tests

• History o liver disease • History o malignancy

Electrocardiogram

• Patients with a history o cardiovascular disease or risk actors or cardiovascular disease who are undergoing intermediate or high-risk surgical procedures • Patients with no risk actors undergoing high-risk surgery

Chest radiograph

• • • • • •

Urinalysis

• New urinary symptoms • Urologic procedures • Implantation o oreign material

History o chronic obstructive pulmonary disease, asthma, or cardiac disease Recent upper respiratory in ection Abnormal history and physical examination f ndings Patients undergoing cardiovascular or thoracic surgery Patient age older than 50 years undergoing upper abdominal surgery Consider or patients who are smokers

Chapter 3

Medical Risk Factors in Surgical Patients

45

Ta b le 3-2: Stra tif c a tio n o No nc a rd ia c Surg ic a l P ro c e d ure s b y Ca rd ia c Ris k Low risk ( 1%)

Breast and other so t tissue, dental, endocrine, eye, gynecologic, minor orthopedic or urologic, plastic surgery

Intermediate risk (1%–5%)

Intraperitoneal, intrathoracic, carotid and endovascular aneurysm repair, head and neck, neurologic, major orthopedic

High risk ( 5%)

Aortic and other major vascular procedures

II. ASA c la s s if c a tio n: ASA physical status classif cation used to Quic k Cut assess the degree o systemic illness in patients prior to surgery is Increasing ASA score shown in able 3-3. correlates with postoperative III. In e c tio n c o ntro l: Surgical site in ections are one o the most morbidity and mortality as well as a longer duration o surgery, common postoperative complications; however, use o antibiotics increas ed intraoperative blood in the perioperative setting has been shown to decrease their loss, longer requirement or incidence. postoperative ventilatory A. Dosing: One preoperative dose is su cient or most cases and support, and longer hospital should be dosed within 60 minutes o the surgical procedure admiss ion. except or vancomycin, which should be dosed 60–120 minutes prior to surgery. B. Choice: should target the most likely pathogens based on the Quic k Cut surgical site Antibiotic us e C. Duration: Prolonged duration o antibiotic use is discouraged. s hould not exceed 24 hours or mos t s urgical procedures . D. Redosing: should be based on the hal -li e o the drug, duration o the surgical procedure, and degree o blood loss IV. Ve no us thro m b o e m b o lis m (VTE): one o the most common Quic k Cut complications ollowing surgery Pulmonary A. Risk actors: include advanced age; prolonged immobility; embolis m is the mos t malignancy; history o V E; ractures o the pelvis, hip, or LE; common caus e o preventable type o surgery; major trauma; obesity; stroke; and myocardial death a ter s urgical in arction (MI) procedures . B. Preoperative prophylaxis: Guidelines are based on severity o the surgery and patient comorbidities ( able 3-4). 1. High-risk patients: Low-dose un ractionated heparin (LDUH) or low-molecular-weight heparin (LMWH) should be started preoperatively; otherwise, initiate as early in the postoperative period as possible. a. Graduated compression stockings (GCS) and intermittent pneumatic compression (ICP): start preoperatively to decrease venous stasis, improve blood ow velocity, and increase f brolytic activity b. Postoperative: Early ambulation in this period is essential. c. High-risk orthopedic procedures: Consider extending prophylaxis or 30 days a er surgery.

Ta b le 3-3: Am e ric a n So c ie ty o Ane s the s io lo g is ts P hys ic a l Sta tus Cla s s if c a tio n Cla s s

De s c rip tio n

I

Healthy patient

II

Mild systemic disease with no unctional limitation

III

Severe systemic disease with def nite unctional limitation

IV

Severe systemic disease that is a constant threat to li e

V

Moribund patient unlikely to survive 24 hours with or without operation

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Chapter 3

Evaluation o the Surgical Patient with Cardiac Disease

Ta b le 3-4: Guid e line s o r Ve no us Thro m b o e m b o lis m P re ve ntio n in P a tie nts Und e rg o ing Surg e ry Le ve l o Ris k

P re ve ntio n Stra te g y

Lo w ris k Minor surgery in patients younger than age 40 years with no risk actors

Early mobilization

Mo d e ra te ris k Minor surgery with risk actors Surgery in patients age 40–60 years with no risk actors

LDUH every 12 hours, LMWH

3,400 units daily, GCS, or IPC

Hig h ris k Surgery in patients older than age 60 years Surgery in patients age 40–60 years with risk actors

LDUH every 8 hours, LMWH

3,400 units daily, or IPC

Hig he s t ris k Surgery in patients with multiple risk actors Hip or knee arthroplasty or hip racture Major trauma or spinal cord injury

LMWH 3,400 units daily, ondaparinux, oral vitamin K antagonists, or GCS/IPC and LDUH/LMWH

LDUH, low-dose un ractionated heparin; LMWH, low-molecular-weight heparin; GCS, graduated compression stockings; IPC, intermittent pneumatic compression. Adapted rom Guyatt GH, Akl EA, Crowther M, et al; American College o Chest Physicians Antithrombotic Therapy and Prevention o Thrombosis Panel. Antithrombotic therapy and prevention o thrombosis: American College o Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141(2)(Suppl):7S–47S.

2. Patients with recent V E events: I anticoagulation must be discontinued or an extended period, placement o an in erior vena cava (IVC) f lter should be considered; major indications or IVC f lter placement include the ollowing: a. Patients who are re ractory to medical anticoagulation and develop V E while on medical therapy Quic k Cut b. Patients who develop complications o anticoagulation IVC f lter placement is us ed in patients who such as bleeding and thrombocytopenia cannot or s hould not be c. Contraindication to anticoagulation such as recent traumatic anticoagulated. brain injury or recent major abdominal hemorrhage d. Free- oating thrombus in the ileo emoral region at increased risk o dislodging and leading to V E

EVALUATION OF THE SURGICAL PATIENT WITH CARDIAC DISEASE Ge ne ra l As p e c ts

Quic k Cut I. Ris k a s s e s s m e nt: Extensive research has ocused on Perioperative preoperative assessment o cardiac risk and prevention o cardiac mortality remains the postoperative complications. Postoperative MI is associated with leading caus e o death a ter hospital mortality rates o 15%–25%. anes thes ia and s urgery. II. P rim a ry g o a l: Identi y comorbid conditions that may adversely impact operative outcomes and attempt to optimize or correct these conditions preoperatively.

As s e s s m e nt o Ca rd ia c Dis e a s e a nd Ris k Fa c to rs o r Ca rd ia c Dis e a s e I. P a s t m e d ic a l his to ry: should ocus on history o cardiac disease, cardiac interventions, and other medical conditions that are risk actors or the development o cardiovascular disease A. Presence o comorbid conditions: Diabetes mellitus (DM), pulmonary disease, and chronic kidney disease (CKD) may increase the risk o perioperative cardiac complications. B. Other: Obtain complete list o current medications and assess unctional status.

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Medical Risk Factors in Surgical Patients

47

II. Phys ic a l e xa m ina tion: Assess body habitus, jugular venous distention, LE edema, cyanosis, surgical scars, and presence o indwelling pacemakers or automatic implantable cardioverter-def brillators (AICDs). A. Vital signs: including BP in both arms B. Auscultation o heart sounds: Evaluate or rhythm, murmurs, or other signs o cardiac dys unction. C. Peripheral pulses: Presence o peripheral vascular disease (PVD) may indicate coronary artery disease (CAD) even in the asymptomatic patient. III. Ca rd ia c his to ry A. Hypertension (H N): Mild (stage 1) or moderate (stage 2; Quic k Cut systolic blood pressure [SBP] 180 mm Hg and diastolic blood In patients with mild pressure [DBP] 110 mm Hg) is not an independent risk actor, to moderate HTN, elective but stage 3 (SBP 180 mm Hg and DBP 110 mm Hg) is a risk s urgery does not need to be actor or the development o cardiac complications. delayed or BP control. B. Angina: able 3-5 shows the Canadian Cardiovascular Society angina classif cation system based on the degree o symptoms with physical activity; patients with class III or class IV angina have an increased risk o cardiac complications during surgery. C. Valvular heart disease: Critical aortic stenosis is associated with increased risk o perioperative cardiac complications; these patients cannot increase cardiac output because o out ow obstruction. 1. Aortic or mitral regurgitation: Operative risk is related to the status o le ventricular unction. 2. Prosthetic heart valves: Patients are at risk or valve thrombosis and thromboembolic complications. D. Congestive heart ailure (CHF): increases risk o pulmonary edema E. Pacemakers and AICDs: may be a ected intraoperatively by electrocautery devices IV. ECG ind ic a tio ns : chest pain, history o CAD, CHF, DM, H N, PVD, morbid obesity, valvular heart disease, and exercise intolerance A. Exclusions: ECG is not routinely needed in minimal-risk procedures and in patients aged younger than 65 years. B. iming: ECG within 1 year is adequate or most patients and most surgical procedures; however, in patients with CAD, an ECG should be obtained within 30 days or ollowing the last episode o cardiovascular symptoms i within 1 year. C. Abnormal f ndings: evidence o prior MI, bundle branch block (BBB), bi ascicular block, atrioventricular (AV) block, prolonged Q , right ventricular hypertrophy, arrhythmia

P re o p e ra tive Ris k As s e s s m e nt Stra tif c a tio n To o ls I. Am e ric a n Co lle g e o Ca rd io lo g y/Am e ric a n He a rt As s o c ia tio n: Patients undergoing noncardiac procedures are stratif ed into three groups based on risk o developing cardiac complications: low risk ( 1%), intermediate risk (1%–5%), and high risk (5%). II. Go ld m a n Ris k Ind e x (Orig ina l Ca rdia c Ris k Ind e x): identif ed perioperative atal and non atal cardiac events; divides patients into our risk classes based on points obtained rom history, physical exam, preoperative testing, and type o operation ( able 3-6)

Quic k Cut Multiple tools predict perioperative cardiac ris k and help sugges t the need or preoperative tes ting. They rely on clinical ris k actors , unctional capacity, and procedure-s pecif c actors .

Ta b le 3-5: Ca na d ia n Ca rd io va s c ula r So c ie ty Cla s s if c a tio n o Ang ina Cla s s

De s c rip tio n

0

Asymptomatic

I

Angina only during strenuous or prolonged physical activity

II

Slight limitation, angina only during vigorous physical activity

III

Moderate limitation, symptoms with activities o daily living

IV

Severe limitation, inability to per orm activity without angina or angina at rest

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Chapter 3

Evaluation o the Surgical Patient with Cardiac Disease

Ta b le 3-6: Go ld m a n Ris k Ind e x Ris k Fa c to r

P o ints

Active heart ailure: preoperative third heart sound or jugular venous distention

11

Myocardial in arction in the past 6 months

10 7

5 premature ventricular complexes/min be ore surgery Rhythm other than sinus

7

Age older than 70 years

5

Emergency surgery

4

Signif cant aortic stenosis

3

Intraperitoneal, intrathoracic, or aortic surgery

3

Markers o poor general medical condition (e.g., renal dys unction, liver disease, lung disease, electrolyte imbalance)

3

From Goldman L, Caldera DL, Nussbaum SR, et al. Multi actorial index o cardiac risk in noncardiac surgical procedures. New Engl J Med. 1977; 297(16):845–850.

III. Re vis e d Ca rd ia c Ris k Ind e x (m o d if e d ro m the Orig ina l Ca rd ia c Ris k Ind e x): assigns predictors o cardiac complications rom history and type o surgery A. History: ischemic heart disease, CHF, cerebrovascular disease (stroke or transient ischemic attack), diabetes requiring insulin use, or CKD (creatinine 2 mg/dL) B. ype o surgery: suprainguinal vascular, intraperitoneal, or intrathoracic C. Risk or cardiac death, non atal MI, and non atal cardiac arrest: based on number o predictors 1. 0 predictor: 0.4% 2. 1 predictor: 0.9% 3. 2 predictors: 6.6% 4. Greater than 3 predictors: greater than 11% IV. Ne w Yo rk He a rt As s o c ia tio n (NYHA): unctional classif cation A. Class I: Patients with cardiac disease without physical activity limitations; ordinary physical activity does not cause undue atigue, palpitations, or dyspnea. B. Class II: Patients with cardiac disease that slightly limits physical activity but who are com ortable at rest; ordinary physical activity results in atigue, palpitations, or dyspnea. C. Class III: Patients with cardiac disease resulting in marked limitation o physical activity but who are com ortable at rest; less than ordinary activity causes atigue, palpitations, or dyspnea. D. Class IV: Patients with cardiac disease who cannot do any physical activity without discom ort; symptoms are present even at rest or with minimal exertion.

Ad d itio na l No ninva s ive a nd Inva s ive Ca rd ia c Te s ting I. Ec ho c a rd io g ra m : may be considered in patients with prior abnormal ECG f ndings, known history o CAD or CHF, dyspnea with unknown cause, and to evaluate le ventricular unction II. No ninva s ive m yo c a rd ia l p e r us io n a s s e s s m e nt: indicated or patients with a unctional capacity less than 4 metabolic equivalents o exercise (ME s) or unknown capacity (e.g., unable to climb a ight o stairs) and or patients with moderate unctional capacity undergoing high-risk surgery III. Exe rc is e s tre s s te s ting : measures unctional capacity to identi y the presence o cardiac arrhythmias or myocardial ischemia and estimates perioperative cardiac risk and long-term prognosis

Quic k Cut Noninvas ive myocardial per us ion as s es s ment is not recommended or patients undergoing intermediateris k s urgical operations with no clinical ris k actors or or patients undergoing low-ris k s urgical procedures .

Chapter 3

Medical Risk Factors in Surgical Patients

IV. No ninva s ive s tre s s te s ting : includes radionuclide myocardial imaging, stress echocardiography, and dobutamine echocardiography A. Perioperative cardiac risk: directly related to extent o jeopardized myocardium identif ed B. Patients with unstable myocardial ischemia: Per orm coronary angiography or stabilize with aggressive medical treatment rather than stress testing.

49

Quic k Cut Noninvas ive s tres s tes ting can predict perioperative cardiac events in patients s cheduled or noncardiac s urgery who are unable to exercis e.

P e rio p e ra tive Ma na g e m e nt a nd Ap p ro a c he s to Ris k Re d uc tio n I. Mo d if a b le ris k a c to rs : For elective surgical procedures, health and li estyle modif cations should be implemented preoperatively. A. Health management: Control BP, cholesterol, and DM and use antiplatelet agents or anticoagulation. B. Li estyle modif cation: aerobic exercise greater than 150 minutes per week, smoking cessation, weight loss, and diet modif cation II. P e rio p e ra tive b e ta -b lo c ke r the ra p y: Beta-blockers are e ective in preventing severe BP uctuations and can reduce the number and duration o perioperative coronary ischemic episodes. A. Indications: patients who are already on beta-blockers, particularly those with history o arrhythmia or MI and patients Quic k Cut undergoing intermediate-risk surgery with clinical risk actors Many patients are or ischemic heart disease candidates or perioperative B. Initiation: I beta-blockers are indicated, they should be started beta blockade. at least 2 weeks be ore elective surgery. C. itration: should be titrated to a heart rate o 60–80 beats per minute in the absence o hypotension and should be tapered o slowly to minimize risk o withdrawal III. P e rio p e ra tive a lp ha -a d re ne rg ic a g o nis ts : used as anesthetic adjuvants and analgesics A. Primary e ect: sympatholytic, reducing peripheral norepinephrine release B. Advantages: reduce requirement or intravenous (IV) or inhaled anesthetics and has been shown to decrease MI and perioperative mortality rates in patients undergoing vascular Quic k Cut surgery Traditionally, -adrenergic agonists were C. Clonidine: selective agonist or alpha2-adrenoreceptors used only as anti-hypertensives. 1. Oral antihypertensive e ects: result rom central and Now, their use is increasing peripheral attenuation o sympathetic out ow or sedative, anxiolytic and 2. Withdrawal: May precipitate hypertensive crises; labetalol analgesic e ects.” can be used to treat clonidine withdrawal. D. Dexmedetomidine: highly selective alpha2-receptor agonist available as an IV solution 1. Usual dosing: in usion o 0.3–0.7 g/kg/hr 2. E ects: shown to increase sedation, analgesia, and amnesia; decreases heart rate, cardiac output, and circulating catecholamines; minimizes need or narcotics when used perioperatively in patients with obstructive sleep apnea (OSA) IV. Co ro na ry a rte ry re va s c ula riza tio n: should be per ormed in patients with stable angina who have signif cant le main coronary artery stenosis or three-vessel disease A. Other indications: recommended or patients with high-risk unstable angina, non–S -segment elevation MI, and acute S elevation B. Elective noncardiac surgery: not recommended within 4 weeks Quic k Cut o coronary revascularization Routine prophylactic C. Elective noncardiac surgery: not recommended within coronary revas cularization is 4–6 weeks o bare-metal coronary stent implantation or within not recommended or patients 12 months o drug-eluting coronary stent implantation with s table CAD be ore D. Elective procedures with signif cant risk o perioperative noncardiac s urgery. bleeding: should be de erred until patients have completed an

50

Chapter 3

Evaluation o the Surgical Patient with Cardiac Disease

appropriate course o thienopyridine therapy (ticlopidine or clopidogrel) 1. For patients treated with drug-eluting stents: Aspirin should be continued i possible. 2. Antiplatelet therapy: should resume as soon as possible in the postoperative period to prevent late stent thrombosis V. Ma in te na n c e o no rm o the rm ia : Body temperature 36.6°C 0.5°C is recommended or most procedures except during periods in which mild hypothermia is intended to provide organ protection.

Quic k Cut De er elective operations or 1 year a ter drug-eluting s tent implantation and a minimum o 1 month or bare-metal s tent implantation.

VI. 3-Hyd ro xy-3-m e thylg luta ryl-c o e nzym e A (HMG-Co A) re d uc ta s e inhib ito rs : should be started or patients who have known vascular disease, elevated low-density lipoprotein cholesterol, or ischemia A. Should be continued: or patients undergoing noncardiac surgery and or those who are already taking statins B. Other indications: Statin use may also be considered or patients undergoing vascular and intermediate-risk surgical operations.

Inva s ive He m o d yna m ic Mo nito ring I. Arte ria l line : Allows or continuous direct BP monitoring and requent arterial blood gas (ABG) sampling; consider in critically ill patients and in patients in whom large volume shi s or blood loss is expected. II. P ulm o na ry a rte ry c a the te r (Swa n-Ga nz): consider in patients at risk or major hemodynamic disturbances or in elderly patients with known cardiac history A. Precautions: Patient disease, surgical procedure, and practice Quic k Cut setting should be weighed prior to insertion. Pulmonary B. Data interpretation: Lack o experience in interpreting artery catheters are not recommended or routine us e. pulmonary artery catheter data may cause more harm than benef t. III. Tra ns e s o p ha g e a l e c ho c a rd io g ra p hy (TEE): consider in critically ill patients to help determine the cause o an acute or persistent hemodynamic abnormality A. Advantages: superior to transthoracic echocardiography ( E) in providing structural and unctional detail B. Disadvantages: invasive procedure that requires intubation

Ba c te ria l End o c a rd itis P ro p hyla xis I. In g e ne ra l: no longer recommended based solely on the risk o acquiring in ective endocarditis (IE) II. Ind ic a tio ns : Cardiac conditions associated with high adverse outcomes rom IE include prosthetic cardiac valve, previous IE, congenital heart disease, and cardiac transplant recipients who develop cardiac valvulopathy. III. Re g im e n: Amoxicillin PO or ampicillin, ce azolin, or ce riaxone IV; i allergic to penicillin, use clindamycin or azithromycin.

P o s to p e ra tive Co m p lic a tio ns I. MI: Most perioperative MIs occur during the f rst 3–5 days when patients shi extracellular uid intravascularly in a process known as autodiuresis. A. Signs and symptoms: Postoperative MIs may be associated with new-onset CHF, arrhythmias, or changes in mental status rather than chest pain. B. Emergency surgery: places patients at a higher risk or perioperative cardiac events than elective surgery

Quic k Cut Bacteremia rom a minor procedure, s uch as dental work, is unlikely.

Quic k Cut Antibiotic prophylaxis solely to prevent IE is not recommended or genitourinary or gastrointestinal tract procedures.

Quic k Cut Patients with a his tory o an MI, pathologic Q waves on preoperative ECG, or an MI within the pas t 30 days are at major ris k or MI.

Chapter 3

Medical Risk Factors in Surgical Patients

II. Arrhythm ia s : Majority o surgery patients exhibit abnormalities in heart rate or rhythm; however, only 5% o these are clinically signif cant. III. P ulm o na ry e d e m a : may occur in patients with a history o CHF due to volume overload and H N IV. Thro m b o e m b o lic e ve nts : May occur in patients with prosthetic heart valves in whom anticoagulation has been discontinued; anticoagulation should be restarted as soon as possible.

EVALUATION OF THE SURGICAL PATIENT WITH LUNG DISEASE P ulm o na ry Func tio n As s e s s m e nt

51

Quic k Cut The hos pital mortality rate o patients who have a pos toperative MI a ter noncardiac s urgery is 20% .

Quic k Cut Pos toperative arrhythmias may be caus ed by metabolic abnormalities , is chemia, and hypoxia, and thes e problems s hould be identif ed and corrected.

I. Ge ne ra l a s p e c ts : Patients with chronic lung disease are more susceptible to postoperative pulmonary complications that may include atelectasis, pneumonia, exacerbation o chronic lung disease, and respiratory ailure requiring mechanical ventilation. Because these complications are associated with longer hospital stays and increased morbidity and mortality, identi ying pulmonary risk actors preoperatively allows appropriate testing and risk modif cation may be undertaken prior to surgery. II. His to ry a nd p hys ic a l e xa m ina tio n: should alert the physician that pulmonary disease exists A. Patient history: Age older than 50 years has been identif ed as an independent risk actor or postoperative pulmonary complications. B. Review o systems: chronic cough, excessive sputum production, wheezing, exercise intolerance, and dyspnea C. Social history: tobacco use D. Medical history: chronic obstructive pulmonary disease (COPD), obesity, OSA, pulmonary H N, asthma, emphysema, prior lung surgery, neuromuscular disorders, CHF, and recurrent bronchitis or pneumonia E. Physical examination: scoliosis; chest wall abnormalities; abnormalities on auscultation including wheezing, rales, and rhonchi; prolonged expiration; cyanosis; f nger clubbing; jugular venous distention; and scars rom prior surgery Quic k Cut III. P re o p e ra tive s tud ie s : Laboratory and imaging evaluation should Ches t x-rays s hould be obtained only in select patients at higher risk or postoperative be per ormed in patients pulmonary complications. with known cardiopulmonary A. Chest radiograph: Routine preoperative chest x-rays are not dis eas e or in patients older necessary in all patients. than age 50 years who are B. ABGs: Assess the adequacy o ventilation and oxygenation. undergoing upper abdominal, thoracic, or aortic aneurys m C. ASA risk classif cation: Greater than class II con ers a more s urgery. than our- old increased risk o postoperative pulmonary complications. D. Pulmonary unction tests (PF s): In the absence o a history Quic k Cut signif cant or COPD or asthma, routine preoperative spirometry No s ingle PFT is an has not been shown to predict postoperative pulmonary abs olute contraindication to complications in extrathoracic surgery. s urgery. E. Preoperative spirometry and ABGs: may be considered in patients with f ndings that suggest pulmonary disease such as planned thoracic procedures, productive cough and dyspnea, Quic k Cut greater than 20/pack/year history o cigarette smoking, abnormal Failure o PFTs to chest radiograph f ndings, and morbid obesity improve a ter bronchodilator F. Patients undergoing thoracic surgical procedures: Specif c therapy may be an indication criteria have been established or the minimum pulmonary o high pulmonary ris k. unction necessary to tolerate pulmonary resection.

P re o p e ra tive Ris k Mo d if c a tio n I. Ce a s e c ig a re tte s m o king : should be stopped at least 6–8 weeks be ore elective surgery in order to signif cantly reduce postoperative complications

52

Chapter 3

Evaluation o the Surgical Patient with Lung Disease

II. COP D: Antibiotics should be administered prior to surgery in patients with acute bronchitis, productive cough, or purulent sputum production. Elective surgery should be delayed until a er treatment and symptoms have resolved. III. As thm a : Patients should be managed preoperatively with antibiotics, bronchodilators, beta2 agonists, and steroids.

Quic k Cut The importance o ambulation and incentive s pirometry us e s hould be reviewed with patients preoperatively.

IV. Ob e s ity: Obese patients have a restrictive respiratory pattern that leads to an increased incidence o postoperative atelectasis.

Op e ra tive Co ns id e ra tio ns I. Ane s the s ia : General anesthesia may cause a small but signif cant drop in unctional residual capacity or up to 2 weeks postoperatively. A. Neuromuscular blockade: Impairs ciliary and diaphragmatic unction; to minimize residual blockade ollowing surgery, avoid use o long-acting agents. B. Endotracheal intubation and inhalation anesthetics: may exacerbate bronchospasm C. Mechanical ventilation: leads to an increased risk o pneumothorax in susceptible patients due to barotraumas D. Neuraxial blockade (spinal or epidural anesthesia): results in a lower rate o pulmonary complications when compared to general anesthesia II. Op e ra tive a c to rs : in uence the risk o pulmonary complications A. Surgical location: T oracotomy and upper abdominal surgeries are associated with the greatest risk o postoperative pulmonary Quic k Cut complications. Higher abdominal B. Minimally invasive surgery: May reduce postoperative incis ions have an increas ed pulmonary complications due to improvement in postoperative ris k o pulmonary complications relative to lung volumes and a decrease in postoperative pain. lower abdominal incis ions . Intraoperative CO2 retention may occur due to insu ation. C. ype o incision: Horizontal incisions have a lower incidence o respiratory complications including hypoxemia and atelectasis when compared to vertical incisions. D. Length o surgery: Surgery lasting more than 3 hours and emergency surgery are associated with increased pulmonary complications.

P e rio p e ra tive Ma na g e m e nt I. Lung e xp a ns io n: Lung expansion techniques reduce postoperative pulmonary complications; these include incentive spirometry, cough, deep breathing, continuous positive airway pressure (CPAP), postural drainage, chest physiotherapy, and intermittent positive pressure breathing.

Quic k Cut The maximal reduction in pulmonary complications is achieved when patient teaching on interventions is s tarted preoperatively.

II. Extub a tio n: Following the completion o surgery; adequate ventilation and oxygenation must be maintained, the airway must remain patent, and aspiration must be prevented with suctioning and head turning. A. Protocol-based weaning o mechanical ventilation: decreases ventilator time and reduces the incidence o ventilator-associated pneumonia B. Reintubation: can be prevented with aggressive management including bronchodilator therapy, requent suctioning, and noninvasive ventilation with CPAP or bilevel positive airway pressure (BiPAP) III. Ad e q ua te p a in c o ntro l: helps to minimize pulmonary complications by improving patient com ort A. Medication: Avoid excessive narcotic or benzodiazepine use to minimize oversedation and respiratory depression. B. Epidural anesthesia: can provide excellent postoperative pain control and may reduce pulmonary complications

Quic k Cut Adequate pain control allows or earlier ambulation and improves the ability o patients to cough and per orm deep breathing exercises.

Chapter 3

Medical Risk Factors in Surgical Patients

P ulm o na ry Co m p lic a tio ns I. Ate le c ta s is : most common postoperative pulmonary complication A. Hypoxemia with atelectasis: usually begins on the second postoperative day B. Early hypoxemia: may signal hypoventilation rom residual anesthesia, airway edema, or obstruction

53

Quic k Cut Pos toperative pulmonary complications are almos t as common as pos toperative cardiac complications , and they can lead to increas ed hos pital lengths o s tay and increas ed mortality a ter s urgery.

II. P ne um o nia : typically occurs within 5 days o surgery A. Cause: requently caused by gram-negative bacteria and Staphylococcus aureus B. reatment: includes collection o respiratory cultures and initiation o antibiotics

III. Othe r s ig nif c a nt c o m p lic a tio ns : include bronchospasm (which can be treated with short-acting inhaled beta2 agonists), pulmonary edema, pneumothorax, pulmonary embolism, adult respiratory distress syndrome, and aspiration

EVALUATION OF THE SURGICAL PATIENT WITH RENAL DISEASE Re na l Func tio n As s e s s m e nt I. His to ry: should ocus on medical conditions that are risk actors or the development o kidney disease such as a known history o CKD, prior episodes o acute kidney injury (AKI), any surgical procedures on the kidney and urinary tract, and nephrotoxic medications A. Underlying systemic diseases: include di use atherosclerosis, DM, H N, autoimmune diseases, and collagen vascular disease B. Medications: T orough review is important to identi y any nephrotoxic medications that have the potential to contribute to AKI. C. Other: Prior history o bleeding problems; determine i the patient is dialysis dependent.

Quic k Cut Patients with CKD commonly need s urgery: Acces s or dialys is is nearly univers al, as well as general s urgical problems .

Quic k Cut Cardiovas cular dis eas e is the mos t common caus e o mortality in patients with CKD.

II. P hys ic a l e xa m ina tio n: should ocus on the ollowing: A. Signs o volume overload: pulmonary rales, jugular venous distension, and peripheral edema B. Signs o cardiovascular disease: cardiac murmurs, diminished peripheral pulses, jugular venous distension, or peripheral edema C. Evidence o coagulopathy: including petechiae and ecchymoses D. Central nervous system changes: including lethargy and altered mental status E. Pericardial or pleural rubs and decreased basilar breath sounds: may indicate pleural e usions

III. La b o ra to ry te s ting a nd d ia g no s tic s tud ie s : should include the ollowing: A. Basic metabolic panel: Assess or electrolyte abnormalities and blood urea nitrogen (BUN) and creatinine levels. B. CBC: to evaluate or anemia; iron studies i anemia is present C. Bleeding time D. Calculations: Creatinine clearance and glomerular f ltration rate (GFR) to determine renal unction may be per ormed using the Crockcro -Gault ormula and the Modif cation o Diet in Renal Disease (MDRD) Study Equation. 1. Crockcro -Gault ormula: Quic k Cut (140 age) lean body weight [kg] Standard ormulas Cr [mg/dL] 72 es timate the degree o 2. For women: renal unction and allow appropriate dos ing o (140 age) lean body weight [kg] .85 medications . Cr [mg/dL] 72

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Chapter 3

Evaluation o the Surgical Patient with Renal Disease

Ta b le 3-7: Na tio na l Kid ne y Fo und a tio n Cla s s if c a tio n o Chro nic Kid ne y Dis e a s e Sta g e

De s c rip tio n

GFR (m L/m in p e r 1.73 m 2 )

1

Kidney damage with normal or increased GFR

2

Kidney damage with mild decreased GFR

60–89

3

Moderately decreased GFR

30–59

4

Severely decreased GFR

15–29

5

Kidney ailure

90

15 (or dialysis)

GFR, glomerular f ltration rate.

3. MDRD Study Equation: GFR, in mL/min per 1.73m 2 186.3 SCr (exp[ 1.154]) age (exp[ 0.203]) (0.742 i emale) (1.21 i black) E. Other: Drug levels should be measured, chest radiograph should be obtained to assess volume status, and ECG should be obtained and compared to prior ECGs. IV. Cla s s if c a tio n o CKD: def ned as either kidney damage or decreased kidney unction or at least 3 months ( able 3-7) A. Proteinuria: principal indicator o kidney damage B. GFR: single best measure o kidney unction C. Level o kidney unction: determines stage o CKD regardless o underlying diagnosis

P re o p e ra tive Ma na g e m e nt I. Fluid a nd e le c tro lyte ho m e o s ta s is : altered in patients with renal disease and results in H N and the ollowing: A. Sodium and water retention: can exacerbate CHF and peripheral edema B. Hyperkalemia: Attempts should be made to normalize K levels. 1. reatment: Sodium bicarbonate, insulin and glucose in combination, and beta agonists may be given to temporarily shi K intracellularly. 2. Exchange resins: Sodium polystyrene sul onate (Kayexalate) may be given orally or by enema. 3. Dialysis: may also be used C. Metabolic acidosis: may be corrected by either bicarbonate administration or with dialysis D. Hypocalcemia: due to decreased active vitamin D ormation E. Hyperphosphatemia: caused by secondary hyperparathyroidism II. He m a to lo g ic unc tio ns : altered A. Anemia: Occurs as a result o decreased erythropoietin production; erythropoietin may be given preoperatively i the surgery is elective. B. Coagulation de ects are expected to occur as a result o altered platelet adhesion and aggregation in uremic patients. III. Ca rd ia c a nd o the r va s c ula r a b no rm a litie s : more common and include atherosclerosis, pericarditis, and pericardial e usions IV. Nutritio na l s ta tus : impaired due to decreased body stores o nitrogen and protein, which may lead to poor wound healing V. Dia lys is : Routine hemodialysis should be per ormed to prevent Quic k Cut volume overload, metabolic acidosis, and hyperkalemia. Hemodialys is s hould A. Peritoneal dialysis exchanges: Should occur up until the time o be per ormed within 24 hours surgery; the peritoneal dialysate should be drained immediately o elective s urgery. prior to surgery. B. emporary hemodialysis: may be used a er abdominal surgery

Op e ra tive Va ria b le s I. Ane s the s ia : Renal ailure a ects the metabolism o di erent anesthetic drugs due to changes in renal excretion and protein binding. A. Inhalational agents: Decrease GFR and urinary excretion o sodium. Fluoride ion accumulation with the use o some agents can lead to renal toxicity.

Chapter 3

Medical Risk Factors in Surgical Patients

55

B. Muscle relaxants: Succinylcholine administration leads to increases in serum K , and atracurium undergoes enzymatic degradation in plasma and can be sa ely used in patients with renal insu ciency. C. Benzodiazepines: Highly protein-bound agents; renal ailure causes decreased protein binding and increased accumulation o Quic k Cut the active orm, which leads to prolonged sedation. Narcotics may have D. Morphine: Should be used cautiously due to its prolonged sedative prolonged e ects in patients with renal dys unction, making e ects. Propoxyphene and meperidine should be avoided in patients entanyl the narcotic o choice. with renal ailure due to accumulation o neurotoxic metabolites. II. Va s c ula r a c c e s s A. Arteriovenous f stulas and gra s: Special care must be taken to protect the access site o dialysis patients. 1. Position: Arm should be positioned to avoid prolonged pressure and possible thrombosis. 2. Blood draws and BP monitoring: should be per ormed on the opposite limb 3. Evaluation: Gra should be evaluated preoperatively and postoperatively to ensure patency. B. Central line placement: Central venous access should be placed on the opposite side o existing vascular access or dialysis.

Quic k Cut Central line placement in the s ubclavian vein s hould be avoided to prevent s ubclavian s tenos is that may a ect the ability to create uture vas cular acces s f s tulas and gra ts .

III. Ane m ia a nd b lo o d lo s s : Severe anemia should be corrected; blood trans usion should be avoided i possible to prevent antibody ormation and hyperkalemia. IV. Hyp o te ns io n: should be avoided to prevent decreased renal per usion and acute tubular necrosis (A N) V. Antib io tic s : must be dosed appropriately or renal unction

P o s to p e ra tive Co m p lic a tio ns I. Ge ne ra l a s p e c ts : Postoperative complications are common in patients with CKD, most commonly hyperkalemia, AKI, in ection, hemodynamic instability, bleeding, arrhythmias, anemia, and loss o vascular access. II. Hyp e rka le m ia : Can be managed by shi ing K intracellularly or by eliminating K rom the body. I ECG changes (e.g., peaked waves, P wave loss, widened QRS) occur, IV calcium should be given to protect against ventricular f brillation and cardiac arrest. III. Co a g ulo p a thy: can be managed with desmopressin (DDAVP), conjugated estrogens, and cryoprecipitate IV. AKI: more common in patients with CKD A. Risk actors: include increasing age, depressed cardiac unction, existing kidney disease, H N, PVD, DM, emergency surgery, and cardiovascular procedures B. Management: should ocus on avoiding nephrotoxins, correcting electrolyte abnormalities and acid–base disorders, and maintaining renal per usion through euvolemia

EVALUATION OF THE SURGICAL PATIENT WITH LIVER DISEASE He p a tic Func tio n As s e s s m e nt I. Tho ro ug h his to ry a nd p hys ic a l e xa m ina tio n: will help to provide in ormation regarding possible liver disease A. History: should ocus on any prior episodes o liver dys unction, upper gastrointestinal bleeding, hereditary liver disorders, exposure to in ections agents (e.g., blood trans usions, tattoos), prior adverse reactions to inhalational anesthetics, and other risk actors (e.g., alcohol abuse, drug abuse)

Quic k Cut Surgical mortality in patients with end-s tage renal dis eas e ranges rom 1% to 4% ; however, the ris k increas es f ve- old or emergency s urgical procedures .

Quic k Cut The mos t common caus e o AKI is ATN.

Quic k Cut The s everity o liver dys unction and the nature o the s urgical procedure correlate with operative ris k.

Quic k Cut Hepatic ins u f ciency increas es the ris k o complications and death in the pos toperative period.

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Chapter 3

Evaluation o the Surgical Patient with Liver Disease

B. Physical examination: should include an assessment o the ollowing: 1. Clinically evident eatures o liver dys unction: jaundice, ascites, peripheral edema, muscle wasting, testicular atrophy, palmar erythema, spider angiomas, gynecomastia, hepatosplenomegaly, and liver nodularity 2. Signs o portal H N: including caput medusa (dilated periumbilical vessels) or splenomegaly 3. Evidence o hepatic encephalopathy: including asterixis and changes in mental status II. La b o ra to ry te s ting a nd d ia g no s tic s tud ie s : Routine assessment o liver unction in surgical patients is only necessary i Quic k Cut there is clinical suspicion or underlying liver disease. Laboratory s tudies may be normal des pite the A. Use ul tests: include aspartate aminotrans erase (AS ), alanine pres ence o s ignif cant liver aminotrans erase (AL ), bilirubin (total, direct, and indirect), dis eas e. alkaline phosphatase, albumin, and prothrombin time B. Platelet count: may be abnormal in patients with portal H N C. Hepatitis serologies: should be sent in patients where exposure to these viral agents is suspected III. Live r b io p s y: may be per ormed preoperatively to assess degree o cirrhosis

Op e ra tive Ris k As s e s s m e nt a nd Stra tif c a tio n I. Und e rlying live r d is e a s e : includes the ollowing: A. Acute hepatitis: Increases surgical morbidity and mortality. Surgery should only be per ormed in patients with acute hepatitis i it is emergent. B. Chronic hepatitis: Also increases operative morbidity and mortality; however, elective procedures may be per ormed in patients whose liver unction is well compensated. C. Cirrhosis: Operative outcomes are in uenced by the degree o hepatic dys unction and the type o surgical procedure. D. Obstructive jaundice: In patients with distal biliary obstruction who are not undergoing liver resection, biliary drainage does not seem to decrease signif cantly perioperative morbidity. For proximal biliary obstruction where liver resection will be per ormed as part o the surgical procedure, preoperative biliary drainage may be more important. II. Se ve rity o unde rlying live r dis e a s e : T e Child- urcotte-Pugh score and the Model or End-Stage Liver Disease (MELD) score are two classif cation systems that can be used to assess degree o hepatic dys unction. A. Child- urcotte-Pugh classif cation system: Calculated rom the patient’s serum bilirubin, albumin level, prothrombin time, Quic k Cut degree o ascites and encephalopathy. Operative mortality or MELD has replaced elective surgical procedures is 10% in Child class A, 30% in Child’s clas s if cation in clinical Child class B, and greater than 50% in Child class C patients. practice. The MELD s core B. MELD score: Linear regression model calculated rom a patient’s may als o be predictive: For every 1-point increas e in bilirubin level, creatinine, and international normalized ratio the MELD s core, there is a (INR) is most commonly used to strati y patients or liver 1% increas e in operative transplantation. Operative mortality in patients with a MELD mortality. score less than 8 is 5% but may increase to greater than 50% in patients with a MELD score greater than 20. III. Typ e o s urg ic a l p ro c e d ure : Morbidity and mortality in patients with hepatic dys unction is greatest or open abdominal and cardiac procedures; emergency surgery is also associated with increased morbidity and mortality.

Ane s the tic Co ns id e ra tio ns I. Ge ne ra l a s p e c ts : Decreased hepatic per usion at baseline increases the susceptibility o the liver to hypoxemia and hypoper usion intraoperatively. Hepatic dys unction may also alter drug metabolism and prolong the e ects o medications. II. Inha la tio n a ne s the tic s : reduce splanchnic per usion and hepatic blood ow to some extent A. Iso urane: associated with minimal hepatic metabolism and does not impair hepatic blood ow and is there ore the inhalational anesthetic o choice in patients with liver dys unction B. Halogenated inhalational agents: should be avoided in patients with a history o hepatotoxicity a er inhalational anesthesia

Chapter 3

Medical Risk Factors in Surgical Patients

57

III. Mus c le re la xa nts : Neuromuscular blockade may be prolonged a er administration o nondepolarizing muscle relaxants. Atracurium and cisatracurium are recommended as they undergo peripheral enzymatic degradation and are not metabolized in the liver. IV. Na rc o tic s a nd b e nzo d ia ze p ine s : Drug action can be prolonged in patients with hepatic dys unction due to altered metabolism. A. Narcotics metabolized in the liver: Morphine, hydrocodone, and oxycodone should be avoided. Fentanyl may be used because its metabolism is not a ected by hepatic dys unction. B. Benzodiazepine metabolism: Midazolam and diazepam are a ected by hepatic dys unction. T e clearance rate o oxazepam and temazepam are not a ected because they are not metabolized in the liver.

P e rio p e ra tive Ma na g e m e nt I. Fluid a nd e le c tro lyte b a la nc e : Perioperative hypotension Quic k Cut should be avoided to prevent worsening hepatic unction. Perioperative care A. Ascites: can be managed with diuretics, uid and sodium s hould ocus on correcting restriction, and paracentesis phys iologic abnormalities and B. Hypomagnesemia: common in patients with chronic liver providing s upportive care as disease and should be corrected organ dys unction develops . C. Lactate metabolism impairment: may result in signif cant acid– base disturbances that may require uid resuscitation or dialysis II. Co a g ulo p a thy A. Prothrombin time: May be elevated secondary to vitamin K Quic k Cut def ciency (lack o actors II, VII, IX, and X) or ailure o Prothrombin time synthetic unction. reatment may be instituted with vitamin K is a s ens itive marker or or resh rozen plasma. s ynthetic unction o the liver. B. T rombocytopenia: may be present in patients with portal H N and splenomegaly and can be treated with platelet trans usion as needed III. He p a tic d ys unc tio n: Worsening hepatic unction is the most common postoperative problem in patients with liver disease and may mani est as worsening hepatic encephalopathy, jaundice, ascites, coagulopathy, and hypoglycemia. A. Encephalopathy: May be treated with protein restriction and the use o lactulose. Narcotics and sedatives that precipitate hepatic encephalopathy should be avoided. B. Jaundice: Correctable causes such as biliary obstruction should be identif ed and managed. C. Ascites: can be managed with diuretics, sodium and water restriction, and paracentesis D. Coagulopathy: can be treated with vitamin K, resh rozen plasma, cryoprecipitate, desmopressin acetate, and platelet trans usion E. Hypoglycemia: may occur in patients with worsening liver ailure and should be treated with glucose in usion

Chapter 4

Li e-T reatening Disorders: Acute Abdominal Surgical Emergencies Laura S. Buchanan and Jose J. Diaz

ACUTE ABDOMEN De f nitio n a nd His to ry

Quic k Cut Many s urgical cons ults addres s times ens itive and li e-threatening dis eas e, o ten requiring rapid evaluation, res us citation, and def nitive management.

I. Ac ute s urg ic a l a b d o m e n: acute onset o severe abdominal pain and usually merits emergent or urgent surgical evaluation II. P a in c ha ra c te ris tic s : can give clues to pathology (Fig. 4-1) A. Gradual, midabdominal, nonspecif c progressive pain: suggests visceral irritation rom a worsening process B. Severe, sudden onset o pain: suggests per oration and may be Quic k Cut localized or dif use Emergent means C. Gradual pain that has sudden severe component: can suggest immediate; urgent re ers to per oration o previous pathology such as appendicitis minimal delay. D. Crampy, intermittent pain: suggests bowel obstruction III. Die t a nd b o we l c ha ng e s A. Anorexia, nausea, and vomiting: commonly accompany an Quic k Cut acute intra-abdominal in ammatory process Childhood B. Changes in bowel habits: nonspeci c in most conditions intus s us ception may produce 1. Bloody diarrhea: suggests ischemia or in ection, as in a characteris tic bloody diarrhea clas s ically re erred to ischemic colitis, Salmonella, or intussusception as “currant jelly” s tools . 2. Absence o bowel movement or atus: signi cant in obstruction IV. Sys te m ic s ig ns A. Chills and ever: nonspeci c but raise concern or sepsis secondary to abdominal pathology 1. Uncomplicated appendicitis/diverticulitis: typically associated with low-grade ever 2. Per oration: usually has ever greater than 38°C B. Unplanned weight loss: raises concern or undiagnosed Quic k Cut malignancy A rigid abdomen is s ynonymous with di us e C. Abdominal distension: concern or possible pathologic bowel peritonitis and almos t always distension or an intra-abdominal mass indicates the need or D. Rigid abdomen: common in cases o gastrointestinal (GI) tract emergent s urgery. per oration

58

Chapter 4

Li e-T reatening Disorders: Acute Abdominal Surgical Emergencies Ra pid ons e t of s eve re, cons ta nt pa in

Abrupt, excrucia ting pa in Myoca rdia l infa rction Bilia ry colic

Pe rfora te d ulce r

Ure te ra l colic

Rupture d a ne urys m

Acute pa ncre a titis

Me s e nte ric thrombos is, s tra ngula te d bowe l Ectopic pre gna ncy

Inte rmitte nt, colicky pa in, cre s ce ndo with fre e inte rva ls

Gra dua l, s te a dy pa in Acute chole cys titis, a cute chola ngitis, a cute he pa titis Appe ndicitis, a cute s a lpingitis

Ea rly pa ncre a titis (ra re ) Dive rticulitis

S ma ll bowe l obs truction Infla mma tory bowe l dis e a s e

Fig ure 4-1: Acute abdomen. (From Doherty GM, Boey J H. The acute abdomen. In: Way LW, Doherty GM, eds . Current Surgical Diagnosis and Treatment, 11th ed. New York: McGraw-Hill; 2003:506, with permis s ion.)

V. P e rtine nt m e d ic a l his to ry A. Previous abdominal surgery: predisposes to adhesive disease Quic k Cut with potential obstruction Adhes ions are 1. Malignancy history may be elicited in this portion o questioning. the mos t common caus e 2. Previous episodes o similar symptoms may have undergone o bowel obs truction in the medical evaluation and records can be obtained. United States . B. Previous illness in other systems: may be causal or associated with the current episode 1. Urinary tract in ection (U I) and obstruction: can present as with acute abdominal pain 2. T e reproductive system (especially in women): can mimic acute abdominal pathology with ovarian cyst rupture, endometriosis, and mittelschmerz (pain with ovulation). 3. Atrial f brillation: suggests an embolic process causing intestinal ischemia 4. Diabetes mellitus: Associated with in ection; sudden poor glucose control can indicate sepsis.

P hys ic a l Exa m I. Sys te m ic s ig ns : Can include ever, tachypnea, hypotension, and dysrhythmias, all o which contribute to severity o illness and indicate that the patient may need resuscitation. Observation can reveal jaundice, dehydration, and mental status changes. II. Abdom ina l e xa m : includes observation, auscultation, and palpation A. Observation: may reveal obvious hernias, local erythema, distension, or asymmetry B. Auscultation: Abscess o bowel sounds suggests peritoneal in ammation, whereas increased, requent, or high-pitched sounds can indicate obstruction. C. Palpation: should be done so as to minimize distress to the patient by beginning away rom the point o maximal pain D. Peritoneal signs: Indicate visceral irritation and include rebound pain, involuntary guarding, and pain with slight motion o the bed. T ese patients will be lying still, usually at.

Quic k Cut Phys ical exam is critical in this group o patients . The rectal exam is es s ential as it may help localize pain.

Quic k Cut Hernias that may not be vis ible on ins pection can remain palpable; cons equently, exam s hould include the inguinal area and groin.

59

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Chapter 4

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III. Re c ta l e xa m : can localize tenderness Quic k Cut A. Presence o blood: raises concern or ischemia, malignancy, or A digital rectal hemorrhoids exam is an es s ential part o B. Prostatitis (can cause generalized abdominal pain): may be the examination o patient diagnosed with rectal exam pres enting with abdominal or perineal pain—it is not IV. Sp e c if c s ig ns : Speci c ndings include the ollowing: optional. A. Murphy sign: Pain in the right upper quadrant (RUQ) with inspiration while the examiner palpates under the right costal margin as seen in acute cholecystitis; the patient will cease Quic k Cut inspiratory ef ort during this maneuver. In men, tes ticular B. McBurney sign: Pain at McBurney point (one third the distance tors ion requires emergent rom the anterior iliac spine to the umbilicus) typically a er intervention and can migration rom the periumbilical region is characteristic o pres ent with s udden lower appendicitis (Fig. 4-2). abdominal pain. Pelvic exam in women can s ugges t C. Rovsing sign: Pain (or rebound pain) in the right lower quadrant intrauterine pregnancy, (RLQ) with palpation o the le lower quadrant (LLQ) is typical ectopic pregnancy, pelvic in appendicitis. in ammatory dis eas e (PID), D. Obturator sign: Pain with internal rotation o a exed leg is and ovarian mas s . associated with appendicitis and pelvic abscess. E. Psoas sign: Pain with hip extension or hip exion against pressure is seen in retrocecal appendicitis. F. Markle sign: Pain with shaking the bed or patient’s oot is a sign o generalized peritoneal in ammation. G. Charcot triad: Fever, jaundice, and RUQ pain occurs in cholangitis. H. Reynold pentad: Fever, jaundice, RUQ pain, mental status change, and shock/sepsis indicates a severe orm o cholangitis. I. Chandelier sign: Pain with manual palpation o the cervix during bimanual exam is due to pelvic peritonitis, such as PID or abscess. J. Cullen sign: Bluish ecchymosis in the periumbilical region is caused by retroperitoneal hemorrhage. K. Kehr sign: pain in the le shoulder, re erred rom irritation pathology in the le upper quadrant (LUQ), including splenic rupture or subdiaphragmatic abscess

Dia g no s tic Te s ting I. La b o ra to ry e va lua tio n A. Complete blood count (CBC) with di erential: Can reveal anemia and dehydration and suggest in ection. A normal or low white count can be seen in the setting o in ection in immunosuppressed patients including elderly and diabetic patients. B. Serum electrolytes: can detect chemical abnormalities typically secondary to the abdominal process including acute renal injury, acidosis, and alkalosis C. Elevated lactate levels: Can indicate underresuscitation, ischemia, or necrotic tissue. It is also elevated in liver ailure.

Umbilicus

Ante rior s upe rior ilia c s pine

Fig ure 4-2: McBurney point. (Lippincott Nurs ing Advis or. Philadelphia: Lippincott Williams & Wilkins ; 2009.) Retrieved rom http://clineguide. ovid.com/gateway? res ourcenurs ingadvis or&docid =cc978-1-58255-511-9)

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Li e-T reatening Disorders: Acute Abdominal Surgical Emergencies

61

D. Urine analysis: can rule in or out a U I or kidney stone Quic k Cut E. Amylase and lipase: Can suggest pancreatitis. Amylase is less Hematuria in the speci c and can be elevated with other intestinal pathology. s etting o s evere abdominal F. Coagulation studies: essential or all patients suspected o pain s ugges ts kidney s tones . needing operative intervention G. Beta-human chorionic gonadotropin: indicated or all women o childbearing potential II. Im a g ing : Determined by the patient presentation, but all patients Quic k Cut with acute abdomen should have an upright chest x-ray, abdominal Upright ches t x-ray at plate, and at and upright abdominal x-rays or a lateral is the bes t plain f lm or the decubitus view. diagnos is o ree air, which A. Findings indicates per oration o a hollow vis cus and is a s urgical 1. Free air: air typically seen under the diaphragm (Fig. 4-3) emergency. a. Per orations: present in 80% o proximal per orations (gastroduodenal) but only 25% o distal per orations (colonic) b. Abdominal manipulation: less common causes such as peritoneal dialysis or recent laparoscopic surgery 2. Pneumatosis intestinalis: appears as small bubble-like air collections within the intestinal wall; may indicate ischemia or contained per oration 3. Pneumobilia: appears as air tracking within the liver and is caused by connections between the biliary and intestinal system, cholangitis, gallstone ileus, or recent endoscopic retrograde cholangiopancreatography (ERCP) 4. Portal venous gas: seen with necrotic tissue in the drainage bed o the portal system, typically the small intestine, appendix, or colon 5. Sentinel loop air (in adults): abnormal; can be due to obstruction, or it can indicate pathology in a nearby organ B. Abdominal ultrasound: imaging test o choice or cholecystitis 1. Findings a. Gallbladder wall thickening and pericholecystic uid b. Shadows rom gallstones: may also be evident 2. In pregnancy: o en used or evaluation o potential appendicitis

Ga s tric fundus a ir Dome of live r

Fig ure 4-3: Free air. The s traight arrows at the top le t repres ent the diaphragm. The horizontal arrow at le t points to the ree air. On the right, the uppermos t arrows s how the diaphragm, and the curved arrows illus trate the outline o the s tomach. The lone central arrow s ignif es the gas troes ophageal junction. (Smith W. Radiology 101, 4th ed. Philadelphia: Lippincott Williams & Wilkins ; 2013.)

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C. Computed tomography (C ) o the abdomen/pelvis: Gives more speci c in ormation than any other single study; however, it o en takes longer to obtain and ideally requires oral (PO) and intravenous (IV) contrast, which may be contraindicated in an acutely ill patient.

Di e re ntia l Dia g no s is

Quic k Cut CT s cans are us e ul but s hould never replace a detailed his tory and phys ical examination.

I. RUQ p a in A. Cholecystitis: Pain is typically worse with atty oods, o en with Quic k Cut history o previous episodes o similar pain and cholelithiasis. When es tablis hing 1. Diagnosis: improved with RUQ ultrasound a di erential diagnos is or 2. reatment: antibiotics and cholecystectomy abdominal pain, cons ider B. Hepatitis: acutely can present with RUQ pain and tenderness location f rs t. 1. Diagnosis: con rmed with liver unction tests (LF s) and serology testing 2. reatment: supportive and nonsurgical C. Peptic ulcer disease: includes gastric and duodenal ulcer disease and is associated Helicobacter pylori in ection 1. Presentation: pain, bleeding, obstruction, or per oration 2. reatment: includes antimicrobials as well as proton pump inhibitors (PPIs) D. Pancreatitis: Pain can result in patients sitting, leaning orward to achieve pain relie . 1. Diagnosis: Serum amylase and lipase are elevated. C scanning Quic k Cut with IV contrast is necessary to determine i necrosis is present. Acute pancreatitis is mos t commonly caus ed by 2. reatment: Patients require aggressive uid resuscitation and alcohol intake or galls tones . monitoring. E. Liver mass: ypically causes pain only i stretching the hepatic capsule. Biliary obstruction rom a mass is characteristically painless jaundice. F. Gastritis: Can present with acute abdominal pain. More serious causes o pain must be eliminated and supportive care of ered. G. Choledocholithiasis: caused by gallstones lodging in the common bile duct and usually associated with some element o biliary obstruction 1. Diagnosis: Elevated bilirubin and transaminases are suspicious when imaging reveals direct evidence o choledocholithiasis or common bile duct dilation. Diagnosis is con rmed with magnetic resonance Quic k Cut cholangiopancreatography (MRCP) or ERCP. Choledocholithias is can lead to pancreatitis . 2. reatment: ERCP is also potentially therapeutic with sphincterotomy and stone extraction. H. Cholangitis: In ection o the biliary system ascending into the intrahepatic system associated with Charcot triad and Reynold pentad; 95% o cases are associated with gallstones. I. Pyelonephritis and nephrolithiasis: ypically present with ank pain, and nephrolithiasis typically has associated hematuria. Quic k Cut Appropriate history and laboratory evaluation should lead to Appendicitis is known as the “great masquerader” these diagnoses. because its presentation can J. Appendicitis: Pain may have an atypical location, especially in be so variable. pregnant women with displacement caused by an enlarged uterus. II. RLQ p a in A. Appendicitis: ypically starts periumbilical with radiation to McBurney point. ime course is usually short hours to a day. Patient may have normal or only slightly elevated white blood cell count with little or no ever. B. Diverticulitis: ypically a le side or pelvic pain can present with right-side pain. C. Cecal volvulus: torsion o a redundant cecum resulting in a closed loop obstruction and pain rom ischemia D. Colon cancer: Can present as pain, obstruction, or per oration. Fecal occult screening and routine colonoscopies increase detection be ore the mass becomes symptomatic. E. Meckel diverticulum: Occurs in 2% o population, only 2% o which are symptomatic, and most occur within 2 o the ileocecal valve. F. Renal system: Other conditions include U I, nephrolithiasis, and pyelolithiasis. G. Reproductive system: gynecologic pain, prostatitis, and testicular torsion

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63

III. LUQ p a in A. Peptic ulcer disease B. Gastritis C. Splenic rupture or in ammation D. Hiatal hernia E. Boerhaave syndrome F. Mallory-Weiss tear IV. LLQ p a in A. Diverticulitis: can present with uncomplicated in ammation, contained abscess, ree per oration, or bleeding B. Sigmoid volvulus: results rom torsion o the sigmoid colon C. Colon cancer D. U I, nephrolithiasis, pyelonephritis E. Gynecologic, prostatitis, testicular torsion V. Me d ic a l c o nd itio ns m a s q ue ra d ing a s a s urg ic a l a b d o m e n A. Pneumonia B. Myocardial in arction C. Pericarditis D. Malignancy E. Diabetic ketoacidosis F. Acute hepatitis G. Rare causes: include acute polyserositis, rheumatic ever, porphyria, sickle cell crisis, and lead intoxication

OBSTRUCTION His to ry I. Sym p to m s : Include nausea, vomiting, crampy abdominal pain, and decreased or absence o atus and stool (all o which, in the absence o pain, suggest ileus). History o similar episodes or slow progression o symptoms suggests a chronic etiology. II. P re vio us s urg ic a l his to ry: Extremely important because Quic k Cut obstruction with previous abdominal surgery is usually adhesive Most SBO due to disease and can potentially improve with non-operative adhesions can be resolved with management. However, in the absence o previous surgery, the nasogastric decompression source o obstruction may be malignancy, per oration, or volvulus and supportive care. and requires intervention.

P hys ic a l Exa m I. Ab d o m ina l e xa m : Signi cant or distension. Emesis character including nonbilious, bilious, and eculent can suggest location o obstruction. II. Inc a rc e ra te d he rnia s : Detailed exam should look or hernias, including inguinal and emoral.

Dia g no s tic Stud ie s I. La b o ra to ry a na lys is : important because patients o en present not only with dehydration but also with signi cant electrolyte and acid–base abnormality II. Ab d o m ina l x-ra y: may reveal air in a nonanatomic location with a hernia A. Cecal and sigmoid volvulus: have characteristic distended colon loops visible on plain lm B. Small bowel obstruction (SBO): Normal abdominal x-ray shows air in the gastric and colon area, but distended, air- lled loops o small bowel are consistent with SBO (Fig. 4-4). Multiple air- uid levels on plain radiographs also indicate obstruction.

Di e re ntia l Dia g no s is I. Me c ha nic a l o b s truc tio n: due to physical blockage o the intestine by internal or external mass, stricture, or intestinal twisting and can occur in the small or large intestine A. erminology 1. Acute obstruction: can occur over hours and rapidly progress 2. Chronic obstruction: develops over weeks to months and is characterized by malnutrition and chronic illness

64

Chapter 4

A

Obstruction

B

Fig ure 4-4: A,B: Small bowel obs truction. Part A is a s upine f lm, and Part B is an upright x-ray. Note the air- uid levels vis ible in Part B. (From Yamada T, Alpers DH, Laine L, et al. Textbook of Gastroenterology, 4th ed. Philadelphia: Lippincott Williams & Wilkins ; 2003.)

3. Strangulating obstruction: Occurs when the blood supply Quic k Cut to the af ected segment o bowel is compromised, leading Strangulated hernias to gangrene and per oration. Signs o strangulation include require emergent s urgery to continuous pain, ever, tachycardia, peritoneal signs, acidosis deal with is chemia. and leukocytosis, and indicate progressive ischemia. 4. Incarceration: Re ers to a hernia that cannot be reduced; an incarcerated hernia may also be strangulated. 5. Closed loop obstruction: Both limbs o a segment o bowel Quic k Cut Strangulation re ers are obstructed. to the viability o the hernia b. Distention: As the more proximal bowel distends, contents . symptoms o obstruction develop. c. Closed loop: more prone to per oration because it cannot decompress 6. Partial obstructions: Allow small or intermittent amounts o matter through; these may respond well to conservative management. a. Clinically: Patients may pass small amounts o gas or stool. Quic k Cut b. Radiographically: Gas or contrast will be seen passing The lead point o into the colon. intus s us ception in adults is 7. Intussusception: Occurs when the bowel olds within its own pres umed to be a tumor and mus t be inves tigated. lumen (think o a sock removed hastily and olded into itsel ). May occur spontaneously in pediatric patients, but in adults, the lead point is suspicious or tumor. 8. Per orating obstruction: occurs when the proximal bowel Quic k Cut The cecum is the overdistends, resulting in per oration largest diameter portion o the B. Location: can partially be indicated by exam ndings large bowel, and by Laplace 1. Gastric outlet obstruction: Results in early satiety and law may be more prone to nonbilious emesis. T is is typically a chronic onset. per oration. (Laplace law: 2. Small intestinal obstruction: will result in bilious or eculent tension pressure diameter.) emesis

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Li e-T reatening Disorders: Acute Abdominal Surgical Emergencies

65

3. Large intestinal obstruction: may not result in emesis until late in its course a er the entire proximal small bowel has dilated C. Causes 1. Adhesions resulting rom previous surgery: Most common cause; partial adhesive obstructions are rst managed conservatively. 2. Malignancy: Without history o prior surgery, a mass is the most common diagnosis; treatment requires removal or bypass and tumor-speci c treatment. 3. Hernias: common source o obstruction caused by migration o an intestinal segment through the hernia de ect a. Internal hernias: occur when a bowel segment migrates Quic k Cut through an internal opening within the abdominal cavity Mechanical b. reatment: reduction o hernia contents and hernia repair obstructions can be 4. Less common causes: include congenital lesions (webs, extraluminal (adhesion, hernias) or intraluminal (mass, bezoar). malrotation), in ammatory lesions (Crohn disease, diverticulitis), oreign bodies, radiation, and trauma II. Func tio na l o b s truc tio n: inability to move intestinal contents Quic k Cut typically due to impaired motility In contras t to A. Ileus (paralytic or adynamic): dif use intestinal lack o motility mechanical obs truction, 1. Causes: occurs a er surgery, peritoneal irritation, and immotility is typically painles s electrolyte abnormality until per oration occurs . 2. reatment: includes uid and nutritional support as well as electrolyte replacement B. Colonic pseudo-obstruction (Ogilvie syndrome): impaired motility o the colon commonly seen a er back or hip surgery

HEMORRHAGE Te rm ino lo g y I. GI b le e d ing : Common emergent surgical consult. In all patients, Quic k Cut priority is placed on resuscitation and, when necessary, trans usion. With all hemorrhagic Upper GI bleed is de ned as bleeding proximal to the ligament o s ources , initial treatment reitz; lower GI bleed includes all other GI locations. includes control o hemorrhage, res us citation, II. He m a te m e s is : Emesis o blood that is bright red or the color o and revers al o coagulopathy. cof ee grounds. It is due to bleeding proximal to the ligament o reitz. III. He m a to c he zia : passage o bright red blood rom the rectum and can be due to bleeding rom an upper or lower source IV. Me le na : passage o black stools due to blood in the GI system and also can occur with upper or lower GI hemorrhage V. Curra nt je lly s to o l: mixture o blood and mucus typically described in children with intussusception

Eva lua tio n

Quic k Cut I. Lo c a liza tio n: First step in evaluation; upper GI hemorrhage may Upper GI hemorrhage present as hematochezia, melena, or even bright red blood per can present as lower bleeding. rectum. A. Nasogastric (NG) and gastric lavage: Evaluates or gastric and duodenal sources. NG lavage must contain bile to be negative. I there is no bile in the NG lavage, then a duodenal bleed may still be missed. B. Endoscopy: Can visualize the stomach, duodenum, and colon. T erapeutic interventions can of er treatment as well. C. Radiographic imaging: Includes tagged red cell scan and angiography; these are more use ul in lower GI bleeding. D. Capsule endoscopy or push enteroscopy: can visualize the small intestine in stable patients with resolved or intermittent bleeds

66

Chapter 4

Hemorrhage

II. Di e re ntia l Quic k Cut A. Upper GI bleed: Most common causes are peptic ulcers, The patient’s his tory esophagogastric varices, vascular mal ormations, and Malloryhelps es tablis h the mos t likely Weiss tears. diagnos is . 1. History o ulcer disease or nonsteroidal anti-in ammatory drug use: bleeding peptic ulcer 2. History o gastroesophageal re ux disease (GERD): esophagitis 3. History o heavy alcohol use: bleeding varices or gastritis 4. Recent retching: Mallory-Weiss tear 5. Weight loss: upper GI malignancy B. Lower GI bleed: Includes all other sources o GI bleeding including jejunum, ileum, colon, and rectum, whereas upper GI bleeding can present with only lower bleeding. Blood is cathartic and passes quickly through the intestine. Upper sources o bleeding must be evaluated and ruled out. 1. Common causes: Lower bleeding is most commonly diverticular hemorrhage and bleeding vascular mal ormations. 2. Less common causes: include malignancy, polyps, hemorrhoids, ssures, ischemic colitis, Meckel diverticulum (most common source in pediatrics), in ectious colitis, and in ammatory bowel disease (IBD) III. Tre a tm e nt: requires resuscitation, localization o bleeding source, cessation o immediate hemorrhage, and prevention o uture episodes A. Initial approach: Because patients with GI bleed may present in hemorrhagic shock, the initial approach must include assessment o ABCs (airway, breathing, circulation), establishment o two large-bore IV lines, and administration o appropriate uids/blood, depending on illness severity. B. Localization: determined by history, physical, and diagnostic testing 1. Rectal exam: Every exam or bleeding must include a rectal exam. 2. NG tube or lavage and aspiration: can diagnose an upper GI source but does not rule out an upper GI source i negative 3. Esophagogastroduodenoscopy (EGD): can both localize and Quic k Cut treat or rule out upper GI sources o hemorrhage Dieula oy les ion 4. agged red blood cell scan: identi es active bleeding by gross caus es GI bleeding and is a location (LUQ) but will not give speci cs o anatomic location vis ible, expos ed s ubmucos al a. Detect bleeds o 0.5 mL/min but requires a delay o up to ves s el. several hours while the study is being per ormed b. Because the tagged cells remain in circulation, i the study is negative, and the patient rebleeds, the test can be repeated within 24 hours. 5. Angiography: can identi y the vessel with bleeding and potentially embolize to provide treatment; can detect bleeding at a rate o 0.5–1.0 mL/min 6. Colonoscopy: can be di cult in an unprepped colon ull o blood but i success ul can also be therapeutic with clips, epinephrine injections, and cauterization C. Nonsurgical treatment: includes endoscopy, angiography, and embolization 1. Vasopressin in usion: will not stop bleeding but may temporize to give time or treatment 2. Ulcer treatment: includes PPI drip and treatment or H. pylori D. Surgical therapy: indicated or persistent hemorrhagic shock ( ails Quic k Cut resuscitation) and recurrent bleeding despite maximal therapy Only 10% o upper 1. Gastroduodenostomy: per ormed i no lesion has been GI bleeds require s urgical identi ed intervention. 2. Proximal gastrectomy: per ormed i no source is seen 3. Subtotal colectomy: per ormed i lower GI bleeding has not been localized be ore operative intervention, but this procedure his high mortality and can be complicated by rebleeding i the source is not included in the resected colon

Study Questions or Part I

Study Questions or Part I Directions: Each of the numbered items in this section is followed by several possible answers. Select the ONE lettered answer that is BES in each case. 1. A healthy adult presents or a pre-employment physical. What will be the largest component o

his or her body by mass? A. B. C. D. E.

Protein Water Calcium Sodium Potassium

2. An 80-year-old man with a history o ischemic cardiomyopathy is hypotensive and oliguric a er

major abdominal surgery. Initial uid resuscitation produces only transient improvements. He is trans erred to the intensive care unit or urther management. A pulmonary artery catheter could be used to measure all o the ollowing except: A. B. C. D. E.

Le atrial lling pressure Cardiac output Ejection raction Mixed venous oxygen saturation Systemic vascular resistance

3. A 25-year-old man is injured in the arm with a kni e. What is the rst mechanism responsible or

hemostasis? A. B. C. D. E.

Extrinsic clotting system Vessel constriction Intrinsic clotting system Platelet activation Fibrinolytic system

4. A 27-year-old woman is experiencing perioral and extremity numbness the morning a er a neck

operation. What is the cause o her symptoms? A. B. C. D. E.

Hypokalemia Hypercalcemia Hypocalcemia Hypochloremia Hyperkalemia

5. A 55-year-old woman undergoes laparotomy or small bowel obstruction. During lysis o

adhesions, an enterotomy is made in the obstructed, but viable, bowel, and a large amount o ecal-looking bowel contents are spilled into the abdomen. T e incision would now be considered what kind o wound? A. B. C. D. E.

Clean contaminated Secondary In ected Contaminated Clean

67

68

Study Questions or Part I

6. A critically ill 55-year-old man is in septic shock in the intensive care unit a er removal o a

nonviable small bowel. What is the most reliable measurement o arterial blood pressure? A. B. C. D. E.

Arterial line diastolic Noninvasive systolic Arterial line mean Arterial line systolic Noninvasive mean

7. Delayed primary closure would be the most appropriate wound closure technique or which o

the ollowing procedures? A. B. C. D. E.

Removal o per orated appendix Repair o wound dehiscence 1 week a er elective le colectomy Emergency drainage o a diverticular abscess with sigmoid resection and end colostomy Vagotomy and pyloroplasty or bleeding duodenal ulcer Repair o an incisional hernia 12 weeks a er an elective le colectomy complicated by a wound in ection and a resultant incisional hernia

8. A 55-year-old man with insulin-dependent diabetes presents to the emergency department with

acute abdominal pain. His heart rate is 130 beats per minute, his blood pressure is 90/60 mm Hg, and his oral temperature is 101.8°F. His respiratory rate is 28 breaths per minute (bpm). T e abdominal examination demonstrates dif use peritonitis. What should be the rst step in the evaluation and management o this patient? A. B. C. D. E.

Volume resuscitation Abdominal radiograph IV antibiotics C scan Immediate laparotomy

9. A 57-year-old man underwent a laparoscopic splenectomy or idiopathic thrombocytopenic

purpura (I P). He subsequently develops a persistent output o 100 mL daily o amylase-rich uid rom a drain placed at the time o surgery. All o the ollowing would be expected to prevent spontaneous resolution o this problem except: A. B. C. D. E.

Octreotide administration Pancreatic duct stricture In ection Nonabsorbable suture in distal pancreatic duct Epithelialization o the tract

10. For appropriate procedures, antibiotic prophylaxis or bacterial endocarditis should be

administered in patients with a history o which o the ollowing? A. B. C. D. E.

Mitral valve prolapse without regurgitation Automatic implantable cardiac de brillator placement Aortic valve replacement Coronary artery bypass gra Surgically repaired ventricular septal de ect

11. Which o the ollowing procedures would be expected to have the greatest impact on

postoperative pulmonary unction? A. B. C. D. E.

Low anterior resection Femoropopliteal bypass Subtotal gastrectomy Open cholecystectomy otal abdominal hysterectomy

Study Questions or Part I

12. Which o the ollowing is a criterion or emergent preoperative dialysis?

A. B. C. D. E.

Potassium (K ) 5.0, without arrhythmia Arterial pH 7.30, anion gap 8 Pericardial riction rub Blood urea nitrogen 105 Creatinine 5.5

13. Preoperative coagulation studies should be obtained on which o the ollowing patients?

A. B. C. D.

A 35-year-old woman on aspirin, prior to varicose vein surgery A 65-year-old diabetic man, prior to inguinal hernia repair A 70-year-old jaundiced woman, prior to choledochojejunostomy A 45-year-old woman prior to bilateral prophylactic mastectomy with transverse rectus abdominis myocutaneous ap reconstructions E. A 50-year-old man with stable angina, prior to coronary artery bypass Directions: T e group of items in this section consists of lettered options followed by a set of numbered items. For each item, select the lettered option(s) that is(are) most closely associated with it. Each lettered option may be selected once, more than once, or not at all.

Que s tio ns 14–17 Match the clinical situation with the appropriate type of drain. 14. Nasogastric decompression

A. Jackson-Pratt closed drain

15. Spontaneous pneumothorax

B. No drain

16. Dif use peritonitis rom per orated duodenal ulcer

C. Underwater seal drain

17. Splenectomy or ruptured spleen

D. Sump drain

18. A 50-year-old woman with chronic obstructive pulmonary disease is hospitalized with small

bowel obstruction. On the evening o her second day, she is acutely anxious and is breathing at a rate o 24 bpm. A er pain medications and reassurance, her oxygen saturations are 92% on 2 L o oxygen, and her tachypnea increases to 30 beats per minute. On exam, she has labored breathing but no other acute ndings. What is the best course o action? A. B. C. D. E.

Increase oxygen by nasal cannula to 3 L Elective intubation Diuresis with urosemide Additional narcotics to suppress breathing rate Computerized tomography o abdomen to assess bowel obstruction

19. A 24-year-old man presents with a traumatic wound to the le extremity. It had been injured in

a all 4 days previously. At home, the patient noted increased redness, pain, and swelling, with the discharge o some oul-smelling pus. In the emergency department, he has a temperature o 102°F, heart rate o 132 beats per minute, and systolic blood pressure o 85 mm Hg. T e leg is tensely distended, extremely tender, and there is some purulent drainage around a region o necrotic skin. T e most appropriate treatment or this patient is: A. B. C. D. E.

Oral antibiotics IV isotonic uids Phenylephrine Low-dose dopamine Intubation and drainage o the abscess

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Study Questions or Part I

20. A 30-year-old man presents with a mass in his right groin. It is not tender and is a bulge that is

more prominent on standing and with exercise. On examination, you nd a 3-cm protrusion into the right scrotum that completely resolves with gentle pressure. T e most appropriate management is: A. B. C. D. E.

Broad-spectrum antibiotics umor markers, including alpha- etoprotein Elective surgical repair Observation only C scan o the abdomen and pelvis

21. A 52-year-old woman undergoes unevent ul partial colectomy or a large polyp o the sigmoid

colon. During the procedure, placement o a Foley catheter demonstrates good urine output. Four days later, she develops a ever. Which o the ollowing is the LEAS likely cause o her ever? A. B. C. D. E.

Pneumonia Wound in ection U I Perirectal abscess Deep venous thrombosis (DV )

22. A 30-year-old man presents or elective repair o a right-sided inguinal hernia. He has no

signi cant medical history, and his physical examination is positive only or the presence o a reducible right-sided hernia. T e operative plan is an open inguinal hernia repair with mesh. T e most appropriate preoperative workup or this patient is: A. B. C. D. E.

Chest x-ray, electrocardiogram (ECG) CBC, basic metabolic panel (BMP) Urinalysis Noninvasive stress test Coagulation pro le only

23. A 60-year-old woman has diabetes and end-stage renal disease on hemodialysis. She undergoes

emergency surgery or per orated peptic ulcer, which is unevent ul. On postoperative day 2, she has chest pain and an ECG, which shows peaked waves. T e best initial maneuver is: A. B. C. D. E.

IV calcium IV insulin Oral potassium Oral calcium IV morphine

24. A 40-year-old woman presents with acute abdominal pain. She describes the pain as high in the

epigastrium, perhaps moving a little to the right side. T e pain comes with meals and has been present on and of over the past 6 months. A er lunch today, the patient developed severe pain, low-grade ever, and nausea. Her vital signs show no ever, heart rate o 85 beats per minute, and normal blood pressure. On exam, she is markedly tender under the right costal margin and cannot take a ull breath during that part o the examination. T e best initial test or this patient is: A. B. C. D. E.

Abdominal C scan RUQ ultrasound Abdominal magnetic resonance enterography (MRE) EGD Liver–spleen scanning

Study Questions or Part I

25. An 18-year-old man presents with 12 hours o abdominal pain. It was originally periumbilical

then migrated to his right side. Over the past 2 hours, he has developed some nausea but has not had any emesis. On examination, he has pain on the right side when palpating the le side. T e name or this sign is: A. B. C. D. E.

McBurney sign Obturator sign Psoas sign Markle sign Rovsing sign

26. A 15-year-old boy is admitted with a history and physical ndings consistent with appendicitis.

Which nding is most likely to be positive? A. B. C. D. E.

Pelvic crepitus Iliopsoas sign Murphy sign Flank ecchymosis Periumbilical ecchymosis

27. A 50-year-old man is admitted with massive bright red rectal bleeding. He recently had a barium

enema that demonstrated no diverticular or space-occupying lesion. Nasogastric suction reveals no blood but does produce yellow bile. T e patient continues to bleed. What is the next diagnostic step? A. B. C. D. E.

Repeat barium enema Colonoscopy Upper GI series Mesenteric angiography Small bowel ollow-through with barium

28. A 15-year-old boy awakens with sudden onset o RLQ and scrotal tenderness accompanied by

nausea and vomiting. Which o the ollowing is the most appropriate diagnosis and represents a surgical emergency? A. B. C. D. E.

Acute prostatitis Acute epididymitis orsion o the testicle Acute appendicitis Gastroenteritis

29. Massive bleeding rom the lower GI tract is occurring in a 55-year-old man who is otherwise

healthy. A er continued bleeding equivalent to one unit o blood, what should be the initial management? A. Emergency laparotomy and total colectomy and ileoproctostomy B. Emergency laparotomy and colostomy with operative endoscopy C. Arteriography to identi y the bleeding site a er anoscopy and sigmoidoscopy have ruled out a distal site D. In usion o vitamin K and resh rozen plasma E. Colonic irrigation with iced saline solution

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Study Questions or Part I

Que s tio ns 30–31 A 45-year-old man is seen in the emergency department a er vomiting bright red blood. He has no previous symptoms. He drinks one alcoholic beverage a day. 30. What is the most reliable method or locating the lesion responsible or the bleeding?

A. B. C. D. E.

Upper GI series Exploratory laparotomy Upper endoscopy Arteriography Radionuclide scanning

31. A er several hours in the hospital, he begins to have recurrent bleeding. He is trans erred to a

critical care bed and is persistently hypotensive despite trans usion o 9 units o packed red blood cells. Which is the most appropriate next step in management o this patient? A. Upper endoscopy with attempt at cauterization o bleeding B. ransport to the interventional radiology unit to identi y and embolize bleeding source C. Placement o a Blakemore tube to temporarily tamponade bleeding and to allow or stabilization o blood pressure D. Laparotomy to control bleeding E. In usion o vasopressin and additional units o blood 32. A 45-year-old woman who has had a hysterectomy presents to the emergency department with

abdominal pain and vomiting. A mechanical small bowel obstruction is seen on the abdominal radiograph. What is the most likely cause or this obstruction? A. B. C. D. E.

Carcinoma o the colon Small bowel cancer Adhesions Incarcerated inguinal hernia Diverticulitis

33. A 25-year-old man is admitted with a history o sudden onset o severe midepigastric abdominal

pain. Upright chest radiograph reveals ree intraperitoneal air. What is the therapy or this patient? A. B. C. D. E.

Upper endoscopy Barium swallow Gastrogra n swallow Observation Laparotomy

Answers and Explanations

Answers and Explanations 1. The a ns we r is B (Chapter 1, Fluid and Electrolytes, Normal Body Composition, I A). T e

normal adult human body is made up o 50%–70% water. T e water is contained in three primary compartments o the body: intracellular, extracellular, and intravascular. On average, two thirds o the body is made o water; in the hypothetical 70-kg man, this is 46 L. O this 46 L, two thirds is intracellular (30 L), and one third is extracellular (16 L). O the extracellular portion, three ourths is interstitial (12 L), and one ourth is intravascular (4 L). T is approximation gives a good starting point when beginning to estimate uid resuscitation, replacement, and maintenance. 2. The a ns we r is C (Chapter 1, T e Intensive Care Unit, Specialized Intensive Care Unit Care

and Monitoring, II C 2). A pulmonary artery catheter can be use ul in distinguishing cardiac dys unction rom other causes o shock in certain patients. It will allow the treating physician to measure le atrial lling pressure rom the port in the tip via back pressure through the lungs. Cardiac output is measured via thermal dilution. Mixed venous oxygen saturation can be measured by drawing a sample rom the catheter. Systemic vascular resistance can be calculated rom the cardiac output, mean arterial pressure, and central venous pressure. 3. The a ns we r is B (Chapter 1, Coagulation, Hemostasis Mechanism Phases, I A). T e rst

mechanism activated when there is damage to a vessel is constriction, which is an ef ort to stop blood ow. T is is ollowed by platelet activation, which produces a platelet plug. T e intrinsic and extrinsic pathways are then activated to orm a brin clot. T e brinolytic system is the body’s mechanism to dissolve established clots. 4. The a ns we r is C (Chapter 1, Fluid and Electrolytes, Water and Electrolyte De cits and Excesses,

V A 1). Hypocalcemia can induce neuromuscular irritability, including perioral and extremity numbness. T is can progress to carpopedal spasm and tetany. T e most common cause o hypocalcemia is parathyroid surgery to treat hypercalcemia, resulting in rebound hypocalcemia. 5. The a ns we r is D (Chapter 2, Wounds, Wound Classi cation, I–IV). T e wound described is

a contaminated wound due to the gross spill o contaminated material. A clean wound is one made through normal, antiseptically prepared skin and encounters no in ected or colonized areas. A clean-contaminated wound is similar to a clean wound except that a contaminated or potentially contaminated area (e.g., bowel, bronchus, urinary tract), which has been prepared to the best o one’s ability and presents minimal contamination, has been opened. An in ected wound is one that already has an established in ection present. Secondary is a type o wound closure and not a classi cation o a wound. 6. The a ns we r is C (Chapter 1, T e Intensive Care Unit, Specialized Intensive Care Unit Care

and Monitoring, II C 1). T e arterial line mean pressure is the most accurate and is the most physiologically use ul measurement o blood pressure. It may be very accurate but o en has limited clinical use ulness and must be used cautiously. Noninvasive blood pressures are not very accurate in critically ill patients. Noninvasive blood pressure measurements are notoriously high in hypotensive patients and low in hypertensive patients. 7. The a ns we r is A (Chapter 2, Wounds, Wound Repair, II C). Delayed primary intention is

appropriate or contaminated wounds, such as a ruptured appendix without abscess ormation. Wound dehiscences are closed with retention sutures that include all layers, including the skin, because the ascial strength has been compromised. In ected wounds are packed open to heal by secondary intention, as with drainage o a diverticular abscess. Clean and clean-contaminated wounds can be closed primarily, as with incisional hernia repair (clean) and vagotomy/ pyloroplasty (clean contaminated).

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Answers and Explanations

8. The a ns we r is A (Chapter 1, Shock, De nition, II D). Intra-abdominal sepsis in a

diabetic patient may be complicated by the development o ketoacidosis and dehydration. T e patient presents with a condition that will likely require emergent surgical intervention. Initial management should be directed at restoration o the patient’s circulating blood volume and optimization o his physiologic status prior to possible laparotomy. T e serum glucose, electrolytes, and pH should be determined and abnormalities corrected. Measurement o hourly urine output will allow assessment o the adequacy o resuscitation. Abdominal radiographs should be obtained to look or ree intraperitoneal air, and broad-spectrum IV antibiotics should be administered, but uid resuscitation takes top priority. A C scan may not be indicated in the patient who, on physical examination and history, clearly has peritonitis. 9. The a ns we r is A (Chapter 2, Gastrointestinal Fistula, III D). Enterocutaneous stulas typically

respond to conservative management and spontaneously close when conditions are avorable. Octreotide has been shown to decrease pancreatic stula output and clearly does not inhibit resolution. Distal obstruction (pancreatic duct stricture), in ection, oreign body (nonabsorbable suture), and epithelialization all inhibit resolution. 10. The a ns we r is C (Chapter 3, Evaluation o the Surgical Patient with Cardiac Disease, Bacterial

Endocarditis Prophylaxis, II). In 1997, the American Heart Association updated guidelines to clari y recommendations or antibiotic prophylaxis or the prevention o bacterial endocarditis. In general, appropriate prophylaxis should be given to patients with underlying structural cardiac de ects (e.g., prosthetic cardiac valves, signi cant valvular disease, hypertrophic cardiomyopathy, complex congenital heart disease, surgically constructed systemic-pulmonary shunts) who undergo procedures leading to bacteremia with organisms likely to cause endocarditis (e.g., major dental work or invasive procedures o the respiratory, GI, or genitourinary tracts). 11. The a ns we r is C (Chapter 3, Evaluation o the Surgical Patient with Lung Disease, Operative

Considerations, II A). Major upper abdominal surgery per ormed via a vertical midline incision would be expected to have the greatest impact on postoperative pulmonary unction. Other operative actors would include thoracotomy, residual intraperitoneal sepsis, age older than 59 years, prolonged preoperative hospitalization, colorectal or gastroduodenal surgery, procedure longer than 3.5 hours, and higher body mass index. Lower abdominal and extremity surgery are associated with ewer pulmonary complications when compared with thoracic and upper abdominal surgery. 12. The a ns we r is C (Chapter 3, Evaluation o the Surgical Patient with Renal Disease, Preoperative

Management, V). Indications or emergent dialysis include li e-threatening hyperkalemia, severe metabolic acidosis secondary to retained organic acids, uremic pericarditis, and volume overload. T e serum creatinine and blood urea nitrogen levels re ect the underlying renal dys unction but will not necessarily mandate emergent preoperative dialysis. 13. The a ns we r is C (Chapter 3, able 3-1). Preoperative evaluation with routine coagulation

studies is neither cost-ef ective nor routinely indicated. Patients with a history o postsurgical bleeding or ongoing acute hemorrhage, patients on oral anticoagulation, patients with liver disease or hepatobiliary obstruction, malnourished patients, and patients unable to give an adequate history should have prothrombin time, partial thromboplastin time, and platelet counts checked preoperatively. 14–17. The a ns we rs a re 14-D, 15-C, 16-B, a nd 17-A (Chapter 2, Surgical ubes and Drains,

Drains, I C). Sump drains are needed to adequately decompress the stomach. When the pleural space requires drainage, a chest tube is placed and connected to an underwater seal so that air and uid cannot re ux into the chest. T is is needed because o the negative intrathoracic pressure generated with each inspiration. Dif use peritonitis cannot be drained, as the peritoneal contents quickly “wall of ” oreign bodies such as drains; discrete intraperitoneal collections can be drained. Splenectomy jeopardizes the pancreatic tail, which is in close proximity to the splenic hilum. When the area is obscured, as with the hematoma accompanying splenic rupture, the integrity o the pancreas cannot be assured, and the potential pancreatic uid leak is drained with a closed-suction drain such as a Jackson-Pratt drain.

Answers and Explanations

18. The a ns we r is B (Chapter 1, T e Intensive Care Unit, Specialized Intensive Care Unit Care

and Monitoring, II). T e patient is clearly showing signs o increased work o breathing and is hyperventilating at an unsustainable rate. It would be reasonable to give anxiolytics or to order a chest radiograph to assess this patient. Increasing the oxygen by nasal cannula may result in marginal improvement in saturation but will not address any underlying condition. Diuresis is appropriate or uid overload. Narcotics will suppress breathing rate but only at signi cant doses and run the risk o hypoventilation. C scan o the abdomen will not be diagnostic and may remove the patient rom an appropriately monitored setting. 19. The a ns we r is E (Chapter 1, Shock, De nition, II D). T e patient is showing signs o septic

shock. T e primary treatment is source control (drainage o the leg abscess), systemic antibiotics, and supportive care (intubation and uid resuscitation). Oral antibiotics alone would be insu cient to treat this critically ill patient. Although IV uids would help support the patient, they do not address the in ection. Phenylephrine is use ul or neurogenic shock, and low-dose dopamine support is not necessary in this instance. 20. The a ns we r is C (Chapter 2, Hernias, Inguinal Hernia, IV). T e patient presents with signs

and symptoms o an inguinal hernia. T e presence o a hernia is an indication or surgical repair. Antibiotics may be indicated in cases o in ection, but the patient has no signs o lymphadenopathy. umor markers are use ul in the workup o testicular masses suspicious or malignancy. In general, imaging is not needed prior to undertaking hernia repair. 21. The a ns we r is D (Chapter 2, Postoperative Complications, Postoperative Fever, I). T e 5 W’s

provide common causes o ever: wound, wind (pneumonia), water (U I), walking (DV ), and “wonder drugs” (typically antibiotics). Other in ections may cause ever, but in the immediate postoperative setting, a new abscess remote rom the operative site is unlikely. 22. The a ns we r is C (Chapter 3, General Aspects or Evaluation and Management o the Surgical

Patient, Preoperative esting, I, and able 3-1). T e patient does not require preoperative cardiac testing given his age, lack o symptoms, and low–cardiac risk surgery. CBC and BMP are reserved or cases in which there is a clinical suspicion o disease or higher risk surgery. Coagulation parameters are necessary in those on anticoagulation or those with a history o bleeding. Urinalysis is indicated in those patients where a oreign body implant is planned, in this case, mesh. 23. The a ns we r is A (Chapter 3, Evaluation o the Surgical Patient with Renal Disease, Preoperative

Management, I B). T e patient is showing signs and symptoms o hyperkalemia. T e ultimate treatment is elimination o potassium, best accomplished through dialysis. For immediate cardiac protection, IV calcium stabilizes cardiac myocytes and prevents ventricular brillation. IV insulin helps shi potassium intracellularly and is use ul as part o the treatment. IV morphine helps with myocardial in arction. 24. The a ns we r is B (Chapter 4, Acute Abdomen, Diagnostic esting, II B). T e patient has signs

and symptoms consistent with acute cholecystitis and demonstrates a positive Murphy sign. T e initial test o choice is an RUQ ultrasound, which may demonstrate a thickened gallbladder wall, pericholecystic uid, ductal dilatation, or gallstones. Abdominal C scan is reasonable or patients with abdominal pain but is neither sensitive nor speci c or biliary pathology. MRE is a reasonable test or small bowel disease, such as Crohn disease. EGD may evaluate gastric pathology such as ulcer, but the clinical situation does not t this patient. In acute cholecystitis, hepatic iminodiacetic acid (HIDA) scanning is reasonable but a er an ultrasound is per ormed. 25. The a ns we r is E (Chapter 4, Acute Abdomen, Physical Exam, IV C). T e patient presents with

a classic history or appendicitis. All o the listed signs may be present in acute appendicitis. Rovsing sign is pain on the right when palpating the le side, as the peritoneum is distended internally to touch the in amed appendix. McBurney sign is pain at McBurney point in the RLQ. Obturator sign is pain on internal rotation o the leg. Psoas may re ect retrocecal appendicitis, pain on extension o the leg. Markle sign represents dif use peritonitis, with pain on shaking the bed.

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Answers and Explanations

26. The a ns we r is B (Chapter 4, Acute Abdomen, Physical Exam, IV E). T e iliopsoas sign is

pain in the lower abdomen and psoas region that is elicited when the thigh is exed against resistance. It suggests an in ammatory process, such as appendicitis. Crepitus suggests a rapidly spreading gas- orming in ection. Murphy sign is elicited by palpating the RUQ during inspiration and suggests acute cholecystitis. Flank and periumbilical ecchymoses suggest retroperitoneal hemorrhage. 27. The a ns we r is D (Chapter 4, Hemorrhage, Evaluation, III B). T e most likely cause o massive

lower GI bleeding in the absence o diverticula is an angiodysplastic lesion o the colon, particularly the right colon. An upper GI series and small bowel studies should be done only a er an exhaustive colonic workup has ailed to demonstrate the source o bleeding. Colonoscopy in the ace o massive bleeding is unreliable and di cult and carries the risk o colonic per oration. In addition, it will not usually demonstrate an angiodysplastic lesion. A repeat barium enema is also unlikely to help. T e most help ul study in this patient would be selective mesenteric angiography. 28. The a ns we r is C (Chapter 4, Acute Abdomen, Physical Exam, IV). T e history described would

be more typical or either testicular torsion or acute epididymitis, o which only torsion represents a surgical emergency. orsion o the testicle is likely the result o an abnormal attachment o the tunica vaginalis around the cord that allows the testis to twist (bell-clapper de ormity). Compromise o the blood supply causes exquisite pain and produces gangrene and atrophy o the testis unless the torsion is treated immediately. orsion is usually seen in young males, most o en occurring spontaneously and even during sleep. It is associated with an onset o severe pain and is accompanied by nausea, vomiting, and abdominal pain. Acute prostatitis may present with vague abdominal pain. A more typical presentation or appendicitis would be pain preceded by nausea or anorexia. T is presentation is not typical or gastroenteritis (which is not a surgical emergency). 29. The a ns we r is C (Chapter 4, Hemorrhage, Evaluation, III B 6). Arteriography is most o en

used as the initial evaluation step or continued bleeding a er anorectal bleeding sources have been eliminated by endoscopy. Arteriography allows identi cation o diverticular bleeding as well as an angiodysplastic lesion o the right colon. Surgery is generally not indicated until 4–6 units o blood have been shed. Coagulation products are o no use unless the patient has abnormal clotting studies. Saline lavage o the colon is not a routine procedure. 30–31. The a ns we rs a re 30-C (Chapter 4, Hemorrhage, Evaluation, III B 3) a nd 31-D (Chapter 4,

Hemorrhage, Evaluation, III D). Upper endoscopy is the most reliable method or precisely locating the site o upper GI bleeding. Endoscopy can almost always be used unless bleeding is massive. Patients who are unstable or have blood losses requiring more than 6 units o blood within a 24-hour period require surgical intervention. Unstable patients should not typically be transported to interventional radiology. A Blakemore tube is only use ul or bleeding esophageal varices. T is patient, who does not have a history indicative o cirrhosis, is unlikely to have bleeding rom varices. 32. The a ns we r is C (Chapter 4, Obstruction, Dif erential Diagnosis, I C 1). Obstructing adhesive

bands a er abdominal surgery are the most common cause o intestinal obstruction. T ey may be dif use or solitary. A partial small bowel obstruction o en responds to conservative management with nasogastric decompression and hydration. Complete small bowel obstruction typically requires operative intervention. 33. The a ns we r is E (Chapter 4, Acute Abdomen, Diagnostic esting, II A 1). Free air within

the peritoneal cavity signals per oration o a hollow viscus. It is present in about 80% o gastroduodenal per orations. Because ree peritoneal air is rarely secondary to other causes, additional studies in this patient would not be necessary be ore laparotomy.

T oracic Disorders

Part II

Chapter Cuts and Caveats CHAP TER 5 P rinc ip le s o Tho ra c ic Surg e ry: Symptoms o malignancy or a radiologic abnormality suspicious or a neoplasm (e.g., coin lesion on a screening chest x-ray, symptoms o dyspnea, or enlarged lymph nodes on physical exam) necessitate aggressive diagnosis because a delay can result in signif cant growth or metastasis and increase mortality. Small cell carcinoma is considered a systemic disease that begins in the lung and metastasizes early. It is rarely amenable to surgical resection, and chemotherapy is the primary treatment. Non–small cell carcinoma begins as a more local disease that spreads to local and regional lymph nodes be ore becoming systemic, making surgical resection more likely to be curative. Mesothelioma usually presents in a late stage with low cure rates, but early stages can be cured with extrapleural pneumonectomy. Spontaneous pneumothorax occurs in young asthenic adults due to a rupture o apical blebs. First episodes are treated with chest tube, but recurrent or bilateral episodes undergo thoracoscopic excision o the blebs and pleural abrasion. Empyema is treated with (1) antibiotics, (2) pus evacuation, and (3) re-expansion o the lung. With mediastinal masses, the location accurately ormulates the di erential diagnosis and ocuses the clinical evaluation: Anterior location suggests lymphoma, thyroid, teratoma/germ cell tumors, or thymoma (which can present with myasthenia gravis, be diagnosed with antiacetylcholine receptor antibodies, and be cured with resection); middle suggests lymphoma, sarcoid, metastatic lung cancer, and cysts; and posterior suggests neurogenic tumors.

CHAP TER 6 He a rt: Many new technologies and minimally invasive interventions are being used to treat coronary artery and valvular disease. Initial treatment o coronary artery disease should consist o li estyle changes. More aggressive interventions should be used based on the symptoms, extent o disease, and the risk/benef t ratio or the intervention. Cardiac catheterization is the basis or determining coronary artery anatomy as well as many endoluminal interventions. Patients with le main coronary artery disease have a reduced survival, making it a primary indication or coronary artery revascularization. T e internal mammary artery gra , which has a 90% or better patency rate at 10 years, has superior patency over other gra s. Mechanical valves have a long li etime but require long-term anticoagulation to prevent thromboembolic events. Biologic prosthesis valves have a shorter li etime but no need or anticoagulation. Acute pericardial tamponade may occur with as little as 100 mL o uid and can be relieved by pericardiocentesis. raumatic tamponade usually requires surgical exploration.

Chapter 5

Principles o T oracic Surgery Jinny Ha and Whitney Burrows

GENERAL P RINCIP LES OF THORACIC SURGERY Tho ra c ic Ca vity Ana to m y

I. Che s t wa ll: Formed by the sternum, ribs, vertebral column, Quic k Cut intercostal muscles, intercostal vessels, and nerves (Fig. 5-1). Its in erior The intercos tal bundle runs on the border is the diaphragm; it is lined internally by the parietal pleura. unders ur ace o the ribs . II. Me d ia s tinum : anatomic region between the pleural cavities or the length o the thorax (Fig. 5-2) A. Anterior compartment: extends rom the undersur ace o the sternum to the pericardium and contains the thymus gland, lymph nodes, ascending and transverse aorta, and great veins B. Visceral compartment: extends rom the pericardium to the anterior longitudinal spinal ligament and contains the pericardium, heart, trachea, hilar structures o the lung, esophagus, phrenic nerves, and lymph nodes C. Paravertebral sulci: potential spaces that contain the sympathetic chains, intercostal nerves, and descending thoracic aorta

Ve in Arte ry Ne rve

Inne rmos t inte rcos ta l mus cle

Exte rna l inte rcos ta l mus cle Inte rna l inte rcos ta l mus cle

Fig ure 5-1: Ches t wall. (Adapted rom Way L. Thoracic wall, pleura, lung, and medias tinum. In: Way LW, ed. Current Surgical Diagnosis and Treatment, 10th ed. Stam ord, CT: Appleton & Lange; 1983:319.)

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Chapter 5

Principles o T oracic Surgery

79

S upe rior Ante rior

Middle P os te rior

Fig ure 5-2: Anatomic compartments o the medias tinum.

III. Lung s a nd tra c he o b ro nc hia l tre e A. Right lung: has three lobes—the upper, middle, and lower— separated by two f ssures (Fig. 5-3) B. Le lung: has two lobes—the upper and the lower 1. Lingula: portion o the upper lobe 2. Single oblique f ssure: separates lobes

Quic k Cut On the right s ide, the m a jo r (o b liq ue ) f s s ure s eparates the lower lobe and the m ino r (ho rizo nta l) f s s ure s eparates the upper lobe.

Tra che a Ma ins te m bronchus

Loba r bronchus Minor fis s ure

S e gme nta l bronchus Oblique fis s ure Lingula

Ma jor fis s ure

Ca rina

Fig ure 5-3: Lungs and tracheobronchial tree. (Courtes y o Thomas C. King and Craig R. Smith. Columbia Pres byterian Hos pital, New York.)

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Chapter 5

General Principles o T oracic Surgery

C. Bronchopulmonary segments: Intact sections o each lobe that have a separate blood supply; there are 10 on the right and 8 on the le . D. racheobronchial tree: Formed rom respiratory epithelium with rein orcing cartilaginous rings; the branching bronchial tubes are progressively smaller, down to a diameter o 1–2 mm. E. Blood supply: dual 1. Pulmonary artery: Blood is unoxygenated. 2. Bronchial artery: Blood is oxygenated. F. Lymphatic vessels: present throughout the parenchyma 1. Lymphatic ow in the pleural space: rom parietal to visceral pleura 2. Lymphatic drainage within the mediastinum: cephalad

Ge ne ra l Tho ra c ic P ro c e d ure s

Quic k Cut The lungs have a dual blood s upply: oxygenated blood rom the bronchial arteries and unoxygenated blood via the pulmonary arteries .

Quic k Cut Generally, lymphatic drainage a ects ips ilateral nodes , but contralateral f ow o ten occurs rom the le t lower lobe.

I. End o s c o p y A. Laryngoscopy: Occasionally important when carcinoma o the lung is suspected. umor involvement o the recurrent laryngeal nerves signif es inoperability. B. Bronchoscopy: use ul or diagnostic and therapeutic purposes 1. Diagnostic uses: include the ollowing: a. o conf rm a lung or tracheobronchial tumor b. o identi y the source o hemoptysis c. o obtain specimens or culture and cytologic examination rom an area o persistent pulmonary atelectasis or pneumonitis d. o obtain tissue biopsy 2. T erapeutic uses: include the ollowing: a. o remove a oreign body b. o remove retained secretions (e.g., rom aspiration o gastric contents) c. o drain lung in ections, such as abscesses 3. ypes: include the ollowing: a. Rigid bronchoscopy: allows visualization o the trachea and main bronchi to the individual lobes (1) Excellent or biopsies o endobronchial lesions and or clearing o thick secretions Quic k Cut (2) Per ormance o rigid bronchoscopy under local Flexible anesthesia requires considerable skill. bronchos copy is es pecially b. Flexible f beroptic bronchoscopy: used more requently us e ul when the patient is (1) Particularly help ul or visualizing lobar bronchi and intubated, as it pres erves the biopsy in small bronchopulmonary segments airway during the procedure. (2) Although rigid bronchoscopy is pre erred, it may also be used or clearing secretions. C. Mediastinoscopy: Lighted hollow instrument is inserted behind the sternum at the tracheal notch and directed along the anterior sur ace o the trachea in the pretracheal space. 1. Diagnostic uses: include the ollowing: a. Direct biopsy o paratracheal and subcarinal lymph nodes Quic k Cut b. Use ul or diagnosing sarcoidosis, lymphoma, and Medias tinal nodes various ungal in ections are important to s tage the 2. Mortality rate: less than 0.1% patient accurately. 3. Complications: include hemorrhage, pneumothorax, and injury to the recurrent laryngeal nerves, although the incidence is extremely low III. Sc a le ne no d e b io p s y: per ormed be ore the use o computed tomography (C )/positron emission tomography (PE ) scans and f ne-needle aspiration (FNA) or lung cancer; used i FNA is nondiagnostic IV. Dia g no s tic p le ura l p ro c e d ure s A. T oracentesis: Pleural e usions are examined or organisms in suspected in ections and cytologically in suspected malignancies. Positive cytologic f ndings prove a tumor to be inoperable.

Chapter 5

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B. Pleural biopsy: Either percutaneous or open pleural biopsy Quic k Cut yields a positive diagnosis in 60%–80% o patients with Pneumothorax is tuberculosis or cancer when a pleural e usion or pleural-based the main complication o mass is present. thoracentes is and pleural biops y. V. Lung b io p s y A. Diagnostic uses: Percutaneous lung biopsy may be used or either a localized peripheral lesion or a di use parenchymal process. B. ypes: include the ollowing: Quic k Cut 1. C -directed FNA biopsy: may obtain tissue or tumor CT-directed FNA that diagnosis, but sampling errors do exist is biopsy negative or a tumor a. Other uses: may also be use ul or in ections and does not rule out the exis tence in ammatory processes o a tumor due to the potential b. Complications: pneumothorax and hemorrhage or s ampling error. 2. Open lung biopsy: necessary i needle biopsy ails at diagnosis VI. Tho ra c ic e xp o s ure : provided by various thoracic incisions, including the ollowing: A. Median sternotomy: exposes heart, pericardium, and structures in the anterior mediastinum (Fig. 5-4) B. Posterolateral thoracotomy: exposes lung, esophagus, and posterior mediastinum (Fig. 5-5) C. Axillary thoracotomy: or limited exposure o the upper thorax during procedures such as f rst-rib resection, upper lobe biopsy, or sympathectomy D. Anterolateral thoracotomy: or rapid exposure in cases o unstable cardiovascular status that cannot tolerate a lateral incision; also allows or excellent airway control (Fig. 5-6) E. Anterior parasternal mediastinotomy (Chamberlain procedure, le side): 2- to 3-cm parasternal incision allows mediastinoscope into the mediastinum or, more commonly, direct visualization and biopsy o mediastinal lymph nodes (para-aortic [level 6] and aortopulmonary window [level 5]).

S upe rior ve na ca va As ce nding a orta P ulmona ry a rte ry

Right a tria l a ppe nda ge Right ve ntricle

Dia phra gm

Fig ure 5-4: Median s ternotomy. (Adapted rom Kirklin J W, Barratt-Boyes BG. Hypothermia, circulatory arres t, and cardiopulmonary bypas s . In: Kirklin J W, Barratt-Boyes BG, eds Cardiac Surgery. New York: Wiley; 1986:62.)

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S ca pula re tra cte d

Fifth rib S ixth rib Rhomboid ma jor Tra pe zius

Fig ure 5-5: Pos terolateral thoracotomy. (Adapted rom Bryant LR, Morgan CV J r. Ches t wall, pleura, lung, medias tinum. In: Schwartz SI, Shires GT, Spencer FC, eds . Principles of Surgery, 5th ed. New York: McGraw-Hill; 1989:634.)

VII. Vid e o -a s s is te d tho ra c ic s urg e ry (VATS): well-tolerated Quic k Cut procedure or numerous pleural and pulmonary diseases that The greates t permits major procedures to be per ormed through minor advantage o VATS is the incisions, using a combination o conventional and unique avoidance o a rib-s preading instrumentation thoracotomy. A. Procedure: Lighted rigid scope connected to a video display is passed into the pleural space. B. Applications: include the diagnosis or management o the ollowing: 1. Idiopathic exudative pleural e usion 2. Known malignant pleural e usion 3. Di use interstitial lung disease 4. Recurrent pneumothorax or persistent air leak

Fig ure 5-6: Anterolateral thoracotomy.

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5. Indeterminate peripheral solitary pulmonary nodules 6. Mediastinal cyst 7. Anatomic lobectomy (in experienced hands only)

CHEST WALL DISORDERS Che s t Wa ll De o rm itie s I. Pe c tus e xc a va tum ( unne l c he s t): Depression o the sternum is the most common chest wall de ormity. A. Symptoms: usually asymptomatic but it may cause some cardiopulmonary symptoms Quic k Cut B. Surgery: may be per ormed or moderate to severe de ormities Surgery may between age 8 years to prior to end o adolescence be per ormed to correct pectus excavatum; bracing 1. Modif ed Ravitch: open is typically us ed or pectus 2. Nuss procedure: closed or minimally invasive approach that carinatum. involves inserting a metal bar through lateral incisions to raise the sternum II. P e c tus c a rina tum (p ig e o n b re a s t): Protrusion de ormity o the anterior sternum, rarely causing symptoms. Bracing is an option, with surgery per ormed or cosmetic reasons. III. P o la nd s ynd ro m e : unilateral absence o costal cartilages, pectoralis muscle, and breast. Surgery is indicated or protection o the underlying thoracic structures and or cosmesis. IV. Tho ra c ic o utle t s ynd ro m e (TOS) A. Clinical presentation: Can mani est into three di erent orms Quic k Cut (neurogenic, arterial, and venous) but symptomatology can overlap TOS is caus ed 1. Neurogenic: combination o motor and sensory symptoms by compres s ion o the rom compression o the brachial plexus. Patients can have neurovas cular bundle— upper extremity (UE) weakness or pain a ecting the neck, the brachial plexus and s ubclavian artery and vein. shoulder, and arm. 2. Arterial: Symptoms are related to compression o the subclavian artery, which can include pain, pallor, paresthesia, and UE coolness. 3. Venous: presents with unilateral swelling o UE with associated cyanosis or rubor due to compression or thrombosis o subclavian vein B. Diagnosis: Clinical; based on a detailed history and physical Quic k Cut examination. Cervical spine f lms to rule out disk disease and Surgery or TOS chest x-ray to evaluate or bony abnormalities (i.e., cervical rib) may involve rs t-rib res ection, should be per ormed. anterior s calenectomy, or C. reatment: initially conservative, using a ocused physical brachial plexus neurolys is . therapy program or 4–6 weeks

Che s t Wa ll Tum o rs I. Be nig n tum o rs A. Chondroma: Most common benign tumor o the chest wall; it occurs at the costochondral junction. B. Fibrous dysplasia o the rib: Occurs posteriorly or on the lateral portion o the rib. It is not pain ul, and it grows slowly. C. Osteochondroma: occurs on any portion o the rib II. Ma lig na nt tum o rs : include f brosarcoma, chondrosarcoma, osteogenic sarcoma, myeloma, and Ewing sarcoma III. Tre a tm e nt: involves wide excision and reconstruction using autologous gra s, prosthetic gra s, or both

P LEURAL AND P LEURAL SPACE DISORDERS Sp o nta ne o us P ne um o tho ra x I. Ep id e m io lo g y: usually occurs in tall, thin males ages 10–30 years. Other risk actors include smoking, chronic obstructive pulmonary disease (COPD), amily history, Mar an syndrome, homocystinuria, and thoracic endometriosis.

Quic k Cut Spontaneous pneumothorax occurs when a s ub p le ura l b le b ruptures into the pleural s pace and allows s econdary lung collaps e.

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II. Sym p to m s : include pleuritic chest pain and dyspnea III. Dia g no s is : made by physical examination and chest radiograph IV. Tre a tm e nt: chest tube drainage o the pleural space A. Indications or surgery: include recurrent pneumothorax (ipsilateral), persistent air leak or 3–5 days, incomplete lung expansion, hemopneumothorax B. Procedure: stapling o apical blebs and pleural abrasion

Quic k Cut Surgery is generally res erved or pneumothorax that does not res olve with ches t tube drainage.

P le ura l E us io ns I. Tra ns ud a tive e us io ns : result rom systemic disorders that cause an increased hydrostatic pressure (congestive heart ailure [CHF]) or states associated with decreased oncotic pressure (hypoalbuminemia) allowing the accumulation o protein-poor plasma f ltrate in the pleural space. reatment is directed toward the underlying process; thoracentesis provides diagnosis and symptomatic relie . Quic k Cut II. Exud a tive e us io ns : result rom the local pleural pathology, which increases the permeability o the pleura, allowing accumulation o a protein-rich plasma f ltrate within the pleural space. reatment usually requires chest tube drainage and/or pleurodesis.

Trans udative e us ions are s ys temic and protein poor; exudative e us ions are local and protein rich.

P le ura l Em p ye m a I. P a tho p hys io lo g y: evolves in three stages A. Exudative phase: Onset to 7 days; uid is initially produced. B. Fibrinopurulent phase: Days 7–21; deposits o f brin on the pleura orm loculations, and the uid is turbid or purulent. C. Chronic or organized phase: More than 21 days; f brin and pleura use and thicken around the periphery o the uid, resulting in rank abscess ormation and/or pleural rind or peel. II. Dia g no s is : Made by thoracentesis in a patient with pleural e usion, leukocytosis, and ever; the aspirated pleural uid is sent or biochemistry studies, and i on gross examination the uid is very cloudy or smells oul, an empyema is likely to be present. III. Tre a tm e nt: Recent use o image-guided catheters ollowed by pleural lytic therapy using tissue plasminogen activator has demonstrated impressive results in success ully draining empyemas. A. Early empyemas: may be treated with aspiration and hhantibiotics B. Established empyemas: Usually have thicker uid and need continuous closed drainage. Loculated empyemas may require surgical drainage via VA S or open thoracotomy. C. Chronic empyemas: I unresponsive to chest tube drainage, may require open drainage via localized rib resection, especially or debilitated patients.

P le ura l Tum o rs a nd Me s o the lio m a I. Ove rvie w: Majority o pleural lesions are metastases rom other primary malignancy. II. Lo c a lize d b e nig n m e s o the lio m a s : Are not related to asbestos exposure; these lesions are treated by wide local excision. III. Ma lig na nt m e s o the lio m a : Related to prior asbestos exposure and presents with a pleural e usion. It has a poor prognosis; the role o surgery is primarily or diagnosis and palliation.

Quic k Cut Pus in the pleural s pace us ually accumulates s econdary to pulmonary in ection.

Quic k Cut Stages o empyema: I, exudative phas e; II, brinopurulent phas e; and III, chronic or organized phas e.

Quic k Cut Pos itive pleural cultures , low pH ( 7.1), low glucos e ( 50 mg/dL), and high lactate dehydrogenas e content ( 1,000 IU/dL) are cons is tent with empyema.

Quic k Cut Decortication and evacuation o empyema s hould be per ormed or lung re-expans ion in chronic empyema.

Quic k Cut Primary tumors o the pleura are rare.

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P ULMONARY INFECTIONS Lung Ab s c e s s I. Etio lo g y: Aspiration o oropharyngeal contents is the most common cause. It occurs in the dependent segments o the lung; these in ections are most o en mixed ora, but anaerobic organisms may predominate.

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Quic k Cut Symptoms o lung abs ces s are s imilar to thos e as s ociated with pneumonia. Radiographs will demons trate a cavitary les ion with an airf uid level.

II. Tre a tm e nt: Intravenous antibiotics are the mainstay or lung abscesses. A. Image-guided percutaneous drainage: o en e ective or large abscesses B. Indications or surgery: include ailure o the abscess to resolve with antibiotic therapy, hemorrhage, inability to rule out cavitating carcinoma, giant abscess ( 4–6 cm in diameter), or rupture into pleural space resulting in a pyopneumothorax

SOLITARY P ULMONARY NODULES (COIN LESIONS) Ove rvie w I. P re s e nta tio n: well-circumscribed lesions usually less than 3 cm in diameter that are completely surrounded by normal lung parenchyma II. Initia l a s s e s s m e nt: should always start with a thorough history and physical with ocus on smoking history, history o cancer, hemoptysis, and age

Quic k Cut Solitary pulmonary nodules have a broad di erential, including congenital, inf ammatory, neoplastic, and vascular etiologies.

Im a g ing I. Thin-s e c tion CT: important or characterizing a pulmonary nodule A. Margins: Irregular, lobulated, or spiculated edges are suggestive o malignancy. B. Calcif cations: ypically associated with benign lesions; di erent patterns o calcif cation can be seen in granulomatous disease and hamartomas. C. Growth: Comparison with previous imaging is important. Size stability more than 2 years is highly associated with benign lesions.

Quic k Cut Co ro na ra d ia ta s ig n, which is the s piculated appearance o a les ion rom ne linear s trands extending outward, is highly s us picious o a malignancy.

II. P ET s c a n: has sensitivity o 95% and lower specif city o 80% A. False negatives: can occur or bronchoalveolar carcinomas, carcinoids, and tumor less than 1 cm in diameter B. False positives: can occur in the setting o recent in ection or granulomatous diseases

Inva s ive Dia g no s tic Te c hniq ue s I. Bro nc ho s c o p y: with endobronchial biopsy and/or brushings can be use ul or centrally located lesions II. Tra ns tho ra c ic FNA: Can be used or peripherally located lesions. Possible complications include hemorrhage and pneumothorax. III. Exc is io na l b io p s y: allows or def nitive pathologic diagnosis

BRONCHOGENIC CARCINOMA Ove rvie w I. Ep id e m io lo g y: Bronchogenic carcinoma is the leading cause o cancer death among men and women in the United States. A. Locally advanced or metastatic disease: 75% o patient presentations B. Age: Middle-aged and elderly; 90% o cases occur between ages 40 and 80 years.

Quic k Cut Lung cancer is the leading caus e o cancer death and has a 5-year s urvival rate o 15% .

II. Ris k a c to rs : 90% o all lung carcinomas are related to smoking; occupational and environmental carcinogens include asbestos, tar, radon, soot, nickel, arsenic, and chromium.

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P a tho lo g y I. His to lo g ic d is trib utio n: Most common lung neoplasm is a Quic k Cut metastatic lesion rom another primary malignancy (secondary The mos t common lung cancer). Lung cancers are classif ed into two major types. lung neoplas m is a metas tatic A. Small cell lung carcinomas: 20% o primary lung cancers depos it rom another primary B. Non–small cell lung carcinomas: 80% o primary lung cancers malignancy. II. No n–s m a ll c e ll lung c a rc ino m a s A. Adenocarcinoma: Now the most common lung carcinoma; lesions are typically located in the periphery and arise rom bronchioles and terminal alveolar units. B. Noninvasive adenocarcinoma: ormerly called bronchoalveolar carcinoma; variant o adenocarcinoma 1. Forms (three): solitary nodule, multinodular orm, and a di use/pneumonic orm 2. Overrepresented in nonsmokers C. Squamous cell carcinoma: second most common subtype 1. Location: Most occur centrally in the lung f elds and arise rom the respiratory mucosa o lobar and segmental bronchi. 2. umor characteristics: Bulky and is associated with obstruction; it undergoes central necrosis and cavitation. III. Sm a ll c e ll a na p la s tic (o a t c e ll) c a rc ino m a : highly malignant; represents 15%–25% o all malignant lung tumors A. Histology: reveals clusters, nests, or sheets o small, round, oval, or spindle-shaped cells with dark nuclei and a scanty cytoplasm 1. Electron microscopy: reveals neurosecretory cytoplasmic granules 2. Classif cation: neuroendocrine tumors o the amine precursor uptake and decarboxylation (APUD) system B. Staging classif cations: early metastasis by lymphatic and vascular routes 1. Limited disease: localized to one hemithorax with ipsilateral regional node involvement Quic k Cut 2. Extensive disease: metastasis outside the hemithorax Treatment or nonC. reatment: Involves a combination o chemotherapy and s mall cell lung cancer is primarily s urgical. Treatment radiotherapy. Surgery may be indicated in those with early lesions. or s mall cell carcinoma is D. Prognosis: overall quite poor chemotherapy and radiation. IV. Othe r ra re tum o rs : Undi erentiated large cell carcinoma, bronchial adenoma, papilloma, and sarcomas are rare.

Clinic a l P re s e nta tio n I. Pulm o na ry s ym ptom s : may include unrelenting cough, dyspnea, Quic k Cut chest pain, hemoptysis, wheezing, and pneumonic symptoms A chronic, II. Extra p ulm o na ry s ym p to m s unrelenting cough is the mos t common s ymptom o lung A. Metastatic extrapulmonary mani estations: include weight cancer. loss, malaise, headache, nausea and vomiting related to brain metastases, and bone pain B. Nonmetastatic extrapulmonary mani estations (paraneoplastic syndromes): secondary to hormonelike substances that are elaborated by the tumor and include Cushing syndrome, hypercalcemia, myasthenic neuropathies, hypertrophic osteoarthropathies, and gynecomastia Quic k Cut III. P a nc o a s t tum o r: invades the superior sulcus involving the Horner s yndrome is thoracic outlet and results in shoulder pain rom invasion o ptos is , mios is , enophthalmos , muscle, radicular arm pain rom invasion o C8 and 1 nerve and anhidros is . roots, and Horner syndrome

Dia g no s is a nd Sta g ing I. Ab no rm a l c he s t ra d io g ra p h: Most common f nding; more likely to represent carcinoma in patients age 40 years and older. T e tumor may present as a nodule, an inf ltrate, or as atelectasis. II. CT s c a n: reveals the extent o the tumor and the possibility o mediastinal lymph node metastasis

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III. P ET s c a n: routinely used to assess the primary tumor and the mediastinal lymph nodes and to screen or metastatic disease IV. Bro nc ho s c o p y: assesses or bronchial involvement and resectability in central lesions, and tissue is obtained or cytologic examination V. Me d ia s tino s c o p y o r m e d ia s tino to m y: obtains mediastinal lymph nodes or pathologic examination and aids in staging VI. P e rc uta ne o us ne e d le b io p s y: may be used or peripheral lesions to obtain tissue or cytologic examination VII. Sta g ing : undamental or the evaluation o treatment protocols and based on in ormation obtained during the preoperative evaluation, f ndings at mediastinoscopy, thoracotomy, and pathologic f ndings o the surgical specimens. Def nitions o tumor size ( ), lymph node metastasis (N), and distant metastasis (M) comprise the NM classif cation o carcinoma o the lung by the revised International Clinical Staging System ( able 5-1).

Ta b le 5-1: Tum o r-No d e -Me ta s ta s is Cla s s if c a tio n o Lung Ca nc e r T (p rim a ry tum o rs ) TX: Tumor is proved by the presence of malignant cells in bronchopulmonary secretions but is not visualized on a radiograph or by bronchoscopy or any tumor that cannot be assessed, such as one in a retreatment staging. TO: No evidence of primary tumor TIS: Carcinoma in situ T1: Tumor that is 3 cm in greatest dimension, surrounded by lung or visceral pleura and with no evidence of invasion proximal to a lobar bronchus at bronchoscopy T1a : Tumor 2 cm in size T1b : Tumor 2–3 cm in size T2: Tumor 3 cm but 7 cm in greatest dimension or a tumor of any size that either invades the visceral pleura or has associated atelectasis or obstructive pneumonitis that extends to the hilar region that involves less than an entire lung; at bronchoscopy, the proximal extent of demonstrable tumor must be within a lobar bronchus or at least 2 cm distal to the carina. T2a : Tumor 3 but 5 cm in size T2b : Tumor 5 cm but 7 cm in size T3: Tumor 7 cm in size or one that directly invades into the chest wall (including superior sulcus tumors), diaphragm, mediastinal pleura, parietal pericardium, or phrenic nerve or a tumor in the main bronchus 2 cm from the carina without involving the carina; also, any associated atelectasis or obstructive pneumonitis involving the entire lung or a separate nodule in the same lobe T4: Tumor of any size with invasion of the mediastinum or involving the heart, great vessels, trachea, esophagus, vertebral body, or carina; in addition, satellite tumor nodules that occur within a different ipsilateral lobe N (no d a l invo lve m e nt) N0: No demonstrable metastasis to regional lymph nodes N1: Metastasis to lymph nodes in the peribronchial or the ipsilateral hilar region, or both, including direct extension N2: Metastasis to ipsilateral mediastinal lymph nodes and subcarinal lymph nodes N3: Metastasis to contralateral mediastinal lymph nodes, contralateral hilar lymph nodes, ipsilateral or contralateral scalene, or supraclavicular lymph nodes M (d is ta nt m e ta s ta s is ) M0: No (known) distant metastasis M1: M1a : Separate tumor in a contralateral lobe; tumor with pleural nodules or malignant pleural effusions M1b : Distant metastasis

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Tre a tm e nt I. Surg ic a l tre a tm e nt A. Pulmonary resection: Such as lobectomy, extended lobectomy, or pneumonectomy, is the mainstay o curative therapy or early-stage bronchogenic carcinoma. A regional lymphadenectomy is routinely per ormed primarily or prognostic (staging) purposes rather than therapeutic intent. 1. Lobectomy: used in disease localized to one lobe 2. Extended resections and pneumonectomy: used when the tumor involves a f ssure or centrally located tumors 3. Wedge resections or bronchial segmentectomy: may be used in localized disease in high-risk patients B. Contraindications or thoracotomy: 50% o all patients with Quic k Cut lung carcinomas are not candidates or thoracotomy. A “popcorn” 1. N2 disease: extensive ipsilateral mediastinal lymph node appearance on x-ray involvement, particularly high paratracheal and subcarinal s ugges ts ha m a rto m a , an 2. N3 disease: any contralateral mediastinal lymph node overgrowth o cartilage that is the mos t common benign involvement lung les ion. 3. Other: distant metastases, malignant pleural e usion, superior vena cava syndrome, recurrent laryngeal nerve involvement, phrenic nerve paralysis, or poor pulmonary unction (relative contraindication) II. Ad juva nt the ra p y: Further treatment using radiotherapy, chemotherapy, or both is indicated or some advanced-stage tumors. A. Postoperative adjuvant chemotherapy: now indicated in all resected non–small cell lung cancer patients stage Ib and higher, demonstrating a small but statistically signif cant survival benef t B. Preoperative chemotherapy and radiation therapy: can be given to select patients with IIIa (N2) disease to sterilize their mediastinal node disease

BRONCHIAL ADENOMAS Ove rvie w

Quic k Cut The term a d e no m a is a mis nomer becaus e all o thes e les ions are all m a lig na nt ne o p la s m s that aris e rom the tracheobronchial tree.

I. Cha ra c te ris tic s : Carcinoid tumors, which comprise 80%–90% o bronchial adenomas, occur mainly in the proximal bronchi (20% mainstem bronchi, 60% lobar or segmental bronchi, and 20% peripheral parenchyma). A. Carcinoid tumors: arise rom basal bronchial stem cells, which, in the process o malignant trans ormation, di erentiate in the direction o neuroendocrine tissue B. Growth: T ey grow slowly and protrude endobronchially, o en causing some degree o bronchial obstruction. C. Peptide production: can produce many di erent types, most commonly serotonin, which can, but very rarely does, lead to carcinoid syndrome i released into systemic circulation II. Sig ns a nd s ym p to m s : Cough, recurrent in ection, hemoptysis, pain, and wheezing. Patient may report a long history o recurrent pneumonia or asthma. III. Dia g no s is : Chest x-ray may reveal a mass with or without associated atelectasis or pneumonia. C better describes the local extent or the presence o distant metastasis. A tissue sample via bronchoscopy or FNA can be per ormed. IV. Tre a tm e nt: surgical excision A. Lobectomy: Most commonly per ormed procedure; rarely does it require a pneumonectomy. B. Octreotide: can be used or patients with unresectable disease with symptoms o carcinoid syndrome V. P ro g no s is : should be greater than 85% 5-year survival or typical carcinoid tumors, decreasing to less than 50%–70% or the atypical variant

Ad e no id Cys tic Ca rc ino m a (Cylind ro m a ) I. Cha ra c te ris tic s : comprises 10% o bronchial adenomas A. Location: occurs more centrally in the lower trachea/carina area and in the orif ces o the mainstem bronchi B. Metastases: tends to occur late, but about one third o patients present with metastases

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II. Tre a tm e nt: En bloc excision o the tumor, including peribronchial tissue and regional lymph nodes. Radiation therapy should be considered in all inoperable patients and in those with residual tumor a er resection. III. P ro g no s is : less avorable than in the case o a carcinoid tumor

Muc o e p id e rm o id Ca rc ino m a I. Cha ra c te ris tic s : account or less than 1% o bronchial adenomas A. Location: Distribution in the tracheobronchial tree is similar to that with carcinoid tumors. B. Most are low grade. II. Tre a tm e nt: Principles that are outlined or carcinoid tumors apply to low-grade mucoepidermoid carcinoma. High-grade variants should be approached and managed like other bronchial carcinomas.

METASTATIC TUMOR Tre a tm e nt

Quic k Cut Metas tatic tumors are common to the lung, which may be the only s ite o metas tas es rom a nonpulmonary primary tumor.

I. Tre a tm e nt: Most metastatic tumors to the lung are not resected. In highly selected cases, surgery is indicated. II. Sing le o r m ultip le m e ta s ta tic tum o rs : can be removed rom the lung as part o the treatment protocol III. Co m ple te re s e c ta b ility: Associated with longer survival than unresectable disease. Long-term survival more than 5 years can be 20%–30% o all patients with completely resected pulmonary metastases.

TRACHEAL DISORDERS Ana to m y I. Struc ture : rachea is 11 cm rom the cricoid to the carina and 1.8–2.3 cm in diameter. A. Cartilage: Encircled by 18–22 cartilaginous rings. T e cricoid cartilage is the only complete tracheal ring; the remaining rings have a membranous portion posteriorly. B. Mobility: Vertical; when the neck is extended, 50% o the trachea is in the neck; when the neck is exed, the entire trachea is behind the sternum. II. Blo o d s up p ly: Segmental and shared with the esophagus; blood is supplied by the in erior thyroid, subclavian, superior intercostal, internal mammary, and the innominate arteries and the bronchial circulation.

Tra c he a l Ne o p la s m s I. Typ e s A. Primary neoplasms: rare 1. Squamous cell carcinomas: Most common variant o these rare tumors. T ey may be exophytic, may cause superf cial ulceration, or may be multiple. 2. Adenoid carcinoma: grows slowly 3. Other: include carcinosarcomas, pseudosarcomas, mucoepidermoid carcinomas, squamous papillomas, chondromas, and chondrosarcomas B. Secondary tumors: usually rom the lung, esophagus, or thyroid gland II. Dia g no s is : Bronchoscopy provides diagnosis. A. Radiographic studies: include chest x-ray, C scan, tracheal tomogram, and uoroscopy or laryngeal evaluation B. Pulmonary unction testing: mandatory i carinal or pulmonary resection is contemplated III. Tre a tm e nt: racheal resection; up to 50% may be removed. A. Resection: Adequate mobilization can usually be obtained by exing the patient’s neck, although laryngeal or hilar release techniques are sometimes necessary. An end-to-end anastomosis is per ormed. B. Incisions 1. Cervical incision: used or resection o the upper hal o the trachea 2. Posterolateral thoracotomy: used or the lower portion o the trachea 3. Combined cervical incision and median sternotomy: can expose entire trachea IV. P ro g no s is : similar to that or resectable carcinoma o the lung

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MEDIASTINAL LESIONS Ante rio r Co m p a rtm e nt Le s io ns

Quic k Cut Fi ty percent o patients with thymomas have as s ociated myas thenia gravis .

I. Thym o m a s : T ymic tumors are among the most common tumors o the anterosuperior mediastinum in the adult. A. Incidence: T ymomas are most common in the f h and sixth decades o li e; males and emales are equally a ected. B. Diagnosis: Most patients are asymptomatic, and the tumor is Quic k Cut discovered incidentally on a routine chest radiograph. Thymic tumors that are not as s ociated with 1. Symptoms: when present, relate to invasion by malignant myas thenia gravis require thymomas and consist o chest pain, dyspnea, or superior exploration and total removal vena cava syndrome o the tumor. 2. Chest x-ray: Lateral view is help ul because small tumors may be obscured by the great vessels in posteroanterior chest radiographs. C. Surgical treatment: Most are removed through a sternal-splitting median sternotomy. II. Te ra to m a s A. Incidence: Occur most requently in adolescents; 80% are benign. B. Etiology: Originate rom the branchial cle pouch in association with the thymus gland. Ectodermal, endodermal, and mesodermal elements are present. C. Diagnosis: Radiographically may appear as smooth-walled cystic lesions or as lobulated solid lesions. Calcif cation is o en present. D. reatment: surgical excision Quic k Cut III. Lym p ho m a s : Symptoms include cough, chest pain, ever, and Fi ty percent o weight loss. patients with lymphoma A. Diagnosis: chest radiograph and lymph node biopsy, using have medias tinal lymph node either mediastinoscopy or anterior mediastinotomy involvement. B. reatment: nonsurgical IV. Ge rm c e ll tum o rs : Rare; occur with an incidence o less than 1% o all mediastinal tumors. T ey metastasize to pleural lymph nodes, the liver, bone, and the retroperitoneum. A. Histologic types: seminoma, embryonal cell carcinoma, teratocarcinoma, choriocarcinoma, and endodermal sinus tumor B. Symptoms: chest pain, cough, and hoarseness caused by invasion o the vagus nerves C. Diagnosis: combination o radiographs and serum tumor markers (beta-human chorionic gonadotropin and alpha- etoprotein) D. reatment 1. Seminomas: complete surgical resection ollowed by postoperative radiotherapy 2. Nonseminomas: combination chemotherapy E. Adjuvant therapy: Seminomas are very radiosensitive, and the other cell types may benef t rom chemotherapeutic agents.

Vis c e ra l Co m p a rtm e nt Le s io ns I. P e ric a rd ia l c ys ts : Usually asymptomatic and are seen on a chest radiograph. Surgery is usually done as a diagnostic procedure. II. Bro nc ho g e nic c ys ts : Generally arise posterior to the carina and may cause pulmonary compression, which can be li e-threatening, particularly in in ancy. T e usual treatment is surgical excision. III. As c e nd ing a o rtic a ne urys m s : included as middle mediastinal masses due to the location o the great vessels in this compartment

THORACIC TRAUMA Im m e d ia te Li e -Thre a te ning Injurie s I. Airwa y o b s truc tio n: Quickly leads to hypoxia, hypercapnia, acidosis, and cardiac arrest. T e highest priority is rapid evaluation

Quic k Cut Visceral compartment lesions are usually cystic, most commonly pericardial cysts or bronchogenic cysts.

Quic k Cut Fewer than 25% o patients with ches t injuries require s urgical intervention.

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and securing the upper airway by clearing out secretions, blood, or oreign bodies; endotracheal intubation; or cricothyroidotomy. II. Te ns io n p ne um o tho ra x: implies that the pleural air collection Quic k Cut is under positive pressure, signif cant enough to cause a marked Tension mediastinal shi away rom the a ected side and cardiopulmonary pneumothorax is an emergency that requires immediate needle collapse decompression and presents A. Causes: Check-valve mechanism allows air to escape rom the with hypotension. lung into the pleural space, which cannot be vented and can cause sudden death. B. Clinical presentation: Collapsed lung results in chest pain, shortness o breath, and decreased or absent breath sounds on the a ected side. Hypotension results rom mediastinal shi , which compresses the vena cava and obstructs venous return to the heart. C. reatment: T orax must be decompressed by an intercostal tube with underwater seal and suction. III. Op e n p ne um o tho ra x: Open wound in the chest wall has exposed the pleural space to the atmosphere. A. Clinical presentation: Open wound allows air movement through the de ect during spontaneous respiration, causing ine ective alveolar ventilation. B. reatment: Involves covering the wound and inserting a thoracostomy tube. Later, debridement and closure o the wound may be necessary. IV. Ma s s ive he m o tho ra x: occurs with the rapid accumulation o blood in the pleural space, which causes both compromised ventilation as well as hypovolemic shock A. reatment: entails securing intravenous access and beginning volume resuscitation and placement o a thoracostomy tube B. Complications 1. Fibrothorax: I the hemothorax is inadequately drained, this may develop and requires decortication. 2. Hemorrhage: indication or surgical exploration

Quic k Cut Surgery is indicated i a ches t tube placed or hemorrhage has an initial output o more than 1 L or drainage o more than 200 mL/hr over 4 hours .

V. Ca rd ia c ta m p o na d e : occurs with the rapid accumulation o blood in the pericardial sac, which causes compression o the cardiac chambers and decreased diastolic f lling resulting in decreased cardiac output A. Clinical presentation: hypotension, tachycardia, and jugular venous distention with mu ed heart sounds B. reatment: prompt pericardial decompression either by pericardiocentesis (i in extremis) or surgical pericardiotomy VI. Fla il c he s t: Blunt chest trauma, causing extensive anterior and Quic k Cut posterior rib ractures or sternocostal disconnection, results in Flail ches t is de ned paradoxical chest wall movement. as at leas t two ractures A. Clinical presentation: Paradoxical chest wall movement in two or more ribs , which inter eres with the mechanics o respiration and can cause acute produces a ree f oating alveolar hypoventilation. Morbidity is related to underlying lung s egment o ches t wall. injury. B. reatment: Adequate pain control (intercostal blocks or epidural narcotics) and aggressive pulmonary toilet. Mechanical ventilation may be required in severe cases.

P o te ntia lly Li e -Thre a te ning Injurie s I. Tra c he o b ro nc hia l d is rup tio n: usually occurs within 2 cm o the carina A. Diagnosis: made by bronchoscopy; suspected with the ollowing: 1. Collapsed lung ails to expand, ollowing placement o a thoracostomy tube. 2. Massive air leak persists. 3. Massive progressive subcutaneous emphysema is present. B. reatment: primary repair II. Ao rtic d is rup tio n: Results rom a deceleration injury in which the mobile ascending aorta and arch move orward, whereas the descending thoracic aorta remains f xed in position by the mediastinal

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Chapter 5

III.

IV.

V.

VI.

T oracic rauma

pleura and intercostal vessels. T is movement causes a tear at the Quic k Cut aortic isthmus, just distal to the takeo o the le subclavian artery. The mos t common A. Clinical presentation: Usually results in racture o the intima area o blunt aortic injury is at and media with the adventitia remaining mainly intact. However, a point o xed attachment, complete disruption o all layers can occur with the hematoma at the s ite o the ligamentum contained only by the intact mediastinal pleura. arterios um, jus t dis tal to the takeo o the le t s ubclavian B. Chest radiograph f ndings: widened mediastinum, indistinct artery. aortic knob, depressed le mainstem bronchus, apical cap, deviation o trachea to the right, and le pleural e usion C. Diagnosis: conf rmed by an aortogram or C angiography D. reatment: Involves strict blood pressure control with short-acting antihypertensives and open repair with interposition gra . Some centers treat with placement o endovascular stents. Dia p hra g m a tic d is rup tio n: results rom blunt trauma to the chest and abdomen, producing a radial tear in the diaphragm, beginning at the esophageal hiatus A. Diagnosis: Chest radiograph shows evidence o the stomach or colon in the chest. B. reatment: Immediate placement o a nasogastric tube (i not already in place) will prevent acute gastric dilatation, which can produce severe, li e-threatening respiratory distress. 1. Next step: urgent transabdominal repair with simultaneous treatment o any intra-abdominal injuries 2. ransthoracic repair: I rupture is not diagnosed until 7–10 days later, this is recommended to ree any adhesions to the lung that might exist. Es o p ha g e a l d is rup tio n: usually results rom penetrating rather than blunt trauma A. Clinical presentation: causes rapidly progressive mediastinitis B. reatment: wide mediastinal drainage and primary closure with tissue rein orcement (pleura, intercostal muscle, or stomach) Ca rd ia c c o ntus io n: results rom direct sternal impact; ranges in severity rom clinically silent to cardiac rupture A. Functional complications: arrhythmias, myocardial rupture, ventricular septal rupture, le ventricular ailure, and coronary artery rupture or thrombosis B. Diagnosis: electrocardiography, cardiac enzymes, and echocardiogram C. reatment: cardiac and hemodynamic monitoring, appropriate pharmacologic control o arrhythmias, and inotropic support i cardiogenic shock develops P ulm o na ry c o ntus io n: most common injury associated with thoracic trauma A. Causes: Blunt trauma produces capillary disruption with subsequent intra-alveolar hemorrhage, edema, and small airway obstruction. B. Diagnosis: chest radiograph, arterial blood gas, and clinical symptoms o respiratory distress C. reatment: uid restriction, supplemental oxygen, vigorous chest physiotherapy, adequate analgesia (epidural narcotics), and prompt chest tube drainage o any associated pleural space complication

Chapter 6

Heart

A. Claire Watkins, D. Bruce Panasuk, William R. Alex, Richard N. Edie, and James S. Gammie

ACQUIRED HEART DISEASE Ove rvie w I. Ep id e m io lo g y A. Heart disease: leading ause death (38%) in N rth Ameri a B. Myocardial in arction (MI): 3 milli n annually in the United States; m rtality rate

10%–15%

II. Sig ns a nd s ym p to m s A. Dyspnea: aused by pulm nary ngesti n, resulting r m in reased lef atrial pressure B. Peripheral edema: result signi ant right-sided ngestive heart ailure (CHF) C. Chest pain: aused by angina pe t ris, MI, peri arditis, a rti disse ti n, pulm nary in ar ti n, pulm nary emb lism (PE), r a rti sten sis D. Palpitations: ardia arrhythmia; f en indi ates is hemia E. Hemoptysis: ass iated with mitral sten sis, pulm nary hypertensi n, and pulm nary in ar ti n F. Syncope: result mitral sten sis, a rti sten sis, heart bl k, r arrhythmia G. Fatigue: result de reased ardia utput (CO) III. P hys ic a l e xa m ina tio n: sh uld in lude the ll wing: A. Blood pressure: measured in b th arms and legs B. Peripheral pulses Quic k Cut 1. Pulsus parvus et tardus: may be seen with a rti sten sis Puls us parvus 2. Aortic insuf ciency: auses wide pulse pressure with a et tardus : a s low ris ing and “water-hammer pulse” (sh rt, intense peripheral pulses) weak puls e C. Neck vein distention: rrelates with internal jugular vein lling; may be aused by ardia tamp nade, tri uspid regurgitati n, r right heart ailure D. Heart 1. Inspection and palpation: the pre rdium a. Normal point o maximum impulse (PMI): elt at the mid lavi ular line, f h inter stal spa e b. Le ventricular hypertrophy: PMI is in reased and displa ed laterally. c. Right ventricular hypertrophy: parasternal heave 2. Auscultation: quality heart t nes, type rhythm, Quic k Cut murmurs, rales, and gall ps EF is a measure IV. P re o p e ra tive m a na g e m e nt: Obtain baseline hest radi graph and ele tr ardi gram (ECG). A. Echocardiography: de nes ventri ular un ti n and eje ti n ra ti n (EF) and assesses r valvular disease

o le t ventricular unction; greater than 50% is normal. EF(% ) stroke volume (SV) 100 end diastolic volume (EDV).

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B. Cardiac catheterization: Right heart atheterizati n is used t determine pulm nary artery pressure (PAP), CO, pulm nary apillary wedge pressure (PCWP), and the presen e lef -t -right shunts (“step up”). Lef heart atheterizati n in ludes r nary artery angi graphy and ventri ul graphy (t determine EF). C. Pulmonary unction studies: patients with kn wn pulm nary disease

Quic k Cut Cardiac catheterization is the gold s tandard or def ning coronary artery anatomy and dis eas e.

V. Ca rd ia c a rre s t A. Causes: in lude an xia/hyp xemia, is hemia/ r nary thr mb sis/MI, and ele tr lyte disturban es (i.e., my ardial depressants, su h as anestheti agents, antiarrhythmi drugs, r digitalis; ndu ti n disturban es, and vag t ni maneuvers) B. Immediate cardiopulmonary resuscitation (CPR): ABCs Quic k Cut 1. Airway: end tra heal intubati n; surgi al airway i airway Anoxic brain injury bstru ti n res ults a ter 3–4 minutes 2. Breathing: ventilat ry and xygen supp rt with an Ambu bag o cardiac arres t. CPR can r a ventilat r maintain cerebral per us ion. 3. Circulation a. Cardiac massage: Cl sed hest ardia mpressi ns. With ardia tamp nade, a ute massive hem th rax, r an Quic k Cut unstable sternum, pen hest massage is usually required. Acidos is and b. Electrical de brillation: i ardia arrest is r m hypocalcemia suppress the myocardium, thereby ventri ular brillati n impairing ventricular c. Drug therapy: C mm nly used agents in lude the unction. Hyperkalemia and ll wing: hypomagnes emia excite (1) Epinephrine: in tr pe, hr n tr pe, vas press r the myocardium and are (2) Calcium: ptimizes in tr pi e e ts arrhythmogenic. (3) Sodium bicarbonate: t treat ass iated a id sis (4) Vasopressor agents: t supp rt bl d pressure (5) Atropine: t reverse brady ardia d. Blood volume: repla e i ne essary VI. Extra c o rp o re a l c irc ula tio n (c a rd io p ulm o na ry b yp a s s ): pr vides the surge n with a m ti nless heart and a bl dless eld while simultane usly per using the di erent rgan systems with xygenated bl d (Fig. 6-1) A. Technique: Bl d is drained r m the ven us system, passed Quic k Cut thr ugh an xygenat r and a heat ex hanger, and pumped ba k In the OR, the high anteri rly. potas s ium concentration B. Myocardial protection: Hypothermia and cardioplegia are in cardioplegic s olutions allows arres t o the heart and pr te tive during the is hemia indu ed by the pr edure. minimization o myocardial 1. Widespread total body in ammatory response: initiates energy cons umption. hum ral ampli ati n systems, in luding the agulati n as ade, brin lyti system, mplement a tivati n, and the kallikrein-kinin system. Quic k Cut 2. Vasoactive substance release: epinephrine, n repinephrine, Major complications histamine, and bradykinin o cardiopulmonary bypas s 3. Sodium and ree water retention: auses di use edema include s troke and other VII. P ro s the tic va lve s (Fig . 6-2): an be tissue r me hani al materials A. Tissue valves: P r ine a rti valves r b vine peri ardial tissue d n t require l ng-term anti agulati n but have limited durability and may ail gradually ver time. A rti tissue valves an be expe ted t last 10–20 years, and mitral tissue valves last 10–15 years. B. Mechanical valves: require li etime anti agulati n therapy t prevent thr mb sis/emb lism but typi ally last r li e C. Risks: Str ke risk 1%–2% per year. B th tissue and me hani al valves have a similar risk pr stheti valve end arditis.

embolic events , vas cular injury or aneurys m, air embolis m, hemolys is , and platelet dys unction.

Quic k Cut The ris k o s troke is higher or mitral valves than aortic valves .

Chapter 6

Heart

O 2 ble nde r Membrane oxygenator

CO 2

O2 Warmed H2 O input He a t e xcha nge r

P ostmembrane pressure monitor P ostmembrane pressure monitor

Fluids He pa rin P ump Venous reservoir

Fig ure 6-1: Extracorporeal membrane oxygenation (ECMO) s etup.

Key a a nte rior b pos te rior c le ft d right e s e pta l

Heart Valves (Superior view)

Ante rior P ulmona ry va lve

a Ante rior inte rve ntricula r a .

d Aortic va lve

c

L. corona ry a .

R. corona ry a .

Circumfle x a .

Conus a rte rios us br.

L. ve ntricle d

c

Bicus pid va lve (mitra l va lve )

R. ve ntricle b R. ma rgina l a . a

a

e b b Gre a t ca rdia c v. Coronary s inus P os te rior

Fig ure 6-2: Heart valves . (As s et provided by Anatomical Chart Co.)

Tricus pid va lve

95

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Chapter 6

A quired Heart Disease

Ta b le 6-1: Mitra l Va lve Re p a ir ve rs us Mitra l Va lve Re p la c e m e nt Re p a ir

Re p la c e m e nt

Operative mortality

1%

6%

Anticoagulation

Not required

Mandatory or 3 months or tissue, li e or mechanical

Reoperation Stroke risk

10% at 20 years 0.04%/year

10–15 years or tissue 1%–2%/year

D. Valve selection: Ch sing between a me hani al and a tissue valve depends n the risk l ng-term anti agulati n versus the risk re perati n. E. Heart valve repair: P ssible r m st patients underg ing mitral valve surgery. Repair is superi r t repla ement ( able 6-1).

Ao rtic Va lvula r Dis e a s e I. Ao rtic s te no s is A. Etiology: Patients with a hist ry rheumatic ever rarely have is lated sten sis but usually have a mixed lesi n sten sis and insu ien y. 1. Congenital: Bi uspid a rti valves ur in 1%–2% the p pulati n. T ese usually devel p al i hanges by the urth de ade and sympt ms by the sixth de ade. Quic k Cut 2. Acquired: M st mm n heart valve disease requiring Bicus pid aortic surgery; it results r m pr gressive degenerati n and valve is s trongly as s ociated al i ati n valve lea ets. with aortic and other arterial B. Pathology: Lea et thi kening and al i ati n results in a aneurys mal dis eas e. de reased r ss-se ti nal valve area. 1. Symptoms: usually begin when the valve area is less than 1 m 2 (n rmal is 2.5–3.5 m 2) Quic k Cut 2. Signi cant pressure load on the le ventricle: results Aortic s tenos is is in n entri lef ventri ular hypertr phy and eventual SAD: s yncope, a ngina, and my ardial dys un ti n d ys pnea. C. Clinical presentation: Patients with sympt mati a rti sten sis (angina, syn pe, arrhythmia, and dyspnea) require a rti valve repla ement due t the likelih d sudden death. D. Diagnosis 1. Physical examination: Classi syst li res end –de res end murmur is heard best in the se nd right inter stal spa e but may radiate t the ar tid arteries. A narr wed pulse pressure al ng with pulsus parvus et tardus is requently und. 2. Echocardiography: estimates the degree sten sis, any ass iated insu ien y, and quality lef ventri ular un ti n 3. Cardiac catheterization: identi es the presen e n mitant r nary artery disease (CAD), whi h is present in 50% surgi al patients E. Treatment: Surgi al rre ti n is re mmended r patients with sympt ms and nsists ex isi n the diseased valve and repla ement with a pr stheti valve. II. Ao rtic ins u f c ie nc y: Eti l gies in lude myx mat us degenerati n, a rti disse ti n, ba terial end arditis, rheumati ever, and a rti r t aneurysm. A. Pathology: Valve lea et br sis and sh rtening (rheumati Quic k Cut ever), a rti annulus dilatati n (Mar an syndr me r a rti Uncorrected aortic aneurysm), r myx mat us lea et degenerati n imp ses a annulus dilation may lead to signi ant volume load n the lef ventri le leading t lef le t ventricular ailure with ventri ular dilatati n. pulmonary conges tion. B. Clinical presentation: Early sympt ms in lude palpitati ns se ndary t ventri ular arrhythmias and dyspnea n exerti n; later, severe CHF is seen, and death results r m pr gressive ardia ailure.

Chapter 6

Heart

97

C. Diagnosis Quic k Cut 1. Physical examination The longer the a. Murmur: Chara teristi diast li murmur is heard al ng duration o the dias tolic the lef sternal b rder and radiates t the axilla. murmur, the wors e the b. Pulse pressure: Of en in reased; water-hammer pulses are valvular ins u f ciency. hara teristi . 2. Echocardiography: used t quantitate the degree insu ien y and t assess lef ventri ular eje ti n per rman e Quic k Cut 3. Cardiac catheterization: used t determine the presen e Puls e pres s ure ass iated CAD s ys tolic dias tolic blood pres s ures E. Treatment: A rti valve repla ement surgery t av id de mpensati n is re mmended r patients with severe insu ien y and any ne the ll wing sympt ms: lef ventri ular syst li dys un ti n (EF 50%), severe lef ventri ular dilati n (end-syst li dimensi n 55 mm, end-diast li dimensi n 75 mm), underg ing an ther ardia surgery, and a ute nset.

Mitra l Va lve Dis e a s e I. Mitra l s te no s is : Alth ugh nly 50% patients rep rt a hist ry rheumati ever, this nditi n is th ught t be the ause alm st all mitral sten sis. A. Pathology: Interval between rheumati ever and the mani estati n mitral sten sis is 10–25 years. 1. Underlying pathologic changes: usi n the mmissures and lea et thi kening with r with ut sh rtening the h rdae tendineae 2. Cross-sectional area o the mitral valve: n rmal 4–6 m 2; mild sten sis 2–2.5 m 2; m derate 1.5–2 m 2; and severe 1–1.5 m 2 3. Pathophysiologic changes: in reased lef atrial pressure, pulm nary hypertensi n, atrial brillati n, de reased CO, and in reased pulm nary vas ular resistan e B. Clinical presentation: Dyspnea is the m st signi ant sympt m, indi ating pulm nary ngesti n and in reased lef atrial pressure. 1. Other mani estations: par xysmal n turnal dyspnea and rth pnea, hr ni ugh and hem ptysis, pulm nary edema, systemi arterial emb lizati n (usually r m a lef atrial thr mbus), and atrial brillati n 2. Long-standing pulmonary hypertension: may result in right ventri ular ailure and se ndary tri uspid regurgitati n C. Diagnosis 1. Physical examination: ypi al patient is thin and a he ti ; Quic k Cut aus ultati n reveals the classic triad an api al diast li Think o mitral rumble, an pening snap, and a l ud rst heart s und. s tenos is in a thin patient with 2. Chest x-ray: typi ally sh ws a pr minent pulm nary dys pnea, opening s nap, and vas ulature in the upper lung elds a dias tolic rumble. 3. ECG: may be n rmal r may sh w P-wave abn rmalities, signs right ventri ular hypertr phy, and right axis deviati n 4. Echocardiography: used t determine the m rph l gy the valve and the severity the sten sis 5. Cardiac catheterization: used t al ulate the mitral valve r ss-se ti nal area, the mitral valve end-diast li pressure gradient, PAP, and any ass iated valvular r r nary artery disease D. Treatment: Surgery is re mmended r all patients with sympt mati sten sis. T e h i e perative appr a h depends n the extent these hanges. 1. Commissurotomy: Opening the used mmissures an be Quic k Cut a mplished under dire t visi n during surgi al mitral valve In s elected patients , repair r per utane usly by ball n mitral valvul plasty. balloon valvuloplas ty and open commis s urotomy have 2. Mitral valve replacement: required r severe disease the equivalent res ults . h rdae tendineae and papillary mus les II. Mitra l ins u f c ie nc y A. Etiology: degenerative mitral valve disease 1. Ventricular dilation: als alled functional mitral regurgitation, alters valvular ge metry; urs with is hemi r idi pathi ardi my pathy 2. Other: in e tive end arditis and rheumati ever

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A quired Heart Disease

B. Pathology: Myx mat us degenerati n is the m st mm n ause and is hara terized by lea et thi kening and h rdal el ngati n. Stru tural alterati ns llagen and abn rmal a umulati n pr te gly ans in the lea et tissue are als seen. 1. Mitral valve prolapse: present in 2%–3% the p pulati n, but m st d n t devel p signi ant mitral regurgitati n and d n t require surgery 2. Insuf ciency secondary to rheumatic ever: Path genesis is similar t that in mitral sten sis. 3. Pathophysiologic changes: in reased lef atrial pressure during syst le, late-appearing pulm nary vas ular hanges (e.g., in reased pulm nary vas ular resistan e), and in reased lef ventri ular str ke v lume (SV) C. Clinical presentation: Many years may elapse between the rst Quic k Cut eviden e insu ien y and sympt m devel pment. O patients 1. Symptoms: dyspnea n exerti n, atigue, and palpitati ns undergoing cardiac s urgery, 2. Atrial brillation: Distenti n the lef atrium auses 12% have atrial f brillation; 25% develop pos toperative elevated lef atrial pressure. atrial f brillation. D. Diagnosis 1. Physical examination: reveals a h l syst li bl wing murmur at the apex that radiates t the axilla, a mpanied by an a entuated api al impulse 2. Echocardiography: an a urately quantitate the degree mitral regurgitati n and an dem nstrate underlying anat mi Quic k Cut abn rmalities the valve (e.g., lea et pr lapse, ruptured Lea ets extending h rdae tendineae, annular dilati n, lea et restri ti n, annular greater than 2 mm above the mitral valve annulus is al i ati n, presen e vegetati ns, et .), degree lef atrial echocardiographic evidence enlargement, extent lef ventri ular dys un ti n, and the o prolaps e. presen e ass iated tri uspid regurgitati n 3. Cardiac catheterization: determines presen e CAD E. Treatment: Only patients with severe regurgitati n sh uld be Quic k Cut nsidered r surgery. Care ul e h ardi graphi assessment There is no e ective the degree regurgitati n sh uld be per rmed. medical therapy or mitral 1. Surgical indications: severe regurgitati n in additi n t the regurgitation. ll wing (h wever, gr wing eviden e dem nstrates that asympt mati patients with severe mitral regurgitati n enj y impr ved l ng-term survival with early perati n): Quic k Cut a. Symptoms: New Y rk Heart Ass iati n (NYHA) lass II The New York Heart r ab ve ( able 6-2) As s ociation s ys tem is us e ul b. Evidence o le ventricular dys unction: EF less than to clas s i y heart ailure. 60%, ventri ular dilati n (end-syst li dimensi n 40 mm), and devel pment atrial brillati n r signi ant pulm nary hypertensi n 2. Mitral valve repair: per rmed when p ssible either by quadrangular rese ti n the p steri r lea et r inserti n an annul plasty ring ( l th- vered ring that stabilizes and s metimes de reases the size the mitral valve annulus)

Tric us p id Va lve , P ulm o nic Va lve , a nd Multip le Va lvula r Dis e a s e s I. Tric us p id s te no s is a nd ins u f c ie nc y A. Etiology 1. Organic tricuspid stenosis: always aused by rheumati ever, m st mitral valve disease

mm nly ass iated with

Ta b le 6-2: Ne w Yo rk He a rt As s o c ia tio n Func tio na l Cla s s if c a tio n o He a rt Fa ilure Class I

No symptoms

Class II

Mild symptoms during ordinary activity

Class III

Signif cant symptoms during any activity

Class IV

Symptoms even while at rest

(Symptoms are typically angina and dyspnea.)

Chapter 6

Heart

99

2. Functional tricuspid insuf ciency: result right ventri ular Quic k Cut dilatati n se ndary t pulm nary hypertensi n and right Tricus pid s tenos is ventri ular ailure, m st mm nly r m mitral valve disease ollows rheumatic ever; 3. Tricuspid insuf ciency: s metimes seen in ar in id tricus pid ins u f ciency res ults syndr me, lupus, r se ndary t blunt trauma r t ba terial rom mitral valve dis eas e. end arditis (intraven us [IV] drug abuse) B. Pathology 1. Stenosis secondary to rheumatic ever: Path genesis is similar t that in mitral valve disease. 2. Elevation o right atrial pressure secondary to stenosis: leads t peripheral edema, jugular ven us distenti n, hepat megaly, and as ites C. Clinical presentation 1. Isolated tricuspid insuf ciency: usually well t lerated 2. Right-sided heart ailure: When this urs, sympt ms (e.g., edema, hepat megaly, and as ites) devel p. D. Diagnosis 1. Physical examination: Pr minent jugular ven us pulse may be bserved. a. Tricuspid insuf ciency: Pr du es a syst li murmur at the l wer end the sternum; the liver may be pulsatile. b. Tricuspid stenosis: pr du es a diast li murmur in the same regi n 2. Chest x-ray: enlargement the right side the heart 3. Echocardiography: estimates the am unt tri uspid valve path l gy and sh uld in lude an evaluati n any ass iated a rti r mitral valve lesi ns and right heart un ti n 4. Cardiac catheterization: m st a urate guide t diagn sing tri uspid disease Quic k Cut E. Treatment: In mild t m derate insu ien y ass iated with Is olated tricus pid mitral valve disease, pini n varies n erning the need r surgery. dis eas e, es pecially tricus pid ins u f ciency, may be well 1. Extensive insuf ciency associated with mitral valve tolerated without s urgical disease: C nsensus is that either valve repair (usually with an intervention. annul plasty ring) r (rarely) valve repla ement is appr priate. 2. Signi cant stenosis: mmissur t my r valve repla ement II. P ulm o nic va lve d is e a s e Quic k Cut A. Pathology: A quired lesi ns are un mm n; ar in id The vas t majority o syndr me may pr du e pulm ni sten sis. pulmonic valve dis orders are B. Treatment: surgi al repair r valve repla ement when warranted congenital abnormalities . by the degree dys un ti n III. Multip le va lvula r d is e a s e A. Pathology: Multiple valves may be inv lved in rheumati ever. Quic k Cut B. Treatment: inv lves repair r repla ement all valves with Patients with multivalvular dis eas e have s igns signi ant dys un ti n

Co ro na ry Arte ry Dis e a s e

and s ymptoms dictated by the mos t s everely a ected valve.

I. Etio lo g y a nd e p id e m io lo g y: m st mm n ause death in the United States; ur times m re prevalent in men than in w men, alth ugh the in iden e in w men is rapidly in reasing Quic k Cut A. Atherosclerosis: Pred minant path geneti me hanism; CAD accounts or 500,000 deaths per year. un mm n auses in lude vas ulitis, radiati n injury, and trauma. B. Risk actors: T se identi ed by epidemi l gi studies in lude hypertensi n (risk minimized when bl d pressure 140/90 mm Hg), sm king, hyper h lester lemia (risk minimized when h lester l 200 mg/dL, l w-density lip pr tein 100 mg/dL, and high-density lip pr tein 40 mg/dL), amily hist ry heart disease, diabetes, and besity. II. P a tho p hys io lo g ic e e c ts : Is hemi disease the my ardium auses de reased ventri ular mplian e and ardia ntra tility and my ardial ne r sis; ventri ular dys un ti n ll wing is hemia urs se ndary t irreversible my ardial ne r sis. A. Hibernating myocardium: dys un ti nal mus le that impr ves with revas ularizati n B. Stunned myocardium: temp rary dys un ti n ll wing revas ularizati n

100

Chapter 6

A quired Heart Disease

III. Clinic a l p re s e nta tio n: CAD may take ne the ll wing rms: A. Angina pectoris: ypi ally presents as substernal hest pain lasting 5–10 minutes. Pre ipitated by em ti nal stress, exerti n, r ld weather and is relieved by rest. 1. Stable angina: un hanged r a pr l nged peri d 2. Unstable angina: sh ws a hange r m a previ usly stable pattern r new- nset angina 3. Other: angina at rest and p stin ar ti n angina B. MI: is hemi ECG hanges and tr p nin elevati n C. Other: CHF r sudden death IV. Dia g no s is : Angina pe t ris due t CAD is m st f en made r m Quic k Cut the patient’s hist ry. A 75% s tenos is A. Cardiac catheterization: Diagn sti g ld standard r CAD. in coronary artery cros s L ati n and size r nary lesi ns an be b th diagn sed s ectional area is the point at which a les ion s ignif cantly and treated. Lef ventri ular un ti n may be assessed by the impedes coronary blood ow. ventri ul gram and hem dynami measurements. B. ECG: N rmal in up t 75% patients when they are at rest with ut pain. S -segment hanges and -wave hanges may be seen, and eviden e a previ us in ar ti n may be apparent. C. Exercise stress testing: evaluates indu ible is hemia, ventri ular dys un ti n, and ass iated ECG hanges D. Radio thallium scan o the heart: delineates is hemi and in ar ted areas my ardium V. Tre a tm e nt A. Medical treatment: Management CAD is initiated with medi al Quic k Cut therapy in patients with stable angina and with n eviden e CHF. Medical 1. Drugs: aspirin, beta-bl kers, statins, ald ster ne bl kade, management o CAD ocus es and antihypertensives on control o ris k actors . 2. Additional therapy: l w- at diet, sm king essati n, and a graded exer ise pr gram B. Catheter-based coronary interventions 1. Balloon angioplasty: Ball n dilati n t relieve the bstru ti n. Sten sis f en re urs. 2. Coronary stenting: Metal stent is pla ed in the lesi n t keep it r m l sing ver time (“resten sis”). Stent may be “bare metal” r may be ated with a drug (e.g., sir limus) that elutes ver time t prevent resten sis. C. Coronary artery bypass surgery (CABG): nstru ti n bypass graf s t d wnstream segments the a e ted r nary arteries t re-establish n rmal bl d w t the my ardium Quic k Cut 1. Common gra s (Fig. 6-3): lef internal mammary artery CABG 10-year t lef anteri r des ending (LAD) r nary artery, reversed patency rates : internal saphen us vein graf s nstru ted r m the as ending a rta t mammary artery more than the target vessel, and radial artery r right internal mammary 90% , s aphenous vein 50% . artery graf s

Le ft s ubcla via n a rte ry Inte rna l ma mma ry a rte ry gra ft (A) S a phe nous ve in gra ft (B) Blocka ge Blocka ge s

Fig ure 6-3: Coronary artery bypas s s urgery. (From Ros dahl CB, Kowals ki MT. Textbook of Basic Nursing, 10th ed. Philadelphia: Lippincott Williams & Wilkins ; 2011.)

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2. Indications: lef main disease greater than 50% sten sis, Quic k Cut pr ximal LAD r ir um ex disease greater than 70% sten sis, CABG is highly triple-vessel disease (espe ially with EF 50%), pr ximal s ucces s ul at relieving angina LAD with ther vessel disease, angina re ra t ry t medi al pectoris ; more than 90% o management, r ailed per utane us r nary interventi n patients are s ymptom ree 3. Increased survival: with lef main disease and triple-vessel 1 year a ter s urgery. disease with de reased ventri ular un ti n r with diabetes 4. Prognosis: Overall m rtality is 2%–3%; risk is in reased in patients with renal ailure, urgen y perati n, pulm nary disease, peripheral vas ular disease, and hist ry str ke r diabetes. VI. Surg ic a l tre a tm e nt o MI c o m p lic a tio ns : Me hani al mpli ati ns MI are in reasingly rare with early revas ularizati n. A. Ventricular aneurysms: My ardium rem dels ll wing in ar ti n and an thin r be me aneurysmal. 1. Indications or repair: CHF, ventri ular arrhythmias, r (rarely) systemi thr mb emb lizati n 2. Coronary revascularization: may als be warranted at the same time B. Ruptured ventricle: Rare; the untreated m rtality rate is 100%. C. Rupture o the interventricular septum (postin arct ventricular septal de ect [VSD]): arries m rtality rate 50% Quic k Cut with ut immediate perati n Placement o an D. Papillary muscle dys unction or rupture: P steri r papillary intra-aortic balloon pump can mus le is usually inv lved. help maintain patients with 1. Treatment: mitral valve repla ement r repair in arct-related VSD or papillary 2. Long-term survival: depends n the extent my ardial mus cle rupture until s urgery. damage

Ca rd ia c Tum o rs I. Be nig n tum o rs : Myx mas are the single m st mm n benign ardia tum rs. M st are l ated in the lef atrium. Others in lude rhabd my sar mas (m st mm n in hildh d), papillary elast br mas, and lip mas as well as either pedun ulated r sessile myx mas (50% benign ardia tum rs), 75% whi h are l ated in lef atrium II. Ma lig na nt tum o rs : Overall, a unt r 20%–25% all primary Quic k Cut ardia tum rs. Sar mas and angi sar mas are the m st mm n. Malignant tumors III. Me ta s ta tic tum o rs : ur m re requently than primary ardia originating rom the heart tum rs (benign r malignant) carry a very poor prognos is . A. Autopsy studies: sh w ardia inv lvement by metastati disease in 10% an er deaths B. Types: Renal ell ar in ma, neur blast ma, melan ma, lymph ma, and leukemia are the tum rs that m st f en metastasize t the heart. IV. Clinic a l p re s e nta tio n: Myx mas typi ally result in emb lizati n. Additi nal presentati ns in lude CHF, peri ardial e usi n and tamp nade, and arrhythmia. V. Tre a tm e nt: surgi al ex isi n

Ca rd ia c Tra um a

Quic k Cut I. P e ne tra ting injury (thro ug h the a nte rio r c he s t wa ll): m st Pericardial e us ions likely t injure the right ventri le (blood) can be vis ualized A. Bleeding into the pericardium: mm n on s ubxiphoid windows o B. Pericardial tamponade: may result; mani ested by distended a ocus ed as s es s ment with ne k veins, hyp tensi n, pulsus parad xus, and distant heart s onography or trauma exam. s unds II. Blunt tra um a : usually m re extensive than is appre iated A. Diagnosis: Hist ry a signi ant bl w t the hest, with r with ut ra tured ribs r sternum, sh uld reate a high index suspi i n a ardia ntusi n r in ar ti n. 1. Serial ECGs and cardiac enzyme studies: sh uld be btained 2. Echocardiography: helps determine my ardial injury 3. New murmurs: sh uld be investigated with imaging 4. Monitoring: similar t a patient with MI be ause similar my ardial injury

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B. Treatment: Blunt trauma may ause rupture treatment by valve repla ement r repair.

a tri uspid, mitral, r a rti valve, requiring

P e ric a rd ia l Dis o rd e rs I. P e ric a rd ia l e us io n: Peri ardium resp nds t n xi us stimuli by in reasing uid pr du ti n; v lume as small as 100 mL may pr du e sympt mati tamp nade i the uid a umulates rapidly, whereas larger am unts may be t lerated i the uid a umulates sl wly. A. Treatment: peri ardi entesis r by tube peri ardi st my via a subxiph id appr a h B. Chronic e usions (e.g., those that occur with malignant involvement o the pericardium): may require peri ardie t my via lef th ra t my r stern t my II. P e ric a rd itis A. Acute pericarditis 1. Causes: staphyl al r strept al in e ti n (a ute Quic k Cut py geni peri arditis is un mm n and is usually ass iated Dres s ler s yndrome with a systemi illness), viral in e ti n, uremia, traumati is pericarditis up to 2 weeks hem peri ardium, malignant disease, and nne tive tissue ollowing an acute MI. dis rders Treatment is nons teroidal 2. Treatment: Manage the underlying ause. Open peri ardial anti-in ammatory drugs . drainage may be required. M st ases res lve with ut seri us sequelae. B. Chronic pericarditis: Eti l gy is f en imp ssible t establish. It may g unn ti ed until it results in the hr ni nstri tive rm, ausing hr ni tamp nade. C. Chronic constrictive pericarditis: presents with dyspnea n exerti n, easy atigability, marked jugular ven us distenti n, as ites, hepat megaly, and peripheral edema 1. Diagnosis: Peri ardium may be me al i ed, whi h is Quic k Cut evident n hest x-ray. Cardia atheterizati n may be needed ECG changes s een t n rm. in pericarditis include ST 2. Treatment: On e the diagn sis has been established in the elevations in all leads , not one sympt mati patient, peri ardie t my sh uld be undertaken dis tribution. with r with ut ardi pulm nary bypass.

CONGENITAL HEART DISEASE Ove rvie w I. Inc id e nc e : 3 in 1,000 births II. Etio lo g y: f en unkn wn A. Rubella (occurring in the rst trimester o pregnancy): kn wn t ause patent du tus arteri sus (PDA) B. Down syndrome: ass iated with end ardial ushi n de e ts III. Typ e s in d e c re a s ing o rd e r: VSD, transp siti n the great vessels, tetral gy Fall t, hyp plasti lef heart syndr me, atrial septal de e t (ASD), PDA, ar tati n the a rta, and end ardial ushi n de e ts IV. Co m m o n p re s e nta tio ns : easy atigability and de reased exer ise t leran e, p r eeding habits and p r weight gain, requent pulm nary in e ti ns, and signs yan sis (indi ating a right-t -lef shunt) V. P hys ic a l e xa m ina tio n: Abn rmalities in gr wth and devel pment sh uld be identi ed. A. Cyanosis and clubbing o the ngers: may be n ted B. Heart examination: sh uld pr eed in the same manner as in the adult 1. Systolic murmurs: requently und in in ants and small hildren and may n t be lini ally signi ant, but a gall p rhythm is great lini al imp rtan e 2. CHF in children: requently mani ested by hepati enlargement VI. Dia g no s is : E h ardi gram and f en atheterizati n are required.

P a te nt Duc tus Arte rio s us I. P a tho p hys io lo g y: Hyp xia and pr staglandins E1 (PGE1) and E2 (PGE2) a t t keep the du tus pen in uter . In the n rmal-term in ant, bl d ir ulati n thr ugh the pulm nary vas ular bed results in elevated xygen levels and pr staglandin breakd wn, whi h results in l sure the du tus within days.

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II. Clinic a l p re s e nta tio n A. Common complaints: dyspnea, atigue, and palpitati ns, signi ying CHF and/ r pulm nary hypertensi n B. May be seen in combination with other de ects: VSD and ar tati n the a rta III. Dia g no s is based primarily n the physi al ndings and e h ardi gram A. Physical examination: Classi ntinu us “ma hinery-like” murmur may be absent until age 1 year. 1. Pulses: widened pulse pressure and b unding peripheral pulses 2. Cyanosis: right-t -lef shunt r m pulm nary vas ular disease IV. Tre a tm e nt A. Surgical management: ligati n the du tus, reserved r Quic k Cut premature in ants with severe pulm nary dys un ti n, in ants wh Mos t preterm in ants su er r m CHF within the rst year li e, and asympt mati weighing les s than 1.5 kg will hildren with a patent du tus that persists until age 2–3 years have a PDA. B. Indomethacin: T is pr staglandin inhibit r an a hieve l sure in premature in ants with sympt mati simple PDA.

Co a rc ta tio n o the Ao rta I. Ove rvie w: severe narr wing, l ated adja ent t the du tus arteri sus that may be atal in the rst ew m nths li e A. Associated intracardiac de ects: Up t 60% patients have PDA, VSD, and bi uspid a rti valve. B. Incidence: twi e as mm n in males II. Clinic a l p re s e nta tio n: f en asympt mati r varying peri ds time A. CHF: sh rtly af er birth B. Other: Heada hes, epistaxis, l wer extremity (LE) weakness, and dizziness may be seen in the sympt mati hild. III. Dia g no s is A. Physical ndings: upper extremity (UE) hypertensi n, absent r diminished LE pulses, and a syst li murmur B. Chest x-ray: may reveal “rib n t hing” in lder hildren, representing llateral pathways via inter stal arteries C. Echocardiography: suggests the degree w limitati n and ther ass iated an malies D. Cardiac catheterization: usually re mmended t de ne l ati n and any ass iated ardia de e ts IV. Tre a tm e nt: surgi al rre ti n r sympt mati patients r asympt mati hildren ages 5–6 years A. Operative procedures: rese ti n and end-t -end anast m sis, pr stheti pat h graf , and sub lavian arterial ap (in whi h Quic k Cut the distal sub lavian artery is transe ted and a pr ximal-based In in ants with sub lavian artery ap is used t enlarge the a rta at the level s evere coarctation, IV PGE1 can provide dis tal per us ion the ar tati n) through maintaining a PDA. B. Complications: residual hypertensi n, spinal rd injury due t is hemia during surgery, p st perative mesenteri vas ulitis related t hypertensi n, and p st perative aneurysm at the site the perative repair

Atria l Se p ta l De e c ts I. Cla s s if c a tio n A. Ostium secundum de ect: m st mm n ASD, und in the midp rti n the atrial septum B. Sinus venosus de ect: l ated high up n the atrial septum, f en ass iated with an malies pulm nary ven us drainage C. Ostium primum de ects: mp nents atri ventri ular septal de e ts, l ated n the atrial side the mitral and tri uspid valves II. P a tho p hys io lo g y: Atrial pressures are equal n b th sides a large ASD (Fig. 6-4). A. Direction o shunt: Be ause atrial emptying urs during ventri ular diast le, dire ti n shunt at the atrial level is

Quic k Cut ASD is twice as common in emales .

Quic k Cut Patent oramen ovale is not cons idered an ASD. The s epta primum and s ecundum ail to us e and leave a patent valve in the os s a ovalis , which occurs in 30% o normal hearts .

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Aorta P ulmona ry a rte ry Right a trium

Le ft a trium

Atrial septal defect

Fig ure 6-4: Atrial septal de ect. In an ASD, an abnormal communication exists between the atria, allowing blood to be s hunted rom the le t atrium to the right atrium through the atrial septum. This hole is us ually the area o the oramen ovale, which normally closes at birth. (From Rosdahl CB, Kowals ki MT. Textbook of Basic Nursing, 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2011.)

Ve na ca va

determined by the relative mplian es the ventri les. Be ause the right ventri le is m re mpliant, the w is lef t right a r ss an ASD. B. Increased pulmonary blood ow: Causes mild gr wth retardati n, and pulmonary vascular obstructive disease may devel p, whi h results in the right ventri le be ming less mpliant than the lef , with bl d w Quic k Cut shunting right t lef a r ss the ASD. Eis enmenger III. Clinic a l p re s e nta tio n s yndrome is a s equence o A. In ancy and early childhood: mild dyspnea and easy atigability events : 1, congenital le t to right s hunt ( rom s eptal B. Children: redu ed exer ise t leran e and re urrent respirat ry de ect or PDA); 2, s ubs equent in e ti ns pulmonary hypertens ion; C. Adults: atrial brillati n and CHF 3, this increas ed pres s ure D. Other: Patients may present with neur l gi sympt ms revers es the s hunt; and 4, ( erebr vas ular a ident r transient is hemi atta k) r cyanotic s ymptoms develop. Eisenmenger syndr me. IV. Dia g no s is A. Physical examination: syst li murmur in the lef se nd r third inter stal spa e and a xed, split, se nd heart s und B. Chest x-ray: m derate enlargement the right ventri le and pr minen e the pulm nary vas ulature C. ECG: right ventri ular hypertr phy D. Echocardiography: de nes the ASD and n tes the dire ti n shunting E. Cardiac catheterization: Determines the “step-up” in xygen saturati n in the right atrium. T e am unt lef -t -right shunt may be al ulated. V. Tre a tm e nt: Based n the size the lef -t -right shunt; s me ( 6 mm) may l se sp ntane usly. Surgery arries a m rtality risk less than 1%; ideal timing is age 4–5 years, be re the hild g es t s h l. A. Indications or ASD closure: Pulm nary bl d w is m re than 1.5 times greater than the systemi bl d w, neur l gi events, heart ailure, arrhythmia, r right ventri ular v lume verl ad. B. Approach: Cl sure may be attempted per utane usly in the atheterizati n lab rat ry.

Ve ntric ula r Se p ta l De e c ts I. Cla s s if c a tio n: Figure 6-5. A. Membranous de ect: m st mm n ventri ular, 70%–80% B. Muscular de ects: may be single r multiple (10%–15%) C. Inlet de ect: atri ventri ular anal type, end ardial ushi n de e t, 5% is lated de e ts D. Outlet de ects: 5%–10% (als alled supracristal r conoseptal defects)

Quic k Cut VSD is the mos t common congenital cardiac les ion.

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Outle t s e pta l

Conove ntricula r

Ante rior mus cula r

Midmus cula r

Inle t s e pta l Apica l mus cula r

Fig ure 6-5: Location o congenital s eptal de ects . (Reprinted with permis s ion rom Kais er LR, Kron IL, Spray TL. Mastery of Cardiothoracic Surgery. Philadelphia: Lippincott-Raven; 1998:688.)

II. P a tho p hys io lo g y: Ventri ular pressures an be equal n either side a large VSD (Fig. 6-6). A. Direction o shunt: Determined by the relative resistan es the pulm nary and systemi ir uits. Be ause the pulm nary vas ular resistan e is l wer than the systemi vas ular resistan e, w is lef t right a r ss a VSD. B. Increased pulmonary blood ow: Lef -t -right shunting leads t pulm nary hypertensi n, de reased right ventri ular mplian e, and Eisenmenger syndr me (irreversible pulm nary vas ular bstru tive disease).

Aorta To right lung

To le ft lung P ulmona ry a rte ry

Le ft ve ntricle

Ve na ca va Right ve ntricle

Ventricular septal defect

Fig ure 6-6: Ventricular s eptal de ects . In a VSD, a hole is in the wall o the s eptum that s eparates the le t and right ventricles . Normally, deoxygenated blood ows through the s uperior vena cava and in erior vena cava into the right atrium, right ventricle, and pulmonary artery. In a VSD, s ome oxygen-rich blood rom the le t ventricle ows through the de ect and recirculates through the lungs . (From Ros dahl CB, Kowals ki MT. Textbook of Basic Nursing, 10th ed. Philadelphia: Lippincott Williams & Wilkins ; 2011.)

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C. Other adverse e ects o pulmonary overcirculation: p r eeding, ailure t thrive, requent respirat ry tra t in e ti ns, and in reased pulm nary vas ular resistan e III. Clinic a l p re s e nta tio n: Children with large de e ts usually have Quic k Cut dyspnea n exerti n, easy atigability, and an in reased in iden e Fi ty percent o pulm nary in e ti ns. Severe ardia ailure may be seen in in ants VSDs are as s ociated with but is less mm n in hildren. PDA, aortic coarctation, or tetralogy o Fallot. IV. Dia g no s is A. Physical examination: harsh pansyst li murmur B. Chest x-ray and ECG: sh w eviden e biventri ular hypertr phy i large C. Cardiac catheterization: determines the severity the lef -t -right shunt, pulm nary vas ular resistan e, and the l ati n V. Tre a tm e nt: surgi al l sure A. Indications: sympt mati r utlet r inlet VSDs; asympt mati Quic k Cut hildren with signi ant shunts wh have n t had sp ntane us A contraindication l sure by age 2 years, PAP 0.5 times greater than systemi to repair o an ASD or VSD is bl d pressure, r pulm nary bl d w greater than 1.5 times f xe d , irre ve rs ib le pulmonary systemi bl d w hypertens ion. B. Operative mortality risk ( 5%): related t the degree pre perative pulm nary vas ular disease

Te tra lo g y o Fa llo t I. P a tho p hys io lo g y: One the m st mm n cyanotic congenital heart disorders; nsists bstru ti n the right ventri ular ut w tra t, a large anteri r VSD, right ventri ular hypertr phy, and an verriding a rta (Fig. 6-7). A. Pentalogy o Fallot: with the additi n an ASD (whi h is little physi l gi signi an e) B. Direction o shunt: Be ause resistan e t right ventri ular ut w ex eeds the systemi vas ular resistan e, the shunt is right t lef , resulting in desaturati n the bl d and yan sis. II. Clinic a l p re s e nta tio n: Cyanosis and dyspnea on exertion are r utinely seen. Children s n learn that by squatting, they an temp rarily alleviate these sympt ms. T ese are ‘ et spells.’ A. Squatting: in reases the systemi vas ular resistan e, whi h de reases the magnitude right-t -lef shunt and auses an in rease in pulm nary bl d w

Tetralogy of Fallot S te nos is of pulmona ry a rte ry

Hype rtrophy of right ve ntricle

Aorta ove rriding both ve ntricle s

Ve ntricula r s e pta l de fe ct

Fig ure 6-7: Tetralogy o Fallot. Tetralogy o Fallot is characterized by the combination o our de ects : (1) pulmonary s tenos is , (2) VSD, (3) overriding aorta, and (4) hypertrophy o the right ventricle. It is the mos t common de ect caus ing cyanos is in children who s urvive beyond 2 years o age. Symptom s everity depends on the degree o pulmonary s tenos is , the s ize o the VSD, and the degree to which the aorta overrides the s eptal de ect. (From Ros dahl CB, Kowals ki MT. Textbook of Basic Nursing, 10th ed. Philadelphia: Lippincott Williams & Wilkins ; 2011.)

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B. Cyanosis: Seen at birth in 30% the ases, by the rst year in Quic k Cut 30%, and later in hildh d in the remainder. P ly ythemia and Tet s pells : epis odes lubbing a mpany it. o s evere cyanos is incited C. Exercise tolerance: limited be ause the inability t in rease by dehydration, crying, or pulm nary bl d w s training that may be relieved by s quatting. III. Dia g no s is A. Physical examination: Reveals lubbing the digits and yan sis. A harsh syst li murmur pulm nary sten sis is f en heard. B. Cardiac catheterization: determines the level pulm ni ut w bstru ti n and the size the pulm nary arteries IV. Tre a tm e nt: tal rre ti n is undertaken af er age 4–6 m nths. A. Surgery: Risk depends n patient’s age and the degree yan sis; pri r t rre ti n, su ient hydrati n and av idan e upper respirat ry in e ti ns are imperative. B. Palliative options prior to repair or high-risk, symptomatic patients: ball n pulm nary valvul plasty and systemi -t -pulm nary (Blal k- aussig) shunt

Tra ns p o s itio n o the Gre a t Arte rie s I. P a tho p hys io lo g y: urs when the a rta arises r m the m rph l gi right ventri le and the pulm nary artery arises r m the m rph l gi lef ventri le, resulting in tw independent parallel ir uits II. Surviva l: depends n mmuni ati n between the right and lef sides the heart thr ugh an ASD, VSD, r PDA III. Dia g no s is : e h ardi gram and ardia atheterizati n (in the setting additi nal intra ardia r extra ardia an malies r inadequate shunting) IV. Tre a tm e nt A. Balloon atrial septostomy: per rmed t a ilitate mixing bl d with inadequate shunting; ll wed by de nitive surgi al rre ti n B. Arterial switch: divisi n the great arteries with trans er the r naries and pr per anast m ses the a rta t the lef and pulm nary artery t the right ventri les

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Study Questi ns r Part II

Study Questi ns r Part II Directions: Each of the numbered items in this section is followed by several possible answers. Select the ONE lettered answer that is BEST in each case. 1. A 19-year- ld man is br ught t the emergen y r

m. He has n signi ant medi al hist ry, but he d es sm ke ne pa k igarettes per day. He is mplaining dyspnea and has a bl d pressure 150/70 mm Hg. Breath s unds are diminished n the lef . What is the best initial treatment r this patient? A. B. C. D. E.

Chest tube drainage Supplemental xygen nly Needle de mpressi n the lef hest C mputed t m graphy (C ) s an the th rax Emergent surgi al expl rati n

2. In the same patient, whi h

A. B. C. D. E.

the ll wing is an indi ati n

r surgery?

Family hist ry re urrent sp ntane us pneum th rax Persistent air leak af er 3 days hest tube drainage Identi ati n an api al bleb n hest C Eviden e li e-threatening respirat ry mpr mise n initial presentati n Hist ry ne pri r epis de su ess ully treated with nservative management n the ntralateral side

3. A patient is br ught t the emergen y department with a stab w und t the right hest in the

urth inter stal spa e in the midaxillary line. T e patient is hyp tensive, mplains sh rtness breath, and is und t have absent breath s unds n the right side the hest. Whi h step sh uld me next in the management this patient? A. B. C. D. E.

Chest radi graph Chest tube inserti n Needle th ra entesis L al w und expl rati n Peri ardi entesis

Que s tio ns 4–5 A hest radi graph a 55-year- ld man inv lved in a high-speed m t r vehi le a ident sh ws a widened mediastinum and pneum mediastinum. EKG sh ws sinus ta hy ardia with requent premature ventri ular ntra ti ns. 4. All

A. B. C. D. E.

the ll wing maneuvers are appr priate at this time except: A rt gram Br n h s py C ntinu us ardia m nit ring Lef th ra t my End tra heal intubati n

5. Expe ted physi l gi

A. B. C. D. E.

hanges due t blunt hest trauma in lude all but whi h

Elevated Pco 2 In reased mplian e Elevated alve lar–arterial (A-a) gradient De reased ventri ular ntra ti ns Elevated shunt ra ti ns

the ll wing?

Study Questi ns r Part II

Que s tio ns 6–7 A 70-year- ld patient n antibi ti therapy r ne r tizing ba terial pneum nia is und t have a large pleural e usi n. 6. In additi n t

A. B. C. D. E.

ntinued antibi ti s, what sh uld be the next step in management

Sputum ulture and sensitivity Chest tube inserti n T ra entesis T ra t my and de rti ati n Rib rese ti n and pen drainage

7. A sample

pleural uid is l udy and thi k, with a pH therapeuti step? A. B. C. D. E.

this patient?

7.2. What sh uld be the next

Vide -assisted th ra s pi surgery with tal pleur desis Chest tube drainage Repeat th ra entesis T ra t my and de rti ati n Rib rese ti n drainage

8. A r utine hest radi graph

r a 55-year- ld man with a 50 pa k-year sm king hist ry sh ws a peripherally l ated 1.5- m n n al i ed lesi n the upper l be the lef lung. N eviden e this lesi n appeared n a hest radi graph 5 years earlier. What sh uld be the next step in this patient’s management? A. B. C. D. E.

Observati n with serial hest radi graphs T ra t my Br n h s py Bi psy Sputum yt l gy

9. A 35-year- ld man is inv lved in a high-speed m t r vehi le

llisi n. He arrives in the emergen y r m in respirat ry distress. Radi graphs taken during the initial evaluati n reveal an air- uid level in the lef hest. Management in ludes all the ll wing except: A. B. C. D. E.

Establishment a se ure airway Immediate pla ement a nas gastri tube Urgent th ra t my t repair the injury Pla ement adequate peripheral vas ular a ess Urgent lapar t my t repair injury

10. Whi h

A. B. C. D. E.

the

ll wing rms

ngenital heart disease is m st

mm n?

ransp siti n the great vessels etral gy Fall t ASD PDA VSD

11. A 32-year- ld man is re erred

r a 1- m lesi n the right upper l be the lung. T e lesi n appears al i ed. Previ us hest radi graph taken 1 year pri r dem nstrates the lesi n t be present at the same size. Further w rkup and treatment w uld in lude whi h the ll wing? A. B. C. D. E.

C s an–guided bi psy Radiati n therapy Surgi al ex isi n Antibi ti s Observati n with repeat hest x-ray

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110

Study Questi ns r Part II

12. A 57-year- ld male patient with a 60 pa k-year sm king hist ry is re erred

mass in the right upper l be. C s an dem nstrates n eviden e What sh uld urther w rkup r treatment in lude? A. B. C. D. E.

r a 1.5- m s litary lymph n de inv lvement.

Radiati n therapy Open lung bi psy Chem therapy Right upper l be t my Repeat hest x-ray in 6 m nths

13. A 22-year- ld emale is re erred

r evaluati n a 2- m middle mediastinal mass dis vered n r utine hest radi graph. What is the m st likely diagn sis? A. B. C. D. E.

Br n h geni yst Lymph ma Neur geni tum r T ym ma Aden ar in ma

14. A 78-year- ld previ usly healthy man is admitted t the emergen y department

mplaining angina, dyspnea, and near syn pe. ECG is n rmal, and a l ud syst li murmur is heard in the se nd right interspa e with radiati n t the ar tids. What is the m st likely diagn sis in this patient? A. B. C. D. E.

MI Peri arditis Mitral regurgitati n A rti sten sis A rti insu ien y

15. Whi h

A. B. C. D. E.

the ll wing is n t a risk a t r

r CAD?

Hypertensi n Sm king Diabetes Renal ailure Hyper h lester lemia

16. A 72-year- ld emale patient is admitted with unstable angina. Cardia

severe triple-vessel CAD. T e ptimal treatment ll wing? A. B. C. D. E.

atheterizati n reveals this patient w uld in lude whi h the

C r nary artery bypass surgery Observati n Medi al management (nitrates, beta-bl kers) C r nary angi plasty issue plasmin gen a tivat r

17. A 72-year- ld male patient with a hist ry

syn pe and dyspnea presents r evaluati n r peripheral vas ular surgery. Physi al examinati n reveals a syst li res end –de res end murmur that radiates t the ar tid arteries. As he is sympt mati , his diseased valve w uld typi ally have an area less than whi h the ll wing? A. B. C. D. E.

1 m2 1.5 m 2 2 m2 3 m2 4 m2

Study Questi ns r Part II

18. A 29-year- ld man is evaluated

r a erebral vas ular a ident. Physi al examinati n reveals a syst li eje ti n murmur at the lef se nd interspa e and a xed split se nd heart s und. What is the m st likely diagn sis? A. B. C. D. E.

VSD ASD Mitral sten sis A rti insu ien y Ventri ular aneurysm

19. A 40-year- ld man is in a maj r m t r vehi le

llisi n with eje ti n r m the driver’s seat. On arrival, his bl d pressure is 70/40 mm Hg, with a pulse 125 beats per minute. He has a hest tube inserted whi h releases 1,500 mL bl d and n hange in vital signs. T e m st appr priate appr a h t this patient is: A. B. C. D. E.

Median stern t my C s an with IV ntrast Lef p ster lateral th ra t my Right p ster lateral th ra t my Anter lateral th ra t my

20. A 46-year- ld p st

e w rker presents with mplaints numbness and asi nal pain in the lef arm. Exam reveals a n rmal pulse and n edema the lef arm, but sympt ms seem t be w rse when the patient stret hes her arm ab ve her head. T e best initial test is: A. B. C. D. E.

Chest x-ray Serum p tassium Angi graphy C s an the lef sh ulder Pulm nary un ti n tests (PF s)

21. A 70-year- ld emale with a hist ry

50 pa k-years igarette sm king presents with a hr ni ugh. Physi al exam reveals arse breath s unds bilaterally, and hest x-ray suggests l w lung v lumes with a 2- m spi ulated lesi n in the periphery the lef l wer l be. Bi psy suggests aden ar in ma, and a metastati w rkup is negative. T e m st appr priate treatment is: A. B. C. D. E.

Chem therapy Radiati n therapy Lef l wer l be t my Lef pneum ne t my Wedge ex isi n

22. A 54-year- ld emale presents with 6 m nths

mild sh rtness breath, l wer extremity edema, and asi nal heart palpitati ns. ECG reveals n rmal sinus rhythm. E h ardi gram sh ws m derate t severe mitral regurgitati n, EF 50%, and m derately dilated lef atrium. Cardia atheterizati n reveals n rmal r nary arteries. What is the best therapeuti pti n r this patient? A. B. C. D.

Diuresis and repeat e h ardi gram in 6 m nths Mitral valve repla ement Anti agulati n and H lter m nit r Mitral valve repair

111

112

Study Questi ns r Part II

23. A 65-year- ld male su ers an S -elevati n MI and is treated with a drug-eluting stent in the mid

LAD artery, aspirin, l pid grel, simvastatin, and met pr l l. He remains hem dynami ally stable and initially re vers ardia un ti n with an EF 45% n h spital day 3. H wever n h spital day 5, he is sh rt breath and edemat us with mild hyp tensi n and a new harsh h l syst li murmur. Whi h the ll wing will n t be help ul in his ntinued management? A. B. C. D. E.

Intra-a rti ball n pump E h ardi gram Surgi al repair V lume resus itati n rans er t an intensive are unit

Answers and Explanati ns

Answers and Explanati ns 1. The a ns we r is A (Chapter 5, Pleural and Pleural Spa e Dis rders, Sp ntane us Pneum th rax).

T e patient has signs and sympt ms sp ntane us pneum th rax. Af er a n rmat ry x-ray, treatment with a hest tube is the best initial treatment. Needle de mpressi n is indi ated in ases tensi n pneum th rax. Additi nal imaging, su h as with C , is n t initially indi ated but may be required i there is n res luti n. Supplemental xygen may help with pneum th rax res rpti n but is n t su ient t all w mplete res luti n. 2. The a ns we r is E (Chapter 5, Pleural and Pleural Spa e Dis rders, Sp ntane us Pneum th rax,

IV A). Indi ati ns r de nitive surgi al management sp ntane us pneum th rax in lude re urren e (ipsilateral r ntralateral), persistent air leak greater than 3–5 days, in mplete expansi n the lung, and hem pneum th rax. 3. The a ns we r is C (Chapter 5, T

ra i rauma, Immediate Li e-T reatening Injuries, II C). T e patient has signs and sympt ms nsistent with a tensi n pneum th rax. T is li e-threatening situati n sh uld be treated immediately by needle th ra entesis. A hest tube inserti n sh uld ll w this maneuver. A hest radi graph is n t ne essary t n rm the diagn sis and will nly delay treatment. L al w und expl rati n has n r le in the management stab w unds the hest. Peri ardi entesis is the h i e when eviden e indi ates peri ardial tamp nade.

4–5. The a ns we rs a re 4-D (Chapter 5, T ra i rauma, P tentially Li e-T reatening Injuries, II D) a nd 5-B (Chapter 5, T ra i rauma, Immediate Li e-T reatening Injuries, VI). Causes

r the hest radi graph and ECG ndings are multiple and in lude a rti rupture, ardia tamp nade, tra he br n hial disrupti n, hyp xia, and ardia ntusi n. A m re pre ise diagn sis w uld be mandat ry be re undertaking th ra t my be ause perative strategy w uld depend n whi h injury is present. Blunt th ra i trauma with r with ut ail hest results in hest wall mus le damage and pain, with resultant splinting and l ss hest wall elasti ity. Intra-alve lar hem rrhage and interstitial edema redu e pulm nary paren hymal elasti ity. T ere re, b th lung and hest wall mplian e de rease. Pco 2, A-a gradient, and shunt ra ti ns w uld pr bably be elevated, and ventri ular ntra ti ns w uld pr bably be de reased. 6–7. The a ns we rs a re 6-C (Chapter 5, Pleural and Pleural Spa e Dis rders, Pleural E usi ns, II) a nd 7-B (Chapter 5, Pleural and Pleural Spa e Dis rders, Pleural Empyema, III B). T e patient

devel ping a pleural e usi n in the setting an underlying pneum nia requires th ra entesis r diagn sis. T e hara ter the uid des ribed is nsistent with that present in an empyema. Initial treatment an empyema sh uld inv lve l sed hest tube drainage. T ra t my and de rti ati n r rib rese ti n may be required when the empyema is n t adequately drained by the hest tube r is therwise n t amenable t l sed drainage. Vide -assisted th ra s pi surgery pleur desis is n t standard treatment r an empyema. 8. The a ns we r is D (Chapter 5, S litary Pulm nary N dules [C in Lesi ns], Invasive Diagn sti

e hniques). T e patient has a s litary pulm nary n dule. He is lder than age 40 years, and the hara teristi s d n t av r a benign lesi n, su h as n entri al i ati n. In additi n, the lesi n was n t present n the hest radi graph 5 years earlier. Diagn sis is mandat ry r determining whether the lesi n is malignant. T is an be d ne by needle bi psy r th ra s pi bi psy. 9. The a ns we r is C (Chapter 5, T

ra i rauma, P tentially Li e-T reatening Injuries, III). T is patient is presenting with a diaphragmati disrupti n, as eviden ed by the identi ati n the st ma h in the hest. reatment inv lves standard resus itati n prin iples, (airway, breathing, ir ulati n), pla ement a nas gastri tube t prevent a ute gastri dilatati n (whi h an pr du e severe, li e-threatening respirat ry distress), and urgent transabd minal repair the diaphragmati de e t. I diagn sis is delayed by 7–10 days, transth ra i repair is pre erred t a ilitate the reeing any adhesi ns t the lung.

113

114

Answers and Explanati ns

10. The a ns we r is E (Chapter 6, C ngenital Heart Disease, Overview, II). T e m st

rms ngenital heart disease are, in de reasing rder, VSD, transp siti n tetral gy Fall t, hyp plasti lef heart syndr me, ASD, and PDA.

mm n the great vessels,

11. The a ns we r is E (Chapter 5, S litary Pulm nary N dules [C in Lesi ns], Imaging, I C).

Is lated lung n dules less than 1.0 m are kn wn as in lesi detailed hist ry, n ting any use t ba pr du ts r previ radi graphs sh uld be btained. A al i ed lesi n that has n suggests a benign pr ess. In this patient, bservati n with hange in the lesi n is an indi ati n r bi psy.

ns. W rkup sh uld in lude a us malignan y. Any pri r hest t enlarged ver a 2-year peri d ll w-up x-ray is indi ated. Any

12. The a ns we r is D (Chapter 5, Br n h geni Car in ma, reatment, I A). T e appr priate

treatment is surgi al l be t my. Observati n with repeat hest x-ray is n t warranted with a sm king hist ry. T is patient is in lini al stage I, based n tum r size and n dal status. T ere is n lear bene t in bi psying the lesi n. Chem therapy and radiati n may be indi ated in ertain stage IIIa lesi ns r in l ally advan ed disease. 13. The a ns we r is A (Chapter 5, Mediastinal Lesi ns, Vis eral C mpartment Lesi ns, II). T e m st

mm n middle mediastinal mass is a br n h geni yst. Lymph ma, thym ma, and germ ell tum rs are mm nly l ated in the anteri r mediastinum. Middle mediastinal lesi ns in lude br n h geni and peri ardial ysts. Metastati aden ar in ma may inv lve the pleural sur a es; h wever, lesi ns are f en small and multiple. 14. The a ns we r is D (Chapter 6, A quired Heart Disease, A rti Valvular Disease, I D). Angina,

syn pe, and dyspnea are the lassi sympt ms a rti sten sis. Physi al examinati n generally reveals a syst li eje ti n murmur in the se nd right inter stal spa e. An ECG and serial ardia enzymes sh uld be btained t rule ut ardia is hemia. T e murmur a rti insu ien y is diast li with a lini al pi ture heart ailure. 15. The a ns we r is D (Chapter 6, A quired Heart Disease, C r nary Artery Disease, I B). Risk

a t rs r CAD are the same as th se r vas ular disease in general—sm king, diabetes, besity, hypertensi n, and hyper h lester lemia. Alth ugh renal ailure is f en ass iated with CAD, this is be ause the requent ass iati n with ther risk a t rs, su h as hypertensi n and diabetes. 16. The a ns we r is A (Chapter 6, A quired Heart Disease, C r nary Artery Disease, V C 2). T is

patient has severe triple-vessel r nary disease. Studies have sh wn a signi ant survival advantage r patients in this ateg ry wh are treated with surgi al revas ularizati n rather than with medi al management r angi plasty. Additi nal bene t may be realized in patients with mpr mised ventri ular un ti n. 17. The a ns we r is A (Chapter 6, A quired Heart Disease, A rti Valvular Disease, I B 1). T is

patient has a rti sten sis. Sympt ms usually begin when the valve area is less than 1 m 2. 18. The a ns we r is B (Chapter 6, C ngenital Heart Disease, Atrial Septal De e ts, III D).

E h ardi gram sear hing r thr mbus r septal de e t sh uld be btained in a y unger patient wh su ers r m a erebral vas ular a ident. A se nd interspa e murmur and xed splitting the se nd heart s und are lassi ndings in ASD. Anti agulati n r 4–6 weeks with ele tive repair the ASD is the indi ated treatment. 19. The a ns we r is E (Chapter 5, T

ra i rauma, Immediate Li e-T reatening Injuries, IV B). Anter lateral th ra t my is the pr edure h i e. T e patient meets riteria r perative interventi n as the initial hest tube utput ex eeds 1 L. T e best initial in isi n in the hem dynami ally unstable patient is anter lateral th ra t my.

20. The a ns we r is A (Chapter 5, Chest Wall Dis rders, Chest Wall De rmities, IV A 1). T e patient

has signs and sympt ms nsistent with neur geni th ra i utlet syndr me. T ere may be a ervi al rib ausing mpressi n the bra hial plexus. Chest x-ray is the initial diagn sti study, ll wed by a urse physi al therapy t alleviate the mpressi n. T e patient’s sympt ms are unlikely t be aused by an ele tr lyte disturban e. Angi graphy is n t indi ated given

Answers and Explanati ns

the n rmal pulse exam. Sh ulder lms may rule ut ra ture, but C w uld be indi ated questi ns ligament us injury. PF s are use ul r lung path l gy nly.

r

21. The a ns we r is C (Chapter 5, Br n h geni Car in ma, reatment, I A 1). T e best de nitive

management a lung an er is ex isi n, and rmal l be t my is the pr edure h i e. Wedge ex isi n is used in ases patients that are t high risk t t lerate anat mi rese ti n, and pneum ne t my is reserved r th se patients with m re di use disease in ne lung. Chem therapy and radiati n have a r le in advan ed disease palliati n. 22. The a ns we r is D (Chapter 6, A quired Heart Disease, Mitral Valve Disease, II E 2). T is

patient meets Ameri an Heart Ass iati n/Ameri an C llege Cardi l gy riteria r surgi al rre ti n mitral regurgitati n given her sympt ms, depressed EF and likely atrial brillati ns. In the setting mitral regurgitati n, an EF bel w 60% represents de reased un ti n. Mitral valve repair is pre erred t repla ement when p ssible. Alth ugh treating v lume verl ad and atrial brillati n will be imp rtant aspe ts in the medi al management mitral insu ien y, surgi al rre ti n is indi ated and ut mes are impr ved with earlier interventi n. 23. The a ns we r is D (Chapter 6, A quired Heart Disease, C r nary Artery Disease, VI C). T is

patient is presenting with a p stin ar ti n VSD. M st immediately, an e h ardi gram will be ne essary t determine the l ati n and size the VSD. Given his mild hyp tensi n, an intraa rti ball n pump will help supp rt hem dynami s until repair an be d ne. Catheter-based repairs are n t likely t be help ul, as riable, injured my ardium surr unding the VSD d es n t er suitable atta hment p int r any per utane us devi es. T e diagn sis a p stin ar t VSD mandates surgi al repair, whi h sh uld be d ne within 24 h urs t ptimize survival. V lume resus itati n in the setting impending ardi geni sh k will nly serve t advan e the disease state.

115

Part III

Vascular Disorders

Chapter Cuts and Caveats CHAP TER 7 Arte ria l Dis e a s e : An untreated IA is associated with a 40% chance o a second IA or stroke within 2 years. CEA, i done or more than 70% stenosis, lowers the 2-year major stroke rate to 9%, whereas medical treatment with antiplatelet therapy has a 26% rate. T e CEA perioperative risk o a major stroke is 1%–3% and is dependent on the surgeon. Acute arterial embolism of en is secondary to cardiac thrombi, such as with atrial brillation, acute MI, and valvular disease. Occlusive disease o the distal aorta and iliac and emoral arteries (in low disease) may produce claudication, rest pain, or tissue loss. When it is limb threatening, it should be evaluated and revascularized. In low disease should generally be revascularized be ore out low disease. Claudication is reversible ischemia o the leg and is managed by li estyle modi cation, including a supervised exercise program; smoking cessation; control o diabetes, hyperlipidemia, and hypertension; and antiplatelet therapy. Revascularization is reserved or patients in whom the claudication inter eres with an active li estyle. T e hallmarks o ischemia are the 6 P’s: pain, pulselessness, paralysis, pallor, paresthesias, and poikilothermia. Rest pain is constant pain, usually across the ore oot, and indicates severe ischemia. issue loss is imminent, and urgent evaluation and revascularization is appropriate. T ere are three important acets to a vascular bypass patency: (1) in ow: i blood ow into the bypass is not strong, the bypass will thrombose; (2) the conduit: i the conduit has a technical problem, such as a twist, kink, narrowing, or anything else that impedes ow, the bypass will thrombose; and (3) out ow: i the vessels distal to the bypass are obstructed or any reason, the bypass will thrombose. Revascularization longer than 6 hours af er acute ischemia may result in a severely impaired limb or even require amputation. Compartment syndrome may occur ollowing revascularization and is caused by increased tissue pressure (20–40 mm Hg) obstructing capillary blood ow to the tissues (because the compartment pressure does not reach arterial pressure, the patient will not present with the signs o arterial occlusion and may have a normal distal pulse). Both open and endovascular repairs o the aorta have excellent long-term durability. Endoleaks are leaks in the space between an endograf and the native vessel, and most should be repaired. Elective repair o AAA at least 5.5 cm in men and 5 cm in women in greatest diameter is appropriate i the patient is likely to tolerate the procedure and has a li e expectancy o more than 2 years. More than 95% o AAAs arise in rarenally.

T e presence o AAA and new-onset abdominal pain should be urgently evaluated or leak or rupture and repaired i present: ~50% o ruptured AAAs result in death prior to treatment. Repaired ruptured AAAs have a high incidence or postoperative complications, especially MI and acute renal ailure. Descending thoracic aortic dissection is usually treated with medical therapy to control hypertension. Surgical or endovascular repair is reserved or leaks, rupture, or occlusion o aortic branches. Proximal dissection is a surgical emergency due to risk o coronary occlusion, aortic regurgitation, and tamponade.

CHAP TER 8 Ve no us a nd Lym p ha tic Dis e a s e : Surgery is a proin ammatory state, and all surgical patients are at increased risk o lower extremity DV . Many patients may have no symptoms or physical ndings. Initial DV treatment is anticoagulation with heparin ollowed by war arin. Risk actors or DV are summarized in the Virchow triad: stasis, hypercoagulable states, and endothelial injury. Proven lower extremity DV prophylaxis includes intermittent pneumatic compression devices and low-dose anticoagulation. IVC lters may prevent lower extremity DV s rom becoming a PE in special situations: those who ail anticoagulation or those who cannot tolerate anticoagulation (such as hemorrhagic stroke or trauma). Upper extremity DV : usually re ers to thrombosis o the axillary or subclavian vein. Secondary UEDV is increasing in incidence due to increased use o upper extremity catheters. Pulmonary embolus may occur in up to 1/3rd o patients, and post-thrombotic syndrome o the arm is common; thus anticoagulation with heparin ollowed by war arin is appropriate in most cases. Primary UEDV (Paget-Schroetter Syndrome) is rare and typically related to extreme arm exercise in sports (e ort thrombosis) or thoracic outlet syndrome. It may be amenable to urgent catheter-directed thrombolytic therapy aimed at preventing post-thrombotic syndrome, ollowed by investigation or etiology. PE is diagnosed with C pulmonary angiogram. PE patients are best treated with systemic anticoagulation.

117

Chapter 7

Arterial Disease Garima Dosi and Robert S. Crawford

GENERAL P RINCIP LES P a tho p hys io lo g y Athe ro s c le ro s is I. Cha ra c te ris tic s : starts as a atty streak and can progress to complex plaques, characterized by intimal ulceration or intraplaque hemorrhage II. Clinic a l m a ni e s ta tio ns : Can be distal rom embolization or local rom stenosis causing partial blockage and diminished distal ow or occlusion and complete luminal blockage. Also determined by the acuity o the lesion and presence o collateral circulation. III. Ris k a c to rs : diabetes mellitus (DM), tobacco use, hypertension (H N), and hyperlipidemia

LOWER EXTREMITY ARTERIAL OCCLUSIVE DISEASE Cla s s if c a tio n I. Ba s e d o n le s io n lo c a tio n: Figure 7-2 shows the lower extremity (LE) arterial tree. A. Suprainguinal aortoiliac occlusive disease (AIOD): involves the aorta and iliacs up to the level o inguinal ligament B. In rainguinal disease: arteries distal to inguinal ligament ( emoral, popliteal, and tibial systems), including emoropopliteal disease and in rageniculate tibial disease II. Ba s e d o n s ym p to m a to lo g y: includes noncritical and critical limb ischemia A. Intermittent claudication: Symptoms are reproducible; rest brings relie . T is is not a limb-threatening condition. 1. Inciting event: walking or exercise 2. Primary symptom: pain in a ected muscle groups (cal ) 3. Risk o major limb amputation: 1% per year B. Neurogenic claudication: Patient presents with history o back pain. Pain radiates down the leg, with associated paresthesia, and can occur with standing.

118

Quic k Cut Vas cular s urgeons encounter a wide variety o clinical mani es tations o arterial dis eas e; Figure 7-1 demons trates that the les ions have s ome common pathophys iologic eatures .

Quic k Cut Atheros cleros is is the mos t common caus e o arterial occlus ive dis eas e and can a ect any vas cular bed in the body.

Quic k Cut In acute arterial occlus ion, collateral circulation does not have time to develop, res ulting in acute is chemia and tis s ue los s .

Quic k Cut Fewer than 5% o patients with intermittent claudication progres s to critical limb is chemia.

Quic k Cut Vas culogenic claudication requires ambulation; neurogenic claudication may occur while s tanding or at res t.

Chapter 7

Arterial Disease

119

Arte ria l dis e a s e

Occlus ive (e.g., s te nos e s, occlus ion, e mbolic)

Tra uma tic tra ns e ction

Ane urys ma l (e.g., AAA, TAAA)

Conge nita l: a rte riove nous ma lforma tions

Conne ctive tis s ue dis orde rs (e.g., Rayna ud, Ta kaya s u)

Nontra uma tic: a the ros cle ros is

Fig ure 7-1: The spectrum o arterial dis ease. AAA, abdominal aortic aneurysm; TAAA, thoracoabdominal aortic aneurysm.

Common ilia c a rte ry Exte rna l ilia c a rte ry Inte rna l ilia c a rte ry Common fe mora l a rte ry De e p fe mora l a rte ry S upe rficia l fe mora l a rte ry

Poplite a l a rte ry Ante rior tibia l a rte ry Tibiope rone a l trunk

Pos te rior tibia l a rte ry Pe rone a l a rte ry

Dors a lis pe dis a rte ry De e p pla nta r bra nch of a rcua te a rte ry

Anterior

Posterior

Fig ure 7-2: The arterial tree o the lower extremity.

120

Chapter 7

Aortoiliac Occlusive Disease (AIOD)

C. Critical limb ischemia: Limb-threatening condition; 30% o patients progress to major amputation within a year. 1. Characteristics: ischemic rest pain or tissue loss (nonhealing ulcers or gangrene) 2. Mortality: 25% die within 1 year rom cardiovascular complications.

Eva lua tio n a nd Wo rkup o P a tie nts with P e rip he ra l Arte ria l Dis e a s e

Quic k Cut Signs and s ymptoms o acute arterial ins u f ciency are the 6 P’s : p ain, p allor, p ares thes ia, p aralys is , p uls eles s nes s , and p oikilothermia.

I. Eva lua tio n: starts with a detailed history and thorough physical exam II. Ca rd io p ulm o na ry s ta tus : critical, as many have signi cant coronary disease III. Dup le x s c re e ning o c a ro tid a rte rie s : may demonstrate concomitant cerebrovascular atherosclerosis IV. Re na l a s s e s s m e nt: Blood urea nitrogen (BUN) and creatinine levels are required, as most patients will require some orm o contrast evaluation either by digital subtraction angiography (DSA) or computed tomography angiography (C A). V. Athe ro s c le ro tic ris k a c to rs : Initiate best medical management o DM, H N, hyperlipidemia, and smoking cessation.

Na tura l His to ry o Untre a te d Dis e a s e I. Co lla te ra l c irc ula tio n: develops around the area o stenosis or Quic k Cut occlusion to provide distal blood ow Many patients are able to live normal lives II. Sup e rf c ia l a rte ry o c c lus io n: Collateral vessels rom pro unda des pite a s uperf cial emoral emoris reconstitute the popliteal artery. artery occlus ion due to collateral ow. III. Ge nic ula te c o lla te ra ls : develop around the knee to provide collateral blood ow IV. In AIOD: Collaterals arise rom iliac, lumbar, and internal mammary arteries.

AORTOILIAC OCCLUSIVE DISEASE (AIOD) Ge ne ra l As p e c ts I. Ana to m ic lo c a tio n: Atherosclerosis usually begins in the in rarenal aorta; over time, this can extend and may result in total occlusion. II. Exte nt: Patients can either have isolated AIOD or have multisegment disease with involvement o in rainguinal vasculature. III. Ris k a c to rs : T ose with isolated AIOD are usually young emales with history o smoking and hypercholesterolemia; patients with di use multisegment disease are usually older male with DM and H N. IV. Clinic a l p re s e nta tio n: Blue toe syndrome can be the presenting Quic k Cut symptom in AIOD. The hallmark o A. Intermittent claudication: Distribution is in the buttock and AIOD is diminis hed or abs ent thigh and suspected in patients with near-normal ankle-brachial emoral puls es . index (ABI) who complain o claudication. Exercise ABI is help ul in uncovering the level o the lesion. B. Leriche syndrome: buttock claudication, impotence, and diminished emoral pulses; seen in males C. Blue toe syndrome: Produced by small cholesterol emboli; patients may have ocal areas o ischemia in the eet. More common in patients with aneurysmal disease that have extensive mural thrombus.

Dia g no s tic Inve s tig a tio ns I. ABI: correlates with patient’s unctional status and can be elevated in noncompressible medial calcinosis as in end-stage renal disease and DM A. Procedure: Blood pressure is measured in both arms, then at the ankle. B. Calculation: Divide systolic ankle pressure by highest o the two brachial pressures ( able 7-1).

Chapter 7

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121

Ta b le 7-1: Sta nd a rd ize d Cla s s if c a tio n o Dis e a s e Ba s e d o n Ankle -Bra c hia l Ind e x 1.13–1.0

Normal

0.9–1.0

Minimal arterial disease; asymptomatic

0.5–.09

Claudication, mild to moderate disease

0.5

Rest pain; severe disease

An ABI o approximately 1 is normal. Higher values indicate calcif ed vessels, and lower values indicate the presence o arterial disease.

II. Noninva s ive va s c ula r la b s tudie s : involves measurement o segmental pressure and wave orm analysis at each arterial segment (thigh, cal , ankle, and toes) and duplex evaluation o the lower limb arteries A. Segmental pressure and pulse volume recording (PVR): will demonstrate di erences in pulse pressure Quic k Cut B. iming: Segmental pressure measurements may be per ormed A di erence o af er graded exercise treadmill test. 20 mm Hg between s egments is diagnos tic o a unctionally III. CTA: most common test or localizing lesions but with limitations s ignif cant les ion. o radiation exposure and possible renal insu ciency rom intravenous (IV) contrast IV. Ma g ne tic re s o na nc e a ng io g ra p hy (MRA): has same advantages as C A but more expensive A. Gadolinium contrast: carries the risk o nephrogenic systemic brosis in patients with renal insu ciency B. Other limitations: False negatives can occur in patients with previous endovascular interventions. V. DSA: still considered the gold standard; commonly per ormed during a planned intervention

Tre a tm e nt I. Me d ic a l the ra p y: First line o therapy or all patients with claudication; best management o their atherosclerotic risk actors and smoking cessation should be instituted in all patients as well as antiplatelet therapy with aspirin. A. HMG-CoA reductase inhibitors: recommended even in Quic k Cut patients with acceptable lipid pro les due to the additional Cilos tazol is the only cardiovascular protective e ects drug that has s hown s ome improvement in abs olute B. Cilostazol: Phosphodiesterase-3 inhibitor that causes vasodilation walking dis tance in patients through smooth muscle cell relaxation and inhibition o platelet with intermittent claudication. aggregation. Contraindicated in congestive heart ailure (CHF). II. Gra d e d e xe rc is e p ro g ra m : Very e ective at encouraging development o collaterals and alleviating symptoms. Ambulation should be an early part o any treatment algorithm or claudication. III. Op e ra tive inte rve ntio n: Indications include li estyle-limiting Quic k Cut claudication, ischemic rest pain, or evidence o tissue loss. Aortoiliac A. Angioplasty/stent: per ormed via trans emoral or brachial approach interventions are the mos t 1. Advantages: Distal aorta and iliacs can be treated with balloon durable endovas cular angioplasty and stent placement; 5-year patency rate is excellent. procedures . 2. Site-related complications: bleeding or hematoma, pseudoaneurysm; arteriovenous stula, iliac artery dissection, thrombus ormation, and distal embolization Quic k Cut B. Open procedures: may include direct reconstruction or extraBecaus e o its anatomic approaches i the patient has severe comorbidities or e f cacy and durability, aortobi emoral bypas s is the in ection gold s tandard or treatment 1. Aortobi emoral bypass: Five-year patency o this procedure o AIOD. is 90% and 75% at 10 years. Procedure is as ollows: a. Step 1: midline laparotomy and aortic exposure b. Step 2: Proximal anastomosis is per ormed between the graf (Dacron or polytetra uoroethylene [P FE]) and aorta in end-to-end or end-to-side ashion.

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c. Step 3: Limbs o the bi urcated prosthetic graf are tunneled retroperitoneally and anastomosed to emoral arteries. 2. Femoral- emoral bypass: Per ormed or unilateral iliac disease; the contralateral emoral artery serves as arterial in ow. a. Procedure: Prosthetic graf is tunneled either subcutaneously or in space o Retzius and anastomosed to emoral arteries. b. Patency: 5-year rate o 75% 3. Axillobi emoral bypass: Per ormed in patients with AIOD who are high-risk candidates or open aortic revascularization; axillary artery serves as the arterial in ow. Five-year patency rate o 60%–85%.

FEMOROP OP LITEAL OCCLUSIVE DISEASE Ge ne ra l As p e c ts I. Ana to m ic e xte nt a nd lo c a tio n: Occlusive disease is most requently seen in the super cial emoral artery (SFA). II. Dis e a s e s e ve rity: ranges rom ow-limiting stenosis to complete occlusion in the super cial emoral and popliteal arteries III. Ris k a c to rs : Atherosclerosis is the most important risk actor; other causes include popliteal entrapment, dissection, embolization, or aneurysmal degeneration.

Quic k Cut The mos t common location or emoral occlus ive dis eas e is in the dis tal SFA at the level o Hunter canal.

IV. Clinic a l p re s e nta tio n: Majority o patients are asymptomatic; the pro unda emoral artery provides important ow to the thigh musculature and through collaterals can sustain near-normal activity. Other presentations are as ollows: A. Intermittent claudication: crampy cal pain with ambulation; intensity o symptoms depends on severity o disease B. Critical limb ischemia: ischemic rest pain, nonhealing ulcer, or Quic k Cut gangrene Res t pain, ulcers , 1. Rest pain: Pain that occurs with no activity; patients usually and gangrene are s igns o describe pain in the more dependent areas such as the toes or imminent limb los s , and on the dorsum o the oot. intervention to res tore ow is needed urgently. 2. Most common complaint: pain that occurs at night and is relieved by dangling the leg rom the bed V. P hys ic a l e xa m ina tio n: In contrast to patients with AIOD, they have palpable emoral pulses but diminished popliteal and pedal pulses. Some patients with severe limb ischemia may have leg pallor on oot elevation and develop rubor in the dependent position.

Dia g no s tic Stud ie s I. No ninva s ive va s c ula r s tud ie s : include the ollowing: A. ABI: Pressure drop o greater than 20 mm Hg indicates signi cant hemodynamic arterial obstruction. B. Exercise treadmill testing: can be used in patients with claudication with normal resting ABI C. Wave orm analysis: Doppler wave orms and PVR

Quic k Cut In healthy patients , ankle pres s ure s hould remain normal or increas e a ter exercis e.

II. DSA: usually reserved or patients as part o planned intervention and gives excellent detail o the target lumen (Fig. 7-3) A. Procedure: Contrast media is injected using catheters placed either by trans emoral or the transbrachial percutaneous approach. Images are recorded under uoroscopy. B. Associated complications: include dye-associated nephrotoxicity, allergy, and site complications as listed earlier III. CTA o a b d o m e n a nd p e lvis with e xtre m ity runo : gives near-equal static in ormation, especially with new three-dimensional (3D) reconstruction techniques; however, there is no dynamic in ormation. Avoids the access site complications associated with DSA and is especially good to delineate calcium within vessels

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123

S tump

Fig ure 7-3: A: Bas eline angiography o the right s uperf cial emoral artery (SFA) revealing a complete occlus ion at the os tium with a s hort s tump. B: Angiography ollowing las er atherectomy with res toration o ow. The SFA was then pos tdilated with a 5.0-mm balloon at low pres s ure. C: Final SFA angiography revealing a widely patent SFA with no evidence o dis s ection or need or s tenting. (From Cas s erly IP, Sachar R, Yadav J S. Practical Peripheral Vascular Intervention, 2nd ed. Philadelphia: Lippincott Williams & Wilkins ; 2011.)

Tre a tm e nt Op tio ns

Quic k Cut

I. Be s t m e d ic a l the ra p y: See earlier discussion (e.g., smoking The adequacy o cessation, lipid control, cilostazol). in ow, the s uitability o the out ow, and the type and II. P e rc uta ne o us inte rve ntio ns : Angioplasty and stenting convey a quality o the conduit all good outcome and durability (up to 80% patency over 3 years). in uence the outcome o the III. Op e n s urg ic a l o p tio ns : can involve endarterectomy or bypass procedure. A. Local endarterectomy o the common emoral and pro unda with patch angioplasty: highly e ective in patients with severe ocal lesions Quic k Cut B. Bypass: Five-year primary patency o emoropopliteal above and In general, patency below knee bypass with greater saphenous vein is 70%–90%. rates are better or above-theknee procedures than below 1. Inf ow: common emoral artery knee. 2. Outf ow: typically the popliteal artery above or below the knee 3. Conduit: As a rule, autogenous vein bypass is pre erred over prosthetic bypass; prosthetic graf s have overall poor patency when used or below-knee vessels.

INFRAGENICULATE TIBIAL DISEASE Ge ne ra l As p e c ts I. Clinic a l p re s e nta tio n a nd a na to m ic e xte nt: usually multisegmental; patients are usually high risk due to other associated medical comorbidities A. Characteristics: commonly seen with DM and end-stage renal disease B. Presentation: Patients typically present with oot ulcers or gangrene.

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II. Tre a tm e nt: For selected patients, endovascular interventions can achieve wound healing. A. Bypass: For rest pain or tissue loss, open bypass is the procedure o choice. 1. Distal target: any o the three tibial arteries (anterior tibial, posterior tibial, or peroneal) or to the pedal arteries o the oot 2. ibial bypasses: Autogenous vein conduit has superior patency rate as compared to prosthetic graf . B. DSA: important to identi y the appropriate in ow and out ow vessel

ACUTE ARTERIAL INSUFFICIENCY

Quic k Cut Toe pres s ure o greater than 40 mm Hg is needed to heal a oot wound.

Quic k Cut The ultimate goal o peripheral bypas s is to provide inline ow to the dis tal oot.

Etio lo g ie s I. Em b o lis m : Debris (thrombus, lipid, tumor, etc.) dislodges rom proximal source and obstructs a distal artery. Majority have a cardiac origin. A. Cardiac origins: mural thrombus in patients with atrial brillation, ventricular thrombus af er myocardial in arction (MI), rheumatic valvular abnormalities, vegetations on prosthetic valves, atrial myxoma B. Noncardiac embolic sources: atherosclerotic or aneurysmal, peripheral artery aneurysm (popliteal artery), thoracic outlet syndrome, iatrogenic atheroembolization af er percutaneous vascular interventions II. Thro m b o s is : In situ thrombosis in patients with atherosclerotic arterial disease can produce acute ischemia. III. Hyp e rc o a g ula b le s ta te s : can cause in situ thrombosis in the absence o atherosclerosis IV. Ao rtic o r a rte ria l d is s e c tio n: Extension o a dissection can cause acute arterial insu ciency. V. Othe r: acute occlusion o previously patent bypass graf

Quic k Cut The mos t common caus e o late gra t ailure is neointimal hyperplas ia.

Quic k Cut Acute arterial ins u f ciency is a vas cular emergency, as rapid res toration o blood ow is required to prevent irrevers ible tis s ue los s , limb los s , and even death.

Quic k Cut Thrombos is is the mos t common caus e o acute arterial ins u f ciency.

Clinic a l P re s e nta tio n I. Sym p to m s : depend on the size o the artery occluded and the presence o collateral circulation II. La rg e o r m a c ro e m b o lus : usually gets lodged at bi urcation sites such as the common emoral artery (super cial emoral/pro unda bi urcation) or popliteal artery (tibioperoneal/anterior tibial bi urcation) III. Mic roe m boli: usually a ect more distal tibial or digital vessels, and patients present with blue toe syndrome

Eva lua tio n I. P ro m p t p hys ic a l e xa m ina tio n: helps determine the level o Quic k Cut occlusion Comparis on with the contralateral extremity and II. CTA with runo : can provide use ul in ormation about the level identif cation o motor and o the occlusion and about options or revascularization s ens ory def cits are important parts o the vas cular exam. III. Dup le x: operator dependent but can be used to make a quick diagnosis (i.e., to locate a thrombus at the emoral bi urcation) IV. On-ta b le a ng io g ra p hy: used when endovascular intervention needs to be per ormed and to con rm patency af er any intervention

Ma na g e m e nt I. Antic o a g ula tio n: always the rst step in critical limb ischemia; IV heparin is the drug o choice II. P e rc uta ne o us thro m b e c to m y a nd thro m b o lys is : pre erred in acute limb ischemia patients with intact motor and sensory unction A. Absolute contraindications to thrombolytic therapy: recent stroke or brain surgery within 2 months, major surgery within 2 weeks, and patients at signi cant risk o bleeding B. iming: T rombolytic therapy requently takes more than 24 hours or e ect.

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III. Op e n thro m b e c to m y/e m b o le c to m y: Per ormed using Fogarty catheters that are advanced into the artery through the embolus, and balloon is in ated. As the catheter is withdrawn with the in ated balloon, the thrombus is extracted. IV. Co m b ine d e nd o va s c ula r a nd o p e n p ro c e d ure s : Recently, an open approach combined with endovascular adjuncts such as angioplasty or stenting. Initial angiography can be ollowed by an open embolectomy, culminating with stenting o in ow, direct in usion o tissue plasminogen activator (tPA) into the artery, and a bypass to below-the-knee arterial target. V. Com p a rtm e nt s yndro m e : Results rom reper usion injury to the Quic k Cut ischemic muscle. Postrevascularization patients need to be watched The clas s ic closely or myoglobinuria and associated nephrotoxicity. is chemic time as s ociated with A. Presentation: pain on passive stretch, cal tenderness, and loss o compartment s yndrome is sensation in the rst web space 6 hours . B. Untreated: can lead to permanent neurologic sequelae such as oot drop C. Fasciotomy: therapeutic and based on clinical suspicion

AMP UTATIONS Ge ne ra l As p e c ts

Quic k Cut

I. Ind ic a tio ns : nonambulatory bed-bound patients, Primary amputation nonreconstructible disease, extensive tissue loss, medical is o ered to patients with critical limb is chemia as f rs tcomorbidities that make revascularization procedures risky, wet line therapy when bypas s is gangrene with sepsis not pos s ible or not des irable. II. Te c hnic a l c o ns id e ra tio ns : Amputation level must maximize the rehabilitation potential o each individual patient. A. Goal: to remove all the in ected or necrotic tissue and to achieve a healing stump o appropriate length so as to t prosthesis B. Level o amputation: determined by the patient’s preoperative unctional status and the involved extremity’s underlying arterial circulation

Sp e c if c Am p uta tio ns I. To e a m p uta tio n: Can be per ormed across a phalanx or metatarsal bone (ray amputation). Associated with minimal gait disturbance. II. Tra ns m e ta ta rs a l a m p uta tio n: involves transection o all ve Quic k Cut metatarsal bones midshaf with a posteriorly based ap Ambulation requires III. Be lo w-kne e a m p uta tio n: ibia and bula are transected 10 cm progres s ively more energy below tibial tuberosity and coverage obtained by a longer posterior with more proximal levels o amputation. ap. Energy expenditure or ambulation is increased 10%–40% over bipedal gait. IV. Ab o ve -kne e a m p uta tio n: Femur is transected at distal one third o shaf . Energy expenditure or ambulation is increased 50%–70% over bipedal gait.

EXTRACRANIAL CEREBROVASCULAR DISEASE Ge ne ra l As p e c ts I. Inc id e nc e a nd e tio lo g y: Stroke is the third leading cause o death in the United States. Atherosclerosis o extracranial carotid arteries usually a ects the carotid bi urcation and the origin o the internal carotid artery and may predispose to stroke (Fig. 7-4). II. As ym p to m a tic : Patients are evaluated on the basis o their degree o stenosis. Patients may have an incidental carotid bruit. III. Sym p to m a tic : Clinical symptoms are as ollows. A. Amaurosis ugax: ransient monocular blindness due to embolization to retinal artery. Hollenhorst plaques (cholesterol atheroemboli) in retinal artery on unduscopy are diagnostic. B. ransient ischemic attack ( IA): sudden onset neurologic event lasting less than 24 hours with complete resolution

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Extracranial Cerebrovascular Disease S troke

Is che mic 87%

Thrombos is

Embolis m

La cuna r

He morrha gic 13%

S ys te mic hypope rfus ion

Intra ce re bra l he morrha ge

S uba ra chnoid he morrha ge

Fig ure 7-4: The etiologies o s troke (cerebrovas cular accident).

C. Reversible ischemic neurologic de cit (RIND): ocal neurologic de cit lasting more than 24 hours but resolving within a week D. Stroke: in arction o brain tissue resulting in permanent neurologic de cit E. Vertebrobasilar insu ciency: Symptoms are due to ischemia in brain supplied by vertebral arteries (posterior circulation) and may produce loss o vision, ataxia, gait disturbances, or vertigo.

Quic k Cut Stroke is in arction in an arterial dis tribution typically producing contralateral hemipares is .

Dia g no s tic Stud ie s I. Ma in o b je c tive s : to identi y the precise location o the de ect and its mechanism o origin II. Typ e s : include the ollowing: A. Computed tomography (C ) o the head without contrast: Quic k Cut initial test o choice to be obtained in any symptomatic patient to CT s cans may be als ely negative in the early identi y the mechanism (i.e., ischemic or hemorrhagic) period; MRI may be more B. Magnetic resonance imaging (MRI): more sensitive in detecting s ens itive. early ischemic changes but time-consuming and may induce claustrophobic reactions C. Cerebrovascular duplex: primary screening modality or detecting and grading the severity o lesions in extracranial carotid and vertebral arteries D. Cerebral angiography: de nes the vessel de ect and can be used as the rst step or interventions to remove thrombus using interventional methods E. Echocardiography: use ul in evaluation o a cardiac source o embolism

Ma na g e m e nt I. Me d ic a l m a na g e m e nt: aspirin, statin therapy, strict control o Quic k Cut H N and DM, and smoking cessation The primary goal o treatment o cerebrovas cular II. Surg ic a l re p a ir: Indications depend on whether the patient disease is prevention o stroke. is symptomatic or asymptomatic and on the degree o stenosis determined by preoperative testing. A. Asymptomatic: Asymptomatic carotid atherosclerosis study (ACAS) has demonstrated 5.9% risk reduction over 5 years in stroke incidence in asymptomatic patients with 60%–99% stenosis who underwent carotid endarterectomy (CEA) and best medical management compared to medical management alone. B. Symptomatic: North American symptomatic endarterectomy trial (NASCE ) demonstrated a 2-year decrease in stroke incidence rom 26% to 9% in symptomatic patients with greater than 70% stenosis with CEA and best medical management compared to medical management alone. Quic k Cut C. Contraindications: disabling stroke with altered level o Routine practice is consciousness, occluded internal carotid artery, presence o to o er CEA to patient who are s ymptomatic and have at medical comorbidities with short li e expectancy leas t 50% carotid s tenos is . D. CEA: involves removal o atherosclerotic plaque rom within the distal common, internal, and external carotid arteries 1. Procedure: Can be per ormed under local anesthesia with regional cervical block or general anesthesia. Done with or without a shunt depending on assessment o collateralization o cerebral blood ow (stump pressure, neuromonitoring, patient response).

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2. Patch: Patch closure is more durable than CEA without patch. 3. Complications: stroke, IA, bleeding, cranial nerve injury (vagus and hypoglossal) E. Carotid angioplasty and stent: Indications include surgically inaccessible lesion (skull base), previous carotid surgery (restenosis), irradiated neck, and severe comorbid cardiopulmonary conditions that preclude open carotid repair. Currently has a higher rate o complications than CEA.

AORTIC DISSECTION Ge ne ra l As p e c ts

Quic k Cut

I. P a tho p hys io lo g y: ear in the intima resulting in blood to ow Dis s ection occurs when the blood can ow in between the layers o aortic wall. rue lumen and alse lumen are between the layers o the created with ormation o intimal ap. T oracic aortic aneurysms ves s el wall rather than ins ide tend to dissect; abdominal aortic aneurysms do not. the lumen. II. Cla s s if c a tio n b a s e d o n tim ing : acute or chronic A. Acute: within 2 weeks rom the onset o symptoms 1. Complicated: must include the presence o rupture, Quic k Cut impending rupture, or evidence o end-organ ischemia and is Acute dis s ection is a surgical emergency a li e-threatening emergency and requires immediate 2. Uncomplicated: No evidence o ischemia or rupture. intervention. Standard o care is medical management and tight blood pressure control. B. Chronic: diagnosis more than 2 weeks af er symptom onset III. Cla s s if c a tio n b a s e d o n a na to m y: Figure 7-5 A. DeBakey classi cation: based on location o tear and extent o involvement o aorta with dissection 1. DeBakey type I: involves the entire aorta rom the root down into the descending aorta and is a surgical emergency 2. DeBakey type II: involves the ascending aorta and is a surgical emergency 3. DeBakey type III: Starts distal to the subclavian artery. reatment is dictated by occurrence o complications. B. Stan ord: based on location o entry tear only 1. Stan ord type A: entry tear located in ascending aorta and is a surgical emergency 2. Stan ord type B: entry tear located distal to origin o lef subclavian artery; medical management IV. Ris k a c to rs : H N (main), aortic wall structural anomalies, bicuspid aortic valve, hereditary conditions (e.g., Mar an syndrome), cocaine abuse V. Clinic a l p re s e nta tio n: usually have signi cant H N A. Pain: Severe, “tearing” chest, back, or abdominal pain. Patients usually describe “worst ever” pain. Misdiagnosis is common, as other causes (MI, pulmonary embolism) are usually ruled out rst. DeBakey classification Type I

Type II

Type A Stanford classification

Type III

Type B

Fig ure 7-5: DeBakey and Stan ord clas s if cation s ys tems or aortic dis s ection.

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Arterial Aneurysms

B. End-organ hypoper usion: may cause symptoms when the dissection compromises blood ow through branch vessels

Dia g no s is a nd Ma na g e m e nt I. CTA o c he s t a b d o m e n a nd p e lvis : gold standard diagnostic modality o choice II. Tra ns e s o p ha g e a l e c ho c a rd io g ra p hy (TEE): excellent to delineate anatomy and extent o involvement o the ascending aorta, arch, coronaries, and aortic valve with type A dissection III. Typ e A d is s e c tio ns : Urgent open surgical repair o ascending aorta with prosthetic graf replacement is treatment o choice. IV. Unc om plic a te d type B a ortic dis s e c tion: Medical management with strict blood pressure control with IV antihypertensive medications in intensive care setting (goal: mean blood pressure 60–70 mm Hg) is treatment o choice. V. Ind ic a tio ns o r typ e B d is s e c tio n: presence o end-organ malper usion, progression o dissection despite best medical Quic k Cut management, impending rupture, or increase in size o aneurysm The mos t important late complication o VI. Tho ra c ic e nd o va s c ula r a o rtic re p a ir (TEVAR): has become chronic aortic dis s ection is the technique o choice or surgical repair o type B aortic aneurys mal dilation. dissections (when indicated)

ARTERIAL ANEURYSMS Ge ne ra l As p e c ts I. De f nitio n: Permanent localized dilation o an artery. Aneurysmal Quic k Cut degeneration can a ect any artery o human body. Aneurys ms have a II. Cla s s if c a tio n: Aneurysms can be classi ed according to location, diameter at leas t 50% greater morphology, or etiology. than the native artery. A. Location: in rarenal aortic aneurysm, thoracoabdominal aortic aneurysm, splenic artery aneurysm, popliteal artery aneurysm, etc. B. Morphology: usi orm (involving the entire circum erence o artery), saccular (outpouching along one wall o the artery) C. Etiology: in ammatory, in ectious, congenital, degenerative, post-traumatic III. Ab d o m ina l a o rtic a ne urys m (AAA): In rarenal degenerative usi orm aneurysm is the most common type and is considered aneurysmal when diameter is greater than 3 cm. A. Complications: include rupture, embolization to the lower extremities (blue toe syndrome), dissection within an existing aneurysm, and stulization to adjacent structures (viscera, ureters) B. Growth: on average, rate o 0.2–0.3 cm per year C. Risk actors: Advanced age, male gender, smoking, amily Quic k Cut history. Other less consistent risk actors are H N, coronary Rupture is the artery disease (CAD), white race, and hypercholesterolemia. mos t eared complication o aneurys ms , as it may res ult in D. AAA rupture: Risk actors include H N, chronic obstructive s udden death. pulmonary disease (COPD), emale gender, current smoking status, and current steroid use. 1. AAA diameter: Rupture risk increases signi cantly with increases in aortic diameter ( able 7-2). 2. Shape: Eccentric or saccular-shaped aneurysms have higher risk o rupture. E. Screening: Criteria or one-time abdominal ultrasound include amily history o aneurysm or males aged 65–75 years who smoked at least 100 cigarettes in their li etime. F. Asymptomatic: Most aneurysms are diagnosed incidentally on physical examination as palpable pulsatile mass in periumbilical region or on abdominal imaging. G. Symptomatic: may have symptoms rom compression such as early satiety rom duodenal compression, hydronephrosis rom ureteral compression, or venous thrombosis rom iliocaval compression 1. Small aneurysms: may present with LE ischemic symptoms rom distal embolization o thrombus present within the aneurysm sac 2. Ruptured aneurysms: present with severe abdominal/back pain, tender pulsatile abdominal mass, and signs o shock

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129

Ta b le 7-2: Ab d o m ina l Ao rtic Ane urys m Rup ture Ris k AAA Dia m e te r (c m ) 4

Rup ture Ris k (% /ye a r) 0

4–5

0.5–5

5–6

3–15

6–7

10–20

7–8

20–40

8

30–50

AAA, abdominal aortic aneurysm.

H. Diagnosis: includes MRI and the ollowing: 1. Abdominal x-ray: may show “egg shell sign” due to calci cation o the aneurysm wall 2. Abdominal ultrasound: Valuable noninvasive tool or diagnosis, screening, and monitoring AAA. It is not use ul in cases o ruptured aneurysm. 3. Abdominal C scan with contrast: Gold standard diagnostic test; it accurately identi es the presence, size, and extent o aneurysm. I. Indications or repair: any symptomatic AAA (irrespective o size), AAA with size 5.5 cm or greater (in emale patients and those with Mar an syndrome, the size cuto is 5 cm), and rapidly expanding aneurysm (i.e., 5 mm growth in 6 months) J. ypes o surgical repair: include the ollowing: 1. Endovascular repair: per ormed via percutaneous access or emoral cutdown and requires the ollowing speci c anatomic criteria: a. Aortic neck: length ( 15 mm), diameter that provides appropriate proximal sealing zone, and angle less than 60 degrees b. Diameter o access arteries: Common and external iliac Quic k Cut artery should be su cient to pass the delivery system. All patients with an endovas cular repair require c. Calci cation: should be less than 50% o aortic li elong s urveillance. circum erence in the proximal and distal seal zone to prevent endoleak (persistent blood ow outside the endoluminal graf but inside the walls o aneurysm sac) Quic k Cut 2. Open surgical repair: can be per ormed either via midline Endovas cular repair transperitoneal or lef retroperitoneal approach and involves has lower perioperative opening the aneurysm sac and suturing the prosthetic graf mortality as compared to to normal aorta. T e aneurysm wall is then wrapped around open AAA repair. the graf . K. Postoperative complications: include the ollowing: 1. Acute renal ailure: Depending on the position o the clamp in Quic k Cut open repair, risk is higher i clamp is supra- or juxtarenal. For Bloody diarrhea all patients, also related to the administration o contrast dye. a ter AAA repair is is chemic 2. Acute LE ischemia: Caused most commonly by distal colitis until proven otherwis e. embolization in open and access site complications in Per orm s igmoidos copy to conf rm and res ect nonviable endovascular repair. Requires emergent repair. bowel promptly. 3. Ischemic colitis: More commonly seen in sigmoid ollowing ruptured AAA repair. Every attempt should be made to preserve the large in erior mesenteric artery (IMA). Can also Quic k Cut occur with coverage o IMA during endovascular repair. Spinal cord is chemia 4. Spinal cord ischemia: Incidence is very low af er in rarenal may be related to interruption aortic aneurysm repair but higher with thoracoabdominal o the artery o Adamkiewicz, aortic aneurysm repair. Some actors related to spinal cord which aris es between T8 ischemia are duration o aortic cross-clamping, episodes o and T12. hypotension, and cholesterol embolization.

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Chapter 7

Mesenteric Vascular Disease

5. Sexual dys unction: rom injury to sympathetic nerves near aortic bi urcation 6. Pelvic ischemia and gluteal claudication: May be seen i both hypogastric arteries are ligated or covered with graf . Per usion to one o the hypogastric arteries must be preserved. 7. Endogra migration and endoleak: associated with endovascular repair and can lead to increase in aneurysm size and eventual rupture. 8. Aortic gra in ection: usually a late complication; may present decades af er surgery a. Presentation: dull abdominal pain, ever, leukocytosis b. Diagnosis: C scan shows presence o air and uid Quic k Cut collection around the graf . The mos t common c. reatment: consists o broad-spectrum antibiotics, organis m in aortic gra t removal o in ected graf via open surgery, and in ection is Staphylococcus aureus. reconstruction via extra-anatomic bypass 9. Aortoenteric stula: presents as gastrointestinal bleeding a. Diagnosis: endoscopy b. reatment: graf explant and extra-anatomic bypass along with repair o enteric stula 10. Aneurysm or pseudoaneurysm: at proximal or distal anastomosis 11. Patients with open repair: may have complications related to the laparotomy, such as adhesive small bowel obstruction or hernia ormation IV. Sp le nic a rte ry a ne urys m : Risk actors include emale gender, Quic k Cut multiple pregnancies, and portal H N. Splenic artery A. Clinical presentation: Majority o patients are asymptomatic. aneurys ms are the mos t Patients with rupture usually present with sharp pain, abdominal common vis ceral aneurys ms . distension, and hemorrhagic shock. T e aneurysm usually rst ruptures in lesser sac ollowed by ree intraperitoneal rupture (double rupture phenomenon). Quic k Cut B. Indications or repair: symptomatic or ruptured aneurysm, size The rate o s plenic greater than 2 cm, and any size in a women o childbearing age artery aneurys m rupture C. Endovascular treatment: coil embolization or stenting across is greater than 90% with the aneurysm pregnancy. D. Open surgical repair: Proximal and distal ligation o splenic artery with or without aneurysmectomy; or aneurysms located in distal splenic artery, splenectomy is per ormed. V. P o p lite a l a rte ry a ne urys m s : Mostly seen in men; 2.50% are bilateral. A. Asymptomatic clinical presentation: palpable pulsatile mass behind knee Quic k Cut B. Symptomatic: Popliteal aneurysms can cause distal One third o patients embolization, can compress nearby structures, or can acutely with popliteal aneurys ms als o have AAA. thrombose, resulting in acute lower leg ischemia. C. Indications or repair: symptomatic aneurysm o any size; asymptomatic aneurysm greater than 2.5 cm in diameter D. Mode o repair: Patients who present with acute limb ischemia are started on therapeutic anticoagulation. Emergent arteriography is performed. 1. Open repair: ligation o aneurysm and arterial bypass or excision o aneurysm and interposition graf to restore distal circulation 2. Endovascular repair: Newer treatment option when anatomy is easible; most surgeons reserve this orm o treatment or patients who are high operative risk. 3. T rombolysis: Consider in stable patient with intact sensory and motor unction but must be ollowed by staged, de nitive repair.

MESENTERIC VASCULAR DISEASE Ana to m y I. Ma in b lo o d s up p ly: celiac axis, superior mesenteric artery (SMA), IMA II. Co lla te ra l c irc ula tio n: pancreaticoduodenal between celiac and SMA; marginal artery between IMA and SMA

Quic k Cut The marginal artery o Drummond and the arc o Riolan are the collateral arcades between the SMA and the IMA.

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Ac ute Me s e nte ric Is c he m ia I. Ep id e m io lo g y: Patients tend to be elderly with signi cant comorbidities. II. Cla s s if c a tio n: based on etiology A. Cardiac source (atrial brillation): most common cause o Quic k Cut embolic occlusion o mesenteric vessels. T e emboli usually The SMA is the mos t lodge distal to the origin o proximal jejunal branches and common abdominal artery middle colic artery, which spares the proximal jejunum and a ected rom embolus due ascending colon. to its oblique origin rom the B. Acute thrombosis: In 20% o cases, pre-existing severe anterior s ur ace o aorta. atherosclerotic stenotic lesion thrombosis is seen. T e entire small and large bowel supplied by SMA is a ected, as the origin o vessel is occluded. C. Nonocclusive mesenteric ischemia: Due to di use mesenteric vasospasm in absence o arterial or venous occlusion. Most commonly seen in patients with severe cardiopulmonary insu ciency and shock. D. Mesenteric venous thrombosis: Involves thrombosis o superior mesenteric vein with or without extension into portal or splenic vein. It can be spontaneous or secondary to abdominal injury, hypercoaguable states, in ammation, or in ection. III. Clinic a l p re s e nta tio n: Peritonitis is seen late once in arction o Quic k Cut bowel occurs. Pain out o IV. Dia g no s is : High index o suspicion along with prompt treatment proportion is the clas s ic phys ical examination f nding be ore bowel in arction sets in is key to prevent mortality. in mes enteric is chemia. A. Plain abdominal x-rays: may show ileus in early cases o mesenteric ischemia or pneumatosis in advanced cases B. Duplex ultrasound o mesenteric vessels: Use ul in identi ying stenoses o celiac and SMA. It is mostly used in chronic mesenteric ischemia. C. C A: good to assess the patency o mesenteric arteries and vein and also use ul in assessing the state o the bowel and other intra-abdominal pathology D. Mesenteric angiogram: provides diagnosis and potential treatment such as angioplasty and stent, thrombolysis, or injection o vasodilator agents V. Tre a tm e nt: depends on the etiology o acute mesenteric ischemia A. Bowel in arction: All patients need exploratory laparotomy and resection o nonviable bowel. Usually, a second look laparotomy is per ormed within 24 hours to ensure viability o residual bowel. B. Embolism: Embolectomy is per ormed; postprocedure, therapeutic anticoagulation is mandatory. C. Acute arterial thrombosis: Aortomesenteric bypass is per ormed. D. Nonocclusive mesenteric ischemia: usually treated with supportive care including bowel rest, antibiotics, and uid resuscitation. Surgical exploration is indicated i peritonitis develops. E. Mesenteric venous thrombosis: systemic anticoagulation; operation i bowel necrosis occurs

Chro nic Me s e nte ric Is c he m ia I. Etio lo g y: Seen in patients with slowly progressive stenosis/occlusion o origin o mesenteric vessels. Atherosclerosis is the most common etiology. II. P a tho p hys io lo g y: In normal individuals, blood ow to intestine Quic k Cut increases 30–90 minutes af er ood ingestion. T is increased blood In chronic mesenteric ow is required or metabolism and absorption. ischemia, the postprandial hyperemic response is III. Clinic a l p re s e nta tio n: Most commonly seen in middle-aged attenuated, resulting in women with a long history o smoking. Patients are usually “mesenteric angina.” cachectic with typical symptoms o postprandial epigastric pain, ear o ood, and weight loss. IV. Dia g no s is : Modalities include the ollowing: A. Mesenteric duplex ultrasound: screening tool with greater than 80% sensitivity and speci city B. C A: diagnostic modality o choice or chronic mesenteric ischemia C. Mesenteric angiogram: Gold standard diagnostic tool. I a stenosis is amenable to endovascular intervention, it can be per ormed at same time.

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Renal Artery Stenosis

V. Tre a tm e nt: All patients with chronic mesenteric ischemia must undergo revascularization to prevent bowel in arction and to improve nutritional status. A. Endovascular revascularization: involves balloon angioplasty and stent placement across the area o stenosis B. Open revascularization: per ormed either by transaortic mesenteric endarterectomy or by aortomesenteric bypass 1. Conduit or bypass procedure: can be prosthetic graf or greater saphenous vein 2. Inf ow or bypass: Can be supraceliac aorta (antegrade bypass) or in rarenal aorta or iliacs (retrograde bypass). Usually both celiac and SMA are bypassed beyond the area o occlusion.

RENAL ARTERY STENOSIS Ge ne ra l As p e c ts I. De f nitio n: Renovascular H N is de ned as systemic H N resulting rom renal arterial compromise. II. Dia g no s is : Renal artery stenosis (RAS) is suspected as cause with abrupt onset or exacerbation o chronic H N, adults on Quic k Cut multiple antihypertensive medications with modest control o RAS can caus e blood pressure, angiotensin-converting enzyme (ACE) inhibitor– re ractory HTN and can als o lead to kidney ailure. induced azotemia, ash pulmonary edema out o proportion to lef ventricular ailure, and H N in children. III. P a tho p hys io lo g y o re no va s c ula r HTN: Stenosis at the level o the renal artery is sensed by receptors in kidney, which secretes renin. Renin increases angiotensin, which causes vasoconstriction and also stimulates the adrenal cortex to secrete aldosterone. Aldosterone increases blood volume and increase blood pressure (Fig. 7-6). IV. Etio lo g y o RAS: associated risk actors or atherosclerosis A. Atherosclerosis: involves the ostium or proximal one third o Quic k Cut renal artery; bilateral involvement, males greater than emales Atheros cleros is B. Fibromuscular dysplasia: Younger women; involves middle caus es 90% o RAS. or distal portion o renal artery. Right side greater than lef side; 30% o cases bilateral. T ese lesions respond very well to endovascular intervention, with greater than 75% cure o H N at 1 year. C. Other causes: traumatic or spontaneous dissection or disruption, vasculitis, thromboembolic disease, renal artery aneurysm, extrinsic compression, radiation injury V. Clinic a l pre s e nta tion: Asymptomatic RAS is diagnosed incidentally; symptomatic presents with sudden worsening o renal ailure, sudden worsening o previously controlled H N, or sudden-onset H N.

Dia g no s is a nd Tre a tm e nt I. Func tio na l te s ts : include the ollowing: A. Captopril scintigraphy: noninvasive test that uses technetium-99m–labeled diethylene triamine pentaacetic acid (D PA) along with administration o the ACE inhibitor, captopril; sensitivity 75% and speci city 90% S te nos is

Kidney

Re nin

Angiote ns in II

Va s ocons triction

Adrenal cortex

RR 10

Hype rte ns ion Blood volume

Aldos te rone

Fig ure 7-6: Pathophys iology o renovas cular hypertens ion. Renal artery s tenos is activates the renin-angiotens in s ys tem, which produces aldos terone. Elevated blood volume and vas ocons triction trans late into elevated blood pres s ures .

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B. Renal vein renin assay: invasive test that documents the contribution o each kidney to plasma renin II. Ana to m ic im a g ing te s ts : include the ollowing: A. Duplex ultrasound evaluation o renal arteries: Initial diagnostic modality o choice. Painless, noninvasive, no exposure to ionizing radiation or nephrotoxic contrast agent, low cost, and had sensitivity o 85% and speci city o greater than 90%. B. C A and MRA: Less invasive, expensive, need or IV contrast. C A carries the risk o radiation exposure, and MRA overestimates the degree o stenosis. C. Conventional renal angiography: Gold standard test o choice or diagnosis o RAS. Invasive procedure with need or IV contrast and potential contrast-induced nephropathy. Has an advantage that therapeutic intervention can be per ormed at same time. III. Tre a tm e nt: include the ollowing: A. Percutaneous angioplasty and stent placement: Minimally Quic k Cut invasive procedure or treatment o stenosis located at proximal Percutaneous or midportion o renal artery. T e pre erred mode o treatment angioplas ty and s tent when applicable. May require bilateral treatment or e ective placement is the pre erred cure o H N. treatment or RAS. B. Aortorenal bypass: using either autogenous (reversed saphenous vein) or prosthetic conduit (e.g., P FE) C. T romboendarterectomy o renal artery: old technique; seldom used D. Nephrectomy: in patients with unilateral disease (small and non unctioning kidney) and unctional contralateral kidney

MISCELLANEOUS Ra yna ud P he no m e no n I. Cha ra c te ris tic s : Episodic, exaggerated vasospastic response Quic k Cut to cold or emotional stimuli, typically seen in ngers. A ected Raynaud digits show a classic series o color changes, initial pallor (due to phenomenon progres s es as white-blue-red or pallor, vasospasm), ollowed by cyanosis (due to deoxygenation o the cyanos is , and hyperemia. static blood), and then by rubor (due to reactive hyperemia rom restoration o blood ow). A. Primary Raynaud phenomenon (Raynaud disease): seen in an otherwise healthy individual with no underlying disease B. Secondary Raynaud phenomenon: associated with an underlying systemic disease (mostly autoimmune disorders like scleroderma, systemic lupus erythematosus, giant cell arteritis, etc.) II. Ma na g e m e nt: Li estyle modi cation includes avoidance o cold and emotional stress, smoking cessation, and discontinuation o vasoconstricting substances such as ca eine and cocaine. A. Medical treatment: includes calcium channel blockers B. Surgical sympathectomy: limited to severe or re ractory cases

Gia nt Ce ll Arte ritis (Te m p o ra l Arte ritis ) I. Cha ra c te ris tic s : Large vessel vasculitis a ecting the aorta and the extracranial branches o the carotid artery. ypically a ects older women o northern European descent. II. Clinic a l p re s e nta tio n: Constitutional symptoms such as ever and atigue; jaw claudication is characteristic symptom and may have ocular symptoms. III. Dia g no s is : emporal artery biopsy is the standard. IV. Tre a tm e nt: medical with corticosteroids

Ta ka ya s u Dis e a s e I. Cha ra c te ris tic s : Large vessel vasculitis a ecting aorta and its major branches and pulmonary artery. A ects young emales; commonly seen among Asians. II. Clinic a l p re s e nta tio n: constitutional symptoms such as ever, myalgia, and weight loss; vessel in ammation resulting in vessel pain/tenderness and vessel brosis and aneurysmal degeneration

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Miscellaneous

III. Dia g no s is : DSA is the gold standard. IV. Me d ic a l m a na g e m e nt: consists o immunosuppression with corticosteroids as rst line o treatment V. Re va s c ula riza tio n: should be per ormed when disease activity is minimal

Thro m b o a ng iitis Ob lite ra ns /Bue rg e r Dis e a s e I. Cha ra c te ris tic s : A ects small- and medium-sized arteries and veins o extremities; characterized by normal proximal pulses but diminished distal pulses. Strong association with smoking and more commonly seen in young males. II. P re s e nta tio n: Patient presents with ischemic symptoms such as claudication or paresthesias. III. Ang io g ra p hy: Corkscrew collaterals around the area o occlusion may be seen. IV. Tre a tm e nt: Main e ective therapy is smoking cessation.

Chapter 8

Venous and Lymphatic Disease Edwin Kendrick and Rajabrata Sarkar

ACUTE DEEP VENOUS THROMBOSIS Ep id e m io lo g y I. Inc id e nc e : Cases o recurrent, atal, and non atal deep venous thrombosis (DV ) exceed 900,000 cases annually in the United States. A. Untreated proximal DV : associated with a 30%–50% risk or pulmonary embolism (PE) and a 12% mortality rate B. DV without prophylaxis: Overall incidence is 20% in general surgical patients, 25% in elective neurosurgical patients, and nearly 50%–60% in patients undergoing orthopedic surgery. II. P a tho p hys io lo g y: Virchow triad A. Hemodynamic changes: stasis or turbulence B. Hypercoagulability C. Endothelial abnormality

Clinic a l Find ing s I. Sig ns a nd s ym p to m s : lower extremity pain, pain on passive dorsif exion (Homans sign), edema, erythema, local warmth, prominent super cial veins, and peripheral cyanosis II. Lo c a tio ns o thro m b o s is : include ilio emoral, cal , and upper limb deep veins as well as ovarian, renal, mesenteric, hepatic, and retinal veins; vena cava; and cerebral venous thrombosis

Dia g no s tic Te s ts

Quic k Cut 30% o DVT patients experience a recurrence in a 10-year time s pan.

Quic k Cut Almos t 1 million DVT are diagnos ed in the United States annually.

Quic k Cut The Virchow triad is s tas is , coagulopathy, and endothelial injury.

Quic k Cut Up to 50% o DVT patients are as ymptomatic, and DVT may be unidentif able with imaging.

I. Dup le x ultra s o no g ra p hy (US): replaced contrast venography (CV) as the diagnostic test o choice A. Function: It may distinguish among vascular and nonvascular pathologies (i.e., adenopathy, Baker cyst, and hematoma). B. Benef ts: lack o radiation, portability, noninvasiveness, and relative cost-e ectiveness II. D-d im e rs : Degradation products o cross-linked brin. Its high sensitivity makes its major clinical usage exclusion o a DV diagnosis Quic k Cut on the basis o a negative result. An elevated D-dimer is nonspeci c. D-dimer may be used as a screening test or DVT. III. Ma g ne tic re s o na nc e ve no g ra p hy (MRV): Has the greatest sensitivity and speci city in imaging iliac, pelvic, and central vein thrombosis compared to CV or US. Disadvantages include

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Fig ure 8-1: DVT, contras t venogram. Intraluminal f lling de ect outlined by contras t (arrow) diagnos tic or acute DVT on a lower extremity venogram. (From Ges chwind J F, Dake MD. Abrams’ Angiography, 3rd ed. Philadelphia: Lippincott Williams & Wilkins ; 2013.)

relative cost, patient cooperation (claustrophobia), study time required, and gadolinium-associated nephrogenic systemic brosis (seen in renal ailure patients). IV. CV: Figure 8-1 A. Uses: used historically as a “golden backup” in cases o initial diagnostic uncertainty B. Disadvantages: include radiation exposure, contrast nephrotoxicity, allergic reactions, radiation exposure, phlebitis, and increased cost

Initia l Tre a tm e nt I. Ob je c tive : prevent PE and propagation o the DV II. Antic o a g ula tio n: Acute DV s should be treated with Quic k Cut low-molecular-weight heparin (LMWH), ondaparinux, or Acute DVT s hould be un ractionated heparin (UFH) and war arin as soon as the diagnosis treated with anticoagulation. is con rmed by objective imaging techniques or until the diagnosis can be con rmed i clinical suspicion is very high. A. A er a 5- to 10-day overlap o anticoagulation: War arin remains the sole therapy when the international normalized ratio (INR) is within the target (2.0–3.0) or at least 24 hours. B. Anticoagulation 3 months with compression therapy: recommended i it is the rst DV , a proximal DV , a surgery-provoked DV , or due to a nonsurgical transient risk actor C. Longer therapy: recommended or an unprovoked DV , recurrent DV , prior PE, or active cancer (use LMWH) D. Disadvantage: Bleeding risk is associated with usage o all anticoagulants. Approximate bleeding risks with LMWH include postoperative bleeding (6%), major hemorrhage (3%), and wound hematoma (4%). III. In e rio r ve na c a va (IVC) f lte r: Figure 8-2 A. Uses: In patients with DV who cannot be anticoagulated (e.g., recent neurologic surgery, ongoing bleeding, etc.), place a Quic k Cut lter immediately to prevent PE. IVC f lters are us ed B. Retrieval: Consideration should be given to placement o a when anticoagulation is retrievable lter, which can be removed once the risk o PE is contraindicated. subsequently decreased.

Ad d itio na l The ra p y I. Go a l: directed at removal o the thrombus to preserve venous valve unction and prevent long-term complications such as post-thrombotic syndrome (P S). T is therapy is reserved or good risk, active younger patients without contraindications to thrombolytic therapy (e.g., recent surgery or bleeding).

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Fig ure 8-2: Retrievable IVC f lter. Note the retrieval at the upper end o the f lter. The f lter has our “petals ” or centering in the IVC.

II. Thro m b o lys is A. Catheter-directed thrombolysis (CD ) with tissue plasminogen activator agents: indicated or ilio emoral DV s (Fig. 8-3) B. Pharmacomechanical thrombolysis (CD with mechanical thrombectomy): e ective option with an anticipated 75%–90% success rate o rapid recanalization o the venous system. Disadvantages include bleeding (5%–11%) and the need or anticoagulation to prevent immediate rethrombosis. III. Op e ra tive ve no us thro m b e c to m y: In rainguinal balloon catheter thrombectomy is used in patients with worsening venous edema or venous gangrene in whom thrombolysis is not possible. Disadvantages include invasiveness o the procedure with general anesthesia and the need or anticoagulation to prevent immediate rethrombosis.

P re ve ntio n I. Le g e le va tio n: has a dual physiologic e ect; it reduces swelling (improving venous return) and venous pressure (gravitational e ect) II. Me c ha nic a l A. Graduated compression stockings: reduce the cross-sectional Quic k Cut area o the veins and increase the velocity o venous blood f ow IPC devices increas e both venous ow (50% reduction in P S development) and f brinolys is . B. Intermittent pneumatic compression (IPC): improves venous hemodynamics and stimulates brinolytic activity C. Foot compression devices: indicated in patients with a high risk or venous thromboembolism (V E) in whom the use o anticoagulants and IPCs are contraindicated

P roge s te rone , ve in ove rflow

Ve in dis te ns ion

Re flux (va lve incompe te nce )

Acute DVT Acute S VT

Va lvula r da ma ge

Chronic ve in obs truction

Ve nous hype rte ns ion

Fig ure 8-3: Pos t-thrombotic s yndrome. Etiopathogeny o chronic venous ins u f ciency and its relation to pos tthrombotic s yndrome. (From Ges chwind J F, Dake MD. Abrams’ Angiography, 3rd ed. Philadelphia: Lippincott Williams & Wilkins ; 2013.)

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Acute Pulmonary Embolism

III. P ha rm a c o lo g ic : Anticoagulation with LMWH, UFH, or ondaparinux is the standard o care or V E prevention in surgical and medical patients. Rivaroxaban is now licensed in the United States or V E prevention a er hip or knee arthroplasty.

Co m p lic a tio ns I. Ac ute c o m p lic a tio ns A. Phlegmasia alba dolens: nonischemic limb with massive pitting edema and blanching B. Phlegmasia cerulea dolens: reversible phase o ischemic venous occlusion (pain ul blue leg) with predisposition or limb loss C. Venous gangrene: irreversible phase o ischemic venous occlusion II. Chro nic c o m p lic a tio n: Post T rombotic Syndrome (P S) A. Clinical mani estations o venous hypertension and valvular dys unction: include limb swelling, limb atigue or pain, venous claudication, pigmentation (dermatoliposclerosis), eczema, erythema, or rank ulceration o the skin B. Incidence: 40% o DV patients will have some degree o P S, Quic k Cut and 4% will develop severe mani estations with ulceration. Severe PTS may be C. Consequences: decreased physical activity abilities and a lower treated with iliac vein s tenting. quality o li e D. T erapy: includes elevation o extremity at rest/night, pain management, compression therapy, wound care, and angioplasty/stenting o iliac vein stenosis (present in 50%–75% o P S patients)

Antic o a g ula tio n The ra p y Co m p lic a tio ns I. He p a rin-ind uc e d thro m b o c yto p e nia : antibody response against neoantigens expressed on platelet actor 4 (PF4) upon binding to heparin A. Clinical diagnosis: thrombocytopenia, thrombosis, or both during or immediately a er heparin use B. Laboratory diagnosis: heparin-induced platelet aggregation assays, heparin antibody test, and serotonin release assay C. reatment: immediate cessation o all orms o heparin and rapid initiation o a direct thrombin inhibitor (e.g., argatroban, lepirudin, or bivalirudin) or anticoagulation II. Ble e d ing ris k: See the sections “Anticoagulation” and “T rombolysis.” III. Os te o p o ro s is : LMWH and UFH

Quic k Cut Heparin is s o commonly us ed that it may be overlooked, s uch as in intravenous us hes .

Quic k Cut Caution—war arin alone is not protective or HIT and can res ult in s evere thrombotic complications .

ACUTE P ULMONARY EMBOLISM Ep id e m io lo g y a nd Etio lo g y I. Inc id e nc e : Occurs in 650,000 American patients annually and Quic k Cut accounts or up to 15% o all in-hospital deaths. Approximately The initial 50%–80% o symptomatic DV patients have evidence o an pres entation o PE is s udden asymptomatic PE. death in 25% o cas es . II. Etio lo g y A. T rombotic embolism: Approximately 90% arise rom Quic k Cut the lower extremity veins; major risk actors include Mos t pulmonary previous V E, surgery, trauma, malignancy, chemotherapy, emboli aris e rom lower chronic heart or respiratory ailure, paralytic stroke, extremity veins . hypercoagulability, pregnancy, and hormone/contraceptive therapy. B. Nonthrombotic PE: With the exception o severe air and at embolism, the hemodynamic consequences are usually mild. reatment is mostly supportive but may di er according to the type o embolic material and clinical severity.

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Clinic a l Find ing s

Quic k Cut I. As ym p to m a tic P E: reported in high requency in DV patients PE may include II. Sym p to m a tic P E: Severity depends on the amount o nonocclusive thrombi, mas s ive occluded pulmonary circulation and the patient’s underlying occlusions, or in arction. cardiopulmonary reserve. III. P o o r p ro g no s tic ind ic a to rs : marked dyspnea, anxiety, and low oxygen saturation; elevated troponin (indicating right ventricular [RV] microin arction, RV dys unction on echocardiography, or RV enlargement on chest computed tomography [C ] scan) IV. He m o d yna m ic c o m p ro m is e a nd d e a th: results rom an increase in pulmonary artery pressure with acute RV ailure; decreased le ventricular stroke volume, cardiac output, and organ per usion; and hypotension

Dia g no s tic Te s ts

Quic k Cut As with DVT, a negative D-dimer virtually excludes a diagnos is o PE.

I. D-d im e r: Negative D-dimer sa ely excludes PE in patients with a low or moderate clinical probability (99% negative predictive); an elevated D-dimer is nonspeci c. II. CT: Multidetector computed tomography (MDC ) or computed tomography angiography (C A) showing a thrombus up to the segmental level can be taken as adequate evidence o PE in most instances (Fig. 8-4). In patients with a low or moderate clinical probability, a negative MDC or C A should be combined with a compression ultrasonography. III. Com pre s s ion ultra s onogra phy (CUS): Lower extremity CUS is used to reduce the overall alse-negative rate o C in suspected PE patients. CUS yields a positive proximal DV result in 20% o patients with PE. IV. Ve ntila tio n-p e r us io n s c intig ra p hy (V/Q s c a n): Normal per usion scan is sa e or excluding PE. A high-probability V/Q scan may establish the diagnosis o PE in patients with a high degree o suspicion. V. P ulm o na ry a ng io g ra p hy: reliable but invasive clinically use ul test when MDC /C A and CUS results are both negative in patients with a high suspicion or PE VI. Ec ho c a rd io g ra p hy: help ul in emergency situations such as shock or hypotension; it serves or urther prognostic strati cation but is not diagnostic or PE

Initia l Tre a tm e nt I. Antic o a g ula tio n: initiated without delay in patients with con rmed acute PE and those with a high or intermediate clinical probability o an acute PE while the diagnostic workup continues A. Initial treatment with LMWH, UFH, or ondaparinux and war arin: should continue or at least 5 days and until the INR is greater than or equal to 2.0 or at least 24 hours

As ce nding Aorta S upe rior Ve na Ca va

Quic k Cut All PE patients s hould undergo rapid ris k s tratif cation with hemodynamic and res piratory s upport as needed.

Ma in P ulmona ry Arte ry S upe rior Le ft P ulmona ry Ve in

S e gme nta l P ulmona ry Emboli S e gme nta l P ulmona ry Emboli Right P ulmona ry Arte ry

Fig ure 8-4: Pulmonary embolis m. CT axial images o pulmonary embolus .

De s ce nding Thora cic Aorta

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Chronic Venous Disorders: Varicose Veins and Chronic Venous Insu ciency

B. War arin therapy: should continue or at least 3 months C. Asymptomatic PE: Identical initial and long-term anticoagulation is recommended. II. P ulm o na ry CDT o r s ys te m ic thro m b o lys is : rst-line treatment in hemodynamic compromised patients unless there are major contraindications A. T rombolysis: should not be delayed because irreversible cardiogenic shock may ensue B. Risks: invasiveness, major bleeding (13%), and intracranial/ atal hemorrhage (1.8%) III. P e rc uta ne o us c a the te r e m b o le c to m y: mechanical embolectomy or ragmentation o proximal pulmonary arterial clots; recommended in hemodynamic compromised patients with contraindications or thrombolysis or when thrombolysis ailed IV. Surg ic a l p ulm o na ry e m b o le c to m y: recommended in hemodynamic compromised patients with contraindications or thrombolysis or when thrombolysis ailed

P re ve ntio n I. IVC f lte rs : should not be placed routinely in patients receiving anticoagulant therapy Quic k Cut A. Anticoagulant therapy contraindicated: Filters may be placed An IVC f lter is not a per ect s ubs titute or in these patients with acute PE. anticoagulation. B. I the risk o bleeding resolves: Patients with lters should receive a conventional course o anticoagulant therapy. II Ris ks A. Early complications: insertion site thrombosis (10%), bleeding, and vessel per oration B. Late complications: recurrent DV (20%), P S (40%), and vena cava occlusion in 33% o patients in 10 years, regardless o the use and duration o anticoagulation

Chro nic Co m p lic a tio n I. Chro nic thro m b o e m b o lic p ulm o na ry hyp e rte ns io n (CTEP H): Pulmonary vascular remodeling may cause severe pulmonary hypertension out o proportion to pulmonary vascular thrombosis (a severe and rare consequence o PE). II. Me d ic a l m a na g e m e nt: associated with poor outcomes III. P ulm o na ry thro m b o e nd a rte re c to m y: provides excellent results and should be considered as rstline treatment whenever possible IV Ma na g e m e nt: Patients should have li elong anticoagulant treatment targeted to an INR o 2.0–3.0.

CHRONIC VENOUS DISORDERS: VARICOSE VEINS AND CHRONIC VENOUS INSUFFICIENCY Ep id e m io lo g y a nd P a tho p hys io lo g y I. Va ric o s e ve ins : Prevalence is 5%–30% in the adult population; caused by hereditary weakness o the venous valves in the super cial veins o the legs. Most patients can identi y a amily member with the condition. II. Chro nic ve no us ins u f c ie nc y (CVI) Present in 5 million people in the United States. Risk actors include varicose veins, amily history o varicose veins, and prior DV . III. P a tho p hys io lo g y: With venous valve ailure, the super cial veins become distended, which causes the next valve in the vein to become incompetent as the valve leaf ets are pulled apart (Fig. 8-5). A. Volume overload: causes distention o the deep system, with resulting incompetence o the deep venous valves by the same Quic k Cut distension process Venous B. issue swelling: irritates adjacent nerves, causing pain, commonly overdis tens ion leads to described as a throbbing ache relieved by elevation o the limb valvular incompetence.

Clinic a l Find ing s I. Va ric o s e ve ins : Most common complaints are a cosmetically displeasing appearance, ankle swelling, cal vein and localized cutaneous pigmentation, eczema, and limb heaviness or ache that occurs a er prolonged standing.

Chapter 8

Venous and Lymphatic Disease

141

Blood flow towa rd he a rt

Va lve preve nts ba ckflow

Blood pools

A.

Normal vein

B.

Varicose vein

Fig ure 8-5: Varicos e veins . Many older people, particularly women, have varicos e veins . A: In a healthy vein, the valves help blood to ow back toward the heart and prevent it rom pooling. B: In varicos e veins , the valves no longer unction properly, allowing the blood to pool. (From Carter PJ . Lippincott Textbook for Nursing Assistants, 3rd ed. Philadelphia: Lippincott Williams & Wilkins ; 2011.)

II

P hle b itis : Stasis in the varicose veins predisposes to phlebitis, which causes pain, swelling, and discom ort; it does not embolize to cause PE, but ascending phlebitis o the greater or short saphenous vein can propagate into the deep venous system and cause DV . III. CVI: Patients may be incapacitated by venous claudication or have severe skin pigmentation changes and ulceration.

Dia g no s is I. P hys ic a l e xa m ina tio n: Examining the great saphenous vein (GSV) and small saphenous vein (SSV) in the standing and rendelenburg positions accurately identi es the presence o venous disease in the vast majority o patients. II. Dup le x US: used or detection o venous ref ux disease in chronic venous disorder patients; widely adopted as a standard o care because o its precision and reproducibility III. Am b ula to ry ve no us p re s s ure (AVP ): Venous pressure in a dorsal oot vein is measured a er the execution o 10 tiptoe Quic k Cut maneuvers in a standing position. AVP is the gold s tandard or meas urement o IV. P le thys m o g ra p hy: noninvasive method o estimating changes in venous hemodynamics . volume in an extremity when assessing or CVI

Tre a tm e nt a nd P re ve ntio n I. CEAP (c linic a l, e tio lo g ic , a na to m ic , p a tho p hys io lo g ic ) c la s s if c a tio n: standardized system or evaluating venous insu ciency II. P rim a ry b e ne f t: Venous interventions can con er long-term improvement in symptoms and ulcer recurrence. III. The ra p e utic o p tio ns : based on clinical assessment and classi cation A. No treatment B. raditional therapy: conservative management with compression stockings, skin care, and li estyle changes C. Surgical therapy: Endovenous ablation (i.e., laser or thermal); sclerotherapy; a combination o venous ligation, axial stripping, and stab phlebectomy. Venous angioplasty and stenting is per ormed in selected patients with advanced CVI who have recurrent ulceration or swelling with severe and disabling symptoms.

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Chapter 8

Lymphedema

SUP ERFICIAL VENOUS THROMBOP HLEBITIS Ep id e m io lo g y a nd P a tho p hys io lo g y I. Etio lo g y: most commonly occurs in the saphenous veins and their tributaries, ollowed by the upper extremity cephalic and basilic veins. T e GSV is a ected in 70% cases, ollowed by the SSV in 20% and bilateral lower extremity super cial venous thrombophlebitis (SV ) in 10%. II. P a tho p hys io lo g y: Related to Virchow triad (endothelial injury, venous stasis, and hypercoagulable states). T e most common predisposing risk actor or the development o SV is varicose veins as discussed earlier.

Clinic a l Typ e s I. SVT with va ric o s e ve ins II. SVT o s up e rf c ia l e xtre m ity ve ins : Upper extremity SV are treated with NSAIDs. Lower extremity SV raise the possibility o DV , and demand urther investigation. III. Tra um a tic thro m b o p hle b itis : catheter or medication induced IV. Se p tic a nd s up p ura tive thro m b o p hle b itis : in ection associated V. Mig ra to ry thro m b o p hle b itis : o en carcinoma or vasculitis associated VI. Mo nd o r d is e a s e : SV o the breast, chest, or dorsal penile vein

Dia g no s is , Tre a tm e nt, a nd P re ve ntio n I. Dia g no s is : based on the presence o erythema and tenderness in the distribution o the super cial veins with a palpable cord (thrombosis) II. The ra p y: aimed at preventing potential serious complications Quic k Cut such as propagation to DV /PE, preventing recurrence o SV , and Treatment decreasing pain and acute inf ammation o s uperf cial venous A. raditional treatment: ambulation, warm soaks, and thrombophlebitis (SVT) is nonsteroidal anti-inf ammatory drugs (NSAIDs) s upportive with NSAIDs . B. Serial duplex scans: used in patients with phlebitis o the GSV or SSV where the possibility o proximal propagation to DV is possible C. Anticoagulation: indicated in extensive SV or SV in the GSV or SSV that is ascending toward the deep system D. Surgical excision: plays a role in suppurative thrombophlebitis where in ection is suspected or con rmed

LYMP HEDEMA Ge ne ra l Cha ra c te ris tic s I. Clinic a l p re s e nta tio n: characterized by the interstitial accumulation o protein-enriched f uid as a consequence o relative impairment o lymphatic drainage II Ep id e m io lo g y: Lymphatic outf ow dys unction may result rom either primary or acquired (secondary) anomalies. A. Primary lymphedema: Females are a ected 2- to 10- old more commonly than males. Peaks are classi ed based on genetics ( amilial vs. sporadic) and time o onset (congenital, praecox, tarda). 1. Congenital: Onset is be ore age 1 year and may be amilial (Milroy disease) or non amilial. 2. Lymphedema praecox: Onset is rom age 1 to 35 years and Quic k Cut Lymphedema may be amilial (Meige disease) or non amilial. s econdary to intervention or 3. Lymphedema tarda: Onset is a er age 35 years. in ection is ar more common B. Secondary lymphedema: most common orm o lymphatic disease than primary lymphatic 1. Developed countries: Iatrogenic causes predominate as dis eas e. consequence o lymphatic trauma or dissection, cancer, or radiotherapy or cancer (e.g., breast cancer). Other causes include large burns, pregnancy, and bacterial and ungal in ections. 2. Developing countries: Filariasis (parasitic in estation with the Wuchereria bancrof i) is the most requent cause o secondary lymphedema (elephantiasis).

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143

III. P a tho p hys io lo g y: Lymphatic circulation provides the normal conduit or return o interstitial f uid and protein to the central circulation. Lymphedema will ensue i the production o lymph exceeds the maximal transport capacity o the lymphatic conduits. Accumulation o protein and cellular metabolites in the extracellular space generates water accumulation, collagen deposition, and elevated interstitial pressure. IV. Clinic a l f nd ing s : depend largely on the duration and severity o the disease A. Edema: extends to the distal aspects o the eet, resulting in “square toes” (Stemmer sign), which is pathognomonic or the loss o cutaneous elasticity with an inability to tent the skin o the interdigital web space B. Skin changes 1. Acute: Skin is usually a pinkish red color with a mildly elevated temperature. 2. Chronic: results in thickened skin with areas o hyperkeratosis, licheni cation, and development o peau d’orange C. Pain: Aching or heaviness o the limb is the most requent complaint; signi cant pain is rare.

Dia g no s is I. Clinic a l p re s e nta tio n, his to ry, a nd p hys ic a l f nd ing s : O en establish the diagnosis. Diagnosis is di cult in the early stages when edema is mild or intermittent. II. P hys ic a l e xa m ina tio n: inspection or cutaneous and subcutaneous brosis, peau d’orange, and Stemmer sign III. Lym p ho s c intig ra p hy: reliable and reproducible method to con rm the diagnosis. A radiolabeled macromolecular tracer is injected within one o the interdigital spaces o the a ected limb.

Tre a tm e nt, P re ve ntio n, a nd Co m p lic a tio ns I. Tre a tm e nt: Nonsurgical management options should be considered initially. A. Mechanical reduction: elevation, therapeutic exercise, manual massage, and compression therapy (i.e., wraps, pumps, or garments) B. Surgical therapy: should be considered only a er a trial o conservative therapy II. P re ve ntive m e a s ure s : skin hygiene, clothing precautions, trauma avoidance, and in ection control III. Co m p lic a tio ns : in ection, malnutrition and immunode ciency (loss o protein, triglycerides, lymphocytes, etc.), and malignancy (i.e., development o lymphangiosarcoma a er radiation therapy in breast cancer patients with resultant long-standing arm edema)

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Study Questions or Part III

Study Questions or Part III Directions: Each o the numbered items in this section is ollowed by several possible answers. Select the ONE lettered answer that is BEST in each case. 1. A 65-year-old woman with a long history o atrial brillation presents to the emergency

department with a history o sudden onset o severe, constant abdominal pain. A er the onset o pain, she vomited once and had a large bowel movement. No f atus has been passed since that time. Physical examination reveals a mildly distended abdomen, which is di usely tender, although peritoneal signs are absent. en years ago, she underwent an abdominal hysterectomy. What is the most likely diagnosis in this patient? A. B. C. D. E.

Acute cholecystitis Per orated duodenal ulcer Acute diverticulitis Acute embolic mesenteric ischemia Small bowel obstruction secondary to adhesions

2. A 60-year-old woman develops weakness in her right arm and leg, and she has some di culty

speaking. T is condition resolves a er 5 minutes, and she has no residual symptoms. Her physician does not hear a carotid bruit, and her electrocardiogram is normal. A carotid duplex ultrasound shows a 75% stenosis o the le carotid artery and an 80% stenosis o the right carotid artery; both are con rmed by a carotid arteriogram. What should be the next step in the management o this patient? A. B. C. D. E.

Right carotid endarterectomy Le carotid endarterectomy Super cial temporal artery to middle cerebral artery bypass Percutaneous transluminal angioplasty o the le carotid artery Bilateral carotid endarterectomy

Que s tio ns 3–4 A 70-year-old man who is a new patient presents with a history o insulin-dependent diabetes mellitus; renal insu ciency (serum creatinine, 2.5); chronic obstructive pulmonary disease; and two myocardial in arctions, the most recent being 1 year ago. His ejection raction is 35%, and he has a right below-the-knee amputation, which he says was secondary to “peripheral vascular disease.” Now, the patient has a large pulsatile nontender abdominal mass. 3. All o the ollowing studies would be appropriate except:

A. B. C. D. E.

C scan o the abdomen Pulmonary unction tests Arteriogram Colonoscopy Persantine thallium scan

His workup demonstrates a 6-cm in rarenal abdominal aortic aneurysm with a 4-cm le common iliac artery aneurysm and normal renal arteries. He has normal external iliac arteries bilaterally, with relatively normal emoral vessels. Pulmonary unction tests indicate a orced expiratory volume in 1 second (FEV1) to be 75% o the predicted value. T e Persantine thallium scan shows an old scar but no reper usion de ect.

Study Questions or Part III

4. What is the next step in this patient’s management?

A. Letting the patient live with the aneurysm because he is too high a surgical risk or elective surgery B. Checking the size o the aneurysm with ultrasound every year until it starts to enlarge C. Not per orming surgery until he develops back pain because he is currently asymptomatic D. Per orming an aortobiiliac bypass E. Repairing the abdominal aortic aneurysm with a tube gra 5. A 67-year-old woman notices a swollen right leg ollowing a 6-hour plane f ight. Which o the

ollowing would be a reasonable next step or the treating physician? A. B. C. D. E.

Prescribe compression stockings and leg elevation. Start 6 months o war arin anticoagulation. Prescribe one baby aspirin per day. Order a venous duplex evaluation. Order a pelvic C scan to look or lymphadenopathy.

Que s tio ns 6–8 A 59-year-old patient undergoes a craniotomy or a benign meningioma. On the 10th postoperative day, he is noted to have a swollen le cal and thigh. 6. What is the least accurate method to diagnose the cause o the swollen leg?

A. B. C. D. E.

Physical examination Le leg venogram 125 I Fibrinogen scan Impedance plethysmography Duplex US

7. I DV is documented, initial treatment should include which o the ollowing?

A. B. C. D. E.

Subcutaneous un ractionated heparin therapy Intravenous heparin therapy T rombolytic therapy with urokinase Aspirin therapy War arin treatment

8. A er recovery rom the acute illness, the patient returns in 6 months, complaining o persistent

leg swelling. Which o the ollowing would be the optimal long-term management as initial treatment? A. B. C. D. E.

Chronic diuretic therapy Venous thrombectomy Venous bypass using an autologous vein Venous bypass using a prosthetic gra Support hose

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Study Questions or Part III

9. A 24-year-old woman presents to your o ce. She is a heavy smoker, approximately 2½ packs per

day. She complains o pain in the le thigh with exercise. On exam, she has a normal le leg, with diminished pulses on the le compared to the right. An ankle-brachial index (ABI) is 0.8 on the le , 1.0 on the right. T e best initial management is: A. B. C. D. E.

Aortobi emoral bypass gra ing Aortoiliac bypass with reversed saphenous vein issue plasminogen activator (tPA) T erapeutic heparin Smoking cessation

10. T e same patient in the a orementioned scenario returns to your o ce a er 2 years with

worsening symptoms. In act, the patient reports constant pain, even without exercise. Repeat ABI on the le is 0.4, 1.0 on the right. T e most appropriate intervention is: A. B. C. D. E.

Aspirin, 325 mg/day tPA Angiography with stent placement Aortoiliac bypass with polytetraf uoroethylene LMWH

11. A 68-year-old man without past medical history is ound to have an incidental carotid bruit on

routine physical examination. Physical examination is otherwise benign, and the patient denies any symptoms. An ultrasound o the neck demonstrates a unilateral 80% stenosis at the junction o the common carotid and internal carotid arteries. What is the best management or this patient? A. B. C. D. E.

Carotid endarterectomy with patch angioplasty Carotid angiography with stent placement Aspirin, 325 mg Carotid endarterectomy with primary repair Cilostazol

12. A 75-year-old woman has progressive weight loss over the past year since the death o her spouse.

She has also some baseline abdominal pain, which is worsened with large meals. Her physical exam is benign, but the patient complains o abdominal pain during the exam. T e best single test or this patient is: A. B. C. D. E.

Upper gastrointestinal (GI) series C angiogram Mesenteric angiography Right upper quadrant ultrasound Magnetic resonance imaging (MRI) o the abdomen

13. A 41-year-old woman undergoes an unevent ul right hemicolectomy or stage II cecal cancer.

On the third postoperative day, she develops new, unilateral leg swelling; local warmth; and pain with passive dorsif exion. What is the most appropriate initial management? A. B. C. D. E.

War arin Aspirin (325 mg) LMWH Retrievable IVC lter Un ractionated subcutaneous heparin

Study Questions or Part III

14. A 60-year-old man has an acute DV at the time o repair o a emur racture. A er treatment, he

has complete resolution o symptoms. T ree years later, he returns with swelling o the same leg, local pain, and some skin ulceration. A D-dimer level is normal. T e most likely diagnosis is: A. B. C. D. E.

Acute DV Heparin-induced thrombocytopenia Pulmonary embolus Post-thrombotic syndrome Phlegmasia alba dolens

15. A 28-year-old woman undergoes le modi ed radical mastectomy or locally advanced breast

cancer. wo weeks later, she develops pain and swelling o her le arm. On exam, her arm appears di usely swollen. T e skin is pink and radial pulses are strong and equal bilaterally. T e best initial test is: A. B. C. D. E.

US Lymphoscintigraphy Magnetic resonance angiography (MRA) Contrast angiography C o the chest

147

148

Answers and Explanations

Answers and Explanations 1. The a ns we r is D (Chapter 7, Mesenteric Vascular Disease, Acute Mesenteric Ischemia, III).

T e triad o a cardiac arrhythmia, the sudden onset o severe abdominal pain, and gut emptying is a classic indicator o embolic mesenteric ischemia. T is combination constitutes a surgical emergency, and the patient should be treated promptly with vigorous rehydration ollowed by arteriography to con rm the diagnosis. Rapid embolectomy o the superior mesenteric artery could save this patient, provided that no delay occurs in her de nitive surgical treatment. Cholecystitis usually presents with right upper quadrant pain and diverticulitis with le lower quadrant pain. A per orated ulcer will have associated di use abdominal tenderness but also will have signs o peritoneal irritation (guarding and rebound). A small bowel obstruction usually presents with colic or intermittent pain. 2. The a ns we r is B (Chapter 7, Extracranial Cerebrovascular Disease, Management II).

T e symptomatic artery is usually repaired rst because it carries the highest risk o stroke. Percutaneous transluminal angioplasty o the carotid artery is presently under investigation as an alternative to carotid endarterectomy, but it is not considered to be the standard o care at this point. Percutaneous transluminal angioplasty is sometimes used or smooth, regular lesions associated with bromuscular dysplasia. T e super cial temporal artery to middle cerebral artery bypass has not been shown to be e ective or this patient’s disease. Bilateral carotid endarterectomy is usually not per ormed because o the risk o recurrent laryngeal nerve trauma, which, i bilateral, could result in a tracheostomy. 3–4. The a ns we rs a re 3-D (Chapter 7, Arterial Aneurysms, General Aspects, III H), a nd 4-D (Chapter 7, Arterial Aneurysms, General Aspects, III I). Colonoscopy is not indicated

i the patient’s stool is heme negative. C can help to evaluate the proximal extent o the aneurysm. Pulmonary unction tests can help to assess risk and to help plan perioperative care. An arteriogram acts as a road map, showing the renal arteries in relation to the aneurysm and the extent o occlusive disease in the iliac and emoral arteries. A Persantine thallium scan helps to de ne perioperative cardiac risk. Elective repair o an abdominal aortic aneurysm (AAA) can be per ormed with a mortality rate lower than 5%. T e leading cause o death in these patients with AAA is rupture. A 6-cm AAA has a 35% rupture rate, and surgery should be recommended unless the patient has a li e expectancy o less than 1 year. Rate o enlargement is not a sa e predictor o risk o rupture. Patients with symptomatic or rupturing AAA have a 75% mortality rate when operated on as an emergency. An aortobiiliac gra is the appropriate procedure in this patient, rather than a tube gra , to repair the associated iliac aneurysm. With no iliac occlusive disease, an aortoiliac bypass avoids groin incisions. 5. The a ns we r is D (Chapter 8, Acute Deep Venous T rombosis, Diagnostic ests, I). A swollen leg

ollowing a period o immobilization is a typical history leading to a DV . Although lymphedema or other causes can also lead to leg swelling, a pelvic C scan would not be the next step or this patient. Physical examination is reliable only 50% o the time or DV , so an accurate diagnostic study such as a venous duplex ultrasound is needed be ore starting long-term anticoagulation. I no other reason or the swelling can be ound, a pelvic C scan may be reasonable. Leg elevation is help ul to reduce swelling, but compression stockings are not recommended in the acute phase or ear o dislodging the clot. Aspirin is o no proven bene t in treating DV . 6–8. The a ns we rs a re 6-A (Chapter 8, Acute Deep Venous T rombosis, Clinical Findings, I, Diagnostic ests, I–IV), 7-B (Chapter 8, Acute Deep Venous T rombosis, Initial reatment, II), a nd 8-E (Chapter 8, Acute Deep Venous T rombosis, Complications, II D). Physical examination

is the least likely method to diagnose the cause o acute leg swelling. Currently, such a patient would undergo duplex US or venography to con rm the presumed diagnosis o DV . Impedance plethysmography can detect increased resistance to venous f ow but does not identi y the cause. 125I Fibrinogen scanning can identi y ongoing thrombosis, but the scan takes 24 hours to complete and is there ore not use ul in acute situations.

Answers and Explanations

Intravenous heparin therapy is the most appropriate initial treatment. Subcutaneous un ractionated heparin therapy in its current orm is not acceptable treatment or DV . T rombolytic therapy would be contraindicated in a patient with a recent craniotomy because it would increase the risk o hemorrhage. Aspirin therapy has no role in the treatment o DV . War arin can be used once the patient is discharged but not as the initial treatment. ransition rom intravenous heparin to war arin therapy should occur on the ourth or h day o heparin administration. Support hose is the mainstay o treatment or patients with chronic postphlebitic syndrome. T rombectomies have been unsuccess ul, and the e cacy o venous bypass has yet to be established. T ere is interest in transplanting venous valves and segments o a vein to replace short-segment thromboses, but this area is still experimental. Prosthetic gra s have no role in venous reconstruction. Chronic diuretic therapy may be use ul or short-term therapy but is certainly not optimal long-term management or this problem. 9. The a ns we r is E (Chapter 7, Lower Extremity Arterial Occlusive Disease, Classi cation, II A;

Aortoiliac Occlusive Disease, reatment, I–II). T e best initial treatment or claudication is control o risk actors. For this patient, smoking cessation is the rst line o treatment but also promotes success should any other intervention need to be undertaken. T e patient does not require anticoagulation or thrombolysis but may bene t rom antiplatelet therapy and a graduated exercise program. Bypass is premature. 10. The a ns we r is C (Chapter 7, Aortoiliac Occlusive Disease, reatment, III A). T e patient

appears to have a hemodynamically signi cant unilateral lesion. In this instance, iliac stenting produces e ective relie and durable results. Bypass is an option, but the overall complication rate is higher or open surgery than or the endovascular approach. Aspirin is use ul as an adjunct but not as primary therapy or a patient with rest pain. tPA and heparin does not have a role unless there is an acute thrombosis. 11. The a ns we r is A (Chapter 7, Extracranial Cerebrovascular Disease, Management, II). T e patient

meets criteria or endarterectomy, as it has been shown to have a reduced risk o stroke versus maximum medical therapy. Patch angioplasty is pre erred over primary repair to minimize risk o recurrence. Angiography and stenting has not yet produced equivalent results. Either stenting or medical therapy such as aspirin may be bene cial in the patient who is not a candidate or surgery. 12. The a ns we r is B (Chapter 7, Mesenteric Vascular Disease, Chronic Mesenteric Ischemia, IV).

T e patient has high suspicion or chronic mesenteric ischemia. Although mesenteric duplex is a reasonable screening test, C angiogram is the de nitive test o choice. An upper GI series is unlikely to provide speci c in ormation in this case, and a right upper quadrant ultrasound is too ocused to suggest hypoper usion o the gut. MRI may yield static in ormation on the character o the bowel but not necessarily the vessels. 13. The a ns we r is C (Chapter 8, Acute Deep Venous T rombosis, Initial reatment). T e patient

presents with signs and symptoms o an acute DV , or which the treatment is anticoagulation. War arin is use ul in the long-term but is never started rst due to the potential complication o skin necrosis. Aspirin and other NSAIDs may be used or super cial venous thrombosis but is insu cient or DV . IVC lters have a role in those who cannot be anticoagulated but are not primary therapy. Subcutaneous heparin is used in prophylaxis, not treatment. 14. The a ns we r is D (Chapter 8, Acute Deep Venous T rombosis, Complications, II). T e

patient presents with the long-term sequelae o DV , known as post-thrombotic syndrome. Skin ulceration would not be expected in an acute DV . T e timing o heparin-induced thrombocytopenia is in close association with the dosing o heparin. PE should present with respiratory symptoms. Phlegmasia is an acute complication o DV , and phlegmasia alba dolens would present with pitting edema and blanching. 15. The a ns we r is B (Chapter 8, Lymphedema, Diagnosis, III). T e patient is presenting with signs

and symptoms o lymphedema secondary to disruption o the axillary lymphatics. T e test o choice is lymphoscintigraphy. US is reasonable to rule out a DV , but this is less likely in the clinical scenario. MRA and conventional angiography are used to assess the arterial system, which seems normal in this patient. C o the chest is unlikely to be use ul in this instance.

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Part IV

Gastrointestinal Disorders Chapter Cuts and Caveats

CHAP TER 9 Es o p ha g us : Every patient with dysphagia should undergo EGD to rule out carcinoma. Squamous cell cancer is most common in the upper and middle third o the esophagus, adenocarcinoma in the lower third. Esophageal ref ux is remarkably common. Most patients respond to acid suppression therapy, and those that do not can be treated with minimally invasive surgery. Fundoplication is e ective at re-establishing a physiologic barrier to ref ux. Preoperative manometry to ensure good esophageal motility is essential in these patients. Barrett esophagus is replacement o distal squamous epithelium with columnar epithelium that can undergo malignant trans ormation. It should be monitored or degree o dysplasia. Severe dysplasia and carcinoma in situ should be resected. Barrett is associated with chronic GERD but is not cured by an antiref ux procedure. Carcinoma o the esophagus is treated with multimodal protocols, with surgery reserved or early stages. Achalasia is the most common motility disorder, associated with dysphagia and regurgitation. Its ndings are dilated esophagus, loss o peristalsis, and increased LES tone showing a bird’s beak on barium swallow and treated by endoscopic dilation or surgical transection o the LES (Heller myotomy).

CHAP TER 10 Sto m a c h a nd Duo d e num : T e management o peptic ulcer disease is initially medical: acid suppression therapy and treatment or H. pylori will cure most patients. Prophylaxis with PPIs to prevent stress ulcer and UGI bleeding should be considered or patients with mechanical ventilation, coagulopathy, sepsis, multiorgan ailure, prior UGI bleed, and neurologic trauma, among others. Gastric ulcers are associated with the risk o cancer. Gastric cancer is usually diagnosed late due to nonspeci c symptoms. Reconstructions a er gastrectomy cause unique physiologic problems such as dumping syndrome. A duodenal ulcer that has recently bled and has a visible artery in its base has a high risk or rebleeding. GIS s are common in the stomach and treated by resection to grossly negative margins. MAL lymphoma is the only malignancy success ully treated with antibiotics.

CHAP TER 11 Sm a ll Inte s tine : Many small bowel obstructions are due to adhesions and will resolve with bowel rest, correction o f uid and electrolytes, and time. Partial small bowel obstruction is usually best managed

conservatively with NG decompression and IV f uid support. Surgery is usually indicated i it ails to resolve or i certain clinical ndings are present, such as localized abdominal tenderness, a hernia, ever, markedly elevated WBC, acidosis, large f uid requirements, or a closed loop obstruction on radiograph. umors o the small bowel such as carcinoid tumor can present with obstruction. Ischemic bowel is a di cult diagnosis and should be suspected when atrial brillation, acute MI, hypercoagulable state, low-f ow state, or an abdominal bruit is present with severe abdominal pain. T e common complications o IBD that may lead to surgical intervention include obstruction, bleeding, stula ormation, and ailure o medical therapy.

CHAP TER 12 Co lo n, Re c tum , a nd Anus : UC has an increasing risk or dysplasia and colonic malignancy with active disease over 10 years. Cancer develops in f at areas in contrast to the polyp–cancer progression in the usual colon cancers. A retrocecal appendix may not exhibit the usual clinical course o RLQ pain. Adenomatous polyps lead to colon cancer i unchecked—most polyps are initially amenable to endoscopic resection. Colorectal cancer is the third leading cause o cancer death, and screening with ecal occult blood testing or endoscopy allows early detection. Adjuvant chemotherapy improves survival in stage III colon cancer. Rectal cancer has a high risk o local recurrence at the site o resection. Rectal cancers respond to radiation therapy, whereas colonic cancers do not. Diverticulitis typically involves the sigmoid colon. Initial uncomplicated attacks are usually treated medically with antibiotics, but most complicated cases ultimately require surgical resection. Patients with clinical diverticulitis must have colon cancer ruled out. T e site o lower GI bleeding must be con rmed be ore surgery. Massive lower GI bleed is usually secondary to diverticulosis or AV mal ormations o the cecum. C. dif cile is a common cause o antibiotic-associated diarrhea; it is detected by PCR and treated with metronidazole.

CHAP TER 13 Live r, Ga llb la d d e r, a nd Bilia ry Tre e : Liver ailure has an elevated INR due to de ciency o actors II, VII, IX, and X, which is corrected with FFP in an acute bleed and vitamin K. It also is associated with thrombocytopenia due to hypersplenism. T e natural history o asymptomatic gallstones is benign, and cholecystectomy is not recommended. Symptomatic gallstones are treated with laparoscopic cholecystectomy. Biliary obstruction due to stones may present as pain ul jaundice and should be treated with removal o the stones by ERCP in most cases ollowed by cholecystectomy or operative common duct exploration at the time o cholecystectomy. Acute cholecystitis should be treated with antibiotics ollowed by cholecystectomy in several days in most cases. Painless jaundice is associated with distal biliary obstruction rom tumors. Resected ampullary cancer has the best long-term survival o the pancreatobiliary cancers obstructing the distal CBD. Cystic liver lesions are usually simple cysts, are not usually symptomatic, and do not require surgery. In the presence o ever and sepsis, the cystic structure may have internal echoes on US and represent an abscess, which is usually drained percutaneously. T e most common solid liver masses are hemangiomas, which do not require surgery. T e most common malignant tumor o the liver is metastatic carcinoma. T e primary should be sought. Resection o metastatic colonic carcinoma to the liver with no metastasis outside the liver as demonstrated by PE scan can result in long-term survival. Hepatocellular carcinoma is the most common primary liver cancer and is associated with cirrhosis o any cause as well as elevated serum alpha- etoglobulin.

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Most blunt liver trauma can be managed nonoperatively. Portal hypertension may lead to bleeding esophageal varices, which may be lethal.

CHAP TER 14 P a nc re a s : Pancreatitis may produce both exocrine and endocrine de ciency. Ranson criteria mark the severity o the pancreatitis. T e most common etiologies are alcohol and gallstones, but it may be a result o viral in ection, drug reactions, or other causes. Supportive care is the rule. Gallstone pancreatitis is best treated by alleviating the obstruction, f uid resuscitation, and antibiotics. Surgery is reserved or cases o pancreatic necrosis. Small pseudocysts may resolve spontaneously; large pseudocysts o en require internal drainage. Most pancreatic cancer occurs in the head o the pancreas presents late as painless jaundice. T e usual treatment is the Whipple operation. Pancreatic resections are complex and have the potential or high morbidity.

CHAP TER 15 Sp le e n: T e spleen unctions both in hematology (RBC and platelet clearance) as well as immunology (removal o encapsulated organisms). I P is the most common reason or elective splenectomy. All patients should be immunized or meningococcus, pneumococcus, and H. inf uenza prior to splenectomy. Accessory spleens occur commonly and may result in recurrence o disease. T e pancreatic tail may be injured during splenectomy, resulting in pancreatic stula. T e spleen is requently injured during blunt trauma and o en can be salvaged with nonoperative management.

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Chapter 9

Esophagus Jonathan P. Pearl

INTRODUCTION Ana to m y (Fig . 9-1) I. Lo c a tio n: T e esophagus is 24 cm in length, extending rom vertebral level C6 to 11. A. Upper esophageal sphincter: at esophageal origin, composed o the cricopharyngeal muscle; courses behind the aortic arch and descends into the thorax on the right B. Esophageal hiatus: Esophagus deviates anteriorly and enters the abdomen through the hiatus. C. Gastroesophageal junction (GEJ): T e tubular esophagus meets the saccular stomach here ( 40 cm rom the incisors), where it is anchored by the phrenoesophageal ligament. II. His to lo g y A. Esophageal mucosa: consists o squamous epithelium except or Quic k Cut the distal 1–2 cm, which is columnar epithelium The es ophagus is B. Two layers o muscle line the esophagus: An inner circular and unique in the gas trointes tinal outer longitudinal layer. T e upper one third is striated muscle, (GI) tract in that it does not whereas smooth muscle predominates in the lower two thirds. eature s eros a.

Cricoid origin

1

Aortic a rch

2

L. ma in bronchus

3

L. a trium

4

Es opha ge a l hia tus

5

Fig ure 9-1: Es ophageal anatomy. (From Dudek RW. High-Yield Gross Anatomy, 4th ed. Baltimore: Lippincott Williams & Wilkins ; 2010.)

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Esophageal Motility Disorders

Va s c ula ture I. Arte rie s : Arterial supply to the esophagus is rom branches o the in erior thyroid; the bronchial, intercostal, in erior phrenic, and le gastric arteries; and direct esophageal branches rom the aorta. II. Ve ins : An extensive subepithelial venous plexus empties superiorly into the hypopharyngeal veins and in eriorly into the gastric veins. Segmental drainage occurs also via the azygous and hemiazygous systems. III. Lym p ha tic d ra ina g e (to the ne a re s t lym p h no d e s ): Upper esophageal lymphatics drain into the cervical or mediastinal nodes, whereas distal esophageal drainage is o en to the celiac nodes.

Quic k Cut The venous s ys tem is more variable than the arterial s ys tem.

Inne rva tio n I. Sym p a the tic a nd p a ra s ym p a the tic s ys te m s : T e esophagus is supplied by the pharyngeal plexus, vagus, upper and lower cervical sympathetic, and splanchnic nerves. II. Aue rb a c h (m ye nte ric ) a nd Me is s ne r (s ub m uc o s a l) p le xus e s : inf uence esophageal motility

P hys io lo g y I. Up p e r e s o p ha g e a l s p hinc te r (UES): T is 3–5 cm high-pressure zone at the esophageal upper border is composed primarily o the cricopharyngeus muscle and relaxes during swallowing to allow ood bolus passage. II. P e ris ta ls is : T ese wavelike movements in the central portion o the esophagus pass down the body o the esophagus and become stronger toward the lower portion. A. Primary peristalsis: propels ood down the esophagus Quic k Cut B. Secondary peristalsis: I a ood bolus ails to progress, local Es ophageal stretch receptors trigger secondary peristalsis to move it. peris taltic pres s ures range rom 25 to 80 mm Hg. III. Lowe r e s opha ge a l s phinc te r (LES): T is 3–5-cm highpressure zone at the esophageal lower portion unctions to prevent gastroesophageal ref ux (GER). No distinct sphincter muscle exists in this area, but manometry readily demonstrates the physiologic high-pressure Quic k Cut zone. LES pressure is inf uenced by several actors and substances. The LES is a zone A. LES pressure increase: occurs with a protein meal, stomach rather than a dis tinct mus cle. alkalinization, gastrin, vasopressin, and cholinergic drugs B. LES pressure decrease: occurs with secretin, nitroglycerine, glucagon, chocolate, atty meals, and gastric acidi cation

ESOP HAGEAL MOTILITY DISORDERS Cric o p ha ryng e a l Dys unc tio n a nd Ze nke r Dive rtic ulum I. P a tho p hys io lo g y A. Cricopharyngeal dys unction: UES ails to relax properly. 1. T e problem may be an incoordination between UES relaxation and simultaneous pharyngeal contraction. 2. T is may result in pharyngoesophageal (Zenker) diverticulum. B. Pharyngoesophageal (Zenker) diverticulum 1. “False” diverticula consist only o mucosa rather than the entire esophageal wall. 2. Symptoms: dysphagia, halitosis, undigested ood regurgitation, nocturnal aspiration, and recurrent aspiration pneumonia 3. Diagnosis a. History and physical examination: raise the suspicion or Zenker diverticulum b. Esophagram: Using water-soluble contrast can provide the diagnosis.

Quic k Cut A true diverticulum is an outpouching o all layers o the wall.

Quic k Cut Endos copy is contraindicated when Zenker diverticulum has been documented radiographically becaus e the ris k o per oration is high. I a diverticulum is not s een on contras t s tudies , then endos copy is indicated to rule out other es ophageal dis orders .

Chapter 9

4. Treatment a. Cricopharyngeal myotomy: through a neck incision b. Endoscopic stapler: T is alternative to open surgery divides the diverticulum wall. c. Diverticulopexy: Large diverticula may require myotomy combined with suspension o the diverticulum to prevent oodstu rom entering the residual sac.

Ac ha la s ia I. P a tho p hys io lo g y: unknown etiology A. Coordinated peristalsis is absent in the body o the esophagus. B. Resting LES pressure is high, and the LES ails to relax during swallowing. C. T e body o the esophagus becomes dilated, and the muscle hypertrophies in an attempt to orce material through the dys unctional LES. II. Sym p to m s : Dysphagia, regurgitation, and weight loss. Respiratory symptoms caused by aspiration may be present. III. Dia g no s is A. Radiographic studies: typically reveal a dilated midesophagus with a “bird’s beak” appearance o the lower esophagus (Fig. 9-2) B. Esophageal manometry: shows absence o peristalsis C. Esophagoscopy: Required to rule out cancer and to document the extent o esophagitis. Retained ood is commonly ound at endoscopy, and the LES may be di icult to traverse.

Esophagus

155

Quic k Cut Zenker diverticulum is treated s urgically.

Quic k Cut The primary problem in achalas ia is the ailure o the LES to relax. Contractions may be low or high amplitude depending on where the patient is in the cours e o the dis eas e.

Quic k Cut Cha g a s d is e a s e , which is caus ed by the organis m Trypanosoma cruzi, caus es a s ymptom complex s imilar to achalas ia.

Quic k Cut The s ine qua non o achalas ia is abs ence o peris tals is on es ophageal manometry.

Fig ure 9-2: Barium s wallow s tudy demons trating clas s ic “bird’s beak” appearance (arrow) o achalas ia. (From Eis enberg RL. Gastrointestinal Radiology: A Pattern Approach, 3rd ed. Philadelphia: Lippincott-Raven Publis hers ; 1996.)

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Esophageal Motility Disorders

IV. Tre a tm e nt: aims to disrupt the lower esophageal musculature to Quic k Cut allow unimpeded ood passage into the stomach Dilatation o A. Nonsurgical the es ophagus with an 1. Pneumatic dilatation: A high-pressure endoluminal balloon endoluminal balloon carries a dilates the lower esophagus. s ubs tantial ris k o per oration. 2. Botulinum toxin: injected into the lower esophageal musculature to provide temporary relaxation B. Surgical (Heller myotomy): T is involves division o the outer longitudinal and inner circular layers o the distal 6 cm o esophagus. T e myotomy is carried onto the proximal 3 cm o the stomach. 1. Myotomy: relieves dysphagia in 80%–90% o patients 2. Esophagomyotomy: usually combined with an anterior Dor undoplication or a partial posterior Toupet undoplication to ameliorate postoperative ref ux C. Peroral endoscopic myotomy (POEM): Endoscopically divides the inner circular layer o musculature. Early data are encouraging.

Di us e Es o p ha g e a l Sp a s m I. P a tho p hys io lo g y A. Characterized by strong nonperistaltic contractions B. Normal sphincteric relaxation and may be associated with GER II. Sym p to m s : may be spontaneous or may be induced by cold or hot liquids, stress, or carbonated beverages Quic k Cut Remember that the A. Chest pain: may be con used with angina pectoris es ophagus can be a s ource o B. Dysphagia: to liquids and solids ches t pain. III. Dia g no s is A. Manometry: reveals high-amplitude simultaneous contractions with a normal sphincteric response to swallowing B. Contrast esophagram: may show a corkscrew appearance o the esophagus IV. Tre a tm e nt A. Medical therapy: calcium channel blockers and smooth muscle relaxants (e.g., nitrates) B. Endoscopic therapy: Botulinum toxin injected into the spastic segment may provide relie . C. Surgery: indicated in patients who continue to have chest pain and dysphagia a er medical therapy or who have an associated pathologic entity (e.g., a diverticulum)

Es o p ha g e a l Re f ux I. Etio lo g y: Common—may a ect up to 80% o the population to varying degrees. T e normal barrier against ref ux is provided by multiple actors. A. LES: normally provides a high-pressure zone B. Esophagogastric junction: normally rests within the abdominal cavity, and the positive intraabdominal pressure adds tone to the LES C. Angle o His (acute angle created between the junction o the lower esophagus and the cardia o the stomach): When the angle is disrupted, as with a hiatal hernia (Fig. 9-3), gastric contents more easily traverse the LES. D. Esophageal motility: Some ref ux is physiologic, but a normally unctioning esophagus clears the ref uxate. In cases o esophageal dysmotility, peristalsis is not adequate to clear the ref uxed secretions. II. Sym p to m s : Substernal pain, heartburn, and regurgitation. Extraesophageal symptoms include sore throat, hoarse voice, Quic k Cut halitosis, and dental caries. Typical ref ux s ymptoms are heartburn and III. Dia g no s is ches t pain. A. History and physical B. Esophagoscopy: may reveal varying degrees o esophagitis C. 24-hour pH probes: placed in the lower esophageal area to measure exposure o the esophagus to acid D. Intraesophageal impedance monitoring: detects nonacid ref ux IV. Tre a tm e nt A. Li estyle modif cations: weight loss, head-o -the-bed elevation during sleep, Avoiding carbonated beverages, and abstinence rom smoking and alcohol

Chapter 9

Esophagus

157

Es opha gus Thora x S toma ch Dia phra gm

Abdome n

Body of s toma ch

A Es opha gus Thora x S toma ch

Dia phra gm

Abdome n

Body of s toma ch

Fig ure 9-3: Major types o paraes ophageal hernia. (From Porth CM. Essentials of Pathophysiology: Concepts of Altered Health States, 3rd ed. Baltimore: Lippincott Williams & Wilkins ; 2010.)

B

B. Medical management 1. Acid-suppressing medications: include proton pump inhibitors and histamine receptor blockers 2. Baclo en (gamma-aminobutyric acid receptor agonist): may diminish transient LES relaxation and reduce symptoms in patients with re ractory ref ux C. Surgical treatment 1. Indications a. Symptoms re ractory to medical treatment b. Patient desires to avoid li elong pharmacotherapy, even i responsive to medication. c. Less common indications include laryngopharyngeal symptoms, esophageal strictures, or Barrett esophagus (see next section). 2. Antire ux operations: designed to mechanically restore the barrier to ref ux and involve wrapping the lower esophagus with gastric undus and restoring the distal esophagus to its original intra-abdominal position with the GEJ below the diaphragm. T e ollowing are most common. a. Nissen undoplication (360-degree wrap o the gastric undus around the distal esophagus): usually per ormed laparoscopically with avorable results b. Belsey Mark IV operation (270-degree wrap): per ormed through a le thoracotomy c. Hill posterior gastropexy (includes a posterior 180-degree undoplication, which is then anchored to the arcuate ligament o the diaphragm): emphasizes restoration o the LES to the intra-abdominal position

Ba rre tt Es o p ha g us I. De nitio n A. Intestinal metaplasia: occurs in the distal esophagus B. Columnar intestinal mucosa: replaces the normal squamous mucosa

Quic k Cut Go b le t c e lls are the characteris tic nding in intes tinal metaplas ia.

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Esophageal umors

II. Etio lo g y A. Caused by exposure o the lower esophagus to acid or nonacid ref ux B. Occurs in 5%–20% o patients with gastroesophageal ref ux disease (GERD) C. Approximately 0.5% o patients per year will develop cancer. III. Dia g no s is : Detected at endoscopy by its characteristic tongues o salmon-colored mucosa in the lower esophagus. When suspected, multiple biopsies are recommended to assess or dysplasia or malignancy. IV. Ma na g e m e nt A. Barrett without dysplasia: surveilled with endoscopy and biopsy every 3 years B. Low-grade dysplasia 1. Can be surveilled annually or progression to high-grade dysplasia 2. Endoscopic radio requency ablation (RFA) or undoplication: may cause dysplasia to regress but there has been an inconsistent response C. High-grade dysplasia 1. Esophagectomy: common management method due to risk o progression to cancer 2. Endoscopic mucosal resection and RFA: aggressive, but these therapies are in their nascent stages

ESOP HAGEAL STRICTURES Ca us tic Stric ture I. Etio lo g y: caused by ingesting caustic agents, such as lye, drain openers, and oven cleaners II. Dia g no s is A. History: caustic ingestion and complaints o chest pain, cough, Quic k Cut drooling, or shortness o breath With a his tory B. Endoscopy: indicated within 24 hours to determine damage extent o caus tic inges tion, it is important to identi y airway III. Tre a tm e nt compromis e early. A. Supportive therapy: T is mainstay o treatment includes broadspectrum antibiotics and respiratory support. B. Esophageal contrast radiographs: per ormed at 10–14 days a er ingestion to assess or stricutres 1. Strictures occur in 5%–10% o patients who have ingested lye. 2. Endoscopic dilatation: begins 3–4 weeks a er ingestion C. Surgery: reserved or cases o per oration or chronic stricture re ractory to dilation

Stric ture s Se c o nd a ry to Es o p ha g itis a nd Re f ux I. P a tho p hys io lo g y: recurrent alternating pattern o mucosal destruction most o en in the distal esophagus due to gastric acid ref ux and subsequent healing A. Schatzki rings: benign strictures o the lower esophagus likely caused by ref ux but may have a congenital component B. Cases o long-standing uncontrolled ref ux may cause a long, narrow stricture. II. Dia g no s is A. History: Ref ux symptoms with dysphagia development suggests strictures. B. Esophagoscopy (with stricture biopsy): determines disease extent and can rule out malignancy C. Radiographs: con rm the diagnosis III. Tre a tm e nt A. Esophageal dilatation: rst-line treatment B. Corticosteroids: Some strictures respond to injections. C. Antire ux operations: may eliminate the inciting actors, and, in some cases, the stricture may recede D. Esophagectomy: indicated i dilatation and an antiref ux operation do not relieve the obstruction

ESOP HAGEAL TUMORS Be nig n Tum o rs I. Le io m yo m a s : intramural smooth muscle tumors that account or two thirds o all esophageal benign neoplasms A. Symptoms: Dysphagia occurs with lesions over 5cm as they grow within the muscular wall. B. Diagnosis 1. History: Dysphagia is typical. 2. Barium swallow: reveals a localized smooth lling de ect in the esophageal wall

Chapter 9

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159

3. Esophagoscopy: con rms the diagnosis i there is a bulge into the esophagus with normal overlying mucosa 4. Biopsy: contraindicated because it violates the mucosa, making subsequent surgical therapy more di cult 5. Endoscopic ultrasound (EUS): help ul to con rm the intramural location o the lesion C. Surgical treatment: rarely indicated or leiomyomas 1. Tumor enucleation (in symptomatic patients): occurs without mucosa violation 2. Limited esophageal resection: indicated i the tumor lies in the lower esophagus and cannot be enucleated II. Be n ig n in tra lu m in a l tu m o rs : usually mucosal polyps, lipomas, f brolipomas, or myxof bromas A. Symptoms: dysphagia, occasional regurgitation, and weight loss Quic k Cut B. Diagnosis Endos copy s hould 1. Radiographs: suggest the diagnosis not be us ed to remove 2. Esophagoscopy: con rms the diagnosis and can rule out benign intraluminal tumors malignancy becaus e o the pos s ibility o C. Surgical treatment: Esophagotomy, tumor removal, and es ophageal per oration. esophagotomy repair comprise the surgical treatment.

Ma lig na nt Tum o rs I. Inc id e nc e a nd p re va le nc e : Annual incidence in the United States is 4.5 cases per 100,000 people. A. Esophageal cancer accounts or 1% o all malignancies in the United States. B. In 2013, there were an estimated 18,000 cases with 15,000 deaths attributed to the disease. II. Etio lo g y (unkno wn): Associated actors are tobacco use, excessive alcohol ingestion, nitrosamines, poor dental hygiene, and hot beverages. Certain pre-existing conditions also increase the likelihood o developing esophageal cancer (e.g., Barrett esophagus). III. P a tho lo g y A. Types 1. Adenocarcinoma: Accounts or 60% o cases in the United States; GERD is the primary risk actor. Barrett metaplasia Quic k Cut progresses to low-grade dysplasia then high-grade dysplasia Barrett es ophagus is and cancer. a precancerous condition. 2. Squamous cell carcinoma: Most common orm worldwide. Risk actors include smoking, alcohol ingestion, and nitrate ingestion. B. Tumor spread: Esophageal malignancies metastasize through both the lymphatic system and the bloodstream, with metastases occurring in liver, bone, and brain. IV. Dia g no s is A. History: Dysphagia and weight loss are almost always present. B. Contrast study o the esophagus: may demonstrate tumor location and extent C. Esophagoscopy: essential or tissue diagnosis and determining tumor extent D. Computed tomography (CT) scan o the chest and abdomen: done to evaluate local lymphatic spread and to search or distant metastases E. EUS: done to assess the depth o the invasion and or staging F. Bronchoscopy (in patients with proximal esophageal lesions): done to assess the possibility o tracheobronchial tree Quic k Cut invasion Overall 5-year s urvival o es ophageal cancer

V. Tre a tm e nt: Survival is poor and depends on stage. is 20% , with almos t no 5-year A. Surgical therapy s urvivors o s tage IV dis eas e. 1. Transhiatal esophagectomy (through a laparotomy and cervical incisions): A complete thoracic esophagectomy is per ormed bluntly with reconstruction o GI continuity with the stomach. 2. Ivor Lewis esophagectomy (through a right thoracotomy and laparotomy): Reconstruction is also accomplished with the stomach.

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Mallory-Weiss Syndrome

B. Neoadjuvant therapy (with radiation and chemotherapy prior Quic k Cut to surgery): Considered standard treatment by many experts. The es ophagus may T e e ects on outcomes and survival are not ully understood. be replaced with s tomach, 1. Chemotherapy: May shrink tumor size and treat or even a s egment o colon, micrometastases. Most tumors respond to cisplatin-based a ter es ophagectomy. regimens, but complete responses are rare. 2. Radiotherapy: May improve local control o disease at the expense o higher rates o postoperative complications. T ere may be little e ect on overall survival. 3. Palliation (in patients who have advanced disease with either invasion o the tracheobronchial tree or advanced metastases): Endoscopically placed metallic stents may allow swallowing o saliva and so oods.

ESOP HAGEAL P ERFORATION Etio lo g y I. Ca us e s A. Iatrogenic: Instrumentation (e.g., esophagoscopy or dilatation) accounts or 50% o all esophageal per orations. B. Trauma (blunt or penetrating): causes 20% C. Boerhaave syndrome (postemetic esophageal rupture): causes 15% II. Es o p ha g e a l rup ture : results in acute mediastinitis

Quic k Cut Acute medias tinitis can be atal.

Dia g no s is I. His to ry: Patients give a recent history o instrumentation o the esophagus or severe vomiting. Almost all patients complain o severe chest pain. II. P hys ic a l e xa m ina tio n A. Crepitus (in the neck): results rom mediastinal air B. Hamman sign (crunching sound heard over the heart): caused by mediastinal air behind the heart III. Che s t ra d io g ra p hy: reveals mediastinal air and, possibly, a widened mediastinum A. Lower esophageal per oration: Air may be present under the diaphragm. B. Hydropneumothorax (usually le side): may be present i the pleura has been violated IV. Contra s t e s opha gra m : study per ormed i per oration is suspected V. CT s c a n: also a very use ul diagnostic modality Quic k Cut

Tre a tm e nt I. Per orm primary repair with tissue buttress rein orcement, combined with wide mediastinal and pleural drainage II. Surg ic a l a p p ro a c h A. Upper esophageal per orations: approached through the le neck B. Midesophageal per orations: repaired through the right chest C. Lower per orations: treated via le thoracotomy or laparotomy

Contras t es ophagram is pre erred over es ophagos copy or identi ying a per oration.

MALLORY-WEISS SYNDROME P a tho p hys io lo g y I. Ac ute up p e r GI he m o rrha g e (p re s e nting s ig n): Bleeding results rom a partial-thickness tear in the lower esophagus near the esophagogastric junction. II. Ma llo ry-We is s le s io ns : may result rom retching or vomiting

Dia g no s is a nd Tre a tm e nt I. End o s c o p y: locates the tear and rules out other causes o bleeding II. Tre a tm e nt: begins with standard resuscitation A. Endoscopy with hemostasis: mainstay o treatment and e ective in most cases B. Surgery (rarely indicated): I endoscopy is not e ective, a laparotomy with anterior gastrotomy and suture ligation o the mucosal tear will stop the bleeding.

Chapter 10

Stomach and Duodenum Cherif Boutros, Ernest L. Rosato, and Francis E. Rosato Jr.

STOMACH Func tio n a nd Em b ryo lo g y I. Func tio ns : storage, emulsif cation, initial digestion by acidif cation and salivary amylase, and ood transmission to the duodenum II. De ve lo p m e nt Quic k Cut A. Rotation: causes the le vagus to lie in the anterior position and The rate o growth o the s tomach le t wall the right vagus to lie in the posterior position outpaces the right, orming B. Mesentery: Ventral and dorsal mesenteries o the oregut the greater and les s er become the lesser and greater omentums, respectively. curvatures .

Surg ic a l Ana to m y I. His to lo g y: Mucosal morphology is composed o distinctly di erent types o glands by stomach region (cardia, undus, body, and antrum). Quic k Cut A. Fundus and body: contain gastric glands with specialized cell The s tomach can be types divided into a proximal region that mainly produces acid and 1. Mucous cells: provide an alkaline coating or the epithelium, peps in and a dis tal s tomach which acilitates ood passage and provides mucosal that mainly s ecretes gas trin. protection 2. Chie cells: Secrete pepsinogen, the precursor to pepsin, which aids in protein digestion. Chie cells are stimulated by cholinergic impulses, gastrin, and secretin. 3. Oxyntic (parietal) cells: stimulated by gastrin to produce hydrochloric acid and intrinsic actor B. Antrum: Contains G cells, which secrete gastrin and are part o the amine precursor uptake and decarboxylase system o endocrine cells. Gastrin stimulates hydrochloric acid and pepsinogen secretion and gastric motility. II. Sto m a c h d ivis io ns : our divisions (Fig. 10-1) Quic k Cut A. Cardia: most proximal portion o the stomach, where it The angle created attaches to the esophagus, and containing the gastroesophageal by the undus and the junction (GEJ), which is typically ound 2–3 cm below the le t lateral border o the diaphragmatic hiatus and contains the lower esophageal es ophagus is re erred to as sphincter (LES) the a ng le o His . B. Fundus: most cephalad extension o the stomach, bounded by the diaphragm superiorly and the spleen laterally C. Body (corpus): Largest portion o the stomach and consisting o the lesser and greater curves. T e incisura angularis creates an abrupt angle along the lesser curvature and marks the beginning o the antrum. D. Antrum: distal 25% o the stomach that begins at the incisura angularis and ends at the pylorus

161

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Stomach

Ga s troe s opha ge a l junction

Fundus

Ca rdia

Incis ura a ngula ris P ylorus Body

Antrum

Fig ure 10-1: Anatomy o the s tomach.

III. Sto m a c h s p hinc te rs : two sphincter mechanisms A. LES (physiologic sphincter): high-pressure zone o muscular Quic k Cut activity in the distal esophagus Failure o the LES to relax res ults in achalas ia; B. Pylorus (anatomic sphincter): controls ood ow rom the ailure to remain contracted stomach into the duodenum res ults in re ux. IV. Arte ria l s up p ly: extremely rich blood supply provided mainly by two arcades running along the lesser and the greater curvature (Fig 10-2) A. Lesser curvature arcade: consists o the right (branch o the Quic k Cut common hepatic artery) and le gastric (branch o the celiac Sacrif cing three o trunk) the our main arteries can s till B. Greater curvature arcade: consists o the right gastroepiploic leave a viable s tomach. (branch o the gastroduodenal artery) and the le gastroepiploic artery (branch o the splenic artery) C. Short gastric arteries ( rom the splenic artery): supply directly the gastric undus V. Ve no us d ra ina g e : in general, parallels the arterial supply A. Lef gastric vein (coronary vein): drains into the portal system and Quic k Cut has multiple anastomoses with the lower esophageal venous plexus Acetylcholine is the primary neurotrans mitter us ed B. Portal hypertension: Venous connections provide a detour or by the e erent vagal f bers . blood and orm esophageal varices that may lead to massive upper gastrointestinal (UGI) hemorrhage. VI. Va g a l inne rva tio n (p a ra s ym p a th e tic s ys te m ): T e vagus nerve stimulates parietal cell secretion, gastrin release, and gastric motility. A. Lef vagus nerve: lies anterior to and le o the esophagus and Quic k Cut gives a hepatic branch to the liver, gallbladder, and biliary tree, The c rim ina l ne rve and a undal branch o Gra s s i is a proximal B. Right vagus nerve: lies posterior to and right o the esophagus branch o the right pos terior vagus . It can be eas ily and supplies branches to the posterior stomach and a celiac mis s ed, and may lead to ulcer branch to the pancreas, small bowel, and right colon recurrence i not divided. C. Truncal vagotomy: Division o the main trunk o vagus nerves has the best chance to control acid production by eliminating all gastric branches; however, it is associated with gallstone ormation (impaired gallbladder motility with loss o the hepatic branches o the le vagus) and diarrhea (loss o the celiac branches rom right vagus).

Chapter 10

Stomach and Duodenum

163

P os te rior ga s tric a rte ry S hort ga s tric a rte rie s

As ce nding e s opha ge a l a rte ry Le ft phre nic a rte ry

S ple nic a rte ry

Le ft ga s tric a rte ry Ce lia c trunk Right ga s tric a rte ry P rope r he pa tic a rte ry Ga s troduode na l a rte ry

Le ft ga s troe piploic a rte ry

P os te rior s upe rior pa ncre a ticoduode na l a rte ry Infe rior pa ncre a ticoduode na l a rte ry Ante rior s upe rior pa ncre a ticoduode na l a rte ry

Right ga s troe piploic a rte ry S upe rior me s e nte ric a rte ry

Fig ure 10-2: Arterial s upply and venous drainage o the s tomach. (From McKenney MG, Mangonon PC, Moylan J P, eds . Understanding Surgical Disease. Philadelphia: Lippincott–Raven Publis hers ; 1998:118. Us ed by permis s ion o Lippincott Williams & Wilkins .)

VII. Lym p ha tic d ra ina g e : extensive but can be divided into our general zones A. Zones: superior gastric, pancreaticolienal, suprapyloric, and in erior gastric B. Oncology: Lymph node dissection or gastric cancer is classif ed in three categories (D1–D3). 1. D1: en bloc gastric resection with surrounding gastric lymph nodes 2. D2: en bloc gastric resection with lymph nodes at the origin o the arteries supplying the stomach Quic k Cut 3. D3: urther dissection o lymph nodes beyond D2 In cancer (e.g., para-aortic) operations , “D” re ers to

P EP TIC ULCER DISEASE

the extent o lymph node dis s ection.

Ga s tric a nd Duo d e na l Dig e s tio n I. Ga s tric a c id s e c re tio n: mediated by a complex interplay o Quic k Cut neuronal and hormonal in uences; the secretory response during Ulcers res ult rom eating is divided into three phases an imbalance between acid A. Cephalic phase: initiated by the sight, smell, and thought o ood production and mucos al de ens e. B. Gastric phase: initiated by mechanical distention o the antrum, with additional gastrin release C. Intestinal phase (not well understood): Intestinal actors, such as cholecystokinin, are mild stimulators o acid production. II. Ne g a tive a c id e e d b a c k m e c ha nis m s : include a decline in vagal stimulation, increased acid content, and duodenal negative eedback. An antral pH o 2 inhibits gastrin release. Acid chyme in the duodenum stimulates secretin release, which urther inhibits gastrin secretion.

Ga s tric Ulc e rs I. Inc id e nc e : more common in men, the elderly, and lower socioeconomic groups II. Etio lo g y: Damage to the gastric mucosal barrier appears to be the most important actor, which can be secondary to the ollowing. A. Bile re ux to the stomach

Quic k Cut Duodenal ulcers are twice as common as gas tric ulcers .

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III.

IV.

V.

VI.

Peptic Ulcer Disease

B. Drugs: including nonsteroidal anti-in ammatory drugs Quic k Cut (NSAIDs), salicylates, steroids, ethanol, and the combination o Ulcers res ult rom smoking and salicylate ingestion an imbalance in gas tric acid C. Helicobacter pylori in ection: weakens the protective production and mucos al gastric mucous barrier, increases the basal and stimulated de ens e. concentrations o gastrin, and impedes gastric healing a er injury, resulting in gastric ulcer ormation Dia g no s is A. History o burning midepigastric pain (stimulated by or ollows eating): common presentation B. UGI radiographs: shows barium in an ulcer crater but is seldom used C. Endoscopy: detects 90% o ulcers and allows multiple biopsy samples to be taken to rule out cancer or control bleeding D. H. pylori: conf rmed by urease breath test, tissue biopsy, or antibody titer measurement Lo c a tio n/typ e A. Type 1 (most common): along the lesser curve at the incisura angularis B. Type 2: body o the stomach in combination with duodenal ulcers; associated with acid oversecretion C. Type 3: develop in the pyloric channel within 3 cm o the pylorus; associated with acid oversecretion D. Type 4: located high in the stomach adjacent to the esophagus E. Type 5: secondary to chronic NSAID and aspirin use and can occur anywhere throughout the stomach Ma lig na nc y Quic k Cut Ten percent A. Gastric cancer will ulcerate in 25%o cases: making it o gas tric ulcers are mandatory to prove by biopsy that an ulceration is not carcinoma malignancies with ulceration. B. A gastric ulcer and carcincoma are two separate entities: A gastric ulcer does not degenerate into carcinoma Tre a tm e nt A. Medical treatment: Used initially; most ulcers will heal in 8–12 weeks. 1. Eliminate irritants o the gastric mucosa: Avoid ethanol, tobacco, and drugs. 2. Sucral ate: sul ated sucrose that binds to the ulcer crater and Quic k Cut enhances the mucosal barrier Antis ecretory medications (H2 blockers and 3. Histamine (H2) blockers: e ectively reduce gastric output PPIs ) are among the mos t 4. Proton pump inhibitors (PPIs): block the enzyme involved commonly pres cribed drugs in the parietal cell secretion o acid worldwide. 5. H. pylori treatment: Requires antisecretory agents, antibiotics (amoxicillin or clarithromycin and metronidazole), and/or bismuth; 90% cure rates are reported with dual antibiotic and omeprazole treatment (“triple therapy”) and have decreased ulcer recurrence. B. Surgical treatment: indicated in the ollowing situations: 1. Intractability: Ulcer ails to heal a er 3 months o medical Quic k Cut therapy or recurs within a year despite adequate therapy. Bleeding is the 2. Bleeding: not controlled by endoscopy or medical therapy major caus e o death in ulcer 3. Per oration: Def nitive ulcer surgery should be per ormed dis eas e. i no preoperative shock, no li e-threatening comorbidities, per oration less than 48 hours, known H. pylori negative, and ailed medical treatment. 4. Gastric outlet obstruction 5. Malignancy: Biopsy proven, or i unable to exclude C. Surgical procedures: ype o ulcer, location, and condition o the patient determines the operative procedure at the time o surgery (Fig. 10-3). 1. Type 1 ulcer: distal gastrectomy with reconstruction a. Gastroduodenal anastomosis (Billroth I gastrectomy): i the duodenum can be mobilized (see Fig. 10-3A) b. Gastrojejunal anastomosis (Billroth II gastrectomy): i the duodenum cannot be mobilized (see Fig. 10-3B)

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Stomach and Duodenum

A

B

C

D

E

F

165

Fig ure 10-3: Common gas tric s urgical procedures : (A) vagotomy and antrectomy (Billroth I), (B) vagotomy and antrectomy (Billroth II), (C) Roux-en-Y gas trojejunos tomy, (D) vagotomy and pyloroplas ty, (E) vagotomy and gas trojejunos tomy, and (F) parietal cell vagotomy.

2. Types 2 and 3 ulcers: vagotomy with antrectomy with extension to include excision o the ulcer 3. Type 4 ulcer a. Antrectomy with extension o resection to include the ulcer: or ulcers greater than 2 cm rom GEJ b. Csendes procedure: For ulcers less than 2 cm rom the GEJ, resection o the gastric antrum and body up to the GEJ (subtotal gastrectomy). Roux-en-Y gastrojejunostomy is done along the resection line (see Fig. 10-3C). 4. Type 5 ulcer: Surgical intervention is reserved or emergency situations (i.e., per oration or hemorrhage). Primary closure, omental patch, or wedge excision combined with cessation o NSAIDs and acetylsalicylic acid (ASA) are standard treatments.

Duo d e na l Ulc e rs I. Etio lo g y: may result rom inappropriate gastrin secretion rom a tumor mass (gastrinoma) Quic k Cut A. Mucosal resistance: may be altered by bacteria (H. pylori) and is Mos t duodenal the most common etiology o ulceration ulcers res ult rom acid B. Gastrinoma also called Zollinger-Ellison syndrome: usually hypers ecretion. (70%–90%) present in a triangular area (gastrinoma triangle) ormed by the junction o second and third portion o the duodenum, cystic duct and common bile duct junction, and the pancreatic neck II. Dia gnos is : Gastrinoma is diagnosed by inappropriately high gastrin level (150–1,000 pg/mL) while not taking PPI therapy. A secretin test (rise o gastrin level 200 pg/mL a er secretin in usion) conf rms the diagnosis. A. History o epigastric pain (radiating to the back): Usual presentation; pain is relieved by ood and typically wakes the patient at night.

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B. Studies: Esophagogastroduodenoscopy (EGD) is the major diagnostic tool. UGI radiographs may also be used. C. Serum gastrin level measurements: Obtained in patients with recurrent ulceration a er surgery, ulcers that ail to respond to medical management, suspected endocrine disorders (multiple endocrine neoplasia I), and Zollinger-Ellison syndrome. Normal serum gastrin levels are less than 200 pg/mL. D. H. pylori: conf rmed by urease breath test, tissue biopsy, or antibody titer measurement III. Lo c a tio n: Most duodenal ulcers are located in the f rst portion o the duodenum. Ulcers on the posterior wall may bleed rom erosion o the gastroduodenal artery penetrating ulcers. Ulcers on the anterior wall may per orate reely into the abdominal cavity. IV. Ma na g e m e nt A. Medical treatment: usually success ul with uncomplicated duodenal ulcer 1. Avoidance o aspirin, ca eine, alcohol, and tobacco: recommended 2. Stress reduction: may be benef cial 3. Eradication o H. pylori 4. Pharmacologic therapy (Table 10-1): mainstay a. H2-receptor antagonists/PPIs: Used most commonly or initial treatment. Most duodenal ulcers heal in 6–8 weeks with such therapy. b. Maintenance therapy: Recommended; ulcer recurrence a er discontinuing medical therapy occurs in 50%–80% o patients. B. Surgical treatment (Table 10-2): Reserved or patients who Quic k Cut have ulcers that ail to respond to medical therapy or who have Acid s uppres s ion is complications (e.g., per oration or bleeding). T ere are a number the initial treatment o mos t ulcer dis eas e. o surgical options; the goal o each is to reduce acid secretion; there ore, most approaches concentrate on interrupting vagal stimulation, antral gastrin secretion, or both. 1. Antrectomy with truncal vagotomy: procedure associated with the lowest recurrence rate (see Fig. 10-3B) 2. Truncal vagotomy and pyloroplasty: A er vagotomy, the motility o the stomach and pylorus is impaired, creating a unctional obstruction. For this reason, a drainage procedure, such as a pyloroplasty (see Fig. 10-3D) or gastrojejunostomy (see Fig. 10-3E), is required. 3. Parietal cell vagotomy (highly selective vagotomy): Only the gastric branches o the vagus nerve are divided (see Fig. 10-3F). a. Drainage: Because innervation o the pylorus is maintained, a drainage procedure is not necessary.

Ta b le 10-1: The ra p y o P e p tic Ulc e r Dis e a s e Ag e nt

E ect

Ad va nta g e s a nd Dis a d va nta g e s

De c re a s e g a s tric a c id ity Antacids

Neutralize gastric acid; also may increase mucosal resistance

Inexpensive; readily available

H2 -receptor antagonists (e.g., cimetidine)

Inhibit histamine receptor on parietal cell, which decreases acid output

Excellent results; mainstay therapy; once daily evening Dosing or maintenance therapy

Proton pump inhibitors (e.g., omeprazole)

Inhibit ATPase proton pump, which is f nal step in acid secretion rom parietal cell

Quicker healing but more expensive than preceding agents

Cytoprotective topical agent (e.g., sucral ate)

Binds to proteins in ulcer to orm protective barrier

Not proven or gastric ulcers

Antibiotics (e.g., amoxicillin)

Eradicate Helicobacter pylori

Inexpensive; important in preventing recurrences in patients with H. pylori

Inc re a s e m uc o s a l d e e ns e

ATPase, adenosine triphosphatase.

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167

Ta b le 10-2: Co m p a ris o n o Mo rb id ity a nd Mo rta lity Ra te s o Di e re nt Surg ic a l Op tio ns o P e p tic Ulc e r Surg e rie s Mo rb id ity

Antre c to m y a nd Trunc a l Va g o to m y

Trunc a l Va g o to m y a nd P ylo ro p la s ty

Ulcer recurrence rate

1%–2%

10%

Dumping syndrome

10%–15%

10%

Mortality

1%–2%

0.5%–1%

Hig hly Se le c tive Va g o to m y 10%–30% 5% 0%

b. Recurrence rates: Somewhat higher ( 10%) but the morbidity is less as compared with truncal vagotomy with antrectomy. T is procedure is o en per ormed laparoscopically, urther decreasing its morbidity. C. Complications: include per oration, hemorrhage, and obstruction 1. Per orations: Occur most commonly with ulcers on the anterior sur ace o the duodenum. Gastric per orations are less common. a. Typical symptoms: include sudden onset o severe abdominal pain, pain radiating to the shoulder, nausea, and vomiting b. Signs: Include a rigid, boardlike abdomen and shock. An upright chest x-ray commonly demonstrates ree air under the diaphragm. c. Treatment (1) Observation: May be occasionally used i the patient is hemodynamically stable and the initial event occurred several hours previously. A monitored setting, antibiotics, and intravenous (IV) uids are required. (2) Simple operative closure (of en with a patch o omentum [Graham patch]): usual treatment (3) De nitive treatment (e.g., by vagotomy with antrectomy): may be indicated in low-risk patients with minimal spillage o the peritoneal cavity, especially i they give a long history ( 3 months) o ulcer symptoms—or proven ailure o the medical treatment 2. Hemorrhage: Occurs in 15%–20% o patients with ulcers. Medical management controls the hemorrhage in most cases. Quic k Cut a. Endoscopy: Necessary to evaluate the site o the A “vis ible ves s el” in hemorrhage. T ermal techniques using electrocoagulation, the ulcer crater is an ominous laser, or heater probe or injection o sclerosing or s ign and is as s ociated with a vasoconstrictive agents may also be used endoscopically. higher ris k o rebleeding. b. Surgery: Surgical intervention is usually needed to control massive hemorrhage, def ned as blood loss 2 liters, hemodynamically unstable despite resuscitation, or continued blood loss requiring more than 6 units o trans used blood in a 24 hour period. (1) Control o the bleeding vessel: Oversewing o the bleeding point is done via a longitudinal opening through the pylorus. (2) Gastroduodenal artery ligation: i oversewing ails to Quic k Cut control the vessel Pyloroplas ty a ter (3) Truncal vagotomy (division o the two main vagal vagotomy is us ed to aid in trunks): also done to reduce acid stimulation (see s tomach emptying becaus e the vagotomy changes the Fig. 10-3C) mechanical unction o the (4) Pyloroplasty (widening o the pylorus): Pyloric incision pylorus . is closed transversely a er ligation. (see Fig 10-3D) (5) Vagotomy with antrectomy: option in low-risk patients 3. Gastric outlet obstruction: may be caused by chronic scarring o the pyloric channel due to prepyloric ulcers a. Symptoms: Obstruction causes symptoms o crampy abdominal pain, nausea, and vomiting. b. Signs: Stomach is usually markedly dilated. Prolonged vomiting due to obstruction can lead to electrolyte disorders, particularly hypokalemic metabolic alkalosis rom the large hydrochloric acid losses.

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Gastric Cancer

c. Initial treatment: several days o nasogastric suction to allow the stomach to decompress d. Surgery: Vagotomy with antrectomy or vagotomy with drainage is the standard procedure.

GASTRIC CANCER Ga s tric Ad e no c a rc ino m a

Quic k Cut Approximately 90% –95% o gas tric tumors are malignant, and o the malignancies , 95% are adenocarcinomas . Other his tologic types include s quamous cell, carcinoid, gas trointes tinal s tromal tumor (GIST), and lymphoma.

I. Epide m iology a nd e tiology: Leading cause o cancer-related death worldwide in the 20th century, gastric adenocarcinoma is now ranked second only to lung cancer. T e overall incidence may be decreasing. II. Ris k a c to rs A. Preventable actors 1. Nutritional actors: ood preparation (smoked, salt cured); oods low in vitamin A and C and high in salt 2. Occupational actors: exposure to rubber, coal, or radiation 3. Habits: cigarette smoking 4. In ection: H. pylori, Epstein-Barr virus 5. Precancerous lesions: adenomatous polyps, chronic atrophic gastritis, dysplasia, intestinal metaplasia, Ménétrier disease B. Genetic actors: type A blood, pernicious anemia, amily history, hereditary nonpolyposis colorectal cancer (HNPCC; Lynch syndrome), Li-Fraumeni syndrome C. History: previous gastric resection Quic k Cut III. P a tho lo g y: classif ed according to its histologic characteristics Di us e gas tric carcinoma has a higher A. Intestinal type: well-di erentiated, glandular tumor ound most incidence o lymph node commonly in the distal stomach metas tas is than does the B. Di use type: poorly di erentiated, small cell inf ltrating tumor intes tinal type. with submucosal inf ltration and ound most commonly in the proximal stomach IV. Clinic a l p re s e nta tio n a nd wo rkup Quic k Cut A. Symptoms: Include epigastric pain, anorexia, atigue, vomiting, and Gas tric cancer weight loss. Proximal tumors can present with dysphagia, whereas s ymptoms are vague and more distal tumors may present as gastric outlet obstruction. nons pecif c, s o mos t patients Symptoms tend to occur late in the course o the disease. are diagnos ed at advanced B. Signs: include palpable supraclavicular (Virchow) or s tage. periumbilical (Sister Mary Joseph) lymph nodes C. Diagnosis: Upper endoscopy with biopsy is considered the best test. D. Preoperative evaluation: aims to assess local spread to adjacent organs (e.g., spleen, diaphragm, omentum, colon), “drop metastases” to the ovary (Krukenberg tumor) or the pelvis (Blumer shel on rectal exam), or distant disease (e.g., to liver, lung) 1. Computed tomography (CT) scan: to look or local extension, ascites, and distant metastases 2. Endoscopic ultrasound: has been shown to be use ul in determining depth o penetration and in detecting nodal metastases 3. Whole body positron emission tomography: applied increasingly to identi y metastatic or recurrent disease 4. Staging laparoscopy: may detect small peritoneal metastases and is required be ore most neoadjuvant protocols V. Sta g ing : Uni orm and accurate staging is essential to dictate treatment options and predict prognosis and assess outcome. T e most commonly used is the American Joint Committee on Cancer based on tumor-node-metastasis classif cation ( able 10-3). VI. Tre a tm e nt: Gastric carcinoma is better managed in a multidisciplinary approach to discuss management o each patient according to the disease stage, patient comorbidities, and available resources. A. General approach 1. Early disease (Tis and T1a): can be o ered endoscopic mucosal resection with close endoscopic surveillance 2. Local disease limited to (T1b N0): should be o ered surgical resection with regional lymph node dissection in a f t patient

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Ta b le 10-3: Am e ric a n J o int Co m m itte e o n Ca nc e r TNM Cla s s if c a tio n Gastric adenocarcinoma that extends to the GEJ is classif ed and managed as esophageal cancer. P rim a ry tum o r (T) Tx Cannot be assessed T0 No evidence o tumor Tis No invasion o the lamina propria T1a Tumor invades lamina propria T1b Invades the submucosa T2 Invades the muscular layer T3 Invades subserosal connective tissue T4a Invades the serosa T4b Invades adjacent structures Re g io na l lym p h no d e s (N) Nx Cannot be assessed N0 No LN metastasis N1 Metastasis in 1–2 regional LNs N2 3–6 LN metastasis N3a 7–15 LN metastasis N3b 16 LN metastasis Dis ta nt m e ta s ta s is (M) M0 No distant metastasis M1 Distant metastasis

Stage 0

Tis

N0

M0

Stage IA Stage IB

T1 T2 T1

N0 N0 N1

M0 M0 M0

Stage IIA

T3 T2 T1 T4a T3 T2 T1

N0 N1 N2 N0 N1 N2 N3

M0 M0 M0 M0 M0 M0 M0

T4b T3 T2 T4b T4b T4a T3 T4b T4b T4a

N1 N2 N3 N0 N1 N2 N3 N2 N3 N3

M0 M0 M0 M0 M0 M0 M0 M0 M0 M0

Any T

Any N

M1

Stage IIB

Stage IIIA

Stage IIIB

Stage IIIC

Stage IV

TNM, tumor-node-metastasis; GEJ , gastroesophageal junction; LN, lymph node. Used with permission rom American J oint Committee on Cancer. Exocrine and endocrine pancreas. In: Edge SB, Byrd DR, Compton CC, et al, eds. AJ CC Cancer Staging Manual, 7th ed. New York: Springer; 2010.

3. Locally advanced disease (T2 or with regional lymph node metastasis): should be managed by multidisciplinary approach with possible neoadjuvant chemotherapy or chemoradiation therapy 4. Metastatic disease: should be o ered palliative chemotherapy B. Surgical resection with curative intent 1. Subtotal or total gastrectomy: depending on tumor location 2. Wide margins ( 5 cm on the stomach): Necessary because extensive submucosal tumor spread can occur. Lesions o the undus and cardia may require resection o the spleen, pancreas, or transverse colon to completely remove the cancer. 3. Lymphadenectomy: Extent is controversial. Removal o the omentum and its nodes is included. Radical lymphadenectomy that includes distant nodal basins has not been shown to improve survival and may increase morbidity. C. Palliative resections: Indicated in the presence o obstructing or bleeding gastric cancers. reatment may include resection, bypass alone, or either one in conjunction with adjuvant therapies. D. Adjuvant chemotherapy (5- uorouracil/leucovorin or taxane and radiation therapy): a er potentially curative resection improves median survival and is the current standard o care VII. P ro g no s is : depends largely on the depth o invasion o the gastric wall, involvement o regional nodes, and presence o distant metastases but still remains poor A. Survival: decreases dramatically i the tumor is through the serosa or into regional nodes B. Recurrence rates af er gastric resection: high, ranging rom 40% to 80%

Ga s tric Lym p ho m a I. Etio lo g y: T e stomach is the most common site o primary intestinal lymphoma; however, gastric lymphoma is relatively uncommon. Patients at risk or developing lymphomas are those who are immunocompromised or have an H. pylori in ection.

Quic k Cut Overall 5-year s urvival a ter the diagnos is o gas tric cancer is 10% –20% .

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II. Dia g no s is : Endoscopy with biopsy and endoscopic ultrasound or staging. As with all lymphomas, assessment o distant disease should include bone marrow biopsy; C o chest, abdomen, and pelvis; and an upper airway exam. H. pylori testing should be done. III. Tre a tm e nt A. Medical treatment: Combining chemotherapy and radiation is now the most accepted therapy. Quic k Cut 1. Chemotherapy: Most common combination is MALT lymphoma cyclophosphamide, hydroxydaunomycin, vincristine, and is currently the only cancer prednisone (CHOP). that is e ectively treated with 2. Mucosa-associated lymphoid tissue (MALT) lymphoma: antibiotics . treated e ectively by the eradication o H. pylori in ection alone B. Surgical treatment: reserved or residual disease or complications

Ga s tric Sa rc o m a s I. Etio lo g y: arise rom the mesenchymal cells o the gastric wall and constitute 3% o all gastric cancers II. GISTs : Most common; arise rom mesenchymal cells o the gastrointestinal (GI) tract, usually the pacemaker cell o Cajal. GIS s are ound predominately in the stomach. III. His to lo g ic d ia g no s is : conf rmed by immunohistochemical staining or CD 117, a cell sur ace antigen IV. P re s e nta tio n: varies rom incidental f ndings to symptomatic large tumors causing obstruction, pain, bleeding, or metastases V. Tre a tm e nt: complete surgical removal with negative margins; no need or lymph node dissection A. Clinical behavior and malignant potential: based on several actors, including mitotic count greater than 5 per 50 high-power f elds; size greater than 5 cm; and cellular atypia, necrosis, or local invasion B. Tumor recurrence or unresectable disease: Can be treated by imatinib mesylate, which inhibits the c-KIT gene–associated tyrosine kinase receptor responsible or tumor growth. Patients with tumors with high malignant potential are o ered adjuvant imatinib therapy.

P OSTGASTRECTOMY SYNDROMES Alka line Re ux Ga s tritis I. II. III. IV.

Etio lo g y: most common problem postgastrectomy, occurring in 25% o all patients Sym p to m s : postprandial epigastric pain, nausea, vomiting, and weight loss Dia g no s is : endoscopy demonstrates the gastritis and a ree re ux o bile Tre a tm e nt: conversion o the Billroth I or II gastrectomy (see Fig. 10-3A,B) to a Roux-en-Y anastomosis (see Fig. 10-3C)

A e re nt Lo o p Synd ro m e I. Etio lo g y: caused by intermittent mechanical obstruction o the a erent loop o a gastrojejunostomy II. Sym p to m s : include early postprandial distention, pain, and nausea, which are relieved by vomiting o bilious material not mixed with ood III. Tre a tm e nt: Provide good drainage o the a erent loop, usually by conversion to a Roux-en-Y anastomosis.

Dum p ing Synd ro m e

Quic k Cut

Dumping s yndromes I. Etio lo g y: A ects most postgastrectomy patients but is a signif cant are caus ed by rapid emptying problem in only a ew. It exists in either an early or late orm with o nutrients into the s mall the early orm being more common. bowel. A. Early dumping syndrome: occurs within 20–30 minutes ollowing ingestion o a meal 1. Characteristics: More common a er partial gastrectomy with Billroth II reconstruction. It results rom the rapid movement o a hypertonic ood bolus into the small intestine. 2. Symptoms: Rapid uid shi s into the small bowel cause distention and a subsequent autonomic response along with the release o several humoral agents responsible or GI symptoms such as nausea, bloating, abdominal cramps, and explosive diarrhea.

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171

B. Late dumping syndrome: Occurs 2–3 hours a er a meal and is Quic k Cut ar less common, causing mostly vasomotor symptoms. T e large Thes e s ymptom carbohydrate load passed into the small intestine causes on overcomplexes can be dis abling— release o insulin resulting in pro ound hypoglycemia. the tendency to pas s out when attempting to inges t II. Tre a tm e nt meals can change every A. Conservative nonsurgical measures: Change o dietary habits as pect o eating habits . control symptoms in the majority o cases. Patients are advised to avoid a high-carbohydrate diet and not to drink uids with meals. Octreotide may be used to control symptoms. B. Surgical treatment: I conservative management ails, surgery aims to delay gastric emptying, including interposition o an antiperistaltic jejunal loop between the stomach and small bowel or conversion to a long limb Roux-en-Y reconstruction.

P o s tva g o to m y Dia rrhe a I. Cha ra c te ris tic s : common in its mild orm but seldom is a disabling problem II. Sym p to m s : usually improve during the f rst year a er surgery

BENIGN STOMACH LESIONS Ga s tric P o lyp s

Quic k Cut

Gas tric polyps are I. Hyp e rp la s tic p o lyp s : Most common gastric polyp and arise us ually ound incidentally. most o en in the setting o chronic atrophic gastritis. T ey are nonThey can typically be excis ed neoplastic, and treatment consists o polypectomy. via endos copy. II. Ad e no m a to us p o lyp s : Associated with a 20% risk o malignancy, especially i greater than 1.5 cm. reatment consists o endoscopic polypectomy. Surgery is required or evidence o invasion on polypectomy specimen, or sessile lesions more than 2 cm, and or polyps with symptoms o bleeding or pain.

Die ula o y Ga s tric Le s io n I. Etio lo g y: an abnormally large tortuous artery located in the submucosa II. Cla s s ic p re s e nta tio n: sudden onset o massive upper GI bleeding with associated hypotension III. Tre a tm e nt: Endoscopy is both diagnostic and therapeutic; surgery is rarely needed.

Be zo a rs I. De f nitio n: agglutinated masses o hair (trichobezoars occur most commonly in young, neurotic women), vegetable matter Quic k Cut (phytobezoars), or a combination o the two orms within the Bezoars are stomach collections o material that II. Sym p to m s : include nausea, vomiting, weight loss, and abdominal remain in the s tomach. pain III. Co m p lic a tio ns : include obstruction and ulceration IV. Tre a tm e nt: generally requires endoscopic or surgical removal, although enzymatic dissolution o some bezoars has been success ul

GASTRITIS Unc o m p lic a te d Ac ute Ga s tritis I. Etio lo g y: Likely due to a number o irritating agents, particularly aspirin and ethanol. Hemorrhage can occur and be massive. II. Tre a tm e nt: Removal o the inciting agent and antacid therapy usually result in prompt healing.

Stre s s Ulc e ra tio n I. Etio lo g y: Ischemia o the gastric mucosa is the inciting event. T e injury is compounded by the e ect o the intraluminal acid. Although stress ulceration is common in critically ill patients, only 5% develop signif cant gastric bleeding.

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II. Lo c a tio n: Characteristically shallow mucosal lesions start in the undus. T ey then spread distally and can involve the entire stomach. III. Clinic a l p re s e nta tio n: A ected patients requently have sepsis, Quic k Cut multiple organ system ailure, severe trauma, a complicated Stres s ulceration postoperative course or are on assisted ventilation. is common in critically ill A. Curling ulcer: stress ulceration that occurs in burn patients patients . B. Cushing ulcer: stress ulceration occurring in patients with head injury IV. Tre a tm e nt A. Prophylaxis: Antacids given as needed to keep the gastric pH greater than 5. H2-receptor antagonists and PPIs are equally e ective at maintaining an adequate gastric pH. B. Medical treatment: Correcting the underlying problems (e.g., sepsis) and vigorous use o antacids. Cimetidine is not help ul once bleeding has occurred. C. Surgical treatment: Rarely necessary and associated with a high mortality. In the case o uncontrollable bleeding, near total gastrectomy is usually the best option. D. Radiographic embolization: done to identi y and control the main artery bleeding

Chapter 11

Small Intestine Katherine G. Lamond

INTRODUCTION Ana to m y I. Struc ture : T e small intestine extends rom the pylorus to the cecum (Fig. 11-1). A. Duodenum: most proximal portion, which extends rom the pylorus to the ligament o reitz B. Jejunum: begins just beyond the ligament o reitz C. Ileum: most distal portion o the small bowel D. T e duodenum is considered retroperitoneal, whereas the jejunum and ileum are intraperitoneal. E. Length: otal 3 m; the duodenum measures 30 cm, the jejunum is 110 cm, and the ileum is 160 cm. II. Va s c ula ture : Arterial supply to the small intestine stems primarily rom the superior mesenteric artery (SMA), which branches into the jejunal and ileal arteries. T e duodenum is also supplied by branches o the celiac axis. A. Jejunal mesenteric arteries: have only one or two arcades with long vasa recta (small arteries directly adjacent to the bowel wall) B. Ileal arteries: have multiple arcades that extend closer to the bowel with short vasa recta

Duode noje juna l junction Duode num

LUQ RLQ Ile oce ca l junction Ce cum Appe ndix

Parts of small intestine Duode num J e junum Ile um

Anterior view

Fig ure 11-1: J ejunum and ileum. LUQ, le t upper quadrant; RLQ, right lower quadrant. (From Moore KL, Agur AMR, Dalley AF. Clinically Oriented Anatomy, 7th ed. Baltimore: Lippincott Williams & Wilkins ; 2013.)

173

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Introduction

III. Sm a ll inte s tine wa ll la ye rs ( o ur): as shown in Figure 11-2 A. Mucosa: Consists mostly o absorptive columnar epithelium and mucus-producing goblet cells. Nutrient absorption takes place via epithelial cells. 1. Villi: have a sur ace area o 500 m 2 Quic k Cut 2. Mucosal cells: proli erate rapidly with a li e span o 5 days The s ubmucos a B. Submucosa: strongest layer; contains nerves, Meissner plexus, blood is the layer that provides vessels, lymphoid tissue (Peyer patches), and f brous and elastic tissue s trength in intes tinal C. Muscularis: consists o two muscle layers with the Auerbach anas tomos is . plexus sandwiched in between 1. Outer layer: runs longitudinally along bowel length 2. Inner layer: circular D. Serosa: outermost layer and derived embryologically rom the peritoneum IV. Inte rna l s truc ture A. Plicae circulares: T ese spiral olds o mucosa and submucosa are more prominent proximally; they may help delineate the small bowel on a plain x-ray. B. Jejunum: larger in diameter, thicker walled, and has more prominent plicae circulares and less mesenteric at than the ileum C. Peyer patches (or lymphoid tissue): more prominent distally in the ileum

P hys io lo g y I. Func tio n: T e primary unctions o the small intestine are digestion and absorption. Food, uid, and secretions rom the stomach, liver, and pancreas reach the small intestine. T e total volume may reach 9 L/day, and all except 1–2 L will be absorbed. II. Mo tility A. wo types o contractions occur a er a meal. 1. o-and- ro motion: mixes chyme with digestive juices, which prolongs exposure to the absorptive mucosa 2. Peristalsis: moves all intestinal contents distally Villus

Mucos a S ubmucos a S e ros a Longitudina l mus cle Circula r mus cle Circula r mus cle Longitudina l mus cle S ubmucos a l ple xus

Figure 11-2: Vasculature o the small intestine. (From Rhoades RA, Bell DR. Medical Physiology: Principles for Clinical Medicine, 4th ed. Baltimore: Lippincott Williams & Wilkins; 2012.)

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B. Migrating motor complex (MMC): When asting, strong Quic k Cut contractions occur in the duodenum every 2 hours to empty Mo tilin is the gut residual ood. hormone involved with the C. Parasympathetic stimulation promotes contractions and MMC. digestion, whereas sympathetic stimulation is inhibitory. III. Ab s o rp tio n: Vitamins, at, protein, carbohydrates, water, and electrolytes are all absorbed in the small intestine. A. Water:Absorbed by passive absorption and osmosis throughout the small intestine: Jejunum ileum duodenum. B. Electrolytes 1. Potassium: absorbed by passive di usion through intercellular pores in the jejunum 2. Sodium: absorbed and actively transported, whereas chloride ollows passively 3. Calcium: actively transported in the jejunum and enhanced by vitamin D and parathyroid hormone 4. Iron: mainly absorbed in the duodenum and enhanced by an acid environment a. T e erric orm (Fe3 ) must be reduced into the errous ion Fe2 . b. Vitamin C (ascorbic acid) can assist with the active transport o iron. C. Fat: Absorption occurs mainly in the jejunum. 1. Pancreatic lipase: digests at, which becomes emulsif ed in bile salt micelles 2. Micelles: release atty acids and monoglycerides to the epithelial cells 3. Epithelial cells: A er absorption, these cells resynthesize triglycerides, which are assembled into chylomicrons and transported directly to the lymphatics. 4. All other nutrients are transported directly into the portal venous system. D. Carbohydrates: digested by salivary and pancreatic amylase 1. Enzymes o the mucosal cell sur ace urther reduce sugars to the monosaccharides. 2. Galactose and glucose: absorbed by active transport 3. Fructose: absorbed by dif usion E. Protein 1. Pepsin: Digestion begins in the stomach with this enzyme and continues in the small bowel by pancreatic proteases. 2. Brush border: Digestion is completed here, yielding tripeptides, dipeptides, and amino acids; all are absorbed by active transport. F. Fat-soluble vitamins: A, D, E, and K are absorbed rom micelles by the mucosa. G. Vitamin B12 (or cobalamin): complexed with intrinsic actor and absorbed in the terminal ileum H. Vitamin C, thiamine, and olic acid: Actively transported; the remaining water-soluble vitamins are absorbed by passive di usion.

DISEASES Sm a ll Bo we l Ob s truc tio n

Quic k Cut I. Ca us e s Adhes ions are the A. Adhesions (scar tissue): cause obstruction through mechanical principal caus e o s mall bowel kinking obs truction (SBO) in the B. Hernias (including ventral, incisional, umbilical, and direct United States . and indirect inguinal): Femoral hernias are particularly prone to incarceration and bowel necrosis. C. Malignancy: adenocarcinoma or lymphoma D. Less likely causes: gallstone ileus (obstruction o the terminal ileum by a gallstone), Crohn disease (see Crohn Disease), intussusception, and volvulus II. Sym ptom s : crampy abdominal pain, nausea, vomiting, and distention; may lack atus or bowel movements III. Dia g no s is A. History and physical: Focused evaluation must include a surgical history, and physical exam must rule out hernias. B. Radiology: Abdominal x-rays show dilated loops o small bowel on supine f lms and air- uid levels on upright f lms (Fig. 11-3). Small bowel ollow-through or computed tomography (C ) scan can also be used to f nd the obstruction or determine the nature o the lesion.

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Fig ure 11-3: Small bowel obs truction, plain f lm. (From Da ner RH. Clinical Radiology: The Essentials, 3rd ed. Philadelphia: Lippincott Williams & Wilkins ; 2007.)

IV. Tre a tm e nt: resuscitation with intravenous (IV) uids, nasogastric tube decompression, and urinary catheter placement to monitor urine output A. Abdominal exploration: per ormed in patients with peritoneal signs, leukocytosis, ever, hypotension, acidosis, a hernia or ailure o resolution o obstructive symptoms B. Partial SBO: may be treated with the a orementioned therapies and monitoring, and may not require surgery unless it progresses to complete SBO C. Complete bowel obstruction: more likely to require operative intervention. Evidence o a closed loop obstruction, or vascular compromise and impending per oration, demands immediate operation.

Tum o rs

Quic k Cut I a patient with bowel obs truction does not have hypotens ion, ever, acidos is , leukocytos is , a hernia or a clos ed loop obs truction, they may be watched with s upportive care or 1-2 days .

Quic k Cut Complete bowel obs truction is more likely to need s urgery in the s ame admis s ion

I. Be nig n ne o p la s m s : usually asymptomatic and rare A. Surgery: indicated or bleeding, obstruction, or intussusception B. Adenomas: rare in small intestine, yet 10 times more common Quic k Cut than malignant tumors (autopsy data) Surgery is indicated 1. Duodenum: most common site or symptomatic benign 2. T ree types: tubular, villous (highest malignancy potential), les ions . and Brunner gland 3. Usually discovered incidentally or as a source o gastrointestinal (GI) bleeding, obstruction, or intussusception 4. reatment: endoscopic or surgical resection B. Hamartomatous polyps: ound in patients with Peutz-Jeghers syndrome (mucocutaneous pigmentation accompanied by widespread intestinal polyposis, with little malignant potential) C. Juvenile (retention) polyps: benign hamartomas and not true neoplasms; more common in the rectum and may autoamputate

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D. Gastrointestinal stromal tumors (GIS ): mesenchymal Quic k Cut neoplasms o the small bowel, ormerly called leiomyomas GISTs are commonly 1. Most commonly benign and present with bleeding, encountered in s urgical obstruction, or intussusception practice. 2. Origin: cells o Cajal, which stain positive or CD 117 on immunohistochemical analysis 3. Ileum: most common site Quic k Cut 4. reatment: wide surgical resection Between 10% and a. Metastases: debulked (i possible) or palliation 30% o GISTs are malignant, b. Imatinib mesylate: yrosine kinase inhibitors may be bas ed on tumor s ize greater than 5 cm, greater than e ective or patients with unresectable or metastatic GIS . 5 mitotic f gures per 50 highE. Other: lipomas, hemangiomas, f bromas, and neurof bromas, power f elds , necros is , and/or which may present with bleeding, obstruction, or abdominal pain the pres ence o metas tas es . II. Ma lig na nt ne o p la s m s A. Overview 1. Incidence: adenocarcinoma (40%), carcinoid (30%), lymphoma (20%), and sarcoma a. Metastases rom other intra-abdominal malignancies are also possible, especially with peritoneal carcinomatosis. b. Metastases rom extra-abdominal malignancies are rare except or malignant melanoma. 2. Symptoms: bleeding, diarrhea, per oration, or obstruction (which may be caused by intussusception) Quic k Cut 3. Diagnosis: commonly made late in the course o disease Malignant because symptoms are o en subtle and insidious in onset tumors cons titute 75% o s ymptomatic s mall bowel 4. Imaging: enteroscope or capsule endoscopy tumors . 5. reatment: segmental resection with adequate margins and mesenteric lymphadenectomy B. Adenocarcinoma: most common in the duodenum and proximal jejunum Quic k Cut 1. Pancreaticoduodenectomy (when located in the f rst and A radical second portions o the duodenum): Unresectable tumors pancreaticoduodenectomy at this location can be palliated by gastrojejunostomy or an is als o called a Whipple intraluminal stent. operation. 2. umors o the distal duodenum and small bowel: wide local bowel resection 3. Metastases to surrounding lymph nodes: o en ound at presentation a. Node-negative disease: Five-year survival may be as high as 80%. b. Node-positive disease: Five-year survival is only 10% as there is no e ective adjuvant therapy. C. Carcinoid tumors: Derived rom enterochroma n cells, which are part o the amine precursor uptake and decarboxylation (APUD) system and secrete various vasoactive amines. Found in Appendix Ileum Rectum. 1. Prognosis and treatment: related to tumor size and the presence o metastases at diagnosis a. Small bowel umors smaller than 1 cm (75%): 2% incidence o metastases b. Small bowel umors larger than 1 cm (20%): 50% rate o metastases c. Small bowel umors larger than 2 cm (5%): 80%–90% rate o metastases 2. Only small bowel carcinoids tend to be multicentric (30%). Early on, they tend to be pedunculated, and may cause intermittent small bowel obstruction 3. Appendiceal carcinoid treatment: these carcinoid tumors have an excellent prognosis. a. umor less than 2 cm at tip o appendix: appendectomy b. umor 2 cm or larger or involving base o appendix: right hemicolectomy 4. Carcinoid syndrome: Serotonin secreted by Kulchitsky cells (enterochroma n cells) causes ushing, diarrhea, and Quic k Cut bronchoconstriction and may progress to tricuspid and Carcinoid s yndrome pulmonary valvular disease. indicates metas tatic dis eas e to the liver. a. Only occurs in patients with liver metastases (10%) because the liver otherwise clears these substances via portal venous drainage

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b. Diagnosis: conf rmed by elevated urinary levels o 5-hydroxyindoleacetic acid (5-HIAA), the breakdown product o serotonin c. reatment: Resection o the primary tumor and metastases. Liver metastases may require palliative therapies, such as alpha blockers ( ushing), octreotide, intra-arterial chemotherapy, or chemoembolization. d. Prognosis: Overall 5-year survival rate is 70%. I liver metastases are present at diagnosis, the 5-year survival rate is 20%. D. Small bowel lymphomas: usually arise in the ileum 1. Non-Hodgkin B-cell lymphomas: most primary lesions 2. Increased incidence: with Crohn and Wegener diseases, systemic lupus erythematosus, AIDS, and celiac sprue 3. Symptoms: abdominal pain, atigue, and weight loss 4. Complications: bowel per oration, hemorrhage, obstruction, and intussusception 5. reatment: Wide local resection, radiation, and chemotherapy. Liver biopsy and distant nodal biopsies are done or accurate staging. 6. Overall 5-year survival rates: 20%–40% E. Leiomyosarcoma: most common o the small bowel sarcomas 1. Di cult to di erentiate rom leiomyoma 2. reatment: resection

Cro hn Dis e a s e I. De f nitio n: also called regional enteritis and granulomatous ileitis; chronic, transmural granulomatous in ammatory disease that can involve any area o the GI tract (mouth to anus) II. Dis trib utio n: T e small bowel alone is involved in 25% o patients, both the small and the large bowel in 50%, and the colon alone in 25%. T e distal ileum is involved in 70% o all cases and may also be called terminal ileitis. III. Dia g no s is Quic k Cut A. Peak age o onset: Between the second and ourth decades, ages An enterocutaneous 15–35 years. Incidence is higher in Ashkenazi Jews. f s tula in an otherwis e healthy B. Symptoms: Abdominal pain, diarrhea (usually not bloody), lethargy, young patient is likely to ever, weight loss, and anorectal disease. Anal f ssures, f stulas, ulcers, s ignal Crohn dis eas e. or perirectal abscesses are seen in 50% o patients with colonic involvement and in 20% o patients with small bowel disease. C. Signs: Abdominal mass, anemia, and malnutrition. Extraintestinal mani estations include in ammatory ocular (uveitis, iritis), joint (arthralgias, arthritis), skin (erythema nodosum, pyoderma gangrenosum), and biliary (primary sclerosing cholangitis) conditions. D. Radiographic f ndings: Contrast study may include areas o stricture separated by “skip areas” o uninvolved bowel (string sign). E. Endoscopic f ndings: “cobblestone” appearance and skip lesions o the mucosa and possible f stulas F. Gross appearance: thickened, shortened mesentery, grayish pink to purple discoloration o the bowel, and creeping at (circum erential growth o mesenteric at around the bowel wall) G. Pathology: mucosal ulceration that progresses to transmural in ammation and noncaseating granulomas in the bowel wall and lymph nodes IV. Di e re ntia l d ia g no s is : ulcerative colitis (limited to colon), lymphoma, and in ectious enteritides (tuberculosis, amebiasis, Yersinia, Campylobacter, Salmonella) V. Me d ic a l tre a tm e nt: Combination o 5-aminosalicyclic acid, sul asalazine, prednisone, antispasmodics, low-residue diet, and intermittent antibiotics may improve symptoms. A. otal parenteral nutrition ( PN): may induce remission and can lead to f stula closure B. In iximab: umor necrosis actor-alpha inhibitor helps enterocutaneous f stulas close and may provide short-term remission. VI. Surg ic a l tre a tm e nt: Reserved or complications but may be necessary in 80% o patients. Goals o surgery are to resect as little bowel as possible; margins o resection need only be to grossly uninvolved bowel. I resection is hazardous, bypass or exclusion o the involved segment may be necessary. A. Surgical indications: obstruction, abscess, megacolon, hemorrhage, f ssures, enterocutaneous f stula B. Intestinal obstruction: Usually caused by stricture and in ammation. Short strictures can be repaired by a stricturoplasty to avoid bowel resection.

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C. Abscesses and f stulas: Common. Abscesses may be intra- or Quic k Cut retroperitoneal. Fistulas may orm rom bowel to skin, bladder, Use antivagina, urethra, or other loops o bowel. in ammatory medicine or the D. Perianal disease: Oral (PO) metronidazole therapy. In general, treatment o Crohn disease surgery should be limited because wound healing is poor. and surgery or the treatment o 1. Perirectal abscesses: require drainage complications o Crohn disease. 2. Anal f stulas and f ssures: may require surgery i severe E. Per oration, hemorrhage, intractable symptoms, cancer, and growth retardation (in children): less common indications or surgery VII. P ro g no s is : 50% o patients who require surgery will require another procedure again within 5 years. VIII. Ca nc e r ris k: somewhat increased risk o small bowel and colon adenocarcinoma associated with the severity and chronicity o in ammation

Dive rtic ula r Dis e a s e I. Duo d e na l d ive rtic ula A. Relatively common (seen on 10%–20% o upper GI radiographs), but most are asymptomatic B. Periampullary diverticula ( 70%): can impair the emptying o bile through the ampulla, resulting in cholangitis, pancreatitis, and common bile duct stones II. J e juno ile a l d ive rtic ula : rare A. May cause obstruction ( rom intussusception), bleeding, or per oration B. May also cause malabsorption rom bacterial overgrowth within the diverticulum III. Me c ke l d ive rtic ulum : most common diverticulum o the GI tract A. T e rule o 2’s: incidence 2%o the population, location Quic k Cut 2 eet rom the ileocecal valve, male/ emale ratio 2:1, age at Remember the rule diagnosis f rst 2 years o li e (i bleeding), and length 2 cm o 2’s or Meckel diverticulum. B. rue diverticula: involves all layers o bowel wall C. Bleeding: Due to heterotopic gastric mucosa in the diverticulum, which causes ulceration in adjacent ileal mucosa. Pancreatic mucosa may also be ound. D. Complications: bowel obstruction ( rom intussusception), bleeding, and acute in ammation, which may be indistinguishable rom appendicitis E. Surgery: I ound incidentally, relative indications or resection include patient age younger than 40 years, diverticulum larger than 2 cm in length, and f brous bands between the diverticulum and the umbilicus or mesentery.

Sho rt Gut Synd ro m e I. De f nitio n: Complication o extensive small bowel resection due to volvulus, vascular accident, or repeated surgical resections. Diagnosis is made based on symptoms, not a specif c bowel length. II. Sym p to m s : diarrhea, steatorrhea, weight loss, and nutritional def ciencies III. Tre a tm e nt A. PN: Small bowel hypertrophy occurs while on PN, and allows Quic k Cut increased PO intake. A PO regimen should include the ollowing: Short gut s yndrome 1. High-calorie, low- at, low-residue, or elemental diet is as s ociated with les s than 2. H 2-receptor blockers or proton pump inhibitors to reduce acid 100 cm o unctional s mall 3. Vitamin supplementation including B12 i the distal ileum is absent bowel. 4. Length: likely need at least 75 cm to survive without o PN or 50 cm o bowel with a competent ileocecal valve B. Surgical therapy (rarely per ormed): Reversal o a short segment o distal small bowel to slow intestinal transit time. Small bowel transplant in extreme cases.

Ra d ia tio n Injury (Two P ha s e s ) I. Ac ute -p ha s e injury: Caused by mucosal injury; symptoms include nausea, vomiting, and diarrhea and are transient. Bleeding or per oration is rare. II. Chro nic injury: caused by obliterative vasculitis, which appears months to years a er exposure A. Minor symptoms: abdominal pain, malabsorption, and diarrhea B. Major complications: Bowel obstruction, per oration, abscess, f stula, and hemorrhage. All o these may require surgery. C. Surgery is technically di cult owing to f brosis and scarring.

Chapter 12

Colon, Rectum, and Anus Julia Terhune and Andrea C. Baf ord

INTRODUCTION Ana to m y I. Co lo n (la rg e inte s tine ): 3–5 f in length and divided into several parts: the cecum, ascending colon, transverse colon, descending colon, and sigmoid colon A. Arterial blood supply, venous drainage, and lymphatic channels: based on embryologic origin 1. Arterial blood supply (Fig. 12-1) a. Superior mesenteric artery (SMA): branches supply midgut structures (cecum, ascending colon, and proximal transverse colon) b. In erior mesenteric artery (IMA): branches supply hindgut Quic k Cut structures (distal transverse, descending, and sigmoid colon) Colonic blood s upply to the midgut (cecum c. Splenic f exure: watershed area susceptible to ischemia to midtrans vers e colon) comes with hypotension and there ore an undesirable location or rom the SMA and to the an anastomosis hindgut (midtrans vers e colon 2. Venous drainage to s igmoid) rom the IMA. a. Superior mesenteric vein: drains the right colon and joins the splenic vein to orm the portal vein b. In erior mesenteric vein: carries blood rom the lef colon to the splenic vein 3. Lymphatic drainage: Lymphatics ollow the arteries.

Middle colic a rte ry

Right colic a rte ry

S upe rior me s e nte ric a rte ry Infe rior me s e nte ric a rte ry Le ft colic a rte ry

Ile ocolic a rte ry Hypoga s tric a rte ry

S upe rior re cta l a rte ry

Middle re cta l a rte ry

Infe rior re cta l a rte ry

180

Fig ure 12-1: Arterial s upply o right (as cending) colon via branches o s uperior mes enteric artery and le t (des cending) colon and rectum via branches o in erior mes enteric artery. Dis tal rectum s upplied by branches rom hypogas tric artery.

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B. Bowel wall Quic k Cut 1. Layers: mucosa, submucosa, muscularis, and visceral Metastases rom peritoneum (serosa) colon cancers generally spread 2. Crypts o Lieberkühn: distinguishing histologic eature o the through lymphatic paths in colonic mucosa; there are no villi progressive ashion with closer 3. enia coli: three distinct bands that orm the outer longitudinal nodes involved f rst. muscle o the colon, which is incomplete 4. Haustra: outpouchings o the colonic wall between the tenia coli II. Re c tum : extends rom the sigmoid colon to the anus and is 15 cm in length A. Arterial blood supply: See Figure 12-1. 1. Superior rectal artery (IMA’s terminal branch): supplies the Quic k Cut upper and middle rectum The rectum’s blood 2. Middle and in erior rectal arteries (branches rom the supply comes rom both the internal iliac artery): supply lower rectum IMA and the internal iliac artery. B. Venous drainage 1. Superior rectal veins: drain the upper and middle rectum, emptying into the portal vein via the in erior mesenteric vein Quic k Cut 2. Middle and in erior rectal veins: drain the lower rectum Becaus e rectal and anal canal via the internal iliacs to the in erior vena cava veins ultimately drain to both 3. Lower rectal and anal cancers: drain to the inguinal and the portal vein and the vena cava through the internal iliac iliac systems. or emoral s ys tems , rectal C. Lymphatic drainage tumors can metas tas ize 1. In erior mesenteric nodes: Filter lymph rom the upper into either the portal or the and middle rectum channels that parallel the arterial s ys temic circulation. supply. 2. Iliac nodes: Filter lymph rom the distal rectum channels adjacent to the middle and in erior rectal arteries. Quic k Cut 3. Inguinal nodes: May be involved in lower rectal and anal The rectum has cancers complete layers o inner D. Bowel wall circular and outer longitudinal mus cle and no tenia coli. 1. In contrast to the colon, complete layers o inner circular and outer longitudinal muscle line the rectum. 2. T e proximal one third o the rectum is covered with peritoneum; the lower one third is extraperitoneal. 3. Valves o Houston: three mucosal olds that project into the rectal lumen III. Anus : erminal portion o the intestinal tract surrounded by the anal sphincters, which regulate continence and de ecation. T e levator ani is palpable as the anorectal ring. A. Epithelial lining 1. Anal margin: normal squamous hair-bearing skin around the anus 2. Anal verge: junction between the anal canal and the perianal skin 3. Anatomic anal canal: Begins at the anal verge and ends at the dentate line. It is lined by anoderm, a modi ed squamous epithelium devoid o skin appendages. 4. Dentate line: located 1–2 cm above the anal verge a. Structures cephalad to the dentate line: endodermal in Quic k Cut origin, supplied by the autonomic nervous system, and Areas cephalad to drained via the systemic circulation the dentate line are ins ens ate. b. Structures below the dentate line: ectodermal in origin, supplied by the somatic nervous system, and drained via the portal circulation 5. ransitional zone (6–12 mm): resides above the dentate line and is where squamous epithelium gradually changes to cuboidal epithelium and then to columnar epithelium B. Columns o Morgagni: longitudinal mucosal olds located just above the dentate line, where they meet to orm the anal crypts C. Anal glands (small): exist beneath the anoderm between the internal and external sphincters and communicate with the anal crypts via anal ducts

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D. Anal canal: surrounded by two muscular sphincters, which provide continence 1. Internal sphincter (continuation o the rectum’s inner circular muscle): smooth muscle with involuntary control and autonomic innervation 2. External sphincter: striated muscle under voluntary control with somatic innervation

P hys io lo g y

Quic k Cut I. Wa te r a nd e le c tro lyte a b s o rp tio n Sodium is actively A. Ileal chyme: T e colon receives 900–1,500 mL each day, o abs orbed in the colon, which all but 100–200 mL is absorbed. whereas water is pas s ively 1. Sodium: actively absorbed across the colonic mucosa abs orbed. 2. Water: absorbed passively, accompanying Na molecules across the mucosa II. Ba c te ria l e rm e nta tio n (o und ig e s te d c a rb o hyd ra te s ): produces short-chain atty acids, which provide energy or the colonic mucosa III. Fe c e s s to ra g e A. Nondigestible waste: stored in the colon until voluntary evacuation occurs B. Bacteria: comprises 90% o the dry weight o eces, each gram containing 1011 to 1012 bacteria, with anaerobes being predominant 1. Bacteroides: anaerobic bacterium; the most common colonic organism 2. Escherichia coli: most common colonic aerobe IV. Co lo nic g a s : Comes rom intraluminal bacterial ermentation and rom swallowed air; ve gases constitute 98%: nitrogen, oxygen, carbon dioxide, hydrogen, and methane.

EVALUATION His to ry

I. Sym p to m s Quic k Cut Hematochezia is A. Change in bowel habits: including incontinence bright red blood per rectum. B. Bleeding: passage o bright red blood (hematochezia) or dark, Melena is dark, tarry s tools . tarry stools (melena) C. Pain: abdominal or anal II. Sig ns A. Rectal discharge: anal or perianal B. Presence o a mass: anal or perianal III. Ca nc e r, c o lo re c ta l p o lyp s , o r inf a m m a to ry b o we l d is e a s e (IBD): personal or amily

P hys ic a l Exa m ina tio n I. P a tie nt c o m p la int d rive n: T e patient with severe anal pain may not be able to tolerate digital or anoscopic examination, and i the cause o pain is not revealed by simple inspection (e.g., ssure or thrombosed hemorrhoid), examination under anesthesia may be necessary. II. Ano re c ta l e xa m ina tio n: usually per ormed with the patient in prone jackkni e or lef lateral position A. Inspection: Skin abnormalities, masses, protrusions, and drainage sites should be noted. B. Palpation: T e perineum, anal canal, and lower rectum should be gently palpated with a gloved, well-lubricated index nger. Sphincter tone, areas o tenderness, and any masses should be noted. C. Anoscopy: best method to evaluate hemorrhoids and other anal canal lesions D. Proctosigmoidoscopy: Rigid proctosigmoidoscope is used to inspect the mucosa or any abnormalities, such as in ammation or tumors.

Ra d io g ra p hic Stud ie s

Quic k Cut

I. Ba rium e ne m a : cost-e ective but cannot reliably detect small Do not us e barium i colonic per oration is tumors or other abnormalities and has been surpassed by computed s us pected. tomography (C ) scans and by exible endoscopy, which permit detection and treatment II. Wa te r-s o lub le c o ntra s t e ne m a : I colonic per oration is suspected, barium enema is contraindicated because extravasation o barium and eces can cause

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severe peritonitis. Water-soluble material is sa er, although quickly diluted, giving these studies lesser diagnostic quality than barium studies. III. CT s c a n: Can demonstrate bowel wall thickening, pericolic in ammation, and/or stulas/abscesses. C scan is also use ul in large bowel obstructions and or detecting metastases in patients with known colorectal cancer (CRC). IV. Ma g ne tic re s o na nc e im a g ing (MRI): o ers little advantage over C scans or colonic disease evaluation but is use ul or assessing anorectal stulas/abscesses and rectal cancer staging V. P o s itro n e m is s io n to m o g ra p hy (P ET): ypically used or staging af er recurrence to detect metastatic disease af er the primary is resected. Occasionally used initially in cases o suspected metastatic disease. VI. De e c o g ra p hy: Dynamic radiologic study used to evaluate de ecation. T e distal colon and rectum are imaged as the patient eliminates barium.

Fle xib le End o s c o p y I. Fle xib le s ig m o id o s c o p y: A 65-cm exible tool examines the distal colon and rectum. II. Co lo no s c o p y A. Enables evaluation o the entire colorectal mucosa in greater than 90% o patients with a 160- or 185-cm exible instrument. Lesions can be biopsied and polyps removed. B. Indications 1. IBD: evaluation and surveillance 2. Di erentiation: between benign conditions (e.g., diverticulitis) and cancer 3. CRC: screening and surveillance 4. Precancerous polyps: detection and removal 5. Gastrointestinal (GI) symptoms: bleeding, abdominal pain, iron de ciency anemia 6. Acute lower GI bleeding: localization and treatments 7. Sigmoid volvulus: reduction

Quic k Cut Flexible endos copy permits a more extens ive evaluation o the bowel than is pos s ible with s hort, rigid ins truments and allows detection o s mall les ions or mucos al irregularities .

Quic k Cut Flexible s igmoidos copy evaluates the dis tal colon and rectum, whereas colonos copy evaluates the entire colon and rectum.

Fe c a l Oc c ult Blo o d I. De te rm ina tio n A. Stool is placed on guaiac-impregnated paper. I hemoglobin is present, a blue color appears when a peroxide-containing developer is added. B. A daily GI blood loss o 20 mL produces a positive result. II. Fa ls e -p o s itive s : Some oods (red meat, radishes, tomatoes) and medications (aspirin, nonsteroidal anti-in ammatory drugs [NSAIDs]) may cause alse-positive results. III. Fa ls e -ne g a tive s : Others (e.g., vitamin C [ascorbic acid]) can produce alse-negatives.

Quic k Cut A pos itive ecal occult blood tes t requires inves tigation to determine the caus e.

P hys io lo g ic Stud ie s I. Ano re c ta l m a no m e try: describes anal sphincter unction in the workup o ecal incontinence and constipation. It can also detect the rectoanal inhibitory ref ex, which is absent in Hirschsprung disease. II. Ele c tro m yo g ra p hy (p ud e nd a l ne rve c o nd uc tio n ve lo c ity): demonstrates injury to the pudendal nerves that supply the anal sphincter

End o re c ta l Ultra s o und I. Re c ta l c a nc e r: shows depth o invasion into the bowel wall and adjacent lymph nodes II. Ana l s p hinc te r injury: reveals site in the incontinent patient III. Co m p lic a te d a na l s tula s : shows their paths

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Benign and Malignant Colorectal umors

BOWEL P REPARATION Die t, P urg a tive s , a nd Ene m a s

Quic k Cut A mechanical bowel preparation is required or barium enema and colonos copy. Although the role o bowel preparation prior to s urgery is controvers ial (i.e., it has not been cons is tently s hown to reduce in ectious complications ), it is s till us ed more o ten than not be ore elective colectomy.

I. Die t: Clear liquids or 24 hours be ore the procedure II. P urg a tive s A. Cathartics or laxatives: used to purge the large intestine o stool B. Mannitol, castor oil, and bisacodyl tablets: largely abandoned due to complications and poor patient tolerance C. Polyethylene glycol (PEG): isotonic lavage solution that acts as an osmotic purgative; 4 L, ingested within 4 hours, is recommended or adequate cleansing D. Sodium phosphate solution: previously avored over PEG due to the smaller volume needed 1. Concern over an association with kidney damage has reduced its usage. 2. aking the two doses at least 6 hours apart minimizes this risk. III. Ene m a s : cleanse the distal colon and rectum; made up o saline, sodium phosphate solution, or soap suds

Antib io tic s I. Ne o m yc in a nd e rythro m yc in b a s e (typ ic a l re g im e n): Oral antibiotics are sometimes given the day be ore surgery to reduce the bacterial count in the large intestines. II. Bro a d -s p e c trum intra ve no us (IV) a ntib io tic : administered within 60 minutes o the start o most colorectal procedures

BENIGN AND MALIGNANT COLORECTAL TUMORS P o lyp s

Quic k Cut Prophylactic antibiotics s hould not be continued beyond 24 hours .

Quic k Cut Pedunculated polyps are on s talks (“peduncles ”), whereas sessile polyps are at.

I. De nitio n: any abnormal projection rom the sur ace o the intestinal mucosa A. Pedunculated polyps: attached to the bowel wall by a stalk B. Sessile polyps: at growths II. Be nig n p o lyp s A. Hyperplastic polyps (most common): Small (90% are 3 mm) lesions o thickened mucosa without cellular atypia. T ey are not premalignant but are of en removed in order to rule out adenomatous changes. B. Hamartomatous polyps: Non-neoplastic growths that consist o an abnormal mixture o normal tissue. Juvenile polyps are rare hamartomas that occur more requently in children and may cause GI bleeding or intussusception. C. Inf ammatory polyps: non-neoplastic growths resulting rom tissue reaction to in ammation, such as pseudopolyps in ulcerative colitis and benign lymphoid polyps III. Ne o p la s tic p o lyp s A. Adenomatous polyps (three types): precancerous neoplasms o the colonic mucosa without invasion beyond the basement membrane 1. ubular adenomas (75%–85%): branched glands of en on a stalk 2. Villous adenomas (5%–10%): long, rondlike projections 3. ubulovillous adenomas (10%–25%): elements o both tubular and villous adenomas B. Adenoma–carcinoma sequence: Evidence has shown that adenomatous polyps can progress rom benign neoplasia to malignancy. 1. Synchronous adenomatous polyps: seen in CRC patients 2. Histopathology: shows10-year transition rom adenoma to carcinoma Quic k Cut a. Peak incidence (discovery): age 50 years Polypectomy reduces the ris k o CRC. b. Peak incidence (cancer development): age 60 years C. Familial adenomatous polyposis (FAP): progresses to colon cancer i not treated

Chapter 12

D. Molecular genetic studies: show our main genetic alterations in colorectal adenomas and carcinomas (ras mutations and deletions rom chromosomes 5, 17, and 18) E. Malignant potential: More than 95% o CRCs arise rom neoplastic polyps. 1. Size: Risk increases with size ( 1 cm, 1%; 1–2 cm, 10%; 2 cm, 50%). 2. Histology: tubular, 5%; tubulovillous, 20%; villous, 40% 3. Sessile appearance

Colon, Rectum, and Anus

185

Quic k Cut Ris k o malignancy depends on his tology and s ize in increas ing order: tubular, tubulovillous , villous ; les s than 1 cm, 1–2 cm, greater than 2 cm.

IV. Tre a tm e nt: Neoplastic polyps should be removed because o their malignant potential. A. Endoscopic polypectomy: Ideal or pedunculated polyps. A malignant polyp may be treated by endoscopic polypectomy i all o the ollowing characteristics are present. 1. T e polyp is pedunculated. 2. T e cancer is con ned to the head (i.e., does not invade the stalk). 3. Venous and lymphatic channels have not been invaded. 4. T e polyp is moderately or well di erentiated histologically. B. ransanal polypectomy: Rectal polyps may be removed surgically through the anus. C. Segmental colectomy with regional lymphadenectomy: Required or polyps that cannot be excised endoscopically and show positive resection margins and submucosal invasion. Removal o the polyp through a colotomy, or a surgically made opening in the colon, is a historical procedure that has no place in polyp disease Quic k Cut treatment. Peutz-J eghers

P o lyp o s is Synd ro m e s

s yndrome produces hyperpigmented s kin s pots and GI tract hamartomas .

I. P e utz-J e g he rs s ynd ro m e : autosomal dominant disorder characterized by hyperpigmented spots on the lips, buccal mucosa, ace, and digits and hamartomas throughout the GI tract A. Complications: Polyps may cause GI bleeding and intussusception. B. Cancer risk: increased risk o malignancy o the intestine (typically the duodenum, and not at the hamartoma) and other Quic k Cut organs All patients with FAP C. reatment: Symptomatic polyps should be removed, preserving ultimately have a colectomy. as much intestine as possible. Regular endoscopic surveillance is also necessary. II. FAP : Patients develop hundreds o adenomatous polyps as early as puberty and will ultimately develop CRC, usually by age 40 years. A. Genetic transmission: autosomal dominant syndrome with high penetrance 1. Almost all cases are caused by germline mutations o the adenomatous polyposis coli (APC) gene, a tumor suppressor gene on chromosome 5. 2. No amily history o the disease in one third o patients. B. Clinical presentation: Polyps are not present at birth; 50% o patients develop adenomas by age 15 years and 95% by age 35 years. 1. Other complications: Polyps may cause bleeding or, rarely, intussusception. 2. Extraintestinal mani estations: common; include epidermoid cysts, osteomas, abdomen and mesentery desmoid tumors, retinal pigmentation, and periampullary and thyroid carcinoma C. Screening: First-degree relatives should be tested or APC gene mutation and begin annual endoscopic screening at age 10–12 years. D. reatment: I untreated, virtually all patients will develop colon cancer on average at age 34–43 years. 1. otal proctocolectomy with ileostomy: removes all colorectal mucosa, and the patient must wear an appliance 2. Colectomy with ileorectal anastomosis (relative rectal sparing): T e ileum is anastomosed to the rectum. a. Patients are examined by proctoscopy every 6–12 months, and all rectal polyps must be removed. b. Celecoxib (selective cyclooxygenase-2 inhibitor): causes polyp regression in some FAP patients

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3. otal proctocolectomy with ileal pouch–anal anastomosis: removes all colorectal mucosa at risk or cancer without requiring requent proctoscopic examinations a. Complications: Sepsis and impotence are more likely with this procedure. b. Disadvantages: more requent stools and higher incidence o anal incontinence and nocturnal seepage III. Ga rd ne r s ynd ro m e : FAP with osteomatosis, epidermoid cysts, and skin bromas IV. Turc o t s ynd ro m e : FAP with central nervous system malignancies

Co lo re c ta l Ca rc ino m a

I. Inc id e nc e : CRC is the most common malignancy o the GI tract Quic k Cut and the second most common nonskin cancer in men and women. CRC is the third mos t lethal cancer in men and A. Women: third most lethal cancer af er lung and breast women. B. Men: third most lethal cancer af er lung and prostate C. Americans have an 5% probability o developing CRC. D. Incidence rises with age: Most cancers are detected af er age 50 years.

II. Site : Incidence o cancers in the right colon as compared to the lef has increased; there ore, screening should be o the entire colon and not just the rectosigmoid. III. Etio lo g y: A number o actors are considered important in CRC development. A. Polyp–cancer sequence B. IBD 1. Ulcerative colitis (UC): causes increased CRC risk, 18% at 30 years af er pancolitis onset 2. Crohn colitis: causes increased CRC risk, but the degree is not well de ned C. Genetics: increased incidence in rst-degree relatives o CRC patients, especially with age less than 50 years at diagnosis 1. FAP 2. Hereditary nonpolyposis colorectal carcinoma (HNPCC): Quic k Cut most common hereditary CRC syndrome and accounts or HNPCC is the mos t 3%–5% o all CRC common inherited CRC s yndrome, caus ed by DNA a. Characteristics mis match repair gene. (1) Autosomal dominant inheritance (2) Proximal colon cancers predominate. (3) Increased risk o both synchronous and metachronous colon cancers (4) Early age o onset (average age is 44 years) (5) Increased incidence o mucinous or poorly di erentiated carcinomas (6) Improved survival stage or stage compared with those who have sporadic tumors b. Extracolonic malignancies: increased incidence o endometrium, ovary, breast, stomach, hematopoietic, small bowel, and skin cancers c. DNA mismatch repair gene mutation: Mismatch repair genes include hMSH2, hMLH1, hPMS1, hPMS2, and hMSH6. Alterations in these genes lead to microsatellite instability (MSI). d. Clinical diagnosis: based on the Amsterdam criteria (1) T ree or more relatives with CRC, spanning two Quic k Cut generations, one o whom is a rst-degree relative Colonos copy is (2) One or more CRC cases diagnosed be ore age 50 years necessary a ter resection to e. Screening recommendations: Individuals should undergo assess or a second primary colonoscopy every 1–2 years beginning at age 20 years and (which occurs 5% o the time). yearly past the age 35–40 years or 10 years younger than the age at which the relative was diagnosed. D. CRC risk actors 1. Family CRC history: With a rst-degree relative who has had CRC, the risk or developing CRC is three to nine times Quic k Cut that o the general population. Previous his tory 2. Race: A rican Americans have a higher risk than do people o o cancer or polyps , even i other races. adequately treated, increas e 3. Personal CRC or polyp history: Even i adequately treated, CRC ris k. they increase the likelihood o developing new cancers.

Chapter 12

IV.

V.

VI.

VII.

Colon, Rectum, and Anus

187

4. Personal IBD history Quic k Cut 5. Age: More than 90% o people ound to have CRC are older Increas ed calcium than age 50 years. and vitamin D intake have 6. Diet: High- at (especially rom animal sources), low- ber been s hown to decrease CRC diets may increase CRC risk. incidence. 7. Activity level: Sedentary individuals have a higher risk o developing CRC. 8. Obesity: Risk o dying o CRC is increased in overweight people. 9. Diabetes: increases risk o developing CRC Quic k Cut 10. Alcohol intake and smoking: CRC has been linked to Right-s ided les ions alcohol and tobacco use. are notable or melena Clinic a l p re s e nta tio n: depends on the location, size, and extent o and anemia, whereas le tthe tumor s ided les ions produce a change in bowel habits and A. Right-sided cancers: present with melenic stools, atigue, and hematochezia. iron de ciency anemia B. Le -sided cancers: present as a change in bowel habits, hematochezia, and/or cramping abdominal pain (caused by partial obstruction) P a tie nt e va lua tio n: includes abdominal and rectal examinations and studies A. Digital examination: use ul to assess the location, size, and extent o tumor invasion o the distal rectum 1. Firm lesions suggest carcinoma, whereas sof polyps are likely benign. 2. I a tumor eels xed or “tethered” to the adjacent pararectal tissues, malignant invasion o the bowel wall is likely. B. Rigid proctosigmoidoscopy: determines the distance o a rectal tumor rom the anal verge C. Endorectal ultrasound: provides in ormation concerning the depth o invasion into the bowel wall by a rectal tumor and involvement o lymph nodes D. Colonoscopy (with biopsy o the lesion and inspection o the remaining colon): necessary to con rm the diagnosis and exclude synchronous lesions E. Laboratory studies: include carcinoembryonic antigen (CEA), liver enzymes, and hemoglobin/ hematocrit F. Imaging: C scan is used to evaluate the chest and abdomen or metastases. MRI is used to stage rectal cancers and to evaluate the liver or metastases. Sta g ing : T e American College o Surgeons’ Commission on Cancer has urged adoption o the NM staging system ( ables 12-1 and 12-2), which identi es the depth o tumor invasion ( ), regional lymph node status (N), and the presence o distant metastases (M). Tre a tm e nt: Surgical resection is necessary or most CRC cases. Important aspects o surgery include the ollowing. A. T orough abdominal exploration to search or metastases B. Removing the colon segment containing the tumor with the lymphovascular pedicle, which contains the lymph nodes that drain the cancer C. Anastomosis without tension between segments o bowel with satis actory blood supply D. Rectal cancer operations: require special considerations Quic k Cut Surgical treatment 1. Upper third (10–15 cm above the anus) and middle third o rectal cancer: upper and (5–10 cm above the anus) tumors: can be treated by resection middle third, LAR; lower third, through the abdomen with anastomosis between the lef colon APR or TATA. and the remaining rectum, or low anterior resection (LAR) 2. Lower third lesions: Several options may be considered. a. Resection o the rectum, anus, and anal sphincters (by a combined abdominal and perineal approach): requires construction o a colostomy abdominoperineal resection (APR, also called the Miles procedure). b. Resection o the rectum with coloanal anastomosis: May require distal rectal mobilization and anastomosis via a transanal approach (transabdominal, transanal or A A resection). A temporary diverting ileostomy allows the anastomosis to heal without the risk o sepsis rom uncontrolled anastomotic leak.

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Ta b le 12-1: TNM Cla s s i c a tio n o Co lo re c ta l Ca nc e r TNM Cla s s i c a tio n P rim a ry tum o r (T)

Re g io na l lym p h no d e s (N)

Dis ta nt m e ta s ta s is (M)

Ab b re via tio n

De nitio n

TX

Primary tumor that cannot be assessed

T0

No evidence o primary tumor

Tis

Carcinoma in situ

T1

Tumor that invades submucosa

T2

Tumor that invades muscularis propria

T3

Tumor that invades the muscularis propria into the subserosa or into nonperitonealized pericolic or perirectal tissues

T4

Tumor that per orates the visceral peritoneum (a) or directly invades other organs (b)

NX

Regional lymph nodes that cannot be assessed

N0

No regional lymph node metastasis

N1

Metastasis in one to three pericolic or perirectal lymph nodes

N2

Metastasis in our or more pericolic or perirectal lymph nodes

N3

Metastasis in any node along the course o a named vascular trunk

MX

Presence o distant metastases not able to be assessed

M1

No distant metastases

M2

Distant metastases

TNM, tumor-node-metastasis.

c. Local excision: used or select, very avorable rectal cancers (small [ 3–4 cm], 1N0, moderately or well-di erentiated tumors, without lymphovascular invasion) F. Adjuvant therapy 1. Colon cancer: Chemotherapy, of en as combinations o 5-f uorouracil (5-FU) and leucovorin with oxaliplatin Quic k Cut (FOLFOX) or irinotecan (FOLFIRI), is currently FOLFOX is a recommended or stage II poor prognostic histologic combination o 5-FU, characteristics or III disease patients with inadequate lymph leucovorin, and oxaliplatin. FOLFIRI combines 5-FU, node sampling. leucovorin, and irinotecan. 2. Rectal cancer: Neoadjuvant chemoradiation as well as adjuvant chemotherapy is recommended or stages II and III rectal cancers. Preoperative radiation therapy may shrink tumors and reduce local recurrence. 3. Monoclonal antibodies (e.g., bevacizumab, cetuximab): have shown clinical e cacy in patients with metastatic CRC, both alone and in combination with FOLFOX VIII. P ro g no s is : determined by 5-year survival and clearly related to disease stage ( able 12-2) IX. Fo llo w-up Quic k Cut A. Physical examination: seldom reveals early tumor recurrences Ninety percent o CRC recurrences happen in B. Colonoscopy: Done 1 year af er surgery to assess or local the f rs t 2 years . recurrence and to detect any new polyps. Af er a negative colonoscopy, the examination should be repeated every 3–5 years to detect any new polyps.

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Colon, Rectum, and Anus

189

Ta b le 12-2: Sta g e a nd P ro g no s is o Co lo re c ta l Ca nc e r Sta g e

Duke s Cla s s i c a tio n

T Le ve l

N Le ve l

M Le ve l

Cure Ra te

0

—

Tis

N0

M0

100%

I

A

T1 or T2

N0

M0

90%

II

B

T3 or T4

N0

M0

80%

III

C

Any T

N1, N2, or N3

M0

60%

IV

D

Any T

Any N

M1

5%

T, tumor; N, regional lymph nodes; M, distant metastases.

C. CEA: most sensitive indicator o recurrent CRC the incidence o a second CRC occurring af er the rst is as high as 5%, with most occurring within ve years 1. CEA may also be elevated in patients with cirrhosis, pancreatitis, renal ailure, UC, and other types o cancer and can also be in uenced by smoking. 2. Most surgeons recommend obtaining CEA levels every 3 months during the rst 2 postoperative years, every 6 months during the third to f h postoperative years, and annually thereaf er. 3. Rising CEA level: indication or urther workup (of en a PE scan) D. Early recurrence detection: could improve survival 1. Isolated hepatic metastases: may be resected with a 25% 5-year survival 2. Solitary pulmonary metastases: may be resected with a 20% 5-year survival E. Chemotherapy and radiation therapy: palliative or recurrent nonresectable CRC

Ca rc ino id Tum o rs I. Etio lo g y: Arise rom neuroectodermal cells and have the ability to incorporate and store amine precursor (5-hydroxytryptophan) and to decarboxylate this substrate, which produces several biologically active amines (e.g., amine precursor uptake and decarboxylation [APUD] tumors). he GI tract is the most common site, and (in decreasing order o requency) carcinoids arise in the appendix, ileum, rectum, stomach, and colon. he tumors are usually small, submucosal nodules. II. Co lo n c a rc ino id s : account or less than 2% o GI carcinoids; they may be multicentric, and they may cause carcinoid syndrome rom liver metastases III. Re c ta l c a rc ino id s : account or cause carcinoid syndrome

15% o GI carcinoids; they are usually solitary, and they do not

IV. Tre a tm e nt: related to tumor size A. umors 2 cm: seldom metastasize and can be locally excised B. umors 2 cm: usually malignant and should be treated by radical resection

DIVERTICULAR DISEASE Te rm ino lo g y I. Dive rtic ulum : abnormal sac or pouch protruding rom the wall o a hollow organ A. rue diverticulum: diverticulum composed o all layers o bowel wall (rare in the colon) B. False diverticulum: diverticulum lacking a portion o the bowel wall (common in the colon) II. Dive rtic ulo s is : presence o diverticula III. Dive rtic ulitis : in ammation associated with diverticula

Quic k Cut Dive rtic ulo s is is the pres ence o diverticula; d ive rtic ulitis is in ammation o diverticula.

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Diverticular Disease

Dive rtic ulo s is I. Etio lo g y: unclear II. Ep id e m io lo g y: Incidence o this acquired disorder increases with age. A. Common in Western societies and rare in unindustrialized nations B. Populations who eat high- ber, low-sugar oods (e.g., sub-Saharan A ricans) have a low incidence o diverticulosis. C. Rare in persons younger than age 30 years D. Present in 75% o people older than age 80 years III. P a tho g e ne s is : herniations o mucosa through the colonic wall A. Diverticula occur at sites where arterioles traverse the wall. B. T ey usually lack a muscular layer (i.e., they are alse diverticula).

Quic k Cut

Colonic diverticula are typically false diverticula.

IV. Sig m o id c o lo n: most common site or diverticula; it is rare or diverticula to occur in the rectum V. Inc re a s e d intra lum ina l p re s s ure (in the c o lo n): thought to be associated with a low- ber diet and has been proposed as the cause o mucosal herniation A. Segmentation (o isolated areas o colon): can produce high pressures B. Highest pressure across the colon wall occurs in the sigmoid colon, which is the region where diverticulosis occurs VI. Mus c ula r hyp e rtro p hy (o the c o lo n wa ll): of en accompanies diverticula and is especially common in the involved sigmoid colon

Dive rtic ulitis I. P e ric o lic in e c tio n: Per oration o one or more diverticula causes extravasation o colonic bacteria, leading to a wide spectrum o disease. A. Pericolic phlegmon: localized in ammation B. Intra-abdominal abscess C. Generalized purulent peritonitis: rom ruptured abscess D. Feculent peritonitis: persistent ecal leakage rom the per oration E. Fistula ormation: including stulas rom the colon to the bladder, vagina, skin, and other sites II. Clinic a l p re s e nta tio n: variable, depends on per oration site and in ection extent A. Le lower quadrant (LLQ) abdominal pain: most common symptom and may radiate to the suprapubic area, groin, or back Quic k Cut B. Abdominal or pelvic mass: may be caused by a phlegmon or abscess LLQ pain is mos t C. Fever and leukocytosis: common common s ymptom o D. Associated ileus: may cause small bowel distention and vomiting diverticulitis . E. Generalized peritonitis: may be present in severe cases F. Colovesical stula: may cause pneumaturia, dysuria, pyuria, or ecaluria or may lead to vaginal drainage o pus or stool III. Initia l e va lua tio n: C scan o the abdomen and pelvis is the most help ul test to con rm the suspected diagnosis and/or extent o diverticulitis. A. IV contrast: given be ore the C scan to simultaneously evaluate the kidneys and ureters, making intravenous pyelography (IVP) unnecessary B. C -guided percutaneous drainage: to drain an abscess C. Air in the bladder: suggests a colovesical stula D. Contrast enema: Avoided i diverticulitis is suspected; hydrostatic pressure can worsen the extravasation o contrast and eces through the per oration. E. Leukocyte count: Obtain initially as a baseline and serially to evaluate the response to treatment. F. Frequent abdominal examinations: determine disease activity IV. Sub s e q ue nt e va lua tio n: Colonoscopy is indicated to exclude cancer as the cause o the per oration. A. Barium enema: less use ul than colonoscopy because small tumors may be masked by diverticula B. Cystoscopy: can be per ormed i a colovesical stula is suspected to rule out a bladder cancer

Quic k Cut Colonos copy is per ormed after acute in ammation res olves .

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Colon, Rectum, and Anus

191

V. Tre a tm e nt: depends on disease severity, number o previous attacks, presence o complications, and the patient’s overall condition A. Phlegmon o the sigmoid colon: Initial treatment includes IV uids, bowel rest (with nasogastric tube decompression i ileus is present), and broad-spectrum IV antibiotics. B. Intra-abdominal abscess: reatment is as above plus C -guided percutaneous abscess drainage. 1. Immediate surgery or acute diverticulitis with abscess carries an increased likelihood o complications and need or colostomy. 2. I the abscess can be success ully drained, the patient usually recovers su ciently to permit an elective single-stage sigmoidectomy with colorectal anastomosis. C. Purulent or eculent peritonitis: includes IV uids, nothing orally, broad-spectrum IV antibiotics, and urgent surgical resection 1. Hartmann procedure: resection o the diseased segment o bowel, rectal stump closure, and colostomy creation, as it is not sa e to make an anastomosis in the presence o severe in ection 2. T e colostomy can be taken down and the colon anastomosed to the rectum, when the patient has recovered, usually af er at least 12 weeks . D. Fistulas caused by diverticulitis: same as or uncomplicated diverticulitis plus surgical resection af er the acute in ammation has subsided 1. Sigmoidectomy and primary colorectal anastomosis: usually possible i acute in ammation has resolved 2. T e structure at the other end o the stula is repaired primarily. E. Sigmoidectomy and primary colorectal anastomosis: Can be done a er recurrent attacks o diverticulitis ollowing recovery Quic k Cut rom the acute episode. However, considerable clinical judgment The us ual indication is required to determine indications. or s urgery is a complication 1. Af er one attack, approximately one third o patients will have o diverticulitis (per oration a second attack, af er which another one third will have a or abs ces s , hemorrhage, or s tricture). Uncomplicated third episode. diverticulitis may not need to 2. Younger patients: Longer li e span means a higher be res ected. cumulative risk or recurrent diverticulitis; there ore, surgery may be recommended earlier. 3. Elective colon resection: typically advised i an episode o complicated diverticulitis is treated nonoperatively F. Additional surgical considerations: Removing all colon Quic k Cut containing diverticula is unnecessary; remove only the portion In res ections or diverticulitis , the proximal with hypertrophied muscular segment. line o res ection is uninvolved 1. With signi cant pelvic inf ammation: Ureteral catheters bowel; the dis tal line is the may be placed prior to surgery to aid in identi ying a ureteral rectum, which is s a e to us e injury should one occur. becaus e diverticulitis does 2. Anastomosis: In order to avoid recurrence, anastomose at the not involve the rectum. level o the rectum; the distal sigmoid colon almost always has a hypertrophied muscular wall.

He m o rrha g e I. Ano the r m a jo r c o m p lic a tio n o d ive rtic ula r d is e a s e : An arteriole adjacent to a diverticulum may rupture, causing massive bleeding. II. P re s e nta tio n: Abdominal pain is rare; patients usually pass large Quic k Cut amounts o bright red blood via the rectum. Rapid blood loss may Diverticular bleeds result in shock. are typically s ingle epis odes III. Dia g no s tic te s ts : accompany resuscitation o bris k, bright red bleeding. A. Immediate patient stabilization: IV crystalloids and blood products i necessary. A nasogastric tube is inserted to rule out gastroduodenal hemorrhage; anoscopy is done to rule out an anorectal source o bleeding. B. Laboratory studies: baseline complete blood count and coagulation studies C. Nuclear scan (labeled red blood cell scan): done i the patient’s condition permits D. Colonoscopy: Use ul or bleeding localization and treatment. Endoscopic clipping and epinephrine injection are examples o hemostasis techniques.

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In ammatory Bowel Disease

E. Mesenteric arteriogram: used i the nuclear scan or colonoscopy indicates the bleeding site and in patients with brisk bleeding 1. With a known site, the branch can be embolized or vasopressin in used to constrict the mesenteric artery and lower portal pressure. 2. Segmental colectomy: indicated i bleeding persists and angiography or colonoscopy has identi ed the hemorrhage site 3. otal abdominal colectomy with ileostomy: indicated i bleeding persists and the site cannot be detected by arteriography

ANGIODYSP LASIA Ge ne ra l Co ns id e ra tio ns I. Cha ra c te ris tic s : T is acquired vascular lesion is also a major cause o colonic hemorrhage. Other names include angiectasis, arteriovenous mal ormation, and vascular ectasias. A. Site: Lesions occur most commonly in the right colon. B. Incidence: increases in requency with age Quic k Cut 1. Occur rarely in persons younger than 40 years Angiodys plas ias are 2. Lesions are probably present in most people older than more common in patients o 70 years. advanced age than in younger C. Cause: may be the result o chronic, intermittent submucosal patients , and are mos t vein obstruction requent in the cecum. They can caus e mas s ive lower GI D. Hemorrhage tends to be slower than that rom diverticulosis. bleeding. Stools may be melenic or bright red, depending on the rate o hemorrhage. II. Eva lua tio n a nd tre a tm e nt: Similar to that or patients with bleeding diverticulosis. However, angiodysplasias tend to bleed intermittently, in contrast to diverticular bleeds, which tend to be a single episode o massive bleeding. A. Colonoscopy: Some angiodysplastic lesions can be detected as “cherry red spots” on the mucosa and can be eradicated by endoscopic electrocoagulation. B. Segmental colectomy: indicated with persistent or recurrent bleeding that can be isolated to a colonic segment by nuclear scans, arteriography, or colonoscopy C. otal abdominal colectomy with ileostomy: may be required as a li esaving measure i bleeding persists and the site cannot be identi ed

INFLAMMATORY BOWEL DISEASE Ge ne ra l Co ns id e ra tio ns I. P re s e nta tio n: wo major types o IBD can cause colitis, Crohn disease (CD) and UC, and their presentations overlap considerably ( able 12-3). In 15% o cases, neither pathologic nor clinical distinction can be made and is called indeterminate colitis. II. Etio lo g y: remains unknown or both diseases Quic k Cut A. Genetic, environmental, in ectious, and autoimmune Dis tinguis hing mechanisms have been suggested, but a clearly de ned cause has between CD and UC (when not been identi ed. pos s ible) is important B. Both diseases can occur at any age but tend to present in young becaus e the medical and s urgical treatments are adults. III. Se ro lo g ic m a rke rs : can help distinguish between CD and UC

di erent or each.

Ulc e ra tive Co litis I. Inf a m m a tio n: Limited to the mucosa. T e rectum is virtually always involved, with in ammation extending proximally or variable distances. In ammation is continuous. II. Invo lve m e nt: No perianal disease or small bowel involvement exists with UC. III. His to lo g y: Crypt abscesses may be present but not granulomas. Pseudopolyps may be present.

Quic k Cut UC demons trates mucos al in ammation only, not ull-thicknes s in ammation. Perianal or s mall bowel involvement is abs ent.

Chapter 12

Colon, Rectum, and Anus

193

Ta b le 12-3: Inf a m m a to ry Dis e a s e o the Co lo n Cha ra c te ris tic s

Ulc e ra tive Co litis

Cro hn Co litis

Us ua l lo c a tio n

Rectum, le t colon

Any segment o colon; ileocolic disease most common

Re c ta l b le e d ing

Common, continuous

Less common, intermittent

Re c ta l invo lve m e nt

Almost always

Fis tula

Rare

Common

Ulc e rs

Shaggy, irregular, continuous distribution

Linear with transverse f ssures (“cobblestone”)

Bo we l s tric ture

Rare; should raise suspicion o cancer

Common

Ca rc ino m a

Signif cantly increased incidence

Mildly increased incidence

p e rinuc le a r a ntine utro p hil c yto p la s m ic a ntib o d ie s (p ANCA)

60%–70%

5%–10%

a nti–Sa c c ha rom yc e s c e re vis ia e a ntib o d ie s (ASCA)

10%–15%

60%–70%

50%

UC, ulcerative colitis.

IV. Extra inte s tina l m a ni e s ta tio ns : include ankylosing spondylitis and sacroiliitis, peripheral arthritis, erythema nodosum and pyoderma gangrenosum, aphthous stomatitis, iritis and episcleritis, and primary sclerosing cholangitis V. Ris k o r c o lo n c a nc e r: occurs with chronic disease A. T e risk is minimal until 10 years af er onset, and then it increases by 1% per year thereaf er. B. T e risk is highest in patients with pancolitis. C. Dysplasia (o the mucosa): associated with an increased risk o cancer. Cancer in UC does not ollow the usual polyp-carcinoma sequence and occurs in the at areas. D. Surveillance colonoscopy (with multiple mucosal biopsies to search or dysplasia): done annually in patients who have had UC more than 10 years VI. Clinic a l p re s e nta tio n: Disease severity ranges rom occasional episodes o diarrhea to ulminant colitis. Quic k Cut UC pres ents with A. Bloody diarrhea is the most common symptom. Rarely, bleeding bloody diarrhea, crampy pain, can be massive and li e threatening. and weight los s . B. Mucus and pus: may accompany the passage o loose stools C. Cramping abdominal pain, malaise, ever, weight loss, and anemia: common D. Fulminant colitis: severe disease characterized by the ollowing: 1. Dilatation o the colon 2. Abdominal pain, tenderness, and distention 3. Fever, leukocytosis, and hypoalbuminemia 4. Signi cant risk o colonic per oration VII. Eva lua tio n: Depends on disease severity. Mild cases can be evaluated on an outpatient basis, whereas ulminant colitis with toxic megacolon is a li e-threatening situation requiring Quic k Cut hospitalization, intensive medical treatment, and emergency surgery In the pres ence o i medical treatment ails. ulminant colitis , colonos copy and barium enema s hould A. Proctoscopy: most valuable test to establish the diagnosis be avoided becaus e thes e 1. Continuous mucosal inf ammation (beginning at the level s tudies may wors en the o the dentate line): highly suggestive o UC patient’s condition. 2. Mucosal biopsies: con rm the diagnosis and/or exclude Crohn and in ectious colitis

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B. Stool samples: Culture or pathogens and examine or ova and parasites to rule out in ectious colitis. C. Serologic markers: or IBD (mainly perinuclear antineutrophil cytoplasmic antibody); see able 12-4 D. Colonoscopy: used to evaluate entire colon i symptoms are mild E. Small bowel contrast studies or enterography: obtained to rule out small bowel involvement, which would indicate CD VIII. Me d ic a l tre a tm e nt: A “step-up” approach based on disease severity and extent is used. A. Oral and topical aminosalicylates (5-aminosalicylic acid [5-ASA], mesalamine): Used as primary therapy in patients with Quic k Cut mild to moderate UC. T ese avoid the toxicity o sul apyridine, Aminos alicylates which is present in sul asalazine. (5-ASA and mes alamine) are B. Immunomodulating agents: used or more severe, medically f rs t-line treatments or UC. resistant disease 1. Steroids: e ective or short-term treatment, but side e ects prevent their long-term use 2. IV cyclosporine: more commonly used to induce, rather than maintain remission 3. Others: 6-mercaptopurine/azathioprine, methotrexate Quic k Cut In iximab is a (same e ects as or CD) monoclonal antibody agains t C. Biologics: Monoclonal antibodies to the proin ammatory TNF. cytokine tumor necrosis actor ( NF), such as inf iximab, are e ective in inducing remission in patients with re ractory UC. D. Broad-spectrum antibiotics: indicated or ulminant colitis IX. Surg ic a l tre a tm e nt A. Indications: hemorrhage, ulminant colitis or toxic megacolon unresponsive to intensive medical treatment, medically re ractory disease, colonic stricture (at least 30% incidence o cancer), and dysplasia or cancer B. Procedures 1. otal proctocolectomy with a permanent ileostomy 2. Restorative proctocolectomy: proctocolectomy with anal sphincter preservation and ileal pouch anal anastomosis (IPAA) a. Most common operation or UC and usually accompanied by a temporary ileostomy, which is closed 8–12 weeks af er the initial operation b. Rarely used in patients with CD because o the risk o recurrent disease in the ileal pouch 3. Abdominal colectomy with closure o the rectal stump: Hartmann procedure a. Indicated with ulminant colitis b. Completion proctectomy and IPAA can be per ormed at a later time. 4. otal proctocolectomy with continent ileostomy: Kock pouch a. Due to incidence o complications, this procedure has been largely replaced by IPAA. b. An ileal pouch is ashioned with a nipple valve that is attached to the abdominal wall and requires intubation to evacuate the ileum several times daily.

Cro hn (Gra nulo m a to us ) Co litis I. Inf a m m a tio n: important eature o CD A. ransmural inf ammation: Full thickness o the bowel wall is in amed. B. Noncontinuous inf ammation: “Skip areas” o normal bowel may separate in amed regions. II. Invo lve m e nt: T e small bowel is requently involved (especially the terminal ileum). Anal or perianal disease (e.g., stulas, abscesses, ssures) is present in approximately one third o patients. Rectal sparing may be present. III. His to lo g y: Granulomas are present in 50% o surgical specimens.

Quic k Cut CD eatures ullthicknes s , noncontinuous in ammation. Small bowel and perianal involvement is common.

IV. End o s c o p ic nd ing s : Linear ulcers may join transverse ssures to give a “cobblestone” appearance to the mucosa.

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V. Extra inte s tina l m a ni e s ta tio ns : generally the same as or UC, except that sclerosing cholangitis is less common VI. Ca nc e r ris k: increased in the diseased segments but less de ned than with UC VII. Clinic a l p re s e nta tio n: typically, abdominal pain, diarrhea, and weight loss A. Malaise, ever, and leukocytosis: common B. Abdominal abscesses and stulas: may occur ( stulas between the involved bowel and the bladder, vagina, skin, or other segments o intestine) C. Fulminant colitis: may be as severe as with UC 1. Megacolon: T e colon usually does not dilate with ulminant CD, which is thought to be because o the transmural in ammation with wall thickening. 2. Per oration risk: Same as in UC; there ore, patients must be treated with the same vigor. VIII. Eva lua tio n: As with UC, evaluation depends on disease severity. A. Physical exam: abdominal examination to evaluate areas o tenderness or mass and anorectal examination to detect abscesses, ssures, or stulas B. Laboratory studies: include serologic markers or IBD, mainly anti–Saccharomyces cerevisiae antibody (see able 12-4), and stool sample or culture, ova, and parasite to rule out in ectious causes o colitis C. Radiographic studies: Upper GI series with small bowel ollow-through or enterography is important to evaluate small bowel involvement and/or C scan i an abscess or per oration is suspected. D. Endoscopy: Proctoscopy is important; i rectal mucosa is not involved, UC is essentially excluded. Colonoscopy is the most sensitive diagnostic modality or colonic involvement. IX. Me d ic a l tre a tm e nt A. Budesonide, 5-ASA agents, and antibiotics: common Quic k Cut treatments or mild to moderate CD Budes onide, a B. Immunomodulating agents: more severe, re ractory disease glucocorticoid with high topical activity and f rs t-pas s 1. Steroids: help ul or acute disease but have many wellmetabolis m in the liver, has established side e ects been s hown to be as e ective 2. 6-Mercaptopurine/azathioprine: have a slow onset o as traditional s teroids with action and are there ore most use ul or maintaining disease les s adrenal s uppres s ion. remission 3. Methotrexate: contraindicated in pregnancy 4. IV cyclosporine: may be help ul, but most patients on therapy ultimately come to colectomy Quic k Cut C. Biologics: Anti- NF agents are increasingly being used to In iximab is particularly e ective or induce and maintain remission in patients with steroidf s tulizing CD. dependent or re ractory CD. T ese agents are particularly e ective in treating patients with stulizing disease. D. otal parenteral nutrition ( PN): Permits bowel rest and induces remission in some patients with signi cant CD. T is Quic k Cut remission rate is much higher than the rate or patients with Anorectal abs ces s es severe UC treated by PN. or f s tulas require s pecial E. Metronidazole and ciprof oxacin: bene cial or perianal disease s urgical cons iderations (pus X. Surg ic a l tre a tm e nt s hould be drained, but large A. Indications: intestinal obstruction, abdominal abscesses and incis ions are avoided to prevent s phincter injury). stulas, per oration, debilitating disease re ractory to medical treatment, ulminant colitis, hemorrhage (rare), and cancer (less common than with UC) B. Surgical considerations: High recurrence rate ( 50% within 10 years) ollows intestinal resection. T e most likely site o Quic k Cut recurrence is at the anastomosis rom the previous operation. Bowel cons ervation in CD s urgery is critical 1. Surgery goal: Conserve bowel. becaus e recurrence is a. Only grossly involved bowel should be resected. common and numerous b. Stricturoplasty: o conserve bowel, this is done rather res ections can lead to s hort than resection to relieve obstruction in short strictures. gut s yndrome. 2. Abdominal abscesses: drained percutaneously prior to surgery

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Ischemic Colitis

3. otal proctocolectomy with ileostomy: May be required or severe rectal disease. IPAA is used rarely due to the risk o disease recurrence. 4. PN: allows bowel rest or 7–10 days preoperatively to promote resolution o intra-abdominal in ammation and potentially reduce the risk o injury to adjacent organs

P SEUDOMEMBRANOUS COLITIS (ANTIBIOTIC-ASSOCIATED COLITIS) Ep id e m io lo g y a nd Clinic a l P re s e nta tio n I. Ac ute d ia rrhe a a s s o c ia te d with the us e o a ntib io tic s : Clindamycin and ampicillin are most of en implicated, but almost every antibiotic has been implicated. Frequently, the antibiotic has been discontinued be ore diarrhea development. II. Co m m o n in ho s p ita ls a nd nurs ing ho m e s : Epidemics have been reported and also af er intestinal operations, especially when antibiotic bowel preparations have been used.

P a tho g e ne s is a nd P re s e nta tio n I. Antib io tic s a lte r the no rm a l c o lo nic b a c te ria l p o p ula tio n. II. Clos trid iu m d if c ile : Normally suppressed by colonic bacteria, this pathogen emerges and causes mild diarrhea to severe li e-threatening colitis. A. Exotoxins: C. di cile elaborates two exotoxins, enterotoxin A and cytotoxin B. B. Pseudomembranes: Yellow plaques may cover the mucosa. 1. Pseudomembranes are composed o brin and debris rom cells and bacteria. 2. T e absence o pseudomembranes does not rule out in ection.

Dia g no s is I. His to ry: History o diarrhea af er treatment with an antibiotic is suspicious. II. Sto o l s a m p le : or C. di cile toxin titer or real-time PCR III. P ro c to s c o p y o r c o lo no s c o p y: may reveal pseudomembranes, which are diagnostic

Tre a tm e nt I. Ca us a tive a ntib io tic : Discontinue. II. Me tro nid a zo le (o ra l o r IV) a nd va nc o m yc in (o ra l): equally e ective; however, the daily cost or metronidazole treatment is much lower III. Co ns tip a ting a g e nts (e .g ., lo p e ra m id e ): Avoid constipating agents. IV. Re c urre nc e : common (25%) and requires retreatment with metronidazole, vancomycin, or newer agents such as ri aximin V. Ab d o m ina l c o le c to m y with ile o s to m y: of en necessary or rare ulminant cases

ISCHEMIC COLITIS Etio lo g y I. Wa te rs he d a re a s : Points o communication between collateral arteries are theoretically at increased risk or ischemia. T ese points include the splenic f exure and the midsigmoid colon; however, any segment o the colon may be involved. Rectal involvement is very rare. II. P re d is p o s ing a c to rs : include the ollowing: A. Surgery: especially aortic surgery with IMA ligation B. Vascular disease: atherosclerosis, vasculitis, and collagen vascular diseases C. Hypercoagulable states: such as polycythemia vera D. Low-f ow states: particularly in the setting o myocardial in arction, sepsis, or congestive heart ailure E. Medications: digitalis, oral contraceptives, antihypertensive medications, and vasopressors

Quic k Cut Is chemic colitis occurs mos t commonly at the s plenic exure and mids igmoid colon becaus e they are waters hed areas o the vas cular s upply.

Quic k Cut Is chemic colitis may res ult in dus ky, mildly is chemic mucos a, partial thicknes s injury with moderate is chemia, or ull-thicknes s necros is .

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Ta b le 12-4: Co lo nic Is c he m ia P ha s e o Is c he m ia

Tra ns ie nt Is c he m ia

Chro nic o r P a rtia l-Thic kne s s Is c he m ia

Ga ng re ne

De ning e a ture s

Involves only mucosa, which o ten looks dusky and hemorrhagic on endoscopy

O ten results in stricture ormation

Entire bowel wall is nonviable.

Sym p to m s

Cramping abdominal pain with passage o small amount o blood

More severe abdominal pain with tenderness, ever, leukocytosis

Severe abdominal pain requently with peritonitis, acidosis, sepsis

Tre a tm e nt

Supportive care with treatment and/or correction o causative actors

More intensive monitoring, intravenous uids, and broad-spectrum antibiotics. Surgical resection i symptomatic stricture develops.

Emergent resection o any nonviable bowel is necessary and almost always requires a colostomy.

P a tho g e ne s is a nd Tre a tm e nt I. Sup p o rtive c a re : IV uids, antibiotics II. Surg ic a l re s e c tio n o r no nvia b le b o we l (s e e Ta b le 12-4)

VOLVULUS Ove rvie w I. De nitio n: twist or torsion o an organ on its pedicle II. Sym p to m s : produced by occluding the bowel lumen (obstruction) or occluding the blood supply (ischemia) III. Inc id e nc e : Low in the United States. It is the most common cause o colon obstruction in A rica, where there is a signi cantly lower rate o diverticular disease, perhaps related to dietary ber intake.

Sig m o id Vo lvulus I. Etio lo g y: Sigmoid volvulus accounts or more than 80% o cases o colonic volvulus. A. Patient characteristics: Average age is 60 years. Patients with this condition of en reside in nursing homes or mental Quic k Cut institutions. Twis ting o the bowel B. Predisposing conditions: include an elongated sigmoid colon and mes entery in volvulus with an ample, reely mobile mesentery and a narrow point o obs tructs the lumen and can xation about which the colon can twist compromis e blood s upply. II. P a tho g e ne s is : T e sigmoid colon usually twists counterclockwise around the axis o the mesentery. ogether, this causes obstruction o the colon lumen and may also cause vascular compromise leading to ischemic bowel.

Ce c a l Vo lvulus I. Etio lo g y: occurs much less requently than sigmoid volvulus A. Patient characteristics: more common in women, and patients are of en younger than 40 years B. Cause: incomplete peritoneal xation o the right colon ( or axial torsion) or a redundant cecum that can op into the lef upper quadrant (LUQ) in the cecal bascule II. Othe r c o ntrib uting a c to rs : may include cancer o the distal colon, malrotation, prior surgery, and pregnancy III. P a tho g e ne s is : T e cecum and ascending colon usually twist clockwise. Bowel and vascular obstruction occurs in a manner similar to that described or sigmoid volvulus.

Dia g no s is I. His to ry: usually indicates increasing abdominal distention, discom ort, and obstipation II. P hys ic a l e xa m ina tio n: Reveals abdominal distention and tympany; rebound tenderness suggests gangrenous bowel.

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III. Ab d o m ina l ra d io g ra p hs A. Sigmoid volvulus: Massively distended sigmoid colon, with both ends in the pelvis and the bow near the diaphragm in the right upper quadrant (“bent inner tube sign”) is seen. B. Cecal volvulus: of en reveals a large distended cecum that occupies the LUQ (“co ee bean” or “kidney” shape) IV. Ba rium e ne m a : reveals the pathognomonic obstructing twist (“bird’s beak de ormity”)

Tre a tm e nt

Quic k Cut

Radiology key words : Sigmoid volvulus looks like a “bent inner tube”; cecal volvulus looks like a “co ee bean.” Volvulus on a barium enema res embles a “bird’s beak.”

I. S ig m o id vo lvu lu s : Endoscopic decompression should be attempted or nonstrangulated sigmoid volvulus but should be terminated i necrotic mucosa is observed or i the volvulus cannot be reduced by gently inserting a rubber tube or the sigmoidoscope itsel past the point o torsion. I there is necrosis, or i it is not possible reduce the volvulus, resection in the operating room is necessary. Af er success ul reduction, the tube should be lef in place to prevent recurrence be ore surgical resection is per ormed. A. Elective sigmoidectomy with colorectal anastomosis: recommended af er success ul decompression, typically during the same hospital admission B. Sigmoidectomy with colostomy (Hartmann operation): indicated i decompression cannot be achieved or i there is gangrenous bowel II. Ce c a l vo lvulus : Colonoscopic decompression is risky and rarely success ul; there ore, surgical resection is necessary to prevent recurrences. A. Right colectomy with primary anastomosis: generally indicated i the bowel is viable B. Cecopexy: rarely per ormed due to high recurrence rates

ANORECTAL DYSFUNCTION Inc o ntine nc e I. Etio lo g y: inability to control elimination o rectal contents A. Anal sphincter mechanical de ects: include iatrogenic injury (e.g., episiotomy or previous stulotomy) and anorectal trauma (e.g., impalement injuries) B. Neurogenic causes: include pudendal nerve injury due to prolonged labor and systemic neurologic disease (e.g., multiple Quic k Cut sclerosis) Incontinence can be C. Systemic disease: including that a ecting the sphincters due to caus es unrelated to (e.g., scleroderma, diabetes) the s phincters (e.g., diarrhea, D. Causes unrelated to the anal sphincter: include severe diarrhea, ecal impaction with over ow, severe proctitis with decreased rectal capacity, ecal impaction s evere proctitis , etc.). with over ow incontinence, and large rectal tumors II. Eva lua tio n: History and anorectal examination of en su ce to establish the diagnosis. A. Anterior sphincter de ect and patulous anus: may be con rmed by a thorough examination and endorectal ultrasound o the anal musculature, i necessary B. Physiologic evaluation: help ul i the cause o incontinence is not obvious 1. Anal manometry: documents resting and squeeze pressures, sphincter length, and minimal sensory volume o the rectum 2. Pudendal nerve terminal motor latency: detects neurogenic impairment III. Surg ic a l tre a tm e nt: Sphincter de ects may be surgically corrected by overlapping sphincter repair with some success. A. Gracilis muscle transposition or arti cial anal sphincter implantation: or more extensive loss o the anal sphincter; however, complication rates are high B. Sacral nerve stimulation and injectable biomaterials: newer methods C. Colostomy: may be required or severe sphincter injuries or or neurogenic or systemic causes o incontinence

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Ob s truc te d De e c a tio n (P e lvic Flo o r–Outle t Ob s truc tio n) I. Ana l s te no s is : May be caused by circum erential hemorrhoidectomy, trauma, or radiation. reatment generally entails repeated dilatation or advancing ull-thickness skin pedicles into the anal canal. II. P ub o re c ta lis (a nis m us ) no nre la xa tio n: unctional disorder characterized by paradoxical contraction o the puborectalis muscle at the time o de ecation A. Symptoms: include a sense o incomplete evacuation and severe straining during de ecation B. Incidence: occurs in women nine times more of en than in men C. Normal colonic transit time: measured by radiopaque marker tracking through the colon (Sitz marker study) D. Diagnosis: con rmed by de ecography and manometry, which demonstrate the ailure o the muscle to relax appropriately E. reatment: Nonsurgical; bio eedback is the treatment o choice. III. Inte rna l intus s us c e ption (inte rna l re c ta l prola ps e ): Characterized by the distal rectum telescoping into itsel , causing partial obstruction. Patients complain o urge to de ecate, rectal ullness, and pelvic pain. A. Solitary rectal ulcer: Of en seen in this syndrome, located in the anterior rectal wall. Chronically, it may cause ischemia resulting in colitis cystica pro unda, which is the entrapment o mucinsecreting glands beneath the mucosa. It is important to distinguish this benign lesion rom cancer. B. Abnormal rectal xation: accompanies intussusception and permits the rectum to descend C. Medical treatment: su ces or most patients and consists o increased dietary ber, stool sof eners, and glycerine suppositories or enemas D. Surgical treatment: Rectopexy with or without rectosigmoid resection. Indications include the ollowing. 1. Debilitating symptoms: despite maximum medical therapy 2. Impending anal incontinence: due to stretch injury to the pudendal nerves caused by constant straining and perineal descent 3. Chronic bleeding: rom a solitary rectal ulcer IV. Re c ta l p ro la p s e : Protrusion o the ull thickness o the rectum Quic k Cut (and occasionally the sigmoid colon) through the anus in concentric Rectal prolaps e mucosal olds should be distinguished rom prolapsed internal mus t be dis tinguis hed rom hemorrhoids, which have radial olds in the prolapsing mucosa. prolaps ed hemorrhoids : A. Etiology: Patients requently have diastasis o levator ani, a deep Prolaps e has concentric mucos al olds , whereas cul-de-sac, redundant sigmoid colon, patulous anal sphincters, hemorrhoids have radial olds . and/or loss o rectal sacral attachments. B. Epidemiology: increased incidence in patients in mental institutions, women who have had a hysterectomy, and elderly women C. Symptoms: include mucosa-lined bowel protruding through the anus, bleeding, anal pain, mucous discharge, and ecal incontinence caused by stretch o the anal sphincters or the pudendal nerves D. reatment: Surgical; incarceration and strangulation are rare but can occur. 1. Rectopexy with or without rectosigmoid resection: treatment o choice or patients in satis actory health and with satis actory anal continence 2. Perineal proctectomy (Altemeier procedure): For patients with signi cant comorbidities, an abdominal incision is avoided; however, recurrence rates are higher. 3. Anal encircling: Placing a band o synthetic material (wire or mesh) subcutaneously around the anus is o historical interest only. 4. Colostomy: or total incontinence

BENIGN ANORECTAL DISEASE He m o rrho id s

Quic k Cut

Hemorrhoids I. Etio lo g y: Cushions o vascular and connective tissue develop, occur in three pos itions : which are thought to protect the sphincter during de ecation and right anterolateral, right permit complete closure o the anus during rest. pos terolateral, and le t lateral. A. Vascular tissue engorgement: causes these cushions/complexes to enlarge B. Hemorrhoidal enlargement: Prolonged straining during de ecation and increased abdominal pressure are thought to produce symptoms.

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II. Cla s s i c a tio n A. Internal hemorrhoids are located above the dentate line and are covered by rectal mucosa; there ore, they are typically not pain ul. Internal hemorrhoids are graded as ollows: 1. First degree: bleed, but do not prolapse 2. Second degree: bleed and prolapse, but reduce spontaneously 3. T ird degree: bleed and prolapse, and must be manually reduced 4. Fourth degree: protrude through the anus and cannot be reduced B. External hemorrhoids reside below the anal verge and are lined by squamous epithelium. A thrombosis within an external hemorrhoid may cause acute swelling and anal pain. III. Sym p to m s : Bleeding and prolapse are the predominant symptoms o internal hemorrhoids. Acutely prolapsed and incarcerated internal hemorrhoids may cause pain. External hemorrhoids cause discom ort, pruritus, and pain i thrombosed. IV. Tre a tm e nt: depends on the symptoms A. Medical therapy: includes increasing dietary ber and uid, stool sof eners, and avoidance o straining B. Rubber band ligation: of en used to treat rst-, second-, and third-degree hemorrhoids and selected cases o ourth-degree hemorrhoids 1. T e rubber bands must be placed above the dentate line or Quic k Cut severe pain will result. Rubber band 2. Caution must be exercised to avoid unintentional ligation o ullligation is the mos t common thickness rectal tissue, which can result in li e-threatening sepsis. treatment or internal C. Sclerotherapy and in rared photocoagulation: less requently hemorrhoids and can only be used or rst-, second-, and third-degree hemorrhoids us ed or internal hemorrhoids . D. Hemorrhoidectomy: May be required or re ractory hemorrhoids and most ourth-degree hemorrhoids. Options include the ollowing. 1. Surgical excision: o one or more hemorrhoidal columns with the mucosa lef open or sutured closed 2. Stapled hemorrhoidectomy: Excises a ring o mucosa and submucosa above the hemorrhoids and returns the anal cushions to their anatomic position. T is procedure has been associated with chronic postoperative pain and is there ore seldom used today. E. T rombosed hemorrhoids: May require excision or pain relie i patient presents within 48–72 hours o thrombosis, when pain is most intense. However, most cases resolve within 2 weeks without any speci c therapy.

Ana l Fis s ure I. De nition: An anal ssure is a tear in the anoderm, commonly caused by constipation. Approximately 90% o ssures are in the posterior midline, where anal per usion is the lowest, and 10% are in the anterior midline. II. Sym p to m s : anal pain and bleeding associated with de ecation III. P hys ic a l nd ing s : may include the ollowing: A. Fissure or ulcer: distal to the dentate line with underlying exposed internal sphincter muscle B. Sentinel skin tag: externally and/or hypertrophied anal papilla internally C. Spasm or hypertrophy o the internal sphincter: in chronic cases IV. Tre a tm e nt: Most ssures will heal with medical treatment. A. Medical: Stool sof eners, increased dietary ber, and warm sitz baths are bene cial. 1. Nitroglycerin or diltiazem: opical application has been shown to increase blood ow to the ischemic internal sphincter muscle and acilitate ssure closure. 2. Botulinum toxin: Injection into the internal sphincter muscle temporarily paralyzes the muscle and allows the ssure to heal. B. Surgical: Lateral internal sphincterotomy may be done or ssures re ractory to medical therapy. T is can be done via an open or a closed technique and is highly curative.

Ano re c ta l Ab s c e s s a nd Fis tula I. P a tho g e ne s is : Abscess is the acute stage and stula is the chronic stage o the same disease process. A. Cryptoglandular in ections: T ey begin in the anal glands that empty into the anal crypts.

Quic k Cut Anorectal abs ces s is acute in ection; anorectal f s tulas are the s equelae o chronic in ection.

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Leva tor a ni

Inte rs phincte ric

Is chiore cta l

Pe ria na l

Inte rna l s phincte r

Exte rna l s phincte r

Fig ure 12-2: Perirectal abs ces s es develop rom f s tulous tracts that begin in rectal ulcers o anorectal glands . Thes e f s tulae extend into the inters phincteric s pace and then ollow tis s ue planes to a variety o pelvic locations where abs ces s es may orm. (From Yamada T, Alpers DH, Kaplowitz N, et al. Textbook of Gastroenterology, 4th ed. Philadelphia: Lippincott Williams & Wilkins ; 2003.)

B. Intersphincteric abscesses: Most abscesses originate between the internal and external sphincters (Fig. 12-2). 1. Perianal abscess: downward extension 2. Ischiorectal ossa abscess: lateral extension through the external sphincter 3. Supralevator abscess: upward extension (rare) II. Sig ns a nd s ym p to m s : anorectal pain, usually re erred to as throbbing pain, requently with ever and leukocytosis A. Swelling and f uctuance: late signs B. Pus and blood drainage: signi es spontaneous rupture and is usually associated with pain relie III. Tre a tm e nt: Incision and drainage (I&D) should be per ormed promptly af er the diagnosis is made. A. Ischiorectal ossa: may contain a large volume o pus be ore uctuance is obvious Quic k Cut B. Antibiotics: required only i immune status is compromised Des pite adequate (e.g., diabetes, leukemia) or there is extensive cellulitis drainage, nearly 50% o IV. Ano re c ta l s tula : communication between the anorectal lumen patients will develop anorectal f s tula. and the perianal skin A. Internal opening: must be identi ed to allow proper treatment 1. Posterior anal crypt: most common site o the internal opening 2. Goodsall rule: Envision a transverse line that bisects the anus. External openings that are posterior to this line will curve and connect to the posterior midline crypt, whereas external openings anterior will communicate to an anterior crypt by a short, radial tract. B. Fistulotomy: Used to treat simple anal stula. Both openings are identi ed and the tract unroo ed. C. Complicated stulas (involve signi cant sphincter muscle): Require procedures that eradicate the internal opening; stulotomy would likely cause incontinence.

P ilo nid a l Dis e a s e I. P a tho p hys io lo g y: Exact mechanism is unclear, although it is characterized by hair rom the skin o the postsacral superior gluteal clef becoming trapped below the sur ace, leading to oreign body reaction and acutely causing local in ection (i.e., abscess) or chronically draining sinuses. II. Tre a tm e nt: I&D or acute abscess and excision with closure by primary or secondary intent or a chronic sinus tract. Complex ap procedures may be necessary or recurrence af er these measures.

Hid ra d e nitis Sup p ura tiva I. P a tho p hys io lo g y: in ection o the apocrine sweat glands A. Subcutaneous sinus tracts: orm rom in ected glands and can spread to the perineum, scrotum, or labia B. Distinguish rom cryptoglandular disease: does not involve the anal canal, whereas cryptoglandular disease originates there II. Clinic a l p re s e nta tio n: varies rom acute sinus tracts to complicated stulas and abscesses III. Tre a tm e nt: Excision o involved skin, requently without primary closure. Recurrence is common.

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Perianal and Anal Canal Neoplasms

Co nd ylo m a Ac um ina tum (Ano -g e nita l wa rts )

Quic k Cut I. Etio lo g y: Causative agent is human papillomavirus (HPV). HPV s trains 16 A. ransmission: usually sexual, with increased incidence in patients and 18 are as s ociated with who practice anoreceptive intercourse travels together with HIV increas ed ris k o anal cancer. B. Anal cancer: Certain viral strains (HPV-16 and HPV-18) ound in condyloma are associated with increased risk. II. Clinic a l p re s e nta tio n: Lesions vary rom tiny excrescences to cauli owerlike masses. A. Site: may be sessile or pedunculated and are usually located on the perianal skin, penis, vulva, vagina, or cervix or in the anal canal B. Symptoms: pruritus, perianal moisture, discom ort, and the presence o masses III. Tre a tm e nt: Local excision and electrocoagulation may be done and o er the best chance o cure. A. opical treatments: bichloroacetic acid or imiquimod B. Surveillance: Patients should be ollowed closely because o the risk o progression to cancer when carcinogenic viral strains are identi ed and the high risk o recurrence.

P ERIANAL AND ANAL CANAL NEOP LASMS Ana l Ma rg in (b e lo w De nta te Line ) I. Ne o p la s m s : include squamous cell carcinoma, basal cell carcinoma, Bowen disease, and perianal Paget disease II. P re s e nta tio n a nd tre a tm e nt: able 12-5

Ana l Ca na l (a b o ve De nta te Line ) I. Epide rm oid c a rc inom a : includes squamous cell, basaloid, cloacogenic, and mucoepidermoid carcinoma A. Clinical presentation: may be bleeding, pain, or anal mass B. Diagnosis and evaluation: includes physical examination to assess tumor size, depth o invasion, ulceration, and regional lymph nodes and anoscopy and/or proctoscopy with biopsy, Quic k Cut Endorectal endorectal ultrasound, and C scan o the pelvis and liver ultras ound is the primary C. reatment: Most lesions require combined modality therapy imaging modalities or local consisting o 5-FU and mitomycin C with external beam radiation. s taging o rectal and anal 1. Super cial early-stage lesions: can be e ectively treated with cancers . As both the depth o local excision only the les ion and the local lymph nodes can be as s es s ed. 2. APR: reserved or treatment ailures with greater than 50% 5-year survival D. Prognosis: Combined treatment has an overall response rate o 90% and a 5-year survival rate greater than 80%.

Ta b le 12-5: Ana l Ma rg in Ne o p la s m s Tum o r Typ e

P re s e nta tio n

Tre a tm e nt

Sq ua m o us c e ll c a rc ino m a

Polypoid, ungating, or ulcerated mass; pruritus; bleeding

Local excision or radiation i large or recurrent

Ba s a l c e ll c a rc ino m a

Central ulceration with irregular, raised pearly borders

Local excision; radiation or abdominal perineal resection or rare, advanced lesions

Bo we n d is e a s e (squamous cell carcinoma in situ)

Variable skin changes: erythematous, crusty, scaly plaques; itching; burning; bleeding; 10% develop squamous cell carcinoma

Wide local excision or topical 5-FU

P e ria na l P a g e t d is e a s e (intraepithelial adenocarcinoma)

Erythematous, eczematous rash with white ulcerations; intractable pruritus; high incidence o visceral carcinoma

Wide local excision or topical retinoic acid; i underlying rectal cancer— abdominoperineal resection

5-FU, 5- uorouracil.

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203

II. Ad e no c a rc ino m a : most commonly an extension rom cancer in the distal rectum A. Cancer arises rom anal glands and ducts: It may mani est outside the lumen o the anal canal and present as an anal stula. B. reatment: generally similar to that or rectal cancer, with preoperative chemoradiation ollowed by APR III. Me la no m a : T e anal canal is the third most common site (af er skin and eyes). Not all anal melanomas are darkly pigmented (i.e., some are amelanotic). A. Symptoms and presentation: Anal mass, pain, and bleeding are most common. Regional lymphatic and distant metastases are common at diagnosis. B. reatment: APR versus wide local excision is controversial, although the key to surgical treatment is a complete excision. T e 5-year survival rate is less than 15%.

Chapter 13

Liver, Gallbladder, and Biliary ree Daniel Medina and Srinevas K. Reddy

GENERAL ASP ECTS Ana to m y a nd P hys io lo g y

204

I. He pa tobilia ry e m bryology: Hepatic diverticulum orms as an embryologic outpouching o the oregut. A. Cranial portion: orms the liver and the larger branches o the intrahepatic ducts B. Caudal portion: orms the gallbladder, cystic duct, and common bile duct II. Live r: weighs 2% o total body weight and is composed o two lobes (lef and right), each subdivided into multiple segments (Fig. 13-1) Quic k Cut A. Hepatic lobes: divided by the interlobar ssure, an invisible line The s egmental anatomy o the liver is between the gallbladder ossa anteriorly and the in erior vena determined by the vas cular cava posteriorly s upply and biliary tree and B. Falci orm ligament: marks the segmental ssure between the does not have obvious median and lateral segments o the lef lobe and is the only external landmarks . externally visible boundary C. Arterial supply: emanates rom the common hepatic artery, which is a branch o the celiac axis 1. Lef hepatic artery: arises rom the lef gastric artery in 20% Quic k Cut The oxygenated o the population blood s upply to the liver is 2. Right hepatic artery: arises rom the superior mesenteric 25% arterial and 75% portal. artery (SMA) in 20% o the population D. Venous supply: emanates rom the portal vein, which carries partially oxygenated blood rom the splanchnic circulation 1. Route: Like the arterial supply, the portal supply also ollows Quic k Cut the hepatic segmental anatomy. A replaced right 2. Venous drainage: occurs through lef , middle, and right hepatic artery aris es rom the SMA ins tead o the proper hepatic veins emptying into the in erior vena cava at the level hepatic artery. o the diaphragm III. Bilia ry tre e : Bile produced by the liver drains into lef and right hepatic ducts, whose con uence orms the common hepatic duct (Fig. 13-2). A. Common bile duct: ormed by the cystic and common hepatic ducts B. Pancreatic duct: typically joins the common bile duct be ore they enter the duodenum through the ampulla o Vater, surrounded by the sphincter o Oddi, which controls bile ow IV. Ga llb la d d e r: located on the in erior aspect o the liver and divided into the undus, body, in undibulum, and the neck A. Histology: Wall is composed o smooth muscle and brous tissue; the lumen is lined with high columnar epithelium. B. Arterial supply: through the cystic artery, which is usually a branch o the right hepatic artery

Chapter 13

Liver, Gallbladder, and Biliary ree

Infe rior ve na ca va

Right he pa tic ve in

Le ft a nd inte rme dia te (middle ) he pa tic ve ins

II

VII 3°

VIII

3°

T

I 3°

IV 2°

3°

2°

III

3°

U

VI

Right a nd le ft (1°) bra nche s of he pa tic a rte ry P orta l ve in He pa tic a rte ry P orta l tria d Bile duct

M

V

Ga llbla dde r R

Anterior view

M = Ma in porta l fis s ure U = Umbilica l fis s ure R = Right porta l fis s ure 2° = S e conda ry bra nche s of porta l tria d s tructure s T = Tra ns ve rs e he pa tic pla ne 3° = Te rtia ry bra nche s of porta l tria d s tructure s

A

Ca ntlie line

VIII

VII

Right live r

II

IV

V

B Anterior view

Ga llbla dde r

Ve na ca va

Le ft live r

III

VI

D Anterior view

Ca uda te lobe

V GB IV

VI

III

II I

VII Right lobe

Le ft lobe

C Anterior view

Ga llbla dde r

VIII

E Inferior view

Fig ure 13-1: Segmental liver anatomy. GB, gallbladder. (From Moore KL, Agur AMR, Dalley AF. Clinically Oriented Anatomy, 7th ed. Baltimore: Lippincott Williams & Wilkins ; 2013.)

C. Venous return: via cystic veins that drain to the portal vein and directly into the liver D. Lymphatic drainage: goes both to the liver and to hilar nodes E. Innervation: rom the celiac plexus V. P hys io lo g y: Generally, the unction o the liver may be classi ed in the ollowing categories. A. Metabolic: detoxi cation, glycogenolysis, ammonia conversion, drug processing, recycling o byproducts, gluconeogenesis, lipogenesis, and cholesterol synthesis B. Neurologic: Liver ailure leads to encephalopathy due to increased toxin level (e.g., ammonia). C. Cardiovascular: angiotensinogen synthesis

205

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General Aspects

Ga llbla dde r

Common he pa tic duct Cys tic duct Common bile duct P yloric s phincte r

Acce s s ory pa ncre a tic duct

P a ncre a s

P a ncre a tic duct Duode na l pa pilla Duode num

Ulce rs ca us e d by Zollinge r-Ellis on s yndrome

Fig ure 13-2: Biliary anatomy. (From Es cott-Stump S. Nutrition and Diagnosis-Related Care, 7th ed. Baltimore: Lippincott Williams & Wilkins ; 2011.)

D. Gastrointestinal (GI): bile production, at emulsi cation, and absorption o essential molecules rom the GI tract Quic k Cut E. Endocrine: thrombopoietin and insulinlike growth actor 1 The unction o the synthesis and insulin metabolism hepatobiliary s ys tem is quite F. Hematologic: etal erythrocyte production; synthesis o complex, and overall unction coagulation and anticoagulation actors cannot yet be replaced by G. Immunologic: acute phase reactants, complement synthesis, and artif cial means . part o the reticuloendothelial system VI. Bile p ro d uc tio n: Approximately 600 mL o bile are produced daily (normal range: 250–1,000 mL/day). A. Composition: electrolytes and water, bile pigments, protein, lipids, phospholipids (e.g., lecithin), cholesterol, and chenodeoxycholic acid conjugated with taurine and glycine primarily B. Storage: gallbladder, which absorbs water and electrolytes de acto, concentrating bile by 10- old C. Release: Coordinated release o bile requires simultaneous Quic k Cut The s phincter o contraction o the gallbladder and relaxation o the sphincter o Oddi is tonically contracted, Oddi. T e process is predominantly under humoral control, via which allows bile to enter cholecystokinin (CCK), but vagal and splanchnic nerves also the gallbladder by backf lling play a role. through the cys tic duct.

He p a to b ilia ry Stud ie s I. Live r unc tio n te s ts (LFTs ): re ect the ollowing: A. Synthetic unction: albumin, brinogen, clotting actors B. Clearance: ammonia, indirect bilirubin C. Excretory unction and patency o the biliary tree: direct bilirubin, alkaline phosphatase D. Hepatocyte injury: direct bilirubin, transaminases

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207

II. He p a to b ilia ry im a g ing : assesses hepatic, biliary, and extrahepatobiliary lesions; overall unction; and biliary obstruction A. Sul ur-colloid liver-spleen scan: Visualizes the reticuloendothelial system (i.e., di erentiates adenoma rom ocal nodular hyperplasia). Rarely per ormed. B. Ultrasound: detects parenchymal lesions and assesses hepatic vascular ow, gallbladder calculi, biliary ductal dilation, gallbladder wall thickening, and the presence o pericholecystic uid C. Computed tomography (CT) and magnetic resonance imaging (MRI): Visualize parenchyma and adjacent tissues with great clarity and are use ul in the delineation o tumors as well as resection planning. Gadoxetate sodium is a contrast agent used in MRI that is highly speci c or ocal nodular hyperplasia (FNH). D. Arteriography: de nes arterial supply usually prior to lesion embolization E. Hepatobiliary iminodiacetic acid (HIDA) scan (cholescintigraphy): employs technetium-99m (99m c), which is excreted in the bile 1. HIDA scan: provides images o the liver, the biliary tree, and the intestinal transit o bile 2. Diagnostic: use ul in diagnosing acute cholecystitis, choledochal cyst, bile leaks (af er cholecystectomy), and Quic k Cut common bile duct obstruction The normal ejection 3. In conjunction with CCK injection: HIDA scan helps raction o the gallbladder is 35% . diagnose biliary dyskinesia and acalculous cholecystitis. F. Magnetic resonance cholangiopancreatography (MRCP): provides the highest resolution o the hepatobiliary and pancreatic structures G. Endoscopic retrograde cholangiopancreatography (ERCP): Combines endoscopic and uoroscopic techniques directed at the biliopancreatic tree. ypically per ormed or biopsy, stenting (e.g., common bile duct and pancreatic duct obstruction), stone extraction, papillotomy, and sphincterotomy. H. Endoscopic ultrasound (EUS): lymph node visualization and biopsy III. Ne e d le b io p s y: provides liver tissue or histology and cultures

HEPATIC TUMORS Be nig n Tum o rs I. He m a ng io m a : Usually asymptomatic and discovered incidentally. May cause symptoms by compressing adjacent structures or distending the liver capsule (Fig. 13-3). T ey are rarely resected except when they are clearly symptomatic.

Quic k Cut Hemangioma is the mos t common benign hepatic tumor.

Fig ure 13-3: MRI o hemangioma (arrows). (From Smith WL. Radiology 101, 4th ed. Baltimore: Lippincott Williams & Wilkins ; 2013, courtes y o Alan Stolpen, MD.)

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Chapter 13

Hepatic umors

II. He p a to c e llula r a d e no m a (he p a tic a d e no m a ): uncommon benign tumor usually seen in women using oral contraceptives (OCPs); also ound in men and women who take anabolic (androgenic) steroids Quic k Cut A. Symptoms: Usually ound incidentally, may cause symptoms by Thirty percent o compressing adjacent structures but may hemorrhage into the patients with hepatocellular peritoneal cavity. T e mortality rate or rupture is 9%. adenoma (hepatic adenoma) pres ent with s pontaneous B. Pathology: Sof tumors with sharply circumscribed edges, no rupture. true capsule, and histologically normal hepatocytes. MRI is the diagnostic test o choice. C. Treatment: includes avoidance o OCPs, anabolic steroids, and pregnancy 1. Large adenomas: should be resected, particularly in anticipation o pregnancy 2. In case o rupture: reatment is embolization or operation ( or resection or hepatic artery ligation), depending on patient stability. III. FNH: common; occurs more of en in women and has a weak association with OCPs A. Symptoms: Usually incidentally diagnosed; spontaneous rupture is rare. FNH is notorious or the presence o central scarring and Quic k Cut radiating septations. On MRI with B. Histology: Contains hyperplastic hepatocytes with in ammatory gadoxetate, FNH is eas ily (Kup er) cells. Bile duct epithelium is a prominent nding. dis tinguis hed rom normal C. Diagnosis and treatment: similar to those or hepatocellular parenchyma. adenoma

Ma lig na nt Tum o rs I. He p a to c e llula r c a rc ino m a (he p a to m a ): Hepatoma is the most common primary malignant liver tumor (Fig. 13-4). A. Incidence: Highest in A rica and Asia. Male/ emale ratio is 2:1. B. Etiology: associated with chronic hepatitis B virus/hepatitis C virus, cirrhosis rom any etiology, hemochromatosis, schistosomiasis, and carcinogens such as chlorinated hydrocarbons, nitrosamines, polyvinyl chloride, organochloride pesticides, a atoxins C. Symptoms: Small hepatocellular carcinomas are usually asymptomatic. 1. I symptomatic: Malaise, ever, and jaundice may also be present. 2. Signs: include hepatomegaly (88%), weight loss (85%), a tender abdominal mass (50%), or ndings associated with cirrhosis (60%) D. Diagnosis: includes abnormal LF s, elevated alpha- etoprotein, and cross-sectional imaging

Quic k Cut Primary hepatic malignant tumors account or 0.7% o all cancers . In men, 90% o primary liver tumors are malignant; in women, only about 40% are malignant (due to the higher prevalence o hepatic adenoma and FNH).

Quic k Cut Larger and more advanced hepatomas o ten present as a dull, aching pain in the right upper quadrant (RUQ).

Fig ure 13-4: CT s can demons trating hepatoma (arrow) . (From Erkonen WE, Smith WL. Radiology 101, 3th ed. Baltimore: Lippincott Williams & Wilkins ; 2009.)

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209

E. De nitive treatment: consists o resection or transplantation 1. Survival: Resection among eligible patients has a 5-year survival 40%. 2. Other: Chemotherapy and ablation are usually palliative measures. II. Intra he p a tic c ho la ng io c a rc ino m a : arises rom the bile duct epithelium and represents 5%–30% o all primary hepatic malignancies A. Presentation: Patients have RUQ pain, jaundice, hepatomegaly, and occasionally a palpable mass. B. Etiology: associated with parasitic in ections (e.g., Clonorchis sinensis), primary sclerosing cholangitis C. Treatment: Resection when possible; otherwise, survival is poor.

Me ta s ta tic Ma lig na nt Tum o rs I. Ove rvie w: Liver is the second most common site o metastasis Quic k Cut (exceeded only by regional lymph nodes) or all primary cancers o One third o all the abdomen. T e ratio o metastatic to primary liver tumors is 20:1. abdominal cancers ultimately II. Dia g no s is : may be di cult because liver metastases are of en s pread to the liver, which is the mos t common s ite o asymptomatic hematogenous s pread. A. Tests: No single laboratory blood test predicts liver metastases in patients with subclinical disease. Currently, LF s and carcinoembryonic antigen have been used albeit with low speci city. B. Imaging techniques: T ese are expensive as screening tests, but are currently the most reliable nonsurgical method o detecting liver metastases. III. Tre a tm e nt: Depends on the type o primary tumor. Because colorectal cancer has generated the most reliable statistics, those gures are cited here. A. Chemotherapy with 5- uorouracil therapy: 10%–30% response Quic k Cut rate and a median survival less than 1 year Many cancers metas tas ize to the liver. Only B. Hepatic arterial in usion: has not improved patient survival colorectal metas tas is to the C. Radiation and cryoablation: palliative liver are potentially res ectable D. Resection: Most e ective mode o therapy but is limited to (i they are anatomically patients who have unilobar liver lesions and no evidence o avorable and there is no extrahepatic disease; 5-year survival rate approaches 40% in extrahepatic dis eas e) patients meeting these criteria.

HEPATIC ABSCESSES AND CYSTS Ab s c e s s e s

Quic k Cut Bacterial abs ces s es o the liver are typically s econdary to intra-abdominal in ection, s uch as cholangitis , appendicitis , or diverticulitis .

I. Ba c te ria l a b s c e s s e s : most common A. Common organisms: Escherichia coli, Bacteroides, Streptococcus, and Enterococcus B. Clinical presentation: includes sepsis, ever and chills, leukocytosis, anemia, abnormal LF s, RUQ tenderness, and occasionally hemobilia C. Treatment: Drainage and antibiotics usually su ce; surgical intervention is rarely required. II. Am e b ic a b s c e s s : second most common hepatic abscess and the most common abscess in the developing world A. Organism: In ection with Entamoeba histolytica reaches the portal vein rom intestinal amebiasis. B. Clinical presentation: includes ever, leukocytosis, hepatomegaly, RUQ pain C. Diagnosis: Occasionally, liver enzyme levels are elevated. Indirect hemagglutination titers or Entamoeba are elevated in Quic k Cut most patients with intestinal in estation and in 98% with hepatic Amebic abs ces s abscess. rophozoites (the active stage) are occasionally present is us ually s terile on routine culture and is treated by in the periphery o the abscess. metronidazole. D. Treatment: Metronidazole; surgical drainage is not usually necessary.

Hyd a tid Cys ts I. Ove rvie w: Result rom in ection with the parasite Echinococcus granulosus, which is endemic in southern Europe, Middle East, Australia, and South America. Dogs are the de nitive host.

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Chapter 13

Hepatic Abscesses and Cysts

II. Clinic a l p re s e nta tio n: Cysts can develop anywhere in the body, but two thirds occur in the liver and one hal in the lungs. T ey rupture into the peritoneal cavity, resulting in urticaria, eosinophilia, and anaphylactic shock. Symptoms include hepatomegaly, RUQ pain, and eosinophilia. III. Dia g no s is : history, imaging, and a positive serum antigen IV. Tre a tm e nt: Symptomatic cysts require surgical removal. T e surgical approach consists o care ul isolation o the operative eld, ollowed by aspiration o the cyst. T e site should be sterilized with 0.5% silver nitrate solution or hypertonic saline.

He p a tic Tra um a I. Mo rta lity: Due to its high blood ow, proximity to the in erior Quic k Cut vena cava (IVC), nearby vital structures, and propensity to develop Injury to the in ections, overall mortality is 10%–20%. retrohepatic IVC has a mortality o greater than 50% , II. Dia g no s is : By imaging and mechanism. Injuries are classi ed in regardles s o treatment. ve levels based on the degree o parenchymal injury seen on crosssectional imaging. III. No ns urg ic a l m a na g e m e nt: In a hemodynamically stable patient with evidence o bleeding, the source can be visualized Quic k Cut Mos t patients angiographically and embolized. with low-grade to moderate IV. Surgic a l m a na ge m e nt: At surgery, hemostasis is usually obtained via liver injuries can be s a ely packing. Less common methods to control bleeding include tractotomy, admitted and obs erved and resectional debridement, anatomic resection, and hepatic artery ligation. do not need liver-s pecif c intervention. V. La te c o m p lic a tio ns : Subcapsular and intrahepatic hematomas can be care ully observed, but many ultimately require drainage. A. Perihepatic collections: usually become in ected whether o blood or bile and must be drained B. Biliary stulas: May track to the skin or into the chest (biliopleural, bronchobiliary stula). reatment is similar to that or GI stulas. C. Traumatic arteriovenous stulas (AVFs): Result usually rom penetrating trauma. Large stulas are best treated by arterial embolization. D. Arteriobiliary stulas: treated via arteriography and embolization

P o rta l Hyp e rte ns io n

I. P a tho p hys io lo g y: abnormal elevation o portal venous pressure Quic k Cut In portal greater than 5–6 mm Hg hypertension, submucosal A. Increase in portal pressure: leads to collateral development to varices are likely to hemorrhage decompress the portal system into the systemic circulation (esophageal varices, B. Dilated veins or varices: likely to develop when pressure is hemorrhoidal bleeding). greater than 20 mm Hg II. Intra he p a tic e tio lo g y: most common A. Cirrhosis (alcohol and hepatitis C virus): causes 85% o portal hypertension in the United States B. Schistosomiasis: Common cause worldwide. Portal hypertension develops when parasitic ova in small portal venules cause a presinusoidal block. C. Other: Wilson disease, hepatic brosis, and hemochromatosis are occasional causes. III. P re he p a tic e tio lo g y: rare; more commonly encountered in children (e.g., portal vein obstruction due to thrombosis, congenital atresia, or stenosis rom extrinsic compression) IV. P o s the p a tic e tio lo g y: also rare A. Budd-Chiari syndrome: characterized by hepatic vein thrombosis; may be idiopathic or secondary to a hypercoagulable state as occurs with tumors, hematologic disorders, OCP use, and trauma B. Other: Any process leading to severe right ventricular ailure, splenic disease, and splenic AVFs/ shunts also lead to posthepatic portal hypertension. V. Clinic a l p re s e nta tio n: includes encephalopathy, GI hemorrhage, malnutrition, and ascites VI. Me d ic a l m a na g e m e nt o a c ute va ric e a l he m o rrha g e : includes the ollowing A. Esophagogastroduodenoscopy (EGD): Should be per ormed as soon as possible to nd the site o bleeding and determine the presence o varices. Upper GI hemorrhage in cirrhotic patients

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211

results rom varices (35%), erosive gastritis (40%), peptic ulcer disease (15%), and esophageal tears (Mallory-Weiss syndrome, 10%). 1. Variceal banding with small rubber bands: treatment o choice 2. Sclerotherapy: controls bleeding temporarily in 80%–90% o patients and is associated with minimal mortality B. Pharmacotherapy: vasopressin (vasoconstricts the Quic k Cut splanchnic circulation), nitroglycerin (lowers portal pressure Variceal hemorrhage independently), somatostatin (splanchnic vasoconstriction) is the principal li e-threatening complication o portal C. Sengstaken-Blakemore tube: nasogastric tube with esophageal hypertens ion and requires and gastric balloons or tamponade o varices emergency intervention. D. Transjugular intrahepatic portosystemic shunt (TIPS): now the pre erred procedure or controlling variceal bleeding (Fig. 13-5) VII. Surg ic a l m a na g e m e nt: Acute massive bleeding re ractory to nonsurgical maneuvers requires emergency intervention. However, emergent surgical procedures are rarely per ormed currently due to high mortality.

A

Quic k Cut TIPS has es s entially replaced s urgical portos ys temic s hunts .

B

He pa tic ve in

P orta l ve in

C

E He pa tic ve in

P orta l ve in

D

Fig ure 13-5: Trans jugular intrahepatic portos ys temic s hunt. A wire is pas s ed through an hepatic vein branch, acros s the liver parenchyma, and into a portal vein branch. The parenchymal path is dilated and a s tent is placed acros s it to maintain patency o the newly created venous conduit. This conduit allows the portal blood to ow reely into the s ys temic venous s ys tem, thus lowering portal pres s ure and the propens ity to bleed rom es ophageal varices . (From Mulholland MW, Lillemoe KD, Doherty GM, et al. Greenf eld’s Surgery, 4th ed. Baltimore: Lippincott Williams & Wilkins ; 2005.)

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VIII. Ele c tive m a na g e m e nt: aims at preventing rebleeding A. Nonoperative management: IPS, EGD banding/sclerosing B. Operative shunts: rarely per ormed 1. Nonselective portosystemic shunts: portacaval, mesocaval, and their variations 2. Selective portosystemic shunts: distal splenorenal (Warren) C. Liver transplantation: only therapy that addresses the underlying liver disease and restores the patient’s hepatic unctional reserve to normal IX. Hyp e rs p le nis m : Common in patients with portal hypertension Quic k Cut and should be treated nonoperatively; 50% o patients who Splenectomy or undergo shunting show improvement. hypers plenis m s hould be per ormed only in cas es o X. As c ite s : complication o hepatic disease/cirrhosis s plenic vein thrombos is . A. Etiology: Results rom sinusoidal hypertension, hypoalbuminemia, abnormal hepatic and abdominal lymph production, and abnormal salt and water retention by the kidneys. Impaired hepatic metabolism o aldosterone leads to salt and water retention. B. Management: Consists o salt/water restriction and diuretics; peritoneal-jugular shunting and IPS may be used to treat re ractory ascites.

GALLBLADDER PATHOLOGY Cho le lithia s is I. Ga lls to ne s : Form as a result o bile precipitation. Most stones (70%) are made up o cholesterol, bilirubin, and calcium. Quic k Cut A. Stone type: cholesterol stones (increase in the cholesterol to Symptomatic bile salts or lecithin ratio predisposes to stone ormation), cholelithias is us ually requires pigmented stones (bilirubin; associated with hemolysis and cholecys tectomy. hemoglobinopathies), calcium bilirubinate stones (associated with in ection or in ammation o the biliary tree) B. Prophylactic treatment: scant evidence to justi y II. Surg ic a l tre a tm e nt: Calci ed or porcelain gallbladder should be removed because the risk o malignancy, although the incidence is less than 5% in recent series. III. Co m p lic a tio ns o c ho le c ys te c to m y: retained stone (which can be extracted with ERCP) and common bile duct injury (which requires surgical hepatobiliary reconstruction)

Cho le c ys titis I. Ga llb la d d e r inf a m m a tio n: In 85%–90% o patients, cholecystitis is caused by calculi, bile stasis, and bacteria. II. Chro nic c ho le c ys titis : Complaints include nausea, vomiting, and intermittent RUQ pain. Symptoms may be associated with eating atty oods. Laboratory studies are generally normal; treatment is elective cholecystectomy. III. Ac ute c ho le c ys titis : Most cases are due to an impacted stone in the gallbladder neck/cystic duct with resultant obstruction. A. Clinical presentation: Fever, nausea and vomiting, RUQ tenderness with/without rebound tenderness, and Murphy sign are common. B. Diagnosis and treatment: Ultrasound is diagnostic; per orm laparoscopic cholecystectomy, i possible, either immediately (i.e., within 72 hours) or as interval surgery (4–6 weeks). IV. Ac a lc ulo us c ho le c ys titis : acute or chronic cholecystitis in the Quic k Cut Some complications absence o stones o cholecys titis /cholelithias is A. Acute orm: occurs as a complication o burns, sepsis, trauma, or require urgent s urgery collagen vascular disease. ypically occurs in ICU patients. including emphys ematous / B. Diagnosis and treatment: HIDA scan is especially help ul with gangrenous gallbladder and the diagnosis; treatment is cholecystectomy or percutaneous per orated gallbladder. cholecystostomy i the patient is too ill to tolerate surgery.

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213

Ga llb la d d e r Tra um a I. Tre a tm e nt: usually managed with cholecystectomy during exploratory laparotomy II. As s o c ia te d vis c e ra l injurie s : common; most requently involve the liver

BILIARY TREE PATHOLOGY Cho le d o c ho lithia s is I. Sto ne s in the c o m m o n b ile d uc t: can be single or multiple and are ound in 10%–20% o patients who undergo cholecystectomy II. Clinic a l p re s e nta tio n: RUQ pain that radiates to the back and right shoulder, intermittent obstructive jaundice, acholic stools, or bilirubinuria III. De nitive d ia g no s is : ultrasonography, ERCP, and labs IV. Tre a tm e nt: ERCP be ore or af er cholecystectomy, intraoperative cholangiogram, biliary-enteric connection (e.g., choledochoduodenostomy or choledochojejunostomy)

Cho la ng itis I. Etio lo g y: ascending in ection o the bile ducts, associated with obstruction due to stones or benign stricture II. Clinic a l p re s e nta tio n: Charcot triad o ever, jaundice, and RUQ pain is present in 70% o cases. III. Tre a tm e nt: includes antibiotics, resuscitation with uids/ electrolytes, and relie o the obstruction

Quic k Cut Mos t s tones ound in the ducts are ormed in the gallbladder.

Quic k Cut Common bile duct s tones pos t cholecys tectomy are arbitrarily def ned as retained s tones i they pres ent within a year. A ter one year, they are thought to be primarily occuring and not retained.

Quic k Cut E. coli is the mos t commonly cultured organis m in cholangitis .

P rim a ry Sc le ro s ing Cho la ng itis I. Etio lo g y: Disease o unknown etiology that a ects the biliary tract, resulting in stenosis or obstruction o the ductal system. PSC is associated with ulcerative colitis. Progressive obstruction results in biliary cirrhosis and liver ailure. II. Clinic a l p re s e nta tio n: Symptoms include RUQ or painless jaundice, usually without ever/chills, pruritus, atigue, and nausea; associated with ulcerative colitis. III. Dia g no s is : ERCP or a transhepatic cholangiogram IV. Tre a tm e nt: includes internal biliary drainage (stenting), hepatobiliary reconstruction, -tube, and orthotopic liver transplantation

Bilia ry Ne o p la s m s I. Ove rvie w : Benign tumors o the gallbladder are rare (papilloma, adenomyoma, ibroma, lipoma, myoma, myxoma, Quic k Cut and carcinoid). The only truly curable gallbladder II. Ca rc ino m a o the g a llb la d d e r: Accounts or 4% o all carcinoma is when the carcinomas; 80% o these are adenocarcinomas. tumor is ound incidentally at A. Clinical presentation: Patient usually complains o pruritus, cholecys tectomy. anorexia, weight loss, and RUQ pain. Jaundice occurs late. B. Treatment: Generally surgical, although less than 10% are resectable. I gallbladder cancer is ound in a specimen removed or benign disease, proceed as ollows. 1. Con ned to the mucosa (T1): No urther treatment is necessary. 2. Invasive disease ( T1): Partial hepatectomy af er appropriate imaging workup is indicated. III. Ca nc e r o the b ile d uc ts A. Risk actors: sclerosing cholangitis, chronic parasitic in ection o the bile ducts, gallstones (present in 18%–65% o cases), and exposure to T orotrast (a contrast agent used in the 1950’s) B. Diagnosis: may be made by percutaneous transhepatic cholangiography, ERCP, C , or MRI 1. Location: umor may be in the distal common bile duct, common hepatic duct, cystic duct, or the right or lef hepatic duct (most common location).

214

Chapter 13

Biliary ree Pathology

2. Metastasis: initially to the regional lymph nodes (16%), spreads by direct extension into the liver (14%), or metastasizes to the liver (10%) C. Treatment: Proximal lesions require hepatic resection and biliary reconstruction. Distal tumors usually require a Whipple operation.

Quic k Cut Cholangiocarcinoma o the con uence o the hepatic ducts is termed a Klatskin tumor.

Cho le d o c ha l Cys ts I. Ove rvie w: Congenital mal ormations o the pancreaticobiliary Quic k Cut tree. Diagnosis is with ultrasound, ERCP, and MRCP. The mos t common II. Cla s s i c a tio n: as ollows pres enting s ymptom o A. Type I: Fusi orm dilatation o the common bile duct. reated a choledochal cys t is with cholecystectomy, cyst excision, and a Roux-en-Y intermittent jaundice. choledochojejunostomy. B. Type II: Diverticulum o the common bile duct. reated by excision o the common bile duct diverticulum. C. Type III: Choledochocele involving the intraduodenal portion o the common bile duct. reated by cyst excision and choledochoduodenostomy or by transduodenal sphincteroplasty. D. Type IV: Cystic involvement o the intrahepatic bile ducts (Caroli disease); may be atal. Patients require liver transplantation. III. Tre a tm e nt: In adults, all choledochal cysts are removed due to the 5% risk o developing malignancy.

Othe r I. Bilia ry tre e tra um a : Most extrahepatic bile duct injuries are iatrogenic, occurring during cholecystectomy. Diagnosis by ERCP. reatment with end-to-end (duct-to-duct) anastomosis may be done at the time o initial injury; otherwise, a Roux-en-Y choledochojejunostomy is necessary. II. Intra p e rito ne a l e xtra va s a tio n o b ile : Extravasation o sterile bile results in chemical peritonitis. In ected intraperitoneal bile induces a ulminant and requently atal peritonitis.

He p a tic Re s e c tio n

Quic k Cut Only 15% o intraoperative biliary injuries are diagnos ed at the time o s urgery.

Quic k Cut I. Rig ht o r le t he p a tic lo b e c to m y: T e right and lef lobes are Hepatic res ections divided by the interlobar ssure, a plane running between the rely on the hepatic s egmental gallbladder ossa and the IVC anatomy. II. Tris e g m e nte c to m y: removes the entire right lobe and the median segment o the lef lobe across the anatomic division o the alci orm ligament (leaving only the lef lateral segment) III. Le t la te ra l s e g m e nte c to m y: removes the segment o liver to the lef o the alci orm ligament IV. We d g e re s e c tio ns : Per ormed or small lesions near the liver sur ace that do not require a ull lobectomy. T ese resections do not adhere to anatomic boundaries but are sa e because a limited amount o tissue is transected.

Chapter 14

Pancreas

H. Richard Alexander, Peter E. Darwin, and Ronald J. Weigel

ANATOMY AND P HYSIOLOGY Cha ra c te ris tic s I. Orie nta tio n: T e pancreas is a 12–15-cm long solid organ that lies in a slightly oblique transverse orientation in retroperitoneum o the upper abdomen (Fig. 14-1). T e anterior border o the pancreas is covered by a smooth glistening membrane, the visceral peritoneum, which must be divided to gain access to the gland. Quic k Cut II. Divis io ns : our anatomic portions o the gland The pancreas has a A. Head: lies in the right upper quadrant (RUQ) and is nested into light pink color dis tinct rom the medial border o the duodenum adjacent retroperitoneal at. B. Neck: lies directly over the superior mesenteric vein (SMV) C. B dy: lies to the lef o the SMV D. Tail: lies adjacent to the hilum o the spleen in the lef upper quadrant Infe rior ve na ca va P orta l ve in Common bile duct

Aorta S ple nic a rte ry S ple nic ve in

P orta he pa tis

Ga llbla dde r Ga s troduode na l a rte ry Acce s s ory pa ncre a tic duct (S a ntorini) Acce s s ory a mpulla Ma jor pa pilla

Ta il

Ma in pa ncre a tic duct (Wirs ung) He a d

Body Uncina te proce s s S upe rior me s e nte ric ve in S upe rior me s e nte ric a rte ry

Fig ure 14-1: Anatomy o the pancreas . The normal anteropos terior thicknes s o the head is les s than 2.5 cm; the neck, 1.5 cm; the body, 2 cm; and the tail, 2.5 cm.

215

216

Chapter 14

Anatomy and Physiology

Im p o rta nt Ana to m ic Re la tio ns hip s I. He a d : Head is slightly lower (caudal) than the tail; it lies over the aorta and is used to the medial wall o the duodenal C-loop. Just cephalad to the head are the porta hepatis structures including the common bile duct, portal vein, and proper hepatic artery. A. C mm n bile duct and pancreatic duct: Course through the head o the pancreas and enter through a common channel into the medial wall o the duodenum via the ampulla o Vater. Flow Quic k Cut through the common channel is regulated by the sphincter o Oddi. There is a clos e B. N menclature inc nsistency: Within the head o the pancreas, proximity (s ometimes with a common channel) between the distal common bile duct and the proximal pancreatic duct are the pancreatic duct and the adjacent to each other. T e pancreatic duct contains multiple side common bile duct. Pathology branches at regular intervals. a ecting one duct may C. Pancreatic head: has a common blood supply with the medial s econdarily a ect the other. wall o the du denal C-l p D. B dy and tail: derive their blood supply rom the splenic artery II. Unc ina te p ro c e s s : small portion o the head that lies posteriorly to the SMV III. Ne c k: lies over the SMV, which joins the splenic vein at the superior border o the pancreas to orm the portal vein IV. Bo d y: lies adjacent to the posterior wall o the stomach, orming the posterior border o the lesser omental bursa or lesser sac V. Ta il: close to the splenic hilum

Va s c ula ture I. Ge ne ra l: Well-vascularized organ that derives most o its blood supply rom the celiac axis branches. Venous drainage is exclusively through the portal venous system to the liver. In ammatory and neoplastic conditions o the pancreas can result in thrombosis or encasement o adjacent vascular structures. II. He a d a nd ne c k: derive their blood supply rom the gastroduodenal artery (GDA) and a branch rom the superior mesenteric artery (SMA) A. GDA: branch o the common hepatic artery; it courses behind the duodenum and branches into the pancreaticoduodenal arcade B. Branch r m the SMA: joins the arcade to create a very rich and redundant blood supply to this area o the gland C. Ven us drainage: via numerous venous tributaries directly entering the SMV III. Bo d y a nd ta il: derive their blood supply rom the splenic artery, which is one o the three branches o the celiac axis and courses Quic k Cut along the superior border o the gland Due to the A. Splenic artery: typically has a serpiginous course, and numerous arrangement o blood vessels, small branches enter the gland along its superior border the in erior pancreatic body and B. Ven us drainage: via the splenic vein, which is slightly caudal to tail can be mobilized with ease. the artery and typically contained more or less within the body o the gland C. SMV and SMA: Vein lies at the in erior border o the pancreatic Quic k Cut neck; immediately adjacent and slightly posterior to the lef lies A replaced right the artery. hepatic artery (incidence 25% )

Duc ta l Ana to m y I. P a nc re a tic d uc ts : drain pancreatic secretions into the duodenum II. Ma jo r a nd m ino r s ys te m s A. Duct Wirsung: empties into the ampulla o Vater in conjunction with the distal common bile duct; the major system B. Duct Sant rini: empties into a minor papilla 2 cm above and medial to the ampulla o Vater; the minor system

P hys io lo g ic Func tio ns I. Exo c rine p a nc re a s : Makes 800–1,000 mL daily o alkaline bicarbonate-rich uid (pH 8) that contains proteases, lipases,

or a replaced common hepatic artery (incidence 2.5% ) aris ing rom the SMA can complicate pancreatic dis s ection.

Quic k Cut The pancreas has both exocrine and endocrine unctions .

Chapter 14

Pancreas

217

and other enzymes or digestion. Under pathologic conditions, the integrity o the exocrine ductal system may be breached; leakage o enzyme-rich uid into the retroperitoneum can result in sepsis, hemorrhage, and in ammation with secondary shif s in uids. II. End o c rine p a nc re a s : Synthesizes various hormones; most important are the islet cells that produce various peptide hormones such as insulin.

PANCREATITIS De f nitio n a nd Cla s s if c a tio n I. P a nc re a titis : in ammatory process in the pancreas II. Cla s s if c a tio n: divided into our categories to clari y the di erent syndromes that are ound and to improve the standardization o treatment and prognosis A. Acute pancreatitis 1. Characteristics: arises in a previously asymptomatic patient and subsides with appropriate treatment; it can involve other regional tissues or remote organ systems 2. Clinically based classif cati n: rom the International Symposium on Acute Pancreatitis a. Severe acute pancreatitis b. Mild acute pancreatitis c. Acute uid c llecti n Quic k Cut d. Pancreatic necr sis Chronic pancreatitis e. Acute pseud cysts can be as s ociated with . Pancreatic abscess exocrine ins u f ciency (malabs orption), endocrine B. Acute relapsing pancreatitis: series o recurrent episodes o ins u f ciency (diabetes ), or acute pancreatitis in an otherwise asymptomatic patient both. C. Chr nic relapsing pancreatitis: chronic in ammation with chemical evidence o pancreatitis, which uctuates in its intensity without a period o resolution D. Chr nic pancreatitis: Shows unrelenting symptoms due to Quic k Cut pancreatic in ammation and brosis; the pancreatic duct and An alcoholic with parenchyma may show calci cation. pancreatitis s till needs to have

Etio lo g y

galls tones ruled out.

I. Ac ute : Approximately 75% o pancreatitis cases can be explained on the basis o biliary tract disease or alcohol abuse, although the exact mechanism or the production o pancreatitis remains theoretical. A. Gallst ne pancreatitis: T ought to be induced by the in ammation that results rom passage o stones into the common bile duct. Most of en, the gallstone has passed by the time the patient is studied. 1. Pancreatic duct and bile duct: empty into a common papilla 2. Obstructi n: Entire common channel can be obstructed i a large calculus becomes impacted in the papilla. 3. Re ux: Bile ows into the pancreatic duct. Experiments have shown that re ux can induce pancreatitis; however, it is unclear whether this re ux occurs in humans. B. Alc h l-induced pancreatitis: may be the result o various mechanisms 1. Alc h l: implicated in the direct damage o acinar cells and the increased enzyme concentration in pancreatic secretion 2. St nes: development encouraged by high-protein concentration with calcium carbonate precipitation in the protein- lled spaces 3. In ammati n and f br sis: Multi ocal ductal obstruction and increased intraductal pressure along with increased permeability caused by alcohol destroys parenchyma. C. C ngenital abn rmalities and hereditary pancreatitis: Duct strictures, pancreas divisum, and metabolic disorders (e.g., hypertriglyceridemia and hypercalcemia) are actors in a small percentage o cases. D. Iatr genic: Pancreatitis can be caused by instrumentation (e.g., endoscopic retrograde cholangiopancreatography [ERCP]), trauma, or certain drugs (steroids, sul onamides, urosemide, and thiazides).

218

Chapter 14

Pancreatitis

E. In ecti us: Mumps, coxsackievirus, cytomegalovirus, herpes simplex virus, mycoplasma, legionella, salmonella, ungi, and parasites have been implicated. F. Malignancy: Pancreatic ductal obstruction rom cancer may present as acute pancreatitis. G. Du denal ulcer: Penetrating ulcer may mani est as acute pancreatitis. H. Idi pathic: Up to 20% o cases have no identi able cause. II. Chro nic A. T xic-metab lic: Alcohol, tobacco smoking, occupational hydrocarbon exposure, hypercalcemia, and hyperlipidemia are actors that may contribute to in ammation/ brosis. B. Genetic: Cystic brosis transmembrane regulator (CFTR) and other genetic mutations (PRSS1 and SPINK) are associated with chronic pancreatitis. C. Idi pathic: Majority o cases worldwide have no de nable etiology. D. Aut immune: Immunoglobulin G4–related pancreatitis may present as either acute or chronic disease. Associated ocal pancreatic enlargement and biliary obstruction may mimic pancreatic carcinoma.

Ac ute P a nc re a titis I. Clinic a l p re s e nta tio n: varies rom mild abdominal discom ort to pro ound shock with hypotension and hypoxemia, depending on the severity o the in ammatory process A. Pain: Most patients have mild to moderate abdominal tenderness, classically epigastric pain radiating to the back. B. Severe cases: Rigid abdomen with epigastric guarding, rebound tenderness, and marked abdominal pain may be present. C. Retr perit neal hem rrhage: caused by severe pancreatic in ammation and necrosis, which can lead to large third-space uid losses, hypotension, tachycardia, and shock with blood dissection (i.e., the blood extravasates between tissue planes) 1. Turner sign: Blood dissection extends to the ank, resulting in ank ecchymoses. 2. Cullen sign: Blood dissects up the alci orm ligament and creates a periumbilical ecchymosis. II. His to ry: Patient commonly mentions recent consumption o a heavy meal, many times with generous quantities o alcoholic beverages. T e pain typically begins 1–4 hours af er a meal and is of en less severe when the patient is slumped orward. Quic k Cut The increas e III. Dia g no s is : aided by the ollowing studies: in amylas e level is not A. Serum amylase level: increased in 95% o patients with acute proportional to the s everity o pancreatitis the pancreatitis . 1. False-p sitives: Approximately 5% o all amylase determinations; 75% o patients with abdominal pain and an increased amylase level have pancreatitis. Quic k Cut 2. Advantages: Some in erences can be made rom the amylase The pancreas must level. Higher amylase levels (usually over 1,000 Somogyi be intact and unctional to units) may indicate gallstone pancreatitis synthesize amylase and release 3. Origin: Some circulating amylase is not o pancreatic origin; it into the circulation; there ore, patients with acute pancreatitis major alternative source is the salivary glands. superimposed on chronic B. Amylase-t -creatinine clearance rati : Amylase determinations pancreatitis may not show an are more sensitive identi ers when the amylase clearance rate increase in serum amylase. is compared with the creatinine clearance rate and a ratio is established. 1. Amylase-t -creatinine greater than 5: strongly suggestive o Quic k Cut pancreatitis An elevated 2. Rapid renal clearance amylase: Using the ratio avoids lipas e level is als o s een in this problem, which tends to reduce serum levels below the pancreatitis . point where a simple serum amylase determination would be positive. 3. Impaired renal uncti n: A ects the creatinine clearance rate sooner than the amylase clearance rate. Even in this situation, however, the amylase-to-creatinine clearance ratio appears to be more sensitive than the serum amylase level.

Chapter 14

Pancreas

219

C. Radi graphic imaging 1. Upper abd minal plain f lms: Relatively insensitive or diagnosis. Signi cant ndings include the ollowing. a. Calcif cati n (in the area the lesser sac and pancreas): may indicate chronic pancreatitis, which is most of en ound in association with alcoholism b. Gas c llecti n (in the lesser sac): suggests abscess ormation in or around the pancreas c. “Cut ” sign: Area o colonic spasm adjacent to an in amed pancreas causes the gas in the transverse colon to end abruptly. 2. Barium studies: may show upper gastrointestinal (GI) abnormalities a. Du denal C-l p: may be widened by pancreatic edema b. Hyp t nic du den graphy: may show the “pad” sign, a smoothing out o the duodenal mucosal olds by the edematous pancreas and the in ammatory response on the medial aspect o the C-loop 3. Angi graphy: Use ul or delineating pancreatic and hepatic blood supply be ore radical surgery. Largely superseded by spiral computed tomography (C ) scan and magnetic resonance imaging (MRI). D. Ultras und (US) imaging: especially use ul in the diagnosis o Quic k Cut pancreatitis US may be 1. Anat mic and vascular landmark changes: can be delineated particularly us e ul in the initial a. Acute pancreatitis: suggested by swelling greater than the workup o pancreatitis to rule out galls tones . normal anteroposterior thickness and loss o tissue planes between the pancreas and the splenic vein b. Other pancreatic an malies: may also be ound (e.g., a change in duct size or calci cation) c. Chr nic pancreatitis: of en mani ested by the presence o calci cation or pseudocysts containing uid or showing a complex cystic structure d. Ascites (easily diagn sed by US): may or may not be present in chronic pancreatitis 2. Ech genicity: a ected by various pancreatic disorders a. Decreased: Most diseases decrease the echogenicity because they include edema and in ammation. b. Increased: generally due to gas or calci cation 3. Fluid densities: lying within the pancreas indicate cysts, abscesses, or possibly lymphoma 4. Ch lelithiasis: May be identi ed, suggesting gallstone pancreatitis. US may also show the presence o cholecystitis or a dilated common bile duct. 5. US limitati n: cannot be per ormed when excessive bowel gas is present, as with an ileus E. Pancreatic CT scan: extremely help ul; provides higher resolution than US, and it is not limited by the masking e ect o Quic k Cut intestinal gas Dynamic CT can be 1. Advantages: Improvements in availability, speed, and us ed to diagnos e pancreatic necros is . resolution in C have made it the most important imaging modality in initial diagnosis and treatment o pancreatitis. 2. CT severity index (including percent gland necr sis): provides valuable prognostic in ormation and allows exclusion o addition pathology and complications ( able 14-1) F. Magnetic res nance (MR) 1. MR pancreat grams and ch langi grams: Widely available and are very use ul or delineating anatomy be ore surgery. T ey can provide excellent detail o the pancreatic duct and bile ducts. 2. MR angi graphy: increasingly available and has replaced invasive angiography or planned pancreatic surgery G. ERCP: In the rst 5 days o severe acute pancreatitis, use is dangerous and is associated with an increased mortality rate. However, patients with acute biliary pancreatic and concurrent cholangitis bene t rom urgent endoscopic intervention ( able 14-2). IV. P ro g no s is : aided by certain signs that are associated with a higher mortality rate and, there ore, are use ul prognostic indicators A. Pr gn stic indicat rs (Rans n signs): able 14-3 B. Other: Acute Physi l gy and Chr nic Health Evaluati n II (APACHE II) score ( able 14-4), Atlanta classi cation or severe acute pancreatitis, Balthazar score, and C severity index assist in identi ying those at high risk or morbidity and mortality.

220

Chapter 14

Pancreatitis

Ta b le 14-1: Ra d io lo g ic Se ve rity As s e s s m e nt Ba ltha za r Co m p ute d To m o g ra p hy Sc o re Gra d e

Co m p ute d To m o g ra p hy Find ing s

A

Normal

B

Focal or di use enlargement o pancreas

C

B

peripancreatic inf ammation

D

C

single f uid collection

E

D

two or more f uid collections and/or presence o gas Co m p ute d To m o g ra p hy Se ve rity Ind e x

Co m p ute d To m o g ra p hy Gra d e

As s ig ne d Sc o re

P e rc e nt Ne c ro s is

As s ig ne d Sc o re

A

0

None

0

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1

30

2

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2

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3

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4

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4 6

Ma xim um s c o re 10 p o ints • Co n ic ting d a ta re g a rd ing e xte nt o ne c ro s is a nd c linic a l o utc o m e Re tro s p e c tive s tud y o 268 p a tie nts , CTSI 5: • 8 m o re like ly to d ie • 17 m o re like ly to ha ve p ro lo ng e d ho s p ita l s ta y • 10 m o re like ly to ne e d ne c ro s e c to m y CTSI, computed tomography severity index.

V. Tre a tm e nt: Certain measures are considered standard, but not all o them are indicated in each case. T e patient’s symptoms dictate much o the treatment. A. Nas gastric sucti n: Used to control nausea and vomiting, decrease pancreatic stimulation, and decrease GI distention rom an ileus. T is suction also makes the patient more com ortable, although it does not appear to shorten the hospital stay. B. Intraven us (IV) uids: Used to replace the third-space uid loss rom edema and extravasation into the peripancreatic spaces. Crystalloid solutions are usually adequate. 1. Patient m nit ring: Include strict input/output measurement (with a Foley catheter). 2. Severe cases with unstable hem dynamics: Invasive hemodynamic monitoring is used.

Ta b le 14-2: Ro le o End o s c o p ic Re tro g ra d e Cho la ng io p a nc re a to g ra p hy P a nc re a titis Ac ute

P e rs is te nt

Co m p lic a te d

Co nva le s c e nt

Re c urre nt

Dia g no s is

Cause is in question

Status o main duct; indication or surgery

Assessment o pseudocysts and stulas

Cause is in question (e.g., lymphoma)

Anatomic assessment (e.g., pancreatic divisum)

Tre a tm e nt

Sphincterotomy or biliary obstruction

Sphincterotomy; stone extraction

Stent or internal drainage

Sphincterotomy in selected highrisk patients

Sphincterotomy or stent in selected patients

Reprinted with permission rom Neoptolemos J P. In: Bradley EL III, ed. Acute Pancreatitis: Diagnosis and Therapy. New York: Raven Press; 1994:75.

Chapter 14

Pancreas

221

Ta b le 14-3: Ra ns o n’s 11 Crite ria o r De te rm ining the Se ve rity o P a nc re a titis On Ad m is s io n Age WBC

55 years 16,000/mm 3

Glucose LDH SGOT

200 mg/dL

350 IU/L 250 SF units %

Initia l 48 Ho urs HCT decrease

10 percentage points

BUN increase

5 mg/dL

Ca 2

8

Pao 2

60 mm Hg

g/dL

Base de cit 4 mEq/L Estimate f uid 6,000 mL

WBC, white blood cell count; LDH, lactate dehydrogenase; SGOT, serum glutamine-oxaloacetic transaminase; HCT, hematocrit; BUN, blood urea nitrogen; Ca 2 , calcium ion; Pao 2 , partial pressure o oxygen in arterial blood.

C. Antibi tics: May reduce the risk o abscess ormation and o lesser sac collections, which of en progress to abscess ormation. Prophylactic antibiotics are usually reserved or those cases with necrosis in an attempt to maintain sterile tissue. D. Pao 2 m nit ring and serial chest radi graphs: For patients who have severe pancreatitis, respiratory distress is common, as are pleural e usi ns, which are more of en on the lef and contain high concentrations o amylase. E. Withh ld ral eedings: Until laboratory test results return to Quic k Cut normal and pain is gone or 48 hours. In cases without severe ileus, Exacerbations o enteral elemental eedings are pre erred to parenteral nutrition. pancreatitis are common with F. Surgery premature oral eedings . 1. Indicati ns a. T c nf rm the diagn sis: In severe cases that do not respond to medical management. Symptoms can be mimicked by visceral per oration, mesenteric arterial occlusion, and other intra-abdominal catastrophes. b. T relieve biliary r pancreatic duct bstructi n (1) Early biliary tract perati n: May increase mortality Quic k Cut in patients who have severe pancreatitis. I possible, The o ending s tone surgery should be delayed until the pancreatitis has will have pas s ed by the time subsided. o s urgical exploration in greater than 90% o patients . (2) C ntinued patient status deteri rati n: Surgical expl rati n may bec me necessary. (3) End sc pic clearance c mm n bile duct st nes: m st en the pre erred r ute Quic k Cut c. T drain the lesser sac: Drainage increases morbidity and Pancreatic collections occur in patients should be per ormed only af er septic complications have with extens ive necros is . occurred. It is not e ective as a prophylactic measure. The approach is to s ample (1) Indicati n: improves prognosis when sepsis has them endos copically or already occurred and lesser sac collections and percutaneous ly, but drainage pancreatic necrosis are present is only per ormed or pus . (2) Established lesser sac abscesses: Drains can be inserted af er opening the lesser omentum widely. (3) Irrigati n catheters: can also be used as part o the therapeutic plan (4) Dependent drainage thr ugh the transverse mes c l n: use ul approach when the upper abdomen is obliterated by in ammation and adhesions 2. Operative pr cedures a. Ch lecystect my: may be required in patients who have gallstone pancreatitis and persistent acute pancreatitis that does not respond to supportive measures b. Resecti n ( r acute pancreatitis): Dangerous and not indicated. Removing necrotic pancreas (nonanatomic dissection) may be required in pancreatic abscess. T ese operations have a high mortality rate.

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222 Pancreatitis

Chapter 14

Pancreas

223

c. Perit neal lavage: can be use ul in excluding other severe Quic k Cut intra-abdominal processes and can be therapeutic in severe Severe pancreatitis pancreatitis is us ually managed non• Catheters: can be placed percutaneously, and operatively except or antibiotics can be included in the lavage solution pers is tent biliary obs truction • Lapar t my: When per ormed or diagnosis and lesser due to s tones , abs ces s or s eps is , or ailure to improve. sac exploration, accompanying peritoneal lavage can be undertaken. • C mplicati ns: include a deterioration o pulmonary unction, which can be compromised by abdominal distention rom the dialysis solutions. A high glucose load in the dialysis solution can induce severe hyperglycemia.

Re la p s ing P a nc re a titis I. Etio lo g y: commonly occurs in nonalcoholic patients and results rom biliary tract disease—either calculi in the ducts or in ammation and spasm o the sphincter o Oddi II. Dia g no s is : can be made by demonstrating the presence o biliary stones or biliary sphincter dys unction A. US: use ul or diagnosing biliary calculi Quic k Cut B. Micr sc pic examinati n the bile: Bile is aspirated Relaps ing through a suction tube placed in the duodenum and examined pancreatitis can res ult rom s tones or in ammation or white blood cells (WBCs), cholesterol crystals, and caus ing s pas m o the microspheroliths. s phincter o Oddi. III. Tre a tm e nt: based on the cause A. Patient with biliary calculi: Procedures include cholecystectomy, common bile duct exploration, biliary manometry, and sphincteroplasty plus pancreaticobiliary septum resection. B. Perisphincteric disease: gallbladder removal and a wide sphincteroplasty that includes the pancreaticobiliary septum C. P stch lecystect my patients: Of en have a positive provocative test and can be treated success ully by sphincteroplasty. A negative provocative test requires workup, including ERCP. Alcoholism should be ruled out. D. Patients with severe intrinsic disease: respond poorly to sphincteroplasty

Chro nic P a nc re a titis

Quic k Cut

I. P a tho lo g ic f nd ing s : include brosis and calci cation throughout Calcif cation o the the gland pancreas indicates chronic pancreatitis . A. Early changes: plugging o the small pancreatic ducts with proteinaceous material containing eosinophils B. With disease pr gressi n: Calci cation becomes prominent; multiple areas o ductal dilatation can result. C. Ductal dilatati n: in its end stages, produces a “chain-o -lakes” appearance D. C mm n bile duct bstructi n r du denal bstructi n: can occur in advanced cases as a result o in ammation in surrounding areas II. Ca us e : Almost always alcohol related. However, certain congenital anomalies can produce chronic ductal obstruction and chronic pancreatitis. III. Clinic a l p re s e nta tio n A. Hist ry unrelenting pain: usually the major indication or surgical intervention B. End crine insu ciency: Damage may be severe enough to cause impaired glucose tolerance or true diabetes. C. Ex crine pancreatic insu ciency: results in malabsorption, with consequent weight loss and steatorrhea D. Plain f lms: may show the calci cations in the ductal system or may aid in delineating neighboring areas that are caught in the in ammatory process E. Severe disease (in the head the pancreas): can mimic carcinoma and cause bile duct obstruction F. Splenic vein thr mb sis: may cause upper GI bleeding

224

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IV. Me d ic a l tre a tm e nt: Analgesia and endocrine replacement as needed are typical. A. Ex crine replacement with pancreatic enzymes: Pancrelipase or pancreozymin in high doses (i.e., 5 g our Quic k Cut times daily) can suppress pancreatic secretion by the eedback Surgery or chronic pancreatitis is cons idered phenomenon. when there is a dominant B. General nutriti nal measures: including alcohol avoidance s tricture, or re ractory pain. C. Octre tide: may be o bene t in select cases V. Surg ic a l tre a tm e nt: Depends on the condition o the pancreatic ducts, as determined by ERCP (Fig. 14-2). I ERCP is not possible and the patient must undergo an operation, pancreatograms can be obtained. A. Puest w perati n: Dilated chain-o -lakes duct is treated by wide unroo ng o the duct and dilated ductules, with drainage o the entire open pancreas into a de unctionalized jejunal loop. A side-to-side procedure may be used, or the surgeon may choose an invagination in which the pancreas is placed into the jejunal loop. B. Distal pancreatect my: used to treat a distal ductal obstruction C. Duval perati n: Proximal ductal obstruction can be treated by amputating the tail o the pancreas and draining the pancreas retrograde into a de unctionalized jejunal loop. T is is not as e ective or long lasting as lateral pancreaticojejunostomy. D. Patient with severe pain and a f br tic, n ndilated duct: Possible surgical procedures include the ollowing. 1. Child perati n: 95% pancreatectomy 2. Splanchnicect my: either abdominal or thoracic a. Technique: T is procedure serves only to relieve the pain o pancreatitis by dividing the splanchnic nerves, with no direct e ect on the underlying disorder. b. Disadvantage: also eradicates the pain rom appendicitis and other intra-abdominal problems, which may delay diagnosis o an abdominal emergency 3. Du denum-sparing pancreatic head resecti n: Approach has become a popular option or patients who have had ailed sphincteroplasties.

Child ope ra tion; re s e ct 95% Duva l Duode num

Re s e ct ta il; dra in proxima l duct to Roux-e n-Y loop

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P ue s tow; s ide -to-s ide pa ncre a ticoje junos tomy Liga me nt of Tre itz Re trope ritone a l duode num P a ncre a tic duct Roux-e n-Y loop

Fig ure 14-2: Surgical treatments or chronic pancreatitis: the Puestow, Duval, and Child operations.

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4. T tal pancreatect my and islet cell transplant: limited to select patients with hereditary relapsing pancreatitis and preserved endocrine unction

P s e ud o c ys t

Quic k Cut I. P a tho lo g ic f nd ing s Ps eudocys t is a late A. Lesser sac c llecti n: Pseudocyst orms as a result o brosis, complication o pancreatitis . thickening, and organization o the organs bordering the collection. B. N t lined by epithelium: Pseudocyst consists only o the in ammatory response o the neighboring organs. C. Related rgans: Stomach, duodenum, colon, and transverse mesocolon orm the walls. T e major organ involved is generally the stomach, which orms the anterior sur ace o the pseudocyst. D. Maturati n (3–5 weeks): not truly ormed until the walls are su ciently organized to become rm anatomic structures E. Natural hist ry: Depends on its size. Small pseudocysts may resolve; large pseudocysts with mature organized walls generally do not resolve. II. Clinic a l p re s e nta tio n A. Maturati n phase: Patient recovers rom a bout o pancreatitis but develops a persistent increase o amylase, a low-grade ever, a Quic k Cut minimally increased WBC count, and chronic pain. Bleeding into a B. C ntinu us min r bleeding: Causes a gradual decrease in ps eudocys t is an indication hemoglobin. More signi cant bleeds are associated with acute or angiographic intervention. pain or hemorrhagic shock. III. Dia g no s is : Pseudocysts are usually diagnosed by US or C scan. IV. Tre a tm e nt: Goal is to allow the maturation phase to continue until the walls o the pseudocyst have matured. Quic k Cut A. Diet: total parenteral nutrition ( PN) or an elemental diet or Maturation-phas e 3–4 weeks until maturation has occurred treatment s ometimes mus t be cut s hort becaus e o s eps is B. Surgical treatment mature pseud cysts or hemorrhage within the 1. Internal drainage: Best approach is through the anterior ps eudocys t. stomach wall to locate the rm connection that usually exists between the posterior stomach and the pseudocyst. a. Aspirate the cyst thr ugh the st mach wall: First step; af er which, an opening is made between the stomach and the pseudocyst and is sutured or hemostasis. b. Res luti n: Pseudocyst then drains into the stomach and generally resolves. 2. De uncti nalized (R ux-en-Y) l p jejunum: I the pseudocyst is not xed to an organ that lends itsel to internal drainage, suture a loop o jejunum to the pseudocyst wall to establish internal drainage. 3. External drainage: Used i the pseudocyst is not ound to be Quic k Cut mature and i suturing o the pseudocyst wall is not sa e. T e Ps eudocys ts are external drainage results in a pancreatic stula, which usually bes t drained internally; heals with continued PN. Pancreatic stula may be quite abs ces s es (in ected di cult to treat. ps eudocys ts ) are drained 4. Excisi n: rare; however, may be indicated i the pseudocyst is externally. small and is located distally in the tail o the pancreas C. End sc pic drainage: Mature collections within 1 cm o the stomach or duodenum can be drained internally via endoscopic ultrasound (EUS) guidance.

PANCREATIC MALIGNANCIES P a nc re a tic Ad e no c a rc ino m a

Quic k Cut Pancreatic cancer has a f ve-year s urvival rate les s than 5% .

I. Inc id e nc e : Approximately 43,000 new cases o pancreatic adenocarcinoma in 2009; incidence is 11.4 per 100,000 and has not changed in 10 years. A rican Americans have a higher rate than the white population. A. M rtality: Fourth most common cause o cancer death in the United States. Most patients have advanced disease at diagnosis, and the 5-year survival or all patients diagnosed with the disease is only 5%.

226

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Pancreatic Malignancies

B. Median age (in the United States): Age 72 years; only 10% o patients are age younger than 50 years. C. Risk act rs 1. Envir nmental act rs: most notably tobacco, as well as chlorinated hydrocarbon solvents and organochlorine insecticides 2. Patient-related act rs: diabetes mellitus, obesity, and the chronic in ammatory conditions cirrhosis or pancreatitis II. Clinic a l p re s e nta tio n Quic k Cut A. Sympt ms: Vague and nonspeci c, including anorexia, About 80% o weight loss, and atigue. Back pain is an ominous symptom pancreatic cancers occur in that requently indicates a locally advanced condition with the head; there ore, painles s malignant in ltration o the retroperitoneal splanchnic nerve jaundice rom dis tal bile duct obs truction is a common plexus. pres enting s ymptom. B. Obstructive jaundice: Patients will typically also experience acholic stools and dark urine. When jaundice is severe, patients will complain o severe pruritus and of en present with excoriation o the skin rom nocturnal scratching. C. Excreti n: Patients may report loose malodorous stools that oat in the bowl secondary to malabsorption o at rom exocrine insu ciency. D. Superf cial r deep thr mb phlebitis (Tr usseau sign): May be the initial presentation. It is migratory and ultimately develops in as many as 10% o patients. E. L cati n: Symptoms at the time o presentation are related to tumor location within the pancreas. 1. Head: Most common site; tumors here produce weight loss and obstructive jaundice in 75% o patients. a. Jaundice: Usually painless; skin excoriation related to pruritus may be present. b. Pain: when present, is usually upper abdominal and radiates to the back c. Physical exam: Usually normal outside o jaundice. Ascites, hepatic mass or hepatomegaly, and palpable lymphadenopathy in the lef supraclavicular region (Virchow node) or periumbilical (Sister Mary Joseph nodes) are physical ndings consistent with metastatic disease. d. C urv isier gallbladder: RUQ nontender mass may represent a passively dilated gallbladder secondary to bile duct obstruction. 2. B dy r tail: less common and generally present at a more advanced stage because tumors do not produce local symptoms III. Dia g no s is : Routine screening o asymptomatic populations Quic k Cut is currently not easible. Progress in serologic testing or tumor Pancreatic head markers provides hope or the uture. cancer may involve the SMV becaus e the vein is A. Abd minal ultras n graphy: Commonly used as the rst immediately adjacent to test to assess the etiology o jaundice. Uni ormly dilated ductal the head o the pancreas system without evidence o cholelithiasis or choledocholithiasis pos teriorly. is consistent with malignant obstruction. B. Pancreatic pr t c l c ntrast-enhanced CT: de nitive imaging test to assess or resectability o the primary tumor and or the presence o metastases C. Percutane us f ne-needle aspirati n (FNA) under CT guidance: can diagnose malignancy but should only be done rarely due to the risk o disseminating cancerous cells D. ERCP: Flexible side-viewing duodenoscope cannulates the pancreatic duct. Contrast medium is injected, and radiographs are taken. 1. Advantages: Small pancreatic cancers can be ound, and specimens via brushing can be collected rom the pancreatic duct or cytologic examination. 2. Success ul cannulati n: Requires a skilled endoscopist. A stent is usually placed to relieve the biliary obstruction. 3. EUS with FNA: pre erred technique or obtaining tissue or diagnosis a. Advantages: Yields very precise in ormation regarding relationship o the primary tumor to surrounding structures such as the hepatic artery or SMV. T is provides very high resolution o small lesions and can allow transduodenal needle biopsies. b. It is less speci c or staging o lymph node metastases.

Chapter 14

Pancreas

227

E. Percutane us transhepatic ch langi graphy: evaluation o patients who have obstructive jaundice and who cannot undergo ERCP 1. Pr cedure: With the patient under local anesthesia, a long Quic k Cut small-bore needle is inserted through the liver into a dilated The value o hepatic duct, and contrast medium is injected to identi y the EUS in tumor s taging is in site o obstruction. determining vas cular invas ion and local lymph nodes . 2. Jaundice: relieved preoperatively by passing a catheter It does not detect liver or through the site o obstruction peritoneal metas tas es , or 3. P tential c mplicati ns: bleeding rom the needle track in other f ndings o unres ectable the liver and sepsis cancer. IV. Tre a tm e nt A. Pancreatic du denect my (Whipple pr cedure): standard surgical treatment or adenocarcinoma o the head o the pancreas when the lesion is curable by resection (Fig. 14-3) 1. Resectability: Many patients are deemed unresectable, as evidenced by metastatic disease identi ed by abdominal imaging and con rmed by percutaneous biopsy. Resectability is con rmed at operation using several criteria. a. Metastases: No metastases in the abdominal cavity; avored sites o metastatic disease include liver and peritoneal dissemination.

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Fig ure 14-3: Whipple procedure. A: The head o the pancreas , dis tal common bile duct, gas tric antrum, and duodenum are removed. B: The GI tract, pancreatic duct, and bile duct are recons tructed.

228

Chapter 14

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F.

Pancreatic Malignancies

b. P rta hepatis structures intact: umor has not invaded this area including the hepatic artery or SMV as it passes behind the neck o the pancreas. c. Lapar sc py: Increased use to rule out peritoneal seeding be ore proceeding with laparotomy in selected patients. T is procedure is indicated in patients with tumors involving the body and tail o the pancreas and in patients with a cancer antigen 19-9 level 400 ng/mL or more. 2. Tissue diagn sis: not required be ore de nitive resection in patients who have a high suspicion o cancer; however, in cases o a question regarding the diagnosis or the mass cannot be immediately resected, tissue is required be ore de nitive nonoperative treatment can be initiated 3. “Classic” Whipple pr cedure: Removal o the head o the pancreas, duodenum, distal common bile duct, gallbladder, and distal stomach. An alternative is the pylorus-preserving Whipple in which the transection o the GI tract is across the duodenum just distal to the pylorus. Quic k Cut a. GI tract rec nstructi n: creation o a gastrojejunostomy The Whipple (or duodenojejunostomy), choledochojejunostomy, and procedure is a radical pancreaticojejunostomy pancreaticoduodenectomy. b. Operative m rtality rate: Should be 2% or lower in centers where this operation is requently per ormed. According to recent publications, the lower mortality rate is realized in institutions doing at least 20 o these procedures annually. c. C mplicati n rate: Considerable (25%); the most common include hemorrhage, abscess, and leakage ( stula) at the pancreaticojejunostomy. Distal pancreatect my (usually with splenect my and lymphadenect my): per ormed or carcinoma o the midbody and tail o the pancreas and or benign mucinous pancreatic tumors 1. Staging: should include laparoscopy 2. In selected patients: Procedure can be laparoscopically or robotically although data do not show better patient outcomes with minimally invasive techniques. T tal pancreatect my: proposed but not commonly done or the treatment o pancreatic cancer 1. Advantages: removal o a possible multicentric tumor and avoidance o pancreatic duct anastomotic leaks 2. Survival rates: not markedly better, and the operation has not been widely adopted 3. Disadvantage: In addition, it has resulted in a particularly brittle type o diabetes, thus decreasing quality o li e. Palliative pr cedures: Per ormed more requently than curative ones because so many patients are incurable. With advances in endoscopic techniques, most palliative procedures can be o ered nonoperatively. 1. End sc pic stenting the c mm n bile duct r gastric utlet bstructi n: Because survival or patients with unresectable or recurrent cancer is short, these are usually e ective in relieving symptoms or the li e span o the patient. 2. Percutane us transhepatic biliary stents: can sometimes be used to provide internal biliary drainage or obstructive jaundice, thereby avoiding a major operation 3. Celiac axis bl ck: Combined alcohol and lidocaine administered in the periaortic sof tissues just adjacent to the celiac axis can relieve pain rom malignant in ltration o the sensory splanchnic nerves. Chem therapy: Has been used in the treatment o patients with advanced pancreatic adenocarcinoma. Even with active treatment, the overall survival is usually less than 1 year. 1. Gemcitabine: Most commonly used; antimetabolite that inhibits DNA synthesis. It can be combined with erlotinib, an epidermal growth actor inhibitor. 2. FOLFIRINOX: Recently adopted combination o our agents has been used in patients with a modest improvement in survival. Ne adjuvant (treatment be re perati n) chem radiati n: used in selected patients who have “borderline” resectable tumors 1. Adjuvant therapy (a er surgery): Chemotherapy, radiation, or a combination o the two is o ered to patients at risk o recurrence. 2. Overall survival: modest improvement compared to surgery alone; typically only a ew months

Chapter 14

V. P ro g no s is : e xtre m e ly p o o r A. Overall: Five-year survival rate is less than 5%, and cures are extremely rare. T e median survival af er resection and neoadjuvant or adjuvant therapy is 20–22 months. B. Unresectable tum rs r metastases: Median length o survival is 6 months. C. Resectable tum rs ( ew): Results o surgery are not good; 20% o patients who undergo resection will live 5 years.

Pancreas

229

Quic k Cut The poor prognos is is due in part to the di f culty in making a diagnos is while the tumor is at an early s tage: Only 10% o pancreatic adenocarcinomas are res ectable at the time o diagnos is .

Othe r P a nc re a tic Ma lig na nc ie s I. Cystic and solid lesions o the pancreas are not rare, but most are not malignant. II. Serous cystic neoplasms are slow growing, with low malignant potential. When asymptomatic, they may be ollowed radiographically. III. Mucinous cystic neoplasms commonly harbor carcinoma and should be resected. IV. Intraductal papillary mucin-producing neoplasia (IPMN) is characterized by mucin production through the pancreatic duct and into the ampulla. Main duct lesions have as poor a prognosis as pancreatic adenocarcinoma.

Chapter 15

Spleen

Daniel E. Mansour, Mayur Narayan, and Ajay Jain

INTRODUCTION Ana to m y I. Lo c a tio n: Largest secondary lymphoid organ in the body, the Quic k Cut spleen is located in the lef upper quadrant o the abdomen (lef The protected hypochondrium), below the diaphragm, and is protected by the location o the s pleen makes 8th–11th ribs. it nonpalpable, unles s it is A. Borders: bordered by the lef kidney posteriorly, the diaphragm pathologically enlarged. superiorly, and the undus o the stomach and the splenic exure o the colon anteriorly; also closely approximates the tail o the pancreas B. Major ligaments 1. Gastrosplenic ligament: connects greater curvature and splenic hilum 2. Splenorenal ligament: connects hilum and kidney 3. Splenophrenic ligament: suspends posterior aspect rom diaphragm 4. Splenocolic ligament: attaches in erior pole to the colon II. Va s c ula ture A. Splenic artery: main blood supply (Fig. 15-1) 1. Origin: branch o the celiac axis 2. Course: travels along the superior border o the pancreas; typically has a tortuous, corkscrew-line course 3. Branches: At the hilum, it branches into trabecular arteries, which terminate in small vessels to the splenic pulp. B. Short gastric arteries: arise rom the spleen and supply the undus o the stomach, then course through the gastrosplenic ligament connecting the hilum and the greater curvature C. Splenic vein: crosses at the lower border o the pancreas and joins the superior mesenteric vein to orm the portal vein

His to lo g y a nd Func tio n I. His to lo g y: Capsule comprising dense connective tissue surrounds the spleen. Septations (trabeculae) arising rom the capsule subdivides the pulp o the spleen into three discrete zones (red pulp, marginal zone, and white pulp) with distinct architecture and unctions. A. White pulp: Contains lymphocytes, macrophages, and plasma cells in a reticular network surrounded by an outer marginal zone; also contains separate areas or cells and B cells. Its primary unction is immunologic. B. Marginal zone: Vascular space between the pulps that contains macrophages, which can engul blood-borne pathogens. It also contains B cells that can generate antibodies. C. Red pulp: Comprises 75% o splenic volume and consists o cords o reticular cells with sinuses in between. Its primary unction is to serve as a blood f lter; it also helps recycle iron.

230

Chapter 15

Spleen

231

S toma ch

S ple nic a rte ry S hort ga s tric a rte rie s

P orta l ve in

S ple e n

P a ncre a s Ta il of pa ncre a s S ple nic ve in S upe rior me s e nte ric ve in Infe rior me s e nte ric ve in

Fig ure 15-1: Anatomic relations hips o the s pleen.

II. Func tio ns A. Filtration: removes oreign materials, cellular debris, and damaged erythrocytes rom circulation B. Immunity: Removes bacteria rom the circulation, including poorly opsonized or encapsulated pathogens. It serves as a site or antigen presentation as well as -cell and B-cell activation and is the major site o immunoglobulin M (IgM) production. C. Reservoir: In a minor capacity, the spleen serves as a reservoir or platelets and red blood cells (RBCs).

PATHOLOGY De f nitio ns I. Hyp e rs p le nis m : unctional hyperactivity that results in a loss o one or more hematologic cell populations A. Primary hypersplenism: Functional change in the absence o hematologic disorders or in ection. It is rare, more commonly a ects women, and is a diagnosis o exclusion. B. Secondary hypersplenism: more common and secondary to another disease process II. Sp le no m e g a ly: gross enlargement o the spleen

Sym p to m s I. II. III. IV.

Ane m ia : causes pallor, atigue, and dyspnea Le uko p e nia : recurrent in ections Thro m b o c yto p e nia : bruising and epistaxis Sp le no m e g a ly: I present, may cause pain secondary to capsular distention. Also may present with rupture and hemorrhage.

Ca us e s o Se c o nd a ry Hyp e rs p le nis m I. P o rta l hyp e rte ns io n: most common cause A. Symptoms: of en accompanied by congestion and splenomegaly B. reatment: splenectomy generally not indicated

Quic k Cut Splenomegaly is increas ed s ize; hypersplenism is increas ed unction. It is pos s ible to have s plenomegaly without hypers plenis m and vice vers a.

Quic k Cut Symptoms o conditions a ecting the s pleen are chief y related to underlying cytopenia or s plenomegaly.

Quic k Cut Portal hypertens ion is the mos t common caus e o hypers plenis m.

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Pathology

II. Sple nic ve in throm bos is : Pancreatic pathology (pancreatitis) is the most common cause. A. Symptoms: classically presents with upper gastrointestinal bleeding due to associated gastric varices B. reatment: Splenectomy is curative. III. He re d ita ry s p he ro c yto s is : inherited (autosomal dominant) Quic k Cut dys unction or de ciency in spectrin, an RBC cytoskeletal protein Acces s ory s pleens A. Symptoms occur in 20% o people and 1. Jaundice and splenomegaly: due to RBC lysis are unctional. I acces s ory 2. Gallstones and biliary colic: may result rom bilirubin stone s pleens are pres ent but not ound and removed at ormation s urgery, dis eas es s uch as ITP B. Diagnosis: physical exam, laboratory abnormalities (anemia, will recur. elevated serum bilirubin, elevated reticulocyte count), blood smear showing spherocytes C. reatment: Splenectomy is curative but should be delayed until af er age 4 years, i possible, to avoid septic complications. IV. He re d ita ry e llip to c yto s is : Related to and managed like hereditary spherocytosis but less severe. Autosomal dominant inherence; involves spectrin and other RBC cytoskeletal proteins. V. Sic kle c e ll a ne m ia : hemolytic anemia due to change rom glutamic acid to valine in the sixth amino acid position o the beta chain in hemoglobin A. Symptoms: Cell de ormity under low oxygen conditions allows sequestration, causing in arction and splenomegaly. B. reatment: splenectomy reserved or patients with massive splenomegaly during sequestration crisis early in li e VI. Id io p a thic a uto im m une he m o lytic a ne m ia : caused by autoantibody ormation against RBC membrane proteins A. Incidence: more common in women B. Symptoms: similar to other hemolytic anemias (jaundice, anemia) C. Diagnosis: direct Coombs test result is positive; reticulocytosis and increased indirect bilirubin in serum D. reatment 1. Medical treatment: Mainstay therapy is high-dose corticosteroids (response in 75% o patients). 2. Splenectomy: help ul in some patients re ractory to medical therapy (up to 80%) VII. Othe r c o ng e nita l he m o lytic a ne m ia s : splenectomy generally not curative but may be considered or reducing trans usions A. Enzyme def ciencies: such as glucose-6-phosphate dehydrogenase (G6PD) and pyruvate kinase de ciencies B. T alassemia major: Autosomal dominant inheritance characterized by de ective hemoglobin synthesis. Causes severe anemia and hepatosplenomegaly. VIII. Id io p a thic thro m b o c yto p e nic p urp ura (ITP ): autoimmune disorder o unknown etiology, characterized by platelet destruction resulting in low platelet count A. Acute orm: More common in children ollowing a viral upper respiratory illness; 80% recover spontaneously. B. Chronic orm: most common in adults and women C. Symptoms: Unexplained ecchymoses or petechiae. Splenomegaly is rare. D. Clinical diagnosis: platelet count less than 100,000; megakaryocytes in bone marrow E. reatment 1. Medical: First-line therapy includes platelet trans usion, gamma-Ig, corticosteroids, and Rho(D) Ig. Quic k Cut 2. A er splenectomy ailure: rituximab and romiplostim Only 20% o ITP 3. Splenectomy: indicated in patients re ractory to medical patients have a s us tained therapy or with intracranial hemorrhage; produces sustained res pons e to corticos teroids . remission in 75%–85% IX. Thro m b o tic thro m b o c yto p e nic p urp ura (TTP ): rapidly progressive and usually atal; characterized by thrombocytopenia, microangiopathic hemolytic anemia, and neurologic complications A. Clinical presentation: ever, petechiae, hemolytic anemia, neurologic symptoms, and renal ailure B. Diagnosis: con rmed by peripheral blood smear, with schistocytes, nucleated RBCs, and basophilic stippling

Chapter 15

Spleen

233

C. reatment: Plasma exchange (plasmapheresis) is rst-line Quic k Cut therapy. Splenectomy reserved or patients with relapse or Felty s yndrome is requiring multiple plasma exchanges. the clas s ic triad o rheumatoid D. Prognosis: poor long-term survival rate ( 10%) arthritis , s plenomegaly, and neutropenia. X. Fe lty s yndrom e : complication o long-standing rheumatoid arthritis, characterized by rheumatoid arthritis, splenomegaly, and neutropenia A. Symptoms: recurrent in ections and chronic leg ulcers B. reatment: splenectomy per ormed or symptomatic neutropenia, anemia requiring trans usions, and severe thrombocytopenia XI. Enzym e d e f c ie nc ie s a nd m e ta b o lic d is e a s e s (unus ua l) A. Enzyme def ciencies: G6PD and pyruvate kinase de ciencies B. Gaucher disease: lysosomal storage disease

Eva lua tio n o Hyp e rs p le nis m I. P e rip he ra l b lo o d s m e a r: Decreased number o RBCs, white blood cells (WBCs), or platelets or abnormal RBC morphology. Reticulocytosis is seen secondary to increased RBC turnovers. II. Bo ne m a rro w b io p s y: may allow detection o increased hematopoetic progenitor cell populations to compensate or hypersplenism and cytopenia III. Ra d io lo g ic im a g ing Quic k Cut A. Ultrasound: can help assess the size and texture o the spleen Ultras ound is us ually and perisplenic uid such as blood the rs t choice in trauma B. Computed tomography (C ) scan: use ul in assessing the size s cenarios . o the spleen as well as determining any structural abnormalities; also helps with guidance o percutaneous procedures and may show other pathology such as lymphadenopathy or varices C. Nuclear imaging: may be use ul in locating accessory splenic tissue causing ongoing cytopenia af er unsuccess ul splenectomy or I P

Sp le nic Cys ts I. Etio lo g y: may be idiopathic or induced by trauma II. Tre a tm e nt: Partial splenectomy or cyst marsupialization should be per ormed whenever possible to preserve splenic unction.

Sa rc o id o s is

Quic k Cut Surgery is only indicated with s plenic cys ts or s ymptoms s uch as pain or mas s e ect (s uch as early s atiety rom gas tric compres s ion).

I. Etio lo g y: multisystem in ammatory disease o unknown etiology characterized by noncaseating granulomas in multiple tissues (especially lungs and lymph nodes) II. Tre a tm e nt: splenectomy typically only indicated to rule out cancer

In e c tio n I. Sp le nic a b s c e s s : uncommon but has a high mortality rate (40%–100%) A. Causes: Most common organisms are Staphylococcus aureus or Quic k Cut Streptococcus. Treatment or 1. In arction: resulting in necrosis and suprain ection splenic in ection is generally 2. Intra-abdominal in ection rom other source. medical, although surgery may 3. Hematogenous seeding: in intravenous drug users or during be indicated or abscess or overwhelming bacteremia (e.g., in endocarditis) disease localized to the spleen. B. Diagnosis: clinical evidence o sepsis ( ever, elevated WBC, etc.), in conjunction with C ndings suggestive o splenic abscess C. reatment: Initiate broad-spectrum antibiotics. Splenectomy has been considered the gold standard or re ractory cases, but percutaneous drainage is increasingly a viable option. II. Vira l in e c tio ns : Mononucleosis, HIV, and hepatitis may cause transient splenomegaly and hypersplenism. III. P a ra s itic in e c tio ns : Malaria, leishmaniasis, or trypanosomiasis may cause splenomegaly. An echinococcal cyst may develop in the spleen. Partial or total splenectomy is curative. IV. Fung a l in e c tio n: Histoplasmosis produces characteristic areas o calci cation within the spleen.

234

Chapter 15

echnical Aspects o Splenectomy

Ne o p la s tic Dis e a s e s I. P rim a ry s p le nic tum o rs (s a rc o m a , he m a ng io m a , a nd ha m a rto m a ): rare A. Symptoms: of en asymptomatic but may cause symptoms i large enough to cause capsular stretch and pain B. reatment: Splenectomy indicated or indeterminate or suspicious lesions (to con rm or exclude malignancy). Benign, stable hemangiomas (as determined by arterial and venous phase contrast C ) do not necessarily require splenectomy. II. Me ta s ta tic d is e a s e : Isolated splenic metastases are rare. III. He m a to lo g ic m a lig na nc ie s A. Hodgkin disease: reatment includes radiation therapy alone, chemotherapy alone, or a combination o both. Overall, there is a good long-term survival rate. B. Staging laparotomy: Splenectomy used to be part o the staging but is now rarely indicated because the additional in ormation does not alter therapy. IV. No n-Ho d g kin lym p ho m a A. Staging: uses the same classi cation as or Hodgkin disease B. Splenectomy: may be indicated in select patients to treat hypersplenism or to relieve symptoms o massive splenomegaly

Quic k Cut Splenectomy is no longer required to s tage Hodgkin lymphoma.

V. Le uke m ia s A. Symptoms: Patients with chronic lymphocytic leukemia (CLL), chronic myelogenous leukemia (CML), and hairy cell leukemia may develop hypersplenism and thrombocytopenia. B. reatment: Splenectomy may bene t in cases that are re ractory to medical therapy.

Othe r Le s io ns I. Sp le nic rup ture : traumatic cause or spontaneous because o massive splenomegaly due to an associated disease II. Sp le no s is : May occur spontaneously af er rupture; shed splenic tissue can engraf in the body and can maintain pathologic hypersplenic state af er therapeutic splenectomy.

Quic k Cut Iatrogenic trauma occurring in the operating room accounts or 20% o all s plenectomies .

III. Sp le nic a rte ry a ne urys m s IV. Ec to p ic s p le e n: Results rom a long splenic pedicle; splenic location can vary within the abdomen. V. Ac c e s s o ry s p le e ns : present in 20% o population; greater than 80% located near the splenic hilum and vascular pedicle and less requently in the tail o the pancreas and in the mesentery

Tre a tm e nt

Quic k Cut Blunt trauma is the leading caus e o s plenectomy. Many cas es o traumatic s plenic injury can be managed nonoperatively.

I. Tre a tm e nt: depends on the underlying condition II. Ta b le 15-1: summarizes the role o surgery in various pathologic conditions

TECHNICAL ASP ECTS OF SP LENECTOMY Op e n Sp le ne c to m y I. Ste p 1: Mobilize the spleen to midline by dividing the splenic attachments (splenophrenic, splenocolic, splenorenal ligaments) either sharply or bluntly. II. Ste p 2: Care ul dissection o the hilum and application o vascular clamps should be per ormed to avoid injury to the tail o the pancreas. III. Ste p 3: Once the splenic hilum is controlled, identi cation and ligation o the short gastrics should be per ormed.

Quic k Cut Open s plenectomy may be per ormed through midline laparotomy or a le t s ubcos tal incis ion.

Quic k Cut Blindly applying a clamp to the s plenic hilum may injure the pancreatic tail.

Chapter 15

Spleen

235

Ta b le 15-1: Ab s o lute a nd Re la tive Ind ic a tio ns o r Sp le ne c to m y Typ e o P a tho lo g y

Ab s o lute Ind ic a tio ns

Re la tive Ind ic a tio ns

Primary splenic disorders

Symptomatic splenic cyst

Primary hypersplenism

Disorders o splenic blood f ow

Bleeding esophagogastric varices associated with splenic vein thrombosis

Portal hypertension with severe hypersplenism

Hematopoietic disorders

Hereditary spherocytosis

Hereditary elliptocytosis Thalassemia major Sickle cell anemia Congenital erythropoietic porphyria

Immune disorders

None

Idiopathic autoimmune hemolytic anemia Idiopathic thrombocytopenic purpura Thrombotic thrombocytopenic purpura Felty syndrome Systemic lupus erythematosus

In ltrative disorders

None

Myeloid metaplasia Sarcoidosis

In ectious diseases

Splenic abscess Echinococcal cyst

Gaucher disease

Neoplastic diseases

Primary splenic tumors

Staging laparotomy or Hodgkin disease or non-Hodgkin lymphoma Chronic lymphocytic leukemia Chronic myelogenous leukemia Hairy cell leukemia

Miscellaneous

Massive splenic trauma Spontaneous rupture

La p a ro s c o p y I. Op e ra tive s te p s : similar to a laparotomy, but care must be taken to avoid rupture and consequent splenosis II. Te c hniq ue : Because splenosis can lead to recurrence o the underlying disease, surgeons must avoid spillage o any part o the splenic specimen; tear-resistant nylon bags are available.

COMP LICATIONS AFTER SP LENECTOMY Injury to Surro und ing Struc ture s I. Ga s tric wa ll: Injury occurs in course o controlling the short gastric vessels. Gastric wall necrosis with delayed per oration with overzealous short gastric ligation may occur. II. Ta il o the p a nc re a s : Injury can occur during clamping or stapling o the artery and vein at the hilum, resulting in postoperative pancreatic leak, pancreatitis, abscess, or phlegmon ormation. I recognized, a drain should be lef postoperatively. III. Co lo nic injury

Quic k Cut Laparos copy can als o be us ed or elective s plenectomy.

Quic k Cut Atelectas is o the le t lower lung is the mos t common complication.

Quic k Cut Remember, the tail o the pancreas is intimately as s ociated with the s plenic hilum.

Ove rwhe lm ing P o s ts p le ne c to m y In e c tio n/Se p s is I. Etio lo g y a nd inc id e nc e : Occurs because spleen is no longer able to opsonize encapsulated bacteria; incidence is very rare ( 1%). A. Causative organisms: encapsulated bacteria, including Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus inf uenzae

236

Chapter 15

Complications af er Splenectomy

B. iming: Most septic episodes occur within 2 years af er splenectomy. C. Risk: greatest i splenectomy occurs during the rst 2–4 years o li e II. Clinic a l p re s e nta tio n: nonspeci c, mild, in uenza-like symptoms, which can rapidly progress to high ever, shock, and death III. P re ve ntio n a nd tre a tm e nt A. Vaccines: should be administered 2 weeks prior to elective Quic k Cut splenectomies or anytime ollowing an unplanned splenectomy Ideally, with and include polyvalent pneumococcal vaccine and vaccines or unplanned s plenectomy, N. meningitidis and H. inf uenzae vaccination s hould be given B. Prophylactic penicillin: Daily doses are commonly prior to dis charge in order to ens ure it is not mis s ed. recommended or children until age 5 years or at least 5 years post splenectomy. C. I symptoms begin: Initiate penicillin therapy immediately.

Othe r

Quic k Cut Trivalent vaccine is

I. P o s to p e ra tive he m o rrha g e : may result rom inadequate commercially available. hemostasis o the splenic pedicle or the short gastric vessels II. Sub p hre nic a b s c e s s : usually accompanied by a lef pleural e usion III. Thro m b o c yto s is : Common; i the platelet count is greater than 1 million, antiplatelet therapy may be considered to prevent spontaneous thrombosis.

Study Questions or Part IV

Study Questions or Part IV Directions: Each o the numbered items in this section is ollowed by several possible answers. Select the ONE lettered answer that is BES in each case. 1. A 47-year-old woman presents with dysphagia to both solids and liquids equally. She has

experienced a 10-kg weight loss over the last several months. A barium swallow reveals a bird’s beak narrowing in the distal esophagus. What is the underlying cause o her symptoms? A. B. C. D. E.

Disorganized, strong nonperistaltic contractions in the esophagus Failure o the lower esophageal sphincter to relax Hiatal hernia Barrett esophagus Esophageal stricture secondary to untreated gastroesophageal re ux

2. A 45-year-old male executive is seen because he is vomiting bright red blood. T ere are no

previous symptoms. T e man admits to one drink a week and has no other signi cant history. In the hospital, he bleeds ve units o blood be ore endoscopy. What is the most likely diagnosis? A. B. C. D. E.

Gastritis Duodenal ulcer Esophagitis Mallory-Weiss tear Esophageal varices

3. An 80-year-old male patient is re erred or dysphagia with re ux o undigested ood. T e patient

occasionally notices a bulging in his lef neck. Which o the ollowing is the most appropriate de nitive treatment? A. B. C. D. E.

Barium swallow Upper endoscopy Cricopharyngeal myotomy C scan o the chest Liquid diet

4. A 42-year-old emale patient is diagnosed with gastroesophageal re ux and is started on medical

therapy. Which o the ollowing would be an indication or surgical antire ux procedure? A. B. C. D. E.

Development o esophageal stricture Barrett esophagus with severe dysplasia Esophagitis by biopsy High lower esophageal sphincter pressure demonstrated by esophageal manometry Slow and uncoordinated swallowing by barium study

5. A 75-year-old male patient presents to the emergency room 2 hours af er developing severe

chest pain with repeated episodes o vomiting. He is tachycardic and ebrile. A chest radiograph demonstrates a lef pleural e usion. Emergent barium swallow reveals extravasation o contrast into the lef chest. Proper de nitive treatment o this patient would include which o the ollowing? A. B. C. D. E.

Observation Emergent surgical intervention Placement o lef chest tube Intravenous antibiotics and admission to the hospital Upper endoscopy

237

238

Study Questions or Part IV

Que s tio ns 6–7 A 65-year-old patient has been treated with pharmacologic therapy or an antral gastric ulcer or 12 weeks. A repeat upper gastrointestinal series shows approximately 50% shrinkage o the ulcer. 6. What urther management should the patient undergo at this time?

A. B. C. D. E.

Continued pharmacologic therapy with a repeat upper gastrointestinal series in 8–12 weeks A change in pharmacologic therapy with a repeat upper gastrointestinal series in 12 weeks An upper endoscopy with multiple biopsies otal gastrectomy Surgery with limited excision o the ulcer

Af er urther diagnostic workup, the patient is ound to have a gastric adenocarcinoma. Metastatic workup is negative. 7. T erapy with curative intent would involve which o the ollowing?

A. B. C. D. E.

Radiation therapy ollowed by chemotherapy alone Distal gastrectomy ollowed by adjuvant chemoradiotherapy otal gastrectomy otal gastrectomy and splenectomy Local excision o the ulcer with clear margins ollowed by radiotherapy

8. Which o the ollowing statements is true about the per ormance o a parietal cell vagotomy?

A. B. C. D. E.

It divides the vagus nerve at the gastroesophageal junction. It maintains innervation o the pylorus so that a drainage procedure is not required. T e recurrence rate is less than 5%. It cannot be per ormed laparoscopically. It is contraindicated or bleeding or per orated ulcers.

9. What innerves the stomach resulting in parietal cell secretion and gastrin release?

A. B. C. D. E.

Phrenic nerve Vagus nerve Greater splanchnic nerves Celiac ganglion 4 root

10. Which o the ollowing is true regarding intestinal absorption o nutrients?

A. B. C. D.

Bile or bile salts are essential or absorption o vitamin B12. An iron-de cient individual can absorb up to 80% o dietary iron. Parathormone increases the intestinal absorption o dietary calcium. Intestinal epithelial cells resynthesize triglycerides be ore their release into the portal circulation. E. riglycerides are absorbed intact in a bile salt micelle–dependent process.

Study Questions or Part IV

Que s tio ns 11–12 A previously healthy 43-year-old man presents with a 6-month history o nonbloody diarrhea, ever, and 10-lb weight loss and now develops urosepsis. On evaluation, an enterovesical stula ( rom the ileum to the bladder) is ound. At laparotomy, ndings include in ammation and “ at wrapping” o three separate segments o ileum. Each segment is approximately 20 cm in length and is separated by less than 20-cm segments o normal-appearing bowel (skip areas). T e distal most o the three segments is more severely in amed than the others and involves the terminal ileum all the way to the cecum. T is segment o ileum is densely adherent to the right superior aspect o the bladder. 11. Which o the ollowing is true?

A. B. C. D. E.

All o the abnormal-appearing bowel should be resected. T is patient has complications o Meckel diverticulitis. All o the bladder wall involved in the in ammatory process must be removed. Extensive resection can reduce the potential or a recurrence to less than 10%. Closure o the stula and resection o the involved bowel are pre erred.

12. T e patient returns to the o ce 3 years later complaining o abdominal pain, abdominal

distention, bloating af er meals, and intermittent constipation interspersed with diarrhea. He has lost 20 pounds during the last 3 months, which he ascribes to the a orementioned abdominal symptoms. An upper gastrointestinal series with a small bowel ollow-through reveals one area o tight stricture in the distal small bowel. T e stricture appears to be 10 cm in length. Which o the ollowing is true? A. All strictures require resection; bypass o the involved segment is not an option. B. Postoperatively, this patient’s chance o another recurrence requiring surgery is 50%. C. Because this patient requires surgery or the second time, his risk o cancer is extremely high, and he should have an extensive small bowel resection. D. Postoperative anastomotic strictures typically cause symptoms years later. E. Because o the patient’s prior surgery, olate replacement is essential.

Que s tio ns 13–15 A 32-year-old male with long-standing Crohn disease presents with a complete obstruction o the small bowel. At laparotomy, scarring o the distal ileum and cecum cause an obstruction. A 10-cm segment o mid small bowel shows moderate nonobstructive Crohn disease. 13. Which operative procedure should be per ormed at this time?

A. Radical resection o the involved segment o mid small bowel, all o the ileum, the cecum, and the right colon B. Resection o the distal ileum and right colon with the involved mesentery and lymph nodes C. Bypass o the obstructing segment with a side-to-side anastomosis between the ileum and the right colon and no resection D. Stricturoplasty o the obstruction plus resection o the short involved segment o mid small bowel E. Resection o the distal ileum and cecum 14. Postoperatively, the patient requires an indwelling bladder catheter or 5 days to treat urinary

retention. He does well until the 10th postoperative day, at which point he develops a ever o 103°F, right lower quadrant (RLQ) pain, and an ileus. T e midline wound is not in amed. Which o the ollowing is most likely to have developed? A. B. C. D. E.

Blind loop syndrome Pyelonephritis Recurrent Crohn disease Intra-abdominal abscess Pseudomembranous enterocolitis

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Study Questions or Part IV

15. Af er success ul surgery and discharge rom the hospital, which o the ollowing is true?

A. I the diseased bowel is removed, therapy with prednisone and metronidazole can best prevent a recurrence. B. T e chance o a cure is greater than 60%. C. T e recurrence rate is higher than 50% during the next 5–10 years. D. I the terminal ileum is removed, the risk o recurrence is decreased. E. I the terminal ileum is removed, the patient will require long-term therapy with oral iron to prevent anemia.

Que s tio ns 16–17 A 63-year-old man presents with a 3-day history o increasing cramping abdominal pain, constipation, and intermittent vomiting. He continues to pass gas. Other than the present complaints, he has been healthy. Examination reveals a distended abdomen with high-pitched bowel sounds. No localized tenderness is ound and no rectal masses are present. T e stool is heme positive. 16. Diagnostically, the rst step should be to per orm which o the ollowing?

A. B. C. D. E.

otal colonoscopy Mesenteric angiography Flat plate and erect abdominal radiographs Upper gastrointestinal radiographs with small bowel ollow-through Barium enema

17. T erapeutically, the rst step should be which o the ollowing?

A. B. C. D. E.

A Fleet enema, clear liquids by mouth, and care ul observation Emergency colonoscopy or colonic decompression Intravenous uids, nasogastric suction, and care ul observation Colonoscopic decompression with use o a rectal tube, i necessary Immediate exploratory laparotomy

Que s tio ns 18–19 A 60-year-old patient who is nishing a course o antibiotic therapy or bacterial pneumonia develops cramping abdominal pain and pro use watery diarrhea. A diagnosis o pseudomembranous or antibiotic-associated colitis is suspected. 18. Which o the ollowing is the quickest way to establish the diagnosis?

A. B. C. D. E.

Stool culture Barium enema Stool titer or Clostridium di cile toxin Proctoscopy Blood culture

19. What would the initial treatment involve?

A. B. C. D. E.

Metronidazole Vancomycin Imodium Cephalexin otal abdominal colectomy

Study Questions or Part IV

20. During exploration or a transverse colon tumor, a surgeon incidentally notices a 2-cm

diverticulum o the small bowel located 2 f proximal to the ileocecal valve. Which o the ollowing statements is not true? A. T is diverticulum should be resected when ound due to an associated increased risk o malignancy. B. T is is an example o the most common type o diverticulum o the gastrointestinal tract, present in 2% o the population. C. It is more commonly ound in men than women. D. When symptomatic in children, it presents as a source o bleeding. E. It can cause obstruction via intussusception. 21. A 55-year-old man presents with a 24-hour history o increasingly severe lef lower quadrant

abdominal pain. On examination, he has tenderness localized in the lef lower quadrant with rebound. Fever and leukocytosis are present. T e clinical suspicion o diverticulitis would best be con rmed by which o the ollowing? A. B. C. D. E.

Barium enema Colonoscopy C scan o the abdomen and pelvis Magnetic resonance imaging o the abdomen and pelvis Chest radiograph

22. A 45-year-old woman with diabetes presents with a 2-day history o acute perirectal pain. On

examination, a tender uctuant mass is present to the lef o the anus. What treatment should be administered at this time? A. B. C. D. E.

Broad-spectrum antibiotic therapy Abscess drainage and excision o the stulous tract Incision and drainage o the abscess Continued observation reatment o Crohn disease

Que s tio ns 23–24 A 34-year-old emale patient in previous good health presents in the emergency department with spontaneous intraperitoneal hemorrhage. Her only medication is an oral contraceptive that she has been taking or the past 5 years. During resuscitation, a bedside ultrasound reveals a large amount o intraperitoneal blood and a 3-cm mass in the right lobe o the liver. 23. What is the likely cause o her hemorrhage?

A. B. C. D. E.

Hepatoma Hemangioma Focal nodular hyperplasia Hepatic cell adenoma Metastatic neoplasm

T e patient continues to bleed and requires trans usion. 24. What urther treatment should be undertaken?

A. B. C. D. E.

Observation in the intensive care unit Right hepatic artery ligation Right hepatic lobectomy Angiographic embolization o hepatic artery C portogram

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Study Questions or Part IV

25. A 45-year-old man presents to the emergency room with 24 hours o lef lower quadrant

abdominal pain. Examination reveals ever and ocal tenderness in the lef lower quadrant but no generalized peritoneal signs. C scan reveals a collection containing air and uid. Optimal management o this patient includes which o the ollowing? A. B. C. D. E.

Admission or intravenous antibiotics and serial abdominal exams Urgent operation with resection o diseased bowel and primary anastomosis Urgent operation with resection o diseased bowel and diverting colostomy Colonoscopy to rule out the possibility o a per orated cancer ollowed by C -guided drainage C -guided drainage ollowed by bowel resection once the patient has ully recovered

Que s tio ns 26–28 A 52-year-old alcoholic man with known cirrhosis presents to the emergency department with hematemesis. 26. Af er resuscitation and stabilization, which procedure should take place?

A. B. C. D. E.

Arteriography Upper gastrointestinal series Endoscopy agged red cell scan Liver biopsy

Workup reveals acutely bleeding esophageal varices. 27. What should the next treatment be?

A. B. C. D. E.

ransjugular intrahepatic portosystemic shunt Emergency portacaval shunt Splenectomy Sclerotherapy Gastroesophageal devascularization

Af er appropriate therapy, the bleeding ceases and the patient stabilizes. He is ound to be a Child’s C alcoholic cirrhotic who has been abstinent or 1 year. Evaluation or an orthotopic liver transplant has begun. 28. I his variceal bleeding recurs, it could be managed by all except which o the ollowing?

A. B. C. D. E.

Portacaval shunt Mesocaval shunt Sclerotherapy ransjugular intrahepatic portosystemic shunt Selective Warren shunt

29. A 73-year-old previously healthy man presents to the emergency room with several days o

jaundice ollowed by 12 hours o right upper quadrant pain and ever. He is mildly hypotensive. C scan o the abdomen reveals dilatation o the biliary tree. T e next step in management includes which o the ollowing? A. B. C. D. E.

Laparoscopic cholecystectomy Open cholecystectomy and tube placement Open cholecystectomy and choledochojejunostomy Fluid resuscitation, antibiotics, and endoscopic retrograde cholangiopancreatography (ERCP) Fluid resuscitation and hepatitis serologies

Study Questions or Part IV

Que s tio ns 30-31 A 33-year-old man with no signi cant past medical history presents to the emergency room with abdominal pain and nausea. He is a ebrile, and laboratory studies reveal a serum amylase level o 1,200 U/L. 30. Which o the ollowing would not be part o initial management?

A. B. C. D. E. 31.

Intravenous hydration Nasogastric decompression Abdominal imaging with ultrasound and/or C scan ERCP to evaluate pancreatic duct anatomy Intravenous narcotic pain medicine

en days into his course o pancreatitis, this patient is ound to have a uid collection measuring 4 cm in diameter near the tail o his pancreas. He had a recurrence o his abdominal pain when he was restarted on a diet 2 days prior but is otherwise asymptomatic. He remains on total parenteral nutrition. Appropriate management o this collection would include which o the ollowing? A. B. C. D. E.

C -guided aspiration to assess or in ection Endoscopic drainage via an ultrasound-guided cystogastrostomy Operative debridement and external drainage C -guided percutaneous drainage Observation alone

32. A 59-year-old patient undergoes exploration or a 4-cm mass in the head o the pancreas that

has caused obstructive jaundice. T e patient had a biliary stent endoscopically placed prior to the procedure with complete resolution o jaundice. At the time o surgery, two small liver metastases are noted. Which o the ollowing is not part o appropriate management at this point? A. B. C. D. E.

ransduodenal pancreatic biopsy Hepaticojejunostomy Gastrojejunostomy Cholecystectomy Celiac ganglion nerve block

33. A 65-year-old patient presents with a history signi cant or obstructive jaundice and weight

loss. A workup reveals a 2.5-cm mass in the head o the pancreas; needle aspiration reveals adenocarcinoma. Which o the ollowing ndings on preoperative C scan would preclude operative exploration or curative resection? A. B. C. D. E.

Presence o replaced right hepatic artery Loss o at plane between tumor and portal vein Loss o at plane between tumor and superior mesenteric artery Occlusion o gastroduodenal artery Occlusion o superior mesenteric vein

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Study Questions or Part IV

Directions: T e group o items in this section consists o lettered options ollowed by a set o numbered items. For each item, select the lettered option(s) that is(are) most closely associated with it. Each lettered option may be selected once, more than once, or not at all. Match the portion o the stomach, duodenum, or pancreas to the appropriate arterial supply. 34. Body and tail o pancreas

A. Lef gastric artery

35. Duodenum and head o pancreas

B. Right gastroepiploic artery

36. Proximal lesser curvature o stomach

C. Splenic artery

37. Distal greater curvature o stomach

D. Vasa brevia (short gastric arteries)

38. Fundus o stomach

E. Superior mesenteric artery

39. A 35-year-old man complains o severe heartburn. He has been on acid suppression over

the counter or 5 years without relie . Endoscopy demonstrates esophagitis, and a pH study documents pathologic re ux. T e best treatment or this patient is: A. B. C. D. E.

Heller myotomy Proton pump inhibitor Nissen undoplication Repeat endoscopy in 3 months Elevation o head o bed

40. A 20-year-old healthy woman undergoes outpatient endoscopy or abdominal pain. T e stomach

is unremarkable on endoscopic examination. In the recovery area, she has normal vital signs and oxygen saturation levels, but she complains o severe chest pain, and there is a crunching sound on cardiac auscultation. T e most likely etiology or the patient’s pain is: A. B. C. D. E.

Esophageal per oration Acute myocardial in arction Pulmonary embolism Missed peptic ulcer Pneumonia

41. A 59-year-old man has upper abdominal pain, atigue, and a 20-lb weight loss over 6 months

despite eating a regular diet. Esophagogastroduodenoscopy (EGD) is per ormed, revealing a 4-cm proximal gastric adenocarcinoma. Positron emission tomography (PE ) scan suggests bilateral lung nodules in addition to the gastric mass. T e best treatment or this patient is: A. B. C. D. E.

Gastrojejunostomy Gastrectomy with Roux-en-Y reconstruction Palliative chemotherapy Radiation to the abdomen Pulmonary resection ollowed by total gastrectomy

Study Questions or Part IV

42. A 60-year-old woman with in requent medical care presents to the emergency department with

diaphoresis, tachycardia, and abdominal pain. Abdominal x-ray reveals ree air, and the patient is taken to the operating room. Despite uid resuscitation, the patient remains tachycardic. A 1.5-cm ulceration with per oration is ound in the distal stomach. What is the best course o action? A. Close the patient, and begin cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP) chemotherapy. B. Primary repair C. Selective vagotomy and antrectomy D. Local excision (wedge resection) E. Distal gastrectomy with Roux-en-Y reconstruction 43. A 49-year-old man presents with abdominal pain over the past year. He describes a burning,

epigastric pain that is partially alleviated by eating. As a result, he has gained 12 lb. He has taken over-the-counter antacids with signi cant relie , but he reports that his symptoms are worsening. What is the best initial study or diagnosis? A. B. C. D. E.

EGD Computerized tomography Abdominal x-ray Small bowel ollow-through Magnetic resonance cholangiopancreatography

44. A 64-year-old woman presents with abdominal pain. T e patient had a previous laparotomy

or trauma one decade ago. She now has dull, di use pain, nausea, one episode o emesis, and ongoing atus. She appears distended, with no hernias, and in no distress. Abdominal x-ray shows multiple air- uid levels. T e best treatment or this patient is: A. B. C. D. E.

Intravenous uids and nasogastric decompression EGD Capsule endoscopy Urgent laparotomy PE

45. A 64-year-old woman presents with abdominal pain. T e patient had a previous laparotomy or Crohn

disease one decade ago. She now has dull, di use pain, nausea, one episode o emesis, and ongoing atus with multiple loose stools. She has a heart rate o 100 beats per minute, a systolic blood pressure o 120 mm Hg, RLQ tenderness on exam, and no distension. T e best treatment or this patient is: A. B. C. D. E.

Intravenous uids and nasogastric decompression EGD Computerized tomography Urgent laparotomy PE

46. Small intestinal at absorption is best characterized by:

A. B. C. D. E.

Passive absorption in the distal duodenum Active absorption in the distal duodenum Absorption by micelles in the jejunum Digestion by amylase and directly absorbed in jejunum Active transport across distal ileum as a complex

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Study Questions or Part IV

47. A 67-year-old woman undergoes screening colonoscopy and is ound to have a sessile

adenocarcinoma in the sigmoid colon. T ere is no evidence o metastatic disease on C o the chest and abdomen. T e most appropriate next step is: A. B. C. D. E.

Annual colonoscopy Endoscopic polypectomy FOLFOX chemotherapy Segmental colectomy with lymphadenectomy Abdominoperineal resection (APR)

48. A 23-year-old woman has crampy abdominal pain and a new perianal stula. Workup should

include all o the ollowing except: A. B. C. D. E.

WBC count and C-reactive protein (CRP level) Colonoscopy Exam under anesthesia Antineutrophil cytoplasmic antibody (ANCA)/anti–Saccharomyces cerevisiae antibody (ASCA) Capsule endoscopy

49. A 45-year-old man with a penicillin allergy undergoes elective ventral hernia repair with mesh

and receives clindamycin. wo days later, he develops severe stool requency with some lef -sided abdominal pain but no ever or tachycardia. T e best initial treatment is: A. B. C. D. E.

Loperamide Intravenous vancomycin Oral metronidazole Oral ri ampin Colectomy

50. A 34-year-old woman is involved in a minor motor vehicle collision and undergoes C scan.

T ere is no visceral injury, but a 1-cm mass is noted in the periphery o the right lobe o the liver. T e radiologist notes that there is a central scar visible. A sul ur colloid scan shows only the appearance o normal parenchyma. T e most appropriate treatment or this lesion is: A. B. C. D. E.

Observation only Oral contraceptive therapy Hepatic artery ligation Open liver biopsy Surgical excision

51. A 55-year-old woman is re erred or cholecystectomy. T ree years previously, she had some pain

and was diagnosed with gallstones on an outpatient ultrasound but de erred operation. She now has had a history o 1 month o jaundice and right upper quadrant pain. On exam, she has normal vital signs, obvious scleral icterus, and a rm liver palpable our ngerbreadths below the costal margin. T e best next step in her management is: A. B. C. D. E.

Laparoscopic cholecystectomy Right upper quadrant ultrasound Open cholecystectomy C scan Hepatobiliary iminodiacetic acid (HIDA) scanning

Study Questions or Part IV

52. A 40-year-old woman presents with a history o gallstones and a recent history o right upper

quadrant pain af er eating atty meals. She has had dark-colored urine and some pruritus. Liver unction tests demonstrate an elevated total bilirubin level o 4 mg/dL and transaminitis. T e next appropriate step in her management is: A. B. C. D. E.

Laparoscopic cholecystectomy ERCP HIDA scanning Cholecystostomy tube Hepaticojejunostomy

53. A 34-year-old man without previous medical history presents with acute abdominal pain o

2 days’ duration radiating to the back. On exam, he has epigastric tenderness. Laboratory exam is most signi cant or an elevated WBC count o 15,000/mm 3 and an amylase o 1,100 U/L. T e most likely reason or his pancreatitis is: A. B. C. D. E.

Alcohol ingestion Steroid use Gallstones Viral in ection Pancreas divisum

54. T e same patient rom question number 53 is admitted and started on intravenous uids and

antibiotics. Af er 24 hours, he becomes tachycardic, hypotensive, and has minimal urine output. His pain increases dramatically, with rebound tenderness on exam, and a repeat WBC count is 24,000/mm 3. T e most appropriate intervention is: A. B. C. D. E.

Upper gastrointestinal series EGD ERCP Surgical debridement C -guided biopsy

55. T e most direct connection between the spleen and the stomach is via:

A. B. C. D. E.

T T T T T

e pancreaticosplenic ligament e short gastric arteries e greater omentum e celiac axis e gastroepiploic artery

56. A 68-year-old patient has a history o splenectomy 2 years prior to presentation. T e most likely

indication or elective splenectomy in an adult is: A. B. C. D. E.

Primary hypersplenism Hereditary spherocytosis Hereditary elliptocytosis Sickle cell trait I P

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Answers and Explanations

Answers and Explanations 1. The a ns we r is B (Chapter 9, Esophageal Motility Disorders, Achalasia, II–III). T is patient

is presenting with classic symptoms o achalasia. T e dysphagia to both solids and liquids is classic, as is the bird-beak narrowing on radiographs. T e underlying de ect is ailure o the lower esophageal sphincter to relax, causing increased pressure in the esophagus and dys unctional swallowing. Disorganized, strong nonperistaltic contractions in the esophagus are characteristic o di use esophageal spasm. Strictures typically have dysphagia to solids well be ore liquids cause symptoms. 2. The a ns we r is B (Chapter10, Peptic Ulcer Disease, Duodenal Ulcers, IV C 2). Massive upper

gastrointestinal bleeding is usually due to a bleeding source proximal to the ligament o reitz. T e cause is most likely to be a posterior duodenal ulcer that is eroding into the gastroduodenal artery. Gastritis, esophagitis, a Mallory-Weiss tear, and esophageal varices are less likely causes o massive upper gastrointestinal bleeding. 3. The a ns we r is C (Chapter 9, Esophageal Motility Disorders, Cricopharyngeal Dys unction and

Zenker Diverticulum, I B 4 a). T is patient’s symptoms are consistent with a Zenker diverticulum. A barium swallow would be diagnostic but not therapeutic. Endoscopy is contraindicated secondary to the risk o diverticular per oration by the endoscope. Surgical myotomy o the cricopharyngeus muscle with resection or suspension o the diverticulum is the treatment o choice. C scan o the chest is not necessary. Changing the diet would not alter the underlying pathology. 4. The a ns we r is A (Chapter 9, Esophageal Motility Disorders, Esophageal Re ux, IV C 1).

Development o esophageal strictures is an indication or surgical antire ux procedures. Uncomplicated Barrett esophagus is a controversial indication or an antire ux procedure, as available studies do not agree as to whether or not surgery reverses the mucosal changes associated with Barrett esophagus. Con rmed severe dysplasia is an indication or esophagectomy, not antire ux surgery. Gastroesophageal re ux is associated with a lower esophageal sphincter pressure. Esophageal dysmotility is a contraindication to re ux surgery. Esophagitis should heal with appropriate medical management. 5. The a ns we r is B (Chapter 9, Esophageal Per oration, reatment, I–II). T is patient’s history,

physical examination, and diagnostic studies are consistent with an acute esophageal per oration, and the situation represents a surgical emergency. Whenever possible, primary surgical repair is indicated regardless o the time since per oration. I sepsis and regional in ammation preclude primary repair, resection with cervical esophagostomy and gastrostomy and jejunostomy tube insertion should be per ormed. Restoration o alimentary continuity with stomach or colon can then be per ormed in 2–3 months. 6–7. The a ns we rs a re 6-C (Chapter 10, Peptic Ulcer Disease, Gastric Ulcers, III C), 7-B

(Chapter 10, Gastric Cancer, Gastric Adenocarcinoma, VI B). Benign gastric ulcers should heal in 8–12 weeks with maximal medical therapy. I the ulcer does not heal completely during this time period, repeat endoscopy should be per ormed with biopsy. I gastric adenocarcinoma is diagnosed in this location, the optimal surgical therapy or this condition would be a distal gastrectomy with D1 (regional) lymph node dissection. More extensive surgery, such as total gastrectomy or splenectomy, would be reserved or more proximal gastric lesions. Neither radiation therapy ollowed by chemotherapy alone without surgery or limited surgery ollowed by radiotherapy is a treatment plan with curative intent. 8. The a ns we r is B (Chapter 10, Peptic Ulcer Disease, Duodenal Ulcers, IV B 3). Parietal cell

vagotomy, also termed highly selective vagotomy, maintains the nerves o Latarjet that innervate the pylorus. By dividing only the branches that innervate the parietal cells, pyloric unction is preserved and out ow o the stomach is maintained. It is a technically demanding operation, in that ailure to adequately sever the appropriate nerves will result in recurrences o more than 10%. However, parietal cell vagotomy can be per ormed or bleeding or per orated ulcers.

Answers and Explanations

9. The a ns we r is B (Chapter 10, Stomach, Surgical Anatomy, VI A). T e vagal nerves are one

o the principal stimulants o gastric acid secretion through direct stimulation o the parietal cells and via gastrin release rom antral cells. Although the splanchnic and celiac ganglions are important in gastric motility and sensation, they do not stimulate acid secretion. T e 4 root and phrenic nerve are not involved in gastric nervous supply. 10. The a ns we r is C (Chapter 11, Introduction, Physiology, III). Both parathormone and vitamin D

increase intestinal absorption o dietary calcium. Bile salts are essential or absorption o ats and atsoluble vitamins. Vitamin B12 is a water-soluble vitamin that complexes with intrinsic actor, which is a protein produced by the stomach, and the protein–vitamin B12 complex is absorbed in the terminal ileum. T e range o iron absorption is only 10%–26% o dietary iron. riglycerides are not absorbed intact but must rst be broken down into ree atty acids and monoglycerides. Once absorbed, they are resynthesized into triglycerides, but they are not released into the portal circulation. Rather, the triglycerides are packaged as chylomicrons and released into the lymphatic circulation. 11. The a ns we r is E (Chapter 11, Diseases, Crohn Disease, III–IV). T e diagnosis o Crohn

disease is supported by the enterovesical stula, the presence o “ at wrapping” o the bowel, in ammation, and the clinical history. o prevent ongoing contamination o the urinary tract, the stula must be closed, and resection o the involved segment o bowel would be the standard approach. Regarding the extent o resection, the 50% risk o recurrence is not decreased by more extensive resections; thus, the less bowel removed, the better. In this case, with three widely separated segments o ileum involved, removal o all involved bowel could result in loss o more than hal o the ileum and would not be advisable. Crohn disease does not directly involve the bladder and thus resection o the bladder wall is unnecessary except when needed to close the opening o the stula. Meckel diverticulum occurs proximal to the terminal ileum; it would not a ect multiple bowel segments and does not cause “ at wrapping.” 12. The a ns we r is B (Chapter 11, Diseases, Crohn Disease, VII). T is patient presents with

recurrent Crohn disease in the orm o an obstruction rom stricture, which is the most common mani estation that requires surgery. Af er surgery, the risk o recurrent mani estations o Crohn disease requiring reoperation is 50%, and the risk remains 50% af er each surgical procedure. Strictures, unlike stulas and per orations, can be treated via bypass o the involved segment o bowel, although resection is pre erred except when the risk is too great. T e risk o cancer is related to the chronicity o the disease and would almost never require extensive small bowel resection, which may leave the patient with short bowel syndrome (a di cult disorder to treat in this population). Postoperative anastomotic strictures cause symptoms very early postoperatively, not years later. I this patient had previously had a resection o the terminal ileum, he would develop a de ciency o vitamin B12, not olate. 13–15. The a ns we rs a re 13-E (Chapter 11, Diseases, Crohn Disease, VI), 14-D (Chapter 11, Diseases, Crohn Disease, VI C), 15-C (Chapter 11, Diseases, Crohn Disease, VII). When surgery

is necessary to treat complications o Crohn disease, the operations are “conservative,” as de ned by the length o the resection. T ere ore, when an obstructive lesion is present, only a short length o bowel needs to be resected. In the case described, the distal ileum and cecum should be removed. Radical resections are not necessary, as they do not reduce the risk o recurrence and may ultimately contribute to short bowel syndrome i several resections are required over long periods. In addition, resection o mesentery and lymph nodes (e.g., or a cancer operation) is unnecessary. Bypass procedures without resection are reserved or only the most di cult cases where resection cannot be undertaken sa ely. A stricturoplasty is appropriate occasionally or short symptomatic strictures in the small bowel only. T e second postoperative week is the usual time or the development o serious complications, such as abdominal wound dehiscence, intestinal anastomotic breakdown, and intraperitoneal abscess. Blind loop syndrome occurs rarely, and although it does cause pain and diarrhea, it does not cause ever and ileus. Pyelonephritis usually causes ank pain and pyuria. Crohn disease does not recur immediately or cause the signs unless complications have occurred. Pseudomembranous enterocolitis causes tenderness over the transverse colon and occasionally over the descending colon, with diarrhea. O the choices listed, an intra-abdominal abscess is the most likely diagnosis.

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Answers and Explanations

T e prognosis o Crohn disease, which requires surgery, is not good because 50% o patients require additional surgical procedures within 5 years o the rst operation. T ere ore, the chance o cure is less than 50%. Medical therapy (including anti-in ammatory agents and antibiotic drugs) has not proved e ective or preventing recurrence o the disease. Removal o the terminal ileum has no e ect on disease recurrence or iron absorption; however, the absorption o vitamin B12 is signi cantly impaired. 16–17. The a ns we rs a re 16-C (Chapter 11, Diseases, Small Bowel Obstruction, III B), 17-C

(Chapter 11, Diseases, Small Bowel Obstruction, IV). Flat plate and erect radiographs o the abdomen should be per ormed rst. Further studies may be needed based on the results o this initial survey. As with all bowel obstructions, the initial treatment involves nasogastric suction, intravenous uids, and resuscitation with care ul attention to correcting metabolic and electrolyte abnormalities. Once a patient has been adequately resuscitated, the decision to either observe care ully or intervene operatively can be made. 18–19. The a ns we rs a re 18-D (Chapter 12, Pseudomembranous Colitis [Antibiotic-Assisted Colitis], Diagnosis, II–III), 19-A (Chapter 12, Pseudomembranous Colitis [Antibiotic-Assisted

Colitis], reatment, II). Crampy abdominal pain and diarrhea af er a course o antibiotic therapy is highly suggestive o antibiotic-associated or pseudomembranous colitis. Diagnosis can be made either by proctoscopy, which demonstrates pseudomembranes, or by stool titer or Clostridium di cile toxin. Proctoscopy establishes the diagnosis immediately. Barium enema is contraindicated. T e antibiotics should be stopped, and the patient should be started on metronidazole. Oral vancomycin is also e ective, but it is more expensive. Colectomy is rarely required only in severe cases. 20. The a ns we r is A (Chapter 11, Diseases, Diverticular Disease, III E). Meckel diverticulum is

the most common diverticulum o the gastrointestinal tract and goes by the rule o 2’s: 2 f rom ileocecal valve, 2% incidence, 2 cm long, and 2:1 male to emale ratio. T ey can cause bleeding due to heterotropic gastric mucosa as well as intussusception and obstruction. An asymptomatic Meckel diverticulum should not be resected. 21. The a ns we r is C (Chapter 12, Diverticular Disease, Diverticulitis, III). C scan o the abdomen

and pelvis is the most help ul test to con rm the suspected diagnosis o diverticulitis. Free air is detected on the chest radiograph in less than 3% o patients with diverticulitis. Contrast enema should generally be avoided in the initial stages o diverticulitis. Colonoscopy to exclude a sigmoid cancer may be o value af er the condition o the patient has stabilized. 22. The a ns we r is C (Chapter 12, Benign Anorectal Disease, Anorectal Abscess and Fistula, III).

T is patient presents with a classic history and physical ndings o perirectal abscess. Antibiotic therapy will not cure an abscess. De nitive drainage is required. T is therapy will be curative in approximately 50% o the patients, and the remainder will develop a stula. However, the physician should deal with the abscess itsel at the initial presentation. Attempts to de nitely address any stula tract at initial presentation is not recommended due to potential complications such as injury to the sphincter muscles and di culties with continence. 23–24. The a ns we rs a re 23-D (Chapter 13, Hepatic umors, Benign umors, II A), 24-D

(Chapter 13, Hepatic umors, Benign umors, II C). Although many liver tumors undergo spontaneous hemorrhage, this condition occurs most requently with hepatic cell adenomas. Up to 30% o patients present with spontaneous rupture into the peritoneal cavity as their initial nding. When the patient continues to bleed, emergency liver resection af er an acute rupture would be associated with high morbidity and mortality. Although hepatic artery ligation may control the bleeding, this can probably be accomplished less invasively by radiologic embolization. Once the bleeding is controlled and the patient recovers, elective resection should be undertaken to avoid uture hemorrhage. 25. The a ns we r is E (Chapter 12, Diverticular Disease, Diverticulitis, V B 2). Cases o diverticulitis

complicated by per oration and abscess ormation are best managed by percutaneous drainage in the absence o evidence o di use peritonitis. Young patients (typically considered as being younger than 50 years o age) with a single severe case such as this should be considered or an

Answers and Explanations

interval resection o the diseased section o bowel because o the very high risk o subsequent severe episodes. Older patients are of en re erred af er a second episode. Colonoscopy should not be routinely per ormed during the acute phase o an episode o diverticulitis but should be per ormed prior on an interval basis. Operative intervention during the acute phase is reserved or cases that either present with di use peritonitis, per oration, or continued worsening o the clinical picture in spite o appropriate nonoperative therapy. Primary anastomosis is typically avoided in the setting o severe in ection and contamination. 26–28. The a ns we rs a re 26-C (Chapter 13, Hepatic Abscesses and Cysts, Portal Hypertension, VI A), 27-D (Chapter 13, Hepatic Abscesses and Cysts, Portal Hypertension, VI B), 28-A

(Chapter 13, Hepatic Abscesses and Cysts, Portal Hypertension, VII). Acute variceal bleeding commonly occurs because o portal hypertension rom underlying cirrhosis. Other causes o upper gastrointestinal bleeding that must also be considered in these patients include gastritis and peptic ulcer disease. Upper gastrointestinal endoscopy is the most rapid way o making the diagnosis o the site and identi ying the cause o upper gastrointestinal bleeding. Once the diagnosis has been made, sclerotherapy is the pre erred method o managing acute variceal bleeding. It is success ul in 90% o patients. Portacaval shunt, mesocaval shunt, sclerotherapy, transjugular intrahepatic portosystemic shunt, and selective Warren shunt or recurrent bleeding would potentially be success ul in preventing long-term hemorrhage. However, portacaval shunt would make a subsequent liver transplant extremely di cult and hazardous. 29. The a ns we r is D (Chapter 13, Biliary ree Pathology, Cholangitis, II). Cholangitis is a potentially

li e-threatening disease. T is patient is present with Charcot triad o pain, ever, and jaundice. 30–31. The a ns we rs a re 30-D (Chapter 14, Pancreatitis, Acute Pancreatitis, III D 8), 31-E (Chapter 14, Pseudocyst, II A, IV). Uncomplicated acute pancreatitis is best managed

conservatively with nasogastric decompression, intravenous hydration, bowel rest, and pain medicine. Imaging with ultrasound, C scan, magnetic resonance imaging, or magnetic resonance cholangiopancreatography can be use ul in establishing a possible etiology (gallstones) or detecting complications. ERCP should not be used routinely during the acute presentation due to the risk o ERCP-associated pancreatitis complicating the acute situation. ERCP should be reserved or speci c cases where there is evidence o biliary obstruction. Evaluation o pancreatic duct anatomy can be help ul on an interval basis to help assess causes o chronic or recurrent pancreatitis. 32. The a ns we r is A (Chapter 14, Pancreatic Malignancies, Pancreatic Adenocarcinoma, IV D, E).

When patients are unresectable due to distant metastases at the time o surgery, a surgeon must accomplish several things. A biliary bypass (hepaticojejunostomy) palliates the obstructive jaundice, and a cholecystectomy is per ormed in conjunction with this. A gastric bypass (gastrojejunostomy) prevents the gastric outlet obstruction observed in 19% o unresected periampullary cancer patients. A celiac axis nerve block has been shown to signi cantly reduce cancer-related pain. A surgeon must also make a tissue diagnosis, in this case by taking a biopsy o one o the liver metastases. An additional pancreatic biopsy is unnecessary and adds additional risks. 33. The a ns we r is E (Chapter 14, Pancreatic Malignancies, Pancreatic Adenocarcinoma, IV A 1).

Findings that determine unresectability on preoperative C scan include encasement o the superior mesenteric artery or proximal celiac axis and occlusion o the superior mesenteric vein or portal vein. umor abutting these vessels but not encasing or occluding them is not a contraindication to resection. T e gastroduodenal artery is ligated during a pancreaticoduodenectomy, thus its occlusion does not preclude resection. A replaced right hepatic artery is not uncommon and must be preserved. T is does not, however, preclude resection. 34–38. The a ns we rs a re 34-C, 35-E, 36-A, 37-B, a nd 38-D (Chapter 10, Stomach, Surgical

Anatomy, IV, and Chapter 14, Anatomy and Physiology, Vasculature, II, III). T e blood supply o the viscera is important in gastrointestinal surgery. T ree o the our main arteries can be sacri ced, and blood ow to the stomach will still be preserved through collateral circulation. T e proximal lesser curvature is supplied by the lef gastric artery (arising rom the celiac axis). T e right gastric artery (arising rom the common hepatic artery) supplies the distal lesser curvature. T e lef and right gastroepiploic arteries supply the proximal and distal greater curvature, respectively. T e

251

252

Answers and Explanations

duodenum and head o the pancreas are supplied by the superior and in erior pancreaticoduodenal arteries that arise rom the gastroduodenal and superior mesenteric arteries, respectively. T e body and tail o the pancreas are supplied by branches o the splenic artery. 39. The a ns we r is C (Chapter 9, Esophageal Motility Disorders, Esophageal Re ux, IV C 2 a). T e

patient is a candidate or surgical antire ux therapy, having documented re ux and having ailed a trial o medical therapy. Heller myotomy is the appropriate surgery or achalasia. Elevating the head o bed is an antire ux measure but unlikely to provide the patient with signi cant relie . 40. The a ns we r is A (Chapter 9, Esophageal Per oration, Etiology, Diagnosis). T e most common

cause o esophageal per oration is instrumentation (endoscopy). T e crunching sound is the result o mediastinal air. Myocardial in arction is unlikely in a young patient, and pulmonary embolism is not consistent with her normal saturation. Peptic ulcer does not typically cause acute chest pain, and pneumonia, although possible, should be more evident by other physical signs. 41. The a ns we r is C (Chapter 10, Gastric Cancer, Gastric Adenocarcinoma, VI C). T e patient

presents with metastatic disease, and the best option is palliative chemotherapy. Bypass, such as gastrojejunostomy, may be used in cases o unresectable obstruction. Gastrectomy may be used or earlier stage tumors, and aggressive therapy such as total gastrectomy has not increased survival. Radiation therapy is not e ective in the treatment o gastric cancer. 42. The a ns we r is D (Chapter 10, Peptic Ulcer Disease, Gastric Ulcers, VI C). T e patient remains

hemodynamically compromised, so the procedure o choice is wedge resection and not de nitive ulcer procedures involving ormal resection. T e ulcer specimen can be examined or evidence o malignancy. CHOP chemotherapy is reserved or cases o gastric lymphoma and not used in the setting o acute per oration. Primary repair, or suture closure, does not address the question o malignancy. 43. The a ns we r is A (Chapter 10, Peptic Ulcer Disease, Gastric Ulcers, III). T e patient has signs

and symptoms o ulcer disease. T e most sensitive test or ulcer symptoms is EGD. C is unlikely to provide in ormation on luminal disease. Abdominal x-ray is use ul or per oration but unlikely to have ndings in uncomplicated cases. Small bowel ollow-through assesses the small bowel, although an upper gastrointestinal series with barium may identi y stomach ulceration. Magnetic resonance cholangiopancreatography is a reasonable test or hepatobiliary disease but has no role in ulcer patients. 44. The a ns we r is A (Chapter 11, Diseases, Small Bowel Obstruction, IV B). T e patient has signs

and symptoms o a partial small bowel obstruction, likely due to adhesions rom his previous surgery. Initial management consists o supportive care, with intravenous uids or volume resuscitation, correction o electrolyte imbalances, and placement o a nasogastric tube or decompression. EGD will be nondiagnostic or most o the small bowel. Capsule endoscopy provides a glimpse o the mucosa and is most use ul in identi ying mass lesions. Laparotomy may be indicated i the patient progresses to a complete bowel obstruction. PE scans identi y areas o increased metabolic uptake (tumor). 45. The a ns we r is C (Chapter 11, Diseases, Crohn Disease, III). T e patient has the hallmarks o

a are o Crohn disease. T e most appropriate means o diagnosis would be C scanning, then treatment with anti-in ammatory medicines. Intravenous uids are rarely contra-indicated, but the patient does not have obstruction or ileus that would warrant nasogastric tube placement. EGD would not be use ul in small bowel diagnosis in this instance. Laparotomy would be overly aggressive and may not help the patient. PE is most use ul in detecting malignancy, which is not a primary concern in this case. 46. The a ns we r is C (Chapter 11, Introduction, Physiology, III C). Fat is processed in micelles to

be absorbed in the intestine. Carbohydrate is digested by amylase and absorbed directly. B12 is actively transported in the terminal ileum as a complex with intrinsic actor. 47. The a ns we r is D (Chapter 12, Benign and Malignant Colorectal umors, Colorectal Carcinoma,

VII). T e patient has a known malignancy, and in this case, the primary treatment is surgical. Annual surveillance may be employed in the postoperative setting. Chemotherapy may be used or advanced-stage disease. APR is the technique o choice or low rectal tumors only.

Answers and Explanations

48. The a ns we r is E (Chapter 12, In ammatory Bowel Disease, Ulcerative Colitis, VII). T e

patient may have in ammatory bowel disease, worked up with markers o in ammation (WBC, CRP, erythrocyte sedimentation rate), antibodies (ANCA/ASCA), and colonoscopy. Capsule endoscopy is used to assess the lumen o the small bowel and may be indicated but not as part o the initial workup. 49. The a ns we r is C (Chapter 12, Pseudomembranous Colitis [Antibiotic-Assisted Colitis],

Pathogenesis and Presentation, II). T e patient has antibiotic-associated colitis. T e most likely o ending organism is Clostridium di cile. Antidiarrheal agents such as loperamide (Imodium) are contraindicated. Intravenous vancomycin is not e ective, and ri ampin may be used only rarely in some re ractory cases. Colectomy is reasonable in cases o megacolon, but antibiotic therapy should be attempted rst. 50. The a ns we r is A (Chapter 13, Hepatic umors, Benign umors, III). T e patient presents with

the characteristic ndings o ocal nodular hyperplasia. It is an incidental nding, with no speci c treatment required or small lesions, as spontaneous rupture is rare. T ere is an association with oral contraceptives, so they should be avoided. Hepatic artery ligation is a use ul technique in cases o rupture only. Surgical excision is reserved or larger or symptomatic lesions. 51. The a ns we r is D (Chapter 13, Biliary ree Pathology, III). T e patient requires more diagnostic

workup prior to undertaking operation. T e jaundice, palpable liver, and pain is suggestive o an obstructed biliary tree. C scan is the most appropriate among the listed choices, as it would demonstrate an anatomic cause, although MRI or ERCP would be appropriate as well. Right upper quadrant ultrasound may demonstrate ductal dilatation but will not provide su cient in ormation or de nitive diagnosis. HIDA is most use ul or cholecystitis. Cholecystectomy may be indicated, but a mass lesion should be ruled out rst. 52. The a ns we r is B (Chapter 13, Biliary ree Pathology, Choledocholithiasis, IV). T e patient

is demonstrating evidence o choledocholithiasis. ERCP o ers the best anatomic in ormation con rming the presence o stones and the ability to alleviate the obstruction through sphincterotomy. Laparoscopic cholecystectomy is an option but unlikely to address her main symptoms and relatively contraindicated without urther intervention. HIDA scanning is unlikely to o er any relevant in ormation beyond con rming obstruction o the biliary tree. A cholecystostomy tube will also alleviate obstruction but is generally reserved or those with cholangitis who are too ill to tolerate more invasive procedures. T e hepaticojejunostomy is an e ective means o biliary bypass but only in the circumstance o benign biliary stricture rather than stone disease. 53. The a ns we r is C (Chapter 14, Pancreatitis, Etiology, I). Gallstones represent the single most

important cause o pancreatitis. Alcohol use is another prime etiology but is less likely given the rise in amylase. Steroids cause pancreatitis uncommonly, and this patient has not report its use. Viral in ection is less likely without a prodrome. Pancreas divisum is a rare, congenital cause. 54. The a ns we r is D (Chapter 14, Pancreatitis, Acute Pancreatitis, V F). T is patient presents as

shock, likely due to in ected pancreatitis or pancreatic necrosis. T e patient is likely to deteriorate without prompt debridement. Upper gastrointestinal would be nondiagnostic as would EGD. ERCP is contraindicated, as it is likely to worsen the acute process. Biopsy is reasonable, but given the acute decompensation, surgical debridement is pre erred. 55. The a ns we r is B (Chapter 15, Introduction, Anatomy, II B). T e short gastric arteries arise rom

the spleen. T ey serve an important anastomotic network in cases o portal vein thrombosis when they may lead to gastric varices. T e gastrosplenic ligament is an important contributor to splenic stabilization; there is no pancreaticosplenic ligament. 56. The a ns we r is E (Chapter 15, Pathology, Causes o Secondary Hypersplenism, VIII).

Hereditary spherocytosis and hereditary elliptocytosis are indications or splenectomy but very uncommon. Sickle cell disease, not trait, may be an indication i splenomegaly is present. Primary hypersplenism is an indication or splenectomy but exceedingly rare.

253

Part V

Breast and Endocrine Disorders

Chapter Cuts and Caveats CHAP TER 16 Bre a s t: Because breast cancer is so common, sel -examinations and screening mammography are important elements or early detection. Screening mammography reduces breast cancer mortality. A strong amily history o breast cancer (multiple amily members) or diagnosis at a young age may be associated with genetic mutations including BRCA1 and BRCA2. T e presence o these mutations may af ect the treatment choices made by the patient. I a breast biopsy is negative, it is imperative to con rm that the correct lesion was biopsied. T is can be accomplished by physical exam, specimen radiography, intraoperative US, or postoperative radiologic evaluation i necessary. In lesions diagnosed as ductal carcinoma in situ, 10%–20% have an in ltrative component at excision. Lobular carcinoma in situ con ers an increased risk o breast cancer in both breasts. Survival rates are the same or patients treated with aggressive resection (mastectomy) versus breast conservation (lumpectomy and radiation). umors o en drain to particular nodes rst, called the sentinel nodes. In breast cancer, this is most commonly in the axilla and can be detected by the injection o dye or radiotracer into the lymphatics. I this node is negative or tumor, then the remaining axillary nodes are negative. T is technique has saved many patients the morbidity o an axillary lymph node dissection. Local advanced breast cancer and in ammatory breast cancer requires multimodal therapy including induction chemotherapy, surgical resection, and postoperative radiation therapy. Nipple discharge is considered concerning i unilateral, bloody, or spontaneous. T e most common cause is intraductal papilloma, and the treatment is excision.

CHAP TER 17 Thyro id , P a ra thyro id , Ad re na l Gla nd s , a nd Thym us : T e rst steps o diagnosis o a thyroid nodule include a thorough history, exam or nodes and vocal cord unction, FNA, and neck ultrasound. FNA is the diagnostic method o choice or most thyroid nodules. T e most eared complication o thyroid surgery is injury to the recurrent laryngeal nerve. Compromise o bilateral recurrent laryngeal nerves leads to a loss o the airway.

Follicular thyroid carcinoma spreads through vessels, is associated with systemic metastasis, and is o en treated with lobectomy and isthmusectomy. Papillary carcinoma is the most common thyroid cancer and has a high cure rate. Papillary and medullary carcinomas are multicentric, spread to regional lymph nodes, and are treated with total thyroidectomy. P H is a major regulator o calcium. Primary hyperparathyroidism is due to adenoma and should be treated or symptomatic patients and asymptomatic patients with a serum calcium greater than 11.5 mg/dL. Secondary hyperparathyroidism is associated with renal ailure, is due to our-gland hyperplasia, and is associated with a low serum calcium. Adrenal masses should be removed when large ( 5 cm) or when biologically active. Pheochromocytoma is the major tumor o the adrenal medulla; always treat with alpha blockade be ore surgical intervention. MEN syndromes arise rom a genetic de ect and produce lesions in the thyroid, parathyroid, pancreas, or pituitary. T ymectomy may improve symptoms in patients with myasthenia gravis.

255

Chapter 16

Breast

Emily Bellavance, Steven Feigenberg, and Jessica Joines

INTRODUCTION Ana to m y I. Bo rd e rs : Figure 16-1 A. Superior border: clavicle B. Medial border: lateral border o the sternum C. In erior border: in ramammary old/sixth rib D. Lateral border: latissimus dorsi E. Posterior border: pectoralis major II. Va s c ula ture : Because the breast is well-vascularized, the breast surgeon needs to be aware o a number o important vessels. A. Arterial supply 1. Axillary artery a. T oracoacromial artery b. Lateral thoracic artery 2. Internal mammary artery a. Anterior intercostal per orators B. Venous return 1. Axillary vein (primary) 2. Posterior intercostal veins 3. Internal mammary veins C. Lymphatic drainage: ollows venous drainage (Fig. 16-2) 1. Axillary chain: divided into three levels in relation to the pectoralis minor muscle 2. Rotter nodes: between pectoralis major and minor muscles 3. Internal mammary chain: ollows the internal mammary vessels and provides medial drainage

BREAST EVALUATION P hys ic a l Exa m ina tio n I. Vis ua l ins p e c tio n: Patient sits, raises arms upward, and then presses on hips to contract the pectoralis major muscle. A. Symmetry and nipple retraction: should be seen B. Skin changes: Observe color, texture, dimpling, edema (peau d’orange), and ulceration (visible tumor). II. P a lp a tio n: With patient in supine position with ipsilateral arm above head, palpate or masses or asymmetric densities. A. Nipple discharge: elicited with pressure on the of ending duct; may also be spontaneous B. Nodes: Examine axillary, cervical, internal mammary, and supraclavicular nodal basins.

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Breast

257

III II I

Fig ure 16-1: Anatomy o the breas t. The das hed line repres ents the pectoralis minor mus cle. I, II, and III repres ent the levels o lymph nodes . (Modif ed rom Harris J R, Lippman ME, Morrow M, et al. Diseases of the Breast, 2nd ed. Philadelphia: Lippincott Williams & Wilkins ; 2000.)

Ra d io lo g ic Exa m I. Ma m m o g ra m : able 16-1 A. Baseline mammogram: starting at age 40 years B. High-risk patients: start screening at earlier age C. Mammography: shows breast architecture, asymmetry, skin thickening, irregular masses, and microcalci cations II. Ultra s o und : Not recommended or routine screening; axillary ultrasound is use ul in assessing lymph nodes. III. Ma g ne tic re s o na nc e im a g ing (MRI): very sensitive but not a speci c evaluation o the breast; can detect the extent o tumor within the breast or lymph node basins and residual tumor a er lumpectomy or systemic therapy

Bio p s y I. Ne e d le b io p s y A. Fine-needle aspiration (FNA): limited use or breast lesions detected on exam or imaging; axillary node biopsy in cancer patients B. Core-needle biopsy: pre erable or breast lesions ( able 16-2) 1. Stereotactic biopsy: uses mammographic equipment to deploy a core needle into mammographic abnormalities 2. Ultrasound-guided biopsy: uses ultrasound to identi y lesion and deploy core needle in ultrasound-detected abnormalities

Quic k Cut

Breas t biops y is neces s ary or diagnos is o palpable or image-detected abnormalities .

Quic k Cut Cys t as piration is both diagnos tic and therapeutic.

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Breast Evaluation

Fig ure 16-2: The arterial s upply may aris e rom axillay, s ubclavian, and internal mammary origin. Veins als o drain into both axillary and internal mammary s ys tems . Lymphatics (not s hown) loos ely ollow the venous pathways . (Modif ed rom Harris J R, Lippman ME, Morrow M, et al. Diseases of the Breast, 2nd ed. Philadelphia: Lippincott Williams & Wilkins ; 2000.)

II. Surg ic a l b io p s y (e xc is io na l b io p s y): completely removes the lesion A. Excisional biopsy af er benign needle biopsy: See able 16-2. B. Needle-localized excisional biopsy: excisional biopsy a er the radiologist places a localizing wire in the breast to identi y the site

Quic k Cut A ter image-guided biops ies , pathology f ndings and imaging res ults mus t be reviewed to as s es s their concordance.

Ta b le 16-1: Ind ic a tio ns o r Exc is io n Fo llo wing Co re Ne e d le Bio p s y Failure to sample calcif cations Diagnosis o atypical ductal hyperplasia Diagnosis o atypical lobular hyperplasia or lobular carcinoma in situ* Lack o concordance between imaging f ndings and histologic diagnosis Radial scar (a proli erative breast lesion not related to surgery) Papillary lesions Flat epithelial atypia *Surgical excision or atypical lobular hyperplasia and lobular carcinoma in situ is controversial. From DeVita VT, Lawrence TS, Rosenberg SA. Cancer: Principles and Practice of Oncology, Vol 1. 8th ed. Philadelphia: Lippincott Williams & Wilkins; 2005.

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259

Ta b le 16-2: Ind ic a tio ns o r Surg ic a l Bio p s y a te r Co re -Ne e d le Bio p s y Wo m a n’s Ris k Le ve l

Ma m m o g ra p hy

MRI*

Normal

Annual starting at age 40 years

LCIS, ADH, ALH

Annual a ter diagnosis

Personal history o breast cancer

Annual a ter diagnosis

BRCA ; multiple f rst-degree, second-degree relatives; bilateral in f rst-degree premenopausal relative; breast/ovarian cancer amily history

Annual starting at 10 years younger than youngest relative but not younger than age 25 years

Annual

Hodgkin lymphoma treated with mantle radiation

Annual starting 8 years a ter treatment

Annual

*MRI and mammogram should be scheduled 6 months apart to screen patients twice yearly because cancers in these patients may be rapidly growing. MRI, magnetic resonance imaging, LCIS, lobular carcinoma in situ; ADH, atypical ductal hyperplasia; ALH, atypical lobular hyperplasia. From DeVita VT, Lawrence TS, Rosenberg SA. Cancer: Principles and Practice of Oncology, Vol 1. 8th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.

BENIGN BREAST DISEASE In e c tio us a nd Inf a m m a to ry Bre a s t Dis e a s e s I. Ce llulitis a nd m a s titis : In ection o the breast is usually associated with lactation. A. Bacteria (Staphylococcus or Streptococcus): enter via the nipple B. reatment: 10–14-day course o antibiotics and improvements o breast eeding technique. Lesions that do not resolve require urther workup or abscess or in ammatory malignancy.

Quic k Cut Patients can continue to breas t eed during mas titis treatment.

II. Ab s c e s s : collection o purulent uid within breast parenchyma treated by surgical drainage or aspiration with a course o antibiotics III. Chro nic s ub a re o la r a b s c e s s : A sinus tract develops rom the lacti erous duct to the areola. A. reatment: requires complete excision o the sinus tract B. Recurrence: common IV. Mo nd o r d is e a s e : phlebitis o the thoracoepigastric vein A. Etiology: Palpable, tender cord runs along the upper quadrants o the breast along the course o the vein. B. reatment: sel -limited course, so treatment is nonsteroidal anti-in ammatory drugs (NSAIDs) and warm compresses

Be nig n Le s io ns I. Fib ro c ys tic c ha ng e s : Benign nodularity with or without pain. Any dominant masses should be evaluated with imaging. II. Fib ro a d e no m a : benign tumor o the breast with brous stromal tissue with an epithelial component; most common in younger women III. P hyllo d e s tum o rs : broepithelial breast tumors with more connective tissue abnormalities than broadenoma A. Malignancy: rare; related to number o mitoses per high-power eld B. reatment: wide local excision or mastectomy C. Sclerosing adenosis: proli eration o acini in the lobules, which may appear to have invaded the surrounding breast stroma D. Fat necrosis: associated with trauma or radiation therapy to the Quic k Cut breast but may simulate cancer with a mass or skin retraction Needle as piration E. Mammary duct ectasia: dilatation o the subareolar ducts, which is per ormed or large may ll with cellular debris; may present as palpable retroareolar s ymptomatic cys ts . mass or nipple discharge

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Malignant Diseases

F. Cysts: diagnosis made by ultrasound 1. Color a. Simple cyst: clear or green uid and is benign b. Galactocele: milk- lled, benign cyst c. Bloody cyst: may represent atypia or malignancy 2. Cyst resolution a. Complete resolution: Per orm ollow-up ultrasound. b. Incomplete resolution: reat as a breast mass and excise. G. High-risk lesions: con er an increased risk o breast cancer Quic k Cut 1. Atypical ductal hyperplasia (ADH): epithelial proli erative Ta m o xi e n or lesion o duct 5 years can reduce the ris k o 2. Lobular neoplasia developing breas t cancer by a. Atypical lobular hyperplasia (ALH) 86% in patients with ADH. (1) Extent: epithelial proli erative lesion in less than one hal o lobular acini (2) Risk o upgraded pathology on excision: 1%–20% b. Lobular carcinoma in situ (LCIS) (1) Extent: epithelial proli erative lesion in greater than or equal to one hal o lobular acini (2) Risk o upgraded pathology on excision: 4%–25% (3) Prevention: amoxi en can reduce risk o breast cancer by 50%. Postmenopausal women with LCIS can decrease risk o breast cancer with raloxi ene. 3. Flat epithelial atypia: Columnar cell lesion in terminal duct lobular units; risk o cancer on excision is 10%–15%. 4. Intraductal papilloma: Polyp o the breast duct; risk o adjacent atypia or malignancy on excision is 10%. Quic k Cut 5. Radial scar: Complex sclerosing lesion; risk o upgraded Surgical excis ion is pathology to cancer on excision is 8%–30%. recommended or ADH, at

Nip p le Dis c ha rg e I. Fe a ture s : Usually a benign condition secondary to brocystic change or papilloma; benign discharge is bilateral with clear, green, or white uid that occurs with breast stimulation/palpation. II. Eva lua tio n a nd tre a tm e nt: Mammogram and ultrasound rule out an associated mass; drainage rom an isolated nipple duct should be excised.

Ma s ta lg ia

epithelial atypia, intraductal papilloma, and radial s car.

Quic k Cut Dis charge is s us picious or intraductal papilloma i it is unilateral, bloody, or s pontaneous .

I. Cyc lic p a in: Correlates with the menstrual cycle; treatment includes supportive bra and analgesics. II. No nc yc lic p a in A. reatment: Restrict caf eine intake; wear a supportive bra; and take NSAIDs, vitamin E (400 IU/ day), and tamoxi en or danazol ( or severe cases). B. Cancer: Must be excluded as a cause o pain. All patients should have a thorough exam and mammogram. Ultrasound is indicated or ocal pain.

MALIGNANT DISEASES Ep id e m io lo g y a nd Ris k Fa c to rs I. Ep id e m io lo g y: A woman has a one in eight chance o developing breast cancer. A. Incidence: In 2013, 240,000 women were diagnosed with breast cancer in the US, and 40,000 women died o breast Quic k Cut cancer. Female gender B. Mortality rate: decreased signi cantly in the last two decades and increas ed age are the due to earlier detection and improvements in treatment s tronges t ris k actors or breas t cancer. II. Ris k a c to rs : able 16-3 A. Family history: produces a three old higher risk 1. First-degree relatives (i.e., mother, daughter, sister): Are af ected. Risk is higher i the relative is premenopausal.

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261

Ta b le 16-3: Ris k Fa c to rs o r the De ve lo p m e nt o Bre a s t Ca nc e r No nm o d i a b le Ris k Fa c to r

Mo d i a b le Ris k Fa c to r

Female sex

Obesity

Age

Alcohol consumption

Family history

Age o parity

High-risk breast lesions

Sedentary li e style

Chest wall radiation

Exogenous estrogen

Early menarche

Smoking

High breast density Inherited mutation

2. Hereditary breast and ovarian cancer: Breast cancer gene Quic k Cut (BRCA) has two orms. BRCA con ers an a. BRCA-1: 60%–80% li etime risk o breast cancer; 40% risk 70% li etime ris k o breas t o ovarian cancer cancer. b. BRCA-2: 40%–80% li etime risk o breast cancer; 10%–20% risk o ovarian cancer B. Reproductive actors: early menarche, nulliparity, age o rst childbirth older than 30 years, late menopause C. Exogenous estrogen: has been shown to increase the risk o breast cancer in postmenopausal women D. Risk estimation: Modi ed Gail model is the most commonly used statistical model to estimate breast cancer risk; it accounts or risk related to age, age o menarche, age o parity, history o prior breast biopsies, amily history in a rst-degree relative, and ethnicity. Other models may be used based on patient’s personal and amily history.

Ris k Re d uc tio n with Me d ic a tio n (Che m o p ro p hyla xis ) I. Se le c tive e s tro g e n re c e p to r m o d ula to rs (SERMs ) A. amoxi en: estrogen receptor agonist/antagonist that blocks Quic k Cut estrogen receptors in the breast and stimulates receptors in SERMs or AIs can uterus, liver, and vagina be us ed to reduce a woman’s 1. Risk reduction: 50% in eligible patients; greater than 80% ris k o breas t cancer. Eligible in ADH patients women have a greater than 2. Side e ects: vasomotor symptoms (hot ashes, night sweats), 1.7% 5-year ris k o breas t cancer by Gail model; or increased risk o endometrial cancer, and thromboembolic events his tory o LCIS. B. Raloxi ene: reduces risk in eligible postmenopausal women, similar to tamoxi en but with ewer side ef ects II. Aro m a ta s e inhib ito rs (AIs ): block the enzyme that converts androgens to estrogen and are there ore ef ective in postmenopausal women in whom estrogen is derived rom androgen conversion rather than rom ovaries A. Exemestane: can decrease risk in eligible postmenopausal women by 60% B. Adverse e ects: osteoporosis, arthralgia, hot ashes, and night sweats

Bre a s t Ca nc e r Sym p to m s I. Ea rly c a nc e rs : o en asymptomatic II. Bre a s t m a s s III. P a in: rarely a symptom but should be completely evaluated to eliminate the possibility o a malignancy IV. Me ta s ta tic d is e a s e : may also be the initial symptom A. Axillary nodes: wo percent o patients present with axillary nodes but no identi able primary breast tumor. I the results o

Quic k Cut A breas t mas s is one o the more common pres enting s ymptoms o breas t cancer, but it is a late f nding.

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Malignant Diseases

all studies are negative, treatment is modi ed radical mastectomy or whole breast radiation with axillary dissection. B. Distant organ metastasis: to the bone, brain, liver, or lungs may cause presenting symptoms

No ninva s ive Bre a s t Ca nc e rs I. Duc ta l c a rc ino m a in s itu (DCIS): Con ned to ductal cells; no invasion o the underlying basement membrane occurs. reatment options ollow. A. Partial mastectomy: excision with clear margins 1. Local recurrence: varies and is related to grade, tumor size, and margin width 2. Fif y percent o recurrences are invasive. B. Lumpectomy and radiation: Radiation reduces risk o recurrence by 50%. C. otal (simple) mastectomy: Removal o breast tissue and areola/ nipple; reconstruction can be done at the time o mastectomy. D. amoxi en: taken or 5 years; reduces risk o invasive and noninvasive in-breast recurrence and risk o contralateral breast cancer by 50%

Quic k Cut O all types o breas t cancer, 20% are noninvas ive.

Quic k Cut Breas t cons ervation therapy includes partial mas tectomy, als o called lumpectomy.

II. P a g e t d is e a s e : Histologically vacuolated cells (Paget cells) are seen in the epidermis o the nipple and result in an eczematous dermatitis. A. DCIS or invasive carcinoma: present in the underlying ducts B. Evaluation: mammography and ultrasound to assess or a subareolar mass C. reatment: lumpectomy to include nipple areolar complex with adjuvant radiation or mastectomy

Inva s ive Bre a s t Ca nc e r I. Fa vo ra b le his to lo g ic typ e s : tubular carcinoma, mucinous carcinoma, and papillary carcinoma II. Le s s a vo ra b le le s io ns A. Medullary cancer: involves lymphocytic in ltration and a well-circumscribed lesion B. In ammatory breast cancer: Histology shows tumor-plugged subdermal lymphatics. Diagnosis is clinically based on in ammatory signs on exam (e.g., warmth, swelling, and pain).

Sta g ing I. Clinic a l s ta g ing A. Diagnostic mammogram: to de ne primary tumor, identi y additional oci, and evaluate contralateral breast B. Breast ultrasound: to de ne primary tumor axillary node C. Chest radiograph: to detect pulmonary or bone metastasis D. Computed tomography (C ) scan o the chest: may be obtained or node-positive or higher than or equal to stage III patients E. Alkaline phosphatase: sensitive or hepatic metastasis F. Bone scan: i nodes are clinically positive or i nodes are clinically negative but the patient has symptoms o bone pain and stage III or higher G. Head C scan: i neurologic signs or symptoms are present Quic k Cut

II. Clinic a l/p a tho lo g ic s ta g ing : ables 16-4 and 16-5

Tre a tm e nt I. Surg e ry: recurrence risk varies and is related to many actors including age, nodal status, tumor size, margin status, and lumpectomy with radiation; typically reduces risk o recurrence by 60%–75% A. Mastectomy: Removal o the breast tissue and nipple/areolar complex. Patients with a large tumor in relation to breast size may have superior cosmetic results with mastectomy. 1. Modi ed radical mastectomy: includes removal o breast and levels I and II axillary lymph nodes (see able 16-1)

Treatment or invas ive breas t cancer includes s urgery, chemotherapy, radiation, and/ or hormonal therapy.

Quic k Cut There is no s urvival di erence between breas t cons ervation and mas tectomy.

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263

Ta b le 16-4: Am e ric a n J o int Co m m itte e o n Ca nc e r Tum o r-No d e -Me ta s ta s is Sta g ing o Bre a s t Ca nc e r T T0

Tum o r Size In situ

T1

2 cm

T2

2cm to

T3

5 cm

T4

N

5 cm

Direct extension to chest wall/skin

No d e Me ta s ta s is

M

N0

None

Nm i

Microscopic

N1

Mobile in level I, II axilla

N2

Fixed in level I, II axilla

N3

Level III axillary, internal mammary, supraclavicular

2 mm

Dis ta nt Me ta s ta s is

M0

None

M1

Any

2. Skin-sparing mastectomy: Nonareolar breast skin is Quic k Cut preserved; with immediate reconstruction provides more Patients who cosmetic result and does not increase recurrence risk. choos e breas t cons ervation 3. Radical mastectomy: includes the pectoralis major and therapy s hould undergo minor muscles and levels I–III axillary nodes radiation, as it prolongs B. Axillary sampling: must accompany surgery to accurately stage s urvival. patient 1. Sentinel node biopsy: or clinically negative nodes; radiotracer and/or vital blue dye is used to identi y the rst Quic k Cut nodes drained by the breast Radical mas tectomy does not improve s urvival a. Advantages: allows minimal dissection with a substantial over other types o breas t decrease in morbidity (lymphedema) s urgery. b. Node(s) examined or cancer: I negative or metastatic disease, no urther lymphadenectomy per ormed. I positive, axillary dissection is per ormed. Quic k Cut 2. Axillary dissection: or patients with clinically positive nodes Surgery is not or with positive sentinel nodes curative or patients with a. Level I and II nodes: removed in relation to the axillary in ammatory breas t cancer, vein (see Figure 16-2) paras ternal tumors , and thos e b. Skip metastasis (i.e., involved level III nodes with with metas tatic dis eas e. negative levels I and II nodes): occurs in less than 5% o cases c. Long thoracic nerve: Preserved to prevent denervation o the serratus anterior muscle, which results in a winged scapula. T oracodorsal nerve and blood supply to the latissimus muscle are also preserved. II. Ad juva nt ra d ia tio n: whole breast radiation involves 45–50 Gy; used in breast conservation to decrease recurrence rates A. Advantages: reduces local recurrences and improves survival ollowing a mastectomy in patients with large tumors ( 5 cm), positive nodes, or with chest wall involvement B. Postmastectomy setting: Nodal radiation is uni ormly administered to the axilla, supraclavicular ossa with or without the internal mammary nodes, and the chest wall.

Ta b le 16-5: Ana to m ic Sta g e a nd P ro g no s tic Gro up s Sta g e 0

In situ disease

M0

Sta g e 1

T1N0, T0–1Nmi

M0

Sta g e 2

T2N0, T3N0, T1N1, T2N1

M0

Sta g e 3

T3N1, any T4, any N2, any N3

M0

Sta g e 4

Any T, any N

M1

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III. Ad juva nt c he m o the ra p y: Candidates have node-positive, tumor larger than 1 cm, estrogen receptor/progesterone receptor (ER/PR)–negative, HER2/neu receptor–positive pathology. A. Common chemotherapy drugs: cyclophosphamide, doxorubicin, docetaxel, and paclitaxel or 3–6 months B. rastuzumab: used to treat HER2/neu (epidermal growth actor receptor 2)–positive cancers C. Side e ects: myelosuppression, alopecia, and cardiomyopathy (doxorubicin and trastuzumab) IV. Ad juva nt ho rm o na l the ra p y: or ER/PR patients A. Premenopausal: tamoxi en ovarian suppression or ablation Quic k Cut B. Postmenopausal: AIs Hormonal therapy is us ed in ER or PR patients . V. Ne o a d juva nt the ra p y: systemic therapy given be ore surgical therapy or local disease A. In ammatory breast cancer: requires chemotherapy be ore surgery (modi ed radical mastectomy), ollowed by radiation B. Large, xed tumors or large nodal disease: can downstage disease and enable resectability or decrease tumor size and allow breast conservation

Fo llo w-up o r Op e ra b le Bre a s t Ca nc e r (Ip s ila te ra l a nd Co ntra la te ra l Bre a s ts ) I. Ob s e rva tio n: or tumor recurrence and complications A. Annual or biannual breast examination: by a physician B. Annual mammogram C. Other: Chest radiographs, C scans, and tumor markers are not needed unless clinical suspicion arises. II. Lym p he d e m a o the a rm : en percent to 30% develop arm edema a er axillary dissection, which is worsened by radiation i greater than 10 lymph nodes are removed. A. reatment: Because each in ection increases lymphatic obstruction by obliterating the remaining open channels with brosis, even minor skin in ections should be evaluated by a physician; chronic edema can be treated with an elastic sleeve. B. Complications: Chronic edema lasting 10 years or longer can rarely lead to the development o lymphangiosarcoma in the af ected arm.

Re c urre nt Dis e a s e I. Me ta s ta tic d is e a s e : present in 10% o patients with recurrence Quic k Cut II. Sta nd a rd tre a tm e nt (o a n is o la te d b re a s t re c urre nc e Mos t recurrences a te r p rim a ry ra d ia tio n the ra p y): mastectomy occur in the s ame quadrant III. Che s t wa ll re c urre nc e s as the original les ion. A. Af er mastectomy: Isolated chest wall recurrences are treated with radiation therapy and resection. B. Ipsilateral recurrences (af er breast conservation with adjuvant radiation): mastectomy IV. Dis ta nt m e ta s ta s is A. Hormone therapy: Patients with hormone-positive breast cancer who respond to one hormone treatment modality generally continue to respond to sequential hormone therapy. B. Chemotherapy: or patients with recurrent disease who are ER or who do not respond to hormone therapy 1. Common drugs: anthracyclines (doxorubicin), taxanes (paclitaxel), and antimetabolites (capecitabine) 2. emporary avorable responses (e.g., decrease in tumor size or pain relie ): occur in 70% o patients with stage IV disease

Sp e c ia l Ca s e s I. Bre a s t c a nc e r in p re g na nc y A. Incidence: occurs in 1.5% o women during childbearing years B. Diagnosis: usually delayed secondary to normal nodularity that orms in breasts during pregnancy 1. Suspicious mass: should have ultrasound, then core biopsy 2. Vital blue dye or sentinel node: contraindicated 3. Radiotracer: appears to be sa e

Quic k Cut Chemotherapy can be adminis tered in late pregnancy; radiation is always contraindicated.

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II. Ma le b re a s t A. Gynecomastia: unilateral or bilateral enlargement o the breast tissue directly behind the nipple 1. ypes (three) a. Prepubertal gynecomastia: rare; caused by adrenal and Quic k Cut testicular carcinoma Breas t enlargement b. Pubertal gynecomastia: 60%–70% o prepubertal boys in the healthy male adoles cent c. Senescent gynecomastia: due to decreased testosterone does not require treatment and will regres s with age. and increased estradiol and luteinizing hormones 2. Causes a. Idiopathic b. Drug therapies: thiazide diuretics, digoxin, theophylline, antidepressants, and hormones c. Alcohol and marijuana abuse d. Disease conditions: cirrhosis, renal ailure, and malnutrition 3. Evaluation and treatment: Evaluate or mass with mammography and physical exam; biopsy any dominant mass. a. Negative biopsy: reat underlying medical condition; provide reassurance. b. esticular tumor: Rarely, gynecomastia can be secondary to testicular tumor. Check serum estrogen, beta-human chorionic gonadotropin, estrogen, and dehydroepiandrosterone; per orm testicular exam. B. Cancer: Accounts or 1% o all breast cancers; average age is 63–70 years and most are ER . 1. Kline elter syndrome: associated with male breast cancer (testicular hormone actors) 2. Symptoms: Most patients present with a painless unilateral mass. 3. Workup: identical to that or emale breast cancer 4. reatment a. Simple mastectomy: most common b. Breast conservation with radiation: an option c. Sentinel node biopsy: axillary dissection d. amoxi en: or ER/PR cancers 5. Survival: similar to emale breast cancer stage or stage

Ch pter 17

T yroid, P r thyroid, Adren l Gl nds, nd T y us John A. Olson Jr.

THYROID GLAND Va s c ula ture

Quic k Cut Surgery remains the mains tay o treatment or s us pected or proven thyroid cancer and compres s ive goiters .

I. Arte ria l s up p ly: Figure 17-1 A. Superior thyroid artery: First br nch o the extern l c rotid rtery supplies the upper pole o the thyroid. B. In erior thyroid artery: rises ro the thyrocervic l trunk o the subcl vi n rtery nd supplies the lower pole C. T yroidea ima artery: occ sion lly rises ro the ortic rch nd connects to the thyroid isth us in eriorly II. Ve no us d ra ina g e : interconnecting series o veins without v lves Quic k Cut A. Superior thyroid veins: dr in long the course o the superior The nodes in the thyroid rteries into the intern l jugul r vein tracheoes ophageal groove B. Middle thyroid vein: dr ins directly into the intern l jugul r (level 6) are mos t important C. In erior thyroid veins: dr in ro the lower pole nd isth us in the s pread o thyroid either directly into the intern l jugul r or the inno in te vein malignancies becaus e involved nodes may s ignal III. Lym p ha tic d ra ina g e : to cervic l nodes loc ted in the centr l tumor extens ion into the neck between the c rotids nd tr che (level 6), long the course recurrent laryngeal nerve. o the intern l jugul r vein (levels 2A, 2B, 3, 4), in the posterior tri ngle (level 5), or to the p r tr che l nodes in the edi stinu ( or erly level 7) (Fig. 17-2)

Ne rve s

Quic k Cut

In 1% o individuals , the laryngeal nerve is nonrecurrent and enters the larynx by cros s ing the TE groove at the midpole o the thyroid.

I. Re c urre nt la ryng e a l ne rve (RLN): br nch o the v gus (cr ni l nerve [CN] X) th t runs in the tr cheoesoph ge l ( E) groove t the postero edi l spect o the thyroid A. On the right: RLN recurs round the subcl vi n rtery nd runs n oblique course, crossing the in erior thyroid rtery be ore entering the E groove. B. On the lef : RLN recurs round the lig entu rteriosu in Quic k Cut the edi stinu nd runs course p r llel to the E groove. The RLN provides C. Divisions: RLN divides t v ri ble loc tions into n nterior motor unction and s ens ory br nch nd posterior br nch. innervation o the glottis and D. Function: Anterior br nch innerv tes the dductor uscles trachea. (thyro rytenoid, inter rytenoid, nd l ter l crico rytenoid), nd posterior br nch innerv tes the bductor uscles (posterior crico rytenoid).

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Anterior view Thyroid ca rtila ge Le va tor gla ndula e thyroide a e P yra mida l lobe Inte rna l jugula r ve in S upe rior thyroid a rte ry S upe rior thyroid ve in Common ca rotid a rte ry

Cricothyroid mus cle Cricoid ca rtila ge

Is thmus of thyroid gla nd Lobe of thyroid gla nd Middle thyroid ve in Thyroide a ima a rte ry

Es opha gus Tra che a Infe rior thyroid ve in

Le ft bra chioce pha lic ve in

Ape x Lateral view of right lobe

Ca ps ule of pre tra che a l fa s cia Ca ps ule of thyroid gla nd Lobe of thyroid gla nd

Is thmus of thyroid gla nd

S upe rior pa ra thyroid gla nd

Infe rior pa ra thyroid gla nd

Ba s e

Fig ure 17-1: Blood s upply o the thyroid gland. Each lobe o the thyroid has two main arteries and three veins . (From Snell RS. Clinical Anatomy by Regions, 9th ed. Baltimore: Lippincott Williams & Wilkins ; 2011).

267

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Abnor

lities o T yroid Descent

Fig ure 17-2: Lymph node s tations o the neck. Metas tas es rom thyroid cancer f rs t involve the central compartment (level 6) and then s pread to the lateral compartment (predominantly levels 3 and 4). (From Dimick J B, Upchurch GR, Sonnenday CJ . Clinical Scenarios in Surgery. Baltimore: Lippincott Williams & Wilkins ; 2012).

E. Injury: ost co only occurs where the nerve crosses the in erior thyroid rtery or where it penetr tes the cricothyroid e br ne 1. Unilateral injury: results in voc l cord p r lysis c using Quic k Cut signif c nt ho rseness s well s sensory loss resulting in Bilateral recurrent dysph gi nd spir tion laryngeal nerve injury may 2. Precautions: Injury is voided by identi ying the nerve long require tracheos tomy. its course. II. Sup e rio r la ryng e a l ne rve (SLN): Inti tely intertwined with the br nches o the superior thyroid rtery; it br nches into n Quic k Cut intern l nd n extern l br nch. Superior laryngeal A. Function: Intern l br nch o the SLN is sensory to the l rynx, nerve injury res ults in vocal nd the extern l br nch is otor to the cricothyroid uscle. weaknes s and may be B. Injury: c n be injured during obiliz tion o the upper pole, es pecially noticeable in especi lly when the lobe is enl rged s ingers .

P a ra thyro id Gla nd s I. Lo c a tio n: Superior p r thyroids re typic lly loc ted t the junction o the upper nd iddle one third o the thyroid on the postero edi l spect (Fig. 17-3). T e upper gl nd is typic lly ne r the in erior thyroid rtery nd is posterior to the RLN. In erior p r thyroids re ne r the lower pole o the thyroid, usu lly nterior to the RLN. II. Injury: usu lly results ro disruption o the blood supply or ro their in dvertent re ov l during thyroid surgery

Quic k Cut Devitalizing all parathyroid glands caus es hypoparathyroidis m, unles s the parathyroids can be reimplanted.

ABNORMALITIES OF THYROID DESCENT Ro ute o De s c e nt I. No rm a l d e s c e nt: T yroid igr tes downw rd ro its point o origin t the or en cecu t the b se o the tongue through the hyoid bone nd the thyrogloss l duct. II. Ab no rm a l d e s c e nt: y result in ectopic pl ce ent o thyroid tissue in the tongue, idline o the neck, or edi stinu Quic k Cut A. Glottic (lingual) thyroid: occurs when the thyroid does not Lingual thyroid may descend into the neck nd re ins t the b se o the tongue be the only unctioning thyroid 1. Symptoms: Obstruction or di culty with speech is usu lly tis s ue in the individual. rel ted to goiter or tion in the lingu l ss. 2. Diagnosis: By inspection or indirect l ryngoscopy. A r dioiodine (131I) sc n should be per or ed to identi y the ss s thyroid tissue.

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269

0.3%

0.3% 13%

11% 3% 1%

1.6%

20%

38% 1%

Fig ure 17-3: Normal locations o the parathyroid glands . The s uperior glands are almos t always located on the dors al as pect o the thyroid at the level o the cricoid cartilage. The in erior glands are more variable but are mos t commonly ound on the lateral as pect o the lower pole o the thyroid. (From Moore KL, Agur AMR, Dalley AF. Clinically Oriented Anatomy, 7th ed. Baltimore: Lippincott Williams & Wilkins ; 2013.)

6% 4% Anterior view

3. Management: T yroxine ( 4) should be the f rst step bec use glottic thyroid tissue is usu lly hypo unctioning. Surgic l re ov l should be considered when there re obstructive sy pto s. B. Mediastinal thyroid (substernal goiter): Most re loc ted in the nterosuperior edi stinu nd y represent substern l extensions ro n enl rged thyroid or nor l thyroid tissue, resulting ro berr nt e bryologic descent o the thyroid into the edi stinu . 1. Evaluation: Usu lly, co puted to ogr phy (C ) sc ns re best. 2. Substernal extensions: y be c used by deno tous hyperpl si nd re not usu lly lign nt; usu lly occur in older ge groups a. Symptoms: E co pression nd dysph gi or dyspne b. Management: In gener l, they do not respond to edic l ther py. Oper tion is usu lly dvised to relieve pressure sy pto s.

Quic k Cut In ambiguous cas es , 131 I s can o the medias tinum may be cons idered becaus e normal unctioning thyroid tis s ue will take up 131 I.

Quic k Cut Almos t all s ubs ternal goiters can be removed through a cervical incis ion without the need or s ternotomy becaus e their blood s upply is derived rom the neck.

THYROID DYSFUNCTION REQUIRING SURGERY Thyro id Ho rm o ne s I. Triio d o thyro nine (T3 ) a nd T4 : Follicular cells o the thyroid re derived pri rily ro the oor o the oregut nd produce 3 nd 4. A. Hormone synthesis and release: Iodine nd tyrosine co bine to or 3 nd 4; both o these hor ones bind to thyroglobulin nd re stored in the gl nd. 1. Release: Under the control o thyroid-sti ul ting hor one ( SH) ro the pituit ry. SH is rele sed upon sti ul tion by thyrotropin-rele sing hor one ( RH) ro the hypoth l us. 2. Feedback regulating RH and SH release: edi ted by circul ting levels o 3 nd 4 B. Action: incre se et bolic r te nd oxygen consu ption, Quic k Cut incre se glycogenolysis (elev ted blood sug r), nd enh nce E ects o thyroid ctions o c techol ines hormones can be muted 1. Result: incre sed pulse r te, c rdi c output, nd blood ow by beta-blockers s uch as 2. Symptoms: Nervousness, irrit bility, uscul r tre ors, nd propranolol. uscle w sting c n lso occur.

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II. Thyro c a lc ito nin: P r ollicul r cells (C cells) re derived ro the ulti obr nchi l body nd re p rt o the ine precursor upt ke nd dec rboxyl tion (APUD) cell syste th t produces c lcitonin (whose unction is unknown).

Gra ve s Dis e a s e (Di us e To xic No n-no d ula r Go ite r) I. P a tho g e ne s is : Autoi une dise se resulting ro de ect in cell- edi ted i unity. Longcting thyroid sti ul tor (LA S) incre ses the size o the thyroid nd its production o thyroid hor one. II. Clinic a l p re s e nta tio n A. Hypermetabolic state: Sy pto s include p lpit tions, swe ting, intoler nce to he t, irrit bility, inso ni , nervousness, weight loss, nd tigue. Signs include n udible bruit over the gl nd, h nd nd tongue tre ors, nd c rdi c rrhyth i s. B. Abnormal deposition o mucopolysaccharide and round cell in ltration: is ch r cterized by exophth l os, che osis, nd eyelid nd pretibi l ede III. Dia g no s is : conf r ed by incre sed tot l seru 4, 3, nd 3 resin upt ke ( 3RU) A. Free 4 index: Incre se o the 3RU v lue ti es the tot l seru 4 nd o r dio ctive iodine upt ke (RAIU) distinguish this ro thyrotoxicosis without hyperthyroidis . B. 131I thyroid scan: shows enl rged thyroid with uni or elev ted upt ke throughout C. Other: Seru cholesterol level is decre sed, nd the blood sug r nd ALP re incre sed. IV. Me d ic a l tre a tm e n t: Initi lly, ntithyroid ls to control thyroid hor one rele se nd block the syste ic e ects o elev ted 4 nd Quic k Cut 131 . T is is usu lly ollowed by thyroid bl tion with I or surgery. 3 Antithyroid drugs A. Antithyroid drugs: e ective in 50% o p tients, especi lly are rapidly e ective and can revers e s ymptoms in a s hort those with sy pto s o short dur tion nd with s ll gl nd time. 1. Action: lter v rious st ges o iodine et bolis a. Methimazole and Propylthiouracil (P U):Methi zole is f rst-line tre t ent to control high seru thyroid levels, except in pregn ncy bec use it is ter togenic. Both it nd P U ct through co petitive inhibition o peroxid se, blocking the oxid tion o iodide to thyroid hor one. P U is reserved or pregn ncy nd thyroid stor bec use it lso blocks the peripher l conversion o 4 to 3, which provides r pid response. P U h s the potenti l or serious liver toxicity. b. Iodine: High concentr tions block the rele se o thyroid hor ones, but the e ect only l sts 10–14 d ys. Quic k Cut c. Propranolol: Bet - drenergic blocker reduces the Methimazole second ry e ects o hyper et bolis . is f rs t line treatment or 2. Recurrence: high i the drugs re stopped Graves Dis eas e. PTU is not recommended due to the ris k 3. oxicity: Drugs ust be discontinued i ever, r sh, rthr lgi , o liver toxicity. lupus-like syndro e, or gr nulocytosis occurs. B. Ablative doses o 131I: Or l d inistr tion is e ective nd usu lly pre erred in Gr ves dise se. 1. Advantages: 131I bl tion obvi tes the need or surgery nd does not ppreci bly incre se the risk o c rcino . 2. Contraindications: pregn ncy or pl nned pregn ncy; l rge, sy pto tic goiters; concurrent thyroid nodules t risk or Quic k Cut lign ncy; Gr ves ophth l op thy (rel tive); nd p tients When neces s ary, the in need o r pid resolution o their hyperthyroidis pre erred operation or Graves V. Surg ic a l tre a tm e nt: usu lly the second-line bl tive option or Gr ves dise se A. Indications: T yroidecto y is indic ted when 131I tre t ent is contr indic ted. B. Objectives: Re ove thyroid tissue to correct the hyperthyroidis . Currently, ost experts reco end per or ing either ne r-tot l thyroidecto y (tot l lobecto y on one side nd subtot l lobecto y on the other) or tot l thyroidecto y.

dis eas e is total thyroidectomy.

Quic k Cut Patients with near total thyroidectomy require s upplementation hormones , but the ris k o pers is tent hyperthyroidis m is minimal.

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271

C. Preoperative preparation: o ini ize the risk o thyroid stor , the p tient should be euthyroid be ore oper tion. 1. Antithyroid drugs: Given until the p tient is clinic lly nd bioche ic lly euthyroid ( ree 3 5 pM/L). Lugol solution or s tur ted pot ssiu iodide (SSKI) is given or 7–10 d ys be ore surgery to decre se gl nd v scul rity. 2. Beta blockade: used i there is t chyc rdi or hypertension despite ntithyroid edic tions D. Propranolol: e ective in r pidly restoring the euthyroid st te nd in reducing v scul rity; ust be given or 4–5 d ys postoper tively to prevent thyroid stor bec use the h l -li e o circul ting thyroid hor one is 5–10 d ys E. Complications 1. T yroid storm: severe hyper et bolic st te th t c uses hyperpyrexi nd t chy rrhyth i s due to uncontrolled hyperthyroidis a. Incidence: r rely ound, unless p tient h s undi gnosed hyperthyroidis nd h s surgery or so e unrel ted e ergency b. reatment: l rge doses o ntithyroid drugs, hydrocortisone, iodine, nd propr nolol 2. Hemorrhage: possible due to incre sed v scul rity in hyper ctive thyroid gl nd a. Airway obstruction: c used by he orrh ge resulting in tr che l co pression nd l rynge l ede b. reatment: Secure the irw y, ev cu te the clot, nd control the bleeding. 3. Hypoparathyroidism: usu lly develops within the f rst 24 hours er surgery nd results in subnor l seru c lciu concentr tion a. Symptoms o hypocalcemia: Nu bness nd tingling perior lly or in the f ngers nd toes, nervousness, nd nxiety. Evidenced by positive Chvostek sign ( ci l twitch with t pping on the ci l nerve) or rousse u sign (c rpoped l sp s with blood pressure cu insu tion). b. reatment o hypocalcemia: Intr venous (IV) or l c lciu s lts. Activ ted vit in D (c lcitriol) Quic k Cut ther py y be required i the seru int ct Intact PTH and p r thyroid hor one (P H) level is low. IV c lciu serum calcium levels should be checked a ter thyroidectomy. should be voided unless severe hypoc lce i (C 7.5 g/dL) nd sy pto s re present. 4. RLN injury: produces voc l cord p r lysis a. Unilateral injury: Usu lly ni ested by ho rseness. I the nerve is int ct (p resis), the p tient usu lly recovers nor l voice within 3 onths. I the injury is per nent, ther py to edi lize the true voc l cord is necess ry. b. Bilateral: Airw y obstruction results due to p r lysis o the voc l cords in the idline dducted position, requiring e ergency intub tion or tr cheosto y. I the nerves re int ct, recovery usu lly occurs in 3–6 onths. 5. Injury to the external branch o the SLN: T is nerve is otor to the cricothyroid uscle nd c n be injured during lig tion o the br nches o the superior thyroid rtery, c using voice tigue nd loss o ti bre nd projection.

P lum m e r Dis e a s e (To xic Multino d ula r Go ite r) I. Cha ra c te ris tic s : Hyperthyroid st te c used by sever l hyper unctioning nodules in ultinodul r gl nd. Most co only ound in wo en older th n ge 50 ye rs nd is usu lly ssoci ted with history o pre-existing nontoxic ultinodul r goiter. II. Clinic a l p re s e nta tio n: Hyper et bolic sy pto s tend to be subtler th n in Gr ves dise se; however, c rdiov scul r ni est tions o hyperthyroidis , such s t chyc rdi , p lpit tions, nd rrhyth i s ( tri l f brill tion) re ore co on. Signs re rrhyth i s, occ sion l uscle w sting, nd the presence o ultinodul r goiter. III. La b o ra to ry s tud ie s : 3 nd 4 levels re incre sed, nd RAIU is incre sed in the nodules, which will not be suppressed by exogenously d inistered 4. IV. Tre a tm e nt: Options or tre t ent re s outlined or Gr ves dise se. 131I tends to be less e ective or toxic ultinodul r goiter th n or Gr ves dise se. A. Preoperative preparation and perioperative management: s e s or Gr ves dise se except or the use o iodides, which y worsen the hyperthyroidis B. otal thyroidectomy: pre erred tre t ent, especi lly i the goiter is l rge or there re co pressive sy pto s

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Chapter 17

T yroid Dys unction Requiring Surgery

To xic Ad e no m a I. Clinic a l p re s e nta tio n: hyperthyroidis due to n utono ously hyper unctioning solit ry nodule in n otherwise nor l gl nd A. Symptoms: Initi lly, the p tient y be sy pto tic bec use hor one production by the rest o the gl nd will be suppressed. Eventu lly, sy pto s o hyperthyroidis c n occur s the nodule continues to secrete thyroid hor one. B. Signs: Solit ry thyroid nodule y be p lp ble in n otherwise nor l gl nd. II. La b o ra to ry s tud ie s : 3 nd 4 levels re incre sed, RAIU is incre sed in the nodule (hot nodule), nd hor one secretion will not be suppressed by exogenous 4. III. Tre a tm e nt: Surgic l excision o the nodule (lobecto y) is the s est nd ost expeditious tre t ent. 131 I bl tion is lso good option. Prep r tion or surgery is s outlined or Gr ves dise se.

Thyro id Go ite r

Quic k Cut I. Ove rvie w: Enl rge ent o the thyroid gl nd re collectively re erred Thyroid goiters to s goiters, which y be di use or ocal nd y be either s ooth can be di us e or ocal, or nodul r. T yroid unction y be nor l or bnor l. and s urgery is indicated or compres s ive s ymptoms . II. Ca us e s : Di use goiters with nor l or decre sed unction h ve benign c uses. Foc l or nodul r goiters with nor l unction y be due to neopl s s. III. Co llo id a nd io d ine -d e f c ie nc y g o ite rs : occur in requently in the United St tes A. Clinical presentation: bulky, so enl rge ents B. reatment: Surgery is indic ted or co pressive sy pto s, coexistent nodules concerning or lign ncy, or occ sion lly, cos etic concerns. T yroid hor one suppression is gener lly not e ective nd should be discour ged. IV. Thyro id itis : In tion c n be cute, sub cute, or chronic. A. Acute suppurative thyroiditis: unco on disorder c used by the he togenous spre d o icroorg nis s into the thyroid gl nd 1. Clinical presentation: p in nd tenderness 2. Diagnosis: f ne-needle spir tion (FNA) 3. reatment: open dr in ge or loc lized resection with ntibiotics B. Subacute thyroiditis (giant cell, granulomatous, or de Quervain thyroiditis): T ought to be vir l nd is o en preceded by n upper Quic k Cut respir tory in ection. Course is sel -li ited, l sting 2–6 onths. Reidel thyroiditis is Nonsteroid l nti-in tory drugs (NSAIDs) re used. usually stony hard on physical C. Chronic thyroiditis: occurs in two jor or s, H shi oto nd exam and di f cult to distinguish rom thyroid malignancy. Reidel Riedel thyroiditis is the only chronic 1. Hashimoto thyroiditis (struma lymphomatosa): Rel tively thyroiditis treated surgically. co on utoi une disorder th t occurs predo in ntly in wo en. T yroid unction is nor l or hypothyroid. re t ent is usu lly long-ter 4 supple ent tion. 2. Riedel ( brous) thyroiditis: Rel tively r re or in which the p renchy is repl ced with dense f brous tissue. re t ent is surgic l. V. No d ula r thyro id e nla rg e m e nts : Di use ultinodul r goiter is the ost co on or nd is the c use o p lp ble nodule in the thyroid in s uch s 10% o the dult popul tion. A. Clinical presentation: T ese goiters re c used by deno tous hyperpl si o the thyroid gl nd, thought to be due to long-st nding sti ul tion o the thyroid by SH. T yroid unction studies re nor l, s re thyroid ntibodies. B. reatment: I there re no clinic l signs o lign ncy nd the gl nd is not sy pto tic, no tre t ent is necess ry. Surgery is indic ted or co pressive sy pto s. Quic k Cut

Thyro id Ne o p la s m s I. Ove rvie w: Frequently, solit ry or pro inent thyroid nodule is detected on physic l ex in tion in n sy pto tic p tient. Although ost solit ry thyroid nodules re benign, the pri ry concern is thyroid c ncer.

The mos t common reas on or thyroid s urgery today is to diagnos e or treat a s us pected thyroid neoplas m that cannot be diagnos ed by other means .

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273

Ta b le 17-1: Ind ic a tio ns o r Fine -Ne e d le As p ira tio n o Thyro id No d ule s P a tie nt Ris k Ca te g o ry

Ultra s o und Fe a ture

Size

High*

Any

5 mm

Average

Any

1.5 cm

Average

Microcalcif cations Hypoechoic Irregular margin Taller than wide Abnormal lymph nodes

1 cm †

Average

Spongi orm Mixed solid-cystic Cystic

2cm 1.5–2.0 cm NR‡

*Patients with a amily history o thyroid cancer, prior exposure to head and neck radiation, prior history o thyroid cancer status post thyroid lobectomy, or multiple endocrine neoplasia type 2 kindred member. † Consider biopsy or smaller lesions depending on clinical suspicion. ‡ May be done or relie o compressive symptoms. NR, not reported.

II. As s e s s m e nt o thyro id no d ule s : ble 17-1 A. Patient’s age: In children, 10%–15% o thyroid nodules re lign nt; during the childbe ring ye rs, ost nodules re benign; incidence o c ncer in nodules incre ses by 10% per dec de er ge 40 ye rs. B. Patient’s sex: T yroid c ncer is ore co on in wo en th n in en, but benign thyroid nodules re lso ore co on in wo en, nd the likelihood th t nodule will prove to be lign nt is gre ter in en th n in wo en. C. Other risk actors: ily history o thyroid lign ncy nd history o exposure to ther peutic r di tion, which incre ses incidence 5–10- old III. Cha ra c te ris tic s o the no d ule A. Consistency: Fir ness suggests lign ncy. B. In ltration (into the surrounding thyroid or overlying structures, such as the strap muscles): suggests lign ncy C. Nodulation: Solitary nodules h ve 5% ch nce o being lign nt. Multiple nodules re present in s ny s 40% o proven c ses o thyroid lign ncy. D. Growth patterns: Nodules th t suddenly incre se in size should be suspected o being thyroid neopl s s. Quic k Cut IV. Ip s ila te ra l lym p h no d e e nla rg e m e nt: Suggests thyroid Ips ilateral vocal cord lign ncy. In children, s ny s 50% o thyroid c ncers re f rst paralys is in a patient with detected bec use o cervic l ly ph node enl rge ent. a thyroid nodule is almos t V. Mo b ility o the vo c a l c o rd s : Bec use voc l cord p r lysis y always diagnos tic o a thyroid malignancy that has inf ltrated not be ssoci ted with voice ch nges, the cords should be ssessed the RLN. preoper tively by either indirect or direct l ryngoscopy in ll p tients undergoing thyroid oper tions. Ex in tion should be repe ted postoper tively i voice bnor lities occur. VI. Dia g no s tic s tud ie s : T yroid nodules re co on; workup ust Quic k Cut e ciently seek to deter ine whether nodule is unction l or likely Nearly all thyroid to be lign nt (Fig. 17-4). cancers are non unctioning and have a normal TSH. A. Blood work: Seru SH is the f rst test or thyroid nodules. 1. Suppressed SH: P tient should be ev lu ted or hyperthyroidis nd then be scheduled or technetiu 99 (99 c) pertechnet te/ 131I thyroid sc n. Quic k Cut 2. Seru c lcitonin: specif c bio rker or edull ry c rcino Ultras ound cannot reliably distinguish benign rom o the thyroid (M C) malignant thyroid nodules. B. US: Using high- requency line r tr nsducer (7.5–14 Hz), nodules c n be identif ed s cystic, solid, or co plex. Fe tures

274

Chapter 17

T yroid Dys unction Requiring Surgery Thyroid nodule * TSH, diagnostic thyroid US +/– lateral neck US

TS H norma l/ e le va te d

TS H low

US-guided FNA†

131

I uptake and scan

Autonomous function (hot)

Nonfunctioning (cold/wa rm)

Rx hype rthyroidis m (ca nce r ra re )

FNA, followe d by s urge ry if not de finitive

Be nign

Follow +/– re pe a t FNA

Inde te rmina nt

Ma ligna nt

Thyroide ctomy

* De te cte d clinica lly or incide nta lly on ima ging. † Crite ria for FNA lis te d in Ta ble 16-2.

Fig ure 17-4: Algorithm or the evaluation and management o the as ymptomatic thyroid nodule. TSH, thyroid-s timulating hormone; US, ultras ound; FNA, f ne-needle as piration.

th t y be suggestive o lign ncy include the presence o c lcif c tions, solid echo-texture, indistinct borders, loc l inv sion, or incre sed v scul rity. C. Needle biopsy (o the thyroid): llows or the histop thologic or Quic k Cut cytop thologic ex in tion o cells s n id in the di gnosis o Needle biops y is the thyroid nodules nd in pl nning ther py mos t us e ul diagnos tic tool or dis tinguis hing benign rom 1. FNA and cytology: Cells re spir ted by pplying malignant thyroid nodules . suction to syringe tt ched to 21- to 25-g uge needle. echnique requires interpret tion by well-tr ined thyroid cytop thologist but h s good degree o ccur cy nd specif city ( lse-neg tive r te 3%) in di gnosing lign nt lesions nd is ssoci ted with ew co plic tions. 2. Core biopsy and histology: Using 14- or 18-g uge especi lly designed needle ( ru-Cut), cylinder o tissue is obt ined then f xed nd st ined or histop thologic n lysis. Due to rel tively high incidence o bleeding co plic tions, the technique is r rely per or ed. D. Radioisotope scanning (o the thyroid): Indic ted in p tients with nodules nd suppressed SH. M y be done with 131I or with 99 c. Quic k Cut 1. Isotope tracers: ken up by nor lly unctioning thyroid Us e FNA or tissue, which ppe rs s “hot” re ; nodules th t do not t ke cold nodules as 20% will up tr cer ppe r s “cold” re s. be neoplas tic. 2. Hot nodules: should be sc nned with 131I to deter ine their unction VII. Op e ra tive a p proa c h: Surgic l re ov l is the inst y o tre t ent Quic k Cut or nodules t high risk or h rboring lign ncy. P r thyroid gl nds For a s olitary nodule nd RLN should lw ys be identif ed nd preserved. conf ned to one lobe, the A. Extent o the operation: depends on the histologic type, extent minimal diagnos tic operation is total removal o that lobe o the tu or s deter ined ro the preoper tive ssess ent nd and the is thmus . the oper tive f ndings, nd the tu or’s biologic ggressiveness B. Lymph node resection: indic ted when nodes re grossly involved VIII. Typ e s o thyro id m a lig na nc y: ble 17-2 Quic k Cut A. Papillary thyroid carcinoma (P C): ccounts or 80% o ll Papillary is the mos t thyroid c ncers in children nd 60% in dults; ects wo en common his tologic type in twice s o en s en patients who have radiation 1. Characteristics: Slow r te o growth; 50% spre d to region l expos ure. ly ph tics; 40% o tu ors re ulticentric in origin.

Chapter 17

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275

Ta b le 17-2: Typ e s o Thyro id Ca nc e r a nd Tre a tm e nt Ca nc e r Typ e

% Thyro id Ca nc e r

P ro g no s is

Tre a tm e nt

Papillary

80%–85%

Excellent

Thyroidectomy, TSH suppression,

/

131

I ablation

Follicular

10%–15%

Good

Thyroidectomy, TSH suppression,

/

131

I ablation

Medullary

5%

Intermediate

Thyroidectomy

Poor

Multimodality therapy

Anaplastic

2%

LND

TSH, thyroid-stimulating hormone; LND, lymph node dissection.

2.

reatment: otal thyroidectomy is the tre t ent o choice or ost P C 1 c . a. Cervical lymphadenectomy: indic ted or gross ly ph node et st sis b. 131I therapy: to bl te the thyroid re n nt nd tre t icroscopic node dise se; indic ted or inter edi te nd Quic k Cut high-risk p tients (e.g., ge 45 ye rs, tu ors 2 c , Patients with wellly ph node et st sis) encaps ulated papillary tumors 3. Prognosis: excellent with occult or well-enc psul ted have a 20-year s urvival rate greater than 90% . intr thyroid l c rcino ; poor when there is extr thyroid l inv sion or i the p tient is older th n ge 45 ye rs B. Follicular thyroid carcinoma (F C): ccounts or 10%–15% o ll thyroid lign ncies; ore co on in re s where iodine-def ciency goiter is prev lent 1. Incidence: A ects wo en twice s o en s en; rel tive requency incre ses er ge 40 ye rs. 2. Characteristics: slow-growing nd usu lly uni oc l tu or spre ds pri rily through the bloodstre nd unco only ( 10%) to region l ly ph nodes 3. reatment: otal thyroidectomy is the tre t ent o choice or ost F C 1 c . a. Lymph node metastasis: Occurs in 10%; ly ph denecto y is indic ted or gross ly ph node et st sis. b. 131I therapy: to bl te the thyroid re n nt nd tre t icroscopic node dise se; indic ted or inter edi te- nd high-risk p tients who lso benef t ro SH suppressions 4. Prognosis: good with ini l v scul r inv sion (80% 20-ye r surviv l r te); poor with gross inv sion (20-ye r surviv l r te 20%) C. M C: ccounts or less th n 5% o ll thyroid c ncers nd ost co only occurs spor dic lly but lso c n be ili l s p rt Quic k Cut o ultiple endocrine neopl si (MEN) syndro e type II Calcitonin is a 1. Characteristics: E rly spre d to the ly ph nodes is us e ul tumor marker to detect ch r cteristic nd spre d to liver nd bone is lso co on. recurrence o MTC. Arises ro the C cells o the thyroid nd produces c lcitonin. 2. reatment: otal thyroidectomy and central compartment (bil ter l level 6) is indic ted or ll M C p tients; lateral compartment-oriented cervical lymphadenectomy is Quic k Cut indic ted or p tients with gross denop thy. In MEN2, the 3. Prognosis: poorer th n or P C or F C nd is rel ted to st ge development o MTC can be a. Overall survival: 86% t 5 ye rs nd 65% t 10 ye rs prevented by prophylactic total thyroidectomy. b. Poor prognostic actors: dv nced ge, NM st ge III or IV, reoper tion, nd h ving MEN2B D. Anaplastic thyroid carcinoma (A C): ccounts or less th n 2% o ll thyroid c ncers but is the ost co on c use o thyroid c ncer–specif c de th 1. Incidence: ost co on between ges 50 nd 70 ye rs nd is three ti es ore co on in wo en th n en 2. Characteristics: c n be reli bly di gnosed by FNA or core biopsy, which shows s ll cells, gi nt cells, or spindle cells; y rise ro pre-existing, well-di erenti ted thyroid neopl s 3. Growth: Usu lly r pid, involving the tr che nd esoph gus; they et st size e rly, so they re usu lly unresect ble.

276

Chapter 17

P r thyroid Gl nds

4.

5. E. T o 1.

2. 3. 4.

5.

reatment: S ll A C ( 5 c ) li ited to the thyroid h ve the gre test ch nce o prolonged surviv l with total thyroidectomy ollowed by djuv nt che other py nd r di tion ther py. a. Patients with locally advanced disease: y benef t ro up- ront che or di tion b. Secure airway: O en the i edi te need or A C p tients. r cheosto y y be per or ed, but endotr che l stenting is pre erred. Prognosis: Poor, with t l outco e in l ost ll, reg rdless o tre t ent. P lli tion is i ed t int ining p tency o the esoph gus nd the irw y. yroid lymphoma: wo percent o ll thyroid lign ncies, ecting ostly wo en 50–70 ye rs ge. Chronic H shi oto thyroiditis is the princip l risk ctor. Characteristics: R pidly enl rging goiter with neck p in, Quic k Cut dysph gi , ho rseness, dyspne , nd cough. Physic l f ndings Phys ical include f r thyroid goiter with f x tion to surrounding examination alone cannot structures. di erentiate goiter rom Diagnosis: FNA nd core biopsy re the inst ys. P tients thyroid lymphoma. should undergo C sc n o the neck, chest, nd bdo en to ev lu te the extent o dise se. ype: l ost exclusively o the non-Hodgkin type nd o Quic k Cut B-cell origin Unles s the tumor reatment: Co bin tion o che other py nd r di tion. is s mall and conf ned to the Surgery h s li ited role. r cheosto y should be thyroid lobe, s urgical excis ion o lymphoma is generally not considered in ny p tient with ctu l or i pending irw y indicated. co pro ise. Prognosis: Outco e is dependent on st ge nd gr de o ly pho . Over ll 5-ye r surviv l h s been esti ted to be 35%.

PARATHYROID GLANDS Ove rvie w I. Em b ryo lo g y: Most individu ls h ve two superior nd two in erior Quic k Cut p r thyroid gl nds th t di er in their e bryologic origin. There is no current A. Superior parathyroid glands: Arise ro the ourth br nchi l s atis actory replacement pouch in close proxi ity to the origin o the thyroid nd descend or PTH, and the patient into the neck. Bec use o the e bryologic origin, bnor l with hypoparathyroidis m p r thyroid loc tions y be either intr thyroid l or within the is doomed to a li etime o epis odic, s ymptomatic posterior edi stinu ne r the E groove. hypocalcemia. B. In erior parathyroid glands: Arise ro the third br nchi l pouch in rel tionship to the thy ic nl ge nd cross the superior gl nds in their descent into the neck. T ey re requently ssoci ted with the thy us gl nd in the nterosuperior edi stinu . II. Ana to m y: Most people h ve our p r thyroid gl nds, but s ew s three gl nds nd s ny s f ve h ve been identif ed. T e ver ge p r thyroid gl nd weighs ro 40 to 70 g. A. Superior parathyroid glands: Usu lly lie t the junction o the upper nd iddle one third o the thyroid gl nd on its postero edi l sur ce or in the E groove; they usu lly lie posteriorly to the RLN nd re in close proxi ity to the thyroid. Occ sion lly, they y even be intr thyroid l. B. In erior parathyroid glands: Lie within circle with 3-c di eter, the center o which is the point where the RLN crosses the in erior thyroid rtery; usu lly nterior to the RLN. T ey y be in close proxi ity to or within the cervic l li b o the thy us gl nd. C. Arterial supply: Derived inly ro the in erior thyroid rtery. Quic k Cut Superior p r thyroid gl nds receive their blood supply ro the Both parathyroid superior thyroid rtery in 10%. D. Venous drainage: is into the superior, iddle, nd in erior thyroid adenomas and hyperplas ia primarily involve chie cells , veins making the pathologic E. Histopathology: Nor l p r thyroid gl nd h s signif c nt dis tinction di f cult. ount o t interspersed with chie nd oxyphil cells.

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T yroid, P r thyroid, Adren l Gl nds, nd T y us

277

P a ra thyro id Ho rm o ne I. Ca lc ium m e ta b o lis m : P H is jor regul tor o c lciu et bolis . A. Action: P H cts in conjunction with ctiv ted vit in D3 to regul te the pl s concentr tion o the ionized or o c lciu . T ere is reciproc l rel tionship between the seru c lciu nd P H secretion— s seru c lciu levels decre se, the secretion o P H incre ses. B. A ected organs: P H exerts its biologic e ect on bone ( obilizes c lciu ro bone), intestine (incre ses intestin l bsorption o c lciu ), nd kidney ( ctive re bsorption o c lciu in the dist l nephron). II. Inc re a s e d , uno p p o s e d P TH s e c re tio n: Clinic l e ects include hyperc lce i , ltered c lciu excretion (initi lly, hypoc lciuri occurs due to incre sed re bsorption, which reverts to hyperc lciuri in chronic hyperp r thyroid st tes when the hyperc lce i exceeds the ren l threshold), hypophosph te i , nd hyperphosph turi . III. La b o ra to ry te s ts : Seru

P H levels c n be

e sured by r dioi

uno ss y.

Hyp e rp a ra thyro id is m I. P rim a ry hyp e rp a ra thyro id is m (P HP T): rel tively co on Quic k Cut disorder th t ost co only occurs spor dic lly PHPT is the A. Etiology and pathology: Most PHP c ses re due to mos t common caus e o solit ry deno ; 10%–15% re due to our-gl nd hypercalcemia in patients hyperpl si ; P C ccounts or less th n 1% o PHP ; 0.4% outs ide the hos pital. o c ses re due to ultiple deno s involving ore th n one gl nd. B. Clinical presentation: Most p tients re clinic lly sy pto tic. Quic k Cut 1. Kidney stones: Nephrolithi sis occurs in 50%. PHPT s ymptoms 2. Bones: Osteitis f bros cystic (von Recklingh usen ollow the mnemonic “s to ne s , b o ne s , m o a ns , a nd dise se o bone) is ound ostly in second ry nd terti ry a b d o m ina l g ro a ns .” hyperp r thyroidis . 3. Moans: Psychi tric ni est tions—person lity disorders or r nk psychosis— re unco on. 4. Abdominal groans: Peptic ulcer dise se y occur, usu lly ssoci ted with hyperg strine i ; cholelithi sis or p ncre titis y lso occur. M ny p tients h ve nonspecif c sy pto s, such s we kness, e sy tig bility, leth rgy, constip tion, nd rthr lgi . C. Diagnosis 1. Laboratory studies: Incre sed seru c lciu is the Quic k Cut cornerstone o di gnosis, which should be shown on t le st A s erum PTH level two blood speci ens dr wn on di erent occ sions. that is inappropriately high a. Other causes o high serum calcium: include et st tic or the s erum calcium level is bone dise se, yelo , s rcoidosis, the use o thi zide diagnos tic or PHPT. diuretics, ilk- lk li syndro e, hypervit inosis, thyrotoxicosis, nd Addison dise se b. Serum 25-hydroxy vitamin D: should be e sured to exclude second ry hypop r thyroidis c. Other: Seru phosphorus level is decre sed, nd the seru chloride-to-phosphorus r tio usu lly exceeds 33:1. 2. Radiographic studies: Pl in r diogr phs re r rely indic ted. Historic lly, in x-r ys, the proxi l ends o the long bones y show bony re bsorption or brown tu ors. Ultr sound, C , or scintigr phy y be used to ssess the p r thyroid gl nds. D. Indications or surgery: ble 17-3 1. Symptomatic patients: All should be considered or surgery. Quic k Cut 2. Asymptomatic patients: i younger th n ge 50 ye rs, Few patients with seru c lciu levels gre ter th n 1 g/dL bove the nor l hyperparathyroidis m are truly r nge; decre se in bone density (T score 2.5 t ny site), as ymptomatic i care ully hyperc lciuri ; decre se in cre tinine cle r nce less th n ques tioned. 60 L/ in or p tients who re un ble to h ve close edic l ollow-up

278

Chapter 17

P r thyroid Gl nds

Ta b le 17-3: Ind ic a tio ns o r Surg e ry in Hyp e rp a ra thyro id is m HP T Typ e

Sym p to m Sta tus

P a tie nts Elig ib le

Tre a tm e nt

Primary

Symptomatic “Vaguely” symptomatic Asymptomatic

All Most† NIH guidelines ‡ met NIH guidelines not met

Parathyroidectomy* Parathyroidectomy* Parathyroidectomy* Observation

Secondary

Symptomatic** Asymptomatic

All PTH 300–500 pg/mL despite maximal medical therapy

Subtotal parathyroidectomy or total parathyroidectomy with autotransplantation

Tertiary

Asymptomatic Symptomatic

Ca All

2

12 mg/dL

Parathyroidectomy†† Parathyroidectomy††

*Directed parathyroidectomy with intraoperative parathyroid hormone monitoring or our-gland exploration. † Symptoms improve 30%–50% o the time. ‡ (Any) Ca 2 1 mg/dL elevation, age younger than 50 years, T score less than 2.5 any site, glomerular fltration rate less than 60 mL/min, or ollow-up unlikely. **Symptoms in secondary hyperparathyroidism (SHPT) that warrant parathyroidectomy include calciphylaxis, bone pain, osteodystrophy, and severe pruritus. †† Four-gland exploration. HPT, hyperparathyroidism; “vaguely symptomatic,” patient with musculoskeletal, neuropsychiatric, and abdominal complaints; NIH, National Institutes o Health; PTH, parathyroid hormone.

E. Preoperative localization o the parathyroid glands: help ul Quic k Cut to per it ini l ccess ppro ch, def ne the n to y Localization in p tients who h ve h d prior surgery, nd id in def ning s tudies s hould not be us ed the p thology in p tients who h ve persistent or recurrent to diagnose PHPT, only to hyperc lce i identi y the adenoma once 1. Ultrasonography (US): will def ne n enl rged p r thyroid in the diagnos is has been made. ost c ses; le st expensive f rst test or p r thyroid loc liz tion 2. Scintigraphy: Using 99 c sest ibi c n loc lize 75% o p r thyroid deno s. a. Delayed images: show persistent upt ke by enl rged p r thyroid gl nds b. Sestamibi scanning: use ul in de onstr ting ectopic gl nds, such s the edi stinu c. Single positron emission computerized tomography (SPEC ): y reve l wh t tr dition l pl n r i ging does not 3. C : p rticul rly success ul in loc lizing enl rged p r thyroids in the edi stinu 4. Magnetic resonance imaging (MRI): See s to be s success ul s C in loc lizing p r thyroids on the 2-weighted i ge. Cost is high. 5. Selective venous sampling and P H assay: Bec use the study is costly nd ti e consu ing, it is reserved only or p tients with neg tive noninv sive i ging. Retrogr de injection o the thyroid veins is per or ed. a. High P H level: Disproportion tely high P H in one or ore o the venous s ples helps to loc lize the lesion to one side o the neck. b. Four-gland hyperplasia: suggested by signif c nt incre se in s ples obt ined ro veins on both sides o the neck F. Surgical treatment: P r thyroid surgeon ust be ble to reli bly identi y ll our p r thyroid gl nds. 1. Solitary adenoma: Should be co pletely excised. Currently, loc liz tion techniques nd intr oper tive ss y o P H levels llow or ini l ccess ppro ch to p r thyroid deno s in ost p tients. a. P H levels: Dr wn t the beginning o the oper tion, nd then li ited dissection is per or ed to excise the deno . Following excision, ddition l P H levels re dr wn t specif c interv ls. (1) Signi cant drop: Due to the short h l -li e o P H (5 inutes), drop occurs i ll bnor l p r thyroid Quic k Cut tissue h s been re oved. A drop o the PTH (2) I the levels do not drop su ciently: Abnor l tissue level to les s than 50% o the re ins. highes t level and into the b. I tumor cannot be ound in the normal locations: normal range is as s ociated Explor tion should continue in regions where ectopic with a 95% –98% cure rate. p r thyroids y be ound, including the deep thy us,

Chapter 17

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the prevertebr l sp ce behind the esoph gus, behind the upper pole o the thyroid, nd intr thyroid l. 2. Four-gland hyperplasia: n ged s ollows a. Subtotal parathyroidectomy (leaving a well-vascularized remnant [50–100 mg o parathyroid tissue] to provide or normal parathyroid unction): Intr oper tive P H levels re obt ined to ensure th t n dequ te excision o p r thyroid tissue h s been per or ed. T ere is 5% recurrence r te. b. otal parathyroidectomy (with autotransplantation o minced parathyroid tissue): T ere is re l d nger o per nent hypop r thyroidis . G. Postoperative management: Hypoc lce i usu lly develops er success ul ther py. Asy pto tic hypoc lce i gre ter th n 8 g/dL requires no tre t ent. 1. Symptomatic hypocalcemia: C lciu less th n 8.0 g/dL lw ys requires tre t ent. a. reatment: should begin with IV c lciu glucon te b. Mildly symptomatic patients: M y be given or l c lciu . Quic k Cut T e g strointestin l (GI) tr ct is ble to bsorb xi u Patients with o 30% o ingested or l c lciu d ily, which corresponds s ignif cant bone dis eas e require prolonged calcium to doses o c lciu s lts r nging ro 3–4 g/d y. s upplementation to permit 2. Vitamin D: y be needed i hypoc lce i re ins s keletal remineralization. sy pto tic despite c lciu supple ent tion II. Se c o nd a ry hyp e rp a ra thyro id is m (SHP T): Found in chronic ren l ilure. T ese p tients re un ble to synthesize the ctive or o vit in D nd develop chronic hypoc lce i nd hyperphosph te i . A. Multiple gland enlargement: results ro chronic hypoc lce i sensed by the p r thyroid B. Unresponsiveness to calcium and vitamin D: C lciu -sensing nd vit in D receptors re requently downregul ted. C. Clinical presentation: Sy pto s include tigue, uscle we kness, pruritus, bone p in, joint p in, nd et st tic so tissue c lcif c tions c using tissue necrosis (c lciphyl xis). Untre ted SHP y result in sy pto tic ren l osteodystrophy ( dyn ic bone, osteo l ci , nd osteitis) with risk o r cture. D. Diagnosis: incre sed seru int ct P H level, hypoc lce i , vit in D def ciency, hyperphosph te i , nd elev ted lk line Quic k Cut phosph t se (ALP) Secondary E. Imaging studies: US, 99 c sest ibi, or C sc n hyperparathyroidis m is always F. Medical treatment: indic ted in ost p tients nd includes as s ociated with our-gland phosph te binders, vit in D n logues, nd c lci i etics such hyperplas ia. s cin c lcet G. Surgical treatment: Subtot l p r thyroidecto y or tot l p r thyroidecto y with utotr nspl nt tion o p r thyroid Quic k Cut tissue is indic ted or p tients who re re r ctory to edic l Tertiary ther py or who h ve intr ct ble sy pto s. hyperparathyroidis m occas ionally occurs a ter III. Te rtia ry hyp e rp a ra thyro id is m (THP T): Hyperp r thyroidis trans plantation, res ulting in th t persists in p tients who h ve chronic ren l dise se despite hypercalcemia. success ul ren l tr nspl nt; it produces the s e sy pto s s PHP . A. Etiology: Autono ous clones o unresponsive, hypersecretory p r thyroid cells develop ro the p r thyroid hyperpl si o long-st nding ren l dise se. B. Diagnosis: Seru P H is elev ted; hyperc lce i , hypophosph te i , nd elev ted ALP re co on. C. Imaging studies: y include ultr sound, 99 c sest ibi, or 4D C sc n D. Surgical treatment: When persistent longer th n 12 onths ollowing tr nspl nt tion, HP is tre ted by subtot l p r thyroidecto y or tot l p r thyroidecto y with utotr nspl nt tion.

ADRENAL GLAND Ove rvie w I. Em b ryo lo g y: consists o two distinct p rts, the cortex nd the medulla, e ch o which h s di erent e bryologic origin A. Medulla: Fro ectoder l cells o neur l crest origin; other extra-adrenal medullary tissue c n be ound in the p r g ngli ,

Quic k Cut The adrenal glands are the s ource o s everal hormones and catecholamines and play a key role in blood pres sure regulation.

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in the org n o Zuckerk ndl just below the origin o the in erior esenteric rtery, nd in the edi stinu . B. Adrenal cortex: derived ro esoder l cells, which c n occ sion lly beco e sep r ted nd or adrenocortical rests nd re ost co only ound in the ov ry or testis II. Ana to m y: wo dren l gl nds, e ch lying on the edi l spect o the superior pole o kidney; their nor l co bined weight is 10 g. A. Histology: T ree distinct re s c n be recognized in the cortex. 1. Zona glomerulosa: outer zone th t produces iner locorticoids (e.g., ldosterone) 2. Zona asciculata: produces cortisol nd glucocorticoids 3. Zona reticularis: inner zone where androgens nd estrogens re de Quic k Cut Arterial anatomy to B. Arterial supply: ro three pri ry sources—the phrenic rtery, the adrenal is variable, but ort , nd ren l rteries there is us ually a s ingle large C. Venous drainage: Short ( 1 c ) right dren l vein dr ins into adrenal vein. the ven c v , nd the le dren l vein joins the phrenic vein to e pty into the le ren l vein. D. Adrenal portal system: Venous blood ro the cortex, cont ining high levels o glucocorticoids, dr ins into the edull , helping to induce the enzy e phenyleth nol ine-N- ethyltr ns er se, which ethyl tes norepinephrine to or epinephrine.

Ad re na l Ho rm o ne s a nd Ca te c ho la m ine s I. Ste ro id ho rm o ne s (thre e c la s s e s ): glucocorticoids, iner locorticoids, nd sex steroids ( ndrogens nd estrogens) A. Glucocorticoids: Most i port nt physiologic lly is cortisol, which h s diurn l v ri tion, with the highest seru levels occurring round 6:00 a .m. Quic k Cut Cortis ol exerts a 1. Regulation: Adrenocorticotropic hor one (AC H; negative eedback on ACTH corticotropin) is produced by the nterior pituit ry gl nd. at the hypothalamic-pituitary AC H sti ul tes the production o cortisol by the dren l. level. a. Corticotropin-releasing actor (CRF): produced by the hypoth l us nd sti ul tes rele se o AC H ro the pituit ry b. Free cortisol: is the ctive hor one 2. Metabolism: Cortisol is et bolized in the liver by conjug tion with glucuronide, which renders it w ter soluble or urin ry excretion. T e level o urin ry 17-hydroxycorticosteroids re ects glucocorticoid production nd et bolis . B. Mineralocorticoids: M jor hor one produced is aldosterone. 1. Regulation: Aldosterone production is regul ted by the renin- ngiotensin syste nd ch nges in pl s concentr tions o sodiu nd pot ssiu . a. Renin: rele sed by the juxt glo erul r cells o the kidney in response to decre sed blood pressure; converts angiotensinogen ( de in the liver) to angiotensin I b. Angiotensin I: is converted to angiotensin II by angiotensin-converting enzyme, which is produced by endotheli l cells c. Angiotensin II: sti ul tes the dren l cortex to rele se aldosterone d. Sympathetic nervous system (SNS): c n lso sti ul te rele se o ldosterone 2. Metabolism: Aldosterone is et bolized in si il r nner to cortisol. It is excreted in the urine in s ll qu ntities nd c n be e sured by r dioi uno ss y. C. Sex steroids: Androgens nd estrogens re produced in the zona reticularis o the dren l cortex. T e urin ry level o 17-ketosteroids re ects ndrogen production. Estrogens c n be e sured directly in the urine. II. Ca te c ho la m ine s : Adrenal medulla is the site o c techol ine production, including dop ine, norepinephrine, nd epinephrine. A. Regulation: C techol ine production is under the control o the SNS. B. Metabolism (Fig. 17-5): Levels o et nephrine, nor et nephrine, v nillyl ndelic cid (VMA), nd c techol ines c n be e sured in the urine. Fr ction ted c techol ine et bolites y be e sured in pl s .

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Tyrosine Tyros ine hydroxyla s e Dopa Dopa de ca rboxyla s e

Mona mine oxida s e , ca te chol-O-me thyltra ns fe ra s e

Homovanillic acid—HVA

Dopamine Dopa mine -βhydroxyla s e Norepinephrine P he nyle tha nola mine N-me thyltra ns fe ra s e

Mona mine oxida s e , ca te chol-O -me thyltra ns fe ra s e

Vanillylmandelic acid—VMA

Epinephrine

Fig ure 17-5: Schematic or catecholamine production. HVA, homovanillic acid. (From Philip PA, David PG. Principles and Practice of Pediatric Oncology, 6th ed. Baltimore: Lippincott Williams & Wilkins ; 2010.)

Ad re no c o rtic a l Ins u f c ie nc y (Ad d is o n Dis e a s e ) I. P rim a ry d is e a s e : results in di inished or bsent unction o the dren l cortex c used by utoi une dise se, bil ter l dren l tuberculosis, dren l ung l in ections, or bil ter l dren l he orrh ge (second ry to eningococc l septice i , postp rtu , or in p tients on ntico gul nt ther py) II. Se c o nd a ry d is e a s e : trophy o the dren l cortex second ry to decre sed pituit ry AC H (Cushing syndro e) c used by AC H suppression by corticosteroid drugs or pri ry pituit ry p thology (Cushing dise se) A. Clinical presentation: Sy pto s include norexi , l ise, weight loss, poor toler nce o stress, hypoglyce i , hypotension, nd occ sion lly, skin hyperpig ent tion. B. Aldosterone de ciency: results in volu e depletion, hypon tre i , hyperk le i , zote i , nd cidosis C. Perioperative steroid replacement: H ndled on n individu l b sis nd depends on the length o steroid ther py, the dos ge t ken, nd the gnitude o the pl nned procedure. In gener l, the t rget is 100–150 g o hydrocortisone IV d ily or 2–3 d ys; preoper tive or l dos ge is resu ed er 3 d ys.

Hyp e rc o rtis o lis m

Quic k Cut Patients with Addis on dis eas e cannot tolerate the s tres s o s urgery without receiving corticos teroid s upport.

Quic k Cut Cus hing s yndrome is mos t commonly caus ed by s uppres s ion o the cortex s econdary to exogenous corticos teroids .

Quic k Cut A patient who has taken s teroids regularly or any period during the pas t year is as s umed to have inadequate adrenal res erve.

I. Cus hing s ynd ro m e : results ro chronic lly incre sed cortisol levels A. AC H dependent 1. Pituitary source (Cushing disease): ccounts or 70% o the c ses o endogenous Cushing syndro e nd is ore co on in iddle- ged wo en. Overproduction o AC H by the pituit ry results in bil ter l dren l hyperpl si ; ost co e ro pituit ry deno . 2. Ectopic Cushing syndrome: ccounts or 15% o the c ses nd is ore co on in older en a. Cause: AC H is produced by n extr - dren l, extr pituit ry neopl s , ost co only s ll cell c rcino o the lung but c n lso occur with bronchi l c rcinoids, thy o s, nd p ncre s or liver tu ors. b. AC H level: quite high ( 500 ng/ L) B. AC H independent: Adren l Cushing syndro e ccounts or 15% o the c ses. 1. Cause: Excess cortisol produced utono ously by the dren l cortex due to n deno , c rcino , or bil ter l nodul r dyspl si nd ectopic cortisol-producing tu ors; re ining

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Ta b le 17-4: Ad re na l Ca us e s o Hyp e rte ns io n Na m e (s )

Ho rm o ne (s )

Ad re na l So urc e

Dia g no s tic Te s t(s )

Aldosteronoma (Conn syndrome)

Aldosterone

Cortex: zona glomerulosa

Aldo/PRA Aldo suppression AVS

Cortisol-producing adenoma (Cushing syndrome)

Cortisol

Cortex: zona asciculata

1 mg dexamethasone suppression test ACTH

Pheochromocytoma

Epinephrine Norepinephrine

Medulla

PFMs 24-hr catecholamines

Aldo, serum aldosterone; PRA, plasma renin activity; aldo suppression, aldosterone response to salt loading; AVS, adrenal vein sampling or aldosterone/cortisol; ACTH, adrenocorticotropic hormone; PFMs, plasma ractionated metanephrines.

2. 3.

4.

5. 6.

7.

drenocortic l tissue trophies, nd AC H levels re low bec use o suppression by the excess cortisol. Clinical presentation: Most co on ni est tions re listed in ble 17-4. Diagnosis: Nor l diurnal rhythm o cortisol secretion is usu lly lost. Cushing syndro e is st te o cortisol excess. Quic k Cut a. Best test or hypercortisolism: elev ted ( 2 g/ No one tes t is dL) orning s ple er suppressing dose o 1 g conclus ive or Cus hing dex eth sone the night be ore s yndrome: Laboratory tes t res ults and clinical b. Alternative test: Me sure s liv ry cortisol t idnight, pres entation mus t be which is nor lly less th n 1.6 ng/ L. cons idered together to make c. Elevated ( 55 g/day) 24-hour urinary ree cortisol: an accurate diagnos is . reli ble index o hypercortisolis due to the incre sed ren l cle r nce o un et bolized cortisol Pathogenesis: Pl s AC H level gives good indic tion i Cushing syndro e is AC Hdependent or independent. a. Extremely low values: ound with dren l Cushing syndro e due to the suppressive e ects o cortisol b. Very high levels: occur with ectopic Cushing syndro e due to the utono ous AC H production c. Normal values: Present in 50% o pituit ry Cushing syndro e d. Intermediate range: Di erenti ting ectopic ro pituit ry Cushing syndro e c n be di cult. (1) High-dose dexamethasone suppression test: P tient is given dex eth sone, 8 g/d y or 2 d ys, nd the urine is collected or e sure ent o 17-hydroxycorticosteroids. In pituit ry dise se, the 17-hydroxycorticosteroid levels will usu lly decre se to less th n 50% o nor l, where s they will show no suppression in the ectopic syndro e. (2) Also help ul: Corticotropin-rele sing hor one (CRH) sti ul tion, jugul r nd peripher l AC H levels, nd pl s lipotrophic hor one y lso be help ul. Localization o pituitary and ectopic tumors: MRI nd C re the best tests to identi y s ll pituit ry deno s; chest f l usu lly shows n ectopic neopl s ; however, C or MRI y be necess ry. Localization o adrenal tumors: C or MRI c n correctly identi y gre ter th n 90%, including deno s less th n 1 c in di eter, c rcino s, nd bil ter l hyperpl si . (1) Radioisotope scanning: R diocholesterol n logue NP-59 (iodo ethylnorcholesterol) c n loc lize unctioning drenocortic l tu ors. T is test is r rely used. (2) Adrenal vein sampling or cortisol: c n lso loc lize the source o cortisol production Curative therapy or pituitary Cushing syndrome a. rans-sphenoidal resection o the tumor: procedure o choice b. Pituitary irradiation rom an external source: H s been e ective in up to 80% o children. However, the cure r te is only bout 15%–20% or dults.

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c. Bilateral total adrenalectomy: now reserved or c ses in which no pituit ry deno is ound, r di tion h s iled, or when the p tient c nnot toler te the prolonged r di tion process (1) Advantage: i edi te nd co plete control o the Quic k Cut cushingoid st te Bilateral (2) Disadvantages: Incre sed orbidity nd ort lity. In adrenalectomy produces a permanent Addis onian s tate. 15% o the c ses, n AC H-secreting pituit ry tu or develops (Nelson syndrome). 8. Ectopic Cushing syndrome treatment: Directed to the underlying neopl s . Re ov l o the tu or is cur tive; however, bec use o the di use n ture o s ll cell lung c ncers, o en only p lli tive ther py c n be o ered. 9. Adrenal Cushing syndrome treatment: tot l dren lecto y Quic k Cut vi l p roscopic or open techniques Laparos copic a. Approach: tr ns bdo in lly or retroperitone lly vi the adrenalectomy has become nk or b ck the pre erred approach or b. Large or aggressive lesions: Open dren lecto y vi adrenal les ions les s than 6 cm n nterior or nk ppro ch is dvis ble or signif c nt in s ize. heterogeneity, nod l involve ent, nd loc l so tissue or v scul r inv sion. c. Partial resection: I ll o the lign nt tissue c nnot be re oved, p lli tive ther py is i proved. 10. Palliative chemotherapy: o ered to those patients who have unresectable malignancies and to those undergoing radiation treatments a. Remission: obt ined in 60% o the c ses, but rel pse is r pid er drug cess tion b. Agents: y include bro ocriptine nd cyprohept dine or itot ne

P rim a ry Hyp e ra ld o s te ro nis m (Co nn Synd ro m e ) I. Ove rvie w: excess secretion o ldosterone by the dren l s result o unil ter l deno (85%), bil ter l deno s (5%), nd hyperpl si (10%) II. Typ e s : In pri ry hyper ldosteronis , pl s renin levels re nor l or low. In the second ry or , the ldosterone incre se is second ry to incre sed pl s renin ro decre se in pressure on the ren l juxt glo erul r cells. Co on c uses include ren l rtery stenosis, lign nt hypertension, nd ede tous st tes, such s congestive he rt ilure, cirrhosis, nd the nephrotic syndro e. III. Sig ns a nd s ym p to m s : Incre sed ldosterone le ds to hypertension, polyuri nd polydipsi , nd he d ches.

Quic k Cut It is important to distinguish hyperaldosteronism due to an adenoma rom that due to hyperplasia because surgical excision is curative or most cases o adenoma but not hyperplasia.

uscle we kness, tigue,

IV. Dia gnos is : Spironol ctone should be discontinued 6 weeks be ore testing, s it c n ect l bor tory v lues. A. Plasma electrolytes: Seru pot ssiu v lue less th n 3.5 Eq/L nd urin ry pot ssiu excretion gre ter th n 30 Eq/d y supports di gnosis o pri ry hyper ldosteronis . B. Screening: Concurrent seru ldosterone nd pl s renin. Pl s ldosterone concentr tion (PAC) o gre ter th n 20 ng/dL nd PAC/pl s renin ctivity (PRA) r tio o gre ter th n 30 re di gnostic or ldosterono with 90% sensitivity. C. Con rmation: Achieved by de onstr ting in ppropri te ldosterone secretion with s lt lo ding, which involves 24-hour urine collection or sodiu nd ldosterone er 3 d ys o high-sodiu diet. IV s line in usion test or c ptopril ch llenge test is lso reli ble ethod but re not usu lly required. V. Lo c a liza tio n o a d e no m a s A. High-resolution adrenal C : best test or loc liz tion o n dren l tu or B. Adrenal vein sampling (to lateralize the source o aldosterone production): use ul in p tients when there is no dren l Quic k Cut bnor lity on C but technic lly di cult CT will detect 1. echnique: Percut neous tr ns e or l c nnul tion o an aldos terone-producing both dren l veins is per or ed nd IV AC H (50 g/hr) adenoma in 90% o cas es . is d inistered. Si ult neous dren l vein blood s ples

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or ldosterone nd cortisol re t ken be ore nd er AC H injection, nd their r tios re deter ined. 2. Results: PAC is rkedly higher ( t le st our- old) on the side o n deno , where s there is little or no le –right gr dient present in c ses o bil ter l dren l hyperpl si . VI. Surg ic a l tre a tm e nt: For p tients who h ve pri ry hyper ldosteronis due to n drenocortic l deno , the tre t ent o choice is l p roscopic dren lecto y; it is i port nt to restore pot ssiu levels be ore surgery. VII. Me d ic a l m a na g e m e nt with s p iro no la c to ne : Direct Quic k Cut nt gonis to ldosterone t the kidney tubule gr du lly le ds to Favorable response reduction in blood pressure nd return to nor l pot ssiu to spironolactone in potassium levels; used in pri ry hyper ldosteronis c used by dren l and blood pressure may predict success ul improvement a ter hyperpl si nd in the preoper tive restor tion o nor l seru adrenalectomy. pot ssiu levels in p tients who h ve deno s.

P he o c hro m o c yto m a I. Ove rvie w: Function lly ctive tu ors th t develop ro the neur l crest–derived chro n tissue; “10% rule” h s been pplied to these tu ors ( ble 17-5). A. Characteristics: produce excess ounts o c techol ines; c n occur s p rt o MEN2 nd re usu lly bil ter l in these p tients B. Malignancy: ost o these tu ors (90%) re benign; higher incidence o lign ncy with extr dren l tu ors 1. Determination: Histologic ex in tion is not n ccur te e ns; presence o et st ses or direct inv sion by the tu or deter ines lign ncy. 2. Cause: Pheochro ocyto s y be due to ut tions in succin te dehydrogen se genes II. Lo c a tio n: Ninety percent re ound in the dren l edull ; 10% o these re bil ter l. O the extr dren l tu ors, ost re ound in the org ns o Zuckerk ndl, the extr - dren l p r g ngli , the urin ry bl dder, nd the edi stinu . III. Sig ns a nd s ym p to m s : Hypertension results ro the excess Quic k Cut production o c techol ines. Other f ndings include tt cks o Hypertens ion he d ches, swe ting, p lpit tions, tre or, nervousness, weight loss, rom pheochromocytoma is intermittent in hal o cas es . tigue, bdo in l or chest p ins, polydipsi nd polyuri , nd convulsions. IV. Dia g no s is : Urin ry levels o et nephrine nd VMA re the ost reli ble di gnostic screening tests. A. Fractionated plasma and urinary catecholamine levels: c n incre se the ccur cy o the di gnosis to virtu lly 100% B. Provocative tests: Using hist ine, tyr ine, or gluc gon is potenti lly h z rdous nd seldo used. V. Loc a liza tion o the tum or: C nd MRI h ve e erged s the ost ccur te loc lizing tools. Scintigr phy with 131I-l beled m-iodobenzylgu nidine (MIBG), which structur lly rese bles norepinephrine, h s been help ul or s ll extr - dren l tu ors. Selective venous s pling is r rely necess ry. VI. P re p a ra tio n o r s urg e ry: should include drenergic block de Quic k Cut with both lph - nd bet -blockers Alpha blockade A. Adrenergic blockade: help ul to provide preoper tive control should precede beta blockade o hypertension, reduce the risk o dr tic swings in blood in pheochromocytoma patients. pressure during surgery, nd provide v sodil tion, llowing restor tion o nor l blood volu e 1. Alpha blockade: Achieved f rst; phenoxybenz ine ther py is begun 2 weeks be ore surgery, st rting with 40 g/d y nd djusting the dose until hypertension is controlled.

Ta b le 17-5: Te n-P e rc e nt Rule o P he o c hro m o c yto m a 10% Malignant

10% Multiple

10% Bilateral

10% Familial

10% Extra-adrenal

10% Children

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2. Beta blockade: Propr nolol is st rted bout 3 d ys be ore surgery, to control t chyc rdi , t dose o 40 g/d y. B. Newer drug regimens to manage hypertension: selective lph -1- drenergic nt gonists (ter zosin nd dox zosin) nd c lciu ch nnel blockers (ni edipine nd nic rdipine) VII. Op e ra tio n : P tient should be onitored with n rteri l nd centr l venous pressure line bec use o the potenti l or wide blood pressure ch nges; l p roscopic, tr ns bdo in l ppro ch is pre erred. A. Sporadic pheochromocytomas: Adren lecto y is the procedure o choice. B. Malignant pheochromocytomas: Surgic l excision o the tu or. Che other py or ther peutic MIBG 131I c n be used or extensive et st tic dise se. C. Component o MEN: Bil ter l cortex dren lecto y should be considered.

Ad re na l Cys ts a nd Othe r Ad re na l Tum o rs I. Inc id e nta l a d re na l m a s s e s : Discovered t utopsy in up to 9% o p tients. With the growing use o C nd MRI sc nning, n incre sed nu ber o these “incident lo s” re being discovered during li e. A. Routine screening: includes tests or pheochro ocyto Quic k Cut (pl s r ction ted et nephrines), hypercortisolis Incidental adrenal (low-dose overnight dex eth sone suppression test), nd mas s es mus t be as s es s ed hyper ldosteronis (PAC/PRA r tio) or hormonal production and B. Imaging: Ch r cteristics on C indic te the likelihood o malignancy. lign ncy. u ors gre ter th n 5 c re t risk o c ncer nd should be re oved. C. Routine biopsy: should be voided unless p tient h s prior risk o lign ncy (e.g., lung or el no ) nd pheochro ocyto h s been ruled out bioche ic lly II. Ad re no c o rtic a l c a rc ino m a : r re (incidence o 0.5–2 c ses per illion per ye r), very ggressive ( ost p tients present with dv nced dise se), nd produce requent hor one overproduction syndro es (hypercortisolis , hyper ldosteronis , or viriliz tion) A. Diagnosis: Contr st-enh nced C o the bdo en nd chest is i port nt to di gnose loc l tu or inv sion nd et st tic Quic k Cut lesions s well s to conf r unctioning contr l ter l kidney. Comp le te re s e c tion o loc a lly c onf ne d tumor B. reatment: Surgic l resection is the inst y or ll st ges; is the only c ha nc e or however, dist nt or loc l spre d is evident in 65% o c ses t c ure rom a d re noc ortic a l present tion. c a rc inoma . C. Prognosis: Poor; edi n surviv l ollowing di gnosis or ll p tients is 18 onths. III. Ad re na l c ys ts : o c c ur in re q ue ntly A. ypes: Most re either endotheli l cysts (ly ph ngio tous or ngio tous) or pseudocysts, resulting ro he orrh ge into nor l dren l tissue or into n dren l neopl s . R rely re they retention cysts or cystic deno s. B. Symptoms: L rge cyst c n present s p lp ble ss nd c n c use dull ching or GI sy pto s due to pressure. C. Diagnosis: C nd MRI re the best ethods v il ble. D. reatment: Bec use neopl s c nnot be excluded, these cysts should be surgic lly excised.

TUMORS OF THE ENDOCRINE PANCREAS P a tho p hys io lo g y I. P a nc re a tic ne uro e nd o c rine tum o rs (P NETs ): Arise ro nor l neuroendocrine cells loc ted in the p ncre tic islets. Most re spor dic, but they c n be heredit ry. II. Cla s s if c a tio n: ccording to their clinic l virulence A. Well-di erentiated tumors: h ve slow-growing, indolent course B. Poorly di erentiated tumors: high gr de nd y be very ggressive III. Func tio na lity: Most PNE s re non unction l; however, they y secrete v riety o hor ones including insulin, g strin, gluc gon, nd v so ctive intestin l peptide (VIP).

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Ins ulino m a I. P a tho g e ne s is : u or origin ting ro the bet cells o the p ncre tic islets th t rele ses bnor lly high ounts o insulin. Most re solit ry nd benign deno s; 10% re lign nt with the potenti l to et st size. II. Clinic a l p re s e nta tio n: Hypoglyce i y result in biz rre beh vior, unconscious episodes, p lpit tions, nervousness, nd other sy pto s o sy p thetic disch rge. III. Dia g no s is : H ve the p tient st or 72 hours then e sure the insulin nd glucose levels. Me sure ent o elev ted insulin C peptide nd sul onylure in blood is used to identi y i trogenic insulin nd or l hypoglyce ic overdose, respectively.

Quic k Cut The Whipple triad includes (1) epis odes o neuroglycopenic s ymptoms (abnormal mentation, anxiety, irritability, diaphores is , tremulous nes s , atigue) precipitated by as ting; (2) hypoglycemia during the epis odes , us ually with blood glucos e levels les s than 60 mg/dL; and (3) relie o s ymptoms by glucos e adminis tration.

IV. Surg ic a l tre a tm e nt: b sed on preoper tive loc liz tion o the tu or, which y be detect ble on C or MRI Quic k Cut A. Endoscopic US: best i ging test bec use ost re less th n 1.5 c An increas ed ins ulin B. Percutaneous catheterization (o the portal vein with serial level in the pres ence o a insulin measurements): c n loc lize the tu or to the he d, low glucos e level (ins ulin-tobody, nd t il glucos e ratio greater than C. Surgical resection: Only cur tive tre t ent; options re 0.25) e ectively conf rms an ins ulinoma. enucle tion or dist l p ncre tecto y. D. Surgical exploration (o the entire pancreas): O en needed to identi y s ll r diogr phic lly occult insulino . Intr oper tive US is help ul. E. Extent: When islet cell hyperpl si is present, n 80%–90% subtot l p ncre tecto y will usu lly control the sy pto s; i the tu or is not loc lized, blind p ncre tecto y should be voided.

Ga s trino m a (Zo lling e r-Ellis o n Synd ro m e ) I. P a tho g e ne s is : Neuroendocrine tu ors th t rise ro enteroendocrine cells o the p ncre s or intestine (duodenu ); ost g strino s re spor dic but y be co ponent o MEN type I nd c n precede develop ent o hyperp r thyroidis . II. Clinic a l p re s e nta tio n: Sy pto s result ro oversecretion o g strin, the consequence o which is peptic ulcer tion due to high g stric cid secretion, which y c use bdo in l p in, GI bleeding, per or tion, or g stric outlet obstruction. III. Inhib itio n o p a nc re a tic e nzym e s : Le ds to di rrhe , ste torrhe , nd incre sed intestin l Pro ound dehydr tion nd lnutrition y be present.

otility.

IV. Dia g no s is : M de b sed on the presence o the clinic l syndro e, not whether the tu or st ins or g strin. Zollinger-Ellison syndro e (ZES) should be considered in ny p tient with n ulcer th t is re r ctory to intensive tre t ent with nt cids, H 2-receptor blockers, or proton pu p inhibitors (PPIs); recurrent peptic ulcer er st nd rd surgic l procedure or peptic ulcer dise se; nd peptic ulcer dise se nd re r ctory di rrhe . A. Laboratory ndings: provide the di gnosis 1. Fasting gastrin level: Gre ter th n 1,000 pg/ L (nor l 110 pg/ L) in the presence o g stric cid (g stric pH 2.0) kes di gnosis o ZES. 2. Secretin stimulation testing: M y cl ri y the c use o odest elev tions in g strin. In ZES, n in usion o secretin will incre se g strin by 120–200 pg/ L or ore. B. Localization o the tumor: Endoscopic US is the best test to identi y s ll g strino s in the duoden l w ll nd p ncre s. 1. C scan and MRI: best cross-section l i ging studies 2. Somatostatin receptor scintigraphy (SRS) with 111-indium-penetreotide with SPEC : less ccur te th n C but used to deter ine et st tic sites V. Tre a tm e nt: ust control g stric hyper cidity nd should re ove ll gross tu or A. Gastrinoma triangle: def ned by the junction o the cystic nd co on bile ducts superiorly, the junction o the second nd

Quic k Cut Mos t (80% ) gas trinomas are located in the “g a s trino m a tria ng le .”

Chapter 17

T yroid, P r thyroid, Adren l Gl nds, nd T y us

287

third portions o the duodenu in eriorly, nd the junction o the neck nd body o the p ncre s edi lly B. Standard surgical approach: Re ove ll identif ble tu ors ( requently ulti oc l), tr nsillu in te the duodenu , open the duodenu nd resect sub ucos l tu ors, nd re ove surrounding ly ph nodes. C. ZES in the setting o MEN1: Unco only cured surgic lly; edic l ther py is pre erred until tu ors re ch 2 c in size. D. otal gastrectomy: Previously the cl ssic tre t ent or re r ctory ZES. It should be per or ed r rely. VI. P ro g no s is : Good i the GI hyper cidity c n be controlled; lthough two thirds o the c us tive tu ors re lign nt, they re very slow growing.

VIP o m a (P a nc re a tic Cho le ra ) I. Ove rvie w: syndro e o severe secretory di rrhe (low [ 50 OS /kg] os otic g p in stool s ple) due to hypersecretion o VIP II. Clinic a l p re s e nta tio n: lso known s WDHA syndrome bec use Quic k Cut o w tery di rrhe ; hypok le i (with result nt pro ound uscul r I you s ee WDHA, we kness due to the high pot ssiu content in the stool), nd think VIPoma. achlorhydri III. P a tho g e ne s is : PNE is solit ry in 80% o c ses nd is usu lly loc lized to the body or t il o the p ncre s; 50% re lign nt. IV. Dia g no s is : Most VIPo s re gre ter th n 3 c in size t di gnosis nd y be e ectively loc lized with C sc nning. V. Tre a tm e nt: So tost tin receptor n logues (octreotide or l nreotide) re usu lly very e ective in controlling the secretory di rrhe . Surgic l excision o the pri ry tu or is indic ted or loc lized dise se. VI. P ro g no s is : st ge dependent nd o en poor due to the presence o et st sis t the ti e o di gnosis

Gluc a g o no m a s I. Ove rvie w: r re PNE s th t produce gluc gono syndro e II. Clinic a l pre s e nta tion: Sy pto s o gluc gono syndro e include necrolytic igr tory erythe (NME) (erythe tous pl ques Quic k Cut I you s ee necrolytic on the ce, perineu , nd extre ities), weight loss, di betes ellitus, migratory erythema, think ne i , di rrhe , venous thro bosis, nd neuropsychi tric sy pto s. glucagonoma. III. P a thog e ne s is : Due to tu ors o the p ncre tic lph islet cells; ost gluc gono s origin te in the p ncre tic t il nd re lign nt. IV. Dia g no s is : de by e sure ent o seru gluc gon, which usu lly exceeds 500–1,000 pg/ L A. C or MRI: used to loc lize the tu or B. Endoscopic US: use ul to guide biopsy nd ev lu te or suspicious denop thy V. Tre a tm e nt: Surgic l resection o ll loc lized gross dise se, including liver et st ses. As ost p tients (50%–100%) h ve et st tic dise se, tre t ent is ost o en p lli tive. For p tients with widespre d dise se, octreotide y be help ul.

MULTIP LE ENDOCRINE NEOP LASIA Typ e s (Thre e ) I. MEN typ e 1 (Ta b le 17-6): r re utoso l do in nt condition predisposing ected individu ls to tu ors o the p r thyroid gl nds, nterior pituit ry gl nd, nd enterop ncre tic endocrine cells A. Clinical de nition: two or ore pri ry MEN1 tu or types or the occurrence o single tu or type in e ber o MEN1 kindred B. Cause: Inherit nce o ut ted enin gene on chro oso e 11q13. T e ex ct unction o this gene is unknown but it is thought to ct s tu or suppressor. Quic k Cut C. Hyperparathyroidism: present in 90% or ore o the p tients MEN1 is the three usu lly be ore ge 50 ye rs, with ost h ving ultiple P’s : p arathyroid dis eas e, p r thyroid gl nd deno s p ituitary adenomas , and D. Pituitary adenomas: present in 20%–60% o c ses nd re p ancreatic tumors . usu lly l ctotroph deno s

288

Chapter 17

Multiple Endocrine Neopl si

Ta b le 17-6: Multip le End o c rine Ne o p la s ia Synd ro m e s Synd ro m e

Clinic a l P re s e nta tio n

Tre a tm e nt

Ge ne /Te s t

MEN1

Primary hyperparathyroidism Prolactinoma Gastrinoma/insulinoma/PPoma/VIPoma/glucagonoma/ non unctional enteropancreatic tumor

Parathyroidectomy Bromocriptine Pancreatectomy/duodenal tumor enucleation

Menin

MEN2A

Medullary thyroid cancer Pheochromocytoma Primary hyperparathyroidism

Thyroidectomy/CLND Adrenalectomy Parathyroidectomy

RET

MEN2B

Medullary thyroid cancer Pheochromocytoma Ganglioneuroma

Thyroidectomy/CLND Adrenalectomy None

RET

MEN, multiple endocrine neoplasia; PP, pancreatic polypeptide; VIP, vasoactive intestinal peptide; CLND, central cervical lymph node dissection; RET, rearranged during trans ection tyrosine kinase proto-oncogene.

E. Enteropancreatic tumors (PNE ): present in up to 80% o p tients 1. Common: G strino is the ost co on sy pto tic tu or nd occurs in up to 60% o MEN1 p tients. I ge-detected non unctioning tu ors o the p ncre s re s co on. 2. Less common: Sy pto tic insulino , gluc gono , nd VIPo c n occur. 3. Metastasis: Both unctioning nd non unctioning PNE y et st size to liver; lign nt PNE is the ost co on c use o MEN1-specif c ort lity. II. MEN typ e 2A: Co prises M C, pheochro ocyto , nd, in MEN 2A, p r thyroid hyperpl si . MEN2 syndro es re c used by ut tion o the RE gene, which ps to 10q11.2 nd cts s do in nt oncogene. A. Medullary thyroid carcinoma: Occurs in ll p tients; it is usu lly ulti oc l nd preceded by non lign nt hyperpl si o the C cells. Seru c lcitonin levels re incre sed. B. Pheochromocytomas: 40% o p tients; o en bil ter l, synchronous, nd usu lly benign; o en presenting l ter th n edull ry thyroid c ncer C. Parathyroid hyperplasia (with consequent hyperparathyroidism): develops in 60% o p tients with MEN 2A nd is o en ilder th n the p r thyroid hyperpl si o MEN 1 III. MEN typ e 2B: s in MEN 2A, edull ry thyroid c rcino nd pheochro ocyto A. Features: r noid body h bitus nd the develop ent o ultiple neuro tous ucos l nodules B. Presentation: f rst or second dec de o li e with uch ore ggressive course

Dia g no s is I. MEN1: Hyperp r thyroidis in MEN1 is typic lly sy pto tic nd is usu lly detected by l bor tory bnor lities (c lciu nd P H). A. Clinical presentation: P tients with MEN1 y present with sy pto s o peptic ulcer tion rel ted to the p ncre tic g strino or with sy pto s rel ted to the pituit ry tu or. B. Genetic testing: Mut tions in enin testing is v il ble to ny index p tient with clinic l MEN1 nd ll f rst-degree rel tives o known MEN1 ut tion c rriers. C. Asymptomatic biochemical screening: involves c lciu nd y include other ore det iled hor on l screening or g strin, sting glucose, insulin, insulinlike growth ctor 1, prol ctin, nd chro ogr nin A II. MEN2A: Should be suspected in ny p tient with M C; p tient should be re erred or genetic counseling nd testing or ut tion o the RE proto-oncogene. Finding o n incre sed seru c lcitonin level le ds to the di gnosis. A. Hyperparathyroidism: usu lly detected by incre ses in the seru c lciu nd P H levels B. Pheochromocytomas or adrenal medullary hyperplasia: y be sy pto tic but should be detect ble by bioche ic l screening III. MEN2B: Most p tients re di gnosed in e rly childhood; bec use it is ggressive, e rly di gnosis is i port nt so th t e ective tre t ent c n begin pro ptly. Di gnosis is si il r to th t or MEN2A. T e e rly ppe r nce o ucos l neuro s nd the r noid body h bitus ids di gnosis.

Chapter 17

T yroid, P r thyroid, Adren l Gl nds, nd T y us

289

Tre a tm e nt I. MEN1: PHP in MEN1 involves ll gl nds, usu lly sy etric lly. Surgery is not cur tive but p r thyroidecto y y reduce circul ting P H. Choice o ppro ch is l rgely b sed on surgeon tr ining nd experience. A. Subtotal (3.5 gland) parathyroidectomy: Le ving nor l-sized well-v scul rized re n nt o p r thyroid tissue is co on ppro ch. B. otal parathyroidectomy (with nondominant orearm Quic k Cut parathyroid autotransplantation): y lso be per or ed Autotrans plantation C. PNE s (located within the pancreas and duodenum): o parathyroid tis s ue to the Resection is per or ed to reduce thre t o lign nt spre d nd orearm has the advantage o to reduce hor on l sy pto s. Resection o non unctioning avoiding repeat neck s urgery PNE s should be considered with gre ter th n 2 c lesion. i recurrence develops . 1. ZES: enucle tion o the tu or loc ted in the g strino tri ngle 2. Insulinoma: enucle tion o tu ors in the p ncre tic he d nd y include dist l subtot l p ncre tecto y D. Pituitary tumors: Usu lly tre ted edic lly with bro ocriptine. r ns-sphenoid l hypophysecto y y be needed in so e c ses. II. MEN2A: P tients with known MEN2A– ssoci ted RE ut tions should receive prophyl ctic tot l thyroidecto y, which is cur tive. A. Pheochromocytoma or adrenal medullary hyperplasia: Adren lecto y (pre er ble l p roscopic) be ore thyroidecto y bec use these hor one-producing disorders c n le d to hypertensive crises during thyroidecto y. B. Hyperparathyroidism: c n be tre ted t the ti e o tot l thyroidecto y by either subtot l p r thyroidecto y or tot l p r thyroidecto y nd ore r p r thyroid utotr nspl nt tion III. MEN2B: re ted si il rly with MEN2A. Bec use MEN2B ssu es such n ggressive course, pro pt nd e ective tre t ent is i port nt.

THYMUS GLAND Ove rvie w I. Intro d uc tio n: T y us is the origin o v riety o tu ors nd is signif c ntly involved in the develop ent o cellul r i unity. A. Cortex: consists pri rily o ly phocytes, which ppe r to igr te to the edull nd then e igr te ro the thy us B. wo limbs: extend into the neck nd re o en ssoci ted with the in erior p r thyroid gl nds II. Func tio ns : Essenti l or the develop ent o cellul r i unity, which controls del yed hypersensitivity re ctions nd tr nspl nt rejection. Histologic bnor lities in the thy us (e.g., ly phoid hyperpl si or thy ic tu ors) re requently ound in ssoci tion with utoi une dise ses.

Mya s the nia Gra vis

Quic k Cut I. Ove rvie w: Autoi une dise se o neuro uscul r tr ns ission Myas thenia th t c uses skelet l uscle we kness. T e ost co on sy pto s gravis exacerbations may re ptosis, double vision, dys rthri , dysph gi , n s l speech, nd be precipitated by upper we kness o the r s nd legs. res piratory in ections . II. No rm a l ne uro m us c ula r tra ns m is s io n: Acetylcholine (ACh) is produced t the nerve ter in l o the yoneur l junction nd binds to receptor sites on the uscle endpl tes, which triggers uscle contr ction. III. Ne uro m us c ula r tra ns m is s io n in m ya s the nia g ra vis : ACh receptor ntibodies develop, resulting in reduced uscle contr ction. IV. Tre a tm e nt: Sust ined i prove ent is chieved with edic tion in only 33% o p tients without surgery nd in 85% o p tients er thy ecto y. A. Medical treatment: P tients respond to drugs th t sti ul te the neuro uscul r junction, such s neostig ine nd pyridostig ine. B. Surgical treatment: Re ov l o the thy o is dvised, lthough the e ect on the y stheni is unpredict ble. However, even in p tients without thy ic tu ors, thy ecto y ppe rs to be the tre t ent o choice.

290

Study Questions or P rt V

Study Questions or P rt V Directions: Each o the numbered items in this section is ollowed by several possible answers. Select the ONE lettered answer that is BEST in each case. 1. A 40-ye r-old

n h s subtot l thyroidecto y per or ed or Gr ves dise se. Sever l hours l ter, he co pl ins o di culty bre thing. On ex in tion, he h s stridor nd rkedly swollen, tense neck wound. Wh t should be one o the f rst steps in the n ge ent o this p tient? A. B. C. D. E.

Intub te with n endotr che l tube. Per or tr cheosto y. Control the bleeding site in the oper ting roo . Open the wound to ev cu te the he to . Aspir te the he to .

2. A 50-ye r-old hypertensive

n h s def nitive bioche ic l evidence o pheochro ocyto . C sc n nd MRI do not reve l ny bnor lities, nd MIBG sc nning is not re dily v il ble. Wh t should be the next step in the n ge ent o this p tient? A. B. C. D. E.

Abdo in l explor tion Continued clinic l observ tion Medi stinoscopy Selective venous s pling Medi stin l explor tion

3. A 55-ye r-old wo

n with progressive but episodic uscle we kness is di gnosed s h ving y stheni gr vis. Her chest r diogr ph is nor l nd reve ls no evidence o edi stin l ss or tu or. Wh t is the ost def nitive tre t ent th t c n be o ered to this p tient? A. B. C. D. E.

Prednisone Neostig ine T y ecto y Pl s pheresis Atropine

4. A f rst-degree rel tive o

Which screening A. B. C. D. E.

p tient ound to h ve dv nced M C is re erred or urther ev lu tion. e sure is the choice or detection o edull ry thyroid p thology?

C re ul physic l ex in tion Seru c lcitonin level Sti ul ted seru c lcitonin level (c lciu G strin level C rcinoe bryonic ntigen (CEA) level

5. I

nd pent g strin)

f rst-degree rel tive o p tient with MEN2A syndro e is ound to h ve edull ry p thology requiring surgic l explor tion o the thyroid gl nd, wh t should the preoper tive screening include? A. B. C. D. E.

Seru cortisol level F sting glucose nd insulin C sc n o the he d Urin ry ldosterone nd renin Urin ry VMA nd et nephrines

Study Questions or P rt V

6. A 60-ye r-old e

le p tient h s workup or episodic sy pto s o p lpit tions, nervousness, nd biz rre beh vior, ll o which tend to occur during sting st tes. Bioche ic lly, she is di gnosed s h ving n insulino . Wh t is the best choice or loc lizing this tu or? A. B. C. D. E.

C sc n MRI Selective rteriogr phy Percut neous c theteriz tion o the port l vein with selective venous s Surgic l explor tion nd intr oper tive ultr sound

pling

7. A 55-ye r-old e

le p tient is ev lu ted or new onset o di betes ellitus. Her edic l history is l rgely unre rk ble. Her physic l ex in tion is unreve ling except or the presence o n erythe tous skin r sh. Her urther ev lu tion should include n investig tion o the possibility o which o the ollowing? A. B. C. D. E.

Insulino Gluc gono G strino C rcinoid tu or P ncre tic choler

8. A 23-ye r-old wo

n h s p lp ble ss in her le bre st. Ultr sound suggests cystic lesion. On spir tion, so e d rk uid is retrieved, but the ss does not co pletely resolve. Wh t is the next step in tre t ent? A. B. C. D. E.

Observ tion NSAIDs Repe t spir tion Excision Si ple stecto y

9. T e best tre t ent or duct l c rcino

A. B. C. D. E.

in situ is:

Observ tion nd re ssur nce Lu pecto y P rti l stecto y with r di tion Si ple stecto y Modif ed r dic l stecto y

10. T e nerve th t supplies the l tissi us dorsi

uscle nd

y be injured during xill ry node

dissection is: A. B. C. D. E.

Long thor cic T or codors l C7 Intercost l br chi l L ter l br chi l

11. A 30-ye r-old

n h s hypertension nd h s co pl ints o we kness nd tigue. His physic l ex in tion is unre rk ble. Routine l bs re nor l except or pot ssiu o 3.0 Eq/L. He undergoes bdo in l C sc n, which de onstr tes 3-c le dren l ss. T e best next step in n ge ent is: A. B. C. D. E.

MRI o the bdo en with 2 i ging Urin ry cortisol onitoring Bet block de Adrenocorticotropic hor one sti ul tion L p roscopic dren lecto y

291

292

Study Questions or P rt V

12. A 56-ye r-old wo

n is undergoing surgery or le -sided p r thyroid deno . T e initi l p r thyroid level is 100 pg/ L. A er incision, the in erior gl nd is identif ed nd re oved, nd the p r thyroid level t 10 inutes lls to 90 pg/ L. T e next step is: A. B. C. D. E.

Closure o incision Monitoring o 20- inute P H levels Explor tion o the le superior gl nd ot l p r thyroidecto y with utotr nspl nt tion St t c lciu e sure ent

13. Which o the ollowing is not ssoci ted with n incre sed incidence o inv sive duct l c rcino

o the bre st? A. B. C. D. E.

Sclerosing denosis Lobul r c rcino in situ Atypic l duct l hyperpl si Epitheli l hyperpl si P pillo tosis

Que s tio ns 14–17 Match the correct treatment with each inf ammatory or in ectious process o the breast. 14. M stitis

A. Surgic l dr in ge

15. Abscess

B. Excision o sinus tr ct

16. Chronic sub reol r bscess

C. Antibiotics

17. Mondor dise se

D. NSAIDs

18. T e pre erred tre t ent or new-onset pubert l gyneco

A. B. C. D. E.

R dic l excision with l tissi us dorsi Observ tion Suction lipecto y oxi en ther py Si ple stecto y

sti is:

p

Que s tio ns 19–20 A 65-ye r-old wo n with no other signif c nt p st edic l history presents with l rge ss in the right bre st. T e ss e sures pproxi tely 6 c in di eter nd ppe rs to be f xed to the chest w ll. In ddition, bulky denop thy is present in the right xill ry region. T e p tient st tes th t the ss h s been enl rging or the l st sever l ye rs. 19. Following

A. B. C. D. E.

ogr phy, wh t should be the next step in this p tient’s ev lu tion?

FNA Incision l or core biopsy Excision l biopsy Modif ed r dic l stecto y R dic l stecto y

Study Questions or P rt V

T e di gnosis or this p tient is inv sive duct l c rcino . A ogr reve ls no other lesions in the right bre st nd no bnor lities in the le bre st. A chest r diogr ph, bone sc n, nd liver unction tests re nor l. 20. Wh t should the next step in the

A. B. C. D. E.

n ge ent o this p tient involve?

Neo djuv nt che other py R di tion ther py to the bre st nd xill R dic l stecto y Modif ed r dic l stecto y Si ple stecto y

293

294

Answers nd Expl n tions

Answers nd Expl n tions 1. The a ns we r is D (Ch pter 17, T yroid Dys unction Requiring Surgery, Gr ves Dise se, V E 2).

Postoper tive bleeding er thyroidecto y c n c use irw y co pro ise due to tr che l co pression. T e f rst step should be to open the wound to ev cu te the he to , ollowed by return to the oper ting roo to control the bleeding site. Atte pts to per or either endotr che l intub tion or tr cheosto y y be di cult until the extern l co pression o the he to is relieved. 2. The a ns we r is D (Ch pter 17, Adren l Gl nd, Pheochro ocyto

, V). Although 90% o pheochro ocyto s re loc ted in the dren l gl nds, they c n occur in ny tissue th t is derived ro neuroectoder . When C sc n nd MRI do not identi y tu or, MIBG sc nning c n be help ul; however, this is not lw ys v il ble. Selective e sure ents o c techol ines dr wn t v rious levels ro the ven c v nd its jor br nches should be obt ined be ore surgic l explor tion.

3. The a ns we r is C (Ch pter17, T y us Gl nd, My stheni Gr vis, IV B). My stheni gr vis is

n utoi une dise se o neuro uscul r tr ns ission th t c uses skelet l uscle we kness. P r sy p tho i etic drugs h ve been ound to i prove uscle strength in these p tients. Prednisone h s lso been used with so e success bec use o the utoi une n ture o this dise se. Pl s pheresis y be e ective in prep ring the p tient preoper tively. T e tre t ent o choice or ll or s o y stheni , except purely ocul r, ppe rs to be thy ecto y. An incre sed percent ge o p tients h ve per nent re ission. T e response to edic tion is i proved in p tients who do not chieve co plete re ission. 4. The a ns we r is B (Ch pter 17, T yroid Dys unction Requiring Surgery, T yroid Neopl s s,

VI A 2). All f rst-degree rel tives o p tients with M C should be screened or this disorder bec use it c n occur in ili l p ttern. Physic l ex in tion o the thyroid gl nd should be per or ed or the detection o ny nodules. An incre sed seru c lcitonin or n incre sed sti ul ted seru c lcitonin test will lso indic te underlying edull ry p thology, either hyperpl si or c rcino . T e sti ul ted tests will detect dise se t n e rlier, ore cur ble st ge. Incre sed g strin levels re ssoci ted with ZES nd re not p rt o this MEN type 2 syndro e. CEA is elev ted in so e GI lign ncies. 5. The a ns we r is E (Ch pter17, Adren l Gl nd, Pheochro ocyto

, IV). M C y present s spor dic or ili l or ssoci ted with MEN type 2A or 2B. Both re ssoci ted with pheochro ocyto s. I pheochro ocyto is present, it should be di gnosed nd tre ted f rst to void the orbidity o cervic l explor tion in p tient with untre ted pheochro ocyto . Urin ry VMA nd et nephrines should be ev lu ted preoper tively.

6. The a ns we r is E (Ch pter 17, u ors o the Endocrine P ncre s, Insulino

, IV). T e p tient h s h d def nitive bioche ic l di gnosis o insulino . T ese tu ors c n be present nywhere in the p ncre s. Bec use they re usu lly s ll in size, rteriogr phy, C , nd MRI re less sensitive th n they would be or l rger tu ors. With c re ul surgic l explor tion nd intr oper tive ultr sound, pproxi tely 90% o these tu ors c n be loc lized t the ti e o surgery.

7. The a ns we r is B (Ch pter 17, u ors o the Endocrine P ncre s, Gluc gono

s, II). Gluc gonproducing tu ors o the p ncre s secrete gluc gon in l rge ounts. P tients tend to present with new onset o di betes ellitus (hyperglyce i ). A ected individu ls lso ch r cteristic lly h ve igr tory erythe tous skin r sh.

8. The a ns we r is D (Ch pter 16, Bre st Ev lu tion, Biopsy, II). Cysts th t do not resolve co pletely

on spir tion should be tre ted s solid lesions nd excised. NSAIDs re use ul in Mondor dise se (thro bophlebitis). Repe t spir tion y be tte pted, but cyst th t recurs once is likely to recur g in. M stecto y is too r dic l ther py.

Answers nd Expl n tions

9. The a ns we r is C (Ch pter 16, M lign nt Dise ses, Noninv sive Bre st C ncer, I A). Excision

with cle r

rgins is the st nd rd o c re, nd r di tion reduces the risk o recurrence by 50%.

10. The a ns we r is B (Ch pter 16, M lign nt Dise ses, re t ent, I B 2 c). T e thor codors l

supplies the l tissi us. T e long thor cic supplies serr tus nterior, nd injury produces winged sc pul . 11. The a ns we r is E (Ch pter 17, Adren l Gl nd, Pri

ry Hyper ldosteronis [Conn Syndro e], VI). T e p tient h s signs nd sy pto s o ldosterono nd i ging consistent with le dren l deno . Further cross-section l i ging is unnecess ry. Cortisol testing is used or suspicion o dren l hyper unction or insu ciency but is not needed in this c se. Bet block de y be use ul or n ge ent o hypertension but would not be indic ted in the initi l n ge ent o pheochro ocyto . In pr ctice, n ldosterone level could be checked preoper tively to conf r the di gnosis, then l p roscopic le dren lecto y.

12. The a ns we r is C (Ch pter 17, P r thyroid Gl nds, Hyperp r thyroidis , I F 1). T e p tient h s

evidence o loss o p r thyroid tissue but not su cient response to consider the bnor l gl nd re oved. It is expected th t there is both 50% reduction in the P H level s well s ove ent into the nor l r nge. Given th t this did not occur, explor tion o the re ining gl nds is the next step. ot l p r thyroidecto y is overly ggressive, nd onitoring o ddition l l b v lues o P H or c lciu does not lter the decision- king process. 13. The a ns we r is A (Ch pter 16, Benign Bre st Dise se, Benign Lesions, III G). Epitheli l

hyperpl si , typic l duct l hyperpl si , nd p pillo tosis re proli er tive lesions o the bre st th t c rry n incre sed risk o inv sive duct l c rcino o the bre st. P pillo tosis is si ply description o the p ttern the cells ssu e (p pill ry). Lobul r c rcino in situ o the bre st c rries n incre sed risk bil ter lly or n inv sive bre st c ncer, which c n be duct l or lobul r. Sclerosing denosis is proli er tion o the cini th t ppe r to inv de, but it is not lign nt or pre lign nt lesion. 14–17. The a ns we rs a re 14-C, 15-A, 16-B, a nd 17-D (Ch pter 16, Benign Bre st Dise se,

In ectious nd In tory Bre st Dise ses, I–IV). Cellulitis o the bre st ( stitis) requires tre t ent with ntibiotics to cover Staphylococcus nd Streptococcus in ection. An cute bscess requires surgic l dr in ge. A chronic recurrent bscess requires excision o the sinus tr ct to void recurrence. Mondor dise se is phlebitis o the superf ci l veins, nd lthough sel -li ited, tre t ent with NSAIDs c n llevi te the disco ort. 18. The a ns we r is B (Ch pter 16, M lign nt Dise ses, Speci l C ses, II A 3). Gyneco

sti represents bre st growth in le due to hor on l i b l nce. T e initi l present tion during puberty should be observed, s the lesion o en regresses. Sy pto tic c ses c n be tre ted edic lly with t oxi en or surgic lly with suction lipecto y. More ggressive surgery such s stecto y is not w rr nted.

19–20. The a ns we rs a re 19-B (Ch pter 16, Bre st Ev lu tion, Biopsy, I B) nd 20-A (Ch pter 16,

Inv sive Bre st C ncer, re t ent, V B). Although FNA c n be per or ed, it y not be conclusive to w rr nt urther tre t ent. A core-needle biopsy c n e sily be per or ed on o this size. Excision is in ppropri te in sses l rger th n 5 c . Def nitive surgic l ther py should not be per or ed until er neo djuv nt che other py is given.

ss

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Special Subjects Chapter Cuts and Caveats

CHAP TER 18 He a d a nd Ne c k Surg e ry: T e most common neck lesion is a reactive lymph node. All adults with a persistent neck mass have a malignancy until proven otherwise. Most head and neck cancers are squamous cell and are treated with surgery, radiation, or chemotherapy. Cosmetic and unctional def cits may be requent. Congenital lesions are abnormal variants o normal structures. T yroglossal duct cysts are midline structures that rise and all with swallowing. T ey should be resected i symptomatic, a er making sure there is adequate residual thyroid tissue. onsillectomy was once an extremely common operation and is now reserved or those with repeated in ections, as the risk o surgery outweighs the benef ts or most patients.

CHAP TER 19 Ba ria tric Surg e ry: Obesity a ects more than one third o Americans and an increasing percentage o children and adolescents. Obesity creates metabolic comorbidities and decreases li e span. BMI is the most use ul marker or obesity; people quali y or bariatric surgery with BMI greater than 40 kg/m 2 or 35 kg/m 2 with medical comorbidities. Bariatric procedures are classif ed as primarily restrictive or malabsorptive. Roux-en-Y gastric bypass is the most common operation and is a blend o the two. Gastric banding and sleeve gastrectomy are restrictive, and the duodenal switch operation is malabsorptive. Postoperative bariatric patients are susceptible to a variety o unique complications, including internal hernia, marginal ulceration, and nutritional def ciencies. achycardia in a postoperative patient is a surgical complication until proven otherwise. T e patient must be assessed or anastomotic leak and DV /PE.

CHAP TER 20 Minim a l Ac c e s s Surg e ry: Minimally invasive surgery relies on technology to decrease the size o the access incisions; visual cues largely replace tactile ones. T e f rst steps in minimally invasive procedures are establishment o pneumoperitoneum and diagnostic laparoscopy. Pneumoperitoneum is an artif cial state that has a mechanical (pressure) component that can mimic abdominal compartment syndrome. T e use o carbon dioxide gas also creates an acidosis. T is does not have a signif cant clinical impact or brie procedures in patients who have minimal physiologic compromise.

Most general surgical procedures have minimally invasive options, including surgery on the gallbladder, appendix, intestines, and hernias. Robotic procedures are especially use ul in anatomically conf ned cases, such as low pelvic surgery or prostatectomy.

CHAP TER 21 Surg ic a l Onc o lo g y: Oncology is increasingly multidisciplinary. Benign and malignant re er to behavior, not outcomes—benign lesions may be atal, and malignant processes may be indolent. Oncogenes drive the cell cycle; tumor suppressor genes provide a natural checkpoint. Dysregulation o either may lead to cancer. Imaging, serum markers, and genomics can all provide diagnosis well in advance o clinical symptoms. Screening can reduce mortality in breast, colon, cervical, and prostate cancer. T e NM system provides a common language to group and stage tumors.

CHAP TER 22 Tra um a a nd Burns : Primary survey: ABCs. Remember the ABCDE o trauma: airway, breathing, circulation, disability, everything else. Hemodynamically unstable patients should not go to the C scanner. Intubate all patients with a low GCS or those with massive injury. Fatal hemorrhage occurs in f ve major locations: chest, abdomen, retroperitoneum, thigh, and externally. Hypovolemia is the most common cause o hypotension in trauma and is treated with uid resuscitation. However, tension pneumothorax and cardiac tamponade cause hypotension, are not associated with hypovolemia, and are not treated with uid resuscitation. T ey should be considered early during resuscitation. FAS exam reliably detects ree uid and can provide an early, sa e means o diagnosing the need or operation. Initial resuscitation o burn victims may be massive: use 4 mL/kg/% BSA over the f rst 24 hours. Use the rule o 9’s to estimate BSA. Hypothermia may cause coagulopathy and resultant bleeding a er trauma. Simple pneumothorax usually presents with dyspnea and is not emergent, whereas a tension pneumothorax presents with hypotension and requires emergent decompression.

CHAP TER 23 Org a n Tra ns p la nta tio n: Calcineurin inhibitors have considerable nephrotoxicity. Organ transplantation is considered or irretrievable end-organ dys unction. T e main complications o immunosuppression are susceptibility to in ections and the development o malignancy. Kidney transplants are the most success ul solid organ transplants. Although dialysis is a replacement option, patients live longer with kidney transplants than on dialysis; there ore, all endstage renal patients are considered transplant candidates. Although outcomes are superior with living donors, deceased donors and extended criteria donors have produced acceptable results. Because no alternative exists to replace a dys unctional liver, transplantation remains the only option or severe liver ailure but is raught with complications due to the extent o disease in most o these patients. Most acute rejection occurs in the f rst year a er transplant and may be related to in ection or inadequate immunosuppression. T e cornerstones o immunosuppression are corticosteroids, but immune modulators have been developed that a ect all aspects o -cell unction and di erentiation. Islet cell transplantation may provide the cure o diabetes without the heavy immunosuppression o whole organ transplant. o date, results are promising.

297

CHAP TER 24 P e d ia tric Surg e ry: Pediatric surgery represents a separate discipline, since the physiology o children di ers rom that o adults. Congenital hernias may be associated with other conditions and require care ul assessment be ore repair. In general, umbilical hernias are not repaired, as they may close spontaneously. Inguinal hernias are repaired with high ligation o the sac. Diaphragmatic hernias are repaired but with caution, as pulmonary dys unction may also be present. Many specif c problems can arise within the neonatal GI tract. Malrotation and necrotizing enterocolitis may require urgent surgery and may result in long-term problems such as short gut syndrome. Failure to pass meconium in the f rst 24 hours suggests a diagnosis o Hirschsprung disease, which is conf rmed on rectal biopsy. Projectile vomiting in a 1-month old in ant may represent hypertrophic pyloric stenosis. reatment is a surgical pyloromyotomy a er correction o any metabolic derangements. Wilms tumor and neuroblastoma are the two most common childhood solid tumors. Gastroschisis is an abdominal wall de ect with no sac and has rare associated congenital anomalies. Omphalocele has a sac and has a high association with congenital anomalies. Esophageal atresia is most commonly a proximal esophageal pouch and distal tracheoesophageal ( E) f stula and is associated with cardiac and VAC ERL anomalies. Intestinal malrotation usually presents with bilious vomiting. Duodenal atresia shows an abdominal double-bubble sign, is corrected by duodenoduodenostomy and is commonly associated with other congenital anomalies. Jejunal and more distal bowel atresia occur rom in-utero vascular accidents and have ew associated congenital anomalies.

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Chapter 18

Head and Neck Surgery Andrea Hebert and Jef rey S. Wol

COMP ONENTS OF THE HEAD AND NECK EXAM Ge ne ra l I. Bre a thing : Note whether the patient is breathing com ortably and the presence o stridor, stertor, or the use o accessory muscles. II. Vo ic e : Note the quality o the patient’s voice (e.g., hoarseness or mu ed or breathy qualities) and any dysarthria. III. Swa llo w: Note i the patient is able to tolerate secretions or i he or she is drooling.

Quic k Cut Stridor is a highpitched s ound produced by turbulent f ow through a partially obs tructed upper airway. Stertor is lower pitched, s noring-type s ound.

He a d I. Ge ne ra l A. rauma: visible ecchymosis, edema, bony abnormalities, or lacerations B. Masses/lesions: skin lesions, biopsy sites or surgical scars, edema, f rmness, induration, uctuance, or erythema II. Eye s A. Examination: Be sure to note extraocular motion and pupillary response and to report nystagmus. B. ests 1. Visual acuity: i the patient is complaining o any change in vision 2. Visual f eld test: i the patient is complaining o diplopia III. Ea rs : Standard o ce assessment o hearing includes the Weber and Rinne tests. A. Weber test: uning ork is struck and placed on the midline o the patient’s head to determine i the sound lateralizes and identif es unilateral hearing loss. B. Rinne test: involves placing the vibrating tuning ork on Quic k Cut the mastoid process and comparing the perception to Per orm a Weber that o the sound directly adjacent to the ear; also helps and Rinne exam i the patient discriminate between conductive and sensorineural has any otologic complaints . hearing loss C. Auricle: Note any de ormity, tenderness to palpation o the tragus or mastoid, or tenderness with tugging o the pinna. D. External auditory canal: Note any canal stenosis, debris, erythema, or otorrhea. E. ympanic membrane: Note whether intact, the presence and characteristics o uid behind the tympanic membrane, presence o middle ear masses, and whether the membrane retracts. IV. No s e : Per orm anterior rhinoscopy on all patients. A. Septum: Examine or deviations or lesions. B. Nasal cavity: Note in erior turbinate hypertrophy, nasal masses or polyps, and the presence o rhinorrhea.

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V. Ora l c a vity/o ro p ha rynx: Note any masses or lesions and speci y the color, riability, and tenderness. Note any ulceration and palpate with a gloved f nger to determine so ness or f rmness. A. eeth: Note the quality o the dentition and the presence o any tenderness. B. Assess: Look or any erythema, edema, palatal asymmetry, or tonsillar deviation. Note any uvular deviation and trismus. VI. La rynx: Per orm a laryngeal mirror exam i not per orming f beroptic laryngoscopy. VII. Ne c k: Palpate or lymphadenopathy or thyroid masses. Note surgical scars, crepitus, or decreased range o motion. VII. Ne uro lo g ic : Per orm a complete cranial nerve (CN) exam.

BENIGN LESIONS OF THE HEAD AND NECK Ove rvie w I. Re a c tive lym p h no d e : most common neck mass and most o en secondary to bacterial or viral in ections II. Ma lig na nc y: Most neck masses in children are benign; in adults, neck masses are more likely to be malignant.

Wo rkup o r Ac q uire d Le s io ns I. De ta ile d his to ry: Obtain details about the ollowing. A. Family history: malignancy and personal history o cancer B. Risk actors: smoking; alcohol consumption; exposure to radiation, sawdust, or other potential carcinogens; and exposure to human papillomavirus (HPV) 16 or 18 C. Recent illnesses: upper respiratory in ection (URI), sinusitis, or tonsillitis; otitis or conjunctivitis; and dental problems II. P hys ic a l e xa m ina tio n: See earlier discussion. III. La b o ra to ry te s ts : may include tuberculin test or tuberculosis, heterophil titer (monospot test) or mononucleosis, thyroid unction tests or thyroid scan, serologic tests or syphilis, and viral titers (especially or Epstein-Barr virus, which is associated with nasopharyngeal carcinoma and Burkitt lymphoma) IV. Ra d io lo g ic s tud ie s : may include so tissue radiographs o the neck, barium swallow, chest x-ray, or scanning procedures such as computed tomography (C ) and magnetic resonance imaging (MRI) V. End o s c o p y: indicated i a primary neoplasm is suspected VI. Tre a tm e nt: depends on the f ndings (Fig. 18-1) A. Antibiotics: i a bacterial in ection is suspected B. Consultation: may be help ul 1. Dental consultation: i the teeth seem to be a source 2. Dermatology consultation: i skin lesions are present C. Surgical biopsy: may be indicated i a mass does not shrink signif cantly over 6 weeks and a source o in ection is not ound 1. Fine-needle aspiration (FNA): used with suspected malignancy 2. Excisional biopsy: indicated or persistent cervical adenopathy

NECK ABSCESSES Typ e s

Quic k Cut The mos t common neck mas s is a reactive lymph node.

Quic k Cut The “rule o 7’s ” provides a guide or etiology o neck mas s es : A mas s that has been pres ent or 7 days is inf ammatory; 7 months , malignant; 7 years , congenital.

Quic k Cut Scrofula is mycobacterial lymphadenitis in the neck.

Quic k Cut Endos copic biops y and radiologic s tudies s hould precede any open biops y o the neck.

Quic k Cut FNA can diagnos e carcinoma but is us ually inadequate to de ne lymphoma.

Quic k Cut A patient pres enting with ever and an erythematous , pain ul, f uctuant neck mas s mos t probably has an abs ces s .

I. P e rito ns illa r a b s c e s s e s (q uins y): most common abscesses in the parapharyngeal space ( able 18-1) A. Cause: arise as a complication o acute tonsillitis B. Clinical presentation: Ipsilateral palatal edema, contralateral deviation o the uvula, “hot potato” voice, trismus, and dysphagia. T e patient may have only a low-grade ever or be a ebrile.

Chapter 18

Head and Neck Surgery

Ma s s

Child

Adult

Infla mma tory

(+)

P hys ica l e xa mina tion

(−)

Antibiotics ; la bora tory te s ts

(+)

Ra diology; pos s ible biops y

Endos copy; biops y of s us pe cte d prima ry tumor

P os s ible infla mma tory ma s s

(−) (+)

Re s olve s Obs e rve

(−)

(+)

Ra diology; pos s ible biops y; e xcis ion

(−)

Antibiotics ; la bora tory te s ts

(+)

FNA or biops y

(−) Re s olve s

Obs e rve

FNA or biops y

Fig ure 18-1: Bas ic algorithm or treatment o head and neck cancer. FNA, ne-needle as piration.

Ta b le 18-1: Ne c k Ab s c e s s e s Sig ns a nd Sym p to m s Pain Swelling Dysphagia Dyspnea Leukocytosis Fever Air in soft tissue radiograph Tre a tm e nt Airway protection Incision and drainage Antibiotics

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II. P a ra p ha ryng e a l s p a c e a b s c e s s e s : Arise rom the posterior teeth or tonsils and can a ect the carotid sheath structures and multiple CNs. T ey can cause mediastinitis and carotid “blowout” (i.e., erosion o the artery wall leading to massive hemorrhage). III. Re tro p ha ryng e a l a b s c e s s e s : arise rom in ected retropharyngeal nodes or extension rom other spaces and can lead to airway obstruction or mediastinitis IV. Lud wig a ng ina : abscess that occupies the sublingual space that generally arises rom a dental source. Can cause death rom airway obstruction, commonly requires tracheostomy V. Be zo ld a b s c e s s e s : arise rom in ection in the mastoid

CONGENITAL MASSES Le s io ns o Thyro id Orig in

Quic k Cut Neck in ections mus t be drained but s hould only be done by thos e amiliar with neck anatomy owing to the carotid artery, airway, and the cranial nerves .

Quic k Cut Abs ces s es in the head and neck can caus e airway compromis e, and intubation or tracheos tomy may be neces s ary.

I. Ove rvie w: T yroid gland originates at the oramen cecum and descends centrally to the level o the thyroid and cricoid cartilages ( able 18-2). A. T yroglossal duct: May pass in ront o , through, or behind the hyoid bone; it is generally obliterated but may persist. Solid tumors o thyroglossal duct origin occur almost exclusively within the tongue and above the hyoid bone. B. T yroidal primordium: Some may remain at any site in the duct and give rise to cysts, f stulas, accessory thyroid tissue, and neoplasms. II. Thyro g lo s s a l f s tula s , c ys ts , a nd s inus e s : Occur in the midline; 20% are suprahyoid, 15% occur at the hyoid, and 65% are in rahyoid. A. Fistulas: almost always the result o in ection with spontaneous or surgical drainage B. Cysts: Present by age 10 years in 50% o cases; no sexual predominance exists, but they are most o en ound in caucasians. 1. Size: usually measure 2–4 cm in diameter and gradually Quic k Cut increase in size, although the size may uctuate Imaging is important 2. Behavior: rise and all with the larynx during swallowing to ens ure a normal thyroid C. Sinus tract: may orm as direct connection to the skin and result gland is pres ent els ewhere in persistent drainage be ore excis ion o a thyroid D. reatment: total surgical excision res t. III. Thyro id re s ts : may be lingual or may occur in the neck A. Endotracheal ectopias: may occur B. Palpation: o the normal position o the thyroid o en reveals no evidence o thyroid tissue C. reatment: dictated by the degree o obstruction and by the presence o other thyroid tissue D. T yroid scan: Ensures that unctional thyroid tissue exists in the usual location; 75% o patients have no other unctional thyroid.

Bra nc hia l Cle t Ano m a lie s I. Em b ryo lo g y: In week 4, f ve ridges and grooves appear on the ventrolateral sur ace o the embryonic head that orm the branchial arches and cle s, respectively, and the pharyngeal pouches develop internally at the same level as the external grooves.

Ta b le 18-2: Co ng e nita l Ne c k Ma s s e s Typ e

Lo c a tio n

Exa m ina tio n

Tre a tm e nt

Thyroglossal cysts

Midline

Firm, nontender

Surgical excision

Branchial cleft cyst

Preauricular anterior

Firm, nontender

Surgical excision

Teratoma

Anywhere

Firm

Surgical excision

Hemangioma

Anywhere

Diffuse

Observation; laser treatment

Cystic hygroma

Posterior triangle

Diffuse

Partial excision

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303

II. Typ e s A. Sinus (incomplete f stula): has either an internal or an external opening B. Complete f stula: has both internal and external openings C. Cyst: has neither internal nor external openings D. Combinations (o any o the preceding types): can occur III. Ana tom y: Anomalies are generally located along the anterior border Quic k Cut o the sternocleidomastoid (SCM) muscle or deep to it; they can occur Second brachial anywhere between the external auditory canal and the clavicle. cle t anomalies are the mos t A. First cle anomalies: always superior to the hyoid bone common and pres ent with an 1. Fistula: i present, courses superiorly and end near the external opening two thirds external auditory canal o the way down the anterior border o the SCM mus cle. 2. Cyst and tract: may lie in the parotid gland, with a variable relationship to the acial nerve B. Second cle anomalies: most common type 1. External opening: approximately two thirds down the SCM muscle anteriorly i present 2. Fistula: i present, ascends with the carotid sheath and ends at the tonsillar ossa C. T ird cle anomalies: rare 1. External opening: occurs in the same position as in a second cle f stula 2. ract: ascends along the carotid sheath and opens in the piri orm sinus D. Fourth cle anomalies: have never been seen in their entirety IV. Cha ra c te ris tic s : generally smooth, round, nontender masses A. Size increase: common during URI B. In ected cyst: may abscess or rupture spontaneously to orm a sinus C. Symptoms: determined by size and location o the anomaly 1. Large cysts: may cause dysphagia, stridor, and dyspnea 2. Small cysts: o en undiscovered until adulthood because o their slow rate o growth and minor symptoms

Quic k Cut Cons ider a neck mas s to be a branchial cle t anomaly i it is located laterally, increas es in s ize with URIs , and has been pres ent s ince birth.

V. Tre a tm e nt: Complete excision without damage to the surrounding vital structures is the def nitive treatment. A. iming: Excision is delayed until antibiotic treatment is completed. B. Incision and drainage: avoided, i possible, because it makes subsequent excision more di cult

Te ra to m a s I. De f nitio n a nd typ e s : growths that consist o multiple tissues oreign to the part o the body in which they arise A. Epidermoid cysts: most common type; lined by squamous epithelium and have no adnexa B. Dermoid cysts: epithelium-lined cavities containing skin appendages (e.g., hair, glandular tissue, and ollicles) C. eratoid cysts (rare in the head and neck): lined with simple stratif ed squamous or respiratory epithelium and contain cheesy keratinous material

Quic k Cut Epidermoid cys ts ectoderm; dermoid cys ts ectoderm and mes oderm; teratoid cys ts ectoderm, mes oderm, and endoderm

II. Ce rvic a l te ra to m a s : most commonly present at birth A. Characteristics: usually 5–12 cm, semicystic, and unilateral B. Symptoms: In ants usually have stridor, apnea, or cyanosis because o tracheal compression, and dysphagia may also be present. Some in ants are asymptomatic at birth but become symptomatic within weeks or months. C. Associated anomalies: increased incidence o maternal hydramnios but no increase in associated in ant anomalies D. reatment: Early excision in in ants is mandatory. III. Ma lig na nt te ra to m a s (o the ne c k): rare; occur exclusively in adults with a very poor prognosis IV. Na s a l d e rm o id s : commonly apparent shortly a er birth A. Location: Nasal dorsum is the most common site, but they may occur in the tip o the nose or the columella (the external end o the nasal septum).

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Ta b le 18-3: Co ng e nita l Na s a l Ma s s e s As s o c ia te d Co ng e nita l Ano m a lie s

Ca n Be Mid line

As s o c ia te d with In e c tio ns o Skin

De rm o id

No

Yes

Yes

Yes

Yes

No

Glio m a

No

Yes

No

Yes

No

No

Enc e p ha lo c e le

Yes

Yes

No

Yes

No

Yes

Me ning itis Ris k

Sinus Tra c t

Co m p re s s ib le

B. Characteristics ( able 18-3): male predominance o 2:1; must be di erentiated rom encephaloceles and gliomas C. reatment: Early removal is important; recurrences secondary to incomplete removal are common.

Va s c ula r Tum o rs I. He m a ng io m a s : Most common tumors o the head and neck in children. Girls are more o en a ected, and lesions are usually solitary. A. Capillary hemangiomas: Include nevus ammeus (port-wine stain) and strawberry nevus and are characteristically ound in the dermis. T ey have an early period o evolution, a er which they o en regress. T ey may develop suddenly and grow quite large. B. Cavernous hemangiomas: More permanent; spontaneous regression is more likely or hemangiomas present at birth than in those appearing later. C. Arteriovenous hemangiomas: occur almost exclusively in adults and have a predilection or the lips and perioral skin D. Invasive hemangiomas: occur in the deep subcutaneous tissues, deep ascial layers, and muscles 1. Presentation: Present as neck masses, predominantly in children; masseter and trapezius are the muscles most commonly involved. Intramuscular hemangiomas most commonly present in young adults as palpable, mobile, noncompressible masses. 2. Characteristics: end to recur a er excision but do not metastasize; they are generally without thrills, pulsations, or bruits; and pain secondary to compression o other structures is usually present. E. Subglottic hemangiomas: Usually capillary in type. Owing to Quic k Cut their location, they o en present at birth with stridor and usually When evaluating with cutaneous involvement. a newborn with s tridor, F. reatment conducting a thorough s kin 1. Congenital cutaneous hemangiomas: Many lesions regress exam is important. spontaneously, but several treatment options exist or those that do not. a. Medical: Glucocorticosteroids, inter eron al a, vincristine, and imiquimod have been used or treatment. Propranolol has been shown to induce involution o in antile hemangiomas. b. Excision: Laser excision is pre erred in areas with cosmetic or unctional concern (pulsed dye laser is used). Surgical excision can also be per ormed. 2. Subglottic lesions: may require tracheotomy, steroids, propranolol, and, in some cases, laser excision 3. Extensive lesions: Surgery may be needed. 4. Radiation therapy: Used to suppress tumor growth in areas that are inaccessible surgically; however, the use o radiation alone is controversial and is known to increase risk o thyroid, breast, and skin cancers. II. Cys tic hyg ro m a s : ound predominantly in the neck and are usually noted at birth A. Location: T ey are more common in the posterior triangle and may extend up into the cheek or parotid region and down into the mediastinum or axilla. 1. Large masses: extend past the SCM muscle into the anterior compartment and may cross the midline 2. Floor o the mouth and base o the tongue: may be involved

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B. Signs and symptoms: di culty nursing, acial or neck distortion, respiratory distress, brachial plexus compression with pain or hyperesthesia, and a sudden increase in size secondary to spontaneous hemorrhage, which can be atal C. Characteristics: Can be progressive, static, or regressive and generally transilluminate; no gender predilection exists, or right or le side. 1. Small lesions: unilocular and f rm 2. Large tumors: loculated, shi able, and compressible Quic k Cut 3. Cyst walls: Usually tense, and because the loculi tend to The greater the communicate, rupture o one locule can cause all o them lymphangiomatous component to partially collapse. o a hygroma, the more likely it D. reatment: Surgery is the mainstay o treatment, but recurrences is to recur. are common because resection is o en incomplete. III. Ora l a nd p e rio ra l lym p ha ng io m a s : Relatively common lesions usually ound at birth or soon a er. T ey behave very much like cystic hygromas.

ACQUIRED LESIONS To ns illa r a nd Ad e no id a l Hyp e rtro p hy I. Ob s truc tive hyp e rtro p hy: Patients benef ting rom tonsillectomy with adenoidectomy are those with airway obstruction, sleep apnea, dysphagia, or ailure to thrive. II. Ad e no id e c to m y: per ormed in children with chronic nasal obstruction, especially when they also demonstrate chronic serous otitis media or orthodontic problems

Le uko p la kia , Erythro p la kia , a nd Ke ra to s is I. De f nitio n: Leukoplakia presents as white lesions that occur on the mucosa o the mouth, pharynx, or larynx. Erythroplakia is a similar red patch. II. Etio lo g y: T ese lesions are associated with repeated trauma Quic k Cut (e.g., rom poorly f tting dentures and decayed teeth), smoking, or Leukoplakia and use o alcohol. erythroplakia are cons idered III. Tra ns o rm a tio n: Leukoplakia is precancerous, with a precancerous les ions ; biops y trans ormation rate ranging rom 11% to 36%. Erythroplakia has and clos e obs ervation are recommended. a higher trans ormation rate. Little correlation exists between the clinical appearance and their histology. IV. Dia g no s is : Biopsy, to rule out squamous cell carcinoma, should be per ormed in high-risk patients (smokers and drinkers) and i the lesion persists a er the removal o an irritative ocus. V. Tre a tm e nt: Benign leukoplakic lesions require no treatment but do require continued observation.

P a p illo m a s I. Sq ua m o us p a p illo m a s o the o ra l c a vity: usually occur as one lesion but may be multiple and are common on the palate and aucial arches A. Characteristics: usually pedunculated and cauli owerlike in appearance B. Recurrence: rare a er excision II. Na s a l (s c hne id e ria n) p a p illo m a s A. Benign lesions o the sinonasal tract: rom the schneiderian mucosa and classif ed into three types: ungi orm, oncocytic, and inverted B. Inverted papillomas: ypically arise rom the lateral nasal wall Quic k Cut and can invade the sinuses and orbits. Grossly, the lesions appear Inverted papillomas bulky and deep red to gray in color and vary in consistency; are unilateral, aris e rom the unlike allergic polyps, they are unilateral. lateral nas al wall, and can 1. Characteristics: Patients generally present with nasal trans orm into s quamous cell obstruction, a postnasal drip, and headaches. T ese lesions carcinoma. occur mainly in men age 50–70 years. 2. Malignant trans ormation: Incidence is 10%. 3. reatment: Complete excision that includes the lateral nasal wall and ethmoid sinus. Recurrence is common; there ore, li elong ollow-up is usually recommended.

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III. La ryng e a l p a p illo m a s : most common laryngeal tumors o childhood and may be ound at any age A. Juvenile type: occurs predominantly in childhood and tends to involute at puberty 1. Etiology: Viral; HPV 6 and 11 are the most common viral strains. 2. Characteristics: Multiple papillomas typically occur and may involve the airway rom the epiglottis to the bronchi. Quic k Cut T e vocal olds are usually involved; hoarseness and Laryngeal papilloma, obstruction occur late. or respiratory papillomatosis, 3. reatment: Laryngoscopic removal, o en by the use o is as s ociated with HPV6 and surgical microdebridement, is the mainstay o therapy. 11 and typically pres ents as a. racheotomy: may be necessary but predisposes to hoars enes s in a child. papilloma seeding b. Recurrence and spread: common B. Adult type: In this orm, the papilloma is generally single. 1. Recurrence: As in the juvenile orm, the papilloma tends to recur ollowing excision. 2. Malignant trans ormation: in recurrent lesions, particularly in patients exposed to radiation

Na s a l P o lyp s I. Inc id e nc e : rare be ore age 5 years and occur more commonly in men II. Etio lo g y: believed to be an allergic response A. Samter triad: T ey may be associated with asthma and an idiosyncratic reaction to aspirin. B. In children: should prompt a sweat test to rule out cystic f brosis III. Cha ra c te ris tic s : In ammatory polyps are almost always bilateral and may recur; paranasal sinus involvement is common. IV. Tre a tm e nt: Polyps are excised i they obstruct the nasal airways or the sinus drainage pathways; patients are placed on a topical steroid medication to prevent recurrence, and management o their allergies is vital.

P e rip he ra l Ne rve Tum o rs I. Sc hwa nno m a s : solitary, encapsulated tumors surrounded by a nerve that are primarily located centri ugally and are o en pain ul and tender II. Ac o us tic ne uro m a s : constitute a type o slow-growing schwannoma A. Etiology: arise rom CN VIII, usually within the internal auditory canal (IAC) Quic k Cut B. Signs and symptoms: may include hearing loss, tinnitus, As ymmetric imbalance, and vertigo s ens orineural hearing los s C. Evaluation: esting includes an audiogram and MRI with is common and requires gadolinium enhancement. that acous tic neuroma be D. reatment: Because these tumors grow slowly, they can ruled out with MRI o the internal auditory canal. be observed in the right clinical context. Other treatment options are surgical resection or radiation therapy. III. Vo n Re c kling ha us e n ne uro f b ro m a to s is (NF I): Neurites (axons) pass through the tumor; lesions are usually multiple, unencapsulated, located centripetally, and characteristically asymptomatic. A. Etiology: Caused by a nerve growth actor gene on chromosome 17q11.2; inheritance is autosomal dominant. B. Malignant trans ormation: 8% C. Signs and symptoms: Ca é au lait spots, vitiligo, gliomas (especially optic), osseous changes, Lisch nodules (iris hamartomas), meningitis, spina bif da, syndactyly, hemangiomas, axillary or inguinal reckles, NF I in a f rst-degree relative, or retinal and visceral mani estations may be present. IV. Ce ntra l ne uro f b ro m a to s is (NF II): Classically, slow-growing, bilateral acoustic neuromas or neurof bromas cause hearing loss or dizziness and lead to a diagnosis by age 20 years. A. Etiology: Chromosomal abnormality involves encoding o a suppressor protein schwannomin. Inheritance is autosomal dominant, but almost 50% o cases are new mutations. B. Diagnosis: may also be established by a unilateral CN VIII mass and a relative with NF II or any two o the ollowing: glioma, juvenile posterior subscapular lenticular opacity, meningioma, neurof broma, or schwannoma.

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C. Signs and symptoms: Ca é au lait spots, hearing loss and balance issues. Lisch nodules, and cutaneous neurof bromas are uncommon. D. Wishart type: early-onset rapid growth and other f bromatous Quic k Cut tumors in addition to CN VIII masses I an important nerve mus t be cut at s urgery, E. Gardner type: later onset, slow growth rate; usually bilateral it s hould be generally acoustic neuromas only reanas tomos ed or a nerve V. Tre a tm e nt: Most neurogenous tumors o the head and neck can be gra t s hould be interpos ed. excised sa ely without sacrif cing nerves.

No nd e nta l J a w Le s io ns I. Fib ro us d ys p la s ia : Developmental anomaly o the bone that mani ests as a de ect in osteoblastic di erentiation and maturation. Any bone(s) in the body can be a ected, including the cranio acial skeleton. A. Characteristics: active growth in childhood and stabilization in adulthood B. Signs and symptoms: bone enlargement; the maxilla is more commonly involved than the mandible. C. Radiographs: reveal sclerosis, lytic lesions, or unilocular lesions D. reatment: Obvious de ormity, pain, or inter erence with unction suggests the need or surgery; conservative resection appears to be the best treatment. E. Malignant trans ormation: possible but uncommon II. To rus : Benign bony growth, occurring at the midline o the palate (maxillary torus) or bilaterally lingual to the bicuspid (mandibular Quic k Cut torus). T ey grow slowly and generally have no signif cance except Tori are common that they may inter ere with the f tting o dentures. benign bony growths that III. Os te o m a s : Slow-growing, benign tumors in the sinuses, jaws, occur on the palate or the or external ear canals. T ey may require excision i they produce mandible. symptoms.

La ryng e a l Le s io ns I. La ryng o c e le : Dilatation o the laryngeal saccule, producing an air sac that communicates with the laryngeal ventricle. Pressure increases the size o a laryngocele (e.g., coughing, straining, playing a wind instrument). A. Laryngopyocele: in ected laryngocele that can be atal i it results in asphyxia or i the purulent contents are aspirated B. Location: Laryngoceles may be unilateral or bilateral. T ey may also be internal (within the larynx), external (presenting in the neck), or both (combined). 1. Internal laryngocele: causes bulging o the alse cord and aryepiglottic old 2. External laryngocele: appears as a neck swelling at the level o the hyoid and anterior to the SCM muscle C. Characteristics 1. Internal laryngoceles: cause hoarseness, breathlessness, and stridor on enlargement 2. External laryngoceles: increase in size with coughing or the Valsalva maneuver; are tympanic to percussion and may produce hissing as the laryngocele empties air into the larynx when the air pressure is reduced D. Diagnosis: C and MRI scans E. reatment 1. Symptomatic laryngoceles: excised 2. Laryngopyoceles: Incision, drainage, and subsequent excision. Antibiotics are also appropriate. II. La ryng e a l we b s A. Characteristics: May be congenital or ollow vocal old trauma. When extensive, they present with stridor, weak phonation, and eeding problems in in ants. B. reatment: Excision or division is generally the pre erred treatment, and placement o a stent or keel is o en required. III. Vo c a l no d ule s : bilateral benign masses that usually occur at the junction o the true vocal olds A. Etiology: associated with vocal abuse B. reatment: Best treated by modi ying the patient’s speaking or singing technique through voice therapy. Surgery is rarely necessary

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IV. Vo c a l p o lyp s Quic k Cut A. Characteristics: usually unilateral and o en do not regress with Vocal polyps are speech therapy unilateral and do not improve B. reatment: Recommended therapy is care ul excision with with s peech therapy; vocal microscopic visualization and avoidance o injury to the underlying nodules are bilateral and are lamina propria; in selected cases, the laser may be help ul. treated with s peech therapy. V. La ryng e a l g ra nulo m a s (intub a tio n g ra nulo m a s ): occur over the vocal processes o the arytenoid cartilages A. Etiology: Generally the result o trauma, usually rom an endotracheal tube, and are usually associated with re ux laryngitis. Voice abuse may be a actor. B. reatment: Antire ux and speech therapies o en help them regress. 1. Persistent granulomas: best treated by excision a er a period o voice and medical therapy 2. Botulinum toxin: used or selected, recurrent cases VI. Aryte no id d is lo c a tio n: generally is the result o endotracheal tube or external trauma A. Characteristics: So , breathy voice a er extubation. Flexible f beroptic exam will reveal an immobile vocal cord. B. reatment: Prompt reduction is advisable; otherwise, the arytenoid usually becomes f xed in the dislocated position. However, late reduction (a er months or years) can be success ul. VII. Co nta c t ulc e rs : mucosal disruptions usually located posteriorly on the vocal olds A. Etiology: sometimes result rom trauma (e.g., rom intubation), occasionally rom vocal abuse, and o en rom gastric re ux laryngitis or heavy coughing B. reatment: antire ux medication and behavioral changes such as elevation o the head o the bed; avoidance o ca eine, chocolate, late-night snacks, and atty oods 1. Antacid therapy: usually results in prompt resolution 2. Antibiotics: may be help ul i in ection is present

HEAD AND NECK INFECTIONS To ns illitis a nd Ad e no to ns illitis I. To ns ille c to m y with a d e no id e c to m y: Once the most common operation per ormed in the United States. It remains quite prevalent but is now per ormed only or specif c indications. A. Obstructive hypertrophy: See earlier discussion. B. Recurrent in ection: Patients with documented recurrent adenotonsillitis are improved a er tonsillectomy with adenoidectomy. II. P e rito ns illa r a b s c e s s : onsillectomy is o en suggested a er treatment or inpatients with a history o previous tonsillitis.

Atyp ic a l Myc o b a c te ria In e c tio n

Quic k Cut Many common in ections such as ear in ections (otitis) can be treated with antibiotics alone.

Quic k Cut A his tory o three to s ix epis odes o adenotons illitis annually is a relative indication or tons illectomy with adenoidectomy.

I. Cha ra c te ris tic s : Presents as an in amed mass or draining sinus in the head and neck, commonly associated with the parotid or submandibular glands and is most common in children and adolescents. Pulmonary involvement is rare. A. Results: Fixation o overlying skin and sinus ormation are common. B. Biopsy: can lead to a chronically draining sinus tract II. Tre a tm e nt: Surgical excision or curettage and drainage. Antimycobacterial drug therapy is not indicated because this is not systemic but a localized problem.

MALIGNANT LESIONS OF THE HEAD AND NECK Ove rvie w I. Cha ra c te ris tic s : able 18-4 shows the basic characteristics o head and neck cancer. II. Ep id e m io lo g y: Primary malignant neoplasms o the head and neck, excluding skin cancer, account or 5% o new cancers each year in the United States. A. Incidence: Male to emale ratio is 3:1 to 4:1, and most lesions occur in patients older than age 40 years.

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Ta b le 18-4: Ba s ic Cha ra c te ris tic s o He a d a nd Ne c k Ca nc e r Mo s t P ro m ine nt Lo c a tio n

Ris k o

Sym p to m

Ris k Fa c to r

Ce rvic a l Me ta s ta s e s

Nose and sinus

Mass

Nickel, wood

Moderate

Nasopharynx

Neck mass; serous otitis media

Epstein-Barr virus

High

Oral cavity

Pain

Tobacco, alcohol

Moderate

Oropharynx

Dysphagia

Tobacco, alcohol, HPV 16 and 18

High

Larynx

Hoarseness

Tobacco

Glottic, low; supraglottic, high

Hypopharynx

Dysphagia

Tobacco, alcohol

High

Salivary glands

Mass

Radiation

High-grade, high; other, low

B.

ypes: Approximately 80% o primary head and neck Quic k Cut malignancies are squamous cell carcinomas; the remainder The number o includes thyroid cancers, salivary neoplasms, lymphoma, and patients with a s econd other less common tumors. primary malignancy o the upper aerodiges tive tract at III. Ris k a c to rs : obacco use, alcohol consumption, and exposure to the time o initial pres entation radiation are etiologic actors in most squamous cell carcinomas o has been reported to be as the head and neck. high as 17% . A. Smoking: Approximately 85% o patients with head or neck cancer smoke or ormerly smoked cigarettes at the time o diagnosis. B. HPV: associated with some head and neck squamous cell carcinomas, most commonly strains 16 and 18

Eva lua tio n I. His to ry: Evaluation o the patient starts with a care ul history, especially head or neck malignancy. A. Exposure to etiologic agents: such as tobacco, alcohol, sawdust, other toxins, and irradiation B. Associated symptoms: hoarseness or sore throat o more than 3 weeks’ duration, dysphagia, otalgia, dyspnea, nonhealing Quic k Cut ulcers, hemoptysis, and neck mass Otalgia is o ten a re erred pain, s econdary to C. Nutritional status involvement o CNs IX and X. 1. Malnourishment: Either because o alcoholism or an obstructive tumor; some patients may require nutritional supplements. 2. Severe malnourishment: Consider re eeding syndrome. Quic k Cut Treatment needs to D. Family history: critical with inherited actors (i.e., medullary be individualized to the needs thyroid cancer) o the patient as well as their II. P hys ic a l e xa m ina tio n: must include an inspection o all the skin ability to comply with the and mucosal sur aces o the head and neck treatment plan. A. Intranasal examination and indirect mirror examination: o the nasopharynx and hypopharynx B. Care ul palpation: o the oral cavity, base o the tongue, and oropharynx C. Fiberoptic examination: o the nose, pharynx, and larynx is indicated in all patients who are being evaluated or cancer

Tre a tm e nt I. Surg e ry (Fig . 18-2): Indicated or many patients with head and neck cancer. T e e ects o radiation are avoided, and radiation can be saved or recurrent disease or other primary cancers. T e choice o surgery can be in uenced by many actors. A. Malnourishment: can increase the perioperative risk o morbidity

Quic k Cut Treatment is bas ed on the s ite and pathology o the primary cancer and the extent o the local, regional, and dis tant dis eas e.

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S te rnocle idoma s toid mus cle

Inte rna l jugula r ve in Ca rotid a rte ry Va gus S pina l a cce s s ory ne rve

A

B

Fig ure 18-2: Types o neck dis s ection, including traditional neck dis s ection and various levels o modi cation. In a radical neck dis s ection (A), the s ternocleidomas toid mus cle, internal jugular vein, and s pinal acces s ory nerve are removed. In the mos t cons ervative modi cation (B), only the as cial compartment with the lymphatic tis s ue is removed, and all o the s tructures are s pared.

B. Coexistent systemic disease: Diabetes, chronic obstructive pulmonary disease, coronary artery disease, etc. increase the surgical risk. C. Results: Necessary procedures can be disf guring and can leave the patient with severe unctional def cits and is best per ormed in institutions that can provide the ull range o rehabilitative services. 1. Resection o the larynx: alters communication 2. Surgery on the tongue, oropharynx, hypopharynx, or mandible: can alter or prevent swallowing D. Contraindication: Surgery or a cure is generally contraindicated in patients with distant metastases. II. Ra d ia tio n the ra p y: Radiation alone is adequate treatment or many early lesions. A. Benef ts: It can provide a cure without the unctional or cosmetic def cits associated with surgery, can treat multiple primary lesions simultaneously, and can prophylactically treat regional nodes that are clinically negative. B. Planned postoperative radiation: can signif cantly increase the Quic k Cut survival rate or patients with advanced lesions A dental examination C. Hyper ractionation (more than one daily treatment) and and possibly extraction is required be ore radiotherapy. concomitant chemotherapy: Studies show that these techniques Dental treatment during and up can enhance the response to radiation therapy, but they increase to 2 years a ter radiotherapy the risk and severity o local side e ects. can be hazardous because D. Complications: mucositis, xerostomia, loss o taste, dermal o decreased vascularity and and so tissue f brosis, dental caries, and bone and so tissue consequent delayed healing. necrosis III. Che m o the ra p y: not curative as a single treatment modality in head and neck squamous cell carcinoma A. Neoadjuvant treatment: to reduce the tumor burden be ore radiation or surgery B. Concomitant radiation therapy: to increase response rates in advanced tumors Quic k Cut C. Palliation: in patients with unresectable tumors or distant metastases The choice o a IV. Re ha b ilita tio n: should be planned at the same time as treatment surgical f ap depends on the size o the de ect, history o A. Surgical aps: Cosmetic and unctional de ects are reconstructed peripheral vascular disease, at the time o the cancer resection whenever possible. prior s urgeries, or procedures 1. Local aps: nasolabial, orehead in the desired donor region 2. Distant pedicled skin aps: deltopectoral, omocervical and general health and 3. Pedicled myocutaneous aps: pectoralis major, latissimus nutritional status o the patient. dorsi, trapezius

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B. Esophagectomy: Gastric “pull-up” (raising the stomach into the chest to replace the esophagus) or colon interposition are options or reconstruction. C. Free microvascular aps: have a high rate o complications but can be very e ective D. Prosthetic rehabilitation: necessary when portions o the maxilla, orbit mandible, or palate are resected E. Voice restoration: When the larynx is removed, intensive rehabilitation is required to re-establish the voice with an electrolarynx that is applied to the neck sur ace, regurgitated air (esophageal speech), or with a prosthesis placed in a tracheoesophageal f stula. F. Swallowing training: Many patients who undergo partial laryngectomy, pharyngectomy, or glossectomy need this to avoid aspiration.

NECK CANCER Ana to m y I. Divis io ns : anterior and posterior triangles A. Anterior triangle: Bounded by the midline o the neck, the in erior mandible border, and the anterior SCM muscle. It can be subdivided urther into submandibular, submental, superior carotid, and in erior carotid triangles. B. Posterior triangle: Bounded by the posterior border o the SCM muscle, the anterior border o the trapezius, and the clavicle. It is divided urther into supraclavicular and occipital triangles. II. Lym p ha tic d ra ina g e : Fascial planes o the neck enclose the lymphatic system and are important when discussing spread o in ections and malignancy in the head and neck. A. Superf cial ascia: subcutaneous and envelops the platysma B. Deep ascia: three parts: 1. Superf cial layer: invests the SCM and trapezius muscles and the parotid and submandibular glands 2. Middle layer: divided into muscular and visceral divisions a. Muscular division: invests the strap muscles and pharyngeal constrictors and buccinators b. Visceral division: also called the pretracheal ascia; envelopes the trachea, esophagus, and thyroid 3. Deep layer: divided into the alar ascia anteriorly and the prevertebral ascia posteriorly C. Retropharyngeal space: lies anterior to the alar ascia and is an important plane when discussing spread o malignancy and in ection D. Neck lymph nodes: Many drain specif c areas o the upper aerodigestive tract. T ese are divided into six levels based on location and drainage patterns. 1. Deep jugular and spinal accessory chains: where most lymph nodes lie 2. Jugular chain divisions: superior, middle, and in erior groups

Ne c k Ma s s Eva lua tio n in Ad ults with No P rim a ry Ca nc e r Se e n o n Exa m

I. His to ry a nd p hys ic a l e xa m ina tio n: Care ul history is taken, Quic k Cut A workup or and the head and neck are examined or evidence o a possible malignancy s hould be primary cancer. undertaken in all adults with II. Dia g no s is : I the primary cancer is not identif ed on the initial a pers is tent neck mas s . examination, the subsequent workup should include the ollowing. A. Imaging: Chest x-ray, barium swallow, and C scan o the neck are indicated in most patients. MRI or ultrasound o the neck is guided by f ndings on the history and physical examination. 1. MRI: particularly use ul in def ning deeply invasive tongue, pharynx, and larynx tumors 2. C o the sinuses: can be used to search or primary tumors 3. Staging: C or MRI o the chest and abdomen are o en used. B. FNA: should be per ormed to provide a tissue diagnosis C. Panendoscopy: direct laryngoscopy, esophagoscopy, bronchoscopy, and nasopharyngoscopy to identi y any obvious lesions or biopsy 1. Random biopsies: I the result o the endoscopic survey is negative, biopsy o the nasopharynx (right, middle, and le ), piri orm sinuses, tongue base, and a tonsillectomy may also be considered. 2. Next step: I all biopsies have negative results, proceed with open neck biopsy and rozen section.

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Tre a tm e nt I. Typ e s o ne c k d is s e c tio n: Figure 18-3 Quic k Cut A. Radical neck dissection: en bloc dissection o the cervical FNA biops y o a lymphatics that includes removal o the SCM muscle, internal s olid neck mas s is o ten the jugular vein, or spinal accessory nerve rs t s tep in its workup. I B. Modif ed ( unctional, conservative) neck dissection: removes the les ion is a metas tas is , a ull head and neck exam, in the cervical lymphatics within their ascial compartments conjunction with imaging, that spares the SCM muscle, internal jugular vein, and spinal may demons trate the primary accessory nerve tumor C. Segmental neck dissection: re ers to removal o less than f ve nodal groups on one side o the neck (e.g., submandibular triangle dissection, supraomohyoid dissection) II. Ele c tive ne c k d is s e c tio n: surgical treatment with no known cervical disease; controversial because radiation therapy can provide prophylaxis or metastatic neck disease in many cases A. Choice between surgery and radiation: usually depends on the treatment o the primary tumor B. In general: per ormed or a primary cancer that has at least a 20% chance o occult metastasis

NASAL CAVITY AND PARANASAL SINUS CANCER Ana to m y a nd Cla s s if c a tio n I. Ba s ic s truc ture : Sinuses are contiguous with the nasal cavity through natural ostia, and the nose and sinuses are lined with a respiratory mucosa, which is pseudostratif ed columnar with goblet cells and cilia. II. Lym p ha tic d ra ina g e : to the parapharyngeal or retropharyngeal nodes III. Lo c a tio n: Most tumors (59%) are in the maxillary sinus, 24% are in the nasal cavity, 16% in the ethmoid, and 1% in the rontal/sphenoid sinuses.

A

Fig ure 18-3: A: Level o res ection in an en bloc compos ite res ection o the oral cavity, oropharynx, or both (the clas s ic commando procedure). B: The s pecimen includes the primary cancer, a s egmental mandibulectomy, and the radical neck dis s ection.

B

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IV. Cla s s if c a tio n: Nasal and sinus cancers are locally invasive. Nodal metastases are unusual and tend to occur late, even with extensive local disease. A. Squamous cell carcinoma: 80% B. Adenocarcinomas: including adenoid cystic carcinoma, 10%–14%

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Quic k Cut Squamous cell carcinoma is the most common malignancy o the nasal cavity and paranasal sinuses.

Clinic a l Eva lua tio n I. P re s e nting s ym p to m s : can include nasal obstruction; epistaxis; localized pain; tooth pain; CN def cits; mass in the ace, palate, or maxillary alveolus; proptosis; and trismus II. Dia g no s is : Extent o the disease is determined by physical examination and radiographic studies. A. C scan: use ul or identi ying bony erosions and orbital or intracranial extension B. MRI: can be used or intraorbital and intracranial invasion

Quic k Cut Be s us picious or a malignancy in a patient who pres ents with unilateral nas al obs truction, epis taxis , localized acial pain, or CN de cits (III, IV, VI, or VII).

Tre a tm e nt a nd P ro g no s is I. Ma xilla ry s inus c a nc e r A. Less advanced cancers: Subtotal or radical maxillectomy. Adjuvant radiation may be used. B. Advanced cancers: Usually receive a combination o surgical resection ollowed by chemotherapy and/or radiotherapy. Orbital exenteration and skin resection are per ormed when necessary. II. Ethm o id s inus o r na s a l c a vity tum o rs : combination o surgical resection and chemotherapy and/ or radiation III. Exte ns ive c a nc e rs : Combined cranio acial resection or selected patients. Chemotherapy is used or treatment or palliation. IV. Ce rvic a l lym p h no d e m e ta s ta s e s : treated with radiotherapy or surgery V. P ro g no s is A. Overall cure rate: 30%–35% B. 5-year survival rate: less advanced lesions, 70%; decreases to 15%–20% with more advanced disease

NASOP HARYNX CANCER Ove rvie w I. Ana to m y: Nasopharynx is the most cephalad part o the pharynx; its roo is ormed by the basioccipital and sphenoid bones, and its posterior wall is ormed by the atlas. A. Walls: Roo and posterior wall are covered by mucosa, and the adenoid tissue is embedded; the lateral wall contains the orif ce o the eustachian tube, and, just posterior to that, the ossa o Rosenmüller. B. Limits: Choanae def ne the anterior limit, and the ree edge o the so palate provides the in erior limit. C. Lymphatic drainage: to the lateral retropharyngeal, jugulodigastric (tonsillar), and high spinal accessory nodes II. Ep id e m io lo g y: High incidence among people living in China. People o Chinese ancestry who live in other countries do not have the same incidence, suggesting an environmental risk actor (i.e., consumption o smoked f sh) contributing to the increased incidence. A. Elevated Epstein-Barr virus titer: high incidence among persons with nasopharyngeal cancer B. Age: occurs at younger ages than do most solid head and neck tumors III. Cla s s if c a tio n: Eighty-f ve percent o nasopharyngeal tumors are epithelial; 7.5% are lymphomas. Epithelial tumors commonly arise in the ossa o Rosenmüller.

Clinic a l Eva lua tio n I. P re s e nting s ym p to m s : Epistaxis, cervical adenopathy, serous otitis media, and nasal obstruction (headache, diplopia, acial numbness, trismus, ptosis, and hoarseness may also be present); 70% o patients will have nodal disease, 40% will have CN involvement.

Quic k Cut An adult with a unilateral middle ear e us ion s hould have nas opharyngos copy to rule out a nas opharyngeal mas s .

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II. Dia g no s is : conf rmed by biopsy o a metastatic lymph node A. Staging: C and MRI B. Elevated Epstein-Barr virus titer: Monitoring o the titer should show a decrease with success ul treatment and an increase with recurrences.

Tre a tm e nt a nd P ro g no s is I. Ra d ia tio n: Primary treatment or all epithelial nasopharyngeal tumors. T e dose is delivered to the nasopharynx and to both sides o the neck. Improved responses are possible with combined chemotherapy and radiation in patients who can tolerate the increased toxicity. II. Ra d ic a l ne c k d is s e c tio n: per ormed or residual nodes i the primary tumor is controlled III. 5-ye a r s urviva l ra te : 40% in patients without positive nodes and 20% in patients with positive nodes

ORAL CAVITY CANCER Ove rvie w I. Ana to m y: Oral cavity extends rom the lip anteriorly to the aucial arches posteriorly and includes the lips, buccal mucosa, gingivae, retromolar trigones, hard palate, anterior two thirds o the tongue (the oral tongue), and oor o the mouth. II. Lym p ha tic d ra ina g e : to the submental, submandibular, and deep jugular nodes III Etio lo g y: Ninety percent o patients are heavy users o tobacco (either smoking or chewing); 80% o patients are heavy drinkers.

Quic k Cut The s even s ubs ites o the oral cavity are the lips , buccal mucos a, gingivae, retromolar trigone, hard palate, oral tongue, and the f oor o the mouth.

Clinic a l Eva lua tio n I. P re s e nting s ym p to m s : Can include loose teeth, pain ul or nonhealing ulcers, odynophagia, otalgia (with posterior lesions), and cervical adenopathy. T e lip is the most common site o carcinoma, ollowed by the oral tongue and oor o the mouth. II. Dia g no s is : Pain, which is a late symptom, occurs a er ulceration develops. A. Mandibular radiographs: assess the bony involvement by adjacent tumors B. Nodal metastases: Common, especially in the oor o mouth and oral tongue with more advanced primary tumors; much are microscopic (occult) disease. C. Metastases: uncommon; usually occur late in cancer o the lip or the buccal mucosa

Tre a tm e nt a nd P ro g no s is I. Sm a ll tum o rs with no lym p h no d e invo lve m e nt: can be treated with either local excision or radiotherapy

Quic k Cut Mos t malignancies o the oral cavity are treated with s urgery, with or without radiation.

II. La rg e r le s io ns : should be treated with combined surgery and radiation A. Surgery: involves an en bloc resection and neck dissection B. echnique: Either a partial mandibulectomy is included or the tumor is “pulled through” medially to the mandible into the neck (i.e., the tumor is removed en bloc, leaving the mandible intact). III. Tum o rs a tta c he d to the m a nd ib le : May be removed with a partial thickness o mandible (i.e., the lingual plate or alveolar process). T e mandibular arch is kept intact when possible. IV. Tum o rs d e m o ns tra ting b o ny e ro s io n in the m a nd ib le : removed with a ull-thickness portion o bone V. 5-ye a r s urviva l ra te : overall, or cancer o all oral cavity sites, is 65% A. Lip cancer: Rates as high as 90% have been reported. B. ongue lesions: Prognosis is worse i the lesion is posterior. 1. Anterior (mobile) tongue lesions: O en diagnosed when they are small; overall 5-year survival rate is more than 65%. 2. Posterior lesions: less than 40%

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OROP HARYNX CANCER Ove rvie w I. Ana to m y A. Boundaries: ree edge o the so palate superiorly, the tip o the epiglottis in eriorly, and the anterior tonsillar pillar anteriorly B. Contents: so palate, tonsillar ossae and aucial tonsils, lateral and posterior pharyngeal walls, and base o the tongue C. Parapharyngeal space: directly lateral to the oropharynx; contains the glossopharyngeal, lingual, and in erior alveolar nerves; pterygoid muscles; internal maxillary artery; and carotid sheath and is a site o early extension o an oropharyngeal tumor that also provides a pathway or the tumor to spread to the base o the skull Quic k Cut D. Lymphatic drainage: Primarily to the jugulodigastric (tonsillar) Tobacco, alcohol nodes; tumors o the so palate, lateral wall, and tongue base also us e, and HPV 16 and 18 spread to the retropharyngeal and parapharyngeal nodes. expos ures are ris k actors or oropharyngeal s quamous cell II. Etio lo g y: Alcohol and tobacco use are commonly ound together carcinoma. in patients with oropharyngeal cancer. A. HPV strains 16 and 18: associated with squamous cell cancer o the oropharynx with increasing incidence Quic k Cut B. Local mucosal irritation, malnutrition, and immune de ects: A s ynergis tic e ect also implicated

Clinic a l Eva lua tio n

s eems to exis t between alcohol and tobacco in oropharynx cancer, but it has not been de ned.

I. Pre s e nting s ym ptom s : Most common is a persistent sore throat, which is requently accompanied by ipsilateral otalgia (re erred pain via the tympanic branch o the glossopharyngeal nerve), vague sensation o throat irritation, restriction o tongue motion (“hot potato voice”), odynophagia, and bleeding. A. Malnourishment: Most patients are signif cantly malnourished. B. Cervical adenopathy: Nodal metastases are ound in 70% o patients with cancer o the base o the tongue and in 60%–80% o patients with tonsillar cancer; most o these nodes are palpable. II. Initia l e xa m ina tio n: Must include care ul palpation o the base o the tongue. Many small tumors are di cult to see but may be palpated easily. III. Dia g no s is : O en made late in the course; many patients are asymptomatic until tumors are large; others are treated conservatively or incorrectly diagnosed lesions. A. Endoscopy under general anesthesia: or all lesions be ore treatment is chosen B. C and MRI: use ul in determining tumor extension

Tre a tm e nt a nd P ro g no s is I. Sm a ll le s io ns : most commonly treated with radiotherapy II. La rg e le s io ns : Combined therapy o ers improved survival rates and is indicated when nodal metastasis is present. III. Co m p o s ite re s e c tio n (the ja w-ne c k o r c o m m a nd o p ro c e d ure ): most commonly used to resect large lesions o the oropharynx and involves a neck dissection and a partial mandibulectomy in conjunction with excision o the tumor (Fig. 18-3) and reconstruction (Fig. 18-4). A. racheotomy: routine treatment B. otal glossectomy: Occasionally, the larynx is spared a er in young and otherwise healthy patients. C. Laryngectomy: per ormed when either the tumor invades the pre-epiglottic space or the entire tongue base and both hypoglossal nerves are removed IV. Tra ns o ra l ro b o tic s urg e ry (TORS): now used at some centers or surgical resection o oropharyngeal tumors A. Reduced morbidity: due to ability to resect the tumor without splitting the mandible B. Decreased need or eeding tubes ollowing resection: demonstrated by some studies V. P ro g no s is : Related to the HPV status o the tumor; patients who have HPV tumors generally have a better prognosis than those who have HPV– tumors.

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Hypopharynx and Cervical Esophagus Cancer

Fig ure 18-4: Recons truction o a circum erential pharyngeal de ect with a jejunal ree gra t. The vas cular pedicle has been anas tomos ed to branches o the external carotid artery and internal jugular vein.

HYP OP HARYNX AND CERVICAL ESOP HAGUS CANCER Ove rvie w I. Ana to m y A. Boundaries: Hypopharynx extends rom the pharyngoepiglottic old to the in erior border o the cricoid area, excluding the larynx. B. Contents: includes the piri orm sinuses, the postcricoid area, and the posterior pharyngeal wall C. Lymphatic drainage: Hypopharynx has a rich lymphatic network. 1. Piri orm sinuses: drain to jugulocarotid and midjugular nodes 2. Posterior pharyngeal wall: drains primarily to retropharyngeal nodes 3. Lower hypopharyngeal areas: drain to paratracheal and low jugular nodes 4. Cervical esophagus: drained by mediastinal nodes II. Cla s s if c a tio n: Ninety-f ve percent o the tumors in this region are epithelial cancers; 60%–75% arise in the piri orm sinuses and 20%–25% on the posterior pharyngeal wall; tumors rarely arise in the postcricoid area. III. Etio lo g y: as with other head and neck tumors, related to heavy use o alcohol and tobacco

Clinic a l Eva lua tio n I. P re s e nting s ym p to m s : riad o throat pain, re erred otalgia, and dysphagia is present in more than 50% o patients. II. Ho a rs e ne s s a nd a irwa y o b s truc tio n: indicate laryngeal involvement III. Sm a ll p o s tc ric o id tum o rs : o en present with mild symptoms o sore throat, globus (a “lump in the throat”), and throat clearing IV. Ce rvic a l lym p h no d e m e ta s ta s e s : ound in 75% o patients with piri orm sinus cancers (41% occult) and in 83% o patients with pharyngeal wall tumors (66% occult) V. Dia g no s is : C scan o the neck with contrast and endoscopy with biopsy complete the workup.

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Tre a tm e nt a nd P ro g no s is I. Ad va nc e d le s io ns : Laryngopharyngectomy and radical neck dissection ollowed by radiotherapy are necessary or most. II. Sm a ll tum o rs tha t s p a re the a p e x o the p iri o rm s inus : Supraglottic laryngectomy can be considered. III. Sm a ll tum o rs : can be treated by radiation therapy alone or by surgical resection via a lateral pharyngotomy IV. Ce rvic a l e s o p ha g us c a nc e r: can require removal o the pharynx, esophagus, and larynx V. P ro g no s is : poor because o extensive submucosal spread and the high incidence o cervical metastasis A. Overall 5-year survival rate: 30% B. I eligible or supraglottic laryngectomy: Five-year survival rate rises to 50%. VI. Che m o the ra p y with ra d ia tio n the ra p y: in organ-sparing protocols

LARYNX CANCER Ove rvie w I. Ana to m y A. Divisions: three regions 1. Supraglottis: extends rom the tip o the epiglottis to include the alse vocal olds and roo o the ventricle 2. Glottis: extends rom the depth o the ventricle to 1 cm below the ree edge o the true vocal old 3. Subglottis: extends rom 1 cm below the ree edge o the true vocal old to the in erior border o the cricoid cartilage B. Lymphatic drainage 1. Supraglottis: rich network that crosses the midline and drains to the deep jugular nodes 2. Glottis: poorly developed sparse lymphatics 3. Subglottis: drains through the cricothyroid membrane to the prelaryngeal (delphian) and pretracheal nodes II. Etio lo g y: More than 90% o patients have a signif cant history o smoking, and heavy alcohol consumption is a common but not def nite etiologic actor. III. Cla s s if c a tio n A. Squamous cell carcinomas: account or 95%–98% o the tumors B. Verrucous carcinoma: variant o squamous cell carcinoma that is locally invasive but almost never metastasizes

Clinic a l Eva lua tio n I. P re s e nting s ym p to m s : Most common symptom is hoarseness. A. Other: Stridor, cough, hemoptysis, odynophagia, otalgia, dysphagia, and aspiration also occur. B. Neck masses: uncommon at the time o presentation II. Dia gnos is : All patients require direct laryngoscopy and biopsy; barium swallow, stroboscopic laryngoscopy, and C scan may be help ul.

Quic k Cut Glottic cancers are us ually diagnos ed relatively early compared to other cancers o the head and neck due to the pres enting s ymptom o hoars enes s .

Tre a tm e nt a nd P ro g no s is I. Ca rc ino m a in s itu: excision o the involved vocal old mucosa and close monitoring II. Ea rly-s ta ge le s ions : Many are treated with radiation because the resultant voice is usually o better quality than the one a er surgical excision (at least initially). However, surgery is still indicated or many patients. A. Removal o the involved vocal old: by traditional techniques or by carbon dioxide laser yields equivalent local control B. Hemilaryngectomy (vertical laryngectomy): or some glottic lesions that involve the anterior commissure because o the increased risk o cartilage involvement C. Limited surgical resection: or some small lesions o the tip o the epiglottis III. La rg e s up ra g lo ttic tum o rs : Supraglottic (horizontal) laryngectomy spares the true vocal olds but removes the epiglottis, aryepiglottic olds, and alse vocal olds.

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Skin Cancer

A

B

Fig ure 18-5: A: Total laryngectomy s pecimen ready or removal, attached only to the tongue bas e. B: Pharyngeal de ect ollowing total laryngectomy. Clos ure is us ually accomplis hed in layers in a T as hion.

IV. Tra ns g lo ttic tum o rs : For supraglottic tumors that spread to a true vocal old, a suprahemilaryngectomy may be considered. Neck dissection, radiation, or both are o en necessary. V. Ad va nc e d tum o rs : Usually require a total laryngectomy, o en combined with neck dissection (Fig. 18-5). Postoperative radiotherapy is usually indicated. VI. Ve rruc o us c a rc ino m a : Conservation laryngectomy, when possible. T ere is no need or elective neck dissection, and the use o radiotherapy is controversial. VII. Co nc urre nt c he m o ra d io the ra p y p ro to c o ls : achieve cure rates comparable to those or traditional combined surgical therapy and allow some patients to avoid total laryngectomy (Fig. 18-6) VIII. P ro g no s is : better than with cancer o other head and neck sites

SKIN CANCER Ba s a l a nd Sq ua m o us Ce ll Ca rc ino m a s I. Etiology: sunlight, radiation, arsenic, burns, scars, and genetic disorders (xeroderma pigmentosum, basal cell nevus syndrome, albinism) II. Clinic a l e va lua tio n: Usually present as slowly enlarging cutaneous or subcutaneous lesions; some lesions orm nonhealing ulcers. Nodal metastasis is uncommon.

Quic k Cut Skin cancer is the mos t common cancer in the United States , with more than 1 million new cas es diagnos ed each year and more than 10,000 deaths .

S ta ge s III a nd IV ca nce r (−)

(+) Comple te re s pons e or >70% pa rtia l re s pons e Cis pla tin/5-fluoroura cil che mothe ra py

S urge ry

Ra dia tion (−) S urge ry

(+) Obs e rve

Fig ure 18-6: Example o organ-s paring neoadjuvant chemotherapy protocol.

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III. Tre a tm e nt: T erapy includes electrodesiccation, curettage, Quic k Cut cryosurgery, excision, Mohs surgery, radiation, and topical Ba s a l c e ll uorouracil. c a rc inoma a c c ounts or A. Squamous cell carcinoma: Surgical excision is pre erred because 80% o s kin c a nc e rs , a nd it allows removal o a margin. s qua mous c e ll c a rc inoma B. Basal cell carcinomas: O the nasolabial olds, medial and lateral a c c ounts or 16% . canthi, or postauricular regions are especially aggressive. T ey can invade multiple tissue planes and, there ore, require an extensive surgical resection. C. Mohs surgery: involves the precise mapping and rozen-section control o the entire resection bed D. Radiation therapy: usually reserved or advanced lesions in areas where surgical excision leaves a cosmetically unacceptable de ect (e.g., the nose, eyelid, and lip) E. All positive nodes: should be treated with neck dissection or radiotherapy

Ma lig na nt Me la no m a I. Ep id e m io lo g y: Accounts or 1% o all cancers; incidence is Quic k Cut increasing by 5%–7% each year. Twenty- ve percent II. Etio lo g y: Sun exposure and heredity play important roles. o all melanomas aris e in the III. P a tho lo g ic va ria nts : lentigo maligna melanoma, superf cial head and neck. spreading melanoma, and nodular melanoma IV. Sta g ing : depth o primary lesion, see part VII Chapter Cuts and Caveats Quic k Cut When des cribing V. Tre a tm e nt: wide excision with treatment o nodal basins or s kin les ions concerning or deeper melanomas melanoma, us e the ABCD A. Sentinel node biopsy: or intermediate depth o invasion to s ys tem: a s ymmetry, b order assess or nodal disease irregularity, c olor (uneven color pattern), and d iameter 1. Lymphoscintigraphy: Radiotracer is injected intradermally greater than 6 mm. around the melanoma lesion. Lymphatic imaging is then per ormed a er injection to conf rm appropriate uptake o the radiotracer. Quic k Cut 2. echnique: Blue dye and radiotracer are injected A s entinel node intradermally at the site o the lesion. T e dye is visible and is the rs t node involved a gamma probe is used to identi y radiotracer activity and an in lymphatic s pread o a incision is made in the area. malignancy. 3. Neck dissection: per ormed or positive nodes 4. Parotidectomy: added or lesions o the anterior scalp, eyelids, auricles, and cheeks because the f rst-level lymphatic drainage is to the periparotid nodes B. Radiation therapy: usually reserved or palliative treatment o recurrent disease C. Chemotherapy: used or disseminated melanoma VI. P ro g no s is : Survival rate is related to the tumor staging; the prognosis in patients with mucosal melanoma is extremely poor.

HEAD AND NECK LYMP HOMA Ove rvie w I. Ep id e m io lo g y: Eighty percent o all malignant lymphomas arise rom nodes, many o which are in the head and neck. A. Hodgkin lymphoma: Seventy percent o patients have cervical lymph node involvement. B. Extranodal presentation: rare in Hodgkin disease but occurs in 20% o patients with non-Hodgkin lymphoma II. Cla s s if c a tio n A. Non-Hodgkin lymphoma: really a group o diseases, which are classif ed into avorable and un avorable types on the basis o therapeutic response B. Hodgkin lymphoma: Histology in uences the prognosis.

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Parotid Gland

Clinic a l Eva lua tio n I. P re s e nting s ym p to m s : Usually a single, enlarged cervical node; most lymphomatous nodes are f rm and rubbery. A. Non-Hodgkin lymphoma: typically presents in upper cervical nodes B. Hodgkin disease: discovered in nodes throughout the cervical chain C. Sites o extranodal involvement in non-Hodgkin lymphoma: Head and neck, particularly in Waldeyer tonsillar ring. Other sites include the nasal cavity, paranasal sinuses, orbit, and salivary glands. D. Systemic symptoms: Approximately 40% o patients with Hodgkin lymphoma have ever, sweats, weight loss, and malaise. II. Dia g no s is : Usually made by excisional biopsy o a lymph node; one o the largest nodes should be removed in its entirety. A. FNA o the lymph node and endoscopy: should be per ormed to rule out squamous cell carcinoma B. I a possible extranodal source has been discovered: Biopsy f rst. C. Frozen-section diagnosis: o little value except to exclude squamous cell carcinoma D. Additional workup aids in staging: Chest radiograph, C scan o the abdomen, and bone marrow biopsy are recommended.

Tre a tm e nt a nd P ro g no s is I. Tre a tm e nt: Combination o chemotherapy agents and radiation therapy are used depending on the stage and pathology.

Quic k Cut Treatment or lymphoma is generally not s urgical.

II. P ro g no s is A. Hodgkin disease: Favorable prognostic actors include localized disease, limited number o anatomic sites, absence o massive disease, and a avorable histology. B. Survival rates: Patients with limited disease have 5-year, relapse- ree rates o 80%–90%; the rate alls to 60%–80% in patients with advanced disease treated with combined therapy; and rates as low as 30% occur in advanced disease. C. Non-Hodgkin lymphoma survival: Radiation therapy or limited disease yields 50%–70% cure rates. 1. With more advanced lesions: Patients with a avorable histology can have a 60%–70% 5-year survival rate and a 30% cure rate. 2. Patients with an un avorable histology: ace a 24%–40% 5-year survival rate with little chance or a cure

UNUSUAL TUMORS Ca ro tid Bo d y Tum o rs I. Cha ra c te ris tic s : Usually present as slow-growing, painless neck masses; 3% are bilateral (increasing to 26% in patients with a amilial tendency or paragangliomas). T e mass may be pulsatile and may have a bruit. II. La rg e tum o rs : can cause dysphagia, airway obstruction, and CN palsies III. Dia g no s is : Angiography shows a tumor blush at the carotid bi urcation that splays the internal and external carotids. IV. Tre a tm e nt: Surgical excision; large tumors may require carotid bypass.

PAROTID GLAND Ove rvie w I. Em b ryo lo g y: Largest o the salivary glands; average gland weighs 25 g. It appears in the ourth week o gestation and originates rom the epithelium o the oropharynx. II. Ana to m y: Covers the masseter muscle, extends beyond the vertical ramus o the mandible, and abuts the external auditory meatus. A. Fascial sheath: Encloses the gland; the tightness o this ascia is responsible or the severe pain that accompanies acute swelling o the gland (acute parotitis). B. Lobes: Classically, the parotid gland was thought to have two lobes, superf cial and deep, which is use ul when discussing the surgical treatment o parotid disease.

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Te mpora l bra nch

Zygoma tic bra nche s

P a rotid gla nd

Ma in trunk of fa cia l ne rve e me rging from s tyloma s toid fora me n Bucca l bra nche s Ma rgina l ma ndibula r bra nch

Ce rvica l bra nch

Fig ure 18-7: Facial nerve branches pas s through the parotid gland.

III. Ste ns e n d uc t: Drains saliva; this duct exits anteriorly, pierces the buccinator muscle, and enters the oral cavity opposite the second upper molar. T e opening is marked by the parotid papilla, which may be elt by the tongue or a f nger. IV. Inne rva tio n (Fig . 18-7): Facial nerve enters the posterior part o the gland immediately a er emerging rom the stylomastoid oramen. A. Divisions (two): Facial nerve divides within the substance o the Quic k Cut gland into two parts (zygomatico acial and cervico acial) at the Generations o pes anserinus or goose’s oot. s tudents have us ed the B. Major branches (f ve): temporal, zygomatic, buccal, mandibular, mnemonic “To Zanzibar By Motor Car” to remember the and cervical branches o the acial nerve. C. Facial nerve and its branches: separate the superf cial and deep portions o the gland (Fig. 18-8) D. Muscles o expression: supplied by the acial nerve on the ipsilateral side o the ace Zygoma ticofa cia l divis ion of fa cia l ne rve

S upe rficia l lobe

De e p lobe Is thmus

Ce rvicofa cia l divis ion of fa cia l ne rve

Fig ure 18-8: Frontal cros s s ection o the parotid gland.

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Parotid Neoplasms

EVALUATION AND MANAGEMENT OF PAROTID MASSES Ove rvie w I. His to ry a nd p hys ic a l e xa m ina tio n: can o en di erentiate among benign, malignant, and in ammatory processes A. Slowly enlarging, distinct mass: can be a benign or malignant neoplasm B. Malignancy: Rapidly enlarging, f rm distinct masses associated with f rm, ipsilateral adenopathy, and masses associated with pain or acial nerve paralysis usually indicate a malignancy. C. In ammatory process: acute, pain ul swelling in one or both glands, associated with ever or systemic symptoms D. Sialadenitis: Intermittent pain and swelling in the gland; a stone may occasionally be palpable on intraoral examination. E. Parotid mass: Metastatic disease in a parotid lymph node (drainage rom the upper two thirds o the ace and the anterior scalp) may present as a mass. II. Dia g no s tic s tud ie s : may provide in ormation that dictates the extent o surgery required, thus permitting better counseling o the patient preoperatively A. Radiologic studies 1. MRI: Can establish i superf cial or deep lobes are involved, Quic k Cut MRI with and suspicious lymphadenopathy, or acial nerve invasion. It may without contras t is generally also help to di erentiate individual histologic lesions. the imaging s tudy o choice 2. C scans: discern many o the same structural details but are when examining parotid not nearly as success ul in di erentiating histologic lesions les ions . B. Invasive tests 1. FNA: provides tissue diagnosis 2. Core-needle biopsy or open biopsy: carries the risk o spreading tumor cells and generally is not indicated

Surg ic a l Ma na g e m e nt I. Be nig n le s io ns : Because most masses are ound in the larger, superf cial lobe, superf cial parotidectomy is usually su cient, but complete excision is required. “Shelling out” a mass o en leads to recurrence. II. Ma lig na nt le s io ns : I the lesion is small, low grade, and completely conf ned to the superf cial lobe, then resection o only that lobe may be su cient. Otherwise, total parotidectomy should be per ormed. A. Facial nerve: Should be sacrif ced i it is involved. Nerve gra ing allows restoration o some unction in 6–12 months. B. Neck dissection: indicated or high-grade lesions C. Postoperative radiation therapy: may be used or un avorable high-grade lesions or in cases where a limited dissection was per ormed

PAROTID NEOP LASMS Be nig n I. Ge ne ra l: Eighty percent o parotid tumors are benign. T e most common presenting eature o these tumors is a painless mass, Quic k Cut and acial paralysis is rare. Very care ul identif cation and surgical Be highly s us picious treatment, which consists o excision that includes a margin o or malignancy i there is a parotid mas s and the patient normal gland, are required. has acial weaknes s . II. P le o m o rp hic a d e no m a s (m ixe d tum o rs ): So named because they contain both stromal and epithelial components; they are the most common benign salivary tumors (60% o all parotid tumors and are slow growing but may be quite large at the time o presentation). III. P a p illa ry a d e no c ys to m a (c ys ta d e no m a ) lym p ho m a to s um (Wa rthin tum o rs ): consist o both epithelial and lymphoid elements A. Presentation: T ey are so (cystic) when palpated and contain mucoid material that may appear purulent. T ey are neoplastic and nonin ammatory.

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B. Incidence: ound in men f ve times as requently as in women Quic k Cut and usually occurs in people ages 40–60 years Ten percent rule C. Etiology: associated with cigarette smoking or Warthin tumors : 10% III. Be nig n lym p ho e p ithe lia l tum o r (Go d win tum o r): are bilateral and 10% are multicentric. Characterized by slowly progressive lymphoid inf ltration o the gland; care must be taken not to con use this lesion with a lymphoma. It is associated with HIV. IV. Oxyp hil a d e no m a s : consist o acidophilic cells called oncocytes, occur most requently in elderly patients, grow slowly, and do not usually grow larger than 5 cm V. Mis c e lla ne o us le s io ns : For example, hemangiomas and lymphangiomas also occur. Hemangiomas that do not regress are treated by resection.

Ma lig na nt I. Muc o e p id e rm o id c a rc ino m a : Arises rom the ducts o the Quic k Cut gland. It is the most common parotid malignancy and constitutes Malignant tumors 9% o all parotid tumors. cons titute 20% o all parotid A. ypes neoplas ms . They are o ten 1. Low-grade tumors: more common orm and are the tumors characterized by pain and seen most requently during childhood acial nerve paralys is . a. Presentation: T ey generally eel so when palpated and appear encapsulated at surgery. b. reatment: excision, with preservation o acial nerve branches that are not directly involved by the lesion c. Prognosis: When treated properly, 5-year survival rate is 95%. 2. High-grade tumors: extremely aggressive, unencapsulated tumors that invade the gland widely a. reatment: otal parotidectomy plus neck dissection (even without palpable nodes); surgery is usually supplemented by postoperative radiation. b. Prognosis: Five-year survival rate is 42% with optimal treatment. II. Ma lig na nt m ixe d tum o rs (c a rc ino m a e x p le o m o rp hic a d e no m a , c a rc ino s a rc o m a ): Second most common type o malignancy and responsible or 8% o all parotid tumors. T e treatment is total parotidectomy; a neck dissection is also done or either palpable adenopathy or a high-grade tumor. III. Sq ua m o us c e ll c a rc ino m a : Rare in the parotid gland; it is important to di erentiate this lesion rom a metastasis arising rom a primary tumor elsewhere in the head and neck such as a skin cancer. A. Presentation: hard on palpation and accompanied by pain and nerve paralysis B. Prognosis: Five-year survival rate is 20%. IV. Othe r le s io ns : include adenoid cystic carcinoma (cylindroma), acinic cell adenocarcinoma, and adenocarcinoma A. reatment: otal parotidectomy; neck dissection is added when obvious nodal disease is present. B. High-grade, recurrent, and inoperable tumors: treated with radiation V. Ma lig na nt lym p ho m a : May arise as a primary tumor in the gland. T e treatment is the same as or other lymphomas.

PAROTID TRAUMA La c e ra tio ns a nd Fo re ig n Bo d ie s I. P a re nc hym a l d a m a g e : usually heals spontaneously i Stensen’s duct is not injured II. Ste ns e n d uc t: the conduit or saliva rom the parotid to the mouth, near the upper second molar. I lacerated or transected, it should be repaired over a small catheter, which will remain in place until the duct heals. III. Fa c ia l ne rve injurie s : May recover spontaneously i only an anterior aspect o a distal branch is injured. I a main trunk is injured, it requires repair by primary anastomosis or nerve gra ing. IV. Fo re ig n b o d ie s (e .g ., b ulle ts ): should be removed

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In ammatory Disorders

INFLAMMATORY DISORDERS Ac ute Sup p ura tive P a ro titis I. Etio lo g y: usually ound in patients who are debilitated and dehydrated and who have poor oral hygiene II. Ca us a l o rg a nis m : usually Staphylococcus aureus, which most likely enters the gland rom the mouth via Stensen duct A. Dehydration: Patient whose salivary glands are not secreting actively is susceptible to rapid growth o the organism in this avorable environment. B. Bacterial proli eration: leads to an intense in ammatory reaction in the gland, with edema and severe pain III. Initia l tre a tm e nt: includes hydration, antibiotics, and measures to promote salivation, such as occasionally sucking on a lemon A. Cultures: taken rom Stensen duct B. Antibiotics: initially directed against S. aureus and are later adjusted as indicated by the results o the cultures IV. Surg ic a l d ra ina g e : required i the process is not arrested by the preceding measures

Ca lc ulo us Sia la d e nitis I. Ove rvie w: Condition caused by stones in the salivary ducts. I obstruction o the duct occurs, in ammation and intermittent pain ul swelling o the gland ollow. II. Dia g no s is : Radiographs may show the stones. In the parotid gland, only 60% o stones are radiopaque. III. Surg e ry: should be postponed i there is an acute in ection present A. Location: When the stone is near the end o the duct, it can be removed transorally; i it is deep in the gland, it can be removed by an external incision. B. Multiple stones and pain recurrence: Remove the entire gland. C. Sialoendoscopy (endoscopy o the ducts o the salivary glands): has become an increasingly common way to diagnose and treat non-neoplastic disorders o the salivary gland, including calculi, strictures, and intraductal masses IV. Va ria nts : Sialadenitis can occur without stones. I symptoms persist, surgery may be necessary to remove the gland.

Chapter 19

Bariatric Surgery Mark D. Kligman

BACKGROUND Ob e s ity

Quic k Cut I. Cla s s if c a tio n a nd c o m o rb id ity Obes ity A. able 19-1: classif es obesity comorbidities have broad B. able 19-2: shows the risk o obesity-related comorbidities rising e ects on both the a ected with increasing body mass index (BMI) individual and s ociety by limiting daily unction, II. P re va le nc e reducing li e expectancy, and A. Incidence: In the United States, obesity a ects 35% o adults; increas ing health care cos ts . 17% o children and adolescents (ages 2–19 years) are also a ected. B. Demographics 1. Ethnicity: Prevalence o obesity is increased in A rican Americans and Hispanics. 2. Socioeconomics: Poverty and poor education are also associated with an increased risk o obesity.

P a tie nt Se le c tio n I. Ge ne ra l c rite ria : Patients must demonstrate the ollowing to quali y or bariatric surgery. A. BMI: greater than 40 kg/m 2 or BMI 35–39.9 kg/m 2 with a signif cant obesity-related comorbidity B. Nonsurgical weight management programs: documented ailure C. Surgical: acceptable operative risk and adequate mental capacity to actively participate in pre- and postoperative care D. Other: absence o current alcohol or illicit drug abuse and o poorly controlled psychosis or depression

Quic k Cut Bariatric s urgery is indicated i BMI exceeds 40kg/m2, or i the BMI 35 and there are medical complications o obes ity

Ta b le 19-1: Cla s s if c a tio n o Ob e s ity Bo d y Ma s s Ind e x (BMI) Ris k o Ob e s ity-Re la te d (kg /m 2 ) Co m o rb id ity Underweight

18.5

Low

Normal

18.5–24.9

Average

Overweight

25.0–29.9

Mild

Class I obesity

30.0–34.9

Moderate

Class II obesity

35.0–39.9

Severe

Class III obesity

40

Very severe

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Ta b le 19-2: Ob e s ity-Re la te d Dis o rd e rs Ca rd io va s c ula r Coronary artery disease Congestive heart ailure Hypertension Dyslipidemia Venous stasis disease P ulm o na ry Obstructive sleep apnea Obesity hypoventilation syndrome Asthma End o c rine Insulin resistance Type 2 diabetes mellitus Polycystic ovarian syndrome Ga s tro inte s tina l Gastroesophageal ref ux disease Nonalcoholic atty liver disease Gallstones

Mus c ulo s ke le ta l Osteoarthritis Ge nito urina ry Stress urinary incontinence Gyne c o lo g ic In ertility He m a to p o ie tic Deep venous thrombosis Pulmonary embolism Ne uro lo g ic Pseudotumor cerebri Stroke

II. Sp e c ia l p o p ula tio ns A. Adolescent patients: Bariatric surgery has been demonstrated to be both sa e and e ective in adolescents. 1. Surgery is currently reserved or high-BMI patients (typically, BMI 50 kg/m 2) with major comorbidities (e.g., diabetes mellitus [DM], obstructive sleep apnea). 2. Patients must reach bone maturity prior to surgery to avoid growth retardation. 3. Family counseling is thought to improve compliance and is mandatory in most programs. B. Elderly patients: Care ul consideration o the current health status and desired goals/results must be undertaken in patients Quic k Cut age older than 65 years. Bariatric s urgery C. Class I obesity: Early data is very promising or extending the may improve diabetes , even indications or bariatric surgery to class I obesity (especially when per ormed in patients or DM treatment), but the practice is not yet considered the with normal BMI. standard o care. III. P a tie nt e va lua tio n: done by a multidisciplinary team that typically includes nutritionists, mental health pro essionals, and exercise physiologists A. Medical subspecialists (most commonly endocrinology, cardiology, or pulmonary medicine): Consultation is based on specif c patient needs. B. Studies: Laboratory testing, radiologic evaluation, endoscopy, cardiac evaluation, and other studies are also based on specif c needs.

SURGICAL TREATMENT OF OBESITY Ba ria tric Op e ra tio n Cla s s if c a tio n Sys te m I. Re s tric tive o p e ra tio ns : procedures that limit oral intake A. Adjustable gastric banding (Fig. 19-1): Proprietary silastic band is placed around the stomach just below the gastroesophageal junction (GEJ), orming the outlet o a small gastric pouch. 1. Mechanism: Balloon attached to the band’s inner sur ace is connected via tubing to a subcutaneous port; when sterile water is injected into the port, the balloon in ates, which narrows the outlet and thus limits ood intake. 2. Advantage: T is operation is easily reversed.

Quic k Cut Bariatric operations are categorized as res trictive, malabs orptive, or both.

Quic k Cut There is a hormonal component to weight management, which is poorly unders tood. The bes t s tudied o thes e hormones is ghrelin.

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Ga s tric pouch Adjus ta ble ga s tric ba nd

S toma ch P ort

Fig ure 19-1: Adjus table gas tric band.

B. Sleeve gastrectomy (Fig. 19-2): creates a narrow tube rom the lesser curvature o the stomach by resection o the greater curvature o the gastric body and undus 1. Mechanism: Sleeve reduces ood intake by impeding its transit through the stomach. 2. Disadvantage: T is procedure is not reversible. II. Ma la b s o rp tive o p e ra tio ns : procedures that limit nutrient absorption A. Biliopancreatic diversion (Fig. 19-3): eatures a 200–500-mL gastric pouch created rom the proximal stomach by resection o the gastric antrum and distal gastric body 1. Mechanism: T e small intestine is divided 200–300 cm proximal to the ileocecal valve to orm the alimentary limb (a combination o the Roux limb and common channel), which is used to drain the gastric pouch. T e biliopancreatic limb is composed o the remaining small intestine and is anastomosed to the alimentary limb 50–150 cm proximal to the ileocecal valve, providing drainage or hepatic Quic k Cut and pancreatic secretions. Roux-en-Y gas tric 2. Complication: commonly causes dumping syndrome bypas s is the s tandard weight B. Biliopancreatic diversion with duodenal switch (Fig. 19-4): los s operation, as it balances Gastric sleeve is used as the gastric pouch, thereby preserving e ective weight los s and ris k the pylorus and eliminating the risk o dumping syndrome as a o complications . complication.

Ga s tric s le e ve

Fig ure 19-2: Sleeve gas trectomy.

Re move d portion of s toma ch

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Re s e cte d s toma ch Ga s tric pouch (200–500 mL)

Roux limb (150–250 cm) Biliopa ncre a tic limb

Common cha nne l (50–100 cm)

Fig ure 19-3: Biliopancreatic divers ion.

III. Co m b ine d re s tric tio n a nd m a la b s o rp tio n (Fig . 19-5): Gastric bypass is essentially a restrictive operation with limited malabsorption in which the volume o the gastric pouch is reduced to 15–30 mL, and the size o the pouch outlet is also limited. A. Mechanism: Alimentary limb is ormed rom the entire small intestine except or the 40–75 cm required to provide drainage or hepatic and pancreatic secretions. B. Advantages: Compared to malabsorptive operations, gastric bypass has similar weight loss with ewer nutritional complications.

P o s to p e ra tive Co ns id e ra tio ns

Quic k Cut Bariatric s urgery may be per ormed by laparos copic or open techniques . Laparos copic gas tric bypas s reduces abdominal wall complications (wound in ections and hernias ) at the expens e o increas ed ris k o perioperative GI hemorrhage, anas tomotic s tricture, and bowel obs truction.

I. Vita m in a nd m ine ra l s up p le m e nta tio n: Begins preoperatively and continues li elong. Supplements commonly include multivitamins, vitamin B12, vitamin D, calcium, and iron. II. Me d ic a l o llo w-up : necessary to adjust medications and to assess nutritional status A. Frequency: at least our times in the f rst postoperative year and annually therea er B. Gastric band patients: additionally assessed or weight loss rate and the band is adjusted as appropriate III. Multid is c ip lina ry o llo w-up : includes nutritional, exercise, and mental health counseling and educates patients or optimal results

Ga s tric pouch (100–200 mL)

Re s e cte d s toma ch

Roux limb (150–250 cm) Biliopa ncre a tic limb Common cha nne l (50–100 cm)

Fig ure 19-4: Biliopancreatic divers ion with duodenal s witch.

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Es opha gus

Ga s tric pouch (15–30 mL)

Bypa s s e d portion of s toma ch

Roux limb (75–150 cm)

Biliopa ncre a tic limb (40–75 cm)

Common cha nne l

Fig ure 19-5: Roux-en-Y gas tric bypas s .

Outc o m e s I. We ig ht lo s s : usually reported as percentage o excess weight loss (EWL) A. EWL: calculated as (current weight ideal body weight)/ Quic k Cut (preoperative weight ideal body weight) 100% Procedures can be compared by the EWL marker. B. Average weight loss: in uenced by the choice o operation 1. Adjustable gastric band: 40%–50% 2. Sleeve gastrectomy: 50%–65% 3. Biliopancreatic diversion (with or without duodenal switch): 65%–75% 4. Gastric bypass: 60%–75% II. Co m o rb id itie s (s e e Ta b le 19-2): improve or enter remission in Quic k Cut 60%–95% o those a ected and is directly related to percentage o In the s everely EWL obes e, weight los s by any III. Surviva l: Bariatric surgery reduces the overall 10-year risk o death means , including s urgical, will improve s urvival. rom disease by 50%.

P OSTOP ERATIVE MORTALITY AND COMP LICATIONS Mo rta lity I. Ra te : Overall mortality rate is 0.2%. II. Ris k: varies by type o operation (malabsorptive combined restrictive) III. Ca us e s : Most common are sepsis, cardiac complications, and pulmonary embolism (PE).

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Co m p lic a tio ns

Quic k Cut I. Ga s tric b a nd ing Malabs orptive A. Early complications (within 30 days o surgery) operations have the highes t 1. T romboembolism mortality rates , res trictive a. Incidence: deep vein thrombosis and PE 0.15% or less, operations have the lowes t mortality rates , and combined much lower than or any other bariatric procedure operations have intermediate b. Diagnosis and treatment: as in non-obese patients mortality rates . c. Prevention: Pharmacologic perioperative prophylaxis is controversial given the rate o thromboembolic events; however, mechanical prophylaxis should be considered in all patients. 2. Per oration (o esophagus/stomach during band placement): rare Quic k Cut 3. Device-related complications: May occur at any time in Minor complications the patient’s postoperative course and commonly require are common with adjus table operative repair. Diagnosis and treatment is based on band s urgery. the specif c type o complication. T e more commonly occurring device-related complications include the ollowing. a. Band penetration (into the gastric lumen): may present as epigastric pain, port site in ection, loss o restriction, or (rarely) GI hemorrhage (1) Diagnosis: established by upper endoscopy, upper GI series, or by abdominal computed tomography (C ) scan (2) reatment: initially involves antibiotic therapy and band removal b. Band slip (band displacement more distally on to the stomach): may present with vomiting due to pouch outlet distortion (1) Diagnosis: conf rmed using plain abdominal f lms, upper GI series, or abdominal C scan (2) reatment: initially involves uid removal rom the band to relieve symptoms, ollowed by surgical revision o the band c. Port in ection: may be caused by direct contamination during band f lls or, secondarily, due to band penetration (1) Evaluation: Abdominal C scan and upper endoscopy are required to rule out band penetration. (2) reatment: initially involves antibiotic therapy and port removal (a) T e band and its tubing are le in the peritoneal cavity, and the skin overlying the port is le to heal secondarily. (b) T e tubing is later retrieved and connected to a new port, completing band salvage. B. Late complications (more than 30 days a er surgery) 1. Device-related complications: (see above) 2. Nutritional def ciencies: rare II. Sle e ve g a s tre c to m y A. Early complications (within 30 days o surgery) 1. Bleeding a. Incidence: less than 1% b. Site: Bleeding can be intraluminal rom the staple line or rom an intraperitoneal source. c. Diagnosis (1) History: Intraluminal bleeding o en presents with hematemesis. (2) Physical examination: O en unremarkable; however, signif cant bleeding can cause hemorrhagic shock. d. reatment (1) Initial therapy: may include resuscitation with uids and blood products and hemodynamic and urinary output monitoring (2) Def nitive treatment (a) Intraluminal bleeding: Controlled using endoscopic techniques; surgical exploration is reserved or ailed endoscopic therapy. (b) Intraperitoneal bleeding: requires surgical exploration to control hemorrhage site

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2. Staple line leak a. Incidence: less than 3% b. Etiology: Most leaks occur near the GEJ and may be associated with partial obstruction in the more distal sleeve. c. Diagnosis Quic k Cut (1) Physical examination (abdominal): Unreliable; The mos t common peritonitis is a late f nding. pres enting s igns o leak a ter bariatric s urgery are thos e o (2) Abdominal C : best diagnostic modality or stable early s eps is —tachycardia and patients tachypnea. (3) Surgical exploration: def nitive diagnostic tool and mandatory or di use peritonitis d. reatment: uid resuscitation, broad-spectrum antibiotics, and nutritional support (1) Wide peritoneal drainage o the leak site: surgically or percutaneously with image guidance; f rst-line treatment (2) Direct repair o the leak site: occasionally success ul Quic k Cut and used in conjunction with wide drainage Direct s uture repair (3) Endoscopic techniques: used to seal leaks, typically in o a GI leak may s ound conjunction with drainage appealing, but the s utures will not hold in the s etting o B. Late complications (more than 30 days a er surgery) peritonitis and inf ammation. 1. Gastric sleeve stricture: rom postoperative scarring or a technical error in sleeve construction a. Incidence: 0.5% b. Clinical presentation: Most common symptoms are nausea and vomiting; typically, patients tolerate uids better than solids. c. Diagnosis (1) Physical examination: Usually unremarkable. Epigastric pain, i present, is mild. (2) Radiologic evaluation: abdominal C , upper GI series, and upper endoscopy d. reatment (1) Endoscopic stenting and surgical stricturoplasty: success ul in some cases (2) Conversion to gastric bypass: usually the best option III. Ga s tric b yp a s s A. Early complications (within 30 days o surgery) 1. Bleeding a. Incidence: 4% b. Site: can be intraluminal, rom an anastomosis or staple line, or intraperitoneal c. Diagnosis (1) History: Hematemesis, hematochezia, or melena suggests an intraluminal source. (2) Physical examination: O en unremarkable; however, signif cant bleeding can cause hemorrhagic shock. d. reatment (1) Initial therapy: may include resuscitation with uids and blood products and hemodynamic and urinary output monitoring (1) Def nitive treatment: determined by hemorrhage site (a) Intraluminal bleeding: O en controllable endoscopically; surgical exploration is reserved or ailed endoscopic therapy, endoscopically inaccessible bleeding sites, or or unstable patients. (b) Intraperitoneal bleeding: o en requires surgical Quic k Cut exploration to control hemorrhage site Anas tomotic leak 2. Anastomotic leak is the mos t eared early a. Incidence: less than 4% complication o bariatric s urgery. Reoperation may be b. Etiology: Most leaks occur 5–14 days rom surgery and are the bes t means o diagnos is . related to tissue ischemia; earlier leaks are usually due to technical error. c. Clinical presentation: Most common presenting signs are those o early sepsis—tachycardia and tachypnea—and patients may appear anxious.

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d. Diagnosis (1) Physical examination (abdominal): Unreliable; peritonitis is a late f nding. (2) Abdominal C : best diagnostic modality or stable patients (3) Surgical exploration: def nitive diagnostic tool and mandatory or di use peritonitis e. reatment: uid resuscitation, broad-spectrum antibiotics, and nutritional support (1) Uncontained leak: Surgical drainage is o en the only necessary intervention; direct repair (or resection) is rarely success ul. (2) Contained leaks: can o en be drained percutaneously under imaging guidance 2. Venous thromboembolism a. Incidence (o DV and PE): each less than 1% Quic k Cut b. Diagnosis and treatment: beyond chapter scope PE accounts or c. Prevention: Perioperative prophylaxis should ollow 50% o all pos toperative American College o Chest Physicians (ACCP) deaths ollowing gas tric recommendations or high-risk general surgery patients. bypas s . (1) Pharmacologic agents (un ractionated heparin or lowmolecular-weight heparin) may be combined with leg compression devices. (2) Prophylactic placement o in erior vena cava f lters is controversial. B. Late complications (more than 30 days a er surgery) 1. Dumping syndrome a. Incidence: Up to 85% o patients experience dumping syndrome at some point in their postoperative course. b. Etiology: usually related to poor ood choices, specif cally oods containing ref ned sugars (e.g., high- ructose corn syrup) or high- at concentrations (especially ried oods) c. Clinical presentation: ollows two patterns (1) Early dumping syndrome: ypically begins 20–30 minutes a er meals and is triggered by the rapid passage o ood with high osmolality into the small intestine. T e hypertonic intraluminal load induces a rapid shi o extracellular uid into the intestinal lumen, producing either GI symptoms (e.g., nausea and vomiting, epigastric ullness, cramping abdominal pain, and diarrhea) or cardiovascular symptoms (e.g., ushing, dizziness, diaphoresis, palpitations, tachycardia, and syncope). (2) Late dumping syndrome: Begins 1–3 hours Quic k Cut a er meals and is triggered by rapid passage o Dumping s yndrome carbohydrates into the small intestine, which may occur a ter any produces a hyperglycemic spike. T e insulin gas trojejunos tomy. released in response is excessive in relation to the total carbohydrate load, subsequently causing hypoglycemia that leads to catecholamine release rom the adrenal gland. Symptoms include tremulousness, diaphoresis, light-headedness, tachycardia, and (rarely) con usion. d. Diagnosis: Care ul history is usually diagnostic. e. reatment (1) Avoid ref ned sugars and atty oods. (2) Somatostatin analogues or acarbose may be help ul or those patients with persistent symptoms o late dumping syndrome despite dietary changes. 2. Anastomotic stricture: occurs almost exclusively at the gastrojejunostomy and may be associated with marginal ulceration a. Incidence: 1%–15% b. Clinical presentation: ypically involves persistent nausea and vomiting; patients o en progressively limit their diet to oods that are able to traverse the stricture (i.e., so oods or liquids). c. Diagnosis (1) Physical examination: o en unremarkable (2) Upper endoscopy: best diagnostic tool d. reatment (1) Endoscopic balloon dilation: highly e ective in providing permanent symptomatic relie (2) Surgical revision: required rarely

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3. Marginal ulcers: occur near the gastrojejunostomy a. Etiology: Factors include increased acid secretion, Helicobacter pylori in ection, nonsteroidal anti-in ammatory drug (NSAID) use, and smoking. b. Incidence: 3%–10% c. Clinical presentation: most commonly epigastric pain associated with postprandial nausea and vomiting d. Diagnosis (1) Physical examination: Patients usually have ocal epigastric tenderness. (2) Upper endoscopy: best method or patients with the typical pain pattern (3) Upper GI series or abdominal C scan: sometimes use ul (4) H. pylori testing e. reatment (1) Uncomplicated ulcers: First-line treatment is medical therapy with cytoprotective agents (sucral ate), proton pump inhibitors, and antibiotics (i H. pylori present); patients should avoid NSAID use and smoking. (2) Nonhealing ulcers: surgical revision o the gastrojejunostomy . Complications: include upper GI hemorrhage and per oration 4. Internal hernia (Fig. 19-6): results rom small intestine trapped in mesenteric de ects created during gastric bypass construction a. Sites (three): Petersen space, transverse mesocolic, or small bowel mesenteric de ects are possible. b. Incidence: 3%–13% c. Clinical presentation: depends on hernia duration and severity (1) Most common symptom: abdominal pain (2) Intestinal obstruction at the hernia site: may produce nausea, vomiting, obstipation, and abdominal distension d. Diagnosis (1) Physical examination: Patients usually have periumbilical or le upper quadrant tenderness. Peritoneal f ndings or rank peritonitis suggest intestinal strangulation. (2) Radiologic evaluation: identif es 80% (a) Abdominal C : test o choice (b) Upper GI series: sometimes help ul (3) Surgical exploration: consider or patients with persistent unexplained abdominal pain despite thorough evaluation e. Di erential diagnosis: adhesive bowel obstruction . reatment: requires surgical exploration with reduction o herniated intestine, resection o nonviable intestine, and closure o all potential hernia sites

A

B

C

Fig ure 19-6: Sites or internal hernia ollowing gas tric bypas s include (A) the trans vers e mes ocolic de ect, (B) Peters en s pace, and (C ) the s mall bowel mes enteric de ect.

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5. Cholelithiasis a. Incidence: Symptomatic cholelithiasis occurs in up to 30% o patients within 3 years ollowing gastric bypass. b. Prevention: two approaches (1) All patients undergo prophylactic cholecystectomy (at the time o gastric bypass): eliminates the possibility o symptomatic gallbladder disease (2) Only patients with symptomatic cholelithiasis have cholecystectomy at the time o gastric bypass: All other patients receive a 6-month course o ursodiol (300 mg by mouth twice daily). T is approach reduces the incidence o subsequent symptomatic gallbladder disease to 2%. 6. Nutritional def ciencies: relatively uncommon in patients who are compliant with postoperative vitamin and mineral Quic k Cut supplementation Nutritional de ciencies are avoidable a. Vitamin B12 def ciency: due to both an overall reduction with routine tes ting and in intrinsic actor production and rom bypass o the site o s upplementation. vitamin B12 production within the stomach b. Calcium and iron def ciency: result rom bypass o the duodenum and proximal jejunum where divalent cations are most e ciently absorbed c. Fat-soluble vitamin def ciency (especially vitamins D and A): due to reduced at absorption in the jejunum and ileum d. Vitamin B1 def ciency (bariatric beriberi): although uncommon, can occur with prolonged episodes o Quic k Cut vomiting; may present with neuropsychiatric abnormalities Vitamin D de ciency (Wernicke encephalopathy) composed o con usion, ataxia, as a complication o gas tric ophthalmoplegia, nystagmus, and impaired short-term bypas s may caus e s econdary hyperparathyroidis m memory or with cardiac f ndings including peripheral edema, dyspnea with exertion, paroxysmal nocturnal dyspnea, and tachycardia IV. Bilio p a nc re a tic d ive rs io n with o r witho ut d uo d e na l s witc h: similar to gastric bypass complications

Chapter 20

Minimal Access Surgery Daniel Medina, Hugo Bonatti, and Stephen M. Kavic

HISTORY Te c hnic a l Ad va nc e s I. Ce lio s c o p y: Kelling was the f rst person to per orm peritoneal “celioscopy” in a canine model with a cystoscope and air insu ation in 1901. In 1910, Jacobaeus used the same technique in humans. II. Im a g e re s o lutio n: Fiberoptic light sources replaced incandescent lights in the 1960s, and the addition o digital cameras greatly improved resolution o images. More recent developments include highdef nition three-dimensional cameras and exible camera heads. III. Sta p ling a nd intra c o rp o re a l e ne rg y d e vic e d e ve lo p m e nt: Quic k Cut based on ultrasound and electricity; allow more e ective division o Minimal acces s tissue, hemostasis, and anastomoses s urgery is heavily technology dependent. IV. Ha nd p o rts : 5-cm incisions and a gelcap through which one hand can be passed while keeping the abdomen air-sealed V. Sing le a c c e s s s urg e ry: relies on a 3-cm incision and an occluding device with multiple ports through which all instruments can be introduced VI. Ro b o tic te c hno lo g y: Independently developed by the National Aeronautics and Space Administration and other institutions; the surgeon remotely and precisely operates various arms that hold modif ed laparoscopic instruments. VII. Hyb rid p ro c e d ure s : per ormed with cooperation o a minimal access surgeon and an interventionist, such as a radiologist or gastroenterologist VIII. Na tura l o rif c e a c c e s s s urg e ry: Instruments are introduced through the stomach, rectum, or vagina; reduces scars, but is not yet the standard o care or most procedures.

Op e ra tive Mile s to ne s

Quic k Cut

Currently, all s urgical I. La p a ro s c o p ic a p p e nd e c to m y: pioneered by Semm (1982); s ubs pecialties including improved diagnosis o pelvic pathology in emale patients. urology, orthopedics , II. La pa ros c opic c hole c ys te c tom y: First per ormed by Erich Muhe cardiothoracic, endocrine, (1985) in Germany, then by Dubois, Mouret, and Perrisat (1987) and trans plant employ minimal acces s approaches . in France. T e procedure was introduced and popularized in the United States by McKernan and Saye, and Reddick in the late 1980s. III. Othe r: By the early 1990s, the technical easibility o a laparoscopic approach was demonstrated or virtually all major abdominal surgical procedures.

GENERAL P RINCIP LES Di e re nc e s b e twe e n Minim a l Ac c e s s a nd Op e n Surg e ry I. Op e ra tive f e ld : Unlike open surgery in which the operative f eld is exposed through a lengthy skin incision, minimal access surgery depends on accessing a natural or created cavity through small incisions.

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II. Vis ua l c o ntro l: Operation is displayed on a video screen, which allows or magnif cation o structures but results in the loss o three dimensions. III. Ins trum e nts : In open surgery, tactile eedback is an essential part o operative control; in minimal access surgery, control is largely visual.

Quic k Cut Minimally invas ive s urgeons rely heavily on vis ual cues to replace the los s o tactile eedback.

Ad va nta g e s a nd Dis a d va nta g e s o Minim a l Ac c e s s Surg e ry I. Ad va nta g e s : include improved visualization o anatomy, less tissue trauma and physiologic stress, less postoperative pain, shorter hospital stay, earlier return to normal activity a er discharge, improved cosmetic result, and decreased perioperative complication rates (e.g., superf cial wound in ection, incisional hernia, and atelectasis) II. Dis a d va nta g e s : decreased tactile sensation, diminished depth perception, reduced degrees o reedom (instrument movement), di cult hemostasis, and resource intensive (cost and training) III. Co s t-e e c tive ne s s : Uncertain; minimal access procedures use expensive equipment and o en disposable supplies, which increases costs. However, this cost increase may be o set by a aster return to normal activity and ewer complications.

P a tie nt P re p a ra tio n I. P re o p e ra tive p re p a ra tio n: Essentially the same as or laparotomy; special attention is paid to the ollowing. A. Underlying medical problems B. Assessment o coagulation status C. Cardiopulmonary disease II. Ge ne ra l a ne s the s ia : employed in nearly all advanced minimal access procedures III. Intra o p e ra tive c o nd uc t: Field is draped widely in case an open exploration is necessary. Quic k Cut A. Antithromboembolic pumps: applied to the lower extremities Phys iologic changes with pneumoperitoneum to minimize the possibility o deep venous thrombosis (DV ) (elevated pres s ure and B. Appropriate anesthetic monitoring: necessary, especially enddecreas ed venous return) tidal CO2 monitoring may increas e the ris k o

Ge ne ra l Op e ra tive Te c hniq ue

pos toperative DVT.

I. Ro o m s e tup : Patient position, video monitor placement, location o the operating team, and equipment testing are critical. II. Es ta b lis hm e nt o intra -a b d o m ina l a c c e s s : Filtered CO2 is used because it is readily available, inexpensive, does not support combustion, and possesses a high di usion coe cient. CO2 is insu ated to a maximum pressure o 12–15 mm Hg in adults. A. Sa e, airtight entry into the peritoneal cavity: may be achieved by various techniques 1. Closed pneumoperitoneum method: Spring-loaded obturator needle (Veress needle) is inserted through the abdominal wall into the peritoneal cavity. a. Lef upper quadrant: sa e entry point b. Desired pressure: Once 12–15 mm Hg is achieved, transparent trocar with coupled camera is advanced under direct visualization through the abdominal wall. 2. Laparoscopic-assisted method: Specialized disposable transparent port is necessary. a. Laparoscope: placed in the operating port while it is advanced directly through the abdominal wall b. Gas: Once the laparoscope is inside, gas is insu ated through the operating port into the peritoneal cavity. 3. Open pneumoperitoneum method: A 2-cm incision is made, and the abdominal wall is dissected under direct vision. A Quic k Cut specialized operating port with a blunt obturator (Hasson Diagnos tic cannula) is inserted, and CO2 is insu ated. laparos copy is the f rs t B. Exploration: T orough visual inspection is made o the sur aces s tep a ter es tablis hment o (i.e., peritoneum, liver, omentum, stomach, and exposed bowel). pneumoperitoneum. T is overview may help to guide the placement o additional ports.

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C. Insertion o accessory operating ports: wo to six ports are necessary to accomplish most laparoscopic procedures. D. Hand-assisted laparoscopic surgery (HALS): also known as “handoscopy”; hybrid alternative to conventional laparoscopy 1. Technique: Small laparotomy incision (6–8 cm) is made, allowing the surgeon to introduce a hand into the abdomen during laparoscopy or exposure and dissection maneuvers. HALS requires a specialized gel device to provide an air-tight seal between the skin incision and the surgeon’s hand. 2. Advantages: restores tactile sensation; improves traction, dissection, and tissue exposure; improves control o bleeding; aids handling and extraction o large, bulky specimens 3. Disadvantages: requires an additional incision that increases surgical trauma; alters port placement and operative strategy; presence o surgeon’s hand minimizes ree space in abdomen

Re la tive Co ntra ind ic a tio ns I. Se ve re c a rd io p ulm o na ry d is e a s e : Increased abdominal Quic k Cut pressure associated with pneumoperitoneum decreases venous Critically ill patients return and worsens pulmonary compliance, potentially leading to and thos e with s ignif cant acidosis, hypotension, and dysrhythmias. comorbidities may be bes t s erved by open s urgery. II. Ge ne ra lize d p e rito nitis : usually best treated with laparotomy III. P rio r a b d o m ina l o p e ra tio ns a nd a d he s io ns : increase the technical di culty and potential danger o laparoscopy, especially at initial injury IV. Se ve re c o a g ulo p a thic s ta te s : Associated risk o hemorrhage is a contraindication or laparoscopy. V. Mo rb id ly o b e s e p a tie nts : Very thick abdominal wall can hinder operating port placement and movement o laparoscopic instruments. VI. Ute rine e nla rg e m e nt (d uring a d va nc e d p re g na nc y): may Quic k Cut preclude su cient intraperitoneal space to per orm laparoscopic The s econd trimes ter is the optimal procedures time or s urgery in pregnant VII. P o rta l hyp e rte ns io n: especially when associated with varices, patients . signif cantly increases the risk o hemorrhage

P hys io lo g ic Cha ng e s As s o c ia te d with P ne um o p e rito ne um I. Ca rb o n d io xid e : produces hypercarbia and acidosis, which quickly resolves II. Inc re a s e d intra -a b d o m ina l p re s s ure (s e c o nd a ry to p ne um o p e rito ne um ): Decreases venous return via compression o retroperitoneal veins, subsequently reducing cardiac output. Decreased venous return predisposes to stasis and DV . III. P ne um o p e rito ne um : may increase systemic vascular resistance and mean arterial pressure IV. Re s p ira to ry unc tio n: a ected by reduced pulmonary compliance (i.e., due to diaphragmatic elevation during pneumoperitoneum)

Co m p lic a tio ns

Quic k Cut

I. Ove ra ll m o rta lity a nd m o rb id ity ra te s : Generally similar to Minimal acces s s urgery has a decreas ed those observed in their corresponding open procedures. Surgical ris k o wound complications site in ections should not exceed 2% in “clean” surgical wounds. relative to open s urgery. II. Co m p lic a tio ns s p e c if c to la p a ro s c o p y: include the ollowing: A. Complications due to access: Abdominal wall vessels may be injured in 2% o cases. 1. Abdominal wall hernias: may occur through 10-mm or larger trocar sites, especially at the umbilicus 2. Organ injury: May occur, especially with adhesions. Placement o an orogastric tube and urinary catheter may reduce the risk o bowel or bladder per oration. B. Complications due to pneumoperitoneum: Pneumomediastinum, pneumothorax, or subcutaneous emphysema are usually the result o excessive insu ation pressures ( 20 mm Hg). 1. Decreased cardiac output and dysrhythmia: can occur due to compression o venous return or hypercarbic acidosis

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2. Postoperative shoulder sel -limited pain: Occurs in Quic k Cut 10%–20% o patients. It is re erred pain believed to be due to Pos toperative either stretching o the diaphragm by the pneumoperitoneum s houlder pain is re erred or direct irritation o the diaphragm by CO2. pain rom the diaphragmatic 3. Gas embolism: may occur due to direct placement o an nerves . insu ation needle into a vessel or CO2 ow directly into an open vessel exposed in dissection C. Complications rom instrumentation: Examples include thermal ( rom electrocautery) or mechanical injury occuring in 1% o cases. T ese complications almost always require reoperation and may be li e threatening i missed.

SELECTED LAPAROSCOP IC P ROCEDURES La p a ro s c o p ic Cho le c ys te c to m y I. Ind ic a tio ns : include biliary colic, symptomatic cholelithiasis, cholecystitis, biliary dyskinesia, or polyps II. Co ntra ind ic a tio ns A. Absolute contraindications: suspicion o malignancy; uncontrolled coagulopathy B. Relative contraindications: severe gallbladder in ammation (acute or chronic), hepatic cirrhosis, portal hypertension, and biliary f stula III. Co m p lic a tio ns A. Common bile duct injuries: occur more commonly ( 0.25%) with laparoscopy than with the open technique (0.1%); requires laparotomy and major biliary reconstruction (Fig. 20-1) B. Bile leak: bile may leak rom the gallbladder bed or cystic duct stump (latter most commonly due to a clip coming o the duct) 1. I suspected: Patient should undergo either an abdominal ultrasound or computed tomography (C ) scan. 2. I present: usually amenable to percutaneous drainage, typically ollowed by endoscopic retrograde cholangiopancreatography (ERCP) to diagnose and treat the leak C. Retained common bile duct stone: Occurs in 10% o patients with Quic k Cut common bile duct stones ound during cholecystectomy. ERCP is The convers ion rate usually diagnostic and therapeutic (e.g., sphincterotomy, stent, etc.). to open cholecys tectomy ranges rom 2% to 10% . IV. Sum m a ry: Laparoscopic cholecystectomy has been demonstrated to be sa e and cost-e ective when compared with open cholecystectomy and is the procedure o choice or most biliary disease.

Fig ure 20-1: The “critical view” o s a ety during laparos copic cholecys tectomy a ter dis s ection o the neck o the gallbladder away rom its bed. The cys tic duct is s een on the le t, and the cys tic artery is on the right. This dis s ection s hould prevent bile duct injuries during laparos copic cholecys tectomy. (From Yamada T, Alpers DH, Laine L, et al. Textbook of Gastroenterology, 4th ed. Philadelphia: Lippincott Williams & Wilkins ; 2003.)

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V. Intra o p e ra tive c ho la ng io g ra p hy (IOC): indicated or the detection o common bile duct stones and the identif cation o biliary anatomy

La p a ro s c o p ic Ap p e nd e c to m y I. Ind ic a tio ns : echnically possible in nearly all patients with suspected appendicitis, including many with per oration. It is also use ul when the diagnosis is uncertain or the patient is emale. II. Re la tive c o ntra ind ic a tio ns A. Appendiceal abscess: best treated by percutaneous drainage and appendectomy several weeks later or with open appendectomy and drainage B. Known or suspected appendiceal tumors III. Co m p lic a tio ns : Same as with open appendectomies; the conversion rate to the open technique ranges rom 3% to 10% and is usually caused by bleeding, abscesses, extensive abdominal contamination, di culty in localization, poor exposure, or appendiceal dissection. (Fig. 20-2) IV. Co ntro ve rs ie s a nd c o nc lus io ns : Laparoscopic appendectomy is sa e and e ective. A. Advantages: slightly shorter hospital stay, lower incidence o wound in ection, and less postoperative pain B. Disadvantages: More expensive and takes longer to per orm than open appendectomy. T e risk o postoperative intra-abdominal abscess also appears to be greater.

La p a ro s c o p ic Ing uina l–Fe m o ra l He rnia Re p a ir I. Ind ic a tio ns : Laparoscopic inguinal repair is used or reducible, recurrent, and bilateral hernias. II. Co ntra ind ic a tio ns A. Absolute: inability to tolerate general anesthesia; in arcted bowel in the hernia sac B. Relative: prior bladder or prostate surgery; hernia repair in children III. Te c hniq ue : can be per ormed rom an intraperitoneal or preperitoneal approach (Fig. 20-3) A. General anesthesia: Required; dissection in the peritoneal cavity increases the risk o bowel injury, adhesion ormation, and postoperative small bowel obstruction. B. Intraperitoneal procedure: can be per ormed with spinal or epidural anesthesia in some patients 1. Step 1: A er diagnostic laparoscopy, the peritoneum is incised above the level o the hernia sac. Blunt dissection is used to created peritoneal aps and to reduce the hernia sac rom the spermatic cord structures. 2. Step 2: Cooper’s ligament is identif ed and mesh secured with tacks. 3. Step 3:.T e peritoneum is closed over the mesh IV. Co m p lic a tio ns : Risk o recurrent hernia a er laparoscopic hernia repair is 1%–5% within the f rst 5 years o surgery. A. Genito emoral and lateral emoral cutaneous nerve injuries: can result in signif cant postoperative groin and thigh pain and are usually caused by inadvertent staple placement too close to the nerves B. Injury to bowel, bladder, or major blood vessels: Although rare, these injuries occur more commonly a er laparoscopic than open repair. V. Ad va nta g e s : earlier return to normal activity; less postoperative pain and numbness VI. Dis a d va nta g e s : longer operative times; higher risk o rare serious injuries (viscera and vessels)

Fig ure 20-2: Laparos copic appendectomy. The arrow points to the appendix. (From Shirkhoda A. Variants and Pitfalls in Body Imaging, 2nd ed. Philadelphia: Lippincott Williams & Wilkins ; 2010.)

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A

B

Figure 20-3: Inguinal canal anatomy as viewed during laparoscopic exploration o the peritoneal cavity. A: The normal anatomy o the inguinal region rom within the peritoneal cavity. Black arrow indicates the closed deep inguinal ring; white arrow, the in erior epigastric vessels. B: An indirect inguinal hernia. Curved black arrow indicates the mouth o the hernial sac; white arrow, the in erior epigastric vessels. (Courtesy o N.S. Adzick.)

La p a ro s c o p ic Ve ntra l He rnia Re p a ir I. Ind ic a tio ns : Any symptomatic abdominal wall ascial de ect, asymptomatic de ects, or “Swiss cheese” abdomen (Fig. 20-4). Commonly, abdominal wall hernias are ventral, incisional, periumbilical, or a combination thereo . II. Co ntra ind ic a tio ns A. Absolute: loss o abdominal domain B. Relative: Incarcerated incisional hernias, patients with cirrhosis or portal hypertension, and patients with a history o long-term peritoneal dialysis (may develop a thick, in ammatory peel in the abdomen). Hernias o the lateral abdominal wall and lumbar region are technically more di cult than anterior hernias. III. Te c hniq ue : Abdomen is usually entered laterally, away rom the hernia. A. Step 1: T ree operating ports are placed laterally on one or both sides o the hernia (additional hernia de ects are commonly seen during laparoscopy that were not appreciated on physical exam). B. Step 2: Size o the hernia de ect(s) is measured, and an appropriate-sized piece o prosthetic mesh is chosen (should be su ciently large to overlap the edges o the hernia de ect by 5 cm in all directions). C. Step 3: Mesh is placed over the de ect and is secured using sutures, tacks, or both.

Fig ure 20-4: Laparos copic umbilical hernia repair. The hernia de ects are eas ily vis ualized as “holes ” in the abdominal wall.

Chapter 20

IV. Co m p lic a tio ns A. Recurrent hernia: Initial data show 5%–10% recurrence rates at 1–2 years a er surgery. B. Seroma: At least 20% o patients develop a uid collection between the mesh and the skin that resolves spontaneously in most cases, although aspiration is occasionally necessary. C. Bowel or bladder injury: occurs in 2% o cases D. In ection: Wound in ection occurs in 1.5%–2% o patients; a ew cases require mesh removal.

Fund o p lic a tio n o r Ga s tro e s o p ha g e a l Re ux Dis e a s e

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Quic k Cut Laparos copic ventral hernia repair has a lower recurrence rates than open ventral hernia repair.

Quic k Cut Minimal acces s techniques can be applied to all oregut procedures , s uch as antire ux procedures per ormed either through the ches t or the abdomen.

I. Ind ic a tio ns : severe gastroesophageal re ux disease (GERD), characterized by the ollowing: A. Failure o medical therapy: with proton pump inhibitors B. Severe nonhealing esophagitis: despite aggressive medical therapy C. Complications o GERD: esophageal stricture, recurrent pneumonia or aspiration, and severe asthma III. Co ntra ind ic a tio ns A. Shortened esophagus: Severe, long-standing GERD causes f brosis and shortening o the esophagus. B. Prior laparoscopic undoplication: considered a relative contraindication IV. Te c hniq ue : All antire ux procedures have two common eatures—repair o a hiatal hernia, when present, and augmentation o lower esophageal sphincter pressure. A. Full (360 degrees) undoplication (Nissen): primarily used or patients with GERD (Fig. 20-5) It is important to assess esophageal motility with manometry or UGI prior to operation. B. Partial 270 degrees undoplication (Toupet): used in patients with poor esophageal motility V. Co m p lic a tio ns : Esophageal per oration ( 1%), pneumothorax or pneumomediastinum; splenic injury; complications all into two general categories. A. Mechanical ailure: results rom either dehiscence o the Quic k Cut suture line or, more commonly, herniation o an intact The s ymptom undoplication through the diaphragm into the chest complex o dys phagia (recurrent hiatal hernia) and poor gas tric emptying B. Fundoplication dys unction: Due to improper construction and is known as “gas bloat resulting in signif cant dysphagia. Vagal nerve injury may also s yndrome” or “pos t-Nis s en s yndrome.” result in poor gastric emptying. VI. Co ntro ve rs ie s a nd c o nc lus io ns : Laparoscopic undoplication is considered the procedure o choice in patients requiring surgical therapy or GERD.

Dia g no s tic La p a ro s c o p y I. Ind ic a tio ns : Used to diagnose abdominal or pelvic pathology. It is the f rst step in any advanced laparoscopic procedure, and may f nd unrecognized conditions. II. Othe r ind ic a tio ns A. Acute pelvic or lower abdominal pain: di erentiate acute appendicitis rom other problems (e.g., pelvic in ammatory disease, ovarian torsion, or hemorrhagic cyst o ovary) B. Tubal ectopic pregnancy: allopian tube excision or incision Quic k Cut with evacuation o the tubal pregnancy Diagnos tic laparos copy is particularly C. Ovarian torsion or in arction: reatment options include us e ul in pelvic dis eas e. detorsion or resection o the ovary. D. In ertility: invaluable in establishing some causes o in ertility, including adhesions, endometriosis, and tubal stricture E. Staging o gynecologic malignancy: Intra-abdominal disease can be staged with aortic and iliac lymph node sampling. F. Ovarian masses: di erentiate benign rom malignant ovarian lesions

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Fig ure 20-5: Nis s en undoplication.

La p a ro s c o p ic Sta g ing o Ma lig na nc y I. “Fo rm a l” s ta g ing p ro c e d ure s : Usually include exploration, lymph node sampling or dissection, liver biopsy, and other interventions as needed or the particular disease process, such as gastrointestinal cancers (esophagus, lung, stomach), genitourinary cancers (testicular, bladder, prostate), lymphoma, and gynecologic cancers. Results may guide treatment prior to def nitive surgery.

Quic k Cut Laparos copic s taging is being us ed with increas ing requency in a variety o di erent cancers .

II. Dire c te d s ta g ing to a s s e s s re s e c ta b ility with c ura tive inte nt: Such as or pancreatic cancer. T e abdomen is inspected or occult metastases not ound by imaging. III. Bio p s y: o specif c abnormalities detected on imaging studies or screening exams

Othe r La p a ro s c o p ic P ro c e d ure s I. La p a ro s c o p ic a d re na le c to m y: regarded as the procedure o choice or most patients with benign adrenal tumors under 10 cm diameter II. La p a ro s c o p ic s p le ne c to m y: ideal in patients without severe splenomegaly or uncorrectable coagulopathy (e.g., well-controlled idiopathic thrombocytopenic purpura [I P]) III. La p a ro s c o p ic live r re s e c tio n: All types o resection, rom wedge resection to true anatomic resection, have been reported. IV. La p a ro s c o p ic d o no r ne p hre c to m y: Considered the procedure o choice or harvest o renal allogra s in appropriate patients. Allogra unction rom laparoscopic donors is equivalent to that o kidneys rom open donors.

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V. La p a ro s c o p ic s urg e ry o r m o rb id o b e s ity: See Chapter 19. VI. La p a ro s c o p ic c o le c to m y: See Chapter 12.

ROBOTIC TECHNOLOGY His to ry a nd Ap p ro a c h I. His to ry: T e technology or robotic surgery was f rst implemented in the late 1980s. By the late 1990s, general surgery, gynecology, urology, and cardiothoracic surgery f elds were employing robotic surgery in major surgical centers. A. Procedures: Generally, procedures amenable to minimal access surgery (e.g., laparoscopy, thoracoscopy) may be per ormed robotically; a ew procedures, such as prostatectomy, may be best per ormed robotically. B. Robot types: During the past two decades, numerous types have been developed that rely on the remote control o the surgeon over the robotic arms, which hold the surgical instruments (Fig. 20-6). T is property o robotic surgery allows remote surgery where the surgeon and the patient are geographically separated. II. Ap p ro a c h: Placement o ports through which the robotic arms manipulate instruments is essentially the same as those o laparoscopic surgery.

Ad va nta g e s , Dis a d va nta g e s , a nd Co nc lus io ns I. Ad va nta g e s : relative to standard laparoscopic surgery, provides improved precision and recovery o three-dimensional vision, ambidexterity, and degrees o reedom II. Dis a d va nta g e s : lack o cost-e ectiveness, requires expensive machinery and a well-trained sta , steep learning curve or the surgeon, and lack o tactile eedback III. Co nc lus io ns : allows or the per ormance o complex procedures in experienced hands, or example, in cardiothoracic surgery (robotic coronary artery bypass), general surgery (Whipple procedure, transplant), bariatric surgery (gastric bypasses), orthopedics (joint surgery), neurosurgery (stereotactic procedures), gynecology (hysterectomy), and urology (prostatectomy)

A

B

Fig ure 20-6: DaVinci robot s ys tem. A: the cons ole. B: “the robot.” (From Ballantyne GH, Mares caux J , Giulianotti PC. Primer of Robotic and Telerobotic Surgery. Philadelphia: Lippincott Williams & Wilkins ; 2004.)

Chapter 21

Surgical Oncology Keli Turner, Natalie A. O’Neill, and Stephen M. Kavic

CANCER De f nitio ns I. Tum o r: abnormal mass o tissue II. Ne o p la s ia : new growth or the development o tumors

Quic k Cut Cancer is the general term or dis eas e caus ed by unregulated growth and s pread o cells .

III. Dys p la s ia : abnormal growth IV. Ma lig na nt: harm ul or having the tendency to displace normal unction V. Be nig n: does not tend to spread to other anatomic areas

Quic k Cut Malignant tumors inf ltrate and metas tas ize.

Gra d e I. Ove rvie w: umor grade is assessed on a microscopic level and represents how much divergence there is between normal cells and the cells o the tumor. A. Well-dif erentiated cells: similar in appearance to normal cells B. Poorly dif erentiated cells: do not resemble the normal cells

Quic k Cut Benign les ions can s till caus e s ignif cant s ymptoms : A ocal les ion near the brains tem may be atal.

II. P ro g no s is : umor grade can indicate prognosis.

Sub typ e s I. Ca rc ino m a : malignant tumor that arises rom epithelium A. Adenocarcinoma: arises rom epithelium and has a glandular component B. Squamous cell carcinoma: arises rom squamous epithelium and has keratinization or other characteristics peculiar to this cell

Quic k Cut In general, the les s di erentiated the tumor, the wors e the prognos is .

II. Sa rc o m a : arises rom mesodermal tissue (mesenchymal cells) III. Lym p ho m a : arises rom the cellular component o lymph nodes (LNs), typically B cells or

cells

CANCER ETIOLOGY AND EP IDEMIOLOGY Ge ne tic Ba s is I. Onc o g e ne s : genes that have the potential to cause cancer, usually by thwarting the normal process o apoptosis A. “Proto-oncogenes”: Become activated to orm oncogenes; mutation in only one gene is required or a gain o unction. B. ras: signal oncogene that encodes a signal transduction protein; commonly mutated in colon cancer

344

Quic k Cut Proto-oncogenes are expres s ed during cellular proli eration (embryonic development or the healing res pons e).

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C. HER-2/ neu : membrane receptor that codes or a protein similar to the receptor or epidermal growth actor; commonly mutated in breast and ovarian cancer D. C-myc: nuclear transcription actor; of en mutated in solid tumors II. Tum o r s up p re s s io n g e ne s : unction to suppress or regulate Quic k Cut cellular proli eration Los s o p53 is the A. Loss o unction: Mutation or deletion in both genes is required. s ingle mos t common genetic B. p53: best known o these genes de ect in human malignancy. III. DNA re pa ir ge ne s : Encode proteins that correct errors in replicated DNA. DNA mismatch repair mutations (MSH2 and MLH1) are associated with hereditary nonpolyposis colon cancer (HNPCC).

Ce llula r Me c ha nis m s

I. Ce ll c yc le : ightly regulated under normal conditions; cancer cells are Quic k Cut Oncogenes drive the characterized by a breakdown in normal regulation o proli eration. cell cycle; tumor s uppres s or II. Me ta s ta s is : may require additional elements, such as modi cation genes provide a natural o the extracellular matrix, altered expression o cellular adhesion checkpoint. molecules, and angiogenic actors III. Ad e no m a –c a rc ino m a s e q ue nc e : See Figure 21-1 IV. Co lo re c ta l c a nc e r: may develop as a result o a number o mutations A. Alterations in the APC gene: T is early change may permit adenoma ormation. B. Mutations in kRas: may lead to adenomatous polyps C. Further mutations in p53: may allow the ormation o Quic k Cut adenocarcinoma

Ca rc ino g e ns I. Che m ic a l A. Tobacco smoke: squamous cell carcinoma o the lung B. Asbestos: mesothelioma o the pleura II. P hys ic a l A. Neck irradiation: papillary thyroid cancer B. Ultraviolet (UV) light: basal cell skin carcinoma III. In e c tio n A. Epstein-Barr virus: Burkitt lymphoma B. Hepatitis B or C: hepatocellular carcinoma IV. Ge o g ra p hic /e p id e m io lo g ic A. Japan: gastric cancer B. China: esophageal cancer

Ep id e m io lo g y

Carcinogens are s ubs tances that are known to be caus ative agents in cancer development.

Quic k Cut No s ingle etiology caus es cancer: multiple actors lead to neoplas tic trans ormation.

Quic k Cut Prevalence is the overall proportion o cas es within a given population.

I. Inc id e nc e : Number o new cases o a particular disease that appear in a given time period. able 21-1 lists the top 10 cancers by Quic k Cut diagnosis. One in our II. Mo rta lity: Parallels cancer incidence but not directly—some Americans will develop s ome tumors are more aggressive biologically ( able 21-2). type o cancer. A. Men: Prostate cancer is the most common malignancy in men. B. Women: Breast cancer is the most common malignancy in women. C. Overall: Lung cancer is the most common cause o cancer death or both sexes. Ge ne a lte ra tion Ce ll type

Los s of AP C Norma l Hype rprolife ra tive e pithe lium e pithe lium

Activa tion Los s of a tumor Los s of p53 Othe r of Ra s s uppre s s or ge ne a ctivity a lte ra tions Ea rly Inte rme dia te La te Ca rcinoma Me ta s ta s is a de noma a de noma a de noma

Fig ure 21-1: The adenoma–carcinoma s equence or colon cancer. Multiple mutations are required to progres s rom normal epithelium to overt cancer. APC, adenomatous polypos is coli gene. (From Swans on TA, Kim SI, Glucks man MJ . BRS Biochemistry, Molecular Biology, and Genetics, 5th ed. Baltimore: Lippincott Williams & Wilkins ; 2009.)

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Ta b le 21-1: Inc id e nc e o Ca nc e r b y Site a nd Ge nd e r Ma le 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Prostate Lung Colon Bladder Melanoma Kidney Lymphoma Oral cavity Leukemia Liver

Fe m a le 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Breast Lung Colon Uterus Thyroid Lymphoma Melanoma Kidney Pancreas Leukemia

SCREENING AND DIAGNOSIS Ove rvie w I. Sc re e ning : Used when a disease process may be detected early enough in its course to allow or optimal management, which relies on a su ciently sensitive test as well as a disease process with signi cant prevalence or a given population. Although a detailed discussion o screening is beyond the scope o this chapter, the American Cancer Society (ACS) recommends screening or the ollowing processes. A. Colorectal cancer: Current guidelines recommend endoscopy (colonoscopy, sigmoidoscopy, or computed tomography [C ]–based virtual colonoscopy) or barium enema starting at age 50 years. Other screening tests may include ecal occult blood testing or stool DNA. B. Breast cancer: Current recommendation remains or annual mammography starting at age 40 years, combined with clinical breast exam every 3 years and routine surveillance with breast sel -examination. C. Cervical cancer: Starting at age 21 years, it is recommended that women have Pap smears every 3 years until age 30 years, then every 5 years in conjunction with a human papilloma virus (HPV) test until age 65 years. D. Prostate cancer: Men older than age 50 years are eligible or prostate-speci c antigen (PSA), but it is not routinely recommended or all men, as there is no proven survival bene t. Quic k Cut II. Dia g no s is : It may take years be ore a tumor is clinically detectable; A s ingle malignant symptoms may be a late appearance o malignancy. cell that undergoes 30 doublings res ults in 1 billion A. Mass ef ect: obstruction or impairment o an adjacent structure cells and a 1-cm diameter due to compression tumor. B. Bleeding: may be related to neovascularization and angiogenesis related to a tumor C. Systemic signs o malignancy: include ever, malaise, and cachexia

Ta b le 21-2: Ca nc e r Mo rta lity Ma le 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Lung Prostate Colon Pancreas Liver Leukemia Esophagus Bladder Lymphoma Kidney

Fe m a le 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Lung Breast Colon Pancreas Ovary Leukemia Uterus Lymphoma Liver Brain

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Ta b le 21-3: Co m m o n Tum o r Ma rke rs Ma rke r

Ma lig na nc y

Alpha- etoprotein

Germ cell tumors, hepatocellular carcinoma

Beta-human chorionic gonadotropin

Choriocarcinoma, testicular cancer

BCR-ABL gene

Chronic myeloid leukemia

CA 19-9

Pancreas, bile duct, stomach

CA 125

Ovarian

Calcitonin

Medullary thyroid

Carcinoembryonic antigen

Colorectal

Chromogranin A

Neuroendocrine tumors

Lactate dehydrogenase

Germ cell tumors

Prostate-specif c antigen

Prostate

Thyroglobulin

Thyroid

D. Tumor markers (Table 21-3): substances typically made by normal cells (but in lower quantities than in cancer cells) that are detectable on laboratory tests and indicate the presence o tumors or tumor-speci c products such as hormones or enzymes 1. Screening: umor markers may be used such as PSA or prostate cancer. 2. Disease recurrence: Some markers may be use ul in the early identi cation o recurrence, such as carcinoembryonic antigen (CEA) in colon cancer.

Im a g ing I. Cros s -s e c tiona l im a ging : Dominant role in the diagnosis and ollow-up o solid tumors. C and magnetic resonance imaging (MRI) both have applications or particular tumor types. Many tumors are initially diagnosed incidentally on imaging obtained or other purposes. II. Func tio na l im a g ing : Positron emission tomography (PE ) is a means o assessing the unctional status o metabolically active tissue. A. Complementary test: Although the images do not provide precise anatomic in ormation, PE describes regions o high metabolic activity, such as rapidly dividing cancer cells. B. Fluorodeoxyglucose (FDG): most commonly used tracer or PE scans C. Combination: PE may be combined with C to produce images at the same time in the same machine. Lesions less than 1 cm may not be easily visible on PE scans.

Quic k Cut Negative cros s s ectional imaging does not exclude a cancer diagnos is .

Quic k Cut PET s cans are mos t us e ul in detecting metas tas es in colorectal, breas t, lung, thyroid and germ cell cancers .

DIAGNOSTIC P ROCEDURES Bio p s y

Quic k Cut

FNA is the pre erred I. Fine -ne e dle a s p ira tion (FNA): Per ormed by pushing a smalltechnique or rapid diagnos is gauge needle, typically 20 gauge or smaller, into the lesion o interest o s uperf cial s olid les ions , and sending material contained in the lumen or analysis to determine s uch as thyroid nodules . the basic cell type. However, FNA cannot reliably diagnose invasive disease, as architecture may not be revealed on a small specimen. II. Co re -ne e d le b io p s y: Larger needle is used, typically 14 gauge, and passed multiple times through the same lesion, which decreases sampling error, but it is slightly more invasive than FNA. T e sample may incorporate some o the tissue around the lesion and provide clues to tumor invasiveness.

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III. Im a g e -g uid e d b io p s y: Percutaneous needle biopsy may be per ormed using imaging guidance when the lesion is not super cial or palpable. echniques include ultrasound-guided, C - or MRI-guided, or stereotactic biopsy. IV. Inc is io na l b io p s y: Such as surgical biopsy with a portion o a lesion removed. T is technique is usually reserved or larger lesions. V. Exc is io na l b io p s y: complete removal o a lesion or diagnostic purposes

Mo le c ula r Dia g no s tic s I. Re c e p to r s ta tus : Certain cancers may carry prognostic and treatment implications. Perhaps best known is the estrogen receptor (ER) and progesterone receptor (PR) status o breast cancer, determined by direct analysis o tumor specimens. II. Ge no m ic s tud ie s : Analyze the structure and unction o a DNA sequence. T e promise o genomics is that speci c genetic sequences may yield prognostic in ormation on tumor behavior or response to therapy. Gene arrays are now available but have not yet been incorporated into common clinical practice. III. P ro te o m ic s : Study o protein structure and their unctions. An increasing body o in ormation is being generated on cancer gene products and their speci c protein signatures that may aid in cancer diagnosis and treatment.

Op e ra tio n I. Op e ra tive inte rve ntio n: may be necessary to determine the diagnosis or the extent o the disease process II. La p a ro s c o p y: has become a standard diagnostic tool or upper abdominal malignancies, as it is more sensitive than cross-sectional imaging or the detection o metastatic disease and less invasive than laparotomy

STAGING Ove rvie w I. P ro g no s is : By standardizing malignancies into groups that have similar behavior, accurate prognostic in ormation can be obtained. II. Tre a tm e nt: Algorithms can be developed or a particular stage o cancer, and these can be rigorously studied, as cancers are grouped into comparable stages. III. Tum o r, no d e s , a nd m e ta s ta s is (TNM) s ys te m (Ta b le 21-4): Most widely used system is based on tumor, nodes, and metastases. A. T: describes the extent o tumor B. N: describes the presence o local or distant LN involvement C. M: describes the presence o distant metastatic disease IV. Clinic a l s ta g ing : made based on biopsy and imaging be ore treatment V. P a tho lo g ic s ta g ing : determined af er de nitive intervention

Quic k Cut Staging is the proces s o grouping cancers bas ed on type and extent o dis eas e.

Quic k Cut TNM is the dominant s taging s ys tem us ed or mos t orms o cancer, and s taging is s pecif c to each cancer type.

SURGICAL TREATMENT Dia g no s tic I. Tis s ue d ia g no s is : Surgical intervention may yield a cancer diagnosis through incisional or excisional biopsy. II. LN s ta tus : important or staging any malignancy, but it is particularly used in breast cancer and malignant melanoma A. LN dissection: Lymphadenectomy involves removing the lymphatic tissue in a known anatomic distribution rom the site o a tumor. B. Sentinel LNs: rst LN in a chain that drains the area o interest 1. Identi cation: Sentinel node can be identi ed through the use o dye (isosul an blue) or radioactive tracer (technetium-99–labeled sul ur colloid) and use o an intraoperative gamma probe.

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Ta b le 21-4: Tum o r, No d e s , a nd Me ta s ta s is Cla s s if c a tio n Sys te m a nd Sta g e Gro up ing o r Ga s tric Ad e no c a rc ino m a Tum o r (T) T0 Tis (in situ) T1 T2 T3 T4

No evidence o primary tumor Tumor limited to mucosa Tumor limited to mucosa or submucosa Tumor to but not through the serosa Tumor through the serosa but not into adjacent organs Tumor into adjacent organs (direct extension)

No d e s (N) N0 N1 N2 N3

No metastases to lymph nodes Only perigastric lymph nodes within 3 cm o the primary tumor Only regional lymph nodes more than 3 cm rom tumor but removable at operation Other intra-abdominal lymph nodes involved

Me ta s ta s e s (M) M0 M1

No distant metastases Distant metastases

Sta g e g ro up ing Stage 0 Stage 1 Stage 2 Stage 3 Stage 4

Tis, N0, M0 T1, N0, M0 T2 or T3, N0, M0 T1–T3, N1 or N2, M0 Any T4, any T3, any N3, any M1

2. Surgical technique: Identi ed sentinel node can be excised and undergo analysis, providing diagnostic in ormation without the morbidity o a ull lymphadenectomy (such as lymphedema). False-negative rate is less than 5%; may be complicated by previous surgery or biopsies that alter the native patterns o lymph drainage.

Quic k Cut Sentinel node techniques were developed to avoid the potentially s ubs tantial morbidity o LN dis s ection.

P ro p hyla c tic I. Bre a s t: Prophylactic mastectomy may be indicated when the Quic k Cut risk o breast cancer approaches 100%; it reduces the risk o breast Prophylactic s urgery cancer by more than 90% but not completely, as some breast tissue may be o ered when the ris k may remain on the chest wall or in the axilla. Candidates include: o developing malignancy A. Bilateral: BRCA-1– or BRCA-2–positive women s eems certain. B. Contralateral: women with invasive breast cancer in one breast II. Ova ry: Prophylactic oophorectomy is o ered in women who are BRCA-1 or BRCA-2 positive; it decreases the risk o ovarian cancer by 90% and the risk o breast cancer by 50% in premenopausal women. III. Thyro id : T yroidectomy is recommended or cases o RE mutation in amilies with multiple endocrine neoplasia (MEN) that causes medullary thyroid carcinoma; typically per ormed in childhood and requires li elong thyroid hormone supplementation. IV. Co lo n: Colectomy is reserved or cases o genetic conditions where the risk o colon cancer is high ( amilial adenomatous polyposis or HNPCC); patients may opt or permanent end ileostomy or internal reconstruction with an Quic k Cut ileoanal pouch anastomosis. Whenever

Cura tive I. Exc is io n: May be adequate or small or low-grade lesions; wide local excision is the pre erred treatment or basal cell skin carcinoma.

pos s ible, oncologic s urgery is per ormed with curative intent.

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II. Ra d ic a l re s e c tio n: Involves the removal o the tumor and its surrounding tissues and may involve removal o multiple LN basins; en bloc resections involve portions o adjacent organs or viscera in direct contact with the tumor.

P a llia tive

Quic k Cut There are s everal common principles in s urgical oncology, including minimal manipulation o the tumor and early ligation o ves s els to avoid vas cular dis s emination, gentle tis s ue handling and dis s ection to minimize local recurrence, and excis ion o lymphatic channels to minimize the ris k o lymphatic s pread.

I. De b ulking : Removal o the majority o a tumor, leaving known residual disease, is per ormed when complete resection would be excessively debilitating; it may increase e cacy o adjuvant therapies due to decreased tumor burden. Most commonly employed in treatment o ovarian cancer. II. Me ta s ta s e c to m y: may alleviate symptoms when control o the primary tumor is obtained; commonly used in resection o liver metastases rom colon cancer III. Sym p to m a tic tre a tm e nt: used to alleviate a speci c symptom rom metastatic disease (e.g., decompression o an obstructing colon mass may prolong li e and minimize su ering in a patient with known metastases)

Fo llo w-up I. Surve illa nc e : Af er surgical resection, patients are monitored closely in order to detect any recurrence o cancer with a combination o history and physical examination, laboratory tests including tumor markers, and imaging. II. Fre q ue nc y a nd tim ing o vis its : Based on the type and stage o the cancer. I a tumor is detected, patients should undergo restaging to determine the most appropriate treatment.

Quic k Cut

MULTIDISCIP LINARY TREATMENT Ad juva nt/Ne o a d juva nt The ra p y I. Ad juva nt the ra p y: systemic treatment in a patient with primary control with the goal to minimize the risk o recurrence or metastasis II. Ne o a d juva nt the ra p y: adjuvant therapy given be ore there is control o the primary tumor (i.e., preoperatively)

Che m o the ra p y

A hallmark o modern care o the cancer patient is the involvement o many dis ciplines to optimize patient outcomes .

Quic k Cut Adjuvant therapy is not a s ubs titute or good s urgical technique.

I. De f nitio n: systemic use o chemical agent to impede or destroy rapidly dividing cancer cells II. Hig h d o s e : Certain medications may be given in higher local doses through regional techniques, such as use o a hepatic artery catheter or liver lesions, isolated limb per usion or lesions o the extremities, or intraperitoneal chemotherapy or peritoneal malignancies. III. Sid e e e c ts : include toxicity to normal cells that undergo division, such as hair and the mucosal sur ace o the gastrointestinal (GI) tract

Ra d ia tio n The ra p y I. De f nitio n: involves the use o energy delivered through external beams or internal implants (i.e., brachytherapy) to damage the DNA o target cells II. Go a l: may be curative or palliative

Othe r

Quic k Cut The precis e regimen o primary and adjuvant treatments depends on the tumor type, location, grade, and s tage as well as patient actors s uch as age, comorbid conditions , and patient pre erences .

I. Im m uno the ra p y: also called biotherapy; systemic modulation o the immune system to combat cancer A. Monoclonal antibodies: More than 12 have been approved by the U.S. Food and Drug Administration (FDA) or use against speci c cancer cells. B. Cancer vaccines: Currently, only one agent is FDA approved—sipuleucel- — or the treatment o prostate cancer.

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II. Ho rm o na l the ra p y: Some malignancies are potentiated by hormones, and hormonal blockade may provide some anticancer bene t. A. Breast cancer: Most are ER positive; tamoxi en blocks the receptor itsel , and aromatase inhibitors block estrogen production. Both have demonstrated a survival bene t. B. Prostate cancer: Androgen inhibitors may be o bene t. III. Ge ne tic the ra p y: In principle, missing or de ective genes could be replaced through trans ection; current genetic therapy remains experimental.

RESEARCH AND TRAINING Clinic a l Tria ls

Quic k Cut

I. Tria l d e s ig n: Surgical oncologists are requently involved in the Phas e I as s es s es development and assessment o new treatments and should be s a ety, phas e II as s es s es amiliar with the basic concepts o trial design. e f cacy, and phas e III compares the tes t treatment A. Phase I: Studies test sa ety; these are of en small studies that to s tandard treatment. establish side e ects as well as a sa e dosage range. B. Phase II: Studies test e cacy; these studies involve more participants and look or a clinical e ect o the treatment. C. Phase III: Studies are comparative to a standard treatment. II. Ins titutiona l re vie w boa rd (IRB): independent review committee that oversees human subject research A. Mandate: Code o Federal Regulations, Part 46 B. Ethical research: guided by three principles (the Belmont report): 1. Bene cence: Research should maximize possible bene ts and minimize possible harms. 2. Justice: T ere should be airness in selection, and those groups that bear the risks o research should bene t rom its conclusions. 3. Respect or persons: Autonomy is the guiding principle, with protection or vulnerable populations.

Tra ining I. Surg ic a l o nc o lo g is ts : should pursue advanced training or their particular eld II. Fe llo ws hip s : currently available beyond surgical residency in general oncologic surgery, hepatobiliary surgery, breast surgery, and complex surgical oncology

Quic k Cut At s ome level, all s urgeons are oncologis ts .

Chapter 22

rauma and Burns

Brandon Bruns and T omas Scalea

TRAUMA Ep id e m io lo g y I. Inc id e nc e : leading cause o death or individuals ages 1–44 years II. Ca us e : More than 50% o these deaths are caused by motor vehicle collisions (MVCs).

P a tie nt Eva lua tio n

Quic k Cut I. P re ho s p ita l: Network o prehospital providers and transport is Caring or injured paramount or optimal trauma patient outcomes. patients in a des ignated II. Initia l e va lua tio n: T e American College o Surgeons (ACS), trauma center has been s hown to improve outcomes through the advanced trauma li e support course (A LS), teaches a and s ave lives . systematic approach to the initial evaluation o trauma patients. A. Primary survey: ABCDE 1. Airway: Ensure the patient is capable o protecting his or her airway; inspect the oropharynx or any potential or obstruction (e.g., blood, teeth); i necessary, establish an airway via tracheal intubation (most guidelines suggest or Quic k Cut a depressed neurologic status with a Glasgow Coma Scale For a GCS 8, plan to intubate. [GCS] score 8). 2. Breathing: Auscultate the bilateral lung f elds or breath sounds; decreased breath sounds may indicate the presence o a pneumothorax. 3. Circulation: Check or emoral and distal pulses, and check the patient’s blood pressure (BP) and heart rate (HR); Quic k Cut tachycardia may precede a drop in BP as the f rst indication o The pres ence o hypovolemia. a emoral puls e indicates 4. Disability (Fig. 22-1): Rapidly assess the patient’s GCS (15 is a s ys tolic BP o at leas t the maximum); i an endotracheal tube is present, add “ ” to 60 mm Hg. the end (e.g., GCS 11 ). 5. Exposure: Patient is ully disrobed or complete physical evaluation. B. Adjuncts: to the primary survey 1. Chest radiograph: Evaluate the chest x-ray systematically, starting with ensuring the correct patient. a. Airway: Inspect the trachea to ensure it is midline; deviation to either side could indicate pneumothorax, hemothorax, or aortic injury. b. Breathing: Ensure lung markings are present; absence indicates the presence o a pneumothorax, and opacif cation o a lung f eld may indicate a hemothorax. c. Cardiac silhouette: Inspect the borders o the heart and mediastinum; classically, a mediastinum greater than 8 cm is suggestive o thoracic aortic injury.

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353

Eye Ope ning S ponta ne ous To s pe e ch To pa in None

4 3 2 1

Ve rba l Re s pons e Orie nte d Confus e d Ina ppropria te words Moa ns None

5 4 3 2 1

Motor Re s pons e Follows comma nds Loca lize s pa in Withdra wa ls De cortica te (Fle xion) De ce re bra te (Exte ns ion) None

6 5 4 3 2 1

Fig ure 22-1: The Glas gow Coma Scale. Score E V M; minimum s core is 3, maximum is 15. (From Zas lau S. Step-Up to Surgery. Baltimore: Lippincott Williams & Wilkins ; 2014.)

d. Diaphragm: Injury to a diaphragm may be suggested by diaphragmatic contour irregularity or the presence o a hollow viscus in the chest. e. Everything else: Examine the bones or racture or misalignment; look or subcutaneous air, which could indicate an occult pneumothorax. 2. Pelvic radiograph: commonly obtained to evaluate or racture, which, in combination with hypotension, may lead the evaluating surgeon to suspect pelvic bleeding as the cause o hypotension 3. Ultrasound: Surgeon-per ormed ultrasound at the bedside enables a rapid assessment o the peritoneal cavity or the presence o uid, which may indicate blood (hemoperitoneum). a. Pericardium: also inspected or the presence o uid, which may indicate blood within the pericardium b. T orax: may be scanned to examine or the presence o pneumothorax or hemothorax C. Secondary survey 1. Physical examination: Full head-to-toe physical examination is done. 2. History: AMPLE a. A: allergies b. M: medications c. P: previous illnesses d. L: last meal e. E: events surrounding injury D. ertiary survey: Once removed rom the chaotic nature o the initial trauma evaluation, the patient undergoes another complete head-to-toe examination 12-24 hours a er arrival.

Sho c k I. Initia l tre a tm e nt: Obtain venous access. A. Options: large-bore (18 gauge or greater) needle in the antecubital ossa, central venous access (subclavian or emoral line), or saphenous vein cutdown B. I unable to obtain venous access: Use intraosseous access.

Quic k Cut Ches t radiograph interpretation is done the s ame way every time: patient identif cation, airway, bilateral lung f elds , cardiac s ilhouette, diaphragm, and everything els e (bones , s ubcutaneous air, oreign bodies ).

Quic k Cut Ultras ound is a very us e ul diagnos tic tool becaus e it is rapid, available, and inexpens ive and may provide an early indication o bleeding.

Quic k Cut The tertiary s urvey o ten leads to the identif cation o dis tal extremity ractures and other injuries mis s ed initially.

Quic k Cut The ultimate goal o the trauma evaluation is to identi y and control s ources o bleeding that lead to s hock.

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II. Ne xt s te p s : Rapid control o bleeding is essential to ensuring patient survival. A. In usion: isotonic crystalloid (lactated Ringer, normal saline, Plasma-Lyte) or blood and blood products B. Identi y bleeding source: Physical examination, chest and pelvic x-rays, and ultrasound all help. C. With uncontrolled blood loss rom an injured extremity: Apply a tourniquet, which may decrease blood loss.

Quic k Cut Patients can bleed to death in f ve locations : ches t, peritoneal cavity, retroperitoneum/pelvis , extremities (mainly the thigh), and the street (i.e., mas s ive blood los s at the s cene).

Re s us c ita tive Tho ra c o to m y I. Ove rvie w: previously called emergency department thoracotomy; per ormed in an emergent setting when the patient loses vital signs to relieve pericardial tamponade (blood within the pericardium causing shock) II. Te c hniq ue : An incision is made in the pericardium, any blood is evacuated, and the aorta is clamped. III. Re s ults : increases blood ow to the brain and coronary arteries and may help stop uncontrolled intra-abdominal or extremity bleeding IV. Ma nua l c o m p re s s io n o the he a rt: may be more e ective than chest compressions when the patient is in hypovolemic shock V. Ind ic a tio ns : controversial and will most likely remain so, but commonly used criteria are the ollowing: A. Penetrating trauma: cardiac arrest and trauma to the chest or abdomen within 15 minutes o arrival to the trauma center (much higher chance o survival i chest injury) B. Blunt trauma: cardiac arrest i the arrest occurs while in ront o the trauma team’s eyes C. Devastating neurologic injury (e.g., transcranial gunshot wound): Many surgeons would not proceed with thoracotomy, although reports o survival and organ donation do exist.

SP ECIFIC INJ URIES He a d a nd Ne c k I. Bra in: Identif cation o a decreased GCS during the primary survey may warn o potential brain injury. A. Pupil examination: Imperative; a dilated and nonreactive pupil may indicate increased pressure secondary to intracranial bleeding. B. Rapid assessment with computed tomography (C ): o en necessary to better characterize the injury C. Initial treatment or intracranial hemorrhage: aimed at decreasing the ICP while preserving cerebral blood ow D. Rapid neurosurgical consultation: will decrease time to def nitive management o injuries II. Ce rvic a l s p ine : Immobilization with a cervical collar should be maintained in all blunt trauma patients until they are able to be ully evaluated and “cleared,” including during rolling and any procedures (e.g., oral–tracheal intubation). A. During secondary survey: Cervical spine is palpated to identi y tenderness or bony de ormity (step-o ). B. Physical examination: can be used to “clear” the cervical spine i the patient is not intoxicated, does not have a “distracting” injury, and does not have a decreased GCS C. C imaging: evaluates or the presence o racture with cervical spine pain or the conditions listed earlier

Quic k Cut Although it is important to es tablis h the ull extent o injury in trauma patients , uns table patients belong in the OR, not undergoing a lengthy radiographic evaluation.

Quic k Cut Res us citative thoracotomy is a high-ris k procedure that is res erved or patients with s ome expectation o s urvival.

Quic k Cut Monro-Kellie doctrine: The brain is enclos ed in the s kull vault; the addition o blood or any s pace-occupying les ion greatly increas es intracranial pres s ure (ICP).

Quic k Cut Avoiding hypotens ion and hypoxia is paramount to prevent brain is chemia, as thes e contribute to wors e outcomes a ter brain injury.

Quic k Cut Firs t-line maneuvers to help decreas e the ICP: analges ia and s edation, head o bed elevation, mannitol (avoid in hypotens ion), hypertonic s aline, and loos ening the cervical collar.

Chapter 22

Angle of ma ndible

Zone III

Cricoid ca rtila ge

Zone II Zone I

rauma and Burns

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Fig ure 22-2: Schematic drawing o the zones o the neck. The junction o zones 1 and 2 is various ly des cribed as being at the cricoid cartilage or at the top o the clavicles . The important implication o a zone 1 injury is the greater potential or intrathoracic great ves s el injury. (From Fis er SM. ABSITE Review, 3rd ed. Baltimore: Lippincott Williams & Wilkins ; 2010.)

III. P e ne tra ting c e re b ro va s c ula r: reatment o vessel injury in the neck is mainly surgical, but interventional radiologic approaches are increasing in requency. T e neck is divided into three zones (Fig. 22-2). A. Zone 1: thoracic inlet to hyoid bone B. Zone 2: Hyoid bone to angle o mandible; classically, injuries here are treated with operative exploration because o the relatively easy surgical access (i.e., not hidden in the thorax [zone 1] or base o skull [zone 3]). C. Zone 3: angle o mandible to cranium IV. Blunt c e re b ro va s c ula r injury (BCVI): Principally carotid artery injury. Risk actors require additional screening or injury identif cation and include cervical spine injury, displaced mid ace racture (Le Fort II and III), pulsatile epistaxis, hanging or clothesline mechanism, basal skull racture, signif cant neck hematoma, and neurologic exam not explained by C o the head. A. Grades o carotid artery injury 1. I: luminal irregularity or dissection, less than 25% narrowing 2. II: luminal irregularity or dissection, 25% or greater narrowing 3. III: pseudoaneurysm 4. IV: occlusion 5. V: transection B. Diagnosis: C neck scans with intravenous (IV) contrast or angiography C. reatment: anticoagulation or antiplatelet therapy

Sp ina l Co rd a nd Sp ina l Co lum n

Quic k Cut All blunt trauma patients are treated as i they have a cervical s pine injury until proven otherwis e.

Quic k Cut Remember, CT o the C-s pine rules out bony injury, not ligamentous injury. Magnetic res onance imaging (MRI) is the pre erred tes t to evaluate or ligamentous injury.

Quic k Cut Clas s ic teaching: zone 1 and zone 3 penetrating neck injuries require additional imaging (computed tomography angiography/ angiography). Zone 2 penetrating neck injuries are treated with s urgical exploration.

Quic k Cut

I. P rim a ry s urve y: During the disability assessment, attention Exces s ive blunt should be paid to the patient’s ability/inability to move all our orce leads to s tretching o the neck ves s els . extremities; the patient should also be rolled and the ull spinal column assessed or the presence o pain or bony de ormity (step-o ). Quic k Cut II. Sp ina l im m o b iliza tio n (in the p re ho s p ita l a nd in-ho s p ita l Carotid artery p ha s e s ): maintain with a backboard and during rolling until injuries lead to an increas ed determination has been made that a spinal racture does not exist ris k o s troke i le t untreated. III. Dia g no s is : Def nitive identif cation o spinal racture is most requently made with C imaging. A. MRI: o en employed to better def ne and visualize injury to the spinal cord itsel B. Steroids: not indicated; shown to increase in ectious complications without decreasing spinal cord edema

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P ne um o tho ra x a nd He m o tho ra x I. De f nitio ns A. Pneumothorax: presence o air in the pleural space (outside o the lung), which causes increased pressure within that hemithorax and di culty with ventilation B. ension pneumothorax: Increased pressure pushes the mediastinum to the contralateral side and causes decreased venous return and decreased BP. C. Hemothorax: presence o blood in the pleural space II. Aus c ulta tio n: Decreased breath sounds during the primary survey may alert the physician to his or her potential. III. Dia g no s is : Chest x-ray assists. C may better evaluate the pathology and can identi y occult pneumothoraces (not visible on x-ray). IV. Tre a tm e nt: Chest tubes drain air or blood and should be placed into the pleural space under sterile conditions during initial trauma evaluation. A. Incomplete drainage o a hemothorax: leads to a retained hemothorax and possible an empyema i not addressed and drained early B. T oracotomy: used to treat massive hemothorax C. Excessive bleeding into the chest: requires surgical evacuation o bleeding and identif cation and control o the bleeding vessel or repair o bleeding structure

Quic k Cut Tens ion pneumothorax is a clinical (not radiographic) diagnos is and is an emergency that requires decompres s ion o the air in the pleural s pace (needle decompres s ion or ches t tube placement).

Quic k Cut Mas s ive hemothorax is o ten def ned as greater than 1 liter o blood rom the ches t tube initially or greater than 200–250 mL o blood per hour, or 4 hours or more, managed with emergent thoracotomy.

Ca rd ia c Injury I. Blunt: Force ul blow to the chest can cause injury to the heart (e.g., steering wheel to chest); these patients should get an electrocardiogram (ECG) during initial trauma evaluation. A. Diagnosis: suggested by an arrhythmia (most requently sinus tachycardia) on ECG B. Echocardiogram: or urther characterization o the injury i the patient’s ECG is abnormal or the patient is hemodynamically abnormal C. reatment: typically nonoperative and consists o inpatient cardiac monitoring or arrhythmia D. Ef ects: Patients can develop structural lesions (cardiac aneurysms, septal wall ruptures, valvular problems). II. P e ne tra ting : Initial evaluation is made during the primary survey adjuncts with ultrasound evaluation o the heart (Fig. 22-3). Quic k Cut A. Diagnosis: Presence o uid within the pericardium may Any penetrating indicate blood, which is highly suggestive o a cardiac injury injury to the “cardiac box” s hould rais e the s us picion o and may cause cardiac tamponade leading to shock; urther a cardiac injury. diagnostic techniques include a “pericardial window” per ormed in the operating room. B. reatment: Operative; the pre erred approach is median sternotomy.

Blunt Tho ra c ic Ao rtic Injury I. Dia g no s is : Initial chest x-ray may suggest the injury. A. Other: widened mediastinum ( 8 cm), pleural cap rom Quic k Cut Mos t patients with bleeding into the pleural space near the apex; loss o blunt injury to the thoracic aortopulmonary window, le mainstem bronchus depressions, aorta die at the s cene. and nasogastric tube displacement to the right B. De nitive diagnosis: contrast-enhanced chest C in most cases today II. Tre a tm e nt: Initial treatment is ocused around decreasing the HR and BP; def nitive treatment may include endovascular treatment, open surgical treatment, or nonoperative management and observation.

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Fig ure 22-3: Schematic drawing o the “cardiac box.” Shaded area repres ents the danger zone or trans medias tinal injury. (From Peitzman AB, Rhodes M, Schwab CW, et al. The Trauma Manual: Trauma and Acute Care Surgery, 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2006.)

Es o p ha g e a l a nd Tra c he a l Injury I. Dia g no s is : physical examination (bubbling in a wound, presence o ood particles), endoscopy (bronchoscopy/esophagoscopy; predominant diagnostic tool in the chest), or swallow study (contrasted x-ray or identif cation o esophageal injury) Quic k Cut Patients with a II. Tre a tm e nt: operative repair pos itive FAST ( uid in the III. E e c ts : racheal injury may lead to excessive subcutaneous peritoneal s pace) and a low emphysema; missed tracheal and esophageal injury can lead to BP or s ignif cant tachycardia mediastinitis and death. (shock) belong in the

Ab d o m ina l Injury I. S o lid o rg a n s (live r a n d s p le e n ): Initial evaluation begins with the ocused abdominal sonography or trauma (FAS ) to assess or ree uid (likely blood) within the peritoneum (Fig. 22-4). A. Hemodynamically normal patient: Further evaluation with abdominal/pelvic C may be pursued. B. Grading: Splenic and liver injuries are graded I–V (with V being the most severe), with more severe injuries likely requiring operative exploration or def nitive treatment. C. reatment: Interventional radiology with embolization may be available in specif c situations.

operating room, not the CT s canner.

Quic k Cut The pres ence o a “blus h” on CT s can with IV contras t indicates extraluminal contras t extravas ation (active bleeding) and may require interventional radiographic embolization or s urgical intervention.

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Fig ure 22-4: Photograph o le t upper quadrant view with a pos itive FAST. This FAST examination o the peris plenic s pace s hows s ignif cant hemoperitoneum and s ugges ts the need or urgent laparotomy. (From Bigatello LM, Alam H, Allain RM, et al. Critical Care Handbook of the Massachusetts General Hospital, 5th ed. Philadelphia: Lippincott Williams & Wilkins ; 2009.)

II. Ho llo w vis c us : Injuries to the stomach, small intestine, and colon comprise this group o injuries. A. Diagnosis: FAS is likely insu cient to diagnose ree uid in the peritoneal cavity in this type o injury. 1. Physical examination: Blunt hollow viscus injury may Quic k Cut present with rank peritonitis, which mandates operative The pres ence o a exploration. “s eatbelt s ign” (s ignif cant 2. Other presentations: Free uid on abdominal/pelvic C in abdominal wall hematoma caus ed by s eatbelt s trap) the absence o solid organ injury requires either operative s hould rais e the s us picion o exploration with exploratory laparotomy; diagnostic a hollow vis cus injury. peritoneal lavage (DPL); serial abdominal exams; or, in some centers, diagnostic laparoscopy. B. reatment: operative repair o injury or resection III. Ab d o m ina l va s c ula r injurie s : include aortic, mesenteric, iliac, and cava injuries that most requently occur as a result o penetrating injury (gunshot and stab wounds) A. Presentation: shock (hypotension, tachycardia, depressed mental status, pallor, cool extremities) and a positive FAS Quic k Cut B. Diagnosis: In blunt or penetrating injury, a positive FAS exam Patients with in the ace o shock requires no urther evaluation and mandates abdominal vas cular injury an emergent trip to the operating room or exploration via commonly eel cold, are very thirs ty, and s ay “I’m going midline incision (exploratory laparotomy). to die”—believe them; they C. reatment: ligation o the bleeding vessel, repair, or bypass might be right . IV. Ge nito urina ry: include injuries to the kidneys, ureters, bladder, and urethra A. Kidney: Most injuries can be managed nonoperatively; operative identif cation o a kidney injury should prompt the surgeon to examine the contralateral kidney to ensure the patient has two kidneys. B. Ureters: Injuries are most o en repaired surgically. C. Bladder: Injuries are urther placed into two categories. 1. Intraperitoneal: Rupture into the peritoneal cavity is repaired surgically. 2. Preperitoneal: Ruptures into the preperitoneal space are most o en managed without an operation and with a urinary catheter or 10-14 days o drainage.

Chapter 22

P e lvic Fra c ture I. Initia l e va lua tio n: plain f lm radiograph (pelvic x-ray) II. P e lvic b ind e r: In a patient with a suspected or verif ed pelvic racture and hypotension, a binder placed around the greater trochanters bilaterally decreases the pelvic volume and minimizes ongoing hemorrhage. III. Tre a tm e nt o r o ng o ing he m o rrha g e a nd s ho c k: may include angioembolization, preperitoneal packing in the operating room, and endovascular aortic occlusion. IV. Tre a tm e nt o r o rtho p e d ic injurie s : may include def nitive or external f xation V. Sp e c ia l c o ns id e ra tio n: Urethral injury is suggested by blood at the urethral meatus, a high-riding “ballotable” prostate, and/or signif cant perineal ecchymosis.

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Quic k Cut Pelvic racture mus t be recognized quickly, as li ethreatening hemorrhage can occur.

Quic k Cut Sus pected urethral injury s hould be urther evaluated with a retrograde urethrogram (RUG). Do not place a Foley catheter, which could convert a partial urethral injury into a ull trans ection.

Extre m itie s I. Fra c ture s : Fractured long bones ( emurs) have the potential to bleed vigorously and lead to shock. A. Diagnosis: Plain f lm x-rays are the mainstay. B. Reduction: Reducing a emur racture (pulling to length) and stabilizing will decrease patient pain and potentially decrease bleeding, but the act o reduction is very pain ul to the patient. C. Arterial injury: Calculation o the ankle-brachial index (ABI) or ankle-ankle index (AAI) can help detect arterial injury (1.0 is normal, 0.9 needs urther evaluation). D. Antibiotic prophylaxis: paramount or open ractures to treat in ection

Co m p a rtm e nt Synd ro m e I. De f nitio n: most commonly ound in the lower leg and orearm but can be ound in any extremity and buttock A. Forearm: classically described as having three compartments— dorsal, ventral, and mobile wad B. Lower leg: classically described as having our compartments— anterior, lateral, superf cial posterior, and deep posterior II. Dia g no s is : most typically made on physical examination by the presence o a tense compartment and the sensation o numbness/ paresthesias/pain

Quic k Cut Dis tal puls e and neurologic exam are essential in the evaluation o any extremity racture.

Quic k Cut The “6 P’s o arterial ins u f ciency” are p uls eles s nes s , p ares thes ias , p oikilothermia, p allor, and p aralys is p ain.

Quic k Cut Puls eles s nes s is the last phys ical exam f nding to occur in compartment s yndrome. Treatment or compartment s yndrome cons is ts o a as ciotomy per ormed in the operating room.

BURNS Burn Injury

Quic k Cut I. Initia l tre a tm e nt: Based on the same principles o initial trauma Becaus e the initial evaluation (airway/breathing/circulation). T e patient must be pres entation o a major removed rom the source o thermal injury, and all burning clothes burn can be quite dramatic, and/or chemicals should be removed. having an orderly approach to A. Avoid hypothermia: Burn wounds can be placed under running management is es s ential. room-temperature water (in an e ort to stop the burning process) but should not be placed under cold water so as not to exacerbate the injury. Burn wounds should then be covered with a sterile sheet to avoid evaporative heat loss and protect the wound. B. Early pain control: IV opioids are warranted, as burn wounds are exceedingly pain ul. C. Other early steps: Give tetanus toxoid and place a nasogastric tube to decompress the stomach (in anticipation o paralytic ileus) and as a means to provide early enteral nutrition, which is vital in the hypercatabolic response to burn injury.

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II. Intub a tio n: Extensive burns to the ace along with singed nasal hairs and carbonaceous sputum should alert the physician to the possibility o airway injury—early intubation is key. III. Re s us c ita tio n: wo large-bore (18 gauge or larger) IV lines should be placed into the bilateral antecubital ossae; lactated Ringer Quic k Cut is the classical uid o choice. Parkland ormula or A. Adults: Parkland ormula or second and third degree burns burn res uscitation: 4 mL B. Fluid resuscitation: Should be tailored to urine output; total body s ur ace area burned calculated requirement o uid is rom the time o burn. (TBSA) weight (kg) 1. iming: First 50% o uid is given in the initial 8 hours, with es timated uid requirements in the f rs t 24 hours the rest in the remaining 16 hours. 2. Urinary catheter: placed to monitor urine output

Eva lua tio n a nd Tre a tm e nt I. Typ e s A. Super cial burns: conf ned to the epidermis, blister, are pain ul, and do not require surgery B. Partial-thickness burns: involve the dermis, are mottled and pale in areas with some preserved epidermal appendages, are pain ul, and require surgery i deep partial-thickness burns C. Full-thickness burns (to the bone or ascia): are leathery or white in appearance, are insensate, and require surgery II. Burn s ize e s tim a tio n: “Rule o 9’s” is used to calculate IV uid requirements (Fig. 22-5). III. To p ic a l a ntim ic ro b ia ls : should be applied a er the ull evaluation o the burn injury to prevent localized bacterial growth. Common agents include the ollowing. A. Silver sul adiazine (Silvadene): painless; may cause neutropenia (rare)

9%

9%

9%

9%

9%

9%

9%

1% 9%

9%

Anterior

9%

9%

Posterior

Fig ure 22-5: Rule o 9’s in es timating body s ur ace area in burn victims . Remember that or this calculation, burns are s cored as s econd degree and above. (From Van Kleunen J P. Step-Up to USMLE Step 2. Baltimore: Lippincott Williams & Wilkins ; 2005.)

Chapter 22

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B. Ma enide acetate (Sul amylon): pain ul application; penetrates Quic k Cut eschar; may cause metabolic acidosis (it is a carbonic anhydrase Sys temic antibiotics inhibitor) should not be adminis tered C. Silver nitrate: used or ace burns; may cause electrolyte in the abs ence o a s pecif c imbalances and stains everything black in ection. IV. Op e ra tive tre a tm e nt: “Early” excision and gra ing o burn wounds is the current standard o care. V. Es c ha ro to m y (e s c ha r [Gre e k : “s c a r”]): may need to be per ormed during initial evaluation in the presence o circum erential wounds because burn eschar can impede per usion or ventilation

Inha la tio n Injury I. Tre a tm e nt: Early intubation may be warranted to protect the patient’s airway rom edema. A. Carboxyhemoglobin level: should be obtained and elevated levels treated with 100% oxygen by acemask B. Bronchoscopy: may be warranted to remove particulate matter II. IV uid re q uire m e nt: Inhalation injury typically requires more than expected to maintain adequate urine output.

Quic k Cut A his tory o burn within a clos ed s pace may alert the phys ician to the pos s ibility o inhalation injury.

Ele c tric a l Burns I. Mus c le d a m a g e : Excessive muscle damage may lead to Quic k Cut compartment syndrome o an extremity, warranting emergent The vis ible contact asciotomy in the operating room. burn will vas tly underes timate A. High-voltage ( 1,000 volts) injuries: should raise the suspicion the degree o mus cular o extensive muscle destruction and cardiac conduction damage that an electrical abnormalities burn has caus ed. B. Myoglobinuria: may be caused by products o muscle breakdown and may lead to a red tint to the urine and places the patient at greater risk o acute kidney injury II. Tre a tm e nt: Myoglobinuria should be treated with titration o resuscitation to a urine output o 100 mL/hr. Diuretics may be indicated to maintain urine output. III. Re ha b ilita tio n: rauma and burn injuries are chronic conditions which require li elong care; rehabilitation can take years and leads to a signif cant loss o productivity.

Chapter 23

Organ ransplantation

Joseph R. Scalea, Max Seaton, Silke Niederhaus, and Jonathan Bromberg

OVERVIEW Re a s o ns o r Tra ns p la nta tio n I. End -o rg a n d ys unc tio n: ransplantation o solid organs is reserved or patients with end-organ dys unction to prolong li e (heart, lung, liver, kidney) and improve quality o li e (all organs). II. Lim ita tio ns : shortage o donor organs and the comorbidities o chronic immunosuppression

Tra ns p la nt Ca nd id a te Eva lua tio n I. Re c ip ie nts : are evaluated, including all disease-related problems II. Othe r p o te ntia lly invo lve d o rg a n s ys te m s m us t b e e va lua te d : Evaluation o a liver transplant candidate includes evaluation or coronary artery disease (CAD) and pulmonary hypertension. A patient with renal ailure rom diabetes may also have signif cant CAD, aortoiliac vascular disease, or unidentif ed carotid stenosis. III. Ge ne ra l he a lth is s ue s : Are evaluated; age, body mass index Quic k Cut (BMI), and adequate social support are relevant actors in Patients with certain cancers that are controlled or determining candidacy or transplant. eradicated are candidates or A. Cancers and in ections: must be ruled out or addressed organ trans plantation. B. Cardiac evaluation: is a must or all transplant recipients IV. Typ ic a l s tud ie s : T e ollowing workup is needed or each organ system A. Pulmonary: chest radiograph. I indicated: pulmonary unction tests, right heart catheterization B. Cardiac: electrocardiogram (ECG) and transthoracic echocardiogram. I indicated, stress test or cardiac catheterization C. Gastrointestinal (GI): Liver unction tests (LF s); computed tomography (C ), ultrasound (US), or magnetic resonance imaging (MRI) o abdomen/pelvis to evaluate vessels and exclude liver masses. In liver patients, esophagogastroduodenoscopy (EGD). In pancreas patients, asting C-peptide. D. Renal/urologic: creatinine. I there is a concern that disease may recur, kidney biopsy (eg, glomerulonephritis) E. Immunologic: tuberculosis (purif ed protein derivative [PPD]); rapid plasmin reagin (RPR) test; serology or hepatitis B and C, cytomegalovirus (CMV), Epstein-Barr virus (EBV), and HIV; and calculated panel reactive antibody (cPRA) to assess sensitization to human leukocyte antigens (HLAs) F. Cancer screening: Colonoscopy i age 50 years. In women, mammography and Papanicolaou (Pap) test as indicated. In men, prostate-specif c antigen as indicated. For liver transplants, alphaetoprotein (AFP).

Te rm ino lo g y I. Ge ne tic re la tio ns hip s : between the donor and the recipient A. Autograf : tissue trans er within the same individual (e.g., skin gra ) B. Isograf : between genetically identical individuals (e.g., identical twins)

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C. Allograf : between genetically nonidentical members o the same species; includes living related and unrelated donors and deceased donor human transplants D. Xenograf : Between di erent species; xenogra s are experimental. II. Surg ic a l te rm s A. Orthotopic graf : Old organ is removed, and the new one is placed in the same position (liver, lung, heart). B. Heterotopic graf : New organ is placed in a di erent position (kidney, pancreas, some hearts).

Do no rs a nd Do no r Se le c tio n I. De c e a s e d d o no rs : have brain injury resulting in irreversible neurologic injury or brain death A. Donors af er brain death (DBD): irreversible cessation o brain unction, as shown on neurologic exam, revealing unresponsiveness and absence o both spontaneous movement and re exes rom the brainstem and higher B. Donors af er cardiac death (DCD): Patients with irreversible neurologic injury who are not brain dead may donate their organs i the amily wishes to withdraw support and donate. Organs are not recovered until cessation o cardiac unction has persisted or 5 minutes, which, depending on the declaring physician, is absence o either a palpable pulse or electrical activity. C. Causes: most o en cerebrovascular disease or trauma D. Exclusions: cancer, in ection, and poor donor organ unction II. Living d o no rs : are individuals motivated by altruism A. Living unrelated donors (e.g., a spouse): share no more genes with a recipient than deceased donors B. Living related donors: share a substantial portion o their genes with the recipient C. Requirements: Living donors must be in good health, have normal unction o the organ under consideration, and be good candidates or anesthesia and the operative procedure. D. Full transplant workup: See “III. General health issues” earlier. E. Risks: Risk o death varies by organ (e.g., 1 in 3,000 or kidneys; 1 in 150 or livers). 1. Kidney: Perioperative mortality or living kidney donors is 0.03%. A living donor provides one kidney; the remaining kidney hypertrophies and achieves 80% o pre-donation creatinine clearance 2. Liver: Donation o the le lateral segment or either lobe o the liver uses open technique, with 0.5%–1% mortality risk. 3. Lung: Live donor lobar lung transplantation is very rare and mostly per ormed to help a waiting child. T e operation is done with an open procedure and involves removal o a lower lobe. For adult recipients, two donors are necessary. III. Do no r o p e ra tio n: Donor organ is removed, wherein the blood supply o the organ is controlled and then the organ is rapidly ushed with a cold (4°C) preservation solution to minimize ischemic injury. IV. Co ld is c he m ia : T e practical limit with current preservation methods is 4 hours or the heart, 6 hours or a lung, 12 hours or the liver, 20 hours or the pancreas, and 36 hours or a kidney.

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Quic k Cut Autogra ts and xenogra ts require immunosuppression to prevent rejection.

Quic k Cut Organ s election is crucial becaus e in ections or cancer rom the donor may be trans mitted to the immunos uppres s ed recipient.

Quic k Cut Strict criteria or brain death mus t be met be ore cons ideration o organ donation. Brain death criteria include: comatos e, apneic, no res pons e to pain, without cranial nerve ref exes or brain s tem ref exes

Quic k Cut Seps is with pos itive cultures is an abs olute contraindication or organ donation.

Quic k Cut The mortality or living kidney donation is very low but not zero.

Quic k Cut Organs are more s ens itive to warm is chemia than to cold is chemia.

Quic k Cut As cold is chemic time increas es , s o does the ris k o permanent damage and delayed or los s o unction o the organ.

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Im m uno lo g ic Co ns id e ra tio ns I. ABO b lo o d g ro up c o m p a tib ility: Same rules apply as those or red blood cell (RBC) trans usions. II. HLAs : histocompatibility antigens A. HLA-A, HLA-B, HLA-C, HLA-DR, HLA-DP, and HLA-DQ (six): Standard tissue typing includes HLA-A, HLA-B, and HLA-DR only. B. HLAs are encoded on chromosome 6: ransplant candidates have six HLAs, def ned by tissue typing (i.e., two each or HLA-A, HLA-B, and HLA-DR). C. Cross-match compatibility: Recipient’s serum is tested or the presence o cytotoxic antibodies directed against sur ace antigens (anti-HLA) on the donor lymphocytes. 1. Positive cross match: implies the presence o pre ormed antidonor antibodies in the serum o the recipient and generally precludes transplantation 2. Panel reactive antibody (PRA): High-PRA patients have pre ormed anti-HLA antibodies against a high proportion ( 80%) o a panel o random human cells, which is used to screen or reactivity. T ere ore, good donors or high-PRA patients are di cult to f nd, resulting in longer waiting times. 3. Donor-speci c antibody (DSA): Anti-HLA antibody in the recipient directed at one or multiple donor alleles, either major histocompatibility complex (MHC) class I or II. DSA is part o the diagnosis o antibody-mediated rejection (AMR).

Quic k Cut Immunologic compatibility o the donor and recipient inf uences the outcome or any type o organ trans plant.

Quic k Cut Cros s -match compatibility mus t be pres ent or kidney, pancreas , and s ome heart trans plants .

Quic k Cut I donor-s peci c antibodies are pres ent in the recipient, the donor organ is unacceptable due to ris k o hyperacute rejection and des truction o the organ.

Re je c tio n I. Hyp e ra c ute re je c tio n: occurs when the serum o the recipient has pre- ormed antidonor antibodies, which adhere to the endothelium, resulting in immediate gra in arction II. Ac ute c e llula r re je c tio n (ACR): Cell-mediated immune response initiated by helper cells (Fig. 23-1). T e pace o proli eration o alloreactive cell clones dictates that acute rejection occurs a er the sixth post-transplant day; a memory immune response can trigger ACR sooner. A. Diagnosis: by gra dys unction and biopsy B. reatment: ACR is usually reversible by a short course o highdose immunosuppressive drugs. C. iming: ACR usually occurs between weeks 1 and 12 posttransplant and rarely a er the f rst year, unless triggered by in ection or inadequate immunosuppression. III. Antib o d y m e d ia te d re je c tio n (AMR): results rom preormed antibody or rom plasma cell production o antibody to the transplanted organ A. Diagnosis: made by the triad o gra dys unction, presence o DSA in the serum, and complement (C4d) staining on biopsy B. reatment: No good treatment exists, but steroids, plasmapheresis, and intravenous immunoglobulin (IVIG) are commonly used. C. iming: 1-12 weeks post transplant IV. Chro nic re je c tio n: Usually happens a er 1 year or later. It has an insidious onset and is multi actorial, involving the cell-mediated and humoral arms o the immune system. V. Im m uno lo g ic to le ra nc e : olerance is a state in which the recipient’s immune system responds normally to all antigens except those o the donor (i.e., the donor antigens are “tolerated”). Small human trials have demonstrated that tolerance is possible.

Quic k Cut A pos itive preoperative cros s match between donor and recipient is highly predictive o hyperacute rejection. I hyperacute rejection occurs , it cannot be treated.

Quic k Cut Antibody mediated rejection leads to gra t ailure much s ooner than acute cellular rejection.

Quic k Cut Chronic rejection is poorly unders tood and cons idered neither treatable nor revers ible.

Quic k Cut The ultimate goal in trans plantation is tolerance, where this is no need or immunos uppres s ion.

Chapter 23

A

B

C

D

Organ ransplantation

365

Fig ure 23-1: Kidney rejection. A: Hyperacute rejection characterized by microthrombi in the glomerular capillaries (large arrow), in ltration with neutrophils (small thin arrow), and endothelial des truction (thick arrow). B: Acute tubulointers titial rejection s howing an inters titial lymphocytic in ltrate, inters titial edema, and in ltration o lymphocytes into the epithelium o the tubules (tubulitis ; arrows). C: Acute vas cular rejection with a s ubendothelial lymphocytic in ltrate (arrow), along with s ome evidence o chronic vas cular rejection. D: Chronic rejection with s evere proli erative endarteritis . (Courtes y o Roger D. Smith, MD.)

Im m uno s up p re s s io n I. Ge ne ra l c ha ra c te ris tic s : Most allogra s require indef nite suppression o the recipient’s immune system to prevent rejection. A. Purpose: to disable components o the immune response (typically lymphocytes) B. Multiple drug therapy: standard; aims or synergistic immunosuppression while minimizing the side e ects II. Cla s s if c a tio n (thre e typ e s ): Induction regimens, maintenance therapy, and antirejection regimens. Specif c immunosuppression medications are described in detail in able 23-1. A. Induction regimens: Aim to avoid rejection within the f rst ew post-transplant weeks. T ey consist o a high-dose steroid taper and an antilymphocyte drug, which can be either lymphocyte depleting (e.g., antithymocyte globulin or alemtuzumab) or nonlymphocyte depleting (e.g., basiliximab). B. Maintenance therapy: provides long-term immunosuppression to prevent rejection and usually include two to three drugs rom separate classes C. Antirejection regimens: high-dose, short-term ( 3 weeks) treatments aimed at reversing acute rejection episodes

Co m p lic a tio ns o Im m uno s up p re s s io n I. In e c tio ns : Nonspecif city o current immunosuppression also impairs host de enses against a diverse group o pathogens and causes opportunistic in ections. A. CMV: common in the early (3–6) months a er a transplant and presents with ever and leukopenia 1. Risk: Varies by prior exposure (serostatus). CMV seronegative recipients o seropositive donors are at the highest risk.

Quic k Cut A broad range o bacterial, viral, ungal, and protozoal organis ms are pos s ible and require prompt diagnos is and treatment becaus e they can be lethal.

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Ta b le 23-1: Im m uno s up p re s s ive Me d ic a tio ns Drug

Cla s s

E ect

Sid e E e c ts

Co m m e nts

Ind uc tio n Ag e nts a nd Antire je c tio n The ra p y Methylprednisolone, dexamethasone, hydrocortisone

Glucocorticoid (IV)

Anti-inf ammatory; inhibits all leukocytes

Obesity, cushingoid acies, poor healing, skin atrophy, striae, acne, diabetes, hypertension, osteoporosis, aseptic necrosis o the hips, cataracts, peptic ulcers, psychosis

Antithymocyte globulin (thymoglobulin, ATGAM)

Depleting polyclonal antibody

Depletes T lymphocytes

Fevers, chills, pulmonary edema, cytokine release syndrome, thrombocytopenia

Requires premedication with steroids, diphenhydramine, and acetaminophen, up to 21 days/ doses

Alemtuzumab (Campath)

Depleting monoclonal antibody (anti-CD52)

Depletes both T and B lymphocytes

Leukopenia

Single dose

Basiliximab (Simulect)

Nondepleting monoclonal antibody (anti-CD25)

Inhibits costimulation by blocking the IL-2 receptor

Rare anaphylaxis

Two doses

Tacrolimus (Progra , FK506)

Calcineurin inhibitor

Inhibits T-cell unction by decreasing IL-2 production

Nephrotoxicity, hypertension, neurotoxicity, tremor, alopecia, diabetes

Vasoconstricts the preglomerular arterioles

Cyclosporine A (Sandimmune, Neoral)

Calcineurin inhibitor

Inhibits T-cell unction by decreasing IL-2 production

Nephrotoxicity, hypertension, hirsutism, diabetes, gingival hyperplasia

Vasoconstricts the preglomerular arterioles

Mycophenolate mo etil (CellCept, My ortic)

Antimetabolite

Inhibits clonal T-cell proli eration by inhibiting purine salvage

Bone marrow suppression; GI disturbances (nausea, diarrhea)

Azathioprine

Antimetabolite

Inhibits clonal T-cell proli eration by inhibiting purine metabolism

Bone marrow suppression; skin cancer

Prednisone, prednisolone

Glucocorticoid (oral)

Anti-inf ammatory; inhibits all leukocytes

Obesity, cushingoid acies, poor healing, skin atrophy, striae, acne, diabetes, hypertension, osteoporosis, aseptic necrosis o the hips, cataracts, peptic ulcers, psychosis

Ind uc tio n Ag e nts

Ma inte na nc e The ra p y

(continued)

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Organ ransplantation

367

Ta b le 23-1: Im m uno s up p re s s ive Me d ic a tio ns (c on tin u e d ) Drug

Cla s s

E ect

Sid e E e c ts

Sirolimus (Rapamycin)

Mammalian target o rapamycin inhibitor

Inhibits T-cell activation

Poor wound healing, hernias, proteinuria, hypercholesterolemia, hypertriglyceridemia, mild bone marrow suppression

Everolimus

Mammalian target o rapamycin inhibitor

Inhibits T-cell activation

Poor wound healing, hernias, proteinuria, hypercholesterolemia, hypertriglyceridemia, mild bone marrow suppression

Belatacept

CTLA-4-Ig usion protein, costimulatory blockade

Blocks costimulation o T-cells by binding to CTLA-4

PTLD, PML

Co m m e nts Should be stopped perioperatively in all patients due to hernia risk

IV only; contraindicated in EBV-mismatched recipients

IV, intravenous; IL-2, interleukin-2; GI, gastrointestinal; CTLA-4-Ig, cytotoxic T-lymphocyte antigen 4 immunoglobulin; PTLD, post-transplant lymphoproli erative disorder; PML, progressive multi ocal leukoencephalopathy; EBV, Epstein-Barr virus.

2. Prophylaxis: valganciclovir 3. reatment: intravenous (IV) ganciclovir or oscarnet i it is resistant B. BK polyoma virus: urothelial virus that can invade a kidney transplant and cause allogra ailure 1. Prophylaxis: does not exist, so monitoring o BK viremia/viruria is per ormed selectively 2. reatment: minimizing immunosuppression C. Pneumocystis carinii pneumonia (PCP): Prophylaxis is given or 1 year with Bactrim, dapsone, or pentamidine. Bactrim also prevents Nocardia in ections. D. Fungal in ections 1. Common: Candidal overgrowth can cause thrush, esophagitis, and yeast in ections. Prophylaxis is 3 months o clotrimazole troches or nystatin swish and swallow. 2. Rare: Aspergillus, Nocardia , histoplasmosis, cryptococcosis, and coccidioidomycosis occur occasionally and must be treated promptly. E. oxoplasmosis: Kittens should be vaccinated and resh transplant patients should not change cat litter. F. uberculosis: can become reactivated a er transplant, so all patients are screened or prior exposure or disease II. Ne o p la s ia : Risks are skin cancer, post-transplant lymphoproli erative disorders (P LDs), and oral squamous cell or emale genital tract cancers. A. Skin cancer: Squamous and basal cell cancers o sun-exposed skin are very common post transplant. Daily sunscreen and annual dermatologic exams are recommended. B. P LD: orm o lymphoma, commonly arising rom B cells and usually associated with EBV 1. Early stages: may respond to acyclovir 2. Later stages: require CHOP chemotherapy (cyclophosphamide, h ydroxydaunorubicin, Oncovin, and prednisone) and rituximab, but the prognosis is poor 3. Oral squamous cell cancers/ emale genital tract cancers: Quic k Cut occur requently in post-transplant patients Papillomavirus is 4. Other: All other cancer screening (such as mammograms or implicated in cancers o the colonoscopy) should ollow current guidelines or all patients. s kin, oral cavity, and emale genital tract. III. P a re ntho o d a te r tra ns p la nta tio n: Organ ailure is associated with endocrine abnormalities that result in ertility problems. T ese abnormalities are reversed a er transplantation. A. Immunosuppression: Pregnancy results in metabolic changes that can result in allogra rejection (and sometimes loss) i not care ully managed. Recipients must be transitioned to

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a mycophenolate- ree regimen at least 2 months prior to conception because this drug is highly teratogenic. B. Outcomes: Premature deliveries and low birth weight in ants are common. Mycophenolate is contraindicated; associated with early miscarriage and cranio acial, limb, cardiac, esophageal, and renal mal ormations.

ORGAN-SP ECIFIC CONSIDERATIONS

Quic k Cut As drug metabolis m increas es , as in pregnancy, higher dos es o immunos uppres s ion are neces s ary to prevent rejection.

He a rt Tra ns p la nta tio n

Quic k Cut I. P re o p e ra tive a s s e s s m e nt: heart ailure survival score (HFSS) Mos t calculated or risk stratif cation immunos uppres s ive regimens A. Indications: End-stage heart ailure (New York Heart Association have little increas ed ris k o class III and IV). Most common causes are dilated and ischemic etal mal ormation except mycophenolate. cardiomyopathies, recurrent li e-threatening arrhythmias, congenital heart disease, and severe valvular disease. B. Contraindications: severe nonreversible pulmonary hypertension; peak oxygen consumption (VO2) 12 mL/kg/min II. Op e ra tive s tra te g y Quic k Cut A. Dissection and cardiectomy: Heart transplantation is mostly The major limitation orthotopic via a median sternotomy. Patients are placed on o cardiac trans plant is chronic rejection, producing cardiopulmonary bypass. s ymptoms o heart ailure and B. Order o reanastomosis: variations exist; le atrium, right accelerated atheros cleros is . atrium, pulmonary artery, then aorta III. P o s to p e ra tive m a na g e m e nt a nd c o m p lic a tio ns A. Location: cardiac surgery intensive care unit (ICU) B. Cardiac output (CO): Monitored and heart rate is maintained at 90–110 beats per minute; epicardial pacing or isoproterenol can be use ul because the heart is no longer innervated. C. Fluid status and volume: Swan-Ganz catheters assess the patient’s physiology and guide volume resuscitation. Urine output and ABGs are also use ul. D. Cardiac tamponade: should be suspected with hypotension, decreased chest tube output, and elevated central venous pressure (CVP) E. Severe rejection: may mani est as ventricular ailure IV. Outc o m e s : Post-transplant mortality is somewhat dependent on etiology; 1-, 2-, and 5-year patient survivals are 87%, 84%, and 75%, Quic k Cut respectively. A rican American recipients have lower s urvival V. Im m uno s up p re s s io n pos s ibly due to higher rates o A. Induction: Patients age younger than 40 years, those with prior hypertens ion pos t orthotopic ventricular assist devices (VADs), A rican Americans, and sensitized heart trans plant (OHT). patients generally require induction. Polyclonal (thymoglobulin) and monoclonal (anti-CD25, anti-CD52) have been described. B. Maintenance: generally tacrolimus, steroids, and antimetabolites VI. Re je c tio n: May mani est as gra dys unction; A rican Americans, those age younger than 40 years, and patients with prior VAD are at higher risk. Endomyocardial biopsy conf rms diagnosis. VII. Alte rna tive s to tra ns p la nta tio n: E cacy o VADs ( or both le and right ventricles) is constantly improving. OH is currently the best option or patients with heart ailure.

P ulm o na ry Tra ns p la nta tio n I. P re o p e ra tive a s s e s s m e nt A. Indications: single lung, bilateral lung, or combined heart-lung 1. Single lung transplant: chronic obstructive pulmonary disease; idiopathic pulmonary f brosis 2. Bilateral lung transplant: cystic f brosis; pulmonary hypertension without right-sided heart ailure 3. Heart/lung transplant: pulmonary hypertension with associated heart ailure (typically right sided); Eisenmenger syndrome B. Contraindications: specif c to pulmonary transplant, nonreversible pulmonary hypertension, and signif cant cardiac disease

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Organ ransplantation

369

II. Op e ra tive s tra te g y A. Single-lung transplantation: Can be done through a posterolateral thoracotomy. T e bronchial anastomosis is per ormed f rst (which is “telescoped”), then the pulmonary arterial and le atrial anastomoses. An omental wrap may be used to prevent leak around the bronchial anastomosis. B. Double-lung transplantation: can be done in two ways: via sequential lung transplant technique, as described or single-lung transplantation, or via a single tracheal, arterial, and venous anastomosis, requiring cardiopulmonary bypass (clamshell incision or midline sternotomy) C. Heart/lung transplantation: ypically per ormed through a median sternotomy. T ese organs are transplanted en bloc. III. P o s to p e ra tive m a na g e m e nt a nd c o m p lic a tio ns A. Location: cardiac surgery ICU B. Graf dys unction: mani ests as hypoxemia, inf ltrative pattern on chest x-ray, and heavy secretions rom the endotracheal tube C. Volume status and physiology: Aggressive diuresis may be required. Urine output, ABGs, and CO measurements help guide volume resuscitation. D. Ventilation: High levels o positive end-expiratory pressure (PEEP) may be used to maintain patency o the small airways; patients may remain on extracorporeal membrane oxygenation (ECMO) until the lungs are unctional. E. Airway complications: Although reduced with surgical Quic k Cut experience and improved technique, 10%–15% o lung recipients Airway complications experience airway complications (leaks, ungal in ections, are the Achilles heel o lung stenosis) because o poor blood supply to the anastomosis. T ese transplantation. complications are less likely with heart/lung transplant. F. In ection: Candida and aspergillus in ections are more serious than bacterial; mostly seen in the f rst 3 months post transplant. Pseudomonas aeruginosa and CMV in ections are common. IV. Outc o m e s : Both donation a er brain death and cardiac death are suitable in lung transplantation. Overall 1-, 2-, and 10-year gra survivals are 80%, 70%, and 50%, respectively. V. Im m uno s up p re s s io n A. Induction: Approximately 50% o patients receiving lung transplants get induction. B. Maintenance: calcineurin inhibitor–based triple therapy VI. Re je c tio n Quic k Cut A. Diagnosis: Conf rmation o suspected rejection is per ormed via In heart/lung transbronchial biopsy and bronchoalveolar lavage. trans plant recipients , rejection B. Acute: associated with lymphocytic inf ltrate and typically seen o lung trans plants may occur early post transplant without rejection o the heart. C. Chronic: characterized by f brosis and obliteration o the small airways and vessels, designated as obliterative bronchiolitis VII. Alte rna tive s to tra ns p la nta tio n: T ere are ew options or end-stage pulmonary disease. Patients who are not candidates or organ transplants are generally re erred to hospice.

He p a tic Tra ns p la nta tio n I. P re o p e ra tive a s s e s s m e nt A. Indications 1. Adult: cirrhosis (hepatitis C virus [HCV], nonalcoholic steatohepatitis [NASH], alcohol, etc.), ulminant hepatic ailure, hepatocellular carcinoma (HCC), and metabolic disorders 2. Pediatric: biliary atresia, Alagille syndrome, and metabolic disease B. Contraindications: Recent or continued alcohol or substance use and poor neurologic status. Complete thrombosis o the entire portal and mesenteric venous system may anatomically Quic k Cut preclude liver transplant. Alcoholis m is a major caus es o cirrhos is . II. Op e ra tive s tra te g y: Figure 23-2 Active alcohol us e is a s trict A. Piggyback: Recipient liver is dissected, leaving a short contraindication to liver recipient hepatic vein cu that can be anastomosed to the trans plantation. in erior vena cava.

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Organ-Specif c Considerations (1) Infe rior ve na cava

Aorta

(4) T tube in common bile duct

(3) He pa tic a rte ry (2) Porta l ve in

Fig ure 23-2: Standard anas tomos es us ed or orthotopic liver trans plant: (1) s uprahepatic in erior vena cava (IVC) and in rahepatic IVC anas tomos es , (2) portal vein anas tomos es , (3) hepatic (s plenic) artery anas tomos is , (4) anas tomos is or biliary drainage. (From Blackbourne LH. Advanced Surgical Recall, 2nd ed. Baltimore: Lippincott Williams & Wilkins ; 2004.)

B. Bicaval: Donor’s supra- and in rahepatic venae cavae are Quic k Cut anastomosed to the recipient’s. T is procedure sometimes uses In the cas e o an venovenous bypass. adult donor to a pediatric C. Living donor: involves transplant o the right liver (adult to adult) recipient, only a portion o the or le lateral segment (adult to child) donor liver is us ed as a “cut down” or “s plit” liver. D. Pediatric: may be rom a live or deceased adult or rom a deceased pediatric donor E. Combined liver-kidney: Li e-saving liver is transplanted f rst. III. P o s to p e ra tive m a na g e m e nt a nd c o m p lic a tio ns A. Location: transplant surgery ICU or surgical ICU B. Volume status and physiology: Hypotension should prompt evaluation or bleeding. C. Coagulopathy: Approximately 20% o patients have a bleeding complication, o en requiring repeat laparotomy and multiple trans usions o blood products to reverse coagulopathy. D. Primary non unction: Rare; despite vascular patency, the new liver ails to unction and requires urgent retransplantation with another organ. E. Hepatic artery or portal vein thrombosis: also rare, 5% o transplants 1. Diagnosis: Elevated LF s, especially ammonia, are suggestive; diagnosis is conf rmed with US or C angiography or by re-exploration. 2. reatment: o en requires retransplantation F. Biliary complications (including strictures and leaks): common, 15% o patients 1. Diagnosis: elevated bilirubin, endoscopic retrograde cholangiopancreatography (ERCP), or bilious drain output 2. Management: includes biliary decompression via stenting or reoperation (Roux-en-Y) IV. Outc o m e s : One-year patient and gra survival are 90%. A. Long-term outcomes: vary by cause o disease, with hepatitis C and HCC having high recurrence rates B. DCD donor organs: have more biliary complications and Quic k Cut slightly poorer long-term gra Liver trans plants V. Im m uno s up p re s s io n tend to be more res is tant to rejection than kidney A. Induction: Unlike most other solid organ transplants, liver trans plants . In s ome cas es , transplants do not receive induction immunosuppression. immunos uppres s ion may B. Maintenance: Initially tacrolimus, steroids, and antimetabolites. be dis continued altogether With hepatitis C or no early rejections, tacrolimus monotherapy (tolerance). may be su cient long term.

Chapter 23

VI. Re je c tio n A. Diagnosis: Liver rejection may mani est with clinical gra dys unction or with elevated liver enzymes. Alkaline phosphatase is typically elevated prior to aspartate aminotrans erase (AS ) and alanine aminotrans erase (AL ). B. Acute: indicated by a lymphocytic inf ltrate C. Chronic: characterized by f brosis or paucity o bile ducts VII. Alte rna tive s to tra ns p la nta tio n: Few options exist or end-stage liver disease. Patients who are not candidates or organ transplants are generally re erred to hospice.

Kid ne y Tra ns p la nta tio n

Organ ransplantation

371

Quic k Cut The elevated enzyme pro le in liver rejection is very s imilar to and o ten indis tinguis hable rom recurrent HCV.

Quic k Cut Hepatocyte trans plantation, s tem cell technologies , and xenotrans plantation are potential uture therapies or end s tage liver dis eas e.

I. P re o p e ra tive a s s e s s m e nt A. Indications: Leading etiologies o end-stage renal disease are diabetes, hypertension, and glomerulonephritis. B. Contraindications: specif c to kidney transplantation, severe iliac atherosclerosis, and signif cant abdominal obesity or severe cardiac or pulmonary disease C. Donors: 30% living; 70% deceased donor II. Op e ra tive s tra te g y: Figure 23-3 A. Recipient: Kidney is transplanted to the extraperitoneal iliac ossa through a curvilinear (Gibson) incision. 1. Adults: Donor renal vessels are anastomosed to the common or external iliac vessels. 2. Children: Aorta and in erior vena cava may be used. Quic k Cut Kidney trans plants B. Urinary drainage: Ureter is anastomosed to the bladder. are mos t commonly s upplied C. Recipient nephrectomy: indicated or chronic persistent by the external iliac ves s els . pyelonephritis, persistent upper tract stones, vesicoureteral re ux, severe unmanageable high-renin hypertension, and polycystic kidney disease III. P o s to p e ra tive m a na g e m e nt a nd c o m p lic a tio ns A. Location: ICU care is usually not required. B. Function: Living donor kidneys should unction immediately with a brisk diuresis (up to 1,000 mL/hr) and drop in creatinine. C. Delayed graf unction (DGF): Up to 40% o deceased donor kidneys do not unction immediately. Management is uid restriction and dialysis. Function usually returns in 1–2 months. D. Oliguria: rare a er living donation and should result in prompt evaluation or obstructive, prerenal, or intrarenal problems (Foley, volume status, thrombosis, acute kidney injury, or rejection) E. Vascular complications 1. Renal artery thrombosis: occurs in 1% o transplants a. Presentation: sudden decline in urine output b. Diagnosis: duplex US c. reatment: requires emergent re-exploration, as it can only be salvaged within minutes o onset Infe rior ve na ca va

Abdomina l a orta

Tra ns pla nte d kidne y

Common ilia c a rte ry

Inte rna l ilia c a rte ry Exte rna l ilia c a rte ry Exte rna l ilia c ve in

Fig ure 23-3: The trans planted kidney. (From Snell RS. Clinical Anatomy by Regions, 9th ed. Baltimore: Lippincott Williams & Wilkins ; 2011.)

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V.

VI.

VII.

VIII.

Organ-Specif c Considerations

2. Renal artery stenosis: Presents as uncontrollable Quic k Cut hypertension and is diagnosed with duplex US and Mos t vas cular arteriography. It is managed with operative repair or complications require urgent angioplasty stenting. or emergent intervention 3. Renal artery aneurysm: Present as pulsatile masses and by open or endovas cular are diagnosed with duplex US (or by a bruit). Management techniques . is surgical repair, stenting, or gra removal and antibiotics ( or mycotic aneurysms). 4. Renal vein thrombosis: occurs in 1%–4% o transplants. a. Presentation: gra pain (due to swelling) and hematuria b. Diagnosis: duplex US c. Management: Immediate surgical exploration. Partial venous thrombosis can be managed with anticoagulation. F. Ureteral obstruction: occurs in 1%–9% o transplants 1. Presentation: oliguria or polyuria with rising creatinine 2. Diagnosis: hydronephrosis 3. reatment: initially, a retrograde ureteral stent or a nephrostomy tube, ollowed by surgical revision via ureteroneocystostomy or ureteroureterostomy G. Urinary leaks and stulas: occurs 5–7 days a er transplantation 1. Presentation: elevated creatinine and a perinephric uid collection 2. Diagnosis: conf rmed with pyelograms or nuclear medicine scans 3. reatment: similar to that or ureteral obstruction discussed earlier H. Lymphoceles: occur in less than 5% o recipients and appear as a perinephric lymph collection Quic k Cut 1. Presentation: decreased urine output and/or rising creatinine Lymphocele can be and ipsilateral leg edema dis tinguis hed rom urinoma 2. Diagnosis: US ( uid collection with or without by s ending a f uid s ample or creatinine level and culture. hydronephrosis) Lymphocele has a low 3. Management: percutaneous or laparoscopic drainage creatinine (equal to s erum); Outc o m e s : Kidney transplant outcomes have improved over the urinoma has high creatinine. last several decades. A. Recipients o living donor kidney: One-year survival approaches 98%–99% and gra hal -li e is 17 years. B. Recipients o deceased donor kidney: One-year survival is 91% with gra hal -li e o 10 years. Im m uno s up p re s s io n A. Induction: Not required but decreases early rejection and is almost universally used. Basiliximab, thymoglobulin, and alemtuzumab are leading induction agents. B. Maintenance: generally tacrolimus, steroids, and mycophenolate, with an early steroid taper Re je c tio n A. Acute rejection: mostly occurs 1 week–3 months a er transplantation; in 10%–15% o patients, within the f rst 6 months a er transplant 1. Presentation: low urine output and rising creatinine 2. Diagnosis: made with a kidney biopsy 3. Management: pulse steroids or antilymphocyte sera or ACR and steroids, possibly pheresis and IVIG or other treatments or AMR B. Chronic rejection: known as chronic allograf nephropathy (CAN), transplant glomerulopathy (TG), and interstitial brosis/tubular atrophy (IFTA); occurs over months to years 1. Presentation: glomerular sclerosis, tubular atrophy, duplication o the glomerular basement membrane, and interstitial f brosis 2. reatment: No cure, but longevity is maximized by adjusting Quic k Cut immunosuppression to minimize nephrotoxicity. Becaus e s urvival improves with trans plantation, Alte rna tive s to tra ns p la nta tio n: Include hemodialysis, all long-term dialys is patients peritoneal dialysis, or medical management only. Patient s hould be re erred or a survival is greatest with transplantation and lower with dialysis trans plant evaluation. (10%–20% annual mortality rates).

Chapter 23

P a nc re a tic a nd Is le t Tra ns p la nta tio n

Organ ransplantation

373

Quic k Cut I. P re o p e ra tive a s s e s s m e nt All type 1 diabetic A. Indications: Solitary pancreas transplants are per ormed patients with renal ailure are mainly or patients with brittle type 1 diabetes (def ned by candidates or s imultaneous hypoglycemic unawareness) and occasionally or patients a er pancreas -kidney trans plants . total pancreatectomy or chronic pancreatitis or trauma or as part o a multivisceral transplant. B. Contraindications: specif c to pancreas transplant, insulin requirement greater than 100 units/day indicating high insulin resistance, severe iliac atherosclerosis, BMI greater than 30 kg/m 2, and poor cardiovascular health C. Donors and outcome: Gra outcomes a ected by donor age, BMI, cause o death, and the appearance o the pancreas. Worse outcomes are seen with donor BMI greater than 30 kg/m2, age older than 50 years, and death due to cerebrovascular accident. II. Op e ra tive s tra te g y A. Simultaneous pancreas-kidney (SPK): Both kidney and pancreas are obtained rom a single donor and transplanted into the recipient with the advantages o better outcomes than pancreas-alone transplant and only one operation needed. B. Pancreas af er kidney (PAK): living donor kidney transplant ollowed months later by deceased donor pancreas transplant 1. Advantages: can avoid dialysis i a live donor is available and maximizes patient survival, which depends on a unctioning kidney 2. Disadvantages: Rejection o pancreas may occur without rejection o kidneys, delaying detection, and requires two operations. C. Pancreas transplant alone (P A): Indicated or brittle diabetics without signif cant nephropathy. T ere is no mortality benef t, but P A signif cantly improves quality o li e. D. Simultaneous pancreas and live donor kidney (SPLK): Patient may receive a living donor kidney and a deceased donor pancreas during the same operation, i the living donor is willing to be “on call.” E. Venous drainage: Portal vein is anastomosed either to the Quic k Cut recipient vena cava or iliac vein (systemic drainage) or to a Becaus e 50% mesenteric vein branch (portal drainage). o ins ulin is cleared by the F. Arterial supply: Pancreatic blood supply is rom the celiac axis rs t-pas s e ect in the liver, portal drainage prevents (splenic artery) and superior mesenteric artery (SMA) (in erior hyperins ulinemia. pancreaticoduodenal arteries). In back table preparation, the internal and external branches o the donor iliac artery Y gra are anastomosed to the splenic artery and SMA. T e common Quic k Cut iliac Y gra is then anastomosed to the recipient iliac artery. Enteric drainage G. Exocrine drainage: Donor duodenum is anastomosed to is mos t common now due the recipient jejunum (enteric drainage) or bladder (bladder to complications o bladder drainage). drainage, which include urinary tract in ections , III. P o s to p e ra tive m a na g e m e nt a nd c o m p lic a tio ns hematuria, urethral s trictures , A. Graf thrombosis: Presents as sudden rise in glucose, is bicarbonate was ting, and diagnosed by duplex US, and treated by excision o the gra . dehydration. emporary anticoagulation is requently used to prevent this complication or to treat partial vein thromboses. B. Postoperative hemorrhage (either intraperitoneal or rom a staple line): can occur in up to 20% o cases C. Anastomotic leaks ( rom the duodenal anastomosis or staple lines): Di cult to repair. reatment includes IV antibiotics and anti ungals, bowel rest, and anastomotic revision (possibly to Roux-en-Y drainage). It may require allogra pancreatectomy. IV. Outc o m e s : One-year gra survival or SPK is 90%, PAK 85%, and P A 85%. V. Im m uno s up p re s s io n A. Induction: Decreases early rejection. T ymoglobulin, alemtuzumab, and basiliximab are leading induction agents. B. Maintenance: generally tacrolimus, steroids, and mycophenolate, with an early steroid taper

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VI. Re je c tio n: no reliable markers; suspected by elevated amylase or lipase (sometimes elevated glucose but o en this is a sign o irreversibility) A. Diagnosis: can only be made by biopsy B. reatment: similar to rejection o kidney transplants VII. Alte rna tive s to tra ns p la nta tio n A. Islet transplantation: Islets are isolated by enzymatically digesting the pancreas and are in used through the portal or mesenteric vein and embolize to the liver (Fig. 23-4). 1. Indications: same as whole pancreas transplant 2. Donors: more lenient criteria (older and more obese patients are acceptable) 3. Mortality: close to zero; still requires immunosuppression 4. Insulin dependence: at highest volume centers, 80%–90% at 1 year but only 20% at 5 years 5. Sensitization: Islet transplants can sensitize patients, making uture kidney or pancreas transplants very di cult to match. Quic k Cut B. Insulin therapy: can be given by individual injections or Is let cell trans plants management using an insulin pump and glucose sensor do not unction as well or las t

Sm a ll Bo we l a nd Multivis c e ra l Tra ns p la nta tio n

as long as s olid pancreas trans plants .

I. Ind ic a tio ns : Patients with short bowel syndrome (SBS) (less than 200 cm o unctioning small bowel) rom congenital abnormalities, Crohn disease, mesenteric thrombosis, trauma, or desmoid tumors. Most patients are on long-term total parenteral nutrition ( PN) and lose access, have line sepsis, or develop cholestatic liver disease due to PN. II. Op e ra tive s tra te g y A. Small bowel only 1. Venous out ow: may be portal or systemic 2. GI anastomosis: per ormed in side-to-side ashion

P a ncre a s Ce ntra l ve in Bra nch of porta l ve in Colla ge na s e dige s tion

Is le ts within s inus oids

Live r Exocrine fra gme nts

P urifie d is le ts

Tra ns pla nta tion of purifie d is le ts into live r through a pe rcuta ne ous ca the te r

Figure 23-4: Islet transplantation. The pancreas is procured as a whole organ rom the donor. The islets are isolated rom the pancreas and are puri ed and in used into a cannula placed in a branch o the recipient’s portal vein. (From Mulholland MW, Maier RV, Lillemoe KD, et al. Greenf eld’s Surgery: Scientif c Principles and Practice, 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2006.)

Chapter 23

III.

IV.

V. VI. VII.

Organ ransplantation

375

3. Ileostomy: end or loop ileostomy 4. Feeding access: with jejunostomy or gastrostomy B. Multivisceral transplant: Can include liver/small bowel or liver/pancreas/small bowel. Donor small bowel is procured with preservation o vessels (either SMA/superior mesenteric vein or aorta and vena cava). P o s to p e ra tive m a na g e m e nt a nd c o m p lic a tio ns : include Quic k Cut bleeding, thrombosis, anastomotic leaks, stomal problems, and Gra t-vers us -hos t dis eas e is more common sepsis in s mall bowel trans plants A. Emergency re-exploration: high rate a er transplant due to the large amount o B. P LD: secondary to EBV lymphoid tis s ue pres ent. C. Graf unction: monitored by absorption studies and direct biopsy Outc om e s : improved quality o li e compared to dependence on PN A. Patient survival: 1-year, 75%; 3-year, 55%–80% C. T ree-year graf survival: 62% Im m uno s up p re s s io n: Induction therapy is commonly used with two or three drug maintenance regimens. Re je c tio n: very common (acute rejection in 30%–55%); diagnosed by malabsorption and ileal biopsy Alte rna tive to tra ns p la nta tio n: PN

Co m p o s ite Tis s ue Allo g ra t a nd Va s c ula rize d Co m p o s ite Allo g ra t Tra ns p la nts

Quic k Cut

Examples o CTA I. De f nitio n: Composite tissue techniques involve transplantation o include ace and hand multiple tissue types (e.g., muscle, bone, vessels, nerves, and skin) trans plantation. in a unctional unit. Composite tissue allogra (C A) requires more specialized surgery and immunosuppression than does solid organ transplant. Quic k Cut II. Ind ic a tio ns : Face: patients with severe acial de ormities due to Recovery o trauma or burns. Hand: amputees vas cularized compos ite III. Op e ra tive s tra te g y: Skin, subcutaneous tissues, bones, muscles, allogra t is time-intens ive and requires care ul coordination nerves, and vessels need to be recovered together. with thoracic and abdominal IV. P o s to p e ra tive m a na g e m e nt a nd c o m p lic a tio ns : include recovery teams . bleeding, thrombosis, and rejection A. Extensive therapy (physical, occupational, swallow, or speech): will be required Quic k Cut B. Graf unction: monitored by unction (degree o active and Failure to continue passive joint movement) and appearance extens ive phys ical therapy V. Outc o m e s may doom the CTA gra t. A. Face transplants (partial or whole): Approximately 25 have been per ormed, with our recipient deaths. B. Hand transplants: have been per ormed with some success, Quic k Cut but there are high costs, rehabilitation requirements, The ps ychological uncertain long-term outcome, and side e ects resulting rom impact o CTA is s ubs tantial immunosuppression and requires continuous evaluation. VI. Im m uno s up p re s s io n: Induction therapy is commonly used with two or three drug maintenance in a variety o regimens. VII. Re je c tio n: common; diagnosed by skin biopsy VIII. Alte rna tive s to tra ns p la nta tio n: amputation o limbs with use o prosthetics or non unctional coverage o open areas by reconstructive surgery (tissue aps and skin gra s)

Chapter 24

Pediatric Surgery

Clint D. Cappiello, Alexis D. Smith, and Eric Strauch

INTRODUCTION Pediatric surgery is a distinct specialty because in ants and children have both dif erent pathology and a dif erent physiologic response than adults.

CONGENITAL HERNIAS

Quic k Cut Remember that children are not jus t s mall vers ions o adults .

Ing uina l He rnia I. Inc id e nc e : occurs in 1%–4% o all children Quic k Cut A. Presentation: Right side 60%, le side 30%, and bilateral 10% o Repair o an inguinal hernia remains the mos t the time; male-to- emale ratio ranges rom 3:1 to 10:1. common general s urgical B. Premature in ants: Incidence is up to 10 greater. procedure in children. C. Increased: in patients with hydrocephalus who are treated with ventriculoperitoneal (VP) shunts, in patients with connective tissue disorders, and in in ants and children on peritoneal dialysis Quic k Cut II. Clinic a l p re s e nta tio n: Figure 24-1 Unlike in adults , a A. Age: O en diagnosed in in ancy, and 35% o patients present congenital inguinal hernia be ore age 6 months. res ults rom a patent B. Classic history: mass or bulge in the groin, scrotum, or labia, proces s us vaginalis , not a breakdown in the inguinal which usually occurs during times o increased abdominal f oor. pressure and usually disappears a er straining or crying has resolved C. I no mass is present: Physician can eel the thickened spermatic Quic k Cut cord, which represents the nondistended hernia sac. A nonreducible III. Inc a rc e ra tio n hernia is incarcerated and A. Boys: Risk associated with a hernia is the chance o intestinal warrants emergent s urgical incarceration. intervention. 1. Intestinal ischemia and obstruction: can occur 2. esticular ischemia: Entrapped bowel becomes edematous and compresses the spermatic vessels. 3. Prematurity: Risk o incarceration in a premature in ant is 2–5 higher than in the older child. B. Girls: Ovarian incarceration can occur as well as incarceration o the intestine. C. reatment: reduction o the incarcerated hernia, hydration o the patient, and herniorrhaphy 1. Premature in ant: hernia repaired during the admission in the rst 24–48 hours Quic k Cut 2. Approach: Reduction is per ormed with or without sedation In in ants younger by gentle, continuous pressure on the incarcerated intestine. than age 1 year, the ris k o 3. I hernia does not reduce: Most hernias will reduce, but i incarceration doubles with delaying repair. not, emergent repair, evaluation o the intestine, and resection o necrotic intestine needs to be per ormed.

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377

Pe ritone a l cavity

Cys t

Va s de fe re ns Pe rs is te nt proce s s us va gina lis Epididymis Te s tis

Pe ritone a l fluid

A

B

Coils of s ma ll inte s tine ins ide pe rs is te nt proce s s us va gina lis, which forms he rnia l s a c

C

Fig ure 24-1: The prototypical congenital inguinal hernia: a s mall bowel loop pres ent in a patent proces s us vaginalis . (From Snell RS. Clinical Anatomy, 7th ed. Philadelphia: Lippincott Williams & Wilkins ; 2003.)

IV. He rnio rrha p hy: A hernia should be repaired soon a er it is diagnosed, unless a major medical reason prohibits. In most children, the hernia can be repaired with outpatient surgery. Premature in ants may have apnea and bradycardia a er surgery and require overnight admission or monitoring. A. Procedure: Open herniorrhaphy in the child consists o identi ying the sac, dissecting the spermatic structures ree, and ligating the sac high at the internal ring o the inguinal canal. Floor repair is rarely needed. B. Laparoscopy: Laparoscopic herniorrhaphy has also gained popularity. Laparoscopic evaluation o the contralateral side can also be per ormed. C. Complications: damage to the vas de erens, vascular injury to the testes, recurrence, and iatrogenic cryptorchidism D. Recurrence rate: reported to be 1%, and the highest requency occurs in premature in ants and patients with incarcerated hernias, connective tissue disorders (e.g., Ehlers-Danlos syndrome), or increased intra-abdominal pressure (VP shunts or peritoneal dialysis catheters)

Dia p hra g m a tic He rnia s I. De f nitio n: Communications through the diaphragm that allow abdominal contents to migrate into the thoracic cavity; incidence is 2.4 in 10,000 live births.

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Congenital Hernias

II. Etio lo g y: Eighty percent are on the le , 20% are on the right. Herniation through the diaphragm on the right side occurs rarely due to the presence o the developing liver. A. Foramen o Bochdalek (most common): Posterolateral diaphragmatic de ect resulting rom a ailure o two muscular groups to use; it occurs most o en in the le hemidiaphragm and is bilateral in less than 10% o in ants. B. Foramen o Morgagni: anterior diaphragmatic de ect; much less common and generally results in less severe problems III. Dia g no s is : Prenatal ultrasound (US) can identi y abdominal viscera in the thorax, and polyhydramnios may occur secondary to oregut obstruction. Postnatal diagnosis o herniation is based primarily on impaired ventilatory capacity. A. Physical examination: reveals tachypnea, dyspnea, use o accessory muscles or ventilation, cyanosis, and nasal aring 1. Breath sounds: decreased or absent on the af ected side 2. Heart sounds: shi ed away rom the af ected side Quic k Cut 3. Bowel sounds: heard in the af ected hemithorax A right-sided cardiac 4. Scaphoid abdomen: caused by the migration o abdominal silhouette (dextrocardia) contents into the chest and res piratory distress B. Chest radiograph: shows signs typical o herniation (Fig. 24-2) signal a le t-sided congential 1. Loculated gas pattern: ound in the af ected hemithorax diaphragmatic hernia until proven otherwis e, due to 2. Mediastinal shif : occurs away rom the hernia bowel entering the le t pleural 3. Atelectasis: occurs in the unaf ected lung space. IV. P re o p e ra tive m a na g e m e nt A. Gastrointestinal (GI) decompression: should be per ormed B. Pneumothorax (in the una ected hemithorax): should be sought and, i present, treated with a chest tube Quic k Cut C. Pulmonary hypertension: causes right-to-le shunting across Preoperative management is aimed at the patent ductus arteriosus (PDA) and oramen ovale both res piratory ins u ciency 1. Hypoxemia: due to hypoplastic lung(s); causes acidosis and pulmonary vas cular 2. Acidosis: causes pulmonary vasculature to constrict, which hypertens ion. decreases blood ow to the lung and increases the right-to-le shunt D. Surgical repair: should proceed only a er the in ant is stable

Fig ure 24-2: Ches t radiograph o a newborn with a le t congenital diaphragmatic hernia. Medias tinal s tructures s hi ted to the right. Abdominal vis cera occupy the le t hemithorax. Nas ogas tric tube locates the s tomach. (From Mulholland MW, Doherty GM, Maier RV, et al. Greenf eld’s Surgery Scientif c Principles and Practice , 4th ed. Philadelphia: Lippincott Williams & Wilkins ; 2006.)

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VI.

VII.

VIII.

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E. High- requency oscillatory ventilation (HFOV): or persistent respiratory distress, hypoxemia, and hypercarbia F. Nitric oxide (NO): potent pulmonary vasodilator that is mixed with the gases used in the ventilator to improve hypoxemia by treating pulmonary hypertension G. Extracorporeal membrane oxygenation (ECMO): consider i acidosis with hypoxemia persists Op e ra tive m a na g e m e nt: based on the ollowing principles: A. Surgical reduction: Herniated contents are reduced surgically back into the abdomen with a subcostal incision or thoracotomy. Recently, a thoracoscopic approach has been success ul. B. Repair: Hernia de ect is repaired either primarily or with prosthetic. C. Monitoring: Acid–base balance and respiratory unction are monitored care ully; aggressive support is continued as needed. P o s to p e ra tive m a na g e m e nt: aimed primarily at maintaining adequate ventilation and per usion and includes the ollowing: A. Respiratory support (on a ventilator): given as needed, and arterial blood gases are monitored B. Atelectasis treatment (o either lung): Retained secretions are prevented. C. Observation or contralateral pneumothorax: reat rapidly i it occurs. D. Adequate GI decompression: provided with an intraoperatively placed nasogastric (NG) tube E. Intra-abdominal compartment syndrome prevention: Silo or abdominal patch may be placed because loss o abdominal domain can make primary repair di cult, and the inability to obtain a tension- ree closure will result in increased abdominal pressure. F. Fluid management: Critical postoperatively, as patients may be hypovolemic initially. Subsequently, diuretics may be used to avoid uid overload. P ro g no s is : depends on preoperative severity and time o presentation Quic k Cut A. Survival rate: 60%–90%; long-term mortality is 10% and is Res olution o usually secondary to persistent pulmonary hypertension. res piratory ins u ciency 1. Ipsilateral lung: almost always hypoplastic and does not aid depends on the maturity o the signi cantly in postoperative respiratory unction contralateral lung and control 2. Lung development: I the in ant survives, the lung will o pulmonary hypertens ion. continue to develop, but a normal complement o alveoli may never be reached. B. Pulmonary unction: Approaches normal as survivors reach adulthood. Studies have shown that survivors are expected to Quic k Cut develop appropriate exercise tolerance. The two main ECMO p a tie nts : survival rate o 43%–80%; should be considered types o abdominal wall as a temporary, potentially li esaving therapy or those or whom no de ects are g a s tro s c his is other option is available and o m p ha lo c e le . In both, the abdominal contents are outs ide o the peritoneal cavity; however, pres entation and management are cons iderably di erent.

ABDOMINAL WALL DEFECTS Typ e s Ta b le 24-1: Co m p a ris o n o Co ng e nita l Ab d o m ina l Wa ll De e c ts Cha ra c te ris tic s

Ga s tro s c his is

Om p ha lo c e le

Size of defect

Smaller ( 4 cm)

Usually larger (4–12 cm)

Presence of sac

No

Yes, if ruptured sac remnant

Contents of sac

Intestine (midgut)

Intestine (midgut, colon), liver, spleen

Location of defect

Right of umbilicus

Central at umbilicus

Associated anomalies

Rare (intestinal atresia)

Common

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Abdominal Wall De ects

Ga s tro s c his is I. Clinic a l e a ture s : usually a small ( 4 cm) opening in the abdominal wall, immediately to the right o the cord, which is located in the normal position ( able 24-1) A. Characteristics: Intestines appear edematous and thickened Quic k Cut with a brinous peel secondary to the in ammatory response In gastroschisis, there to direct intrauterine exposure to amniotic uid and postnatal is no protective sac covering the herniated contents. vascular compromise. B. Herniation: ypically, the entire midgut is herniated; the stomach, urinary bladder, and gonads may also herniate. C. Associated anomalies and syndromes: Rare; intestinal atresia is the most requent (10%–15% o cases) anomaly. Quic k Cut II. P re na ta l d ia g no s is : most commonly made by prenatal US

In ants with gas tros chis is are more likely to be born premature and o ten have intrauterine growth retardation with low birth weights .

III. P re o p e ra tive m a na g e m e nt: encompasses three main principles: respiratory support due to in ants’ prematurity, heat preservation, and uid resuscitation due to the large sur ace area o exposed intestines A. Fluids: In ants are usually hypovolemic and require 125%–150% maintenance intravenous (IV) uids or adequate resuscitation. B. NG decompression and broad-spectrum antibiotics: are initiated C. Intestinal ischemia: may be present due to obstruction o the vascular supply to the intestines

IV. Op e ra tive m a na g e m e nt: Emergent; there is no covering o the GI tract to prevent heat and uid losses. In ants undergo either immediate or delayed primary closure depending on the ability to reduce the herniated viscera. A. Immediate primary closure: involves decompressing the GI Quic k Cut tract and stretching the abdominal wall over the de ect with Rapid coverage o the expos ed vis cera closure immediately a er birth with a plas tic bowel bag is B. Abdominal compartment syndrome: o avoid this imperative to protect the complication, place a pre ormed Silastic pouch (silo) or bowel and minimize heat and temporary coverage. Serial reductions are per ormed at the mois ture los s . bedside until primary closure is easible (usually in 5–7 days).

Om p ha lo c e le I. Clinic a l e a ture s : central abdominal wall de ect located at the umbilicus ranging rom 2 to 12 cm A. Location: Most omphaloceles are lateral old de ects that always occur at the umbilicus and are covered with a sac. (See able 24-1) B. Sac: Covers the extruding visceral contents (always present); Quic k Cut i the omphalocele has ruptured, a sac remnant will be visible. Delayed primary T e sac usually contains the liver and midgut. clos ure is us ed i there is C. Pentalogy o Cantrell: Omphalocele may be a constituent; concern or abdominal compartment s yndrome. others are diaphragmatic hernia, cle sternum, absent pericardium, and intracardiac de ects. D. Associated anomalies: trisomies 13 and 18; Beckwith-Wiedemann syndrome; and cardiac, neural tube, and genitourinary mal ormations II. P re na ta l d ia g no s is : made classically by US, which can also help dif erentiate an omphalocele rom gastroschisis by the presence o a sac

Quic k Cut Approximately 50% o omphalocele patients have one or more as s ociated anomalies .

III. P re o p e ra tive m a na g e m e nt: varies depending on whether the omphalocele sac is intact or ruptured A. All cases: NG decompression, IV uid resuscitation, and broadspectrum antibiotics are instituted in all cases. B. Unruptured omphalocele: Managed initially nonoperatively; the sac is le intact and protected with a sterile dressing. Workup is initiated or associated de ects. C. Ruptured omphalocele: managed with immediate placement o a silo or temporary coverage o the de ect

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IV. Op e ra tive m a na g e m e nt: Can vary greatly; the choice o procedures includes primary closure, staged repair, or, or an unruptured omphalocele, initial nonoperative management. A. Primary repair: Can prove to be problematic with larger omphaloceles. I primary repair is attempted, monitoring or intra-abdominal hypertension is essential. B. Staged repair: Silastic sheeting or preconstructed silo bags can be used to stage the repair. By keeping tension on the prosthetic sac through routine bedside reductions, the abdominal wall can be stretched to accommodate the herniated viscera. 1. Closing the de ect: Prosthetic material or biologic mesh can be used. 2. Closure: usually accomplished within 10 days C. Alternative method o treatment: Cover the de ect with skin aps, leaving the resultant ventral hernia to be repaired later. V. No no p e ra tive m a na g e m e nt: Option or patients with associated pulmonary hypoplasia and cardiac anomalies that may not tolerate reduction. Initial nonoperative management acts as a bridge to delayed closure when the in ant is more stable. A. echnique: Sac is coated with silver sul adiazine (Silvadene) or a silver-impregnated sterile dressing; an eschar orms, with subsequent granulation tissue. T e resultant ventral hernia can be repaired later. B. Risks: sac rupture, requiring subsequent repair in an in ected area; sepsis; undiagnosed intestinal atresia; and prolonged hospitalization

P o s to p e ra tive Ma na g e m e nt I. Mus c ula r p a ra lys is a nd m e c ha nic a l ve ntila tio n: may be required until the abdomen stretches enough to accommodate the viscera or a reoperation to loosen the repair II. Slo w o ns e t o b o we l unc tio n: In ants o en require parenteral nutrition. Bowel unction appears to return aster ollowing repair o an omphalocele.

Quic k Cut Abdominal compartment s yndrome pres ents with oliguria, ventilatory compromis e, decreas ed venous return, and low cardiac output.

P ro g no s is I. Ga s tro s c his is : Although more di cult to manage initially, it has ew long-term problems. A. Mortality rate: greatly improved with the use o total parenteral nutrition ( PN) and is now 5% Quic k Cut B. Intestinal strictures: may develop at evisceration site due to ischemia Mortality is related to C. Short-gut syndrome: may develop i intestinal gangrene is prematurity, s eps is , as s ociated congenital anomalies , and the present and an extensive small bowel resection is required viability o the GI tract at the II. Om p ha lo c e le : Outcome is related to the presence o associated time o s urgery. anomalies; overall mortality rate ranges rom 20% to 60%.

ESOP HAGEAL ATRESIA AND TRACHEOESOP HAGEAL MALFORMATIONS De f nitio n I. Es o p ha g e a l a tre s ia (EA) (with o r witho ut tra c he o e s o p ha g e a l f s tula [TEF]): most common congenital anomaly o the esophagus II. Inc id e nc e : Ranging rom 1:2,500 to 4,500 live births; there is a wide spectrum o lesions. III. As s o c ia te d a no m a lie s : high incidence; dictate overall outcomes and survival

Typ e s o Le s io ns I. P ure EA: proximal and distal blind pouches without a EF; occurs in 7% o patients (Fig. 24-3) II. EA with a p ro xim a l TEF: least common type; occurs in 0.5% o patients III. EA (p ro xim a l p o uc h) with a d is ta l TEF: occurs in 86% o patients Quic k Cut Es ophageal atres ia IV. TEF witho ut a tre s ia (H-typ e f s tula ): occurs in 5% o patients; with proximal pouch and dis tal dif ers in presentation in that patients tend to present at an older age tracheoesophageal s tula is with recurrent pneumonia the mos t common variant. V. P ro xim a l a nd d is ta l TEF: occurs in 1.5% o patients

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Esophageal Atresia and racheoesophageal Mal ormations

A

B

C

D

Fig ure 24-3: Types o es ophageal atres ia. Atres ia with dis tal tracheoes ophgeal s tula (A) is the mos t common.

As s o c ia te d Co ng e nita l Ano m a lie s I. Ca rd io va s c ula r a no m a lie s : Most common; among these, ventricular septal de ects (VSDs) and tetralogy o Fallot are most requent. II. VACTERL: may be ully or partially demonstrated, that is, one or any combination o lesions may occur

Dia g no s is

Quic k Cut As s ociated congenital anomalies occur in 50% –70% o es ophageal atres ia.

Quic k Cut

The VACTERL I. P hys ic a l e xa m ina tio n as s ociation, a wellA. Aspiration o material: can present as excessive salivation as recognized anomaly complex, well as choking and cyanosis with breast eeding involves vertebral and a nal B. Fistula: can result in pneumonitis and respiratory distress de ects , c ardiac anomalies , tracheoe s ophageal s tula, C. Scaphoid abdomen: accompanies pure atresia due to the lack o and renal and limb dys plas ia. distal air in the GI tract II. Dia g no s is : Usually made within the rst 24 hours a er birth. T e af ected in ant classically presents with choking with the rst eeding. A. Plain radiographic lms (o the chest and the abdomen): important in establishing the diagnosis Quic k Cut 1. Chest lm: should con rm the diagnosis by using air as Mos t es ophageal contrast and will demonstrate the blind upper pouch as well atres ias can be diagnos ed as ailure o passage by the NG tube at the beds ide by nding res is tance to pas s age o an 2. Gasless abdomen: characteristic o pure EA NG tube. 3. Long-gap EA: gap greater than 3 cm between the two ends o the esophagus B. Workup: Due to high incidence o concomitant congenital de ects, thorough workup is warranted preoperatively. 1. Physical exam: ocuses on identi ying any de ects (VAC ERL) 2. Echocardiography: best initial screening test or cardiac de ects 3. Additional testing: renal ultrasonography and chromosomal analysis

P re o p e ra tive Ma na g e m e nt I. De c o m p re s s io n o the p ro xim a l p o uc h: requires a sump tube (Replogle tube) with low, continuous suction II. Up rig ht p o s itio n: is maintained III. De la ye d re p a ir: Placement o a gastrostomy tube prevents urther gastric aspiration and provides a route or preoperative eedings with extended delay. IV. Lo ng -g a p EA: Stretching the proximal pouch daily shortens the distance between the esophageal ends in preparation or eventual repair. V. Bro a d -s p e c trum IV a ntib io tic s : initiated

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Op e ra tive Ma na g e m e nt I. P rim a ry re p a ir: Can be undertaken at the time o presentation i the de ect measures less than 2 cm and no signs o pneumonitis are present. Broad-spectrum antibiotic therapy is begun. A. echnique: Extrapleural dissection through the hemithorax opposite the aortic arch is currently avored to prevent empyema rom occurring as the result o an anastomotic leak. 1. Step 1: EF is repaired. 2. Step 2: Primary esophagostomy is per ormed. 3. Step 3: Dissecting the proximal pouch allows or the adequate length o esophagus necessary to create a tension- ree anastomosis. B. Minimally invasive, thoracoscopic EA- EF repair: has been proven to be ef ective and sa e and is gaining popularity II. De la ye d re p a ir: May be needed i a long-gap EA exists, allowing or growth o the in ant and shortening o the gap. Externalized traction sutures may be placed on either end o the esophageal pouches to allow or serial tightening at the bedside over a 10–14-day period in order to approximate the pouches at a quicker rate.

P o s to p e ra tive Ma na g e m e nt I. Go a l: directed at potential pulmonary and esophageal problems A. Extubation: done as soon as possible to protect the tracheal repair B. Pulmonary toilet: necessary to prevent pneumonia or reintubation C. Esophagotracheal suction: done care ully and with a speci cally de ned length o tubing to avoid damage to the anastomosis II. Surviva l: 85%–95% overall survival, with mortality virtually always related to associated comorbidities

P o s to p e ra tive Co m p lic a tio ns I. Ana s to m o tic le a k: Due to excessive tension on the anastomosis and ischemia o the esophageal ends; 95% close spontaneously with adequate drainage by a pleural tube and nutritional support. II. Ana s tom otic s tric ture : common early complication ollowing EF repair in as high as 30%–40% o patients 1. Cause: consequence o gastroesophageal re ux (GER), ischemia at the anastomosis, and ollowing an anastomotic leak 2. reatment: Strictures are treated with serial dilatations. III. GER: most common complication ollowing EF repair; 40%–70% o patients IV. Re c urre nt f s tula s : occur in less than 10% o patients and are usually a sequelae o an anastomotic leak but do require a reoperation or ligation o the stula

P ro g no s is I. Ris k s tra tif c a tio n: identi es in ants at risk or death and long-term morbidity II. Ris k a c to rs : include low birth weight ( 1,500 g), major congenital heart disease and other severe associated anomalies, ventilator dependence, and long-gap EA

INTESTINAL MALROTATION Ove rvie w I. De f nitio n: Abnormal placement and xation o the midgut into the peritoneal cavity. Malrotation can occur independently or can be associated with other mal ormations, such as diaphragmatic hernia, omphalocele, and gastroschisis (Fig. 24-4). II. No rm a l in ute ro d e ve lo p m e nt: Midgut develops extra-abdominally then migrates intraperitoneally, where it undergoes a 270-degree rotation. III. Dis p la c e m e nts c a us e d b y m a lro ta tio n A. Cecum: not in the right lower quadrant (RLQ), and the duodenum does not pass posteriorly to the superior mesenteric artery B. Base o the small bowel: Instead o being xed rom the ligament o reitz to the cecum in the RLQ, the whole midgut is anchored on the superior mesenteric artery. C. Cecum xation: Various stages can be seen, but it is usually xed to the right upper quadrant (RUQ) with the brous bands (Ladd bands) that extend across the duodenum.

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Intestinal Malrotation

Fig ure 24-4: Malrotation.

IV. Se q ue la e A. Intestinal obstruction: can result rom adhesive bands across the duodenum xing it to the RUQ; more common in in ants and neonates but can occur later in li e B. Midgut volvulus: More serious than intestinal obstruction; intestine twists on the superior mesenteric vessels, causing obstruction as well as ischemia, potentially leading to gangrene o the entire small bowel.

Clinic a l P re s e nta tio n I. Bilio us vo m iting : usual presenting symptom and helps to rule out pyloric stenosis or simple colic II. P a s s a g e o b lo o d y s to o l: late occurrence implying ischemia III. Ap p e a ra nc e : In ant may appear normal, with hemodynamic stability, or may be dehydrated and in shock a er the intestine becomes ischemic or necrotic.

Quic k Cut Bilious emes is in a neonate s hould prompt a rapid inves tigation or malrotation and volvulus .

Dia g no s is I. Ra d io g ra p hs : very use ul when making the diagnosis A. Plain lm: May demonstrate the “double bubble” sign, which Quic k Cut is produced by intestinal gas con ned to the stomach and Early diagnos is duodenum, with small amounts o gas in the residual, unused o malrotation is crucial to prevent the development GI tract. In a newborn with bilious vomiting, this sign is an o a volvulus with res ultant indication or surgery. intes tinal gangrene. B. Upper GI series: may demonstrate an abnormally located ligament o reitz, the presence o the duodenum to the le o midline, a duodenal obstruction, or a “beaked” end in the barium column at the point o the intestinal twist II. P ro m p t s urg ic a l e xp lo ra tio n: imperative i the diagnosis o malrotation is suspected but cannot be ruled out

Op e ra tive Ma na g e m e nt I. Surg ic a l p ro c e d ure s : vary with the presence or absence o volvulus and the status o the intestine A. Simple malrotation: treated by the Ladd procedure 1. Release o adhesive bands and mobilization o the duodenum: Goal is to broaden the mesentery o the intestine as much as possible and to separate the duodenum and ascending colon.

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2. Intestinal obstruction/ischemia prevention: Cecum is placed in the le upper quadrant and the duodenum in the right lateral abdomen so that both organs will be in avorable positions. 3. Appendectomy: Because the appendix may not be in its expected position, this procedure eliminates the potential diagnostic challenge and complications; a uture episode o appendicitis may produce. B. Malrotation with volvulus: requires several preliminary steps 1. Step 1: counterclockwise detorsion o the midgut volvulus Quic k Cut 2. Step 2: Bowel is then examined or viability and or areas o Think “turn back the necrosis. hands o time” or detors ion a. Small areas o gangrene: I present, resection is o a volvulus . per ormed, ollowed by the Ladd procedure. b. Extensive ischemia: Bowel is untwisted, and the abdomen is closed and re-explored 24 hours later. T is second look allows marginally viable tissue to recover, with the hope o minimizing the amount o resection. II. La p a ro s c o p ic m a na g e m e nt: reasonable initial approach

P ro g no s is I. Re c urre nc e (a te r s urg ic a l e xp lo ra tio n a nd a La d d p ro c e d ure ): very low ( 2%) II. Lo ng -te rm s e q ue la e : Minimal a er repair o simple malrotation; however, when extensive intestinal resection is required, the result depends strongly on the amount o intestine remaining.

INTESTINAL ATRESIA Duo d e na l Atre s ia a nd Ste no s is I. Ca us e : May occur because the duodenum ails to recanalize in the Quic k Cut early embryonic stages. T e lesion may be complex, partial, or in the Up to 50% o orm o a web. patients with duodenal atres ia II. As s o c ia te d a no m a lie s will have another congenital A. risomy 21: occurs in 30% o in ants with duodenal anomaly o a di erent organ s ys tem. mal ormations B. Cardiac lesions: present in many in ants ( 25%) C. Annular pancreas: 25%, with the pancreas orming a ring around the duodenum 1. Cause: due to ailure o the ventral pancreatic bud to completely rotate dorsally 2. Underlying web/stenosis: true cause o the obstruction, although the annular pancreas may cause extrinsic compression III. Dia g no s is : Prenatal US can diagnose the majority; as with an abdominal radiograph, a double bubble sign is usually present. T e clinical diagnosis is usually made rom two simple ndings. A. Bilious vomiting: occurring in a nondistended in ant B. Double bubble sign (Fig. 24-5): Paucity o distal gas suggests complete obstruction. IV. P re o p e ra tive m a na g e m e nt: Because these lesions have a high association with other more critical anomalies, stabilization and evaluation can be done be ore surgery. A. Gastric decompression and uid resuscitation B. Preoperative antibiotics: administered V. Op e ra tive m a na g e m e nt: Directed at restoring a patent GI tract; repair can be done through a laparotomy or laparoscopy. A. Duodenoduodenostomy: usually can be per ormed B. Duodenojejunostomy: good alternative i duodenoduodenostomy cannot be done C. apering duodenoplasty: may be done rst or patients with a dilated, atretic proximal duodenum D. Gastrojejunostomy: contraindicated E. Web: I present, the duodenum is opened at the site o obstruction, the web is excised, and the duodenum is closed transversely. Care must be taken to identi y the ampulla o Vater because it is also located on the mesenteric side o the web. F. Annular pancreas: Bypass with duodenoduodenostomy. Annular pancreas is never transected, as the injured duct structures will result in a persistent pancreatic leak.

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Intestinal Atresia

Fig ure 24-5: Duodenal atres ia. Supine radiograph demons trates gas in the s tomach (S) and markedly dilated duodenal bulb (D), producing the double bubble s ign. The remainder o the abdomen is gas les s . (From Siegel MJ , Coley BD. Core Curriculum: Pediatric Imaging. Philadelphia: Lippincott Williams & Wilkins ; 2005.)

G. T orough search: done to ensure patency o the entire GI tract Quic k Cut because 3.5% o patients have other atresias A “Double bubble” H. NG tube: used or GI decompression s ign indicates duodenal atres ia. VI. P o s to p e ra tive m a na g e m e nt: simple but requires patience A. GI decompression: important to protect the suture line and to prevent possible aspiration B. GI unction: Return is slow. C. PN: Nutritional support is usually needed. VII. P ro g no s is : Long-term results o surgery are good, with survival approaching 95%. Mortality in these patients is related to prematurity o the in ant and to associated anomalies.

J e juna l, Ile a l, a nd Co lo nic Atre s ia s

I. Ca us e : In utero vascular accidents result in ischemia o a segment Quic k Cut The s everity o the o bowel, with consequent stenosis (5%) or atresia (95%). intes tinal atres ia is related A. Familial intestinal atresias: also exist, with varying patterns o to the s ize o the vas cular inheritance arcade that was a ected in B. Jejunoileal atresias: evenly split between the jejunum and ileum, utero. with the colon uncommonly af ected II. As s o c ia te d a no m a lie s : Because they are not embryonic maldevelopments, associated anomalies are much less common; however, 10% o patients have cystic brosis. III. Clinic a l p re s e nta tio n: Diagnosis is suspected prenatally when there is maternal polyhydramnios or postnatally when an in ant develops abdominal distension and bilious vomiting a er 24 hours o li e or ails to pass meconium. Quic k Cut Jaundice may also develop. The pas s age o A. Degree o abdominal distention: Varies with the level o the meconium does not rule out obstruction. Proximal obstructions lead to less distention, an atres ia becaus e the GI whereas more distal lesions produce generalized distention. tract was intact be ore the B. Small bowel or colonic atresia: All such patients should have an vas cular accident. early evaluation or cystic brosis.

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IV. Dia g no s is : can be made prenatally with US and etal magnetic resonance imaging (MRI) A. Abdominal radiographs: show various degrees o obstruction, depending on the level o the atresia or stenosis; the picture can be con used with meconium ileus 1. Di erences: In atresia, air- uid levels are present; a meconium ileus shows distended bowel and a “soap bubble” Quic k Cut appearance. In intes tinal atres ia, air-f uid levels are always 2. Peritoneal calci cations: suggest intrauterine per oration pres ent on x-ray. Meconium with meconium peritonitis ileus s hows only dis tended B. Contrast studies: help ul in both diagnosis and management bowel. 1. Contrast enema: Will reveal colonic lesions; a microcolon suggests the atresia developed early in gestation. 2. Rules out: Hirschsprung disease, meconium ileus, and other congenital disorders, making diagnosis o the atresia more certain V. P re o p e ra tive m a na g e m e nt: GI decompression and uid replacement. Gastric losses should be replaced and electrolytes corrected i surgery is to be delayed. Begin broad-spectrum antibiotic therapy. VI. Op e ra tive m a na g e m e nt: Surgery is per ormed to re-establish intestinal continuity. A. End-to-end intestinal anastomosis: current procedure o choice 1. Disadvantage: may be di cult to accomplish because o the marked size disparity o the bowel— the proximal bowel is dilated, and the distal, unused bowel is small 2. Repair tips: apering o the proximal bowel or resection o a limited amount o dilated bowel may aid in the repair. B. GI unction: may be slow to return because the distended bowel has been ound to have impaired motility C. NG tube: placed to allow decompression and prevent aspiration D. Atresia and meconium ileus: In a patient with both conditions, the distal intestine may contain inspissated small bowel secretions. T e site o inspissation should be irrigated with a 4% acetylcysteine (Mucomyst) solution to relieve any potential obstruction. VII. P o s to p e ra tive m a na g e m e nt: decompression and patience A. Hyperalimentation: may be needed until the GI tract recovers B. Malabsorption: I present, may prolong the recovery time. VIII. P ro g no s is : Because associated anomalies are ew, survival is a unction o the prematurity o the in ant. A. Survival: Current results show a survival rate o almost 100%. B. Postoperative complications: Most common leading to mortality are intestinal obstruction and anastomotic breakdown.

“Ap p le -P e e l” Atre s ia I. De f nitio n: severe orm o small bowel atresia, so named because o its radiographic appearance II. Ca us e : occurs during a large vascular accident to one or more o the mesenteric arcades in utero III. GI unc tio n: In these patients, return is very prolonged, and malabsorption is common.

HIRSCHSP RUNG DISEASE Ove rvie w I. Ca us e : absence o ganglion cells in the myenteric and submucosal plexus in the intestine A. Ine ective peristalsis: Af ected segment o the bowel is unable to relax. B. Extent: Usually involves the rectum and extends proximally at varying lengths (short-segment vs. long-segment Hirschsprung); however, the entire colon may be involved and is re erred to as total colonic aganglionosis. II. Inc id e nc e : ranges rom 1:4,500 to 7,000 live births A. Classic Hirschsprung disease: male predominance o 4:1 B. otal colonic aganglionosis: slight male predominance III. Ge ne tic s : Approximately 80%–90% o cases are sporadic. A. Inherited amilial predisposition: occurs in 10% o cases B. RE proto-oncogene mutation: accounts or the highest proportion o both amilial and sporadic cases

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Clinic a l P re s e nta tio n I. Ne wb o rns : classically present with a history o delayed passage o meconium A. Meconium: usually passed within 24 hours a er birth in term in ants and within 48 hours in premature in ants B. Other signs: abdominal distention, bilious vomiting, poor eeding, and constipation C. Physical examination: reveals a distended abdomen 1. Loops o stool- lled bowel: occasionally palpated 2. Rectal examination: o en demonstrates a tight anal sphincter with an empty rectal vault II. Old e r c hild re n: constipation, abdominal distention, and ailure to thrive III. Hirs c hs p rung e nte ro c o litis : initial clinical presentation o a small percentage o children with Hirschsprung disease who present with pro use diarrhea, abdominal distention, and ever A. Cause: develops due to intestinal stasis proximal to the aganglionic segment resulting in bacterial overgrowth and translocation B. I suspected: Contrast enemas or diagnosis should be avoided due to risk o intestinal per oration. C. reatment: serial rectal irrigations and IV antibiotics

Quic k Cut The diagnos is o Hirs chs prung dis eas e s hould be s us pected in any patient with a his tory o cons tipation dating back to the newborn period.

Quic k Cut Clas s ically, an explos ion o watery s tool occurs with Hirs chs prung dis eas e ollowing examination.

Quic k Cut Enterocolitis in Hirs chs prung dis eas e can be atal.

Dia g no s is I. Initia l im a g ing with up rig ht a nd d e c ub itus a b d o m ina l ra d io g ra p hs : reveals air- uid levels and a distended bowel with a paucity o air in the rectum (Fig. 24-6) II. Co ntra s t e ne m a : Next diagnostic study o choice and o en acilitates diagnosis; water-soluble contrast is pre erred to barium. A. Classic radiographic ndings: narrow, spastic distal intestinal segment with a proximal dilated segment B. ransition zone: represents the most distal area in which ganglia cells are present 1. Location: most commonly located in the rectosigmoid, but it can occur anywhere in the intestine 2. De nition: ransition zones are less well-de ned in short-segment Hirschsprung as well as in total colonic aganglionosis. III. Ano re c ta l m a no m e try: demonstrates elevated resting anal sphincter pressures and an absence o a relaxation re ex

T

Fig ure 24-6: Hirs chs prung dis eas e. *, dilated normal bowel; T, trans ition zone; **, aganglionic s egment. (From Dudek RW. BRS Embryology, 5th ed. Baltimore: Lippincott Williams & Wilkins ; 2010.)

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IV. Re c ta l b io p s y: Specimens are characterized in the absence o ganglion cells and presence o hypertrophied nerve trunks. A. Bedside suction rectal biopsy: currently the procedure o choice and con ers little risk to the patient B. Considerations: Although the procedure is simple, it produces small submucosal specimens and requires an experienced pathologist or correct interpretation.

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Quic k Cut Rectal biops y is the gold s tandard or diagnos is o Hirs chs prung dis eas e.

Op e ra tive Ma na g e m e nt I. Surg ic a l a p p ro a c h: Variety; a primary pull-through procedure (one-stage) is the pre erred approach, but some in ants require an initial diverting colostomy (two-stage procedure) prior to their de nitive operation due to enterocolitis or marked dilation o proximal normal colon. II. Go a ls o s urg e ry: Each operative procedure has three common goals. A. Resect: involved aganglionic intestine B. Re-establish: unctional GI tract by bringing normal ganglionic bowel to the anus C. Preserve: sphincter unction III. P ro c e d ure s : Most commonly per ormed are the endorectal pull-through, Soave, Swenson, and Duhamel, which can be per ormed either laparoscopically or through an open approach. A. Endorectal pull-through: 1. Step 1: Rectal mucosa is dissected rom the rectal wall transanally up to the peritoneal re ection. 2. Step 2: Abdomen is entered transanally through the rectal wall. 3. Step 3: Proximal normal bowel is pulled through the stripped anorectal segment and is sutured to the anorectal junction. B. Soave procedure: 1. Step 1: Aganglionic colon is excised to the level o the peritoneal re ection. 2. Step 2: Mucosa is removed in the remaining rectum. 3. Step 3: Proximal normal bowel is pulled through the stripped anorectal segment and is sutured to the anorectal junction. C. Swenson procedure: 1. Step 1: Involved colon is excised to within 1 cm o the anal mucocutaneous margin. 2. Step 2: Bowel is then sutured to the cuf o distal anorectal segment, thus establishing GI continuity. D. Duhamel procedure: 1. Step 1: Aganglionic colon is excised to the level o the peritoneal re ection within the abdomen. 2. Step 2: Proximal normal bowel is tunneled between the sacrum and the rectum and is then anastomosed end to side to the low anorectum.

P o s to p e ra tive Co m p lic a tio ns I. Hirs c hs p rung -a s s o c ia te d e nte ro c o litis : major cause o postoperative morbidity and mortality with incidence rates as high as 30% A. Higher risk: in patients with an anastomotic stricture, long-segment disease, or total colonic aganglionosis B. iming: Usually occurs within the year a er the de nitive repair; patients present with explosive oul-smelling diarrhea, ever, and abdominal pain and distention. C. reatment: Fluid resuscitation, broad-spectrum IV antibiotics, and repeated rectal irrigations with saline. Most cases are managed nonoperatively. II. Co ns tip a tio n: Evaluation o constipation or obstruction includes a rectal exam and contrast enema to evaluate or stricture as well as a suction rectal biopsy to assess or persistent aganglionosis. A. Anal dilatation: may be necessary i constipation occurs secondary to the retained aganglionic internal anal sphincter or due to an anastomotic stricture B. Botulinum toxin injection: may be used when elevated internal anal sphincter tone pressures are documented

Quic k Cut Cons tipation or pers is tent obs tructive s ymptoms s hould prompt an evaluation to rule out mechanical obs truction.

III. Fe c a l inc o ntine nc e a nd d ia rrhe a : encountered requently in early postoperative period but improve with bulking agents and usually resolve with time

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DISORDERS OF INFANCY In a ntile Hyp e rtro p hic P ylo ric Ste no s is I. De f nitio n: common cause o gastric outlet obstruction in in ants due to hypertrophy o the muscular layer o the pylorus, classically causing nonbilious projectile vomiting II. Etio lo g y: Unknown; however, both genetic and environmental actors play a role in the pathophysiology. A. Male-to- emale ratio: 4:1 B. Family history: Of spring o a emale with a history o pyloric stenosis have a 10- old greater chance o developing pyloric stenosis, whereas of spring o a male with a history o pyloric stenosis have a 4- old greater chance. C. Environmental actors: breast eeding, seasonal variability, and erythromycin exposure III. Clinic a l p re s e nta tio n: Classic presentation is projectile nonbilious vomiting at ages 2–8 weeks. A. Classic derangement: Vomiting can lead to hypochloremic, hypokalemic metabolic alkalosis. B. Jaundice: present in 10% o in ants IV. Dia g no s is Quic k Cut A. Physical examination: Palpation o the enlarged pylorus, also Patience and termed “the olive,” in the midepigastrium can be diagnostic. pers is tence on phys ical exam B. NG tube: Complete evacuation o the stomach may aid in is es s ential to palpating the nding the mass. enlarged pylorus . C. Ultrasonography: Standard initial imaging technique; diagnosis is con rmed with a pyloric channel length o 16 mm or greater and a pyloric muscle thickness o 4 mm or greater. D. Upper gastrointestinal (UGI) series: help ul when US results are equivocal (Fig. 24-7) 1. Findings: elongated pyloric channel with a “string” sign or “railroad track” sign (one to two thin barium tracts, respectively, through the pylorus) 2. Slowed gastric emptying o contrast V. P re o p e ra tive m a na g e m e nt: Correction o the hypokalemic, Quic k Cut hypochloremic metabolic alkalosis is (contraction alkalosis) Surgery or pyloric essential prior to anesthesia and surgical correction o pyloric s tenos is s hould be de erred stenosis. until the hypochloremic, hypokalemic metabolic A. Goal: decreasing serum bicarbonate level to less than 30 mEq/L alkalos is is corrected: rs t, B. Optimal resuscitation: achieved through IV administration o res tore volume with normal normal saline boluses and 5% dextrose in 0.45 normal saline s aline, and s econd, res tore containing 20 mEq o potassium chloride at 1.5–2 the normal potas s ium as needed. maintenance rate

Fig ure 24-7: The upper GI in this 6-week-old baby s hows elongation and narrowing o the pyloric channel (arrowheads). On the s tomach s ide, notice the rounded indentation (arrows) caus ed by the very hypertrophied pyloric mus cle. This is called the s houlder s ign. Together, this combination o s igns is diagnos tic or pyloric s tenos is . (From Erkonen WE, Smith WL. Radiology 101, 3rd ed. Philadelphia: Lippincott Williams & Wilkins ; 2009.)

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VI. Op e ra tive m a na g e m e nt: Surgical procedure o choice is the Ramstedt pyloromyotomy. A. echnique: Incision o the serosa is made down the length o the enlarged pylorus to the depth o the mucosa. A complete myotomy is demonstrated through bulging o the submucosa through the divided hypertrophied muscle. B. Intraoperative leak test: per ormed to rule out any per oration C. Approach: Pyloromyotomy may be done through an open or laparoscopic approach. Studies have demonstrated equal e cacy and complication rates. VII. P o s to p e ra tive m a na g e m e nt: Patient may be started on eedings o glucose and water or an electrolyte in ant ormula (e.g., Pedialyte) 4–6 hours a er surgery. A. Complications: Vomiting occurs in 50%–80% o patients postoperatively because o gastric atony or acute gastritis but is usually sel -limited and can be minimized with slow advancement o eedings. 1. Duodenal per oration: I recognized intraoperatively, handled by a simple repair and omental patch, NG decompression or 24–48 hours, and antibiotics; unrecognized duodenal per oration can result in signi cant morbidity and mortality. 2. Incomplete pyloromyotomy: Frequent vomiting beyond 1 week may indicate an incomplete pyloromyotomy; treatment is repyloromyotomy. VIII. P ro g no s is : Long-term studies indicate no sequelae such as ulcer disease, ood intolerance, or hiatal hernia occurring a er a pyloromyotomy or in antile hypertrophic pyloric stenosis. In addition, no problems with growth and development occur.

Bilia ry Atre s ia I. De f nitio n: Disease process that results in progressive in ammatory destruction o the bile ducts and occurs in 1 in every 20,000 births. I untreated, the disease progresses to cirrhosis o the liver and is the most common indication or liver transplantation in the pediatric U.S. population. Quic k Cut II. Etio lo g y: Unknown; however, both environmental (viruses) and Untreated biliary hereditary actors have been implicated to cause the nal common atres ia leads to cirrhos is in 3–4 months . pathway o biliary in ammation, luminal obliteration, and brosis. III. Cla s s if c a tio n: three types A. ype I: atresia restricted to the common bile duct ( 12%) B. ype II: level o atresia within the common hepatic duct ( 3%) C. ype III: atresia at the porta hepatis (most common 85%) IV. Clinic a l p re s e nta tio n: In ants usually present with persistent jaundice and pale acholic stools. A. Laboratory studies: reveal conjugated hyperbilirubinemia B. Liver unction studies: may or may not be abnormal, depending on the degree o liver damage rom cholestasis Quic k Cut V. Dia g no s is : Workup is designed to dif erentiate true The mos t important anatomic obstruction o the biliary tree rom other causes o rule o thumb is that hyperbilirubinemia. persistent jaundice beyond A. ORCH (toxoplasmosis, others, rubella, cytomegalovirus, and the rs t month o li e mus t be evaluated. herpes simplex virus): antibody titers B. Serum electrophoretic patterns: examined or alpha-1 antitrypsin de ciency C. Ultrasonography: Biliary atresia is suspected i the gallbladder or ducts are not visualized. D. Hepatobiliary scintigraphy: Nuclear scans using technetium-99m (99m c)–labeled iminodiacetic acid derivatives look or biliary excretion into the GI tract. Failure o the isotope to appear in the intestine within 24 hours is suggestive o biliary atresia. E. Percutaneous liver biopsy: Predominant nding commonly seen in biliary atresia is bile ductular proli eration and in ammation. F. Diagnostic laparotomy or laparoscopy: Per orm i biliary atresia cannot be ruled out by a orementioned methods. 1. Intraoperative cholangiography: I normal patent biliary system is demonstrated, a wedge biopsy o the liver is taken and the surgical procedure is ended. 2. I patency cannot be demonstrated: Porta hepatis is explored to nd the atretic duct and proceed with a biliary drainage procedure.

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P orta he pa tis

He pa tic Arte ry P orta l ve in

Fig ure 24-8: Kas ai procedure or biliary atres ia, with Roux limb. (From Blackbourne LH. Advanced Surgical Recall, 2nd ed. Baltimore: Lippincott Williams & Wilkins ; 2004.)

VI. Tre a tm e nt A. Hepatic portoenterostomy (Kasai procedure): standard operation and mainstay o initial operative interventions (Fig. 24-8) B. Goal: Excise all extrahepatic biliary remnants in order to complete a wide anastomosis o jejunum to the porta hepatis (portoenterostomy) to allow or drainage o the biliary ductules and restore biliary drainage o the liver. VII. P ro g no s is : Currently, without surgical intervention, biliary atresia is atal rom cirrhosis resulting in end-stage liver disease. A. Native liver unction: 40% o patients 10 years a er Kasai portoenterostomy B. Liver transplantation: necessary in 60% o patients or longQuic k Cut term survival Biliary atres ia patients account or more 1. Donor pool: Four percent mortality rate has been noted while than 50% o all pediatric liver on the transplantation list; however, the use o living-related trans plant patients . liver transplant and split-liver deceased donor transplant has increased the donor pool in in ants and children. 2. 2.5-year survival rates: 85%

Ne c ro tizing Ente ro c o litis I. De f nitio n: devastating disease o the neonatal intestinal tract II. Etio lo g y: Likely multi actorial, and several hypotheses exist. It is believed that the immature intestine suf ers rom decreased barrier unction; when coupled with aberrant microbial colonization and

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III.

IV.

V.

VI.

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ischemic injury, the resultant exuberant immune response leads Quic k Cut to necrotizing enterocolitis (NEC). T e current theory revolves The ris k o around an imbalance between intestinal immunity, enterocyte developing NEC is invers ely barrier unction, and altered microbial ora leading to increased proportional to the ges tational permeability. age and birth weight. Ep id e m io lo g y: Prematurity and low birth weight are the most commonly associated risk actors. A. Estimated prevalence: 7% in extremely low- and very-low-birth-weight in ants B. Mortality risk: 20%–30% in these in ants, with the highest risk among in ants requiring surgery Clinic a l p re s e nta tio n: usually occurs within the rst 2 weeks o li e A. First signs: usually intolerance to ormula and abdominal distention, with the passage o hemepositive stools B. Associated perinatal problems: premature rupture o the membranes, prolonged labor, amnionitis, respiratory distress, apneic episodes, cyanosis, or delivery room resuscitation C. Physical exam ndings: correlate with the extent o the disease 1. Mild NEC: Benign exam may be ound. 2. More severe NEC: Abdominal distention and tenderness will increase with severity o the disease. 3. Necrotic or per orated intestine: o en results in abdominal mass or abdominal wall erythema Dia g no s is A. Laboratory ndings: leukopenia, thrombocytopenia (both associated with gram-negative sepsis), anemia, hyponatremia, metabolic acidosis, and coagulopathy B. Abdominal radiographs (anteroposterior and lef lateral decubitus): Facilitate diagnosis and are used to monitor the patient’s clinical course. Findings include the ollowing. 1. Distended, edematous intestines 2. Intramural air (pneumatosis intestinalis): Figure 24-9 3. Portal venous gas 4. Isolated persistent distended loop o bowel or “ xed loop”: persists over serial radiographs 5. Free intraperitoneal air: suggests intestinal per oration Tre a tm e nt: based on Bell’s stages A. Stage I: mild systemic signs 1. Mild systemic signs: apnea, bradycardia, temperature instability 2. Mild intestinal signs: abdominal distention, increased gastric residuals, bloody stools 3. Radiologic signs: nonspeci c or normal

Fig ure 24-9: Necrotizing enterocolitis . Multiple loops o dis tended bowel have bubbly and linear radiolucencies in the bowel wall (pneumatos is intes tinalis ). (From Brant WE, Helms CA. Brant and Helms Solution. Philadelphia: Lippincott Williams & Wilkins ; 2006.)

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B. Stage II: de nitive disease 1. Systemic signs: mild to moderate 2. Additional intestinal signs: absent bowel sounds, abdominal tenderness 3. Speci c radiologic signs: pneumatosis intestinalis, portal venous gas 4. Laboratory changes: metabolic acidosis, thrombocytopenia C. Stage III: advanced disease 1. Severe systemic illness: hypotension, sepsis 2. Additional intestinal signs: abdominal distention, peritonitis Quic k Cut 3. Severe radiologic ndings: pneumoperitoneum Nonoperative management is initial therapy 4. Additional laboratory changes: metabolic and respiratory or mos t neonates s us pected acidosis, disseminated intravascular coagulopathy VII. Me d ic a l m a na g e m e nt: GI decompression, parenteral antibiotic therapy, uid resuscitation, and PN

o having NEC; the cours e is us ually 7–14 days .

VIII. Op e ra tive m a na g e m e nt: Approximately 40% o patients require surgery or NEC complications. A. Abdominal radiograph: Can usually document with a crossQuic k Cut table lateral or le lateral decubitus position; lms are obtained Intes tinal per oration every 4–6 hours or as clinically indicated. is an abs olute indication or B. reatment: Resection o the involved intestine; GI tract is s urgery. diverted with a proximal enterostomy and mucous stula. T e stomas should be placed to prevent tension on the in amed mesentery. C. Isolated per oration or limited disease: Primary anastomosis o the normal bowel is per ormed in neonates, with relatively stable physiology and no evidence o coagulopathy or sepsis. D. Severely ill patient (or in the extremely low birth weight in ant [ 1,000 g]): Major procedure may not be tolerated; placement o peritoneal drains (using local anesthesia) at the bedside can be per ormed. IX. P o s to p e ra tive m a na g e m e nt: Includes continued medical management o the primary disease as well as routine postsurgical care; in ant is treated with antibiotics, GI decompression, and PN. A. Disease progression: Requires urther surgery or additional per orations. Recurrent NEC occurs in 4%–6% o patients. B. Oral eedings: Delayed until a er the acute disease resolves and clinical evidence suggests return o bowel unction. Dietary adjustments may be necessary until the mucosa has regenerated and undergone unctional maturation. C. Enterostomy: Can be closed during the initial hospitalization or a er discharge. Operating prior to 4 weeks postoperatively may prove di cult secondary to in ammation and adhesions. D. Stoma management: Can be di cult; early recognition and treatment o these complications are necessary to prevent urther complications. 1. Local problems: include prolapse, degeneration o the surrounding skin, or mucosal irritation 2. Physiologic problems: Include uid losses, electrolyte abnormalities, and intolerance o the diet. A proximal ostomy will be the most di cult to manage in terms o output and physiologic derangement. E. Strictures: with subsequent intestinal obstruction occurs in 30% o cases 1. iming: usually occurs 3–6 weeks a er the acute episode 2. reatment: resection and primary anastomosis once the patient is prepared nutritionally or surgery X. P ro g no s is A. Mortality rate: Signi cantly dif erent between neonates treated with medical versus surgical management (67% vs. 30%); overall mortality increases with decreasing birth weight. B. Long-term morbidity: Related to the length and unction o the remaining intestine and other comorbidities related to prematurity a er recovery rom NEC. 1. Extensive bowel resection: Patient may develop short-bowel syndrome. 2. Comorbidities: intraventricular hemorrhage, chronic pulmonary insu ciency, and associated cardiac problems 3. Neurodevelopmental problems: ound in 50% o patients

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XI. P re ve ntio n: Although several modalities have been studied and evaluated as possible adjuncts or the prevention o NEC, currently the only recommendations with evidence o both sa ety and e cacy are breast milk and nonaggressive enteral nutrition. It has also been shown that prenatal maternal glucocorticoids decrease the rate o NEC development in premature neonates.

SOLID TUMORS Wilm s Tum o r I. De f nitio n: Involves either the entire kidney or a part o it; bilateral involvement occurs in 4%–13% o cases. II. Etio lo g y: Mesodermal, mesonephric, and metanephric origins have been proposed. III. Inc id e nc e : An estimated 500 new cases o Wilms tumor occur each year in the United States. Wilms tumors account or more than 90% o all pediatric renal tumors.

Quic k Cut The two mos t common s olid tumors o childhood are Wilms tumor and neuroblas toma. Although other tumors occur (e.g., rhabdomyos arcoma, Ewing tumor, os teogenic s arcoma, various brain tumors ), Wilms tumor illus trates the multidis ciplinary approach that is currently us ed in the management o tumors that occur in childhood.

IV. Clinic a l p re s e nta tio n: Asymptomatic ank mass is usually discovered by the parents or during a routine physical examination. T e mass is smooth, lobulated, and commonly mobile. A. Other symptoms: abdominal pain, hematuria, and anorexia B. Hypertension: occurs in 10% o patients secondary to activation o the renin–angiotensin system C. Mean age at diagnosis: 3 years D. Males: umor may invade the spermatic vein, leading to a varicocele. E. Cardiac dys unction: umor can extend into the right atrium via the in erior vena cava. V. As s o c ia te d a no m a lie s : individual congenital anomalies or part o a syndrome A. WAGR syndrome: Wilms tumor, aniridia, genitourinary mal ormation, and mental retardation B. Beckwith-Wiedemann syndrome: congenital growth dysregulation with visceromegaly, macroglossia, omphalocele, and hyperinsulinemic hypoglycemia at birth VI. Dia g no s is : Imaging studies to aid in the diagnosis o Wilms tumor should de ne the nature o the abdominal mass, the organ o origin, the status o the contralateral kidney, the presence o tumor in the renal vein or vena cava, and the presence or absence o distal metastases A. Chest computed tomography (C ) scan: will reveal metastasis to the lung, which is the most common site B. Ultrasonography with a Doppler examination: can identi y the organ o origin, the opposite kidney, and the presence o renal vein or vena cava involvement C. C scan: can identi y the organ o origin i there is bilateral kidney involvement D. MRI: avoids radiation exposure but has not been shown to be superior to C imaging VII. Sta g ing A. Stage I: umor is limited to the kidney and is completely excised; the sur ace o the renal capsule is intact. T e tumor was not ruptured be ore or during removal. T ere is no residual tumor apparent beyond the margins o resection. B. Stage II: umor extends beyond the kidney but is completely removed. T ere is regional extension o the tumor (i.e., penetration through the outer sur ace o the renal capsule into the perirenal so tissues). Vessels outside the kidney substance are in ltrated or contain tumor thrombus. C. Stage III: Residual nonhematogenous tumor is con ned to the abdomen. Lymph nodes on biopsy are ound to be involved in the hilus, the periaortic chains, or beyond. T ere has been dif use peritoneal contamination by tumor, such as spillage or tumor beyond the ank. Implants are ound on the peritoneal sur ace, and the tumor extends beyond the surgical margins either microscopically or grossly. T e tumor is not completely resectable because o local in ltration into vital structures. D. Stage IV: Hematogenous metastases can occur with deposits beyond stage III (e.g., lung, liver, bone, or brain). E. Stage V: Bilateral renal involvement is evident at diagnosis. An attempt should be made to stage each side according to the a orementioned criteria on the basis o the extent o disease be ore a biopsy.

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Ta b le 24-2: Wilm s Tum o r Surviva l Ra te s Wilm s Tum o r 4-Ye a r Surviva l Ra te Sta g e

FH

UFH

I

99%

83%

II

98%

81%

III

94%

72%

IV

86%

38%

V

87%

55%

FH, favorable histology; UFH, unfavorable histology. From American Cancer Society. Survival rates for Wilms tumor by stage and histology. American Cancer Society Web site. http://www.cancer.org/cancer/wilmstumor/detailedguide/wilms-tumor -survival-rates. Accessed February 14, 2015.

VIII. Ma na g e m e nt: involves a multidisciplinary approach Quic k Cut A. Surgery: Mainstay o treatment; timing depends on tumor stage. Becaus e o the 1. Operation includes: exploratory laparotomy, examination good prognos is with Wilms o the opposite kidney, resection o the tumor, and periaortic tumor, even in the s etting node dissection or sampling o extens ive dis eas e, it is 2. Vena caval extension: Requires the removal o the tumor acceptable to res ect other organs . thrombus. T is operation may require a cardiopulmonary bypass to assist in the resection. B. Chemotherapy: critical or cure C. Radiotherapy: Used to treat extensive disease (stages III–V); complications include secondary cancers in children; inter erence with growth and development o bones, joints, and muscles; radiation pneumonitis; radiation enteritis; and cardiotoxicity. IX. P ro g no s is : Survival is related to stage, response to treatment (stages IV and V patients), loss o heterozygosity, and the histology o the tumor, which is reported as avorable (FH) and un avorable (UFH) and dictates treatment protocols. Current 4-year survival rates by stage and histology are shown in able 24-2.

Study Questions or Part VI

Study Questions or Part VI Directions: Each of the numbered items in this section is followed by several possible answers. Select the ONE lettered answer that is BEST in each case.

Que s tio ns 1–2 A 35-year-old man has right-sided serous otitis media and a right upper neck mass. 1. It is most important to evaluate this patient or which o the ollowing? A. B. C. D. E.

Cancer o the right ear Cancer o the right tonsil Cancer o the right maxillary sinus Cancer o the nasopharynx Hodgkin lymphoma

2. Which o the ollowing will be the primary treatment or this tumor?

A. B. C. D. E.

Local excision to negative margins Wide local excision and radical neck dissection Neoadjuvant chemotherapy ollowed by resection o residual tumor Unilateral radiotherapy with combined chemotherapy Bilateral radiotherapy

3. A 65-year-old man is ound to have a small invasive squamous cell carcinoma o the right vocal

cord. T e right vocal cord is paralyzed, and a lymph node in the right anterior neck is 4 cm in diameter. Optimal treatment o the primary tumor should include which o the ollowing? A. B. C. D. E.

otal laryngectomy Vertical hemilaryngectomy Supraglottic (horizontal) laryngectomy Right cordectomy Chemotherapy

Que s tio ns 4–5 A 55-year-old woman presents with complaint o a mass overlying the angle o the right mandible. She says the mass has been slowly enlarging over the past 2–3 years and that the mass is painless. On physical examination, it is rm and overlies the angle o the right mandible and the area between the angle and the tragus o the ear. Neurologic examination o the head and neck is completely normal. 4. Which o the ollowing does this mass most likely represent?

A. B. C. D. E.

Mucoepidermoid cancer o the parotid gland Acute parotitis Benign mixed tumor o the parotid gland (pleomorphic adenoma) Malignant mixed tumor o the parotid gland Hemangioma o the parotid gland

5. What will be the optimal treatment or this lesion?

A. B. C. D. E.

Radiation therapy otal parotidectomy with preservation o the acial nerve otal parotidectomy including resection o the acial nerve Super cial parotidectomy Enucleation

397

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Study Questions or Part VI

6. A 9-year-old girl presents with drainage rom the midline neck. T ere is some surrounding

cellulitis and an apparent 2-cm mass that elevates with swallowing. T e most appropriate de nitive management o this condition is: A. B. C. D. E.

Antibiotics alone T yroid scanning US-guided aspiration Complete surgical excision Radioiodine therapy

7. A 71-year-old man presents with mild hearing loss and tinnitus o the right ear. His symptoms

are new and not particularly troubling to him. MRI demonstrates a solid lesion in the internal auditory canal. T e most appropriate management is: A. B. C. D. E.

Surgical resection Radiation therapy Observation Fine-needle aspiration Radio requency ablation

8. A 60-year-old man has a smoking history o 80 pack-years and presents with a lesion on the tongue.

T e biopsy is consistent with squamous cell carcinoma. A ull workup demonstrates a 1.5-cm solid lesion in the le upper lobe o the lung but is otherwise negative. T e most appropriate management is: A. B. C. D. E.

Radiation therapy Chemotherapy only Radical surgical resection Surgical resection and chemotherapy Re erral to hospice care

9. A 37-year-old man undergoes Roux-en-Y gastric bypass or morbid obesity. He recovers

unevent ully and is discharged home the ollowing day. He returns on postoperative day 6 with abdominal pain, tachycardia, and low-grade ever. His abdominal exam is unremarkable, and his abdominal C scan shows signi cant in ammation in the upper abdomen with some ree uid. T e best initial treatment is: A. B. C. D. E.

Acid reduction with proton pump inhibitors Loperamide Increased pain control with oral narcotics Diagnostic laparoscopy Nonsteroidal anti-in ammatory drugs

10. Which o the ollowing patients meets criteria or bariatric surgery?

A. B. C. D. E.

15-year-old boy with body mass index (BMI) 39.9 kg/m 2 25-year-old woman with BMI 33 kg/m 2 and allergic asthma 35-year-old man with BMI 38 kg/m 2 and a deviated septum 45-year-old woman with BMI 39 kg/m 2, diabetes mellitus, and degenerative joint disease 79-year-old man with BMI 39.9 kg/m 2

11. A 60-year-old woman is taken to the operating room or a laparoscopic cholecystectomy. A er

insu ation o the abdomen with CO2, her respiratory rate increases dramatically and she becomes hypotensive with decreased cardiac output. T e most likely reason or this acute event is: A. B. C. D. E.

Acidosis secondary to carbon dioxide Pneumothorax Volume depletion Oversedation with narcotics Decreased sympathetic activity

Study Questions or Part VI

12. A 35-year-old man undergoes laparoscopic ventral hernia repair with lysis o adhesions. T e

procedure is unevent ul, and he is admitted to the hospital or recovery. A er 3 days, he develops a newly distended abdomen, abdominal pain, and hypotension that does not respond to 1 L o normal saline. T e most likely explanation is: A. B. C. D. E.

Myocardial in arction Missed enterotomy Acidosis secondary to pneumoperitoneum Deep venous thrombosis Gas bloat syndrome

13. A 25-year-old woman presents with a 2-cm palpable le neck nodule. She is asymptomatic

but is anxious about the lump in her neck. She visits her primary care physician, who orders a US, which demonstrates a solid lesion. She presents to your o ce or evaluation. T e most appropriate means o diagnosis is: A. B. C. D. E.

Computerized tomography o the neck Magnetic resonance angiography (MRA) Fine-needle aspiration Incisional biopsy Excisional biopsy

14. T e American Cancer Society (ACS) recommends routine screening or all o the ollowing

except: A. B. C. D. E.

Mammography or breast cancer Pap smear or cervical cancer Prostate-speci c antigen (PSA) or prostate cancer Colonoscopy or colon cancer Fecal occult blood testing or colon cancer

15. A new chemotherapeutic agent is developed to treat advanced lung cancer. T e company begins

a large trial o 1,000 patients comparing the e cacy o the new medication versus a leading medication that has been in use or the last 5 years. T is trial can best be described as: A. B. C. D. E.

Phase 0 Phase I Phase II Phase III Double-blind, randomized controlled trial

16. A 22-year-old man is shot in the chest. He presents to the emergency department with incoherent

mumbling but his eyes open to vocal commands and no response to pain ul stimuli. What is his Glasgow Coma Scale score? A. B. C. D. E.

6 8 10 12 14

17. T e same patient in question number 8 has a systolic blood pressure o 60 mm Hg, a thready pulse, and

has some blood bubbling rom a hole in his lateral le chest. T e most important initial maneuver is: A. B. C. D. E.

Endotracheal intubation Administration o 1 L o crystalloid Occlusive dressings to the wound Blood sample or cross match Examination o the pupils

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Study Questions or Part VI

18. A er stabilization, the patient’s hemodynamics improve but do not normalize. T e patient is

also di cult to ventilate. Chest x-ray shows collapse o the lung on the le side and shi o the mediastinal structures to the right. T e next best maneuver is: A. B. C. D. E.

Administration o 100% oxygen Operative thoracotomy Chest tube insertion Needle decompression o the le chest Administration o sur actant

19. A 27-year-old woman with end-stage renal disease secondary to glomerulonephritis undergoes

renal transplantation in the right iliac ossa. wo months a er operation, she develops some edema o the right leg along with decreased urine output. C scan demonstrates a uid collection near the kidney, and an aspiration o the collection shows a creatinine level equal to serum. T e best next step in management is: A. B. C. D. E.

Diagnostic laparoscopy and internal drainage Open operation and ureteral revision Pulsed corticosteroids Blood trans usion Percutaneous drainage

20. A 42-year-old man with insulin-dependent diabetes mellitus undergoes pancreas transplantation.

A er good initial results, at postoperative day 4, he develops increasing glucose levels requiring insulin. T e best initial means o diagnosis is: A. B. C. D. E.

C scan with contrast MRI-guided biopsy Urine culture Serum antibody levels Retroperitoneal US

21. A 33-year-old man has a kidney transplant. One month later, he presents with decreased urine

output and increased serum creatinine. A renal biopsy is per ormed, which is consistent with acute rejection. T e best initial treatment is: A. B. C. D. E.

Decreased immunosuppressant levels ransplant nephrectomy Plasmapheresis Pulsed corticosteroids C scan with IV contrast

22. A 4-week-old male in ant presents to the emergency department with a 3-day history o vomiting.

T e amily reports that he had an unevent ul birth history and was developing normally. T e emesis has been nonbilious, quite orce ul, and occurring immediately a er eedings. On physical examination, you eel a rm mass in the epigastric region. T e best course o action is: A. B. C. D. E.

Immediate laparotomy Fluid resuscitation and semiurgent operation Laparoscopic pyloromyotomy NG decompression Hydroxy iminodiacetic acid (HIDA) scan and liver unction tests

Study Questions or Part VI

23. A newborn girl presents with a mass at the umbilicus. She is in no distress. Immediately to

the right o the umbilical cord, an apparent loop o bowel is exposed to the air. T e best initial treatment or the management o this patient is: A. B. C. D. E.

Application o silver sul adiazine Echocardiography Immediate operation with primary abdominal wall closure Sterile dressing and repair prior to discharge Skin gra ing

24. A 2-day-old emale in ant has not yet passed meconium. T ere is no relevant maternal or birth

history. On examination, her abdomen is so but distended, and vital signs are normal. Rectal examination is per ormed, and the rectal vault appears empty, but ollowing withdrawal o the nger, a rush o stool emerges. T e best diagnostic test or this patient is: A. B. C. D. E.

Abdominal x-ray Computerized tomography o the abdomen Genetic analysis or CF R Contrast enema with barium Rectal biopsy

25. In which o the ollowing situations would the best results be obtained or an emergency

department thoracotomy? A. B. C. D. E.

Cardiac arrest in a construction worker a er alling rom a scaf old eight stories high Cardiac arrest ollowing a motor vehicle accident with expulsion o the individual rom the car Cardiac arrest ollowing a gunshot wound to the abdomen External cardiac massage that has ailed a er more than 10 minutes in a trauma patient Cardiac arrest ollowing a stab wound to the chest

26. A 21-year-old male is brought to the emergency room a er an assault with a baseball bat. He

has suf ered obvious head trauma. He opens his eyes spontaneously, does not speak but makes incomprehensible sounds, and localizes to pain. What is his Glasgow Coma Scale score? A. B. C. D. E.

8 9 10 11 12

Que s tio ns 27–28 A 50-year-old man is brought to the emergency department immediately a er suf ering ull-thickness burns over the entire sur ace o both upper extremities and the anterior chest and abdomen. His weight is approximately 155 lb. Initial uid resuscitation has been started with lactated Ringer solution. 27. T e initial resuscitation rate should be approximately which o the ollowing?

A. B. C. D. E.

300 mL/hr 600 mL/hr 900 mL/hr 1,200 mL/hr 1,500 mL/hr

T e patient responds to treatment.

401

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Study Questions or Part VI

28. A er 8 hours, the uid rate should be changed to which o the ollowing?

A. B. C. D. E.

300 mL/hr 600 mL/hr 900 mL/hr 1,200 mL/hr 1,500 mL/hr

29. A 2,600-g newborn without any obvious anomalies turns blue during her rst eeding. An attempt

at passing an oral gastric tube to decompress the stomach is unsuccess ul. Which o the ollowing statements is correct? A. T e most likely orm o tracheal esophageal mal ormation is a blind pouch without a tracheal stula. B. No urther workup or other anomalies is indicated owing to the normal appearance o the patient. C. Because the orogastric tube does not pass, it should be removed to prevent gagging. D. Primary repair can be undertaken i the de ect is less than 2 cm in length. E. I the lung elds are clear to auscultation a er the cyanotic episode, an immediate chest radiograph would not aid in the newborn’s management. 30. Which o the ollowing statements about laparoscopic surgery is true?

A. Due to the minimally invasive nature o laparoscopy, preoperative evaluation o patients is less critical than or laparotomy. B. Routine use o orogastric tubes and urinary catheters is unnecessary during advanced laparoscopic procedures. C. T e abdomen is always prepared and draped or potential laparotomy. D. Antithromboembolic pumps are not needed during laparoscopic procedures, as the risk o deep venous thrombosis is less than or laparotomy. E. Spinal anesthesia is su cient or most advanced laparoscopic procedures. 31. Which o the ollowing physiologic changes occurs as a result o carbon dioxide pneumoperitoneum?

A. B. C. D. E.

Decreased pulmonary compliance due to diaphragm elevation and increased abdominal pressure Metabolic alkalosis rom systemic absorption o carbon dioxide Increased cardiac output as a result o increased venous return Decreased systemic vascular resistance Decreased mean arterial pressure

32. A 32-year-old woman undergoes a laparoscopic cholecystectomy or biliary colic. Forty-eight

hours a er the operation, she complains o ever and RUQ pain. Laboratory studies reveal an elevated white blood cell count as well as an elevated total bilirubin. Which o the ollowing is not part o the initial management? A. B. C. D. E.

C scan o the abdomen HIDA biliary scan Surgical exploration Endoscopic retrograde cholangiopancreatography (ERCP) Broad-spectrum antibiotics

33. Which o the ollowing is true about pediatric hernias?

A. T e incidence is roughly equal in males and emales, with males becoming more common as age increases. B. Congenital pediatric hernias are bilateral 50% o the time. C. Inguinal hernias o en close spontaneously in children, and repair should be delayed until 2 years o age. D. Incarcerated hernias in children should never be reduced. Emergency repair is mandatory. E. Right-sided inguinal hernias are twice as common as le -sided inguinal hernias.

Study Questions or Part VI

34. A victim o a motor vehicle accident who was thrown rom the vehicle is brought to the

emergency department. T e patient is unconscious and hypotensive. He is ound to have a dilated le pupil, decreased breath sounds over the right chest, a moderately distended abdomen, an unstable pelvis, and severe bruises over the thighs. A er resuscitation with 2 L o crystalloid and 2 units o type-speci c packed red blood cells, the patient remains hypotensive with a systolic blood pressure in the low 80’s. What is the least likely explanation or this patient’s hypotension? A. B. C. D. E.

External blood loss Bleeding into the chest Retroperitoneal bleeding Severe closed head injury Femoral ractures

35. An adult male is brought to the emergency department or evaluation and treatment ollowing

injury in a house re. T e patient was ound in a closed room. He has singed acial hair and ull-thickness burns over approximately 30% o his body sur ace area. All o the ollowing are important in his initial stabilization and treatment except which? A. B. C. D. E.

Endotracheal intubation IV uid resuscitation Insertion o a ureteral catheter etanus toxoid administration Systemic antibiotics

36. With the increasing use o US, prenatal diagnosis o abdominal wall de ects is becoming more

common. You are asked to consult a amily with this prenatal diagnosis. Which o the ollowing points and discussion is not true? A. Closure may require more than a single operation. B. I gastroschisis is strongly suspected, amniocentesis is essential to rule out chromosomal abnormalities. C. PN is requently used. D. T e outcome o this category o patient is related both to the integrity o the GI tract or to associated anomalies. E. One o the primary goals o treatment with abdominal wall de ects is to protect the exposed contents o the abdomen. 37. Disadvantages o laparoscopy when compared with laparotomy include all o the ollowing except

which? A. B. C. D. E.

Di culty controlling severe bleeding Poorer visualization o the operative eld Greater di culty placing sutures Loss o tactile sensation Higher operating room costs

38. Laparoscopic cholecystectomy is indicated or all o the ollowing conditions except which?

A. B. C. D. E.

Biliary dyskinesia Initial treatment in patients with severe cholangitis Acute cholecystitis Symptomatic cholelithiasis Biliary pancreatitis

403

404

Study Questions or Part VI

QUESTIONS 39–43 For each clinical situation, match the appropriate diagnosis. A. Acute tubular necrosis B. Hyperacute rejection C. Gra versus host disease D. Acute rejection E. Chronic rejection 39. Occurs when there is cross-match incompatibility 40. Usually a temporary condition or poor renal unction that lasts rom 1–14 days related to

preservation, ischemia, and reper usion o the transplanted kidney 41. Can usually be success ully treated with high doses o immunosuppression, such as methylprednisolone 42. More prevalent in small bowel transplantation than in other organ transplants related to the large

amount o lymphoid tissue associated with the gra 43. Slow decline in renal unction over months or years resulting rom humoral and cellular events

that are generally not treatable or reversible

Que s tio ns 44–45 For each question, match the appropriate immunosuppressive agent. A. Corticosteroids B. acrolimus C. Cyclosporine D. Antithymocyte globulin E. Mycophenolate 44. A calcineurin inhibitor that became the mainstay o immunosuppressive regimens in the 1980s

and continues as the basis o many immunosuppressive regimens with toxicities that include hypertension, gingival hyperplasia, and nephrotoxicity 45. An antimetabolite used as part o triple immunosuppression therapy

Que s tio ns 46–49 Match the GI anomaly with the listed statement. A. Malrotation B. Duodenal atresia C. Small bowel (jejunal and ileal) atresia D. Imper orate anus 46. While considering a vascular accident, there is an associated nding o cystic brosis in a patient

with this GI problem. 47. Although part o the VAC ERL complex, it is associated more commonly with renal

mal ormations. 48. Complete intestinal necrosis is the most eared complication. 49. T ere is a high association with trisomy 21.

Answers and Explanations

Answers and Explanations 1–2. The a ns we rs a re 1-D (Chapter 18, Nasopharynx Cancer, Clinical Evaluation, I–II) a nd 2-E

(Chapter 18, Nasopharynx Cancer, reatment and Prognosis, I–II). T e two most common presenting symptoms o cancer o the nasopharynx are enlarged posterior cervical lymph nodes and unilateral serous otitis media. Cancer o the right ear, right tonsil, or right maxillary sinus or Hodgkin lymphoma generally do not cause otitis media and usually occur in an older age group. Hodgkin lymphoma will lead to serous otitis media only i Waldeyer ring involvement has led to eustachian tube dys unction, which is a rare occurrence. Bilateral radiotherapy is the primary treatment or all epithelial nasopharyngeal tumors. 3. The a ns we r is A (Chapter 18, Larynx Cancer, reatment and Prognosis, IV). Any carcinoma

o the vocal cord that leads to xation o the cord or o the hemilarynx is at least 3. Massive involvement o surrounding so tissues will make the tumor stage 4. T e presence o a single ipsilateral lymph node greater than 3 cm but less than 6 cm in diameter makes the stage o the neck node N2a. Multiple small lymph nodes on the same side o the neck as the primary tumor are classi ed N2b, and lymph nodes involving the opposite side o the neck change the staging to N3. 3 tumors cannot be adequately treated with partial laryngectomy in most cases; total laryngectomy is required. Radiation therapy is used postoperatively as a planned combined treatment in most cases. Chemotherapy is used or inoperable cases or in experimental protocols. 4–5. The a ns we rs a re 4-C (Chapter 18, Parotid Neoplasms, Benign, I–II) a nd 5-D (Chapter 18,

Evaluation and Management o Parotid Masses, Surgical Management, I). T e history given is most consistent with a benign neoplasm o the parotid gland. Benign mixed tumors are the most common benign tumors o the salivary glands. Benign salivary tumors account or 60% o all parotid tumors. Malignant tumors, such as a mucoepidermoid cancer, usually grow more rapidly and are more o en associated with acial nerve paralysis. T e absence o pain makes acute parotitis unlikely. Hemangiomas o the parotid gland are much rarer than benign mixed tumors. T e optimal treatment or a benign mixed tumor is removal o the tumor with a margin o normal parotid gland. T is usually can be accomplished with a super cial parotidectomy. Although these tumors o en appear to shell out, removal by simple enucleation results in a very high recurrence rate. Excision o the entire gland with or without the acial nerve is indicated or malignant tumors. Radiation therapy does not have a role in the management o this lesion. 6. The a ns we r is D (Chapter 18, Congenital Masses, Lesions o T yroid Origin, II, D). T e

patient is presenting with signs and symptoms o a thyroglossal cyst. I there is initial in ection, antibiotics are used to temporize. De nitive management is complete surgical excision, including a portion o the hyoid bone. 7. The a ns we r is C (Chapter 18, Acquired Lesions, Peripheral Nerve umors, II D). T e patient

presents with an acoustic neuroma, a subtype o schwannoma. As these are slow-growing tumors, the most appropriate management is expectant, with observation. Should the lesion become more symptomatic, surgical resection or radiation may be indicated. 8. The a ns we r is B (Chapter 18, Malignant Lesions o the Head and Neck, reatment, III C). T e

patient has evidence o metastatic disease and is a candidate or palliative therapy only. Metastatic disease is a contraindication to surgery. Radiation therapy may be use ul or control o primary disease, or in the setting o multiple primary lesions in the same vicinity, but is generally avoided in this setting. Hospice care is reserved or those who are at imminent risk o demise. 9. The a ns we r is D (Chapter 19, Complications III Gastric bypass A 2). In the postoperative

patient, physical examination is relatively unreliable. Patients may present with marginal ulceration, or which the treatment is acid suppression, but typically develop pain weeks a er the operation i routine acid suppression is not provided. Antidiarrheals are not indicated or pain, and urther narcotic therapy is only use ul i the patient has had inadequate pain control at home.

405

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Answers and Explanations

40 kg/m 2 is the conventional threshold or bariatric surgery. In adolescents, a higher cutof is used, and care ul consideration must be given to the elderly. Patients with BMI 35–39.9 kg/m2 with medical comorbidities related to obesity are also candidates or bariatric surgery.

10. The a ns we r is D (Chapter 19, Patient Selection, I–II). BMI

11. The a ns we r is A (Chapter 20, General Principles, Physiologic Changes Associated with

Pneumoperitoneum, I–II). T e patient’s distress is related to the pneumoperitoneum. Insu ation o gas into a vein may result in air embolus, and absorption o CO2 can cause a clinically signi cant acidosis. Pneumothorax may occur with malposition o the needle but is unlikely. Volume de cits usually do not produce such a dramatic picture. Sedation diminishes the respiratory rate, and sympathetic activity is not typically changed by abdominal surgery. 12. The a ns we r is B (Chapter 20, Selected Laparoscopic Procedures, Laparoscopic Ventral Hernia

Repair, IV C). T e patient has signs and symptoms o peritonitis consistent with a delayed per oration. T e injury may have been partial thickness at time o operation and evolved over the ensuing 2 days. Myocardial in arction is possible but should cause chest pain and is less likely in a young patient. Pneumoperitoneum is essentially completely resorbed over the rst 2 postoperative days and would not contribute to an acute event. deep venous thrombosis should produce swelling in the leg or respiratory di culty i a pulmonary embolism develops. Gas bloat may produce abdominal distension but is uncommon in this setting. 13. The a ns we r is C (Chapter 18, Neck cancer, II B). A solid, palpable neck lesion should have

ne-needle aspiration. Incisional and excisional biopsy are premature as the lesion may require more extensive margins or neck dissection. C is a use ul adjunct, but the initial diagnosis is best achieved through FNA. MRA will not provide use ul in ormation at this point. 14. The a ns we r is C (Chapter 21, Screening and Diagnosis, Overview, I D). ACS guidelines are

based on both the test characteristics (the likelihood o cancer detection) as well as the likelihood o impacting the patient’s course and treatment. Among these listed, PSA has not shown a demonstrable survival bene t or mass screening purposes. 15. The a ns we r is D (Chapter 21, Research and raining, Clinical rials, I C). T is is a phase III

study, comparing a new treatment to standard o care. A phase 0 study is an in ormal term used to describe pharmacokinetic studies. Phase I tests the sa ety o a medication. Phase II trials investigate a clinical ef ect. No mention is made o this trial design, so randomization o patients is possible but not de nitive. Similarly, blinding the subjects and the providers to intervention is a technique that is not explicit rom the question. 16. The a ns we r is B (Chapter 22, rauma, Patient Evaluation, II A 4). Eyes: 3 or response to voice.

Verbal: 2 or incomprehensible sounds. Motor: 1 or no response to pain. 17. The a ns we r is A (Chapter 22, rauma, Patient Evaluation, II A). T e primary survey (ABCs)

begins with airway assessment. T e patient is in extremis, and intubation should be the rst priority. Volume resuscitation should also begin promptly, along with the secondary survey assessing or injuries. Pupillary exam is appropriate to help determine neurologic status but should wait. 18. The a ns we r is D (Chapter 22, Speci c Injuries, Pneumothorax and Hemothorax, I B). T e

patient has a tension pneumothorax, and the best initial maneuver is needle decompression via the second interspace. Once released, the patient should have a chest tube placed or ongoing treatment. Increased oxygen levels will not resolve the condition, and thoracotomy is overaggressive and not su ciently prompt to address tension pneumothorax. T ere is no role or sur actant in the management o the adult trauma patient. 19. The a ns we r is A (Chapter 23, Organ-Speci c Considerations, Kidney ransplantation, III

H 3). T e patient is presenting with a symptomatic lymphocele. T e best management is internal drainage, which can be per ormed with minimally invasive techniques. A urinoma should have a markedly elevated creatinine level. T e patient does not show signs o rejection, so corticosteroids are contraindicated. I the patient has a hematoma, evacuation would be reasonable, but ongoing

Answers and Explanations

trans usion is not. For lymphocele, percutaneous drainage results in unacceptably high rates o recurrence. 20. The a ns we r is E (Chapter 23, Organ-Speci c Considerations, Pancreatic and Islet

ransplantation, III A). T e patient may have a catastrophic vascular event. T e initial maneuver is to rule out vascular events by US. C scan cannot assess the in ow and out ow adequately, and nonspeci c ndings would lead to other diagnostic modalities. Biopsy is not speci c enough to yield a diagnosis. Urine culture would not be use ul, even in cases o bladder drainage. Antibody levels are not use ul. 21. The a ns we r is D (Chapter 23, Organ-Speci c Considerations, Kidney ransplantation, VII). For

acute rejection, high-dose corticosteroids with a taper is the treatment o choice. Occasionally, cyclosporine toxicity may cause decreased gra unction, but this is not consistent with the biopsy results. Nephrectomy is the last resort, when the gra is unsalvageable. Plasmapheresis only has role or pre ormed antibodies or hyperacute rejection. Additional contrast will not provide a diagnosis and may allow urther renal injury. 22. The a ns we r is B (Chapter 24, Disorders o In ancy, In antile Hypertrophic Pyloric Stenosis, V).

T e in ant presents with classic signs and symptoms or hypertrophic pyloric stenosis. T e initial management should be correction o electrolyte abnormalities—as the in ant is expected to have hypochloremic, hypokalemic metabolic alkalosis—then operation or pyloromyotomy. Immediate laparotomy is indicated or questions o ischemia, not present in this case. NG decompression is unnecessary, as this represents a high obstruction. Liver scanning and biochemical pro le is indicated in cases o jaundice only. 23. The a ns we r is C (Chapter 24, Abdominal Wall De ects, Gastroschisis, IV). T e patient is

presenting with gastroschisis. As this represents a congenital evisceration, emergent surgery is indicated. Unlike omphalocele, there is no role or nonoperative management. Further, because the risk o major cardiac anomalies is low, operation should not be delayed in search o other de ects. Silver sul adiazine is use ul or nonruptured omphalocele. Inguinal hernias should be repaired prior to discharge. Skin gra ing is rarely indicated in abdominal wall closure. 24. The a ns we r is E (Chapter 24, Hirschsprung Disease, Diagnosis, IV). T e history is consistent

with Hirschsprung disease. T ere is aganglionosis o a portion o colon, resulting in the inability to pass stool. Abdominal plain lms may reveal obstruction and air- uid levels but are nonspeci c. C may also reveal distended loops but does not provide conclusive diagnosis. Cystic brosis may be associated with intestinal atresia but more typically small bowel. Contrast enema certainly suggests the diagnosis, but water-soluble agents are pre erred. Rectal biopsy remains the gold standard o diagnosis. 25. The a ns we r is E (Chapter 22, rauma, Resuscitative T oracotomy, V). Emergency department

thoracotomies should only be per ormed by trained personnel and or speci c indications. T e best results and the highest salvage rates have been obtained with emergency thoracotomy ollowing cardiac arrest rom penetrating injury to the chest (patient E). In general, major blunt trauma (patients A and B) and ailed external cardiac massage lasting or 10 minutes (patient D) are relative contraindications. A patient whose heart stops a er a gunshot wound to the abdomen (patient C) has likely exsanguinated and will not bene t rom an emergency thoracotomy. 26. The a ns we r is D (Chapter 22, Fig. 22-1). He receives 4 points or eye opening, 2 or best verbal

response, and 5 or best motor response. 27-28. The a ns we rs a re 27-B a nd 28-A (Chapter 22, Burns, Burn Injury, III). T e burn involves

approximately 36% o the body sur ace area (BSA). According to the Parkland ormula, 4 mL/ kg o body weight/% BSA burned o lactated Ringer solution should be administered during the rst 24 hours. Hal o this amount should be given during the rst 8 hours a er injury and the remainder over the next 16 hours. 29. The a ns we r is D (Chapter 24, Esophageal Atresia and racheoesophageal Mal ormations,

Operative Management, I). A primary repair at time o presentation can be undertaken i

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Answers and Explanations

the de ect is less than 2 cm in length. A blind proximal pouch with a distant EF is the most common type o mal ormation. T ere is a 40% incidence o associated anomalies in one or more other organ systems. Decompression o the proximal pouch is important to reduce aspiration. A radiograph can help to demonstrate the anatomy. 30. The a ns we r is C (Chapter 20, Selected Laparoscopic Procedures, Laparoscopic

Cholecystectomy, III). Because all laparoscopic procedures have the potential to be converted to laparotomy, preoperative preparation must be as thorough as or open abdominal surgery. T e bladder and stomach are decompressed with a urinary catheter and an orogastric tube, respectively, to avoid injury during creation o the pneumoperitoneum. Prophylaxis against deep venous thrombosis is necessary, as risk actors or that condition are inherent in laparoscopy. General anesthesia is needed or the vast majority o advanced laparoscopic procedures; spinal anesthesia cannot achieve a high enough level without respiratory embarrassment. 31. The a ns we r is A (Chapter 20, General Principles, Physiologic Changes Associated

with Pneumoperitoneum, IV). Physiologic changes associated with carbon dioxide pneumoperitoneum are complex and interdependent, but several generalizations can be made. Pulmonary compliance is decreased rom diaphragmatic elevation and increased intra-abdominal pressure. Hypercarbia causes acidosis, not alkalosis. Cardiac output is usually decreased due to decreased venous return, and blood pressure and systemic vascular resistance are increased. 32. The a ns we r is C (Chapter 20, Selected Laparoscopic Procedures, Laparoscopic

Cholecystectomy, III B 1). Bile duct injuries or bile leaks a er laparoscopic cholecystectomy should not initially be managed by surgical exploration. Resuscitation, antibiotics, and appropriate imaging to de ne the anatomy o the problem are the rst steps. 33. The a ns we r is E (Chapter 24, Congenital Hernias, Inguinal Hernias, I). Sixty percent o

pediatric inguinal hernias are right sided, 30% are le sided, and 10%–15% are bilateral. T e male-to- emale ratio is 6:1. Inguinal hernias do not close spontaneously like umbilical hernias and should be repaired when diagnosed. Incarcerated hernias are managed with reduction ollowed by hydration and repair. 34. The a ns we r is D (Chapter 22, rauma, Shock, II B). Multiple trauma patients with hypotension

and hypovolemic shock are rarely, i ever, hypotensive secondary to head injury. T e treating physician must look or another cause o hypotension, which is almost always blood loss. T e blood loss can be rom ve dif erent areas: (1) external blood loss rom lacerations or an open wound (details should be obtained rom the rescue workers at the scene o the accident); (2) intrathoracic blood loss; (3) intra-abdominal blood loss; (4) retroperitoneal bleeding almost always associated with pelvic ractures; and (5) bleeding into the thighs secondary to emur ractures, which can cause shock. In the patient described, the closed head injury would be the least likely mechanism or this continued hypotension. 35. The a ns we r is E (Chapter 22, Burns, Inhalation Injury, I). T e patient described is at a high

risk or suf ering an inhalation injury. Delayed airway obstruction can develop rapidly during the rst 24–48 hours a er injury. It is best to per orm endotracheal intubation early be ore respiratory problems develop, as later intubation can be di cult. Vigorous IV uid resuscitation is indicated or all patients who have ull-thickness burns involving more than 20% BSA. Because urine output must be ollowed very closely, an indwelling ureteral catheter is mandatory in the management o these patients. etanus toxoid with or without hyperimmune immunoglobulin should be given i the patient’s tetanus immunization status is not current. Systemic antibiotics are usually not indicated in the initial management o burn patients. 36. The a ns we r is B (Chapter 24, Abdominal Wall De ects). T e general category o abdominal

wall de ects consists o gastroschisis and omphaloceles. T e primary goal o treatment is to protect the exposed or potentially exposed GI tract. T is is done either by abdominal wall closure, scari cation o the omphalocele sac, or covering with Silastic or silicon material with staged reduction and closure. Although coverage is complete and the GI tract is unctional, nutrition is usually accomplished by PN. T e outcome or the patient is dictated by the integrity and viability o the GI tract (gastroschisis) or associated anomalies (omphalocele). Chromosomal abnormalities may be present in patients with omphaloceles but not with gastroschisis.

Answers and Explanations

37. The a ns we r is B (Chapter 20, General Principles, Advantages and Disadvantages o Minimal

Access Surgery). It is generally agreed that improved visualization o the operative eld due to magni cation and improved light delivery to remote areas o the abdomen are an advantage o laparoscopy over laparotomy. Di culty controlling severe bleeding, greater di culty placing sutures, loss o tactile sensation, and higher operating costs are clear disadvantages o laparoscopy as compared with laparotomy. 38. The a ns we r is B (Chapter 20, Selected Laparoscopic Procedures, Laparoscopic

Cholecystectomy, I). Laparoscopic cholecystectomy is indicated or most symptomatic biliary conditions, including biliary colic, acute cholecystitis, biliary dyskinesia, and biliary pancreatitis, a er resolution o pancreatitis. However, initial therapy or cholangitis is hydration, broadspectrum antibiotics, and drainage o the common bile duct. Cholecystectomy is per ormed at a later time a er resolution o sepsis. 39–43. The a ns we rs a re 39-B, 40-A, 41-D, 42-C, a nd 43-E (Chapter 23, Overview, Rejection,

I, II, IV). Hyperacute rejection occurs when the serum o the recipient has pre ormed antidonor antibodies. Be ore transplantation, the recipient’s blood is examined or the presence o cytotoxic antibodies speci cally directed against antigens on the donor’s lymphocytes (cross-match test). Hyperacute rejection cannot be treated but can be avoided. Kidney transplants are occasionally associated with a period o acute tubular necrosis, which is a temporary condition thought to be related to conditions that occur during obtaining and preserving the kidney. It occurs rarely in living donor transplants. High doses o immunosuppression—either methylprednisolone or antithymocyte globulin or OK 3—are used to treat acute rejection. T is diagnosis is usually made via the detection and workup o gra dys unction and may include a biopsy. Acute rejection can be treated and is reversible. Chronic rejection usually has an insidious onset and is multi actorial, involving both cell-mediated and humoral arms o the immune system. In lung transplantation, it is known histologically as bronchiolitis obliterans. Generally, there is no known ef ective therapy. Because the small bowel is rich in lymphoid tissue, gra versus host disease has become more prevalent in this group o recipients than in other organ transplants. T is is caused by the proli eration o donor-derived immunocompetent cells with a number o clinical presentations, including skin rash. 44–45. The a ns we rs a re 44-C a nd 45-E (Chapter 23, Overview, Immunosuppression, I,

able 23-1). Calcineurin inhibitors block the calcineurin-dependent pathway o helper -cell activation and include cyclosporine and tacrolimus, which are both used in maintenance immunosuppressive regimens. Cyclosporine became the mainstay o immunosuppressive regimens in the early 1980s and is now in a new ormulation known as Neoral. Associated side ef ects include nephrotoxicity, hypertension, tremor, and hirsutism. acrolimus, which was introduced more recently, is also a pro ound inhibitor o -cell unction, with many similar side ef ects as cyclosporine. Corticosteroids inhibit all leukocytes and have numerous side ef ects, including excessive weight gain, diabetes, and cushingoid acies. Mycophenolate is an antimetabolite that impairs lymphocyte unction by blocking purine biosynthesis via inhibition o the enzyme inosine monophosphate dehydrogenase. 46–49. The a ns we rs a re 46-C, 47-D, 48-A, a nd 49-B (Chapter 24, Intestinal Atresia).

GI anomalies vary greatly. T e dif erence between duodenal atresia and the other small bowel atresias is a developmental (duodenal) accident versus a vascular accident (jejunum and ileum). T ere ore, chromosomal abnormalities (most commonly, trisomy 21) appear with duodenal problems. T e exception to this general rule is the associated incidence o cystic brosis with small bowel atresias. Malrotation, although it causes an obstruction, may also pose a vascular problem. T is is related to the midgut volvulus, which can cause total ischemia to the intestine. Renal mal ormations occur in 40% o the imper orate anus, either as a VAC ERL complex or related to the disease itsel (urethral stula).

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Part VII

Surgical Subspecialties Chapter Cuts and Caveats

CHAP TER 25 Uro lo g ic Surg e ry: Acute vesical outlet obstruction may represent an emergency: Acute urinary retention is best treated by catheter drainage, either a Foley catheter or suprapubic tube. Perineal in ection may spread among ascial planes rapidly, leading to death. T e question o Fournier gangrene should prompt immediate imaging and broad-spectrum antibiotics. rauma to the GU tract is common. Af er trauma, blood at the meatus in a male is a sign o urethral injury and requires imaging prior to catheterization. Most renal trauma can be managed nonoperatively. Most ureteral trauma requires reconstruction. Benign prostatic hypertrophy is common in elderly men and is typically treated medically initially. Symptoms include hesitancy, requency, and decreased power o the urinary stream. T ose that do not respond may undergo trans-urethral surgery. Most testicular tumors are o germ cell origin (deriving rom the cells that make up the reproductive system). T ey typically metastasize to the para-aortic lymph nodes. Early detection through sel -examination may improve survival.

CHAP TER 26 P la s tic a nd Re c o ns truc tive Surg e ry: T e “reconstructive ladder” provides a guide to the optimal management o wounds and sof tissue de ects. Simpler solutions such as local rearrangements are tried rst, ollowed by local aps, then “ ree aps.” T e higher on the ladder, the more di cult the procedure and the greater the likelihood o complications. Flaps may include ascia, muscle, or both. Free aps are more complicated and have higher ailure rates than pedicled aps. In ected wounds do not support skin graf s. Wounds reach most o their ultimate strength by 6 weeks postoperation, which reaches a maximum o 80% o the integrity o nonwounded tissue. Immediate breast reconstruction does not change outcomes in early-stage breast cancer. Reconstructive surgical techniques can be used as adjuncts in abdominal wall reconstruction (complex hernias) as well as de ects o the chest wall. Melanoma is an invasive skin cancer. It is staged by depth, using the Breslow system o absolute distance in millimeters. reatment is generally surgical with wide excision. Adjuvant therapy is used or advanced disease.

CHAP TER 27 Ne uro s urg e ry: T e skull is a rigid container with xed volume, so increases in volume (bleed, tumor, cerebral edema) necessarily cause an increase in pressure. CPP MAP ICP. Epidural hematomas usually arise rom trauma to the middle meningeal artery and present with a lucid interval between bouts o decreased consciousness. Unilateral papillary dilatation of en signi es signi cant cerebral compression. reatment o signi cant hematomas is evacuation. Spinal cord injury results in motor and sensory de cits below the level o the lesion. T ey also may have loss o sympathetic tone (spinal shock). reatment is largely supportive once spinal stabilization has taken place. Symptomatic aneurysms should be treated by open surgery or endovascular occlusion.

CHAP TER 28 Ortho p e d ic s : Compartment syndrome may ollow ractures and crush injuries, is most likely to develop in the leg, and needs prompt decompression to minimize disability. Pressure may be measured directly within each ascial compartment. Open ractures require antibiotics and urgent operative debridement and stabilization. Osteomyelitis is usually treated with long-term antibiotics. All patients with knee dislocations require a peripheral pulse exam and ABI due to the risk o popliteal artery injury. Bony tumors usually represent metastasis rather than primary malignancies.

411

Chapter 25

Urologic Surgery

Jessica Felton, Daniel Reznicek, and Andrew Kramer

UROLOGIC EMERGENCIES Ac ute Urina ry Re te ntio n I. De f nitio n: abrupt inability to pass urine, typically associated with lower abdominal and suprapubic discom ort; usually requires greater than 200 mL o urine in the bladder II. Ca us e : In men, more commonly due to obstruction in the urethra or prostate. In women, a neurogenic bladder component is of en present. III. Tre a tm e nt: must be addressed promptly by either a urethral catheter or suprapubic tube placement

P ria p is m I. De f nitio n: unwanted erection present or more than 4 hours in the absence o sexual excitation II. Typ e s (two ) A. Low f ow (ischemic; most common): Patients have pain, rigid corpus cavernosa, and little or no arterial in ow. B. High f ow (nonischemic; less common): Partial, nonpain ul erections are nonemergent and usually associated with prior trauma. III. Dia g no s is : Physical exam ndings and intercavernosal arterial blood gases help di erentiate between low- and high- ow priapism. IV. Tre a tm e nt A. First-line treatment: For ischemic priapism, aspiration o the corporal blood reduces the pressure and removes the anoxic blood. B. Other: saline irrigation, sympathomimetic injections, and surgical intervention involving shunts created between the corpus cavernosum and spongiosum V. Ris k a c to rs A. Hematologic disorders: Sickle cell disease is responsible or up to one third o all cases. Other hematologic disorders such as leukemia and thalassemia may also precipitate priapism. B. Medications: razodone, hydralazine, and cocaine are commonly tested. Many other medications may also cause priapism. C. Neurogenic: Spinal cord injuries, neuropathies, and even spinal anesthesia can cause priapism.

Te s tic ula r To rs io n I. P re s e nta tio n: usually presents as sudden onset o pain with associated nausea and vomiting, of en in males age younger than 25 years II. Phys ic a l f ndings : pain to palpation and loss o the cremasteric re ex III. Dia g no s is : Always include a scrotal ultrasound in any patient in Quic k Cut whom torsion is suspected due to the small window o opportunity Us e s crotal to save a torsed testicle (Fig. 25-1). ultras ound or rapid diagnos is IV. Tre a tm e nt: immediate surgical exploration, detorsion o the i tors ion is s us pected. a ected side, and bilateral orchidopexy

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Urologic Surgery

413

Fig ure 25-1: Scrotal ultras ound per ormed on a 17-year-old male with acute right s crotal pain or 3 hours . Doppler demons trates adequate f ow in the le t tes ticle and lack o f ow on the right cons is tent with tes ticular tors ion.

Ob s truc tive Uro p a thy I. Em e rg e nt: when urinary tract obstruction (e.g., stone) is causing sepsis or worsening renal unction II. Tre a tm e nt: Upper urinary tract obstruction requires drainage and may include a ureteral stent or percutaneous nephrostomy tube.

P a ra p him o s is I. De f nitio n: Foreskin is retracted over the glans and cannot be reduced to its normal position. II. P hys io lo g y: Entrapped skin ring leads to increasing edema o the glans distally and may cause arterial occlusion and necrosis. III. Tre a tm e nt: Reduction can be attempted af er squeezing the glans rmly or 5 minutes to reduce swelling and then quickly pulling the oreskin orward. Alternatively, a dorsal slit can be per ormed, which releases the skin ring with an incision.

Fo urnie r Ga ng re ne I. De f nitio n: necrotizing asciitis or the perineum and genitalia II. P hys ic a l f nd ing s : Patients have pain out o proportion to the extent o in ection. Crepitus, cellulitis, necrosis, and oul-smelling lesions are usually present. III. Dia g no s is : I in doubt, order a computed tomography (C ) scan rather than ultrasound because C will demonstrate air tracking through the tissue planes. IV. Tre a tm e nt: Broad-spectrum antibiotics and early wide debridement o necrotic tissue are required. Most commonly, it is a mixed in ection with gram-positive, gram-negative, and anaerobic bacteria.

Quic k Cut I concerned about Fournier gangrene, order a s tat CT o the abdomen/pelvis and s tart broad-s pectrum antibiotics .

414

Chapter 25

Urinary ract Stones

URINARY TRACT STONES Typ e s o Urina ry Ca lc uli

Quic k Cut A ra d io p a q ue s tone means it is vis ible on x-ray. Even ra d io luc e nt s tones s how up on CT s cans .

I. Ca lc ium o xa la te s to ne s (m o s t c o m m o n): radiopaque and most commonly idiopathic, but other disorders such as hyperparathyroidism, renal tubular acidosis, and chronic diarrheal states can also cause calcium oxalate stones (Fig. 25-2) II. Uric a c id s to ne s : radiolucent stones caused by insulin resistance, dietary purine excess, and gout III. Cys tine c a lc uli: aintly radiopaque and rare A. Cause: Cystinuria is an autosomal recessive disorder that causes a de ect in renal tubular reabsorption o our amino acids: cystine, ornithine, arginine, and lysine. Only cystine orms calculi. B. Prevention: Overhydration and urine alkalinization to pH 7.5 are the most e ective preventive measures. Oral cystine-binding drugs, such as d-penicillamine or alpha-mercapto-propionylglycine, also help. IV. Struvite c a lc uli: Radiopaque stones usually related to chronic urinary tract in ections (U Is) with urea-splitting bacteria, which maintain alkaline urine. Proteus is the most common causative bacteria.

Clinic a l P re s e nta tio n I. P a in: Most requent symptom caused by ureteral obstruction. T e site o pain is related to the location o the obstructing calculus (e.g., ank pain, lower abdominal pain, testicular pain, or vulvar pain). II. Othe r s ym p to m s : hematuria (visible or microscopic), nausea and vomiting, and irritative bladder symptoms (e.g., rom a ureterovesical junction calculus)

Fig ure 25-2: CT s can per ormed on a 44-year-old male with right-s ided abdominal pain and gros s hematuria. CT s can demons trated an obs tructing s tone near the ureteropelvic junction and hydronephros is .

Chapter 25

Urologic Surgery

415

Dia g no s is

Quic k Cut I. P hys ic a l e xa m ina tio n: Patients are usually uncom ortable and Patients with urinary have costovertebral angle tenderness. calculi o ten have writhing pain and have di culty II. Urina lys is : Hematuria is usually present; a uric acid stone is lying s till, which di ers unlikely to be ound in a patient with a urine pH o 6.5 or higher. rom peritonitis and acute III. No nc o ntra s t a b d o m ina l/p e lvic CT: diagnostic test o choice abdomen in which pain is exacerbated by movement. IV. Ultra s o no g ra p hy: Can be use ul in pregnant emales or children to avoid radiation exposure. It de nes hydronephrosis or an acoustic shadow rom a calculus but is much less sensitive than C . Of en used in conjunction with a plain abdominal x-ray. V. Cys to ure thro s c o p y with re tro g ra d e p ye lo g ra p hy: may be needed to con rm calculus presence and reveal its location i imaging studies are not de nitive

Tre a tm e nt I. Ob s e rva tio n: Reserved or stones with reasonable likelihood o spontaneous passing, which is related to stone size and obstruction Quic k Cut site. Encourage adequate hydration, using a urine strainer, Spontaneous s tone controlling pain, and an alpha blocker to reduce ureteral spasm and pas s age is a unction o s ize: improve stone passage rate. 6 mm 10% , 5 mm 50% , II. Surg ic a l p ro c e d ure s : Advances in endoscopic techniques, 4 mm 90% extracorporeal shock wave lithotripsy (ESWL), and endourology success ully allow most calculi to be removed without open surgical procedures. A. Ureteroscopy and/or stent placement: ransurethral approach into the ureter to stent the kidney and allow the stone to pass or a ureteroscope may be used to treat the stone directly. 1. Calculi can be basketed and removed intact or ragmented with lasers. Quic k Cut 2. Stent is of en lef in the ureter af er stone manipulation to Pneumothorax alleviate obstruction rom edema. is a pos s ible complication with percutaneous B. Percutaneous nephrolithotomy (PCNL): Nephrostomy tube nephrolithotomy. tract in the ank is best suited or large calculi that can be ragmented and removed using ultrasonic, electrohydraulic, or laser lithotriptors. C. ESWL: External energy source is ocused by uoroscopic or Quic k Cut Out o all s tone ultrasound guidance on a calculus to provide a high-pressure procedures (ureteros copy, zone that can ragment the calculus. T e gravel-like ragments ESWL, and PCNL), only pass through the ureter. ureteros copy can be D. Complications: bleeding, perinephric hematoma, “steinstrasse” per ormed with antiplatelet (gravel causing ureteral obstruction), and hypertension agents or anticoagulation. E. Contraindications: coagulopathy, antiplatelet medications, or in ection

BENIGN P ROSTATIC DISORDERS Be nig n P ro s ta tic Hyp e rp la s ia I. De f nitio n: Benign prostatic hyperplasia (BPH) is a benign enlargement o the prostate gland that occurs commonly in aging men. A. Histology: Changes include stromal and epithelial hyperplasia in the transition (periurethral) zone, which can compress the prostatic urethra and obstruct urinary ow. B. Clinical sequela: Lower urinary tract symptoms (LU S) occur in a subset o patients with histologic BPH. Obstruction is thought to be due to both prostate size and urethral tone. II. Dia g no s is : Can only be de nitely made with prostatic tissue evaluated by a pathologist; however, presumptive BPH can be diagnosed based on the patient’s irritative or obstructive symptoms and ndings on digital rectal examination (DRE).

416

Chapter 25

Benign Prostatic Disorders

III. Sym p to m s A. Obstructive voiding symptoms: tend to respond best to treatment 1. Diminished orce o urinary stream despite a ull bladder 2. Hesitancy in initiating ow 3. Sense o incomplete emptying 4. Intermittency or “double voiding” 5. Urinary retention B. Irritative voiding symptoms: thought to be caused by detrusor instability rom chronic obstruction and include requency, urgency, nocturia, and dysuria IV. P hys ic a l e xa m ina tio n a nd d ia g no s tic te s ting A. Gland palpation: to assess size, consistency, and presence or Quic k Cut absence o induration on DRE A rm, non-tender B. ransabdominal ultrasonography or direct catheterization: gland s ugges ts BPH. A to assess residual urine volume in the bladder palpable pros tate nodule C. Pressure f ow studies: Signi cant bladder contraction but s ugges ts pros tate cancer. decreased orce o stream suggest obstruction due to the prostate. Absence o orce suggests an intrinsic detrusor insu ciency. V. Tre a tm e nt: Medical therapy remains the rst-line treatment or presumed BPH. I medical treatment ails, many surgical options or removing the transition zone tissue o the prostate remain. A. Indications or treatment: Most men initiating treatment do so or relie o symptoms rather than any absolute indication. Absolute indications or intervention include the ollowing. 1. Urinary retention 2. Signi cant or recurrent gross hematuria not due to other causes 3. Bladder calculi 4. Bilateral hydroureteronephrosis with renal insu ciency secondary to bladder outlet obstruction 5. Repeated U Is caused by urinary stasis B. Medical therapy: Relieves symptoms in men with mild to moderate disease. Although objective improvement may be minimal, i symptomatic improvement occurs, treatment is success ul. 1. Selective alpha-1 sympatholytics: block alpha-1 receptors in the prostatic capsule and bladder neck area, reducing outlet Quic k Cut resistance and improving symptoms Selective alpha-1 a. Mild to moderate LU S: T ese are the most commonly s ympatholytics include used rst-line treatment with good symptomatic tams ulos in, terazos in, al uzos in and reduce pros tatic improvement. res is tance to urinary f ow. b. Principal side e ect: orthostatic hypotension 2. 5-Alpha reductase inhibitors: block intraprostatic conversion o testosterone to dihydrotestosterone (DH ), reducing prostatic size and improving symptoms with minimal side e ects a. Based on the principle that prostatic growth is androgen dependent b. Objective symptom improvements have been modest, and a trial o 3–6 months may slightly be required to determine e cacy. c. T ese agents reduce the risk o acute urinary retention and the need or transurethral resection o the prostate ( URP). 3. Combination therapy (e.g. 5-alpha reductase inhibitor plus alpha sympatholytics): has been shown in randomized controlled trials to be superior to single-agent therapy or disease progression prevention C. Surgical therapy 1. URP: provides reliable and immediate improvement in both symptoms and voiding dynamics a. Procedure: Wire loop attached to an electrocautery unit is used to resect tissue under direct cystoscopic vision. Regional anesthesia is commonly used. b. Complications: bleeding, in ection, retrograde ejaculation, bladder neck contracture, urethral stricture, and impotence (rarely) c. ransurethral incision ( UI): may be appropriate or patients who have small glands and is associated with a lower incidence o bladder neck contracture and retrograde ejaculation

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Urologic Surgery

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Ta b le 25-1: Dia g no s tic Fe a ture s o P ro s ta titis /Chro nic P e lvic P a in Synd ro m e Sym p to m s

Sys te m ic Sig ns

Inc re a s e d WBCs in EP S

Acute bacterial prostatitis

Yes

Yes

Yes

Yes

Chronic bacterial prostatitis

Yes

No

Yes

Yes

Nonbacterial prostatitis

Yes

No

Yes

No

Prostadynia

Yes

No

No

No

Typ e o P ro s ta titis

P o s itive Culture

WBC, white blood cell count; EPS, expressed prostatic secretions.

2. Open prostatectomy (enucleation): usually reserved or patients with glands greater than 60 g or in whom other pathology exists (e.g., vesical calculus or bladder diverticulum requiring repair) 3. Minimally invasive prostatic surgical options: have evolved dramatically and include techniques such as microwave therapy, laser ablation, and transurethral needle ablation ( UNA)

No nb a c te ria l P ro s ta titis I. De f nitio n: Benign in ammation that may be bacterial or nonbacterial. Patients tend to be younger than those presenting with BPH, and symptoms tend to be more irritative and pain ul rather than obstructive ( able 25-1). II. Sym p to m s : Of en synonymous with “male pelvic pain syndrome,” creating an array o symptoms ranging rom urinary requency, urgency, perineal pain, and dysuria. T e hallmark symptom is pain. III. Tre a tm e nt: although no clear standard-o -care treatment exists, many use a combination o antibiotics, alpha blockers, muscle relaxants, and bio eedback

Quic k Cut With pros tatitis , it is important to rule out acute bacterial in ection. Acute bacterial pros tatitis is always as s ociated with a UTI and requires antibiotics . Cons titutional s ymptoms s uch as ever and chills are us ually pres ent.

GENITOURINARY MALIGNANCIES P ro s ta te Tum o rs I. Ep id e m io lo g y a nd d ia g no s is : Prostate cancer is the most common noncutaneous cancer among men worldwide. T e current li etime risk o prostate cancer or men living in the United States is approximately one in six. A. Present screening modalities: DRE and prostate-speci c antigen (PSA) test 1. DRE: traditional cancer detection method, assessing or induration, or a “nodule,” in the prostate and should be per ormed yearly 2. PSA level: PSA is a serine protease that serves to lique y semen af er ejaculation. a. Roles: diagnostic and in ollowing response to cancer treatment b. When combined with DRE, determination o the PSA level improves the ability to detect cancers. It has a high speci city, but low sensitivity and is good or ruling out those who do not have cancer (low alse-positive rate). B. Prostate biopsy: O ce-based procedure per ormed with transrectal ultrasound ( RUS) guidance in men who have a suspicious DRE and/or an elevated level o PSA. Risks include bleeding (urinary tract or rectal) and in ection. Signi cant complications occur in less than 0.5%–1% o men. II. Tre a tm e nt A. Expectant management (two types) 1. Watch ul waiting: Noncurative treatment; goal is to limit morbidity rom disease or therapy. a. reatment is delayed until symptoms become evident, at which time androgen deprivation therapy (AD ) is initiated. b. Usually or patients expected to live less than 5 years who may develop local symptoms but will not die rom the disease

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Chapter 25

Genitourinary Malignancies

2. Active surveillance: Selective delayed de nitive (curative intent) therapy; this approach care ully monitors the patient with cancer with requent PSAs and biopsies with the goal o undergoing curative therapy when the risks o cancer exceed the risks o treatment (usually low-risk prostate cancers in healthier Quic k Cut patients). The only two B. Surgery: Radical prostatectomy is a treatment or locally curative therapies or con ned tumors in appropriate surgical candidates. T ere pros tate cancer are radiation has been a dramatic shif rom open radical retropubic (either external beam or prostatectomy to minimally invasive techniques, such as brachytherapy) and s urgery. laparoscopic and robotic-assisted laparoscopic prostatectomy. C. Radiation: Radiation can include implantation o radioactive pellets (brachytherapy) or external beam radiation. D. AD : Either surgical or chemical is e ective. Androgens uel prostate growth; there ore inhibiting them prevents prostate cancer growth. Common medications used include gonadotropin-releasing hormone agonists (leuprolide, goserelin) and androgen receptor antagonists (bicalutamide, utamide). III. P ro g no s is A. Survival: Median survival with metastatic disease is 2–2.5 years. Men who have a good biochemical response (PSA nadir less than 4 ng/mL) have a longer survival than those with poor biochemical response (PSA nadir greater than 4 ng/mL). B. Hormone re ractory disease: Disease progression af er androgen ablation therapy. Survival averages 12–18 months. 1. Chemotherapy: o date, no therapies are consistently e ective, but several chemotherapy agents are approved with modest e cacy (mitoxantrone, docetaxel). 2. Other: Immunologic agents have also been developed, and sipuleucel- was the rst therapeutic vaccine to be U.S. Food and Drug Administration (FDA) approved or the treatment o any cancer.

Bla d d e r Ca rc ino m a I. Ep id e m io lo g y a nd Dia g no s is A. Incidence: In the United States, greater than 70,000 new cases per year are diagnosed. Men are more commonly a ected than women (3:1). B. Age: generally, a disease o the elderly; median age 67–70 years C. Risk actors: occupational exposure to aniline dyes, aromatic amines, and naphthylamine; cigarette smoking; phenacetin (analgesic) abuse; chronic in ammation; Schistosoma haematobium cystitis; history o cyclophosphamide Quic k Cut treatment; and history o pelvic irradiation Painles s hematuria D. Clinical presentation: Painless hematuria is the most common is the mos t common pres enting s ymptom o (85%) presenting symptom. Bladder irritability with urinary bladder cancer. requency, urgency, and dysuria is commonly associated with di use carcinoma in situ or invasive cancer. E. Diagnosis: Cystoscopy and urine cytology are the mainstay o detection. II. Tre a tm e nt A. Super cial transitional cell tumor (nonmuscle invasive) 1. Complete transurethral resection: T e tumor is resected in super cial and deep components. Deep resection is per ormed to de ne i muscle-invasive disease is present. All visible tumors should be resected. a. Random bladder and prostatic urethral biopsies: Can determine the multi ocal extent o disease. Pathologic evaluation includes grade o lesion (low or high grade), evidence o invasion into the lamina propria or muscle, and carcinoma in situ (CIS) in random bladder biopsies. b. Serial endoscopic and cytologic ollow-up: Should be done at regular intervals; 70% o patients develop recurrences. 2. Intravesical adjuvant chemotherapy: may reduce recurrence rate to 30%–45% a. T iotepa: alkylating agent b. Mitomycin C: inhibits DNA synthesis (alkylating agent) c. Doxorubicin: inhibits DNA synthesis (anthracycline antibiotic)

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3. Bacillus Calmette-Guerin (BCG): attenuated strain o Mycobacterium bovis that has a stimulatory e ect on immune responses and is the only intravesicular agent to reduce the risk o progression to muscle-invasive disease 4. Alpha inter eron: immune modulator B. CIS: Despite its lack o invasion, CIS represents a high-grade lesion, with a 50% chance o developing into invasive carcinoma. 1. Initial treatment: Intravesical BCG is usually given in 6 weekly instillations. 2. Maintenance therapy: Repeat induction course with incomplete response (normal ollow-up cystoscopy, biopsies, and cytology) to earlier discussion. C. Muscle-invasive disease (invasion into muscularis propria) 1. Radiation therapy: relatively ine ective (20% long-term survival) a. Newer investigational uses o radiation therapy involve attempts at bladder preservation through combination protocols using systemic chemotherapy plus radiation therapy. b. Radiation therapy prior to radical cystectomy has not improved survival or decreased the incidence o local recurrence. 2. Radical cystectomy a. In men: Pelvic lymphadenectomy with cystoprostatectomy is per ormed. Urethrectomy is per ormed with tumor involvement o the prostatic urethra. b. In women: Anterior pelvic exenteration is of en per ormed, in which the bladder, urethra, uterus, allopian tubes, ovaries, and anterior vaginal wall are removed. 3. Urinary diversion: required once the bladder is removed and can be done in several ways a. Conduits: can be created using ileum or transverse colon and allow urine to passively drain into an external collection device on the abdominal wall b. Continent diversion: creation o an intra-abdominal urine reservoir, which requires drainage by passing a catheter through a stoma on the abdominal wall c. Neobladder ormation: Using the small bowel (ileum) or colon, allows men to void via urethra. Preliminary results among women are air, with high rates o incontinence. III. P ro g no s is : varies dramatically between super cial carcinoma (85% o cases) and muscle-invasive carcinoma (15% o cases) A. Organ-con ned lesions: Five-year survival is 70%–75% af er radical cystectomy or invasive disease. B. Metastatic cancer: 50–70% o patients have a partial or complete response to systemic therapy or metastatic disease. Only 10% are durable responses ( 3 years), and 5-year survival rate is 5%–20% or metastatic cancer.

Re na l P e lvis a nd Ure te r Tra ns itio na l Ce ll Ca rc ino m a I. Ep id e m io lo g y a nd d ia g no s is : uncommon, usually unilateral tumor (bilateral in 2%–5%) A. Risk actors: similar to bladder lesions, with addition o Balkan nephropathy B. Progression: Only 2%–4% o people with bladder transitional tumors will develop upper tract lesions; 50% o people presenting with an upper tract transitional tumor will develop a bladder lesion. C. Signs and symptoms: gross hematuria, microscopic hematuria, and ank pain caused by an obstruction D. Diagnosis: C scan, retrograde pyelography, and ureteroscopy are e ective (Figs. 25-3 and 25-4). II. Tre a tm e nt A. Nephroureterectomy 1. raditional radical treatment: removal o the kidney, entire ureter, and a cu o bladder at the ureteral ori ce 2. Conservative excision: may be appropriate or low-grade, low-stage ureteral tumors and involves tumor excision with primary ureteroureterostomy or ureteral reimplantation (into the bladder) or distal ureteral lesions B. Endoscopic treatment: Newer equipment has allowed or endoscopic ureteral resection o low-grade and low-stage tumors. T e role is still evolving but is currently reserved or patients with low-grade papillary tumors in solitary renal units or or patients whose health precludes major surgical intervention. III. P ro g no s is : Depends largely on stage. When completely resected, prognosis remains good. However, upper tracts transitional cell carcinoma ( CC) can quickly become high stage due to its ready ability to invade through the thin wall o the ureter, renal pelvis, and beyond.

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Hydronephrosis

Solid mass

Fig ure 25-3: A 71-year-old male pres ented with gros s hematuria. CT s can here without contras t demons trates le t-s ided hydroureteronephros is . In the dis tal le t ureter, a dens e mas s appears to be caus ing the hydronephros is . Final pathology demons trated urothelial carcinoma.

Access wire

Filling defect

Ureteroscope

Fig ure 25-4: This retrograde ureterogram was made by injecting contras t up the ureter with a ureteros cope. Contras t does not ll up the entire ureter becaus e it contains a mas s . The U-s haped de ect is als o re erred to as a goblet sign. In an obs tructing s tone, the ureter would s pas m around the lling de ect. Here, the ureter is dilated in the area o the mas s .

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Re na l Ce ll Ca rc ino m a I. Ep id e m io lo g y: 65,000 new cases per year A. Incidence: more common in men than in women and has a peak incidence in the f h to seventh decades o li e B. von Hippel–Lindau disease (VHL): associated with renal cell carcinoma

Quic k Cut The renal cell carcinoma clas s ic triad o pain, hematuria, and f ank mas s is now very uncommon with the advent o requent CT s cans —greater than 50% are now ound incidentally.

II. Clinic a l p re s e nta tio n a nd d ia g no s is : commonly discovered during radiographic studies or other complaints (incidental) A. Paraneoplastic syndromes: occur in 20% and include Stau er syndrome (nonmetastatic hepatic dys unction), hypercalcemia (unclear etiology), hypertension, erythrocytosis, and endogenous pyrogen production B. Imaging: of en used in the evaluation, workup, and diagnosis 1. Ultrasonography: use ul or di erentiating a simple renal cyst (i.e., absence o internal echoes; a smooth, thin wall; Quic k Cut and an acoustic shadow arising rom the edges) rom a Any les ion that is complex or solid lesion not a s imple renal cys t on 2. C scan with intravenous (IV) and oral contrast: Most ultras ound requires a CT cost-e ective diagnostic and staging modality; evaluates evaluation. local tumor, venous extension, regional lymph nodes, and liver metastases. Noncontrast C scans of en miss large renal lesions (Fig. 25-5). 3. Magnetic resonance imaging: may be o bene t in those who cannot have contrast and may help de ne involvement o the renal vein 4. Percutaneous aspiration and biopsy: Historically contraindicated due to the possibility o tumor tracking but is now becoming more common. Biopsy is a reasonable method o diagnosis or patients with metastatic disease or tissue con rmation. III. Tre a tm e nt A. Radical nephrectomy (open or laparoscopic): Surgical removal o the ipsilateral adrenal gland, kidney, and investing adipose tissue and ascia. Regional lymphadenectomy may also be per ormed. B. Cardiopulmonary bypass: May be required when renal cell carcinoma invades the renal vein and in erior vena cava and extends to the right atrium. Although this is rare, surgical treatment to excise the tumor is more extensive. IV. P ro g no s is A. Stage I: Five-year cancer-speci c survival rate is greater than 90%. B. Stage II: Five-year survival rate is 75%–80%. C. Stage IV: Median survival is 16–20 months, and the 5-year survival rate is less than 10% or patients with distant metastases.

Te s tic ula r Tum o rs I. De f nitio n: Ninety- ve percent o all testicular tumors are germ cell tumors (GC s). A. Non-GC s: rare; include sex cord, sex stromal, lymphomas, and other rare tumors B. GC s: Major tumors are seminomatous and nonseminomatous tumors. Nonseminomatous germ cell tumors (NSGC s) include embryonal carcinoma, teratoma, choriocarcinoma, and yolk sac tumors, alone or in combination. Secondary tumors include lymphomas. II. Ep id e m io lo g y A. Cryptorchidism (undescended testis): increases testicular malignancy risk B. Incidence: Although testis tumors are generally uncommon, they are the most common malignancy in men ages 20–34 years. C. umor type: age dependent Quic k Cut 1. Yolk sac tumors and teratomas: common in in ants Tes ticular cancer is 2. All cell types: seen in young adults mos t common malignancy in 3. Seminoma: more common in men ages 35–60 years men age les s than 35 years . 4. Lymphomas: predominate in men age greater than 60 years

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A

B

Fig ure 25-5: A: CT s can without contras t demons trates a normal-appearing right kidney. B: Portal venous phas e demons trates a large pos terior les ion with s olid and cys tic components , cons is tent with renal cell carcinoma.

III. Clinic a l p re s e nta tio n a nd d ia g no s is : Painless testicular swelling or enlargement is the classic presenting sign, of en diagnosed by sel -exam. A. Pain (13%–49%): suggests hemorrhage or in arction and may be con used with epididymitis B. Physical examination: may reveal a rm, nontender, or mildly tender distinct mass or di use testicular swelling C. Reactive hydrocele: occurs in 5%–10% o cases D. Ultrasonography: Gold standard in diagnosis. It is very sensitive in determining the size, location, and echogenicity o palpable Quic k Cut testicular abnormalities, particularly i a hydrocele limits the Biops y o tes ticular cancer or diagnos is is physical examination. contraindicated due to the E. Alpha- etoprotein (AFP), beta-human chorionic pos s ibility o the tumor gonadotropin (HCG), and lactate dehydrogenase (LDH): tracking through di erent Serum marker levels are use ul or diagnosis, or ollowing the lymph node drainage. response to treatment, and or identi ying recurrent disease. 1. AFP: may be elevated in patients with yolk sac tumors, embryonal carcinoma, and (rarely) in teratomas 2. Beta-HCG: Elevation may accompany choriocarcinoma, embryonal carcinoma, and seminomas. Seminomas do not elaborate AFP; there ore, an elevation con rms a nonseminomatous component.

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IV. Tre a tm e nt: Varies with cell type and disease stage. Initial treatment is surgical exploration via an inguinal approach to avoid potential contamination o scrotal lymphatic draining during tumor manipulation. A. Seminoma: uniquely radiosensitive and chemosensitive 1. Low-stage seminoma: Postorchiectomy treatment options include close observation, singleagent carboplatin therapy, or radiation therapy. Survival approaches 100%. 2. High-stage seminomas: Current recommendations include up to our courses o chemotherapy with cisplatin, etoposide, Quic k Cut and bleomycin. Seminomas are a. Postchemotherapy radiation: Sometimes considered or common between ages patients with a residual retroperitoneal mass. 35 and 60 years , are uniquely radio- and chemos ens itive, b. Prognosis: Sixty-seven percent complete response rate to and con er great long-term chemotherapy and an overall survival rate o 72% can be s urvival i diagnos ed early. expected. B. NSGC s 1. Low-stage NSGC : reatment involves inguinal orchiectomy ollowed by either modi ed retroperitoneal lymphadenectomy (RPLND), primary chemotherapy, or by an intense surveillance protocol. a. Surveillance: Generally reserved or compliant patients at low risk o micrometastatic disease. Risk actors o the primary testis tumor avoring RPLND include an embryonal carcinoma component, vascular or lymphatic invasion, and extension into peritesticular structures. b. RPLND ( 30%o stage I patients): Surgical removal o speci c high-risk lymphatic tissue. Most patients with micrometastases receive two cycles o adjuvant platinum-based chemotherapy. c. Survival: approaches 92% or both groups 2. High-stage NSGC : Patients with minimal nodal involvement radiographically or ailure to normalize markers postorchiectomy should undergo either RPLND or chemotherapy alone. Intermediate prognosis tumors have 5-year survival o 80%; poor prognosis tumors have a 5-year survival o 48%.

MALE ERECTILE DYSFUNCTION P e nis I. Ana to m y A. Penile erectile tissue: contained within three erectile bodies: two dorsally situated corpora cavernosa and one ventrally located corpus spongiosum B. Urethra: lies within the corpus spongiosum, which consists o cavernous, expansible spaces C. unica albuginea: T ick, brous tissue layer surrounding each o the three corpora. T e ascia o the tunica around the cavernosa is much thicker, which helps support the increased pressure in the corpus spongiosum spaces.

P e nile Ere c tio n a nd De tum e s c e nc e I. He m o d yna m ic s : Arterial ow increases, and increased venous resistance also contributes. II. Ne uro p hys io lo g y: Cavernous nerves mediate neurovascular interaction. A. Erections with genital stimulation: require only an intact sacral re ex B. Parasympathetic nervous system: primary importance; nitric oxide (NO) released rom nonadrenergic, noncholinergic neurons and the endothelium leads to vascular and corporal smooth muscle relaxation

Dia g no s is I. His to ry: very important when evaluating the cause o erectile dys unction A. Nature o onset and problem duration: Important; psychogenic impotence may be abrupt in onset with a li e stress. B. Interview with sexual partner: may prove bene cial C. Nocturnal or early morning erections: may suggest a psychogenic cause D. History o pelvic trauma (including vascular or neurogenic injury): important to discern E. Risk actors: diabetes, hypertension, smoking, heart disease, and hypercholesterolemia

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II. P hys ic a l e xa m ina tio n: Special emphasis on the neurologic and vascular examination. T e penis should be examined or plaques and the testes or size and consistency. III. La b o ra to ry te s ts : testosterone level and serologic tests or systemic disease (e.g., anemia, renal insu ciency) IV. Dia g no s tic te s ts : not indicated in every patient A. Nocturnal penile tumescence: Measurements are taken o nocturnal erections occurring during rapid eye movement sleep. Gauges are placed on the accid penis at bedtime and attached to a monitor overnight that evaluates the number, duration, and rigidity o erections. B. Intracorporeal injections o vasoactive substances (e.g., papaverine, phentolamine, and prostaglandin E): Used to elicit an erection. Response with a normal erection eliminates a signi cant venous leak etiology or erectile dys unction. C. Duplex sonography evaluation: provides an objective measure o arterial penile blood ow and a relative assessment o venous drainage 1. Cavernosal arteries: evaluated or increased width and ow af er intracorporeal vasoactive injection 2. Venous outf ow: Should diminish during erections; i venous out ow is still high on duplex study, suspect a venous leak. V. Tre a tm e nt A. Counseling: required or men with a signi cant psychogenic component B. Oral therapy: has revolutionized treatment 1. Selective phosphodiesterase type 5 inhibitors: enhance erection through the NO/cyclic guanosine monophosphate (cGMP) pathway 2. T ree agents have been FDA approved: sildena l, vardena l, and tadala l C. Vacuum erection device: External pump mechanism that draws blood into the penis to obtain an erection. T e blood is retained by the placement o a constricting rubber ring at the base o the penis. D. Vasoactive intracorporeal injections: sel -administered, with risks composed o bruising, mild scar ormation, or priapism E. Penile implant: Device surgically implanted into the corpora cavernosum. Several styles exist that are either malleable or in atable. 1. Risks: in ection associated with the prosthetic material 2. Mechanism: In atable prostheses have two chambers in the Quic k Cut corpus cavernosum, with a reservoir in the retropubic space Types o penile (o Retzius) and a pump in the scrotum. Saline is inserted into implants include s emirigid the reservoir at the time o the procedure and stays in circuit (noninf atable), inf atable between the cylinders and reservoir or the li e o the device, (s el -contained), and threeregulated by the pump in the scrotum. piece inf atable. 3. Satis action: approaches 95%

VOIDING DYSFUNCTION De f nitio ns I. Vo id ing : complex act involving detrusor contraction with sphincteric relaxation (the micturition re ex), which is coordinated in the pontine micturition center and controlled by cerebral input II. Dys unc tio n: Lesions occurring throughout the nervous system of en pro oundly a ect voiding. Quic k Cut A. Hyperref exia (bladder overactivity): produced by upper motor Hyperref exia is an neuron lesions (suprasacral) exaggerated ref ex res pons e, whereas aref exia is the B. Aref exia (bladder f accidity): produced by lower motor neuron abs ence o a ref ex res pons e. lesions (sacral nerve roots or cauda equina)

Dia g no s is I. His to ry: Detailed historical in ormation regarding requency, urgency, nocturia, sensation o ullness, straining, incontinence, erectile unction, bowel habits, paralysis, paresthesias, history o neurologic and vertebral disease, pelvic surgery, and trauma as well as a review o medications are vital parts o diagnosis.

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II. P hys ic a l e xa m ina tio n: Assessment o sensation; motor unction; and re exes o the lower extremities, perineum, and rectal areas is done. Anal sphincter tone should also be assessed, as should the bulbocavernosal ref ex (contraction o the anal sphincter with compression o the glans or clitoris or with traction on an indwelling urethral catheter). III. Uro d yna m ic s tud ie s A. Filling cystometry: Creation o a pressure–volume curve during bladder lling. Normal bladder sensation, high compliance (accommodation to increasing volumes with minimal increase in pressure), and the absence o uninhibited contractions during lling comprise a normal study. Quic k Cut B. Voiding phase: Assesses ow rate, contractility, and vesical Urodynamics pressure during voiding. Postvoid residual urine is recorded. are help ul or determining C. Electromyelography (EMG) o the striated sphincter: bladder unction (i.e., capacity, Demonstrates sphincteric unction and determines i appropriate compliance, and contractility), sphincter relaxation occurs with voiding. Denervation o the s phincter unction, outlet res is tance, and f ow rate. sphincter may be elicited.

Vo id ing Dys unc tio n P a tte rns I. De trus o r hyp e rre e xia (hyp e rto nic ne uro g e nic b la d d e r): occurs with suprasacral lesions and is characterized by diminished bladder capacity and uninhibitable detrusor contractions A. Presenting symptoms: Irritative, such as urgency and requency. I intravesical pressures become elevated, vesicoureteral re ux and upper tract deterioration may occur. B. reatment: anticholinergics, intermittent bladder catheterization, and (sometimes) surgical bladder augmentation II. De trus o r a re e xia (a to nic b la d d e r): occurs with lesions o the sacral cord, nerve roots, or cauda equina, resulting in loss o the sacral re ex arc A. Symptoms: Increased capacity, decreased intravesical pressure, absence o e cient bladder contractions, and urinary retention with over ow incontinence may result. B. reatment: Medical therapy is generally ine ective. Catheterization (indwelling or intermittent) and urinary diversion are of en used. III. De trus o r e xte rna l s p hinc te r d ys s yne rg ia (DSD): T is condition results rom lesions o the spinal cord and may occur alone or may complicate a hyperre exic or atonic picture. A. Pathophysiology: involves contraction o the external sphincter during bladder contraction, causing a “ unctional” outlet obstruction with poor emptying and high detrusor pressures which may cause kidney damage B. reatment: medication to promote urinary retention (anticholinergics) and intermittent catheterization

Vo id ing Dys unc tio n in Sp e c if c Dis e a s e s I. Sp ina l c o rd injury: Suprasacral lesions usually cause hyperre exia with DSD, and sacral lesions usually cause are exia. II. Ce re b ro va s c ula r a c c id e nts : Result in loss o cortical inhibition with detrusor hyperre exia, mani ested by urgency with urge incontinence. DSD is not eatured, and patients of en contract the sphincter voluntarily. III. P a rkins o n d is e a s e : causes detrusor hyperre exia, resulting in urgency, requency, incontinence, and ailure o the external sphincter to relax, which may complicate the picture IV. Multip le s c le ro s is : Leads to voiding dys unction in 50%–80% o those a ected. Most commonly, urgency, requency, and incontinence are seen; occasionally, retention. Urodynamic studies reveal detrusor hyperre exia in most cases. V. Mye lo d ys p la s ia : various abnormal conditions o vertebral development that a ect spinal cord unction, o which myelomeningocele is most common A. Findings: poorly compliant bladder with high intravesical pressure, weak detrusor contractions, and DSD B. Management: anticholinergic agents to diminish bladder pressures and intermittent catheterization to overcome ailure o the bladder to empty

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VI. Lum b a r d is c d is e a s e : Causes detrusor acontractility and decreased sphincteric activity; obstructive voiding symptoms predominate. Urinary retention may occur. VII. Dia b e tic ne uro p a thy: autonomic neuropathy mani ested by diminished bladder sensation, increased capacity, decreased contractility, and elevated postvoid residual volume

Inc o ntine nc e I. De f nitio n: Leakage o urine should be rst classi ed based on Quic k Cut history. T e etiologies are mani old, and the treatment should be Types o urinary directed toward eliminating the underlying cause or mitigating the incontinence include s tres s , incontinence. urge, overf ow, and total. II. Cla s s if c a tio ns : our types A. Stress urinary incontinence: leakage o urine during Valsalva or increased abdominal pressure 1. Incidence: Although it is more common in women af er childbirth and age causing progressive laxity in the pelvic oor, men also may develop it af er radical prostatectomy or pelvic radiation. 2. reatment: may be behavioral (including uid management and Kegel exercises), medical, and surgical (i.e., urethral slings and other procedures to strengthen the pelvic oor) B. Urge incontinence: Urine leakage due to detrusor overactivity, which may be idiopathic or have an underlying neurologic basis relating to a pre-existing disease state. reatment is of en medical; rst-line therapy is of en anticholinergic agents. C. Overf ow incontinence (also known as paradoxical incontinence): With urinary retention, the addition o even small quantities o increased volume in the bladder cause urine leakage. Some patients do not realize they are in retention with large volumes o urine in the bladder. In these patients, only discovery by bladder scan or catheter placement o a ull bladder is over ow incontinence even suspected. D. Continuous incontinence: Due to a urinary stula that bypasses the urethral sphincter. In emales, it may be due to an ectopic ureter that enters in the urethra or a vesicovaginal stula. Unless the communication between the urinary tract and the outside is repaired, it will continue inde nitely. A temporizing measure may be diverting the urine via nephrostomy tubes, ureteral stents, or urethral catheterization. T e stula is bypassed or the urine is diverted away rom it; patients may achieve dryness until the stula is repaired.

Tre a tm e nt I. P ha rm a c o lo g ic tre a tm e nt: allows manipulation o bladder contractility (via cholinergic receptors in the bladder) and changes in outlet resistance (via alpha-adrenergic receptors in the bladder neck, prostatic capsule, and urethra) II. Ca the te riza tio n A. Indwelling catheter: may have an additional channel to allow in usions such as water or saline to ush clots or topical agents B. Intermittent catheterization: Frees the patient rom continuous appliance usage and lowers the incidence o U Is, meatal erosion, urethral stricture, and epididymitis. Patients develop bacterial colonization, which requires no treatment unless symptoms o in ection occur. III. Urina ry dive rs io n (a wa y rom the bla dde r): Forming an ileal conduit or catheterizable reservoir may be necessary in patients with recurrent urosepsis or renal insu ciency caused by a detrusor problem. IV. Bla d d e r a ug m e nta tio n: Increasing capacity and decreasing intravesical pressure may be required in patients with hyperre exia or in those with small and contracted, poorly compliant bladders secondary to long-standing neurologic disease (e.g., myelomeningocele), radiation cystitis, or chemically induced bladder brosis. Intermittent catheterization is usually required.

Auto no m ic Dys re e xia I. De f nitio n: outpouring o sympathetic activity in response to a erent visceral stimulation in patients with spinal cord injuries with lesions above 6 II. E e c ts : Bladder, urethral, or rectal stimulation may produce pro ound hypertension, bradycardia, diaphoresis, headache, and piloerection in these patients.

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III. Tre a tm e nt: Withdrawal o the stimulant and medication directed at the hypertensive crisis. Prophylaxis with various medications (e.g., chlorpromazine, ni edipine) is sometimes use ul in a ected patients who require urologic manipulation.

UROLOGIC TRAUMA Blunt Tra um a I. Eva lua tio n: Need or radiographic assessment in patients with urologic trauma is based on the mechanism o injury, vital signs, physical examination, and urinalysis. A. Gross hematuria (or microhematuria and a systolic blood pressure [SBP] less than 90 mm Hg): requires radiographic evaluation o the kidneys B. Microhematuria (in patients who have always had an SBP less than 90 mm Hg): does not require a radiographic evaluation unless clinical suspicion is high based on the mechanism o injury (e.g., all rom a height, direct blows, high-speed motor vehicle crashes) C. Penetrating trauma (regardless o the degree o hematuria): requires an evaluation II. Ra d io g ra p hic te s ts : C scan o the abdomen and pelvis, cystogram, retrograde urethrogram, and renal angiography are possibilities.

Re na l Injurie s I. Cla s s if c a tio n: Renal injuries are grades 1 through 5. A. Grade 1 (contusion): no obvious parenchymal injury, but subcapsular hematoma is possible B. Grade 2 (minor lacerations): super cial cortical disruptions that do not involve the collecting system and are less than 1 cm C. Grade 3 (major lacerations): deep corticomedullary lacerations that do not involve the collecting system but are greater than 2 cm D. Grade 4 (deep lacerations): involve the collecting system or cause urinary extravasation E. Grade 5: de ned as either an avulsion o the renal hilum or a shattered kidney II. Ra d io g ra p hic a s s e s s m e nt A. Abdominal/pelvic C scan: rst-line test per ormed to rule out renal injury 1. Dry C : done rst to help demonstrate stones 2. Early venous phase and 10-minute delayed images: Done next; the delayed phase helps de ne the ureteral anatomy. B. Renal arteriography: generally reserved or patients with possible vascular injuries that are not elucidated on the C scan and may require embolization III. Tre a tm e nt Quic k Cut A. Nonoperative: Contusions, minor lacerations, and some major Typically, only grade lacerations can be managed with bed rest, serial hematocrit 5 renal injuries require open evaluation, and hydration. Ureteral stenting may be required in s urgical exploration and only in the s etting o an uns table cases o ongoing urinary extravasation. patient (they have a high ris k B. Angiography and embolization: can control most renal bleeding o as s ociated intra-abdominal C. Surgical exploration: Debridement o nonviable renal tissue, injuries ). The remaining renal closure o the collecting system, coverage o the injury with injuries can be managed nonperinephric adipose tissue, and drainage o the retroperitoneum. operatively, with occas ional s tenting o grade 4 renal Stents are usually not needed. injuries . IV. Re na l tra um a c o m p lic a tio ns A. Post-traumatic hypertension: uncommon but may occur in 5%–10% o patients and is mediated by renin owing to ischemic tissue Quic k Cut B. Associated injuries: more common in patients with penetrating Initial identi cation rather than blunt trauma o as s ociated injuries with 1. Blunt trauma: Right renal injuries are associated with liver appropriate treatment will trauma, and lef renal injuries are associated with splenic injuries. prevent many complications 2. Penetrating trauma: Bowel lacerations, pancreatic injury, and o renal trauma. other vascular injuries occur.

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Ure te ra l Injurie s I. Etio lo g y: Ureteral injuries are caused primarily by penetrating trauma or iatrogenic injury. A. Deceleration injuries: may result in avulsion o the ureteropelvic junction, especially in children B. Blast e ect rom gunshot wounds: Bullet may not have directly transected the ureter, but thermal damage to surrounding structures results rom the bullet wound, and the precarious nature o the ureter’s blood supply make it susceptible to collateral damage. II. Ra d io g ra p hic a s s e s s m e nt: C initially identi es injury site; intraoperative retrograde pyelogram can urther delineate the injury. III. Tre a tm e nt A. Complete ureteral transections: should be explored and repaired B. Partial injuries (or suspected devitalization rom blast e ect): should undergo initial attempts at stenting, either anterograde or retrograde, prior to attempting open repair

Bla d d e r Tra um a (Lo we r Urina ry Tra c t) I. Etio lo g y: Blunt bladder trauma is requently associated with pelvic ractures. Rupture can be extraperitoneal or intraperitoneal, depending on the location o the tear. A. Extraperitoneal: Majority o bladder injuries (80%); these ruptures have a much better prognosis and are easier to manage. B. Intraperitoneal: T ese 20% are due to the continuity o the bladder dome with the peritoneum, whereas the rest o the bladder is extraperitoneal or pelvic. Associated urethral injuries should always be considered as a possibility. II. Eva lua tio n A. Retrograde urethrogram (RUG): Blood at the urethral meatus, Quic k Cut an elevated prostate gland on DRE, or a mechanism o injury The prognos is possibly causing a urethral tear should prompt an RUG be ore o intraperitoneal bladder bladder catheterization. per orations in general is B. Plain lm cystography: Drainage and oblique lms are much wors e, but this may necessary. A cystogram involves maximally (400–500 mL) lling be due to the much higher likelihood o as s ociated the bladder to determine extravasation o contrast medium injuries to vital intraperitoneal (e.g., C or plain lm). s tructures . III. Tre a tm e nt: For intraperitoneal bladder injuries, treatment is immediate surgery, whereas or extraperitoneal injuries, treatment is a long-term Foley catheter in the urethra.

Quic k Cut

Ure thra l Injurie s

Always per orm an RUG be ore ins erting a Foley catheter in s omeone with a his tory o trauma and blood at the urethral meatus .

I. Eva lua tio n : Examination and radiographic assessment are described earlier. A high index o suspicion should be maintained, because passage o a urethral catheter may signi cantly worsen a mild urethral injury by theoretically turning a small laceration into a complete avulsion or disruption. II. Tre a tm e nt A. Penetrating anterior urethral injuries: Should be explored, debrided, and repaired primarily; a urethral catheter should be lef in place af er repair. B. Complete prostatomembranous urethral disruptions ( rom blunt trauma): require open suprapubic tube placement 1. Attempts at primary repair: not warranted 2. Attempts at “realignment” (over a urethral catheter or with f exible cystoscopes): may be indicated 3. Follow-up open repair o post-traumatic strictures: should occur 3–6 months a ter the injury

Quic k Cut

P e nile Injurie s I. Fra c ture o the e re c t p e nis : Caused by direct blunt trauma that signi cantly buckles the corpus cavernosum, resulting in a tear o

Penile racture is mos t commonly as s ociated with s exual activity.

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the tunica albuginea overlying the corpora cavernosa. Urethral tears are associated in some penile racture cases (20%) and should always be ruled out by an RUG. A. Physical ndings: ecchymosis, swelling, and deviation o the penis B. Diagnosis: usually made based on physical examination and the patient’s history, which usually includes the penis buckling during sexual activity, ollowed by rapid detumescence, sharp pain, and immediate bruising and swelling C. reatment: operative repair and closure o any cavernosal tear 1. Surgical exploration: to prevent scarring o the corpus cavernosum and subsequent Peyronie disease (abnormal penile curvature) 2. Urethrogram with repair o the urethral injury: may be necessary II. P e ne tra ting p e nile tra um a : Evaluated and treated similarly to a ractured penis. All such injuries should be explored and repaired.

Te s tic ula r Tra um a I. Blunt tra um a : esticular rupture is the primary injury that requires surgical repair; testicular ultrasound is the gold standard when making this diagnosis. A. Evaluation: Physical examination is integral and can reveal a large hematocele. Extrusion o the semini erous tubules rom the con nes o the tunica albuginea o the testis can be ound with ultrasound or surgical exploration. B. reatment: Repair involves debriding extruded or nonviable semini erous tubules and closure o the overlying tunica albuginea o the testicle. II. P e ne tra ting tra um a : Physical examination and ultrasound may prove help ul. All suspected testicular or spermatic cord injuries should be explored.

Chapter 26

Plastic and Reconstructive Surgery Niluka A. Wickramaratne, Helen G. Hui-Chou, Devinder Singh, and Tripp Holton

OVERVIEW Ba c kg ro und I. De f nitio n: Plastic surgery is a broad f eld that encompasses the reconstruction o body parts altered by birth de ects, trauma, oncologic resections, and advanced age. II. E e c t o wa r: T e f eld truly emerged during the 20th century, when the burden o patients de ormed by war was met by the advances in anesthesia, aseptic techniques, and antibiotics.

Quic k Cut “Plas tic” originates rom the Greek word “plas tikos ,” which means to mold and res hape.

No ta b le Fig ure s I. Sus hruta (c irc a 600 BCE, Ind ia ): known or writing the Sushruta Samhita (Sanskrit: Sushruta’s Compendium), a text describing his many surgical techniques, including the f rst total nasal reconstruction II. Ga s p a ro Ta g lia c o zzi (1545–1599, Ita ly): developed the agliacozzi ap, a tubed, pedicled medial arm ap used or nasal reconstruction (Fig. 26-1) III. Sir Ha ro ld Gille s (1882–1960, Ne w Ze a la nd ): First modern plastic surgeon; he coined the reconstructive term to “replace like with like.” IV. J o s e p h E. Murra y (1919–2012, Unite d Sta te s ): Only plastic surgeon to win a Nobel prize; he became interested in transplantation immunology when studying skin allogra s in burn patients and was the f rst surgeon to per orm a success ul organ transplant in humans.

RECONSTRUCTIVE P LASTIC SURGERY Wo und s a nd De e c ts I. Re c o ns truc tive la d d e r (Fig . 26-2): erm used by plastic surgeons to describe the thought process used to approach wounds and de ects. T ey aim to maximize the restoration o orm and unction while minimizing donor site morbidity. Procedures on the lower rungs tend to be sa er and less costly; as the de ect becomes larger, more complex, or more critical, the surgeon must adopt a more complex reconstructive procedure. II. Ne g a tive P re s s ure Wo und The ra p y (NP WT): commonly re erred to as a wound vacuum-assisted closure; uses suction to

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Quic k Cut Surgeons aim to us e a procedure rom the lowes t rung o the recons tructive ladder pos s ible. It is not ideal to walk “down” the ladder.

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Fig ure 26-1: The Tagliacozzi f ap. One o the s eminal des criptions o a f ap or nas al coverage, it has become the emblem o plas tic s urgery.

promote wound healing o en on large, chronic wounds, which can Quic k Cut be gra ed or closed once a granulation bed orms The negative A. echnique: Wound is dressed with contoured oam, covered pres s ure draws out with an occlusive dressing, and attached to a pump that applies a edematous and in ectious controlled level o negative pressure (typically 75–125 mm Hg). f uid rom the wound bed, enhancing circulation and B. “Microde ormation”: Mechanical orces speed the healing decreas ing the bacterial process by promoting cell migration and proli eration, which burden. accelerates ormation o granulation tissue. III. Skin g ra ts : used to reconstruct superf cial skin wounds too large to close by primary intention and or which secondary healing is Quic k Cut inappropriate Once healed, a A. Wound location: Head and neck wounds o en receive ulls kin gra t replaces the barrier thickness skin gra s (F SGs) to match color and texture; de ects unction in the area o the overlying joints (e.g., the hand) should be treated with F SGs in de ect. order to avoid contractures that limit movement. B. Underlying structures: Wound bed must contain an adequate blood supply to support gra healing. 1. Muscle: has a robust blood supply and supports skin gra s very well 2. Fat: Less vascular; gra has an increased risk o ailure.

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REGIONAL TIS S UE TRANS FER

LOCAL TIS S UE TRANS FER

S KIN GRAFT

DIRECT TIS S UE CLOS URE

ALLOW WOUND TO HEAL BY S ECONDARY INTENTION

Fig ure 26-2: The “re c ons truc tive la d d e r.” The p rogre s s io n o te c hniq ue s is rom the mos t s tra ig ht o rwa rd a t the b ottom to the mos t c omp le x a t the top . The up p e r rungs a re a ls o a c c omp a nie d b y the gre a te s t ris k o c omp lic a tions . In ge ne ra l, s urge o ns a im to us e the lowe s t rung o the la d d e r tha t me e ts the c linic a l ne e d s o the p a tie nt. (Fro m Tho rne CH, Ba rtle tt S P, Be a s le y RW, e t a l. Grab b and S mith’s P las tic S urg e ry, 6th e d . Ba ltimore : Lip p inc ott Willia ms & Wilkins ; 2006.)

3. Exposed bone/tendon/cartilage (lacking periosteum, peritendon, or perichondrium): cannot support gra s C. Split-thickness skin graf s (S SGs): Contain the epidermis and a portion o the dermis. T ey do not contain skin appendages (hair ollicles, sebaceous glands, sweat glands), which are located in the deep dermis and/or Quic k Cut subcutaneous tissue. Split-thicknes s s kin 1. Advantages: Large supply o donor areas (renewable supply as gra ts cannot s ecrete s kin the site re-epithelializes) and decreased primary contracture; oils , s weat, or grow hair. meshing can increase sur ace area and allow drainage o uid that may otherwise separate the gra rom the wound bed. 2. Disadvantages: cosmetically (aesthetically) in erior, Quic k Cut decreased durability, variable pigmentation, and increased Split-thicknes s s kin secondary contracture gra t s ites can be reharves ted 3. Common donor sites: Abdomen, buttocks, and thighs, which a ter they heal. provide a large amount o skin. Even the scalp can serve as a donor site. D. F SGs: Contain the epidermis, dermis, and variable amounts o subcutaneous at. T e donor site must be closed primarily or with an S SG, and, thus, they are usually taken rom areas with redundant skin. T e gra will retain its normal hair growth, secretions, and pigmentation once healed in the recipient site. 1. Advantages: cosmetically superior (even compared to a nonmeshed S SG), less secondary contracture, and increased durability 2. Disadvantages: limited donor sites and increased primary contracture 3. Common donor sites: Postauricular and supraclavicular skin provides an excellent match or acial de ects. Other common F SG donor sites include the medial arm, medial orearm, and groin crease.

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E. Graf healing: Adherence o the gra is very important or Quic k Cut survival. Occurs in three phases. Gra t healing 1. Plasmatic imbibition (days 1–2): Nutrients are absorbed ollows the “3 i’s ”: imbibition, passively rom the blood supply in the recipient wound bed. inos culation, and ingrowth. 2. Inosculation (day 3): ormation o anastomotic connections between the capillaries in the recipient bed and vessels in the dermis o the gra 3. Angiogenesis (day 5): ingrowth o new vessels into the gra F. Regrowth o the graf ’s architecture: occurs at a slower pace, Quic k Cut such that eventually, skin appendages, pigmentation, and Primary contracture innervation may return in F SGs is recoil o elas tic bers ; s econdary contracture is G. Primary contracture: immediate reduction in size o the contraction toward the center gra a er harvesting due to passive recoil o elastic f bers o the wound. located in the dermis; more common in F SGs due to a higher concentration o elastin H. Secondary contracture: centripetal contraction toward the center o the wound that occurs a er the gra is applied to the recipient site; more common in S SGs likely because they lack the cellular structure and matrix composition ound in deeper layers o the dermis I. Graf ailure: causes as ollows: 1. Graf thickness: In a thicker gra , there are more cells, which Quic k Cut means that the gra has a higher metabolic demand. Wounds must have 2. Separation o the graf rom the wound bed (e.g., excess 5 ewer than 10 bacteria per tension): disrupts the nutrient supply because initial gram o tiss ue to s upport a nourishment o the gra occurs via di usion s kin gra t. Typically, these a. Fluid (i.e., blood, serum, or pus) between the graf and wounds have good granulation the wound bed: disrupts imbibition tis s ue, no necrotic tis s ue, and no gross purulence. b. Shear orce and movement between the graf and the recipient bed: disrupts inosculation/ingrowth 3. In ection (e.g., contaminated oreign body): In ected wounds will not allow skin gra s to adhere; critical bacterial concentration is 105 bacteria per gram tissue. IV. Othe r g ra t typ e s : as ollows: A. Fat graf s: sections o dermal at can be inlaid into a de ect or contouring; o en used in breast reconstruction B. endon graf s: numerous tendons in the body (e.g., palmaris longus) can be harvested without loss o unction; o en used to replace damaged tendons in the hand C. Cartilage graf s: Rib, conchal, and septal cartilage gra s can be harvested or ear, nasal, and nipple reconstruction (a er mastectomy). D. Nerve graf : Sural nerve gra s are o en used to repair peripheral Quic k Cut nerve injuries. Nerve regeneration E. Vein graf s: Saphenous vein is o en harvested; vein gra s can be occurs at a rate o 1 mm/day along the gra t until reaching used or arterial or venous replacement. the motor endplate. F. Bone graf s: Guide regeneration o the native bone along the gra (osteoconduction), unlike vascularized bone aps where union between the ap and native bone occurs via osteoinduction (recruitment o osteoblasts). Bone autogra s can be harvested rom sites such as the iliac crest. Cadaveric cancellous bone allogra can also be used. V. Tis s ue e xp a ns io n: used to increase the amount o tissue available or local reconstructive procedures by applying mechanical orce, which provides a reliable source o tissue with preserved hair and sensation and good color and texture match A. Expansion period: wo properties o skin come into play. 1. Biologic creep: cellular growth and regeneration in response to chronic stretching orces 2. Stress relaxation: principle that the orce required to stretch a material a certain length decreases over time B. ypes: two broad categories 1. Internal tissue expansion: Silicone reservoir is placed beneath the skin and in ated over time with saline to expand the overlying tissue. Eventually, a f brous capsule orms around the

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expander, containing most o the new vasculature. Common uses include reconstruction o scalp, ace and breast de ects, and reconstruction a er removal o congenital nevi. 2. External tissue expansion: uses an external device to apply a constant orce on skin a. DermaClose: uses skin anchors placed around a wound to expand surrounding tissue toward the center b. BRAVA: Used or breast reconstruction or augmentation; negative pressure provides threedimensional (3D) tension on the breast. VI. Fla p s : units o tissue that are moved or trans erred to the recipient Quic k Cut site with their own vascular supply (Fig. 26-3) Flaps have their own A. Classi cations: by method o trans er, vascular supply, or vas cularization; gra ts are anatomic components dependent on the recipient B. Local aps: used to close cutaneous wounds near the donor site s ite’s blood s upply. 1. Advancement aps: Flap is moved orward to f ll the de ect, without lateral or rotational movement (e.g., V-Y advancement or single pedicle advancement ap). 2. Rotation ap: Semicircular ap rotated on a pivot point to f ll an adjacent de ect. A backcut (or Burow triangle) is used to acilitate rotation. 3. ransposition ap: rotated on a pivot point to f ll a de ect contiguous with the base o the ap a. Rhombic ap: Note that the lesion can be any shape and is excised leaving a rhombic-shaped de ect. b. Bilobed ap: Commonly used or nasal de ects; the ap uses two lobes, where the primary lobe is used to f ll the de ect and the secondary lobe is used to f ll the donor site o the primary lobe.

Ra ndom fla p

Fa s ciocuta ne ous fla p

Axia l fla p

A

B

C

Myocuta ne ous fla p D

Fig ure 26-3: Major f ap types .

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30°

Limb

30° 60°

30°

Ce ntra l me mbe r Limb A

B

C

Fig ure 26-4: Z-plas ty. This is a very common plas tic s urgical technique or local coverage and s car revis ion.

C.

D. E. F. G.

4. Z-plasty: Similar to the transposition ap, two triangular aps are raised and transposed into the de ect created by the other. Used or scar revision (Figure 26-4). Distant aps: Donor site is not adjacent to the recipient site. 1. Pedicled: Flap is still connected to its original vessels. 2. Free: Flap’s vasculature is divided rom the donor site and reattached at the recipient site using microsurgical anastomosis. Random aps: lack an anatomically def ned vascular system and are ed by the dermal–subdermal plexus Axial aps: Based on a def ned artery and vein, which originate at the base o the ap and run along its axis. Axial aps may be distant or locoregional. Angiosomes: Units o skin and underlying deep tissue that are supplied by a single source vessel. Source vessels supply the skin and subcutaneous tissue via cutaneous per orator arteries. Per orator aps: Cutaneous aps that are supplied by one or more per orator arteries. T ey are named a er either their per orator vessel (e.g., deep in erior epigastric per orator ap) or the anatomic region, i the ap can be harvested with multiple per orators (e.g., anterolateral thigh ap). 1. Direct cutaneous: Per orator only pierces the deep ascia, without passing through any other structures. 2. Indirect septal and septocutaneous: Per orator passes through an intermuscular septum be ore piercing the deep ascia to supply the skin.

Quic k Cut The wider the angles on a “Z” plas ty, the longer the nal s car length.

Quic k Cut Free tis s ue trans er has a higher rate o ailure and requires longer operating time than pedicled f aps .

Quic k Cut Becaus e a random f ap is dependent on ves s els entering the bas e, its widthto-length ratio is limited (typically 1:3).

Quic k Cut The boundaries o s kin that can be reliably harves ted rom a s ingle ves s el are de ned as an angios ome.

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3. Indirect muscle and musculocutaneous: Per orator passes Quic k Cut through muscle be ore piercing the deep ascia; more Per orator f aps common than septocutaneous per orator aps and require caus e les s donor s ite dissection within the muscle to f nd the per orating vessels. morbidity becaus e they allow H. Muscle/myocutaneous: composed o muscle, its ascia, and mus cle to be pres erved. overlying skin; supplied by at least one dominant vascular pedicle, which is usually in a reliable location relative to the muscle I. Fasciocutaneous: Composed o skin and its underlying ascia; Quic k Cut vascular plexus in the ascia is supplied by a per orating artery. The robus t blood T ese aps are less bulky than muscle aps and have less donor s upply o a myocutaneous f ap o ten allows or site morbidity. s ucces s ul healing even i the 1. Scapular ap: based on circum ex scapular artery f ap is us ed in an irradiated or 2. Radial orearm ap: based on radial artery in ected wound. J. Osteomyocutaneous/bone: Vascularized bone aps can be composed o only bone or a combination o bone, skin, and muscle (composite ap). T ese are o en used as ree aps to reconstruct bony de ects o the head, neck, and spine. 1. Iliac crest ap (deep circum ex iliac artery): Iliac crest can be harvested alone or with a skin paddle and a segment o the internal oblique muscle. 2. Fibula ap (peroneal artery): Fibula can be harvested alone or with a skin paddle.

He a d -to -To e Re c o ns truc tio n I. Cra nia l/s c a lp re c o ns truc tio n A. Layers o the scalp and cranium: SCALP 1. Skin 2. Subcutaneous tissue: contains vessels and nerves Quic k Cut Remember 3. Galeal aponeurotic layer: provides strength; continuous with “S-C-A-L-P” (s kin, the rontalis and occipitalis muscles and the temporoparietal s ubc utaneous tis s ue, galeal ascia laterally a poneurotic, loos e areolar 4. Loose areolar tissue: subgaleal ascia; provides mobility; tis s ue, and p ericranium) or contains emissary veins the layers o the s calp. 5. Pericranium: adherent to the calvarium B. Blood supply ( ve paired arteries): supratrochlear, supraorbital, superf cial temporal, posterior auricular, and occipital Quic k Cut C. Sof tissue de ects: Replace “like with like” by using hair-bearing Skin gra ts on the tissue. reatment options include the ollowing. s calp are s us ceptible to pres s ure necros is , s o bols ter 1. Primary closure: small de ects ( 3 cm) can be closed dres s ings mus t be applied primarily with great care. 2. Skin graf ing: o en used as a temporizing measure to allow time or tissue expansion 3. issue expansion: provides a larger amount o scalp tissue with intact sensation and hair growth 4. Local aps: aps should be based on at least one o the named artery systems 5. Free tissue trans er: o en required or large de ects D. Cranial de ects: reatment must provide structural protection or the brain and should maintain normal shape o the calvarium. 1. In ection: I the wound is in ected, reconstruction should be delayed until the in ection is ully treated. 2. reatment options: include the ollowing: a. Alloplastic materials: Can be pre- ormed using computer-aided design; they are pre erred or large de ects and are composed o titanium mesh, polymethyl methacrylate (PMMA), or polyether ether Quic k Cut ketone (PEEK). Autologous bone is b. Autologous bone graf s: serve as a sca old or new bone pre erred over implants due growth rom the edges o the de ect (osteoconduction) to a lower in ection/extrus ion (1) Original bone graf : I the original bone removed rate. during the craniectomy is preserved (either rozen

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or placed in the abdominal subcutaneous tissue), it can be used later to reconstruct the de ect. (2) Other: split calvarial bone gra (outer table rom the parietal bone) or split rib gra II. Eye lid re c o ns truc tio n: Eyelid de ects commonly occur as a result o oncologic resections (Mohs micrographic surgery) or trauma. A. Goals: Restore eyelid blink unction (maintain a unctional lacrimal system, which cleans and lubricates the eye), protect the globe (prevent puncture, exposure keratitis, desiccation, etc.), and achieve adequate aesthetic results. B. echnique: Choice depends on the thickness o the de ect and the amount o eyelid tissue that is missing. 1. Partial-thickness loss: can be closed primarily or with F SGs, which are used to avoid contracture, which can lead to ectropion a. Skin de ects: best reconstructed with skin gra s rom the contralateral eyelid, which provides the best color and thickness match b. De ects o the conjunctiva and tarsal plate: Although usually occur as part o a ull-thickness de ect, they may need to be repaired on their own. 2. Full-thickness de ects: De ects up to 30% o the lid can be closed primarily, but they must be closed in layers to avoid notching. Larger de ects are closed with a variety o local aps. III. Ea r re c o ns truc tio n: A. External ear de ects: arise as a result o trauma, bites, oncologic resections, and congenital mal ormations 1. Microtia (congenital hypoplasia): due to incomplete embryonic development o the ear; may be an isolated de ect or associated with other mal ormations 2. External ear anatomy: Pinna can be divided into subunits that def ne its aesthetic appearance and help guide reconstruction. a. Helix and lobule: create the overall contour o the ear and are important or projection and the appearance o symmetry with the other ear b. Antihelix and antitragus: complex cartilaginous olds that give structure and support to the ear c. Conchal complex: made up o the conchal bowl and cavum conchae; does contain cartilage but is not as important or structural support 3. Goals o reconstruction: Replace the cartilaginous ramework, recreate 3D morphology, and achieve symmetry with the una ected side. B. Subtotal ear de ects: De ects involving only the skin o the ear can be reconstructed with skin gra s or local skin aps. Quic k Cut Full-thickness de ects require reconstruction o both skin and The perichondrium o underlying cartilage mus t underlying cartilaginous structures. Various chondrocutaneous be intact in order or a gra t advancement and rotational aps have been described. to take. C. otal ear reconstruction: o en used or microtia in children and is a multistage procedure 1. Stage 1: Costal cartilage ( rom ribs 6 to 8) is carved to orm the ramework o the ear, using the contralateral ear as a template to match size and shape. 2. Stage 2: Framework is then covered in a pedicled or ree temporoparietal ascial ap and inset in the proper location. 3. Stage 3: Skin gra is used to cover the ascial ap. IV. Na s a l re c o ns truc tio n: Nasal de ects occur most commonly as a result o trauma or oncologic resection. A. Layers: skin, bone and cartilage, and mucosal lining Quic k Cut B. Aesthetic subunits (nine): dorsum, paired sidewalls, tip, paired When a de ect ala, columella, and paired so tissue triangles makes up greater than 50% C. Goals o reconstruction: maintain a patent airway, replace all o a s ingle s ubunit, it is bes t missing layers, and achieve good aesthetic results to extend the de ect and recons truct the s ubunit as a D. Method: depends on the location, size, and depth o the de ect whole. 1. Skin de ects: Small de ects in certain locations (e.g., medial canthal region, typically concave areas) heal very well by secondary intention. Various local aps are used or larger de ects or de ects in other locations (bilobed, nasolabial, or orehead aps).

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2. Lining and structural de ects: Bone and cartilage autogra s (conchal or rib cartilage can be harvested) are used to replace midline and alar structures, supporting the so tissue and restoring projection. Replacing the nasal mucosal lining is very important when reconstructing ullthickness de ects. Failure to do so can result in contracture, stenosis o the lumen, exposure and resorption o cartilage or bone gra s, and alar notching. V. Lip re c o ns truc tio n: Lip de ects are commonly due to tumor resection, congenital cle s, and trauma. A. Lip anatomy: Skin in the vermilion zone (red zone) is unique so skin gra s cannot be used because o a color and texture mismatch. T e epidermis is very thin, allowing the dense capillary plexus to shine through and give the lip its color. B. Goals o reconstruction: Maintain oral competence, including Quic k Cut muscular integrity, sensation, and the aperture o the mouth; Micros tomia is los s preserve normal speech; and achieve good aesthetic results. o the aperture o the mouth. C. Method: Depends on characteristics o the de ect, such as size, thickness, and location. In general, local aps are used to redistribute surrounding lip tissue, which is the only way to replace like with like in the case o vermilion lip tissue. 1. Small de ects (up to 30%) o the upper or lower lip: can be closed primarily, depending on their location 2. Abbé lip switch ap (two stages): originally designed to reconstruct the philtrum in bilateral cle lip de ects a. Stage 1: Full-thickness segment o the una ected lip (not involving the commissure) is raised (using the labial artery as the pedicle) and rotated into the de ect on the other lip. b. Stage 2: Flap’s pedicle is connecting the upper and lower lips and will be divided 2–3 weeks later during the second stage o the procedure. T e donor site is closed primarily. VI. He a d a nd ne c k: De ects o the aerodigestive tract are usually due to malignancy in the oral cavity. Squamous cell carcinoma is the most common type. A. Functions o the pharynx: serves as a passageway or ood and air, swallowing (propelling ood boluses while protecting the airway), and speech (lips and oral cavity shape sounds generated by the vocal cords) B. Goals o reconstruction: Provide bulk in the oropharynx to eliminate dead space during speech and swallowing, replace the lining o the oral cavity, and restore the continuity o the digestive tract. C. Sof tissue reconstruction: Although some de ects can be reconstructed locally, distant aps are o en necessary to provide adequate bulk. When the de ect involves the ull circum erence o the hypopharynx and esophagus, many o these aps can be tubed in order to recreate a lumen. 1. Pedicled pectoralis major ap: based on its dominant blood supply, the thoracoacromial artery 2. Free aps: When used in a tubed conf guration, the skin o anterolateral thigh (AL ), radial orearm (commonly used or oor o mouth de ects involving the base o the tongue), scapular, and parascapular asciocutaneous aps lies on the inside, lining the new lumen. T is provides a strong epithelial layer, which protects the ap rom ood boluses. 3. Free jejunum: Portion o small intestine, oriented in the direction o peristalsis, can be inset with its mesenteric blood supply (See Figure 18-4). D. Bony reconstruction: Head and neck cancers o en require resections that involve the bony skeleton, resulting in large de ects o the mandible and mid ace (maxilla, zygoma, and orbit). 1. Goals o reconstruction: Restore structural support to allow or the normal mechanics o mastication, maintain acial projection, and replace the lining o the oral or nasal cavities. 2. Mandibular reconstruction plates: Can be used on their own to bridge a de ect in the mandible without replacing the bony segment. High ailure rates result rom the metal plate eventually extruding through the so tissue o the mouth or ace, or the plate itsel may racture a er some time due to the orces o mastication. 3. Nonvascularized bone graf s: Segments o autologous bone gra s can be harvested rom various sites (iliac crest, scapula, rib, f bula, and radius) and f xed using metal plates. Only used or small de ects (6 cm or less). High ailure rate due to resorption and in ection because they rely on the surrounding vascular bed or survival. Must be done delayed. 4. Vascularized bone aps: Segment o bone is harvested with its blood supply. T e ree f bula ap (peroneal artery and vein) is most commonly used or mandibular reconstruction. T ese have better success rates than bone gra s or reconstruction plates. T e ap vessels are usually anastomosed to the acial artery and vein using microsurgery.

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VII. Bre a s t re c o ns truc tio n: Reconstruction a er surgical resection Quic k Cut is an important part o breast cancer treatment. T e type o Patients can avoid reconstruction used depends on characteristics o the de ect (size recons truction and us e an o the de ect—i.e., mastectomy or lumpectomy, quality o skin external pros thes is to res tore aps a er the mastectomy) and other patient actors (e.g., patient the orm o the breas t. pre erence, size o the contralateral breast, medical comorbidities, body habitus). A. iming: depends on patient pre erence, tumor biology, and the need or adjuvant radiation therapy 1. Immediate: usually done in early-stage cancers (stages I and II), when radiation therapy is not expected a. Advantages: better cosmetic result (mastectomy skin can be used, skin is not contracted, premastectomy landmarks are available), single-stage procedure, and easier access to recipient vessels when ree tissue trans er is per ormed b. Disadvantages: I postoperative radiation is required, it can cause skin changes (shrinkage, contracture, f rmness and pigment changes), at necrosis, and de ormity, and wound healing complications may delay urther adjuvant therapy. 2. Delayed-immediate: Per ormed in patients at a somewhat increased risk o requiring adjuvant radiation therapy. A tissue expander is placed at the time o mastectomy and f lled as appropriate. I radiation is required, it can be de ated and ref lled a er the therapy. Def nitive reconstruction is per ormed once therapy is complete. a. Advantages: allows or skin preservation even with radiation b. Disadvantages: wo stages are required. 3. Delayed: Reconstruction is per ormed well a er the mastectomy (months to years later). a. Advantage: Postoperative radiation will not a ect the reconstruction. (months to years later) b. Disadvantages: wo-stage procedure, cosmetically in erior, and reconstruction may be more di cult and recipient vessels may be di cult to f nd due to scarring. B. ypes: include oncoplastic breast reduction, implant-based, and autologous tissue trans er 1. Oncoplastic breast reduction: involves per orming adjacent tissue trans er, most commonly in the orm o a reduction mammoplasty at the same time as breast conserving therapy (BC ) Quic k Cut a. Indications: best in patients who require airly large Symmetry can be lumpectomies achieved by reduction in the b. Advantages: allows the plastic surgeon to rearrange breast contralateral breas t. tissue to f ll the de ect while still maintaining symmetry and cosmesis 2. issue expander: Placed under the pectoralis major at the time o the mastectomy or a delayedimmediate reconstruction. A er the expansion process is f nished, the tissue expander is removed and replaced with an implant, or an autologous tissue trans er is done to reconstruct the breast. 3. Saline: silicone shell f lled with saline solution (physiologic) a. Advantages: low capsular contracture rates, leaks are sa ely absorbed by the body, and easier to adjust or size b. Disadvantages: Wrinkling; leakage will cause complete de ation. 4. Silicone: silicone shell f lled with silicone f ller a. Advantages: more natural eel than saline; less wrinkling b. Disadvantages: Higher contracture rates; rupture can cause local in ammation and granuloma ormation. 5. Autologous tissue trans er: Involves using either pedicled or ree ap. Choice o ap depends on the size o the breast, prior surgeries (which limit the availability o donor sites), and any medical comorbidities. a. ransverse rectus abdominis muscle ( RAM): based on Quic k Cut the superior epigastric artery (Fig. 26-5) The TRAM f ap (1) Disadvantage: not commonly per ormed due to provides enough tis s ue or high donor site morbidity (hernia, abdominal wall recons truction or any breas t weakness, and larger potential areas o at necrosis) s ize or body habitus but has (2) Donor site: May require mesh reconstruction; high donor s ite morbidity. concurrent abdominoplasty is per ormed to close the site.

440

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IV

De -e pithe lize zone

II Infe rior e piga s tric ve s s e ls

I

III

S upe rior e piga s tric a rte ry

P os te rior re ctus s he a th Arcua te line Infe rior re ctus re mna nt

Fig ure 26-5: The trans vers e rectus abdominis mus cle (TRAM) f ap. The TRAM is a pedicled f ap, bas ed on the s uperior epigas tric artery. (From J a ee RA, Anesthesiologist’s Manual of Surgical Procedures, 5th ed. Baltimore: Lippincott Williams & Wilkins ; 2014; reproduced with permis s ion rom Spear SL. Surgery of the Breast: Principles and Art. Philadelphia: LippincottRaven; 1998.)

b. Latissimus dorsi: based on the thoracodorsal artery (1) Advantages: can be used or reconstruction o small/ medium breast and/or in conjunction with an implant (2) Donor site: Long-term morbidity is low, although seroma ormation is common. c. Abdominally based aps: Free aps using an abdominal skin paddle are desirable because the donor incision can be closed with a concurrent abdominoplasty and include the ree RAM and deep in erior epigastric per orator, which involves dissecting within the rectus to f nd the per orator, without taking any muscle. d. Recipient vessels: Free aps include internal mammary vessels and thoracodorsal vessels (less common). VIII. Bre a s t d e o rm itie s : include gynecomastia, macromastia, and tuberous breast A. Gynecomastia: enlargement o breast tissue in males 1. Etiology: due to an excess o estrogens relative to androgens; may be due to underlying disease (e.g., cirrhosis, hypothyroidism, adrenal and testicular tumors, hypogonadism, Kline elter syndrome) or certain drugs (e.g., marijuana, anabolic steroids, spironolactone, ketoconazole, cimetidine, or puberty)

Quic k Cut Free TRAM can be done us ing a mus cle-s paring technique, which als o reduces the ris k o hernia ormation.

Quic k Cut Gynecomas tia occurs normally during the neonatal, pubertal, and elderly periods .

Quic k Cut In high-ris k patients , s uch as thos e with BRCA mutations , gynecomas tia may repres ent breas t cancer.

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reatment: Idiopathic gynecomastia should be observed initially because it o en regresses. a. Medical: Aromatase inhibitors (tamoxi en) decrease peripheral conversion o androgens to estrogens. b. Surgical: includes suction lipectomy or surgical excision B. Macromastia: excessive enlargement o the emale breasts 1. Etiology: due to an abnormal growth response to normal circulating amounts o estrogen that causes large increases in f brous and atty tissue but a relatively small increase in glandular tissue 2. Symptoms: neck, back, and shoulder pain; intertriginous rashes, in ections, and maceration at the in ramammary old (IMF) 3. reatment: surgical a. Reduction mammoplasty: Goal is to relieve symptoms by reducing breast volume and reposition the nipple–areolar complex (NAC) at or above the level o the IMF through many possible techniques. T e NAC is le on a dermoglandular pedicle, which preserves blood supply and innervation. Pedicle design and skin patterns are generally independent o each other. (1) Pedicle designs: in erior, superior, central, and medial pedicles (2) Skin patterns: inverted (Wise pattern), vertical, and circumareolar Quic k Cut b. Suction lipectomy: used as an adjunct or contouring Lipectomy alone will C. uberous breast: abnormal breast development, resulting in not addres s breas t projection narrow breast base, high IMF, and large areola due to herniation or nipple pos ition. o the breast parenchyma into the areolar space 1. Location: usually bilateral but may be unilateral 2. reatment: external tissue expansion with at gra ing to increase breast volume; surgery to expand the base o the breast, reduce the size o the areola, and correct the nipple location IX. Che s t wa ll: De ects arise as a result o trauma, tumor resections, in ections, radiation damage, and congenital conditions. A. Mediastinitis: In ection o the sternal wound is a li e-threatening complication o cardiac procedures and requires complex ap reconstruction. B. Structures: Pleural lining is important or maintaining an Quic k Cut airtight seal over the lungs, which prevents pneumothorax and Removal o all f stulas; ribs are important or skeletal structure and support, devitalized or in ected tis s ue protection o vital organs, and proper breathing mechanics; and and hardware is key to the s ucces s o the s ubs equent the sternum is the point o articulation or the ribs and clavicles. recons truction. C. Goals o reconstruction: Restore stability and structure o the ribs and chest wall, obliterate dead space, and restore the pleural lining. D. Structural de ects: Reconstruction o rib de ects is indicated when our or more ribs are involved and the de ect is longer than 5 cm, as these will result in paradoxical motion and poor breathing mechanics. 1. Sof tissue aps: Bridging the space le by the missing ribs or sternum can provide enough stability to allow or normal breathing. a. ensor ascia latae ap: provides strong ascia b. T ick muscle aps: such as the rectus abdominis myocutaneous ap 2. Alloplastic materials: used when more support is needed (typically or lateral chest rib cage rather than sternum) a. Polypropylene or polytetra uoroethylene mesh: can be used or semirigid f xation b. PMMA: even more rigid; can be embedded within mesh layers or additional support E. Sternal wounds: Vacuum-assisted closure is o en used as a bridge to def nitive reconstruction; pedicled aps bring wellQuic k Cut vascularized tissue into the wound, which speeds healing. T e Flap coverage is the sternum does not require rigid f xation or bony union. s tandard therapy or s ternal 1. Pectoralis ap: Considered the workhorse or sternal wound in ections . wounds; the pectoralis major has two vascular systems: the dominant thoracoacromial artery and a set o segmental per orators rom the internal thoracic artery (I A) (also called the internal mammary).

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issue

2. Pectoralis turnover ap: Based medially on the segmental Quic k Cut per orators rom the I A; the pectoralis muscle is Coronary artery separated rom its humeral attachment laterally, and the bypas s gra ting us ually thoracoacromial pedicle is divided at the clavicle; the muscle involves harves ting the le t is ipped medially and inset into the wound. ITA; in thes e patients , the 3. Unilateral advancement ap: Based on the thoracoacromial pectoralis turnover f ap may be limited to the right s ide. artery pedicle; the muscle is divided rom its medial attachments and advanced urther medially into the sternal wound. 4. Rectus abdominis muscle ap: based on the superior epigastric artery 5. Omental ap: Based on the either the le or right gastroepiploic artery; typically avoided in patients with previous abdominal surgeries due to damage or scarring o the omentum. T ere is a potential risk o in ectious spread between the mediastinal and peritoneal cavities or herniation o abdominal organs into the chest. X. Ab d o m e n: echniques are as ollows. Quic k Cut A. Panniculectomy: resection o hanging skin and at o the low The indication or abdomen typically done via a waistline incision (distinguished panniculectomy is generally rom abdominoplasty, as there is no dissection above the to improve hygiene and to umbilicus and no umbilical transposition); may also be done with limit intertrigo (ras hing o s kin olds ). a eur-de-lis pattern, which adds a vertical midline incision and is designed to resect tissue in the vertical and horizontal directions B. Abdominal wall reconstruction: Mainstay is component separation. 1. echnique: Incise the external oblique ascia and divide the underlying muscle, which allows the midline rectus muscle to be advanced toward the midline or closure under less tension. Many surgeons will augment this closure with biologic or permanent mesh placed deep to the repair (sublay) or on top o the repair (onlay). 2. Advantages: Spares innervation to the rectus muscles (innervation lies in the deeper internal obliques) as well as the blood supply, which runs within the rectus (a communication o deep in erior epigastric vessels and the internal mammary or superior epigastric vessels). XI. Lo we r e xtre m ity: echniques are as ollows. A. Groin coverage or vascular graf s: ypically accomplished with the rotation o regional pedicled muscle aps. Use o the adjacent sartorius muscle is o en the f rst choice. Each patient’s anatomy must be determined, as blood supply to the muscle o choice may have been excluded by vascular disease or bypasses. B. rauma: Mainstay o coverage or open wounds o the knee and upper one third o the leg includes use o the medial and lateral gastrocnemius muscles as well as the soleus; lower one-third wounds are very challenging to reconstruct and most require ree ap coverage.

WOUND HEALING AND DISEASES OF SKIN AND SOFT TISSUE P ha s e s o Wo und He a ling I. In a m m a to ry: Platelets secrete in ammatory mediators, attracting neutrophils and macrophages. II. P ro li e ra tive : Fibroblasts enter the wound and lay down collagen, resulting in granulation tissue; epithelialization occurs. III. Ma tura tio n: Collagen cross-linking, collagen remodeling, and Quic k Cut myof broblasts cause wound contraction.

Sc a rs I. Hyp e rtro p hic s c a rs : within the border o scar II. Ke lo id s : exceed border o scar, o en pedunculated

By 6 weeks pos tinjury, the wound will reach its ultimate s trength: 80% o the original.

Wo und s I. Ac ne inve rs a ( o rm e rly hid ra d e nitis s up p ura tiva ): In ection o the subcutaneous tissue in areas o skin bearing apocrine sweat glands (typically in the axilla or groin). reatment involves antibiotics, incision and drainage, and excision with either primary closure or skin gra ing.

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Ta b le 26-1: Sta g e s o P re s s ure Ulc e rs Sta g e

Cha ra c te ris tic s

I

Intact skin with nonblanchable redness of a localized area

II

Partial-thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed

III

Subcutaneous fat is visible.

IV

Full-thickness tissue loss with exposed bone, tendon, or muscle

II. P re s s ure s o re s : evaluation/staging ( able 26-1) A. Management: O -load pressure is essential via a specialty bed (low air-loss mattress) and requent turning protocols; also improve position and treat contractures, optimize nutrition, and manage wound care dressings. B. ypes: Most common sites are sacral, ischial, trochanteric, occipital, heel, etc. III. Dia b e tic o o t ulc e rs : may be treated by compression or Unna boots; notoriously slow to heal IV. Chro nic ve no us s ta s is : Characteristic skin changes and edema are managed symptomatically.

Be nig n Skin Le s io ns

I. Cys ts : very common uid-/matter-f lled cavities in the Quic k Cut Lipomas greater subcutaneous tissues (e.g., epithelial cysts, sebaceous cysts, and than 5 cm are typically epidermal inclusion cysts secondary to puncture o the skin) imaged with magnetic II. Lip o m a s : Fat tumors are most commonly ound on the neck, res onance or computed shoulders, back, and thighs. Excision is indicated or aesthetic and tomography (CT) to evaluate or evidence o malignancy. unctional reasons. III. He m a ng io m a s : T ese vascular tumors are the most common tumors o in ancy, typically ound on the head or neck; they start in Quic k Cut the f rst ew weeks o li e and tend to grow rapidly over the f rst year, Ten percent o then involute at a rate o 10% per year. children have a hemangioma. A. Management: Can be observed; may also be treated with oral or intralesional corticosteroids (will arrest growth but not reverse it), propranolol, or pulsed dye laser. Surgery is typically reserved or lesions that either threaten airway patency or obstruct the visual f eld or in highly sensitive cosmetic areas such as the nasal tip. Pro ound bleeding or ulceration are also indications or excision. B. Kasabach-Merritt syndrome: eatures pro ound Quic k Cut thrombocytopenia occurring in conjunction with a hemangioma Vas cular IV. Va s c ula r m a l o rm a tio ns (VMALs ): May be capillary, venous, mal ormations grow with the lymphatic, or arteriovenous mal ormations present at birth (helps child and do not regres s . distinguish them rom hemangiomas) that grow proportionally with the child. Angioembolization may be used or treatment, sometimes as an adjunct to en bloc resection.

Ma lig na nt Skin Le s io ns

Quic k Cut Bas al cell carcinoma is the mos t common s kin cancer.

I. Ba s a l c e ll c a rc ino m a : commonly occurs on the head and neck; has a pearly appearance with surrounding telangiectasia, and metastasis is rare; treated with Mohs surgery or excision A. Mohs surgery: involves sequential shavings with immediate pathologic analysis B. Cure rate: T is mapped, layer-by-layer excision with immediate yields excellent cure rates ( 95%). II. Sq ua m o us c e ll c a rc ino m a : Exposure to sunlight is the primary risk actor and is associated with premalignant skin lesions and chronic wounds (Marjolin ulcer). A. Presentation: commonly presents on the lips; o en has central ulceration and satellite lesions and may grow rapidly and metastasize via lymphatics and or blood B. reatment: can be treated with Mohs or excision

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III. Me la no m a : History o severe sunburns is a known risk actor. A. Presentation: Lesions look like irregular nevi with asymmetric shape, irregular borders, and changes in size and color. B. Subtypes: Superf cial spreading is the most common; others include nodular, acrolentiginous, and lentigo maligna. C. Staging: Currently staged using the American Joint Committee on Cancer’s tumor-node-metastasis classif cation. Other classif cation systems include the ollowing. 1. Breslow method: involved precisely measuring the depth o the tumor in millimeters. Breslow system is pre erred. 2. Clark classi cation: based on histologically determining the deepest level o the skin in which malignant cells are ound D. Management: Excision is the treatment or stages I–III. Stage IV is treated with chemotherapy and radiation. Recommended margins are as ollows (based upon Breslow thickness). Quic k Cut 1. Melanoma in situ (stage 0): 0.5-cm margins In malignant 2. Lesions greater than 1.0 mm in thickness: 1-cm margins melanoma, the depth o les ion 3. Lesions 1mm: 2-cm margins, possible excision o in millimeters determines the underlying ascia radial margin in centimeters . E. Sentinel lymph node (SLN) biopsy: done to stage nodal disease and determine whether a ull lymph node dissection is indicated to remove cancer burden

CRANIOFACIAL SURGERY P e d ia tric

Quic k Cut

I. Cle t lip a nd c le t p a la te : Most common congenital cranio acial Corrected too late, anomaly. T e primary goal o cle palate repair is the optimization the cle t palate will render o normal speech development. the patient with hypernas al s peech. A. Epidemiology: Unilateral cle lips are nine times more common than bilateral. Cle lips occur twice as commonly on the le as the right. B. Incidence: 0.3 per 1,000 in A rican Americans; 1 per 1,000 in Caucasians; 2 per 1,000 in Asians; and 3.6 per 1,000 in Native Americans C. Embryology: Face orms 4th–10th week o gestation; anomaly develops due to ailure o usion o the two medial nasal prominences o the rontonasal processes to the lateral palatine processes derived rom the maxillary prominences. D. Anatomy: Primary palate is anterior to the incisive oramen and consists o lips, alveolus, and anterior palate; secondary palate is posterior to the incisive oramen and consists o hard and so palate to the uvula. E. Classi cation: described in 1931 1. Veau Class I: isolated so palate cle 2. Veau Class II: isolated hard and so palate 3. Veau Class III: unilateral cle lip and palate 4. Veau Class IV: bilateral cle lip and palate F. reatment: Requires a multidisciplinary approach; a standard team includes a geneticist, plastic surgeon, otolaryngologist, nutritionist/dietitian, speech pathologist, audiologist, dentist/oral surgeon, nurse, psychologist, and social worker. G. iming o repairs: proceeds as ollows: 1. Age 0–3 months: presurgical nasoalveolar molding (NAM) or lip adhesion 2. Age 3 months: primary cle lip repair 3. Age 9–18 months: primary cle palate repair 4. Age 7–9 years: alveolar bone gra (age o mixed dentition) 5. Puberty: orthodontics 6. Adolescence: open rhinoplasty 7. Skeletal maturity: orthognathic surgery H. Complications: velopharyngeal incompetence (di culty in speech), palatal f stulas, and mid ace hypoplasia (mid acial bony development is retarded by manipulation o these areas during cle repair)

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Ad ult

Quic k Cut I. Tra um a : Initial management o acial injuries ollows basic Facial injuries are principles o advanced trauma li e support (A LS) and begins with rarely li e threatening but airway, control o hemorrhage, and evaluation and stabilization o s hould alert the examiner concomitant injuries. to the pos s ibility o airway compromis e, cervical s pine A. Initial evaluation: history, physical exam, and imaging studies injuries , or central nervous 1. rauma history: past medical history, allergies, medications, s ys tem injuries . last meal, and mechanism o injury 2. Physical exam: skin and so tissue rom scalp to neck; sensory examination o trigeminal nerve regions o the ace and oral cavity; motor examination o the acial nerve, ocular and orbital examination, which is o en assisted by ophthalmology to document visual acuity and other injuries to the globe; and intraoral examination o mucosa, dentition, and occlusion o teeth 3. Imaging: Per ormed to evaluate skeletal abnormalities; C scans are the most commonly used modality. A panoramic radiograph evaluates the entire mandible, rom condyle to condyle, in a single image. B. ypes: mandible (order o most common: angle, condyle, Quic k Cut symphysis/parasymphysis), maxilla, nasal bones, and orbital Ophthalmologic ractures cons ultation s hould be cons idered in every cas e o 1. Exam or orbital ractures: First indication o optic nerve orbital trauma. compression may be red color desaturation; direct and consensual pupillary responses; and globe movement. 2. Orbital racture types: orbital oor, medial orbit, and orbital roo C. Management: intermaxillary f xation (IMF) and open reduction and internal f xation (ORIF)

HAND SURGERY Tra um a I. Fra c ture s : phalanx (usually treated by alignment then immobilization), metacarpal (boxer’s racture; typically treated with reduction and splinting), carpal (typically managed with casting), and radius/ulna (long bone ractures usually managed with casting)

Quic k Cut Hand ractures are common and require individualized treatment, as unction o the hand is critical.

II. Am p uta tio ns a nd re p la nts : Indications or digital replant include thumb, single digit distal to exor digitorum superf cialis (FDS) insertion, multiple digits, hand amputation through palm, any part in a child, and proximal arm injury with sharp mechanism. A. Contraindications or replant: single digits proximal to FDS exor insertion; severely crushed, mangled, or contaminated parts; multiple-level amputation; and multiple trauma or severe medical problems B. Finger reconstruction: second toe trans er, f nger lengthening C. T umb reconstruction: lengthening, pollicization, toe-to-thumb trans ers III. Bite injurie s : Human bites may occur in de ensive injury; anaerobic bacteria are common. Dogs and cats are most responsible or animal bites. A. Animal bite organisms: include Pasteurella species, Staphylococcus, Streptococcus, and Capnocytophaga B. reatment or animal bites: involves aggressive debridement o devitalized tissue, administration o appropriate antibiotics, and tetanus and rabies treatment or prophylaxis

Quic k Cut Two percent o the population s u ers an animal bite each year.

Tum o rs a nd Ha nd Ma s s e s I. Be nig n s o t tis s ue m a s s e s : Ganglion cysts are most requent, causing degeneration o connective tissue in joint capsules or tendon sheaths. Aspiration has high recurrence rate. Surgical excision must remove stalk o ganglion. Other lesions include the ollowing. A. Giant cell tumors: Likely reaction to injury, with large yellow subcutaneous mass. reatment is by excision.

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B. Epidermal inclusion cyst: due to prior implantation o epidermal cells into the dermis; presents as a f rm, nontender mass or cyst, and treatment is complete excision C. Glomus tumor: Subcutaneous nodules in subungual region causing cold hypersensitivity and paroxysmal and pinpoint pain. reat with complete excision. II. Ma lig na nt s o t tis s ue m a s s e s : Squamous cell carcinoma is most common; usually occurring on the dorsum o the hand in elderly men and with an aggressive metastatic rate. reat with wide local excision with 5–10-mm margins. Others as ollows. A. Basal cell carcinoma: Pearly lesions with ulceration, telangiectasias, and discoloration. Metastasis is uncommon, and treatment is excision o 5-mm margins or Mohs surgery. B. Melanoma: May be visible on skin or subungual. reatment is wide local excision with margins based on tumor depth or amputation at joint proximal to lesion. III. Be nig n b o ne tum o rs : Enchondroma is most common and is treated with curettage and bone gra ing. Osteoid osteoma and osteochondroma are other tumors. IV. Ma lig na nt b o ne tum o rs : Chondrosarcoma is most common and is treated with en bloc resection with ray amputation or digits. Osteogenic and Ewing sarcoma are others (see Chapter 28).

In e c tio n I. P a ro nyc hia : in ection where the nail and skin meet; most common in ection o the hand A. Acute: associated with Staphylococcus aureus; treatment with Quic k Cut Treatment o elevation o nail plate and incision into nail old paronychia includes B. Chronic: usually ungal (Candida or atypical Mycobacterium); antibiotics and drainage, treatment with topical anti ungals and eponychial marsupialization which us ually requires incis ion (excision o crescent-shaped portion o skin proximal to and elevation o the nail plate. eponychial old; wound allowed to close by secondary intention) II. Fe lo n: abscess o pulp o digit A. Etiology: Occurs a er puncture wound; S. aureus is the most common pathogen. B. reatment: Open longitudinal incision over pulp in the area o maximal uctuance; lateral incision over midline may preserve digital arteries; important to divide septa in pulp to allow drainage and packing. III. He rp e tic whitlo w: Herpes simplex types 1 and 2 in ection; clear vesicles may orm. Medical treatment with acyclovir; no incision is necessary. IV. Fle xo r te no s yno vitis : A. Signs: (Kanavel’s signs) intense pain with any attempt to extend partly exed f nger, f nger held in exion or com ort, uni orm swelling involving the entire f nger, and percussion tenderness along the course o the tendon sheath B. reatment: initially antibiotics, splinting, and hand elevation but highly likely to need incision and drainage V. Me d ia n ne rve c o m p re s s io n (c a rp a l tunne l s ynd ro m e ): typically caused by repetitive motion A. reatment: initially splinting and avoidance o inciting task; may respond to intracanal injections o steroids B. Advanced cases: may be decompressed with open or endoscopic surgery (release o the transverse carpal ligament)

AESTHETIC P LASTIC SURGERY Ove rvie w I. Ra tio na le : Aesthetic or cosmetic procedures are per ormed to Quic k Cut improve a patient’s appearance. Great care must be taken by the Aes thetic s urgery plastic surgeon to identi y appropriate candidates. may be des igned to correct a perceived f aw and/or to II. Ca nd id a te s e le c tio n: As these interventions are truly elective mitigate e ects o aging. in nature, patients with worrisome medical comorbidities as well as patients su ering rom body dysmorphic disorder must be identif ed. It is incumbent on the surgeon to educate the patient about realistic results and potential risks.

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Co m m o n Op e ra tive Ae s the tic P ro c e d ure s

Quic k Cut I. Bre a s t a ug m e nta tio n: per ormed to address micromastia Micromas tia is (small breasts) es s entially a s ubjective A. reatment: Patients are counseled about our undamental diagnos is and is identi ed by options, including size and type o implant (saline or silicone), the patient. anatomic position o the implant relative to the pectoralis major muscle (subpectoral or subglandular—on top o the muscle and below the breast gland), and location o incision ( our most common access sites are the IMF, periareolar region, axilla, and umbilicus—transumbilical breast augmentation [ UBA]). B. Breast ptosis: Simultaneous assessment o descent o the NAC relative to the IMF must be made. In cases o micromastia with minor ptosis, a subglandular augmentation may rotate the nipple upward and improve or even correct the ptosis. C. Complications: Breast augmentation may be complicated Quic k Cut by asymmetry, capsular contracture, diminished nipple Special sensation, in ection, leak or rupture, etc. Due to various issues/ mammography techniques complications, the current reoperative rate 3 years a er breast (Eklund views ) are augmentation is 13% or saline implants and 21% or silicone. recommended to

II. Rhino p la s ty: may be approached through either open or closed technique A. Historically: predicated on reduction o the size o various nasal components (classically shaving/reduction o a dorsal hump) B. Currently: Has evolved into a synthesis o reduction and augmentation with care ul attention paid to placement o cartilage gra s and suturing techniques to def ne and augment various aesthetic components o the nose. It is thought that as many as 20% o rhinoplasties require revision.

maintain s ens itivity or cancer s urveillance in the recons tructed breas t.

Quic k Cut Male and emale aes thetic ideals o the nos e are quite di erent.

III. Ble p ha ro p la s ty: Operative rejuvenation o the upper and/or lower eyelids may include a resection or resuspension o the skin and at times the underlying orbicularis oculi muscle. A. Fat herniation: For many patients, the visible de ormity o the lower lids is actually through the orbital septum, which may be Quic k Cut repositioned, resected, or redraped during skin resection. With all elective B. Care ul preoperative assessment: Eye-related morbidities cos metic procedures , care ul such as dry eyes must be assessed. Blepharoplasty may also be a patient s election is critical. reconstructive operation in the setting o redundant upper eyelid skin (dermatochalasis) leading to impaired visual f elds. IV. Lip o s uc tio n: minimal access approach to body contouring whereby the surgeon aspirates and sculpts areas o the patient’s Quic k Cut undesired at Phys iologic A. ypes: include suction only, power-assisted, ultrasound, and complications can aris e rom mas s ive f uid s hi ts laser orms when lipos uction is high B. echnique: Surgeon typically starts by in using tumescent volume (5 or more liters o solution into the areas to be liposuctioned. T e uid (saline lipoas pirate). or lactated Ringer) will o en contain epinephrine to decrease blood loss and may contain a local anesthetic such as lidocaine to lessen pain. C. Complications: include lidocaine toxicity, contour de ormities or asymmetry, tunneling marks, seroma/ hematoma, insu cient or overaspiration, and injury to deep structures (in the case o abdominal liposuction, this includes entry into the peritoneal cavity with possible per oration o bowel) V. Rhytid e c to m y ( a c e -li t): Skin o the ace and/or neck is undermined to varying extents, and the underlying superf cial musculoaponeurotic system (SMAS) is manipulated (typically elevated or tightened) to correct signs o aging. T e skin and SMAS are ideally pulled in di erent vectors. Evaluation o the aging ace and neck generally includes assessment o hairline and style, brow position, crow’s eet, nasolabial olds, marionette lines, perioral rhytids (wrinkles), jowling, and whether or not the cervicomental angle is acute or obtuse.

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A

B

C

D

E

Fig ure 26-6: Breas t ptos is . (From Thorne CH, Bartlett SP, Beas ley RW, et al. Grabb and Smith’s Plastic Surgery, 6th ed. Baltimore: Lippincott Williams & Wilkins ; 2006.)

VI. Ab d o m ino p la s ty: Removes redundant skin and at rom the lower abdomen typically through a hipto-hip waistline incision. Dissection along the muscular ascia spares the umbilicus, which is transposed through a new midline opening in the abdominoplasty ap, which allows the surgeon to reapproximate the rectus muscles at the midline (linea alba) i previous pregnancy or weight gain has caused a persistent diastasis o the muscles. VII. Ma s to p e xy: Per ormed to correct varying degrees o breast ptosis Quic k Cut (Fig. 26-6); grade determines extent o invasiveness required or a The ideal breast has meaning ul correction o the de ormity. all breast tissue including the nipple remaining above the IMF. A. Grade 1 ptosis: characterized by a nipple at the IMF B. Grade 2 ptosis: has the nipple below the old C. Grade 3 ptosis: has a nipple at the bottom o the breast acing downward when the patient is standing VIII. Bra c hio p la s ty: Excessive skin and at o the upper arm (elbow Quic k Cut Contour and to axilla) can be removed but o en trades an unsightly excess o appearance s urgery comes loose tissue or a sizeable and di cult to camou age scar. As with at the expens e o s cars , most body aesthetic procedures, it can be enhanced by judicious which may be di cult to use o liposuction. A staged approach may be used when signif cant camouf age. adipose tissue is present. IX. Chin a ug m e nta tio n: Changing the shape and position o the chin may be done via osteotomies and repositioning o the bony portion o the chin (mandible) or through the use o alloplastic implants (available in a variety o sizes and shapes and must be tailored by the surgeon to address each patient’s aesthetic need). A. echnique: may be per ormed through intraoral access or a submental incision B. Evaluation: It is critical or the plastic surgeon to evaluate the patient with regard to general acial harmony and specif cally, i the chin de ormity relates to more complex anatomic def ciencies that must be corrected with orthognathic procedures. T e f rst step would be to assess the patient’s dental occlusion. X. Bro w li t: Location and position o eyebrows can a ect a patient’s appearance. Quic k Cut A. Ideal position: in males, generally at or just above the superior Poor brow s haping orbital rim and straight; in emales, arching and above the and pos ition can make a superior orbital rim patient look old or unpleas ant. B. echnique: Can be per ormed endoscopically or via incisions at the hairline or within the rontal hair. During this procedure, certain muscles o the orehead can be excised or transected to improve orehead wrinkling (this wrinkling may also be addressed via botulinum toxin injections).

Bo d y Co nto uring a te r Ma s s ive We ig ht Lo s s I. Ove rvie w: Body contouring/sculpting a er massive weight loss (via any combination o diet, exercise, and/or bariatric surgery) o en consists o a panel o procedures. A. Complications: commonly, hematoma and seroma ormation, widening o scars, wound healing problems, and in ection

Quic k Cut Becaus e obes e patients are high ris k, procedures may be s taged to minimize operative times , pain, and blood los s .

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Plastic and Reconstructive Surgery

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B. Patient expectations: Need to be managed starting with the f rst preoperative assessment. Although some patients may experience amazing results, others will require numerous procedures and have results best appreciated when clothed.

INNOVATIONS AND DEVICES IN P LASTIC SURGERY Ma te ria ls I. Bio lo g ic d e rm a l m a trix: acellular dermal matrix serves as a biologic mesh that may be procured rom human (cadaver) or porcine sources; primarily use ul as a rein orcement in contaminated f elds II. Synthe tic m e s he s : Variety o materials are available to the modern surgeon, varying in composition, arrangement o f bers, pore size, weight, and exibility. III. Bo ne re p la c e m e nt: Beyond autogra , cadaveric bone, calcium hydroxyapatite, titanium, and materials such as PEEK or PMMA may be used.

De vic e s I. La s e r a ng io g ra p hy: used or intraoperative diagnosis o tissue necrosis and determining viability o skin aps II. Do p p le r a nd tis s ue o xim e try: may also be used to assess tissue per usion

Surg ic a l Inno va tio ns I. Va s c ula rize d c o m p o s ite a llo g ra ts (VCAs ): Represent the transplantation o multiple tissue types, including the unctional units o hand or ace transplant. Although they remain experimental, dozens o VCA have been per ormed to date. II. Bio p ro s the tic s : artif cial materials to replace particular organs or organ unctions III. Tis s ue e ng ine e ring : Use o cultured cells to recreate a missing or damaged component is still in its in ancy.

Chapter 27

Neur surgery

Kenneth M. Crandall and Charles A. Sansur

ANATOMY Bra in I. Skull: C ntains v lume 1,500 mL mprising the brain ( 87%), erebr spinal f uid (CSF) ( 9%), and bl d vessels ( 4%) in a rigid mpartment; n rmal cerebral blood f ow (CBF) is 50 mL/100 g brain tissue per minute. II. Mo nro -Ke llie d o c trine : Under n rmal nditi ns, the v lume ea h the three brain mp nents is in equilibrium.

Quic k Cut The Monro-Kellie doctrine as s umes that the cranial vault has a f xed maximum volume.

III. Arte ria l s up p ly A. Anterior circulation: derived r m the internal carotid arteries, giving rise t the middle cerebral and the smaller anterior cerebral arteries, whi h supply the rontal, temporal, and parietal lobes and the deep gray matter Quic k Cut B. Posterior circulation: riginates r m the vertebral arteries The brain is one 1. Basilar artery: rmed r m the vertebral arteries at the f tieth (2% ) o body weight audal margin the p ns but receives one f th (18% ) o 2. Branches: supply the pons, cerebellum, thalamus, and divide the cardiac output. int the p steri r erebral arteries, whi h supply the occipital lobes C. Circle o Willis: Arterial anast m ti ir le rmed by multiple arteries between the maj r bran hes the anteri r and p steri r ir ulati ns. In the event a maj r vessel lusi n, the bl d supply t its territ ry may be supplied by an ther vessel via the ir le Willis. IV. Ve no us d ra ina g e : All ven us bl d r m the brain uses the internal jugular veins. A. Super cial cerebral veins: drain the rtex and sub rti al white matter int the superi r sagittal, transverse, petr sal, r avern us sinuses B. Deep cerebral veins: Drain the deeper stru tures su h as the basal ganglia and thalamus. T ese veins drain int the great vein o Galen be re emptying int the straight sinus.

Sp ina l Co rd I. Arte ria l s up p ly A. Anterior spinal artery: riginates r m the vertebral artery and supplies the anter medial gray matter B. Posterior spinal artery: paired; riginates r m the vertebral artery C. Segmental medullary arteries: Originate at many levels r m bran hes the a rta and vertebral arteries. I mpr mised, spinal rd in ar ti n may result. II. Ve no us re turn: typi ally parallels the arterial supply

450

Quic k Cut The artery o Adamkiewicz is a large medullary artery that may be interrupted during aortic s urgery.

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Ce re b ro s p ina l Fluid

Quic k Cut I. To ta l volum e : Appr ximately 150 mL, with 25 mL l ated in the The entire volume o ventri les. CSF is ntinu usly pr du ed, r ughly 80% by the h r id CSF is replaced three times plexus, and the rest is se reted in the interstitial spa es the brain. a day. II. Flow pa th: CSF f ows r m the lateral ventricles t the third ventri le thr ugh the oramina o Monro and rea hes the urth ventri le via the cerebral aqueduct o Sylvius. It exits the ventri les t the subara hn id spa e thr ugh the oramina o Magendie (midline) and Luschka (lateral). A. Reabsorption: CSF ir ulates ar und the spinal rd and the brain and is reabs rbed int the superi r sagittal sinus via the ara hn id villi. B. Arachnoid villi: a t as ne-way valves that pen at 5 mm Hg

Ne rvo us Sys te m Func tio na l Ana to m y I. Uniq ue p a tho p hys io lo g ic p ro c e s s e s : result r m the mplexity the entral nerv us system’s (CNS) un ti nal rganizati n, the rigidity its b ny en l sures, and its resp nses t injury II. Fo c a l le s io ns : a e t neur l gi un ti n by l al destru ti n nerv us tissue; tissue dist rti n with un ti nal l ss attributable t ax nal stret hing and subsequent synapti damage; hanges in bl d f w, ausing is hemia r ven us ngesti n; and alterati ns in the ele tri al r metab li a tivity a l al area, pr du ing an epilepti us

PATHOP HYSIOLOGY Intra c ra nia l P re s s ure

Quic k Cut Normal ICP ranges rom 5 to 15 mm Hg.

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I. No rm a l ra ng e : 5–15 mm Hg; pr blems an devel p i the intra ranial pressure (ICP) be mes t high r l w. A. Compensatory changes: T ese must set a hange in any mp nent t maintain a n rmal ICP. B. Rate o volume change: has great lini al signi an e 1. Meningioma: T is sl w-gr wing tum r an be me quite large be re sympt ms devel p r ICP in reases. 2. Epidural hematoma: Small, a ute mass lesi ns an ause tremend us in rease in ICP and severe neur l gi de its. III. Re la tio ns hip be twe e n ICP a nd intra c ra nia l volum e : des ribed by an exp nential urve (Fig. 27-1) A. Beyond the f at portion o the curve: Intra ranial mp nents are n l nger able t mpensate r hanges in v lume; there re, a slight in rease in intra ranial v lume pr du es a very large in rease in ICP. Quic k Cut B. Ischemia and herniation: result when de reases in CSF v lume Increas ed ICP an n l nger maintain equilibrium leads to peripheral arterial vas ocons triction and IV. Sym p to m s a nd s ig ns o inc re a s e d ICP (intra c ra nia l hypertens ion to maintain hyp e rte ns io n): heada he, nausea/v miting, n usi n, cerebral per us ion, as papilledema, upward gaze paralysis (Parinaud syndr me), ranial characterized in Cus hing triad nerve (CN) VI palsy, bulging ntanelles and splitting sutures (in (hypertens ion, bradycardia, in ants), lethargy (eventually leading t ma), and Cushing triad and irregular res piration). (hypertensi n, brady ardia, and irregular respirati n)

V Intra cra nia l volume (bra in + blood + CS F)

Fig ure 27-1: This compliance curve repres ents the pres s ure–volume relations hip within the intracranial s pace. The ICP s tays within normal limits until a critical volume (V) is reached, above which the pres s ure increas es exponentially.

Chapter 27

Path physi l gy

Fig ure 27-2: Axial CT s hows di us e cerebral edema. (From Cas tillo M. Neuroradiology Companion, 4th ed. Philadelphia: Lippincott Williams & Wilkins ; 2011.)

V. ICP m e a s ure m e nt A. Direct: ventriculostomy r intraparen hymal/subara hn id m nit ring devi es (“b lts”) B. Indirect: An estimate may be made by lumbar puncture (LP); h wever, this sh uld be av ided in the presen e spa e- upying intra ranial lesi ns due t herniati n. VI. He rnia tio n: When all mpensat ry me hanisms have been exhausted and the ICP ntinues t in rease, the brain “herniates” r shi s t ward the l w-pressure mpartment (the alx and the tent rium divide the interi r the skull int mpartments). Vari us herniation syndromes are re gnized. A. Sub alcine herniation (Fig. 27-2): Displa ement r m ne supratent rial mpartment t an ther may lead t anteri r erebral artery mpressi n and l ss un ti n in the pp site leg and bladder ntr l. B. Transtentorial (uncal) herniation: m st mm n type brain herniati n 1. Cause: urs when the medial temp ral l be is r ed d wn ver the edge the tent rium leading t midbrain mpressi n 2. Neurologic signs: pr gressive deteri rati n ns i usness, Quic k Cut ipsilateral pupillary dilatati n r m ul m t r nerve Progres s ive mpressi n, and ntralateral hemiparesis as a result deterioration in cons cious nes s mpressi n the erebral pedun les and pupillary dilatation is 3. Hemiparesis: May be ipsilateral in a min rity ases, concerning or herniation. whereas pupillary dilatati n is ipsilateral in 80%. T us, pupillary dilatati n is m re reliable in l alizing the lesi n. C. Tonsillar herniation (trans oramen magnum): Cerebellar t nsils herniate thr ugh the ramen magnum resulting in medullary mpressi n, whi h leads t respirat ry depressi n and death.

Auto re g ula tio n

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I. Ove rvie w: Cerebral bl d f w (CBF) versus erebral per usi n pressure (CPP) is sh wn in Figure 27-3. Average CBF: higher t gray than white matter and is in reased in areas high neur nal a tivity II. P re s s ure a uto re g ula tio n: maintains CBF ver a wide range MAP (50–150 mm Hg) (see Fig. 27-3) A. Intact autoregulation: ICP remains stable as bl d pressure hanges within the limits menti ned earlier. B. Disrupted autoregulation: r m intra ranial disease pr esses su h as head injury r tum rs Quic k Cut III. CP P : At CPP 50 mmHg, erebral bl d f w is inadequate t CPP MAP ICP pr vide su ient xygen delivery and t sustain n rmal metab lism.

C

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50 75 100 125 150 175 200 225 Cerebral perfusion pressure (torr)

Fig ure 27-3: Cerebral blood ow vers us cerebral per us ion pres s ure. Due to autoregulation, CBF remains cons tant or CPP between 50 and 150 mm Hg.

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Ce re b ra l Ed e m a I. Ove rvie w: T e brain rea ts t insults by devel ping edema. T e rate hange in edema rmati n is dire tly pr p rti nal t the neur l gi de its and/ r hanges in ICP. A ute edema pr du es m re de its than hr ni edema. II. Typ e s Quic k Cut A. Cytotoxic edema: Devel ps r m disrupted ellular metab lism Cytotoxic edema with a depleti n glu se and xygen st res, ausing retenti n is mos t requently s een in intra ellular s dium and water. T e bl d–brain barrier (BBB) is chemia. Vas ogenic edema remains inta t. Cyt t xi edema is m st mm nly seen ll wing is as s ociated with tumors and in arcts, ardia arrest, and in Reye syndr me. hemorrhage. B. Vasogenic edema: Results r m breakd wn the end thelial tight jun ti ns in the BBB, ausing leakage intravas ular pr teins and plasma int the extra ellular spa e. T is is the m st mm n type edema seen lini ally and may be aused by trauma, brain tum r, in e ti n, and surgery. Ster ids may aid in the redu ti n vas geni edema.

EVALUATING THE NEUROSURGICAL PATIENT Initia l Ma na g e m e nt I. Pa tie nt’s his tory: Imp rtant; timing the nly lues in ertain diagn ses.

sympt ms al ng with amily hist ry

II. Vita l s ig ns : All vital signs are ntr lled by CNS me hanisms. Bl respirati n an be help ul in l alizing a lesi n. A. Hypertension/bradycardia (Cushing triad): devel ps late in brain injury when irreversible neur l gi hanges may have already urred B. Hypotension: may be due t l ss vas ular t ne se ndary t l ss sympatheti ntr l, whi h may be se ndary t hyp thalami , medullary, r spinal rd injury (SCI) III. Coa gula tion s ta tus : Use antiplatelets r anti agulants sh uld be assessed al ng with pr thr mbin time (P )/internati nal n rmalized rati (INR), partial thr mb plastin time (P ), and platelet levels.

Ne uro lo g ic Exa m ina tio n I. Le ve l o c ons c ious ne s s (LOC): Sh uld be determined f rst. Patients may present as alert (wide awake), lethargi (sleepy but easily ar usable), stup r us (resp nsive nly t n xi us stimuli), r unresp nsive (n resp nse t n xi us stimuli). II. Eye e xa m ina tion: Pupils are examined r their size, symmetry, and rea ti n t light. Eye p siti n and m vements are assessed t aid in l alizing the lesi n. Fundus pi exam assesses papilledema. A. Cortical lesion: Pupil size may be n rmal, but r ving eye m vements r gaze deviati n are p ssible. B. Midbrain or oculomotor lesion: may pr du e a unilateral dilated, n nrea tive pupil with the eye deviated d wnward and utward C. Pons lesion: May be ass iated with pinp int pupils (1 mm); h wever, this an als be seen with nar ti sedati n. III. Bra in s te m re f e xe s : Che k ugh, gag, rneal, and ul ephali (d ll’s eye) ref exes and the al ri ( ul vestibular) resp nse t rule ut brain stem damage.

neur l gi disease may be

d pressure, pulse rate, and

Quic k Cut Patients with intracranial hemorrhage or who require neuros urgical procedures s hould have coagulation parameters normalized or ris k atal bleeding.

Quic k Cut A detailed neurologic evaluation s hould be per ormed on all patients . When this is not pos s ible in emergency s ituations or in a comatos e patient, a brie examination will have to s u f ce.

Quic k Cut Brain s tem re exes are very important when examining a comatos e patient becaus e the comatos e patient cannot provide in ormation on higher levels o unction.

IV. Mo to r e xa m ina tio n: In a mat se patient, it may nly be p ssible t assess the resp nse t pain ul stimuli. Decorticate (f exor) r decerebrate (extensor) p sturing help determine l ati n and severity injury. V. Se ns o ry le ve l d e te rm ina tio n: imp rtant in spinal

rd lesi ns

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Chapter 27

Head Injury

VI. De e p te nd o n re f e xe s a nd p la nta r re s p o ns e s : he ked t distinguish a l wer m t r neur n lesi n r m an upper m t r neur n lesi n

HEAD INJ URY Cla s s i c a tio n I. Bra in injurie s : urring a er trauma an be lassi ed as the ll wing: A. Primary: urring instantane usly at the time impa t B. Secondary: resulting r m a hain events triggered by the initial injury by is hemia, hyp xia, and ell-mediated death II. He a d injurie s : an be ateg rized as the ll wing: A. Closed head injury: Brain injury with n eviden e s alp la erati n r ra ture. May result r m high speed, n nimpa t trauma due t rapid brain a elerati n/de elerati n. B. Blunt head injury: With r with ut s alp la erati n r m impa t with a blunt bje t; all s alp la erati ns must be expl red i there is a skull ra ture present. C. Penetrating head injury: se ndary t bullet r kni e w und

Quic k Cut Trauma is the leading caus e o morbidity and mortality in young individuals in the United States .

Quic k Cut In the majority o trauma atalities , head injury is a primary determinant o outcome.

Initia l Ma na g e m e nt a nd As s e s s m e nt I. Im m e d ia te c a re : is n t di erent r head trauma vi tims r m that any ther injured patient and sh uld be in a rdan e with advan ed trauma li e supp rt (A LS) guidelines (see Chapter 22) II. Ra d io g ra p hic s tud ie s A. Head computed tomography (CT) scans: Sh uld be per rmed n all patients with suspe ted head trauma. Diagn sti ndings in lude the ll wing. 1. Hematomas: an be easily diagn sed be ause the way bl d appears, relative t the brain a. Hyperdense: a ute with n rmal hem gl bin b. Isodense: suba ute c. Hypodense: hr ni r a ute with a l w hem gl bin level 2. Epidural hematomas: appear as nvex (lens-shaped) lle ti ns, whi h typi ally d n t r ss suture lines and are usually ass iated with an verlying skull ra ture 3. Acute subdural hematomas (SDHs): Have a n avity t ward the brain and n rm t the shape the brain Quic k Cut sur a e; they may r ss suture lines. All trauma patients 4. Cerebral edema: an be assessed by the size the ventri les, with a s us pected head basal subara hn id isterns, l ss sul i at the nvexity, and injury s hould have head and cervical s pine CT s cans . degree midline shi B. Magnetic resonance imaging (MRI): an sh w damage when a C head s an result is n rmal in a patient with signi ant neur l gi de its 1. Di use axonal injury (DAI): Due t ax nal shearing, injuries are imaged better with MRI mpared t C . 2. Location: T ese lesi ns ur requently in the rpus all sum, sub rti al white matter, and brain stem. C. Cervical spine CT scans (with sagittal and coronal reconstructions): taken t rule ut ass iated spinal injuries 1. Cervical spine racture or neurologic de cit re erable to the cervical spine: absolute contraindication r imm bilizati n devi e ( ervi al llar) rem val r per rman e f exi n/extensi n views 2. Flexion/extension views: In the absen e ervi al ra ture r ervi al spinal rd de it, these may be required t rule ut ligament us injury. D. Cervical spine MRI: In the patient wh has been mat se r l nger than 2 weeks, this an be use ul t assess r ligament us injury, dis herniati n, r SCI.

Inc re a s e d Intra c ra nia l P re s s ure Ma na g e m e nt I. Go a l: Redu e CSF, brain, r bl d v lume within the skull. A. Head elevation: Pr m tes ven us drainage, thereby de reasing ICP. Als , keeping the patient’s head straight pr m tes drainage thr ugh the bilateral jugular veins.

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B. Hyperventilation: Rapidly helps l wer ICP. T e erebral Quic k Cut vessels resp nd qui kly t de reasing the arterial Pco 2, ausing Hyperventilation is vas nstri ti n; the Pco 2 is maintained between 30 and 35 mm Hg. not a long-term option or ICP C. Sedation and paralysis: Blunting the in reases in ICP seen with control. agitati n and m vement; h wever, this als mpr mises the ability t assess the patient’s neur l gi status. T ere re, sh rta ting agents su h as pr p l and entanyl are re mmended. Paralyti s may be a last res rt. D. Increasing the serum osmolality (to 310–320 mOsm): De reases ICP by pulling f uid ut the brain. Serum sm lality and ele tr lytes have t be measured every 6 h urs. 1. Hyperosmolar agents (e.g., mannitol): Administered intraven usly (IV) with a b lus 1.0 g/kg ll wed by in usi n 25–50 g every 4–6 h urs. E e ts an be seen in 5–20 minutes. 2. Diuretics: su h as ur semide 3. Hypertonic saline: elevates the patient’s s dium (n greater than 155 mEq/L) t pull f uid away r m the brain E. Ventriculostomy: an rapidly de rease a patient’s ICP, parti ularly i hydr ephalus is present, via CSF rem val F. Barbiturates: May be used i all the previ usly menti ned e rts ail t l wer the ICP. T ey w rk by de reasing brain metab lism and there re intra erebral bl d v lume; h wever, they are als ass iated with hyp tensi n, whi h an w rsen brain injury. day, they are nly given t sele t patients. G. Decompressive craniectomy: Rem val part the skull all ws the brain t expand and is used when the a rementi ned medi al therapies have ailed. II. ICP m o nito r: Pla ement is ne essary t evaluate the neur l gi Quic k Cut status and ICP therapy in the un ns i us patient. Maintenance o A. Criteria or placement: Glasg w C ma S ale (GCS) s re 8 adequate CPP prevents r less in a patient with an abn rmal head C or GCS less than 8, irrevers ible is chemic injury. a n rmal head C , age lder than 40 years, hyp tensive, and/ r has de erebrate/de rti ate p sturing B. Devices 1. Ventriculostomy (intraventricular catheter [IVC] or external ventricular drain [EVD]): G ld standard, giving the m st a urate measurement; all ws CSF rem val t help l wer the ICP. T ere is a risk hem rrhage and in e ti n, espe ially with pr l nged use. Quic k Cut 2. Intraparenchymal monitors/subarachnoid monitors: FiberA ventriculos tomy pti ICP pr bes use ul when a ventri ul st my atheter provides cons tant monitoring o ICP and allows or ann t be pla ed. S metimes they s rew int the skull via therapeutic drainage. a b lt me hanism. T ey have a l wer risk in e ti n and paren hymal hem rrhage mpared t IVC. III. Co ns um p tive c o a g ulo p a thy: Severe brain injury auses release tissue thr mb plastin, whi h a tivates the extrinsi l tting pathway and an lead t abn rmalities in l tting and even disseminated intravas ular agul pathy (DIC). T e patient’s P /INR, P , and platelet levels sh uld be m nit red and rre ted a rdingly.

Quic k Cut

Patients with IV. Se izure p ro p hyla xis : Risk p st-traumati epilepsy rrelates evidence o intracranial with severity and l ati n underlying brain injury. hemorrhage s hould receive A. Risk actors: subdural, epidural, r intraparen hymal s eizure prophylaxis or at ( ntusi n) hem rrhages; depressed skull ra ture; GCS less than leas t 1 week. 10; and penetrating brain injury B. Phenytoin: Give 1.0 g IV r by m uth as l ading d se, ll wed by 300 mg per day. D se r hildren is 10 mg/kg initially, ll wed by maintenan e at 5 mg/kg per day. C ntinue r 7 days, unless the patient has had a seizure.

Sc a lp Injury Ma na g e m e nt I. Sc a lp : Highly vas ular; patients an l se large v lumes bl d i la erati ns are n t pr mptly addressed. II. De b rid e m e nt: T r ughly debride pri r t l sure, espe ially i a skull ra ture is present.

Quic k Cut Pos t-traumatic epileps y may res ult rom s evere brain injury.

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Chapter 27

Head Injury

III. Fra c ture s : an be lassi ed as ll ws: A. Linear, stellate, or comminuted: des ribe mplexity the ra ture line B. Depressed ractures: have a skull p rti n that is displa ed inward C. Compound ractures: Overlying s alp is la erated. D. Basilar ractures: raverse the base the skull; patients may have e hym sis behind the ear (Battle sign), whi h may be ass iated with t rrhea r hem tympanum. Anteri r basilar ra tures result in peri rbital e hym sis (ra n’s eyes) and p ssibly rhin rrhea. IV. Op e ra tive inte rve ntio n A. Depressed skull ractures: May be ass iated with dural tear and underlying brain damage. Depressed skull ra tures greater than 1 m are usually surgi ally elevated. B. Compound ractures: require a th r ugh debridement and l sure t prevent subsequent in e ti n

Tra um a tic Ce re b ro s p ina l Fluid Le a ks I. Dia g no s is : Assess the f uid r beta-2 trans errin; i bl d is mixed with the CSF, all w s me t drip nt a gauze and assess r the “halo sign.” II. P o s t-tra um a tic CSF s tula s : Ninety- ve per ent l se sp ntane usly with nservative management, whi h in ludes elevating the head. A. Lumbar CSF drain: pla ed in s me ases t divert CSF drainage and pr m te stula healing Quic k Cut B. Craniotomy with closure o the dural de ect: may be ne essary Mos t traumatic CSF i lumbar drainage ails leaks res olve without s urgical C. Broad spectrum, prophylactic antibiotics: re mmended t intervention. prevent ass iated in e ti n

Tra um a tic Intra c e re b ra l He m o rrha g e s a nd Ce re b ra l Co ntus io ns I. Intra c e re b ra l he m a to m a s : result r m vessel tearing in white matter and are due t penetrating trauma r a elerati n–de elerati n injuries II. Ce re b ra l c o ntus io ns : Super ial hem rrhages ur when the anteri r temp ral and r ntal l bes strike the r ugh edges the tent rium r skull. A. Coup injury: urs when the skull strikes the brain underlying the site impa t B. Contrecoup injury: O urs dire tly pp site t the impa t site when the brain strikes the inner table the skull n the pp site side al ng the r e ve t r. T us, i a pers n were stru k n the ba k the head, the up injury w uld be t the ipital l be and the r nt temp ral tips w uld sustain the ntre up injury. III. Ma na g e m e nt: ypi ally nsists m nit ring the patient l sely in the intensive are unit (ICU) and repeating the C s an t assess r hanges. Surgi al de mpressi n may be ne essary when in reased ICP be mes re ra t ry t medi al management r i the hemat ma signi antly expands.

Extra -a xia l He m o rrha g e s I. Epidura l he m a tom a : lle ti n bl d between the b ne and dura, Quic k Cut usually arterial origin (high pressure), aused by la erati n the Epidural hematomas middle meningeal artery with an ass iated ra ture temp ral b ne are convex (lens -s haped) A. Less common etiologies: Bleeding r m the middle meningeal on CT and are caus ed by dis ruption o a meningeal vein r dural ven us sinus. Y unger patients are at higher risk artery. be ause their dura are less adherent t the inner table the skull. B. Diagnosis: Classi ally, patients present with a lucid interval. T e patient is kn ked ut immediately a er injury ( n ussi n e e t), then regains ns i usness but has a heada he, and then l ses ns i usness ver minutes t h urs as the hemat ma expands and reates mass e e t (h wever, this presentati n is seen in nly 10%–15% ases). C. Head CT: hara teristi appearan e a nvex, lens-shaped high density adja ent t b ne D. Treatment: Very small epidural hemat mas with ut lini al de its an be nservatively managed with serial C s ans and l se lini al bservati n. Sedati n sh uld be minimized be ause this may alter the patient’s neur l gi exam. T se that are ass iated with neur l gi de its r that ause mass e e t must be eva uated.

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B

A

Fig ure 27-4: Contras t-enhanced CT s can o extra-axial hematomas . A: Epidural hematoma. Note the lenticular s hape. B: Subdural hematoma on the patient’s right s ide. Note the cres cent s hape o the hematoma. (From Haines DE. Neuroanatomy in Clinical Context. Wolters Kluwer; 2014.)

II. SDH: lle ti n a ute r hr ni bl d that a umulates between Quic k Cut the dura and the ara hn id Acute SDHs are A. Etiology: ypi ally r m disrupted bridging veins between the concave (cres cent-s haped) dura and the rti al sur a e. Older patients are at an in reased on CT and are caus ed by risk due t brain atr phy ausing in reased vulnerability t the dis ruption o bridging veins . bridging veins. Chronic SDH an als devel p r m membranes rmed r m hemat ma breakd wn. B. Acute SDH: Presents as an ev lving and expanding mass lesi n. O en, mental status deteri rates with w rsening neur l gi de its. 1. Diagnosis: On C , a hyperdense n ave mass is present between the brain and the skull (Fig. 27-4). 2. Treatment: i de reased mentati n r al neur l gi sympt ms, usually requires rani t my and l t eva uati n C. Chronic SDH: en a subtle, sl w, pr gressive deteri rati n (e.g., heada he, hemiparesis, aphasia) ver weeks r m nths, whi h en presents as dementia in the elderly patient 1. Diagnosis: On C s an, the n ave mass appears either is dense r hyp dense depending n the hr ni ity the hemat ma; 50% are bilateral. 2. Treatment: Can en be treated initially with burr h le drainage the l t; rea umulati n an require rani t my r de nitive drainage and rem val the membranes.

SP INAL CORD INJ URY Ove rvie w I. Ep id e m io lo g y: 4:1 prep nderan e SCI am ng males t emales A. Cause: M st ur as the result m t r vehi le llisi ns and alls. B. Incidence: One milli n pe ple have traumati SCI ea h year in the United States.

Quic k Cut SCI is one o the leading caus es o death and dis ability in the f rs t decades o li e.

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II. Exte nt o injury: depends n the m rph l gy and the l ati n the ra ture, the presen e pre-existing degenerative disease (e.g., ngenital anal sten sis, herniated dis s, r ligament us hypertr phy), and the patient’s age and ass iated systemi injuries III. Cla s s i c a tio n: mplete r in mplete Quic k Cut A. Complete SCIs: N m t r r sens ry un ti n bel w the level Complete SCI the injury (in luding re tal). T is has a dismal pr gn sis; patients have no motor or s ens ory unction below the 1% exhibit signi ant re very i sympt ms remain r level o the injury. 24 h urs. B. Incomplete SCIs: Rapid surgi al de mpressi n may help rest re un ti n in these patients. Spe i SCI syndr mes in lude the ll wing. 1. Central cord injury: Results r m a n ussive bl w t Quic k Cut The hallmark the rd, typi ally in patients with pre-existing sten sis. pres entation o SCI is De its in the upper extremities are greater than in the l wer pres ervation o light touch, extremities and peripheral mus ulature (e.g., the hands) are pos ition s ens e, and vibration. usually m re severely a e ted than pr ximal mus ulature (e.g., the sh ulders). 2. Anterior SCI: Usually inv lves damage t the anteri r spinal artery, resulting in in ar ti n r is hemia the anteri r tw Quic k Cut thirds the rd. Signi ant mus le weakness is seen. The hallmark 3. Brown-Séquard syndrome: typi ally urs r m hemise ti n pres entation in Brownthe rd a er penetrating trauma

Ma na g e m e nt I. Sp ine im m o b iliza tio n: Patients sh uld be put in a hard ervi al llar and n a hard b ard in the eld be ore the patient is trans erred t the h spital. II. P ro p e r tra ns e r te c hniq ue s : L g-r lling and s p stret hers while maintaining ervi al tra ti n ensure that ull spinal pre auti ns are being maintained. III. Sta b iliza tio n: A LS pr t ls (A, B, C, D, E) apply. A. Complete SCI: Patient may n t eel pain ass iated with a br ken limb r with an internal hem rrhage. B. Vital signs: Observati n is riti al. C. Cervical or high thoracic SCIs: Patients may have neur geni sh k se ndary t interrupti n the sympatheti pathways. 1. Signs: T ese patients will devel p hyp tensi n in ass iati n with brady ardia, se ndary t un pp sed vagal t ne. 2. Management: Patients en require v lume resus itati n and may als need press r agents. IV. Ne uro lo g ic e va lua tio n: Emergen y medi al pers nnel may dis l se whether the patient ever exhibited m t r un ti n. A. Detailed motor and sensory exam: must be assessed in all ur extremities t determine m t r and sens ry level B. Ref exes: Sa ral ref exes are imp rtant be ause sparing the sa ral segment the rd—pr gn sis r re very is better i the patient exhibits sa ral sparing. Abd minal, remasteri , and sphin teri ref exes (e.g., bulb avern sus and anal twit h) must als be assessed. V. Ra d io g ra p hic s tud ie s : Patients with suspe ted injury require ervi al spine imaging. A. CT scan: Sagittal and r nal re nstru ti ns are re mmended. Ba k pain r neur l gi sympt ms l alizing t the th ra i and lumb sa ral spine may require additi nal C imaging.

Séquard s yndrome is ips ilateral los s o motor unction, light touch, and vibration with a contralateral los s o pain and temperature.

Quic k Cut About 15% o patients s u er s ome improper manipulation o the s pine be ore they arrive at the hos pital.

Quic k Cut Methylprednis olone has not been s hown to improve outcomes in SCI and is as s ociated with complications .

Quic k Cut Any trauma patient with neck pain, neurologic def cit, or a high-ris k mechanis m o an injury s hould be cons idered to have a cervical cord injury.

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B. MRI: I a b ny abn rmality is identi ed with C s an, an additi nal evaluati n with MRI may be ne essary, whi h an reveal spinal rd abn rmalities and extra-axial abn rmalities (e.g., epidural hemat ma, ruptured dis , r ligament us injury). C. CT myelogram o the spine: may be ne essary in patients with ntraindi ati ns t MRI (e.g., ardia pa emaker) VI. Tre a tm e nt A. Immobilization: N n perative management is p ssible i the ra ture is n t severe, alignment is preserved, and neural elements are n t mpressed. 1. Minor ractures or ligamentous injuries: hard ervi al llar 2. More complex ractures: may heal by the patient wearing a hal devi e r at least 3 m nths B. Open reduction and internal xation: de nitive management r unstable spine ra tures 1. Immediate surgical intervention: required in patients with in mplete SCI and in patients wh exhibit pr gressive neur l gi deteri rati n with an MRI s an suggestive spinal rd r nerve r t mpressi n 2. Fusion: all ws patients t be m re qui kly m bilized and rehabilitated, whi h de reases m rbidity r m mpli ati ns se ndary t SCI VII. Co m p lic a tio ns : Patients with SCIs an su er r m several Quic k Cut pr blems. Patients with SCI A. Hypotension: in the a ute setting have many complications , B. Ileus: an last 10–14 days which contribute to morbidity and mortality. C. Renal: st nes, pyel nephritis, and renal ailure D. Deep venous thrombosis (DVT): an lead t pulm nary emb lus (PE) 1. DVT prophylaxis: C mpressi n b ts are imperative. O en, patients als re eive IVC lters. 2. Medical: T ese patients are als pla ed n a pr phyla ti regimen sub utane us r l w-m le ular-weight heparin. E. In ections: urinary tra t in e ti ns, pneum nia, and r m de ubitus ul ers

Intra c e re b ra l He m o rrha g e I. Hyp e rte ns ive intra c e re b ra l he m o rrha g e : Als kn wn as Quic k Cut hemorrhagic stroke, these ur within the brain paren hyma, Intracerebral usually at the site smaller, per rating arteri les. hemorrhage is les s common A. Locations: basal ganglia, thalamus, erebellum, and p ns than is chemic s troke but has B. Diagnosis: Usually, a hist ry l ng-standing hypertensi n a wors e prognos is . and a relatively sudden nset al neur l gi de its, with r with ut de reased mentati n. T ese patients typi ally have heada he. 1. Unenhanced CT scan: Study h i e; di erentiates r m is hemi str ke, whi h may present similarly; h wever, the treatment is quite di erent. 2. Blood counts and coagulation unction: sh uld be rre ted 3. Vascular imaging: May rule ut ther auses hem rrhage (vas ular mal rmati ns, aneurysms). C ntrasted MRI will evaluate r tum rs and avern us mal rmati ns. C. Treatment: typi ally supp rtive by ntr lling hypertensi n and rre ting any bleeding dis rder t prevent l t expansi n and urther neur l gi de line 1. Supratentorial hemorrhages: M st are ass iated with signi ant de its. Surgery is reserved nly r th se in reas nable nditi n with surgi ally a essible lesi ns. 2. In ratentorial hemorrhages: requently require emergent eva uati n t prevent brain stem mpressi n II. Va s c ula r m a l o rm a tio ns : ypi ally present with either hem rrhage r seizure. Hem rrhages an present as intra erebral r subara hn id with a ute neur l gi hanges and heada he. A. Types 1. Arteriovenous mal ormation (AVM): M st mm n type; mp sed shunts between vessels. N rmal brain is n t usually seen. 2. Telangiectasia: Capillary tu s are separated by n rmal brain mm nly in the p ns; it is unlikely t bleed.

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3. Cavernous mal ormations (cavernomas): Pa ked sinus idal vessels with ut n rmal brain that an ur anywhere in the brain and are en multiple. Familial rms have been d umented. 4. Developmental venous anomalies: Extensive ven us netw rks and a n rmal variant ven us drainage. T ese are benign lesi ns but may be ass iated with avern mas. B. Diagnosis 1. Noncontrasted CT scan: rst study t rder in any patient Quic k Cut with a ute neur l gi hanges Conventional 2. Vascular imaging: Ne essary whenever a vas ular angiogram is the gold mal rmati n is suspe ted. C nventi nal angi gram is the s tandard in vas cular imaging. standard; C and magneti res nan e angi gram are used m re requently. C. Treatment: depending n the size and l ati n the mal rmati n, may in lude surgery, end vas ular emb lizati n, and radi surgery ( r a mbinati n) in additi n t the ll wing: 1. Ventriculostomy: may be required t ntr l in reased mass e e t and ICP, espe ially i bl d has leaked int the ventri les and hydr ephalus is present 2. Hypertension: sh uld be managed aggressively 3. Seizure activity: treated r pr phylaxed III. Othe r c a us e s : Ass iated with ther disease pr esses, su h as a brain tum rs (e.g., renal ell ar in ma, melan ma), erebral vas ulitis, anti agulati n therapy, bl d dys rasias (e.g., thr mb yt penia, leukemia), systemi lupus erythemat sus, r Sturge-Weber syndr me. C ntrasted MRI s an may be help ul.

Sub a ra c hno id He m o rrha g e I. Ca us e : M st mm nly aused by head trauma; h wever, it may Quic k Cut als be sp ntane us (e.g., aneurysm r AVM). Trauma is the mos t A. Spontaneous SAH due to aneurysm rupture: Usually ass iated common overall caus e o with sudden, severe heada he (w rst heada he li e), v miting, s ubarachnoid hemorrhage sti ne k, ph t ph bia, altered mental status, and s metimes a (SAH). Aneurys ms are the mos t common caus e o hist ry an earlier severe s - alled “herald heada he.” Certain s pontaneous SAH. aneurysms are ass iated with spe i neur l gi ndings. 1. Posterior communicating artery aneurysm: ass iated with CN III palsy 2. Internal carotid–ophthalmic aneurysm: ass iated with Quic k Cut m n ular visual eld ut All patients B. Diagnosis: C dem nstrates nearly 90% all SAH. raumati complaining o an acute, SAH is typi ally seen n the rti al sur a e, whereas aneurysmal s evere headache s hould be evaluated or SAH with a SAH is n entrated in the basilar isterns ( ir le Willis). CT s can. 1. Negative CT: i n mass e e t, sa e t pr eed with LP, whi h may dem nstrate high red bl d ell unt and xanth hr mia 2. Positive CT or LP: Angi gram will be needed t determine the number aneurysms (15% have multiple aneurysms) and whether a rrelati n exists between aneurysm size/shape and risk rupture. 3. Repeat angiogram: Fi een per ent patients d n t exhibit an angi graphi ally identi able s ur e SAH and need an ther n e the subara hn id bl d has dissipated. II. Typ e s A. Berry aneurysms: m st mm n; weak areas the bl d vessel wall, typi ally at a bi ur ati n B. Mycotic aneurysms: arise se ndary t in e ti n, mm nly end arditis C. Atherosclerotic aneurysms: rm e tati r usi rm dilati n III. Tre a tm e nt: Pr mpt treatment ruptured aneurysms is required, as they have the pr pensity t rehem rrhage, parti ularly in the rst 2 weeks. A. Craniotomy and surgical clipping: Standard management Berry aneurysms. A small metalli lip is pla ed at the ne k t deny f w t the weakened, dilated d me. B. Endovascular obliteration: Fast be ming a main treatment pti n, parti ularly in l ati ns di ult t a ess surgi ally. Small metal ils are ed int the aneurysm d me thr ugh

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A

B Fig ure 27-5: Oblique cerebral angiogram. A: Right intracranial aneurys m. B: A ter an endovas cular coiling o the aneurys m, there is no longer any ow to the aneurys m dome.

angi graphi ally guided mi r atheters (Fig. 27-5). T e bvi us risk this te hnique is vessel per rati n with atastr phi nsequen es. C. ICU: SAH patients require extensive are t address a h st pr blems, su h as hypertensi n, hyp natremia, ardia arrhythmias, vas spasm, str ke, and hydr ephalus. D. Antibiotic therapy: an res lve my ti aneurysms IV. P ro g no s is : Rate hem rrhage r m an unruptured aneurysm is 1%–3% per year; 10%–15% patients die be re they rea h h spital are, and an ther 40%–50% die during their a ute h spitalizati n. O th se surviving patients, 50% are able t return t their rmer li estyle; the rest survive with impairment.

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CENTRAL NERVOUS SYSTEM TUMORS Ove rvie w I. Ove ra ll inc id e nc e : 10,000–13,000 new brain tum r ases in the Quic k Cut United States per year; 4,000 ases spinal rd tum rs Brain tumors are the mos t common s olid tumors in II. Bim o d a l d is trib utio n: r the requen y brain tum rs the pediatric population. A. First age peak: urs in hildh d (age 3–10 years) 1. Location: Fi y per ent pediatri brain tum rs ur in the p steri r ssa, and 50% are supratent rial. 2. Common brain tumors in children: pil yti astr yt ma, medull blast ma, rani pharyngi ma, and brain stem gli ma B. Second age peak: O urs in the sixth de ade; 75% adult brain tum rs are supratent rial. C mm n adult brain tum rs in lude metastasis, malignant gli mas, meningi mas, and pituitary aden mas. III. Cla s s i c a tio n: N men lature r CNS is en n using; m st are named based n their ellular rigin. A. Glial tumors (gliomas): nstitute nearly 50% brain tum rs; Quic k Cut derive r m glial cell lines GBM is the mos t 1. Histologic grading: in reasing malignan y r m l w-grade common adult primary brain astr yt ma t anaplasti astr yt ma t gli blast ma tumor. multi rme (GBM) 2. Other types: Glial tum rs als in lude lig dendr gli mas and ependym mas. B. Nonglial cell tumors: meningiomas (whi h arise r m ara hn id ells), schwannomas ( r m S hwann ells), medulloblastomas ( r m primitive neur e t dermal remnants), pituitary tumors ( r m h rm nal ells in the pituitary gland), pineal tumors ( en r m germ ells), and tum rs arising r m the bl d vessels (hemangioblastomas and metastatic tumors)

Dia g no s is I. P re s e nta tio n: Patients present with sympt ms via several Quic k Cut me hanisms. The more eloquent A. Mass e ect: Brain and spinal rd are relatively int lerant the region where the tumor spa e- upying lesi ns, whi h mpete with n rmal tissue within aris es , the more dramatic the the rigid skull r spinal anal—again, CNS tissues are mu h m re patient’s s ymptoms . t lerant sl w-gr wing lesi ns than rapid v lume hange. B. Eloquence: um rs in el quent areas the brain be me sympt mati early. C. Blood vessel compression: May deprive n rmal areas the CNS r m vital nutrients. Highly metab li tum rs may als “steal” bl d r m surr unding brain. D. Metabolic impairment: Chemi al messengers pr du ed an inter ere with n rmal “h st” brain un ti n. E. Seizures: aused either by dire t me hani al irritati n r by a e ting n rmal brain metab lism F. CSF outf ow obstruction: leads t hydr ephalus II. Ne uro lo g ic e va lua tio n: L k r a hist ry a ute nset r pr gressive neur l gi de its; asymmetry may aid in l alizati n, and an examinati n that indi ates spe i l bar dys un ti n is highly suspi i us r a al lesi n, su h as a brain tum r. III. Ad d itio na l s tud ie s : Required t hara terize the lesi n. C ntrasted C and MRI s ans must dem nstrate disrupti n the BBB (a requent mani estati n in the vi inity a tum r).

Sp e c i c Bra in Tum o rs I. As tro c yto m a s : M st mm n brain tum r in adults; they are sl w-gr wing and in ltrating with p rly de ned b rders. A. Peak incidence: during the urth de ade li e B. Clinical presentation: seizures, heada hes, in reased ICP, and al neur l gi de its C. Imaging: C and MRI s ans sh w irregular n nh m gene us enhan ement with edema surr unding the tum r (Fig. 27-6).

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D

Fig ure 27-6: A–D: MRI o glioblas toma multi orme. The borders o this les ion enhances brightly with contras t. The arrows point to the hypointens e core s ignif es central necros is (a s ign o aggres s ivenes s ).

D. Treatment: hem therapy as well as the ll wing: 1. Aggressive surgical resection: H wever, mplete rese ti n is nearly imp ssible given the in ltrative nature the tum r. 2. Radiation therapy: p ssibly in luding high-d se radi surgery t the site the tum r E. Prognosis: Highly rrelated with hist l gi grade; h wever, age, m rbidities, and neur l gi insult play a r le. II. Ep e nd ym o m a s : generally well- ir ums ribed tum rs that ur in the vi inity ventri les; may metastasize t ther l ati ns thr ugh the CSF A. Clinical presentation: en in ludes in reased ICP, hydr ephalus, and ther al neur l gi sympt ms B. Imaging: C ntrasted MRI r C s an sh ws an irregularly enhan ing lesi n with a well-de ned b rder in the vi inity the ventri le. Additi nal imaging the entire neuraxis is imp rtant t rule ut metastasis. C. Treatment: aggressive surgi al rese ti n and radiati n D. Prognosis: Median survival is 5 years. III. Olig o d e nd ro g lio m a s : sl w-gr wing gli mas that en have al i ati n A. Clinical presentation: m st mm nly seizures; en a al neur l gi de it B. Imaging: C and MRI s ans reveal al i ed areas in nearly 40%–50%.

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C. Treatment: rese ti n, with r with ut radiati n therapy D. Prognosis: Survival rate is 3–10 years depending n grade. IV. Me ning io m a s : Arise r m the ara hn id layer the meninges and a unt r 15% intra ranial ne plasms. Lesi ns are usually adja ent t the dura with a well-de ned b rder and mpress (rather than invade) the brain. Meningi mas are very sl w gr wing and may be me in redibly large be re pr du ing sympt ms. A. Clinical presentation: heada he, al neur l gi de its, and seizures B. Imaging: C and MRI s ans reveal h m gen us, intensely enhan ing mass and a well-demar ated b rder with n rmal tissue (Fig. 27-7). C. Treatment: surgi al ex isi n, alth ugh stere ta ti radi surgery an be used r di ult t rea h lesi ns D. Prognosis: Usually g d; h wever, a t rs su h as l ati n, extent rese ti n, and grade uld reate a p rer pr gn sis. V. Me ta s ta tic tum o rs : Appr ximately 20% an er patients will Quic k Cut devel p intra ranial metastases, m st mm nly r m the lung, Metas tatic brain breast, kidney, and melan mas. tumors are common and A. Clinical presentation: in reased ICP, bstru tive hydr ephalus, typically pres ent as multiple al neur l gi de it, and sp ntane us intra erebral hem rrhage enhancing les ions on MRI. B. Imaging: C and MRI s ans reveal multiple well- ir ums ribed, enhan ing masses surr unded by erebral edema. C. Treatment: rese ti n i the lesi n is s litary r the hist l gy is in questi n, ster ids, and wh le-brain radiati n D. Prognosis: With treatment, 50% patients with a single intra ranial metastasis will live r 1 year a er diagn sis.

Fig ure 27-7: T2 -weighted coronal MRI s hows le t s phenoid wing meningioma. (From Penne RB. Wills Eye Institute—Oculoplastics, 2nd ed. Philadelphia: Lippincott Williams & Wilkins ; 2011.)

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VI. Me d ullo b la s to m a s : Malignant tum rs the erebellum and the urth ventri le r m primitive neur e t dermal ells. T ese tum rs present during the rst and se nd de ades li e, with a male pred minan e. A. Clinical presentation: erebellar and brain stem dys un ti n, hydr ephalus, and in reased ICP B. Imaging: C ntrasted C and MRI s ans dem nstrate a n nh m gen us, enhan ing midline mass usually adja ent t r in the urth ventri le. C. Treatment: Extensive surgi al rese ti n and radiati n therapy t the site and the entire neuraxis t prevent CSF seeding. Radiati n therapy ann t always be used in y ung hildren, and hem therapy remains the treatment h i e a er surgery. D. Prognosis: 5–10 year survival but highly dependent n age, extent rese ti n, and sensitivity t hem radiati n VII. He m a ng io b la s to m a s : m st mm n primary intra-axial tum r Quic k Cut in the p steri r ssa in adults; an be ass iated with v n HippelCerebral Lindau disease (al ng with hemangi blast mas in ther rgans) hemangioblas tomas may be A. Clinical presentation: Cerebellar dys un ti n and p ssibly as s ociated with von Hippelhydr ephalus; 10% patients have erythr yt sis se ndary t Lindau dis eas e. erythr p ietin se reti n r m the tum r. B. Imaging: C and MRI s ans usually reveal an enhan ing mural n dule within a yst, and angi graphy reveals an intense vas ular blush. C. Treatment: Surgi al rese ti n is the treatment h i e. D. Prognosis: generally g d VIII. Ve s tib ula r s c hwa nno m a s (a c o us tic ne uro m a s ): arise r m the vestibular p rti n CN VIII A. Clinical presentation: T ese benign tum rs usually present with tinnitus, hearing l ss, and ev lving unsteadiness. CN VII may be mpr mised, leading t a ial weakness. B. Imaging: Enhan ed C and MRI s ans en dem nstrate the a usti neur ma arising r m the internal audit ry meatus. C. Evaluation: Brain stem audit ry ev ked p tentials and audi metri testing are very use ul r evaluating these lesi ns. D. Treatment: rese ti n, stere ta ti radi surgery, r b th E. Prognosis: Related t tum r size and extent rese ti n. B th hearing preservati n al ng with a ial nerve un ti n are imp rtant in determining treatment and pr gn sis.

P ituita ry Tum o rs I. Clinic a l p re s e nta tio n: Pituitary tum rs tend t present in several ways. A. Mass e ect: T r ugh mpressi n the pti hiasm. Classi ally, the patient presents with bitemp ral hemian psia. Quic k Cut B. Endocrinopathy: H rm nal ver- r underpr du ti n ausing Large pituitary Cushing syndr me (se ndary t ex ess adren rti tr pi tumors clas s ically produce h rm ne se reti n), a r megaly (se ndary t ex essive gr wth bitemporal hemianops ia. h rm ne se reti n), hyperpr la tinemia, r hyp pituitarism. H wever, 30% patients have a n nse reting aden ma. C. Apoplexy: T is is an a ute hem rrhage int a pituitary tum r. C mm nly, these patients will have heada he, impaired visi n, extra ular mus le dys un ti n, and end rin pathy. II. Dia g no s tic te s ts A. Laboratory analysis: the pituitary-related h rm nes B. Contrasted CT and MRI scans: dem nstrate the tum r al ng with the surr unding brain stru tures and b ny anat my III. Tre a tm e nt A. Prolactin-secreting adenomas: Medi al therapy, su h as bromocriptine (a d paminergi ag nist), is the rst-line therapy. B. Surgical resection: reatment h i e r m st n n–pr la tin-se reting tum rs and pr la tin mas that are pr gressively sympt mati despite medi al therapy. T is is espe ially true r tum rs mpressing the pti hiasm with visual eld de its. 1. Tumors with little suprasellar extension: End s pi trans-sphen idal r ute (nasal r sublabial) an be used. 2. Larger tumors: Crani t my may be required.

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C. Stereotactic radiosurgery: may be used as an adjun t a er partial surgi al rese ti n and is e e tive in ntr lling 90% pituitary aden mas that remain a er surgery

CONGENITAL NERVOUS SYSTEM LESIONS Sp ina l Dys ra p his m I. Sp ina b i d a : results r m ailure the vertebral ar hes t use A. Diagnosis: It may be t tally asympt mati and be und in identally n spinal radi graph (spina bi da ulta), r it may be sympt mati . B. Associated congenital anomalies: an in lude dermal sinus, diastemat myelia (splitting the rd int halves), r a tethered spinal rd II. Me ningoc e le : T is rare lesi n is a sa like p steri r midline herniati n the dura mater and is usually n t ass iated with any neur l gi de its. Repair is indi ated primarily r smeti reas ns.

Quic k Cut Spinal dys raphis m is us ually de ective us ion o a raphe and is as s ociated with f ndings on general phys ical examination highly s ugges tive o an underlying abnormality, s uch as a tu t o hair, nevus , lipoma, abnormal blood ves s els , a dimple, or a s inus tract.

III. Mye lo m e ning o c e le : Herniati n the dura mater and neural elements p steri rly as a result in mplete l sure the neural tube. T is lesi n may be ass iated with hydr ephalus. A. Surgical treatment: Aimed at l sure the de e t. A ventri ul perit neal (VP) shunt may be ne essary i hydr ephalus is present. B. Neurologic de ects: C mm n; severity is related t the l ati n the lesi n. Higher lesi ns have a w rse pr gn sis.

Hyd ro c e p ha lus I. Ove rvie w: Hydrocephalus literally means “water head,” and the abn rmality may be ngenital r a quired. It is aused by an bstru ti n t the f w ( bstru tive hydr ephalus) r reabs rpti n ( mmuni ating hydr ephalus) CSF. II. Etio lo g y: M st mm n auses are as ll ws. A. Complications o intraventricular hemorrhage: in prematurity B. Aqueductal stenosis C. Chiari mal ormation 1. Type I: M st mm n; erebellar t nsils are l w lying within the ramen magnum. 2. Type II: ass iated with myel mening ele; d wnward herniati n the urth ventri le 3. Types III and IV: rare and either ause severe neur l gi de its r are in mpatible with li e D. Dandy-Walker syndrome: agenesis the erebellar vermis and the ramina Magendie and Lus hka III. Clinic a l nd ing s : In ants may present with bulging ntanelles, s alp vein dilatati n, rapidly in reasing head ir um eren e, de reased upward gaze (sun-setting eyes), papilledema, lethargy, irritability, v miting, and ataxia. IV. Tre a tm e nt: C s an r ranial ultras und (in ne nates) sh ws a dilated ventri ular system. MRI may be use ul in determining the eti l gy. A. VP shunt: M st mm nly used meth d diverting CSF. Other Quic k Cut l ati ns diversi n in lude the atria the heart and the Ventriculoperitoneal pleura. s hunting is the mos t common B. Endoscopic third ventriculostomy: inv lves the reati n a treatment or hydrocephalus as the peritoneum can h le in the f r the third ventri le, thus diverting the CSF reabs orb s ignif cant amounts ar und an bstru ti n (su h as aquedu tal sten sis) o exces s CSF.

FUNCTIONAL NEUROSURGERY Mo ve m e nt Dis o rd e rs I. Ove rvie w: Many advan ements have been made in the treatment m vement dis rders (su h as Parkins n disease and essential trem r). Initially, lesi ns were made t destr y the abn rmally un ti ning areas brain. day, thr ugh deep brain stimulati n (DBS), ele tr des are pla ed int the brain and nne ted t a stimulat r t help m dulate the abn rmal areas.

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II. P a rkins o n d is e a s e : dis rder aused by destru ti n d pamine-generating ells in the brain, leading t a mal un ti n in the basal ganglia A. Presentation: resting trem r, rigidity, and bradykinesia Quic k Cut B. Treatment: Alth ugh there is n ure, sympt ms are managed DBS o the initially using medi ati ns, whi h may have severe side e e ts. s ubthalamic nucleus is us ed Certain patients are andidates r DBS the subthalamic in the treatment o Parkins on dis eas e. nucleus. T e gl bus pallidus internus is an ther therapeuti target but has less an e e t. III. Es s e ntia l tre m o r: Chara terized by severe intenti n trem r when a patient tries t per rm an a ti n. Similar t Parkins n disease, the sympt ms have been signi antly impr ved thr ugh DBS (stimulating the ventral intermediate nu leus the thalamus).

Ep ile p s y I. Etio lo g y: Re urrent seizures an be a debilitating nditi n with multiple eti l gies. II. Tre a tm e nt: Mainstay in ludes antiepilepti drugs, all whi h an have seri us side e e ts. Frequently, seizures an be me re ra t ry t these medi ati ns. Diagn sti tests su h as ele tr en ephal graphy and MRI help determine i there is a parti ular us their seizures, whi h may resp nd t surgi al rese ti n.

DEGENERATIVE SP INE DISEASE Ove rvie w I. Ana to m y: Intervertebral dis s ntain a s br us enter, kn wn as the nucleus pulposus surr unded by a t ugh br us layer alled the annulus br sis. A. Herniated or “slipped” discs: ur when the nu leus pulp sus herniates thr ugh a rupture in the annulus br sis B. Location: ypi ally, the dis herniates either underneath r thr ugh the p steri r l ngitudinal ligament. It an then exert pressure n the the al sa , spinal rd, r, m re mm nly, ne the nerve r ts. II. Ra d ic ulo p a thy: C mpressi n a nerve r t pr du es sympt ms in the dermat mes and mus le gr ups that the nerve r t supplies.

Ce rvic a l Dis c He rnia tio n I. Clinic a l p re s e nta tio n: typi ally presents initially as ne k pain, se ndary t inf ammati n the dis apsule and the adja ent p steri r l ngitudinal ligament A. Pain: may be l ated between the s apula, then radiate up int the ne k and head (even ausing heada hes) Quic k Cut B. Radicular signs and symptoms: en a mpany ervi al dis Radiculopathy herniati n when nerve r t mpressi n urs and in lude pain res ults rom nerve root that radiates int the arm, numbness, weakness, and l ss ref exes compres s ion and us ually C. Location: M st requently at the C6/C7 level, ll wed by the requires s urgical releas e or C5/C6 level. Ea h level inv lved pr du es lassi sympt ms relie o s ymptoms . based n the nerve r ts they mpress ( able 27-1). D. Diagnosis: MRI is help ul in evaluating radi ul pathy. II. Tre a tm e nt: Initial management is analgesi s, n nster idal anti-inf ammat ry drugs (NSAIDs), mus le relaxants, rest, physi al therapy, and ster id inje ti ns. I nservative therapy is unsu ess ul, surgi al de mpressi n and p ssible usi n may be required. A. Central and lateral herniation: Anteri r appr a h is used t rem ve the dis and de mpress the spinal rd and nerve r ts. T e tw adja ent vertebral b dies are then used t gether. F r singlelevel disease in patients with n rmal ervi al urvature, a disc replacement (t tal dis arthr plasty) may als be per rmed. B. Far lateral herniation: P steri r appr a h is used with lamine t my and ramin t my. P steri r usi n is s metimes ne essary depending n the extent de mpressi n.

Ce rvic a l Sp o nd ylo s is I. Etio lo g y: aused by pr gressive degenerati n hanges the j ints and ste phyte rmati n

the dis s and ligaments ass iated with arthriti

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Ta b le 27-1: Ce rvic a l Dis c Synd ro m e s Dis c Sp a c e : C4–C5 Ne rve Ro o t: C5

Dis c Sp a c e : C5–C6 Ne rve Ro o t: C6

Dis c Sp a c e : C6–7 Ne rve Ro o t: C7

Dis c Sp a c e : C7–T1 Ne rve Ro o t: C8

Se ns o ry lo s s

Lateral arm

Radial aspect orearm; thumb; index f nger web space

Posterior arm; index f nger; long f nger

Ulnar two f ngers; medial orearm

Mo to r we a kne s s

Shoulder abductors; shoulder external/ internal rotators

Biceps; brachial radialis; supinator/ pronator

C6–C7 wrist extensors; elbow extensors

Finger exors; ulnar deviator o the hand

Cha ng e s in DTRs

Biceps re ex diminished

Biceps and radial re exes diminished

Triceps re ex diminished

Finger exor re ex diminished

DTR, deep tendon re ex. Adapted rom Freedman AH, Wilkins RH. Neurosurgical Management for the House Of cer. Baltimore: Lippincott Williams & Wilkins; 1984.

II. Clinic a l p re s e nta tio n: T is degenerati n sl wly narr ws the anal and neural ramina ausing gradual mpressi n the rd and nerve r ts. T ese patients en have disease at multiple levels the ervi al spine. A. Radicular symptom: aused by the impingement and identi al t that seen with dis herniati n B. Myelopathy: Hyperref exia, gait instability, and di ulty with ne m t r tasks results r m the gradual narr wing the anal, Quic k Cut mpressing the spinal rd. Myelopathy res ults C. Imaging: MRI helps assess the dis s, ligaments, and hanges in the rom s pinal cord compres s ion. spinal rd. C s ans are help ul in evaluating the b ny anat my. III. Tre a tm e nt: T ese patients may als be managed nservatively i there are n m t r de its. I sympt ms are debilitating and persist despite these measures, either anteri r r p steri r surgery may be needed. Surgery uld take the rm an anteri r usi n, p steri r lamine t my with r with ut usi n, r p steri r lamin plasty.

Lum b a r Dis c He rnia tio n I. Ove rvie w: As in the ervi al spine, dis herniati n represents extrusi n nu leus pulp sus thr ugh annulus br sis. ypi ally, nerve r ts exit thr ugh a neural ramen ne segment bel w the herniated dis (L5/S1 dis herniati n irritates the S1 nerve r t). II. Clinic a l p re s e nta tio n: Patients usually have a hist ry ba k pain al ng with radi ular sympt ms, en rep rting pain exa erbated by sitting r straining (Valsalva maneuver) See able 27-2.

Ta b le 27-2: Lum b a r Dis c He rnia tio n Synd ro m e Dis c Sp a c e : L1–L2 Ne rve Ro o t: L2

Dis c Sp a c e : L2–L3 Ne rve Ro o t: L3

Dis c Sp a c e : L3–L4 Ne rve Ro o t: L4

Dis c Sp a c e : L4–L5 Ne rve Ro o t: L5

Dis c Sp a c e : L5–S1 Ne rve Ro o t: S1

Dis c s p a c e : S1–S2 Ne rve Ro o t: S2–S3

Dis trib utio n o s e ns o ry lo s s

Anterior thigh; inguinal ligament

Anterior thigh

Anterior thigh; medial leg to the medial malleolus

Lateral leg; dorsum o oot to big toe

Lateral leg; oot to small toe; sole o oot

Buttocks; perineal region; genitalia

Mo to r we a kne s s

Hip exion; hip abduction

Hip abduction; knee extension

Knee extension; oot inversion

Foot and toe extension

Foot and toe exion

Intrinsic muscles o the oot

Re f e x c ha ng e s

—

—

Decreased knee jerk

Decreased or absent knee jerk

Decreased or absent ankle jerk

Sphincteric dys unction

Adapted rom Freedman AH, Wilkins RH. Neurosurgical Management for the House Of cer. Baltimore: Williams & Wilkins; 1984.

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C Fig ure 27-8: A–D: Spinal cord signal changes. A,B: A 32-year-old man with a 12-year history o progressive upper and lower extremity myelopathy. Magnetic resonance imaging (MRI) demonstrated congenital anomalies at C1–C2, with associated hypertrophy o the ligamentum avum causing severe dorsal spinal cord compression. C: Computed tomographic myelogram demonstrates abnormal bony projections on the ventral sur aces o the C1 and C2 laminar arches, causing compression. He underwent posterior decompression o C1 and C2 (D) with excellent improvement in symptoms. E: A 52-year-old woman with bilateral hand clumsiness. Sagittal MRI demonstrates patchy spinal cord signal changes at C5 and C6 (arrows) along with spondylotic cord compression. (From Bridwell KH, DeWald RL. Textbook of Spinal Surgery, 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2011.)

III. P hys ic a l e xa m ina tio n: Reveals intense lumb sa ral spasm. Quic k Cut Frequently, a p sitive “straight leg raising” sign, as well as radi ular Mos t lumbar dis c signs and sympt ms, are present. herniations improve without IV. Tre a tm e nt: Patients are rst treated nservatively. s urgical intervention. A. Imaging: I sympt ms d n t impr ve, MRI an determine nerve r t mpressi n (Fig. 27-8). I an MRI ann t be btained, C myel graphy is an alternative. B. Discectomy: typi ally needed thr ugh a p steri r appr a h i the pain d es n t resp nd t nservative management r the patient has signi ant neur l gi de its

Lum b a r Sp o nd ylo s is

Quic k Cut I. Ove rvie w: Chr ni degenerati n an ause arthr pathy, dis Cauda equina degenerati n, and ligament us hypertr phy leading t narr wing s yndrome is a neuros urgical the anal. emergency requiring prompt decompres s ion. II. Clinic a l pre s e nta tio n: T e patient des ribes ba k and leg pain that is a hing in nature, exa erbated by pr l nged standing r walking, and ameli rated by sitting (neurogenic claudication). M re severe entral sten sis an present as cauda equina syndrome, with signi ant leg weakness, saddle anesthesia, and b wel/bladder dys un ti n.

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III. Dia g no s is : MRI s an remains the best te hnique t visualize the dis s, ligaments, and nerve r ts. C s an is used t assess the b ny anat my. IV. Tre a tm e nt: C nservative therapy is again the primary treatment. As the disease pr gresses, surgi al de mpressi n by lamine t my (and usually usi n) may be required.

SP INE TUMORS Ove rvie w I. Cla s s i c a tio n: Generally, by their l ati n being intramedullary (intrinsi t the spinal rd), extramedullary, intradural, r extradural. Similar t the brain, they are urther lassi ed based n Quic k Cut Spinal cord tumors their hist l gi ell rigin. may be as s ociated with a A. Intramedullary tumors: intrinsi t the spinal rd and s yrinx. typi ally present with gradually pr gressive neur l gi de its and myel pathy 1. Astrocytomas: All grades, as in the brain, an als ur within the spinal rd. M st requently, they ur in the ervi al r th ra i regi ns and may be ass iated with a syrinx. 2. Ependymomas: O en ur in the ervi al spine and an als be ass iated with a syrinx. A se nd gr up ependym mas inv lves nus (myx papillary ependym ma). B. Intradural, extramedullary tumors: pr du e sympt ms thr ugh nerve r t mpressi n ( ausing radi ul pathy and myel pathy) 1 Meningiomas: m st requently ur in the th ra i spine and are managed similarly t their intra ranial unterparts 2. Schwannomas: Arise r m S hwann ells, whi h are ass iated with the nerve r ts. T ese present as dumbbell-shaped tum rs pr truding thr ugh ut the neural ramen (they an be intradural r extradural). O en, s hwann mas may be multiple. II. Dia g no s is : usually established by neur l gi examinati n and then pr eeding with radi graphi studies A. MRI scan with and without contrast: study h i e r all tum rs 1. Intramedullary tumors: present as an enhan ing mass expanding the spinal rd 2. Intradural and extradural lesions: typi ally enhan e and mpress the spinal rd B. CT scan: an be help ul in assessing b ny anat my parti ularly in metastati disease (whi h has a pr pensity t invade b ne) III. Me ta s ta tic tum o rs : M st mm nly en untered extradural spinal column tum r, typi ally riginating r m the vertebral b dy; they m st requently are ass iated with primary tum rs r m lung, breast, and pr state. T ese tum rs are best treated aggressively with de mpressi n and usi n (in m st ases) en ll wed by radiati n. IV. P rim a ry b o ne tum o rs : Alth ugh rare, en bl rese ti n these lesi ns is urative and sh uld be re mmended when p ssible. Radiati n and hem therapy als play a r le in p st perative management.

P ERIP HERAL NERVES Ca rp a l Tunne l Synd ro m e I. Etio lo g y: results r m median nerve entrapment as it traverses under the carpal ligament at the wrist II. P re s e nta tio n: Patients typi ally present with hand pain and numbness ver the palmar thumb and rst tw digits. Weakness, parti ularly with thumb pp siti n may als be present. III. Dia g no s tic s tud ie s : an in lude ele tr my graphy (EMG)/nerve ndu ti n vel ity (NCV) abn rmalities and physi al exam ndings, su h as a Tinel sign (pain with per ussi n the arpal ligament) Quic k Cut IV. Tre a tm e nt: C nservative management with wrist splints is rst Carpal tunnel attempted and patients with ntinued sympt ms may require s yndrome produces median surgi al de mpressi n the nerve by utting the arpal ligament. nerve neuropathy.

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C4

C5

C6

P os te rior cord

C7

Axilla ry Long thora cic

Ra dia l

C8 La te ra l cord T1

Me dia n ne rve Me dia l cord

T2

Ulna r

Fig ure 27-9: Simplif ed diagram o the brachial plexus .

Cub ita l Tunne l Synd ro m e I. Etio lo g y: results r m ulnar nerve entrapment as it traverses the ubital tunnel in the elb w II. P re s e nta tio n: Patients present with pain and numbness n the ulnar sur a e the hand al ng with hand weakness. III. Dia g no s is a nd tre a tm e nt: Diagn sti w rkup is similar t that r arpal tunnel syndr me and treatment inv lves de mpressing the nerve in the ubital tunnel.

Bra c hia l P le xus I. Ana to m y: ex eedingly mplex anat mi stru ture that inv lves a transiti n r m the ervi al r ts (C5– 1) int the axilla and ur main nerves—mus ul utane us, axillary, median, and ulnar (Fig. 27-9) II. Clinic a l p re s e nta tio n: Injuries an result r m trauma r ne plasia. M st typi ally, bra hial plex pathy is seen in the setting trauma where the ne k is severely stret hed and avulsi n injury urs t the plexus (tearing the nerve r ts r m the spinal rd). III. Eva lua tio n: In ludes physi al exam al ng with extensive EMG/NCV studies. Can inv lve a C myel gram and an MRI t evaluate the nerve r ts and bra hial plexus. IV. Tre a tm e nt a nd p ro g no s is : Nerve r t avulsi ns generally have a very p r pr gn sis. With residual m t r and sens ry un ti n, the patient has an ex ellent han e regaining un ti n the nerve r t. H wever, i the nerve r t is severed, then the patient may need a nerve transp siti n t rest re un ti n. Furtherm re, a d rsal r t entry z ne (DREZ) pr edure may need t be per rmed t treat pain.

Chapter 28

Orthopedics Oliver annous and Robert Sterling

ORTHOP EDIC EMERGENCIES Sp ina l Ep id ura l Ab s c e s s

Quic k Cut Without rapid diagnos is and treatment, orthopedic emergencies threaten li e or limb unction.

I. De f nitio n: extradural collection o purulence located within the spinal canal II. Ep id e m io lo g y: most commonly occurs in the thoracic or lumbar spine A. Risk actors: intravenous (IV) drug abuse, immunodef ciency (HIV, immunosuppressive medications, end-stage renal disease), prior spinal osteomyelitis or discitis, recent spine surgery, or recent systemic in ection; may spread hematogenously or locally B. Most common organisms: Staphylococcus aureus and gram-negative rods III. Dia g no s is : Symptoms include bowel/bladder incontinence, local or radicular pain, saddle anesthesia, and lower extremity (LE) weakness. T oracic abscess patients may present with myelopathic symptoms (wide-based spastic gait, dermatomal chest pain, LE spasticity, or paraparesis). A. Physical exam: LE weakness, absent rectal tone and/or volition, LE clonus, or positive Babinski re ex Quic k Cut B. Imaging: Magnetic resonance imaging (MRI) is the test o MRI with gadolinium choice. Computed tomography (C ) myelogram is the next best is the mos t s ens itive imaging modality to di erentiate imaging modality i an MRI is contraindicated. abs ces s rom cerebros pinal IV. Tre a tm e nt: In the presence o neurologic def cits, emergent spinal f uid. canal decompression and evacuation o the abscess is indicated. A small abscess without neurologic def cit may be treated with a course o IV antibiotics and bracing with requent clinical ollow-up.

P e lvic Ring Injurie s with He m o d yna m ic Ins ta b ility I. Typ e s : Injuries that disrupt the sacroiliac (SI) joint can cause hemorrhage rom the pelvic venous plexus. Fractures into the greater sciatic notch can lacerate the superior gluteal artery. II. Dia g no s is : anteroposterior (AP) pelvic x-ray demonstrating pubic symphysis widening (Fig. 28-1) or SI joint widening, persistent hemodynamic instability not attributable to another cause a er initial management with pelvic compression binder, expanding pelvic hematoma seen on C scan, or active bleeding seen on pelvic arteriogram III. Initia l m a na g e m e nt: includes aggressive uid resuscitation, application o a pelvic binder centered on the greater trochanters, intra-abdominal source o hemorrhage ruled out, and emergent pelvic stabilization o a hemodynamically unstable patient A. External pelvic f xation: decreases pelvic volume to improve tamponade B. Pelvic angiogram with embolization o actively bleeding vessels: i external f xation and uid replacement ail

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473

Fig ure 28-1: Pubic s ymphys is widening in a pelvic ring injury.

IV. De f nitive s ta b iliza tio n: occurs semi-electively a er the patient stabilizes A. Closed/open reduction o the SI joint, sacrum, or posterior ilium: undertaken with internal f xation B. Open reduction and internal f xation (ORIF): o the anterior ring or continued external f xation is achieved (Fig. 28-2)

Co m p a rtm e nt Synd ro m e I. De f nitio n: Increased interstitial uid pressure within an osseo ascial compartment. T is causes microcirculatory compromise, leading to necrosis o the muscle within the compartment and dys unction o the nerves.

Fig ure 28-2: AP pelvic x-ray s howed plating o the s ymphys is and s acroiliac joint s crew xation.

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II. Ca us e s : racture, crush injuries, arterial injury, tight cast/dressing, Quic k Cut burns, gunshot injury, intramuscular hematoma Pain out o III. Dia g no s is primarily clinical proportion to the injury is A. Pain: escalating pain in the extremity in spite o increasing pain s ugges tive o compartment medication administration, pain out o proportion to the injury, s yndrome. pain with passive stretch o the myotendinous units within the compartment, pain and tenseness on palpation (less reliable f nding) B. Intracompartmental pressure measurement: used when clinical exam is unclear or in unreliable/ unconscious patients 1. Absolute pressure measurement: greater than 30 mm Hg 2. Pressure less than 30 mm Hg below the diastolic blood pressure IV. Tre a tm e nt: emergent surgical release o all involved compartments

Ne c ro tizing Fa s c iitis I. De f nitio n: rapidly ascending in ection caused by group A Streptococcus that can lead to limb loss and death i treatment is delayed II. Dia g no s is : progressive so tissue in ection that may have crepitus Quic k Cut Air in the s o t tis s ues III. Im a g ing : X-ray with subcutaneous air; C scan can aid in may be detected on phys ical diagnosis by showing abscess and/or gas in the so tissues; MRI can exam or on plain radiographs . demonstrate asciitis. IV. Tre a tm e nt: aggressive surgical debridement o all in ected tissue and parenteral antibiotics

Fra c ture s a nd Dis lo c a tio ns As s o c ia te d with Va s c ula r Injury

Quic k Cut

Fractures and dis locations as s ociated with vas cular injury cons titute limb-threatening injuries .

I. Com m on s ite s inc lude the ollowing: distal emur, proximal tibia, supracondylar humerus (primarily in children), knee dislocations II. Dia g no s is : Suspicion is based on proximity with clinical signs o vascular injury suggested by ankle-brachial indices (ABIs) less than 0.8 ( able 28-1) and require arterial duplex ultrasonography or C angiography; or intraoperative angiogram. III. Tre a tm e nt: placement o a temporary vascular shunt ollowed by orthopedic stabilization o the racture; subsequent ormal vascular repair/reconstruction IV. Outc o m e : amputation rate near 100% i warm ischemia time exceeds 6 hours

Sc a p ulo tho ra c ic Dis s o c ia tio n I. De f nitio n: traumatic dissociation o the scapula rom the thorax II. P re s e nta tio n: usually seen on chest x-ray as lateral displacement o the scapula (Fig. 28-3) A. Vascular injuries: occur in up to 90% o cases and o en include the subclavian or axillary arteries B. Brachial plexus injuries: present in up to 95% o cases III. Outc o m e s : ail extremity rate o 50%, amputation rate o 20%, and mortality rate o 10%

Ta b le 28-1: P hys ic a l Sig ns o a Ma jo r Arte ria l Injury Absent or comparably weak pulses Distal cyanosis Expanding hematoma Pulsatile bleeding Comparably cold extremity Distal paralysis and paresthesias Bleeding not controlled with direct pressure

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Fig ure 28-3: X-ray s howing lateral dis placement o the s capula indicative o s capulothoracic dis s ociation.

ORTHOP EDIC URGENCIES

Quic k Cut

Op e n Fra c ture I. De f nitio n: any racture that has been exposed to the external environment, usually not only through the skin but also through hollow visceral organs (Fig. 28-4) II. Ma na g e m e nt: Splinting is done initially with removal o gross contamination and placement o sterile dressings. A. Medical: Administration o a f rst-generation cephalosporin (vancomycin in patients who are allergic to penicillin). Use o an

Urgencies are not immediately li e or limb threatening, but s igni cant delay in diagnos is and treatment can res ult in los s o limb or joint unction and prolonged treatment.

Fig ure 28-4: Open orearm racture with both radius and ulna expos ed.

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aminoglycoside and penicillin should be considered or patients with large wounds or or those with soil or arm contamination. etanus prophylaxis is administered. B. Def nitive: Def nitive irrigation and debridement are per ormed in the operating room with stabilization.

Quic k Cut Open racture requires urgent treatment to decreas e the ris k o os teomyelitis .

Se p tic Arthritis I. P re s e nta tio n: rapid onset o atraumatic pain in a joint II. Etio lo g y: ypically hematogenous origin; immunocompromised Quic k Cut patients are at increased risk. Septic arthritis requires urgent treatment III. P hys ic a l e xa m ina tio n: joint e usion, exquisite tenderness to to prevent pos tin ectious palpation, and severe pain with minimal motion o the joint arthritis . IV. Dia g no s is : conf rmed by needle aspiration with synovial uid analysis ( able 28-2) A. Synovial uid white blood cell (WBC) count: More than 50,000 with greater than 90% polymorphonuclear leukocytes (PMNs) suggest the diagnosis. B. Crystals: Fluid must be inspected or crystals; an acute gout are can have an exceptionally high WBC count with mostly PMNs. C. Di erential diagnosis: includes aseptic arthritis (rheumatoid, psoriatic, etc.) and gout V. Tre a tm e nt: Surgical debridement and lavage o the joint (open or arthroscopic). Antibiotic therapy should not be instituted be ore obtaining adequate specimens or a culture and sensitivity.

Ta b le 28-2: Exa m ina tio n o the Syno via l Fluid No rm a l

Gro up I No nin a m m a to ry

Gro up II In a m m a to ry

Gro up III Se p tic

Gross appearance

Transparent, clear

Transparent, yellow

Opaque or translucent, yellow

Opaque, yellow to green

Viscosity

High

High

Low

Variable

White cells/mm 3

200

2,000

Polymorphonuclear leukocytes

25%

50%

50%,

Culture

Negative

Negative

Negative

Glucose (mg/dL)

Almost equal to blood

Almost equal to blood

Associated conditions

—

Degenerative joint disease Trauma* Neuropathic arthropathy* Hypertrophic osteoarthropathy† Pigmented villonodular synovitis* SLE† Acute rheumatic ever† Erythema nodosum

5,000–75,000 90%

25, lower than blood Rheumatoid arthritis Connective tissue diseases (SLE, PSS, DM/PM) Ankylosing spondylitis Other seronegative spondyloarthropathies (psoriatic arthritis, Reiter syndrome, arthritis o chronic inf ammatory bowel disease) Crystal-induced synovitis (gout or pseudogout) Acute rheumatic ever

50,000, o ten 100,000 95% O ten positive 50, lower than blood Bacterial in ections Compromised immunity (disease-or medication-related) Other joint disease

*May be hemorrhagic. † Group I or II. SLE, systemic lupus erythematosus; PSS, progressive systemic sclerosis; DM/PM, dermatomyositis/polymyositis. Reprinted with permission rom Rodnan GP, Schumacher HR. Examination o synovial f uid. In: Primer on Rheumatic Diseases, 8th ed. Atlanta: Atlanta Arthritis Foundation; 1983:187.

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Hip Dis lo c a tio n

Quic k Cut I. P re s e nta tio n: History o moderate to severe trauma to the Urgent reduction extremity and inability to move the hip. Most dislocations are o hip dis location decreas es posterior and the leg is internally rotated at the hip and shorter than the ris k o emoral head the contralateral limb. os teonecros is . II. Dia g no s is : Pelvic or hip x-ray demonstrates the dislocation (Fig. 28-5); C scan can demonstrate emoral head or acetabular racture. III. Tre a tm e nt: Expedient reduction under general anesthesia; C scan to evaluate or emoral head or acetabular racture a er reduction.

P e ne tra ting Injurie s to J o ints I. Dia g no s is : Intra-articular injection o sterile saline at a point distant to the laceration with leak at the injury site aids in the diagnosis. II. Tre a tm e nt: ormal irrigation and debridement (open or arthroscopically) to prevent in ectious arthritis

Quic k Cut Urgent irrigation and debridement o penetrating injuries to joints prevents in ectious arthritis .

Fig ure 28-5: X-ray demons trating pos terior hip dis location.

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TRAUMA Ove rvie w I. Ad va nc e d tra um a li e s up p o rt (ATLS): In the management o trauma patients, it is important to remember A LS guidelines with strict adherence to the ABCs (airway, breathing, circulation; see Chapter 22). II. Exte nt o injury to the m us c ulo s ke le ta l s ys te m : varies Quic k Cut according to the patient’s age, the direction o the energy causing the Orthopedic trauma, and the magnitude o the trauma injuries are more likely to A. Patient’s age: suggests the weak link in the musculoskeletal be limb threatening than li e system threatening. 1. In skeletally immature patients: Weak link is the growth plate at the ends o the long bones. 2. Young but skeletally mature patients (16–50 years o age): may be more likely to sustain ligamentous injuries because the relative strength o the mature bone exceeds that o the supporting so tissues 3. In late middle-aged or elderly patients (with signif cant osteopenia): Injuries to the ligaments are uncommon; ractures o the metaphyseal portions o long bones are prevalent (i.e., distal radius, hip). T e metaphyseal area is at risk because the likelihood o osteopenia is much greater in this metabolically active area. B. Direction o the trauma: may determine which structures are Quic k Cut injured (e.g., knee-dash injury that occurs in motor vehicle Patterns o injury collisions requently causes ractures o the patella and emur as may occur, leading to well as posterior hip ractures or dislocations) predictable groups o damage C. Magnitude o the trauma: related to the energy imparted bas ed on the mechanis m o 2 (E ½ mv ), where m mass and v velocity injury. 1. High-energy injuries (e.g., in motor vehicle accidents): tend to cause comminuted, complex skeletal injuries, which may be open ractures 2. Low-energy injuries: requently occur in the elderly or during sports and are more likely to cause simple, isolated injuries o ligaments, muscles, or bones

Fra c ture I. De s c rip tio n: Radiographic appearance may give insight into the type o trauma that produced a particular racture. Other descriptors are as ollows. A. Location: may be the diaphysis (sha ), the metaphysis (juxta-articular), or through the joint sur ace (articular) B. Orientation: may be transverse, oblique, spiral, segmental, comminuted, or incomplete such as greenstick in the growing skeleton (Figs. 28-6 and 28-7) C. Displacement: may be expressed in terms o bone diameters (e.g., 1 bone diameter o displacement 100% displacement) in sha ractures and in millimeters o step-o in articular ractures (e.g., tibial plateau ractures) D. Impaction: requently occurs in the proximal humerus and may indicate stability E. Angulation: should use the apex o the racture as a point o re erence (i.e., apex dorsal) F. Rotation: o en best assessed clinically but may be appreciated on radiograph G. Open or closed: open, or compound (old terminology), indicates a so tissue injury in the region o the racture with exposure to the external environment 1. Communication: All wounds in the proximity o ractures should be assumed to communicate with it. 2. Classif cation: Gustilo classif cation ( able 28-3) II. Stre s s ra c ture : Implies a racture resulting rom abnormal stresses on normal bone ( atigue racture) or normal stresses on abnormal or osteopenic bone (insu ciency racture). Osteoporosis is a common cause o an insu ciency racture. A. Common sites in patients with normal bone: tarsal bones (calcaneus), metatarsals, and tibial sha B. Common sites in patients with osteopenic bone: emoral neck, oot, pelvis, and vertebrae

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Fig ure 28-6: Long bone racture patterns . (Redrawn with permis s ion rom Rang M. Children’s Fractures, 2nd ed. Philadelphia: J B Lippincott; 1983:5.)

C. Diagnosis: Plain radiographs are help ul i reactive healing has occurred. 1. Bone scans: quite sensitive but not specif c 2. MRI: Very sensitive and has increased specif city i a linear signal change is present; 2 image will most commonly demonstrate edema in the area o racture. III. P a tho lo g ic ra c ture s : occurring in a weakened bone due to metabolic bone disease or a tumorous condition (i.e., a primary Quic k Cut bone malignancy, myeloma, or metastatic disease) Pathologic ractures are ractures that occur in IV. Im p e nd ing p a tho lo g ic ra c ture s : Lytic de ect in bone, o en due abnormally weakened bone. to a metastasis, weakens the bone but has not yet caused a racture. Prophylactic stabilization is o en per ormed to prevent a racture.

Fig ure 28-7: Fracture patterns in children. (Redrawn with permis s ion rom Rang M. Children’s Fractures, 2nd ed. Philadelphia: J B Lippincott; 1983:2.)

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Ta b le 28-3: Gus tilo Cla s s if c a tio n o Op e n Fra c ture s Gra d e

De s c rip tio n

Gra d e 1

Skin opening o 1 cm or less, quite clean; most likely rom inside to outside; minimal muscle contusion; simple transverse or short oblique ractures

Gra d e 2

Laceration 1 cm long, with extensive so t tissue damage, f aps, or avulsion; minimal to moderate crushing components; simple transverse or short oblique ractures with minimal comminution

Gra d e 3

Extensive so t tissue damage including muscles, skin, and neurovascular structures; o ten a high-velocity injury with a severe crushing component • 3A: Extensive so t tissue laceration, adequate bone coverage; segmental ractures, gunshot injuries • 3B: Extensive so t tissue injury with periosteal stripping and bone exposure; usually associated with massive contamination • 3C: Vascular injury requiring repair

Reprinted with permission rom Behrens F. Fractures with so t tissue injuries. In: Browrer BD, J upiter J B, Levine AM, et al, eds. Skeletal Trauma, Philadelphia: WB Saunders; 1992:313.

Fra c ture s in Child re n I. Gro wth p la te ra c ture s : Because the growth plate is cartilaginous, it represents a weak point at the ends o the bone. A. Classif cation: Salter-Harris classif cation (Fig. 28-8) B. ypes: All types o growth plate ractures may be associated with growth arrest, and the parents should be advised o this. 1. ypes 1 and 2: Do well with closed reduction and cast immobilization; however, some may require pin or screw f xation. Growth arrest is unlikely. 2. ypes 3 and 4: Frequently require open reduction and f xation because they are intra-articular ractures; they are at greatest risk o causing growth arrest. II. Buc kle (o r to rus ) ra c ture s : incomplete ractures that occur in the metaphysis o bones adjacent to (but not involving) the growth plate (Fig. 28-9) A. Most common site: distal radius B. reatment: o en require only cast immobilization III. Gre e ns tic k ra c ture s : Fractures in the sha o a bone that extends through only one side or one aspect o the cortex. Casting is employed or treatment to maintain reduction with close ollow-up, as reangulation can occur and require completion o the racture to maintain proper alignment (see Fig. 28-9).

Fig ure 28-8: The Salter-Harris clas s i cation o growth plate ractures . (Redrawn with permis s ion rom Salter RB, Harris WR. Injuries involving the epiphys eal plate. J Bone J oint Surg. 1963;45A:587.)

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Fig ure 28-9: X-ray s howing extra-articular dis tal radius racture.

IV. Child a b us e ra c ture s : Care ul history obtained rom the child’s Quic k Cut parents, caregiver, and siblings, as well as a complete physical Any child who examination, is important when di erentiating ractures caused by pres ents with a his tory accidents rom those caused by child abuse. incompatible with the injury A. Common presentation: spiral long bone ractures in the absence s hould be cons idered as a o a consistent injury history pos s ible child abus e injury. B. Diaphyseal emur racture: Any child younger than 36 months with this racture should be evaluated or child abuse. C. Multiple ractures o varying age and stage o healing: o en Quic k Cut diagnostic o child abuse I any s us picion D. Radiograph skeletal survey should be per ormed: o abus e is pres ent, s ocial AP projection o the trunk and extremities plus anterior, s ervice/child protective posterior, and lateral views o the skull cons ultation is mandatory. V. Sup ra c o nd yla r ra c ture s o the hum e rus : Care ul neurovascular examination must be done be ore and a er any attempts at reduction are made. Quic k Cut A. Displaced ractures: require urgent attention due to the Supracondylar potential or compression or entrapment o the brachial artery ractures o the humerus that can lead to limb ischemia and compartment syndrome may lead to compartment B. reatment o nondisplaced ractures: long-arm casting or s yndrome. 4–6 weeks C. reatment o displaced ractures: closed (occasionally open) reduction with pin stabilization and long-arm casting with pin removal in 4–6 weeks

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VI. Fra c ture s o b o th o re a rm b o ne s A. Age younger than 10 years: closed reduction and molded plaster immobilization with close observation acutely or compartment syndrome B. Age older than 10 years: Attempt closed reduction, but ORIF may be necessary. Remodeling o the diaphysis is minimal a er age 10 years so anatomic reduction is necessary. VII. Dis ta l ra d ius ra c ture s : Distal radial metaphysis is a requent site or buckle ractures; distal radial epiphyseal plate is a requent site or growth plate ractures (which, i displaced, should have a closed reduction under anesthesia with cast immobilization). VIII. Fe m ur ra c ture s A. Children age younger than 6 months: most o en treated with Pavlik harness or early spica casting B. Children age 7 months–5 years: Post racture overgrowth is common so 1–2-cm shortening is accepted. 1. Overlap less than 2–3 cm: treatment with spica casting 2. Overlap greater than 3 cm: surgical treatment with exible nails or external f xation to maintain length C. Children age 5–11 years: Surgical treatment with exible intramedullary nails is indicated. D. Children age older than 11 years: Surgical treatment with exible intramedullary nails, rigid intramedullary nail, or submuscular plating is indicated. IX. Fra c ture s o the tib ia : associated with compartment syndromes A. Examination: All patients with tibia ractures should be examined or any skin disruption, and the neurovascular status o the leg should be evaluated and documented. B. reatment: Managed in children with plaster immobilization. I open wounds are present, external f xation allows access or wound care.

Fra c ture s in Ad ults I. Fra c ture s o the d is ta l ra d ius , p ro xim a l hum e rus , hip , a nd s p ine : all common in elderly persons with osteoporosis A. Distal radius racture: See section III below. B. Proximal humerus ractures: Early motion a er callus development is essential to decrease shoulder sti ness. 1. Simple ractures: sling and swathe immobilization 2. Comminuted ractures: ORIF or prosthetic replacement C. Hip ractures: ORIF or arthroplasty is associated with better long-term unction and patient survival. D. Osteopenic compression ractures o the spine: Managed with bracing or 3–4 months. Metastatic disease should be ruled out as a cause. II. Hum e ra l s ha t ra c ture s : Isolated racture is usually treated with a sling and humeral racture brace. A. Fracture in conjunction with multiple trauma (LE ractures or ipsilateral orearm ractures): usually treated with surgical f xation to enable upper extremity (UE) weight bearing or crutch/walker use B. Associated radial nerve palsy: o en recovers spontaneously III. Dis ta l ra d ius ra c ture s A. Extra-articular ractures (see Fig. 28-9): reated by closed reduction and immobilization in a wellmolded cast; racture comminution may necessitate surgical f xation. B. Intra-articular ractures: treated by reduction and stabilization with pinning, external f xation, or internal f xation to restore the joint anatomy IV. Sc a p ho id ra c ture s : o en occurs in the young, as energy sustained rom a all is trans erred to the scaphoid and resisted by the distal radius (Fig. 28-10) A. Diagnosis: Wrist pain, especially in the anatomic snu ox a er Quic k Cut a all on an outstretched wrist, should arouse suspicion o this Scaphoid ractures carpal bone injury. are the mos t common B. reatment: Healing is o en delayed owing to a precarious ractures o the wris t bones . blood supply to the bone, which is largely covered with articular cartilage. 1. Nondisplaced ractures: thumb-spica casting 2. Displaced ractures: surgical open reduction and f xation

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Fig ure 28-10: X-ray demons trating s caphoid racture.

V. Bo xe r’s ra c ture s ( ra c ture o the o urth o r f th m e ta c a rp a l ne c k): rom a closed f st striking on the ulnar side o the hand A. Angular de ormity: well tolerated up to 40 degrees in the ourth metacarpal neck and 60 degrees in the f h B. Malrotation: poorly tolerated as it causes the f ngers to overlap C. reatment: casting unless severe angulation or malrotation is present VI. Sp ina l ra c ture s : Initial evaluation and treatment includes evaluation or neurologic injury with a complete motor, sensory, and Quic k Cut re ex examination; complete spinal C is indicated to rule out these All uncons cious ractures. All patients suspected o having a spinal injury should be patients involved in motor immobilized on a long spine board with a cervical collar and head vehicle or motorcycle accidents s hould be as s umed blocks. to have a s pinal injury until A. Cervical spine ractures: requently associated with quadriplegia proven otherwis e. and requently multiple levels o injury B. T oracic spine ractures: Simple compression ractures o en in elderly osteopenic patients secondary to minimal trauma (e.g., coughing) may be due to metastatic disease; high-energy mechanisms are associated with more complex racture can result in paraplegia. C. Lumbar spine ractures 1. Presentation: L1–L2 mixed neurologic can be seen rom injury to the conus medullaris (upper motor neuron) or cauda equina (lower motor neuron); below L2, typically involves only nerve roots.

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2.

VII. VIII.

IX.

X.

A

reatment: Urgent decompression o neural elements in Quic k Cut patients with incomplete or progressive neural def cits Acute blunt trauma or injuries at the level o the cauda equina is the optimal s pinal cord injury high-dos e approach. methylprednis olone protocol a. Steroids: I begun within 3 hours o injury, continue or has been as s ociated with 23 hours. I begun 3–8 hours postinjury, continue or improved neurologic recovery. 48 hours. A er 8 hours, steroids do not improve return o unction. b. Spinal stabilization: Per ormed to prevent worsening o a neural def cit and restore alignment. Patients with complete quadriplegia or paraplegia should also be considered as candidates or spinal stabilization with instrumentation on a less urgent basis to allow early rehabilitation. P e lvic ra c ture s : See “Pelvic Ring Injuries with Hemodynamic Instability” earlier. Fe m o ra l s ha t ra c ture s : Early stabilization decreases pulmonary complications. A. raction (on a short-term basis): i the patient is too critically ill or surgery (e.g., severe coagulopathy, marked elevation o intracranial pressure) B. External f xation: Indicated or initial stabilization o the racture in an unstable trauma patient. Formal stabilization should be per ormed as soon as the patient’s condition is stable. C. Intramedullary stabilization: treatment o choice or isolated emoral sha ractures (Fig. 28-11) Tib ia l ra c ture s A. Isolated closed racture treatment: Plaster immobilization and early weight bearing; intramedullary nail f xation can acilitate early return to ambulation. B. Multiple injuries or open tibial racture treatment: intramedullary rods; external f xation Ankle ra c ture s : A. Lateral malleolus racture alone: Cast treatment is the mainstay; surgical treatment i the ankle mortise is wide on initial x-rays. B. Medial malleolus racture alone: o en a vertical or oblique racture, which leaves the ankle unstable; surgical treatment with reduction and f xation C. Medial malleolus and lateral malleolus racture: Surgical reduction and f xation is indicated to maintain racture reduction (Figure 28-12).

B

Fig ure 28-11: Mids ha t s piral emur racture and image a ter intramedullary nail placement.

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Fig ure 28-12: Ankle racture involving both medial and lateral malleoli.

XI. Ca lc a ne us ra c ture s : o en due to axial loading (during a motor vehicle accident or all rom a height); may be associated with a contralateral ankle or vertebral racture A. C scan: per ormed to characterize the racture pattern due to the complex osteology o the calcaneus B. Poor prognostic actors: age older than 50 years, manual labor, worker’s compensation, bilateral calcaneal ractures, smokers, or peripheral vascular disease C. reatment: casting or stress ractures, nondisplaced ractures, high-risk patients; surgical reduction and f xation or displaced or impacted ractures (o en delayed [7–10 days] to allow swelling to decrease)

Dis lo c a tio ns I. Sho uld e r: especially common in young adults and result in labral tear A. Presentation: Frequently recur in patients age younger than 40 years. In patients age older than 40 years, a tear o the rotator cu should be suspected. May have associated axillary nerve palsy. B. Management: Immediate reduction and sling immobilization; early physical therapy. Arthroscopic labral repair is indicated or recurrent dislocators or high-demand athletes. II. Hip : See “Hip Dislocation” earlier. III. Kne e : implies severe ligamentous injury around the knee and Quic k Cut dislocations should raise awareness or potential popliteal artery All knee dis locations injury (Fig. 28-13) s hould rais e s us picion o popliteal artery injury. A. Etiology: Ligamentous knee injuries occur most commonly in sports-related activities. otal ligamentous disruptions and dislocations are usually the result o violent injuries.

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Fig ure 28-13: AP knee x-ray demons trating joint s pace widening (es pecially laterally) with s ubluxation cons is tent with multiple ligament injuries .

B. Management: First step is to evaluate the neurovascular status o the LE. T en, the ligaments and capsule around the knee are evaluated. Gentle reduction o the joint should be per ormed. 1. ABI: All patients with knee dislocations require a pulse evaluation and documentation o the ABI. A patient with an abnormal ABI requires ormal angiographic evaluation o ow through the popliteal artery. 2. Delayed ligamentous reconstruction: per ormed a er the appropriate vascular intervention to restore knee stability

ARTHRITIS Cla s s if c a tio n I. P rim a ry o s te o a rthritis : Primary pathology is in the articular cartilage. A. Most common sites: hip, knee, and spine B. Heberden nodes: o en seen on physical exam

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II. P o s t-tra um a tic a rthritis : isolated joint degeneration ollowing trauma to that joint III. Rhe um a to id a rthritis a nd its va ria nts : include the autoimmune group o in ammatory diseases in which the hyaline articular cartilage is secondarily attacked by a local invasive pannus that primarily involves the synovium IV. Crys ta l d e p o s itio n d is e a s e s : Include gout and calcium pyrophosphate deposition disease. T ese diseases usually present as an isolated hot, in amed joint. V. In e c tio us a rthritis : See “Septic Arthritis” earlier.

No no p e ra tive Ma na g e m e nt I. P ha rm a c o lo g ic m a na g e m e nt: maximized by consultation with a rheumatologist A. Nonsteroidal anti-in ammatory drugs (NSAIDs): especially important in osteoarthritis, which can be treated conservatively or years. Crystalline and degenerative joint diseases require NSAIDs during acute are-ups, but the natural history o these diseases is not altered by long-term management with these drugs. B. Corticosteroids: used in rheumatoid and osteoarthritis to reduce in ammation; used systemically in multiple joint or generalized disease; used locally by injection into a single joint in patients with degenerative or post-traumatic rheumatoid arthritis C. Disease-modi ying antirheumatic drugs (DMARDs): First line o treatment or rheumatoid arthritis and should be initiated on initial diagnosis. May result in disease remission and signif cant improvement in long-term outcomes. D. Biologic agents (tumor necrosis actor antagonists and interleukin receptor antagonists): second-line agents and used in combination with DMARDs when f rst-line treatment is ine ective II. Exe rc is e a nd s p linting : Have an important place a er the acute joint in ammation has been controlled. A ull range o joint motion and muscle strength is maintained by exercising the joint through a painless arc o motion. Splinting in a unctional position prevents establishment o contractures. III. Inje c tio n (o c o rtic o s te ro id , d ire c tly into s ym p to m a tic jo ints ): can be an e ective measure to provide temporary relie o symptoms

Op e ra tive Ma na g e m e nt I. Os te o to m y: Correction o malalignment may alter the mechanics enough to give signif cant relie rom pain. T e disease process must not have completely destroyed the joint or osteotomy to be success ul. A. Goal: Osteotomy is designed to trans er weight bearing onto relatively normal articular sur ace in the setting o nonin ammatory arthritis. B. emporizing measure: Osteotomy about the hip and knee can be per ormed in patients too young to consider arthroplasty but who wish to preserve motion. II. Arthro d e s is : Commonly used in the small joints o the wrist, hand, oot, and ankle. Arthrodesis o the shoulder, hip, and knee are less well tolerated. A. echnique: Joint sur aces are excised and the bones on each side heal together in a f xed position. Quic k Cut B. Indications: pain relie Any patient who has a high unctional demand C. Results: very durable and long lasting s hould be cons idered or III. Arthro p la s ty (to ta l jo int re p la c e m e nt): Relieves pain, arthrodes is rather than or preserves motion, and is the most common surgical treatment or arthroplas ty. arthritis. It can be used or joints destroyed by any o the arthritides, but major joints such as the hip, knee, shoulder, and elbow are common sites. A. Indications: pain relie predominantly in patients who are usually older and less active B. Postin ectious arthritis: relative contraindication because o the increased risk o in ection around the implant C. Outcome: ypical “li e expectancy” or a hip or knee arthroplasty implant is 20 years, depending on the unctional requirements and weight o the patient. Failure is at a rate o 1% per year.

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In ections

INFECTIONS Ac ute Os te o m ye litis I. Clinic a l p re s e nta tio n: Hematogenous osteomyelitis is common in childhood. A. Children: In the metaphysis o children’s bones, there is a unique capillary venous sinusoid underneath the growth plate. Minor trauma predisposes to sludging and allows minor bacteremic conditions to initiate an in ection. B. Progression: In ection can track beneath the periosteum. Loss Quic k Cut o blood supply devitalizes the bone, and the resulting necrotic Seques trum bone is called a sequestrum. T e elevated periosteum lays down becomes a nidus or extensive new bone, which is termed an involucrum. recurrence o in ection i it is C. Septic arthritis: can result i the metaphysis is intra-articular, not adequately debrided. such as in the case o the hip or shoulder, allowing eruption o the in ection out o the medullary space to enter into the synovial cavity II. P e d ia tric e tio lo g y A. Neonates: S. aureus and gram-negative rods predominate B. Young children (age 2–5 years): requently caused by Haemophilus, Staphylococcus, and Streptococcus species C. Older children (age 5 years or older): S. aureus is the predominant causal organism. D. History: Child with a history o minor trauma who does not improve must be considered to have possibly developed osteomyelitis. A child’s re usal to bear weight on an extremity demands a workup or osteomyelitis or septic arthritis. III. Ad ult e tio lo g y: Patient whose immune system is suppressed and patients with sickle cell disease are predisposed to osteomyelitis rom hematogenous spread o unusual organisms. A. Gram-negative in ections: Patients with immunosuppression and IV drug users are susceptible particularly to Pseudomonas aeruginosa . B. Salmonella : Patients with sickle cell anemia have a particularly high incidence o this type o osteomyelitis. C. Gonococcal septic arthritis: most common organism in adolescent, sexually active patients IV. Dia g no s is : Care ul physical examination, complete blood count (CBC), sedimentation rate, and bone scan help to conf rm the diagnosis. Needle aspiration o the a ected bone or joint is the def nitive diagnostic test. V. Tre a tm e nt: Includes appropriate IV antibiotics and surgical drainage. Initial antibiotic treatment should be selected to cover the most likely causes o organisms and should always include coverage or Staphylococcus.

Chro nic Os te o m ye litis I. Etio lo g y: Uncommon; however, it is seen in patients who have had severe open ractures, in immunosuppressed patients, and in patients with pressure ulcerations secondary to paraplegia. II. Clinic a l p re s e nta tio n: Osteomyelitis involving the bony cortex is a particularly di cult problem. WBCs, as well as antibiotics, have only limited access to the site o in ection. A. Early treatment: Attempts to cure chronic osteomyelitis involve a thorough debridement o in ected nonviable bone (sequestrum), open wound care, and a prolonged course o IV Quic k Cut antibiotics. Cortical bone has minimal vas cularity and is B. Late treatment: A er all devascularized bone and so tissue even les s well vas cularized in have been removed, and once a stable wound base has been the ace o os teomyelitis . established, the overlying so tissue and bone de ect need to be addressed. 1. Flaps: Bone de ect can be packed with antibiotic-impregnated beads ( requently, tobramycin or gentamicin beads) ollowed by rotational or ree vascularized tissue coverage. Later, the ap can be elevated, the beads can be removed, and cancellous autogra ing can be per ormed.

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2. Ring: A ring external f xator may be used to transport bone to f ll de ects. Occasionally, the wounds can be le open during transport, and they will close spontaneously once the de ect is closed. 3. Gra s: Use o vascularized bone gra s, such as the ree vascularized f bula or f bular transposition gra , is an option or large bone de ects.

TUMORS P rim a ry Bo ne Tum o rs I. Clinic a l p re s e nta tio n: Patients with a neoplastic bone lesion Quic k Cut present with pain, swelling, or occasionally, a pathologic racture. Bony les ions may T is applies to bony metastases as well as or primary tumors o bone. res ult rom primary tumors , II. Dia g no s is : In addition to di erentiating a primary tumor rom metas tas es , or metabolic a metastatic lesion o bone, some metabolic processes, such as proces s es . hyperparathyroidism and in ection, must be care ully considered. A. Physical examination: demonstrates the tumor mass B. Plain radiographs: o en suggest the etiology and nature o the bone lesion based on its location, appearance, and the response o the surrounding normal bone (Fig. 28-14) 1. Malignancy: expected i the f lms show a large tumor, aggressive destruction o bone, ine ective reaction o the bone to the tumor, and extension o the tumor into so tissue 2. Benign lesions: expected i the f lms show a small, well-circumscribed lytic lesion; thick, sclerotic rim o reactive adjacent bone; and no extension into so tissue III. Wo rkup : Includes a C scan and MRI o the involved extremity to stage the tumor and delineate its extent and anatomic relationships. A technetium-99m (99m c) scan is help ul in determining metastatic involvement o distant parts o the skeleton. Quic k Cut A. Suspected malignancy: C scan o the chest is important to rule Incomplete workup out pulmonary metastases. or a poorly planned biops y o a primary bone tumor may B. Biopsy: should be per ormed a er staging has been completed prove atal or the patient or and should be planned so that the incision can be excised with a res ult in los s o limb. def nitive resection

Fig ure 28-14: Schematic o the dis tal emur. Numbered s ites repres ent tumor locations : (1) cortical brous dys plas ia and adamantinoma, (2) os teoid os teoma, (3) chondromyxoid broma, (4) os teochondroma, (5) os teos arcoma, (6) chondroblas toma, (7) giant cell tumor, (8) nonos s i ying broma, (9) enchondroma or chondros arcoma, (10) bone cys t or os teoblas toma, (11) bros arcoma or malignant brous his tiocytoma, (12) brous dys plas ia, and (13) Ewing s arcoma or other s mall round tumors . (Redrawn with permis s ion rom Mos er RP, Madewell J E. An approach to primary bone tumors . Radiol Clin North Am. 1987;25[6]:1079–1080.)

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IV. Tre a tm e nt: Surgical treatment continues to be the mainstay o management or both benign and malignant tumors o the extremities. T e surgical margin varies signif cantly with the aggressiveness o the lesion. A. Benign tumors: can be treated by intralesional or intracapsular excision o the tumor with or without chemical cautery, electrocautery, or cryotherapy and with or without bone gra ing o the de ect B. Malignant tumors: require at least a 2-cm margin C. Metastases: Isolated pulmonary metastases o sarcoma should be considered or surgical resection because the literature shows that this occasionally results in a cure and certainly a prolonged li e span in these patients. V. Ad juva nt the ra p y o r m a lig na nt tum o rs : Radiotherapy and chemotherapy may have important roles as adjunctive therapy in anticipation o limb-sparing procedures. A. Radiation: Some tumors (e.g., Ewing tumors) are very sensitive to radiotherapy. Some protocols include radiation therapy initially, but in general, radiation therapy is not an important part o the protocol. B. Chemotherapy: Ewing tumors are well known to be very sensitive to various chemotherapeutic regimens. Osteosarcoma is sensitive to some chemotherapeutic agents, and presurgical treatment can lessen the size o the tumor. VI. Typ e s o p rim a ry b o ne tum o rs : A. Osteosarcoma: More than 60% o patients with these tumors are age 10–20 years. 1. Clinical presentation: Sixty percent occur about the knee at either the distal emur or the proximal tibia. ypically, pain and tume action is present. 2. Imaging: Radiographically, the lesion is commonly lytic, but it may be a characteristically blastic lesion o the bone and produce a classic sunburst appearance. MRI and C scans show that the lesion is ill def ned with so tissue extension. 3. Histology: umor may be predominantly f brogenic, chondrogenic, or osteogenic; each o the three cell types Quic k Cut predominates in approximately equal numbers. The s ine qua non o os teos arcoma is production 4. reatment o malignant os teoid by the a. Neoadjuvant chemotherapy (given be ore surgery): tumor s troma. Can narrow surgical margins and acilitate limb salvage. A high tumor kill rate observed in the resected specimen correlates avorably with long-term survival. b. Surgical resection: Cornerstone o management; amputation or limb salvage surgery may be required. c. Adjuvant chemotherapy: has a benef cial e ect and has increased 5-year survival rates rom 10% to 20% with surgery alone to almost 60% with combined therapy B. Ewing sarcoma: disease o childhood and adolescence, occurring evenly among individuals age younger than 20 years 1. Clinical presentation: ypically, signif cant tume action and pain in the involved area; history, physical examination, and radiographic f ndings mimic those o osteomyelitis. 2. Imaging: Radiologically, the lesion is seen to be a lytic bone lesion characteristically involving the diaphysis with some periosteal reaction. 3. Histology: Small round cells, which may orm pseudorosettes reminiscent o neuroblastoma. Chromosomal translocation t11:22 is associated. 4. reatment: Relative roles o chemotherapy, radiation therapy, and surgical therapy are being evaluated. T ese tumors are sensitive to both chemotherapy and radiotherapy, and together these modalities have a signif cant cure rate. Patients are at risk o orming osteosarcoma in the radiated bone during early adulthood. C. Multiple myeloma: most common primary malignancy o bone that occurs in patients who are 30 years and older with a peak Quic k Cut incidence at age 50–60 years Multiple myeloma 1. Clinical presentation: Characterized by overproduction o is the mos t common primary monoclonal immunoglobulins or immunoglobulin subchains bone tumor in adults . (Bence Jones, or M, protein); initial presentation is o en a pathologic racture, requently o the spine or long bones.

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2. Diagnosis: should be suspected when lytic lesions are ound in a patient with anemia, elevated sedimentation rate, and elevated serum calcium levels a. Labs: Diagnosis can be made by serum or urine electrophoresis or immunophoresis in 95% o cases, but 5% o patients with myeloma are nonsecretors o M protein. b. Biopsy o the bone marrow: o identi y secreting and nonsecreting tumors and to show plasma cells replacing the marrow. T e percentage o bone marrow replacement o ers some prognostic in ormation. c. Plain radiography: reveals punched-out lytic lesions, with little adjacent reactive bone, that occur requently in the spine, pelvis, proximal emur, and skull d. Bone scans: ypically “cold” in the absence o pathologic racture; skeletal survey is indicated to evaluate or other bony lesions. 3. reatment: combination o chemotherapy and radiation therapy with palliative surgical f xation o pathologic ractures to improve the patient’s quality o li e VII. Me ta s ta tic d is e a s e : umors metastatic to the skeleton are signif cantly more common than primary musculoskeletal tumors. Primary tumors that most commonly metastasize to bone include carcinomas o the breast, lung, prostate, thyroid, and kidney, or indeed, almost any type o tumor. A. Diagnosis: Most bony metastatic disease presents with pain in the involved bone. Metastatic bone disease may be the initial presentation o a malignancy. 1. Radiographs: Show most bone lesions to be lytic. With some breast tumors and most prostatic tumors, the bone lesion has a blastic appearance. 2. Bone scans: Help ul when a single symptomatic lytic lesion is ound on initial radiographs. I the bone scan shows multiple lesions, the likelihood o metastatic disease is high. 3. Skeletal metastases o unknown origin: best worked up with a history and physical examination; blood tests including CBC, thyroid-stimulating hormone, and calcium level; urine analysis; whole-body bone scan; plain radiographs o the chest and the involved bone; and a C scan o the chest, abdomen, and pelvis B. reatment: radiation therapy 1. Prophylactic bone f xation: indicated when a bone lesion places the bone at signif cant risk o racture without treatment 2. Pathologic ractures: generally should be f xed internally using a combination o metal implants plus methylmethacrylate bone cement to manage bone loss

ADULT ORTHOP EDICS Sho uld e r a nd Elb o w I. Ro ta to r c u te a r: Rotator cu consists o the supraspinatus, in raspinatus, teres minor, and subscapularis muscles. Acute tears occur in overhead throwing athletes or patients age older than 40 years with shoulder dislocation. Chronic degenerative tears are usually seen in patients older than 60 years. A. Symptoms: include shoulder pain exacerbated by overhead activity, night pain, and shoulder weakness B. Diagnosis: MRI is the imaging o choice to conf rm clinical suspicion or rotator cu tears. Ultrasound may be an e ective alternative but is dependent on the com ort level o the user. C. reatment: Physical therapy, NSAIDs, and steroid injection are the f rst line; arthroscopic rotator cu repair is indicated or ailed conservative treatment. II. Ante rio r s ho uld e r ins ta b ility: Most common cause is an anterior shoulder dislocation. A. Associated lesions: Bankart (tear o the anterior labrum) and Hill-Sachs (impaction o the posterior humeral head onto the anterior glenoid) lesions B. Recurrence: high rate—up to 90% in f rst-time dislocators age younger than 25 years III. La te ra l e p ic o nd ylitis : tendinosis (tendon degeneration) o the origin o extensor carpi radialis brevis (ECRB) tendon at the lateral epicondyle o the humerus; most common cause o elbow pain and attributed to overexertion o the orearm with repetitive wrist extension and orearm pronation/ supination A. Presentation: elbow pain exacerbated by resisted wrist extension and gripping activities B. Physical exam: reveals tenderness to palpation o the origin o ECRB on the lateral epicondyle

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C. reatment: Activity modif cation, physical therapy, NSAIDs, and steroid injections. A proximal orearm band may help alleviate symptoms, as it o oads tension rom the ECRB tendon. Surgical debridement o the tendon is warranted in patients re ractory to a orementioned management a er several months o symptoms.

Ha nd I. Ca rp a l tunne l s ynd ro m e : compression o the median nerve at the wrist; most common UE compressive neuropathy, a ecting up to 10% o the population A. Symptoms: numbness and paresthesias in the median nerve distribution B. Physical exam: may reveal thenar atrophy and positive inel sign at the wrist (tapping above the carpal aggravates symptoms) C. Diagnosis: Clinical; nerve conduction velocity (NCV) and Quic k Cut electromyography (EMG) may help conf rm the diagnosis. Carpal tunnel D. reatment: Wrist splinting, activity modif cation, or steroid s yndrome is initially managed injection into the carpal tunnel. I this ails, surgical release o the by res t and s plinting. transverse carpal ligament is indicated. II. Trig g e r f ng e r: Clicking and catching o the exor tendons at the A1 pulley (annular ligament at the metacarpophalangeal joint). Symptoms respond well to steroid injection. Surgical release o the A1 pulley indicated or ailed injections. III. P a ro nyc hia : in ection at the nail old; most common hand in ection A. Acute in ection: occurs secondary to trauma such as nail biting or manicure; most commonly S. aureus B. Chronic in ection: occurs with prolonged exposure to water or chemicals; most commonly Candida albicans C. reatment: removal o the nail plate, irrigation, and antibiotics/anti ungals IV. Fle xo r te no s yno vitis : in ection o the synovial sheath o the exor tendons o the hand Quic k Cut A. Symptoms: Kanavel signs ound on exam Kanavel s igns are: B. reatment: incision and drainage o the exor tendon sheath; • f exed pos ture o the IV antibiotics and observation o clinical improvement a ected nger V. Ga ng lio n c ys t: mucin-f lled cyst that involves a joint or tendon • pain with pas s ive s tretch o the digit sheath usually caused by trauma or degeneration; commonly • s aus age-like s welling occurs at the dorsal or volar wrist • tendernes s to palpation A. Presentation: Appears as a f rm, well-circumscribed mass that over the f exor tendon transilluminates over a light source. Symptoms may include • and pos s ible s pread by pain that radiates to the f ngers with wrist motion or direct communication with the s ynovial s heaths o the trauma to the cyst. thumb and s mall nger. B. reatment: Observation; aspiration has a high recurrence rate. Surgical cyst resection indicated or ailed observation and persistent pain.

Hip I. Tro c ha nte ric b urs itis : Pain over the lateral aspect o the hip thought to be due to in ammation in the bursa between the greater trochanter and the iliotibial band. endinosis o the gluteus medius and minimus tendons is o en the primary cause o trochanteric bursitis. A. Symptoms: Include lateral hip pain that may radiate to the buttocks, groin, or lower back. Pain is exacerbated by stair climbing or rising rom a seated position. Patients o en complain o inability to sleep on the a ected side. B. Physical exam: reveals tenderness to palpation over the trochanter and pain with resisted abduction C. reatment: NSAIDs, physical therapy, and steroid injection are o en e ective.

Kne e I. Ante rio r c ruc ia te lig a m e nt (ACL) te a r: ACL is the major ligament that stabilizes the tibia rom translating anteriorly beneath the emur. Most common mechanism is a noncontact pivoting injury; patients eel a “pop” in the knee and o en results in acute hemarthrosis. A. Physical exam: reveals a positive Lachman test (increased anterior tibial translation with the knee exed to 30 degrees)

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II.

III.

IV.

V.

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Orthopedics

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B. reatment: Nonoperative treatment with activity modif cation Quic k Cut and physical therapy is acceptable or low-demand patients. ACL Major ligamentous reconstruction indicated or active patients who want to return injuries can o ten be to sports and those with persistent instability. diagnos ed on phys ical examination alone. P o s te rio r c ruc ia te lig a m e nt (P CL) te a r: PCL stabilizes the tibia rom posterior translation beneath the emur. It is injured with a posteriorly directed orce onto the tibia such as a dashboard injury. A. Physical exam: reveals a positive posterior drawer test B. reatment: Bracing is indicated or low-demand patients. PCL reconstruction is indicated or PCL injuries combined with other ligamentous injury. Me d ia l c o lla te ra l lig a m e nt (MCL) te a r: MCL stabilizes the knee against valgus stress; most commonly injured ligament o the knee. reatment is physical therapy and bracing or partial tears. Operative repair or reconstruction or complete tears or combined ligamentous injuries. La te ra l c o lla te ra l lig a m e nt (LCL) te a r: LCL stabilizes the knee against varus stress; injury o the LCL is usually combined with other ligamentous injuries. reatment is physical therapy and bracing or partial tears. Operative repair or reconstruction or complete tears or combined ligamentous injuries. Me nis c a l te a r: variable etiology, location, and morphology A. Classif cation: degenerative, traumatic, or both B. Location: may occur in the medial (most common) or lateral compartments C. Involvement: may involve the lateral one third (vascularized), middle one third, or inner one third (avascular) zones o the meniscus D. ear pattern: may be vertical, horizontal, radial, bucket-handle, parrot beak, or complex E. Presentation: medial or lateral-sided joint pain with mechanical symptoms (clicking or locking o the knee) F. Physical exam: may reveal an e usion, joint line tenderness, and a positive McMurray test G. reatment: NSAIDs and physical therapy; surgical treatment or mechanical symptoms (catching/ locking) or persistent pain 1. Partial meniscectomy: or tears not amenable to repair 2. Meniscal repair: or tears in the peripheral (vascular) zone 3. Meniscal transplantation: option or young patients with normal mechanical alignment o the knee and no ull-thickness cartilage de ects Qua d ric e p s a nd p a te lla r te nd o n te a r: most o en occurs in middle-aged and older patients, especially those with diabetes mellitus or renal disease A. Physical examination: Mild swelling and tenderness; patient is unable to initiate extension against gravity with the knee at 90 degrees o exion. B. reatment: surgical repair

Fo o t a nd Ankle I. Ankle s p ra ins : typically inversion injuries that involve the anterior talof bular ligament (A FL) and less requently the calcaneof bular ligament (CFL) A. reatment: rest, ice, compression, and elevation (RICE) B. Functional mobilization: achieved with a stirrup brace with weight bearing as tolerated II. Ac hille s te nd o n d is rup tio ns : usually young to middle-aged patients who typically eel a sharp pain or hear an audible “pop” A. Physical examination: T ompson test is per ormed with the patient prone and the examiner squeezing the cal looking or plantar exion o the oot. Greatly decreased or absent exion is a positive sign o rupture. B. reatment: controversial 1. Casting: yields higher rerupture rates 2. Surgical treatment: increased in ection rate at the site

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Study Questions or Part VII

Study Questions or Part VII Directions: Each of the numbered items in this section is followed by several possible answers. Select the ONE lettered answer that is BES in each case. 1. A 47-year-old patient with a history o le -sided nephrectomy or trauma 20 years ago presents

with right ank pain and hematuria. Laboratory studies reveal a creatinine o 2.5 mg/dL. Which o the ollowing is the appropriate management plan? A. B. C. D. E.

Hydration overnight, ollowed by repeat evaluation o serum creatinine Intravenous pyelography (IVP) C scan o abdomen and pelvis with oral and IV contrast Ultrasonography ollowed by urgent cystoscopy Percutaneous nephrostomy tube placement

2. Which o the ollowing are potential sequelae o benign prostatic hyperplasia?

A. B. C. D. E.

Bladder stone ormation Recurrent urinary tract in ections secondary to prostatitis Prostate cancer Bladder cancer Organic impotence

3. A 68-year-old man undergoes a C scan o the abdomen as part o the evaluation or some mild

abdominal tenderness a er a motor vehicle collision. T e scan reveals no evidence o trauma, but a 4-cm solid le renal mass is noted. T ere is evidence o thrombus in the in erior vena cava. Which o the ollowing treatments is not indicated? A. B. C. D. E.

Preoperative chemotherapy and radiation to downstage tumor Resection o the le adrenal gland Resection o the para-aortic lymph nodes Resection o the le kidney Incision o vena cava and removal o thrombus

4. A 23-year-old man has a solid mass in his le testis. When it is removed, the pathology reveals

an embryonal carcinoma with a teratoma. A C scan o the chest and abdomen reveals 8 cm o lymphadenopathy in the periaortic nodes. What is the recommended treatment? A. B. C. D. E.

Modif ed nerve-sparing retroperitoneal lymph node dissection Full bilateral retroperitoneal lymph node dissection Chemotherapy with paclitaxel ( axol), gemcitabine, and cisplatin Chemotherapy with cisplatin, etoposide, and bleomycin Chemotherapy plus retroperitoneal radiation

5. Which testicular cancer cell type is extremely radiosensitive?

A. B. C. D. E.

Embryonal carcinoma Yolk sac tumor Seminoma Choriocarcinoma eratocarcinoma

Study Questions or Part VII

6. A 21-year-old male patient is brought to the emergency department or evaluation a er a motor

vehicle accident. As part o this secondary survey, the patient is ound to have blood at the urethral meatus. What is the next maneuver? A. B. C. D. E.

Foley catheter insertion ollowed by cystogram Urethrogram IVP C scan Diagnostic peritoneal lavage

Directions: T e group of items in this section consists of lettered options followed by a set of numbered items. For each item, select the lettered option(s) that is(are) most closely associated with it. Each lettered option may be selected once, more than once, or not at all. 7. A 70-year-old man presents to the outpatient clinic with complaints o di culty in voiding. He

reports some hesitancy in initiating ow, as well as a sense o incomplete emptying. He has not had any ever or chills and complains o only a mild dull pain in the lower midline. What is the most likely source o his symptoms? A. B. C. D. E.

Simple urinary tract in ection Pyelonephritis Prostatic cancer Benign prostatic hyperplasia Ureteral stones

8. T e patient has normal vital signs and no pain on physical examination. Ultrasound examination

in the previous patient demonstrates 150 mL o urine remaining in the bladder ollowing voiding. T e best initial treatment or the management o this patient is: A. B. C. D. E.

Narcotics Cipro oxacin amsulosin (Flomax) Cystoscopy Open prostatectomy with lymph node dissection

9. A 34-year-old man is involved in a motorcycle crash and sustains signif cant damage to legs and

skin. He has a large skin de ect over the majority o the back o the hand. T e most appropriate def nitive management or this patient is: A. B. C. D. E.

Split-thickness skin gra ing Primary closure Biologic dressing Vacuum-assisted closure Full-thickness skin gra ing

10. A 9-year-old boy alls o his bicycle, strikes the edge o a curb, and shears o a portion o his

upper lip. On examination, he is hemodynamically stable without evidence o any internal injury. T e right upper lip has a large ap that is nearly transected and ischemic and approximately 20% o the overall lip length. A er debridement o devitalized tissue, the best management or this de ect is: A. B. C. D. E.

Healing by secondary intention Primary closure Nasolabial rotational ap Buccal ap Free ap rom LE

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11. A 27-year-old man is struck on the side o the head during a company so ball game. T e patient

complains o headache, has had two episodes o emesis, and is somewhat lethargic. T e most likely source o his problems is: A. B. C. D. E.

Elevated intracranial pressure Contrecoup injury Cranial nerve V injury Cranial nerve VII injury Basilar skull racture

12. T e same patient rom question number 11 was initially brie y unconscious at the scene then

regained consciousness. Although under evaluation, his mental state deteriorates. T e most likely explanation or this is: A. B. C. D. E.

Subdural hemorrhage Subarachnoid hemorrhage Epidural hematoma Basilar skull racture Inner ear disruption

13. A 30-year-old woman is stabbed in the back and presents to the emergency department in a highly

anxious state. Her heart rate is 120 beats per minute and her blood pressure is 100/50 mm Hg. On exam, she does not have motor unction in her right leg, which is also numb. On the le leg, she does not react to pain ul stimuli and is insensate to temperature. T e most likely etiology o her problem is: A. B. C. D. E.

Central cord syndrome Neurogenic shock Anterior spinal cord injury Di use axonal injury Hemisection o the spinal cord

14. A 20-year-old man is in a motor vehicle collision and has a racture o the le tibia. On exam, he

has a nondisplaced racture and terrible pain in the leg, which seems to be getting worse despite narcotic pain medication. T e pulse in the leg is present but diminished relative to the other side. T e patient also complains o numbness in the a ected oot. T e best initial treatment is: A. P. C. D. E.

Fluid resuscitation Parenteral narcotics Operative release o the compartments o the leg External f xation C angiography

15. An 18-year-old girl alls rom atop a piece o urniture onto a hard sur ace but stops her all on an

outstretched hand. She only complains o pain in her wrist. What is the most likely injury? A. B. C. D. E.

Distal radial racture Distal ulnar racture Lunate bone racture Scaphoid bone racture Boxer’s racture

16. A 25-year-old man has been playing basketball when another player ell atop his knee. He elt a

popping sensation, ollowed by acute pain. On exam, the lower leg moves orward reely at the knee joint. T e patient has a weakly palpable pulse in the leg, and the ABI is 0.6 (and 1.0 on the una ected side). T e most appropriate next step is: A. B. C. D. E.

Angiography Knee brace immobilization Urgent arthroscopy Heparinization Serial pulse examinations

Study Questions or Part VII

17. A 47-year-old woman is undergoing a le mastectomy or a large breast cancer. Postoperative

chemotherapy is planned. Which o the ollowing is not true? A. B. C. D. E.

A tissue expander can be placed at the time o the initial operation to provide reconstruction. A latissimus dorsi ap can provide adequate tissue or reconstruction. Reconstruction must be delayed until a er treatment or the primary tumor is complete. A contralateral reduction mammoplasty can provide symmetry. Nipple reconstruction is typically per ormed as a separate procedure.

18. A 68-year-old woman has a Mohs excision on the tip o her nose. A ull-thickness skin gra with

a tie-over dressing is used. On the f h postoperative day, the dressing is removed, and the gra is pink. What is the most likely reason or this? A. B. C. D. E.

Imbibition Inosculation In ection Fibrination Collagenesis

19. Which o the ollowing is the best treatment or melanoma?

A. B. C. D. E.

Surgical excision Chemotherapy Radiation therapy Immunotherapy Regional hyperthermic per usion

20. A 21-year-old male su ers a severe comminuted racture o the right LE with considerable so

tissue loss a er a motorcycle accident. He has exposed bone and tendon in his wound a er external f xation. Which is the appropriate management? A. B. C. D. E.

Split-thickness skin gra Full-thickness skin gra Allogra ollowed by ull-thickness skin gra Z plasty Muscle ap

21. T e son o a 74-year-old woman calls her primary care physician or advice. He says that his mother

has been complaining o headache and vertigo or several hours and is vomiting. Apart rom a deep venous thrombosis in her le leg 2 months ago, she has been healthy. T ey shared dinner the night be ore, and she had been f ne. She now is asking or a prescription or the same motion sickness pills that she used to help her son when she drove him to camp. What should the physician do? A. B. C. D. E.

Call in a prescription or droperidol. Make arrangements to see the patient in clinic tomorrow. Make arrangements to see the patient in clinic today. Recommend that the patient be taken to the emergency department in an ambulance. Order a ventilation/per usion scan to rule out pulmonary embolism.

22. Which o these statements is true?

A. Brain metastases occur more requently than primary brain tumors. B. T e Cushing response is the tachycardia and hypertension seen with mass lesions o the pituitary. C. T e Cushing response is bradycardia and hypotension seen with terminal brain herniation. D. T e Cushing response is the maintenance o cerebral per usion pressure against variations in systemic blood pressure. E. Primary brain tumors are more common than metastatic brain tumors.

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Que s tio ns 23–24 A 38-year-old previously healthy emale presents with a single partial seizure. Physical examination is unremarkable. A C head scan shows a lesion that enhances with contrast measuring 1.5 1 cm in the tip o the right temporal lobe surrounded by a rim o local edema. 23. What is the best way to proceed?

A. B. C. D. E.

Stereotactic needle biopsy Open biopsy umor resection Electroencephalography (EEG) Brain MRI, chest radiograph

24. I this patient’s lesion is resected and it turns out to be a glioblastoma, which o the ollowing is true?

A. B. C. D. E.

T e patient’s median expected survival is 2 years. Additional surgery is not meaning ul. T e patient’s prognosis is unchanged by radiation therapy. Age is an important prognostic actor or this tumor. T e clinical presentation o the tumor was uncommon or this patient.

25. Which o the ollowing major joint dislocations constitutes the direst surgical emergency?

A. B. C. D. E.

Hip dislocation Knee dislocation Shoulder dislocation Elbow dislocation Subtalar dislocation

26. A 37-year-old intoxicated man is struck by the bumper o a car while he is crossing the street.

He sustains a comminuted closed proximal one-third tibia and f bula ractures. T e ractures are stabilized with an external f xator 1 hour a er the man arrives at the trauma bay. Approximately 2 hours a er surgery, he has a severe pain that is not controlled by IV morphine. T e physical examination demonstrates 2 dorsalis pedis and posterior tibial pulses, increased swelling o the leg, decreased sensation and paresthesias o the f rst web space, and exquisite pain with active and passive motion o the toes. What should be the next step in treatment? A. B. C. D. E.

Four compartment asciotomies o the leg Femoral angiography with runo Elevation o the leg above the heart Continued observation Repeat plain radiographs o the leg

27. Which o the ollowing describes the most appropriate treatment regimen or a newly diagnosed

primary osteogenic sarcoma o the distal emur? A. B. C. D. E.

Above-knee amputation and chemotherapy Radiation therapy Limb salvage surgery with marginal excision Neoadjuvant and adjuvant chemotherapy with surgical excision A combination o chemotherapy and radiation therapy

28. A patient is involved in a high-speed motor vehicle collision. T e patient has a Glasgow Coma

Scale (GCS) score o 7 on arrival. Which o the ollowing is not urgently indicated? A. B. C. D. E.

Emergent intubation Placement o an intraventricular catheter Nasogastric tube to prevent aspiration Spinal cord immobilization Urgent C scan o the brain

Answers and Explanations

Answers and Explanations 1. The a ns we r is D (Chapter 25, Urologic Emergencies, Obstructive Uropathy, and Urinary

ract Stones, reatment). An obstruction calculus in a patient with a single kidney represents an indication or emergency surgery. Hydration alone is insu cient and may lead to permanent renal impairment. Radiographic studies with IV contrast may cause nephrotoxicity with impaired renal unction. Percutaneous nephrostomy tube placement should be reserved or cases in which cystoscopy and retrograde pyelography and stent placement ail. 2. The a ns we r is A (Chapter 25, Benign Prostatic Disorders, Benign Prostatic Hyperplasia, V A 3).

Bladder stone ormation due to urinary stasis is a known sequelae o benign prostatic hyperplasia (BPH), and with severe obstructive symptoms, patients can have bilateral hydroureteronephrosis and renal ailure, commonly known as obstructive azotemia. Recurrent prostatitis is caused by bacterial or nonbacterial in ection o the prostate and has no correlation with BPH. Bladder and prostate cancer or organic impotence are not directly associated with BPH. 3. The a ns we r is A (Chapter 25, Genitourinary Malignancies, Renal Cell Carcinoma, III). Renal

cell carcinoma is very chemotherapy resistant. A le radical nephrectomy includes the le kidney, adrenal gland, and investing and ascia as well as a regional lymphadenectomy. Removal o tumor thrombus rom the in erior vena cava is indicated. 4. The a ns we r is D (Chapter 25, Genitourinary Malignancies, esticular umors, IV B). Men with

metastatic nonseminomatous testicular carcinoma, and in this case with bulky retroperitoneal disease, are best treated initially with systemic chemotherapy. T e agents o choice are cisplatin, etoposide, and bleomycin. 5. The a ns we r is C (Chapter 25, Genitourinary Malignancies, esticular umors, IV A).

Seminomas are uniquely radiosensitive among testicular tumors. Other nonseminomatous tumors, on the other hand, respond to chemotherapy and are generally radioresistant. 6. The a ns we r is B (Chapter 25, Urologic rauma, Bladder rauma [Lower Urinary ract], II A).

T e f nding o blood at the urethral meatus or an elevated prostate gland suggests a urethral tear. Passage o a Foley catheter may exacerbate a urethral tear. IVP and C scan detect injuries to the kidney, ureters, and bladder but not injuries to the urethra. T e patient must have a care ully per ormed urethrogram be ore any other urologic manipulation. 7. The a ns we r is D (Chapter 25, Benign Prostatic Disorders, Benign Prostatic Hyperplasia, III).

Benign prostatic hyperplasia is a common condition that presents with signs and symptoms due to the mechanical impingement o the urethra. Common symptoms include obstructive symptoms, such as those described in the question earlier, as well as irritative symptoms, such as requency, urgency, nocturia, and dysuria. Physical exam demonstrates an enlarged, f rm gland, and diagnosis may be conf rmed on biopsy. 8. The a ns we r is C (Chapter 25, Benign Prostatic Disorders, Benign Prostatic Hyperplasia, V).

T e initial treatment o benign prostatic hypertrophy is medical. Alpha blockade, such as with tamsulosin, is appropriate. Narcotics are use ul in the management o kidney stones. Antibiotics are appropriate or urinary tract in ection and suspected bacterial prostatitis. Cystoscopy is an excellent diagnostic maneuver or lesions o the bladder. Prostatectomy is typically reserved or cases o malignancy. 9. The a ns we r is E (Chapter 26, Reconstructive Plastic Surgery, Wounds and De ects, III A). A er

initial debridement and wound care to minimize contamination, the def nitive management o a unctional area across a joint is ull-thickness skin gra ing. Split-thickness gra s are contraindicated due to the risk o contracture and reduced mobility. Primary closure is a great technique or small de ects but produces too much tension in areas o substantial loss. Vacuumassisted closure su ers the same risk o loss o unction, and biologic dressings probably have their greatest use as temporary closure in burn patients.

499

500

Answers and Explanations

10. The a ns we r is B (Chapter 26, Reconstructive Plastic Surgery, Head-to- oe Reconstruction, V).

Lip de ects that are up to one third o the lip length are amenable to primary closure. Secondary intention produces signif cant de ormity. Local aps are unacceptable cosmetically, and ree aps rom dissimilar areas have no role in reconstruction. 11. The a ns we r is A (Chapter 27, Pathophysiology, Intracranial Pressure, IV). T e patient is

displaying classic signs o elevated intracranial pressure, including headache, nausea, and decreased levels o consciousness. Contrecoup injury may occur opposite the site o direct injury but in and o itsel does not explain the patient’s symptoms. rigeminal and acial nerve injuries are uncommon and do not lead to the listed symptoms. T e mechanism o injury is highly unlikely to damage the base o the skull. 12. The a ns we r is C (Chapter 27, Head Injury, Extra-axial Hemorrhages, I D). T e patient had a

“lucid interval” typical o the arterial injury associated with epidural hematomas. Subarachnoid hemorrhage usually produces a “thunderclap” headache that does not remit, and subdural hematomas produce chronic, progressive symptoms. Basilar skull racture may produce characteristic bruising patterns on the ace and head. 13. The a ns we r is E (Chapter 27, Spinal Cord Injury, Overview, III B 3). Brown-Séquard syndrome,

or hemisection o the spinal cord, typically results rom penetrating trauma, with loss o motor unction and sensation to light touch and vibration ipsilaterally, with loss o pain and temperature sensation contralaterally. Central cord lesions typically a ect upper extremities more than lower. T e patient does not meet parameters or shock. Anterior spinal cord problems lead to muscle weakness but preservation o sensation. Di use axonal injury leads to di culty with mentation rather than ocal sensory de ects. 14. The a ns we r is C (Chapter 28, Orthopedic Emergencies, Epidural Abscess, IV). T e patient is

presenting with early signs and symptoms o compartment syndrome. It would be reasonable to measure compartment pressures, but the treatment is emergent decompression. Overly aggressive uid resuscitation may worsen the symptoms, and narcotics may only mask the pain leading to worsening necrosis. External f xation is a good option i an open racture is present but will not address this patient’s problems. 15. The a ns we r is D (Chapter 28, rauma, Fractures in Adults, IV). T e scaphoid bone is the most

commonly injured bone o the wrist, typically injured during a all. T is represents an urgent situation, as the blood supply to this region is notoriously tenuous. Radiographs should be obtained immediately. I the racture is nondisplaced, a thumb-spica cast is appropriate; displaced ractures require operative f xation. 16. The a ns we r is A (Chapter 28, rauma, Dislocations, III B 1). A knee dislocation places the

popliteal artery at risk. T e priority is on diagnosis, with a ormal angiogram or patients with an abnormal ABI. A knee brace may be used but is insu cient to address the limb-threatening injury to the artery. Arthroscopic surgery may help with the ligaments but again ignores the vasculature. Heparin is not indicated until a diagnosis is made. 17. The a ns we r is C (Chapter 26, Head-to- oe Reconstruction, Breast Reconstruction, VII A).

Breast reconstruction can be per ormed either at the time o mastectomy or as a delayed procedure. iming is not dependent on adjuvant treatment. 18. The a ns we r is B (Chapter 26, Reconstructive Plastic Surgery, Wounds and De ects, III E 2). Skin

gra s are initially held in place by f brin bonds. Imbibition is rom passive movement o nutrient to the gra rom the donor tissue. When inosculation, or vascular budding, occurs, the gra turns pink rom return o circulation to the gra . 19. The a ns we r is A (Chapter 26, Wound Healing and Diseases o Skin and So

issue, Malignant Skin Lesions, III D). Surgical excision remains the def nitive treatment or melanoma. All o the other options are adjuvant treatments.

20. The a ns we r is E (Chapter 26, Reconstructive Plastic Surgery, Head-to- oe Reconstruction, XI

A). Bone denuded o periosteum and tendons does not support skin gra s. T ese areas require muscle aps or coverage.

Answers and Explanations

21. The a ns we r is D (Chapter 27, Spinal Cord Injury, Intracerebral Hemorrhage, I B). T e patient

has symptoms re erable to the central nervous system. Her age makes stroke likely. Having had a recent venous thrombosis, she will likely be on anticoagulant therapy. T us, a hemorrhage should be suspected. T ere is no in ormation about motor weakness; there ore, the cerebellum is a more likely location than the cerebrum. T e vertigo also implicates the cerebellum. T e posterior ossa is a very tight compartment, intolerant o mass e ects. Uncontrolled hypertension leads to progression o clot size and is the mechanism or rapid symptom progression and death. Even without clot growth, there is a risk or development o hydrocephalus. T e patient needs to be evaluated emergently, her blood pressure normalized i elevated, and a C scan per ormed to look or the suspected cerebellar hemorrhage. She will then need either surgery or observation in the intensive care unit. Pulmonary embolism is ar less likely than stroke and usually presents with dyspnea. T us, the ventilation-per usion scan is not indicated. T e son is not vomiting, so the ood they had shared is unlikely to be causing her symptoms. Droperidol is given intravenously and would be o little use to the patient at home even i all she really needed was an antiemetic. 22. The a ns we r is A (Chapter 27, Pathophysiology, Intracranial Pressure, IV). T e Cushing

response is the combination o bradycardia and hypertension. Metastatic cancers greatly outnumber primary brain neoplasms. Even i only one f h o cancers cause brain metastases, these still outnumber primary tumors. 23. The a ns we r is E (Chapter 27, Central Nervous System umors, Specif c Brain umors, I B). Late-

onset seizure should be considered to be caused by a brain tumor until proven otherwise. C head scan appearance is only suggestive o etiology; it cannot be ully depended on to distinguish between primary tumors and metastases. MRI can reveal additional small lesions o en not visible on C . Multiple lesions would suggest metastases rather than primary tumor, as primary parenchymal tumors are usually but not always solitary. A lesion ound on chest radiograph suggests a brain metastases because primary brain tumors do not spread to the lungs. I MRI shows multiple lesions, the surgeon can target the sa est one or biopsy. I there is only one lesion, suggesting a primary brain neoplasm, its location in the tip o the nondominant hemisphere allows or radical resection. 24. The a ns we r is D (Chapter 27, Central Nervous System umors, Specif c Brain umors, I B).

Younger patients with glioblastomas tend to survive longer than the elderly, and supratentorial location is more common than in ratentorial location in adults. T e median expected survival or a patient with a glioblastoma is 1 year. Aggressive cytoreductive surgery improves survival. T e di cult issue is the postoperative quality o li e. Survival is improved by radiation, although the time gained is weeks or months, not years. T e tumor was located in the anterior temporal lobe where seizures are a common presentation. 25. The a ns we r is B (Chapter 28, rauma, Dislocations, III). Dislocation o the knee is

accompanied by a 30%–33% incidence o injury to the popliteal vasculature (and nerve). A pre- and postreduction neurovascular examination is mandatory, and any suggestion o altered per usion (ABI 0.9, decreased pulses, signs o ischemia) requires an evaluation o the vascular supply distal to the knee. Frank tears or intimal injuries can occur. Dislocation o the hip can lead to avascular necrosis o the emoral head, especially i reduction is delayed or longer than 12 hours; however, this injury is not limb threatening. Shoulder dislocation is associated with axillary nerve trauma and rotator cu tears in older people. Simple (no racture) elbow or subtalar dislocations tend to be stable ollowing reduction. 26. The a ns we r is A (Chapter 28, Orthopedic Emergencies, Compartment Syndrome, III).

Compartment syndrome is common a er high-energy trauma, particularly that which has a component o crushing injury. T e diagnosis is made clinically by pain out o proportion to that expected rom the injury and pain with passive stretch o muscles in the involved compartment. Intracompartmental pressure monitoring can be used to conf rm the diagnosis or to make it in an obtunded patient. Femoral angiography would be indicated i vascular injury were suspected. Elevation o the leg can actually exacerbate compartment syndrome by decreasing the arterial in ow pressure i elevation is excessive. Plain radiographs and continued observation are not indicated because excessive delay in treatment can result in irreversible ischemia. Fasciotomies must be per ormed to relieve the compartment syndrome.

501

502

Answers and Explanations

27. The a ns we r is D (Chapter 28, umors, Primary Bone umors, VI A 4). Primary osteogenic

sarcoma occurs most requently in adolescence and young adulthood and appears most commonly about the knee (distal emur and proximal tibia). T e combination o neoadjuvant (be ore surgery) and adjuvant chemotherapy, with surgical resection to achieve at least a wide (2-cm cu o normal tissue) surgical margin, has increased the 5-year disease- ree survival rate to more than 60%. Radiation is not indicated when clean surgical margins are obtained. 28. The a ns we r is C (Chapter 27, Head Injury, Initial Management and Assessment, Increased

Intracranial Pressure Management). A GCS less than 8 requires intubation and intracranial pressure monitoring. Spinal cord immobilization should be practiced or all trauma patients. A C scan will greatly aid diagnosis. Although gastric decompression may be part o this patient’s management, this is a secondary concern. In act, placement o a tube be ore imaging may complicate a basilar skull racture.

Appendix A

Grade “A” Cuts: Use ul Surgical Kn wledge Pairings by System ASSOCIATIONS WITH HIGH VALUE FOR THE SURGICAL STUDENT Ca rd io va s c ula r

Think

A rtic dissecti n—pr ximal (type A)

Surgery

A rtic dissecti n—distal (type B)

Bl

Deep ven us thr mb sis (DV )/pulm nary emb lism (PE)

Best strategy is preventi n

ransient ischemic attack and car tid lesi n C mpleted str ke Abd minal a rtic aneurysm

d pressure c ntr l

Endarterect my Usually n surgery

5 cm

Repair

Abd minal a rtic aneurysm (AAA) and pain

Rupture; emergent repair

A rtic graf and gastr intestinal (GI) bleed

Rule ut (R/O) a rt enteric stula

A rtic graf and ever

R/O graf in ecti n

A rt iliac cclusive disease

Imp tence, butt ck claudicati n

Extremity rest pain r tissue l ss

Urgent revascularizati n

Ankle-brachial index (ABI) 0.4–0.7

Claudicati n

ABI

Rest pain

0.4

Extrinsic c agulati n cascade

Pr thr mbin time, bl cked by war arin

Intrinsic c agulati n cascade

Partial thr mb plastin time, bl cked by heparin

P pliteal aneurysms

Limb-threatening (thr mb sis)

Fem ral aneurysms

N t limb-threatening

Iliac veins

Have n valves

Virch w triad

Stasis, intimal injury, hyperc agulability

503

504

Appendix A

Es o p ha g us

Think

Dysphagia

Must d end sc py, R/O cancer

“Bird’s beak” es phagram

Achalasia

Nissen und plicati n

reats gastr es phageal re ux disease (GERD), n t Barrett dysplasia

P r peristalsis and GERD

C nsider Nissen with cauti n, may have dysphagia

High-grade Barrett

25% risk

Cancer in Barrett

Curative by resecti n

Es phageal cancer

EUS t stage; early disease is resectable

Zenker diverticulum

Cric thyr id t my

Es phageal per rati n

Diversi n, tube th rac st my

Es phageal per rati n

M st c mm nly iatr genic

Alkali injury

Lique acti n necr sis

Hist l gic layer absent in es phagus

Ser sa

Scler derma

Av id surgery

Sto m a c h/Duo d e num

carcin ma

Think

Gastric varices

Splenic vein thr mb sis

N nhealing gastric ulcer

Resecti n

Bleeding ulcer

End sc pic interventi n

Anteri r du denal ulcer

Per rates, patch with mentum

P steri r du denal ulcer

Bleeds, high rebleed rate

Gastr intestinal str mal tum r (GIS )

Resecti n

Muc sa-ass ciated lymph id tissue lymph ma Ulcer and high gastrin levels Severe besity (b dy mass index

ulcer, R/O cancer

/

imatinib

reat Helicobacter pylori (antibi tics) Z llinger-Ellis n syndr me

40 kg/m 2)

Bariatric surgery

M st eared bariatric surgery c mplicati n

Anast m tic leak

Gastric cancer

Surgery r R0 and R1 n dal disease

Nutriti nal de ciencies af er bariatric surgery

Vitamin B12, Ca, Fe, at-s luble vitamins

F ur maj r gastric arteries (tw gastric, tw gastr epipl ic)

Only ne st mach

M st imp rtant stimulus r secretin release

Gastric acid

M st imp rtant stimulus r gastrin release

A meal

M st imp rtant stimulus r parietal cell

Acetylch line, histamine, gastrin

Live r

ur necessary t preserve viability

Think

Cyst—simple

N surgery

Cyst with internal ech

Bacterial abscess

Cyst with “anch vy paste”

Amebic abscess

Cyst with calci cati ns

Echinococcus

Abscess eti l gy

Bacteremia, GI per rati n, intraven us drug abuse

S lid mass—m st c mm n benign lesi n

Hemangi ma

S lid mass—m st c mm n cancer

Metastasis

S litary c l rectal metastasis

P sitr n emissi n t m graphy t pr ve is lated, then resecti n

Hepatic aden ma

Has risk

rupture, f en surgery

Appendix A

Grade “A” Cuts: Use ul Surgical Kn wledge Pairings by System

F cal n dular hyperplasia (FNH)

Central stellate scar n c mputed t m graphy (C )

F cal n dular hyperplasia

N surgery

Alpha- et pr tein

Hepat cellular carcin ma

Bleeding es phageal varices

End sc pic banding

Re ract ry bleeding es phageal varices

ransjugular intrahepatic p rt systemic shunt

High MELD sc re r end stage liver disease

Seri us liver ailure (think transplant)

Bleeding with cirrh sis

L w act rs II, VII, IX, X, and platelets

Replaced right hepatic artery

Arises r m SMA

Bilia ry-P a nc re a s

Think

Jaundice—pain ul

Gallst nes

Jaundice—painless

Cancer

Primary scler sing ch langitis

Ulcerative c litis

Muc sal gallbladder cancer

Curable with ch lecystect my

Ch langi carcin ma

Usually n t resectable

Ampullary cancer

Of en curative resecti n is p ssible

Fever, jaundice, right upper quadrant pain

Ch langitis

Gallbladder wall edema and gallst nes

Acute ch lecystitis

Acute pancreatitis eti l gy

Gallst nes r alc h l

Chr nic pancreatitis

Ductal stricture (“chain

Pancreatic pseud cyst

M st res lve; therwise cyst—gastr st my

Pancreatic pseud cyst

C mmunicates with pancreatic duct

CA 19-9

Pancreatic cancer marker

Sm a ll Inte s tine

505

lakes”) and calci cati n

Think

Small b wel bstructi n (SBO) and hernia

Surgery

SBO m st c mm n cause in the United States

Adhesi ns

Cl sed l p bstructi n

Surgical emergency

Acute abd men

Alm st always surgical

Meckel diverticulum

Bleed (heter t pic gastric muc sa)

Intussuscepti n in adults

P lyp id mass as lead p int; resect

Cr hn disease

Creeping at, transmural in ammati n, perianal disease

Cr hn disease with bleed, stricture, per rati n, r stula Surgery Carcin id

the small b wel

Obstructi n, bleeding; m re aggressive

Carcin id

the appendix

Curable with resecti n, less aggressive

Co lo n

Think

Cecal v lvulus

Lef upper quadrant distended l p, surgical resecti n

Sigm id v lvulus

Right upper quadrant l p, dec mpressi n, then surgery

V lvulus

“Bent inner tube” sign n x-ray

Retr cecal appendix

20% ccurrence, n McBurney tenderness

Vascular watershed areas

Splenic exure, rect sigm id

Bl

C l n sc py—assess r ischemic c litis (IMA injury)

dy diarrhea af er AAA repair

Clostridium dif cile c litis

Diagn sis: p lymerase chain reacti n r pseud membranes Surgery i re ract ry t antibi tics (metr nidaz le)

506

Appendix A

Ulcerative c litis Ulcerative c litis

Increased risk

c l n cancer ver time

xic megac l n risk, pseud p lyps, n skip lesi ns

Ulcerative c litis

Cured by t tal pr ct c lect my

Ulcerative c litis

Sequence: in ammati n-dysplasia-cancer in at areas

C l n cancer

Sequence: APC p lyp-cancer

C l n cancer

Stage III gets adjuvant chem therapy

C l n cancer

5% incidence

Rectal cancer

Radiati n sensitive

Rectal cancer

Ne adjuvant s metimes used—stage III

Anal cancer

De nitive treatment is medical (n t surgery)

Pneumaturia

Fistula t bladder r m diverticulitis

Diverticular bleeding

Usually st ps sp ntane usly

End o c rine /Bre a s t

KRAS mutati ns-aden mat us

sec nd primary lesi n

Think

Multiple end crine ne plasia (MEN) 1

Pancreas, pituitary, parathyr id lesi ns

MEN 2A

Medullary carcin ma the thyr id (M C), phe , parathyr id hyperplasia

MEN 2B

M C, phe , mar an id habitus

T yr id n dule

Fine-needle aspirati n (FNA)

Papillary cancer

95% 5-year survival with thyr idect my, spreads by lymph n des

F llicular cancer

80% 20-year survival with thyr idect my, bl spread

Medullary thyr id carcin ma

P r pr gn sis, t tal thyr idect my

Primary hyperparathyr idism

Single aden ma, resecti n

Sec ndary hyperparathyr idism

Hyperplasia

Primary hyperald ster nism

L k

T ymect my

May cure myasthenia gravis

Phe chr m cyt ma

Adrenal medulla; alpha bl ck be re surgery

Ductal carcin ma in situ

Resecti n and radiati n therapy

L bular carcin ma in situ

Marker

Partial mastect my (lumpect my)

Equivalent survival t mastect my

In ammat ry breast cancer

Intradermal metastases, initial chem radiati n

Bl

Intraductal papill ma

dy nipple discharge

all glands in renal ailure

r ald ster ne-pr ducing adrenal aden ma.

r increased risk

N nres lving breast abscess

Breast cancer

Winged scapula af er axillary dissecti n

L ng th racic nerve injury

P e d ia tric s

d-b rne

bilateral breast cancer

Think

Abd minal wall de ect—gastr schisis

N ass ciated an malies, perate

Abd minal wall de ect— mphal cele

High ass ciated an malies, identi y be re repair

M st c mm n es phageal atresia

Pr ximal p uch with distal trache es phageal stula

Ile c lic intussuscepti n

Currant jelly st

Malr tati n

Bili us v miting

Pyl ric sten sis

Pr jectile v miting

Du denal atresia

D uble bubble sign, du denal bypass

ls, reduce with enema

Appendix A

Grade “A” Cuts: Use ul Surgical Kn wledge Pairings by System

Jejunal atresia

In uter vascular accident; resecti n

Hirschsprung disease

N mec nium in 24 h urs, rectal bi psy

Midline neck mass

T yr gl ssal duct cyst

Tra um a

Think

Cushing triad in traumatic brain injury

Bradycardia, hypertensi n, irregular respirati n

Cl sed head injury

Increases sympathetic t ne

Spinal c rd injury

Decreases sympathetic t ne

Penetrating neck trauma

Z ne II—OR; z ne I r III—imaging be re therapy

Rapid decelerati n injury

A rtic tear at ligamentum arteri sum

Initial w und healing

ype III c llagen pred minates

Initial w und

Po 2 at center

Electrical burn

Can underestimate injury; rhabd my lysis

Carb nace us sputum

Inhalati nal injury; intubate

Circum erential burn

Eschar t my (p ssible extremity ischemia)

Only burn antibi tic t penetrate eschar

Ma enide

Unc nsci us patient neck clearance

Clinical exam unreliable, use C

Bl

Urethral injury; urethr gram

d at meatus

M st sensitive sign M st c mm n

renal trauma

rm

w und is zer

Hematuria

sh ck

Hyp v lemia

M st c mm n rgan damaged in blunt trauma

Spleen; usually n n perative salvage

Splenect my

Vaccinate: Haemophilus in uenzae, pneum c ccus, mening c ccus

M st sensitive tissues t pressure

Skin

Othe r P a iring s d

r

muscle

Rectal, pr state, pancreatic, es phageal cancer staging

C with intraven us c ntrast; g d C with ral c ntrast; g d C chest; g d

at

Think

End sc pic ultras und; g

r

Vascular tum rs; necr tic pancreas; abscess (“rim-enhancing”); “blush” equals bleeding

r

B wel versus abscess

r

Es phageal injury/leak, c in lesi n, PE

F cused assessment with s n graphy r trauma (FAS ); g d r

Abd minal trauma, pericardial e usi n ( uid bleeding in trauma)

End sc pic retr grade ch langi pancreat graphy (ERCP); g d r

C mm n bile duct st nes, bile leak, pancreatic duct gram (pseud cyst) Carries a 2% incidence pancreatitis

Ultras und; g

DV (duplex), visceral vessel assessment

agged red bl

d

r

d cell scan; g d

echnetium-99 scan; g

d

r

GI bleeding, hepatic hemangi ma (magnetic res nance imaging [MRI] and C angi graphy als diagn stic)

r

Hepatic imin diacetic acid scan (HIDA); g d

T yr id, Meckel, biliary tree r

Acute ch lecystitis, biliary dyskinesia

Suspected spinal c rd injury

C r b ny injury MRI r ligament us injury

Rapid c rrecti n

May cause central p ntine myel sis

Order

507

hyp natremia

cell arrival in w und

P lym rph nuclear leuk cyte, macr phage, lymph cyte, br blast

508

Appendix A

Chr nic w unds

Pressure s res, diabetic

Reverse ster id e ect n w und healing

Vitamin A

Kel id

Gr ws bey nd b rder

War arin-induced skin necr sis

Pr tein C de ciency

Catheter-related bl

C ag-negative Staphylococcus

dstream in ecti ns

t ulcer, ven us leg ulcers riginal scar

Sp ntane us bacterial perit nitis

Gram-negative bacteria

In ecti n with lactati n

Staphylococcus aureus

Acute sialadenitis

S. aureus

Small intestinal cell uel

Glutamine

C l n cyte uel

Sh rt-chain atty acids

Sh rt-chain atty acids

Acetate, butyrate, pr pi nate

Maj r hist c mpatibility c mplex II

Antigen-presenting cells (macr phages, dendritic cells), end thelium

Index

509

Index Page numbers ll wed by f and t indicate f gures and tables, respectively.

A AAA. See Abd minal a rtic aneurysm Abbé lip switch lap, 438 ABCDE assessment, 352 Abd men, acute surgical, 58–66 c nditi ns masquerading as, 63 cuts and caveats n, 2 de initi n , 58 diagn stic testing in, 60–62 diet and b wel changes in, 58 di erential diagn sis , 62–63 hem rrhage and, 65–66 imaging , 61–62, 61f lab rat ry evaluati n , 60–61 LLQ pain in, 63 LUQ pain in, 63 bstructi n and, 63–65 pain characteristics , 58, 59f pertinent medical hist ry in, 59 physical exam , 59–60 RLQ pain in, 62 RUQ pain in, 62 study questi ns n, 70–72, 75–76 systemic signs , 58 Abd minal a rtic aneurysm (AAA), 128–130, 129t Abd minal exam, 59 Abd minal injury, 357–358, 358f FAST assessment , 357, 358f h ll w viscus, 358 s lid rgan, 357, 358f vascular, 358 Abd minally based laps, r breast rec nstructi n, 440 Abd minal rec nstructi n, 442 Abd minal wall de ects, 379–381, 379t Abd minal wall hernias, 38–39 Abd minal wall rec nstructi n, 442 Abd min plasty, 448 ABGs. See Arterial bl d gases ABI. See Ankle-brachial index ABO bl d gr up, 15, 364 Ab ve-knee amputati n, 125 Abscesses, 40 amebic, 209 an rectal, 200–201, 201f appendiceal, 339 Bez ld, 302 breast, 259 Cr hn disease and, 179, 195–196 cutane us, 40 hepatic, 209 intra-abd minal, 40, 191 lung, 85 neck, 300–302, 301t

parapharyngeal space, 302 perit nsillar, 300, 308 retr pharyngeal, 302 spinal epidural, 472 splenic, 233 subphrenic, 236 Abs rbable suture, 32, 33t Abs rpti n, in small intestine, 174–175 Acalcul us ch lecystitis, 212 ACC. See American C llege Cardi l gy Acetylch line, in myasthenia gravis, 289 Achalasia, 155–156, 155f, 162 Achilles tend n disrupti ns, 493 Acid(s), weak, 11 Acid–base balance bl d gas assessment , 12t disturbances in, 11–12. See also specific types regulat ry systems r, 11 Acid sis, 11–12 hyp c agul pathy in, 14 metab lic, 11–12, 12t, 54 respirat ry, 11, 12t ACL. See Anteri r cruciate ligament (ACL) tear Acne inversa (hidradenitis suppurativa), 40, 201, 442 Ac ustic neur ma, 306, 465 Acquired heart disease, 93–102 ACR. See Acute cellular rejecti n ACT. See Activated cl tting time ACTH. See Adren c rtic tr pic h rm ne Activated cl tting time (ACT), 14 Activated partial thr mb plastin time (aPTT), 14 Acute arterial insu iciency, 124–125 Acute cellular rejecti n (ACR), 364, 365f Acute c r nary disease, trans usi n therapy in, 16 Acute kidney injury (AKI) p st perative c mplicati ns in, 55 surgical patients with, 53–55 Acute n rm v lemic hem diluti n, 16 Acute Physi l gy and Chr nic Health Evaluati n II (APACHE II), 219, 222t Acute suppurative par titis, 324 Acute suppurative thyr iditis, 272 Acute surgical abd men. See Abd men, acute surgical Acute urinary retenti n, 412 Adamkiewicz, artery , 450 Addis n disease, 281 Aden carcin ma, 344 anal, 203 es phageal, 159 gastric, 168–169

lung, 86 nasal and paranasal, 313 pancreatic, 225–229 small intestine, 177 Aden cyst ma, papillary, par tid, 322–323 Aden idal hypertr phy, 305 Aden id carcin ma, 89 Aden id cystic carcin ma, br nchial, 88–89 Aden idect my, 308 Aden ma(s) br nchial, 88–89 c l rectal, 184–185 hepat cellular, 208 parathyr id, 276–279 par tid gland, 322–323 pituitary, 287, 465–466 small intestine, 176 t xic (thyr id), 272 Aden ma–carcin ma sequence, 345, 345f Aden mat us p lyp sis c li (APC) gene, 185 Aden mat us p lyps, 171, 184 Aden t nsillitis, 308 ADH. See Antidiuretic h rm ne; Atypical ductal hyperplasia Adjustable gastric banding, 326, 327f c mplicati ns , 330 utc mes , 329 Adjuvant treatment, 350 Ad lescents, bariatric surgery in, 326 Adrenal c rtex, devel pment , 279–280 Adrenal cysts, 285 Adrenalect my, lapar sc pic, 342 Adrenal glands, 279–285 anat my , 280 cuts and caveats n, 254–255 embry l gy , 279–280 path l gy , 281–285 study questi ns n, 290–291, 294–295 Adrenal h rm nes, 280 Adrenal medulla, devel pment , 279–280 Adren c rtical carcin ma, 285 Adren c rtical insu iciency, 281 Adren c rtical rests, 280 Adren c rtic tr pic h rm ne (ACTH), 280–283 Advanced trauma li e supp rt (ATLS), 352, 454, 478 Advancement lap, 434, 442 Aesthetic plastic surgery, 446–449 a ter massive weight l ss, 448–449 candidate selecti n r, 446 c mm n pr cedures in, 447–448 rati nale r, 446 A erent l p syndr me, 170 A terl ad, 27–29

509

510

Index

AHA. See American Heart Ass ciati n AICD. See Aut matic implantable cardi verter-de ibrillat r AIOD. See A rt iliac cclusive disease Airway assessment, 352 Airway c ntr l, in intensive care unit, 21–22 Airway bstructi n, 21–22, 90–91 AIs. See Ar matase inhibit rs AKI. See Acute kidney injury Alc h l-induced pancreatitis, 217, 223 Ald ster ne, 280 Ald ster n ma (C nn syndr me), 282t, 283–284 Alemtuzumab, 366t ALH. See Atypical l bular hyperplasia Alkaline re lux gastritis, 170 Alkal sis, 12 metab lic, 9, 12, 12t respirat ry, 12, 12t Allergic reacti n, t trans usi n, 15 All gra t c mp site tissue, 375 de initi n , 363 vascularized c mp site, 375 Alpha-adrenergic ag nists, peri perative, 49 Alpha- et pr tein germ cell tum rs and, 90 testicular tum rs and, 422 Alve lar minute ventilati n, 22 Amaur sis ugax, 125 Ambulat ry ven us pressure (AVP), 141 Amebic abscess, 209 American C llege Cardi l gy (ACC), risk assessment t l , 47 American Heart Ass ciati n (AHA), risk assessment t l , 47 American S ciety Anesthesi l gists (ASA), physical status classi icati n , 45, 45t Amine precurs r uptake and decarb xylati n (APUD) system, 177, 189 AMPLE hist ry, in trauma assessment, 353 Amputati ns in arterial disease, 125 digit (hand), 445 AMR. See Antib dy-mediated rejecti n Amylase pancreatic, 175, 218 salivary, 175 Anab lic envir nment, 17 Anal canal, 182 Anal canal ne plasms, 202–203 Anal cancer, 202–203 Anal ducts, 181 Anal issure, 200 Anal glands, 181 Anal sten sis, 199 Anaplastic thyr id carcin ma (ATC), 275–276, 275t Andr gens, 280 Anemia in chr nic kidney disease, 54, 55 hem lytic, 232 sickle cell, 232 in splenic path l gy, 231–232 Anesthesia r patient with liver disease, 56–57

r patient with lung disease, 52 r patient with renal disease, 54–55 Aneurysm(s) abd minal a rtic, 128–130, 129t arterial, 128–130 ascending a rtic, 90 ather scler tic, 460 berry, 460 internal car tid– phthalmic, 460 myc tic, 460 renal artery, 372 rupture, and subarachn id hem rrhage, 460 splenic artery, 130 Angina classi icati n , 47, 47t Ludwig, 302 in surgical patient, 47 Angina pect ris, 100 Angi dysplasia, 192 Angi graphy, 66 Angi graphy, laser, 449 Angi plasty, 100, 121, 127 Angi s mes, 435 Angi tensin-c nverting enzyme, 280 Angi tensin I, 280 Angi tensin II, 280 Angi tensin gen, 280 Angle His, 156, 161 Animal bites, 445 Ani n gap, 11 Ankle-brachial index (ABI), 120, 121t, 122, 359, 486 Ankle dis rders, in adults, 493 Ankle ractures, 484, 485f Ankle sprains, 493 Annular pancreas, 385 An -genital warts, 202 An rectal abscess, 200–201, 201f An rectal disease, benign, 199–202 An rectal dys uncti n, 198–199 An rectal istula, 200–201 An rectal man metry, 183 An rectal ring, 181 An sc py, 182 Anteri r cerebral artery, 450 Anteri r c mpartment, mediastinum anat my , 78, 79f lesi ns , 90 Anteri r cruciate ligament (ACL) tear, 492–493 Anteri r parasternal mediastin t my, 81 Anteri r sh ulder instability, 491 Anteri r spinal artery, 450 Anter lateral th rac t my, 81, 82f Antiarrhythmic drips, 26 Antibi tic(s) b wel preparati n, 184 pr phylactic, 40, 45, 50, 52, 55, 236 Antibi tic-ass ciated c litis, 196 Antib dy(ies) m n cl nal, in cancer treatment, 350 in rgan transplantati n, 364 Antib dy-mediated rejecti n (AMR), 364 Antic agulati n, pre perative, 45–46, 46t Antidiuretic h rm ne (ADH), inappr priate secreti n , 7–8

Anti- act r Xa activity, 14 Antithr mbin III, 13 Antithr mbin III mutati ns, 15 Antithym cyte gl bulin, 366t Antithyr id drugs, 270–271 Anus anat my , 181–182 cuts and caveats n, 151 evaluati n , 182–183 physi l gy , 182 A rtic aneurysms abd minal, 128–130, 129t ascending, 90 A rtic c arctati n, 103 A rtic disrupti n, 91–92 A rtic dissecti n, 124, 127–128 classi icati n , 127, 127f diagn sis and management , 128 type A, 128 type B, 128 A rtic injury abd minal, 358 blunt th racic, 356 A rtic insu iciency, 93, 96–97 A rtic regurgitati n, 47 A rtic sten sis, 96 A rtic valve replacement, 97 A rtic valvular disease, 96–97 A rt bi em ral bypass, 121–122 A rt iliac cclusive disease (AIOD), 118, 120–122 APACHE II sc re, 219, 222t Ap plexy, 465 Appendect my, lapar sc pic, 335, 339, 339f Appendiceal abscess, 339 Appendicitis, abd minal pain in, 62 “Apple-peel” atresia, 387 aPTT. See Activated partial thr mb plastin time Aqueductal sten sis, 466 Arachn id villi, 451 Are lexia, bladder, 424–425 Ar matase inhibit rs (AIs), 261, 351 Arrhythmia p st perative, 51 preventi n in ICU, 26 Arterial aneurysms, 128–130 Arterial bl d gases (ABGs) in acid–base dis rders, 12t pre perative, 51 in weaning r m ventilat r, 23 Arterial catheter, 24, 50 Arterial disease, 118–134 amputati ns in, 125 a rt iliac cclusive, 118, 120–122 em r p pliteal cclusive, 122–123, 123f in rageniculate tibial, 123–124 l wer extremity cclusive, 118–120 path physi l gy , 118 peripheral, 120 spectrum , 119f untreated, natural hist ry , 120 Arterial dissecti n, 124 Arterial insu iciency, acute, 124–125 Arteri ven us istulas, 55 Arteri ven us istulas, traumatic, 210 Arteri ven us hemangi mas, 304

Index Arteri ven us mal rmati n (AVM), 459 Arteritis, giant cell (temp ral), 133 Arthritis, 486–488 classi icati n , 486–487 n n perative management , 487 perative management , 487 p st-traumatic, 487 rheumat id, 487 septic, 476, 488 Arthr desis, 487 Arthr plasty, 487 Aryten id disl cati n, 308 ASA. See American S ciety Anesthesi l gy Ascending a rtic aneurysms, 90 Ascites, 57, 212 ASDs. See Atrial septal de ects Assist r v lume c ntr l (AC/VC), in ventilat r supp rt, 22 Asthma, surgical patients with, 52 Astr cyt ma, 462–463, 463f, 470 ATC. See Anaplastic thyr id carcin ma Atelectasis, 39, 53, 235 Ather scler sis, 99, 118, 120 Ather scler sis, car tid artery, 125–127, 126f Ather scler tic aneurysm, 460 ATLS. See Advanced trauma li e supp rt At nic bladder, 425 Atrial septal de ects (ASDs), 103–104, 104f Atypical ductal hyperplasia (ADH), 260 Atypical l bular hyperplasia (ALH), 260 Atypical myc bacteria in ecti n, 308 Auerbach (myenteric) plexus, 154, 174 Auricle ear, examinati n , 299 Auscultati n, 93, 356 Aut gra t, 362 Aut immune pancreatitis, 218 Aut l g us banked bl d, 16 Aut matic implantable cardi verter de ibrillat r (AICD), 47 Aut n mic dysre lexia, 426–427 Aut regulati n, 452 Aut trans usi n, 16 AVFs. See Arteri ven us istulas AVM. See Arteri ven us mal rmati n AVP. See Ambulat ry ven us pressure Axial lap, 434f, 435 Axillary nerve, 471, 471f Axillary th rac t my, 81 Axill bi em ral bypass, 122 Azathi prine, 366t

B Bacterial end carditis, pr phylaxis against, 50 Bacteroides, 182 Bacteroides fragilis, 40 Ball n angi plasty, 100 Bariatric beriberi, 334 Bariatric surgery, 325–334 r ad lescent patients, 326 classi icati n , 326–328 c mbined restrictive and malabs rptive perati ns in, 328, 329f cuts and caveats n, 296 r elderly patients, 326 malabs rptive perati ns in, 327, 328f m rtality in, 329

nutriti nal c nsiderati ns in, 328, 334 utc mes , 329 patient selecti n r, 325–326 p st perative c mplicati ns , 329–334 p st perative c nsiderati ns in, 328 restrictive perati ns in, 326–327, 327f study questi ns n, 398, 405–406 Barium enema, 182 Barrett es phagus, 157–158, 159 Basal cell carcin ma, 443 anal, 202, 202t hand, 446 head and neck, 318–319 Basal metab lic rate (BMR), 17 Basic metab lic panel, 44t, 53 Basilar artery, 450 Basilar skull ractures, 456 Basiliximab, 366t Bassini repair, 38 Battle sign, 456 Beckwith-Wiedemann syndr me, 395 Belatacept, 367t Bell’s stages, necr tizing enter c litis, 393–394 Bel w-knee amputati n, 125 Belsey Mark IV perati n, 157 Bend ractures, 479f Benign, de initi n , 344 Benign pr static hyperplasia (BPH), 415–417 Benz diazepines r patient with liver disease, 57 r patient with renal disease, 55 Beriberi, bariatric, 334 Berry aneurysms, 460 Beta-bl cker therapy, peri perative, 49 Beta-human ch ri nic g nad tr pin germ cell tum rs and, 90 testicular tum rs and, 422 Beta-2 trans errin, 456 Bez ars, 171 Bez ld abscesses, 302 Bicarb nate, in acid–base balance regulati n, 11 Bile intraperit neal extravasati n , 214 pr ducti n , 206 Bile duct cancer, 213–214 Biliary atresia, 391–392, 392f Biliary tree anat my , 204, 206f cuts and caveats n, 151–152 embry l gy , 204 ne plasms , 213–214 path l gy , 213–214 physi l gy , 205–206 trauma t , 214 Bili pancreatic diversi n, 327, 328f, 329, 334 Bili pancreatic diversi n with du denal switch, 327, 328f, 329, 334 Bili us emesis, 384 Billr th I gastrect my, 164, 165f Billr th II gastrect my, 164, 165f Bil bed lap, 434 Bi l gic agents, r arthritis, 487 Bi l gic dermal matrix, 449 Bi pr sthetics, 449

511

Bi psy, 347–348 breast, 257–258, 258t, 259t excisi nal, 348 head and neck, 300, 311 image-guided, 348 incisi nal, 348 liver, 56 lung, 81 pleural, 81 pr state, 417 scalene n de, 80 sentinel n de, 263, 319, 348–349, 444 thyr id, 273–274 Bi therapy, 350 Bite injuries, 445 BK p ly ma virus, 367 Bladder carcin ma, 418–419 Bladder laccidity, 424 Bladder veractivity, 424–425 Bladder trauma, 358, 428 Blast e ect, r m gunsh t w unds, 428 Bleeding time, 13, 53 Blephar plasty, 447 Bl d gases in acid–base dis rders, 12t pre perative, 51 in weaning r m ventilat r, 23 Bl d l ss, acute unexpected, 16 Bl d pressure high. See Hypertensi n l w. See Hyp tensi n m nit ring in ICU, 24–25 Bl d trans usi n, 15–16 alternatives t , 16 disease transmissi n in, 15–16 indicati ns r, 16 risks , 15–16 Blue t e syndr me, 120 Blunt trauma cardiac, 356 cerebr vascular (BCVI), 355 chest, 354 head, 454 renal, 427 testicular, 429 th racic a rtic, 356 ur l gic, 427 BMI. See B dy mass index BMR. See Basal metab lic rate B dy c nt uring/sculpting, 448–449 B dy mass index (BMI), 325, 325t B dy sur ace area (BSA), in burn injuries, 360, 360f B dy weight, water calculati n with, 5 B erhaave syndr me, 63, 160 B il ( uruncle), 40 B ne lap, 436 B ne gra ts, 433 B ne in ecti ns, 488–489 B ne marr w bi psy, in hypersplenism, 233 B ne replacement materials, 449 B ne tum rs, 489–491 adjuvant therapy r, 490 benign, 490 diagn sis , 489, 489f hand, 446 malignant, 490

512

Index

B ne tum rs (continued) metastatic, 490, 491 primary, 489–491 surgical treatment , 490 B wel adhesi ns, 59 B wel changes, acute surgical abd men and, 58 B wel intussuscepti n, 58, 64, 176 B wel bstructi n, 63–65, 197–198 B wel preparati n, 184 B wen disease, 202, 202t B xer’s racture, 483 BPH. See Benign pr static hyperplasia Brachial plexus anat my , 471, 471f injuries , 471, 474 Brachi plasty, 448 Bradycardia, in neur surgical patient, 453 Braided sutures, 32, 33t Brain anat my , 450 arterial supply , 450 aut regulati n , 452 path physi l gy in, 451–453 ven us drainage , 450 Brain death, d n rs a ter, 363 Brain herniati n, 452 Brain metastases, 464 Brain stem re lexes, 453 Brain trauma, 354, 454–457 ICP management in, 454–455 initial management and assessment , 454 primary, 454 radi graphic studies , 454 sec ndary, 454 seizure pr phylaxis in, 455 Brain tum rs, 462–466 classi icati n , 462 diagn sis , 462 epidemi l gy , 462 Branchial cle t an malies, 302–303, 302t BRAVA, 434 BRCA-1/BRCA-2 genes, 261 Breast, 256–265 anat my , 256, 257f, 258f benign disease , 259–260 cuts and caveats n, 254 de rmities , 440–441 evaluati n , 256–258 palpati n , 256 physical examinati n , 256 radi l gic exam , 257 study questi ns n, 291–295 visual inspecti n , 256 Breast abscess, 259 Breast augmentati n, 447 Breast bi psy, 257–258 c re-needle, 257, 258t, 259t ine-needle aspirati n, 257 surgical (excisi nal), 258 Breast cancer, 260–265 epidemi l gy , 260 ll w-up r perable, 264 h rm nal therapy r, 351 in lammat ry, 262 invasive, 262 in male breast, 265

medullary, 262 metastatic, 261–262, 264 n ninvasive, 262 in pregnancy, 264 pr phylactic surgery t prevent, 349 recurrent, 264 risk act rs r, 260–261, 261t risk reducti n with medicati n, 261 screening r, 346 staging , 262, 263t sympt ms , 261–262 treatment , 262–263 Breast cysts, 260 Breast pt sis, 447, 448, 448f Breast rec nstructi n, 439–441, 440f Breathing, assessment , 299, 352 Bresl w meth d, melan ma staging, 444 Bridging veins, 457 Br nchial aden mas, 88–89 Br nchial artery, 80 Br nchial tubes, 80 Br nch genic carcin ma, 85–88 clinical presentati n , 86 diagn sis and staging , 86–87, 87t path l gy , 86 treatment , 88 Br nch genic cysts, 90 Br nch pulm nary segments, 79f, 80 Br nch sc py, 80 Br w li t, 448 Br wn-Séquard syndr me, 458 Brush b rder, 175 Buckle ractures, 479f, 480, 481f Budd-Chiari syndr me, 210 Buerger disease, 134 Bu ering systems, 11 Burns, 359–361 cuts and caveats n, 297 electrical, 361 evaluati n and treatment , 360 luid resuscitati n in, 360 ull-thickness, 360 initial treatment , 359 partial-thickness, 360 rule 9’s in, 360, 360f study questi ns n, 401–403, 407–408 super icial, 360 t pical antimicr bials r, 360–361 Bursitis, tr chanteric, 492 Butter ly ractures, 479f

C CABG. See C r nary artery bypass gra t Cachectic patient, nutriti nal status evaluati n in, 18 CAD. See C r nary artery disease Cajal cells, 177 Calcaneus ractures, 485 Calcium de iciency, in bariatric surgery patients, 334 digesti n and abs rpti n , 175 imbalances , 10. See also Hypercalcemia; Hyp calcemia in hyperparathyr idism, 277–279 in hyp parathyr idism, 276 in thyr id dys uncti n, 271

IV c ncentrati ns , 6, 6t in surgical patients with renal disease, 54 Calcium xalate st nes, 414 Calcium pyr ph sphate dep siti n disease, 487 Calcul us sialadenitis, 324 Cal ric requirements, 17–18 Cal rimetry, indirect, 18 Cancer. See also specific types adjuvant/ne adjuvant therapy r, 350 adren c rtical, 285 anal, 202–203, 202t bile duct, 213–214 bladder, 418–419 b ne, 489–491 breast, 260–265, 346, 351 cellular mechanisms in, 345 cervical, 346 chem therapy r, 350 clinical trials n, 351 c l rectal, 62–63, 186–189, 345, 345f, 346 de initi ns in, 344 diagn sis , 346–347 diagn stic pr cedures r, 347–348 epidemi l gy , 345, 345t es phageal, 159–160, 316–317 eti l gy , 344–345 gallbladder, 213 gastric, 164, 168–170 genetics , 344–345 genetic therapy r, 351 genit urinary, 417–423 hand, 446 head and neck, 308–311 h rm nal therapy r, 351 imaging , 347 kidney renal cell carcin ma, 421, 422f Wilms tum r, 395–396, 396t lapar sc pic staging , 342 laryngeal, 317–318, 318f liver, 208–209, 208f lung, 85–88 lymph n de status in, 348–349 m rtality in, 345, 345t multidisciplinary treatment , 350–351 nasal and paranasal, 312 nas pharyngeal, 313–314 neck, 311–312 ral cavity, 314 r pharyngeal, 315 pancreatic, 225–229 par tid gland, 323 pr state, 346, 351, 417–418 radiati n therapy r, 350 recurrence , trans usi n and, 16 renal pelvis and ureteral, 419, 420f screening r, 346 skin, 443–444 basal cell carcin ma, 202, 202t, 318–319, 443 hand, 446 head and neck, 318–319 melan ma, 177, 203, 319, 444, 446 squam us cell carcin ma, 318–319, 443 transplant-related, 367 small intestine, 177–178

Index splenic, 234 staging, 348 subtypes , 344 surgery r, 348–351 curative, 349–350 cuts and caveats n, 297 diagn stic, 348–349 ll w-up in, 350 palliative, 350 pr phylactic, 349 research and training n, 351 thyr id, 272–276, 288 tum r markers in, 347, 347t Cancer vaccines, 350 Capillary hemangi mas, 304 Capsule end sc py, 65 Carb hydrates, digesti n and abs rpti n , 175 Carb n di xide, in acid–base balance regulati n, 11 Carb xyhem gl bin level, 361 Carbuncle, 40 Carcin carcin ma, par tid gland, 323 Carcin embry nic antigen (CEA), 187, 189 Carcin gens, 345 Carcin id syndr me, 189 Carcin id tum rs br nchial, 88 c l rectal, 189 small intestine, 177–178 Carcin ma, 344. See also specific types Carcin ma ex ple m rphic aden ma, 323 Cardiac arrest, 94 Cardiac b x, 356, 357f Cardiac catheterizati n, 94 Cardiac c ntusi n, 92 Cardiac death, d n rs a ter, 363 Cardiac (heart) disease acquired, 93–102 epidemi l gy , 93 physical indings , 93 pre perative management , 93–94 signs and sympt ms , 93 c ngenital, 102–107 surgical patient with assessment disease and risk act rs in, 46 bacterial end carditis pr phylaxis r, 50 cardiac hist ry , 47 c m rbid c nditi ns in, 46 c r nary artery revascularizati n r, 49–50 ECG indicati ns in, 47 evaluati n , 46–51 general aspects , 46 HMG-C A reductase inhibit rs r, 50 invasive hem dynamic m nit ring , 50 m di iable risk act rs in, 49 n ninvasive and invasive cardiac testing in, 48–49 n rm thermia maintenance in, 50 peri perative alpha-adrenergic ag nists r, 49 peri perative beta-bl cker therapy r, 49

peri perative management and risk reducti n r, 49–50 physical exam , 47 p st perative c mplicati ns in, 50–51 pre perative risk assessment strati icati n t ls r, 47–48, 48t Cardiac hist ry, 47 Cardiac injury, 101–102, 356 Cardiac massage, 94 Cardiac utput, 368 Cardiac risk in n ncardiac pr cedures, 44, 45t in patients with cardiac disease. See Cardiac disease, surgical patient with Cardiac silh uette, 352 Cardiac tamp nade, 28, 91, 368 Cardiac tum rs, 101 Cardi genic sh ck, 27, 28t Cardi plegia, 94 Cardi pulm nary bypass, 94, 95f Cardi pulm nary resuscitati n (CPR), 94 Car tid angi plasty, 127 Car tid arteries, 450 ather scler sis , 125–127, 126f duplex screening , 120 injury t , 355 Car tid b dy tum rs, 320 Carpal tunnel syndr me, 446, 470, 492 Cartilage gra ts, 433 Catab lic rate, 17 Catech lamines, 280, 281f Catheter(s), 34–35. See also specific types Catheter-related in ecti ns, 34 Cauda equina syndr me, 469 Cavern us hemangi mas, 304 Cavern us mal rmati ns (cavern mas), 460 CBC. See C mplete bl d c unt CBF. See Cerebral bl d l w CEA. See Carcin embry nic antigen Cecal v lvulus, 62–63, 197–198 Cecum, intestinal malr tati n and, 383 Celi sc py, 335 Cell cycle, and cancer, 345 Cellulitis, 41, 259 Central c rd injury, 458 Central nerv us system (CNS) anat my , 450–451 aut regulati n in, 452 c ngenital lesi ns , 466 cal lesi ns , 451 uncti nal anat my , 451 path physi l gy in, 451–453 tum rs , 462–466 classi icati n , 462 diagn sis , 462 epidemi l gy , 462 metastatic, 462, 464 Central neur ibr mat sis, 306–307 Central ven us catheters, 34, 55 Cerebellum, 450 Cerebral aqueduct Sylvius, 451 Cerebral arteries, 450 Cerebral bl d l w (CBF), 452, 452f Cerebral c ntusi ns, 456 Cerebral edema, 453, 454 Cerebral in arcts, 453 Cerebral per usi n pressure (CPP), 452, 452f

513

Cerebral veins, 450 Cerebr spinal luid (CSF), 451 l w , 451 bstructed, tum rs and, 462 traumatic leaks , 456 v lume , 451 Cerebr spinal luid istula, 456 Cerebr vascular accident. See Str ke Cerebr vascular disease, extracranial, 125–127 Cerebr vascular injury blunt (BCVI), 355 penetrating, 355 Cervical cancer, screening r, 346 Cervical disc herniati n, 467 Cervical disc syndr mes, 467, 468t Cervical es phageal cancer, 316–317 Cervical spine ractures, 483 Cervical spine trauma, 354 Cervical sp ndyl sis, 467 Cervical terat mas, 303 Chagas disease, 155 Chamberlain pr cedure, 81 Chandelier sign, 60 Charc t triad, 60 Chem therapy, 350 Cherry red sp ts, c l nic, 192 Chest radi graph pre perative, 44t, 51 in trauma assessment, 352–353 Chest trauma, resuscitative th rac t my in, 354 Chest tubes, 33 Chest wall anat my , 78, 78f de rmities , 83 tum rs , 83 Chest wall rec nstructi n, 441–442 CHF. See C ngestive heart ailure Chiari mal rmati n, 466 Chie cells, 161, 276 Child abuse ractures, 481 Children ractures in, 480–482 surgery in. See Pediatric surgery Chin augmentati n, 448 Chl ride imbalances , 9–10. See also Hyperchl remia; Hyp chl remia IV c ncentrati ns , 6, 6t Ch langi carcin ma, intrahepatic, 209 Ch langitis, 62, 213 Ch lecystect my, lapar sc pic, 335, 338– 339, 338f Ch lecystitis, 62, 212 acalcul us, 212 acute, 212 chr nic, 212 Ch lecyst kinin, 163, 206 Ch led chal cysts, 214 Ch led ch lithiasis, 62, 213 Ch lelithiasis (gallst nes), 62, 212, 232 bariatric surgery and, 334 Ch lera, pancreatic, 287 Ch lescintigraphy, 207 Ch ndr ma, chest wall, 83 Chr nic all gra t nephr pathy (CAN), 372

514

Index

Chr nic kidney disease (CKD) classi icati n , 54, 54t pre perative management , 54 surgical patients with, 53–55 Chr nic lymph cytic leukemia (CLL), 234 Chr nic myel gen us leukemia (CML), 234 Chr nic bstructive pulm nary disease (COPD), surgical patients with, 52 Chr nic rejecti n, 364, 365f Chr nic thyr iditis, 272 Chr nic ven us insu iciency (CVI), 140–141 Chr nic ven us stasis, 443 Chyme, 182 Cil staz l, 121 Circle Willis, 450 Circulati n, in trauma assessment, 352 Cirrh sis p rtal hypertensi n with, 210 surgical patients with, 56 CKD. See Chr nic kidney disease Clark classi icati n, melan ma staging, 444 Claudicati n intermittent, 118, 120, 122 neur genic, 118, 469 vascul genic, 118 Clean-c ntaminated w unds, 30 Clean w unds, 30 Cle t lip and cle t palate, 444 Clinical staging, 348 Clinical trials, n cancer, 351 CLL. See Chr nic lymph cytic leukemia Cl nidine, peri perative, 49 Cl sed drains, 33 Cl sed ractures, 478 Cl sed head injury, 454 Cl sed l p bstructi n, 64 Cl sed pneum perit neum meth d, 336 Clostridium difficile, 196 Clostridium perfringens, 41 Clostridium tetani, 40 Cl t rmati n, 13 Cl tting cascade, 13 Cl tting act rs, 13 CML. See Chr nic myel gen us leukemia CNS. See Central nerv us system C agulati n, 13–15 mechanisms , 13 in neur surgical patient, 453 pre perative testing , 44t C agulati n cascade, 13 C agul pathy, 13–14 c nsumptive, 455 hist ry , 13 hyperc agul pathic, 15 hyp c agul pathic, 14 lab rat ry evaluati n , 13–14 medically induced, 14 physical indings , 13 in surgical patients with liver disease, 57 in surgical patients with renal disease, 54, 55 C arctati n a rta, 103 C in lesi ns, 85 C ld ischemia, r d n r rgan, 363 C lect my, subt tal, 66 C litis

C C C C C

C C C C C

C

C C C C C C C C C C C C C C C C C C C

ulminant, 193, 195 granul mat us (Cr hn). See Cr hn disease indeterminate, 192 ischemic, 196–197, 197t pseud membran us (antibi ticass ciated), 196 ulcerative, 192–194 litis cystica pr unda, 199 llagen, in w und healing, 30 llateral circulati n, 120 ll id g iter, 272 l n anat my , 180–181 bl d supply , 180, 180f cuts and caveats n, 151 evaluati n , 182–183 gases , 182 injury t , 358 physi l gy , 182 l nic agangli n sis, t tal, 387 l nic atresia, 386–387 l nic (large intestinal) bstructi n, 65, 197–198 l nic pseud - bstructi n, 65 l n sc py, 183 in c l rectal cancer, 187–188 in Cr hn disease, 194–195 in gastr intestinal bleeding, 66 in pseud membran us c litis, 196 in ulcerative c litis, 193–194 l rectal carcin ma, 186–189 abd minal pain in, 62–63 cellular mechanisms in, 345, 345f clinical presentati n , 187 eti l gy , 186–187 evaluati n , 187 ll w-up in, 188–189 incidence , 186 pr gn sis , 188 pr phylactic surgery t prevent, 349 screening r, 346 staging , 187, 188t, 189t treatment , 187–188 ulcerative c litis and, 193 l rectal tum rs, 184–189 l t my, 185 lumns M rgagni, 181 mmand (jaw-neck) pr cedure, 315, 316f mminuted skull ractures, 456 mm n bile duct, 204, 206f, 216 mm n bile duct st nes, 62, 213 mpartment syndr me, 125, 359, 473–474 mplete bl d c unt (CBC), 44t, 53 mp site tissue all gra t, 375 mp und skull ractures, 456 mpressi n st ckings, 45 mputed t m graphy (CT), abd minal/ pelvic, 62 mputed t m graphy-directed FNA, lung, 81 ndyl ma acuminatum, 202 ngenital head and neck masses, 302–305, 302t ngenital heart disease, 102–107 ngenital hernias, 376–379 ngenital nasal masses, 303–304, 304t

C C C C C C C C C C

ngenital nerv us system lesi ns, 466 ngestive heart ailure (CHF), 47 nj int tend n, 35, 36f nn syndr me, 282t, 283–284 nsumptive c agul pathy, 455 ntact ulcers, 308 ntaminated w unds, 30 ntinu us cl sure, 31, 32f ntinu us inc ntinence, 426 ntinu us p sitive airway pressure (CPAP), 22–23 C ntractility, cardiac, 27–28 C ntracture, skin gra t, 433 C ntrec up injury, 456 C ntusi n cardiac, 92 pulm nary, 92 C per ligament, 36f, 37 C per ligament repair, 37–38 COPD. See Chr nic bstructive pulm nary disease C re-needle bi psy, 347 breast, 257, 258t, 259t C r na radiata sign, 85 C r nary artery bypass gra t (CABG), 100–101, 100f C r nary artery disease (CAD), 99–101 C r nary artery revascularizati n, 49–50 C r nary stenting, 100 C rp ra cavern sa, 423 C rpus sp ngi sum, 423 C rtical lesi n, 453 C rtic ster ids, r arthritis, 487 C rtic tr pin-releasing act r (CRF), 280 C rtis l, 280 imbalances , 281–283 pr ducti n , 280 C up injury, 456 C urv isier gallbladder, 226 CPAP. See C ntinu us p sitive airway pressure CPR. See Cardi pulm nary resuscitati n CPR. See Cerebral per usi n pressure Cranial/scalp rec nstructi n, 436–437 Crani acial surgery, 444–445 Creatinine clearance, 53 CRF. See C rtic tr pin-releasing act r Cric id cartilage, 89 Cric pharyngeal dys uncti n, 154–155 Cric pharyngeal my t my, 155 Cric thyr id t my, 21 Criminal nerve Grassi, 162 Critical limb ischemia, 120, 122 Cr ckcr t-Gault rmula, 53 Cr hn disease, 178–179, 192, 194–196 clinical presentati n , 192, 193t, 195 evaluati n , 195 medical treatment , 195 surgical treatment , 195–196 Cr ss-match, 364 Crypt glandular in ecti ns, 200 Crypt rchidism, 421 Crypts Lieberkühn, 181 Crystal dep siti n disease, 487 Csendes pr cedure, 165 CSF. See Cerebr spinal luid Cubital tunnel syndr me, 471

Index Cu ed central ven us catheters, 35 Cullen sign, 60, 218 Curative surgery, r cancer, 349–350 Curling ulcer, 172 Currant jelly st l, 58, 65 Cushing disease, 281 Cushing syndr me, 281–283, 282t Cushing triad, 453 Cushing ulcer, 172 Cutane us abscesses, 40 “Cut ” sign, 219 CVI. See Chr nic ven us insu iciency Cyan tic c ngenital heart de ects, 106–107 Cycl sp rine A, 366t Cylindr ma, 88–89 Cyst(s) adrenal, 285 branchial cle t, 302–303, 302t breast, 260 br nch genic, 90 ch led chal, 214 cutane us, 443 derm id, 303 epidermal inclusi n, 446 epiderm id, 303 gangli n, 445, 492 hepatic, 209–210 hydatid, 209–210 pericardial, 90 splenic, 233 terat id, 303 thyr gl ssal, 302, 302t Cystaden ma, par tid, 322–323 Cystic hygr mas, 304–305 Cystine calculi, 414 Cystinuria, 414 Cyst gram, 428 Cyt megal virus, transplant-related, 365–367 Cyt t xic edema, 453

D Dandy-Walker syndr me, 466 DaVinci r b t system, 343, 343f DCIS. See Ductal carcin ma in situ D-dimer, 135, 139 DeBakey classi icati n, a rtic dissecti n, 127, 127f Debulking, 350 Deceased d n rs, 363 Decerebrate (extens r) p sturing, 453 Dec rticate ( lex r) p sturing, 453 Deep gray matter, 450 Deep tend n re lexes, 454 Deep ven us thr mb sis (DVT), 15, 135–138 clinical indings , 135 c mplicati ns , 138 diagn stic tests r, 135–136, 136f epidemi l gy , 135 preventi n , 137–138 in spinal c rd injury, 459 treatment , 136–137, 137f De ecati n, bstructed, 199 De ec graphy, 183 De ibrillati n, 94 Degenerative spine disease, 467–470

Delayed hem lytic reacti n, 15 Delayed primary intenti n, 31 Dentate line, 181 Depressed skull ractures, 456 de Quervain thyr iditis, 272 DermaCl se, 434 Dermis, 30 Derm id cysts, 303 Derm ids, nasal, 303, 304t Detrus r are lexia, 425 Detrus r external sphincter dyssynergia (DSD), 425 Detrus r hyperre lexia, 425 Devel pmental ven us an malies, 460 Dexamethas ne, 366t Dexmedet midine, peri perative, 49 Diabetic t ulcers, 443 Diabetic ket acid sis, 11 Diabetic neur pathy, v iding dys uncti n in, 426 Diagn stic lapar sc py, 341, 348 Dialysis, 54, 372 Dialysis catheters, 34–35 Diaphragmatic disrupti n, 92 Diaphragmatic hernias, 377–379, 378f Diaphragm injury, 353 Diaphyseal emur racture, 481 Diarrhea in lammat ry b wel disease and, 193, 195 p stvag t my, 171 pseud membran us c litis and, 196 Diast lic bl d pressure, 24 DIC. See Disseminated intravascular c agul pathy Dieula y lesi n, 66, 171 Di use es phageal spasm, 156 Di use g iter, 272 Digesti n, 163, 174–175 Directed d n r, 16 Dirty w unds, 30 Disability, in trauma assessment, 352 Disc degenerati n, 467–470 Disc replacement, 467 Disease-m di ying antirheumatic drugs (DMARDs), 487 Disl cati ns, 485–486 hip, 477, 477f knee, 485–486, 486f sh ulder, 485 vascular injury with, 474, 474t Displaced ractures, 478 Disseminated intravascular c agul pathy (DIC), 14 Distal radius racture in adults, 482 in children, 480, 481f, 482 Distant laps, 435 Diuresis, 5 Diverticular disease c l rectal, 189–192 small intestinal, 179 Diverticulitis, 62–63, 189–191 Diverticul sis, 189–190 Diverticulum de initi n , 189 alse, 189 true, 179, 189

515

DMARDs. See Disease-m di ying antirheumatic drugs DNA repair genes, 345 D butamine, 26 D n r(s), 363 deceased, 363 directed (trans usi n), 16 kidney, 363, 371 liver, 363, 370 living, 363 D n r perati n, 363 D n rs a ter brain death (DBD), 363 D n rs a ter cardiac death (DCD), 363 D n r-speci ic antib dy, 364 D pamine, 26 D ppler and tissue ximetry, 449 D wn syndr me heart disease in, 102 intestinal atresia in, 385 Drains, 33–34 c mplicati ns , 34 types , 33–34 DSD. See Detrus r external sphincter dyssynergia Ductal carcin ma in situ (DCIS), 262 Duct Sant rini, 216 Duct Wirsung, 216 Duhamel pr cedure, r Hirschsprung disease, 389 Dumping syndr me, 170–171, 332 Du denal atresia and sten sis, 385–386, 386f Du denal diverticula, 179 Du denal ulcers, 163, 165–168, 218 Du denum aden mas , 176 anat my , 173, 173f cuts and caveats n, 150 Duval perati n, 224 DVT. See Deep ven us thr mb sis Dysplasia, de initi n , 344 Dyspnea, 93

E EA. See Es phageal atresia Ear(s), examinati n , 299 Ear rec nstructi n, 437 Echinococcus granulosus, 209–210 Ech cardi graphy, 48, 93 Ech cardi graphy, transes phageal, 50 Ect pic Cushing syndr me, 281, 283 Ect pic pregnancy, lapar sc py in, 341 Edema cerebral, 453, 454 peripheral, 93 pulm nary, 51, 140 E usi ns pericardial, 101–102 pleural, 84, 221 Eisenmenger syndr me, 104 Ejecti n racti n (EF), 93 Elb w dis rders, 491–492 Elderly patients, bariatric surgery in, 326 Elective surgery, pre perative testing r, 44 Electrical burns, 361 Electr cardi gram, pre perative, 44t, 47 Electr lytes, 3–10 de icits and excesses , 6–10

516

Index

Electr lytes (continued) digesti n and abs rpti n , 175, 182 extracellular, 3 gastr intestinal istula and, 41–42 gastr intestinal l sses , 5, 5t intracellular, 3 maintenance , 3–6 adjustments , 5 IV c ncentrati ns r, 6, 6t n rmal b dy c mp siti n, 3 in surgical patients with liver disease, 57 in surgical patients with renal disease, 54 trans usi n and disturbances in, 15 Elephantiasis, 142 Ellipt cyt sis, hereditary, 232 El quence, brain tum rs, 462 Emb lect my, 125 Emb lism, 124–125 gas, 338 pulm nary, 29, 138–140 Emergency department th rac t my, 354 Emergency surgery acute abd men and, 58–66 pre perative testing r, 44 Emergent, de initi n , 58 Empyema, pleural, 84 Encephal cele, c ngenital nasal, 304, 304t Encephal pathy, hepatic, 57 End carditis, in ective, pr phylaxis against, 50 End crine dis rders. See also specific disorders cuts and caveats n, 254–255 study questi ns n, 290–295 End crine pancreas, 217 tum rs , 285–287, 291, 294 End rectal ultras und, 183, 187, 202 End- rgan dys uncti n, 362 End sc pic retr grade ch langi pancreat graphy (ERCP), 207 in acute pancreatitis, 219, 220t in biliary tree path l gy, 213–214 in chr nic pancreatitis, 224 in pancreatic malignancies, 226 in relapsing pancreatitis, 223 End sc py. See also specific procedures c l n and rectum, 183 gastr intestinal, 65 th racic, 80 End tracheal intubati n, 21–22 in patient with lung disease, 52 End-t -end anast m sis, 89 Enema barium, 182 b wel preparati n, 184 water-s luble c ntrast, 182–183 Energy expenditure, 17 Energy s urces, 17 Entamoeba histolytica, 209 Enteral nutriti n, 19–20 administrati n rate in, 20 administrati n r ute in, 19 c mplicati ns , 20 rmula c mp siti ns in, 19 Enter chr ma in cells, 177 Enter c litis Hirschsprung, 388, 389 necr tizing, 392–395, 393f

Enzyme de iciencies, splenic path l gy in, 233 Ependym mas, 463, 470 Epic ndylitis, lateral, 491–492 Epidermal inclusi n cyst, 446 Epidermis, 30 Epiderm id carcin ma, anal, 202 Epiderm id cysts, 303 Epidural abscess, spinal, 472 Epidural anesthesia, in patient with lung disease, 52 Epidural hemat ma, 451, 454, 456, 457f Epigastric hernias, 38 Epilepsy, 467 Epinephrine, 26 Epipl celes, 38 Ep etin alpha, 16 Epstein-Barr virus (EBV), and nas pharyngeal cancer, 313–314 ERCP. See End sc pic retr grade ch langi pancreat graphy Erectile dys uncti n, 423–424 Erythr plakia, 305 Eschar t my, 361 Escherichia coli c l nic, 182 surgical site in ecti n, 40 Esm l l, 26 Es phageal atresia (EA), 381–383, 382f Es phageal disrupti n, 92 Es phageal hiatus, 153, 153f Es phageal per rati n, 160 Es phageal re lux. See Gastr es phageal re lux disease Es phageal spasm, di use, 156 Es phageal strictures, 158 Es phageal tum rs, 158–160 benign, 158–159 malignant, 159–160, 316–317 Es phagitis, strictures sec ndary t , 158 Es phag gastr du den sc py (EGD), 66 Es phagus, 153–160 anat my , 153–154, 153f cuts and caveats n, 150 hist l gy , 153 innervati n , 154 l cati n , 153 m tility dis rders , 154–158 physi l gy , 154 trauma t , 357 vasculature , 154 Essential trem r, 467 Estr gens, 280 Ethm id sinus cancer, 312–313 Euv lemic hyp natremia, 7–8 Ever limus, 367t Ewing sarc ma, 490 Excisi nal bi psy, 348 Excreti n, water, calculating am unt , 3–5 Exemestane, 261 Exercise stress testing, 48 Ex crine pancreas, 216–217 Exp sure, in trauma assessment, 352 Extens r (decerebrate) p sturing, 453 External anal sphincter, 182 External audit ry canal, 299 Extra-axial hem rrhages, 456–457, 457f Extracellular c mpartment, 3, 4f

electr lyte c mp siti n , 3, 4t luid v lume in, 3 Extrac rp real circulati n, 94, 95f Extrac rp real sh ck wave lith tripsy (ESWL), 415 Extracranial cerebr vascular disease, 125–127 Extrinsic pathway, in cl tting cascade, 13 Extubati n, 23 in patient with lung disease, 52 Exudative e usi ns, 84 Eye(s), examinati n , 299 Eyebr w li t, 448 Eye examinati n, in neur l gic patient, 453 Eyelid rec nstructi n, 437 Eyelid surgery, aesthetic, 447

F Face-li t, 447 Facial nerve, 321–322, 321f Facial nerve injuries, 323 Fact r V Leiden mutati n, 15 Fact r Xa, 13–14 Falci rm ligament, 204 False diverticulum, 189 Familial aden mat us p lyp sis (FAP), 184, 185–186 Familial intestinal atresias, 386 Fasci cutane us lap, 434f, 436 FAST. See F cused abd minal s n graphy r trauma Fat(s) digesti n and abs rpti n , 175 as energy s urce, 17 Fat gra ts, 433 Fat necr sis, breast, 259 Fat-s luble vitamins, 175 Fatty acids, sh rt-chain, 182 Febrile reacti n, t trans usi n, 15 Fecal inc ntinence, 198 Fecal ccult bl d, 183 Feculent perit nitis, 191 Fell wships, nc l gy, 351 Fel n, 446 Felty syndr me, 233 Fem ral canal, 37 Fem ral- em ral bypass, 122 Fem ral hernias, 36f, 37 lapar sc pic repair , 339 Fem r p pliteal cclusive disease, 122–123, 123f Femur ractures, 359 in children, 481, 482 diaphyseal, 481 sha t, 484, 484f Fever, p st perative, 39 Fibrin lysis, 13 Fibr aden ma, breast, 259 Fibr cystic changes breast, 259 Fibr lip ma(s), es phageal, 159 Fibr ma(s), small intestine, 177 Fibr th rax, 91 Fibr us dysplasia jaw, 307 rib, 83 Fibr us thyr iditis, 272 Fibula lap, 436

Index Fick equati n, 17, 18 Filariasis, 142 Filling cyst metry, 425 Fine-needle aspirati n (FNA), 347 breast, 257 head and neck, 300, 311 lung, 81 thyr id, 273–274, 273t Finger rec nstructi n, 445 Fissures anal, 200 pulm nary, 79, 79f Fistula an rectal, 200–201 arteri biliary, 210 arteri ven us, 55, 210 branchial cle t, 302–303 Cr hn disease and, 179, 195–196 diverticulitis and, 191 gastr intestinal, 41–42 p st-traumatic CSF, 456 thyr gl ssal, 302 trache es phageal, 381–383, 382f urinary, kidney transplantati n and, 372 Fistul gram, 42 “5 W’s,” 39 Flail chest, 91 Flap(s), 434–436. See also specific types and procedures axial, 434f, 435 classi icati n , 434, 434f distant, 435 asci cutane us, 434f, 436 l cal, 434 muscle/my cutane us, 434f, 436 ste my cutane us/b ne, 436 per rat r, 435–436 rand m, 434f, 435 Tagliac zzi, 430, 431f Z-plasty, 435, 435f Flat epithelial atypia breast, 260 Flexible iber ptic br nch sc py, 80 Flexible sigm id sc py, 183 Flex r (dec rticate) p sturing, 453 Flex r ten syn vitis, 446, 492 Fluid, b dy, 3–10 adjustments , 5 gastr intestinal istula and, 41–42 maintenance , 3–6 n rmal c mp siti n, 3 p st perative status, 39–40 in surgical patients with liver disease, 57 in surgical patients with renal disease, 54 Fluid resuscitati n, in burn injuries, 360 FNA. See Fine-needle aspirati n FNH. See F cal n dular hyperplasia F cal g iter, 272 F cal n dular hyperplasia (FNH), 208 F cused abd minal s n graphy r trauma (FAST), 357, 358f F ley drain, 33 F lic acid, abs rpti n , 175 F llicular cells, thyr id, 269 F llicular thyr id carcin ma (FTC), 275, 275t F t dis rders, in adults, 493 F t ulcers, diabetic, 443

F ramina Luschka, 451 F ramina Magendie, 451 F ramina M nr , 451 F rearm ractures, 482 F reign b dies, par tid gland, 323 F urnier gangrene, 413 Fracti n inspired xygen (FiO2), 21 Fracture(s), 478–485 angulati n , 478 ankle, 484, 485f b xer’s, 483 calcaneus, 485 child abuse, 481 cl sed, 478 descripti n , 478 displacement , 478 distal radius in adults, 482 in children, 480, 481f, 482 emur, 359 in children, 481, 482 diaphyseal, 481 sha t, 484, 484f hand, 445 hip, 482 humerus pr ximal, 482 sha t, 482 suprac ndylar, 481 impacti n , 478 l cati n , 478 pen, 475–476, 475f, 478, 480t rbital, 445 rientati n , 478, 479f ste p r tic, 482 path l gic, 479 pediatric, 480–482 pelvic (pelvic ring), 359, 472–473 penile (erect penis), 428–429 r tati n , 478 scaph id, 482, 483f skull, 456 spinal, 482, 483–484 stress, 478–479 tibia, 482 in adults, 484 in children, 481 vascular injury with, 474, 474t Free air, in abd minal radi graphy, 61, 61f Free lap, 435, 438 Fr ntal l be, 450 Fruct se, 175 FTC. See F llicular thyr id carcin ma FTSGs. See Full-thickness skin gra ts Full-thickness burns, 360 Full-thickness skin gra ts (FTSGs), 432 Fulminant c litis, 193, 195 Functi nal mitral regurgitati n, 97 Functi nal neur surgery, 466–467 Functi nal bstructi n, 65 Fund plicati n, 157, 341, 342f Fungal in ecti ns splenic, 233 transplant-related, 367 Funnel chest, 83 Furuncle (b il), 40

517

G Gail m del, m di ied, breast cancer risk, 261 Galact cele, 260 Galact se, 175 Gallbladder anat my , 204–205 C urv isier, 226 cuts and caveats n, 151–152 embry l gy , 204 lapar sc pic rem val , 335, 338–339, 338f path l gy , 212–213 physi l gy , 205–206 trauma t , 213 Gallbladder carcin ma, 213 Gallst ne pancreatitis, 217 Gallst nes, 62, 212, 232 bariatric surgery and, 334 Gangli n cysts, 445, 492 Gangrene F urnier, 413 gas, 41 ven us, 138 Gardner syndr me, 186 Gardner-type neur ibr mat sis, 307 Gas emb lism, 338 Gas gangrene, 41 Gastrect my pr ximal, 66 sleeve, 326, 327f c mplicati ns , 330–331 utc mes , 329 syndr mes a ter, 170–171 types , 164–165, 165f Gastric acid, 163 Gastric banding, adjustable, 326, 327f c mplicati ns , 330 utc mes , 329 Gastric bypass, 328, 329f c mplicati ns , 331–334 utc mes , 329 Gastric cancer, 164, 168–170, 169t Gastric lavage, 65 Gastric utlet bstructi n, 64, 167 Gastric p lyps, 171 Gastric sarc mas, 170 Gastric ulcers, 163–165 Gastrin ma, 165, 286–287, 288 Gastritis, 171–172 abd minal pain in, 62–63 alkaline re lux, 170 unc mplicated acute, 171 Gastr du denal artery, 216 Gastr du den st my, 66 Gastr es phageal juncti n (GEJ), 153, 161, 162f Gastr es phageal re lux disease (GERD), 156–157, 157f und plicati n r, 157, 341, 342f strictures sec ndary t , 158 Gastr intestinal bleeding, 65–66 di erential diagn sis , 66 evaluati n , 65–66 l calizati n , 65, 66 l wer, 65–66 termin l gy in, 65

518

Index

Gastr intestinal bleeding (continued) treatment , 66 upper, 65–66 Gastr intestinal dis rders. See also specific disorders cuts and caveats n, 150–152 study questi ns n, 237–253 Gastr intestinal istula, 41–42 Gastr intestinal str mal tum rs (GISTs), 170, 177 Gastr intestinal (GI) tubes, 34 Gastr schisis, 379–381, 379t Gastr splenic ligament, 230 Gastr st my tubes, 34 Gaucher disease, 233 G cells, 161 GCS. See Glasg w C ma Scale General surgery cuts and caveats n, 1–2 essentials , 30–42 gastr intestinal istula in, 41–42 hernias in, 35–39 in ecti ns in, 40–41 p st perative c mplicati ns in, 39–40 study questi ns n, 67–75 tubes and drains in, 33–35 w unds in, 30–32 Geniculate c llaterals, 120 Genit em ral nerve injury, 339 Genit urinary injuries, 358 Genit urinary malignancies, 417–423 Gen mic studies, 348 Germ cell tum rs, 90, 421–423 GFR. See Gl merular iltrati n rate Giant cell arteritis, 133 Giant cell thyr iditis, 272 Giant cell tum rs, 445 Gilles, Sir Har ld, 430 Glasg w C ma Scale (GCS), 352, 353f, 455 Gli blast ma multi rme, 463f Gli mas brain (CNS), 462 c ngenital nasal, 304, 304t Gl merular iltrati n rate (GFR), 53–54, 54t Gl mus tum r, 446 Gl ttic (lingual) thyr id, 268–269 Gl ttis, 317 Glucag n mas, 287, 288 Gluc c rtic ids, 280 Gluc ne genesis, 17 Gluc se, 17, 175 Glyc pr tein (Gp) recept rs, 13 G blet cells, 174 G dwin tum r, 323 G iter, 272 di use, 272 cal, 272 substernal, 269 t xic multin dular, 271 G ldman Risk Index, 47, 48t G n c ccal septic arthritis, 488 G ut, 487 Graded exercise pr gram, 121 Graduated c mpressi n st ckings (GCS), 45 Granul ma, laryngeal (intubati n), 308 Granul mat us c litis. See Cr hn disease Granul mat us ileitis. See Cr hn disease

Granul mat us thyr iditis, 272 Graves disease, 270–271 Gravity drains, 33 Gray matter, cerebral, 450 Great arteries, transp siti n , 107 Great vein Galen, 450 Greenstick ractures, 478, 479f, 480, 481f Gr ss hematuria, 427 Gr wth plate ractures, 480, 480f Gunsh t w unds, blast e ect r m, 428 Gustil classi icati n, pen ractures, 478, 480t Gynec mastia, 265, 440–441

H Haemophilus ste myelitis, 488 Hairy cell leukemia, 234 Hal sign, 456 Hamart ma c l rectal, 185 lung, 88 splenic, 234 Hamart mat us p lyps, 176, 184 Hand-assisted lapar sc pic surgery (HALS), 337 Hand dis rders, in adults, 492 Hand in ecti ns, 446, 492 Hand surgery, 445–446 Hand trauma, 445 Hand tum rs and masses, 445–446 Harris-Benedict equati ns, 18 Hartmann pr cedure, 191, 198 Hashim t thyr iditis, 272 Haustra, 181 Head and neck cancer, 308–311. See also specific types basic characteristics , 309t chem therapy r, 310 epidemi l gy , 308–309 evaluati n , 309 radiati n therapy r, 310 rehabilitati n in, 310–311 risk act rs r, 309 surgery r, 309–310, 310f treatment alg rithm r, 301f treatment , 309–311 Head and neck examinati n, 299–300 Head and neck in ecti ns, 308 Head and neck injuries, 354–355 Head and neck lesi ns r masses acquired, 300, 305–308 benign, 300 c ngenital, 302–305, 302t malignant, 308–311 treatment alg rithm r, 301f vascular, 304–305 Head and neck rec nstructi n, 438 Head and neck surgery, 299–324 cuts and caveats n, 296 study questi ns n, 397–399, 405–406 Head injuries, 454–457 blunt, 454 cl sed, 454 ICP management in, 454–455 initial management and assessment , 454 penetrating, 454

radi graphic studies , 454 seizure pr phylaxis in, 455 Healing. See W und healing Hearing tests, 299 Heart, 93–107 cuts and caveats n, 77 study questi ns n, 108–115 trauma t , 101–102, 356 tum rs , 101 Heart c mpressi ns, 354 Heart disease acquired, 93–102 epidemi l gy , 93 physical indings , 93 pre perative management , 93–94 signs and sympt ms , 93 c ngenital, 102–107 surgical patient with assessment disease and risk act rs in, 46 bacterial end carditis pr phylaxis r, 50 cardiac hist ry , 47 c m rbid c nditi ns in, 46 c r nary artery revascularizati n r, 49–50 ECG indicati ns in, 47 evaluati n , 46–51 general aspects , 46 HMG-C A reductase inhibit rs r, 50 invasive hem dynamic m nit ring , 50 m di iable risk act rs in, 49 n ninvasive and invasive cardiac testing in, 48–49 n rm thermia maintenance in, 50 peri perative alpha-adrenergic ag nists r, 49 peri perative beta-bl cker therapy r, 49 peri perative management and risk reducti n r, 49–50 physical exam , 47 p st perative c mplicati ns in, 50–51 pre perative risk assessment strati icati n t ls r, 47–48, 48t Heart ailure c ngestive, 47 NYHA classi icati n , 98, 98t Heart/lung transplantati n, 368–369 Heart rate (HR), 27 Heart transplantati n, 368 Heart valves anat my , 95f dis rders , 47, 96–99 pr sthetic, 47, 94–96 repair versus replacement, 96, 96t Helicobacter pylori in ecti n and gastric cancer, 168–170 and peptic ulcer disease, 164–168 Heller my t my, 156 Hemangi blast ma, 462, 465 Hemangi ma(s) arteri ven us, 304 capillary, 304 cavern us, 304

Index c ngenital cutane us, 304 cutane us, 443 head and neck, 304 hepatic, 207, 207f invasive, 304 small intestine, 177 splenic, 234 subgl ttic, 304 Hematemesis, 65 Hemat chezia, 65, 182 Hemat ma, 454 epidural, 451, 454, 456, 457f subdural, 454, 457, 457f Hematuria, 427 Hem dialysis, 372 Hem dialysis, temp rary, 54 Hem dialysis catheters, 34–35 Hem diluti n, acute n rm v lemic, 16 Hem dynamic m nit ring ICU patients, 24–25 surgical patients with cardiac disease, 50 Hem gl bin (Hgb), 27–29 Hem lytic anemia, 232 Hem lytic reacti n, delayed, 15 Hem philia A, 14 Hem philia B, 14 Hem ptysis, 93 Hem rrhage acute surgical abd men with, 65–66 diverticular disease and, 191–192 extra-axial, 456–457, 457f intracerebral, 456, 459–460 subarachn id, 460–461, 461f th racic, 91 Hem rrhagic str ke, 459 Hem rrh ids, 199–200 external, 200 internal, 200 pr lapsed internal, 199 Hem stasis cl t rmati n in, 13 mechanism phases , 13 primary, 13 Hem static agents, 16 Hem th rax, 91, 356 Henders n-Hasselbalch equati n, 11 Heparin-induced thr mb cyt penia (HIT), 138 Hepatic abscesses, 209 Hepatic bi psy, 56 Hepatic cysts, 209–210 Hepatic disease hyp c agul pathic state in, 14 surgical patient with anesthetic c nsiderati ns in, 56–57 evaluati n , 55–57 hepatic uncti n assessment in, 55–56 hist ry , 55 lab rat ry testing and diagn stic studies , 56 perative risk assessment and strati icati n , 56 peri perative management , 57 physical examinati n , 55–56 transplantati n in, 369–371. See also Liver transplantati n

Hepatic uncti n tests, 44t, 206 Hepatic mass, abd minal pain with, 62 Hepatic resecti n, 214, 342 Hepatitis abd minal pain in, 62 surgical patients with, 56 Hepatitis B, trans usi n transmissi n , 15 Hepatitis C, trans usi n transmissi n , 15 Hepat biliary imin diacetic acid (HIDA) scan, 207 Hepat biliary system anat my , 204–205, 205f, 206f imaging , 207 physi l gy , 205–206 studies , 206–207 Hepat cellular aden ma, 208 Hepat cellular carcin ma, 208–209, 208f Hepat ma, 208–209, 208f Hereditary ellipt cyt sis, 232 Hereditary n np lyp sis c l rectal carcin ma (HNPCC), 186 Hereditary spher cyt sis, 232 HER-2/ neu recept r, 345 Hernia(s), 35–39 abd minal wall, 38–39 c mplicati ns , 35 c ngenital, 376–379 de initi n , 35 descriptive terms r, 35 diaphragmatic, 377–379, 378f epigastric, 38 eti l gy , 35 em ral, 36f, 37, 339 hiatal, 63, 156, 157f incarcerated, 35, 63, 64 incidence , 35 inguinal, 35–38, 36f, 339, 340f, 376–377 internal, 65 bariatric surgery and, 333, 333f lapar sc pic repair , 339–341, 340f bstructi n with, 63–65 strangulated, 64 umbilical, 38, 340–341, 340f ventral, 39, 340–341, 340f Herniated discs, 467–469 Herniati n syndr mes, brain, 452 Herni rrhaphy, r inguinal hernia, 377 Herpetic whitl w, 446 Hesselbach triangle, 35, 36f, 37 Heter t pic gra t, 363 Hgb (hem gl bin), 27–29 Hiatal hernia, 63, 156, 157f Hibernating my cardium, 99 Hickman catheter, 35 Hidradenitis suppurativa, 40, 201, 442 Hill p steri r gastr pexy, 157 Hip disl cati n, 477, 477f Hip dis rders, in adults, 492 Hip ractures, 482 Hirschsprung disease, 183, 387–389, 388f Hirschsprung enter c litis, 388, 389 Histamine (H 2) bl ckers, r peptic ulcer disease, 164, 166, 166t Hist c mpatibility antigens (HLAs), 364 HIT. See Heparin-induced thr mb cyt penia HIV/AIDS, trans usi n transmissi n , 15

519

HLAs. See Hist c mpatibility antigens HMG-C A reductase inhibit rs, 50, 121 HNPCC. See Hereditary n np lyp sis c l rectal carcin ma H dgkin disease head and neck, 319–320 splenic, 234 H ll w viscus, 358 H riz ntal mattress suture, 31, 32f H rm nal milieu, 17 H rm nal therapy, r cancer, 351, 418 H rner syndr me, 86 HTN. See Hypertensi n Human papill mavirus (HPV), 202, 315 Humerus ractures pr ximal, 482 sha t, 482 suprac ndylar, 481 Hydatid cysts, 209–210 Hydr cele reactive, 422 spermatic c rd, 37 Hydr cephalus, 466 Hydr c rtis ne, 366t Hyperacute rejecti n, 364, 365f Hypercalcemia, 10, 277–279 Hyperchl remia, 10 Hyperchl remic acid sis, 11 Hyperc agul pathic states, 15, 124 Hyperc rtis lism, 281–283 Hyperkalemia, 9 diagn sis/eti l gy , 9 in surgical patients with renal disease, 54, 55 sympt ms , 9 trans usi n and, 15 treatment , 9 Hypernatremia, 8 causes , 8 diagn sis/eti l gy , 8 sympt ms , 8 treatment , 8 Hyper sm lar hyp natremia, 6, 8 Hyperparathyr idism, 277–279 indicati ns r surgery in, 277, 278t in multiple end crine ne plasia, 287–289 primary, 277–279 sec ndary, 278t, 279 tertiary, 278t, 279 Hyperph sphatemia, in surgical patients with renal disease, 54 Hyperplastic p lyps, 171, 184 Hyperre lexia, bladder, 424–425 Hypersplenism, 231–233 de initi n , 231 evaluati n , 233 p rtal hypertensi n and, 212, 231 primary, 231 sec ndary, 231–232 Hypertensi n (HTN) adrenal causes , 282t intracranial, 451 in neur surgical patient, 453 p rtal, 210–212, 231 p st-traumatic, 427 pulm nary, diaphragmatic hernia and, 378

520

Index

Hypertensi n (HTN) (continued) ren vascular, 132–133 in surgical patient, 47 Hypertensive intracerebral hem rrhage, 459 Hyperthyr idism, 270–272 Hypert nic neur genic bladder, 425 Hypert nic saline, 6t Hypertr phic scars, 442 Hyperventilati n, r ICP management, 455 Hyperv lemia, 6 Hyperv lemic hypernatremia, 8 Hyperv lemic hyp natremia, 7–8 Hyp calcemia, 10 in hyp parathyr idism, 276 in surgical patients with renal disease, 54 in thyr id dys uncti n, 271 trans usi n and, 15 Hyp chl remia, 9–10 Hyp c agul pathic states, 14 Hyp dermis, 30 Hyp glycemia, in patients with liver disease, 57 Hyp kalemia, 8–9 diagn sis/eti l gy , 9 sympt ms , 8–9 treatment , 9 Hyp magnesemia, 57 Hyp natremia, 6–7 acute, 7 causes , 6–7 chr nic, 7 diagn sis and categ rizati n , 7–8 sympt ms , 7 Hyp - sm lar hyp natremia, 7–8 Hyp parathyr idism, 271, 276 Hyp pharynx anat my , 316 cancer , 316–317 Hyp tensi n in neur surgical patient, 453 in spinal c rd injury, 459 in surgical patients with renal disease, 55 Hyp thermia burn injuries and, 359 hyp c agul pathy in, 14 therapeutic, 94 Hyp v lemia, 5, 6, 39–40 Hyp v lemic hypernatremia, 8 Hyp v lemic hyp natremia, 7–8 Hyp v lemic sh ck, 27, 28t Hyp xemia with atelectasis, 53 early, 53 Hyp xia, 21

I IBD. See In lammat ry b wel disease ICP. See Intracranial pressure (ICP) ICU. See Intensive care unit Idi pathic aut immune hem lytic anemia, 232 Idi pathic thr mb cyt penic purpura (ITP), 232 Ileal atresia, 386–387 Ileal chyme, 182 Ileum, 173–174, 173f

Ileus, 65 Iliac crest lap, 436 Image-guided bi psy, 348 Immune reacti n, t trans usi n, 15 Immun l gic t lerance, 364 Immun m dulat rs r Cr hn disease, 195 r ulcerative c litis, 194 Immun suppressi n in rgan transplantati n, 365–368 c mplicati ns , 365–368 inducti n, 365 maintenance, 365 medicati ns r, 366t–367t trans usi n and, 16 Immun therapy, r cancer, 350 Impacted ractures, 478 Impending path l gic ractures, 479 Incarcerated hernia, 35, 63, 64, 376 Incisi nal bi psy, 348 Incisi nal hernia, 39 Incisura angularis, 161, 162f Inc ntinence ecal (an rectal), 198 urinary, 426 Indeterminate c litis, 192 Indirect cal rimetry, 18 Inducti n regimen, in immun suppressi n, 365 In ancy, dis rders , 390–395 In antile hypertr phic pyl ric sten sis, 390–391 In ecti n(s). See also specific infections b ne, 488–489 breast, 259 gastr intestinal istula and, 42 hand (nail), 446, 492 head and neck, 308 p stsplenect my, 235–236 splenic, 233 surgical, 40–41 In ecti n c ntr l, pre perative, 45 In ecti us (septic) arthritis, 476, 488 In ective end carditis (IE), pr phylaxis against, 50 In eri r mesenteric artery (IMA), 180, 180f In eri r mesenteric vein, 180 In eri r rectal artery, 180f, 181 In eri r thyr id artery, 266, 267f In eri r thyr id veins, 266, 267f In eri r vena cava (IVC) ilter, 46, 136, 137f, 140 In ertility lapar sc py in, 341 rgan transplantati n and, 367–368 In lammat ry b wel disease (IBD), 192–196. See also Cr hn disease; Ulcerative c litis clinical presentati n , 192, 193t eti l gy , 192 In lammat ry breast cancer, 262 In lammat ry phase, w und healing, 30, 442 In lammat ry p lyps, 184 In liximab r Cr hn disease, 195 r ulcerative c litis, 194 In rageniculate tibial disease, 123–124

In rainguinal disease, 118 In ratent rial hem rrhage, 459 Inguinal hernia, 35–38 anat my and, 35–37, 36f c ngenital, 376–377, 377f diagn sis , 37 direct, 37 herni rrhaphy r, 377 incarcerated, 376 indirect, 37 lapar sc pic repair , 339, 340f pantal n, 37 pediatric, 37, 38 recurrence rates , 38 recurrent, 37 repair , 37–38 sites , 36f special situati ns with, 38 types , 37 Inhalati n injury, 361 INR. See Internati nal n rmalized rati Insensible water l ss, 5 Instituti nal review b ards (IRBs), 351 Insulin ma, 286, 288, 289 Insulin therapy, 374 Intensive care unit (ICU), 21–26 airway c ntr l in, 21–22 hem dynamic and ther invasive m nit ring in, 24–25 intensive patient care in, 21 management speci ic t , 21–26 trans usi n therapy r patient in, 16 vas active medicati ns and antiarrhythmic drips in, 26 ventilat r supp rt in, 22–23 Interleukin recept r antag nists, 487 Intermittent claudicati n, 118, 120, 122 Intermittent pneumatic c mpressi n (IPC), 45 Internal anal sphincter, 182 Internal car tid artery, 450 Internal car tid– phthalmic aneurysm, 460 Internal hernia, 65 bariatric surgery and, 333, 333f Internal inguinal ring, 35, 37 Internati nal n rmalized rati (INR), 13 Interrupted cl sure, 31, 32f Interstitial ibr sis/tubular atr phy (IFTA), 372 Intervertebral discs anat my , 467 degenerati n , 467–470 replacement , 467 Intestinal atresia, 385–387 Intestinal malr tati n, 63, 197–198, 383–385, 384f Intestinal bstructi n, 63–65, 197–198 Intestinal v lvulus, 62–63, 197–198, 384 Intra-abd minal abscesses, 40, 191 Intracellular c mpartment, 3, 4f electr lyte c mp siti n , 3, 4t luid v lume in, 3 Intracerebral hem rrhage, 459–460 Intracerebral hem rrhage, traumatic, 456 Intrac mpartmental pressure, 474 Intracranial hypertensi n, 451 Intracranial pressure (ICP), 451–452, 451f and brain herniati n, 452, 452f

Index increased, management , 454–455 measurement , 452 n rmal range , 451 v lume relati nship , 451, 451f Intracranial pressure m nit r, 455 Intraductal papillary mucin-pr ducing ne plasia (IPMN), 229 Intraductal papill ma (breast), 260 Intrahepatic ch langi carcin ma, 209 Intrinsic pathway, in cl tting cascade, 13 Intubati n, end tracheal, 21–22 Intubati n granul mas, 308 Intussuscepti n, 58, 64, 176, 199 Invasive hemangi mas, 304 Inverted papill mas, 305 I dine, r Graves disease, 270 I dine, radi active, r Graves disease, 270 I dine-de iciency g iter, 272 I n(s), str ng, 11 I n pumps, 3 IPC. See Intermittent pneumatic c mpressi n (IPC) IPMN. See Intraductal papillary mucinpr ducing ne plasia IRBs. See Instituti nal review b ards Ir n, digesti n and abs rpti n , 175 Ir n de iciency, in bariatric surgery patients, 334 Ischemic c litis, 196–197, 197t Ischi rectal ssa abscess, 201 Islet transplantati n, 374 Is gra t, 362 ITP. See Idi pathic thr mb cyt penic purpura IV luids, electr lyte c ncentrati n in, 6, 6t IV nutriti n. See Parenteral (IV) nutriti n

J Jacks n-Pratt drain, 33 Jaundice, 57 hereditary spher cyt sis and, 232 bstructive, 56 pancreatic aden carcin ma and, 226 Jaw lesi ns, n ndental, 307 Jaw-neck (c mmand ) pr cedure, 315, 316f Jejunal atresia, 386–387 Jejun ileal atresia, 386 Jejun ileal diverticula, 179 Jejun st my tubes, 34 Jejunum, 173–174, 173f Jejunum, ree, r rec nstructi n, 438 J int injuries, penetrating, 477 J int replacement, 487 Juvenile (retenti n) p lyps, 176, 184

K Kasabach-Merritt syndr me, 443 Kasai pr cedure, r biliary atresia, 392, 392f Kehr sign, 60 Kel ids, 442 Kerat sis, 305 Ket nes, 17 Kidney cancer renal cell carcin ma, 421, 422f Wilms tum r, 395–396, 396t Kidney disease hyp c agul pathic state in, 14

surgical patients with, 53–55 dialysis in, 54 hist ry , 53 lab rat ry testing and diagn stic studies in, 53–54 perative variables in, 54–55 physical examinati n , 53 p st perative c mplicati ns in, 55 pre perative management , 54 renal uncti n assessment in, 53–54 vascular access in, 55 Kidney ailure acid sis in, 11 acute, surgical patients with, 53–55 Kidney st nes, 62–63, 414–415 Kidney transplantati n, 371–372 alternatives t , 372 d n rs r, 363, 371 lapar sc pic d n r nephrect my r, 342 liver transplantati n with, 370 perative strategy r, 371, 371f pancreas transplantati n with, 373 rejecti n , 372 Kidney trauma, 358, 427 Kline elter syndr me, 265 Knee disl cati n, 485–486, 486f Knee dis rders, in adults, 492–493 Kulchitsky cells, 177

L Labetal l, 26 Lactate, IV c ncentrati ns , 6, 6t Lactate dehydr genase (LDH), testicular tum rs and, 422 Lactated Ringer’s, 6t Lactate metab lism, 57 Lactic acid sis, 11 Ladd pr cedure, 384–385 Lapar sc pic adrenalect my, 342 Lapar sc pic appendect my, 335, 339, 339f Lapar sc pic ch lecystect my, 335, 338–339, 338f Lapar sc pic d n r nephrect my, 342 Lapar sc pic und plicati n, r GERD, 341, 342f Lapar sc pic hernia repair em ral hernia, 339 inguinal hernia, 339, 340f ventral hernias, 340–341, 340f Lapar sc pic liver resecti n, 342 Lapar sc pic splenect my, 235, 342 Lapar sc pic staging malignancy, 342 Lapar sc pic surgery, 335–343. See also specific procedures advantages and disadvantages , 336 cl sed pneum perit neum meth d , 336 c mplicati ns , 337–338 c st-e ectiveness , 336 cuts and caveats n, 296–297 diagn stic, 341, 348 general perative technique in, 336–337 general principles , 335–338 hand-assisted, 337 hist ry , 335 intra-abd minal access r, establishment , 336–337 m rtality and m rbidity in, 337

521

pen pneum perit neum meth d , 336 pen surgery versus, 335–336 perative milest nes in, 335 patient preparati n r, 336 physi l gic changes ass ciated with pneum perit neum in, 337 relative c ntraindicati ns t , 337 study questi ns n, 398–399, 402–403, 406, 408–409 technical advances in, 335 Laplace law, 64 Large intestine. See C l n Laryngeal cancer, 317–318, 318f Laryngeal granul mas, 308 Laryngeal lesi ns, 307–308 Laryngeal nerves, 266–268, 271 Laryngeal papill mas, 306 Laryngeal webs, 307 Laryng cele, 307 Laryng py cele, 307 Laryng sc py, 80 Larynx, examinati n , 300 Laser angi graphy, 449 Lateral c llateral ligament (LCL) tear, knee, 493 Lateral epic ndylitis, 491–492 Lateral em ral cutane us nerve injury, 339 Lateral malle lus racture, 484, 485f Latissimus d rsi muscle lap, 440 LCIS. See L bular carcin ma in situ LCL. See Lateral c llateral ligament (LCL) tear, knee Le t hepatic artery, 204 Le t lung, 79, 79f Le t ventricular hypertr phy, 93 Lei my ma, es phageal, 158–159 Lei my sarc ma, small intestine, 178 Leriche syndr me, 120 Leukemia, splenic, 234 Leuk penia, in splenic path l gy, 231 Leuk plakia, 305 Levat r ani, 181 Level c nsci usness (LOC), 453 Lichtenstein repairs, 38 Linear skull ractures, 456 Lingual (gl ttic) thyr id, 268–269 Lipase, pancreatic, 175 Lip cancer, 314 Lip ma(s) cutane us, 443 es phageal, 159 small intestine, 177 Lip sucti n, 447 Lip rec nstructi n, 438 Liver anat my , 204, 204f bl d supply , 204 cancer , 208–209, 208f cuts and caveats n, 151–152 embry l gy , 204 imaging , 207 injury t , 357 metastases t , 209 physi l gy , 205–206 resecti n , 214, 342 trauma t , 210 tum rs , 207–209

522

Index

Liver abscesses, 209 Liver bi psy, 56 Liver cysts, 209–210 Liver disease hyp c agul pathic state in, 14 surgical patient with anesthetic c nsiderati ns in, 56–57 evaluati n , 55–57 hepatic uncti n assessment in, 55–56 hist ry , 55 lab rat ry testing and diagn stic studies , 56 perative risk assessment and strati icati n , 56 peri perative management , 57 physical examinati n , 55–56 Liver uncti n tests, 44t, 206 Liver mass, abd minal pain with, 62 Liver transplantati n, 369–371 bicaval, 370 r biliary atresia, 392 d n rs r, 363, 370 kidney transplantati n with, 370 perative strategy r, 369–370, 370f piggyback, 369 Living d n rs, 363 L bular carcin ma in situ (LCIS), 260 L bular ne plasia breast, 260 LOC. See Level c nsci usness L wer es phageal sphincter (LES), 154, 162 L wer extremity arterial cclusive disease, 118–120 L wer extremity arterial tree, 118, 119f L wer extremity rec nstructi n, 442 L wer GI bleeding, 65–66 Lucid interval, 456 Ludwig angina, 302 Lumbar disc disease, v iding dys uncti n in, 426 Lumbar disc herniati n, 468–469, 468t, 469f Lumbar hernias, 39 Lumbar spine ractures, 483 Lumbar sp ndyl sis, 469–470 Lumpect my, 262 Lung(s) anat my , 79–80, 79f bl d supply , 80 metastases t , 89 Lung abscess, 85 Lung bi psy, 81 Lung cancer, 85–88 clinical presentati n , 86 diagn sis and staging , 86–87, 87t path l gy , 86 treatment , 88 Lung disease, surgical patient with anesthesia r, 52 evaluati n , 51–53 general aspects , 51 hist ry and physical examinati n , 51 lung expansi n techniques r, 52 perative c nsiderati ns r, 52 pain c ntr l in, 52 peri perative management , 52–53 pre perative risk m di icati n in, 51–52 pre perative studies , 51 pulm nary c mplicati ns in, 53

pulm nary uncti n assessment in, 51 ventilat r supp rt and weaning in, 52 Lung expansi n techniques, 52 Lung transplantati n, 368–369 d n rs r, 363 d uble, 368 heart transplantati n with, 368–369 single, 368–369 Lymphadenitis, myc bacterial, in neck, 300 Lymphangi ma, ral and peri ral, 305 Lymphangi sarc ma, 264 Lymphatic vessels, pulm nary, 80 Lymphedema, 142–143, 264 Lymphedema praec x, 142 Lymphedema tarda, 142 Lymph n de status, in cancer, 348–349 Lymph celes, 372 Lymph epithelial tum r, benign, 323 Lymph id p lyps, 184 Lymph ma(s), 344 gastric, 169–170 head and neck, 319–320 mediastinal, 90 muc sa-ass ciated lymph id tissue (MALT), 170 small b wel, 177–178 splenic, 234 testicular, 421 thyr id, 276

M Macr mastia, 441 Ma enide acetate, 361 Magnesium, IV c ncentrati ns , 6, 6t Magnetic res nance ch langi pancreat graphy (MRCP), 207 Magnetic res nance imaging (MRI), breast, 257 Maintenance therapy, in immun suppressi n, 365 Malabs rptive bariatric perati ns, 327, 328f Malignant, de initi n , 344 Mall ry-Weiss syndr me, 160 Mall ry-Weiss tears, 63, 160 MALT lymph ma. See Muc sa-ass ciated lymph id tissue (MALT) lymph ma Mammary duct ectasia, 259 Mamm graphy, 257, 262 Mamm plasty, reducti n, 441 Mandibular t rus, 307 Mandibular tum rs, 314 Marginal ulcers, bariatric surgery and, 333 Marginal z ne, spleen, 230 Markle sign, 60 Mass e ect, 346, 462, 465 Massive hem th rax, 91, 356 Mastalgia, 260 Mastect my, 262–263, 265 pr phylactic, 349 rec nstructi n a ter, 439–440 Mastitis, 259 Mast pexy, 448, 448f Mattress suturing, 31, 32f Maturati n phase, w und healing, 442 Maxillary sinus cancer, 312–313 Maxillary t rus, 307 McBurney sign, 60, 60f

MCL. See Medial c llateral ligament (MCL) tear, knee McVay meth d, 38 MDRD. See M di icati n Diet in Renal Disease (MDRD) Study Equati n Mean bl d pressure, 24 Mechanical ventilati n, 22–23 m de , 22 in patient with lung disease, 52 rate , 23 respirat ry alkal sis in, 12 r utine starting p int in, 23 weaning and extubati n in, 23, 52 Meckel diverticulum, 62, 179 Medial c llateral ligament (MCL) tear, knee, 493 Medial malle lus racture, 484, 485f Median nerve, 471, 471f Median nerve c mpressi n, 446, 470, 492 Median stern t my, 81, 81f Mediastinal lesi ns, 90 Mediastinal thyr id, 269 Mediastinitis, 441 Mediastin sc py, 80 Mediastin t my, anteri r parasternal, 81 Mediastinum, 78, 79f Medical hist ry, 43 Medical risk act rs, 43–57 ASA physical status classi icati n , 45, 45t assessment , 43 cardiac in n ncardiac surgical pr cedures, 44, 45t in surgical patient with cardiac disease, 46–51 cuts and caveats n, 2 general aspects , 43–46 in ecti n c ntr l and, 45 in patients with liver disease, 55–57 in patients with lung disease, 51–53 in patients with renal disease, 53–55 pre perative testing r, 44–46, 44t study questi ns n, 67–75 Medullary breast cancer, 262 Medullary thyr id carcin ma (MTC), 275, 275t, 288 Medull blast ma, 462, 465 Megac l n, 195 Meissner (submuc sal) plexus, 154 Melan ma, 444 anal, 203 hand, 446 head and neck, 319 intestinal metastases r m, 177 staging , 444 Melan ma in situ, 444 Melena, 65, 182 MEN. See Multiple end crine ne plasia Meningi mas, 451, 462, 464, 464f, 470 Mening cele, 466 Meniscal tear, 493 Mesenteric ischemia acute, 131 chr nic, 131–132 Mesenteric vascular disease, 130–132 Meshes, synthetic, 449 Mes theli ma, 84

Index Metab lic acid sis, 11–12, 12t, 54 Metab lic alkal sis, 9, 12, 12t Metab lic panel, 44t, 53 Metab lic rate, basal, 17 Metastasect my, 350 Metastases t b ne, 490, 491 t brain, 462, 464 cellular mechanisms in, 345 t heart, 101 t liver, 209 t lung, 89 t small intestine, 177 t spine, 470 t spleen, 234 Metastatic breast cancer, 261–262, 264 Methimaz le, 270 Methylprednis l ne, 366t MI. See My cardial in arcti n Micelles, 175 Micr de rmati n, 431 Micr hematuria, 427 Micr tia, 437 Midbrain lesi n, 453 Middle cerebral artery, 450 Middle rectal artery, 180f, 181 Middle thyr id veins, 266, 267f Midgut v lvulus, 384 Midsigm id c l n, 196 Migrating m t r c mplex (MMC), 175 Milr y disease, 142 Mineral c rtic ids, 280 Minimal access surgery, 335–343 advantages and disadvantages , 336 cl sed pneum perit neum meth d , 336 c mplicati ns , 337–338 c st-e ectiveness , 336 cuts and caveats n, 296–297 general perative technique in, 336–337 general principles , 335–338 hist ry , 335 intra-abd minal access r, establishment , 336–337 m rtality and m rbidity in, 337 pen pneum perit neum meth d , 336 pen surgery versus, 335–336 perative milest nes in, 335 patient preparati n r, 336 physi l gic changes ass ciated with pneum perit neum in, 337 relative c ntraindicati ns t , 337 study questi ns n, 398–399, 402–403, 406, 408–409 technical advances in, 335 Minnes ta tubes, 34 Mitral insu iciency, 97–98 Mitral regurgitati n, 47 Mitral sten sis, 97 Mitral valve disease, 97–98 Mitral valve pr lapse, 98 Mitral valve repair, 96, 96t, 98 Mitral valve replacement, 96, 96t, 97 Mittelschmerz, 59 Mixed ven us xygen saturati n (SvO2), 24 M di icati n Diet in Renal Disease (MDRD) Study Equati n, 53–54 M hs surgery, 319, 443

M lecular diagn stics, 348 M nd r disease, 259 M n cl nal antib dies, 350 M n ilament sutures, 32, 33t M n saccharides, 175 M nr -Kellie d ctrine, 450 M rphine, r patient with renal disease, 55 M tilin, 175 M tility dis rders, es phageal, 154–158 M t r examinati n, 453 M vement dis rders, 466–467 MRCP. See Magnetic res nance ch langi pancreat graphy MRI. See Magnetic res nance imaging MTC. See Medullary thyr id carcin ma Muc epiderm id carcin ma br nchial, 89 par tid gland, 323 Muc sa-ass ciated lymph id tissue (MALT) lymph ma, 170 Muhe, Erich, 335 Multil cular abscess, 40 Multiple end crine ne plasia, 287–289 MEN1, 287–289, 288t MEN2A, 288–289, 288t MEN2B, 288–289, 288t Multiple myel ma, 490–491 Multiple scler sis, v iding dys uncti n in, 425 Multiple valvular disease, 99 Multivisceral transplantati n, 374–375 Murphy sign, 60 Murray, J seph E., 430 Muscle/my cutane us laps, 434f, 436 Muscle relaxants r patient with liver disease, 57 r patient with renal disease, 55 Muscul cutane us nerve, 471, 471f Myasthenia gravis, 289 Myc bacteria in ecti n, atypical, 308 Myc phen late m etil, 366t Myc tic aneurysm, 460 Myel dysplasia, v iding dys uncti n in, 425 Myel mening cele, 466 Myenteric (Auerbach) plexus, 154, 174 My cardial in arcti n (MI), 93, 100 peri perative, 39 p st perative, 50 surgical treatment c mplicati ns, 101 My cardial per usi n assessment, n ninvasive, 48 My cutane us lap, 434f, 436 My sitis, Clostridium, 41 Myx ibr ma, es phageal, 159 Myx mas, 101

N Nail in ecti ns, 446, 492 Narc tics, r patient with liver disease, 57 Nasal cavity anat my , 312 cancer , 312–313 Nasal derm ids, 303, 304t Nasal papill mas, 305 Nasal p lyps, 306 Nasal rec nstructi n, 437–438 Nas gastric (NG) lavage, 65, 66

523

Nas gastric (NG) tubes, 34 Nas pharyngeal cancer, 313–314 Nati nal Kidney F undati n, CKD classi icati n , 54, 54t Neck. See also Head and neck anat my , 311 benign lesi ns , 300 c ngenital masses , 302–305, 302t examinati n , 300 lymphatic drainage , 311 mass evaluati n in adults with n primary cancer seen n exam, 311 trauma t , 354–355 z nes , 355, 355f Neck abscesses, 300–302, 301t Neck cancer, 311–312. See also Head and neck cancer Neck dissecti n, 310f, 312, 312f Neck vein distenti n, 93 Necr tizing enter c litis, 392–395, 393f Necr tizing asciitis, 41, 474 Negative pressure w und therapy (NPWT), 430–431 Ne adjuvant therapy, 350 Ne plasia. See also specific types de initi n , 344 transplant-related, 367 Ne plastic p lyps, 184–185 Nephrect my, lapar sc pic d n r, 342 Nephr lithiasis, abd minal pain in, 62–63 Nerve gra t, 433 Nerv us system. See Central nerv us system Neuraxial bl ckade, in patient with lung disease, 52 Neur blast ma, 395 Neur ibr ma(s), small intestine, 177 Neur ibr mat sis type I, 306 type II, 306–307 Neur genic bladder, hypert nic, 425 Neur genic claudicati n, 118, 469 Neur genic sh ck, 27, 28t Neur l gic examinati n, 453–454, 458, 462 Neur ma, ac ustic, 306, 465 Neur muscular bl ckade, in patient with lung disease, 52 Neur surgery, 450–471 cuts and caveats n, 411 uncti nal, 466–467 study questi ns n, 496–498, 500–502 Neur surgical patient evaluati n , 453–454 initial management , 453 New Y rk Heart Ass ciati n (NYHA) classi icati n heart ailure, 98, 98t risk assessment t l , 48 Nicardipine, 26 Nipple discharge, 260 Nissen und plicati n, 157, 341, 342f Nitr gen balance, 18 Nitr glycerin, 26 Nitr prusside, 26 N dular thyr id enlargements, 272 N nabs rbable suture, 32, 33t N n-H dgkin lymph ma head and neck, 319–320 splenic, 234

524

Index

N ninvasive stress testing, 49 N nsemin mat us germ cell tum rs (NSGCTs), 421–423 N n–small cell lung carcin ma, 86 N nster idal anti-in lammat ry drugs (NSAIDs), r arthritis, 487 N repinephrine, 26 N rmal saline (NS), 6, 6t N rm - sm lar hyp natremia, 7–8 N rm thermia, in surgical patients with cardiac disease, 50 N se aesthetic plastic surgery r, 447 c ngenital masses , 303–304, 304t examinati n , 299 NPWT. See Negative pressure w und therapy NSGCTs. See N nsemin mat us germ cell tum rs Nucleus pulp sus, 467 Nuss pr cedure, 83 Nutriti n r bariatric surgery patients, 328, 334 r surgical patient, 17–21 Nutriti nal therapy, 18–21 energy (cal ric) requirements in, 18 enteral, 19–20 g als , 18–19 parenteral (IV), 20–21 pr tein requirements in, 18–19 Nutriti n status evaluati n, 18, 54 NYHA. See New Y rk Heart Ass ciati n

O Oat cell carcin ma, 86 Obese patient nutriti nal status evaluati n in, 18 pre perative risk management in, 52 Obesity classi icati n , 325, 325t c m rbidities in, 325, 325t, 326t epidemi l gy , 325 surgery r. See Bariatric surgery Oblique ractures, 478, 479f Obstructed de ecati n, 199 Obstructing hernia, 35 Obstructi n. See also specific types airway, 21–22, 90–91 intestinal (b wel), 63–65, 175–176, 176f, 197–198 Obstructive jaundice, 56 Obstructive sh ck, 28–29, 28t Obstructive ur pathy, 413 Obturat r hernias, 39 Obturat r sign, 60 Occipital l be, 450 Ocul m t r lesi n, 453 Ogilvie syndr me, 65 Olig dendr gli mas, 463–464 Omental lap, 442 Omphal cele, 379–381, 379t Onc genes, 344–345 Onc l gy. See Cancer; Surgical nc l gy O ph rect my, pr phylactic, 349 Open drains, 34 Open ractures, 475–476, 475f, 478, 480t Open pneum perit neum meth d, 336 Open pneum th rax, 91

Open splenect my, 234 Oral cavity cancer , 314 examinati n , 300 squam us papill ma , 305 Oral lymphangi ma, 305 Orbital ractures, 445 Organ transplantati n, 362–375 candidate evaluati n r, 362 cuts and caveats n, 297 d n rs r, 363 ertility and pregnancy a ter, 367–368 genetic relati nships in, 362–363 immun l gic c nsiderati ns in, 364 immun suppressi n in, 365–368 c mplicati ns , 365–368 inducti n, 365 maintenance, 365 medicati ns r, 366t–367t rgan-speci ic c nsiderati ns in, 368–375 reas ns r, 362 rejecti n , 364 study questi ns n, 400, 404, 406–407, 409 termin l gy in, 362–363 Original Cardiac Risk Index, 47, 48t Or pharynx anat my , 315 cancer , 315 examinati n , 300 Orth pedics, 472–493 adult, 491–493 cuts and caveats n, 411 emergencies in, 472–475 study questi ns n, 496–498, 500–502 trauma in, 478–486 urgencies in, 475–477 Orth t pic gra t, 363 Osm larity, IV luids, 6t Osm tic pressure, b dy luid and electr lyte regulati n by, 3 Oste arthritis, primary, 486 Oste ch ndr ma, chest wall, 83 Oste ma, head and neck, 307 Oste myelitis acute, 488 chr nic, 488–489 Oste my cutane us/b ne lap, 436 Oste p r tic ractures, 482 Oste sarc ma, 490 Oste t my, 487 Ostium primum de ect, 103 Ostium secundum de ect, 103 Otalgia, in head and neck cancer, 309 Ovarian cancer, pr phylactic surgery t prevent, 349 Ovarian in arcti n, 341 Ovarian masses, lapar sc py r, 341 Ovarian t rsi n, 341 Over l w inc ntinence, 426 Overhydrati n, 40 Ovulati n, pain with (mittelschmerz), 59 Oxygenati n (Po 2), 22 Oxygen delivery equati n, 27 Oxygen saturati n (Sao 2), 27–29 Oxygen saturati n, mixed ven us (SvO2), 24 Oxyntic (parietal) cells, 161 Oxyphil aden ma, 323

P 6 P’s, arterial insu iciency, 120 Pacemakers, 47 Packed red bl d cell trans usi n therapy, 15–16 alternatives t , 16 disease transmissi n in, 15–16 indicati ns r, 16 risks , 15–16 Paget disease breast, 262 perianal, 202, 202t Palliative surgery, r cancer, 350 Panc ast tum r, 86 Pancreas, 215–229 anat my , 215–216, 215f annular, 385 cuts and caveats n, 152 end crine, 217 tum rs , 285–287, 291, 294 ex crine, 216–217 malignancies , 225–229 rientati n , 215 physi l gy , 216–217 vasculature , 216 Pancreatic aden carcin ma, 225–229 clinical presentati n , 226 diagn sis , 226–227 epidemi l gy , 225–226 pr gn sis , 229 treatment , 227–228, 227f Pancreatic amylase, 175, 218 Pancreatic ch lera, 287 Pancreatic duct, 204, 206f, 216 Pancreatic enzyme replacement, 224 Pancreatic lipase, 175 Pancreatic neur end crine tum rs (PNETs), 285, 288, 289 Pancreatic du denect my (Whipple pr cedure), 227–228, 227f Pancreatic pr teases, 175 Pancreatic pseud cyst, 225 Pancreatic transplantati n, 373–374 alternatives t , 373 pancreas a ter kidney, 373 pancreas al ne, 373 simultane us pancreas and live d n r kidney, 373 simultane us pancreas-kidney, 373 Pancreatitis, 217–225 abd minal pain in, 62 acute, 217, 218–223 APACHE II sc re in, 219, 222t clinical presentati n , 218 diagn sis , 218–219 ERCP indings in, 219, 220t pr gn sis , 219 radi graphic severity assessment , 219, 220t Rans n criteria in, 219, 221t treatment , 220–223 alc h l-induced, 217, 223 aut immune, 218 chr nic, 217, 218, 223–225 clinical presentati n , 223 eti l gy , 223 medical treatment , 224

Index path l gic indings in, 223 surgical treatment , 224–225, 224f classi icati n , 217 c ngenital abn rmalities and, 217 de initi n , 217 eti l gy , 217–218 gallst ne, 217 genetic, 218 hereditary, 217 iatr genic, 217 idi pathic, 218 in ecti us, 218 relapsing, 217, 223 t xic-metab lic, 218 Panel reactive antib dy (PRA), 364 Panniculect my, 442 Pantal n hernias, 37 Papillary aden cyst ma, par tid, 322–323 Papillary thyr id carcin ma (PTC), 274–275, 275t Papilledema, 453 Papill ma head and neck, 305–306 intraductal (breast), 260 inverted, 305 laryngeal, 306 nasal (schneiderian), 305 squam us, ral cavity, 305 Parad xical aciduria, 9, 12 Parad xical inc ntinence, 426 Paranasal sinuses anat my , 312 cancer , 312–313 Parane plastic syndr mes, 421 Parapharyngeal space, 315 Parapharyngeal space abscesses, 302 Paraphim sis, 413 Parasitic in ecti ns, splenic, 233 Parathyr id aden ma, 276–279 Parathyr id glands, 268, 276–279 anat my , 276 cuts and caveats n, 254–255 embry l gy , 276 injury t , 268 l cati n , 268, 269f Parathyr id h rm ne (PTH), 277 imbalances , 276–279 indicati ns r surgery in, 277, 278t in multiple end crine ne plasia, 287–289 in thyr id dys uncti n, 271 Paravertebral sulci, 78 Parenteral (IV) nutriti n, 20–21 administrati n rate in, 20 administrati n r ute in, 20 c mplicati ns , 21 rmula c mp siti n in, 20 Parietal cells, 161 Parietal l be, 450 Parkins n disease, 467 v iding dys uncti n in, 425 Parkland rmula, r burn resuscitati n, 360 Par nychia, 446, 492 Par tid gland, 320–324 anat my , 320 embry l gy , 320 in lammat ry dis rders , 324

innervati n , 321, 321f masses , management , 322 ne plasms , 322–323 trauma t , 323 Par titis, acute suppurative, 324 Partial bstructi ns, 64 Partial-thickness burns, 360 Patellar tend n tear, 493 Patent ductus arteri sus, 102–103 Path l gic ractures, 479 Path l gic staging, 348 PCL. See P steri r cruciate ligament (PCL) tear PCOP. See Pulm nary capillary cclusi n pressure PCWP. See Pulm nary capillary wedge pressure Pect ralis lap, r sternal w unds, 441 Pect ralis maj r lap, pedicled, 438 Pect ralis turn ver lap, 442 Pectus carinatum, 83 Pectus excavatum, 83 Pediatric ractures, 480–482 Pediatric surgery, 376–396 r abd minal wall de ects, 379–381 r c ngenital hernias, 376–379 crani acial, 444 cuts and caveats n, 298 r dis rders in ancy, 390–395 r es phageal atresia and trache es phageal mal rmati ns, 381–383 r Hirschsprung disease, 387–389 r intestinal atresia, 385–387 r intestinal malr tati n, 383–385, 384f r s lid tum rs, 395–396 study questi ns n, 400–404, 407–409 Pedicled lap, 435 Pedicled pect ralis maj r lap, 438 Pedunculated p lyps, 184 PEEP. See P sitive end expirat ry pressure Pelvic l r– utlet bstructi n, 199 Pelvic racture, 359, 472–473 Pelvic radi graph, in trauma assessment, 353 Pelvic ring injuries with hem dynamic instability, 472–473 radi graphic studies , 472, 473f stabilizati n , 473, 473f Penetrating trauma cardiac, 356 cerebr vascular, 355 chest, 354 head, 454 j int, 477 penile, 429 renal, 427 testicular, 429 urethral, 428 ur l gic, 427 Penile implant, 424 Penis anat my , 423 erectile dys uncti n , 423–424 erecti n and detumescence , 423 racture (erect penis), 428–429 injuries t , 428–429 Penr se drain, 34

525

Pental gy Cantrell, 380 Pental gy Fall t, 106 Pepsin, 161, 175 Pepsin gen, 161 Peptic ulcer disease, 163–168 abd minal pain in, 62–63 pharmac l gic therapy r, 166, 166t surgical treatment , 166–167, 167t Percutane us nephr lith t my (PCNL), 415 Per rating bstructi n, 64 Per rat r laps, 435–436 Periampullary diverticula, 179 Perianal abscess, 201 Perianal ne plasms, 202–203 Pericardial cysts, 90 Pericardial dis rders, 102 Pericardial e usi ns, 101–102 Pericardial tamp nade, 101, 354 Pericarditis, 102 acute, 102 chr nic, 102 chr nic c nstrictive, 102 Pericardium, ultras und , 353 Peric lic in ecti n, 190 Perineal hernias, 39 Peri perative my cardial in arcti n, 39 Peri ral lymphangi ma, 305 Peripheral arterial disease, evaluati n and w rkup in, 120 Peripheral bl d smear, in hypersplenism evaluati n, 233 Peripheral edema, 93 Peripherally inserted central catheters (PICCs), 35 Peripheral nerve(s), 470–471 Peripheral nerve tum rs, 306–307 Peristalsis es phageal, 154 intestinal, 174–175 Perist mal hernias, 39 Perit neal dialysis, 54, 372 Perit neal dialysis catheters, 35 Perit nitis eculent, 191 purulent, 191 rigid abd men with, 58 Perit nsillar abscesses, 300, 308 Per ral end sc pic my t my (POEM), 156 Peutz-Jeghers syndr me, 176, 185 Peyer patches, 174 PFTs. See Pulm nary uncti n tests Pharyng es phageal (Zenker) diverticulum, 154–155 Phase I clinical trials, 351 Phase II clinical trials, 351 Phase III clinical trials, 351 Phenylephrine, 26 Phe chr m cyt ma, 282t, 284–285, 284t, 288–289 Phlegmasia alba d lens, 138 Phlegmasia cerulea d lens, 138 PHPT. See Primary hyperparathyr idism Phyll des tum r, 259–260 Physical exam, pre perative, 43 in patient with cardiac disease, 47 Physical status classi icati n, ASA, 45, 45t Phyt bez ars, 171

526

Index

PICCs. See Peripherally inserted central catheters Pige n breast, 83 Piggyback liver transplantati n, 369 Pil nidal disease, 201 Pineal tum rs, 462 Pituitary aden ma, 287, 465–466 Pituitary tum rs, 462, 465–466 Plantar resp nses, 454 Plasmalyte, 6t Plasma v lume, 3 Plastic surgery, 430–449 aesthetic, 446–449 a ter massive weight l ss, 448–449 candidate selecti n r, 446 c mm n pr cedures in, 447–448 rati nale r, 446 crani acial, 444–445 cuts and caveats n, 410 de initi n , 430 hand, 445–446 inn vati ns and devices in, 449 n table igures in, 430 rec nstructive, 430–442 abd minal, 442 breast, 439–441, 440f chest wall, 441–442 cranial/scalp, 436–437 ear, 437 eyelid, 437 head and neck, 438 lip, 438 l wer extremity, 442 nasal, 437–438 tissue expansi n r, 433–434 r w unds and de ects, 430–436 study questi ns n, 495, 497, 499–500 war’s e ect n, 430 Platelet activati n, 13 Platelet adherence, 13 Platelet c unt, 13, 56 Platelet plug, 13 Ple m rphic aden mas, par tid, 322 Pleural and pleural space dis rders, 83–84 Pleural bi psy, 81 Pleural e usi ns, 84, 221 Pleural empyema, 84 Pleural pr cedures, diagn stic, 80–81 Pleural tum rs, 84 Plicae circulares, 174 Plummer disease, 271 PMI. See P int maximum impulse PNETs. See Pancreatic neur end crine tum rs Pneumat sis intestinalis, 61 Pneum bilia, 61 Pneumocystis carinii pneum nia (PCP), 367 Pneum nia Pneumocystis carinii, 367 p st perative, 39, 53 Pneum perit neum cl sed, 336 c mplicati ns due t , 337–338 pen, 336 physi l gic changes ass ciated with, 337 Pneum th rax, 81, 356 diaphragmatic hernia and, 378

pen, 91 sp ntane us, 83–84 tensi n, 28, 91, 356 P int maximum impulse (PMI), 93 P lyp(s) c l rectal, 184–186 gastric, 171 nasal, 306 small intestine, 176 v cal, 308 P lyp sis syndr mes, 185–186 P ns, 450 P ns lesi n, 453 P rt, 35 P rtal hypertensi n, 210–212 ascites in, 212 eti l gy , 210 hypersplenism in, 212, 231 medical management , 211, 211f path physi l gy , 210 surgical management , 211–212 P sitive end-expirat ry pressure (PEEP), 22–23 P steri r cruciate ligament (PCL) tear, 493 P steri r spinal artery, 450 P ster lateral th rac t my, 81, 82f P stgastrect my syndr mes, 170–171 P st perative c mplicati ns, 39–40 in patients with cardiac disease, 50–51 in patients with lung disease, 53 in patients with renal disease, 55 P st perative ever, 39 P st perative in ecti ns, 40–42 P st-thr mb tic syndr me (PTS), 136, 138 P st-transplant lymph pr li erative dis rder (PTLD), 367, 375 P st-traumatic arthritis, 487 P stvag t my diarrhea, 171 P tassium digesti n and abs rpti n , 175 imbalances , 8–9. See also Hyperkalemia; Hyp kalemia IV c ncentrati ns , 6, 6t maintenance , 6 P upart ligament, 35 Prednis l ne, 366t Prednis ne, 366t Pregnancy breast cancer in, 264 ect pic, lapar sc py in, 341 rgan transplantati n and, 367–368 Prel ad, 27–28 Pre perative antibi tics, 45 Pre perative evaluati n, 43 Pre perative testing, 44–46, 44t Pressure s res, 443, 443t Pressure supp rt (PS), in ventilat r supp rt, 22 Priapism, 412 Primary hyperald ster nism (C nn syndr me), 282t, 283–284 Primary hyperparathyr idism (PHPT), 277–279 Primary intenti n, 30, 31f Primary intenti n, delayed, 31 Primary intestinal lymph ma, 169–170 Primary scler sing ch langitis, 213 Pr ct sc py, 193

Pr Pr Pr Pr

ct sigm id sc py, 182 lactin-secreting aden mas, 465 li erative phase, w und healing, 30, 442 phylactic antibi tics, 40, 45, 50, 52, 55, 236 Pr phylactic cancer surgery, 349 Pr pylthi uracil (PTU), 270 Pr state cancer, 417–418 h rm nal therapy r, 351, 418 screening r, 346, 417 Pr state gland, benign dis rders , 415–417 Pr state-speci ic antigen (PSA), 417 Pr statitis abd minal pain with, 60 n nbacterial, 417 Pr statitis/chr nic pelvic pain syndr me, 417, 417t Pr sthetic heart valves, 47, 94–96 Pr sthetic mesh repairs, 38 Pr tein digesti n and abs rpti n , 175 as energy s urce, 17 nutriti nal requirements , 17 in nutriti nal therapy, 18–19 Pr tein C, 13 Pr tein C de iciency, 15 Pr tein S, 13 Pr tein S de iciency, 15 Pr te mics, 348 Pr thr mbin time (PT), 13, 57 Pr t n pump inhibit rs (PPIs), r peptic ulcer disease, 164, 166, 166t Pr t - nc genes, 344 Pr ximal gastrect my, 66 Pr ximal humerus ractures, 482 PSA. See Pr state-speci ic antigen Pseud cyst, pancreatic, 225 Pseud hyp natremia, 7–8 Pseud membran us c litis, 196 Pseudomonas aeruginosa, 488 Pseud p lyps, 184, 192 Ps as sign, 60 PT. See Pr thr mbin time PTC. See Papillary thyr id carcin ma PTH. See Parathyr id h rm ne PTLD. See P st-transplant lymph pr li erative dis rder PTS. See P st-thr mb tic syndr me p53 tum r suppress r gene, 345 Pub rectalis (anismus) n nrelaxati n, 199 Pudendal nerve c nducti n vel city, 183 Puest w perati n, 224 Pulm nary artery, 80 Pulm nary artery catheter, 24, 25f, 50 Pulm nary capillary cclusi n pressure (PCOP), 24 Pulm nary capillary wedge pressure (PCWP), 24 Pulm nary c ntusi n, 92 Pulm nary edema chr nic c mplicati n , 140 p st perative, 51 Pulm nary emb lism, 29, 138–140 clinical indings , 139 diagn stic tests r, 139, 139f epidemi l gy and eti l gy , 138

Index preventi n , 140 treatment , 139–140 Pulm nary uncti n tests (PFTs), 51, 94 Pulm nary hypertensi n, diaphragmatic hernia and, 378 Pulm nary in ecti ns, 85 Pulm nary n dules, s litary, 85 Pulm nary vascular bstructive disease, 104 Pulm nary vascular resistance (PVR), 24–25 Pulm nic valve disease, 99 Pulsus parvus et tardus, 93 Purgatives, 184 Purulent perit nitis, 191 Push enter sc py, 65 PVR. See Pulm nary vascular resistance Pyel nephritis, abd minal pain in, 62–63 Pyl ric sten sis, in antile hypertr phic, 390–391 Pyl rus, 162, 162f

Q Quadriceps tear, 493 Quinsy, 300

R Radial rearm lap, 436 Radial scar, 260 Radiati n injury, 179 Radiati n therapy, 350 Radicul pathy, 467 Radi active i dine, r Graves disease, 270 Radi lucent st nes, 414 Radi paque st nes, 414 Radius ractures, distal in adults, 482 in children, 480, 481f, 482 Ral xi ene, 261 Rand m lap, 434f, 435 Rans n criteria, 219, 221t ras nc gene, 344 Ravitch pr cedure, m di ied, 83 Raynaud phen men n, 133 Reactive hydr cele, 422 Recept r status, 348 Rec nstructive ladder, 430, 432f Rec nstructive surgery, 430–442 abd minal, 442 breast, 439–441, 440f chest wall, 441–442 cranial/scalp, 436–437 ear, 437 eyelid, 437 head and neck, 438 lip, 438 l wer extremity, 442 nasal, 437–438 tissue expansi n r, 433–434 r w unds and de ects, 430–436 Rectal exam, 60, 66 Rectal intussuscepti n, 199 Rectal pr lapse, 199 Rectal tubes, 34 Rectal ulcer, s litary, 199 Rect anal inhibit ry re lex, 183 Rectum anat my , 181

bl d supply , 180f, 181 cuts and caveats n, 151 evaluati n , 182–183 physi l gy , 182 Rectus abd minis muscle lap, 442 Recurrent laryngeal nerve (RLN), 266–268, 271 Red pulp, spleen, 230 Reducible hernia, 35 Reducti n mamm plasty, 441 REE. See Resting energy expenditure Re lex(es) brainstem, 453 deep tend n, 454 in spinal c rd injury, 458 Re lux. See Gastr es phageal re lux disease Regi nal enteritis. See Cr hn disease Rehabilitati n, in head and neck cancer, 310–311 Rejecti n, 364 acute cellular, 364, 365f antib dy-mediated, 364 chr nic, 364, 365f hyperacute, 364, 365f Relapsing pancreatitis, 217, 223 Rem deling phase, w und healing, 30 Renal artery aneurysm, 372 Renal artery sten sis, 132–133, 132f, 372 Renal artery thr mb sis, 371 Renal cell carcin ma, 421, 422f Renal disease hyp c agul pathic state in, 14 surgical patients with, 53–55 dialysis in, 54 hist ry , 53 lab rat ry testing and diagn stic studies in, 53–54 perative variables in, 54–55 physical examinati n , 53 p st perative c mplicati ns in, 55 pre perative management , 54 renal uncti n assessment in, 53–54 vascular access in, 55 Renal ailure acid sis in, 11 acute, surgical patients with, 53–55 Renal pelvis transiti nal cell carcin ma, 419, 420f Renal st nes, 62–63, 414–415 Renal transplantati n, 371–372 alternatives t , 372 d n rs r, 363, 371 lapar sc pic d n r nephrect my r, 342 liver transplantati n with, 370 perative strategy r, 371, 371f pancreas transplantati n with, 373 rejecti n , 372 Renal trauma, 358, 427 Renal vein thr mb sis, 372 Renin, 280 Replants, amputated digits, 445 Research, cancer, 351 Respirat ry acid sis, 11, 12t Respirat ry alkal sis, 12, 12t Respirat ry e rt, 21 Respirat ry rate (RR), 21 Resting energy expenditure (REE), 17, 18

527

Rest pain, 122 Restrictive bariatric perati ns, 326–327, 327f Resuscitative th rac t my, 354 Reticul cyt sis, 233 Retr grade urethr gram (RUG), 428 Retr pharyngeal abscesses, 302 Reversible ischemic neur l gic de icit (RIND), 126 Revised Cardiac Risk Index, 48 Reyn ld pentad, 60 Rhabd my sarc ma, 101 Rheumatic ever, 96, 98, 99 Rheumat id arthritis, 487 Rhin plasty, 447 Rh mbic lap, 434 Rhytidect my, 447 Richter hernia, 35 Riedel thyr iditis, 272 Right hepatic artery, 204 Right lung, 79, 79f Right ventricular hypertr phy, 93 Rigid abd men, 58 Rigid br nch sc py, 80 Rigid pr ct sigm id sc py, 187 RIND. See Reversible ischemic neur l gic de icit Rinne test, 299 Risk assessment strati icati n, r surgical patients with cardiac disease, 47–48, 48t Risk act rs. See Medical risk act rs R b tic surgery, 335, 343, 343f R tati n lap, 434 R tat r cu tear, 491 R und ligament, 36 R ux-en-Y gastric bypass, 328, 329f R ux-en-Y gastr jejun st my, 165, 165f R vsing sign, 60 Rubella, c ngenital, 102 Rule 9’s, in burn injuries, 360, 360f Running stitch, 31, 32f

S Salivary amylase, 175 Salmonella ste myelitis, 488 Salter-Harris classi icati n, gr wth plate ractures, 480, 480f Samter triad, 306 Sao 2 ( xygen saturati n), 27–29 Sarc id sis, 233 Sarc ma(s), 344 b ne, 490 gastric, 170 small intestine, 177–178 splenic, 234 SBS. See Sh rt b wel syndr me SBT. See Sp ntane us breathing trial Scalene n de bi psy, 80 Scalp/cranial rec nstructi n, 436–437 Scalp injuries, 455 Scaph id ractures, 482, 483f Scapular lap, 436 Scapul th racic diss ciati n, 474, 475f Scars, 442 Schatzki rings, 158 Schist s miasis, 210 Schneiderian (nasal) papill mas, 305

528

Index

Schwann mas, 306, 462, 465, 470 Scler sing aden sis, 259 Scr ula, 300 Sec ndary hyperparathyr idism (SHPT), 278t, 279 Sec ndary intenti n, 31, 31f Segmental ractures, 478 Segmental medullary arteries, 450 Seizure(s), 467 treatment , 467 tum rs and, 462 Seizure pr phylaxis, in head (brain) trauma, 455 Semin mas, 90, 421–423 Sengstaken-Blakem re tubes, 34 Sens ry examinati n, 453, 458 Sentinel n de bi psy, 263, 319, 348–349, 444 Sepsis gastr intestinal istula and, 42 p stsplenect my, 235–236 preventi n , 42 Septic arthritis, 476, 488 Septic sh ck, 27–28, 28t Sequestrum, 488 Sessile p lyps, 184 Sex ster ids, 280 Sh ck, 27–29, 353–354 hem dynamic pr ile analysis in, 28t types , 27–28, 28t Sh rt b wel syndr me (SBS), 374–375 Sh rt-chain atty acids, 182 Sh rt gastric arteries, 230, 231f Sh rt gut syndr me, 179 Sh ulder disl cati n, 485 Sh ulder dis rders, in adults, 491 Sh ulder instability, anteri r, 491 Sh uldice repair, 38 SHPT. See Sec ndary hyperparathyr idism SIADH. See Syndr me inappr priate antidiuretic h rm ne Sialadenitis, 322 Sialadenitis, calcul us, 324 Sickle cell anemia, 232 Sigm id sc py, 183 Sigm id v lvulus, 63, 197–198 Silver nitrate, 361 Silver sul adiazine (Silvadene), 360 SIMV. See Synchr nized intermittent mandat ry ventilati n Sinus tract, 302 Sinus ven sus de ect, 103 Sipuleucel-T, 418 Sir limus, 367t 6 P’s, arterial insu iciency, 120 Skin anat my , 30 gastr intestinal istula and, 42 w unds in, 30–32 Skin cancer, 443–444 basal cell carcin ma, 443 anal, 202, 202t hand, 446 head and neck, 318–319 melan ma, 444 anal, 203 hand, 446 head and neck, 319

intestinal metastases r m, 177 staging , 444 squam us cell carcin ma, 318–319, 443, 446 transplant-related, 367 Skin gra ts, 431–433 c ntracture , 433 ailure , 433 ull-thickness, 432 healing , 433 split-thickness, 432 Skin lesi ns benign, 443 malignant, 443–444. See also Skin cancer Skull, 450 Skull ractures, 456 Sleeve gastrect my, 326, 327f c mplicati ns , 330–331 utc mes , 329 Sliding hernia, 35 Slipped (herniated) discs, 467–469 Small b wel bstructi n (SBO), 63, 64, 64f, 175–176, 176f Small b wel transplantati n, 374–375 Small cell anaplastic ( at cell) carcin ma, 86 Small cell lung carcin ma, 86 Small intestine, 173–179 anat my , 173–174, 173f–174f cuts and caveats n, 150–151 diseases , 175–179 injury t , 358 intestinal malr tati n and, 383 layers , 174, 174f physi l gy , 174–175 tum rs , 176–178 vasculature , 173 Sm king cessati n, pre perative, 51 S dium digesti n and abs rpti n , 175, 182 imbalances , 6–8. See also Hypernatremia; Hyp natremia IV c ncentrati ns , 6, 6t maintenance , 6 in surgical patients with renal disease, 54 S dium-p tassium-ATPase pump, 3 S litary pulm nary n dules, 85 S litary rectal ulcer, 199 Spectrin, 232 Spermatic c rd, anat my , 36, 36f Spermatic c rd hydr cele, 37 Spher cyt sis, hereditary, 232 Sphincter Oddi, 206 Spigelian hernias, 39 Spina bi ida, 466 Spinal anesthesia, in patient with lung disease, 52 Spinal arteries, 450 Spinal c lumn injury, 355 Spinal c rd arterial supply , 450 c ngenital lesi ns , 466 ven us return , 450 Spinal c rd injury, 355, 457–461 anteri r, 458 aut n mic dysre lexia in, 426–427 classi icati n , 458 c mplete, 458

c mplicati ns , 459 epidemi l gy , 457 extent , 458 inc mplete, 458 management , 458–459 neur l gic evaluati n in, 458 radi graphic studies , 454, 458–459 stabilizati n , 458 treatment , 459 v iding dys uncti n in, 425 Spinal dysraphism, 466 Spinal epidural abscess, 472 Spinal ractures, 482, 483–484 Spinal imm bilizati n, 355, 458, 459 Spine anat my , 467 degenerative disease , 467–470 tum rs , 470 Spiral ractures, 478, 479f Spir metry, pre perative, 51 Spir n lact ne, r C nn syndr me, 284 Spleen, 230–236 anat my , 230, 231f cuts and caveats n, 152 uncti n , 231 hist l gy , 230 injury t , 357 ne plastic diseases , 234 path l gy , 231–234 Splenect my abs lute and relative indicati ns r, 235t c mplicati ns a ter, 235–236 lapar sc pic, 235, 342 pen, 234 technical aspects , 234–235 Splenic abscess, 233 Splenic artery, 216, 230, 231f Splenic artery aneurysm, 130 Splenic cysts, 233 Splenic lexure, 180, 196 Splenic in ecti n, 233 Splenic rupture, 63 Splenic vein, 230, 231f Splenic vein thr mb sis, 232 Splen c lic ligament, 230 Splen megaly, 231, 232 Splen phrenic ligament, 230 Splen renal ligament, 230 Split-thickness skin gra ts (STSGs), 432 Sp ndyl sis cervical, 467 lumbar, 469–470 Sp ntane us breathing trial (SBT), 23 Sp ntane us pneum th rax, 83–84 Squam us cell carcin ma, 344 anal, 202, 202t es phageal, 159 hand, 446 laryngeal, 317 lung, 86 nasal and paranasal, 313 par tid gland, 323 skin, 318–319, 443, 446 tracheal, 89 Squam us papill ma, ral cavity, 305 Square t es, 143 Stable angina, 100

Index Staging cancer, 348. See also specific cancers lapar sc pic, 342 TNM system , 348, 349t Stan rd classi icati n, a rtic dissecti n, 127, 127f Staphylococcus aureus ste myelitis, 488 surgical site in ecti n, 40 Starling curve, 24 Starvati n, 17 Statins (HMG-C A reductase inhibit rs), 50, 121 Stellate skull ractures, 456 Stemmer sign, 143 Stensen duct, 321 Stensen duct trauma, 323 Sternal w unds, 441–442 Stern t my, median, 81, 81f Ster id h rm nes, 280 St mach, 161–163 arterial supply , 162, 163f benign lesi ns , 171 cancer , 164, 168–170, 169t cuts and caveats n, 150 embry l gy , 161 uncti ns , 161 injury t , 358 lymphatic drainage , 163 path l gy , 163–172 surgical anat my , 161–163, 162f, 163f vagal innervati n , 162 ven us drainage , 162, 163f Straight sinus, 450 Strangulated hernia, 35, 64 Strangulating bstructi n, 64 Streptococcus ste myelitis, 488 Stress testing exercise, 48 n ninvasive, 49 Stress ulcerati n, 171–172 Stress urinary inc ntinence, 426 Str ke, 125–127, 126f hem rrhagic, 459 v iding dys uncti n in, 425 Str ng i ns, 11 Struma lymph mat sa, 272 Struvite calculi, 414 STSGs. See Split-thickness skin gra ts Stunned my cardium, 99 Subacute thyr iditis, 272 Subarachn id hem rrhage, 460–461, 461 Subcutane us tissue, 30 Subdural hemat ma, 454, 457, 457f Sub alcine herniati n, 452, 452f Subgl ttic hemangi mas, 304 Subgl ttis, 317 Submuc sal (Meissner) plexus, 154 Subphrenic abscess, 236 Subpleural bleb, 83 Substernal g iter, 269 Subthalamic nucleus, 467 Subt tal c lect my, 66 Sucral ate, r peptic ulcer disease, 164 Sucti n drain, 33 Sul amyl n, 361 Sul ur-c ll id liver-spleen scan, 207 Sump drains, 34

Super icial burns, 360 Super icial ven us thr mb phlebitis (SVT), 142 Superi r laryngeal nerve (SLN), 268, 271 Superi r mesenteric artery (SMA), 173, 180, 180f, 216 Superi r mesenteric vein, 180, 216 Superi r rectal artery, 180f, 181 Superi r thyr id artery, 266, 267f Superi r thyr id veins, 266, 267f Suprac ndylar ractures humerus, 481 Supragl ttic tum rs, 317 Supragl ttis, 317 Suprainguinal a rt iliac cclusive disease, 118 Supralevat r abscess, 201 Supratent rial hem rrhage, 459 Surgery. See also specific procedures general cuts and caveats n, 1–2 essentials , 30–42 gastr intestinal istula in, 41–42 hernias in, 35–39 in ecti ns in, 40–41 p st perative c mplicati ns in, 39–40 study questi ns n, 67–75 tubes and drains in, 33–35 w unds in, 30–32 minimal access, 335–343 advantages and disadvantages , 336 cl sed pneum perit neum meth d , 336 c mplicati ns , 337–338 c st-e ectiveness , 336 cuts and caveats n, 296–297 general perative technique in, 336–337 general principles , 335–338 hist ry , 335 intra-abd minal access r, establishment , 336–337 m rtality and m rbidity in, 337 pen pneum perit neum meth d , 336 pen surgery versus, 335–336 perative milest nes in, 335 patient preparati n r, 336 physi l gic changes ass ciated with pneum perit neum in, 337 relative c ntraindicati ns t , 337 study questi ns n, 398–399, 402–403, 406, 408–409 technical advances in, 335 pediatric, 376–396 r abd minal wall de ects, 379–381 r c ngenital hernias, 376–379 crani acial, 444 cuts and caveats n, 298 r dis rders in ancy, 390–395 r es phageal atresia and trache es phageal mal rmati ns, 381–383 r Hirschsprung disease, 387–389 r intestinal atresia, 385–387 r intestinal malr tati n, 383–385, 384f r s lid tum rs, 395–396 risk act rs in. See Medical risk act rs r b tic, 335, 343, 343f

529

subspecialties. See also specific subspecialties cuts and caveats n, 410–411 study questi ns n, 494–502 Surgical abd men. See Abd men, acute surgical Surgical in ecti ns, 40–41 Surgical nc l gy, 348–351 curative, 349–350 cuts and caveats n, 297 diagn stic, 348–349 ll w-up in, 350 palliative, 350 pr phylactic, 349 research and training n, 351 study questi ns n, 399, 406 Surgical physi l gy acid–base disturbances in, 11–12 c agulati n in, 13–15 cuts and caveats n, 1 luid and electr lytes in, 3–10 intensive care unit, 21–26 nutriti n, 17–21 principles , 3–29 sh ck in, 27–29 study questi ns n, 67–75 trans usi n therapy in, 15–16 Surgical site in ecti n (SSI), 40, 45 Sushruta, 430 Sutures, 31–32 abs rbable, 32, 33t braided, 32, 33t characteristics , 32 c ntinu us (running stitch), 31, 32f h riz ntal mattress, 31, 32f interrupted, 31, 32f material , 32, 33t m n ilament, 32, 33t n nabs rbable, 32, 33t simple, 31 size , 32 vertical mattress, 31, 32f SVR. See Systemic vascular resistance SVT. See Super icial ven us thr mb phlebitis Swall wing assessment, 299 Swall wing training, 311 Swan-Ganz catheter, 24, 50 Swens n pr cedure, r Hirschsprung disease, 389 Synchr nized intermittent mandat ry ventilati n (SIMV), 22 Sync pe, 93 Syndr me inappr priate antidiuretic h rm ne (SIADH), 7–8 Syn vial luid analysis, 476, 476t Systemic vascular resistance (SVR), 24–25 Syst lic bl d pressure, 24

T T3 (trii d thyr nine), 269 T4 (thyr xine), 269 Tachycardia, b dy water levels and, 5 Tacr limus, 366t Tagged red bl d cell scan, 66 Tagliac zzi, Gaspar , 430 Tagliac zzi lap, 430, 431f Takayasu disease, 133–134

530

Index

Tam xi en, 261, 262, 351 TEE. See T tal energy expenditure; Transes phageal ech cardi graphy TEG. See Thr mb elast gram Telangiectasia, 459 Temp ral arteritis, 133 Temp ral l be, 450 Temp rary hem dialysis, 54 Tend n gra ts, 433 Tend n re lexes, deep, 454 Tenia c li, 181 Tensi n pneum th rax, 28, 91, 356 Terat id cysts, 303 Terat mas head and neck, 302t, 303–304 mediastinal, 90 testicular, 421 Tertiary hyperparathyr idism (THPT), 278t, 279 Testes, undescended, 421 Testicular t rsi n, 412, 413f Testicular trauma, 429 Testicular tum rs, 421–423 Tetanus injecti n, 40 Tetral gy Fall t, 106–107, 106f Tet spells, 106–107 TEVAR. See Th racic end vascular a rtic repair TFPI. See Tissue act r pathway inhibit r Thalamus, 450 Thalassemia maj r, 232 Therm diluti n, 24 Thiamine, abs rpti n , 175 Th mps n test, 493 Th racentesis, 80–81 Th racic a rtic injury, blunt, 356 Th racic cavity, anat my , 78–80, 78f–79f Th racic dis rders. See also Heart; Th racic surgery cuts and caveats n, 77–78 study questi ns n, 108–115 Th racic end vascular a rtic repair (TEVAR), 128 Th racic utlet syndr me (TOS), 83 Th racic spine ractures, 483 Th racic surgery cuts and caveats n, 77 exp sure and incisi ns in, 81, 81f general pr cedures in, 80–83 principles , 78–92 study questi ns n, 108–115 vide -assisted, 82–83 Th racic trauma, 90–92 immediate li e-threatening, 90–91 p tentially li e-threatening, 91–92 Th racic ultras und, 353 Th rac t my anter lateral, 81, 82f axillary, 81 r massive hem th rax, 356 p ster lateral, 81, 82f resuscitative, 354 THPT. See Tertiary hyperparathyr idism Thr mbect my pen, 125 perative ven us, 137 percutane us, 124

Thr mbin, 13 Thr mbin time, 14 Thr mb angiitis bliterans, 134 Thr mb cyt penia heparin-induced, 138 in patients with liver disease, 57 in splenic path l gy, 231–233 Thr mb cyt sis, p stsplenect my, 236 Thr mb elast gram (TEG), 14 Thr mb lysis, 124, 137 Thr mb sis, 124–125 Thr mb tic thr mb cyt penic purpura (TTP), 232–233 Thr mb xane A, 13 Thumb rec nstructi n, 445 Thym mas, 90 Thymus, cuts and caveats n, 254–255 Thymus gland, 289 Thyr calcit nin, 270 Thyr gl ssal cysts, 302, 302t Thyr gl ssal duct, 302 Thyr gl ssal istulas, 302 Thyr idal prim rdium, 302 Thyr id carcin ma, 274–276 anaplastic, 275–276, 275t llicular, 275, 275t medullary, 275, 275t, 288 papillary, 274–275, 275t pr phylactic surgery t prevent, 349 Thyr id dys uncti n, requiring surgery, 269–276 Thyr idea ima artery, 266, 267f Thyr id enlargements, n dular, 272 Thyr id gland, 266–276 abn rmal descent , 268–269 cuts and caveats n, 254–255 innervati n , 266–268 lymphatic drainage , 266, 268f study questi ns n, 290, 294 vasculature , 266, 267f Thyr id h rm nes, 269–270 Thyr iditis, 272 Thyr id lymph ma, 276 Thyr id ne plasms, 272–276 Thyr id n dules, 272–274. See also Thyr id carcin ma alg rithm r evaluati n and management , 274f assessment , 273 characteristics , 273 diagn stic studies , 273–274 ine-needle aspirati n , 273–274, 273t perative appr ach t , 274 Thyr id rests, 302 Thyr id-stimulating h rm ne (TSH), 269 Thyr id st rm, 271 Thyr tr pin-releasing h rm ne (TRH), 269 Thyr xine (T4), 269 TIA. See Transient ischemic attack Tibia ractures, 482 in adults, 484 in children, 481 Tidal v lume, in ventilat r supp rt, 23 Tinel sign, 470 Tissue engineering, 449 Tissue expansi n, 433–434 Tissue act r pathway inhibit r (TFPI), 13

Tissue ximetry, 449 Tissue-type plasmin gen activat r (t-PA), 13 T e amputati n, 125 T lerance, immun l gic, 364 T nsillar herniati n, 452 T nsillar hypertr phy, 305 T nsillect my, 308 T nsillitis, 308 TORCH syndr me, 391 TORS. See Trans ral r b tic surgery T rus, 307 T rus (buckle) ractures, 479f, 480, 481f TOS. See Th racic utlet syndr me T tal c l nic agangli n sis, 387 T tal energy expenditure (TEE), 17 T tal j int replacement, 487 T tal minute ventilati n, 22 T tal parenteral nutriti n (TPN), 20–21 T upet und plicati n, 341 T xic aden ma, 272 T xic multin dular g iter, 271 T x plasm sis, 367 t-PA. See Tissue-type plasmin gen activat r TPN. See T tal parenteral nutriti n Trachea anat my , 89 dis rders , 89 Tracheal injury, 357 Tracheal ne plasms, 89 Trache br nchial disrupti n, 91 Trache br nchial tree, 79f, 80 Trache es phageal istula (TEF), 381–383, 382f Trache es phageal mal rmati ns, 381–383 Trache st my, 21 TRAM. See Transverse rectus abd minis muscle (TRAM) lap Transes phageal ech cardi graphy (TEE), 50 Trans ramen magnum, 452 Trans usi n therapy, 15–16 alternatives t , 16 disease transmissi n in, 15–16 indicati ns r, 16 risks , 15–16 Transgl ttic tum rs, 318 Transient ischemic attack (TIA), 125 Transiti nal cell carcin ma renal pelvis and ureter, 419, 420f urinary bladder, 418 Transjugular intrahepatic p rt systemic shunt (TIPS), 211, 211f Transmetatarsal amputati n, 125 Trans ral r b tic surgery (TORS), 315 Transplantati n. See Organ transplantati n; specific procedures Transplant gl merul pathy (TG), 372 Transp siti n lap, 434 Transp siti n the great arteries, 107 Transtent rial herniati n, 452 Transudative e usi ns, 84 Transurethral resecti n the pr state (TURP), 416 Transverse ractures, 478, 479f Transverse rectus abd minis muscle (TRAM) lap, 439, 440f Trastuzumab, 264

Index Trauma, 352–359. See also specific injuries abd minal, 357–358, 358f biliary tree, 214 bladder, 358, 428 brain, 354, 454–457 cardiac, 101–102 cuts and caveats n, 297 epidemi l gy , 352 es phageal and tracheal, 357 gallbladder, 213 genit urinary, 358 hand, 445 head, 454–457 head and neck, 354–355 hepatic, 210 rth pedic, 478–486 par tid gland, 323 patient evaluati n in, 352–353 penile, 428 primary survey in, 352 renal, 358, 427 sec ndary survey in, 353 sh ck in, 353–354 spinal, 355, 457–461 study questi ns n, 399–401, 403, 406–408 tertiary survey in, 353 testicular, 429 th racic, 90–92 th racic a rtic, 356 trans usi n therapy in, 16 ureteral, 358, 428 urethral, 358, 428 ur l gic, 358, 427–429 Trem r essential, 467 Parkins n, 467 Trich bez ars, 171 Tricuspid sten sis and insu iciency, 98–99 Trigger inger, 492 Trii d thyr nine (T3), 269 Tris my 21. See D wn syndr me Tr chanteric bursitis, 492 Tr usseau sign, 226 True diverticulum, 179, 189 Truss, 38 TTP. See Thr mb tic thr mb cyt penic purpura Tubercul sis, transplant-related, 367 Tuber us breast, 441 Tubes, gastr intestinal (GI), 34 Tubular aden mas, 176, 184 Tubul vill us aden mas, 184 Tum r(s). See also specific types adrenal, 281–285 b ne, 446, 489–491 central nerv us system, 462–466 c l rectal, 184–189 de initi n , 344 es phageal, 158–160 genit urinary, 417–423 grade , 344 hand, 445–446 head and neck, 308–311 hepatic, 207–209 par tid gland, 322–323 pediatric, 395–396 pituitary, 287, 462, 465–466

531

pr state, 417–418 renal, 395–396, 396t, 421, 422f small intestine, 176–178 splenic, 234 testicular, 421–423 urinary bladder, 418–419 Tum r markers, 347, 347t Tum r necr sis act r antag nists, 487 Tum r–n de–metastasis (TNM) staging, 348, 349t breast cancer, 263t c l rectal carcin ma, 187, 188t gastric cancer, 168, 169t lung cancer, 87, 87t Tum r suppress r genes, 345 Tunica albuginea, 423 Turc t syndr me, 186 Turner sign, 218 TURP. See Transurethral resecti n the pr state Tw -thirds rule, 3 Tympanic membrane, examinati n , 299

Urethral injuries, 358, 428 Urge inc ntinence, 426 Urgent, de initi n , 58 Uric acid st nes, 414 Urinalysis, pre perative, 44t Urinary bladder laccidity , 424–425 veractivity , 424–425 trauma t , 358, 428 Urinary bladder carcin ma, 418–419 Urinary inc ntinence, 426 Urinary retenti n, acute, 412 Urinary tract in ecti n (UTI), 62–63 Urinary tract st nes, 414–415, 414f Urine utput, 5 Ur dynamic studies, 425 Ur l gic emergencies, 412–413 Ur l gic surgery, 412–429 cuts and caveats n, 410 study questi ns n, 494–495, 499 Ur l gic trauma, 427–429 UTI. See Urinary tract in ecti n

U

V

UC. See Ulcerative c litis Ulcer(s) c ntact, 308 diabetic t, 443 du denal, 163, 165–168, 218 gastric, 163–165 marginal, bariatric surgery and, 333 peptic, 62–63, 163–168 pressure, 443, 443t s litary rectal, 199 stress, 171–172 Ulcerative c litis (UC), 192–194 cancer risk in, 193 clinical presentati n , 192, 193, 193t evaluati n , 193–194 medical treatment , 194 surgical treatment , 194 Ulnar nerve, 471, 471f Ulnar nerve c mpressi n, 471 Ultras und abd minal, 61–62 breast, 257, 262 end rectal, 183, 187, 202 hepat biliary, 207 in trauma assessment, 353 Umbilical hernias, 38 lapar sc pic repair , 340–341, 340f Uncal herniati n, 452 Uncinate pr cess, 216 Underwater seal drainage system, 33 Undescended testes, 421 Unilateral advancement lap, 442 Unil cular abscess, 40 Unstable angina, 100 Upper es phageal sphincter (UES), 153, 154 Upper GI bleeding, 65–66 Ureteral injuries, 358, 428 Ureteral bstructi n kidney transplantati n and, 372 st nes and, 414–415 Ureteral transiti nal cell carcin ma, 419, 420f Ureter sc py, 415 Urethra, male, 423

Vaccines, cancer, 350 VACTERL ass ciati n, 381 Vagus nerve, 162 Valves H ust n, 181 Valvular heart disease, 47, 96–99 Varic se veins, 140–141, 141f Vasa recta, 173 Vascular dis rders arterial, 118–134 cuts and caveats n, 116–117 lymphatic, 142–143 study questi ns n, 144–149 ven us, 135–142 Vascular injuries abd minal, 358 ractures and disl cati ns ass ciated with, 474, 474t Vascularized c mp site all gra t transplants, 375, 449 Vascular mal rmati ns (VMALs), 443, 459–460 Vascular resistance pulm nary (PVR), 24–25 systemic (SVR), 24–25 Vascular tum rs, head and neck, 304–305 Vascul genic claudicati n, 118 Vas active medicati ns, 26 Vas dilat rs, 26 Vas genic edema, 453 Vas press rs, 26 VATS. See Vide -assisted th racic surgery Vein gra ts, 433 Ven us an malies, devel pmental, 460 Ven us disease, 135–142. See also specific types acute, 135–140 chr nic, 140–141 Ven us gangrene, 138 Ven us thr mb emb lism (VTE) p st perative, 51 p st perative preventi n , 45 pre perative pr phylaxis r, 45–46, 46t as surgical risk act r, 45 Ventilati n, 22

532

Index

Ventilat r supp rt, 22–23 m de , 22 in patient with lung disease, 52 rate , 23 respirat ry alkal sis in, 12 r utine starting p int in, 23 weaning and extubati n in, 23, 52 Ventral hernias, 39 lapar sc pic repair , 340–341, 340f Ventricular septal de ects, 104–106, 105f Verruc us carcin ma, laryngeal, 317 Vertebr basilar insu iciency, 126 Vertical mattress suture, 31, 32f Vestibular schwann mas, 465 VHL. See v n Hippel–Lindau disease Vide -assisted th racic surgery (VATS), 82–83 Vill us aden mas, 176, 184 VIP ma, 287, 288 Viral in ecti ns, splenic, 233 Virch w triad, 135 Visceral c mpartment anat my , 78, 79f lesi ns , 90 Visceral pr tein measurement, 18 Visual acuity, 299 Visual ield test, 299 Vitamin(s) abs rpti n , 175 de iciencies, in bariatric surgery patients, 334 Vitamin A de iciency, in bariatric surgery patients, 334 Vitamin B12 abs rpti n , 175 de iciency, in bariatric surgery patients, 334 Vitamin B1 de iciency, in bariatric surgery patients, 334 Vitamin C, abs rpti n , 175 Vitamin D de iciency, in bariatric surgery patients, 334 Vitamin supplementati n, r bariatric surgery patients, 328, 334 VMALs. See Vascular mal rmati ns V cal c rds, thyr id n dules and, 273

V V V V V

cal n dules, 307 cal p lyps, 308 ice, assessment , 299 ice rest rati n, 311 iding dys uncti n, 424–427 de initi ns in, 424 diagn sis , 424–425 patterns , 425 in speci ic diseases, 425–426 V lume l ad, 96 V lvulus, 62–63, 197–198, 384–386 v n Hippel–Lindau disease (VHL), 421 v n Recklinghausen neur ibr mat sis, 306 v n Willebrand disease, 14 v n Willebrand act r, 13, 14 VTE. See Ven us thr mb emb lism

W “5 W’s,” 39 WAGR syndr me, 395 Walk, in 5 W’s assessment, 39 War arin, m nit ring therapy with, 13 Warthin tum rs, 322–323 Warts, an -genital, 202 Water, b dy, 3–10 adjustments , 5 b dy weight and, 5 c mpartments , 3, 4f de icits and excesses , 6 in 5 W’s assessment, 39 gastr intestinal istula and, 41–42 gastr intestinal l sses , 5, 5t maintenance , 3–6 calculati ns r am unts in, 3–5 evaluating rates , 5 excreti n and, 3–5 insensible l ss and, 5 n rmal c mp siti n, 3 p st perative status, 39–40 in surgical patients with liver disease, 57 in surgical patients with renal disease, 54 tw -thirds rule , 3 Water, digesti n and abs rpti n , 175, 182 Water-hammer pulse, 93 Water-s luble c ntrast enema, 182–183 WDHA syndr me, 287

Weak acids, 11 Weaning, r m ventilat r, 23, 52 Weber test, 299 Weight l ss bariatric surgery and, 329 massive, b dy c nt uring a ter, 448–449 Whipple pr cedure, 227–228, 227f White pulp, spleen, 230 Wilms tum r, 395–396, 396t Wind, in 5 W’s assessment, 39 Wishart type neur ibr mat sis, 307 W nder drugs, 39 W rk breathing, 21 W und(s), 30–32 classi icati n , 30 clean, 30 clean c ntaminated, 30 c ntaminated, 30 dirty, 30 rec nstructive surgery r, 430–436 W und cl sure, 31–32 interrupted, 31 suture characteristics in, 32 W und healing, 30–31, 442–443 delayed primary intenti n in, 31 phases , 30, 442 primary intenti n in, 30, 31f sec ndary intenti n in, 31, 31f W und in ecti ns, 39 W und repair, 30–31, 31f W und vacuum-assisted cl sure, 430–431

X Xen gra t, 363 X-rays, abd minal, 61, 61f

Y Y lk sac tum rs, 421

Z Zenker diverticulum, 154–155 Z llinger-Ellis n syndr me, 165, 286–287, 289 Z na asciculata, 280 Z na gl merul sa, 280 Z na reticularis, 280 Z-plasty, 435, 435f