Acute Care Surgery: Principles and Practice

Acute Care Surgery Acute Care Surgery Principles and Practice Editor-in-Chief L.D. Britt, MD, MPH Brickhouse Profes...

Author: L.D. Britt | Donald D. Trunkey | David V. Feliciano

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Acute Care Surgery

Acute Care Surgery Principles and Practice

Editor-in-Chief

L.D. Britt, MD, MPH Brickhouse Professor of Surgery and Chairman Department of Surgery Eastern Virginia Medical School Norfolk, Virginia

Editors

Donald D. Trunkey, MD Professor Department of Surgery Oregon Health Sciences University Portland, Oregon

David V. Feliciano, MD Professor of Surgery, Emory University School of Medicine Chief of Surgery, Grady Memorial Hospital Atlanta, Georgia

Editor-in-Chief: L.D. Britt, MD, MPH Brickhouse Professor of Surgery and Chairman Department of Surgery Eastern Virginia Medical School Norfolk, VA, USA

Editors: Donald D. Trunkey, MD Professor Department of Surgery Oregon Health Sciences University Portland, OR, USA

David V. Feliciano, MD Professor of Surgery Emory University School of Medicine Chief of Surgery Grady Memorial Hospital Atlanta, GA, USA

Library of Congress Control Number: 2006925630 ISBN: 10: 0-387-34470-5 ISBN: 13: 978-0-387-34470-6

e-ISBN-10: 0-387-69012-3 e-ISBN-13: 978-0-387-69012-4

Printed on acid-free paper. © 2007 Springer Science+Business Media, LLC All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC., 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein. 9 8 7 6 5 4 3 2 1 springer.com

Preface

The genesis of this project is a direct result of the fact that there is no substantive textbook that addresses the full-spectrum of surgical emergencies. Even in a field in which there is a plethora of excellent textbooks on a variety of surgical topics (including trauma), there is no one reference book with a dedicated emphasis on both traumatic and nontraumatic conditions potentially necessitating surgical intervention in the acute setting. This project became even more unique when its stepwise development paralleled the evolution of a new specialty–acute care surgery. This was far from a serendipitous link. On the contrary, my editorial colleagues and I, along with many of the contributors, have recently been part of a major effort to build the foundation for this new specialty. As with any proposed new specialty, there have been a few rough interfaces with some of the other surgical specialties regarding the scope of practice of the acute care surgeon. Fortunately, the key to this conflict resolution will revolve around what is best for the patient. However, irrespective of these dynamics, there is a worsening crisis in acute care in this nation. The anatomy of the textbook has five parts: Each chapter in the first two parts is preceded by a case scenario and multiple choice questions. At the end of each chapter in Part I (General Principles) and Part II (Principles and Practice of Acute Care Surgery: Organ-Based Approach), there is a critique for the case scenario and the associated answer. This format is designed to have the reader focus on a specific clinical management or system-based problem prior to reading the chapter. An entire section (Part III) is dedicated to administration, ethics, and law as it relates to issues and situations in the acute surgical setting. Another important feature of the book is the emphasis on system development (Part IV). Similar to the current trauma systems throughout the nation, there should be a more comprehensive network to facilitate optimal management of all surgical emergencies. These issues are addressed. Also, in the same section, there is a proposed training curriculum for Acute Care Surgery along with a model of an existing emergency surgical service that could serve as a foundation for the development of a more broad-based specialty. How our international colleagues are addressing emergency surgical needs is highlighted in the final section (Part V). Experts from three different continents provide focused insight into the intricacies of their respective systems with respect to acute care surgery. In summary, this inaugural edition of this textbook is designed to be a comprehensive and definitive reference of the full spectrum of Acute Care Surgery. With contributions from the top experts throughout the world, I do feel this goal has been accomplished. L.D. Britt, MD, MPH Editor-in-Chief

v

A Tribute

This textbook is dedicated to one of the true giants in American surgery. He was a contributor to and a major inspiration for this project. If Dr. Claude Organ were to be described in one statement, it would be the following: “He was a monument to excellence.” With talents that transcended medicine, he was often highlighted as a legitimate renaissance man. Whatever he engaged in, Dr. Organ made better. It could be argued that the popular label “Midas touch” is more applicable to the life and times of Dr. Organ, for he was highly successful in all the arenas he entered. He consistently downplayed the litany of awards and accolades he accumulated

Claude H. Organ, Jr., MD, MS (Surg), FACS, FRCSSA, FRACS, FRCS, FRCSEd Professor Emeritus, Department of Surgery University of California San Francisco-East Bay Oakland, California (Deceased)

vii

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A Tribute

throughout his illustrious career, including being elected Chairman of the American Board of Surgery, President of the American College of Surgeons, and Editorin-Chief of the Archives of Surgery. He was the recipient of the highest award given by the American College of Surgeons: The Distinguished Service Award. Dr. Organ, the author of more than 250 scientific journal articles and book chapters, was an invited lecturer and visiting professor at many of the great institutions throughout the world. This tribute provides only a glimpse of the impact that Dr. Organ had over his 78 year lifespan. Merely highlighting his professional career inadequately covers the full spectrum of his legacy, for the “big picture” view of Dr. Organ also includes that man who portrayed the consummate husband, father, grandfather, friend, colleague, and mentor. Perhaps his crowning achievement is his tremendously accomplished family. Even with this recognition, Dr. Organ would be quick to give the credit for the success of his seven children to his equally talented wife, Elizabeth (Betty). He stated on numerous occasions that his wife was the chief architect of the social and professional development of their children. Each child has become a prominent professional in various fields, including medicine, banking, art, and education. An argument could be made that this is one of the most successful American families – essentially, a guarantee that the Organ legacy will continue. I am one of the many who was mentored by Dr. Organ and who profited from his endless wisdom and guidance. In fact, his last advice to me just prior to his untimely death was a firm charge to me to find a way to accelerate the completion and production of this textbook so that it would match the timing of the unveiling of the new specialty – Acute Care Surgery. With Dr. Organ being such a driving force in the first phase of the development of this project, my editorial colleagues and I can think of no one more deserving of this tribute. L.D. Britt, MD, MPH Editor-in-Chief

Contents

Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . A Tribute . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

v vii xiii

Part I General Principles 1 Initial Assessment and Early Resuscitation . . . . . . . . . . . . . . . . . . . . . . Louis H. Alarcon and Andrew B. Peitzman

3

2 The Operating Theater for Acute Care Surgery . . . . . . . . . . . . . . . . . . Kenneth L. Mattox

24

3

Anesthesia and Acute Care Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . Omid Moayed and Richard P. Dutton

30

4 Fundamental Operative Approaches in Acute Care Surgery . . . . . . . . David J. Ciesla and Ernest E. Moore

43

5 The Perioperative Management of the Acute Care Surgical Patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Craig M. Coopersmith and Timothy G. Buchman

67

6 The Hemodynamically Labile Patient: Cardiovascular Adjuncts and Assist Devices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Edward E. Cornwell III and Preeti R. John

84

7 Principles and Practice of Nutritional Support for Surgical Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Maheswari Senthil, Bobby Rupani, Jondavid H. Jabush, and Edwin A. Deitch

91

8 The Intensive Care Unit: The Next-Generation Operating Room . . . . Philip S. Barie, Soumitra R. Eachempati, and Jian Shou

106

9

Burns . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Basil A. Pruitt, Jr., and Richard L. Gamelli

125

10

Electrical and Lightning Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Raphael C. Lee

161

11

Soft Tissue Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anthony A. Meyer, Jeffrey E. Abrams, Thomas L. Bosshardt, and Claude H. Organ, Jr.

166

ix

Contents

x

12 The Open Abdomen: Management from Initial Laparotomy to Definitive Closure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Fred A. Luchette, Stathis J. Poulakidas, and Thomas J. Esposito

176

13

Acute Care Surgery and the Elderly . . . . . . . . . . . . . . . . . . . . . . . . . . . Patrick K. Kim, Donald R. Kauder, and C. William Schwab

187

14

Acute Care Surgery in the Rural Setting . . . . . . . . . . . . . . . . . . . . . . . . Dana Christian Lynge, Nicholas W. Morris, and John G. Hunter

194

15

Prehospital Care in the Acute Setting . . . . . . . . . . . . . . . . . . . . . . . . . . Norman E. McSwain, Jr.

202

16

Disaster and Mass Casualty Management . . . . . . . . . . . . . . . . . . . . . . . Eric R. Frykberg

229

17

Principles of Injury Prevention and Control . . . . . . . . . . . . . . . . . . . . . M. Margaret Knudson and Larisa S. Speetzen

249

18 Education: Surgical Simulation in Acute Care Surgery . . . . . . . . . . . . . Lenworth M. Jacobs and Karyl J. Burns

263

Part II Organ-Based Approach 19

Pharynx and Larynx . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Ernest M. Myers

277

20

Head and Neck: Pediatrics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Reza Rahbar and Gerald B. Healy

305

21

Esophagus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . George C. Velmahos, Nahid Hamoui, Peter F. Crookes, and Demetrios Demetriades

314

22

Central Nervous System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Peter B. Letarte

332

23

Chest Wall . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . John C. Mayberry and Donald D. Trunkey

348

24

Lungs and Pleura . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Riyad Karmy-Jones and J. Wayne Meredith

362

25

Heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Matthew S. Slater

389

26

Thoracic Aorta . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Peter I. Ellman and Irving L. Kron

400

27

Diaphragm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Michel B. Aboutanos, Therèse M. Duane, Ajai K. Malhotra, and Rao R. Ivatury

420

28

Abdominal Wall . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Jeffrey A. Claridge and Martin A. Croce

435

29

Foregut . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Philip E. Donahue

450

30

Small Intestine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Juliet Lee, Todd Ponsky, and Jeffrey L. Ponsky

471

31

Liver and Biliary Tract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Spiros P. Hiotis and Hersch L. Pachter

479

Contents

xi

32

Pancreas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Juan A. Asensio, Patrizio Petrone, and L.D. Britt

497

33

Spleen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . L.D. Britt

513

34

Intraabdominal Vasculature . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . George H. Meier III and Hosam F. El Sayed

524

35

Colon and Rectum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Herand Abcarian

549

36

Urogenital Tract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Nejd F. Alsikafi, Sean P. Elliott, Maurice M. Garcia, and Jack W. McAninch

561

37

Pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Craig M. Rodner and Bruce D. Browner

589

38

Lower Extremities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Tina A. Maxian and Michael J. Bosse

602

39

Hand and Upper Extremities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . David T. Netscher and Idris Gharbaoui

615

40

Peripheral Vasculature . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . David V. Feliciano

656

Part III Administration, Ethics, and Law 41 Understanding the Latest Changes in EMTALA: . . . . . . . . . . . . . . . . . Our Country’s Emergency Care Safety Net Thomas R. Russell

677

42

Informed Surgical Consent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Linda S. Laibstain and Robert C. Nusbaum

683

43

Advance Directives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . David G. Jacobs

689

44 The Nonviable Patient and Organ Procurement . . . . . . . . . . . . . . . . . . Frederic J. Cole, Jr., Jay N. Collins, and Leonard J. Weireter, Jr.

701

45

715

Ethical Dilemmas and the Law . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Ira J. Kodner, Daniel M. Freeman, Robb R. Whinney, and Douglas J.E. Schuerer

Part IV System and Curriculum Development 46 Development of a Regional System for Surgical Emergencies (RSSE) A.Brent Eastman, David B. Hoyt, and J. Wayne Meredith

743

47

Acute Care Surgery: A Proposed Curriculum . . . . . . . . . . . . . . . . . . . . L.D. Britt and Michael F. Rotondo

752

48 Emergency General Surgery: The Vanderbilt Model . . . . . . . . . . . . . . . José J. Diaz, Jr., Oscar D. Guillamondegui, and John A. Morris, Jr.

754

Part V The International Communities 49

Acute Care Surgery: United Kingdom . . . . . . . . . . . . . . . . . . . . . . . . . . 767 Bernard F. Ribeiro, Simon Paterson-Brown, Murat Akyol, Michael Walsh, Andrew Sim, and Christopher Aylwin

Contents

xii

50

Acute Care Surgery: Australia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Thomas Kossmann and Ilan S. Freedman

786

51

Acute Care Surgery: Japan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Kyoichi Takaori and Nobuhiko Tanigawa

796

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

809

Contributors

Herand Abcarian, MD Department of Surgery, University of Illinois at Chicago, University of Illinois at Chicago Medial Center, Chicago, IL, USA Michel B. Aboutanos, MD, MPH Division of Trauma, Critical Care, and Emergency Surgery, Virginia Commonwealth University Medical Center, Medical College of Virginia Hospitals and Physicians, Richmond, VA, USA Jeffrey E. Abrams, MD Department of Surgery, University of North Carolina, Chapel Hill, NC, USA Murat Akyol, MD University Department of Surgery and The Transplant Unit, The Royal Infirmary of Edinburgh, Edinburgh, Scotland, UK Louis H. Alarcon, MD Departments of Critical Care Medicine and Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA Nejd F. Alsikafi, MD Department of Urology, University of Chicago, Mount Sinai Hospital, Chicago, IL, USA Juan A. Asensio, MD Department of Surgery/Division of Trauma, University of Medicine and Dentistry of New Jersey at Newark, Newark, NJ, USA Christopher Aylwin, BSc, MBBS, MRCS Department of General Surgery, Trauma Service, Royal London Hospital, London, England, UK Philip S. Barie, MD, MBA Departments of Surgery and Public Health, Weill Medical College of Cornell University, New York, NY, USA Michael J. Bosse, MD Department of Orthopaedic Surgery, Carolinas Medical Center, Charlotte, NC, USA

xiii

xiv

Contributors

Thomas L. Bosshardt, MD Department of Surgery, Marian Medical Center, Santa Maria, CA, USA L.D. Britt, MD, MPH Department of Surgery, Eastern Virginia Medical School, Norfolk, VA, USA Bruce D. Browner, MD Department of Orthopaedic Surgery, University of Connecticut Health Sciences Center, Farmington CT, USA; Department of Orthopaedics, Hartford Hospital, Hartford, CT, USA Timothy G. Buchman, PhD, MD Departments of Surgery, Anesthesiology, and Medicine, Washington University School of Medicine, St. Louis, MO, USA Karyl J. Burns, RN, PhD Department of Traumatology, Hartford Hospital/University of Connecticut, Hartford, CT, USA David J. Ciesla, MD Departments of Surgery and Trauma, University of Colorado Health Sciences Center, Denver Health Medical Center, Denver, CO, USA Jeffrey A. Claridge, MD Department of Surgery, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, OH, USA Frederic J. Cole, Jr., MD Department of Surgery, Eastern Virginia Medical School, Sentara Norfolk General Hospital, Norfolk, VA, USA Jay N. Collins, MD Department of Surgery, Eastern Virginia Medical School, Sentara Norfolk General Hospital, Norfolk, VA, USA Craig M. Coopersmith, MD Departments of Surgery and Anesthesiology, Washington University School of Medicine, St. Louis, MO, USA Edward E. Cornwell III, MD Department of Surgery, Johns Hopkins School of Medicine, Johns Hopkins Hospital, Baltimore, MD, USA Martin A. Croce, MD Department of Surgery, Regional Medical Center at Memphis, University of Tennessee, Presley Memorial Trauma Center, Memphis, TN, USA Peter F. Crookes, MD Department of Surgery, University of Southern California, Los Angeles, CA, USA Edwin A. Deitch, MD Department of Surgery, University of Medicine and Dentistry of New Jersey—New Jersey Medical School, University of Medicine and Dentistry of New Jersey— University Hospital, Newark, NJ, USA

Contributors

xv

Demetrios Demetriades, MD, PhD Department of Surgery, Division of Trauma and Surgical Critical Care, University of Southern California, Los Angeles, CA, USA José J. Diaz, Jr., MD, CNS Department of Surgery, Division of Trauma and Surgical Critical Care, Vanderbilt University Medical Center, Vanderbilt University Hospital, Nashville, TN, USA Philip E. Donahue, MD Department of Surgery, University of Illinois at Chicago, John H. Stroger Hospital of Cook County, Chicago, IL, USA Therèse M. Duane, MD Division of Trauma, Critical Care, and Emergency Surgery, Virginia Commonwealth University Medical Center, Medical College of Virginia Hospitals and Physicians, Richmond, VA, USA Richard P. Dutton, MD, MBA Division of Trauma Anesthesiology, R. Adams Cowley Shock Trauma Center, University of Maryland Medical System, Baltimore, MD, USA Soumitra R. Eachempati, MD Department of Surgery, Weill Medical College of Cornell University/New York Presbyterian Hospital, New York, NY, USA A. Brent Eastman, MD Department of Trauma, Scripps Memorial Hospital La Jolla, La Jolla, CA, USA Sean P. Elliott, MD Department of Urology, University of California San Francisco, San Francisco General Hospital, San Francisco, CA, USA Peter I. Ellman, MD Department of General Surgery, University of Virginia, University of Virginia Health Sciences Center, Charlottesville, VA, USA Hosam F. El Sayed, MD, PhD Department of Surgery, Division of Vascular Surgery, Eastern Virginia Medical School, Norfolk, VA, USA Thomas J. Esposito, MD, MPH Department of Surgery, Section of Trauma, Injury Analysis, and Prevention Programs, Loyola University Medical Center, Foster G. McGaw Hospital, Maywood, IL, USA David V. Feliciano, MD Department of Surgery, Emory University School of Medicine, Grady Memorial Hospital, Atlanta, GA, USA Ilan S. Freedman, MBBS Department of Orthopaedic Surgery, The Alfred Hospital, Melbourne, Victoria, Australia Daniel M. Freeman, AB, JD Einstein Institute for Science, Health, and the Courts, Chevy Chase, MD, USA

xvi

Contributors

Eric R. Frykberg, MD Department of Surgery, University of Florida College of Medicine, Shands Jacksonville Medical Center, Jacksonville, FL, USA Richard L. Gamelli, MD Department of Surgery, Loyola University Medical Center, Maywood, IL, USA Maurice M. Garcia, MD Department of Urology, University of California San Francisco, San Francisco, CA, USA Idris Gharbaoui, MD Department of Orthopaedics, University of Texas Health Science Center at Houston, Houston, TX, USA Oscar D. Guillamondegui, MD Department of Surgery, Division of Trauma and Surgical Critical Care, Vanderbilt University, Vanderbilt University Medical Center, Nashville, TN, USA Nahid Hamoui, MD Department of General Surgery, University of Southern California, Los Angeles, CA, USA Gerald B. Healy, MD Department of Otolaryngology, Harvard University, Children’s Hospital, Boston, MA, USA Spiros P. Hiotis, MD, PhD Department of Surgery, New York University School of Medicine, New York, NY, USA David B. Hoyt, MD Department of Surgery, University of California San Diego Medical Center, San Diego, CA, USA John G. Hunter, MD Department of Surgery, Oregon Health and Science University, Portland, OR, USA Rao R. Ivatury, MD, MS Department of Surgery, Virginia Commonwealth University, Virginia Commonwealth University Medical Center, Richmond, VA, USA Jondavid H. Jabush, MD Department of Surgery, University of Medicine and Dentistry of New Jersey—New Jersey Medical School, University of Medicine and Dentistry of New Jersey— University Hospital, Newark, NJ, USA David G. Jacobs, MD Department of Surgery, Carolinas Medical Center, Charlotte, NC, USA Lenworth M. Jacobs, MD, MPH Department of Traumatology, Hartford Hospital/University of Connecticut, Hartford, CT, USA

Contributors

xvii

Preeti R. John, MD, MPH Department of Surgery, Johns Hopkins University, The Johns Hopkins Hospital, Baltimore, MD, USA Riyad Karmy-Jones, MD Department of Cardiothoracic Surgery, Harborview Medical Center, Seattle, WA, USA Donald R. Kauder, MD Department of Surgery, Division of Traumatology and Surgical Critical Care, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA, USA Patrick K. Kim, MD Department of Surgery, Division of Traumatology and Surgical Critical Care, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA, USA M. Margaret Knudson, MD Department of Surgery, University of California San Francisco, San Francisco General Hospital, San Francisco, CA, USA Ira J. Kodner, MD Department of Colon and Rectal Surgery, Washington University in St. Louis, Barnes-Jewish Hospital, St. Louis, MO, USA Thomas Kossmann, MD Department of Trauma Surgery, The Alfred Hospital, Melbourne, Victoria, Australia Irving L. Kron, MD Departments of Surgery and Thoracic and Cardiovascular Surgery, University of Virginia, University of Virginia Health Sciences Center, Charlottesville, VA, USA Linda S. Laibstain, JD Williams Mullen Hofheimer Nusbaum, Norfolk, VA, USA Juliet Lee, MD Department of Surgery, George Washington University, Washington, DC, USA Raphael C. Lee, MD, ScD, DSc (Hon) Departments of Surgery (Plastic), Medicine (Dermatology), Organismal Biology (Biomechanics), and Molecular Medicine, University of Chicago, Chicago, IL, USA Peter B. Letarte, MD Department of Neurosurgery, Hines Veterans Hospital, La Grange Park, IL, USA Fred A. Luchette, MD Department of Surgery, Division of Trauma, Surgical Critical Care, and Burns, Loyola University Medical Center, Foster G. McGaw Hospital, Maywood, IL, USA Dana Christian Lynge, MD, CM Department of Surgery, University of Washington, Seattle Veterans Affairs Medical Center, Seattle, WA, USA

xviii

Contributors

Ajai K. Malhotra, MD Division of Trauma, Critical Care, and Emergency Surgery, Virginia Commonwealth University Medical Center, Medical College of Virginia Hospitals and Physicians, Richmond, VA, USA Kenneth L. Mattox, MD Department of Surgery, Baylor College of Medicine, Ben Taub General Hospital, Houston, TX, USA Tina A. Maxian, MD, PhD Department of Orthopaedic Surgery, State University of New York Upstate Medical University, Syracuse, NY, USA John C. Mayberry, MD Department of Surgery, Oregon Health and Science University, Portland, OR, USA Jack W. McAninch, MD Department of Urology, University of California San Francisco, San Francisco, CA, USA Norman E. McSwain, Jr., MD Department of Surgery, Tulane University School of Medicine, Charity Hospital Trauma Center, New Orleans, LA George H. Meier III, MD Department of Vascular Surgery, Eastern Virginia Medical School, Norfolk, VA, USA J. Wayne Meredith, MD Department of Surgery, Wake Forest University School of Medicine, WinstonSalem, NC, USA Anthony A. Meyer, MD, PhD Department of Surgery, University of North Carolina, Chapel Hill, NC, USA Omid Moayed, MD Division of Trauma Anesthesiology, R. Adams Cowley Shock Trauma Center, University of Maryland Medical System, Baltimore, MD, USA Ernest E. Moore, MD Departments of Surgery and Trauma, University of Colorado Health Sciences Center, Denver Health Medical Center, Denver, CO, USA John A. Morris, Jr., MD Section of Surgical Sciences, Division of Trauma, Vanderbilt University School of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA Nicholas W. Morris, MD Department of General Surgery, Powell Valley Health Care and Hospital, Powell, WY, USA Ernest M. Myers, MD Department of Surgery, Division of Otolaryngology, Head and Neck Surgery, Howard University Hospital, Washington, DC, USA

Contributors

xix

David T. Netscher, MD Department of Surgery, Division of Plastic Surgery, Baylor College of Medicine, Veterans Affairs Medical Center, Houston, TX, USA Robert C. Nusbaum, LLB, JD (Hon) Williams Mullen Hofheimer Nusbaum, Norfolk, VA, USA Claude H. Organ, Jr., MD, MS (Surg) Deceased, Department of Surgery, University of California San Francisco-East Bay, Oakland, CA, USA Hersh L. Pachter, MD Department of Surgery, New York University School of Medicine, New York, NY, USA Simon Paterson-Brown, MBBS, MPh Department of Surgery, The Royal Infirmary Edinburgh, Edinburgh, Scotland, UK Andrew B. Peitzman, MD Department of Surgery, University of Pittsburgh, Pittsburgh, PA, USA Patrizio Petrone, MD Department of Surgery, Division of Trauma Surgery and Surgical Critical Care, Los Angeles County and The University of Southern California Medical Center, Los Angeles, CA, USA Jeffrey L. Ponsky, MD Department of Surgery, University Hospitals and Case Western Reserve University, Cleveland, OH, USA Todd Ponsky, MD Department of Pediatric Surgery, Children’s National Medical Center, Washington, DC, USA Stathis J. Poulakidas, MD Department of Surgery, Loyola University Medical Center, Foster G. McGaw Hospital, Maywood, IL, USA Basil A. Pruitt, Jr., MD Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA Reza Rahbar, DMD, MD Department of Otolaryngology, Harvard Medical School, Boston Children’s Hospital, Boston, MA, USA Bernard F. Ribeiro, MB, BS Department of Surgery, Basildon University Hospital, Basildon, England, UK Craig M. Rodner, MD Department of Orthopaedic Surgery, University of Connecticut Health System, Farmington, CT, USA

Contributors

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Michael F. Rotondo, MD Department of Surgery, The Brody School of Medicine, East Carolina University, Greenville, NC, USA Bobby Rupani, MD Department of Surgery, University of Medicine and Dentistry of New Jersey— New Jersey Medical School, University of Medicine and Dentistry of New Jersey— University Hospital, Newark, NJ, USA Thomas R. Russell, MD American College of Surgeons, Chicago, IL, USA Douglas J.E. Schuerer, MD Department of Surgery, Washington University in St. Louis, St. Louis, MO, USA C. William Schwab, MD Department of Surgery, Division of Traumatology and Surgical Critical Care, University of Pennsylvania Medical Center, Philadelphia, PA, USA Maheswari Senthil, MD Department of Surgery, University of Medicine and Dentistry of New Jersey— New Jersey Medical School, University of Medicine and Dentistry of New Jersey— University Hospital, Newark, NJ, USA Jian Shou, MD Department of Surgery, Weill Medical College of Cornell University, New York, NY, USA Andrew Sim, MBBS, MS Department of Surgery and Remote and Rural Medicine, University of Highlands and Islands, Western Isles Hospital, Stornoway, Scotland, UK Matthew S. Slater, MD Department of Cardiothoracic Surgery, Oregon Health and Science University, Portland, OR, USA Larisa S. Speetzen, BA San Francisco Injury Center, University of California San Francisco, San Francisco, CA, USA Kyoichi Takaori, MD, PhD Department of General and Gastroenterological Surgery, Osaka Medical College, Takatsuki, Osaka, Japan Nobuhiko Tanigawa, MD, PhD Department of General and Gastroenterological Surgery, Osaka Medical College, Takatsuki, Osaka, Japan Donald D. Trunkey, MD Department of Surgery, Oregon Health and Sciences University, Portland, OR, USA George C. Velmahos, MD, PhD, MSEd Department of Surgery, Harvard Medical School/Massachusetts General Hospital, Boston, MA, USA

Contributors

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Michael Walsh, BSc, MS Department of Vascular and Trauma Surgery, The Royal London Hospital, London, England, UK Leonard J. Weireter, Jr., MD Department of Surgery, Eastern Virginia Medical School, Sentara Norfolk General Hospital, Norfolk, VA, USA Robb R. Whinney, DO Department of Surgery, Washington University in St. Louis, St. Louis, MO, USA

Part I General Principles

1 Initial Assessment and Early Resuscitation Louis H. Alarcon and Andrew B. Peitzman

Case Scenario During the initial assessment and early resuscitation phase, a multiple trauma patient (25-year-old man) is determined to be in hemorrhagic shock and has the following findings: • Multiple abrasions (head, torso, and extremities) • Dilated right pupil • Precordial bruises (chest x-ray demonstrates fully expanded bilateral lungs with an endotracheal tube above the carina; a widened mediastinum; obliterated pulmonary-aortic window and aortic knob) • Soft abdomen • Unstable pelvic fracture (pneumatic garment is now inflated) With a worsening hemodynamic status systolic blood pressure at 70 mm Hg and pulse, what is the top management priority for this patient (who required translaryngeal endotracheal intubation in the field because of his comatose state after an initial lucid period)? (A) (B) (C) (D) (E)

Immediate craniotomy Placement of an external pelvic fixator Repair of traumatic aortic rupture Further evaluation by computed tomography Abdominal ultrasonography

During the initial encounter with a patient, determination of severity of illness, identification of lifethreatening conditions, and resuscitation must occur. The Latin word resuscitare is the origin of the term resuscitation and means to reanimate or revive. Resuscitation implies restoring adequate tissue perfusion with oxygenated and nutrient-rich blood. As this chapter emphasizes, it is within the first minutes and hours of patient–physician interaction that subsequent organ dysfunction can be either aborted or allowed to progress. An essential tenet in the early management of the critically ill acute care surgery or trauma patient is immediate initiation of therapy to correct abnormal physiology, as evaluation and diagnosis proceed. The classic approach taught to medical students in the evaluation of a new patient is to complete a detailed history and physical examination and then formulate a differential diagnosis. However, when dealing with the severely ill or injured patient, this approach is not appropriate. Recognition and treatment of life-threatening conditions may be necessary before a definitive diagnosis can be determined. This is the approach adopted by the American College of Surgeons in the Advanced Trauma Life Support (ATLS) course.1 This organized and prioritized philosophy can be applied not only to trauma patients but also to any critically ill surgical or nonsurgical patient.

Triage The purpose of this chapter is to describe the assessment and resuscitation of both acute care surgery and trauma patients. Although differences exist in the initial evaluation and management of these categories of patients, certain principles can be applied to all critically ill and injured patients. Both the similarities and the differences are addressed. The specifics of the subsequent management of these patients are discussed in other chapters.

The word triage is derived from the French word meaning “to sort.” In the context of medicine, it implies the sorting and classification of injured or ill patients according to the severity of illness and prioritization of care according to available resources. Historically, war has provided the impetus to develop and refine triage systems. The lessons learned from the triage and care of casualties of war were eventually adapted to civilian medicine.

3

4

Unique Aspects of the Trauma and Acute Care Surgical Patient Trauma and acute care surgical patients present with acute anatomic and physiologic derangements that can be life or limb threatening. These problems often require immediate identification and treatment, making these patients very different from the patient who presents in a nonacute care setting. The early recognition that a patient is “sick” requires an astute clinician and can sometimes be made by quick examination of the patient. Aggressive and timely resuscitation efforts must be promptly initiated. It must be recognized that the patient has severe physiologic disturbances, and these need to be addressed before a definitive diagnosis can be entertained. This modus operandi, which places emphasis on physiologic stabilization rather than on exhaustive diagnostic maneuvers, is in contradistinction of the classic approach, which is to diagnose first and treat the definitive diagnosis. Thus, critical diagnostic and therapeutic decisions are made based on incomplete information. Another aspect that makes these patients unique is that the acute nature of their illness allows little or no preoperative evaluation. Complete evaluation and optimization of cardiovascular and pulmonary status is not feasible. In addition, these patients often present with full stomachs and/or substance intoxication, which can complicate airway and anesthetic management. The patients may also have injuries that complicate airway management, such as head, cervical spine, maxillofacial, or tracheobronchial trauma. Perhaps contrary to Occam’s razor,2 trauma patients often have multiple injuries. However, these are not random and often do present in predictable constellations based on mechanism of injury. Today, it is clear that the primary goal in the stabilization of trauma and critically ill surgical patients is correction of physiologic derangements. The sequential approach to patients condoned by the ATLS course can be applied to all cases of critically ill patients, acute care surgery, and trauma (Table 1.1).1 The goals of the primary survey are to identify immediate threats to life and to sta-

Table 1.1. Initial evaluation and management of critically ill or injured patients. Primary survey Airway Breathing Circulation Disability Expose the patient Resuscitation Secondary survey Definitive care Source: Data from American College of Surgeons Committee.1

L.H. Alarcon and A.B. Peitzman

bilize the patient. These may require laparotomy or thoracotomy, control of hemorrhage or gastrointestinal contamination, and transfer to the intensive care unit for further optimization of hemodynamics and tissue perfusion. Definitive correction of anatomic disturbances may often need to be postponed until physiologic stabilization has occurred (e.g., the damage-control laparotomy).3

Systematic Evaluation and Treatment The initial priorities in the management of all critically ill or injured patients are the same: verify the patency of the airway, ensure adequacy of breathing and ventilation, and restore circulation to vital organs. Airway, breathing, and circulation (commonly referred to as the ABCs) remain the basic tenets of life support. During the primary survey of the patient, life-threatening conditions are identified and treated immediately in this orderly fashion. This is an essential principle of the ATLS algorithm.1 In the first few seconds of the patient encounter, the gravity of the patient’s condition can be quickly ascertained; this brief assessment will dictate the tempo and aggressiveness of the resuscitation efforts. Patients should be categorized according to hemodynamic status: agonal, unstable, or hemodynamically normal. Terms such as hemodynamic stability should be avoided. While this phrase attempts to convey hemodynamic normalcy over time, it is more appropriate to accurately describe the patient’s condition and its variability over the period of observation. The patient who is unstable hemodynamically is hypotensive, tachycardic, or both. This represents physiologic decompensation and should be recognized as such and corrected expeditiously. The agonal patient is clearly profoundly ill with obvious clinical signs of shock. Such patients will not tolerate inadequate treatment. Time wasted on simply diagnostic procedures will increase the likelihood of a poor outcome for such patients. All maneuvers must be potentially therapeutic. For example, if the agonal patient may have a pneumothorax or hemothorax, this should be diagnosed by chest tube rather than chest radiograph, providing both diagnosis and therapy.

Airway and Breathing The airway is assessed first to ascertain patency. If the patient is able to speak clearly, the airway is not likely to be in immediate threat. However, repeated reassessment is essential. Continuous determination of arterial oxygen hemoglobin saturation via pulse oximetry serves as an adjunct to airway monitoring. However, changes in pulse oximetry temporally lag behind significant alterations in alveolar oxygenation and ventilation4,5 and cannot be solely relied on to make this detection in a timely fashion. Supplemental oxygen should be provided via a mask.

1. Initial Assessment and Early Resuscitation

The basic airway management strategy is to relieve the airway of obstruction. In unconscious patients, the most common cause of airway obstruction is the tongue, which moves posteriorly against the pharyngeal wall. A Glasgow Coma Scale (GCS) of 8 or less strongly suggests the need for a definitive airway immediately. Other causes of glottic obstruction are secretions, blood, vomitus, teeth, and or foreign materials. Edema of laryngeal structures may also lead to airway obstruction, as is seen with anaphylaxis, thermal injury, smoke inhalation, or epiglottitis. Facial, mandibular, or tracheolaryngeal fractures may also compromise the airway and complicate the ability to establish a definitive airway. Partial airway obstruction is evidenced by gurgling, stridor, hoarseness, or choking. The use of accessory respiratory muscles, paradoxical respiratory effort, or gasping signifies respiratory distress due to impending airway obstruction. These patients should have definitive airway control with the placement of an endotracheal tube. For many patients with airway obstruction, simple maneuvers may open the airway and improve the ability of the patient to ventilate. These maneuvers are designed to displace the mandible anteriorly, thus moving the tongue forward and alleviating the obstruction. The head tilt–chin thrust maneuvers may be used initially for nontrauma patients. The head tilt is performed by placing the palm of the hand on the patient’s forehead and the other hand behind the neck. The head is tilted posteriorly. The chin lift is done by hooking the second and third fingers beneath the chin, and pulling the chin upward, bringing the teeth to near occlusion. These maneuvers provide significant anterior displacement of the mandible and significantly open the glottis. To reemphasize, these maneuvers are contraindicated for patients who may have blunt cervical spine injury. The jaw thrust is another maneuver that may relieve airway obstruction, and, if performed correctly, it can be done while maintaining cervical spine immobilization. By grasping the angles of the mandible and lifting anteriorly, the mandible can be displaced anteriorly without movement of the spine. For unconscious patients, these maneuvers in combination with an oropharyngeal airway can facilitate adequate ventilation with a bagvalve-mask device until definitive airway can be established. Appropriate head positioning and a tight seal of the mask on the face are critical for the success of this procedure. Application of cricoid pressure, the Sellick maneuver, reduces but does not eliminate the risk of gastric insufflation, with subsequent vomiting and aspiration. Definitive airway management is best accomplished with tracheal intubation. The decision to intubate is made for patients who show signs of inadequate respiration despite the basic airway maneuvers described previously or for whom these interventions alone are unlikely to sustain

5 Table 1.2. Indications for endotracheal intubation. Absolute indications Airway obstruction or near obstruction (e.g., stridor) Apnea or near apnea Respiratory distress (dyspnea, tachypnea, cyanosis, hypoxemia, hypercarbia) Depressed level of consciousness (GCS ≤ 8) Urgent indications Hypotension or cardiovascular instability Penetrating neck injury with airway compromise Chest wall injury or disturbance that impairs ventilation despite tube thoracostomy Risk of aspiration because of bleeding in the oropharynx or airway and vomiting Relative indications Oromaxillofacial injuries Pulmonary contusion Need for diagnostic or therapeutic interventions in a patient who is at risk for deterioration Potential respiratory failure due to analgesic or sedative requirements

adequate respiration (Table 1.2). The most experienced operator should be designated to perform this task, as patients often will not tolerate prolonged attempts at intubation. Placement of an endotracheal tube is the best method to oxygenate and ventilate a patient, and, once secured, the tube reduces the risk of gross aspiration of gastric contents compared with bag-valve-mask ventilation.6 The decision to secure the airway with a tracheal tube can be made by assessing a number of parameters: airway patency, adequacy of oxygenation, adequacy of ventilation, ability to protect the airway (level of consciousness), and overall severity of the patient’s condition. The preferred route for definitive airway control for most patients is the orotracheal route. The nasal route should be avoided in patients with potential basilar skull or facial fractures. The surgical cricothyroidotomy is employed when the orotracheal route has failed or is deemed inappropriate because of significant midface or mandibular injuries or bleeding. Plans and preparations should always be made for this eventuality, because orotracheal intubation is not always successful. The key to successful tracheal intubation is preparation of the patient and of the necessary equipment. Failure to position the patient appropriately or to test and prepare all necessary equipment is a frequent cause of unsuccessful intubation. For nontrauma patients, the head should be placed in the “sniffing position,” which is facilitated by placing a small pillow or folded towels behind the head (not the back). This position is absolutely contraindicated for trauma patients, who must be presumed to have a cervical spine injury. The need for inline cervical stabilization for trauma patients increases the degree of difficulty in intubating these patients. The use of pharmacologic agents during intubation of patients remains an area of debate. The risks of sedative

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or paralyzing agents are loss of the airway, loss of spontaneous respiratory effort, aspiration of gastric contents, and hypotension or cardiovascular collapse. For these reasons, the ATLS course does not encourage the use of these drugs. However, in skilled hands, rapid-sequence induction with a combination of an inducing agent and a short-acting paralytic agent, is a highly effective method for securing the airway.7–9 The use of sedatives alone, without paralytic agents, may have a theoretical advantage, that is, the patient may continue to breathe spontaneously should the attempt at placing the airway prove unsuccessful. However, this theoretical advantage has not been proved. In fact, in acute care airway situations, complications were greater in number and severity for the nonparalyzed patients compared with standard rapidsequence induction with a paralytic agent and included aspiration, airway trauma, and death.10 Intubation is carried out after preoxygenation and is performed under direct vision during direct laryngoscopy. Successful placement of the endotracheal tube is confirmed by visualization of the tube between the vocal cords as it is placed, detection of exhaled CO2 using a disposable CO2 detector, and auscultation over the epigastrium and chest. A number of alternative techniques are available to establish a secure airway in patients who fail orotracheal intubation (such as nasotracheal intubation, laryngeal mask airway, combi-tube, bronchoscopic intubation, “blind” tactile intubation, the “lighted-stylet,” needle cricothyroidotomy and jet ventilation, and retrograde airway placement). However, these methods are heavily dependent on highly trained individuals performing difficult airway techniques and may not be possible with significant blood or secretions in the airway (e.g., bronchoscopic intubation), and the instrumentation may not be available in the emergent situation. Therefore, the surgical cricothyroidotomy is the preferred backup method for acute care surgical airway treatment.11 This is accomplished by stabilizing the thyroid cartilage with the nondominant hand while making a vertical or horizontal incision over the cricothyroid space, which is often easily palpable. If not palpable, a vertical incision in the approximate area is made and can be extended cephalad or caudally if needed. Palpation confirms the location of the cricothyroid membrane, and a transverse incision is made in this membrane. The back end of the scalpel or a hemostat clamp can be used to dilate the cricothyroidotomy, and an appropriately sized standard endotracheal tube (or tracheostomy tube if available) can be inserted and secured in place. Emergent tracheostomy is not favored because of the greater difficulty associated with this procedure when performed emergently outside of the operating room, requiring greater technical skills and therefore more prone to failure than cricothyroidotomy. However, tracheostomy may be necessary for patients

L.H. Alarcon and A.B. Peitzman Table 1.3. The “deadly dozen” lethal and potentially lethal thoracic and airway injuries in trauma patients that should be detected and treated in the primary and secondary surveys. “Lethal six” Airway obstruction Tension pneumothorax Cardiac tamponade Open pneumothorax Massive hemothorax Flail chest “Hidden six” Thoracic aorta disruption Tracheobronchial injury Blunt cardiac injury Diaphragmatic injury Esophageal injury Pulmonary contusion Source: Data from American College of Surgeons Committee.1

with tracheolaryngeal trauma, as this injury may preclude safe cricothyroidotomy. In the primary survey, a number of life-threatening conditions should be sought and corrected immediately upon detection (Table 1.3).1 Of these, tension pneumothorax, flail chest, massive hemothorax, and open pneumothorax are identified on physical examination, without the need or delay to obtain chest radiography, and should be treated immediately. The initial relief of a tension pneumothorax can be accomplished rapidly by inserting a 14- or 16-gauge needle into the second intercostal space in the midclavicular line. Insertion of a thoracostomy tube into the fourth or fifth intercostal space should then follow. A flail chest results from the fracture of three or more ribs in at least two places. This results in a segment of the chest wall that moves paradoxically with respirations. More important from a physiologic standpoint is the underlying pulmonary contusion,12–15 which can lead to significant hypoxemic respiratory failure. The pulmonary contusion may require intubation and mechanical ventilation if severe or if the patient has labored respirations or respiratory compromise. Patient mortality more than doubles when pulmonary contusion and flail chest are combined compared with either injury alone.13 However, more than half of these deaths are directly attributed to central nervous system injuries, with another third caused by massive hemorrhage, demonstrating that these patients often have significant associated injuries. For patients with major chest wall injuries, adequate analgesia can often best be accomplished with the placement of a thoracic epidural catheter for the continuous infusion of opiates and/or regional anesthetics.16–20 Thoracic epidural anesthesia has been shown to be superior to intravenous administration of opioids via patientcontrolled analgesia devices.21 Pain control is critical in


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the management of chest wall injuries. With inadequate pain control, hypoventilation and splinting may lead to atelectasis or pneumonia and worsen the alveolar hypoventilation and intrapulmonary shunt, resulting in hypoxia and hypercarbia. The use of continuous epidural analgesia is associated with significant improvement in vital capacity and maximum inspiratory pressure in these patients.18

Circulation Assessment of circulation is done by palpation of pulses and checking skin color, temperature, capillary refill, and mentation. As a general guide, the rate and quality of the pulses can provide important information regarding the adequacy of peripheral circulation and volume status. A strong pulse is associated with adequate cardiac output, whereas a weak, thready pulse often indicates hypovolemia and inadequate cardiac output. Arterial blood pressure is measured. However, a significant drop in blood pressure is a late finding in hemorrhagic shock and may require a blood loss of >30% of total blood volume to manifest (Table 1.4). Thus, a patient with a normal blood pressure measurement may be hypovolemic with ongoing hypoperfusion. On the other hand, the hypotensive patient has decompensated physiologically. In trauma patients, a single systolic blood pressure less than 90 mm Hg has an associated mortality rate of 25%. Narrowing of the pulse pressure and mild tachycardia may be the first signs of hypovolemia and may require blood loss of 15% to 30% of total blood volume to become apparent. Normal mentation implies adequate cerebral perfusion, while diminished level of consciousness in the presence of tachycardia and/or hypotension may be associated with shock or hypoxia, irrespective of central nervous system injury. In patients with significant head injuries, secondary brain injury occurs with hypoxia and hypotension, and these two abnormalities need to be

aggressively corrected. Morbidity and mortality rates are doubled for patients with traumatic brain injury who develop hypotension and nearly triple if the combination of hypotension and hypoxia occurs.22 Intravenous access should be established immediately in all patients in shock. This is most efficiently accomplished by the insertion of two large-bore (14 or 16 gauge) peripheral lines in the antecubital fossae. Occasionally, percutaneous central venous access or venous cut-downs at the saphenous vein at the ankle or groin will be necessary, although these procedures are more time consuming and require technical skill and therefore are not preferred when peripheral veins are accessible. The choice of intravenous catheter will determine the rapidity with which fluids or blood products can be administered to the patient. As determined by the law of Poiseuille, flow of a fluid through a catheter and intravenous tubing is proportional to the pressure gradient across the catheter, the fourth power of the catheter radius, and inversely proportional to the length of the catheter and the viscosity of the fluid. For this reason, wide catheters and tubing with short lengths will have the advantage of providing the best intravenous access and permit the most rapid delivery of fluids.23 If the trauma patient has signs of hypovolemia or shock, hemorrhage must be immediately identified and controlled. The possible sites of blood loss in the trauma patient include thorax, abdomen, pelvis, retroperitoneum, external hemorrhage, and long bone fractures. Physical examination, plain radiography, focused abdominal sonography for trauma (FAST), and diagnostic peritoneal lavage are the mainstay diagnostic maneuvers. Empiric placement of thoracostomy tubes is often the most efficient diagnostic and therapeutic maneuver for hypotensive patients with thoracic injuries. If this search for bleeding is unrevealing, other causes of shock to consider are tension pneumothorax, cardiac tamponade, high spinal cord injury (neurogenic shock), and severe blunt myocardial injury (rare).

Table 1.4. Estimated fluid and blood requirements for a 70-kg male patient with varying degrees of blood loss, based on initial presentation. Blood loss (mL) Blood loss (% blood volume) Pulse rate Blood pressure Pulse pressure Respiratory rate Urine output (mL/hr) Mental status Fluid replacement

Class I

Class II

Class III

Class IV

Up to 750 Up to 15% 30 Slightly anxious Crystalloid

750–1,500 15%–30% >100 Normal Decreased 20–30 20–30 Mildly anxious Crystalloid

1,500–2,000 30%–40% >120 Decreased Decreased 30–40 5–15 Anxious and confused Crystalloid and blood

>2,000 >40% >140 Decreased Decreased >35 Negligible Confused, lethargic Crystalloid and blood

Source: Reproduced with permission from American College of Surgeons’ Committee on Trauma, Advanced Trauma Life Support® for Doctors (ATLS®) Student Manual, 7th ed. Chicago: American College of Surgeons, 2004.

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Fluid Resuscitation Restoration of normal circulation implies prevention or reversal of shock. Shock is defined as the inadequate delivery of oxygen and other metabolic substrates necessary for normal function and survival of cells and tissues. It is important to realize that significant cellular hypoperfusion and death can occur despite normal arterial blood pressure. Equating shock with hypotension and cardiovascular collapse is a gross oversimplification that may result in undue patient morbidity. The optimal type, amount, and timing of fluid administration during the resuscitation of injured patients in hemorrhagic hypovolemic shock remain a subject of intense investigation and debate. Understand that the primary goal in management of active hemorrhage, whether trauma or nontrauma, is to stop the bleeding. With truncal hemorrhage that results in hypotension, these patients need rapid control of bleeding in the operating room: operating room resuscitation. For patients with hemorrhagic shock in the prehospital setting, aggressive volume infusion in an attempt to normalize blood pressure may be harmful. Until surgical control of hemorrhage has been achieved, aggressive infusion of fluids may actually disrupt hemostatic clots and cause hemodilution and vasodilation, and it has been shown to worsen outcomes in animal models of hemorrhagic shock.24–30 In a prospective randomized trial of patients with penetrating torso trauma, patients received either delayed fluid resuscitation upon arrival to the operating room or standard resuscitation by the paramedics.Although a number of technical limitations of this study exist, the trial demonstrated that delayed fluid administration was associated with lower patient mortality.31 However, a review of the diverse literature on this topic was unable to demonstrate a survival advantage or disadvantage to early or larger volume of intravenous fluid resuscitation in uncontrolled hemorrhage.32 The literature on this topic is difficult to analyze as a whole because of the inconsistent methodologies employed in the different studies. Overly aggressive resuscitation may also have other deleterious effects. A study of supranormal resuscitation in severely injured trauma patients with >2 L blood loss targeted resuscitation to a supraphysiologic cardiac index (≥4.52 L/min/m2) and oxygen delivery (≥670 mL/min/ m2).33 In this small study, the ability to attain these supranormal hemodynamic values was associated with improved survival and decreased morbidity rates. However, this effect was more a reflection of the patients’ abilities to achieve these parameters in this subset rather than benefits of therapy. Subsequent studies of supranormal resuscitation have not shown benefit.34 In fact may demonstrate a detrimental effect of the supranormal resuscitation strategy. For trauma patients, resuscitation

L.H. Alarcon and A.B. Peitzman

using oxygen delivery ≥500 mL/min/m2 was indistinguishable from oxygen delivery at ≥600 mL/min/m2. Less volume loading was required to attain and maintain oxygen delivery at ≥500 mL/min/m2 than at 600 mL/ min/m2 using a computerized algorithm to standardize resuscitation during the first 24 hours.34 Supranormal resuscitation, compared with standard resuscitation, is associated with more lactated Ringer’s infusion, decreased intestinal perfusion, and increased incidence of abdominal compartment syndrome, multiple organ failure, and death in trauma patients.35 It is clear that both extremes—no fluid versus massive resuscitation—should be avoided as they are detrimental to patient outcome. What is also clear is that surgical control of hemorrhage should be considered part of the initial resuscitation of patients in hemorrhagic shock. Attempts at resuscitation in this situation will be futile and perhaps detrimental, as definitive control of bleeding will be delayed. Much has been written with regard to the choice of fluid used for the resuscitation of patients in shock. Clearly, most critically ill patients will require volume expansion at some point with the goal of restoring intravascular volume and preserving tissue perfusion and oxygenation. Options include isotonic crystalloids, hypertonic fluids, natural and synthetic colloids, blood products, and other novel solutions. At present, the first-line fluid of choice for the resuscitation of patients in shock remains isotonic crystalloids, such as lactated Ringer’s or normal saline solutions. These fluids have a long history of proven effectiveness and are inexpensive, readily available, and easy to preserve. The theoretical advantages of colloids such as albumin solutions include the possibility that they will provide more rapid restoration of intravascular volume with a smaller volume of infused fluid than crystalloids. Colloids may also be associated with less tissue and lung edema and may preserve plasma albumin levels. The potential disadvantages of colloids include their cost and the fact that, in the leaky capillary syndrome seen in many critically ill patients, albumin infusion may not preserve the intravascular oncotic pressure but rather leak into the extravascular space. Hypertonic saline solution combines some of the advantages of crystalloids and colloids. Hypertonic saline may cause less peripheral edema than isotonic fluids, as it draws intracellular fluid into the vascular space. It also may have fewer detrimental effects on immune function. Several studies have examined the role of hypertonic saline compared with isotonic saline in trauma patients, and no clear difference in outcomes could be shown.36–38 However, some benefit may result from infusion of hypertonic saline in patients with penetrating injuries39 or those with combined traumatic brain injury and shock.40 Several studies have attempted to answer the question as to the benefits of colloids and crystalloid solutions.


One large meta-analysis of the use of albumin versus crystalloids showed a trend toward an increased mortality rate for a variety of critically ill patients who received albumin.41 However, in other large meta-analyses of the literature comparing albumin solutions with crystalloids for a wide variety of surgical and nonsurgical indications, no difference in mortality rate was detected based on the these choices of resuscitation fluid.42,43 These metaanalyses include heterogeneous populations of patients and studies of differing designs, confounding the interpretation of the results. At this time, no strong recommendation can be made to support the use of colloids over crystalloids for patients in shock. The availability of newer colloid solutions, such as hydroxyethyl starch (HES) have renewed this debate. Synthetic starch solutions HES have been used clinically to restore intravascular volume in patients with shock. Several HES solutions are available clinically that differ in the molecular mass fractions of HES and in the composition of the electrolyte solution. The studies that have analyzed the use of HES as a resuscitation fluid are encouraging. In a canine model of hemorrhagic shock, fluid resuscitation during uncontrolled bleeding resulted in higher oxygen delivery and lower systemic lactate concentrations when HES (6%) was used compared with lactated Ringer’s solution during resuscitation to a target mean arterial blood pressure of 60 to 80 mm Hg.44 Also, compared with administration of 0.9% saline, volume resuscitation with HES in balanced electrolyte solution (Hextend) is associated with less metabolic acidosis and longer survival in an experimental animal model of septic shock.45 There are concerns regarding the development of coagulopathy with the infusion of HES, because it is known to inhibit platelet function. However, fluid resuscitation with low-molecular-weight HES may reduce the risk of bleeding associated with HES of higher molecular weight and degree of substitution.46 Also, a dilutional effect on coagulation function independent of the type of resuscitation fluid employed has been observed.47 Furthermore, colloids with a more physiologically balanced electrolyte formulation may result in less metabolic acidosis and alteration of intestinal perfusion. In a prospective, randomized, blinded trial with elderly surgical patients, the use of balanced electrolyte HES helped prevent the development of hyperchloremic metabolic acidosis and provided better gastric mucosal perfusion than saline-based HES.48 Clearly, not all resuscitation fluids are equivalent, and patient outcomes will depend on the timing and on the amount and type of fluid employed. Alternative crystalloid resuscitation fluids are being evaluated. One promising option is Ringer’s ethyl pyruvate solution (REPS), which has been assessed in a number of studies using animal models of mesenteric

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ischemia/reperfusion injury,49 hemorrhagic shock,50 and acute endotoxemia.51,52 In these animal models, infusion of REPS, when compared with Ringer’s lactate solution, was shown to improve survival and decrease expression of proinflammatory cytokines. Ringer’s ethyl pyruvate solution merits further evaluation for the resuscitation of patients with hemorrhagic shock, sepsis, and trauma.53 There remains a need for well-designed clinical trials to determine whether colloids or crystalloids are better for the resuscitation of trauma patients. Because of many limitations, the existing meta-analyses must be interpreted with caution. However, with this in mind, a metaanalysis of this literature regarding humans suggests that trauma patients should continue to be initially resuscitated with crystalloids at this time.54,55

Transfusion The use of blood products in the care of critically ill and injured patients has saved many lives. However, evidence-based practices are evolving regarding the use of blood products. A multicenter, randomized clinical trial has clearly shown that, for critically ill patients in the intensive care unit (predominantly nontrauma patients), a restrictive strategy that employs a hemoglobin transfusion trigger of 7 g/dL is as at least as effective and may be superior to a liberal transfusion threshold of 10 g/dL.56 In fact, the 30-day mortality rate was lower for the subgroup of patients with an Acute Physiology and Chronic Health Evaluation (APACHE) II score of ≤20 who were randomized to the restrictive transfusion strategy. Patients who were deemed to have ongoing bleeding were excluded from this study. The same investigators published a subsequent study involving patients with known cardiovascular disease that showed similar 30- and 60-day survival rates for the restrictive and liberal transfusion strategies, with the exception of patients with acute myocardial infarction or unstable angina. For the patients with acute coronary syndromes (not simply a history of coronary artery disease), outcomes with a hemoglobin transfusion threshold of 10 g/dL were improved.57 For the trauma population, red blood cell transfusion has been shown to be a predictor of mortality, independent of severity of shock as determined by arterial base deficit, serum lactate level, shock index, and degree of anemia.58 In addition, there is a dose-dependent correlation between transfusions of packed red blood cells and the development of infection in trauma patients. Multivariate analyses show that transfusion of blood within 48 hours of hospital admission is an independent risk factor for the development of nosocomial infections.59–61 For other critically ill patients, a similar association between blood transfusion dose and nosocomial infections has been demonstrated.62 The administration of blood transfusions is also an independent risk factor for the

10

development of multiorgan failure in trauma patients independent of other indices of shock.63 On the other hand, empiric blood transfusions should be administered to trauma patients in shock who fail to respond to initial resuscitation with crystalloids. As mentioned earlier, this patient group often requires prompt operative control of hemorrhage. Because of these and other known detrimental effects associated with blood transfusion, as well as the limitations related to cost and availability (e.g., in the battlefield or prehospital setting), hemoglobin-based oxygen carriers (HBOCs) are being evaluated as an alternative to blood transfusion. While several varieties of HBOCs have been developed, the polyhemoglobins are the most promising type at this time; these include human recombinant polymerized hemoglobin and bovine hemoglobin glutamer 250.64 The HBOCs have been shown to be effective and safe for the resuscitation of shock in animal models and to improve survival rates better than resuscitation with crystalloids or HES solutions.65–68 Small clinical studies show promise for the use of HBOCs for surgical and trauma patients.69–71 There are currently phase III clinical trials in progress that will attempt to answer this question for human patients,64,72,73 and the HBOCs may become important in the early resuscitation of patients with anemia and shock.

Other Resuscitation Efforts Emergency department resuscitative thoracotomy, surgical exploration for control of active hemorrhage (e.g., repair of ruptured abdominal aortic aneurysm, splenectomy for active hemorrhage from splenic injury), stabilization of pelvic fractures, and control of external bleeding should all be considered part of the stabilization of circulation phase of the primary survey of hemodynamically abnormal and unstable patients. The best results for emergency department resuscitative thoracotomy are obtained for patients with penetrating injuries to the thorax, who had obtainable vital signs, and who suffer rapid deterioration in the emergency department, with up to 20% survivorship.74 Patients with penetrating abdominal injuries had significantly lower survivorship (6.8%), and survivors with blunt thoracic trauma who required emergent thoracotomy were extremely rare (0.5%).74,75 For patients with penetrating thoracic injuries who have vital signs at the scene or in the emergency department, survival is much higher than for those who did not have obtainable vital signs.76,77 Meanwhile, trauma patients who are pulseless and whose electrical cardiac activity is asystolic or agonal (wide complex heart rate 4 mL/kg; FiO2 < 0.5) • Complete reversal of muscle relaxation (sustained head lift) • Hemodynamic stability, not requiring rapid transfusion or bolus fluid therapy • Normothermia • Structurally adequate airway (air leak around endotracheal tube) • No indication for surgery or other procedures that would benefit from continued intubation * The patient must meet all of these criteria.

carbon dioxide levels. When minimal ventilator settings are achieved (FiO2 = 0.40, pressure support of 10 cmH2O) we assess the patient for extubation using the criteria listed in Table 3.4. The anesthesiologist and the surgeon share responsibility for completion of fluid resuscitation in the postoperative patient. Young patients, in particular, may achieve normal vital signs through compensatory vasoconstriction while still significantly hypovolemic. This “occult hypoperfusion syndrome”6 is associated with an increased risk of subsequent organ system dysfunction and failure if not recognized and treated. Adequate systemic perfusion can be confirmed in a number of ways, including normalization of mixed venous oxygen saturation, maximization of cardiac output, and clearance of elevated serum lactate.7 Elderly patients, and those with known cardiovascular disease, present specific challenges in the postoperative period. Not only must adequate systemic oxygen delivery be ensured, but prophylaxis against myocardial ischemia should also be provided. It is reasonable based on current evidence to administer beta-adrenergic-blocking drugs to any elderly patient without specific risk factors throughout the perioperative period.8 This is especially important in the 24 hours immediately following major surgery, when pain, shivering, and fluid shifts can all alter myocardial oxygenation for the worse.

Acute Care Situations Intracranial Emergencies Neurosurgical emergencies arise from conditions that increase intracranial pressure (ICP), reducing cerebral blood flow and thus brain tissue oxygenation. Elevated ICP will result in a decrease in the patient’s level of consciousness and the potential for brain stem herniation and death if not promptly addressed. Trauma is the leading cause of increased ICP, as the result of epidural or subdural hemorrhage, intraparenchymal hemorrhage,

3. Anesthesia and Acute Care Surgery

35

Table 3.5. Common neurosurgical emergencies.* Case Subdural or epidural hematoma Intraparenchymal hemorrhage Depressed skull fracture Unstable cervical spine Acute hydrocephalus

Urgency

Duration

Blood loss

Postoperative pain

Potential for regional anesthesia

1

2

2

3

2 3 2 2

4 3 3 2

1 2 3 4

3 3 2 3

2 (burr hole under local) 4 4 4 4

* Scale is from 1 to 4, with 1 being most urgent, shortest duration, least blood loss, greatest postoperative pain, and greatest potential for regional anesthesia.

or diffuse cerebral edema. Elevated ICP and the need for acute care surgery may also arise from spontaneous intracranial hemorrhage, intracranial malignancies, and impairment of cerebrospinal fluid circulation. Emergent craniectomy is indicated to correct the cause of increased ICP, and there is a strong time dependency of neurologic recovery on the speed with which surgery is performed. Table 3.5 lists the common neurosurgical emergencies. In addition to the usual considerations outlined above, the anesthesiologist must initiate or continue maneuvers to improve cerebral oxygenation. These generally follow the guidelines of the Brain Trauma Foundation9 and consist of the steps listed in Table 3.6. Application of these therapies depends on knowledge of the patient’s intracranial physiology. This may be obtained from monitors of ICP (extradural catheters, intraparenchymal fiberoptic filaments, or ventricular catheters) and/or cerebral oxygenation (jugular venous bulb oxygen saturation, various investigational devices for measuring tissue perfusion). It is important for all anesthesiologists responsible for neurosurgical emergencies to have a working knowledge of the intracranial monitoring devices in use in their institution. This will allow for continued use during the perioperative period and will reduce the chance of iatrogenic complications (e.g., unintended closure of a ventriculostomy drain). Pulmonary management should be directed toward aggressive support of cerebral oxygen delivery. Any patient with a deteriorating mental status should be promptly intubated, even before reaching the operating room. This is both to support ventilation and to avoid aspiration or sudden respiratory arrest during the cerebral CT that commonly precedes an acute care neurosurgery. Although it was once thought that increased levels of positive end-expiratory pressure (PEEP) would impair venous outflow from the brain, thus contributing to elevated ICP, it is now recognized that PEEP and other maneuvers to increase mean airway pressure are appropriate if they result in improved arterial oxygen saturation.10 Hyperventilation acutely lowers ICP by vasoconstriction and reduction of cerebral blood flow. Because this therapy may exacerbate cerebral ischemia on the cellular level, it should be reserved for those

patients in imminent danger of herniation who are en route to acute care surgical decompression.11 At all other times, the anesthesiologist should strive to maintain the patient’s pCO2 at normal levels. Traditional teaching in neurosurgical emergencies was to limit fluid administration in an effort to reduce the development of cerebral edema. This approach is no longer recommended.12 Volume restriction will lead to cerebral vasoconstriction and decreased cerebral blood flow, with disastrous consequences for brain tissue oxygenation. Brain trauma patients who experience even one episode of hypotension have substantially worse outcomes than those who do not.13 Preservation of normal intravascular volume is the goal, which may require aggressive fluid administration to the patient with associated noncranial injuries. Placement of a pulmonary artery catheter or esophageal ultrasound probe to guide fluid volume therapy is appropriate in patients with severe neurologic conditions. Pressor or inotrope therapy may be necessary to support cerebral perfusion pressure, particularly for the patient requiring high-dose barbiturate therapy to reduce cerebral metabolism and ICP. Although the acute care neurosurgical patient will typically have a depressed level of consciousness and may already have been intubated before reaching the operating room, normal anesthetic dosing is still appropriate. Analgesic therapy is important to minimize painmediated spikes in blood pressure and ICP. Muscle Table 3.6. Maneuvers, in approximate order of application, to improve cerebral oxygenation. • Optimization of systemic oxygenation • Hemodynamic support ⴰ Fluid resuscitation to a euvolemic state ⴰ Pressor and/or inotropic therapy • Elevation of the head and torso • Adequate analgesia and sedation • Drainage of cerebrospinal fluid via ventriculostomy • Osmotic therapy ⴰ Mannitol ⴰ Hypertonic saline • Barbiturate coma • Decompressive craniectomy (controversial) • Decompressive laparotomy (anecdotal/investigational)

36

O. Moayed and R.P. Dutton

relaxation, while not required for cranial exposure, is indicated as prophylaxis against sudden patient movement during delicate portions of the surgery, particularly if the patient’s head has been secured in a rigid frame. Longer acting sedative/amnestic medications, such as benzodiazepines, should be avoided because they may cloud the assessment of neurologic status in the postoperative period. Inhaled volatile anesthetics are appropriate for intraoperative anesthesia; reduction in cerebral blood flow is more than counterbalanced by decreased metabolic demand at doses up to 1 MAC (minimum alveolar concentration).14 Postoperatively, if an appropriate dose of analgesic has been administered, it should be possible to awaken and assess the patient without commitment to extubation. Even following the simplest of neurosurgical emergencies, such as relief of hydrocephalus or evacuation of an epidural hematoma, the patient will be slow to arouse. The anesthesiologist must recognize this and plan on continued postoperative mechanical ventilation until baseline neurologic function has recovered.

rologic function after the patient has been positioned for surgery. Uncooperative patients or those with significant pulmonary compromise should undergo rapid-sequence intubation, with the diligent application of manual inline cervical stabilization throughout laryngoscopy and intubation.15 Hemodynamic instability may develop during surgery as the result of blood loss (more common with thoracic or lumbar fractures) or spinal shock (more common with cervical injuries). The anesthesiologist must first ensure that the patient has an adequate intravascular fluid volume (by TEE or pulmonary artery catheter monitoring) and should then add inotropic therapy in a titrated fashion to reverse the inappropriate vasodilation and negative inotropic state caused by the loss of sympathetic transmission. The need for emergent neck exploration can arise following penetrating trauma or soft tissue infection. These cases will provide airway challenges similar to the patient with the unstable surgical spine and should be approached in a similar fashion. If time and patient cooperation allow, then fiberoptic examination and intubation of the airway under topical anesthesia and light sedation are desirable.16 If the patient is in extremis, then a rapidsequence approach is indicated, with a surgeon capable of emergent cricothyroidotomy standing by. Surgical debridement and drainage of a subpharyngeal or cervical abscess will usually be a short procedure, whereas exploration following penetrating trauma may lead to prolonged vascular or tracheal repairs. The anesthesiologist should have a sufficiency of monitoring and intravenous access to deal with all likely contingencies. Extubation following either neck exploration or fixation of a cervical spine fracture should be approached with a great deal of trepidation, as edema and hematoma in the vicinity of the injury can produce rapid and lethal airway compromise following removal of the endotracheal tube.17 In addition to the usual criteria for mental status, respiratory function, hemodynamic stability, and analgesia shown in Table 3.4, the anesthesiologist should also observe whether there is a leak of gas around the endotracheal tube when the cuff is deflated.Although not absolutely diagnostic, the presence of a leak around the

Neck Injury and Unstable Spine Acute care spinal surgery is fortunately rare, as it is only indicated in patients with evolving neurologic deficits. Patients who are neurologically intact, and those with a complete spinal level unlikely to improve after surgery, are best treated on a scheduled basis, when it is easier to ensure the availability of the surgical specialist, the necessary instruments and hardware, and neurophysiologic monitoring. Emergent spinal surgery is commonly indicated for treatment of acute traumatic injuries, but can also be necessitated by an abscess or hematoma compromising the spinal canal. The common acute care procedures involving the neck or chest are listed in Table 3.7. Airway management will be the first challenge for the anesthesiologist, as the potential exists for creating or worsening a spinal cord injury in the patient with an unstable cervical spine. Cooperative patients should receive an awake fiberoptic intubation following topical anesthesia of the upper airway and trachea, with general anesthesia withheld until confirmation of continued neu-

Table 3.7. Common emergencies involving the neck or chest.* Case Threatened airway Abscess Penetrating neck injury Traumatic aortic injury Pulmonary hemorrhage Bleeding after CT surgery

Urgency

Duration

Blood loss

Postoperative pain


1 3 2 2 2 2

1 1 2 3 3 2

4 4 3 1 2 2

3 3 3 1 1 2

2 3 3 4 4 4



tube is reassuring that the airway will not be critically compromised when the tube is removed.

Vascular Emergencies The need for urgent vascular surgery may arise following blunt or penetrating trauma or as the result of atherosclerotic disease progression. Hemorrhagic disease (penetrating trauma to a large vessel, rupture of an aortic aneurysm) is an absolute emergency, whereas ischemic disease (trauma to a smaller vessel, thromboembolism) is urgent in proportion to the risk of infarction in the affected region of the body. Procedures to save a limb or organ threatened by end artery occlusion should be considered emergent. Although elective vascular surgery patients have been shown to benefit from regional or combined regional and general anesthetic techniques,18 this approach is less desirable in the emergency setting. Emergency procedures, especially those following trauma, are less predictable than elective cases and may take significantly longer than expected. The patient is also less well prepared and may be cold, acidotic, and vasoconstricted at the time of arrival in the operating room. Sympathetic blockade, while desirable in the long term, may cause significant short-term hypotension in the hypovolemic patient receiving a spinal or epidural anesthetic. Our own approach is to begin emergency cases with a careful general anesthetic. If the patient is likely to benefit from postoperative epidural analgesia, we will place the catheter at the conclusion of the procedure, following fluid volume resuscitation and normalization of coagulation parameters. The need for systemic anticoagulation will complicate many acute care vascular procedures. This can be problematic for the patient who has multisystem injuries or who is already suffering dilutional coagulopathy secondary to hemorrhage and resuscitation. Close attention to coagulation studies is essential, as well as close communication with the surgeon to establish the degree of anticoagulation required. Acute care vascular surgery patients will be at significant risk for perioperative myocardial ischemia and infarction. Although it may be tempting to delay surgery to pursue cardiac function studies such as dobutamine stress echocardiography, risk-benefit analysis rarely favors this approach.19 First, it is unlikely that any cardiac intervention would be indicated before dealing with the acute care vascular condition. Second, it is appropriate to treat most acute care vascular surgery patients as the highest possible risk in any case. For the anesthesiologist this means a cardiac-friendly general anesthetic (generous narcotic administration, limited use of anesthetics with negative inotropic properties), perioperative betablockade, and the use of a specific cardiac function

37

monitor such as a pulmonary artery catheter or intraoperative TEE. Postoperative intensive care is usually indicated, and it is appropriate to plan for a gradual emergence from anesthesia with extubation only in the comfortable, resuscitated, and hemodynamically stable patient. Tachycardia is the most common risk factor for perioperative myocardial infarction, and any increase in heart rate should be aggressively treated with volume resuscitation, analgesia, and beta-blockade.20

Acute Abdomen Abdominal emergencies include incarceration of hernias, acute appendicitis, diverticulitis, or cholecystitis, perforation of viscous organs, traumatic hemorrhage, bowel obstruction, and ectopic pregnancies. The suggestions for case prioritization presented above apply strongly to abdominal surgery cases, as does the recommendation for the attending anesthesiologist to personally see the patient as soon as possible. A brief visit can help to discriminate those patients who are well compensated and can afford to wait a short while from those who are septic, dehydrated, or otherwise severely compromised. In many situations rapid transportation to the operating room will facilitate intubation, placement of access and monitoring lines, and fluid volume resuscitation even before surgery begins. This is especially true if the patient is coming from an area of the hospital such as the emergency department where aggressive intensive care cannot be provided. Table 3.8 summarizes the common abdominal emergencies. Beyond routine anesthetic concerns, successful facilitation of acute care abdominal surgery will generally depend on accurate management of the patient’s cardiovascular system. Intraperitoneal hemorrhage arising from trauma or a perforated viscous can be rapidly life threatening, but is difficult to quantify until surgery begins. Nonhemorrhagic abdominal emergencies typically involve either acute sepsis (appendicitis, cholecystitis) or obstruction of the bowel. In either case acute inflammation, exacerbated by surgery, will lead to a rapid and profound “third-space” loss of intravascular fluid.21 The anesthesiologist must be prepared for a large volume resuscitation, with adequate intravenous access and the ability to closely monitor the patient’s circulation via central venous or pulmonary artery catheterization, TEE, or frequent laboratory analysis. Postoperatively, caution is advisable in deciding to awaken the patient and wean them from mechanical ventilation. Although most patients undergoing straightforward appendectomy, cholecystectomy, or reduction of an incarcerated hernia can be extubated without difficulty (especially following laparoscopic surgery), patients undergoing more extensive surgeries should be allowed to emerge from anesthesia more gradually. Closure of the

38

O. Moayed and R.P. Dutton

Table 3.8. Common abdominal emergencies.* Case Unstable blunt or penetrating trauma Ruptured AAA Perforated viscous Stable penetrating trauma Appendicitis Acute cholecystitis Bowel obstruction Pelvic abscess Tubal ectopic pregnancy Testicular torsion NASTI, septic shock

Urgency

Duration

Blood loss

Postoperative pain


1

3

1

1

4

1 2 2 4 4 3 4 2 2 3

3 3 3 2 2 3 2 2 1 2

2 3 3 4 3 3 3 3 4 2

1 1 2 2 2 1 2 2 3 2

4 3 3 3 3 3 3 3 2 3

* Scale is from 1 to 4, with 1 being most urgent, shortest duration, least blood loss, greatest postoperative pain, and greatest potential for regional anesthesia. AAA, abdominal aortic aneurysm; NASTI, necrotizing acute soft tissue infection.

abdomen following major surgery may lead to increased intraperitoneal pressure, as injured and inflamed tissue continues to swell in the postoperative period. This abdominal compartment syndrome can significantly impair postoperative pulmonary function, even in the presence of attentive resuscitation,22 Pressure on the diaphragm is less of a problem when the abdomen is left open, but fluid requirements will be substantial, and these patients are rarely stable enough for early extubation. Because muscle relaxation is required for abdominal exploration and subsequent closure, attention must be given to the adequacy of reversal at the end of the case. Acute care abdominal operations are also noteworthy for significant postoperative pain; for the patient who will not be taking oral medications, this leads to the use of intravenous patient-controlled analgesia for the first few postoperative days.23

Necrotizing Fasciitis, Soft Tissue Wounds, and Burns Although usually not as exciting or dramatic as hemorrhagic or neurosurgical emergencies, soft tissue surgery occupies a large percentage of “off-hours” operating room time. Patients with open skin wounds require surgery for initial irrigation and debridement, follow-on surgeries for continued assessment, and an eventual definitive reconstruction and closure. The latter cases are clearly not emergent. Serial every-other-day irrigation and debridement procedures have a low urgency but cannot be completely disregarded because they are essential for moving the patient toward eventual closure and hospital discharge. Initial soft tissue surgeries have greater or lesser acuity depending on the patient’s condition. Aggressive exploration and excision of dead tissue is an essential step in the treatment of the patient in septic

shock from a necrotizing acute soft tissue infection (NASTI) and should be regarded as more urgent for patients who are less stable. Early fasciotomy of an extremity in a patient with compartment syndrome or a circumferential burn may be limb saving.24 Early irrigation and sterile coverage of any skin defect will reduce the incidence and severity of subsequent infectious complications.25 The patient with an indication for emergent soft tissue surgery may be difficult to position on the operating room table and may require an intraoperative change in position to allow for complete surgical exposure. Because diabetes, obesity, and peripheral vascular disease are risk factors that predispose toward soft tissue infections (especially Fournier’s gangrene), anesthetic management is usually not straightforward. General anesthesia is recommended for all but the most peripheral procedures, because surgical times are unpredictable, blood loss may be significant (particularly during the initial debridement), and the possibility of an active bacteremia is a contraindication to spinal or epidural needle placement. Once sepsis is controlled, an epidural catheter can facilitate both repeated operative procedures and ongoing analgesia. Although uncontrolled arterial bleeding is unlikely, steady loss of blood from large areas of exposed fascia can quickly exsanguinate the soft tissue surgery patient. Large-bore intravenous access is recommended, along with the availability of cross-matched blood products and aggressive use of fluid and body warmers. The anesthesiologist should strive to maintain a reasonable hemoglobin concentration (8–10 g/dL), adequate platelet count (>60,000), and normal coagulation factor function, particularly if the duration or extent of surgery is not clear. Especially during the initial, emergent, exploration and debridement it is wise to err on the side of overly vigorous resuscitation. Such patients will likely be getting


39

sicker before they get better, while the requirement for multiple future surgeries will make it likely that any “over-transfused” blood products will simply delay the need for transfusion on another day. As with most acute care surgeries, the anesthesiologist should insist on adequate physiologic performance before considering an early extubation. Because the skin will usually not be closed, but simply covered with a vacuum or wet-to-dry dressing, soft tissue cases can end quickly. Allowing the patient some time in the PACU on mechanical ventilation to equilibrate fluids and fully recover from general anesthesia is often the wisest course of action. The patient presenting in septic shock poses particular challenges. The patient will have a low systolic blood pressure because of both inappropriate vasodilation and myocardial depression induced by bacterial endotoxin. As for the hemorrhaging patient, anesthetic agents, particularly induction drugs, must be carefully titrated. An appropriate target level of anesthesia calculated to produce amnesia and analgesia should be selected, with fluids, inotropes, and vasopressors added as necessary to maintain perfusion pressure. It is difficult during the early stages of sepsis to discriminate hypotension due to vasodilation, which is best managed with fluid administration and judicious use of pressors, from hypotension due to myocardial dysfunction, which is best addressed with inotropes. The use of an intraoperative monitor of cardiac performance, such as a pulmonary artery catheter or TEE, is essential to guide fluid, drug, and anesthetic therapy.

Orthopedic Emergencies Orthopedic operations account for a large percentage of unscheduled surgeries performed in most hospitals. Orthopedic emergencies—exsanguinating pelvic trauma or limb-threatening compartment syndrome—are rare, but urgent and acute orthopedic cases are common. The “urgent” category includes the treatment of open fractures of any bone and closed fractures of the long bones. Irrigation, debridement, and fixation of an open fracture is an urgent procedure, because the risk of osteomyelitis is directly related to the time interval between injury and

definitive operative treatment.26 Other orthopedic injuries may require urgent repair if they are associated with potentially reversible neurologic deficits, as discussed above for spinal surgery. Finally, dislocation of the hip, knee, shoulder, or elbow produces neurovascular compromise of the involved joint and is an indication for urgent sedation or general anesthesia to facilitate emergent reduction.27 Table 3.9 lists the common orthopedic emergencies. Early fixation of closed long-bone fractures is beneficial because it will facilitate patient mobilization and thus reduce the incidence of pulmonary complications.28 Numerous retrospective studies have confirmed this finding, as summarized in the consensus statement of the Eastern Association for the Surgery of Trauma.29 The benefits of early fixation must be weighed against the risks of aggravating other injuries, however, particularly for the patient with a significant traumatic brain injury (TBI). Some authors have found a worsening of outcome for patients with TBI undergoing early fracture fixation, whereas others have found no difference.30,31 All of these studies agree, though, that early fixation is associated with an increased incidence of both hypotension and transient arterial desaturation in the operating room. Decisions regarding fluid resuscitation, anesthetic depth, and ventilator management may have a profound effect on the patient’s ultimate outcome, meaning that close communication among the anesthesiologist, the operating surgeon, and the neurosurgical consultant is highly desirable. The decision to postpone or abbreviate indicated orthopedic procedures is not an easy one but may be necessary to avoid instability in a vulnerable patient who is not yet fully resuscitated. The choice of anesthetic technique for the emergency orthopedic patient depends on the nature of the injury, the underlying health of the patient, and the duration of the intended surgery. Any patient with significant potential for hemodynamic instability should undergo a general anesthetic with endotracheal intubation, for the reasons listed earlier. Purely regional techniques should be reserved for patients with an appropriate mental status and degree of motivation, undergoing surgeries of predictable duration involving a single extremity (i.e.,

Table 3.9. Common orthopedic emergencies.* Case Unstable spine Unstable pelvis, shock Open fracture Closed long bone fracture Acetabular fracture Hip fracture Reduction of dislocated joint

Urgency

Duration

Blood loss

Postoperative pain


2 1 2 3 3 3 2

3 1 2 2 3 2 1

2 1 3 3 3 3 1

2 2 2 2 1 2 3

4 4 2 2 2 1 3


40

O. Moayed and R.P. Dutton Table 3.10. Significant physiologic differences observed in pediatric patients undergoing acute care surgery.

isolated closed ankle fractures). However, the combination of regional and general anesthesia may provide the best of both techniques for patients undergoing extensive procedures. Use of epidural anesthesia for major orthopedic procedures of the femur, hip joint, and pelvis is associated with decreased intraoperative hemorrhage, decreased incidence of deep venous thrombosis, and improved postoperative analgesia.32 Single-shot or catheter blockade of the brachial plexus can bring similar benefits to patients undergoing upper extremity or shoulder surgery. Anesthetic challenges unique to orthopedic procedures include difficulty in finding sites for intravenous and arterial access, complex patient positioning to facilitate surgical exposure, and the physiologic changes produced by manipulation of unstable fractures. Transesophageal echocardiography has demonstrated that all patients undergoing internal medullary fixation of a femur fracture will experience embolization of fat and bone marrow.33 The fat embolus syndrome (FES) occurs when this embolic challenge triggers an autoimmune reaction in the lungs.34 The syndrome is characterized by the sudden onset of pulmonary hypertension, wheezing, hypotension, desaturation, petechiae, and disseminated intravascular coagulation. Treatment is supportive, beginning with the administration of intravenous fluids and epinephrine, and continuing with critical care management of acute respiratory distress syndrome, coagulopathy, and organ system failure. The ability to prophylax against FES with aggressive fluid volume administration before fracture manipulation has been proposed but not definitively confirmed.35 There is no question, however, that the patient who is well resuscitated before the event will fare better during and after the onset of symptoms.

• Reduced cooperation with procedures, especially with younger patients • Reduced functional residual capacity, more rapid desaturation • More compliant lungs and chest wall; usually easier to ventilate • Lower baseline blood pressure and higher resting heart rate • Increased compensation for hemorrhage; blood pressure decreases later than in adults • More reliance on tachycardia to support cardiac output when stressed • Increased heat loss • Increased sensitivity to narcotics and sedatives

the differences between pediatric and adult physiology (Table 3.10). Although the goals of anesthesia are similar, the techniques by which they are achieved may need to be modified from the normal practice for adults. It is extremely important for the anesthesiologist to have knowledge of these differences, have all the equipment needed for pediatric cases, and be comfortable taking care of pediatric patients. Table 3.11 shows the three common emergencies presenting in older children. The need for emergent surgery in children is most often precipitated by trauma, by airway compromise due to infection or foreign body aspiration, or by gastrointestinal tract compromise caused by appendicitis, hernia incarceration, or congenital abnormality. The acuity of the operation will vary as it will for an adult (as discussed earlier), but the practitioner must be wary of the rapid changes in vital signs that can occur in sick children when compensatory mechanisms for pulmonary or cardiovascular compromise are exhausted. Children undergoing acute care surgery will require general anesthesia. Although anesthesia in elective pediatric patients is commonly induced by inhalation of a volatile gas and nitrous oxide before placement of an intravenous catheter, this approach may be more dangerous in the emergency setting. Although potentially traumatizing, placement of an intravenous catheter followed by rapid-sequence induction is the safest course for any child with the potential for hemodynamic instability. An exception to this rule is the child with an upper airway obstruction caused by epiglottitis or foreign body aspiration. Agitation may lead to the complete occlusion of a tenuous airway, meaning that the preferred approach

Pediatric Emergencies Surgical emergencies in neonates are beyond the scope of this discussion, as they should be managed by specialty trained pediatric surgeons and anesthesiologists working in centers with the necessary experience and infrastructure to handle these cases well. Emergencies in older children, however, can present in almost any surgical or anesthetic practice. For the anesthesiologist, the key to successful management is a thorough understanding of Table 3.11. Common pediatric emergencies.* Case Aspirated foreign body Epiglottitis Fracture reduction

Urgency

Duration

Blood loss

Postoperative pain


3 1 4

1 2 2

4 4 4

4 3 3

4 4 3



is a gradual “breathe-down” induction until a deep enough level of anesthesia is reached that an intravenous catheter can be placed and the airway instrumented without a response from the patient.36 Because of their smaller functional residual capacity and higher metabolic rate, apneic children will begin to desaturate much faster than apneic adults, even following adequate preoxygenation. Once airway and intravenous access have been secured, successful anesthesia management in the pediatric patient is largely a matter of attention to detail.Temperature must be closely followed and the patient kept covered and actively warmed to the greatest degree possible. Blood loss must be carefully observed and adequate intravenous fluid therapy provided. Systemic narcotics will have a more profound effect on mental status than in adults and should be administered in a titrated fashion. Infiltration of the surgical site with a local anesthetic is highly recommended as an adjuvant to postoperative pain management. Most pediatric patients will emerge from anesthesia easily and should be extubated as soon as they are awake enough to support an open airway. Postoperative care should be in an age-appropriate unit.

41

4.

5.

6.

7. 8.

9.

10.

Critique This rapid onset of symptomatology in an otherwise healthy young man is malignant hyperthermia (MH) until proven otherwise. Although not highlighted in the vignette, hyperthermia would be associated with this presentation. Because MH is triggered by the use of volatile anesthetic agents in susceptible patients, the first step in treatment is a change in the anesthetic technique. Dantrolene sodium, a muscle relaxant, inhibits calcium release from the sarcoplasmic reticulum of the skeletal muscle, which is considered the key mechanism for this syndrome. Dantrolene sodium should be given intravenously (1–2.5 mg/kg). Although MH can make the patient rapidly unstable, immediate cessation of the operation will not always be practical and safe in the emergency setting.

11.

Answer (D)

17.

References 1. Egbert LD, Battit GE, Turndorf H, et al. The value of the preoperative visit by an anesthetist. JAMA 1963; 185:553. 2. Lubenow TR, Ivankovich AD, McCarthy RJ. Management of acute postoperative pain. In Barash PG, Cullen BF, Stoelting RK, eds. Clinical Anesthesia, 4th ed. Philadelphia: Lippincott, Williams & Wilkins, 2001: 1409–1410. 3. Horlocker TT, Abel MD, Messick JM, Jr, Schroeder DR. Small risk of serious neurologic complications related to

12. 13.

14.

15. 16.

18.

19.

20.

lumbar epidural catheter placement in anesthetized patients. Anesth Analg 2003; 96:1547–1552. Standards approved by the American Society of Anesthesiologists House of Delegates, October 1988, ASA Newsletter, December 1988. Pagel PS, Schmeling WT, Kampine JP, et al. Alteration of canine left ventricular diastolic function by intravenous anesthetics in vivo: ketamine and propofol [published erratum appears in Anesthesiology 1992; 77:222]. Anesthesiology 1992; 76:419–425. Blow O, Magliore L, Claridge JA, et al. The golden hour and the silver day: detection and correction of occult hypoperfusion within 24 hours improves outcome from major trauma. J Trauma 1999; 47:964–969. Abramson D, Scalea TM, Hitchcock, et al. Lactate clearance and survival following injury. J Trauma 1993; 35:584–588. Mangano DT, Layug EL, Wallace A, Tateo I. Effect of atenolol on mortality and cardiovascular morbidity after noncardiac surgery. Multicenter Study of Perioperative Ischemia Research Group. N Engl J Med 1996; 335:1713– 1720. Brain Trauma Foundation, American Association of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care. Guidelines for the management of severe traumatic brain injury. J Neurotrauma 2000; 17:451– 627. McGuire G, Crossley D, Richards J, et al. Effects of varying levels of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure. Crit Care Med 1999; 25:1059–1062. Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trail. J Neurosurg 1991; 75:731–739. Frost EA. Perioperative management of the head trauma patient. Ann Acad Med Singapore 1994; 23:497–502. Chestnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993; 134:216–222. Todd MM, Drummond JC. A comparison of the cerebrovascular and metabolic effects of halothane and isoflurane in the cat. Anesthesiology 1984; 60:276. Podolsky S, Baraff LJ, Simon RR, et al. Efficacy of cervical spine immobilization methods. J Trauma 1983; 23:461–465. Desjardins G, Varon AJ. Airway management for penetrating neck injuries: the Miami experience. Resuscitation 2001; 48:71–75. Epstein NE, Hollingsworth R, Nardi D, Singer J. Can airway complications following multilevel anterior cervical surgery be avoided? J Neurosurg 2001; 94:185–188. Yeager MP, Glass DD, Neff RK, Brinck-Johnsen T. Epidural anesthesia and analgesia in high-risk surgical patients. Anesthesiology 1987; 66:729. Chassot PG, Delabays A, Spahn DR. Preoperative evaluation of patients with, or at risk of, coronary artery disease undergoing non-cardiac surgery. BJA 2002; 89:747– 759. Mecca RS. Postoperative recovery. In Barash PG, Cullen BF, Stoelting RK, eds. Clinical Anesthesia, 4th ed. Philadelphia: Lippincott, Williams & Wilkins, 2001: 1382.

42 21. Buckley FB, Martay K. Anesthesia and obesity and gastrointestinal disorders. In Barash PG, Cullen BF, Stoelting RK, eds. Clinical Anesthesia, 4th ed. Philadelphia: Lippincott, Williams & Wilkins, 2001: 1044–1045. 22. Saggi BH, Sugerman HJ, Ivatury RR, Bloomfield GL. Abdominal compartment syndrome. J Trauma 1998; 45:597. 23. Smythe M. Patient-controlled analgesia: a review. Pharmacotherapy 1992; 12:132–143. 24. Mabee JR. Compartment syndrome: a complication of acute extremity trauma. J Emerg Med 1994; 12:651–656, 1994. 25. Haury B, Rodeheaver G, Vensko J, et al. Debridement: an essential component of traumatic wound care. Am J Surg 1978; 135:238. 26. Bednar DA, Parikh J. Effect of time delay from injury to primary management on the incidence of deep infection after open fractures of the lower extremities caused by blunt trauma in adults. J Orthop Trauma 1993; 7:532. 27. Kellam JF. Hip dislocations and fractures of the femoral head. In Levine AM, ed. Orthopaedic Trauma Association, American Academy of Orthopaedic Surgeons. Orthopaedic knowledge update: Trauma. Rosemont, IL: AAOS, 1996; 281–286. 28. Charash WE, Fabian TC, Croce MA. Delayed surgical fixation of femur fractures is a risk factor for pulmonary failure independent of thoracic trauma. J Trauma 1994; 37:667–672.

O. Moayed and R.P. Dutton 29. Dunham CM, Bosse MJ, Clancy TV, et al. Practice management guidelines for the optimal timing of long-bone fracture stabilization in polytrauma patients: the EAST practice management guidelines work group. J Trauma 2001; 50:958–967. 30. Jaicks RR, Cohn SM, Moller BA. Early fracture fixation may be deleterious after head injury. J Trauma 1997; 42:1–5. 31. Kalb DC, Ney AL, Rodriguez JL, et al. Assessment of the relationship between timing of fixation of the fracture and secondary brain injury in patients with multiple trauma. Surgery 1998; 124:739–744. 32. Holte K, Kehlet H. Effect of postoperative epidural analgesia on surgical outcome. Minerva Anestesiol 2002; 68:157–161. 33. Levy D. The fat embolism syndrome: a review. Clin Orthop Res 1990; 261:281. 34. Bulger EM, Smith DG, Maier RV, Jurkovich GJ. Fat embolism syndrome. A 10-year review. Arch Surg 1997; 132:435–439. 35. McDermott ID, Culpan P, Clancy M, Dooley JF. The role of rehydration in the prevention of fat embolism syndrome. Injury 2002; 33(9):757–759. 36. Gotta AW, Ferrari L, Sullivan C. Anesthesia for otolaryngologic surgery. In Barash PG, Cullen BF, Stoelting RK, eds. Clinical Anesthesia, 4th ed. Philadelphia: Lippincott, Williams & Wilkins, 2001: 996.

4 Fundamental Operative Approaches in Acute Care Surgery David J. Ciesla and Ernest E. Moore

Case Scenario A 55-year-old business woman is seen by the acute care surgeon for diffuse peritonitis. She is diaphoretic and hemodynamically labile. The patient stated that the onset of the sharp abdominal pain was abrupt and occurred 24 hours ago. Which of the following is the management approach of choice? (A) (B) (C) (D) (E)

Celiotomy Magnetic resonance imaging evaluation Computed tomography evaluation Laparoscopy Antimicrobial therapy and intensive care unit monitoring

Acute care surgical conditions present without warning and can encompass the entire field of surgery. Consequently, the acute care surgeon must be able to act decisively with incomplete information and unclear diagnoses. There is little time for preoperative preparation, and strategies often evolve as the operation progresses. Moreover, any anatomic region can present with an emergent condition, and multiple regions can be involved simultaneously. In preparation of this chapter, we reviewed all emergent operations performed at Denver Health Medical Center in 2002 and 2003. We excluded routine conditions such as appendicitis, cholecystitis, and superficial soft tissue infections with which all general surgeons are familiar. Trauma and nontrauma emergencies were categorized according to the anatomic region involved (Table 4.1). Although the abdomen was the most frequently involved region, the spectrum differed between trauma and nontrauma emergencies, with a greater proportion of trauma emergencies requiring attention outside the abdomen. Emergent cases were also classified according to the American Board of Surgery

case reporting system (Table 4.2). The spectrum of surgical emergencies involves multiple aspects of general surgery that require thoracic and vascular expertise in addition to proficiency with alimentary and abdominal processes. The aim of this chapter is to provide a standard operative approach to surgical emergencies based on anatomic regions. The ABCs of acute care resuscitation are well known as airway, breathing and circulation, but we also use this acronym to remind ourselves of the ABCs of acute care surgery. First, Assemble the team. Emergency conditions often require assistance from a myriad of services that not only includes operating disciplines such as anesthesia, neurosurgery and orthopedics but also ancillary services such as a blood bank and perfusionists. Next, Bring a book to the operating room. The nature of surgical emergencies does not allow much preoperative study, and it is critical to have a reference that reminds the acute care surgeon about the vital anatomic relationships in unfamiliar areas. Finally, Consider your protection. In emergent situations, the focus is usually on care of the deteriorating patient at the expense of personal safety. Moreover, actions often proceed much more rapidly than under nonemergent conditions, and there is greater potential for exposure to bodily fluids and contaminated sharps. Therefore, it is best to put on protective boots, eyewear, gloves, and gowns before assuming care of the patient rather than waiting until the situation reaches a crisis. Patients requiring acute care surgery are in varying degrees of physiologic compromise. Metabolic derangements often require a damage control approach where the operation is suspended before definitive surgical therapy can be provided. Damage control can be applied to any anatomic region and is accomplished in three conceptual phases. The first phase involves abbreviated resuscitative surgery to control hemorrhage and contamination. Definitive reconstruction is deferred during this phase in favor of rapid measures to stem life-threatening

43

44

D.J. Ciesla and E.E. Moore

Table 4.1. Anatomic regions involved in acute care surgery. Anatomic region Neck Chest Abdomen and pelvis Extremity

Trauma

Nontrauma

34 (10%) 64 (19%) 191 (58%) 41 (12%)

3 (2%) 21 (11%) 142 (75%) 23 (12%)

Source: Denver Health Medical Center, 2002–2003. From Ciesla DJ, Moore EE, Johnson JL, Moore JB, Cothren CC, Burch JM. The academic trauma center is the model for training the emergency surgeon. J Trauma 2005;58:657–662.

bleeding, restore perfusion where needed, and limit contamination. Wounds are closed temporarily, and the patient is transferred to the intensive care unit with the intent to return to the operating room under more favorable physiologic conditions. The second phase involves arresting of the “bloody viscious cycle” of acidosis, coagulopathy, and hypothermia by completing resuscitation in the intensive care unit. Adjunctive measures to refractory hemorrhage such as angiographic embolization are also carried out during this phase. The third phase consists of retuning to the operating room for definitive management of injuries and wound closure. Definitive wound closure is sometimes further delayed to allow reduction in tissue edema. The decision to truncate the initial operation should be made when it appears likely that further operation is technically challenging without exceeding the patient’s physiologic reserve. General indications include the inability to stop bleeding due to coagulopathy, an inaccessible major venous injury, and the need for prolonged operation in a patient with a suboptimal response to resuscitation.1 Ideally, damage-control measures should be instituted as early as possible. Physiologic guidelines include a persistent base deficit of 10 or less, temperature of 33°C or less, and recalcitrant coagulopathy. The technical aspects of abridged surgery are dictated by the pattern of injuries. Procedures for expeditious vascular control include ligation of accessible blood vessels and selective arterial inflow occlusion using intravascular balloons and clamps. Temporary intraluminal shunts can be used to preserve distal tissue perfusion during resuscitation when there is extensive segmental vessel damage. Solid organ tamponade is achieved through gauze packing, circumferential mesh wrapping, and balloon catheter–type devices. Contamination from perforated intestine can be rapidly controlled by stapled closure or umbilical tape ligation. External tube drainage provides effective control of injuries to the biliary tree, pancreatic duct, and ureters. Once the goals of resuscitative surgery are met, wounds are temporarily closed with the aid of synthetic occlusive material. The specific approach to damage control is based on the anatomic region involved. Key anatomic relationships and technical maneuvers are presented for each anatomic region. We focus on

rapid exposure of key areas that allow surgical control, resection, and reconstruction of anatomic structures. Interfaces between traditional anatomic divisions such as the thoracic outlet and diaphragmatic hiatus often present difficult exposure problems (Figure 4.1). An approach to extending surgical incisions to expose an adjacent region is also provided. It is assumed that the reader is familiar with surgical principles and techniques on the level of a practicing general surgeon. The surgeon must be familiar with a versatile, self-retaining retractor that can be deployed rapidly. This is especially important where retraction is needed to expose the recesses of the abdomen such as the diaphragmatic hiatus and the pelvis.

Key Points 1. Assemble the team. 2. Bring an anatomy book to the operating room. 3. Begin communication with the anesthesiologist early in the case to gauge the physiologic state of the patient. 4. Consider damage control early. 5. Approach vascular injuries sequentially, starting with major arterial injuries and leaving contained hematomas for last. Table 4.2. Spectrum of emergent operations. Surgical emergencies Alimentary tract Stomach Small bowel Colon Abdomen General exploration Abdominal decompression Liver and biliary tract Pancreas Spleen Abdominal wall Vascular Neck Chest Abdomen Upper extremity Lower extremity Thoracic Exploratory thoracotomy Resuscitative thoracotomy Repair diaphragm Lung Heart Head and neck Genitourinary Total

Trauma

Nontrauma

57 (17%) 7 23 27 101 (31%) 30 7 35 9 16 4 87 (26%) 9 11 26 21 20 53 (16%) 6 22 9 5 11 25 (8%) 7 (2%) 330

88 (47%) 16 33 39 49 (26%) 33 11 0 5 0 1 31 (16%) 1 3 4 4 19 18 (10%) 16 0 0 1 1 2 (1%) 1 (1%) 189

Source: Denver Health Medical Center, 2002–2003. From Ciesla DJ, Moore EE, Johnson JL, Moore JB, Cothren CC, Burch JM. The academic trauma center is the model for training the emergency surgeon. J Trauma 2005;58:657–662.

4. Fundamental Operative Approaches

45

Neck Cervicomediastinum

Thoracic Outlet

Chest

Axilla

Thoracoabdominal

Diaphragmatic Hiatus

Alternatively, percutaneous transtracheal ventilation can be accomplished by inserting a large-bore intravenous catheter through the cricothyroid membrane, into the trachea, and attaching it with tubing to an oxygen source capable of delivering 50 psi or greater. A hole cut in the tubing allows for intermittent ventilation by occluding and releasing the hole. Adequate oxygenation can be maintained for greater than 30 minutes. However, because exhalation occurs passively, ventilation is limited; and carbon dioxide retention may occur.

Abdomen Iliofemoral

Pelvic Outlet

Thigh

Popliteal Fossa Leg

Figure 4.1. Interfaces between traditional anatomic divisions frequently present difficult surgical exposure problems.

Neck Emergent Airway Airway management is the first priority in the emergent setting. Surgical control of the airway is essential in the setting where orotracheal or nasotracheal intubation is contraindicated or impossible. The technique has been well described with minor variations. In brief, the cricothyroid membrane is identified by palpation between the thyroid and cricoid cartilage. A midline incision is made over the cricothyroid membrane to avoid injury to the anterior jugular veins and associated bleeding. Furthermore, a vertical incision can be extended superiorly or inferiorly if the cricothyroid membrane is initially misjudged. Confirmation of position is accomplished by palpation through the wound. The trachea is controlled by use of a trach-hook positioned on the inferior border of the thyroid cartilage. A transverse incision in the cricothyroid membrane is then made and enlarged bluntly. Finally, a 6-mm endotracheal tube is placed in the cricothyroidotomy under direct vision and secured to the neck. Relative contraindications to cricothyroidotomy include laryngotracheal separation, and patients less than eight years of age. In such cases, emergent tracheostomy may be necessary.

Exposure Exposure of the midline structures of the anterior neck is accomplished via a collar incision two finger breadths above the clavicles, extending laterally to the anterior boarder of the sternocleidomastoid muscle. The position of the skin incision can be varied according to the level of injury. An extension along the anterior boarder of the sternocleidomastoid muscle provides further lateral and superior neck exposure. Skin flaps deep to the platysma muscle raised superiorly to the thyroid cartilage and inferiorly to the suprasternal notch usually provide adequate exposure of anterior structures. Once exposed, the strap muscles are divided vertically in the midline to enter the pretracheal space. Complete mobilization of the sternothyroid muscles exposes the anterior trachea, thyroid, and bilateral carotid sheaths. The thyroid isthmus can be retracted superiorly or inferiorly or divided between clamps and suture ligated to expose the first three tracheal rings. The strap muscles can also be divided if more lateral exposure of the carotid sheath is required. Unilateral neck exploration of the anterior triangle is accomplished via an incision along the anterior boarder of the sternocleidomastoid muscle from the mastoid process to the head of the clavicle (Figure 4.2). The omohyoid muscle crosses the anterior triangle of the neck deep to the sternocleidomastoid muscle and is retracted or divided as necessary. The carotid sheath is opened along the length of the incision to expose the carotid artery, jugular vein, and the vagus nerve. The facial vein, which marks the level of the carotid bifurcation, is divided and suture ligated. Lateral retraction of the jugular vein exposes the carotid artery. The ansa cervicalis, located within the carotid sheath, can also be divided without consequence. Exposure of the distal carotid artery in zone three is difficult. The first step is division of the ansa cervicalis and mobilization of the hypoglossal nerve. Next, the portion of the posterior belly of the digastric is resected. Removal of the styloid process and attached muscles can be helpful. At this point, anterior displacement of the mandible becomes important. Some authorities have advocated division and elevation of the vertical ramus of the mandible. However, the parotid gland and facial

46

D.J. Ciesla and E.E. Moore Styloid process Int. Carotid A. Ext. Carotid A. Sternocleidomastoid M.

Facial n.

Glossopharyngeal n. Hypoglossal n.

Vagus N. Common Facial V. Ansa Cervicalis

Digastric m. (cut)

Int. Jugular V.

Vagus n.

Sternothyroid M. A

Omohyoid M.

C

B

Figure 44.2. Vital Structures of the neck. (A) The relationship between the facial veein and the carotid bifurcation. The incision can be extended superiorly be behind the ear for distal carotid exposure or inferiorly to a median sternoto omy for proximal exposure. (Reprinted with permission from Ward RE. Injju ury to the cerebral vessels. In Blaisdell WF, Trunckey DD, eds. Traumaa Management. New York: Thieme, 1986: 273.) (B) Key anatomic relation nsships of the distal internal carotid artery. The posterior belly of the digastriicc muscle has been divided and the mandible retracted anteriorly. Note th hee position of the hypoglossal and vagus nerves. (Reprinted with permisssiion of Elsevier from Rutherford RB. Atlas of Vascular Surgery. Philade ellphia: WB Saunders, 1993.) (C) Relative position of the facial, glossophary yn ngeal, and hypoglossal nerves to the internal carotid artery and styloid p process. (Reprinted with permission of The McGraw-Hill Companies fro om m Burch JM, Franciose RJ, Moore EE. Trauma. In Schwartz SI, Shires G GT, Spencer FC, et al., eds. Principles of Surgery, 7th ed. New York: McGra aw w-Hill, 1999: 155–221.)

nerve prevent exposure of the internal carotid to the base of the skull. Excessive anterior traction on the mandible or parotid may damage the facial nerve; consequently, division of the ramus is seldom useful unless the surgeon is willing to resect the parotid and divide the facial nerve. Proximal carotid, subclavian and vertebral arteries are approached through a supraclavicular incision located 1 cm above and parallel to the clavicle (Figure 4.3). The clavicular head of the sternocleidomastoid muscle is divided, the external jugular vein is divided and ligated, and the subclavian vein is retracted inferiorly. The anterior scalene muscle is then detached from the first rib to expose the second and third segments of the subclavian artery. Care must be taken to avoid transection of the phrenic nerve, which is surprisingly thin and traverses the surface of the anterior scalene muscle. This provides exposure of the subclavian artery, proximal vertebral artery, internal mammary artery, and thyrocervical trunk. The vagus nerve passes deep to the subclavian artery adjacent to the common carotid artery. Further exposure can be achieved by resection of the medial half of the

clavicle. Proximal injuries to the right subclavian artery sometimes require median sternotomy, whereas injuries to the proximal left subclavian artery are best approached through a left anterior lateral thoracotomy. The cervical esophagus can be approached from either side thorough an incision along the anterior boarder of the sternocleidomastoid muscle. It is best to approach the distal cervical esophagus through a left neck incision. The sternocleidomastoid muscle is retracted laterally, and the omohyoid muscle is retracted or divided. The facial vein is ligated, allowing lateral retraction of the carotid sheath. When necessary, the inferior thyroid artery and the middle thyroid vein are divided and ligated. Medial retraction of the thyroid and trachea exposes the lateral esophagus. Care is taken to avoid injury to the recurrent laryngeal nerve, which lies in the tracheoesophageal groove. This is especially important if circumferential mobilization of the esophagus is required. Access to the space between the trachea and esophagus as well as the prevertebral space behind the esophagus is now possible.


47

Sternocleidomastoid m.

Internal jugular v. Carotid a. Vagus n.

Middle cervical ganglion

Inferior thyroid a. Inferior cervical ganglion

Phrenic n. Vertebral a. Brachial plexus Trapezius m.

Thoracic duct

Thyrocervical trunk

A

Omohyoid m.

cheal disruption or tracheal transection, the distal trachea has the potential for retraction into the mediastinum. Care must be taken to avoid airway occlusion by retraction of the wound edges during exposure while an endotracheal tube is placed into the distal trachea. The initial maneuver to control active bleeding in the neck is direct pressure ideally using point control with the finger. Attempts at dissection, vessel identification, and clamping may worsen bleeding in an already unstable patient. Blind placement of clamps should specifically be avoided because of the risk of further injury to other vessels and nerves in close proximity. Difficult areas to control include the oropharynx and the base of the neck at the thoracic outlet. Intranasal packing or nasal placement of Foley catheter and balloon inflation can control profuse bleeding from the nose. Tight packing of the pharynx using laparotomy pads can usually control bleeding from the mouth. Endoluminal balloon occlusion using Fogarty-type catheters placed into the open end of a bleeding vessel or larger balloon-type catheters placed directly into the wound can provide effective control of bleeding and allow time for resuscitation or angiographic embolization. This technique is particularly useful for controlling vertebral artery injuries and carotid artery injuries near the skull base.2 Distal perfusion past surgically accessible carotid injuries can be maintained temporarily using vascular shunts. Esophageal contamination of neck wounds can result in lethal mediastinitis. Drainage of esophageal contamination can be temporarily controlled by placement of a nasogastric tube or a large T-tube directly into the esophagus through an esophageal wound. If more extensive drainage is required, a loop esophagostomy can be created, or the esophagus can be divided easily using an endoscopic stapler and the proximal end brought out through the wound as an end esophagostomy.

B Figure 4.3. (A) Vital structures of the proximal neck. (B) Retraction of the carotid sheath and scalene fat pad exposes the subclavian vessels and the anterior scalene muscles. The phrenic nerve is isolated, and the anterior scalene muscle is divided close to the scalene tubercle of the first rib. (A, B reprinted with permission from Wind GG, Valentine RJ. Anatomic Exposures in Vascular Surgery. Baltimore: Williams & Wilkins, 1991.)

Damage Control The principles of damage control in the neck are to secure airway patency, stem blood loss, and control digestive tract contamination. The majority of airways are managed emergently by endotracheal intubation even with suspected tracheal violation. In cases of laryngotra-

Key Points 1. Make a vertical incision and use a 6.0-mm endotracheal tube for emergent cricothyroidotomy. 2. For proximal exposure of major cervical vascular injuries, extend the cervical incision via a median sternotomy. 3. The facial vein lies directly superficial to the carotid bifurcation. 4. The hypoglossal nerve passes between the internal carotid artery and internal jugular vein then turns anteriorly across the lateral surface of the external carotid artery. 5. The recurrent laryngeal nerve is best found in the tracheoesophageal groove at the base of the neck.

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Figure 4.4. Incisions for thoracic emergencies. The choice of incision is based on the underlying injured vessel. Because the identity of the injured vessel is not always known, the surgeon must be prepared to extend the initial incision or perform additional incisions. (Adapted with permission of The McGraw-Hill Companies from Burch JM, Franciose RJ, Moore EE. Trauma. In Schwartz SI, Shires GT, Spencer FC, et al., eds. Principles of Surgery, 7th ed. New York: McGraw-Hill, 1999: 155–221.)

Chest


sternal border and extended along the inframammary/ pectoral crease to the midaxillary line. The incision is carried through the skin and chest wall muscles to the intercostals with a single continuous stroke. Placement of the incision directly on the body of a rib reminds the surgeon to curve the incision medially and laterally along the line of separation of an intercostal space. No attempt should be made to control chest wall bleeding until after resuscitative maneuvers are performed. The chest is entered laterally on top of the fifth rib with either knife to avoid injury to the heart. Two fingers are placed into the pleural space and the intercostal muscles divided between the fingers with scissors to protect the intrathoracic structures. The intercostal incision is extended medially to the sternum and posteriorly to the paraspinous muscles. Exposure can be enhanced by transecting the cartilaginous attachments of ribs above or below the intercostal incision at the left sternal border. A Finochietto retractor is then placed in the wound, with the rack toward the table in case an extension across the sternum is required (Figure 4.5). The base of the left lung is elevated with the left hand, and the inferior pulmonary ligament is divided with a scissors. For profound hypovolemia, the descending thoracic aorta is cross-clamped just inferior to the left pulmonary hilum. Limited blunt dissection is generally

Incisions for thoracic emergencies are positioned according to the specific surgical emergency. In thoracic trauma, the identity of the injured vessel is not always known, and the emergency surgeon must be prepared to extend an incision or perform additional incisions (Figure 4.4).

Resuscitative Thoracotomy Resuscitative thoracotomy is generically defined as that performed to revive patients from imminent or established cardiopulmonary arrest. Although this heroic procedure is most effective for penetrating cardiac wounds, it may be life saving for other exsanguinating intrathoracic injuries, pulmonary venous air embolism, or profound hypovolemic shock caused by massive hemorrhage from any source.The goals of emergency department thoracotomy are to (1) decompress pericardial tamponade, (2) control intrathoracic bleeding and air leak, (3) perform open cardiac massage, and (4) cross-clamp the descending thoracic aorta to redistribute blood flow to the heart and brain and to limit intraabdominal blood loss. Successful resuscitative thoracotomy demands rapid entry into the chest. The skin incision is initiated at the

Figure 4.5. Open the pericardium anterior to the phrenic nerve. (Reprinted with permission of Elsevier from Moore EE. Emergency thoracotomy and aortic cross-clamping. In Moore EE, Eiseman B, Van Way CW, eds. Critical Decisions in Trauma. St. Louis: CV Mosby, 1984: 529.)


required to separate the esophagus from the aorta in the area of clamping. Proximal hilar injuries require prompt vascular control. After division of the inferior pulmonary ligament, the left pulmonary hilum is occluded between the fingers of the left hand. The right hand then places a Satinski clamp across the hilum from superior to inferior guided by the fingers of the left hand. An alternative is the hilar twist where the lung is torsed 180° about the pulmonary hilum after division of the inferior pulmonary ligament. If there is evidence of intrapericardial blood or ineffective myocardial contraction, a generous vertical pericardiotomy is made anterior to the phrenic nerve large enough to deliver the heart for complete inspection or internal cardiac message. Open bimanual cardiac message is performed by placing the right hand behind the heart along the diaphragm and the left hand on the anterior surface of the heart. The heart is compressed with the flat of the hands over a large surface. Direct pressure with the fingertips must be avoided because of the potential for rupturing the ventricular wall. Air embolism is a frequently overlooked lethal complication of pulmonary injury. The patient is placed in the Trendelenburg position to trap the air in the apex of the left ventricle. Emergency thoracotomy is followed by cross-clamping the pulmonary hilum on the side of the injury to prevent further introduction of air. Air is aspirated from the apex of the left ventricle with an 18-g needle and 50-cc syringe. Vigorous open cardiac massage is used to force the air bubbles through the coronary arteries. The highest point of the aortic root is also aspirated to prevent air from entering the coronaries or embolizing to the brain. Sometimes air can be aspirated directly from the right coronary artery. The patient should be kept in the Trendelenburg position and the hilum clamped until the pulmonary venous injury is controlled.

Anterolateral Thoracotomy The left or right anterolateral thoracotomy is the most versatile incision for thoracic surgical emergencies. Because of the uncertain trajectory of bullets, it is the safest approach for gunshot wounds. Patients in extremis should remain in a supine position on the operating room table. Lateral positioning may limit access to the superior mediastinum or lesions in the opposite hemithorax, compromise ventilation of the dependent lung, or allow blood to spill over into the contralateral bronchial tree. A left anterolateral thoracotomy via the fifth intercostal space is preferred for resuscitation because this provides access for opening the pericardium, clamping the descending thoracic aorta or pulmonary hilum, and repair of most cardiac wounds.

49

Transsternal Anterior Thoracotomy The left anterolateral thoracotomy, initially performed for resuscitation, is extended across the sternum through the right fifth intercostal space to provide access to right thoracic wounds or to improve exposure of the left chest. The transsternal incision is particularly important for controlling from the posterior mediastinum. The sternum is traversed with a Lebsche knife; the internal mammary arteries should be suture ligated following restoration of cardiac activity. Massive hemorrhage from pulmonary hilar wounds may be best controlled by intrapericardial ligation of the pulmonary veins as well as isolation of the main pulmonary artery. The primary limitation of this incision is exposure of the superior thoracic aperture. For immediate vascular control of the aortic arch branches, the superior portion of the sternum should be opened with a Lebsche knife and the incision extended to the neck.

Left Book Thoracotomy The left book or trap door thoracotomy is employed for access to the proximal left subclavian artery as it exits the posterior thoracic outlet, but its utility is controversial. The conceptual design is an en bloc left anterolateral thoracotomy, upper sternotomy, and left supraclavicular extension. Although the classic description consists of an initial third interspace incision, which entails an incision above the nipple traversing the breast or pectoralis major, we believe a standard submammary/pectoral skin incision with thoracic entry via the fourth intercostal space is preferable. The anterolateral thoracotomy is continued via the upper sternum and completed with a left supraclavicular incision, transecting the sternocleidomastoid and omohyoid muscles to disengage the trap door. The incision is technically challenging, and the underlying complex anatomy may be difficult to unravel within a large hematoma. Of note, the relatively small phrenic nerve should be isolated on the surface of the anterior scalene before this muscle is divided to access the subclavian artery distal to the thyrocervical trunk. Under urgent conditions of free intrathoracic bleeding from a proximal left carotid or subclavian artery wound, median sternotomy with a left cervical extension may be done more expediently than the trap door configuration. Additionally, in cases where the left subclavian artery is injured outside the thoracic outlet, proximal subclavian control can be achieved through the anterolateral thoracotomy, and definitive repair can be achieved via separate supraclavicular incision without the intervening upper sternotomy.

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Median Sternotomy Median sternotomy has a relatively limited use for acute thoracic emergencies and is largely confined to anterior stab wounds to the heart or thoracic outlet injuries (Figure 4.6). Although a sternotomy provides an excellent view of the anterior surface of the heart, major injuries to the pulmonary hila may be difficult to manage, and posterior mediastinal structures are virtually inaccessible. The safety of median sternotomy can be ensured by preliminary blunt dissections of the retrosternal space via windows developed in the suprasternal notch and below the xiphoid process. The lungs should be deflated during sternal sawing to prevent violation of the pleural spaces. Finally, the initial separation of the sternal incision should be done slowly to avoid injury to the innominate vein, which is in close proximity to the upper sternum.

Median Sternotomy with Right or Left Cervical Extension Rapid exposure of the proximal right subclavian, innominate, or proximal common carotid arteries is best achieved via a median sternotomy with appropriate cervical extension. A right supraclavicular incision is optimal to access the proximal right subclavian and innominate arteries, whereas carotid injuries in zone 1 of the neck are approached via extensions along the anterior border of the sternocleidomastoid muscle on the involved side. The strap muscles are divided to expose the proximal common carotid artery.

A

Left Posterolateral Thoracotomy Posterolateral incisions also have a limited role in thoracic surgical emergencies. The conspicuous exception is an injury to the descending thoracic aorta, which is almost always due to blunt trauma. A large soft tissue incision is warranted under emergent conditions; the skin incision is begun under the left nipple and extended posteriorly below the tip of the scapula. The latissimus dorsi, serratus anterior, and trapezius muscles are divided to free the shoulder girdle. The typical blunt aortic injury occurs just distal to the left subclavian artery and is approached through the fourth interspace, whereas more distal injuries are approached through the sixth interspace. Transection of a rib posteriorly provides adequate exposure without the time required for rib resection.

Exposure Great Vessels The great vessels of the chest are best exposed through a median sternotomy or a bilateral anterolateral thoraco-

B Figure 4.6. The median sternotomy. (A) The incision is made from the suprasternal notch to one side of the xiphoid process. (B) Final exposure of the great vessels through a median sternotomy. The thymus is not shown. (A, B reprinted with permission of Elsevier from Rutherford RB, Atlas of Vascular Surgery. Philadelphia: WB Saunders, 1993.)


tomy with transsternal division. Incision is made over the sternum in the midline from just below the suprasternal notch to below the xiphoid process. Blunt dissection beneath the sternum at the suprasternal notch and xiphoid process protects the underlying structures from injury during sternal division. The thymus is then divided in the midline to expose the anterior pericardium and great vessels. Proximal exposure of the aorta and superior vena cava requires opening the pericardium. The left brachiocephalic vein can be dissected free and retracted to expose the origin of the innominate artery. Extension of a median sternotomy to a right neck incision along the anterior border of the sternocleidomastoid muscle exposes the innominate artery bifurcation, whereas extension to a right supraclavicular incision exposes the proximal right subclavian artery. This exposure requires lateral retraction of the internal jugular vein. Care must be taken to avoid injury to the phrenic nerve and the right vagus nerve, which passes over the anterior surface of the subclavian artery and the recurrent laryngeal nerve as it passes behind the subclavian artery. The proximal left common carotid artery is somewhat more posterior than the innominate artery and is obscured by the left brachiocephalic vein. The innominate vein must be retracted inferiorly and the proximal internal jugular vein retracted laterally. Extension of the incision along the anterior border of the left sternocleidomastoid muscle provides exposure of the more distal left common carotid artery. Because the course of the aortic arch is anterior to posterior, it is difficult to reach the origin of the left subclavian artery through a median sternotomy. If a median sternotomy has been performed, the incision is extended to a trap door incision by transecting the sternum in the third or fourth intercostal space and adding a left supraclavicular incision. In hemodynamically unstable patients, initial control is achieved by applying pressure to the apex of the left chest through a left anterolateral thoracotomy. The superior lobe of the left lung is then retracted inferiorly to expose the aortic arch. The vagus nerve passes over the aortic arch just proximal to the origin of the left subclavian artery. The parietal pleura over the aortic arch is opened posterior to the vagus nerve.

Descending Thoracic Aorta The descending thoracic aorta is exposed via a posterolateral thoracotomy in the fourth intercostal space. The left lung is deflated and retracted anteriorly. The aorta is then visible from the origin of the left subclavian artery to the diaphragmatic hiatus.

Esophagus Surgical emergencies involving the thoracic esophagus (penetrating or barogenic perforation) usually involve

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the distal one third of the esophagus. The distal thoracic esophagus is approached through a left thoracotomy in the sixth intercostal space. The lung is retracted anteriorly after division of the inferior pulmonary ligament. The parietal pleura is then opened over the distal aorta, and the esophagus is dissected circumferentially. The area of esophageal injury is mobilized generously to ensure complete inspection of the injured segment and to allow easy manipulation. The distal esophagus and cardia of the stomach can be exposed by incision in the diaphragm at the esophageal hiatus and pulling the gastroesophageal junction into the chest. Because the aortic arch obscures the esophagus in the left chest, esophageal injuries proximal to the left pulmonary hilum are approached through the right chest. Division of the azygous vein at the superior aspect of the right pulmonary hilum is necessary for proximal exposure of the thoracic esophagus.

Pulmonary Hilum The pulmonary hilum is optimally exposed through a posterolateral thoracotomy with the patient in the lateral decubitus position. However, most emergent operations begin with the patient in the supine position requiring an anterolateral thoracotomy. Placing extra padding under the involved side of the chest helps elevate the hilum with the patient in the supine position. The chest is entered through the fifth intercostal space because the critical anatomy of the lungs is at the hilar level. The intercostal muscles are divided in the rib space from the sternum to the transverse spinous processes. The key maneuver to exposing the hilar structures is traction on the lung to bring the hilar structures out from the mediastinum. The anterior aspect of the pulmonary hilum is exposed by posterolateral retraction of the deflated lung. Dissection of the left pulmonary hilum is begun by incision in the pleura overlying the pulmonary artery. The soft tissue in the space bounded by the aortic arch, the vagus nerve, and the phrenic nerve is opened by sharp dissection. The main pulmonary artery is the most superior structure and is located just under the aortic arch. The superior pulmonary vein is the most anterior structure overlying the bronchus and pulmonary artery. The inferior pulmonary vein is identified within the medial aspect of the inferior pulmonary ligament. It is sometimes necessary to obtain control of the pulmonary veins from within the pericardium. The right pulmonary hilum is exposed in a similar fashion. The azygous vein courses over the superior margin of the right pulmonary hilum and can be divided for enhanced exposure of the right mainstem bronchus. The right pulmonary artery lies immediately anterior to the bronchus. The pulmonary veins are anterior and inferior to the pulmonary artery. The posterior aspect of the pulmonary hilum is exposed by medial retraction of the lung. The bronchus

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is the most posterior structure in relation to the pulmonary artery and vein. The parietal pleura is incised at the transition of the chest wall to visceral pleura on the hilum. The pulmonary arteries lie anterior and lateral to the accompanying bronchus except for the left main pulmonary artery, which passes posterior to the left upper lobe bronchus. All pulmonary arteries are invested within a distinct perivascular sheath, which must be entered to be in the correct dissection plane. The pulmonary veins generally lie anterior and inferior to the artery and bronchus.

Damage Control The quintessential damage-control maneuver in the chest is the resuscitative thoracotomy in the emergency department. The goal is to restore physiology by dramatic but temporary maneuvers so that the patient can survive transport to the operating room where definitive treatment is given. Once in the operating room, several damage-control techniques are used according to the injuries present. Exsanguinating abdominal injuries are addressed through a laparotomy with the aortic crossclamp in place. Patients requiring cross-clamp times exceeding 30 minutes rarely survive. The damage-control maneuvers for thoracic injuries are slightly different from those for the abdomen. The emphasis in the chest is to provide rapid definitive treatment rather than suspend repair until after resuscitation in the surgical intensive care unit (SICU). This is because the physiologic requirements with respect to filling of the heart and expansion of the lungs do not tolerate packing as a method for controlling major bleeding. Bleeding from cardiac wounds is initially controlled during resuscitative thoracotomy by digital pressure using a skin stapler directly on the myocardium. Once transported to the operating room, myocardial injuries are definitively repaired using large permanent sutures and pledgets on the right ventricle. Injuries to the great vessels and aorta are repaired primarily or with synthetic grafts. Placement of intravascular shunts maintains distal perfusion so that the operation can be suspended until resuscitation in the SICU is complete. In the dying patient, ligation of the carotid or subclavian arteries should be considered. Ligation of the subclavian artery is surprisingly well tolerated. If the patient survives, reconstruction using bypass grafts can be performed at a later operation. Anatomic pulmonary resections are associated with a high mortality rate for patients with severe lung injury.3 Nonanatomic resections and tractotomy using stapling devices provide for rapid exposure and control of parenchymal bleeding and air leaks.4,5 Tractotomy is well tolerated because of the extensive collateralization of the lung.


Damage control of esophageal injuries is aimed at preventing mediastinal sepsis. Proximal esophageal drainage is accomplished by placement of an orogastric tube or creation of a cervical esophagostomy. Thoracic drainage is achieved by placement of chest tubes. Placement of gastrostomy or jejunostomy tubes can be delayed until later operation once resuscitation in the SICU is complete. Thoracic incisions can be closed temporarily by using a large monofilament suture to approximate the skin. Laparotomy pads can be placed below the sternum to prevent the cut edges of the bone from injuring the heart. Occasionally, swelling of the postischemic myocardium and lungs as a result of resuscitation will prevent closure of the chest. In such cases, the wound is packed with laparotomy pads and closed with an adhesive impermeable surgical barrier (Ioban, 3M Corp.). Definitive closure is delayed until swelling resolves, usually within 23 to 48 hours.

Key Points 1. For hemodynamically unstable patients, begin with a transsternal left anterior thoracotomy and extend across the sternum if necessary. 2. Place the aortic cross-clamp below the left pulmonary hilum after dividing the inferior pulmonary ligament. 3. Open the pericardium anterior to the phrenic nerve. 4. Clamp the injured pulmonary hilum to control air embolism. 5. The pulmonary arteries are located anterior and lateral to the associated bronchus except for the left main pulmonary artery, which is posterior to the left upper lobe bronchus. 6. Avoid anatomic resections for penetrating trauma in favor of stapled pulmonary tractotomy. 7. Identify the phrenic nerve, which is surprisingly small, on the anterior scalene muscle when dissecting the proximal right subclavian artery.

Abdomen The abdomen is the most frequently involved body region requiring acute care surgery (see Table 4.1). Although the general surgeon routinely performs abdominal operations, acute care surgery often requires exposure of structures not commonly encountered in elective procedures. This section focuses on rapid exposures of difficult areas of the abdomen. Anatomically, the


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abdomen is divided into three zones, the supramesocolic, containing the liver, spleen, and pancreas; the inframesocolic, containing the root of the mesentery; and the pelvis, containing the rectum and iliac vessels. Retroperitoneal structures include the pancreas, kidneys, aorta, and vena cava.

Incision All emergent abdominal explorations in patients older than 6 years are performed using a midline incision because of its versatility (Figure 4.7). The ability to reach all parts of the abdomen and eviscerate the patient is mandatory. The midline laparotomy is easily extended with a transverse incision if enhanced exposure is required laterally or extended superiorly to a median sternotomy or across the costal margin into a rib space when pathology extends into the mediastinum or thorax. A transverse incision above the umbilicus extended well

Figure 4.8. Control of the aorta at the diaphragmatic hiatus. (Reprinted with permission from Champion HR, Robbs JV, Trunkey DD. Rob and Smith’s Operative Surgery, 4th ed. Trauma Surgery, Parts 1 and 2. London: Butterworths, 1989.)

Figure 4.7. Abdominal incisions. Emergency procedures are performed through a midline laparotomy from the xiphoid process to the symphysis pubis. Additional exposure is achieved by extensions to median sternotomy, left thoracotomy, and unilateral or bilateral subcostal incisions. (Adapted with permission from Champion HR, Robbs JV, Trunkey DD. Rob and Smith’s Operative Surgery, 4th ed. Trauma Surgery, Parts 1 and 2. London: Butterworths, 1989.)

onto the flanks may be appropriate for children under the age of 6 years. If the patient has been in shock or is currently unstable, no attempt should be made to control bleeding from the abdominal wall until major sources of hemorrhage have been identified and controlled. The incision should be made with a scalpel rather than with an electrosurgical unit because it is faster. Liquid and clotted blood is rapidly evacuated with multiple laparotomy pads, and the aorta is palpated at the diaphragmatic hiatus to estimate blood pressure and a dialogue initiated with the anesthesiologist to determine the need for temporary aortic occlusion. If exsanguinating hemorrhage originates near the midline in the retroperitoneum, direct manual pressure is applied with a laparotomy pad and the aorta clamped at the diaphragmatic hiatus (Figure 4.8). The stomach and esophagus are retracted to the left to expose the right crus of the diaphragm. The posterior peritoneum is then divided between the right crus and the aorta. The index and middle fingers are placed on either side of the aorta as a guide to place a large curved vascular clamp parallel to the fingers pushed against the spine. Cephalad division of the median arcuate ligament and right crus can extend

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exposure over the lower thoracic aorta. The diaphragm is dissected laterally from the aorta into the posterior mediastinum. Although 5 to 7 cm of aorta can be exposed from this approach, more proximal control requires a left thoracotomy either by extension of the midline laparotomy or by separate incision. Circumferential dissection at this level is not recommended because of the presence of inferior phrenic and segmental arteries that are easily torn. With massive ongoing bleeding, the source is addressed directly with fingers or by firm pressure of a laparotomy pad and fist while exposure is achieved. If the liver is the source of massive hemorrhage, the hepatic pedicle should immediately be clamped (Pringle maneuver) and the liver compressed by tightly packing several laparotomy pads between the injury and the underside of the anterior chest wall. In all other cases, a rapid palpation of the liver and spleen is performed, and, if injuries are confirmed, additional pads are placed in the respective upper quadrants. For patients in cardiopulmonary arrest, closed cardiac message is ineffective in the presence of hypovolemia. Although the heart can be compressed by applying pressure to the underside of the diaphragm against the chest wall, opening the diaphragm and delivering the heart into the abdomen allows more effective open cardiac massage. An incision in the central tendon of the diaphragm to the left of the xiphoid process opens the inferior pericardium. Bimanual compression is then performed through the pericardiotomy. An exception is a suspected penetrating wound to the suprarenal aorta, in which case extension of the laparotomy across the left costal margin to a left thoracotomy is the preferred approach.


Exposure Supramesocolic Viscera Suprarenal Aorta Exposure of the supramesocolic aorta is accomplished by right medial visceral rotation that includes all abdominal contents to the left of the aorta (Figure 4.9). When the operation is initiated through a midline laparotomy, the left colon is mobilized along the lateral retroperitoneal attachments. The splenorenal and splenophrenic ligaments are divided, and the colon, spleen tail of the pancreas, and stomach are rotated medially. The left kidney and ureter can be left posterior or elevated with the adrenal gland and tail of the pancreas. This exposes the upper aorta at the diaphragmatic hiatus and includes exposure of the celiac axis, left renal artery, and origin of the superior mesenteric artery. The supraceliac abdominal aorta is exposed by dividing the left crus of the diaphragm. Dividing the celiac ganglion, which surrounds the celiac trunk at its origin on the aorta, exposes the celiac axis. Exposure of the thoracic aorta from within the abdomen is achieved by entering the left chest through circumferential incision in the diaphragm 3 cm from the intercostal margin. Alternatively, the left chest is entered by extending the midline laparotomy across the costal margin and performing a thoracotomy through an intercostal space. Control of the thoracic aorta is then accomplished by division of the left inferior pulmonary ligament and isolation of the aorta against the vertebral body. The distal abdominal aorta and proximal left iliac artery are exposed by medial reflection of the sigmoid colon and mesentery. Distal exposure of the left iliac artery and the right iliac artery is difficult with this approach and should be accomplished through an anterior transperitoneal approach.

Exploration Formal abdominal exploration should immediately follow control of life-threatening hemorrhage. A systematic evaluation of all abdominal contents is required to ensure that all pathology is identified at the initial operation. Although the sequence of exploration may vary with surgeon preference and the condition of the patient, exploration generally begins with evaluation of the liver and spleen. The root of the mesentery is inspected by retraction of the colon superiorly and evisceration of the small bowel to the right. The stomach, duodenum, small bowel, and colon are examined along with the mesentery. The posterior wall of the stomach can be visualized by entering the lesser sac through the anterior leaf of the gastrocolic omentum. Exploration of the retroperitoneal structures, including the kidneys, pancreas, aorta, and vena cava, is performed when clinically indicated and is described below.

Esophagus Esophageal exposure is maximized by carrying the superior extent of the incision to the junction of the costal cartilages with the xiphoid process. This allows increased lateral retraction of the costal margin opening up the upper abdomen. The left lobe of the liver can usually be retracted superiorly and to the left, which, along with superolateral retraction of the left costal margin and inferior retraction of the stomach, exposes the esophageal hiatus. If the liver is large, division of the left triangular ligament allows retraction of the liver to the right. However, this can result in fracture of the cirrhotic or fatty infiltrated liver. To isolate the esophagus, the gastrohepatic ligament is divided over the caudate lobe of the liver and the lesser sac entered to the right of the lesser curve of the stomach. The gastroesophageal fat pad over the abdominal esophagus is taken off the stomach


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and the phrenoesophageal ligament divided between the cardiac notch and the left crus of the diaphragm. Blunt finger dissection then defines the posterior esophagus from the left in conjunction with blunt dissection from the right through the lesser sac. Placement of an orogastric or nasogastric tube facilitates identification of the esophagus for blunt dissection. Suprahepatic Inferior Vena Cava The inferior vena cava exits the abdomen anterior and to the right of the esophagus and aorta. Exposure of the vena cava above the liver proceeds via midline laparotomy with firm traction of the costal margins superiorly. Extension to a median sternotomy greatly enhances exposure and allows control from inside the pericardium when necessary. The round, falciform, and coronary ligaments are divided to expose the bare area of the liver, and the liver is retracted inferiorly. The hepatic veins should be visible at this point and can be carefully dissected and encircled at their junctions with the vena cava. The suprahepatic vena cava is very short, and exposure is made difficult by the hepatic veins inferiorly and the diaphragm superiorly. If emergent control is required, the incision is extended to a median sternotomy, and the central tendon of the diaphragm is divided over the vena cava. Alternatively, the pericardium is opened vertically and the midline vena cava isolated just inferior to the right atrium. Pancreas and Duodenum

Figure 4.9. Right and left medial visceral rotations. (Reprinted with permission of The McGraw-Hill Companies from Burch JM, Franciose RJ, Moore EE. Trauma. In Schwartz SI, Shires GT, Spencer FC, et al., eds. Principles of Surgery, 7th ed. New York: McGraw-Hill, 1999: 155–221.)

Exposure of the head of the pancreas and the first and second portions of the duodenum usually proceeds simultaneously. A Kocher maneuver is performed by incision along the lateral peritoneal attachments of the duodenum sweeping the second and third portions of the duodenum medially to the inferior vena cava. This allows palpation of the head of the pancreas to the level of the superior mesenteric vessels and visual inspection of the anterior and posterior surfaces of the second and third portions of the duodenum. The Cattell and Braasch maneuver exposes the third and fourth portions of the duodenum by raising the mesentery of the terminal ileum and ascending colon from the posterior abdominal wall. Dissection begins at the lateral attachments of the cecum along the white line of Toldt and proceeds by elevating the mesentery of the ascending colon and ileum that contains the superior mesenteric artery and vein. The entire small bowel and ascending colon can then be reflected medially and superiorly out of the abdomen. Care must be taken to avoid injury to the right gonadal vessels and right ureter, which remain attached to the posterior abdominal wall. Alternatively, the fourth portion of the duodenum can be exposed by first performing a Kocher maneuver followed by division of the ligament of Treitz.

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The ligament of Treitz is a fibromuscular fold of peritoneum suspended from the right crus of the diaphragm and attaches to the fourth portion of the duodenum. It represents the proximal attachment of the small bowel mesentery. Division of the ligament of Treitz allows rotation of the fourth portion of the duodenum from left to right behind the mesenteric vessels. Although this maneuver allows visualization of the anterior surface of the third portion of the duodenum, the posterior surface can be evaluated only by palpation. Exposure of the pancreatic body and tail requires entering the lesser sac (Figure 4.10). Division of the gastrohepatic ligament will allow limited exposure to the head and superior border of the pancreas. Division of the gastrocolic ligament permits full inspection of the anterior surface of the pancreas along its length, including the inferior border. Division of the gastrocolic ligament is most commonly performed by transection of the anterior leaf of the greater omentum with ligation of the anterior epiploic arteries distal to the gastroepiploic arteries. The stomach is then reflected cephalad and the colon with attached greater omentum reflected caudally, thus opening the lesser sac. Wide exposure of the lesser sac occasionally requires extensive division of the gastrocolic ligament. Omental necrosis can result from the devascularization of the arc of Barkow by division of the right and left epiploic arteries along with the anterior epiploic arteries. An alternative approach to the lesser sac involves division of the posterior leaf of the greater omentum from the colon and ligation of the posterior epiploic arteries that variably arise from the transverse, dorsal, or great pancreatic arteries. Some posterior epiploic arteries also enter the colon directly or anastomose with the vasa recta of the middle colic circulation. The posterior leaf of the greater omentum is relatively avascular and is easily divided along the length of the transverse colon. With the stomach and attached greater omentum reflected cephalad and the transverse colon reflected caudally, the entire anterior surface of the pancreas is exposed. This also facilitates mobilization of the splenic flexure of the colon and division of the splenocolic and splenorenal ligaments. For suspected injuries to the pancreas, it is imperative to inspect the posterior pancreatic surface by incision of the peritoneum along the inferior border of the pancreas, taking care to avoid injury to the splenic vein. The spleen is mobilized from lateral to medial to expose the posterior surface of the tail of the pancreas and the splenic hilum. This maneuver also exposes the posterior surfaces of the distal splenic artery and vein. The splenic vein can also be exposed by mobilization of the inferior boarder of the pancreas with superior retraction of the pancreatic body. Dissection of the vein proceeds by dissection along the posterior surface from lateral to medial to the junction with the superior mesen-


A

B Figure 44.10. 10 Exposure of the pancreas pancreas. (A) The gastrocolic liglig ament is opened and the stomach retracted superiorly to expose the head, neck, and body of the pancreas. (B) The spleen is mobilized and reflected medially, exposing the posterior aspect of the spleen and splenic vessels. (A, B reprinted with permission of Excerpta Medica Inc. from Asensio JA, Demetriades D, Berne JD, et al. A unified approach to the surgical exposure of pancreatic and duodenal injuries. Am J Surg 1997; 174:54–60.)

teric vein.The superior and anterior surface of the splenic vein contains multiple tributary veins that drain the pancreas. The inferior mesenteric vein may be encountered entering either the splenic vein or superior mesenteric vein. The splenic and superior mesenteric veins join to form the portal vein behind the neck of the pancreas. One should not hesitate to divide the neck of the pan-


A

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gastrohepatic ligament is divided and the lesser sac entered over the caudate lobe of the liver. If necessary, a Pringle clamp is placed from left to right exiting the foramen of Winslow. The first and second portions of the duodenum are then mobilized by a Kocher maneuver that extends from the right edge of the hepatoduodenal ligament to the inferior vena cava below the right renal vein. Inferior traction of the duodenum improves exposure of the portal structures. The common bile duct and hepatic artery are anterior to the portal vein in the hepatoduodenal ligament. Isolation of the portal vein begins by incision along the right posterior boarder of the hepatoduodenal ligament with extension superiorly to the hilum of the liver and inferiorly to the head of the pancreas. The pyloric, duodenal, right gastric, and coronary veins enter the medial aspect of the portal vein near the head of the pancreas. The common bile duct is identified on the right side of the anterior surface of the portal vein. Following the cystic duct from the gallbladder leads to the common bile duct near the hilum of the liver. The course of the hepatic artery is followed from its origin at the celiac trunk by incision of the posterior peritoneum within the lesser sac and following the artery distally to the gastroduodenal artery, the first major branch. Liver

B Figure 4.11. Posterior retroperitonostomy. (A) An incision is made 2 cm inferior to the twelfth rib through the muscle layers to the retroperitoneal space. (B) The incision is widened to allow exploration of the pancreatic region. (A and B reprinted with permission of Elsevier from Van Vyve et al.6)

creas to expose these veins and control exsanguinating hemorrhage. Access to the pancreatic tail is also achieved by a retroperitoneal peritonostomy (Figure 4.11).6 An incision is made 2 cm inferior to the left twelfth rib with the patient in the right lateral decubitus position. After the muscles are severed, the pancreatic region can be reached by finger dissection of the exposed retroperitoneal space just above the renal fossa. The retroperitoneal opening is widened to allow exploration and extraction of necrotic pancreas and retroperitoneal fat. Portal Structures Emergent exposure of the porta hepatis is accomplished by retraction of the liver and gallbladder superolaterally and the hepatic flexure of the colon inferiorly. Exposure can be facilitated by lateral extension of the midline laparotomy and mobilization of the hepatic flexure. The

The lower costal margins impair visualization and a direct approach to the liver. Exposure of the right lobe is improved by elevating the right costal margin with a large retractor. The right lobe is mobilized by dividing the right triangular and coronary ligaments. Following division of the right triangular ligament, the dissection is continued medially dividing the superior and inferior coronary ligaments. The right lobe is then rotated medially into the surgical field. Mobilization of the left lobe is accomplished in the same fashion. The superior surface is exposed by division of the round ligament between clamps followed by division of the falciform ligament over the surface of the liver to the hepatic veins. Care must be taken when dividing any of the coronary or falciform ligaments because of their proximity to the hepatic veins and retrohepatic vena cava. Exposure of the retrohepatic vena cava requires firm superior retraction of the costal margins. Extension to a median sternotomy can greatly enhance retraction of the ribs and allow wider exposure. The right triangular ligament is then divided and the bare area of the liver exposed. The retroperitoneal attachments are divided as the right lobe of the liver is retracted medially. Several small hepatic veins enter the vena cava directly from the posterior surface of the right and caudate lobes of the liver and must be ligated and divided to avoid bleeding during mobilization of the right lobe. The right hepatic vein is identified as it enters the suprahepatic vena cava.

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Inframesocolic Exposure

Pelvis

Root of the Mesentery

Superior displacement of the small bowel exposes the structures within the pelvis. Limiting the superior extent of the midline laparotomy facilitates packing of the small bowel within the abdomen. Mobilization of the sigmoid colon and rectum is straightforward and proceeds by incision of the posterior peritoneum along the left lateral attachments of the colon, continuing to the peritoneal reflection in the pelvis and to the right of the colon. The peritoneum is divided close to the bowel and dissection performed bluntly with care to avoid injury to the ureter. The presacral space is developed by blunt dissection posterior to the rectum in the sacral hollow. Anterior dissection between the uterus or prostate and the bladder is accomplished in a similar manner. If necessary, the lateral attachments containing the middle and inferior rectal vessels are divided for circumferential dissection of the rectum. The iliac vessels are exposed by incision over the aortic bifurcation and sharp dissection along the anterior surface of the common iliac artery to its division into the external and internal iliac arteries. The right ureter crosses the iliac artery at its bifurcation and should be retracted laterally. The internal and external iliac veins lay posteromedial to the associated arteries. The injured right iliac vein is difficult to expose and may require temporary division of the overlying common iliac artery. The common iliac artery and its branches are exposed by retraction of the sigmoid colon and rectum to the right. The left ureter is retracted laterally and dissection carried out from the aortic bifurcation to the division of the common iliac artery. Penetrating wounds to the aortic bifurcation and iliocaval confluence are difficult to control and are associated with a high mortality rate. The iliocaval confluence is exposed by first dividing the right common iliac artery between clamps and then developing the plane between the iliac artery and iliac vein to the aortic bifurcation (Figure 4.12). The aorta is rotated to the left and the underlying veins exposed. Unilateral exposure of the iliac artery can be accomplished through an anterior oblique flank incision and retroperitoneal dissection. The incision is made at the lateral border of the rectus muscle approximately 3 cm superior and parallel to the inguinal ligament (Figure 4.13). The incision is extended to the midaxillary line and terminates midway between the iliac crest and tip of the twelfth rib. The external and internal oblique muscles are divided and the preperitoneal space entered through the transversus abdominus muscle and transversalis fascia. The preperitoneal space is then developed by blunt dissection over the iliac fossa, exposing the psoas and iliacus muscles.The ureter is retracted with the peritoneum away from the psoas muscle. The iliac vessels are located on the

The anterior approach to the superior mesenteric artery and vein below the transverse mesocolon begins by reflection of the small bowel to the right and retraction of the transverse mesocolon anteriorly and superiorly. A transverse incision is made at the base of the transverse mesocolon from the fourth portion of the duodenum to the patient’s right. The middle colic artery and vein are identified and traced proximally to their origins. The superior mesenteric artery lies to the left of the vein. Division of the ligament of Trietz and superior retraction of the inferior border of the pancreas allows limited exposure of the vessels. This approach allows rapid but limited exposure of the mesenteric vessels and is often appropriate for hemorrhage control or embolectomy. More proximal exposure requires dissection above the transverse mesocolon. Extensive exposure of the origin of the superior mesenteric artery and abdominal aorta is achieved by a right medial visceral rotation.

Infrarenal Aorta The infrarenal aorta is exposed by retracting the transverse colon superiorly and the small bowel to the right. The posterior peritoneum is incised over the anterior aortic surface from the inferior border of the duodenum extending inferiorly to the right side of the aortic midline and onto the right common iliac artery at the aortic bifurcation.The iliac artery is controlled with a vascular clamp, taking care to avoid injury to the underlying iliac vein. No attempt should be made to separate the iliac artery from the vein. The right iliac artery crosses anterior to the left iliac vein just distal to the aortic bifurcation. The left common iliac artery is exposed by lateral retraction of the cut edge of the peritoneum and the artery controlled with a vascular clamp.

Inferior Vena Cava Exposure of the inferior vena cava begins by dividing the lateral attachments of the right colon from the cecum to the hepatic flexure. The right colon is then reflected to the left. A Kocher maneuver is then performed, and the inferior vena cave is exposed from the caudate lobe of the liver to the iliac bifurcation. Circumferential dissection of the vena cava should be avoided in emergent operations because of the risk of injury to the lumbar veins, which enter the vena cava through the posterior wall. The right adrenal vein enters the vena cava above the right renal vein. The caudate lobe of the liver obstructs exposure of the suprarenal vena cava.


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trolled. Packing of injuries of the left lobe may not be as effective, because there is insufficient abdominal and thoracic wall anterior to the left lobe to provide adequate compression with the abdomen open. Because of the technical challenge and high mortality rate of hepatic vascular isolation, direct operative repair of retrohepatic venous injuries is avoided. If massive venous hemorrhage is seen from behind the liver and if reasonable hemostasis can be achieved with perihepatic packing, the patient can be transferred to the interventional radiology suite where hemorrhage from arterial sources are embolized and stents are placed to bridge venous injuries. Perihepatic packing may not control hemorrhage from larger branches of the hepatic artery. The Pringle maneuver is used as an adjunct to packing for the temporary control of the arterial hemorrhage (Figure 4.14). The length of time that a Pringle maneuver can remain in place without causing irreversible ischemic damage to the

Figure 4.12. Exposure of the iliocaval confluence. The distal aorta and common iliac arteries are controlled with clamps. The right common iliac artery is divided between clamps and rotated to the left along with the aorta to expose the iliocaval confluence and the posterior wall of the aorta. (Reprinted with permission of Elsevier from Salam AA, Stewart MT. New approach to wounds of the aortic bifurcation and inferior vena cava. Surgery 1985; 98:105–108.)

medial aspect of the psoas muscle. Proximal exposure to the aortic bifurcation can be achieved with this approach. The external iliac artery can be exposed to the inguinal ligament with extension to a groin incision when necessary to expose the common femoral artery.

Damage Control Liver Perihepatic packing is capable of controlling hemorrhage from most hepatic injuries, and it has the advantage of freeing the surgeon’s hands. The laparotomy pads should remain folded with two or three stacked together. The right costal margin is elevated, and the pads are strategically placed over and around the bleeding site.Additional pads should be placed between the liver, diaphragm, and anterior chest wall until the bleeding has been con-

Figure 4.13. The iliac vessels can be approached through an incision 2 cm above and parallel to the inguinal ligament. The abdominal muscles are divided and the retroperitoneum elevated from lateral to medial. The incision can be extended inferiorly across the inguinal ligament over the femoral canal. (Reprinted with permission from Wind GG, Valentine R, Anatomic exposures in vascular surgery. Baltimore: Williams & Wilkins, 1991.)

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Most sources of venous hemorrhage within the liver can be managed with perihepatic packing. Even retrohepatic vena cava and hepatic vein injuries have been successfully tamponaded by closing the hepatic parenchyma over the bleeding vessel. Venous hemorrhage caused by penetrating wounds that traverse the central portion of the liver can be managed by suturing the entrance and exit wounds with horizontal mattress sutures. For bleeding from minor lacerations that do not respond to compression, topical hemostatic techniques have been successful. Small bleeding vessels are usually controlled with the argon beam coagulator. Topical thrombin can also be applied to minor bleeding injuries by saturating either a gelatin foam sponge or a microcrystalline collagen pad and applying it to the bleeding site.

Figure 4.14. The Pringle maneuver. (Reprinted with permission of The McGraw-Hill Companies from Burch JM, Franciose RJ, Moore EE. Trauma. In Schwartz SI, Shires GT, Spencer FC, et al., eds. Principles of Surgery, 7th ed. New York: McGrawHill, 1999: 155–221.)

liver is unknown, but clamp times exceeding 60 minutes have been successful. Ligation of the right or left hepatic artery is appropriate for patients with recalcitrant arterial hemorrhage from deep within the liver. Its primary role is for injuries where application of the Pringle maneuver results in the cessation of arterial hemorrhage. Arterial ligation is a preferred alternative to a deep hepatotomy. When bilobar arterial bleeding persists, an intrahepatic balloon can be very effective. Our method is to tie a large Penrose drain to a hollow catheter and ligate the opposite end of the drain. The balloon is then inserted into the bleeding wound and inflated with soluble contrast media. If the control of the hemorrhage is successful, a stopcock or clamp is used to occlude the catheter and maintain the inflation. The catheter is left in the abdomen and removed at a subsequent operation 24 to 48 hours later. If recurrent hemorrhage occurs, selective embolization is usually effective. Suturing of the hepatic parenchyma remains an effective hemostatic technique for persistently bleeding lacerations less than 5 cm in depth. The preferred suture is 0 chromic attached to a large curved blunt needle. The large diameter of the suture helps prevent it form pulling through Glisson’s capsule. A simple running technique is used to approximate the edges of shallow laceration. Deeper lacerations may be managed with interrupted horizontal mattress sutures placed parallel to the edge of the laceration. When tying the suture, tension is adequate when visible hemorrhage ceases or the liver blanches around the suture.

Spleen Splenectomy is appropriate for significant splenic injuries in the patient with refractory coagulopathy. Bleeding from minor splenic injuries can be controlled by the argon beam coagulator or absorbable mesh splenorrhaphy in cases where the splenic capsule has been stripped. The mesh need not be sutured to the spleen but can be packed with laparotomy pads.

Kidney Bleeding from moderate parenchymal injuries in the unstable patient usually responds to perirenal packing. For larger injuries, nonviable tissue is debrided, and surface vessels are ligated with absorbable sutures. Surface bleeding from capsular avulsion can be controlled by manual compression and argon beam coagulation. Prompt nephrectomy, however, is appropriate in the multiply injured patient with a major pedicle injury. Injuries to the ureter are not repaired in the unstable patient. Closed suction drains are placed in proximity to the injury for temporary drainage. The transected ureter can be temporarily ligated, preferably with placement of a nephrostomy tube or drained using an exteriorized ureteral stent. Bladder injuries are adequately managed with transurethral or suprapubic Foley catheters. More extensive injuries can be drained with bilateral stents passed retrograde through ureters and exteriorized through the abdominal wall.

Gastrointestinal Tract Contamination from gastrointestinal perforations is contained by rapid closure using full-thickness running monofilament suture or stapling devices. Resection of devitalized tissue is accomplished rapidly by stapled division of the bowel and ligation of the mesentery. No


attempt is made to restore gastrointestinal continuity in the unstable patient; reconstruction is delayed until reoperation following the completion of resuscitation. Biliary or pancreatic diversion is achieved by external tube drainage. Most injuries to the head of the pancreas can be managed by suture ligation of bleeding and packing. Severe injuries involving the ampulla can be managed by delayed pancreaticoduodenectomy.7 The pylorus, pancreatic neck, and proximal jejunum are stapled and divided, the common bile duct is ligated, and biliary drainage is achieved by tube cholecystostomy.

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plastic sheet placed over the bowel extending beneath the abdominal wall lateral to the wound edges. A surgical towel is placed over the drape to the wound edges over which two 10-mm suction drains are placed so that they exit the dressing superiorly. The abdomen is then covered with an adhesive surgical barrier (Ioban, 3M Corp.) to include the wound and surrounding skin. The drains are placed to wall suction to control draining abdominal fluid. The advantages of this closure are the rapidity with which it can be placed and the avoidance of suture damage to the skin edges.

Arteries Larger arteries in the abdomen can often be repaired rapidly by lateral suture. Repair should always be attempted for injuries involving the aorta and the superior mesenteric, proper hepatic, and iliac arteries. When the artery is transected, distal perfusion can be preserved using intraluminal shunts. Placement occurs after achieving proximal and distal control of the injured vessel. The type of shunt used depends on the diameter of the injured artery. A critical step in shunt placement is securing the shunt within the vessel lumen; ligatures securing the shunt should be placed around uninjured segments of artery. Systemic heparinization is usually contraindicated because of bleeding from other injuries, but may be initiated in the SICU when resuscitation is complete and coagulopathy is resolved.

Veins Ligation is the treatment of choice for venous injuries of the abdomen in the unstable patient. Ligation of the inferior vena cava, portal vein, superior mesenteric vein, and iliac veins is appropriate when the alternative is exsanguination. Ligation of the infrarenal vena cava and iliac veins may result in lower extremity venous hypertension, and prompt lower extremity fasciotomy should be considered. Ligation of the superior mesenteric and portal vein results in dramatic but transient bowel edema and requires aggressive fluid loading according to atrial filling pressures.

Wound Closure Because the abdominal compartment syndrome can develop in the damage-control situation, the abdominal incision should not be closed. Damage control situations often result in significant bowel edema or require extensive abdominal packing. Many techniques of temporary abdominal closure using synthetic material have been described. The goal is to provide a tension-free closure that protects but does not irritate the bowel while accommodating the increased abdominal volume. We have adopted an abdominal closure using a fenestrated clear

Key Points 1. Make a big incision. 2. Extend the incision to a median sternotomy or laterally into the chest when more exposure is required. 3. Do not delay left medial visceral rotation for suspected injuries to the suprarenal aorta or its primary branches. 4. Apply a Pringle clamp early to control major bleeding from the liver. 5. Identify the common bile duct, common hepatic duct, and portal vein before dissecting the gastrohepatic ligament. 6. Divide the neck of the pancreas to expose the superior mesenteric and portal vein. 7. Do not circumferentially dissect the aorta, inferior vena cava, or the iliac vessels.

Extremities Exposure The principles of managing vascular emergencies are based on achieving proximal and distal control of the lesion and repair if possible or bypass when necessary. Immediate control is achieved by direct pressure over a bleeding wound or proximal control point. Inclusion of proximal and distal control points in the sterile field allows rapid control of life-threatening hemorrhage while direct pressure is applied to the wound. Tourniquets occlude collateral blood supply and should be used rarely. The uninjured lower extremity should be prepped in case autogenous vein grafts are required for vascular repairs. Although vascular emergencies often call for rapid exposure and restoration of limb perfusion, the procedure must be done carefully with proper vascular technique. Blind clamping may cause injury to adjacent nerves and should be avoided. Heparin should be used routinely unless contraindicated, and completion angiography

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should be performed unless normal palpable pulses are reestablished. The most significant risk factor for limb loss following injury is failed revascularization.8

Upper Extremity The axillary artery is divided into three parts, the first extends from the first rib to the medial boarder of the pectoralis minor muscle, the second part lies under the pectoralis minor muscle, and the third extends from the lateral boarder of the pectoralis minor muscle distally. The axillary artery is approached through an incision 2 cm inferior and parallel to the clavicle centered over the deltopectoral triangle. The incision is extended laterally over the deltopectoral groove, which contains the cephalic vein that enters the subclavian vein at the deltopectoral triangle. The intramuscular groove between the pectoralis major and deltoid muscles is separated along the entire course of the wound. The pectoralis minor muscle is then divided below the coracoid process exposing the underlying neurovascular bundle. The axillary artery is most superficial at the deltopectoral triangle just medial to the coracoid process. The artery lies superior and deep to the axillary vein, which is retracted inferiorly. The nerves and brachial plexus lie deep to the first part of the axillary artery and must be identified to prevent clamp injury. Division of the pectoralis major muscle from its clavicular insertion can enhance exposure. The branches of the axillary artery are preserved because they provide collateral blood flow to the arm. The distal axillary and proximal brachial arteries are approached by extension of the incision over the lateral boarder of the pectoralis major muscle, following the course of the brachial artery in the grove between the biceps and triceps muscles. Separation of these muscles exposes the neurovascular bundle along its entire course to the bicipital aponeurosis. The distal brachial artery is approached through an S incision at the antecubital fossa with the proximal extension positioned medially. The basilic vein is retracted medially, and the bicipital aponeurosis is divided to expose the median nerve and brachial artery. Isolation of the artery requires division of the flanking veins and communicating branches. Following the artery distally most easily identifies the brachial bifurcation. The ulnar artery passes medially deep to the pronator teres muscle. Isolation of the forearm arteries more distal to the brachial bifurcation requires distal counter incisions.

Lower Extremity The common femoral artery begins at the inguinal ligament as a continuation of the external iliac artery. The artery is approached through a longitudinal incision over the femoral vessels such that the superior third of the incision is above the groin crease (Figure 4.15). The fascia

Figure 4.15. Approaches to the superficial femoral artery. Proximal exposure is achieved through an incision above the sartorius muscle, and distal exposure is achieved through an incision below the sartorius. Exposure of the distal profunda femoris artery is achieved through a medial incision and approach between the vastus medialis and adductor longus muscles. (Reprinted with permission of Elsevier from Rutherford RB, Atlas of Vascular Surgery. Philadelphia: WB Saunders, 1993.)

lata is opened inferior to the sartorius muscle and the femoral sheath exposed and opened. Care must be taken to avoid injury to the common femoral vein located medially. The profunda femoral artery arises laterally 3 to 5 cm distal to the inguinal ligament about the level at which the greater saphenous vein joins the common femoral vein. If more proximal control is needed, the incision is extended superiorly and laterally toward the anterior superior iliac spine with division of the inguinal ligament. Exposure of the distal superficial femoral artery is accomplished by extending the incision along the superior border of the sartorius muscle, which is retracted medially. This exposes the entire superficial femoral artery to the adductor hiatus.


Anterior tibial a.

Soleus m. Gastrocnemius m.

Figure 44.16. 16 Exposure E off th the popliteal lit l artery t b by di division i i off th the tibial attachments of the soleus and division of the tendons of the semitendinosus, gracilis, and sartorius muscles. (Reprinted with permission from Wind GG, Valentine RJ. Anatomic Exposures in Vascular Surgery. Baltimore: Williams & Wilkins, 1991.)

The popliteal artery is divided into three anatomic segments, the suprageniculate, midpopliteal, and infrageniculate. Medial approaches to the suprageniculate and infrageniculate sections provide rapid proximal and distal control to the popliteal artery and allow extension to expose the midpopliteal artery. The medial approach to the suprageniculate popliteal artery is through an incision positioned along the groove between the vastus medialis and sartorius muscles. The fascia over the sartorius is incised and the muscle retracted posteriorly. The adductor magnus tendon is separated from the semimembranous muscle to expose the popliteal vessels as they enter the adductor canal. The adductor magnus tendon can be divided to enhance exposure. The vein located laterally to the artery at this point may be paired and contains several bridging veins that must be divided to expose the artery. The collateral geniculate arteries should be preserved whenever possible to preserve collateral blood flow. Extension of the incision over the medial knee and division of the sartorius, semimembranous, semitendinosus, and gracilis muscles and the medial head of the gastrocnemius muscle exposes the midpopliteal artery (Figure 4.16). If divided, these muscles should be tagged with suture to facilitate reapproximation at the conclusion of the case. The infrageniculate popliteal artery is approached through a longitudinal incision of the medial leg 1 cm posterior to the tibia from the medial tibial condyle inferiorly over the proximal third of the leg. The saphenous vein is located in this area and should be preserved. The fascia posterior to the tibia is divided superiorly to the

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insertion of the semitendinosus muscle and the gastrocnemius muscle retracted posteriorly. Division of the muscle attachments of the medial knee allows more proximal exposure as described earlier. Division of the tibial attachments of the soleus allows additional exposure. The popliteal vessels can usually be seen in the depths of the wound at this point, although the distal extent may be covered by the tibial attachments of the soleus muscle, which can be divided as necessary. The popliteal veins are paired at this level with numerous bridging veins that must be divided to provide adequate exposure of the artery. The anterior tibial artery passes through the interosseus membrane between the tibia and fibula. More distal exposure of this artery requires a separate incision through the anterior compartment of the leg. The tibioperoneal trunk and posterior tibial artery are exposed by distal extension of the soleus incision along the posterior surface of the tibia.

Fasciotomy Forearm fasciotomy is performed through a volar incision that begins medial to the biceps tendon proximal to the elbow crease and extends toward the radial side of the arm following the medial boarder of the brachioradialis and continuing across the palm to the thenar crease (Figure 4.17). The fascia over the superficial flexor compartment is opened proximal to the elbow and extended distally across the carpel tunnel into the palm. The superficial radial nerve, radial artery, and brachial radialis are retracted laterally and the underlying muscles of the deep flexor compartment decompressed individually. Decompression of the deep flexor compartment is critical because forearm compartment syndromes most often affect this muscle group. If necessary, the dorsal forearm is decompressed through a straight incision beginning at the lateral epicondyle that extends to the midline of the wrist. Decompression of the quadriceps compartment is accomplished through an anterolateral incision over the length of the thigh. The ileotibial band and fascia overlying the vastus lateralis is divided along its length. The two-incision, four-compartment fasciotomy of the lower leg is performed through a medial incision positioned just posterior to the tibia and a lateral incision positioned just anterior to the fibula (Figure 4.18). The positions of the greater saphenous vein medially and peroneal nerve laterally must be considered when making the fasciotomy incisions. It is essential that all four compartments in the leg be released; thus the incisions should be long enough to afford complete longitudinal incision over the underlying compartments. The superficial posterior compartment is released through the medial incision by dividing the fascia between the tibia and

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D.J. Ciesla and E.E. Moore Median nerve Volar compartment

Radial nerve Mobile wad

Superficial flexors Ulnar nerve

Radius Anterior interosseus nerve Dorsal compartment

Ulna

Deep flexors

Figure 44.17. 17 Forearm fasciotomy. fasciotomy A volar incision is made from the antecubital fossa to the mid palm with division of the transverse carpal ligament. The superficial and deep flexor compartments are then opened. (Reprinted with permission from Champion HR, Robbs JV, Trunkey DD. Rob and Smith’s Operative Surgery, 4th ed. Trauma Surgery, Parts 1 and 2. London: Butterworths, 1989.)

gastrocnemius. The deep posterior compartment is released by detaching the soleus muscle from the tibia, taking care not to injure the popliteal neurovascular bundle. The anterior and lateral compartments are released through the lateral incision centered between the tibia and fibula. The anterior intermuscular septum is identified by transverse incision over the two compartments. Two fasciotomy incisions are then made, one anterior and one posterior to the intermuscular septum along the length of the compartments. Fasciotomy wounds are left open and dressed with application of bulky dressings. Local wound care and wet to dry dressings are applied on postoperative day 1. Primary wound closure is often possible, but splitthickness skin grafts may be required when ischemiareperfusion–induced edema is significant or in crush injuries with extensive tissue destruction.

Damage Control When faced with surgical emergencies involving the extremities, one must always remember to preserve first the life and then the limb. In extreme circumstances, amputation may be the only option available to prevent death. When amputation is not possible, the dead extremity is packed in ice until the patient can tolerate the procedure. Examples include severe metabolic derangement resulting from reperfusion of an ischemic extremity, extensive necrotizing soft tissue infection, multisystem injuries with progressive shock, coagulopathy, and acidosis. Life-threatening hemorrhage from extremity injuries can usually be controlled by direct pressure, proximal and distal control of the bleeding vessel, or balloon catheter tamponade. Simple arterial or venous ligation is also a viable option when the physiologic condition of the patient will not allow definitive vascular repair. Distal perfusion can also be maintained during resuscitation by the use of intraluminal shunts.9 Fracture stabilization is an important component in the treatment of complex extremity injuries. As with complex vascular injuries, definitive fracture fixation is often impossible because of the patient’s physiologic state. The principles of damage control have been extended to orthopedic trauma.10,11 Rapid external fixation of long bone and pelvic fractures can be accomplished in the emergency department, intensive care unit, and operating room. For multiply injured patients with femur fractures, damage-control orthopedic surgery minimizes the additional surgical impact induced by acute femoral stabilization.12

Key Points 1. Extend the inguinal incision across the inguinal ligament. 2. The profunda femoral artery arises on the lateral aspect of the common femoral artery. 3. Retract the sartorius anteriorly for proximal superficial femoral artery control and posteriorly for distal superficial femoral artery control. 4. Divide the semimembranous, semitendinosus, and sartorius muscles to expose the popliteal artery. 5. For combined injuries, place an arterial shunt first, repair the vein and then the artery, and perform a fasciotomy. 6. Use external skeletal fixation in the unstable patient.


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Towards fibular head

Anterior fasciotomy

Peroneus longus muscle Anterior intermuscular septum Tibialis anterior muscle

Lateral fasciotomy

Superficial peroneal nerve

Towards lateral malleolus

Superficial peroneal nerve

A

B

Superficial posterior fasciotomy

Deep posterior fasciotomy

Tibia Saphenous nerve and vein

Opened under soleus bridge Intermuscular septum

To medial malleolus

C Figure 44.18. 18 Four-compartment leg fasciotomy fasciotomy. (A) An incision is made 2 cm lateral to the tibia over the anterior intermuscular septum. (B) The anterior and lateral compartments are released by incision medial and lateral to the intermuscular septum while preserving the superficial peroneal nerve. (C) The superficial and deep posterior compartments are approached through an incision in the medial leg posterior to the saphenous vein. The intermuscular septum between the superficial

D and deep compartments is identified by a transverse incision incision. (D) The superficial compartment is decompressed by opening the fascia over the gastrocnemius muscles followed by decompression of the deep compartment by opening the soleus fascia. The fascial incisions must extend the entire length of the compartment. (A–D, reprinted with permission from Champion HR, Robbs JV,Trunkey DD. Rob and Smith’s Operative Surgery, 4th ed. Trauma Surgery, Parts 1 and 2. London: Butterworths, 1989.)

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Critique With the abrupt onset of the patient’s symptomatology, a perforated hollow viscus is the likely etiology. The 24-hour delay in definitive management has complicated this situation because this patient is now septic. Because the specific etiology is not known, the patient should be taken to the operating room and a midline, vertical incision (celiotomy) made to obtain the optimal exposure for the necessary exploration. This patient has secondary peritonitis, and there is no need for either intensive care unit monitoring or diagnostic evaluations in remote radiologic suites. Surgical intervention is the only option. Answer (A)

References 1. Moore EE, Burch JM, Franciose RJ, Offner PJ, Biffl WL. Staged physiologic restoration and damage control surgery. World J Surg 1998; 22:1184–1190; discussion 1190–1191. 2. Firoozmand E, Velmahos GC. Extending damage-control principles to the neck. J Trauma 2000; 48:541–543. 3. Cothren C, Moore EE, Biffl WL, Franciose RJ, Offner PJ, Burch JM. Lung-sparing techniques are associated with improved outcome compared with anatomic resection for severe lung injuries. J Trauma 2002; 53:483–487.

4. Wall MJ, Jr, Hirshberg A, Mattox KL. Pulmonary tractotomy with selective vascular ligation for penetrating injuries to the lung. Am J Surg 1994; 168:665–669. 5. Wall MJ, Jr, Villavicencio RT, Miller CC, 3rd, et al. Pulmonary tractotomy as an abbreviated thoracotomy technique. J Trauma 1998; 45:1015–1023. 6. Van Vyve EL, Reynaert MS, Lengele BG, Pringot JT, Otte JB, Kestens PJ. Retroperitoneal laparostomy: a surgical treatment of pancreatic abscesses after an acute necrotizing pancreatitis. Surgery 1992; 111:369–375. 7. Eastlick L, Fogler RJ, Shaftan GW. Pancreaticoduodenectomy for trauma: delayed reconstruction: a case report. J Trauma 1990; 30:503–505. 8. Hafez HM, Woolgar J, Robbs JV. Lower extremity arterial injury: results of 550 cases and review of risk factors associated with limb loss. J Vasc Surg 2001; 33:1212–1219. 9. Porter JM, Ivatury RR, Nassoura ZE. Extending the horizons of “damage control” in unstable trauma patients beyond the abdomen and gastrointestinal tract. J Trauma 1997; 42:559–561. 10. Scalea TM, Boswell SA, Scott JD, Mitchell KA, Kramer ME, Pollak AN. External fixation as a bridge to intramedullary nailing for patients with multiple injuries and with femur fractures: damage control orthopedics. J Trauma 2000; 48:613–621; discussion 621–623. 11. Pape HC, Giannoudis P, Krettek C. The timing of fracture treatment in polytrauma patients: relevance of damage control orthopedic surgery. Am J Surg 2002; 183:622–629. 12. Pape HC, Grimme K, Van Griensven M, et al. Impact of intramedullary instrumentation versus damage control for femoral fractures on immunoinflammatory parameters: prospective randomized analysis by the EPOFF Study Group. J Trauma 2003; 55:7–13.

5 The Perioperative Management of the Acute Care Surgical Patient Craig M. Coopersmith and Timothy G. Buchman

Case Scenario In an apneic 70-year-man who is recovering in the intensive care unit after a protracted operative intervention 3 days ago, you notice that his ventilatory management is highlighted as follows: (A) (B) (C) (D) (E)

Volume-cycle ventilation FiO2 is 60% PEEP is 15 cm H2O Pressure support Endotracheal suctioning

Which of the above is the least appropriate?

Successful management of the acute care surgical patient requires comprehensive and complex physiologic monitoring and adaptive intervention that typically spans at least three venues: the emergency department, the operating room, and the intensive care unit. Coordinated care of the patient by emergency medicine physicians, anesthesiologists, and intensivists is as important in obtaining a favorable outcome as the judgment and skill of the operator. The purpose of this chapter is to frame a strategy for perioperative care of the acute care surgical patient in the intensive care unit. The point of view of this chapter is that of the intensivist, who has geographic responsibility for care of multiple patients in the intensive care unit yet must integrate effectively with the other venues that affect each acute care surgical patient in order to achieve optimal outcomes. It is common that the emergency surgeon plays the role of intensivist in the preand postoperative phases of care. The use of the phrase “monitoring and adaptive intervention” and the allusion to a temporal sequence that brings the patient through multiple venues of care is not casual. It is intended to remind all caregivers that the

physiologic response to stress—irrespective of whether the stress is traumatic, pathologic, or therapeutic (the stress of surgery)—has its own dynamics. The purpose of monitoring the patient is not to facilitate titration to a particular endpoint but rather to verify that the patient is on a safe physiologic trajectory. The purpose of adaptive intervention is not to make physiologic parameters “normal” but rather to ensure that care processes favor timely recovery.

A Perspective on Stress and Response With rare exception, the indication for acute care surgery is a stressful event that triggers (and frequently overwhelms) compensatory mechanisms. Whatever the event—an obstructed loop of bowel, rupture of an abdominal aortic aneurysm, a juxtadiaphragmatic gunshot—there is a sequential and tripartite response. The three response phases are felicitously labeled with imperatives: escape, survive, and recover. The escape phase invariably begins before medical intervention. The sympathetic nervous system is activated, releasing preformed epinephrine and norepinephrine that redirect blood flow toward vital organs (and limit hemorrhage when the stress involves bleeding). The release of cortisol initiates the process of metabolic reprogramming, mobilizing carbohydrate stores for immediate tissue use. Pain itself is attenuated. The teleologic explanation is to permit a traumatically injured animal to escape. What is important is not the teleology but rather the consequences that can confound initial evaluation. First, tachycardia, a relatively normal blood pressure, and a narrowed pulse pressure are frequent initial findings. Second, transient modest hyperglycemia (and consequent osmotic diuresis) may be physiologic but also deceptive—the patient appears to have adequate nutrients and hydration available. Third, pain is often obscured. In aggregate, the patient can initially appear to

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be better than the actual physiology. The importance of serial examination, especially of patients who appear to be relatively well, cannot be gainsaid.

Preoperative Care of the Acute Care Surgical Patient Following Initial Resuscitation Acute care surgical operations may be immediate (e.g., abdominal gunshot wound with deep hypotension) or may follow an interval aimed at investigation (e.g., computed tomography scan of a tender abdominal mass) or may follow an attempt at nonoperative management (e.g., nasogastric suction to relieve a small bowel obstruction). Patients undergoing investigations and nonoperative management often receive care in the intensive care unit before operation. For this reason, initial resuscitation is operationally defined as that care required to transport the patient out of the emergency department irrespective of destination. Initial resuscitations that provide stability sufficient for transport are essential but often incomplete, and the intensive care unit often receives partially resuscitated patients who may require urgent or even emergent surgery. Another common scenario is the inpatient who acutely deteriorates. The deterioration may be a complication of a prior operation (such as an anastomotic dehiscence or fascial dehiscence and evisceration). The deterioration may follow failed nonoperative management (such as “conservative” management of a splenic laceration with delayed hemorrhage). Although some limited resuscitation may occur on the wards, the intensivist is often called on to continue the resuscitation while the operating room is prepared. These scenarios and sequences are important because the intensivist plays a pivotal role in advancing the completeness of the resuscitation and the readiness for operation. The frequent tension between “too sick to operate on” (i.e., needs further resuscitation) and “too sick not to operate on” (i.e., should be in the operating room now) is best addressed by rapid and systematic evaluation and intervention with specific attention to operative readiness and to projection of possible outcomes, including complications.

Physiologic Reassessment and the Second Phase of the Stress Response The importance of serial reevaluation cannot be overemphasized.The most important reason to revisit the patient and the data is to evaluate the physiologic trajectory. That evaluation is grounded in familiarity with what happens

C.M. Coopersmith and T.G. Buchman

to the physiology of stress following the escape phase, when survival becomes the priority. Two major physiologic mechanisms—secretion of catecholamines and secretion of cortisol—persist, and global metabolic activity falls while blood is shunted away from nonessential tissues.1 Temperature normally falls, so the “mildly febrile” patient is often “more inflamed”— more septic—than the absolute temperature suggests. Anorexia is common as internal nutrient consumption falls. Pain, discomfort, and general misery are prominent, and activity declines. In the absence of intravenous fluids, thirst is a common symptom. This period is decidedly hypometabolic—in its initial descriptions, this survival phase was called an “ebb” phase.2 More than any other time in the clinical course, it is essential to inquire whether the patient perceives himself or herself to be “better, worse, or the same” since the prior examination. Patients who state that they are “the same”—as miserable as they were before receiving the ordinary interventions of intravenous fluids and pain medications that characterize initial care—are in fact becoming physiologically worse. These patients who are not responding to symptomatic management generally require accelerated evaluation and earlier definitive care.

Preoperative Actions In this section, we assume that a diagnosis has been established, initial resuscitation is at least in progress, and plans have been made to take the patient to the operating room. Several preoperative actions have substantial effects on perioperative care, particularly if they are overlooked or omitted.

Relevant History The urgency of acute care surgery often causes some elements of the history to go unasked or unanswered. Other elements are, in our experience, essential to safe perioperative management. These include the following: • A complete list of current medications and food supplements. Lists can be obtained from patient, family, personal physician, pharmacy, or other health care agencies. The frequency with which important medications (such as thyroid replacement, corticosteroids, insulin, antiseizure agents) are omitted is matched by the failure to ascertain intake of over-the-counter drugs (such as antacids and salicylates) and diet supplements that contain highly active compounds. Although this information may have no bearing on the operation, it has great bearing on the perioperative period.

5. Perioperative Management

• Social history, with specific attention to alcohol consumption. Alcohol remains the most widely used drug to (self)-treat anxiety and depression, and unrecognized alcohol withdrawal syndromes are quite common. Because this may be the last time the patient will be awake enough to answer questions about substance use, it is imperative that the question be asked straightforwardly and answered accurately. • Focused systems review. The focus should be on common postoperative complications. For example, asking about headaches is much less informative than asking about transient neurologic impairment that may not appear on physical examination. Whether the patient has ever had chest pain is probably less important than whether they have had arrhythmias or sustained a myocardial infarction. Whether the legs have ever had swelling is less important than whether the patient has ever had a deep venous thrombosis or pulmonary embolism. And so on. • Functional status and reserve assessment. This is the most frequently overlooked aspect of the history that impacts perioperative care. Inquiry should be made about the patient’s performance status just before the illness that is precipitating operation. Typical questions include exercise tolerance (e.g., climbing stairs and walking); assistance with activities of daily life (e.g., bathing and eating); and recovery time from recent illnesses such as a common cold. Verbatim descriptions of functional status are often more helpful than standard scales such as the New York Heart Association (NYHA) level, but both should be ascertained if at all possible.3 • Advance directives, including appointment of a personal representative. Many patients coming to acute care surgery are older and/or have little physiologic reserve. They should be advised that there may be some period—brief or prolonged—during the postoperative period that they may be too sleepy or weak to communicate reliably with medical staff. Even if the patient has not executed a legal document appointing a personal representative to make decisions when the patient is unable, identifying the patient’s preferred surrogate in the medical record is often key to subsequent care. Similarly, it is always appropriate to ask whether the patient has advance directives and, if so, who has copies of the documents. It is a myth that patients and families are unduly frightened by this question: those who do not have directives will say so, and those who have prepared advance directives want the medical team to know about them.4

Pre-Illness Physiology Acute care patients have physiology that is deranged from their ordinary status. Whether the usual (ordinary)

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status of a particular patient is “textbook normal” is another matter. It is therefore important to solicit whatever information is available about the patient’s usual physiology—heart rate, blood pressure, breathing patterns (including use of home oxygen and external supports), temperature, weight, and physical activity. Recent electrocardiograms and blood studies are also helpful to understand the patient’s physiology. As the population ages and acquires chronic illnesses such as diabetes mellitus, hypertension, and other cardiac and pulmonary diseases, individual parameters frequently change. For example, older obese patients with hypertension often are poorly controlled and “normally” run mean arterial pressures 20 torr or more above textbook values. They may require higher pressures to adequately perfuse vital viscera, and overzealous correction in the postoperative period can prolong and worsen the clinical course. Recent values are often known to patient and family; if not, records from the personal physician can (and should) be obtained.

Specific Signs and Symptoms Surgical cases are usually undertaken emergently because there is immediate threat to life or limb. In many cases, the threat is some form of circulatory shock— hypovolemic, cardiogenic, or septic. Whereas the signs of hypovolemia are familiar, readily recognized by the surgeon and usually treated aggressively upon recognition, and whereas cardiogenic shock usually is identified and managed intraoperatively by the anesthesia team, the severity of sepsis is commonly obscured by survival stress responses, and therefore the physiologic impact is underappreciated by both surgeon and anesthesiologist. Failure to identify and aggressively treat sepsis in the preoperative and intraoperative phases of acute care surgical care can significantly prolong perioperative care and worsen outcomes. The following items should be considered during the preoperative evaluation of the patient: • Is the mental status normal for this patient? Because the emergency surgeon usually has not encountered the patient before the preoperative evaluation, family and friends accompanying the patient (or other medical staff if the patient has been under medical care before consultation) should be consulted. Although hypoxia and hypoglycemia can cause altered mental status in acute care patients, sepsis is the more common cause of acute but mild mental status changes, assuming other parameters of perfusion (heart rate, blood pressure) are near normal. • Is the patient tachypneic? Unless the patient has hypoxemia relative to his or her normal state, perhaps the most common cause for tachypnea in an acute care surgical patient is early sepsis. Other possibilities

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•

•

• •

•


include subclinical pulmonary embolism and diminished tidal volumes caused by pain or weakness. Is there mild jaundice? The picture is usually cholestatic. Scleral icterus may be hard to recognize, but a glance at the urine collecting in the urimeter often suggests that pigment is being spilled. Are the digits grey and cool? Acrocyanosis is a process, not an event. It begins with microvascular thrombosis that can be observed in fingers and toes. This is a manifestation of disseminated intravascular coagulation and can be one of the earliest signs of sepsis in patients with underlying microvascular disease, such as diabetes. Is there mild hyperglycemia? This often occurs just before the appearance of full-blown sepsis. Is there lactic acidemia? Small increases are common in early sepsis and signal mismatch between oxygen delivery and oxygen supply. High values (above 7 mmol/L) suggest (intraabdominal) catastrophe. Does the hemogram show an unexpectedly low value for platelets or absolute lymphocyte numbers? Both megakaryocytes and lymphocytes appear exquisitely sensitive to sepsis. Because many patients have had a complete blood count in the recent past, comparisons are often easy, and a decline in platelet count, absolute lymphocyte count, or both suggests sepsis in the appropriate clinical context.

The reason that the recognition of sepsis is important in the preoperative phase is that early, goal-directed resuscitation has been shown to improve outcome, and both the emergency surgeon and anesthesiologist should plan their care accordingly. Immediate administration of appropriately broad spectrum antimicrobial treatment is necessary but by itself insufficient. Adequate restoration of the erythron, timely use of sympathomimetic amines, and resuscitation to oxygen extraction goals (typically an SvO2 >70%) must occur in parallel with acute care operation. Delaying resuscitation until arrival in the intensive care unit appears to result in sicker patients with prolonged recovery and worse outcomes, in both our hands and others’.5

Discussion of Perioperative Care Environments Acute care surgery is associated with an unpredictable intraoperative course. Although most patients can have acute problems corrected and transfer to the general ward, a significant minority will require postoperative transfer to an intensive care unit. Advising the patient and family preoperatively that this is a common and even routine precautionary measure following acute care surgery will allow intensive care unit admission to be a reassurance as opposed to an unwelcome surprise.

Actions in the Operating Room The acute care surgeon is properly concerned with providing the least risky operation that will set the stage for healing and recovery. Implementation of this “least risky” philosophy has led to several important advances, such as the damage-control laparotomy,6 the open abdomen approach,7 and planned second-look procedures,8 discussed elsewhere in this book. With each of these approaches, the acute care surgeon acknowledges the therapeutic complementation of intensive care unit resuscitation and operative correction. A “least risky” approach also includes anticipating the types of supports that may be needed for prolonged perioperative care in the intensive care unit and providing the safest types of those supports. Considerations in the operating room should include the following: • For patients who are undergoing emergency celiotomy, consideration should be given to placement of transabdominal enteral feeding access and, if appropriate, gastric decompression. Perioperative malnutrition is a common and vexing problem that translates into long intensive care unit stays, long ventilator runs, and increased complication rates (e.g., infection).9 Although nasal gastric and small bowel catheters can be used to supply nourishment to many patients, they are uncomfortable and predispose to complications of their own, such as sinusitis and reflux/aspirationrelated pulmonary infections. Surgical placement of a gastric tube with a small intestinal extension usually requires only a couple of extra minutes in the operating room but can allow for early and precise feeding while minimizing risks associated with gastroparesis and associated reflux. • For all emergency patients, consideration should be given to early placement of a tracheostomy. Here, preoperative functional status can serve as an important guide to anticipating the need for prolonged mechanical ventilation. Patients who are dependent on home ventilatory supports (such as home oxygen or bilevel positive airway pressure [BiPAP]) and patients who are NYHA class IV and require major acute care surgery have a high probability of requiring prolonged ventilatory support. Tracheostomy facilitates many aspects of perioperative respiratory care in the intensive care unit and is often more comfortable for the patient, reducing agitation and thus simplifying sedation regimens as well. The above should not be construed as endorsement of indiscriminate performance of tracheostomy for the average acute care surgical patient but rather as recommendation for earliest possible placement of a tracheostomy where placement seems so likely as to be inevitable.


• Replacement of potentially contaminated vascular cannulae. Acute care surgical patients often require initial resuscitation under less than ideal conditions. This can lead to breaks in aseptic technique during insertion and maintenance of peripheral and central venous cannulae and of arterial cannulae. At the conclusion of an acute care surgical procedure, the various indwelling catheters should be inventoried and assessed for possible contamination. The exigency of the clinical situation may well preclude immediate replacement, but whenever possible critically ill acute care surgical patients should be given the benefit of properly aseptic cannulae.

Preparation of the Intensive Care Unit and its Team for Receipt of a Preoperative Patient With increasing frequency (owing to the severity of illness, the ageing population, and the difficulties in finding an available operating room), the intensive care unit is notified by the emergency department that an acute care surgical patient requires ongoing resuscitation in the intensive care unit before operation. Safe transfer requires preparedness of the intensive care unit, which in turn requires specific communications. A minimum checklist includes the following: 1. Patient identifiers: name, date of birth, medical record number. 2. Illness leading to acute intensive care unit admission. This is more often descriptive than diagnostic, as in “distended abdomen and short of breath.” An accurate description is nevertheless vital to care, because, although it could represent anything from a visceral perforation with pneumoperitoneum to acute intraabdominal hemorrhage, it points to the systems that are perceived to be most acutely compromised. 3. Life supports already in place. These may include ordinary endotracheal tubes and vasoactive infusions but may also include more exotic supports, such as GardnerWells tongs for patients who have sustained cervical spine trauma, high-frequency oscillating ventilators, and continuous venovenous filtration apparatus. 4. Monitors already in place. These may include bladder catheters and arterial and central venous catheters. 5. Timing of operation if known or planned. This is often omitted from the initial communication, yet essential—if the patient will spend only 30 minutes in the intensive care unit before operation, priorities are often altered and personnel often need to be redeployed to focus on immediate needs.

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6. Known allergies. Although the general drug list can await the patient’s arrival, knowing and apprising the team of any drug allergies can prevent serious complications. 7. Current vital signs, including temperature and pulse oximetry data. Several preparations should be routinely made in anticipation of the arrival of an acute care surgical patient. Unless the patient is febrile, the room should be warmed. Whether the patient is intubated or not, an airway management kit and ventilator should be immediately available. At least one bag of a balanced salt solution (normal saline or lactated Ringer’s) should be available: often there is an acute need to infuse fluids and administer critical drugs (paralytics, sedatives, vasoconstrictors) as the patient arrives in the intensive care unit. If the patient is hypovolemic, a rapid infusor should be prepared. The blood bank should be contacted by the intensive care unit team before the patient’s arrival in order to determine whether a current blood specimen is available and, if so, what products have been made available for the patient. (It is insufficient to ask the staff of the emergency department or ward about blood products in readiness: they will report what they believe has been requested of the blood bank, not what is actually available.)

The Hand-Off The intensive care unit team has two immediate tasks: (1) continue the resuscitation and (2) prepare the patient for operation. Often, both tasks must be accomplished concurrently and within a very short interval. Thus, it is important for all members of the intensive care unit team to remain focused on the tasks and to assume responsibilities that are complementary and not duplicative. Limiting the number of caregivers in the intensive care unit cubicle to those with assigned tasks is an important first step. We prefer to limit this number to five: the intensivist at the head of the bed; a respiratory therapist prepared to adjust the ventilator and (if necessary) assist with an emergency intubation; a nurse to tend to the monitoring needs of the patient; a nurse to tend to the treatment needs of the patient; and a scribe to enter the data onto the (paper or electronic) flow sheet. The transporting team bringing the patient to the intensive care unit is asked to help transfer (if necessary) the patient to the intensive care unit bed and then to step outside the cubicle so that the intensive care unit team can accomplish its tasks. Patients frequently become unstable during transport. It is therefore important to assess the basics of airway, ventilation, and perfusion immediately upon arrival. An awake patient who, in response to a question, can

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identify himself or herself by voice has all three. Sedated and intubated patients must be immediately investigated by palpation of a pulse, a pulse oximetry signal, and verification that carbon dioxide is being exhaled. Verification of the presence of end-tidal CO2 is strong evidence that the patient has both ventilation and perfusion.11 For this reason, the CO2 monitor is connected even before application of electrocardiographic leads and monitoring. Provided that the patient is ventilating and perfusing, the seven items in the prearrival checklist should be reviewed next. Once these items are complete and there is understanding of the timing of the operation, the intensive care unit team should focus on the acute illness in the context of the patient’s chronic health status. The duration and severity of the present illness are often reflected in the acute physiologic derangements. The chronic health status, including the roster of medications and treatments (the latter commonly including respiratory treatments such as BiPAP and renal treatments such as dialysis), provides insight into the extent to which current physiology represents a departure from normal. For example, a patient who is maintained on three antihypertensive drugs probably is inadequately resuscitated at a “normal” blood pressure of 120/80 torr. Finally, the complete record of resuscitative medications and treatments and the patient’s responses should be reviewed.All of the above can usually be accomplished in about 3 minutes.

Ongoing Care in Anticipation of Operation Almost as soon as the hand-off is complete, preparations must be made to transport the patient to the operating room. There is substantial risk that, unless attention is focused on the goals of resuscitation to minimize operative risk, some aspects of the patient’s physiology can deteriorate through inattention. The single most useful tool to prevent inattention in this phase of care is to set explicit goals to be attained and maintained, with equally explicit statements for how these goals are to be achieved. For example, it is inadequate to simply state, “give the patient a fluid challenge.” It is necessary to state, “administer 500 mL normal saline over 15 minutes, and report the effect of that challenge on heart rate, blood pressure, central venous pressure, and urine output over the subsequent 30 minutes.” By explicitly listing the goals, the surgeon and intensivist can agree on the resuscitative endpoints. The intensivist should then identify and state the strategies to achieve these goals.

Postoperative Intensive Care This section is organized into two intercalated parts. One describes the third phase of the stress response (recovery), and the other focuses on specific actions that must


be taken at the bedside to minimize the risk that the patient falls off the recovery trajectory. This section is intended to be taken as a whole.

The Third Phase of the Stress Response To recover from critical illness and the surgery required to control the source of that illness, local and remote tissues must be lysed and rebuilt. The plural “tissues” is used deliberately as a reminder that both high-turnover tissues (such as leukocytes) and slower turnover tissues (such as gut mucosa) and even very slow turnover tissues (such as lean muscle) are involved in these processes. It is the superposition of these processes that gives rise to fairly predictable dynamics and energetics.12 Early in the recovery phase, the patient remains deeply catabolic, mobilizing the building blocks necessary for repair. The clinical correlate is the appearance of nitrogen and potassium in the plasma, which are used for protein and cell assembly, respectively. Utilization of these moieties is less efficient than mobilization, and therefore they appear in urine waste. Generally this phase lasts about 4 days, provided that the emergency was readily controlled (e.g., simple appendicitis managed by appendectomy). The first transition during the recovery phase is marked by more efficient use of potassium. Although nitrogen wastage continues, potassium losses in the urine return close to the patient’s baseline. The endocrine correlate is the diminution of plasma levels of cortisol toward normal levels. This phase lasts about 3 days. The second transition during recovery is marked by regain of control over nitrogen losses. The patient remains hypermetabolic—mild fever and tachycardia are still the norm. However, tissue repair accelerates, intestinal transit becomes normal, and the patient usually is well enough to be fully liberated from hospital supports (fluids, devices, incident-specific drugs) and plans made for discharge. It takes about 3 weeks for repair of the acutely injured tissue. The third and generally final transition of the recovery phase involves rebuilding both lean muscle mass and fat stores. This lasts about 1 month. In aggregate, recovery from surgical emergencies is typically a 2-month process. Depending on the chronic health status of the patient before the emergency, and the nature of the surgical emergency, this third phase of the stress response can be accelerated or delayed. Regardless, the three transitions must occur for recovery to continue to completion. When recovery stalls, there has typically been a failure to complete one of the three necessary transitions. Recognizing the transition failure as early as possible, creating a differential of possible causes, and removing whatever roadblock exists is essential to safe recovery.


To recognize transition failures, one must become conversant with the neuroendocrine events that are regulating the dynamics of tissue responses. Numbered and bolded are key ideas that illuminate milestones and problem points in the response to stress: 1. Adrenocorticotropic hormone (ACTH). The escape phase initiates central nervous system (CNS) coordination of the stress response.13 Paraventricular neurons in the hypothalamus secrete corticotrophin-releasing hormone (CRH), thus initiating activation of the hypothalamic-pituitary-adrenal axis (HPA). The CRH arrives at the anterior pituitary gland to stimulate the secretion of ACTH from corticotrophic cells. Secretion of ACTH can be further upregulated by arginine vaopressin; however vasopressin has no intrinsic ACTH-releasing activity. Adrenocorticotropic hormone is not preformed. Rather, it is released proteolytically from a precursor molecule, proopiomelanocortin (POMC). (Another cleavage product of POMC is beta-endorphin, which is likely responsible, at least in part, for the blunted pain perception during the escape phase.) Once the ACTH reaches the general circulation and is transported to the adrenal cortex, it stimulates the latter to produce glucocorticoids, mineralocorticoids, and adrenal androgens. Collectively, ACTH levels are reserved and augmented early in acute stress. When they decline, it is because glucocorticoids—mostly cortisol—provide negative feedback to both the hypothalamus and the pituitary. 2. Glucocorticoids. These molecules have many effects. Skeletal muscle breaks down when they are in excess. Glucocorticoids modulate the stress response at the molecular level in at least three ways, ultimately inhibiting function of proinflammatory cytokines.14 Glucocorticoids also affect growth and thyroid and reproductive functions in the context of acute stress. Their initial effects also promote secretion of growth hormone, suppress gonadotropin secretion (GnRH), and inhibit gonadal tissue. Although these effects might appear partially counterproductive (e.g., lysis of lean muscle) in the context of perioperative care, it must be constantly borne in mind that the stress response evolved to promote recovery following minor or moderate injury versus survival of major life threats. 3. Autonomic nervous system (ANS). While the HPA axis is marshalling the endocrine system, the peripheral autonomic system is also being activated. Because sympathetic (versus parasympathetic) activation is dominant early in the stress response, “sympathetic nervous system” (SNS) and “ANS” are often used synonymously. The stress causes rapid release of the catecholamines epinephrine and norepinephrine from the adrenal medulla into blood. This rise in catecholamine content is responsible for tachycardia and narrowed pulse pressure (via vasoconstriction and elevated diastolic pressure) that is

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often seen following stress. However, the ANS does much more than merely mobilize catecholamines from stores. Efferent cholinergic preganglionic fibers project out from the interomediolateral column of the spinal cord to synapse in the sympathetic ganglia with projections to the smooth muscle of the vasculature, heart, gut, kidney, striated muscle, and fat. Autonomic nervous system function demonstrates dynamic compensation in the perioperative period.15 4. Somatotropin (growth hormone). Growth hormone (GH) comes from the pituitary gland. There are two hypothalamic regulators: a releasing hormone (GnRH) and an inhibitory hormone (somatostatin). Stress causes an initial rise in the average level of GH. Perhaps more important is a fundamental difference from the normal state—GH is continuously detectable. (In the normal unstressed state, GH is undetectable except for a couple of large amplitude diurnal pulses that last no more that a couple of hours.) The downstream effector of GH is principally insulin-like growth factor-1 (IGF-1), which instructs tissue to grow and divide. Insulin-like growth factor-1 is often measured in lieu of GH, because the former does not fluctuate nearly as much as GH itself and in fact can uncouple from GH under catabolic conditions. 5. Aggregate effect. The three axes—HPA, SNS, and somatotropin—are activated in concert at the onset of stress. Collectively, these affect nearly every bodily function, including—but not limited to—arousal, cardiac performance, vascular tone, ventilation, respiration, and urine production. 6. Metabolic disequilibria. The aggregate stress response also rebalances metabolic pathways. The key feature is mobilization of fuels for immediate use. The key hormone is glucagon, which is released as part of the ANS activation. Released from the pancreatic A cells, glucagons acts to raise blood glucose three ways: activation of lipolysis, glycogenolysis, and gluconeogenesis. Glucagon does not act alone—catecholamines and glucocorticoids assist with lipolysis; glucocorticoids assist with gluconeogenesis; and epinephrine triggers breakdown of glycogen. The one hormone that is involved with all three paths to mobilize sugar and free fatty acid for immediate use is glucagon.17 7. Oxidation. The fuels mentioned in the last section are not merely mobilized, they are oxidized in great quantity. This oxidation produces both carbon dioxide and heat, and the latter manifest as fever. Production of carbon dioxide nevertheless lags behind the prodigious oxygen consumption, with typical respiratory quotients of 0.7 for fat and 0.8 for carbohydrate.18 The fact that the respiratory quotient is 50% TBSA)

1.00–1.25 ¥ BEE 1.25–1.5 ¥ BEE 1.5 ¥ BEE 1.75–2.0 ¥ BEE

Approximate caloric requirement Kcal/kg/day 25–30 30–35 30–35 35–40

Protein gm/kg/day

NPC : N*

1.0–1.2 1.4–1.5 1.4–1.8 1.8–2.0

150 : 1 120 : 1 90–120 : 1 80–100 : 1

BEE – Basal Energy Expenditure; NPC : N – Non protein calorie to nitrogen ratio; TBSA – Total body surface area; *6.25 gm of protein = 1 gm of nitrogen

Example: Consider a 5 ft 6 in tall, 60-year-old male weighing 65 kg, who is undergoing emergency laparotomy for perforated viscus. Step I: Based on the Harris-Benedict equation, his BEE = 1353 kcal which is 21 kcal/kg/day. Step II: Multiplied with a stress factor of 1.5 his estimated caloric needs = 2030 kcal which is 31 kcal/kg/day. Step III: Protein requirement of 1.5 g/kg/day = 98 g/day NPC : N = 120 : 1

Figure 77.3. 3 Calculating the caloric and protein needs of surgisurgi cal patients. Step I: Calculate the basal energy expenditure using the Harris-Benedict equation. Step II: Based on patient’s condition, multiply the BEE with a stress factor to derive the total

caloric needs needs. Step III: Multiply the recommended protein (g/kg) for each subgroup of patient population with the patient’s weight to derive the total protein required/day.

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M. Senthil, B. Rupani, J.H. Jabush, and E.A. Deitch

been estimated, protein requirements are determined. This can be done in a number ways. For example, the amount of protein can be based on a specific nonprotein calorie to nitrogen ratio, on body weight, or by estimating protein needs as being 15% to 20% of total calories. Whether one uses a nonprotein to calorie ratio of 100 : 1, grams of proteins/kg, or 15% to 20% of total calories as protein, one gets very similar results, as shown by the following clinical example. Consider a 5 ft 6 in tall, 60-year-old male weighing 65 kg who is undergoing acute care laparotomy for a perforated viscus. Based on the Harris-Benedict equation, his BEE would be 1,353 kcal. His estimated caloric needs would be about 2,030 kcal if his calculated BEE is multiplied with a stress factor of 1.5. If 20% of his nutrition support regimen consisted of protein calories (406 kcal), he would receive about 101 g of protein or 16 g of nitrogen and 1,624 nonprotein calories (25 kcal/kg). This would be equivalent to 1.5 g protein/kg body weight and a nonprotein calorie to nitrogen ratio of approximately 100 : 1. Overfeeding during critical illness may actually be more hazardous than underfeeding in some circumstances (Table 7.1). This idea is supported by the fact that overfed animals have a higher mortality rate and an increased susceptibility to infection than underfed or normally nourished animals. Additionally, in a study of postoperative patients, overfeeding of parenteral carbohydrate (manifest as a respiratory quotient >0.95) was associated with a significantly higher incidence of septic complications and mortality than a similar group of patients whose respiratory quotient was 10

IED = 89† Standard = 87†

p < 0.001* Decreased in IED (8% vs. 22%) p = 0.01

p < 0.001 NS (18.1 vs. 17.7 days)

ICU, intensive care unit; IED, immune-enhancing diet; LOS, length of stay; NS, not statistically significant; PRCT, prospective randomized controlled trial. * Decrease in infection was significant only in elective surgical patients, not in critically ill. † Enteral nutrition started within 36 hours of diagnosis of sepsis.

7. Nutritional Support

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Although there was no statistically significant beneficial effect on mortality, the patients fed the immuneenhancing diets had a significant reduction in the rate of infection, days on the ventilator, and hospital stay. Additionally, a recently published prospective randomized multicenter clinical trial has shown that the administration of an immune-enhancing diet resulted in a significant reduction in mortality as well as in the infection rate in septic intensive care unit patients.39 Based on these studies, it appears that all intensive care unit patients as well as significantly stressed patients should receive a high-protein enteral diet, with the use of immune-enhancing diets being reserved for those patients who are septic or at highest risk of becoming septic (Figure 7.4). The timing of the initiation of enteral feeding may also be important. There are several reasons to believe that a policy of immediate/early enteral feeding will be superior to delayed enteral feeding, even though only limited amounts of enterally administered nutrients may be absorbed during the first few days after insult. This concept is based on the observation that even short periods of starvation or TPN use can lead to atrophy of gut tissue out of proportion to that seen in other organs and that intraluminal nutrients play a major role in the maintenance of gut structure and function. Furthermore, clinically, the transition to an oral diet after a period of TPN or prolonged starvation is often associated with diarrhea and malabsorption, which is believed to be a

direct result of mucosal atrophy. This diarrheal state, by impairing the ability of the patient to tolerate enteral feeding, may result in further limitation of enteral intake and thus promote further mucosal atrophy. Therefore, it is easy to visualize a potential cycle where starvation or TPN, by causing mucosal atrophy, predisposes to malabsorption and diarrhea and thereby impairs the ability of the patient to tolerate subsequent enteral feedings. In fact, a recent prospective randomized clinical trial documented that early enteral nutrition, started within 6 hours of injury and shock, reduced the incidence of organ failure and largely prevented injury-induced increases in gut permeability when compared with patients whose enteral feedings were begun 24 or more hours postinjury.40 Although there is experimental and some clinical evidence that early enteral feeding is beneficial,8,27,40 especially if begun shortly after injury, early enteral feeding is only now beginning to gain more widespread clinical acceptance. This reluctance to institute enteral feedings until after the acute injury phase is over and gastrointestinal function has returned to normal is related largely to the fear that immediate feeding will result in a higher rate of complications than delayed feeding, such as aspiration of gastric contents. Based on studies in burn and trauma patients,27,40 this fear seems to be largely unfounded. Although there have been a few case reports of very early enteral (jejunostomy) feeding being associated with intestinal ischemia in underresuscitated trauma

Enteral Feeding Formulas

Standard isotonic Formula ± Fiber

High protein formulas ± Fiber

Iso – osmotic (300 mosm) Non protein calorie to nitrogen ratio of 150 : 1 Caloric Density 1.0 kcal/ml

Iso or hyperosmolar >450 mosm) NPC : N ratio < 120 : 1 Caloric Density 1.3-2.0 kcal/ml

For use in stable and minimally stressed patients

To avoid protein energy malnutrition

For use in moderately stressed and in most ICU patients

To limit muscle wasting

Figure 7.4. Categories of enteral feeding formulas: major categories of enteral formulas and their compositions, indications, and uses for specific patient populations. BCAA, branched

Immune enhancing formulas

Similar to high protein formulas but with BCAA, glutamine, arginine, omega-3 fatty acids and nucleotides. NPC : N < 100 : 1 Caloric Density – 1.0 kcal/ml

For use in septic, major trauma and highest risk ICU patients

To limit muscle wasting plus improve immune and organ functions

chain amino acids; ICU, intensive care unit; NPC : N ratio, nonprotein calorie to nitrogen ratio.

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patients, the incidence of this complication is significantly less than 1%, and, in a recent review of the literature on this issue, the authors found a similar incidence of bowel necrosis in nonenterally fed high-risk patients.41 Nonetheless, it appears prudent to establish hemodynamic stability and ensure that the patient is out of shock before the initiation of enteral feeding. On the other hand, clinical experience with patients suggests that enteral feeding after an episode of hypotension may prevent or reduce the extent of small bowel ischemia.40,42 Having decided to use enteral nutrition and having established which category of enteral formula to use for a specific patient (see Figure 7.4), it is now time to determine whether the patient should be fed into the stomach or the jejunum. Despite the rhetoric and debate over whether intragastric or postpyloric feeding is superior, in most cases this is a dealer’s choice. Because of convenience, we believe that intragastric feedings should be attempted in most patients and if tolerated then continued. The advantages of intragastric feeding are that hyperosmolar as well as isoosmolar solutions can be administered and bolus feedings can be given. In contrast, hyperosmolar jejunal feedings are not as well tolerated and are more likely to cause distension, cramping, and diarrhea than gastric feedings. Additionally, a continuous feeding regimen must be used with the jejunal administration of nutrients. The main disadvantage of intragastric feeding is the risk of aspiration and the failure to administer adequate nutritional support in patients with gastric ileus. Whether feeding into the stomach or the jejunum, a similar nutrient administration strategy can be applied. Feedings are started at a rate of 25 to 30 mL/hr and advanced slowly over the next 36 to 72 hours to meet caloric and nutrient goals. If gastric bolus feeding is used, then approximately 100 mL of the enteral formula is given and the nasogastric tube is clamped. Gastric residuals are then measured 4 hours later just before the next scheduled bolus feeding.As long as the gastric residuals remains less than 100 to 150 mL, the next bolus feeding is given, the tube clamped, and the process continued. The strategy of measuring gastric residuals every 4 hours should also be used when continuous intragastric feedings are administered to decrease the risk of the patient developing high gastric residuals and hence the increased possibility of pulmonary aspiration. During the initiation and early days of enteral feeding, the patient should be monitored closely for signs of feeding intolerance, such as distension, diarrhea, cramping, or increased gastric residuals. In some patients with borderline gastric ileus, the use of prokinetic agents or erythromycin may be helpful. For patients who have nasogastric or nasojejunal tubes and who are likely to require prolonged enteral nutrition (>30 days), the tubes should be replaced with a feeding gastrostomy or jejunostomy for patient comfort and for


ease of nutrient administration. For most patients, placement of a percutaneous gastrostomy is preferred over a jejunostomy, because operative jejunostomies have a low but significant complication rate of 2% to 3%,43,44 and they are more difficult to use and maintain than gastrostomies. Additional details on feeding tube–related complications as well as the management of specific side effects of enteral feeding are well covered in several recent reviews.44,45

Nutrient Pharmacology Nutrient pharmacology is based on the concept that specific nutrients and growth factors can improve the clinical outcome of critically ill patients by functioning as organ- and tissue-specific fuels or stimulants. In this capacity, these specific nutrients and growth factors support the physiologic function and repair of certain organs and tissues as well as augment the immune system and promote wound healing. These factors include the specific nutrients added to the immune-enhancing diets as well as anabolic agents. Research in this area has been intense, because even immune-enhancing nutritional diets are only partially capable of reversing stress, sepsis, or injury-induced hypercatabolism or ameliorating impaired tissue repair processes and immune as well as organ dysfunction. One novel area of research involves the use of hormones to improve wound healing, improve immune function, and support organ function in addition to limiting the hypermetabolic response. This approach was thought likely to be ultimately successful based on initial clinical studies performed in the mid-1990s showing that growth hormone (GH) accelerates wound healing46 and insulinlike growth factor-1 (IGF-1) may preserve lean body mass47 in patients with major burns. Since then, both GH and IGF-1 have been shown to limit muscle wasting and promote anabolism in a large number of patient populations, including patients who sustained mechanical or thermal trauma as well as those with sepsis, with pancreatitis, or undergoing major gastrointestinal operations.48,49 Because IGF-1 appears to be the mediator of the anabolic effects of GH, the risk of side effects (especially hyperglycemia) is higher with GH, and GH resistance has been documented in septic patients, IGF-1 is a conceptually more attractive candidate hormone than GH. Furthermore, IGF-1 has been shown to limit catabolism as well as gut atrophy and bacterial translocation, indicating that it may be useful in preserving gut function as well as muscle mass. Further concerns were raised about the safety of GH by a recent large prospective randomized trial showing that septic patients and patients with MODS who were randomized to the high-dose GH arm of the study had higher morbidity and mortality rates.50


Like IGF-1, other hormones, such as bombesin,51 neurotensin,52 epidermal growth factor,53 and even basic fibroblast growth factor,54 have also been shown to have beneficial effects on gut structure and function, illustrating the concept that the gut response to dietary manipulations and injury can be hormonally modulated. Vitamin and mineral supplementation are also areas of intense investigation, because these substances have been found to exert a number of important protective effects. Collectively they are called “micronutrients,” as they are found in extremely small amounts in the body. Micronutrients play a key role in cellular function and are critical for wound healing, antioxidant production, and immune function. For example, vitamins C and E are important nutrient antioxidants, vitamins A and C are important in wound healing, and vitamins A, D, C, and E as well as zinc and selenium are important in wound healing. Other potentially beneficial effects of micronutrients and antioxidants are being continuously uncovered. For example, three clinical trials of critically ill surgical patients, two of which were prospective randomized clinical trials, showed that early splanchnic-directed antioxidant therapy was effective in decreasing organ failure and shortening intensive care unit stays.55–57 These studies were based in large part on the idea that splanchnic blood flow is decreased after injury or during shock, resulting in the subsequent development of ischemia-reperfusion–mediated gut injury and inflammation. Although frequently overlooked, deficiencies of specific trace minerals, such as copper, selenium, zinc, and chromium, can result in impaired wound healing, depressed cellular immunity, and augmented oxidantmediated tissue damage. Thus, each of these minerals is briefly discussed. The critical nature of these trace minerals is based on their key roles as cofactors in important cellular pathways and defenses. For example, copper is a cofactor for a number of key enzymes, such as superoxide dismutase, cytochrome C oxidase, and lysyl oxidase, and thus is involved in antioxidant defenses, metabolism, and wound healing. The recommended dose of copper is 1.5 to 3 mg/day for critically ill patients.58 Like copper, selenium also plays a key role in antioxidant defenses, as it is an integral part of the antioxidant enzyme glutathione peroxidase.59 Selenium deficiency has been reported with acute illness.60 low oral intake,61 malnutrition,62 and long-term TPN use.63 Once established, selenium deficiency is associated with oxidant-induced disorders such as cardiomyopathy63 and myositis.64 At present, the recommended dose of selenium for critically ill patients is 100 μg/day. Chromium in its organically complex form, also know as “glucose tolerance factor,” potentiates the action of insulin on carbohydrate and lipid metabolism, thereby fostering an anabolic state.65 Chromium deficiency has been reported with long-term TPN use and is associated

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with the development of new-onset hyperglycemia.66 The recommended dose of chromium is 50 to 200 μg/day, but higher doses might be needed for hypermetabolic patients. Zinc is an essential nutrient for rapidly proliferating cells because it is an integral component of DNA and RNA polymerase. Additionally, zinc is a key cofactor of superoxide dismutase and thus is an important component of the body’s antioxidant defenses and is also required for optimal wound healing.67,68 Finally, not only is zinc deficiency relatively common in critically ill patients but it also has been documented to lead to impaired cellular immunity.69 The recommended zinc dose for critically ill patients is 25 mg/day. Most enteral formulas provide the recommended daily doses of these essential micronutrients; however, patients receiving long-term TPN would require intravenous supplementation to avoid deficiency. Avoiding a deficiency of micronutrients in critically ill patients is vital in decreasing complications and promoting positive outcomes. On the other hand, although a decrease in circulating iron is a constant feature of major injuries70 and was once thought to be an abnormality requiring correction, there is abundant evidence documenting that hypoferremia is actually an important part of the host’s immune antibacterial defenses.71 That is, because microorganisms require iron for cell replication and multiple metabolic functions, the hypoferremic response to injury appears to be a protective response that aids the host by decreasing the availability of iron for use by invading microorganisms. Studies documenting that iron replacement therapy increases the risk of severe infections as well as mortality in both human and animal studies confirm the protective effects of hypoferremia against infection. Consequently, because iron replacement therapy for stressed patients predisposes to infectious complications and deaths, iron replacement therapy is not indicated. In summary, a highly sophisticated “nutrient pharmacology” appears to be evolving, based on which specific nutrients will be given or withheld in order to modulate specific physiologic processes.

Anabolic Agents Despite the fact that optimal nutritional regimens decrease the rate of catabolism, limit muscle wasting, and improve immune function and wound healing, nutritional support alone is not sufficient to completely limit muscle wasting or compensate for the increased catabolic response observed in septic or severely stressed patients. Consequently, the strategy of using anabolic agents in concert with high-protein diets has been employed to further limit muscle wasting. Anabolic agents tested

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include growth hormone and IGF-1 (discussed in the previous section on nutrient pharmacology) as well as testosterone, testosterone analogs, oxandralone, insulin, and most recently the beta-blocker propanolol. Testosterone and testosterone analogues are not considered here, because they have a significant risk of causing hepatotoxicity, can have masculinizing effects, and have been found to be less effective in limiting muscle wasting than other agents. Emphasis on the other anabolic agents is appropriate. Oxandralone is an oral synthetic testosterone analog that has minimal virilizing activity and little hepatotoxicity when compared to testosterone. Several prospective controlled trials have shown that oxandralone combined with a high-protein diet increases lean body mass and limits muscle protein wasting in acute and rehabilitating burn patients by increased protein synthesis.72,73 It has also been used successfully in a variety of catabolic populations, including people with hepatitis and acquired immunodeficiency syndrome wasting myopathy.74,75 More recently, a prospective randomized controlled trial with burn patients showed that oxandralone increases constitutive proteins such as albumin, prealbumin, and retinolbinding protein and reduces acute-phase protein levels.76 When compared with human growth hormone or testosterone, the advantages of oxandralone are that it is orally administered, cost effective with comparable and/or better anabolic effect, and less toxic.77–79 Although the data are limited and most studies showing efficacy in acutely hypercatabolic patients were performed with burn patients, because of its favorable risk-benefit ratio, there is much to recommend the use of oxandralone for the high-risk surgical patient. In fact, oxandralone is approved by the FDA for use as an anabolic agent in trauma and severely stressed patients. The dose of oxandralone is 20 mg/day given as two 10-mg oral doses, and it can be safely administered by mouth or via a nasogastric tube. Because of its well-documented beneficial effects on restoring lost muscle mass during the recovery and rehabilitation phases, oxandrolone should be continued until muscle mass is largely restored in patients who have had prolonged episodes of hypercatabolism and lost significant muscle mass. Insulin, apart from its effect on blood glucose, also appears to have anabolic effects by increasing skeletal muscle glucose uptake and net protein synthesis.80 This anabolic effect of insulin was initially reported using a very high dose of continuous insulin infusion (mean of 32 U/hr) for severely burned children. At this high dosage of insulin, concomitant glucose infusions were required to prevent significant hypoglycemic events. Since then, further studies with burned children have shown that doses of insulin as low as ∼5–10 U/hr are sufficient to promote muscle anabolism without the drawback of hypoglycemia associated with the higher dose insulin


regimen.81,82 Although insulin was given for up to 4 weeks in these studies and was found to limit muscle wasting in the early post-burn period and to promote positive nitrogen balance and reconstitution of lean muscle mass in the later stages of injury, there is almost no information on its effectiveness as an anabolic agent for non-burn patients or adults. This lack of data outside of the burn patient population makes its use for adult surgical patients problematic. On the other hand, the use of continuous insulin therapy to maintain tight plasma glucose control (80 to 110 mg/dL) has been recently shown in a prospective randomized controlled trial to reduce the mortality rate of ventilated surgical intensive care unit patients by almost 50%.17 Until more clinical data accrue on the effectiveness of insulin in various populations of high-risk surgical patients, its routine use cannot be unequivocally recommended. Another area of active research is the use of betablockers in attenuating the stress- or injury-induced hypermetabolic response. The rationale for the use of beta-blockers for hypermetabolic patients is based on the fact that catecholamines are increased severalfold after injury or during stress states, and they have been documented to significantly contribute to the hypercatabolic response as well as increased energy needs. Although the data on beta-blockers for patients with acute surgical illness are still very limited, two recent prospective randomized trials in severely burned children documented that propranolol attenuated the acute hypermetabolic response and reversed muscle protein catabolism by decreasing heart rate and resting energy expenditure as well as increasing muscle protein synthesis.83,84 In these studies, propanolol was administered at a dose sufficient to decrease the heart rate of these burned children by 15% to 20%. As for insulin, there are no studies with adult or non-burn patients testing propanolol as an anabolic agent. However, the ability of beta-blockade to reduce the mortality of patients with cardiovascular disease undergoing surgery is well established.85 In this second scenario, beta-blockade to a heart rate of 80 is thought to improve survival by limiting postoperative cardiac complications. For this reason, the use of betablockers, for at least certain subgroups of high-risk patients, appears beneficial. It is well recognized that hypercatabolism and muscle wasting is a serious consequence of sepsis, trauma, or severe stress states and that, once 10% to 15% of the muscle mass is lost, immune function decreases, wound healing is impaired, and the risk of nosocomial infections, especially pneumonia, is increased. Consequently, providing optimal nutritional support of the high-risk surgical patient is a priority. Accomplishing this goal requires a thorough knowledge of the metabolic response to injury and stress as well as recognition of the various nutritional options available.


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Critique Having been in the hospital for 9 days, this patient definitely needs nutritional support. Unfortunately, the enteral route (gastric or postpyloric) is the preferred conduit for nutrition; however, hemodynamic instability is a contraindication for enteral feeding. Because this patient requires pressor support, she cannot be considered hemodynamically stable. Therefore, the route for nutritional support, in this setting, is parenteral (central). Answer (A)

References 1. Long CL. Metabolic response to injury and illness: estimation of energy and protein needs from indirect calorimetry and nitrogen balance. J Parenter Enteral Nutr 1979; 3:452–456. 2. Hill AG, Hill GL. Metabolic response to severe injury. Br J Surg 1998; 85:884–890. 3. Bessey PQ, Watters JM, Aoke TT, et al. Combined hormonal infusion stimulates the metabolic response to injury. Ann Surg 1984; 200:264–281. 4. Aulick LH, Wroczyski FA, Coil JA, et al. Metabolic and thermoregulatory responses to burn wound colonization. J Trauma 1989; 29:478–483. 5. Deitch EA. Bacterial translocation of the gut flora. J Trauma 1990; 30:S184–S190. 6. Deitch EA. Multiple organ failure: pathophysiology and potential future therapies. Ann Surg 1992; 216:117–134. 7. Deitch EA, Xu DZ, Franko L, et al. Evidence favoring the role of the gut as a cytokine generating organ in rats subjected to hemorrhagic shock. Shock 1994; 1:141–146. 8. Deitch EA. Role of the gut lymphatic system in multiple organ failure. Curr Opin Crit Care 2001; 7:92–98. 9. Mainous MR, Block EF, Deitch EA. Nutritional support of the gut: how and why. New Horiz 1994; 2:193–201. 10. Hulsewe KWE, van Acker BAC, von Meyenfield MF, et al. Nutritional depletion and dietary manipulation: effects on the immune response. World J Surg 1999; 23:536–544. 11. Deitch EA. Infection in the compromised host. Surg Clin North Am 1988; 68:181–197. 12. Alexander JW, MacMillan BG, Stinnett JD, et al. Beneficial effects of aggressive feeding in severely burned children. Ann Surg 1980; 192:505–517. 13. Moore FA, Feliciano DV, Andrassy RJ, et al. Early enteral feeding, compared with parenteral, reduces postoperative septic complications: the results of a meta-analysis. Ann Surg 1992; 216:172–183. 14. Beale RJ, Bryg DJ, Bihari DJ. Immunonutrition in the critically ill: a systematic review of clinical outcome. Crit Care Med 1999; 27:2799–2805. 15. Jeejeebhoy KN. How should we monitor nutritional support: structure or function? New Horiz 1994; 2:131–138.

16. Burke JF, Wolfe RR, Mullany CS, et al. Glucose requirements following burn injury. Ann Surg 1979; 190:274–285. 17. Van Den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl J Med 2001; 345:1359–1367. 18. Greig PD, Elwyn DH, Askanazi J, et al. Parenteral nutrition in septic patients: effect of increasing nitrogen intake. Am J Clin Nutr 1987; 46:1040–1047. 19. Endres S, Ghorbani R, Kelly VE, et al. The effect of dietary supplementation with n-3 polyunsaturated fatty acids on the synthesis of interleukin-1 and tumor necrosis factor by mononuclear cells. N Engl J Med 1989; 320:265–271. 20. Nghia MV, Waycaster M, Acuff RV, et al. Effects of postoperative carbohydrate overfeeding.Am Surg 1987; 53:632– 635. 21. Campbell SM, Kudsk KA. “High tech” metabolic measurements: useful in daily clinical practice? J Parenter Enteral Nutr 1983; 12:610–612. 22. Klein S, Kinney J, Jeejeebhoy K, et al. Nutrition support in clinical practice: review of the published data and recommendations for future research directions. J Parenter Enteral Nutr 1977; 21:133–156. 23. Harris J, Benedict F. A Biometric Study of Basal Metabolism in Man. Washington, DC: Carnegie Institute, 1919. 24. Weissman C, Kemper M, Askanazi J, et al. Resting metabolic rate of the critically ill patient: measured versus predicted. J Anesthesiol 1986; 64:673–679. 25. Wilmore DW, Mason AD Jr, Johnson DW, et al. Effect of ambient temperature on heat production and heat loss in burn patients. J Appl Physiol 1975; 38:593–597. 26. Saito H, Trocki O, Alexander JW, et al. The effect of route of nutrient administration on the nutritional state, catabolic hormone secretion and gut mucosal integrity after burn injury. J Parenter Enteral Nutr 1987; 11:1–7. 27. McDonald WS, Sharpe CW Jr, Deitch EA. Immediate enteral feeding in burn patients is safe and effective. Ann Surg 1991; 213:177–183. 28. McGeer AJ, Detsky AS, O’Rourke K. Parenteral nutrition in cancer patients undergoing chemotherapy: a metaanalysis. Nutrition 1990; 6:233–2340. 29. The Veterans Affairs Total Parenteral Nutrition Cooperative Study Group: Perioperative total parenteral nutrition in surgical patients. N Engl J Med 1991; 325:525–532. 30. Herndon DN, Barrow RE, Stein M, et al. Increased mortality with intravenous supplemented feeding in severely burned patients. J Burn Care Rehabil 1989; 10:309–313. 31. Mochizuki H, Trocki O, Dominioni L, et al. Mechanism of prevention of postburn hypermetabolism and catabolism by early enteral feeding. Ann Surg 1984; 200:297–310. 32. Deitch EA, Sambol JT.The gut-origin hypothesis of MODS. In Deitch EA, Vincent JL, Windsor A, eds. Sepsis and Multiple Organ Dysfunction. Philadelphia: WB Saunders, 2002: 105–116. 33. Meyer J, Yurt RW, Duhaney R, et al. Differential neutrophil activation before and after endotoxin infusion in enterally versus parenterally fed human volunteers. Surg Gynecol Obstet 1988; 167:501–509. 34. Fong Y, Marano MA, Barber A, et al. Total parenteral nutrition and bowel rest modify the response to endotoxin in humans. Ann Surg 1989; 210:449–456.

104 35. Wilmore DW, Smith RJ, O’Dwyer ST, et al. The gut: a central organ after surgical stress. Surgery 1988; 104:917– 923. 36. Speath G, Berg RD, Specian RD, Deitch EA. Food without fiber promotes bacterial translocation from the gut. Surgery 1990; 108:240–247. 37. Alverdy JC, Aoys E, Moss GS. Total parenteral nutrition promotes bacterial translocation from the gut. Surgery 1988; 104:186–190. 38. Heyland DK, Novak, F, Drover, J et al. Should immunonutrition become routine in critically ill patients?: a systematic review of evidence. JAMA 2001; 286:944–953. 39. Galban C, Montejo JC, Mesejo A, et al. An immune enhancing enteral diet reduces mortality rate and episodes of bacteremia in septic intensive care unit patients. Crit Care Med 2000; 28:643–648. 40. Kompan L, Kremzar B, Gadzijev E, et al. Effects of early enteral nutrition on intestinal permeability and the development of multiple organ failure after multiple injury. Intensive Care Med 1999; 25:157–161. 41. Zaloga GP, Roberts PR, Marik P. Feeding the hemodynamically unstable patient: a critical evaluation of the evidence. Nutr Clin Pract 2003; 18:285–293. 42. McClave SA, Chang WK. Feeding the hypotensive patient: does enteral feeding precipitate or protect against ischemic bowel? Nutr Clin Pract 2003; 18:279–284. 43. Sarr MG. Appropriate use, complications and advantages demonstrated in 500 consecutive needle catheter jejunostomies. Br J Surg 1999; 86:557–561. 44. Tapia J, Murguia R, Garcia G, et al. Jejunostomy techniques, indications and complications. World J Surg 1999; 23:596– 602. 45. American Gastroenterological Association Medical Position Statement: guidelines for the use of enteral nutrition. Gastroenterology 1995; 108:1280–1301. 46. Gilpin DA, Barrow RE, Rutan RL, et al. Recombinant human growth hormone accelerates wound healing in children with large cutaneous burns.Ann Surg 1994; 220:19– 24. 47. Cioffi WG, Gore DC, Rue LW, et al. Insulin-like growth factor-1 lowers protein oxidation in patients with thermal injury. Ann Surg 1994; 220:310–316. 48. Wilmore DW. The use of growth hormone in severely ill patients. Adv Surg 1999; 33:261–274. 49. Gibson FAM, Hinds CJ. Growth hormone and insulin-like growth factors in critical illness. Intensive Care Med 1997; 23:369–378. 50. Takala J, Ruokonen E, Webster NR, et al. Increased mortality associated with growth hormone in critically ill adults. N Engl J Med 1999; 341:785–792. 51. Haskel Y, Xu D, Lu Q, et al. Elemental diet-induced bacterial translocation can be hormonally modulated. Ann Surg 1993; 217:634–642. 52. Evers BM, Izukura M, Townsend CM, et al. Neurotensin prevents intestinal mucosal hypoplasia in rats fed an elemental diet. Dig Dis Sci 1992; 37:426–431. 53. Jacobs DO, Evans DA, Mealy K, et al. Combined effects of glutamine and epidermal growth factor on the rat intestine. Surgery 1988; 104:358–364.

M. Senthil, B. Rupani, J.H. Jabush, and E.A. Deitch 54. Gianotti L, Alexander JW, Fukishima R, et al. Reduction of bacterial translocation with oral fibroblast growth factor and sucralfate. Am J Surg 1993; 165:195–200. 55. Barquist E, Kirton O, Windsor J, et al. The impact of antioxidant and splanchnic-directed therapy on persistent uncorrected gastric mucosal pH in the critically injured trauma patient. J Trauma 1998; 44:355–360. 56. Porter JM, Ivatoury RR, Azimuddin K, et al. Antioxidant therapy in the prevention of organ dysfunction syndrome and infectious complications after trauma: early results of a prospective randomized study. Am Surg 1999; 65:478– 483. 57. Nathens AB, Neff MJ, Jurkovich GJ, et al. Randomized, prospective trial of antioxidant supplementation in critically ill surgical patients. Ann Surg 2002; 236:814–822. 58. Demling RH, Debiasse MA. Micronutrients in critical illness. Crit Care Clin 1995; 11:651–673. 59. Rotruck J, Pope A, Ganther H, et al. Selenium: biochemical role as a component of glutathione peroxidase. Science 1979; 179:588–590. 60. Haeker F, Stewart P. Effects of acute illness on selenium homeostasis. Crit Care Med 1990; 18:442–449. 61. McKenzie RL, Rea HM, Thomson CD, et al. Selenium concentration and glutathione peroxidase activity in blood of New Zealand infants and children. Am J Clin Nutr 1978; 31:1413–1418. 62. Levine RJ, Olson RE. Blood selenium in Thai children with protein calorie malnutrition. Proc Soc Exp Biol Med 1970; 134:1030. 63. Fleming CR, Lie JT, Mc Call JT, et al. Selenium deficiency and fatal cardiomyopathy in a patient on home parenteral nutrition. Gastroenterology 1982; 83:689–693. 64. Brown MR, Cohen HJ, Lyons JM, et al. Proximal muscle weakness and selenium deficiency associated with long term parenteral nutrition. Am J Clin Nutr 1986; 43:549–554. 65. Anderson RA, Polansky MM, Bryden NA, et al. Supplemental–chromium effects on glucose, insulin, glucagon and urinary chromium losses in subjects consuming controlled low chromium diets. Am J Clin Nutr 1991; 54:909–916. 66. Brown RO, Forloines-Lynn S, Cross RE, et al. Chromium deficiency after long term parenteral nutrition. Dig Dis Sci 1986; 31:661–664. 67. Kohn S, Kohn D, Schiller D. Effect of zinc supplementation on epidermal Langerhans cells of elderly patients with decubitus ulcers. J Dermatol 2000; 27:258–263. 68. Rostan EF, DeBuys HV, Madey DL, et al. Evidence supporting zinc as an antioxidant for skin. Int J Dermatol 2002; 41:606–611. 69. Bogden JD. Influence of zinc on immunity in the elderly. J Nutr Health Aging 2004; 8:48–54. 70. Deitch EA, Sittig KM. A serial study of the erythropoietic response to thermal injury. Ann Surg 1993; 217:293–299. 71. Weinberg ED. Iron depletion: a defense against intracellular infection and neoplasia. Life Sci 1992; 50:1289–1297. 72. Demling RH, Desanti L. Oxandralone, an anabolic steroid, significantly increases the rate of weight gain in the recovery phase after major burns. J Trauma 1997; 43:47–51. 73. Wolf SE, Thomas SJ, Dasu MR, et al. Improved net protein balance, lean mass and gene expression changes with


74.

75. 76.

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78. 79.

oxandralone treatment in the severly burned. Ann Surg 2003; 237:801–811. Mendenhall CL, Moritz TE, Roselli GA, et al. A study of oral nutritional support with oxandralone in malnourished patients with alcoholic hepatitis: results of a Department of Veterans Affairs cooperative study. Hepatology 1993; 17:564–570. Berger J, Poll L, Hall C, et al. Oxandralone in AIDS wasting myopathy. AIDS 1996; 10:1657–1662. Thomas S, Wolf SE, Murphy KD, et al. The long term effect of oxandralone on hepatic acute phase proteins in severely burned children. J Trauma 2003; 56:37–44. Demling RH. Comparison of the anabolic effects and complications of human growth hormone and the testosterone analog, oxandralone, after severe burn injury. Burns 1999; 25:215–221. Fox M, Minor A, et al. Oxandralone: a potent anabolic steroid. J Clin Endocrinol Metab 1962; 22:921–923. Karim A, Ranney RE, Zagarella BA, et al. Oxandralone disposition and metabolism in man. Clin Pharmacol Ther 1973; 14:862–866.

105 80. Sakurai Y, Aarsland A, Herndon DN, et al. Stimulation of muscle protein synthesis by long- term insulin infusion in severely burned patients. Ann Surg 1995; 222:283– 297. 81. Ferrando AA, Chinkes DL, Wolf SE, et al. A submaximal dose of insulin promotes net skeletal muscle protein synthesis in patients with severe burns. Ann Surg 1999; 229:11– 18. 82. Thomas SJ, Morimato K, Herndon DN, et al. The effect of prolonged euglycemic hyperinsulinemia on lean body mass after severe burn. Surgery 2002; 132:341–347. 83. Herndon DN, Hart DW, Steven EW, et al. Reversal of catabolism by beta-blockade after severe burns. N Engl J Med 2001; 345:1223–1229. 84. Hart DW, Wolf SE, Chinkes DL, et al. B-blockade and growth hormone after burn. Ann Surg 2002; 236:450– 457. 85. Poldermans D, Boersma E, Bax JJ, et al. The effect of bisoprolol on perioperative mortality and myocardial infarction in high risk patients undergoing vascular surgery. N Engl J Med 1999; 341:1789–1794.

8 The Intensive Care Unit: The Next-Generation Operating Room Philip S. Barie, Soumitra R. Eachempati, and Jian Shou

Case Scenario A 39-year-old man is in his seventh day in the intensive care unit on ventilatory support (transoral– translaryngeal endotracheal intubation) after having acute care surgery for a ruptured abdominal aortic aneurysm. Although the patient has brain stem function and is hemodynamically stable, he is unresponsive to voice. The current ventilator settings are as follows: IMV = 12 breaths/min FiO2 = .40 PEEP = 5 cm H2O

PaO2 = 120 mmHg PCO2 = 37 mmHg pH = 7.39

The nurse notes that the patient has no spontaneous breathing and requires frequent suctioning. He has had recent temperature spikes. Chest x-ray demonstrates no atelectasis. Which of the following is the airway management of choice at this time? (A) Transnasal–translaryngeal endotracheal intubation (B) Continue transoral–translaryngeal endotracheal intubation (C) Percutaneous tracheostomy (D) Independent lung ventilation (E) Inverse: E ratio ventilation

For many reasons, the intensive care unit (ICU) is viewed increasingly as an OR itself, a bona fide, convenient alternative to scheduling a case in the main OR. The scope of surgical procedures that can be undertaken at the bedside is broad. For acute care surgical procedures or urgent procedures on critically ill patients who are too unstable for intrahospital transport to the OR, operating at the bedside is plausible. However, no matter how careful the planning or exigent the need, using the ICU cubicle as an OR has inherent limitations not easily overcome. The risks of intrahospital transport for most patients may be overstated. The patient may not be moved, but almost everyone and everything required to perform surgery in the ICU must be brought to the bedside. Space at the immediate bedside is constrained in almost all ICUs, and it may be difficult to place everything in the immediate vicinity. Importantly, infection control practices that are the standard of care in the OR cannot be replicated in the ICU. That which can be accomplished surgically in the ICU, effectively and safely, and under what conditions and constraints, is the subject of this review. Unfortunately, there is little Class I evidence in this subject area; therefore, much of this chapter is based by necessity on retrospective data and expert opinion.

Rationale Demands upon the operating room (OR) are a fixture of modern health care. Operating room time is expensive and scarce and is often allocated in advance in “blocks” to busy surgeons. Timely completion of the elective surgical schedule is important for prudent hospital fiscal management and also for patient and surgeon satisfaction. Surgical emergencies demand priority access to the OR and, because of their inherent unpredictability, are disruptive to the OR schedule. It can be difficult to schedule a nonemergency case on short notice.

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All things considered, operations should be performed in the OR. The modern OR has evolved to become a bastion of integrated special-purpose high technology. Integrated OR teams can support unstable critically ill or injured patients for protracted periods during complex operations in an environment where considerations of patient safety are paramount. Almost any pharmaceutical that can be administered in the ICU is available for administration in the OR. Inhalational anesthetics can be given, which is impossible elsewhere. Drugs to manage

8. The Next-Generation Operating Room

rare complications of anesthesia, such as malignant hyperthermia syndrome, are readily available only in the OR. Monitors and anesthesia ventilators are nearly as sophisticated as those used in ICUs. Overhead lighting is designed for the purpose. Room temperature can be controlled. A dropped instrument can be retrieved, cleaned, resterilized, and returned to the field within 5 minutes. Supplies or instruments not requested in advance are immediately at hand, minimizing costly delays. Yet operations are performed at the bedside, and increasingly often. The reasons are several. Some acute care operations cannot wait. Operating room time may not be available within a reasonable time frame; neither can some surgeons wait. Other procedures are sufficiently minor that mobilization to take the patient to the OR constitutes a waste of resources. The resources in personnel and portable monitoring equipment necessary for transport of the patient to the OR are substantial and often unjustifiable for performance of a brief, minor operation. However, every “road trip” must be assessed not only from as risk-benefit perspective but also from a costbenefit perspective.1 Those patients who should travel are those who must, and no others. Published guidelines2 for intrahospital transport indicate that, at a minimum, the ICU patient’s respiratory therapist and nurse should accompany the patient out of the ICU for the duration of the transport, but to do so might require juggling the ICU staff on the fly to accommodate the departure, or it might be impossible if the patient does not have one-to-one nursing (a rarity). Physician accompaniment is a poor substitute in that the physician is often a junior one with limited familiarity with the patient’s case and has limited skills for troubleshooting the myriad things that can go wrong with infusion pumps, intravenous tubing, and the like. However, the putative lack of safety of the intrahospital “road trip” is probably overstated. Szem et al. observed a cohort of critically ill, mechanically ventilated surgical patients on intrahospital transports and stratified the transports in terms of risk (number of vasoactive drugs infusing and use of therapeutic positive end-expiratory pressure [PEEP]). Transports were less common to the OR than to the radiology suite (where monitoring and support capabilities are often rudimentary in contrast to those available in the OR). Despite the high severity of illness and the high-risk nature of the most common destination, the incidence of transport-related mishaps was only 5%, all of which were minor (e.g., tangled intravenous tubing, low battery). Stevenson et al.4 noted that even the sickest ICU patient can be transported safely if risk and benefits are weighed carefully, patients are stabilized insofar as possible before the transport is undertaken, and monitoring is continuous throughout. All members of the transport team must be educated in patient evaluation; potential risks, complications, and

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interventions; and equipment operation and troubleshooting. All members of the transport team must understand their roles and responsibilities in detail and must communicate effectively. Written policies are useful to define the levels of personnel, training, and support and the equipment necessary for safe patient transport. The same can be said for the roles and responsibilities of the members of the operating team at the bedside. The issues with respect to intrahospital transport of critically ill children have also been examined.5 Transportation of critically ill children may be more hazardous than for adults. In a prospective observational study by Wallen et al.,5 only 24% of transports were uneventful. Physiologic perturbation occurred in 72% of transports, and an equipment-related mishap occurred in 10% of transports. At least one “major” intervention was required in 14% of transports (34% for mechanically ventilated patients vs. 10% for nonventilated patients); however, neither cardiac arrest nor death was observed. Notably, 11% of pediatric patients became hypothermic during the transport episode. Whereas both the intensity of pretransport of therapy (as measured by the Therapeutic Intensity Scoring System, TISS) and the duration of transport were independent risk factors for physiologic deterioration and the need for intervention, equipment malfunction was predicted only by the duration of transport.5

What Resources Are Needed? Preparation of the Unit and Staff First and foremost, the staff of the ICU must be familiar and comfortable with the use of the ICU as an OR.6 If the staff is experienced, the chance of procedure-related complications is much reduced. If the staff is not familiar with the roles and responsibilities they will be asked to assume in the ICU/OR, then an intensive, comprehensive educational program that addresses all common and many less common bedside operations must be implemented. The “learning curve” for physicians of the first few procedures might best be addressed by performing the operation in the OR under conditions that reproduce those expected to prevail in the ICU, but such precautions do not address the educational and training needs of the bedside nurse or respiratory therapist in the ICU. The operations performed at the bedside will vary from ICU to ICU based on the specialty orientation and case mix of the particular unit. An example of procedures performed in a trauma ICU is shown in Table 8.1.7 Among trauma patients, laparotomy in several guises was more common than either tracheostomy or access procedures for enteral feeding.7

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P.S. Barie, S.R. Eachempati, and J. Shou

Table 8.1. Scope of procedures performed at the bedside in the ICU at a level I trauma center. Laparotomy (in 13 patients) Irrigation after drainage of abscess Removal of packs Removal and replacement of packs Drainage of abscess Jejunostomy Tracheostomy Open Percutaneous Percutaneous endoscopic gastrostomy Fasciotomy, lower extremity

43 15 13 10 4 1 24 16 8 10 2

Source: Data from Porter et al.7

Detailed protocols that define roles and responsibilities, medications, monitoring equipment, disposable supplies, and surgical instruments to be needed for each procedure are desirable in part because most of what is required, including nursing services that exceed what the patient’s primary nurse can provide, will need to be brought to the bedside in advance of the procedure. All needed equipment (and reasonably anticipated needs) must be at the bedside before the start of the procedure. Unfortunately, such protocols probably exist in few ICUs. Communication is essential so that if additional nursing personnel will need to be at the bedside for the procedure, adequate coverage for the other patients is ensured. Particular consideration should also be given to whether an anesthesiologist or nurse anesthetist should be part of the bedside team for the procedure. Co-administration of a narcotic, a benzodiazepine, and a neuromuscular blocking agent may constitute full general anesthesia, depending on dosage; administration, monitoring, and available airway management skills must be equivalent in all practice venues. All patients must be monitored adequately, commensurate with the magnitude of the procedure. Continuous pulse oximetry, electrocardiograph tracing, and blood pressure measurement together represent a minimum standard for every procedure, no matter how minor. Invasive hemodynamic monitoring or end-tidal CO2 monitoring may be required for more complex undertakings.

Preparation of the Patient Informed consent must be obtained from the patient or the designated representative according to local norms unless the intervention is for an immediately life-threatening condition. Renal and hepatic function should be ascertained for proper dosing of medications (see below) (Table 8.2). The coagulation system should also be assessed to determine the risk of bleeding and the need to administer coagulation factors or platelets before surgery. It must be remembered that the platelet count

does not reflect platelet function and that conventional tests of platelet function are either unreliable (e.g., template bleeding time) or not immediately available (e.g., thromboelastography). Patients who have received aspirin or another nonsteroidal antiinflammatory agent should be considered for transfusion of platelets to “cover” the procedure, but specific guidelines do not exist. Patients with renal dysfunction (blood urea nitrogen concentration above ∼70 mg/dL) also have platelet dysfunction and can receive either cryoprecipitate or D,D-arginine vasopressin for short-term stabilization of platelet function. Enteral feedings should be held for up to 6 hours before the procedure unless it is very minor and positioning will not increase the risk of aspiration. Preoxygenation (with pure oxygen) of all patients for about 15 minutes before the procedure may also be beneficial.

A Culture of Safety and Accountability The hazards of accidental injury by sharps (e.g., needles, scalpel blades) and the risks of blood-borne transmission of etiologic agents are real. Policies and procedures have been changed in virtually every OR to minimize the risk, which fortunately has been decreasing.8 Overall annual percutaneous injury rates decreased from 21/100 beds to 16.5/100 beds between 1997 and 2001 in a nine-hospital midwestern U.S. hospital system whose facilities, urban and rural, ranged from 113 to 1,400 beds.8 Average annual injury rates were higher in large hospitals, but smaller hospitals had significantly higher proportions of injury in the emergency department, OR, and ICU (12.3% vs. 9.4% for the ICU setting). Intensive care units in teaching hospitals also had higher proportions of percutaneous injuries than did nonteaching hospitals (11.4% vs. 7.8%). In the OR, particular attention is paid to communication among team members, protocols for passing sharp instruments to and from the operative field and instrument table, and meticulous accounting of sharps throughout the operation. Similar attention to detail is mandatory if surgery at the bedside in the ICU will be made as safe as possible for the patient and the operating team. Sterile gowns, sterile double gloves, masks, caps, and eye protection should be used for any bedside procedure where the possibility exists of splashing blood or bodily fluids. In particular, accounting for the whereabouts of sharps at the bedside remains an issue in the authors’ estimation. The mattress must never be used as a “pincushion” for needles. The period of highest risk to practitioners appears to be during “clean up” in the aftermath of minor procedures, when the accounting process for sharps is informal and, indeed, often haphazard. When drapes are collected for disposal at the end of the procedure (usually by the person who performed the procedure, who may


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Table 8.2. The formulary for analgesia, anesthesia, and sedation in the ICU. Agent

Initial IV adult dose

Induction agents Etomidate

6 mg or more

Ketamine

1–2 mg/kg

Propofol

1.5–2.5 mg/kg

Thiopental

1–5 mg/kg

Intravenous sedatives/analgesics Midazolam 0.5–4 mg

Diazepam

2.5–5.0 mg

Lorazepam

1–4 mg

Morphine

2–10 mg

Hydromorphone

0.5–2.0 mg

Fentanyl

50–100 mcg

Meperidine

25–100 mg

Neuromuscular blocking agents Succinylcholine 0.75–1.5 mg/kg

Atracurium Cisatracurium

0.2–0.5 mg/kg 0.2–0.5 mg/kg

Mivacurium

0.15 mg/kg

Pancuronium

0.05–0.1 mg

Comments Maintains CO and BP. Reduces ICP but maintains CPP. Short T1/2; use infusion for maintenance. Possible adrenal suppression. Rapid-onset, short-duration agent for induction of anesthesia. Can be given by continuous infusion for maintenance and at lower dose for sedation without anesthesia. Transiently increases BP and HR. Raises ICP and intraocular pressure. Usually does not depress respiration. Crosses the placenta, but generally safe in pregnancy and for neonates and children. Concurrent narcotics or barbiturates may prolong recovery. Can cause anxiety, disorientation, dysphoria, and hallucinations, which may be reduced by a short-acting benzodiazepine during emergence. Atropine pretreatment is recommended to decrease secretions but may increase incidence of dysphoria. Hepatic metabolism. Provides no analgesia. Potent amnestic effect. Causes apnea and loss of gag reflex. Can cause marked low BP. Infuse at 0.05–0.3 mg/kg/min for prolonged sedation. Minimal accumulation (hepatic insufficiency) facilitates rapid elimination. Account for 1 kCal/mL (lipid infusion) in nutrition prescription. Use of same vial >12 hr associated with bacteremia. Safety for children still debated. Used rarely, now mostly for TBI management. Reduces BP and CPP. Accumulates with prolonged use or infusion, especially with hepatic insufficiency.

Short T1/2, but accumulates during infusion owing to active metabolites. Only benzodiazepine with potent amnestic effect. Can cause low BP and loss of airway. Primarily used for short-term sedation for ICU procedures. Renal elimination. Long T1/2 limits usefulness in ICU except rare cases when very long-term sedation is required. Terminates epileptiform activity effectively. Hepatic elimination. Effective anxiolytic. Preferred agent for continuous infusion of benzodiazepines (starting dose, 1 mg/hr). Can cause low BP, especially with hypovolemia, and paradoxical agitation. Hepatic elimination. Analgesic and sedative effects. Can cause low BP, CO, and apnea. Tolerance and withdrawal possible after long-term use. Can be given as IV infusion or by PCA for analgesia or to facilitate prolonged mechanical ventilation or withdrawal of care. Hepatic elimination. Hydrated ketone of morphine with similar use and risk profiles. Approximately eightfold more potent than morphine. Hepatic elimination. Approximately 50-fold potency compared with morphine, but less likely to cause low BP in appropriate dosage (less histamine release). Versatile for ICU use given IV or by epidural infusion or PCA. Less potent than local anesthetics for epidural analgesia or abrogation of surgical stress response. Can cause truncal rigidity and apnea with inability to ventilate by hand (use neuromuscular blockade to facilitate intubation in that setting). Hepatic elimination. Of little use in the ICU. Low doses cause postoperative shivering, which increases VO2 and HR. Accumulates even in mild renal insufficiency and can cause seizures. Contraindicated with monoamine oxidase inhibitors (hyperthermia, death).

Only depolarizing NBMA (occupies ACh receptor). Rapid onset, effect dissipates within 10 min of single dose. Causes hyperkalemia. Can precipitate malignant hyperthermia syndrome. Increases ICP and intraocular pressure. Contraindicated in TBI, spinal cord injury, neuromuscular disease, and burns. Metabolized by plasma cholinesterase, absence of enzyme (relatively common) causes prolonged paralysis. Short-acting, non-depolarizing NMBAs (competitive inhibitors of Ach). Relatively slow in onset compared with other agents in class. The drugs are similar, except atracurium causes histamine release and can cause high HR, low BP. Cisatracurium now used preferentially; short acting and requires IV infusion for prolonged effect. Effect potentiated by hypokalemia. Many drug interactions. Elimination by Hoffman elimination and ester hydrolysis; thus can be used for patients with renal/hepatic insufficiency. Non-depolarizing NMBA with slow onset and moderate duration of action. Can be given by continuous infusion. Releases histamine; causes bronchospasm. Can cause decreased or increased HR and cardiac dysrhythmias. Faster onset and recovery in children ages 2–12 years. Enhanced blockade in pregnant patients given magnesium for preeclampsia. Inactivated by plasma cholinesterases; prolonged paralysis possible in enzyme-deficient patients. Rapid onset, prolonged effect. Causes hypertension and tachycardia. Used for induction of neuromuscular blockade, but should be converted to a drug such as continuously infused cisatracurium for maintenance. Eliminated by kidneys and liver, resulting in accumulation with repeated doses.

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Table 8.2. Continued Agent

Initial IV adult dose

Rocuronium

0.6 mg/kg

Vecuronium

0.08–0.10 mg/kg

Miscellaneous agents Droperidol 0.625 mg

Haloperidol

2–5 mg

Ketorolac

0.5–1.0 mg/kg

Reversal agents Flumazenil

0.1–0.2 mg

Naloxone

Up to 0.4 mg

Edrophonium with Atropine

0.5–1.0 mg/kg 0.007–0.014 mg/kg

Neostigmine with Glycopyrrolate

0.5–2.0 mg 0.1–0.2 mg

Comments Nondepolarizing NMBA with rapid onset and moderate duration of action. Some potential for histamine release; can cause bronchospasm. Can cause decreased or increased HR and cardiac dysrhythmias. Children less than 1 year of age are more susceptible to the drug. Metabolized by liver. Nondepolarizing NMBA with rapid onset and short duration of action. Less potential for histamine release. Can cause malignant hyperthermia syndrome. Metabolized by liver.

Potent antiemetic effect but used rarely in the ICU. Sedative effects. Can cause low BP, especially in conjunction with vasodilators. Antidopaminergic properties contraindicate use in Parkinson’s disease. Can cause extrapyramidal effects. Hepatic elimination. Used commonly for anxiolysis (often preferred to lorazepam), especially when respiratory depression is undesirable. Not FDA-approved for IV administration, but IV route is commonplace in practice. Antidopaminergic properties contraindicate use in Parkinson’s disease. Can cause Extrapyramidal effects. Hepatic elimination. Parenteral NSAID used in lieu of opioids o, for opioid-sparing effect in combination. Interferes irreversibly with platelet function and can cause incisional or GI hemorrhage and acute renal failure. Use strictly limited to less than 5 days in postoperative period.

Benzodiazepine antagonist. Rapid onset and short duration. Adverse effect of benzodiazepine can persist after drug wears off. Repeated doses of up to 0.8 mg can be used. Abrupt antagonism of chronic benzodiazepines use can precipitate seizures. Opioid antagonist. Rapid onset and short duration. Often diluted 0.4 mg/10 mL and titrated 0.04–0.08 mg at a time to reverse undesirable side effects while preserving analgesia. Repeated doses of up to 0.4 mg or continuous IV infusion can be used. Abrupt antagonism of opioid use can precipitate hypertension, increased HR, pulmonary edema, or myocardial infarction. Edrophonium is an anticholinesterase inhibitor with antidysrhythmic properties. Rapid onset, short duration; therefore, used usually in concert with atropine, which counteracts the increased secretions, decreased HR, and bronchospasm. Not effective for reversal of neuromuscular blockade caused by depolarizing agents. Renal and hepatic elimination (edrophonium). Atropine may cause fever. Cause salivation and severe bradycardia. May cause bronchospasm or laryngospasm. Metabolized by kidneys. Not effective for reversal of neuromuscular blockade caused by depolarizing agents. Because of profound low HR response, given in same syringe with glycopyrrolate (or sometimes atropine). Glycopyrrolate counteracts low HR and unopposed causes increased HR. May cause fever. Glycopyrrolate is contraindicated in GI ileus/obstruction and in neonates.

Ach, acetylcholine; BP, blood pressure; CO, cardiac output; CPP, cerebral perfusion pressure; FDA, U.S. Food and Drug Administration; GI, gastrointestinal; HR, heart rate; ICP, intracranial pressure; ICU, intensive care unit; IV, intravenous; NBMA, neuromuscular blocking agent; NSAID, nonsteroidal antiinflammatory drug; PCA, patient-controlled analgesia; T1/2, elimination half-life; TBI, traumatic brain injury, VO2, oxygen consumption.

have been working only with the patient’s primary nurse), it is easy to overlook an unsecured sharp lurking within the folds of the drape. Even if no injury occurs at the bedside, if a sharp is discarded inadvertently in the trash rather than the ubiquitous “sharps containers,” untold numbers of hospital workers and sanitation workers are placed at risk.

Infection Control Intensive care units are bastions of health care–acquired infections and multidrug-resistant bacterial pathogens. There is substantial foot traffic in the unit and at the bedside, making the environment strikingly different from that of the OR. For these and other reasons, infec-

tion control can be difficult to maintain in the ICU, although adherence is crucial for the safe performance of procedures and operations at the bedside. The application of the principles of infection control and the implementation of preventive strategies is simple and should not be considered as constraining or controlling, if implemented and adhered to as an integral part of the behavior of all staff members who provide direct patient care.9 Specific measures, including hand washing, barrier precautions, pulmonary toilet, positioning, early removal of catheters and drains, and the control of antibiotic use should be integrated fully into the continuous process of improvement of the quality of care. As one example, Jacobs et al.10 observed a 32% infection rate after percutaneous tracheostomy and associated it with a 34%


incidence of “inappropriate” administration of antibiotics for therapy of nosocomial pneumonia. After instituting an antibiotic administration protocol that decreased the incidence of inappropriate antibiotic administration to 4%, the incidence of infection complicating percutaneous tracheostomy was reduced significantly to 11%.

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express purpose of the procedure.Adequate sedation was achieved in all cases, at a mean total dose of 4.23 mg/kg. The mean duration of the ICU stay was 108 minutes. Three patients had hypotension, and three patients had arterial oxygen desaturation, but no instance required endotracheal intubation or therapy other than the administration of fluid.

Anesthesia, Analgesia, and Sedation Almost every bedside procedure requires analgesia, sedation, or anesthesia, alone or in some combination. Published guidelines describe in detail the sustained use of these agents for indications such as prolonged mechanical ventilation or control of increased intracranial pressure.11 Aranda and Hanson12 have described a systematic approach to the use of these agents in the ICU setting. The critical care team should review the anesthesia record as soon as all postoperative patients are admitted to the ICU, looking in particular for signs of allergy, drug interactions, or destabilizing adverse effects that may inform future decision making. A panoply of agents is available for use during bedside procedures and operations (see Table 8.2), and the choice must be based on several factors. Is the patient intubated? Are the patient’s hemodynamics stable and normal? Will the procedure require general anesthesia, or will local anesthesia suffice? If general anesthesia is required, for how long must it be effective? Will neuromuscular blockade be needed? If sedation is planned, will it be conscious sedation or maintained at a deeper level? Will repetitive administration be required for multiple procedures? Will the agents require reversal, or will they be allowed to “wear off”? Will metabolism of the agents be impaired by abnormal organ function? Will the personnel available be able to manage the agent(s) chosen? For children, sedation or anesthesia may be necessary for performance of bedside procedures that may only require local anesthesia when performed in adults. The combination of intravenous midazolam analgesia and ketamine anesthesia is safe and effective for bedside procedures in children, including lumbar puncture, bone/bone marrow aspiration/biopsy, central venous catheter placement, liver biopsy, and thoracentesis.13 Among 127 patients who underwent a total of 295 monitored procedures reviewed by Slonim and Ognibene,13 only 9 complications were noted. In particular, the dysphoric emergence phenomenon that is characteristic of ketamine administration to adults was observed only once. There has been ongoing concern regarding the safety of administration of propofol to children, specifically relating to the risk of lactic acidosis. Wheeler et al.14 reviewed 91 children who received propofol for 110 bedside procedures in a pediatric ICU, some of whom were not critically ill and were moved to the ICU for the

Ultrasound Ultrasound has become almost indispensable in the armamentarium of the surgeon at the bedside.15 With real-time imaging, the information obtained can augment the physical examination, refine the differential diagnosis, or guide an intervention. Although surgeon-performed ultrasound was developed for rapid evaluation of the abdomen of the hypotensive trauma patient, ultrasound can also increase the safety of central venous catheterization, assess the presence, depth, and extent of an abscess, guide and confirm the aspiration of a fluid collection or the gallbladder, or diagnose wound dehiscence before it is apparent on physical examination. The use of ultrasound imaging to detect a pleural effusion has essentially supplanted the lateral decubitus chest radiograph. Moreover, thoracentesis and central venous catheter insertion are facilitated and made safer. As surgeons become more facile with ultrasound imaging, other uses will develop for the assessment of patients in the acute setting.

Bedside Neurologic Surgery Intervention at the bedside may be required for evaluation and management of increased intracranial pressure (ICP). Maintenance of cerebral perfusion is important for management of patients with traumatic brain injury, and determination of both ICP and cerebral perfusion pressure is central to management. Intracranial pressure can be assessed by extradural pressure transduction (e.g., the “bolt”), by parenchymal placement of a fiberoptic catheter, or by placement of a catheter into a lateral cerebral ventricle (e.g., ventriculostomy) via a twist-drill craniotomy (burr hole). The value of the information gained justifies performance of this highly invasive procedure despite the high incidence of complications, including hemorrhage, malposition, occlusion, and an 8% incidence of infection (ventriculitis). Invasive placement of intracranial monitoring devices has traditionally been by neurosurgeons at the bedside in the ICU rather than in the trauma bay or the OR. Infection control is paramount for ventriculostomy catheter insertion, because, although prolonged catheterization increases the risk of infection, neither antibiotic prophylaxis nor scheduled catheter changes reduce the risk.16,17

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However, a dearth of neurosurgical coverage for trauma in many areas has increased interest in the placement of these devices by non-neurosurgeons. In a review of 157 parenchymal ICP monitors placed in 146 patients with intracranial injury, surgical residents placed 87 ICP monitors without attending supervision and 43 with immediate supervision by either general surgeons or neurosurgeons.18 Neurosurgeons placed 26 monitors without the participation of residents. No major technical complications, episodes of catheter-induced intracranial hemorrhage, or infectious complications were reported. Protocols have also been described to train non-neurosurgeons in the safe placement of ventriculostomy catheters.19 Drainage of chronic subdural hematoma at the bedside has also been described,20 using twist-drill craniotomy under local anesthesia. In a prospective observational trial, Reinges et al.20 followed 118 adult patients, 19 of whom had bilateral lesions. Treatment of unilateral chronic subdural hematoma was 92% successful, albeit after a mean of 3.2 taps (0–5) for drainage. Treatment of bilateral hematomas was equally successful but required up to 10 taps for success. The failure rate was 9%, owing to hemorrhage (n = 2), identification of subdural empyema (n = 2), or inadequate drainage (n = 7). A preoperative computed tomography (CT) scan that demonstrated septation of the hematoma was a significant predictor of treatment failure.

Bedside Surgery of the Head and Neck In a review of 1,268 cases, Abbas et al.21 found 10 cases (incidence, 0.8%) for reopening of cervical incisions following thyroid or parathyroid surgery, usually for hemorrhage. In only two instances was emergency reopening at the bedside necessary, but tracheostomy was required for one of those two cases. Notably, the median time interval from the completion of surgery to the intervention for cervical hematoma was 16 hours (range, 2–48 hours). Several anecdotal reports attest to the efficacy of fineneedle aspiration or percutaneous drainage for the management of fluid collections in the neck following surgery or trauma. Fritscher-Ravens et al.22 reported three critically ill patients who underwent successful fine-needle aspiration at the bedside in the ICU, two of whom had a therapeutic intervention. A mediastinal abscess after percutaneous tracheostomy was aspirated in one patient, leading to appropriate antibiotic therapy and complete recovery. A paratracheal hematoma compressing the airway was aspirated in another patient with multiple trauma, thereby avoiding tracheostomy. Yeow et al.23 reviewed 34 patients who had 41 fluid collections drained percutaneously after major head and neck oncologic


surgery. Prior fine-needle aspiration had been “successful” in only 56% of patients, which increased to 91% after closed-suction percutaneous drainage for a mean of 9 days. The collections were approached through the ipsilateral posterior triangle, and no complications were noted.

The Cervicothoracic Interface: Tracheostomy Tracheostomy is perhaps the most commonly performed “real” operation at the bedside in the ICU, but what does reality reflect, given that tracheostomy is increasingly performed using a percutaneous technique through an incision that is less than 1 cm in length? Some tracheostomies are best performed in the OR even now, although some debate persists as to whether bedside open or percutaneous tracheostomy is preferable. Reflecting its commonplace performance, tracheostomy is the area in this review where good-quality data are ample to answer most, if not all, questions. The most common indication of tracheostomy is acute respiratory failure that transitions into ventilator dependence (Table 8.3),24 followed by airway “protection” for the patient who is obtunded or whose gag reflex is impaired or absent. The third most common indication for tracheostomy is maxillofacial trauma. Large series of open tracheostomies at the bedside have been reported with morbidity rates comparable to tracheostomy performed in the operating room.25 For adult patients with difficult anatomy, cricothyroidostomy is a safe long-term alternative to a conventional infrathyroid tracheostomy.26 On the other hand, percutaneous tracheostomy is advocated as a safe, cost-effective bedside procedure, especially when performed with attention to detail (Table 8.4) under direct airway visualization by fiberoptic bronchoscopy,27 although the necessity of bronchoscopy has been questioned owing to a paucity of supporting data. As with the introduction of

Table 8.3. Indications and patient selection criteria for 71 bedside percutaneous tracheostomies in a surgical ICU. Indications Acute respiratory failure Airway protection Maxillofacial trauma Selection criteria Positive end-expiratory pressure (PEEP) 30% total body surface area) or those who cannot tolerate a single procedure to achieve closure, staged excision of burned tissue is performed, and the resulting wounds are closed with available cutaneous autografts or a biologic dressing.99 The technique of burn wound excision is based on the depth of the wound and anatomic site to be excised. Excision of deep partial-thickness wounds to the level of a uniformly viable bed of deep dermis, by the tangential technic pioneered by Janzekovic,100 and immediate coverage with cutaneous autograft results in rapid wound closure with a typically excellent result. This can be done with an unguarded Weck knife, a Goulian-guarded Weck knife, a handheld dermatome, or a powered dermatome set at 0.0016 to 0.0030 of an inch, depending on the area to be excised and the age and gender of the patient. Optimally, the desired wound bed is achieved in one pass of the knife as evidenced by diffuse bleeding. If this endpoint is not realized, another pass of the knife will be

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needed. A frequent error is attempting this technique in wounds of an inappropriate depth and assuming that punctuate bleeding indicates a viable bed. Such wounds will heal with a poor take of the grafted skin as the bed contains marginally viable tissue incapable of supporting the cutaneous autograft. These wounds at the initial graft dressing change may appear to be doing well only to fail at 5 to 10 days postoperatively. Tangential excision as originally reported was employed early in the first week postburn; however, it can be successfully applied any time to a wound that is not infected or heavily colonized. During the performance of this procedure, the amount of blood loss can be minimized with the use of a tourniquet on extremity burns or subeschar clysis containing epinephrine. The decision that the depth of the excision is satisfactory with these adjuncts will be based primarily on the appearance of the wound, an appreciation of which most experienced burn surgeons have had to learn to some degree through trial and error. A modification of tangential excision is wound excision via layered escharectomy. With this technique, the wound is sequentially excised to a viable bed of subcutaneous tissue and elements of deep dermis particularly at the wound margin. This allows relative preservation of body part contour, a graft with ultimately more pliability, decreased limb edema, and a cosmetically more acceptable transition at the juncture of the grafted wound with the unburned skin of the wound margins. An alternative to layered excision is to excise the wound with a scalpel or electrocautery. Using knife excision, the wound is excised to the muscle fascia or to viable deep subcutaneous tissue. Bleeding can be significant with such procedures; therefore, the excision and control of bleeding must be done efficiently. The use of electrocautery to perform the dissection limits the blood loss without compromising the recipient graft site. Imperative with electrocautery excision into the deep fat is avoidance and limitation of thermal injury to the wound bed, which will compromise the “take” of the applied skin graft. The use of the cutting mode with rapid dissection is necessary. When excision to fascia has been performed, the viability of the fascia should be assessed. The surgeon must determine if the fascia requires removal and the underlying muscle used as the graft bed. In the performance of fascial excisions caution should be exercised during the dissection to avoid entrance into a joint or bursa and injury of extensor tendons in the hand or the Achilles’ tendon at the ankle. The blood loss occurring with burn wound excision is related to the time of excision postburn, the area to be excised, the presence of infection, and type of excision (i.e., fascial or tangential). Donor sites can also represent a significant portion of the blood loss. The use of the scalp or previously harvested donor sites is associated with increased bleeding. The quantity of blood loss has been

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estimated to range from 0.45 to 1.25 mL/cm2 burn area excised.101 Adjunctive measures that can be used to control blood loss include elevation of limbs undergoing excision, applications of topical thrombin and/or vasoconstrictive agents in solutions to the excised wound and donor site, clysis of skin graft harvest sites and/or the eschar prior to removal, and application of tourniquets. Spray application of fibrin sealant can also reduce bleeding from the excised wound after release of the tourniquet. Blood loss will be compounded if the patient has become coagulopathic, hypothermic, or acidotic during the procedure. Perioperative cold stress, which may induce hypothermia, can be reduced by maintaining the temperature of the operating room between 30° and 32°C and by using warmed fluids for wound irrigation. The harvest, application, and postoperative care of split-thickness skin grafts and skin graft donor sites are the same as for any other surgical patient. Grafting of the burn wound is usually done at the time of excision. However, there are instances when it is advisable to stage the skin-grafting procedure. The surgeon must be aware of the patient’s status throughout the surgical procedure and if necessary reassess the extent of the planned procedure. It may be best to perform the excision only and to stage the timing of skin graft application. Additionally, if the wound bed is suspect as to its viability, then only excision should be performed. The wound can be dressed with a 5% Sulfamylon solution dressing or covered with allograft skin or any of several biologic dressings and subsequently reevaluated. The cutaneous allograft is a very useful approach when excising facial burns where the goal is to preserve all possible elements and perform the definitive grafting procedure on a “tested” recipient bed. When an infected wound is being excised, no attempt at placing autograft skin should be considered until the infection has been resolved following treatment with topical and systemic antimicrobial agents as determined by culture results and inspection of the wound. The choice of the donor site for the performance of a cutaneous autograft will in some patients be limited to those skin sites that have not been injured with burns. When there is a choice of donor sites, the requirements of the recipient site and the potential for donor site morbidity should be factored into selecting the site of graft harvest. In the grafting of facial burns, color match is an important consideration, and obtaining a graft from a site above the clavicles or the inner aspect of the thigh will provide the best result. For children, harvest of a graft from the scalp results in a donor site that is not particularly painful postoperatively and has no long-term cosmetic consequences. The harvest of grafts from posterior body surfaces provides, in general, a more acceptable wound for most patients. Although the anterior thigh is an often-selected site, it can heal with significant hyper-

B.A. Pruitt, Jr., and R.L. Gamelli

trophic change and cause a patient more problems and distress than the grafted burn. The use of sheets of autograft skin for resurfacing the burn represents the gold standard. This is the only acceptable approach for burns of the face and neck and the best choice in grafting of the hands and breast. Every attempt should be made to use such autografts in children, because they provide the best long-term results. It may not be possible to achieve these objectives for patients with extensive burns or for those in whom the pattern and location of the injury limits donor site availability. The use of meshed cutaneous autografts allows the surgeon to increase the area covered. Skin graft meshing devices of various design and manufacture are available with expansion ratios from 1 : 1 to 1 : 9. The wider the mesh, the greater the wound area covered; however, it will take the wound longer to close by ingrowth from the margins of the mesh reticulum to fill the open interstices during which time there is the very real potential for graft loss and wound infection to occur. Additionally, widely meshed autografts have a greater propensity to form hypertrophic burn scars and may provide a skin surface with unsatisfactory mechanical stability, inadequate pliability, permanently poor cosmetic appearance, and restricted joint mobility. Despite these potential limitations, the use of meshed cutaneous autografts is an important strategy and potentially life-saving approach for patients with extensive body surface area burns. The technique of skin graft harvesting would seem to be a relatively simple procedure, yet it is often not done well. As noted earlier, the harvest site should be the one that will yield a graft with the desirable characteristics and the least donor site morbidity. Grafts should be of sufficient size to achieve wound closure with a minimum of intergraft seams. Powered dermatomes are available with up to 6-inch cutting widths that provide excellent sheets of skin for facial grafts or when meshed, can cover a significant burn area. Donor site preparation is essential to obtain a uniform graft. Powered clysis, can rapidly be accomplished over an extensive harvest site using an air-powered surgical wound irrigating system equipped with a 14- or 16-gauge needle attached to 3-L bags of normal saline. This provides a stable, uniform surface for graft harvest and limits the difficulties encountered when harvesting over contoured surfaces or bony prominences. The thickness of the harvested graft should be related to the site to be grafted, whether the graft is to be meshed, the mesh ratio, and, to some degree, surgeon preference. The desired thickness of the graft also influences donor site selection (i.e., a “thick” graft should be harvested from an area of “thick” skin). Harvest of a “thick” graft from an area of “thin” skin (i.e., the inner arm) can produce a full-thickness wound that will have to be grafted.

9. Burns

Skin grafts through which one can read printed material are primarily epithelial autografts with a minimal amount of dermis (0.004–0.006 inch), whereas those that are more opaque contain a variably greater amount of dermis (0.008–0.012 inch). Thinner grafts yield a better donor site and function well on a dermal wound bed but may not do well when placed on a wound excised to fascia. For elderly patients, thin grafts that contain insufficient numbers of keratinocyte progenitor cells are considered the cause of melting graft syndrome and prolong the time of reepithelialization. Thicker grafts are more pliable, heal with less contraction, and will do better than thin grafts when meshed. The thicker grafts may result in donor site scarring and delay in donor site closure, especially in the elderly patient. The harvested graft should be placed on the prepared burn wound parallel to the major flexion creases and can be attached mechanically with staples or sutures or secured with tissue adhesives such as fibrin glue. A properly placed set of grafts on an extremity should at the end of the operation be able to remain in place as the extremity is put through a gentle range of motion. One of the most important aspects of a skin-grafting procedure is the application of a proper dressing. A highly successful approach is to use multiple layers of a nonadherent linen dressing moistened with a 5% solution of mafenide acetate applied circumferentially to the excised and grafted wounds on an extremity. A bolster produced by using net dressings drawn tightly over the burn dressings and stapled to the skin is used to “fix” the grafts on torso wounds. Graft failure occurs as a result of inadequate excision, inadequate hemostasis, infection, subgraft seroma formation, mechanical sheering during postoperative care, or, rarely, “upside down” application. The first dressing change is typically done 48 to 72 hours postoperatively. If a sheet graft is well intact at that time, a nonadherent dressing is reapplied to protect the wound. In the case of meshed autografts, the moist dressings of mafenide acetate solution, changed daily or more often as required, are continued until the mesh is closed.

Skin Substitutes Although split-thickness cutaneous autografts are the usual method of wound closure, there is often the need for a skin substitute. Alternative wound coverings are used to achieve wound closure when the available donor surface area is not sufficient, when there is a need to test the wound bed, or for primary management of selected partial-thickness wounds. The goal with a skin substitute is to obtain temporary physiologic wound closure and protect the wound from bacterial invasion. The two most commonly used naturally occurring biologic dressings are human cutaneous allograft and porcine cutaneous xenograft. Human allograft skin is commercially avail-

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able as split-thickness grafts in either fresh viable or cryopreserved form. Both of these preparations are capable of becoming vascularized; however, this best occurs with fresh allograft skin. Allograft skin can provide wound coverage for 3 to 4 weeks before rejection.102 Xenograft tissue is available as reconstituted sheets of meshed porcine dermis or as fresh or prepared split-thickness skin. Porcine skin impregnated with silver ions to suppress wound colonization is also available. Xenograft skin can be used to cover partial-thickness injuries or donor sites, which reepithelialize beneath the xenograft.103 Various synthetic membranes have been developed that provide wound protection and possess vapor and bacterial barrier properties. BiobraneTM (Dow-Hickham, Sugarland, TX), is one such product that has been used in the management of partial-thickness and donor site wounds.104 This bilaminate membrane consists of a collagen gel adherent to a nylon mesh as the dermal analog to promote fibrovascular ingrowth and a thin outer silastic film as the epidermal analog to provide barrier properties. Biobrane has also been used as the scaffold for the growth of allogenic fibroblasts that secrete, while in culture, various growth factors along with other mediators.The fibroblasts are then removed by freezing to complete preparation of the membrane. These membranes are currently approved for use in fully excised wounds, donor sites, and superficial partial-thickness burns.105 Another collagen-based skin substitute is the dermal replacement developed by Burke and Yannas, presently in use as IntegraTM (Integra LifeScience Corporation, Plainsboro, NJ).This membrane consists of an inner layer of collagen fibrils with added glycosaminoglycan and an outer barrier membrane of polysiloxane. It is placed over freshly excised full-thickness wounds, and, once fully vascularized, the epidermal analog is removed and the vascularized “neodermis” covered with a thin split-thickness cutaneous autograft.106 A permanent skin substitute for burn care victims represents the search for the Holy Grail. Presently, cultured epithelial autografts are commercially available but are limited in their use because of suboptimal graft take, fragility of the skin surface, and high cost.107 Use of any biologic dressing requires that the excised wound and the dressing that has been applied be meticulously examined on at least a daily basis. Submembrane suppuration or the development of infection necessitates removal of the dressing, cleansing of the wound with a surgical detergent disinfectant solution, and even reexcision of the wound if residual nonviable or infected tissue is present. Following such wound care, the biologic dressing can be reapplied, and, if it remains adherent and intact for 48 to 72 hours without suppuration, that biologic dressing can be removed and the wound closed definitively with cutaneous autografts. The proper management of the patient’s burn wounds is critical to achieve the optimum cosmetic and functional

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outcome and the timely return of the patient to full activity. For patients with major burns, the wound must be properly cared for and closure achieved expeditiously to lessen the level of physiologic disruption that accompanies a major burn. Failure to do so can result in invasive wound infection, chronic inflammation, erosion of lean body mass, progressive functional deficits, and even death.

The Treatment of Special Thermal Injuries Electric Injury This topic is dealt with in Chapter 10.

Chemical Injuries A variety of chemical agents can cause tissue injury as a consequence of an exothermic chemical reaction, protein coagulation, dessication, and delipidation. The severity of a chemical injury is related to the concentration and amount of chemical agent and to the duration with which it is in contact with tissue.108 Consequently, initial wound care to remove or dilute the offending agent takes priority in the management of patients with chemical injuries (Figure 9.8). Immediate copious water lavage should be instituted while all clothing, including gloves, shoes, and underwear, exposed to the chemical are being removed.

Figure 9.8. Failure to remove footwear and institute water lavage to dilute and remove concentrated lye, which had spilled into the boot of this patient, resulted in severe tissue injury during transportation to the hospital. Note extensive liquefaction of tissue, thrombosed vessels (white arrow), and edema of the extensor tendons exposed at the midmetatarsal level on the dorsomedial aspect of the foot (black arrow).


The lavage is continued for at least 30 minutes or until dilution has lowered the concentration of the agent below that which will cause tissue damage or until testing the involved surface with litmus paper confirms that the agent has been removed. For patients in whom extensive surface injury has occurred, the irrigation fluid should be warmed to prevent the induction of hypothermia. Although seldom needed, if a patient with concentrated alkali injuries requires prolonged irrigation and is hemodynamically stable, the patient can be cared for while sitting in a chair under a shower. The appearance of skin damaged by chemical agents can be misleading. In the case of patients injured by strong acids, the involved skin surface may have a silky texture and a light brown appearance that can be mistaken for a sunburn rather than the full-thickness injury that it is. Skin injured by delipidation caused by petroleum distillates may be dry, show little if any inflammation, and appear to be undamaged but found to be a full-thickness injury on histologic examination. Variable degrees of pulmonary insufficiency may occur in patients with cutaneous injuries caused by volatile chemical agents that can also be inhaled, such as anhydrous ammonia, the ignition products of white phosphorus, mustard gas, chlorine, and even the vapors of strong acids. Additionally, pulmonary insufficiency may be caused by the inhalation of the gaseous products of petroleum distillates as may occur in patients who sustain delipidation injuries due to partial immersion in gasoline and other petroleum products. In the case of patients with anhydrous ammonia injury, any powdery condensate adherent to the skin should be brushed off before irrigation. Hydrofluoric (HF) acid injury is most common in those involved in etching processes; the cleaning of air-conditioning equipment, patio grills, and other metallic objects with spray products containing HF; and petroleum refining. After contact with HF acid, there is a characteristic pain-free interval of variable duration with subsequent appearance of focal pallor that progresses to penetrating necrosis, typically accompanied by severe pain. Immediately after injury, calcium gluconate gel should be applied topically or prolonged irrigation with a solution of benzalkonium chloride instituted. The persistent severe pain that may occur in digits injured by HF acid can be relieved by injecting 10% calcium gluconate into the artery supplying that finger. Local tissue injection of calcium gluconate is an alternate route of delivery but may in itself compromise the blood supply of the involved digit. Persistent pain caused by subungual HF acid is best treated by removal of the nail under digital block anesthesia. The pain typically relents and the nail grows back with little or no deformity. If these measures fail to control pain, local excision and skin grafting will be needed to remove the damaged tissue and achieve pain relief.109 Extensive HF

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acid injury may induce systemic hypocalcemia, which is treated by intravenous infusion of calcium. Burns caused by phenol should be treated with immediate water lavage to remove, by physical means, the liquid phenol on the cutaneous surface. Following that lavage, the involved area should be washed with a lipophilic solvent such as polyethylene glycol to remove any residual adherent phenol that is only slightly soluble in water.110 Intensive systemic support is required for patients with extensive phenol burns, in whom absorption of the agent can cause central nervous system depression, hypothermia, hypotension, intravascular hemolysis, and even death. Injuries caused by white phosphorus are usually discussed with other chemical injuries but are actually conventional thermal burns caused by the ignition of the particulate phosphorus. These injuries are most commonly encountered in military personnel injured by explosive antipersonnel devices (grenades), which can cause mechanical tissue damage and drive fragments of white phosphorus into the soft tissues. All wounds containing white phosphorus particles should be covered with a wet dressing that is kept moist to prevent ignition of the particles by exposure to air. If the interval between injury and definitive wound care will be so long as to permit dessication of the wet dressings, the wounds can be briefly washed with a freshly mixed dilute 0.5% to 1% solution of copper sulfate followed by copious rinsing. Such treatment generates a blue-gray cupric phosphide coating on the retained phosphorous particles that both impedes ignition and facilitates identification.111 Whatever form of topical treatment is employed, the wound should be debrided and all retained phosphorous particles, which can be readily identified with an ultraviolet lamp, removed. The removed particles should be placed under water to prevent them from igniting and causing a fire in the operating room. Strong acids and alkali can cause devastating ocular injuries and must be treated immediately, even before leaving the scene of the injury, by irrigation with water, saline, or phosphate buffer. In the hospital, eye irrigation must continue until the pH of the eye surface returns to normal. The rapid penetration of ocular tissue by strong alkalis necessitates prolonged irrigation (12to 72 hours). Such irrigation is best carried out with a modified scleral contact lens with an irrigating side arm. The effects of iritis induced by chemical ocular injury are minimized by installation of a cycloplegic such as 1% atropine following irrigation. If irrigation and removal of the offending agent is delayed, the entire globe may be so damaged as to lose turgor and all visual function. Even with early irrigation, corneal damage can be severe, and late complications of symblepharon and xerophthalmia may occur. An ophthalmologist should be involved in the care of such patients from the time of admission.

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Bitumen Burns Bitumen injuries are commonly caused by hot tar coming in contact with the skin. The injury that results is a thermal contact burn, which is not associated with any significant component of a chemically mediated injury. There is no significant absorption of materials unless the patient is in an explosion and has ingested or inhaled the material. The primary initial treatment is urgent cooling of the molten material with no attempt made to remove the tar. By cold application, the transfer of heat can be limited and the degree of tissue damage minimized.There are various agents that have been advertised as being effective for the removal of tar and asphalt products. These have varied from mayonnaise to simple petroleumbased jellies and seem to be similar in terms of efficacy. Considering that the initial temperature of liquid tars and asphalts are typically in excess of 600°F, early concerns about infection would seem to be unfounded and offer no support for urgent removal with potential destructive consequences to underlying otherwise viable tissue. It is preferable to apply an emulsifying petroleum-based ointment and allow the tar to separate during the first day or two after admission.108

Cold Injuries Injuries occurring secondary to environmental exposure can result in local injuries, frostbite, or systemic hypothermia. During the wintertime in urban environments, the most common mechanism of injury involves homeless persons or an elderly patient who has become disoriented and wandered from home. The pathophysiology of the local injuries consists essentially of crystal formation caused by freezing of both extracellular and intracellular fluids. Consequently, the cells dehydrate and shrink, and blood flow is altered to the exposed area resulting in tissue death. During the thawing of damaged tissues, microemboli that have formed further occlude the microvascular circulation, adding insult to injury.112 It is important to note that the initial clinical presentation of the patient is not likely representative of the ultimate degree of tissue loss. Patients presenting with frostbite will have coldness of the injured body part with loss of sensation and proprioception. On initial examination, the limb may well appear pale or cyanotic or have a yellowwhite discoloration. During rapid rewarming at 40° to 42°C in water for 15 to 30 minutes, hyperemia will occur followed by pain, paresthesias, and sensory deficits. Over the subsequent 24 hours, edema and blistering will develop, and it may be the better part of a week before one can determine the true depth and extent of the injury. In the initial management of the patient, rewarming is critical, but it must be done only when there is no chance

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for an episode of refreezing. If blisters appear, the question of whether they should be preserved or debrided has proponents of both sides of the answer. Some authors suggest that white blisters can be debrided whereas purplish blue blisters should be left intact. The injured extremity should be elevated in an attempt to control edema and padded to avoid pressure-induced ischemia as a secondary insult. Administration of pain medication is based on the patient’s response. Frostbite wounds are tetanus-prone wounds, and therefore tetanus toxoid should be administered based on the patient’s immunization status. Before any definitive plans are made for surgical intervention, sufficient time should be allowed to pass so that a clear demarcation between viable and nonviable tissue is apparent (Figure 9.9). However, it is not in the patient’s best interest to follow the adage of “freeze in January and

Figure 9.9. Spontaneous healing of frostbite injury proximal to the discolored skin on the dorsum of this foot is indexed by decreased hair growth in that area. The demarcation of nonviable tissue shown here permitted amputation at a midfoot level and salvaged the heel pad.


amputate in June.”113 Although it will take some time for definitive delineation of the depth of the injury, once the wounds have begun to mummify the thought that there will be tissue salvage seems more than naive. Patients suffering frostbite injuries should be evaluated for other potential trauma and treated for systemic hypothermia if it is present. The posthospitalization disposition of cold injury patients requires a clear understanding of their preexisting health status and the factors that predisposed them to injury, such as dementia or major psychological disease.114

Radiation Injury Radiation exposure secondary to the detonation of a thermonuclear device is not as likely as is exposure from an industrial or medical accident, misuse of radiation materials, or acts of terrorism. The dispersal of radioactive substances can take several forms, including accidents during storage and mishandling, accidents during transportation of radioactive materials, intentional dispersal either alone or in combination with other agents, and intentional dispersal through an explosive device. In both storage and transport accidents, the dispersal and subsequent exposure to radioactive materials is usually limited to the people immediately involved and is well contained geographically once the event is recognized. It is typically difficult to expose large numbers of individuals to significant doses of radiation at any given time, and the risks are limited to those involved in a given incident. Small-dose radiation exposure does not affect health for many years and is associated with few acute problems, although it is still a significant health risk. In the event of intentional radiation dispersal, the risk of exposure and injury as well as the source involved need to be evaluated. The risk of trauma is related to the primary explosive device itself as well as trauma related to the secondary effects of the explosion, such as shell fragments, structure collapse, or injury from debris. Psychological trauma from witnessing the primary event or from the experience of living through the event, with the associated physical manifestations, may pose a further problem in the handling of a significant number of injured victims. Exposure risk is related to primary contamination from the particles released from the explosive device, secondary contamination from particles that have become mixed with debris, debris dust, and fallout, and tertiary contamination from exposure to particles in contact with patients. Ionizing radiation is composed of two types: radiation that has mass and radiation that is energy only. Exposure to alpha particles, which are relatively large, highly charged particles, slow moving, and penetrate only a few microns into tissue, can be effectively shielded with

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ordinary substances such as paper, cardboard, or clothing. Alpha particles can be a source of secondary and tertiary contamination. Beta particles, made up of either positively or negatively charged species, have greater energy, can penetrate more deeply into tissues, require shielding with material such as aluminum to prevent exposure. Both alpha and beta particles result from the decay of a radioactive source. Gamma and x-rays are produced by radioactive decay or an x-ray source; they have neither mass nor charge; however, they penetrate deeply, and shielding requires the use of such materials as lead, steel, or thick cement. Following removal from the source of radiation, no further exposure occurs, and the patient poses no danger to those providing care. Radiation caused by neutrons requires special consideration. Nuclear reactors are the major source of neutron emission and create radiation that penetrates deeply, causing widespread damage to underlying tissues. Radiation exposure of 2 to 4 gray (Gy) can cause nausea and vomiting, hair loss, and bone marrow injury leading to death from infection up to 2 months after exposure. Exposures of 6 to 10 Gy result in the destruction of the bone marrow and injury to the GI tract with a mortality rate approaching 50% within 1 month. When the exposure is 10 to 20 Gy there is severe injury to the GI tract, and death can occur in as little as 2 weeks. When exposure is above 30 Gy, cardiovascular and nervous system damage occur primarily as a result of hypotension and cerebral edema. There is almost immediate nausea, vomiting, prostration, hypotension, ataxia, and convulsion, and death can occur in a matter of hours. At present there appears to be no effective treatment following radiation exposure. For treatment to be effective, it would need to be given before the exposure. In cases of accidental exposure, treating bone marrow suppression, although successful, has not prevented death, which usually occurs from radiation pneumonitis, GI tract injury, and hepatic and renal failure.115,116 The burn injuries resulting from radiation exposure are usually localized and represent a high radiation dose to the skin. They appear identical to a thermal burn and may present with erythema as with a first-degree burn, which will heal following some sloughing of the skin. With higher dose exposures, blisters may occur as with a partial-thickness burn, and healing occurs in a similar manner. When the radiation exposure has been significant, such as 20 Gy, radionecrosis occurs. If the event leading to the radiation exposure causes surface contamination, decontamination needs to be done before dealing with the wound. This consists of saline irrigation of the wound and treatment with standard aseptic techniques. It is not necessary to excise the wound urgently unless it is contaminated with long-life radionuclides such as alpha-emitting particles. Patients who have greater than a 1 Gy whole-body exposure should be considered for

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early wound closure so that the wound itself does not become the site of a lethal infection.117 To manage radiation-exposed victims effectively, a hospital must have a well-organized plan in place and the appropriate decontamination facility within the emergency room. The goals are to save the patient’s life and to prevent further injury. The decontamination must be done so that the personnel providing care to the patient do not become exposed. All contaminated materials must be carefully handled to prevent contamination of the hospital and its facilities and the public sewage system.

Toxic Epidermal Necrolysis Toxic epidermal necrolysis (TEN) is a rare, lifethreatening mucocutaneous form of exfoliative dermatitis that is often secondary to drug sensitivity.The incidence of TEN has been estimated at 0.4 to 1.2 cases per million population per year.118 These patients may give a history of sore throat, burning eyes, fever, and malaise and present with systemic toxicity. Physical findings can include rash, bullae, and diffuse exfoliation, with the large areas of separation having the appearance of a partial-thickness burn. When lateral stress is applied to the involved skin it separates at the dermal-epidermal junction, Nikolsky’s sign. The resulting wounds give the appearance of a wet surface as seen in a second-degree burn. The mechanism of injury is thought to be keratinocyte apoptosis induced by interactions between the cell surface death receptor Fas and its receptor FasL or CD95L.119 Lyle in 1956 was the first to describes two entities in the initial description of TEN consisting of staphylococcal scalded skin syndrome (SSS) and what today is recognized as TEN.120 Staphylococcal scalded skin syndrome is a generalized exfoliative dermatitis due to infections with staphylococcal organisms. In SSS, the lesion is at the intraepidermal layer with blister formation followed by desquamation of large sheets of skin with relatively rapid reepithelialization over 7 to 10 days. The outcome in patients with SSS is significantly better than that in TEN patients. In TEN, there is necrosis of all layers of the skin and a mortality rate between 30% and 40%, whereas with SSS it is 3% to 4%. Stevens-Johnson syndrome (SJS) is an entity in which there is also extensive epidermolysis, often presenting with target-shaped skin lesions with differentiation from TEN related to the extent of cutaneous involvement. One current delineation classifies patients with less than 10% to 30% cutaneous involvement as SJS and those with greater than 10% to 30% as TEN, particularly if it involves oral-genital and ocular mucosae.121 Whether SJS and TEN represent the same process, differing only in the extent of cutaneous involvement and sites affected, or are pathologically distinct entities has not been determined with any degree of certainty.

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Figure 9.10. The back, buttocks, and upper thighs of this patient with toxic epidermal necrolysis (TEN) have been covered with a translucent collagen-based skin substitute, Biobrane, following cleansing with saline and gentle debridement of exfoliated epidermis. Note focal areas of adherent darkly pigmented epidermis that were left in place and covered with the bilaminate membrane, which provides barrier function, reduces pain, and prevents dessication of the exposed dermal surface to promote healing. The undressed wounds of the arms and legs were covered with Biobrane after this photo was obtained.

Patients with TEN have wound care needs identical to those of patients with extensive second-degree wounds. They exhibit significant fluid losses and have specialized nutritional needs. Care of these patients in a burn center by experienced surgeons has resulted in a significant improvement in outcome.122 General principles of management of these patients include the cessation of potential precipitating drugs, the discontinuance of systemic steroids if recently initiated, ophthalmologic evaluation, and skin biopsy confirmation of the diagnosis.123 Additionally, systemic antibiotics should be reserved for those cases in which infection is highly likely. Replacement of fluid and electrolytes and provision of nutritional support and aggressive wound care are critical elements in the care of these patients. Wound care may consist of the application of a biologic dressing once all of the nonviable tissue is fully debrided or the use of silver-impregnated dressings (Figure 9.10).The most frequent mistakes in the care and management of these patients are underestimating the extent of the cutaneous involvement, airway compromise, and not understanding how rapidly these patients can become critically ill. To date, the results of studies of various modalities that can be employed to control the degree of skin slough have been too inconsistent to recommend their general use.124

Mechanical Injury The combination of burn injury and multisystem trauma occurs in up to 4% to 5% of all burn patients.125,126


Patients suffering combination injuries are typically male, with their injuries having occurred from a flame ignition during an assault or motor vehicle crash. Victims suffering a combination of burns and trauma tend to have a higher incidence of inhalation injury, higher mortality rate, higher injury severity score (ISS), and longer length of stay, despite no differences in total body surface area burned, than patients with only burns. Trauma victims with burns with an inhalation injury have a near threefold increase in their mortality rate.98 Those victims not surviving their injuries typically are significantly older and have a higher ISS and a larger body surface area burn than trauma victims with burns who survive their injuries. The management priorities for patients suffering burns plus trauma must be as for patients with trauma. Understanding the mechanism of injury is vital in determining the probability of associated injuries and provides a guide for the workup of the patient. A formal trauma evaluation should be performed for all burn victims when the history of the event points to the possibility of combined mechanisms of injury. Life-threatening injuries must be promptly treated and fractures immobilized, and the resuscitation fluid needs of the patient should be calculated to include the burn wound–mandated needs and those of the associated trauma. Blood is not part of the initial resuscitation for patients with only burn injuries, but when there is multiple trauma blood transfusions may be necessary in the early management of the patient. Often the presence of a major burn wound results in the patient being viewed as having only a burn, and the standard assessment of a trauma patient is not done. Patients with impaired neurologic status should undergo a computerized axial tomographic scan to rule out intracranial pathology along with evaluation for a spinal injury. This is particularly important if the patient jumped from a burning building to escape the fire, was injured in an industrial accident, or was involved in a motor vehicle crash. Potential thoracic, abdominal, or pelvic injuries should be evaluated with chest, abdominal, and pelvic roentgenograms as well as with abdominal computed tomography and FAST (focused abdominal sonography in trauma) examinations. Diagnostic peritoneal lavage may also be used for the unstable patient to verify the presence of an injury requiring exploratory laparotomy. The nonoperative management of significant injuries of the spleen or liver requires thoughtful consideration for patients with a major burn, and it maybe prudent to opt for surgical management particularly if the abdominal wall is extensively burned. For patients with major long bone injuries, early operative intervention with stabilization will facilitate their overall management as well as that of the burn. In selected circumstances, early burn excision with skin graft wound closure may be the best approach to facilitate the operative management of the orthopedic injury.

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The management of patients with significant burn injuries in conjunction with mechanical trauma requires a highly coordinated plan of care. The patient must be continuously reassessed to avoid missing an injury, and the surgeon must be vigilant to the development of trauma-related complications.

number of formulas permit one to make close approximations of daily energy expenditure in a variety of surgical patients. A formula based on studies of extensively burned patients is useful in estimating burn patient calorie needs.128

Metabolic and Nutritional Support

where EER is estimated energy requirements, BMR is basal metabolic rate, TBS is total burn size, m2 is total body surface area in square meters, and AF is activity factor of 1.25 for burns. A rule of thumb estimate for nutritional needs of patients whose burns involve more than 30% of the body surface is 2,000 to 2,200 kilocalories and 12 to 18 grams of nitrogen per square meter of body surface per day.39

Estimation and Measurement of Metabolic Rate Burn injury alters central and peripheral thermoregulatory mechanisms, the predominant route of heat loss, the distribution and utilization of nutrients, and metabolic rate. All of these postburn metabolic changes must be considered when planning the metabolic support and nutritional management of the hypermetabolic burn patient necessary to minimize loss of lean body mass, accelerate convalescence, and restore physical abilities. Metabolic support includes patient care procedures and environmental manipulations in addition to the provision of adequate nutrition. The perceived temperature of comfort of burn patients (on average 30.4°C) is higher than that of unburned control patients and necessitates maintaining the ambient temperature at that level in the patient’s room to prevent the imposition of added cold stress, which would exaggerate an already elevated metabolic rate.127 Physical therapy with active motion to the extent possible and passive motion to stretch muscles in the absence of spontaneous motion is instituted on admission to minimize muscle wasting secondary to disuse. Analgesic and anxiolytic agents should be used as needed to prevent pain and anxiety-related increases in circulating catecholamine levels, which can further increase metabolic rate. Assiduous monitoring is necessary to facilitate early diagnosis and prompt treatment of infections and thereby reduce their metabolic impact. The importance of excision and grafting of the burn wound has been emphasized by recent studies showing that such treatment reduces resting energy expenditure in burn patients, even if the entire wound cannot be excised and grafted at a single sitting. Even though metabolic rate can be reduced by pharmacologic means, studies indicating that the hypermetabolic response to burn injury is wound directed speak for meeting caloric needs rather than reducing nutrient supply to the burn wound by pharmacologic intervention. One must determine the resting energy expenditure in order to calculate the nutrients required to meet the patient’s needs. Bedside indirect calorimetry is the most accurate means of determining metabolic rate, but a bedside metabolic cart may not always be available. A

EER = [BMR × (0.89142 + 10.01335 × TBS)] × m2 × 24 × AF,

Nutritional Support Meeting the metabolic needs of the burn patient can be accomplished by providing nutritional support via the GI tract or by the intravenous route. After determining what the metabolic needs will be for an individual burn patient, the next question is will the patient be capable of meeting the needs by oral intake? For patients who can eat, it is not likely that a standard hospital diet will meet the calculated needs, and it is often necessary to supplement the patient’s intake with various nutritional supplements. A calorie count should be recorded to verify that the patient is capable of consistently meeting the daily nutrient intake goal. For the patient who is incapable of achieving the necessary nutrient intake or who cannot eat, one must decide how to deliver the feedings. Total parenteral nutrition in the past provided a way by which patients could receive the majority or all of their calorie and protein needs but at present has largely been supplanted by the use of enteral nutritional support. Compared with total parenteral nutrition, enteral nutritional support is technically easier to accomplish, lower in cost, supports the health of the GI tract, and ameliorates the systemic inflammatory response syndrome.129–133 At the time of admission, a patient who will require specialized nutritional support should have either a nasogastric or nasoduodenal tube placed. Patients can safely and effectively be fed by either of these routes with appropriate precautions. It is not required that one use custom-made feedings to meet the patient’s nutrient needs. It is possible by using combinations of currently available commercial products to obtain the necessary blend of nutrients, feeding density, water, and protein requirements while avoiding the cost of compounding specialized enteral feedings. It is preferable to start enteral feedings soon after the patient is admitted. The patient should be fed with the head of the bed elevated to 30°, with feeding residuals checked frequently to avoid

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gastric distention and possible aspiration. A potential advantage of early enteral feedings is modulation of the hypermetabolic response, although the actual ability of early feedings to achieve this goal has been called into question.134–136 When feedings are initiated early postinjury, the desired rate of administration can typically be reached within 24 to 48 hours of admission. There are multiple recommendations regarding the initial concentration, rate, incremental increase, and frequency of the increases. Starting a tube feeding of standard concentration at 20 to 40 mL/hr and advancing the rate a similar amount every 4 hours works well for most patients. The most important issues are that the nursing staff understands the goals, knows how to monitor for feeding intolerance, and appreciates the attention to detail necessary to achieve consistent delivery of the feedings. If a patient is intolerant of gastric feedings and gastric aspirate volume exceeds the total of two hourly feedings, the administration of metoclopramide will often resolve the problem. If the patient fails to respond to metoclopramide, an attempt should be made to place either a nasoduodenal or nasojejunal feeding tube, which will minimize this feeding difficulty and lessen the risk of aspiration. Patients who become septic will often manifest changes in feeding tolerance along with new-onset hyperglycemia or changes in insulin needs as early signs pointing to this problem. For patients receiving central vein alimentation, the risk of catheter sepsis must be evaluated as an etiology for the patient’s septic process. For patients who become intolerant of enteral feedings or develop GI complications that prevent use of the GI tract, total parenteral nutrition will be required. However, with careful attention to detail and a welldesigned, patient-specific enteral feeding protocol, this should rarely be needed in the care of a burn patient.

Monitoring The complications associated with the use of enteral or parenteral support in the burn patient are in large part similar. Burn injury induces insulin resistance, which may lead to hyperglycemia. The maintenance of blood glucose values with aggressive insulin replacement has a favorable impact on the outcome of critically ill patients.137 For critically ill patients the preferable route of administration of insulin is intravenously, with the goal of maintaining plasma glucose values between 80 and 110 mg/dL. There is a well-recognized limit to the caloric load that a critically ill patient can tolerate from carbohydrates, and for the 70-kg patient this is approximately 1,800 kCal per day from glucose.138 Excessive amounts of glucose can result in respiratory quotient (RQ) values >1, which may cause hepatic steatosis and complicate ventilatory management. Sufficient protein to meet metabolic demands must be provided. To estimate protein needs, 24-hour urine urea


nitrogen is measured to which an additional 0.1 to 0.2 g of nitrogen per percent total body surface area burn remaining is added. These determinations can be done on a weekly basis unless there is a special need to perform them more frequently. Numerous studies have been done to determine precise protein needs and the optimum balance of protein to nonprotein calories. For adult patients, 1.5 to 2.0 g protein per kilogram lean body mass per day is a reasonable goal and for children, 3 g protein per kilogram lean body mass.139,140 A nonprotein calorie to nitrogen ratio of 100 : 1 provides the patient with sufficient calories to support protein synthesis in the face of ongoing protein breakdown and reduces net protein loss.141,142 The provision of dietary protein at these levels has been shown to positively impact patient outcome.143 An increasing blood urea nitrogen level must be evaluated in terms of nitrogen overfeeding and the protein load recalculated to avoid uremia and an associated diuresis. Measurements of visceral proteins such as serum transferrin and albumin can be used to monitor the impact of the nitrogen content of the diet on the patient’s nutritional status. These proteins are simply markers that can be followed over time and are probably best utilized in a trend analysis based on weekly determinations because albumin has a half-life of 20 days and transferrin 8 days. Thyroid prealbumin with a half-life of 2 days and retinal binding protein with a 12-hour half-life can be used to track short-term responses in selected patients. To prevent the development of essential fatty acid deficiencies, lipids must be included in the diet but should not exceed more than 40% of the total calorie load or more than 3 g/kg body weight per day. Most enteral diets will contain adequate fat to prevent the development of essential fatty acid deficiency, and parenteral diet formulations typically contain long-chain fatty acids. The serum triglyceride concentration and the triene/tetraene ratio should be measured weekly to assess fatty acid status. If this ratio is greater than 0.4, an essential fatty acid deficiency exists that necessitates adjustment of the dietary fat content.144 Supplemental medium-chain triglycerides can be given enterally but are associated with increased ketone production and may cause diarrhea.39

Complications Serum electrolytes must be monitored to make necessary adjustments in the amount of free water, sodium, chloride, potassium, phosphorus, calcium, and magnesium provided to the patient. Laboratory values should be obtained at initiation of the feedings and daily during the stabilization phase and with each change in the patient’s clinical status. During the first several days after admission, and with the initiation of nutritional support, there can be dramatic shifts in serum and plasma values of electrolytes and minerals. As noted above, hypernatremia can

9. Burns

develop if free water replacement is insufficient to account for insensible water loss through the burn wound, which can be 2.0 to 3.1 mL/kg body weight/% burn/day.145 Hypernatremia can also develop with persistent febrile episodes if free water replacement does not match the patient’s needs. Hyponatremia may represent underreplacement of sodium but typically is related to free water excess. Correction of hyponatremia should be attempted with restriction of free water intake. For adults an increase in body weight of more than 400 g per day reflects water loading and should prompt a review of fluid intake and output records and adjustment of fluid administration.2 Potassium and phosphorus must be given to meet the patient’s needs, which often exceed initial estimates particularly when large loads of glucose are being given along with exogenous insulin. In the course of the patient’s care as the open wound area decreases and the hypermetabolic state slowly resolves, the nutrient load should be adjusted so that balance is maintained between metabolic needs and substrates delivered and the patient is not overfed. Alternatively, if a patient is found to have lost more than 10% of his or her admission weight, it is likely that caloric estimates are not being achieved or were underestimated. Although most experienced clinicians possess the skill to assess patient needs accurately, the performance of bedside indirect calorimetry can provide objective information as to the patient’s resting energy expenditure, respiratory quotient, oxygen consumption, and carbon dioxide production. The results may indicate the need to adjust the total calorie load if the resting energy expenditure has been underestimated or modify the fuel substrate load if the respiratory quotient is approaching or greater than 1. The patient should receive increased amounts of vitamin C, at recommended doses of 1 g/day for adults and 500 mg/day for children, which will aid in wound healing.146 For patients with burns of greater than 20% of the total body surface area, zinc at doses of 220 mg/day will support wound healing as well as white cell function.147 The routine provision of these nutrients avoids complications related to insufficient delivery and obviates the need to measure their levels in the patient. In patients with prior surgery or preexisting medical conditions, special attention may be required to monitor for feeding intolerance and to ensure that adequate amounts of iron, folate, and vitamin B12 are being effectively delivered. For patients who have received extended courses of broad-spectrum antibiotics, vitamin K replacement beyond standard recommendations may be required to avoid the development of nutritionally related coagulopathy. The preservation of lean body mass requires more than just the appropriate amounts and blend of nutrients. Physical activity is important in directing the nutrients to muscle and reducing truncal fat deposition and the risk of hepatic steatosis.

153

In addition to providing appropriate calorie, protein, and nutrient loads to burn patients, it is now possible to modulate the metabolic response. Administration of beta-antagonists to children has been shown to be safe and to have a significant positive effect on outcome.148 The administration of growth hormone, which is depressed following burn injuries, has met with variable results. Herndon et al.149 have reported a positive effect in burned children given growth hormone, but a recent multicenter trial from Europe including critically ill patients showed an increased mortality in treated patients.150 An alternative strategy that seems not to be associated with problems for adults and is efficacious for children is the use of the drug oxandrolone, although a recent study reported that the agent was associated with prolonged need for mechanical ventilation in trauma patients.151–154 Additional strategies that might be utilized are the provision of selected nutrients in increased amounts. Glutamine, arginine, nucleotides, and omega-3 fatty acids have all been used in attempts to improve immune function above that seen with the optimal use of standard nutritional formulations.155–159 The routine use of these measures requires a full understanding of the therapeutic benefits and the potential adverse consequences of each. Additionally, some studies have found such supplements to be ineffective.160 For patients who have established chronic renal failure or develop renal insufficiency during their course of care, changes in the nutritional formulation will have to be made to accommodate their altered clinical status. For patients who require dialysis, the frequency of dialysis should be adjusted so that the protein intake needed to meet metabolic needs can be given. For patients with significant injuries who are receiving large amounts of feeding through the GI tract, the health of the GI tract itself must be continuously monitored. The development of major GI complications, although not common, can adversely impact the patient’s outcome. Complications can include ischemic necrotic bowel disease, intestinal obstruction, the development of Clostridium difficile colitis, and noninfectious diarrhea.161–165 The patient’s clinical status should be continuously monitored, and any changes in abdominal findings on physical examination should be aggressively followed up with appropriate diagnostic radiographic studies, endoscopy, stool cultures, and abdominal exploration before the patient deteriorates and develops an irreversible condition.

Transportation and Transfer Many important advances have been made in the care and management of burn-injured victims during the past 50 years. One of the more significant advances has been the recognition of the benefits of a team approach in the care of critically injured burn patients. The American

154

B.A. Pruitt, Jr., and R.L. Gamelli Figure 9.11. The transfer of patients to burn centers is often done by helicopter as shown here. Note the shiny metallic inner surface (black arrow) of the “space blanket” in which the patient has been wrapped to conserve heat and prevent excessive cooling during transport. The burn surgeon and burn nurse, sitting adjacent to the patient, monitor urinary output and, as needed, adjust the rate of infusion of the fluids suspended above the patient. The vibration, noise, poor light, and limited space that conspire to make monitoring and therapeutic intervention difficult mandate preflight physiologic stabilization of each patient who is to be transferred.

College of Surgeons and the American Burn Association have developed optimal standards for providing burn care and a burn center verification program that identifies those units that have undergone peer review of their performance and outcomes. Patients with burns and/or the associated injuries and conditions listed in Table 9.2 should be referred to a burn center. Once the decision has been made to transfer a patient to a burn center, there should be physician-to-physician communication regarding the patient’s status and need for transfer.166 Institutions should have preexisting interhospital transfer policies in place to facilitate communication and patient transfers. It is critical that the patient be properly stabilized in preparation for the transfer. The flight transfer team should have the capability of providing the care required for a critically injured, severely burned patient throughout the entire transfer procedure. A surgeon, a respiratory therapist, and a licensed practical nurse, all experienced in burn care, comprise such a team for long-distance, fixed wing aircraft transfers. For short-distance transport by rotary wing aircraft, inclusion of a burn physician in the flight team optimizes the safety and quality of care of extensively burned patients, but patients with lesser burns may be adequately cared for by nonphysician helicopter flight team members (a flight nurse and/or an advanced paramedic) who are in ready contact with medical control. A flight team roster should be maintained and published so the surgeons and other members of the team will be available when needed. Physicians and other team members should be assigned to the flight (transfer) team only after 6 to 12 months experience at a burn center, which will enable them to become familiar with the complications that occur in burn patients during resuscitation and develop compe-

tence in the prevention, treatment, and resolution of these problems. During transport the need to perform life-saving interventions such as endotracheal intubation or reestablishing vascular access may be very difficult to accomplish in the relatively unstable and limited space of a moving ambulance or a helicopter in flight (Figure 9.11). This difficulty makes it important to institute hemodynamic and pulmonary resuscitation and to achieve “stability” before undertaking transfer by either aeromedical or ground transport. A secure large-bore intravenous cannula must be in place to permit continuous fluid resuscitation. Patients should be placed on 100% oxygen if there is any suspicion of carbon monoxide exposure. If there is any question about airway adequacy an endotracheal tube should be placed and mechanical ventilation instituted before transfer begins. In-flight mechanical ventilatory support can be provided by a transport ventilator with oxygen supplied from a lightweight Kevlar tank transported in backpack fashion by the respiratory therapist. Patient safety during transport may necessitate chemical paralysis of the patient to prevent loss of the airway or vascular access. In-transit monitoring for helicopter transfer includes pulse rate, blood pressure, electrocardiogram, pulse oximetry, end-tidal CO2 levels, and respiratory rate. For long-distance transfer, the same physiologic indices should be monitored. In addition, the ultrasonic flowmeter should be used to assess the presence and quality of pulsatile flow in all four limbs on a scheduled basis, and excursion of the chest wall should be monitored to identify a need for limb or chest escharotomy, respectively. The hourly urinary output should also be monitored with fluid infusion adjusted as necessary. All patients should

9. Burns

be placed on nothing-by-mouth status, and those with a greater than 20% body surface area burn require placement of a nasogastric tube. In essence, a mini intensive care unit should be established for the duration of the long-distance flight. The burn wound should be covered with a clean and/or sterile dry sheet. The application of topical antimicrobial agents is not necessary before transfer, because they will have to be removed on admission to the burn center. Maintenance of the patient’s body temperature is vital. Wet dressings, which can lead to hypothermia, particularly in small adults and children, should be avoided. The patient should be covered with a heat-reflective space blanket to minimize heat loss. Pain medication is given in sufficient dosage to control the patient’s pain during transport while avoiding respiratory depression, airway comprise, or hypotension. Burn wounds, as tetanus-prone wounds, mandate immunization in accordance with the recommendations of the American College of Surgeons. As in the case of the transfer of any trauma victim, documentation must be thorough, flow sheets should be clearly marked, and a listing of all medications, including intravenous fluids that have been given, must be provided to the receiving physician. In the case of a patient suffering from significant multisystem trauma and burn injuries, it may be necessary to treat the patient’s lifethreatening mechanical injury before transfer if the transport time will be of long duration or the patient is unstable.98

Survival Data During the course of the past half century, early postburn renal failure as a consequence of delayed and/or inadequate resuscitation has been eliminated, and inhalation injury as a comorbid factor has been tamed. Invasive burn wound sepsis has been controlled, and early excision with prompt skin grafting and general improvements in critical care have reduced the incidence of infection, eliminated many previously life-threatening complications, and accelerated the convalescence of burn patients.167 All of these improvements have significantly reduced the mortality rate for burn patients of all ages. At the midpoint of the past century, a burn of 43% of the total body surface would have caused the death of 50 of 100 young adult patients (15 to 40 years) with such burns. Since that time, the extent of burn causing such 50% mortality (the LA50) in 21-year-old patients has increased to 82% of the total body surface and in 40-year-old patients to 72% of the total body surface. In children (0 to 14 years) the LA50 has increased from 51% of the total body surface in the 1950s to 72% today, and in the elderly (>40 years) the LA50 has increased from 23% of the total body surface area to 46% (Table 9.5). Not only has survival

155 Table 9.5. Changes in burn patient mortality at U.S. Army Burn Center, 1945–1991. Percentage of body surface burn causing 50% mortality (LA50) Age group

1945–1957

1987–1991

Children (0–14 years) Young adults (15–40 years)

51 43

Older adults

23

72* 82† 73‡ 46§

* Age 5 years. † Age 21 years. ‡ Age 40 years. § Age 60 years.

improved, but the elimination of many life-threatening complications and advances in wound care have improved the quality of life of even those patients who have survived extensive severe thermal injuries.

Critique It is well known that the Parkland formula is merely a guideline for fluid resuscitation and not a strict rule. The formula is particularly inaccurate for deep partialand full-thickness burns greater than 60% total body surface area. However, volume resuscitation, which substantially exceeds the estimated amount, often reflects the extent of an associated inhalation injury. Answer (B)

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B.A. Pruitt, Jr., and R.L. Gamelli neutralizing and non-acid neutralizing stress ulcer prophylaxis in thermally injured patients. J Trauma 1994; 36:541–547. Swain AH, Azadian BS, Wakeley CJ, Shakespeare PG. Management of blisters in minor burns. Br Med J (Clin Res Ed) 1987; 295:181. Rockwell WB, Ehrlich HP. Should burn blister fluid be evacuated? J Burn Care Rehabil 1990; 11:93–95. Demling RH, Lalonde C. Burn trauma. In Blaisdell FW, Trunkey DD, eds. Trauma Management, vol. IV. New York: Thieme Medical, 1989: 55–56. Hartford CE. The bequests of Moncrief and Moyer: an appraisal of topical therapy of burns B 1981 American Burn Association presidential address. J Trauma 1981; 21:827–834. Hunter GR, Chang FC. Outpatient burns: a prospective study. J Trauma 1976; 16:191–195. Miller SF. Outpatient management of minor burns. Am Fam Physician 1977; 16:167–172. Nance FC, Lewis VL Jr, Hines JL, Barnett DP, O’Neill JA. Aggressive outpatient care of burns. J Trauma 1972; 12:144–146. Heinrich JJ, Brand DA, Cuono CB. The role of topical treatment as a determinant of an infection in outpatient burns. J Burn Care Rehabil 1988; 9:253–257. Smith-Choban P, Marshall WJ. Leukopenia secondary to silver sulfadiazine: frequency, characteristics and clinical consequences. Am Surg 1987; 53:515–517. Gamelli RL, Paxton TO, O’Reilly M. Bone marrow toxicity by silver sulfadiazine. Surg Gynecol Obstet 1993; 177: 115–120. Lindberg RB, Moncrief JA, Mason AD. Control of experimental and clinical burn wound sepsis by topical application of Sulfamylon compounds. Ann NY Acad Sci 1968; 150:950–972. Yin HQ, Langford R, Burrell RE. Comparative evaluation of the antimicrobial activity of Acticoat antimicrobial barrier dressing. J Burn Care Rehabil 1999; 20:195–200. Strock LL, Lee MM, Rutan RL, Desai MH, Robson MC, Herndon DN, Heggers JP. Topical Bactroban (mupirocin) efficacy in treating burn wounds infected with methicillinresistant staphylococci. J Burn Care Rehabil 1990; 11:454–460. Pruitt BA Jr. Burn wound. In Cameron JL, ed. Current Surgical Therapy, 5th ed. St. Louis: CV Mosby, 1995: 872–879. Pruitt BA Jr, McManus AT, Kim JH, Goodwin CW. Burn wound infections: current status. World J Surg 1998; 22: 135–145. Jackson D, Topley E, Caso JS, Lowbury EJ. Primary excision and grafting of large burns. Ann Sur 1960; 152: 167–189. Tompkins RG, Remensynder JP, Burke JF, Tompkins DM, Hilton JF, Schoenfield DA, Behringer GE, Bondoc CC, Briggs SE, Quinby WC. Significant reductions in mortality for children with burn injuries through the use of prompt eschar excision. Ann Surg 1988; 208(5):577–585. Burke JF, Bondoc CC, Quinby WC. Primary burn excision and immediate grafting: a method of shortening illness. J Trauma 1974; 14:389–395.

98. Santaniello JM, Luchette FA, Esposito TJ, Gunawan H, Davis KA, Gamell RL. Ten years experience of burn, trauma and combined burn/trauma injuries comparing outcomes. J Trauma 2004; 57:696–700. 99. McManus WF, Mason AD Jr, Pruitt BA Jr. Excision of the burn wound in patients with large burns. Arch Surg 1989; 124:718–720. 100. Janzekovic Z. A new concept in the early excision and immediate grafting of burns. J Trauma 1970; 10:1103–1108. 101. Desai MH, Herndon DN, Broemeling L, Barrow RE, Nichols RJ, Rutan RL. Early burn wound excision significantly reduces blood loss. Ann Surg 1990; 211:753–759. 102. Herndon DN. Perspectives in the use of allograft. J Burn Care Rehabil 1997; 18:S6. 103. Chatterjee DS. A controlled comparative study of the use of porcine xenograft in the treatment of partial thickness skin loss in an occupational health center. Curr Med Res Opin 1978; 5:726–733. 104. Demling RH. Burns. N Engl J Med 1985; 313:1389–1398. 105. Supple K, Halerz M, Aleem R, Gamelli RL. Transcyte as an alternative dressing for use in the pediatric burn patient. J Burn Care Rehabil 2003; 24(2):S129. 106. Sheridan RL, Choucair RJ. Acellular allodermis in burn surgery: 1 year results of a pilot trial. J Burn Care Rehabil 1998; 19:528–530. 107. Rue LW III, Cioffi WG, McManus WF, Pruitt BA Jr. Wound closure and outcome in extensively burned patients treated with cultured autologous keratinocytes. J Trauma 1993; 34:662–667. 108. Mozingo DW, Smith AA, McManus WF, Pruitt BA, Mason AD. Chemical burns. J Trauma 1988; 28:642–647. 109. Kohnlein HE, Merkle P, Springorum HW. Hydrogen fluoride burns: experiments in treatment. Surg Forum 1973; 24:50. 110. Pardoe R, Minami RT, Sato RM, Schlesinger SL. Phenol burns. Burns 1976; 3:29–41. 111. Pruitt BA Jr. Management of burns in the multiple injury patient. Surg Clin North Am 1970; 50:1283–1299. 112. Bangs CC. Hypothermia and frostbite. Emerg Med Clin North Am 1984; 2:475–487. 113. Miller BJ, Chasmar LR. Frostbite in Saskatoon: a review of 10 winters. Can J Surg 1980; 23:423–426. 114. Britt LD, Dascombe WH, Rodriguez A. New horizons in management of hypothermia and frostbite injury. Surg Clin North Am 1991; 71:345–370. 115. IAEA, June 1996, The Radiological Accident at the Irradiation facility in Nesvizh, IAEA (vienna, Austria), on line at IAEA http://www-pub-iaea.org/MTCD/publications/ PDF/Pub1010_web.pdf. 116. Tsujii H, Akashi M, eds. The Criticality Accident in Tokaimura: Medical Aspects. Proceedings of an International Conference, December 14 and 15. Chiba, Japan: National Institute of Radiological Sciences, 2000. (NIRSM-146). 117. Mettler, FA, Voelz, GL. Major radiation exposure—what to expect and how to respond. N Engl J Med 2002; 346:1554–1561. 118. Roujeau JC, Kelly JP, Naldi L, Rzany B, Stern RS, Anderson T, Auquier A, Basliju-Garin S, Corlea O, Locate F. Medication use and the risk of Stevens Johnson syndrome

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or toxic epidermal necrolysis syndrome. N Engl J Med 1995; 333:1600–1607. Viard I, Wehrli P, Bullani R, Schneider P, Holler N, Salomon D, Hunziker T, Saurat J, Tschopp J, French L. Inhibition of toxic epidermal necrolysis by blockade of CD95 with human intravenous immunoglobulin. Science 1998; 282:490–493. Becker DS: Toxic epidermal necrolysis. Lancet 1998; 351:1417–1420. Rasmussen JE, et al. Erythema multiforme, StevensJohnson syndrome and toxic epidermal necrolysis. Dermatol Nuc Dermatol Nurs 1995; 7:37–43. Heimbach DM, Engrav LH, Marvin JA, Harnar TJ, Grube BJ. Toxic epidermal necrolysis: a step forward in treatment. JAMA 1987; 257:2171–2175. Speron S, Gamelli RL. Toxic epidermal necrolysis syndrome versus mycosis fungoides. J Burn Care Rehabil 1997; 18:421–423. Brown KM, Silver GM, Halerz M, Walaszek P, Sandroni A, Gamelli RL. Toxic epidermal necrolysis: does immunoglobulin make a difference? J Burn Care Rehabil 2004; 25:81–88. Dougherty W, Waxman K. The complexities of managing severe burns with associated trauma. Surg Clin North Am 1996; 76:923–958. Purdue GF, Hunt JL. Multiple trauma and the burn patient. Am J Surg 1989; 158:536–539. Wilmore DW, Orcutt TW, Mason AD Jr, Pruitt BA Jr. Alterations in hypothalamic function following thermal injury. J Trauma 1975; 15:697–703. Carlson DE, Cioffi WG Jr, Mason AD Jr, McManus WF, Pruitt BA Jr. Resting energy expenditure in patients with thermal injuries. Surg Gynecol Obstet 1992; 174:270–276. Alverdy J, Aoys E, Moss GS. Total parenteral nutrition promotes bacterial translocation from the gut. Surgery 1988; 104:185–190. Wilmore D, Long J, Mason A, Skreen RW, Pruitt BA Jr. Catecholamines: mediators of the hypermetabolic response to thermal injury. Ann Surg 1974; 180:653– 669. Kudsk K, Brown R. Nutritional support. In Mattox K, Feliciano D, Moore E, eds. Trauma. New York: McGraw-Hill, 2000: 1369–1405. Demling RH, Seigne P. Metabolic management of patients with severe burns. World J Surg 2000; 24:673–680. Bessey PQ, Jiang ZM, Johnson DT, Smith RJ, Wilmore DW. Posttraumatic skeletal muscle proteolysis: the role of the hormonal environment.World J Surg 1989; 13:465–470. Mochizuki H, Trocki O, Dominion L, Brackett KA, Joffe SN, Alexander JW. Mechanism of prevention of postburn hypermetabolism and catabolism by early enteral feeding. Ann Surg 1984 ;200:297–300. Wood RH, Caldwell F Jr, Bowser-Wallace BH. The effect of early feeding on postburn hypermetabolism. J Trauma 1988: 28:177–183. Chiarelli A, Enzi G, Casadei A, Baggio B, Valerio A, Mazzoleni F. Very early nutrition supplementation in burned patients. Am J Clin Nutr 1990; 51:1035–1039. Van Den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, Vlasselaers D, Ferdinande P,

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Lauwers P, Bouillon R: Intensive insulin therapy in critically ill patients. N Engl J Med 2001; 345:1359–1367. Askanazai J, Rosenbaum S, Hyman A, Silverberg PA, Milic-Emili J, Kinney JM. Respiratory changes induced by the large glucose loads of total parenteral nutrition. JAMA 1980; 243:1444–1447. Peck M. Practice guidelines for burn care: nutritional support. J Burn Care Rehabil 2001; 12:59S–66S. Waymack J, Herndon D. Nutritional support of the burned patient. World J Surg 1992; 16: 80–86. Wolf R, Goodenough R, Burke J, Wolfe M. Response of proteins and urea kinetics in burn patients to different levels of protein intake. Ann Surg 1983; 197:163–171. Matsuda T, Kagan R, Hanumadass M, Jonasson O. The importance of burn wound size in determining the optimal calorie: nitrogen ratio. Surgery 1983; 94:562–568. Alexander J, MacMillan B, Stinnet J, Ogle CK. Beneficial effects of aggressive protein feeding in severely burned children. Ann Surg 1980: 192:505–517. O’Neill JA, Caldwell MD, Meng HC: Essential fatty acid deficiency in surgical patients.Ann Surg 1977; 185:535–542. Harrison HN, Moncrief JA, Duckett JW Jr, Mason AD Jr. The relationship between energy metabolism and water loss from vaporization in severely burned patients. Surgery 1964; 56:203–211. Mayes T, Gottschlich M, Warden G. Clinical nutrition protocols for continuous quality improvement in the outcomes of patients with burns. J Burn Care Rehabil 1997; 18:365–368. Selmanpakoglu ACC, Sayal A, Isimer A. Trace element (Al, Se, Zn, Cu) levels in serum, urine, and tissues of burn patients. Burns 1994; 20:99–103. Herndon DN, Hart DW, Wolf SE, Chinkes DL, Wolfe RR. Reversal of catabolism by beta-blockade after severe burns. N Engl J Med 2001; 345(17):1223–1229. Herndon D, Barrow R, Kunkel K, Broemling L, Rutan R. Effects of recombinant human growth hormone on donor site healing in severely burned children. Ann Surg 1990; 212:424–429. Talala J, Ruokonen E, Webster N, Nielsen MS, Zandsta DF, Vurdelinckx G, Hinds CJ. Increased mortality associated with growth hormone treatment in critically ill adults. N Engl J Med 1999; 341:785–792. Demling R. Comparison of the anabolic effects and complications of human growth hormone and the testosterone analog, oxandrolone, after severe burn injury. Burns 1999; 25:215–221. Demling R, Orgill D. The anticabolic and wound healing effects of the testosterone analog oxandrolone after severe burn injury. J Crit Care 2000; 15:12–17. Demling R, DeSanti L. Oxandrolone, an anabolic steroid, significantly increases the rate of weight gain in the recovery phase after major burns. J Trauma 1997; 43:47–51. Bulger EM, Jurkovich GJ, Farver CL, Klotz P, Maier RV. Oxandrolone does not improve outcome of ventilatordependent surgical patients. Ann Surg 2004; 240:472– 480. Saito H, Trocki O, Wang S, Gonce SJ, Joffe SN, Alexander JW. Metabolic and immune effects of dietary arginine supplementation after burn. Arch Surg 1987; 122:784–789.

160 156. Souba W. Glutamine: a key substrate for the splanchnic bed. Annu Rev Nutr 1991; 11:285–308. 157. Alverdy JC. Effects of glutamine-supplemented diets on immunology of the gut. J Parenteral Enteral Nutr 1990; 14:109S–113S. 158. Ziegler T, Young L, Benfell K, Scheltinga M, Hortos K. Clinical and metabolic efficacy of glutamine supplemented parenteral nutrition after bone marrow transplantation: a randomized, double-blind controlled trial. Ann Intern Med 1992; 116:821–830. 159. Alexander J, Saito H, Trocki O, Ogle C. The importance of lipid type in the diet after burn injury. Ann Surg 1986; 204:1–8. 160. Saffle JR, Wiebke G, Jennings K, Morris SE, Bartor RG. Randomized trial of immune-enhancing enteral nutrition in burn patients. J Trauma 1997; 42:793–802. 161. Kowal-Vern A, McGill V, Gamelli R. Ischemic necrotic bowel disease in thermal injury. Arch Surg 1997; 132:440– 443. 162. Scaife C, Saffle J, Morris S. Intestinal obstruction secondary to enteral feedings in burn trauma patients.


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10 Electrical and Lightning Injuries Raphael C. Lee

Case Scenario A 23-year-old industrial mechanic sustains a highvoltage electrical injury. He has a circumferential fullthickness injury of the right upper extremity. The patient develops hand paraesthesia and then numbness. Which of the following is the management of choice at this time? (A) Decrease fluid resuscitation and elevate the involved extremity (B) Increase fluid resuscitation and administer mannitol (C) Continue to monitor the extremity (D) Perform escharotomy and monitor the extremity (E) Perform escharotomy and fasciotomy of the involved extremity

Pathophysiology and Manifestations Because of the multiple modes of electrical force action on biologic tissues, electrical injury can produce a very complex pattern of injury and resulting clinical manifestations.1,2 Electrical forces cause tissue injury primarily by permeabilization of cell membranes and thermal denaturation of tissue proteins. When high-energy arcmediated contacts occur, there is often a strong thermoacoustic blast force generated, which adds blunt mechanical trauma. Associated falls and skin burns are frequent, adding to victim injury. Electrical current passing through the body imposes electrical forces acting on cell membranes. The longer the cell projects in the direction of current flow, the stronger the force. Large cells, such as skeletal muscle and nerve, experience strong enough forces during electrical shock to disrupt their membranes. This produces the increased permeability to electrolytes in solution that subsequently

leads to metabolic energy depletion, free radical generation, and cellular necrosis. The resistance to current passage is highest at the skin contact points, which explains the occurrence of deep burns at the contact point, as shown in Figure 10.1. Similarly, victims of direct lightning strikes experience a multimodal injury. The current passes in the air between the cloud, and the lightning strikes the victim. Although very little of the lightning current penetrates the body, the current pulse sets up a large magnetic field pulse that readily penetrates the body. The magnitude of this pulse is sufficient to induce large internal currents that cause neuromuscular, cardiac, and central nervous system damage. The thermoacoustic blast (i.e., thunder)–related barotrauma can be significant. Peripheral nerve and skeletal muscle tissues are the most vulnerable to membrane permeabilization by electrical force. The rapidity of this process is such that only millisecond duration contacts are required to generate significant damage accumulation. With more prolonged contacts, on the range of seconds, thermal damage in the subcutaneous tissues occurs. Because the vulnerability to supraphysiologic temperature exposure is similar across different tissue types, victims of prolonged contact suffer direct thermal damage to all tissues in the current path.3 The rate of tissue heating scales with the square of the tissue current density. As a consequence of the variation in current density with extremity cross-sectional area, the anatomic distribution of tissue injury varies considerably. Both heat and electrical forces lead to disruption of cellular membranes, extensive swelling, and compartment syndromes (Figure 10.2).4 The extremities are nearly always involved because most victims that require inpatient hospital care are young industrial or construction workers using their hands. In industrial high-voltage shocks, conduction of electrical current through the body takes place before mechanical contact is made. Electrical contact can occur through the electrical arc. Exposure to the expanding arc

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R.C. Lee Table 10.1. Basic management of electrical injuries.

Figure 10.1. Characteristic appearance of an electrical contact wound. The central area has experienced very high temperatures, resulting in tissue coagulation. It can be expected that this injury extends along the current path beneath the skin. The same pattern results regardless of the direction of the current. The depression of the wound is caused by coagulation, not by the momentum of ionic current passage.

or flash brings the victim in the circuit. The involuntary muscle spasm that results may lead to joint dislocations and spine fractures. When currents of more than 100 mA are passed hand-to-hand or hand-to-foot, there is enough electrical force generated in the heart to cause cardiac arrhythmias.

Approach to Management Electrical injury patients can present complex medical management challenges. In severe cases, the widespread destruction of tissue causes tremendous life-threatening physiologic stress unlike any other form of trauma. On the other extreme are the apparently minor cases, wherein insidious injury to the nervous system presents substantial diagnostic and management challenges. Many electrical shock survivors present with delayed-onset neurologic and neuropsychological problems. In general, medical providers must be aware that electrical shock patients can require involvement of every medical and

• Resuscitation and assessment ⴰ Evaluate and support vital organ function ⴰ Manage cardiac injury if present ⴰ If myoglobinuria present, increase urine output to 2 cc/kg ⴰ Perform fasciotomies as needed within 6 hours of injury ⴰ Use diagnostic imaging (MRI) to assess extent of injury ⴰ Provide tetanus prophylaxis • Initial debridement ⴰ Remove grossly devitalized tissue ⴰ Provide temporary wound coverage ⴰ Provide antibiotic coverage ⴰ Release tense muscle compartments • Wound closure • Provide nutrition support ⴰ Repeat debridement at 24–48 hours ⴰ Close the wound • Neurologic and psychiatric assessment ⴰ Provide pain control ⴰ Perform baseline psychiatric assessment and follow-up ⴰ Perform neuropsychological evaluation at 6 months postinjury • Rehabilitation ⴰ Muscle strengthening and endurance enhancement ⴰ Scar management ⴰ Occupational therapy

surgical specialty. A basic management strategy is listed in Table 10.1.5

Acute Care In the field, the first priority is to disconnect the patient from the electrical power source. When high-capacity circuits are involved, this must not be attempted before the circuit is deenergized. If the circuit is a commercial power distribution line, great care has to be exercised. Highvoltage, high-current-capacity lines can generate enough electrical field in the ground around a victim to cause injury to anyone approaching to aide. In addition, these commercial power circuits have automatic shut-off and automatic power return breakers. These high-voltage circuits can turn on while emergency crews are attempting to extract the victim. Therefore, it is strongly recommended that the emergency crews contact the electrical utility to shut down the line before extracting.

Figure 10.2. The incredibly destructive nature of just a brief contact with high-voltage electrical power is shown. The muscle contraction has ripped the muscle away from the tendons, and there is massive swelling requiring full fasciotomies. Both thermal and nonthermal injuries are evident, resulting in extensive tissue destruction.

10. Electrical and Lightning Injuries

While extracting the victim, it is safest to assume spine injury until proven otherwise. Although this manifestation is unusual, it is well established that fractures and joint dislocations can follow the muscle spasm that occurs during electrical shock. Prolonged cardiopulmonary resuscitation may be necessary before the stunned myocardium regains the ability to sustain a coordinated rhythm. This is particularly true following lightning injury. Large-bore peripheral intravenous lines delivering a balanced salt solution at a rate sufficient to generate a 30 to 50 cc/hr urine output, supplemental oxygen, and a Foley catheter are essential. If the urine is visibly pigmented with hemochromogens, the urine output should be doubled and alkalinized to a pH > 6. As soon as the patient arrives in the emergency care department, clothing and debris on wounds should be removed and the wounds cleaned. Large skin burn wounds are often present because of arc-mediated contacts and clothing ignition. Care should be taken to prevent rapid loss of body heat through open wounds. When skin contact wounds are present or the contact voltage is in excess of 200 volts, transfer to a burn center for definitive evaluation and care should occur.The immediate goal is to support vital organ function to achieve patient stabilization. Begin initial resuscitation with potassium-free solutions such as normal saline, which is preferred until serum chemistries are known. In the absence of significant skin burns the initial fluid administration rate is based on clinical signs such as blood pressure, pulse rate, and clinical intuition. Subsequently the fluid is adjusted as needed to maintain 30 to 50 cc of urine output per hour. If the urine is visibly pigmented, intravenous fluid should be increased to double the hourly urine output until it clears. It is recommended that the urine pH is alkalinized to above 6.0 by adding bicarbonate to the intravenous solutions. Providing adequate nutritional support, especially though enteral tube feedings, is very important. Supplemental oxygen may be helpful to edematous tissues. Cardiac arrhythmia must be immediately controlled by appropriate antiarrhythmic agents and correction of pH and electrolyte abnormalities. Brain injury can manifest with seizures, which may need to be controlled with antiepileptic agents and with correction of serum chemistries.6 Patients who have lost central nervous system control or respiration or airway should be intubated and mechanically ventilated. A feeding tube should be passed to begin gastrointestinal alimentation within 6 hours of injury. Clearly, enteral feeding is contraindicated if abdominal viscera are injured by current. Substantial intraabdominal injuries are known to occur in electrical trauma. Ruptures of colon, gallbladder, and other organs have been reported. Fortunately, these severe intraabdominal injuries are unusual. A paralyzed ventilated patient may need electroencephalographic monitoring to assess the quality of seizure control.

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Diagnostic Evaluation Cardiac arrhythmias must be rapidly detected by examination of the pulses and measurement of blood pressure and then diagnosed by electrocardiogram. The major initial diagnostic challenge is to determine the location and extent of all tissue damage, particularly that which is beneath undamaged skin. Lateral spine x-rays are needed to rule out unstable spine fracture patterns. X-ray images of the extremities involved are also important to rule out skeletal fractures or joint dislocations. Blood chemistries should be immediately evaluated and monitored. Metabolic acidosis and elevated serum potassium level may occur as a consequence of extensive skeletal muscle injury. Over several hours creatine phosphokinase level will rise if there is significant skeletal muscle cell lysis. Thermally damaged tissue is recognizable on gross inspection, whereas tissues damaged by electropermeabilization usually simply appear edematous. Within minutes after injury, tissue edema begins to increase due to increased vascular permeability and release of intracellular contents into the extravascular space. Compartment syndrome and compression neuropathies are common manifestations of an electrically traumatized extremity. Injured skeletal muscle and nerve frequently underlie uninjured skin (see Figure 10.1). If a fast magnetic resonance imaging (MRI) scanner is available, T2weighted images can localize muscle and nerve edema, and gadolinium enhanced T1-weighted images can demonstrate tissues with cell membrane permeabilization.7 It is important to remember that edema cannot form in the absence of tissue perfusion. Thus, where severe heating has left coagulated vessels, tissue injury may exist in the absence of edema. The presence of edema on MRI should guide attention to potential problem areas. Compartment pressures should be measured where edema is present. Tense muscle compartments are not reliably diagnosed by manual palpation. Muscle compartment fluid pressures should be measured and documented. If MRI is not available, then the muscle compartments within the current path between contact points should be monitored for elevated interstitial fluid pressure. Elevated compartment pressures may not manifest until the patient has been resuscitated. It may be necessary to check the pressures every 8 hours for 24 hours. Radionucleotide scanning with Tc99m-pyrophosphate may be useful to localize hidden tissue injury, especially in cases of less extensive injury.7 However, these scans take 4 to 6 hours to complete and are mostly useful in the less severe injuries. Neurologic complaints are almost invariably present. When symptoms exist, neurodiagnostic studies are required to determine the extent of neuromuscular dysfunction. Compound nerve conduction velocity and electromyography are standard studies that are widely

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available. Unfortunately, they lack sensitivity and specificity. Our protocol is to use refractory period spectral analysis, which permits separately measuring the responses of the different nerve fiber types present in compound nerves. Major peripheral nerves contain thousands of fibers that exist in several different types. The large myelinated fast fibers are most susceptible to electrical forces generated by passage of current through the extremity while small-diameter unmyelinated fibers are the least susceptible. Thus, peripheral nerve injury is mixed in pattern. Diagnostic evaluation by refractory period spectral analysis of nerve function is most useful because of its capability to discriminate each axon type separately.8 Unless the victim was water submerged, at least two skin contact wounds are present. Because 60-Hz commercial power frequency current reverses direction every 8 msec, nearly always all wounds serve as both entry and exit points into the body. Therefore, the commonly used terminology of “entrance” or “exit” wounds is basically incorrect. Differences in wound area, depth, and topography are determined by the size and shape of the object with which the victim was in contact. Ophthalmologic examination with emphasis on signs of corneal burns or abrasions should be performed. The ignition of a highenergy arc generates a loud noise or blast, which can lead to tympanic membrane rupture and/or closed head trauma. If there is a history of loss of consciousness, a computerized tomogram of the head is indicated.

Early Management Perfusion to edematous tissue must be restored as soon as possible. Diminished pulses or decreased tissue oxygen detected by transcutaneous pulse oximetry are indications for escharotomy releases. Assessing the need for fasciotomy is an important consideration. The classic clinical signs of pain in acute compartment syndrome cannot be relied on because of the nerve injury that frequently accompanies electrical shock. When there are circumferential (or near-circumferential) extremity skin burns, muscle compartment pressures can be elevated because of eschar compression. If the muscle, abdominal, chest, or other compartment pressures remain elevated after escharotomy, then fasciotomy is indicated in the operative theater under adequate lighting. Because the compartment pressure needs to exceed only 30 mm Hg to reduce gas exchange in the muscle, measurement for a distal arterial pressure drop is not an early indicator of the risk of ischemic muscle injury. A muscle compartment fluid pressure of greater than 30 cm H2O is the indication for fasciotomy. When a muscle compartment requires release in an electrical shock victim, the adjacent ones should also be decompressed. It must be remembered that permanent muscle

R.C. Lee

damage can be appreciated after only 2 hours of warm ischemia, and a no-reflow state can occur after 6 hours of warm ischemia time. To be effective, the epimyesium must also be released under full view. Release of skeletal muscle compartments is often followed by massive bulging of muscle and a readily observed increase in tissue perfusion. Care to avoid tissue drying or desiccation is important. In addition to topical antimicrobial coverage, the wound should be covered using an evaporative barrier. In addition to decompression of extremity muscle compartments, decompression of nerve within edematous fibroosseus conduits (e.g., carpal tunnel, Guyon’s canal, and tarsal tunnel) should be carried out to help prevent compression neuropathy. Unless thermally burned, nerve and tendons should not be debrided at the initial visit to the operating room. Well-fashioned splints are essential to maintain joints in a position of function and to protect vascular perfusion during hospitalization. With modern surgical reconstruction techniques, amputations are required less often now. The risk of infection must be kept in mind. Tetanus prophylaxis should be administered as established by the World Health Organization guidelines. Anaerobic bacterial infection of devascularized skeletal muscle is a commonly expressed concern and intravenous penicillin G and/or hyperbaric oxygen as prophylactic antibiotics are utilized by some but has unproven value. Radiographs taken to rule out fractures may reveal air bubbles in the subcutaneous tissues. This probably results from boiling from Joule heating and may indicate irreversible heat damage. Most importantly, in the triage and acute care setting, soft tissue air bubbles should not be interpreted as a sign of anaerobic sepsis. Debridement of nonviable tissue should be performed in the operating theater as soon as the patient has been stabilized and the evaluations completed. Quinby et al.9 proposed early muscle debridement under histologic control. Although accurate, this method prolongs general anesthesia and may result in increased morbidity. Arteries and veins that are burned should be replaced with healthy vein grafts as soon as possible. A second-look procedure 48 hours later is often needed to be certain of a complete debridement. The most widely practiced approach is to reinspect and debride the wounds in the operating theater within 48 to 72 hours so that systemic toxicity and local infection risk are minimized. Wound closure should wait until the wound is free of all dead and/or marginal tissue and quantitative bacteriologic counts rule out invasive wound sepsis. In most cases, the major vessels have not been heat damaged and can be used to support microvascular free flaps. Wound closure can also be accomplished by local fasciocutaneous flaps or skin grafts. The choice of procedure should be made with the view toward optimizing rehabilitation potential. Local skin and fascial flaps in an injured

10. Electrical and Lightning Injuries

extremity have been shown to be reliable. Doppler presurgical assessment of the vascular pedicles is desirable. Tendons and nerves should be kept physiologically moistened and protected with vascularized tissue as soon as possible. Effective wound closure should be accomplished whenever possible within the first week.

Rehabilitation Rehabilitation into society and gainful employment is the ultimate objective and often the biggest challenge. Survivors of industrial accidents are often young and proud of their capabilities. After injury, they are often limited by pain and worried about their ability to return to gainful employment. For severely injured victims this requires functional muscle and nerve reconstruction as well as correction of scar contractures. Psychological problems are the rule and require involvement of serial neuropsychological assessment and protracted support.10 Persistent neurologic problems are also common and often require therapeutic intervention from a pain management specialist.11 Work force reentry should be guided by consultation with employer, patient, co-workers, and an experienced rehabilitation team.12 Under investigation are therapeutic surfactant copolymers that mimic the effects of natural cellular chaperones that promise to reduce tissue loss after electrical injuries.13

Critique The development of paraesthesia in an extremity with a circumferential full-thickness burn is a compartment syndrome until proven otherwise. In addition to this patient requiring an escharotomy, a fasciotomy is also needed given the mechanism of injury—a highvoltage electrical injury. Muscle damage with subsequent swelling should be suspected. Answer (E)

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References 1. Lee RC. Tissue injury from exposure to power frequency electrical fields. In Lin J, ed. Advances in Electromagnetic Fields in Living Systems, New York: Plenum Press, 1994; 81–127. 2. Capelli-Schellpfeffer M, Lee RC, Toner M, Diller KR. Correlation Between Electrical Accident Parameters and Sustained Injury. IEEE /PCIC Transactions, September 1996. 3. Remensnyder JP. Acute electrical injuries. In Martyn JAJ, ed.Acute Management of the Burned Patient. Philadelphia: WB Saunders, 1990; 66–86. 4. Lee RC, Cravalho EG, Burke JF, eds. Electrical Trauma: The Pathophysiology, Manifestations and Clinical Management. Cambridge: Cambridge University Press, 1992; 133–152. 5. Lee RC, Capelli-Schellpfeffer M, Kelley KM, eds. Electrical injury: a multidisciplinary approach to therapy, prevention and rehabilitation. Ann NY Acad Sci 1994; 720. 6. Dasgupta RA, Schulz JT, Lee RC, Ryan CM. Severe hypokalemia as a cause of acute transient para plegia following electrical shock. Burns 2002; 28:609–611. 7. Fleckenstein JL, Chason DP, Bonte FJ, et al. High-voltage electric injury: assessment of muscle viability with MR imaging and Tc-99 m pyrophosphate scintigraphy. Radiology 1995; 195(1):205–210. 8. Abramov G, Bier M, Capelli-Schellpfeffer M, Lee RC. Alteration in sensory nerve function following electrical shock. Burns J 1996; 22(8):602–606. 9. Quinby WC Jr, Burke JF, Trelstad RL, Caulfield J. The use of microscopy as a guide to primary excision of high-tension electrical burns. J Trauma 1978; 18:423–429. 10. Pliskin NH, Ammar AM, Fink JM, Hill SK, Malina AC, Kelley KM, Meiner BA, Lee RC. Neuropsychological effects of electrical injury. J Int Neuropsychol Soc 2006; 12:17–23. 11. Wilbourn AJ. Peripheral nerve disorders in electrical and lightning injuries. Semin Neurol 1995; 15(3):241–256. 12. Chico M, Capelli-Schellpfeffer M, Kelley KM, Lee RC. Management and coordination of post-acute medical care for electrical trauma survivors. Ann NY Acad Sci 1999; 888:334–342. 13. Lee RC, River P, Pan FS, Ji L, Wollmann RL. Surfactantinduced sealing of electropermeabilized skeletal muscle membranes in vivo. Proc Natl Acad Sci USA 1992; 89:4524– 4528.

11 Soft Tissue Infections Anthony A. Meyer, Jeffrey E. Abrams, Thomas L. Bosshardt, and Claude H. Organ, Jr.

Case Scenario A 57-year-old renal transplantation patient develops a necrotizing soft tissue infection in the perineum. She is febrile, tachycardic, and hemodynamically labile with deterioration of renal function. Which of the following is not essential to the management of the patient? (A) (B) (C) (D) (E)

Fluid resuscitation Antimicrobial therapy Nutritional support Debridement of necrotic tissue Hyperbaric oxygen therapy

Necrotizing soft tissue infections are infections that cause tissue necrosis by both direct cell destruction and ischemia secondary to thrombosis of blood vessels that pass through the fascial and subcutaneous fat to the skin. Infections can occasionally involve muscle as well. Necrotizing soft tissue infections represent a spectrum of infection that may be localized to a relatively small area, take days to progress, and have minimal systemic effects or spread rapidly to involve more than 25% of the body’s surface, with profound hemodynamic instability and death within 12 to 24 hours. Such soft tissue infections mandate acute surgical intervention. These infections have been known by many names, including “hospitalism,” “hemolytic streptococcal gangrene,” “necrotizing erysipelas,” “necrotizing cellulitis,” and “necrotizing fasciitis.” Recently, the name “necrotizing soft tissue infection” (NSTI) has become the accepted name. However, the terminology of NSTI is of secondary concern when physicians are challenged by a pattern with this aggressive illness. Distinguishing the specific category of necrotizing infection serves little purpose. The primary

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emphasis must be focused on rapid recognition and prompt treatment. To limit severe morbidity and to reduce mortality, early treatment with aggressive surgical intervention and appropriate antimicrobial therapy is essential. The NSTIs must be considered a surgical emergency. In an excellent clinical account of NSTI in Civil War medicine, over 60% mortality for serious infections was reported.1–3 Mortality rates reported for this disease process have varied dramatically, depending on the patient population and treatment available. Meleney,4 in a review of cases from China in 1920, reported lower mortality (20%), but described a less aggressive spectrum of disease because patients with more virulent infections would not survive to reach care. Recent series in the United States have also varied in the type of disease process that is seen, the patient population, and outcomes. In general, the mortality rate for NSTI generally remains in the 20% to 40% range.2,5,6 Increased attention has been focused on NSTIs in recent years. This may have to do with studies coming out documenting potentially new and more virulent types of the disease. Other reasons for greater attention may be the sensational accounts of individual cases in the tabloid press, including descriptions of “flesh-eating bacteria” and “flesh-eating viruses.” Clearly, there is evidence that the actual incidence of these infections is increasing.7–9 Hospitals that treat a large number of critically ill patients, such as teaching and public hospitals, have described an increase in the number of NSTI patients. The rise in the incidence of the disease may also be explained by the increasing numbers of immunosuppressed or chronically ill patients, who appear to be more susceptible to these infections, the increased obesity in the population, and a better recognition and diagnosis of the process.10–12 The magnitude by which correct diagnosis is contributing to an increased perceived incidence is yet to be determined. The etiology of the disease remains poorly understood, but it is clear that NSTIs remain a major clinical problem.

11. Soft Tissue Infections

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The pathophysiology will be reviewed to understand why the disease is so morbid and to provide an understanding of how to diagnose and treat this challenging spectrum of soft tissue infections.

Pathophysiology The potential causes of NSTIs include tissue injury, bacterial inoculation, superficial skin infection, and any of the many possible mechanisms for initiating cutaneous infections. There is often tissue damage or injury, including the injury of a surgical incision. Wounds combine a means for introduction of bacteria with a potential medium in which the bacteria can multiply. By whatever mechanism, a bacterial inoculum gets into dermal or subcutaneous tissue and, rather than create a simple abscess or cellulitis, initiates a cascade of cell destruction, inflammation, and ischemia. This creates a means by which the infection moves into normal tissue and causes necrosis and secondary ischemia of more superficial tissue by thrombosis of vessels that pass through the infected tissue.5,13,14 Patients who are at increased risk for NSTIs include diabetics, immunosuppressed patients, and intravenous drug users.15,16 Whether the continued inoculation of contaminated material or the debilitating lifestyle that is associated with intravenous drug use is the principle cause of the infection is unclear.13,17,18 There are many other medical problems that are associated with increased incidence of NSTIs. Diabetics have impaired blood flow to skin and other soft tissue, decreased ability to fight bacterial infection, and other metabolic changes that make them more susceptible to any infection. Patients who undergo immunosuppression to limit transplant rejection or for treatment of cancer are also at increased risk for these severe soft tissue infections. Furthermore, these immunosuppressed patients are more likely to develop infections from atypical organisms than the most common types, which are discussed later.19 There are patients, however, in whom there is no obvious cause who present with a clinical picture suspicious for NSTI. It is important to understand that the lack of an obvious associated medical condition or injury should not preclude a potential diagnosis of NSTI. There is ample evidence that early identification and treatment are important to improving outcome and ultimately decreasing the morbidity of this rapidly progressing infection. It is important also to remember that the management of NSTI in patient groups at increased risk is no different from management in patients without these risks. The presence of risk factors should only make the physician more aggressive at pursuing early diagnosis.

Figure 11.1. Histology of NSTI, demonstrating acute inflammation within muscle bundles.

Microbiology The microbiologies of the organisms cultured from NSTIs in different studies vary widely and are dependent not only on the disease and patient population but also surgical and laboratory techniques as well. The bacteriology of NSTI is well recognized, and the infectious process is independent of specific bacteria.17,20–23 Although NSTIs can be monomicrobial, most are polymicrobial and involve aerobic and anaerobic organisms behaving synergistically. These bacteria can invade the subcutaneous tissue, fascia, and even muscle to result in necrosis and destruction (Figures 11.1 and 11.2). In our series of patients treated at an urban hospital, 78% of cases were polymicrobial and 2.8 organisms were recovered per patient.17 Anaerobes, skin flora, and Gram-negative rods were commonly encountered (Table 11.1). Elliott et al.21

Figure 11.2. Bacterial invasion of the soft tissues by Grampositive cocci.

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A.A. Meyer, J.E. Abrams, T.L. Bosshardt, and C.H. Organ, Jr.

Table 11.1. Bacteriologic findings in patients with necrotizing soft tissue infections. Organism

No. of patients

Anaerobes Mixed anaerobes Clostridium sp.* Diphtheroids Bacteroides fragilis Bacteroides buccae Peptostreptococcus sp. Total

16 8 3 2 2 1 32

Gram-positive cocci Streptococcus viridans Hemolytic group A streptococci Enterococcus faecalis Total

8 7 6 21

Gram-negative rods Mixed gram-negative rods Proteus mirabilis Escherichia coli Eikenella corrodens Enterobacter sp. Serratia marcescens Total

6 4 3 3 1 1 18

Skin flora Staphylococcus coagulase negative Staphylococcus aureus Mixed skin flora Total

14 14 4 32

* Includes C. perfringens, C. septicum, C. sordellii, C. tetani, and C. botulinum. Source: Reprinted with permission from Bosshardt et al.17

analyzed 182 patients with NSTI over an 8-year period, focusing on the microbiology of the infectious process, and found 154 polymicrobial infections out of 182 total cases, with an average of 4.4 microbes per NSTI (based on original wound cultures). The most common organisms, in order, were Bacteroides species, aerobic Streptococcus, staphylococci, enterococci, Escherichia coli, and other Gram-negative rods. Monomicrobial infections are usually caused by hemolytic group A Streptococcus, Staphylococcus aureus, or clostridial species. Group A streptococcal NSTIs not uncommonly involve younger patients and the extremities and are associated with a streptococcal toxic shocklike syndrome. These infections may appear suddenly in

previously healthy patients and are often exceedingly rapid in progression. Organ system dysfunction can be out of proportion to the extent of local signs and symptoms.8,24,25 Recent reports indicate that NSTIs can be caused by group B Streptococcus26 and group G Streptococcus,27 demonstrating that serious invasive streptococcal infections may be on the rise. Clostridial infections are classically associated with myonecrosis (gas gangrene), severe toxicity, and higher mortality. Clostridium perfringens c. novyi and c. septicum are often cultured, and clinical signs include intense pain, swelling, crepitus, and a thin watery discharge.21,28,29 On exploration necrotic, sometimes blackened muscle is encountered. There are many other monomicrobial NSTI pathogens that are less frequently encountered, including Vibrio vulnificus30 and Cryptococcus neoformans.31 Table 11.2 summarizes some of the organisms seen with NSTI, their characteristics, and some general recommendations. It must be remembered, however, that the microbiology of soft tissue infections is not usually known until days after treatment has been initialed, at which time the patient is improving or deteriorating or has died. The identification of the NSTI is not done by the microbiology but by clinical evaluation and surgical exploration of the infected tissue. It is the clinical evidence of tissue destruction by the advancing soft tissue infection causing necrosis rather than infection of necrotic tissue that defines NSTI. The mechanisms that determine whether organisms will only colonize or will cause rapidly progressing tissue destruction and potential death in hours or a few days remain unclear. It is probably a combination of the virulent organism, the local milieu of the infection, the general condition of the patient, and other unknown factors during the early spread of the infection that are most important. Once the organisms start to grow in the tissue, the infection appears to progress on the basis of two principle areas: The first is the destruction and breakdown of normal tissue components by proteolytic and lipolytic enzymes. This causes a breakdown of tissue and provides more nutrients for bacteria that allow the infection to progress. Furthermore, tissue breakdown helps eliminate barriers that would allow normal septations to limit progression of infection to normal healthy tissue.

Table 11.2. Organisms seen with necrotizing soft tissue infection, their characteristics, and general recommendations. Organism group Group A Streptococcus Staphylococcus Bacteroides sp. Gram-negative organisms Candida and other fungi Clostridia

Relative prevalences Common More common with cutaneous origin of infection Most common anaerobe Common in mixed infection Most associated with immunosuppressed patients Relatively uncommon

Clinical problems Often spreads rapidly May have multiple sites Need tissue to process for culture More often seen in postoperative wound infections May require microscopic tissue evaluation for diagnosis Often leads to profound sepsis and rapid death


The second component of tissue destruction is the cytokine release secondary to initiation of these infections. There is evidence that the cascade of cytokines that can be released by these infections impacts the patient both locally and systemically. The massive release of tumor necrosis factor and other tissue destruction cytokines contribute to the necrosis seen in infected tissue. This provides additional nutrients for bacterial growth. Furthermore, the cytokines, lymphokines, and other mediators, including leukotrienes and products of the coagulation and complement cascades, cause vasodilatation, hypotension, and sepsis syndrome, leading to altered organ function and potentially multisystem organ failure.32–34 The eventual outcome of these processes is a rapidly progressing systemic sepsis, triggered by the advancing soft tissue infection. Understanding these physiologic changes is essential to rapidly diagnosing the problem and rationally treating the unique differences in each patient.

169 Table 11.3. Signs and symptoms of necrotizing soft tissue infections. Physical examination Erythema Edema Inflammation Induration Bronzing of skin Vesicles or bullae Crepitance Local anesthesia Pain out of proportion to physical findings Loss of function Foul odor Discolored thin drainage Necrosis Systemic signs Fever Tachycardia Confusion or obtundation Shock Systemic inflammatory response syndrome Multiple-organ dysfunction or failure

Presentation and Diagnosis The presentation of NSTI is highly variable and can range from early sepsis with obvious skin involvement to minimal cutaneous manifestations with a disproportionate (even alarming) underlying necrotizing fasciitis. The infections often develop in deep tissue planes, resulting in the epidermis appearing relatively uninvolved until late in the course of the disease. This may lead to difficulty differentiating serious NSTI from cellulitis or nonnecrotizing infections. The clinical presentation of NSTI usually begins with localized pain and a deceptively benign appearance. Clinical clues (summarized in Table 11.3) that may assist in establishing an early diagnosis are pain out of proportion to physical appearance, edema beyond the area of erythema, small skin vesicles, crepitus, and the absence of lymphangitis. Additional local signs suggesting deep infection include skin induration, dermal thrombosis, epidermolysis, or dermal gangrene. Bullae formation and a thin, gray, foul-smelling discharge from the skin and subcutaneous tissue develop late in the process and are typically associated with systemic manifestations of sepsis, including shock and multiple organ failure.2,17,29,35–38 Figure 11.3 illustrates an advanced case of NSTI secondary to intravenous drug use. The extremities are the predominant location of NSTIs in most large series of patients. The perineum, trunk, and gluteal region are other common anatomic sites. Although no area of the body is safe from NSTI, infections of the chest and head and neck region are less common.6,17,38–42 Early recognition is the sine qua non for the assessment of risk factors. Multiple risk factors increase the

probability of a life-threatening infection.43 Those comorbid conditions include diabetes mellitus, peripheral vascular disease, malnutrition, malignancy, obesity, advanced age, immunocompromised states (AIDS, steroid therapy), and chronic alcohol or intravenous drug abuse (Table 11.4). These factors are associated with underlying defects in immune function, and they all affect patient outcome. In the urban setting, intravenous and subcutaneous injections of illicit substances have become a more prevalent risk factor and should raise one’s suspicion. Our experience with NSTIs treated at an urban medical center revealed that 67% of patients were actively

Figure 11.3. Advanced necrotizing soft tissue infection of the upper extremity secondary to intravenous drug abuse. Large bullae, bronzing and induration, and weeping of thin gray fluid signify severe underlying infection and necrosis.

170 Table 11.4. Risk factors for necrotizing soft tissue infections. Diabetes mellitus Intravenous drug abuse Obesity Malnutrition Chronic alcoholism Peripheral vascular disease Age greater than 60 years Immunocompromised state Steroid therapy HIV/AIDS Malignancy

practicing parenteral drug use.17 Additional studies demonstrated similar results.38,44–46 The etiology of an NSTI is not always obvious and usually involves some form of tissue damage. The most common etiologies include trauma (blunt and penetrating), postoperative wound complications, cutaneous infections, intravenous or subcutaneous illicit substance injection, perirectal abscesses, strangulated hernias, perforated viscous (i.e., diverticulitis), and idiopathic causes.6,17,35,37,38,47 Necrotizing soft tissue infections have also been linked to nonsteroidal antiinflammatory drugs (NSAIDs). However, this association remains unclear, as other comorbidities and risk factors are frequently found.48–50 Necrotizing soft tissue infections must be diagnosed clinically. There has been some investigation of the use of frozen section or other techniques to diagnose NSTI, but, other than with fungi such as Aspergillus, invasive infection is not diagnosed microscopically. The defining characteristic of NSTI is tissue destruction caused by advancing infection, which can be best and quickest determined by clinical assessment, usually in the operating room. Initially when presented with a patient with extensive soft tissue manifestations of infection as evidenced by any one or all five of the classic components of inflammation (pain, swelling, redness, and increased temperature and loss of function), a clinician should consider NSTI. If there are questions as to whether this is indeed an NSTI or a simple soft tissue infection, a reasonable approach is to start treating the patient for a simple soft tissue infection by standard treatments—intravenous antibiotics, elevation and immobilization of the area—and frequently reexamine the area every 4 to 6 hours. The limits of erythema should be marked on the skin with a pen, with attention to determine if the border of infection appears to progress beyond this mark in subsequent examinations. If infection progresses beyond the previous delineated areas of infection, then NSTI should be strongly considered and surgical intervention should be planned immediately. Even failure to improve over a period of 8


to 24 hours with appropriate treatment should be a reason for surgical exploration or very close attention.13 Wong et al.51 have described a diagnostic tool to distinguish what they describe as necrotizing fasciitis from other soft tissue infections. They developed the Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score that includes white cell count, hemoglobin, sodium, glucose, creatinine, and C-reactive protein as variables. However, these are all measures of physiologic derangement and inflammation and are not specific enough for infection. Furthermore, there is no comparison of LRINEC to clinical judgment by an experienced surgeon.51 The use of imaging studies to determine the presence of NSTI is limited by the relatively low percentage of patients who have soft tissue gas or other means of diagnosis. Inflammatory changes in soft tissue may be very clear on computed tomography or magnetic resonance imaging but are very nonspecific and not as useful as an examination by a clinician experienced with NSTIs. Clinical aspiration of fluid to look for bacteria also is insufficient. Cultures often take too long to make a timely diagnosis and the Gram stains are not able to make a diagnosis of necrotizing infection. Operative exploration for diagnosis should be an incision down to the muscular fascia (and through it to fully evaluate the fascia and muscle). The area should be examined for gray-brown fluid (“dishwater pus”), change of the fascia from glistening white to gray, and easy separation of the subcutaneous fat from the fascia. If any of these are found, a presumptive diagnosis of NTSI is made. Ultimately the diagnosis is made with a high index of suspicion and confirmed at the time of surgical exploration of the area involved.44

Clinical Management The clinical management of NSTIs requires rapid and simultaneous resuscitation, antibiotics (and possible other antimicrobial agents), aggressive surgical debridement, and supportive care. It is important to understand that all aspects of treatment must be initiated promptly to limit tissue damage, morbidity, and mortality. Resuscitation should begin immediately for patients who are suspected of having any type of soft tissue infection, even if the diagnosis is unclear and the patient is being closely monitored. The magnitude of resuscitation will depend on the patient’s physiologic status and response to initial treatment. Intravenous fluid resuscitation is essential because these patients are often intravascularly depleted, despite having localized and sometimes even generalized edema. Adequate intravascular volume is important to maintain good tissue oxygen delivery as well as limit the adverse effects of multiple organ failure.


Intravenous lactated Ringer’s solution given in large volumes is the appropriate way to resuscitate these patients. The use of colloid resuscitation is generally not of benefit and may lead to other potential problems, including coagulopathy, if synthetic colloid is used. The amount of fluid resuscitation should be targeted to provide adequate perfusion of organ systems. Urine output remains the best single measure of determining adequacy of resuscitation. The use of pulmonary artery catheters or other means to look at cardiac index can increase risk to the patient given the potential systemic nature of the infection. Furthermore, many patients will have high cardiac output states, and invasive monitoring will be of limited benefit. Patients who have profound cardiac or cardiopulmonary dysfunction may require a pulmonary arterial catheter to monitor and guide treatment when the benefit exceeds the risk. Patients who have evidence of multiple organ dysfunction or failure need support of the affected system(s). This may include intubation and mechanical ventilation for acute respiratory failure, use of vasoactive drugs for profound hypotension, hemofiltration or dialysis for acute renal failure, and other organ-system support as needed. Hyperglycemia should be closely managed to best treat the infection. It is important to integrate the surgical management of the infection with the critical care management of the patient. However, critical care management is an adjunct, not the primary treatment of NSTIs. Delaying surgical management until the patient is “stable” or “improved” by resuscitation in the intensive care unit will fail. Appropriate and aggressive surgical debridement and appropriate antibiotics must be included in the immediate resuscitation plan.

Critical Care Management Hemodynamic support from vasoactive drugs such as dopamine or alpha agents may be useful. Betaadrenergic agents such as dopamine or alpha-adrenergic agents should be used if the patient is unable to maintain a blood pressure sufficient for renal autoregulation. Systolic blood pressures of only 75 to 80 in septic patients are often sufficient, and use of alpha agents to raise the blood pressure even higher may be deleterious to the heart. Patient care should be focused on treating the disease process more than treating the organ-system consequences of the infection. Mechanical ventilation, when needed, should be initiated quickly to prevent complications of respiratory failure and/or aspiration. Good pulmonary toilet will need to be part of this supportive care. Treatment of other organ-system dysfunction, such as coagulopathy, should be initiated immediately as well. Nutritional

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support should be considered as soon as the infection is improving.52,53 Attention is often focused on what antibiotics to use for these patients. Given the sometimes complex nature of the infections, broad-spectrum antibiotics should be started first, with narrowing of the spectrum once the causative organisms are known. Intravenous penicillin G remains the other treatment of choice for group A streptococcal infections, although there is some evidence that clindamycin may provide equal benefit. However, no comparative study has demonstrated a superior response to clindamycin in NSTI. Penicillin G, if chosen, should be given at a high dose, such as 20 to 24 million units a day for adults, to have as rapid an impact as possible. One million units hour of penicillin G in continuous infusion avoids some of the low levels associated with bolus dosing cited by the proponents of clindamycin. Until Gram-negative organisms can be ruled out, coverage for them is important. This can be done with an aminoglycoside or other agent effective against the common Gram-negative organisms in individual hospitals. If previously hospital-acquired organisms such as resistant Staphylococcus are suspected, vancomycin would be recommended for use in the initial antibiotic treatment for these infections. If there is suspicion of Candida or fungi such as Aspergillus, based on either wound inspection or pathology, antifungal agents should be included. The specific antibiotics chosen should be based on the patient’s acute infection, underlying pathology, medical history (including allergies), and the bacteria and other organisms seen in the respective hospitals. Consideration of the antimicrobial sensitivities of different organisms in a specific hospital should also be used when selecting which agents to use. These antibiotics should be adjusted when cultures and sensitivities are complete. Some physicians have recommended the use of intravenous immunoglobulins (IVIG) for NSTI.54,55 It is unclear whether IVIG works as a nonspecific opsonin or by specific binding to a bacterial antigen and activation of specific and nonspecific inflammatory mechanisms. Intravenous IG may also have an effect on the circulating cytokines to control the systemic inflammatory response.There are no comparative trials yet to assess the efficacy of IVIG for NSTIs. The fundamental approach to NSTI still remains aggressive surgical debridement in the acute or initial setting. Operative exploration of the wound not only permits definitive diagnosis of the NSTI but also puts the surgeon in position to provide the most crucial part of the treatment.19,56 Some research suggests that surgery can be delayed or potentially avoided.57 However, most thorough studies conclude that the most important part of the treatment of NSTIs is surgical debridement, and the earlier it is done, the better the outcome.5,58 True NSTIs

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will not be successfully treated without aggressive surgical debridement. For patients who are hemodynamically unstable or who have not yet responded to rapid resuscitation, delay in surgery until “normalization” has been achieved may limit the patient’s chance of survival. Often, patients will respond to resuscitation only after the infected tissue is debrided and the area drained.

Surgical Debridement Surgical debridement of an NSTI has many different techniques; however, wide excision of all inflamed or infected tissue is the most accepted therapeutic approach. Initial debridement should involve an incision in the most inflamed, tender, or indurated area or in a central area of soft mass if one is present. This should be carried down to the fascia. If the fascia is a gray, dull, or a stringy type of tissue as opposed to the normal pearly, tough fascia, a diagnosis of NSTI can be made. Whether or not the fascia is abnormal, it should be incised to examine the muscle underneath. If the fascia is abnormal as described, then the skin and soft tissue above the abnormal fascia should be lifted away to see how far the abnormality extends in the fascia. The necrotic fascia should be excised, and the overlying skin and subcutaneous fascia should be excised with it. This avoids the possibility of leaving large flaps of heavily infected skin, allowing continued spread of the infection and drainage of the inflammatory mediators into the lymphatics and veins. The skin and subcutaneous fascia should be cut back to viable bleeding tissue that appears normal in color and texture. The viable tissue will likely be edematous but it will be otherwise normal. It is uncommon to see classic thick, creamy purulence in NSTIs. The classic description has been “dishwater pus,” which is a brownish-tan fluid that weeps from the infected site. The debridement should be done expeditiously either with a curved Mayo scissors or cautery. The difficulty with cautery is that it is hard to assess the quality of the tissue once it has been cut with the Bovie. If cautery is to be used, cutting current is more likely to be effective with specific attention either to tie off or to coagulate isolated vessels. If the infection is in the extremity and has caused considerable muscle necrosis and/or destruction of neurovascular components, consideration should be given to guillotine amputation.59 No attempt should be made to close any wounds such as extremity stumps in the face of such NSTIs. If the patient is profoundly unstable with an extremity infection, guillotine amputation may be the fastest way to attempt to salvage the patient’s life. It is important that the patient be brought to the operating room as soon as possible. If it is unclear that the


patient has an NSTI and the patient is being closely monitored, observation examinations are important. However, once the diagnosis is made and the suspicion is high, rapid transfer to the operating room for exploration should be done. Attempts to try to do this in unstable patients outside the operating room should be very limited. Once the diagnosis is made, transport the patient to the operating room because the magnitude of debridement, fluid resuscitation, and potential blood loss that could occur are best managed there. Preoperative preparation should include type and cross with at least four units of blood and warming the operating room. The wound exploration and debridement should be considered similar to excision of a large burn area, because the fluid and potential bone losses are similar and the need for maintenance of body temperature is important. After aggressive debridement, it is likely that the patient will actually improve hemodynamically and clinically. It is important, however, that the patient be reexamined in the operating room within 24 hours to assess whether or not the advance of the infection has been stopped.2,6,13 If there is additional necrotic tissue, then it should be again debrided aggressively. Necrotic tissue should not be left for subsequent debridement, hoping that more tissue will not have to be taken. If the tissue has a reasonable chance of being viable, then it should be noted where this is so it can be considered for further debridement if necessary on subsequent exploration. Repeated operative debridements are often necessary; one study reported an average of 3.3 debridements per patient.6 Once a wound appears to be stable and there is no evidence of advancing infection, dressing may occur in an appropriate facility, not necessarily in the operating room. Necrotizing soft tissue infections are often treated in a burn center. Burn centers are often experienced with the massive fluid resuscitation and management of very critically ill and unstable patients required not only in burns but in NSTIs as well. Furthermore, the wound care and wound coverage teams needed for these patients has considerable overlap between burns and NSTIs.12,60,61

Wound Care Dressing the wounds between debridements is best done by using a moist dressing, such as saline or lactated Ringer’s. In general, it is best to avoid topical antimicrobial agents such as Silvadene, which cause discoloration in the tissue and make it difficult to determine whether tissue is viable or nonviable. Other soluble topical antimicrobials that do not stain tissue can be used, but they are not a substitute for adequate excision and debridement


from the NSTI. Antimicrobial solutions that cause cellular damage such as betadine solution should be avoided. Hyperbaric oxygen (HBO) has been proposed as an integral part of treatment of NSTIs.62,63 Although it is used in some centers, there is no prospective evidence that outcomes are superior with HBO compared with standard care approaches. A recent study by Riseman et al.64 compared 12 patients treated before HBO with 17 patients treated after HBO, with an improvement in mortality from 67% to 23%. However, it was not a prospective, randomized, or case-controlled study.64 Some studies examining the use of HBO have described patients who have slow-healing soft tissue wounds with positive surface cultures rather than NSTIs. When HBO can be compared in a comprehensive prospective randomized trial, the appropriateness of this technique for NSTIs can be determined. Once the patient is stable, the subsequent wound coverage should be planned.This is often done using a simple skin graft, but sometimes complex reconstruction such as for perineal wounds may be needed. Perineal infections resulting in large debridement of perianal tissue occasionally requires colostomy but often can be managed without it. If the scrotal skin has to be resected during debridement of the NSTI, the testicles are almost always viable and can be left behind. If they retract into the inguinal canal, they can be mobilized, brought down, and sutured together with absorbable sutures beneath the penis and then skin grafted over to form a new scrotal area. More complex wound coverage can be done in conjunction with plastic surgery when necessary. However, early closure with skin graft is usually advantageous with subsequent reconstruction once the patient is well and recovering not only from the infection but also the other complicated medical problems. Supportive care of the patient during this process is important. Nutritional support is important, especially as the patient is recovering and becomes anabolic again.52 Tube feedings may be necessary for adequate caloric and protein intake because patients may be intubated or unable to take in sufficient calories and protein just by eating. Appropriate vitamins and minerals such as zinc are essential. These patients will have increased caloric and protein demands because of the loss of fluid through the open wounds as well as the hypermetabolism associated with this infection. Patients often need rehabilitation. When amputation is required, contact with a prosthetist to determine how best to eventually shape the stump will be important. Rehabilitation should begin as early as the patient is stable and able to participate and not put off until discharge. It may take months for patients to regain strength even after relatively straightforward management of the NSTI.

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Burn centers again are often useful places to treat these patients because burn centers have many of the elements and the experienced staff necessary to treat this problem. However, treatment could be effectively done in other units that have the surgical expertise, nursing and hospital support, and experience in management of these problems. In summary, an NSTI is a surgical disease that needs to be quickly recognized and aggressively treated. The time required to treat the patients is considerable, and the temptation is often to look for someone else to manage this life-threatening but uncommon problem. However, a well-trained general surgeon with comprehensive skills should be able to manage most of the patients. The pattern of these infections will continue to change as the microbial flora, antibiotic use, and patient population evolves. This disease process will continue to require rapid evaluation and treatment based on clinical experience and a high index of suspicion. New techniques for diagnosis and treatment are still being evaluated. Diagnosis and management of NSTIs will still require the attention and skill of a committed general surgeon.

Critique The mainstay of management of any necrotizing soft tissue infection is early and aggressive surgical debridement. Antibiotics, fluid resuscitation (particularly for a hemodynamically labile, septic patient), and nutritional support are required adjuncts. However, without surgical debridement, the adjuncts will not provide definitive management. Also, there have been no phase III blinded, prospective, randomized trials demonstrating the efficacy of hyperbaric oxygen therapy. Answer (E)

References 1. Dellinger FL. Severe necrotizing soft-tissue infections. Multiple disease entities requiring a common approach. JAMA 1981; 246(15):1717–1721. 2. Malangoni MA. Necrotizing soft tissue infections: are we making any progress? Surg Infect (Larchmt) 2001; 2(2): 145–152. 3. Quirk WF Jr, Sternbach G. Joseph Jones: infection with flesh eating bacteria. J Emerg Med 1996; 14(6):747–753. 4. Meleney. Hemolytic Streptococcus gangrene. Arch Surg 1924; 9:317–364. 5. Ahrenholz DH. Necrotizing soft-tissue infections. Surg Clin North Am 1988; 68(1):199–214. 6. McHenry CR, et al. Determinants of mortality for necrotizing soft-tissue infections. Ann Surg 1995; 221(5):558–565.

174 7. Bisno AL, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med 1996; 334(4):240–245. 8. Chelsom J, et al. Necrotising fasciitis due to group A streptococci in western Norway: incidence and clinical features. Lancet 1994; 344(8930):1111–1115. 9. Demers B, et al. Severe invasive group A streptococcal infections in Ontario, Canada: 1987–1991. Clin Infect Dis 1993; 16(6):792–802. 10. Chao CS, et al. Necrotizing soft tissue infection in heart transplantation recipients: two case reports. Transplant Proc 1998; 30(7):3347–3349. 11. Cheung AH, Wong LM. Surgical infections in patients with chronic renal failure. Infect Dis Clin North Am 2001; 15(3):775–796. 12. Kuncir EJ, et al. Necrotizing soft-tissue infections. Emerg Med Clin North Am 2003; 21(4):1075–1087. 13. Schecter WP, Schecter G. Necrotizing fasciitis of the upper extremity. J Hand Surg 1982; 7:15–20. 14. Lewis RT. Soft tissue infections. World J Surg 1998; 22(2): 146–151. 15. Huang JW, et al. Necrotizing fasciitis caused by Serratia marcescens in two patients receiving corticosteroid therapy. J Formos Med Assoc 1999; 98(12):851–854. 16. Wai PH, et al. Candida fasciitis following renal transplantation. Transplantation 2001; 72(3):477–479. 17. Bosshardt TL, Henderson VJ, Organ CH Jr. Necrotizing soft-tissue infections. Arch Surg 1996; 131(8):846– 854. 18. Ebright JR, Pieper B. Skin and soft tissue infections in injection drug users. Infect Dis Clin North Am 2002; 16(3):697– 712. 19. Hill MK, Sanders CV. Skin and soft tissue infections in critical care. Crit Care Clin 1998 14(2):251–262. 20. Childers BJ, et al. Necrotizing fasciitis: a fourteen-year retrospective study of 163 consecutive patients. Am Surg 2002; 68:109–116. 21. Elliott DC, Kufera JA, Myers RAM. The microbiology of necrotizing soft tissue infections. Am J Surg 2000; 179:361– 366. 22. Giuliano A, et al. Bacteriology of necrotizing fasciitis. Am J Surg 1977; 134:52–56. 23. Sudarsky LA, et al. Improved results from a standardized approach in treating patients with necrotizing fasciitis. Ann Surg 1987; 206:661–665. 24. Wood TF, Pooter MA, Jonasson O. Streptococcal toxic shock-like syndrome: the importance of surgical intervention. Ann Surg 1993; 217:209–214. 25. Wolf JE, Rabinowitz LG. Streptococcal toxic shock-like syndrome. Arch Dermatol 1995; 131:73–77. 26. Gardam MA, et al. Group B streptococcal necrotizing fasciitis and streptococcal toxic shock-like syndrome in adults. Arch Intern Med 1998; 158:1704–1708. 27. Humar D, et al. Streptolysin S and necrotising infections produced by group G streptococcus. Lancet 2002; 359:124– 129. 28. Lewis RT. Soft tissue infections. World J Surg 1998; 22:146– 151. 29. File TM. Necrotizing soft tissue infections. Curr Infect Dis Rep 2003; 5:407–415.

A.A. Meyer, J.E. Abrams, T.L. Bosshardt, and C.H. Organ, Jr. 30. Holow KD, Harner RC, Fontenelle LJ. Primary skin infections secondary to Vibrio vulnificus: the role of operative intervention. J Am Coll Surg 1996; 183:329–334. 31. Marcus JR, et al. Risk factors in necrotizing fasciitis: a case involving Cryptococcus neoformans. Ann Plast Surg 1998; 40:80–83. 32. Fast DJ, Schlievert PM, Nelson RD. Toxic shock syndrome–associated staphylococcal and streptococcal pyrogenic toxins are potent inducers of tumor necrosis factor production. Infect Immun 1989; 57(1):291–294. 33. Muller-Alouf H, et al. Cytokine production by murine cells activated by erythrogenic toxin type A superantigen of Streptococcus pyogenes. Immunobiology 1992; 186(5):435– 448. 34. Muller-Alouf H, et al. Comparative study of cytokine release by human peripheral blood mononuclear cells stimulated with Streptococcus pyogenes superantigenic erythrogenic toxins, heat-killed streptococci, and lipopolysaccharide. Infect Immun 1994; 62(11):4915–4921. 35. Elliott DC, Kufera JA, Myers RAM. Necrotizing soft tissue infections: risk factors for mortality and strategies for management. Ann Surg 1996; 224:672–683. 36. Majeski JA, John JF Jr. Necrotizing soft tissue infections: a guide to early diagnosis and initial therapy. South Med J 2003; 96:900–905. 37. Chapnick EK, Abter EI. Necrotizing soft tissue infections. Infect Dis Clin North Am 1996; 10:835–855. 38. Lille ST, et al. Necrotizing soft tissue infections: obstacles in diagnosis. J Am Coll Surg 1996; 182:7–11. 39. Singh G, et al. Necrotising infections of soft tissues—a clinical profile. Eur J Surg 2002; 168:366–371. 40. Callahan TE, Schecter WP, Horn JK. Necrotizing soft tissue infections masquerading as cutaneous abscess following illicit drug injection. Arch Surg 1998; 133:812–818. 41. Urschel JD, Takita H, Antkowiak JG. Necrotizing soft tissue infections of the chest wall. Ann Thorac Surg 1997; 64:276–279. 42. McMahon J, Lowe T, Koppel DA. Necrotizing soft tissue infections of the head and neck: case report and literature review. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003; 95:30–37. 43. Francis KR, et al. Implications of risk factors in necrotizing fasciitis. Am Surg 1993; 59:304–308. 44. Wall DB, et al. A simple model to help distinguish necrotizing fasciitis from nonnecrotizing soft tissue infection. J Am Coll Surg 2000; 191:227–231. 45. Bangsberg DR, et al. Clostridial myonecrosis cluster among injection drug users. Arch Intern Med 2002; 162:517– 522. 46. McGuigan CC, et al. Lethal outbreak of infection with Clostridium novyi type A and other spore-forming organisms in Scottish injecting drug users. J Med Microbiol 2002; 51:971–977. 47. McHenry CR, et al. Idiopathic necrotizing fasciitis: recognition, incidence, and outcome of therapy. Am Surg 1994; 60:490–494. 48. Kahn LH, Styrt BA. Necrotizing soft tissue infections reported with nonsteroidal antiinflammatory drugs. Ann Pharmacother 1997; 31:1034–1039.

11. Soft Tissue Infections 49. Forbes N, Rankin APN. Necrotizing fasciitis and non steroidal anti-inflammatory drugs: a case series and review of the literature. NZ Med J 2001; 114:3–6. 50. Lesko SM, et al. Invasive group A streptococcal infection and nonsteroidal antiinflammatory drug use among children with primary varicella. Pediatrics 2001; 107:1108– 1115. 51. Wong CH, et al. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med 2004; 32(7):1535–1541. 52. Graves C, et al. Caloric requirements in patients with necrotizing fasciitis. Burns 2005; 31(1):55–59. 53. Green RJ, Dafoe DC, Raffin TA. Necrotizing fasciitis. Chest 1996; 110(1):219–229. 54. Stevens DL. Streptococcal toxic shock syndrome associated with necrotizing fasciitis. Annu Rev Med 2000; 51:271–288. 55. Laupland KB, et al. Intravenous immunoglobulin for severe infections: a survey of Canadian specialists. J Crit Care 2004; 19(2):75–81. 56. Voros D, et al. Role of early and extensive surgery in the treatment of severe necrotizing soft tissue infection. Br J Surg 1993; 80(9):1190–1191.

175 57. Hsiao GH, et al. Necrotizing soft tissue infections. Surgical or conservative treatment? Dermatol Surg 1998; 24(2):243– 248. 58. Bilton BD, et al. Aggressive surgical management of necrotizing fasciitis serves to decrease mortality: a retrospective study. Am Surg 1998; 64(5):397–401. 59. Anaya DA, et al. Predictors of mortality and limb loss in necrotizing soft tissue infections. Arch Surg 2005; 140(2): 151–158. 60. Barillo DJ, et al. Burn center management of necrotizing fasciitis. J Burn Care Rehabil 2003; 24(3):127–132. 61. Edlich RF, et al. Massive soft tissue infections: necrotizing fasciitis and purpura fulminans. J Long Term Eff Med Implants 2005; 15(1):57–65. 62. Clark LA, Moon RE. Hyperbaric oxygen in the treatment of life-threatening soft-tissue infections. Respir Care Clin North Am 1999; 5(2):203–219. 63. Wilkinson D, Doolette D. Hyperbaric oxygen treatment and survival from necrotizing soft tissue infection. Arch Surg 2004; 139(12):1339–1345. 64. Riseman JA, et al. Hyperbaric oxygen therapy for necrotizing fasciitis reduces mortality and the need for debridements. Surgery 1990; 108(5):847–850.

12 The Open Abdomen: Management from Initial Laparotomy to Definitive Closure Fred A. Luchette, Stathis J. Poulakidas, and Thomas J. Esposito

Case Scenario A 67-year-old patient has undergone a prolonged and complicated operation for mesenteric ischemic (embolic etiology). Circulation has just been restored to the ischemic bowel; however, the patient is hypothermic (34°C), acidotic, and coagulopathic. Which of the following is the appropriate management at this time? (A) (B) (C) (D) (E)

Wood’s lamp assessment of bowel viability Repeated on-table angiography after 45 minutes Administration of mannitol Immediate fascial closure of the abdomen Creative abdominal closure

The establishment and management of the open abdomen is now a main component of the armamentarium in acute care surgery. Pringle was the first to report use of the open abdomen for management of soldiers sustaining catastrophic abdominal injuries during World War II. It was abandoned because of the poor results encountered with recurrent bleeding at the time of pack removal and late infections. Lucas and Ledgerwood1 reintroduced the technique with a prospective study conducted from 1968 to 1973. Subsequent patient series reports by Calne et al.,2 Feliciano et al.,3 Svoboda et al.,4 and Carmona et al.5 demonstrated the utility of packing for devastating abdominal injuries with subsequent patient survival. Today, the concept of “damage control” has been well accepted in the management of critically ill and injured patients. Promulgated by Rotondo and colleagues,6 this operative management strategy has become the mainstay in major trauma centers throughout the United States. The strategy has been utilized to avoid and treat the complications of primary and secondary abdominal compartment syndrome (ACS) related to intraabdominal

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hypertension. The acute care surgeon will also encounter ACS in patients presenting with other nontraumatic abdominal catastrophies.7–14 Additionally, the damage-control technique has applications in general surgery, vascular surgery, urology, gynecology, and even thoracic surgery.8,9 Surgeons treating intraabdominal infection at the end of the nineteenth century respected the “enormous increases of intraabdominal tension.”10 Effective treatment for both primary and secondary ACS became available with the introduction of the open abdominal technique,11,12–14 which allowed practitioners to realize the benefits of this new strategy on impaired physiology that resulted from abdominal hypertension.15–17 This has been used adjunctively with open peritoneal lavage for the management of severe feculent peritonitis. With the evolution of the open abdomen for trauma and peritonitis, the challenge of dealing with the temporarily open abdomen and its eventual closure has grown. This chapter details the complex care of such patients and the decision processes culminating in the definitive closure of the abdomen.

Indications for Leaving the Abdomen Open Utilizing the strategy of damage control, physicians have increasingly incorporated truncated operations into routine practice. For trauma patients, the initial procedure of abdominal exploration is designed to control hemorrhage and contamination. For nontrauma indications, these basic principles are also applied most commonly for control of an infectious source. The decision to terminate the initial operation is determined by the patient’s overall capacity to withstand the physiologic stress posed by the extended operative time needed to complete the operation (Table 12.1). The complex decisions dealing with choice of temporary closure, timing of return to the operating room for

12. The Open Abdomen Table 12.1. Indications for the damage-control approach. 1. Inability to achieve hemostasis because of coagulopathy 2. Inaccessible major venous injury 3. Time-consuming procedure in a patient with suboptimal response to resuscitation 4. Management of extraabdominal life-threatening injury 5. Reassessment of intraabdominal contents 6. Inability to reapproximate abdominal fascia because of visceral edema Source: Reprinted with permission from Shapiro et al.47

reconstruction, and definitive closure of the abdomen are dictated by individual patient variables, including the constellation of injuries or other conditions, physiologic reserve, response to resuscitation, and available resources. A critical factor at the first operation is the preservation of the abdominal wall fascia for use at the time of eventual closure. All available synthetic materials can be temporarily secured directly to the skin, recognizing that this may lead to minor skin loss and potential compromise of an ideal cosmetic result. A choice of temporary closure should be based on anticipated needs, including repeated access to the peritoneal cavity, porosity, durability, pliability, interaction with adjacent structures, and cost. The temporary coverage of the exposed viscera allows a bridge to resuscitation and thereby the reversal of shock and other physiologic derangements such as fluid and heat loss and dessication. The most common goal during resuscitation in the intensive care unit is correction of hypothermia and underlying coagulopathy. Aggressive cardiovascular resuscitation with both crystalloid and blood products should also occur in order to optimize oxygen delivery and consumption. One should anticipate progressive pulmonary failure requiring manipulation of ventilatory modes to maintain oxygenation and ventilation. Return to the operating room will be dictated by the time required to achieve restoration of physiologic reserve defined as correction of hypothermia, coagulopathy, and acidosis. This typically requires 24 to 96 hours. The patient’s response to treatment or onset of further problems will determine the time and location of additional operative intervention. Ongoing hemorrhage (transfusion requirement of more than 10 units of packed red blood cells), persistent or worsening acidosis, or the development of ACS will necessitate an early unplanned return to the operating room for intervention. When ACS develops as a result of ongoing resuscitation, the surgeon may decide to proceed with decompression of the peritoneal cavity in the intensive care unit. If there is a concern that the ACS is a result of ongoing hemorrhage, the operating room offers the optimal setting for controlling the hemorrhage in contrast to the intensive care unit.

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Definitive closure of the open abdomen often requires complex planning and the involvement of other surgical disciplines with expertise in wound management. A particularly vexing complication of the open abdomen is an enteral fistula, which is now open to the air without interposing tissue. Management of the open abdominal wound while controlling the fistula output is challenging. The incidence ranges between 2% and 25% of injured patients undergoing damage control management. With this in mind, most acute care surgeons make efforts to close the open abdomen as soon a physiologically possible. This can be performed as early as several days after the original operation or electively at weeks or months after the initial procedure. Delayed operations allow time for catabolism to abate and for the patient’s physiologic reserve to return as signaled by wound contracture and granulation, improving nutritional parameters (nitrogen balance, prealbumen, transferrin) reflected by weight gain, and return of general well being. The choice of procedure or prothesis will vary based on the constellation of injuries and tissue available for reconstruction. Because each patient’s wound is unique, no single technique or prosthesis is ideal for every patient’s situation. Frequently, a combination of techniques must be utilized with some degree of creativity and flexibility because of the complex nature of these wounds and the attendant complications that can be associated with them. Cipolla et al.18 have proposed an algorithm linking the clinical situation with specific techniques used for management of the open abdomen.

Temporary Wound Management Techniques for the Open Abdomen Temporary closures can be categorized into two types: those involving closure of the skin and those that do not. When the skin can be approximated, coaptation can be achieved with a running suture or towel clips. In contrast, there are multiple techniques for temporary closure that leave the skin as well as fascia separated. All include some type of protective barrier applied over the peritoneal contents (Table 12.2). Towel clip closure of the skin is the most rapid of the temporary techniques. The clips are placed at 1-cm intervals. Some surgeons advocate orienting the handles of the towel clip toward the center of the incision. This facilitates dressing coverage of the towel clips and reduces artifact on subsequent radiographs. A surgical cloth is then applied as a wound drape over the towel clips. The entire assembly is held in place with an adhesive plastic drape, thereby reducing ascitic fluid irritation of the abdominal skin. Advantages of a towel clip closure are its rapid technique, low cost, maintenance of core

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F.A. Luchette, S.J. Poulakidas, and T.J. Esposito

Table 12.2. Various techniques for temporary bridging of an open abdomen. Method Skin closure (running monofilament suture or towel clips) Nonadherent materials (Bogotá bag, bowel bag, silicone sheet) Polyglactin 910 (Knitted Vicryl Mesh, Ethicon, Somerville, NJ) Polyglycolic acid (Dexon Mesh, Davis & Geck, Danbury, CT) Removable prosthesis (Wittman patch, Starsurgical, Inc., Burlington, WI) Vacuum-assisted closure KCI USA, Inc., San Antonio, TX)

Material

Expense

The most rapid technique and most effective at reducing heat and fluid loss

Low

Biologically inert, maintains heat and reduces fluid loss, reexploration is easy; evisceration occurs when material tears at suture sites Absorbable, noninfectious, partially incorporated into granulation tissue; complications include tearing at suture line with evisceration and/or enteric fistulae Absorbable, noninfectious, rapidly incorporated into granulation; complications include enteric fistulae Extended time of open abdomen with repeated reexploration in the intensive care unit; limitation is requirement for suturing to fascia Reduced incidence of abdominal compartment syndrome while prolonging time of temporary closure before fascial closure; requires manufacturer’s equipment

Low Moderate

Moderate High High

Modified with permission from: Rutherford EJ, Skeete DA, Brasel KJ. Management of the patient with an open abdomen: Techniques in temporary and definitive closure. Cur Prob Surg 2004;41:824.

temperature, and minimization of fluid losses. Despite close application of the clips, as intraabdominal pressure increases, there may be development of secondary ACS, evisceration of bowel between the towel clips, and pressure necrosis of the skin. The Bogotá bag utilizes a large sterile intravenous (IV) bag, which is usually split open, to cover the abdominal viscera.19–22 The bag can be secured to either the skin or fascia, but preferentially one should use the skin to minimize trauma to the fascia. When securing the bag to the skin, it is preferable to use a tapered needle, which minimizes the tearing of the bag at the suture sites. In comparison, the IV bag may tear when secured to the skin with a cutting needle. Other materials that can be employed in a similar fashion include intestinal bag, steri drape, parachute sheeting,23 silicone sheeting,24 PTFE (polytetrafluoroethylene; Gortex®) patch, or rayon cloth.25 All of these materials minimize fluid loss and are easy to remove, relatively inexpensive, and biologically inert, thus minimizing adhesions. The downside of using these materials is that they all easily tear, creating the potential for subsequent intestinal evisceration. Mesh materials include nonabsorbable and absorbable types. The nonabsorbable have fallen out of favor because of high cost and increased association with fistulae. The absorbable mesh, if left in place, eventually will be incorporated into the granulating wound. There are two commercially available absorbable meshes, polyglactin11,12 and polyglycolic acid.26–30 Both can be secured to either the skin or fascia. Again, it is preferable to utilize the skin and preserve the fascia for later definitive closure. Both types of meshes are resistant to infection,28,29 improve early wound strength,25 and, if used for definitive closure, result in a planned ventral hernia (Figure 12.1). A noteworthy problem with polyglactin11,12 is that the smaller interstices can impair fluid drainage.

Additionally, when secured with a tapered needle, the mesh tends to tear at the suture site. In contrast, polyglycolic acid has large interstices, which more easily allows egress of peritoneal fluid and also less tearing during needle placement. The major disadvantage of all mesh closures is the association with enteric open-air fistulae if the wound is allowed to desiccate. The fistulae can be minimized if the mesh is covered with a moist dressing. With the mesh in place, no further procedures may be required for wound care in the critically ill patient. However, if the patient’s physiologic state permits, the mesh can be reefed (tightened) at the bedside. This gradually draws the fascial edges closer together and may allow early definitive primary closure of the abdomen. If this is not possible, the wound is allowed to granulate through the mesh and contract. This can be covered with a skin graft at a later date or be allowed to naturally epithelialize over time.

Figure 12.1. Ventral hernia after closure of abdomen by secondary intent with skin graft.

12. The Open Abdomen

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Mortality rate has been reduced with use of the “open” abdominal technique in the management of patients with intraabdominal sepsis.31 Several techniques have been described to maintain abdominal integrity and yet allow frequent reexploration and lavage in the critically ill septic patient. These include slide fasteners, zippers, and the Wittman patch.32–36 All were designed to eventually be removed with delayed primary closure. The Wittman patch has been extensively studied and is made of two adherent leaves of polyamiden and polypropylene with a Velcro-type closure (Figure 12.2). The leaves are sutured to the fascia and then secured to each other via the Velcro fastener. At the time of each reexploration, the leaves are trimmed to allow staged closure of the incision. In the final operation, the patch is removed and a definitive closure performed. Advantages of this device include easy reexploration at the bedside, maintenance of abdominal domain, and little need for chemical paralysis. The disadvantages

are the expense and multiple manipulations of the fascia. The vacuum-assisted closure (VAC) for large chronic wounds is used in an effort to promote healing by constant application of negative pressure. It has subsequently been adapted for use in acutely managing the open abdomen.37–41 This is a component dressing beginning with a nonadherent plastic drape placed beneath the anterior abdominal wall peritoneum to protect the abdominal viscera (Figure 12.3).37–41 Multiple perforations are placed in the drape to allow for fluid drainage (Figure 12.4A). Moist surgical wound towels are then placed over the drape and Jackson Pratt drains positioned over the wound towels (Figure 12.4B). The dressing is then secured to the skin with an adhesive plastic drape (Figure 12.4C,D). It is critical to have a good seal to the skin to maintain negative pressure. An alternative is a commercially available dressing (VAC dressing, KCI). In this system, a polyurethane

Figure 12.2. (A) Insertion of Wittman patch for open abdomen on postoperative day 8 after damage-control surgery for trauma. (B) Advancement of Velcro leaflets. (C) Approximation

of fascial edges. (D) Primary closure of abdomen on postoperative day 18. (A–D, reprinted with permission from Cipolla et al.18)

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F.A. Luchette, S.J. Poulakidas, and T.J. Esposito Figure 12.3. Schematic illustration of application of vacuum pack. (Reprinted with permission from Brock et al.38)

Rolled surgical sponge Plastic drape covered with surgical towel

Sump drains Continuous suction

Adhesive-backed plastic

A

C

B

D

Figure 12.4. Barker vacuum dressing. (A) Polyethylene sheet placed over the peritoneal viscera and beneath the parietal peritoneum. (B) A moist surgical towel(s) folded to fit the fascial defect, on top of the polyethylene sheet, but below the skin edges. (C) Bulb suction devices connected to each drain using a Y-adapter. Alternatively, each drain may be attached to an individual bulb suction. (D) Final vacuum dressing after application of occlusive barrier and suction to drains. (A–D, reprinted with permission from Barker et al.37)


Figure 12.5. Vacuum-assisted closure dressing applied to the abdominal wound.

sponge is cut to the appropriate size of the open abdominal wound and placed over a sterile drape. An 18-F suction tube is inserted into the sponge, and then the sponge, tubing, and skin are covered with an adherent occlusive drape. Suction is applied to the sponge continuously from a portable pump. The dressing is changed every 2 to 3 days to allow inspection of the wound and viscera (Figure 12.5). Advantages with either VAC dressing include decreased incidence of ACS, maintenance of abdominal domain, avoidance of chemical paralysis, elimination of temporary fascial suturing, and early fascial closure. Utilization of a nonadherent bowel bag with both the VACassisted dressing and the Wittman patch extend the time interval between dressing changes. Disadvantages of the commercial VAC system include the need for special equipment, expense, and minimal long-term follow-up data. Recent studies have reported use of the VAC device in patients for 21 to 49 days after injury with a primary closure rate of 40% to 92%.46,50 The temporary closure techniques necessitate further operative intervention. Although no single technique is ideal for every patient, priorities should include minimizing loss of abdominal domain while preserving the fascia, expense, minimization of heat and fluid losses, and expeditious closure. Thus, a common sequence in clinical practice is as follows: initial temporary coverage of the viscera followed by mesh or VAC dressing and then possible split-thickness skin graft or natural epithelialization.

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This should be based on adequacy of cardiovascular resuscitation and restoration of oxygen delivery and consumption as well as correction of hypothermia and coagulopathy. Clearly if the patient has ongoing hemorrhage or develops a secondary ACS, they should have these problems immediately addressed either in the operating room or at the bedside in the intensive care unit. In the absence of pressing indications for early reexploration,9,42,43 the reoperation should be scheduled when the probability of achieving complete fascial closure is greatest. This occurs usually 3 to 4 days after the initial celiotomy. Generally, by this time, diuresis and negative fluid balance have occurred. Decreasing abdominal girth and decreasing peripheral edema are evident and represent a reduction in visceral edema and abdominal wall edema. Despite this, often the abdomen cannot be closed, resulting in the acceptance of a subsequent ventral hernia that generally requires planned repair at a later date.44 When packing has been utilized in an effort to control solid organ bleeding, every effort should be made to remove the packing as soon as possible to minimize infectious risk (Figure 12.6). The rate of abdominal abscess formation in association with packing has been recorded as high as 24%.9 This high incidence of infection in these immunocompromised patients may cause physicians to continue prophylactic antibiotics for a protracted course. However, this strategy has been shown to offer no reduction in infectious complications even in the face of intestinal injuries.9,45–47 This may also predispose patients to the risk of superinfection with resistant organisms.9 Thus there is no good evidence to support extended use of antibiotics in solid organ injuries that require packing for control of hemorrhage. For patients requiring open abdomen management for secondary and tertiary peritonitis, many authors report bedside “washout” or peritoneal lavage in an effort to

Timing of Reconstruction and Subsequent Laparotomies Patients undergoing a damage-control laparotomy with gastrointestinal discontinuity should be returned to the operating room as soon as possible for reconstruction.

Figure 12.6. Perihepatic packing with laparotomy pads at the time of reexploration.

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minimize septic complications. Repeated laparotomy can be performed safely in the intensive care unit, but it may not affect the incidence of subphrenic or pelvic abscess.

Techniques for Delayed Primary Closure Ideally, all open abdomens should undergo definitive closure in a timely fashion. Every effort must be made to avoid unnecessary tension on the closure to avoid necrosis, dehiscence, and subsequent incisional hernia. The patient must also not be placed at risk for resultant incidence of secondary ACS. If primary closure can be achieved, there is minimal risk of the infection, enteric fistula, and wound problems that are typically seen with an open abdomen. This delayed primary closure of the original celiotomy wound can be performed days to weeks after the original operation. If delayed primary closure is not possible in a timely fashion, options for wound management include closure with a permanent prosthetic material, closure with autologous tissue, or closure with temporary prosthetic material with an anticipated ventral hernia. The latter approach requires definitive closure months to years after the original wound closure. Most acute care surgeons avoid the use of a permanent wound prosthetic particularly with an open contaminated wound for obvious concerns with infection. Most open abdomens will thus be managed with one of several commercially available biologic materials. Use of an extracellular matrix from animal or human tissue, cadaveric fascia, or autologous tissue in the form of flaps avoids or reduces the frequency of wound infections and/or enterocutaneous fistulae.


with Marlex mesh or Dexon mesh. Furthermore, the occurrence of intraabdominal adhesions was minimal.48,49 Because of the early vascular ingrowth and subsequent resistance to infection, SIS has been successfully utilized in contaminated or potentially contaminated ventral and/or inguinal hernias.50 Unfortunately, there has been limited use of this material as a prosthetic for closure of open abdomens.

Human Acellular Dermis Human acellular dermis (AlloDerm®) has similar biologic properties to porcine SIS. AlloDerm is prepared from cadaveric skin using a unique proprietary method. Once processed, all cellular components are removed, leaving the intact basement membrane and dermal collagen matrix. Thus, this acellular human dermis lacks the ability to induce an antigenic response. AlloDerm functions as a biologic scaffold for ingrowth of autogenous tissue, with many of the same advantages as SIS. It is available in two sizes: 2 × 4 cm and 3 × 7 cm. Before implantation, it must be rehydrated for 10 minutes in warm saline.An additional advantage over SIS is that several pieces of AlloDerm may be sutured together to cover larger defects (Figure 12.7). When compared with PTFE (Gortex®) in an animal model, there was no difference in mechanical wound strength.51 Unfortunately, long-term follow-up data are not yet available.52 However, more acute care surgeons are gaining experience with this new biologic prosthesis for wound closure and find it clinically superior to SIS.

Additional Techniques Tissue expander devices can be useful in facilitating wound closure utilizing native tissue without creation of

Small Intestinal Submucosa Porcine small intestine submucosa (SIS®) is an extracellular matrix composed primarily of type I collagen. It is prepared by removal of the mucosa’s muscularis externa, leaving an acellular submucosa that is preserved by freeze-drying and then sterilized with ethylene oxide. Before full implantation, it is reconstituted in warm saline for 10 minutes. It is available as 1-, 2-, 4-, and 8-ply sheets. This has been studied in both animal models and clinical practice for repair of hernia defects using the 4-ply preparation. Unfortunately, only short-term follow-up data are available.48–50 When histologic analysis was performed after use in repairing animal abdominal wall hernia defects, at 12 and 20 weeks postimplantation, the SIS had been well organized into the host tissue. The SIS was shown to be superior when compared with wounds closed

Figure 12.7. AlloDerm® placement for reconstruction of abdominal wall.


flaps and/or grafts. Large abdominal wall defects may be covered with native tissue after use of tissue expanders. The earliest report of soft tissue expansion described the use of pneumoperitoneum in 1931.53 Current use of this strategy primarily involves soft tissue enhancement, using balloon devices strategically placed in surrounding tissues to increase their capacity to accommodate reconstruction, and closure is used to repair the fascial hernia. Small series have reported good results with short followup periods.54 A recent series of 31 patients, which included seven trauma patients, claimed a success rate of 71%.55 Local advancement flaps in combination with absorbable mesh is another option for abdominal closure. This approach avoids split-thickness skin grafting and minimizes the risk of intestinal fistula.56 It is generally employed when fascial closure is either not possible or would predispose to ACS. This method of closure should only be used when there are no further planned surgical interventions. The flaps are created by separating the skin and subcutaneous tissue from the rectus sheath and external oblique fascia. The dissection is carried to the anterior axillary line from both sides of the open fascia. The fascial opening is then bridged with absorbable mesh, and the skin flaps are sutured in the midline.When there is unnecessary tension on the midline closure, a relaxing counterincision is made at the level of the anterior axillary line. Once the soft tissue edema resolves, these incisions will contract and close by secondary intention without the need for skin grafts. Depending on the size of the resultant ventral hernia, this may require repair of the ventral hernia at a later date. Most commonly this is performed using fascial component separation or standard mesh repair. Autologous flap techniques include rectus femoris flap for the suprapubic area, component separation, free myocutaneous flaps, and tensor fascia lata flaps. Tensor fascia lata is an ideal autologous tissue for management of large infected wounds or a contaminated field. The fascia lata is harvested from the thigh; the thigh wound is closed over suction drains. The fascial graft is oriented so that the deep surfaces are in contact with the peritoneal cavity. Experimental models have demonstrated that the rate of collagen synthesis and deposition is increased fivefold after implantation of this autologous tissue graft. Within 2 weeks, revascularization from the surrounding abdominal wall occurs.57–59 Unfortunately, recurrent hernia rates are rather high and reportedly range from 9% to 29%.57,60,61 Other disadvantages of tensor fascia lata flaps grafts include the creation of an additional wound on the thigh and the requirement for epidermolysis and potential for necrosis of the skin closed over the fascial flap.

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Component Separation Ramirez et al.62 first described component separation in 1990. This technique allows closure of the midline defect with an innovative advancement flap of muscle and fascia. First, a subcutaneous flap of adipose tissue is created by separating the subcutaneous adipose tissue from the fascia of the anterior rectus sheath and continuing laterally onto the external oblique aponeurosis to the level of the midaxillary line. The external oblique is then divided in a longitudinal fashion approximately 2 cm lateral to its insertion into the rectus sheet and separated from the internal oblique (Figure 12.8).This incision should be continued up onto the lower chest and no higher than the origin of the rectus abdominus muscle. With adequate release of the external oblique and internal oblique, the rectus muscles can be closed without significant tension. When additional mobility is required, a second longitudinal incision is placed in the posterior rectus sheet separating the rectus muscle. Bilateral component separation will allow enough mobility to close defects as large as 10 cm in the epigastrium, 20 cm at the level of the umbilicus, and 6 cm at the suprapubic level. The subcutaneous flaps are closed over suction drains to minimize seroma or hematoma formation. Multiple modifications of this technique have been described.43,63,64 Component separation avoids the complications associated with mesh implantation and has a more established profile of reliability than do biologic scaffolds. However, as with tensor fascia lata, the reported rate of recurrent hernia formation is significant, ranging from 22% to 32%.61,65 Appropriate utilization of the open abdomen and strategies for its subsequent closure have been increasingly associated with improved patient outcome. Management of these patients is a complex and challenging endeavor that should be an essential component of the acute care surgeon’s repertoire of skills.

Figure 12.8. Component separation with placement of AlloDerm® to bridge fascial defect.

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After the initial decision to leave the abdomen open, varying intervals of maintaining it temporarily open or transiently closed ensue. Definitive closure can be accomplished at the appropriate juncture either primarily or secondarily in a staged fashion, accepting a planned ventral hernia for some period of time. Noteworthy complications include secondary compartment syndrome; fistulae; intraabdominal and wound infections; tissue necrosis; evisceration; and dehiscence and incisional hernia. Clinical acumen and knowledge of the indications for early termination of the initial operation are imperative and based on guidelines that are well described. Subsequent decisions for timing and number of returns to the operating room are rooted in a sound knowledge of patient physiology; options for staged closure; and the advantages, disadvantages, and potential complications of each as well as their management. This often requires the combination of a number of methods and some degree of flexibility and creativity. The use of native tissue, prosthetics, and general nutritional, pulmonary, immunologic, and psychological support, individually or in combination, are all integral to success.

Critique This is a critical point in the case where continued operative management, even when definitive management has yet to be achieved, is deleterious. The “three dark angels of death” (hypothermia, acidosis, and coagulopathy) are absolute indicators for ending the operation as expeditiously as possible and establishing some type of creative closure (which includes simply packing the abdomen). Several options are usually available, including the creation of a “silo” by cutting a large panel from an irrigation bag. Further management of the patient needs to be done in an intensive care unit setting before any attempt at definitive intervention. Answer (E)

References 1. Lucas CE, Ledgerwood AM. Prospective evaluation of hemostatic techniques for liver injuries. J Trauma 1976; 16:442–451. 2. Calne RY, McMaster P, Pentlow BD. The treatment of major liver trauma by primary packing with transfer of the patient for definitive treatment. Br J Surg 1979; 66:338–339. 3. Feliciano DV, Mattox KL, Jordan GL Jr. Intra-abdominal packing for control of hepatic hemorrhage: a reappraisal. J Trauma 1981; 21:285–290.

4. Svodoba JA, Peter ET, Dang DV, et al. Severe liver trauma in the face of coagulopathy: a case for temporary packing and early reexploration. Am J Surg 1982; 144:717–721. 5. Carmona RC, Peck DZ, Lim RC. The role of packing and planned reoperation in severe hepatic trauma. J Trauma 1984; 24:779–784. 6. Rotondo MF, Schwab CW, McGonigal MD, et al. “Damage control”: an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma 1993; 35:375–383. 7. Wittman DH, Bansal N, Bergstein JM, et al. Staged abdominal repair compares favorably with conventional operative therapy for intra-abdominal infections when adjusting for prognostic factors with a logistic model. Theor Surg [now Eur J Surg] 1994; 25:273. 8. Berger RL, Dunton RF, Leonardi HK, Karlson KJ. Pack and close approach to persistent postcardiopulmonary bypass bleeding. J Am Coll Surg 1994; 178:353–356. 9. Rotondo MR, Zonies DH. The damage control sequence and underlying logic [review]. Surg Clin North Am 1997; 77:761. 10. Noetzel W. Die operativer Behandlung der diffusen eitrigen Peritonitis. Verh Dtsch Ges Chir 1908; 34:638. 11. Wittman DH, Schein M, Condon RE. Management of secondary peritonitis. Ann Surg 1996; 224:10. 12. Wittman DH, Wallace JR, Schein M. Open abdomen, planned relaparotomy, or staged abdominal repair: is there a difference? World J Surg 1994; 268:S49. 13. Wittman DH, Goris RJA, Ranga bashyam N, et al. Laparostomy, open abdomen, etappenlavage, planned relaparotomy and staged abdominal repair: too many names for a new operative method. In Ruedi TM, ed. State of the Art of Surgery. Reinach, Switzerland: International Society of Surgery, 1994:23. 14. Wittman DH. Staged abdominal repair: development and current practice of an advanced operative technique for diffuse suppurative peritonitis. Acta Chir Austriaca [Eur Surg] 2000; 32:171. 15. Neidehardt JH, Kraft F, Morin A, et al. Le traitement “La ventre ouvert” de certaines peritonites et infections parietals abdmoninales graves: etudes et technique. Chirurgie 1979; 105:272. 16. Maetani S, Tobe T. Open peritoneal drainage as effective treatment of advanced peritonitis. Surgery 1981; 90:804. 17. Porter JM, Ivatury RR, Nassoura ZE. Extending the horizons of “damage control” in unstable trauma patients beyond the abdomen and gastrointestinal tract. J Trauma 1997; 42:559–561. 18. Cipolla J, Stawicki SP, Hoff WS, et al. A proposed algorithm for managing the open abdomen. Am Surg 2005; 71:202– 207. 19. Myers JA, Latenser BA. Nonoperative progressive “Bogotá bag” closure after abdominal decompression. Am Surg 2002; 68:1029–1030. 20. Feliciano DV, Burch JM. Towel clips, silos, and heroic forms of wound closure. Adv Trauma Crit Care 1991; 6:231– 250. 21. Frenandez L, Norwood S, Roettger R,Wilkins HE 3rd.Temporary intravenous bag silo closure in severe abdominal trauma. J Trauma 1996; 40:258–260.

12. The Open Abdomen 22. Ghimenton F, Thomson SR, Muckart DJ, Burrows R. Abdominal content containment: practicalities and outcome. Br J Surg 2000; 87:106–109. 23. Howdieshell TR, Yeh KA, Hawkins ML, Cue JL. Temporary abdominal wall closure in trauma patients: indications, technique, and results. World J Surg 1995; 19:154–158. 24. Howdieshell TR, Proctor CD, Sternberg E, et al. Temporary abdominal closure followed by definitive abdominal wall reconstruction of the open abdomen. Am J Surg 2004; 188:301–306. 25. Bender JS, Bailey CE, Saxe JM, et al. The technique of visceral packing: recommended management of difficult fascial closure in trauma patients. J Trauma 1994; 36:182–185. 26. Lamb JP, Vitale T, Kaminski DL. Comparative evaluation of synthetic meshes used for abdominal wall replacement. Surgery 1983; 93:643–648. 27. Marmon LM, Vinocur CD, Standiford SB, et al. Evaluation of absorbable polyglycolic acid mesh as a wound support. J Pediatr Surg 1985; 20:737–742. 28. Dayton MT, Buchele BA, Shirazi SS, Hunt LB. Use of an absorbable mesh to repair contaminated abdominal-wall defects. Arch Surg 1986; 121:954–960. 29. Lopez Villata GC, Furio-Bacete V, Ortiz Oshiro E, et al. Experimentally contaminated reabsorbable meshes: their evolution in abdominal wall defects. Int Surg 1995; 80:223–226. 30. Morris JA Jr, Eddy VA, Rutherford EJ. The trauma celiotomy: the evolving concepts of damage control. Curr Probl Surg 1996; 33:609–708. 31. Bradley SJ, Jurkovich GJ, Pearlman NM, Stiegmann GV. Controlled open drainage of severe intra-abdominal sepsis. Arch Surg 1985; 120:629–631. 32. Heddirch GS, Wexler MJ, McLean AP, Meakins JL. The septic abdomen: open management with Marlex mesh with a zipper. Surgery 1986; 99:399–408. 33. Walsh GL, Chiasson P, Hedderich G, et al. The open abdomen: a Marlex mesh and zipper technique. Surg Clin North Am 1988; 1:25–40. 34. Wittman DH, Aprahamian C, Bergstein JM. Etappenlavage: advanced diffuse peritonitis managed by planned multiple laparotomies utilizing zippers, slide fastener, and Velcro analogue for temporary abdominal closure. World J Surg 1990; 14:218–226. 35. Aprahamian C, Wittman DH, Bergstein JM, Quebbeman EJ. Temporary abdominal closure (TAC) for planned relaparotomy (etappenlavage) in trauma. J Trauma 1990; 30:719–723. 36. Wittman DH, Aprahamian C, Bergstein JM, et al. A burrlike device to facilitate temporary abdominal closure in planned multiple laparotomies. Eur J Surg 1993; 159:75–79. 37. Barker DE, Kaufman HJ, Smith LA, et al. Vacuum pack technique of temporary abdominal closure: a 7-year experience with 112 patients. J Trauma 2000; 48:201–207. 38. Brock WB, Barker DE, Burns RP. Temporary closure of open abdominal wounds: the vacuum pack. Am Surg 1995; 61:30–35. 39. Smith LA, Barker DE, Chase CW, et al. Vacuum pack technique of temporary abdominal closure: a four year experience. Am Surg 1997; 63:1002–1008.

185 40. Garner GB, Ware DN, Cocanour CS, et al. Vacuum assisted wound closure provides early fascial reapproximation in trauma patients with open abdomen. Am J Surg 2001; 182:630–638. 41. Stone PA, Hass SM, Flaherty SK, et al. Vacuum-assisted fascial closure for patients with abdominal trauma. J Trauma 2004; 57:1082–1086. 42. Hirschberg A, Mattox KL. “Damage control” in trauma surgery. Br J Surg 1993; 80:1501. 43. Hirschberg A, Mattox KL. Planned reoperation for severe trauma. Ann Surg 1995; 222:3. 44. Fabian TC, Croce MA, Pritchard FE, et al. Planned ventral hernia: staged management for acute abdominal wall defects. Ann Surg 1994; 219:643. 45. Bloomfield G, Saggi B, Blocher C, Sugerman H. Physiologic effects of externally applied continuous negative abdominal pressure for intra-abdominal hypertension. J Trauma 1999; 46:1009–1016. 46. De Waele JJ, Benoit D, Hoste E, Colardyn F. A role for muscle relaxation in patients with abdominal compartment syndrome. Intensive Care Med 2003; 29:332. 47. Shapiro MB, Jenkins DH, Schwab CW, Rotondo MF. Damage control: collective review. J Trauma 2000; 49:969–978. 48. Dejardin LM, Arnoczky SP, Clarke RB. Use of small intestinal submucosal implants for regeneration of large fascial defects: an experimental study in dogs. J Biomed Mater Res 1999; 46:203–211. 49. Badylak S, Kokini K, Tullius B, et al. Morphologic study of small intestinal submucosa as a body wall repair device. J Surg Res 2002; 103:190–202. 50. Franklin JJ Jr, Gonzalez ME Jr, Michaelson RP, et al. Preliminary experience with new bioactive prosthetic material for repair of hernias in infected fields. Hernia 2002; 6:171–174. 51. Menon NG, Rodriguez ED, Byrnes CK, et al. Revascularization of human acellular dermis in full-thickness abdominal wall reconstruction in the rabbit model. Ann Plast Surg 2003; 50:523–527. 52. Dalla Vecchia L, Engrum S, Kogon B, et al. Evaluation of small intestine submucosa and acellular dermis as diaphragmatic prostheses. J Pediatr Surg 1999; 34:167–171. 53. Cady B, Brooke-Cowden GL. Repair of massive abdominal wall defects: combined use of pneumoperitoneum and Marlex mesh. Surg Clin North Am 1976; 56:559–570. 54. Paletta CE, Huang DB, Dehghan K, Kelly C. The use of tissue expanders in staged abdominal wall reconstruction. Ann Plast Surg 1999; 42:259–265. 55. Tran NV, Petty PM, Clay RP, et al. Tissue expansion– assisted closure of massive ventral hernias. J Am Coll Surg 2003; 196:484–488. 56. Fansler RF, Taheri P, Cullinane C, et al. Polypropylene mesh closure of the complicated abdominal wound. Am J Surg 1995; 170:15–18. 57. Disa JJ, Goldberg NH, Carlton JM, et al. Restoring abdominal wall integrity in contaminated tissue-deficient wounds using autologous fascia grafts. Plast Reconstr Surg 1998; 101:979–986. 58. Disa JJ, Chiaramonte MF, Girotta JA, et al. Advantages of autologous fascia versus synthetic patch abdominal

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F.A. Luchette, S.J. Poulakidas, and T.J. Esposito reconstruction in experimental animal defects. Plast Reconstr Surg 2001; 108:2086–2087. Das SK, Davidson SF, Walker BL, Talbot PJ. The fate of free autogenous fascial grafts in the rabbit. Br J Plast Surg 1990; 43:315–317. Feldt-Rasmussen K, Jensen OA. Large ventral herniae treated with free fascial grafts; a follow-up study. Acta Chir Scand 1956; 111:403–408. Girotto JA, Chiaramonte M, Menon NG, et al. Recalcitrant abdominal wall hernias: long-term superiority of autologous tissue repair. Plast Reconstr Surg 2003; 112:106–114. Ramirez OM, Uras E, Dellon AL. “Components separation” method for closure of abdominal-wall defects: an

anatomic and clinical study. Plast Reconstr Surg 1990; 86:519–526. 63. Jernigan TW, Fabian TC, Croce MA, et al. Staged management of giant abdominal wall defects: acute and long-term results. Ann Surg 2003; 238:349–357. 64. Ennis LS, Young JS, Gampper TJ, Drake DB. The “open book” variation of component separation for repair of massive midline abdominal wall hernia. Am Surg 2003; 69:733–743. 65. de Vries Reilingh TS, van Goor H, Rosman C, Bemelmans MH, et al. “Components separation technique” for the repair of large abdominal wall hernias. J Am Coll Surg 2003; 196:32–37.

13 Acute Care Surgery and the Elderly Patrick K. Kim, Donald R. Kauder, and C. William Schwab

Case Scenario You are asked to evaluate an 80-year-old retired railroad porter who stumbled and fell while walking his dog. He has left upper extremity and forehead abrasions. According to his family, he lives alone and is completely independent. The patient denies any medical problems with the exception of diabetes mellitus and benign prostate hypertrophy. He has a normal mental status and is hemodynamically stable. Outside of the abrasion, patient’s physical examination is unremarkable. Which of the following should be the management plan for this patient? (A) (B) (C) (D) (E)

Overnight observation in the hospital Outpatient management Refer patient to a rehabilitation center Obtain plain radiography of the head Obtain head computed tomography scan

Performing acute care surgery in the elderly poses a wide spectrum of challenging problems for the surgeon. The geriatric population is possessed of unique physiology, risk factors, anatomic considerations, and preexisting conditions that significantly impact outcome. Many of these issues arise simply as a result of the “normal” aging process. Those who suffer from conditions that require acute care surgical interventions and are subsequently exposed to the physiologic stress that accompanies them suffer high rates of complications and mortality.1 As the cohort of elders increases, it is increasingly vital for the surgeon to understand how age affects their surgical evaluation and treatment. No broad consensus exists regarding the age at which a person becomes “elderly,” but generally this appellation has been applied to those variably between 55 and 75 years of age. Regardless of when elder years begin, this group continues to comprise a greater proportion of the

American population. In 2000, 35 million Americans were 65 years or older (12.4% of the population). In 2001, the overall life expectancy in the United States was 77.2 years (74.4 years for men and 79.8 years for women).2 By 2030, this number is expected to increase to 71 million (19.6% of the population).3 Acute care surgery in the elderly is associated with strikingly high rates of complications and mortality, carrying a 7- to 10-fold increase in mortality compared with the same procedures performed electively.4,5 Those older than 74 years fare even worse than those between the ages of 64 and 74 years.5 Interestingly, it appears that age contributes less to morbidity and mortality in acute care operations than the emergency nature of the process itself. One study suggests that the differences in mortality between octogenarians and septuagenarians are due to American Society of Anesthesiologists (ASA) grade and delays in surgical treatment, not to age.6 It might be inferred, then, that variations in the physiologic reserve of persons of similar ages, as well as different rates of senescence among an individual’s organ systems, are critical factors that influence outcome. Because age cannot be controlled, it becomes imperative to optimize the other factors during evaluation and definitive treatment.

Normal Physiologic Changes Associated with Aging The physiologic changes associated with aging are well studied. Every organ system has age-related changes that have significance for the surgeon. Collectively, the normal physiologic changes associated with aging and the changes associated with chronic diseases result in diminished physiologic reserve available to handle the stress of acute surgical disease and surgical intervention.7 The cardiovascular system undergoes many changes.7 Aging is associated with decreased responsiveness to beta-adrenergic stimulus, limiting both inotropy and

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chronotropy and, ultimately, cardiac output. The maximum achievable heart rate is decreased. Left ventricular reserve is diminished, resulting in less ability to increase ejection fraction under stress. Left ventricular hypertrophy results in decreased compliance. Ventricle filling is more dependent on atrial contraction, and cardiac output becomes more dependent on end-diastolic volume. Alterations in the arterial vascular system also affect myocardial function. Arterial intimal hyperplasia leads to increased stiffness of arterial walls, occurring independently of atherosclerosis. Diastolic pressure decreases, which worsens perfusion pressure of the myocardium. Progressive aging has a significant effect on pulmonary physiology.7 Alterations in chest wall mechanics and intrinsic changes in the lung parenchyma have an additive effect. As costal cartilage becomes calcified, the chest wall becomes more rigid. Respiratory muscle strength is decreased, and intercostal muscles atrophy and become weaker. All of these factors contribute to decreases in both forced expiratory volume and forced vital capacity. Breathing becomes more dependent on the diaphragm and abdominal muscles. Regarding the lungs themselves, the alveolar–arterial oxygenation gradient is increased, the shunt fraction is increased, ventilation–perfusion mismatch is increased, and diffusion capacity is decreased. All of these factors contribute to decreased arterial oxygenation. Addition of a large abdominal surgical incision in this setting, especially in the emergency situation when there is no opportunity to optimize pulmonary mechanics preoperatively, can have disastrous consequences on pulmonary physiology. The renal system is relatively impaired in the elderly.7 Anatomic changes include glomerulosclerosis, which decreases effective renal cortex mass. Functional changes include decreased glomerular filtration rate, decreased glomerular filtration reserve, decreased reabsorption and secretion by renal tubules, and blunted response to aldosterone and antidiuretic hormone. Intraabdominal surgical conditions are frequently associated with insensible and third-space fluid losses or hemorrhage. The resultant hypovolemia and hypoperfusion of the renal cortex puts the patient at high risk for developing clinically significant renal dysfunction. Gastrointestinal function is relatively preserved in the elderly.7 Most age-related changes involve the esophagus and the colon. Esophageal neuromuscular degeneration contributes to diffuse esophageal spasm, achalasia, and reflux. Dysfunction of the upper esophageal sphincter predisposes patients to aspiration, dysphagia, and pharyngoesophageal diverticula. Lower esophageal sphincter dysfunction contributes to gastroesophageal reflux. The stomach and small bowel structure and function remain relatively unaffected by aging. In the colon, thickening of the colonic muscular wall occurs. Endocrinologic changes are numerous.7 Even among nondiabetic patients, the elderly demonstrate some

P.K. Kim, D.R. Kauder, and C.W. Schwab

degree of insulin resistance, resulting in decreased glucose tolerance. Studies in surgical patients have demonstrated that intensive glycemic control is associated with a decrease in morbidity and mortality compared with more liberal glycemic control,8 but the optimal glycemic range among the elderly who undergo acute care surgery is unknown. An important age-related change in the endocrine system is the decreased sympathetic response to stress, clinically manifested by a decreased vasoconstriction response to cold environments. This makes the elderly patient particularly susceptible to hypothermia in the perioperative period. Finally, regarding the thyroid gland, subclinical hypothyroidism is prevalent in the elderly population.9 Subclinical hypothyroidism in the elderly has been shown to be independently associated with depression, dementia, and coronary disease.10,11 Neurologic and cognitive changes are numerous.7 Physiologic and anatomic changes include cortical atrophy, decreased cerebral blood flow, and decreased cerebral oxygen consumption. Clinically the elderly are more likely to have blunted visual, auditory, and tactile sensation and increased pain threshold. The clinical significance is the increased prevalence of anxiety, agitation, and delirium in the perioperative period. The inappropriate use of narcotic analgesics and sedative/hypnotics can exacerbate underlying deficits. Decreased capacity to follow postoperative instructions related to pulmonary toilet, ambulation, and analgesic management can lead to unfavorable outcomes. Alterations in cerebellar function, as well as balance and gait disturbances, can predispose the patient to falls.

Clinical Presentation of Elderly Patients Initial evaluation of the elderly patient with a suspected surgical emergency may be difficult. For both medical and surgical conditions, the elderly may present atypically or with nonspecific complaints.12 The elderly patient may delay seeking medical attention because of a higher pain threshold, or an atypical or falsely benign presentation, or denial.13–15 Preexisting alterations in mental status or neurologic status (i.e., dementia, delirium, prior stroke, and diabetic neuropathy) may also contribute to delayed presentation by the patient or referral by primary providers. The chief complaint may thus not immediately suggest the correct differential diagnosis. Furthermore, the history of present illness may be difficult to elicit, and the medical history may be complex, incomplete, or frankly inaccurate. Physical examination similarly may be deceptively benign. This may be particularly true of diseases that normally cause peritonitis, such as diverticulitis and appendicitis.16–18 Among patients hospitalized in medical intensive care, altered mental status, absence of

13. Acute Care Surgery and the Elderly

peritoneal signs, analgesics, antibiotics, and mechanical ventilation all contributed to delays in surgical evaluation and treatment.19 Predictably, delays in presentation, referral, diagnosis, and treatment all contribute to dismal rates of morbidity and mortality among the elderly with acute surgical problems.

Preoperative Assessment By its nature, acute care surgery precludes complete preoperative evaluation and risk stratification. Ideally, a complete medical history is obtained, and this information can be helpful in stratifying risk and optimizing the patient in the perioperative period. Eighty percent of the elderly have at least one chronic medical condition, and fifty percent have two or more.20 In decreasing order, the most common chronic conditions are arthritis, hypertension, heart disease, cancer, diabetes, and stroke.20 Of these, heart disease, hypertension, and diabetes have the greatest impact on outcomes following surgery and are the focus of active investigations. The American College of Cardiology/American Heart Association (ACC/AHA) perioperative executive summary provides guidelines for cardiac risk stratification for patients undergoing noncardiac surgery.21 Although the guidelines are primarily focused on patients who undergo elective noncardiac surgery, the same algorithm is used for postoperative risk stratification among patients who undergo acute care procedures. The ACC/AHA paradigm stratifies risk using three components: clinical markers, functional capacity, and surgery-specific risk. Clinical markers are classified as major, intermediate, and minor. Major predictors include acute or recent myocardial infarction (MI), unstable or severe angina, decompensated heart failure, “large ischemic burden” (clinically or by noninvasive testing), significant arrhythmias, and significant valvular disease. Intermediate predictors include mild angina, remote MI, compensated heart failure, diabetes, and serum creatinine level ≥2.0 mg/dL. Advanced age is classified as a minor predictor, along with abnormal electrocardiogram, nonsinus rhythm, history of stroke, uncontrolled hypertension, and low functional capacity. Functional capacity can be measured by metabolic equivalent (MET) levels, in which 1 MET is defined as the oxygen uptake at rest (approximately 3.5 mL/kg/min oxygen uptake).22 Patients who cannot routinely tolerate a demand of 4 METs have increased perioperative cardiac and long-term risks. Four-MET activities include light work around the house, such as dusting or washing dishes, climbing a flight of stairs, or walking at a rate of 4 miles per hour. Regarding surgery-specific risk of sustaining a cardiac event, major acute care surgery in the elderly is a priori considered high-risk surgery (>5% risk of cardiac event) and is grouped with aortic and other major vascular

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surgery, peripheral vascular surgery, and prolonged procedures associated with large fluid shifts and/or blood loss.21 Intermediate-risk procedures (6 cm and not responding to medical therapy Persistent fever and signs of sepsis after 2 weeks of therapy Persistence after 6–8 weeks without reduction in size Recurrent or major hemoptysis Bronchopleural fistula Empyema Cannot exclude cancer

3. Place nasogastric tube or EGD in esophagus as anatomy may be obliterated 4. Small (600 mL/24 hr → 12%–50% mortality with medical management • >600 mL/16 hr → 75% mortality with medical management • “Exsanguinating”: >1,000 mL at >150 mL/hr → 100% mortality with medical management “Clinically significant” → one of the following: • Causes death • Requires hospitalization • Associated with evidence of systemic blood loss, including ↓ hematocrit • Requires transfusion • Presents risk of aspiration and/or airway obstruction

embolization, and endobronchial ablation and/or resection, depending on etiology.

Etiology Considering all forms of hemoptysis, approximately 85% are caused by inflammatory etiologies, with infection predominating.99 The bronchial arteries are the major source of hemoptysis, making up 90% of cases.97 Although tuberculosis continues to be the leading cause of hemoptysis worldwide, chronic inflammatory disease and bronchogenic carcinoma remain the most common causes in western societies.100 Uncommonly, massive hemoptysis may be a consequence of primary airway lesions or primary pulmonary malignancies. Inflammation or infection can result in erosion of adjacent great vessels into the bronchus. The propensity of anastomotic fistula arising after lung transplantation or sleeve resection (particularly of the right upper lobe) underlines the importance of wrapping the anastamosis with viable tissue (such as omentum or pericardium) or interposing intercostal flaps between the airway anastomosis and the pulmonary artery.101 The “classic” airway-related procedure, however, does not involve resection but rather chronic intubation and pressure necrosis, namely, tracheoinnominate artery fistula. The underlying causes range from inappropriate low placement of the tracheostomy to anatomic variations. The published incidence of this potentially fatal complication ranges between 0.5% and 5%.

Diagnosis Prior pneumonia, history of aspiration, smoking history, and prior surgery may all suggest the diagnosis. A travel history should always be sought when possible. Travelers to Asia, the Middle East, and South America may develop hemoptysis as a result of parasitic infection. Catamenial (endometriosis) hemoptysis may be

24. Lungs and Pleura

suspected if recurrent episodes are associated with the patient’s menstrual cycle. For children, bronchial adenoma, vascular anomalies, and foreign body aspiration are the most common cause. For adults, those over the age of 40 years and smokers are at risk for bronchogenic carcinoma. In addition, mitral stenosis and/or pulmonary infarction from embolism should be entertained when the clinical history is consistent. The quality of the bleeding can suggest the source and thus the diagnosis. Brisk, bright red arterial bleeding usually implicates the bronchial circulation, most often secondary to inflammatory etiologies. Rarely, this can imply more major arterial sources, such as innominate artery or aorta, or, even more uncommonly, left atrium or pulmonary vein. Dark blood is more consistent with pulmonary artery bleeding, such as might be seen in the setting of a Rasmussen aneurysm.

379 Initial Management Antibiotics Upright if not intubated Vascular access Correct coagulation disorders O2 Place affected side dependent suspected/known Lateralize CXR 60% accurate Patient correctly identifies site 10–47% Physical exam identifies side correctly 50% incorrectly 3% Localize Flexible and/or rigid bronchoscopy Angiography if not immediately life threatening, otherwise after isolation Isolate Endobronchial blocker DL-ETT

“Occult” Massive Hemoptysis Significant hemoptysis is rarely a diagnostic dilemma. However, it has been estimated that up to 30% of endobronchial clots, primarily in patients who have been ventilated for prolonged periods, with or without tracheostomy, occur without evidence of hemoptysis. In ventilated patients, the most notable manifestations are an acute rise in peak pressure accompanied by a decrease in tidal volume.102 Multiple peripheral clots may result in transmission of elevated airway pressure to the rest of the thorax, resulting in decreased venous return and possibly hemodynamic compromise. More proximal clots, such as those at the end of the endotracheal tube, are usually associated with normal distal airway pressure and limited hemodynamic changes. A rare variation is a large clot that acts as a ball valve on the end of the endotracheal tube, allowing inspiration but preventing expiration. This may manifest as progressive lobar collapse in some areas while other areas are over distended, increasing difficulty in ventilation and recalcitrant hypoxemia. Recurrent pneumothoraces as a consequence of rapid hyperventilation have been reported. Diagnosis can be confirmed by flexible bronchoscopy, and for most cases this will be sufficient to break up the clot. Occasionally, rigid bronchoscopy with or without instillation of thrombolytics will be required.99

Initial Management In the setting of massive hemoptysis, the initial concern should be to protect the airway and to stabilize the patient. Subsequently, lateralization, localization, and isolation to prevent drowning needs to proceed rapidly (Figure 24.10).97 Bronchoscopy plays a central role in managing these patients. Bronchoscopy performed within 48 hours of the onset of hemoptysis is more likely

Treatment

Observation

Embolization

Operation

Figure 24.10. Rough schema for the initial management of massive hemoptysis.

to identify the site of bleeding than if performed later, for both rigid and flexible bronchoscopy. Rigid bronchoscopy has been able to identify the source of bleeding in up to 86% of cases when performed within 48 hours compared with 52% when performed later. Flexible bronchoscopy success rates range from 34% to 93% success rates with early intervention as opposed to 11% to 50% with later procedures.101 Even when angioembolization control of the hemorrhage is being considered, bronchoscopic localization or even lateralization of the bleeding site may ultimately facilitate the angiographer’s efforts to localize the feeding vessel(s). Rigid and flexible bronchoscopy are complimentary. Rigid scopes have better ability to suction large quantities of liquid and clotted blood, to maintain and secure an airway, to provide ventilation continuously, and to provide more technical options, including the use of large forceps to facilitate clot debridement and tumor debulking.97 Flexible bronchoscopy has become more acceptable as an initial procedure, particularly for patients who are already intubated.99 The flexible scope has a greater ability to evaluate the peripheral airways. Limitations include decreased suction capability and visualization through the smaller port in some settings. Also in some settings the endotracheal tube may obscure the source of hemorrhage.

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When both techniques are available, a reasonable approach to bronchoscopy may be, for patients who are hemodynamically stable, already intubated, and in the intensive care unit, to perform flexible bronchoscopy first while arranging for surgical consultation, evaluating coagulation factors, and obtaining blood products. For unstable patients or patients with ongoing severe bleeding, the primary emphasis should be on transferring the patient to the operating room as soon as possible, where both flexible and rigid bronchoscopy can be performed. The desire to perform a flexible bronchoscopy should never impede transfer to the operating room. In the presence of massive hemorrhage, flexible bronchoscopy is insufficient to adequately clear the airway of blood and blood clots. Rigid bronchoscopy will permit both aggressive bronchial toilet and ventilation. Initial control may be obtained by using ice-saline lavage or dilute epinephrine. If these initial maneuvers are successful, but no definite site of bleeding has been identified, flexible bronchoscopy can then be used through the rigid bronchoscope to further examine the bleeding side down to the lobar or segmental level. If significant bleeding continues, the bleeding side/site should be isolated using endobronchial techniques.

Strategies to Prevent Further Airway Contamination A simple method to prevent further airway contamination is to advance the uncut endotracheal tube into the airway of the unaffected lung. This may be difficult if the site of bleeding arises from the left lung, as advancing the endotracheal tube into the right main stem bronchus often results in occlusion of the right upper lobe. However, in critical situations this can be tried as a temporizing measure. This will provide for unilateral ventilation while preventing further aspiration of blood. It does not, however, provide a means of control. Double-lumen tubes may also be utilized. Well positioned, they allow excellent isolation of both lungs and prevent asphyxiation. These, however, may be at times difficult to place and require expertise, particularly in an acute care setting when time is of the essence. Even if successfully placed, technical difficulties such as displacement can lead to further aspiration and death. Garzon and colleagues98 described a series of 62 patients, in which four of seven patients managed with a double-lumen tube ultimately died as a consequence of intraoperative tube dislodgment with subsequent continued aspiration of the unaffected lung during surgery. This was in contrast to six patients managed with left main stem intubation with a single-lumen tube and six further patients managed by single-lumen intubation coupled with balloon blockade of the left lung, none of whom died from aspiration.98 Another drawback of double-lumen intubation relates to

R. Karmy-Jones and J.W. Meredith

the small caliber of each limb of the endotracheal tube which does not permit passage of bronchoscopes of adequate sizes to allow aspiration/toilet of the bleeding airway under direct vision. In this circumstance, one has to resort to “blind” catheter aspiration. The doublelumen tube is ideally utilized at the time of planned surgical resection. Endobronchial blockers can be placed easily in the main bronchi or bronchus intermedius, although occasionally the individual anatomy of the patient will allow more precise control, such as into the orifice of the left lower, left upper, or right upper lobes. Not only will this approach prevent further aspiration of blood, but it also allows easier ventilation and further bronchoscopic assessment and toilet through the endotracheal tube. Inflation of the tracheal cuff helps secure the blocker in position against the tracheal wall, but additional fixation is obtained by tying the blocker to the secured endotracheal tube.A size 8 Fr Fogarty® blocker is usually needed to occlude the main airways. Smaller 4 Fr catheters are preferable for more selective occlusion at the lobar or segmental level. Recently, there have been bronchial blockers designed to be placed through an endotracheal tube, using a side port attachment and loop so that the blocker can be advanced and repositioned as needed. This form also has the ability to suction or irrigate through the blocker. Endobronchial tamponade may by itself suffice to control bleeding.103 The catheter is left inflated for 24 hours while coagulation parameters are corrected and the patient’s condition is stabilized. The balloon is then deflated under bronchoscopic vision. If no further bleeding occurs, it is left in situ and deflated for an additional 24 hours. If there is no further bleeding, the catheter can be removed. Prolonged use of endobronchial blockers or double-lumen tubes may be associated with critical ischemia or obstructive pneumonitis. Antibiotic coverage should be provided.

Diffuse Parenchymal Bleeding Rarely, the source of bleeding is diffuse, bilateral alveolar hemorrhage. In this setting, lung isolation is not sufficient. Bronchoscopy can confirm the bilateral nature of the hemorrhage and clear the airway of gross blood clots, which may allow some decrease in bleeding. Anecdotally applying increased positive end-expiratory pressure of 10 to 20 cm H2O has resulted in diminishing bleeding until systemic therapy can be effective.

Subsequent Treatment In the setting of massive hemoptysis, usually additional interventions are required after isolation. These can include topical or systemic agents (Table 24.9).101,104 In

24. Lungs and Pleura Table 24.9. Adjunctive hemoptysis.

381 pharmacological

treatments

of

Topical • Iced saline lavage → 50 mL aliquots at 4°C • Topical epinephrine → 0.2 mL 1 : 1,000 in 500 mL normal saline • Topical thrombin ± fibrinogen Systemic • Vasopressin → 0.2–0.4 U/min • Tranexamic acid • Steroids/cytotoxic agents/plasmapheresis → for autoimmune disorders • Danazol → for catamenial hemoptysis

most cases the issue will be timing of angioembolization and whether or not surgical intervention, including resection, will be needed.

Angioembolization Angiography can be used as both a diagnostic and a therapeutic tool.105,106 Practically, it is much more efficient if the likely bleeding site has been localized before the study at bronchoscopy or by plain radiographs. A flush aortogram is first obtained to determine the number, location, and size of the bronchial arteries. There are a variety of bronchial artery anatomic variations. Most frequently, the bronchial arteries originate from the thoracic aorta between T3–T8, usually T5–T6. The three most common patterns are (1) a single left and right bronchial artery (30.5%), (2) a single right bronchial with an additional common trunk from which both a right and left bronchial arise (25%), and (3) two left bronchial arteries and a right intercostal origin to a right bronchial artery (12.5%).99 If the bleeding site is from an upper lobe, the ipsilateral subclavian artery, internal thoracic, and at times intercostal arteries may also need to be studied because nonbronchial artery systemic collaterals exist in up to 45% of cases. This is particularly important when pleural thickening, indicating inflammation and a possible site of collateralization, is present. Before embolization can be performed, digital subtraction angiography is used to determine whether or not a spinal arterial branch arises from the involved bronchial artery or arteries. If embolization can be carried out well distal to the spinal artery, embolization may still be feasible. Embolization can be performed using a variety of substances, but polyvinyl alcohol (350 to 590 μm) or gelfoam is preferred by most authors because these materials occlude neither the access vessel nor the smallest distal arterioles, which might lead to tissue infarction. Larger coils and detachable balloon, not only are associated with distal collateralization but, in the event that rebleeding occurs, appear to prevent reaccessing the target vessels. If a bleeding source cannot be iden-

tified or suspected, then a pulmonary angiogram will be required, especially if tuberculosis, other cavitary lesions, or a pulmonary arteriovenous malformation is suspected. The pulmonary artery is identified as the source of massive hemoptysis in only 8% of cases. The initial success rates range from approximately 60% to 100%. Recurrent bleeding occurs in 20% to 30% of cases. Possible reasons for recurrence include the following: 1. Recanulization (usually between 2 and 7 months) 2. Increased blood flow via pulmonary artery–bronchial fistula 3. Diffuse systemic collaterals 4. Subsequent erosion of necrotizing inflammation into the pulmonary artery Repeated procedures directed at the initial bronchial bleeding source or associated collaterals may increase the success rate in selected cases. Recurrent bleeding by 1 year occurs in 20% to 46% of patients, but usually is not massive. By 3 to 5 years, recurrent bleed rates are reported to be 23%. Whether or not embolization should be accepted as definitive therapy depends on the underlying circumstances. Most critically ill patients have multiple problems, and embolization, with or without temporary airway control, may be the best therapy to allow improvement. However, patients with isolated lesions at high risk of rebleed (such as cavitary lesions or localized lung necrosis) may be better served with early resection when they have been stabilized.

Surgical Versus Medical Therapy for Massive Hemoptysis Surgical intervention may be required to manage a specific large vessel bleed (such as tracheoinnominate artery fistula), or if there is a localized airway or parenchymal source that is resectable. Overall mortality rate in the setting of surgical resection (up to 50%) is somewhat lower than the maximum mortality described with medical management (up to 86%), but this probably reflects a degree of bias, as many of the medically managed patients were not considered surgical candidates because of extensive underlying disease processes.107 If bleeding can be controlled and the patient stabilized, the mortality rate associated with surgery can be reduced to approximately 20%. In the acute setting, assuming that the patient is an operative candidate, surgery should be considered if there is ongoing bleeding despite airway control and embolization; if embolization is not technically possible; if bleeding recurs after embolization; and/or if a lesion is noted that has a high likelihood of rebleeding. Surgery is contraindicated if the underlying etiology is diffuse (such as bilateral

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necrotizing pneumonia) or if prebleed lung function is severely compromised (FEV1 < 1.0 L). In summary, airway hemorrhage is a potentially rapidly fatal condition. Death may occur within minutes from asphyxiation before control can be achieved. The primary prognostic factors are the rate of bleeding and the underlying cardiopulmonary status of the patient. Bronchoscopy is central to management, but the goals differ depending on circumstances. For stable patients with minimal hemoptysis, bronchoscopy can be used to diagnose the cause and to be the primary treatment modality. In the setting of massive and/or life-threatening bleeding, bronchoscopy is primarily performed to maintain ventilation and direct endobronchial blockade. Although flexible bronchoscopy is an acceptable mode initially, there should be no delay in performing rigid bronchoscopy when it becomes apparent that bleeding is too vigorous to permit successful airway exploration with the smaller flexible instrument. Once isolation of bleeding has been achieved, the choice needs to be made between embolization and surgical resection.

R. Karmy-Jones and J.W. Meredith

Although not strictly a “parenchymal” problem, tracheoinnominate artery fistula (TIF) deserves to be included in the discussion of acute care lung surgery because it is as an important consideration for hemoptysis and because most patients requiring a tracheostomy do so because of underlying lung pathology. The seriousness of this feared complication of tracheostomy is the high mortality rate (87.6%) if it develops. Tracheoinnominate artery fistula arises as a consequence of proximity between the tube and the artery (below the fourth ring or high riding artery) or of pressure necrosis by the cuff. Tracheal capillary pressure ranges between 20 and 30 mm Hg, and tracheal wall circulation is impaired with cuff pressures at 22 mm Hg and totally obstructed at pressures of 37 mm Hg. High-volume low-pressure tracheal cuffs with cuff pressures 8 cm • Depression of the left main stem bronchus • Loss of paravertebral pleural stripe • Calcium layering at the aortic knob • Deviation of nasogastric tube in the esophagus • Lateral displacement of the trachea Lateral chest x-ray • Anterior displacement of the trachea • Loss of the aortic and pulmonary window • Other findings • Apical pleural hematoma • Massive left hemothorax • Obvious blunt injury to diaphragm

P.I. Ellman and I.L. Kron

forming an aortogram takes time and manpower, requires an interventional radiology team, and in some medical centers requires the patient to be brought to the angiography suite—away from the relative safe haven of the operating room or intensive care unit. It is not uncommon for a patient to exsanguinate and die in the angiography suite.38,47,48 Complications include contrast reactions, renal insufficiency, groin hematomas, and pseudoaneurysms. Given all of these problems, aortography is being used less frequently as a primary means of assessing aortic injury. It clearly has a role for the stable patient who has an equivocal helical CT study. In our institution, we will use aortography for patients who are stable and have equivocal helical CT scans. If the patient is unstable, we plan on using TEE in the operating room as a confirmatory test. Helical CT scanning is currently the best first test to evaluate for BAI in a stable patient. It offers a number of advantages over aortography without giving up too much in the way of sensitivity or specificity; thus, in most centers helical CT scanning has become as the primary means of ruling out BAI. Some medical centers have now made helical CT the definitive test for BAI without the need for further tests, such as aortography or TEE.43,49–51 The speed with which the test can be done, its sensitivity and specificity, and the ease of interpretation make spiral CT a superior test to all three in the initial evaluation of a possible traumatic aortic rupture. Many of these patients also will need an abdominal CT scan to evaluate for intraabdominal trauma, thus making spiral CT even more efficacious. The sensitivity and negative predictive value of the test are approximately 100%.43,45,52,53 The specificity and positive predictive value range between 50% and 89%. Findings that are indicative of traumatic aortic disruption include wall thickening, extravasations of contrast, filling defects, paraaortic hematoma, intimal flaps, mural thrombi, pseudoaneurysm, and psuedocoarctation (Figure 26.2).44 False-positive results can occur because of a ductus diverticulum, but this will usually be present in the absence of an intimal irregularity or mediastinum hematoma. If the study is equivocal then more studies with a higher specificity will need to be done, such as TEE or aortography. Transesophageal echocardiography, like other forms of sonography, is operator dependent. There is a variability in the literature with regard to reports of the sensitivity and specificity of TEE, with some reports suggesting 100% accuracy and others suggesting a sensitivity of only 60%.46,52,54–56 However, in experienced hands it can be a highly accurate way to diagnose BAI, particularly in a patient who is already in the operating room for a lapartotomy. One advantage TEE has over helical CT scanning is that it is portable and can be performed in an unstable patient. Thus, in our center, if a patient with a high index of suspicion for BAI is unstable and requires

26. Thoracic Aorta

403

Figure g 26.2. 26 2 This Thi CT scan demonstrates d t t the th disruption di ti in i the th descending aorta, as well as periaortic blood and hemothorax.

laparotomy, we will plan on performing TEE in the operating room. Contraindications clearly include patients with oropharyngeal, esophageal, or severe maxillofacial injuries, as well as concomitant cervical spine injuries.

Management After the initial period of resuscitation some critical decisions will need to be made. The stability of the patient

will largely dictate management (Figure 26.3). Because these patients will often have multiple injuries rather than an isolated injury to their aorta, management can often be complicated. Unstable patients will likely have abdominal or pelvic bleeding. Patients requiring laparotomy should be brought to the operating room, and intraoperative TEE can be performed to rule out aortic injury. Patients with pelvic bleeding with the need for angiographic embolization can undergo thoracic aortography in the interventional suite at the time of embolization (see the algorithm in Figure 26.3). Currently, the standard of care is immediate thoracotomy and aortic repair for stable patients who do not require concomitant laparotomy, craniotomy, or pelvic stabilization.There are a number of comorbid factors that make an open repair a relative contraindication, including pulmonary contusions (thus going on single lung ventilation may not be possible), abdominal bleeding, and nervous system injuries. These patients should be stabilized before attempts are made for open repair. A stable patient with aortic injury should have an expedient preoperative workup that includes a head and abdominal CT. As stated before, relief of space-occupying lesions in the brain and treatment of intraabdominal hemorrhage take precedence over the repair of aortic injuries. The logic behind this is that they are more likely to lead to death than the aortic injury in this situation. After these issues have been dealt with, the patient’s stability and overall status should be assessed. If a patient appears to be exsanguinating from the aorta, clearly this should be dealt with immediately. If not, after a laparotomy it is probably best to return the patient to the

Stable

Possible BAI • Mechanism of Injury • Chest Xray • Wide mediastinum • Broken 1st rib, clavicle • Loss of aortic knob

+ DPL/Ultrasound

Helical CT Scan + BAI

– BAI

Figure 26.3. An algorithm for the management of blunt aortic injury. BAI, blunt aortic injury; CNS, central nervous system; CT, computed tomography; DPL, diagnostic peritoneal lavage; OR, operating room; TEE, transesophageal echocardiography.

Aortography Or TEE

No further studies

Evaluate for other sources of unstability • Pelvic fx: to angio for embolization of pelvic bleeding • Femoral fractures • Chest bleeding.

• TEE for unstable pt • CT once stability is achieved – BAI

Open repair in OR

– DPL/Ultrasound

Exploratory Laparotomy • Intraoperative TEE

Equivocal

No further studies

Unstable

+ BAI

• Stent graft or delayed repair • Medical therapy for severe CNS trauma

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intensive care unit where he or she can be stabilized and then brought back within the next 24 to 48 hours for aortic repair. Patients who are unstable will most likely have multiple traumatic injuries and are unable to withstand the additional stress of an open repair. Traditionally these patients were stabilized in the intensive care unit and open repair is done within the first 48 to 72 hours after the traumatic event. Operative results have been fraught with relatively high rates of paralysis and death in this patient population. In recent years endovascular stent grafting has emerged as a potential option for these patients. It has been highlighted that endovascular stent grafting is safe and effective in the short term and is particularly advantageous for patients who have significant other injuries who would otherwise not be stable enough for an open repair.57,58 Some medical centers are now using endovascular repair regardless of the severity of other injuries.59 It should be noted that most reports are anecdotal, with relatively small numbers, but the results are encouraging.57–59 Given the relative rarity of this phenomenon, a multiinstitutional prospective trial over a number of years would most likely be needed to objectively compare open repair with endovascular stent grafting. In the short term, it appears that the risk of paralysis is also lower with this method. Although the rates of paralysis of open repair are in the range of approximately 10%, there has yet to be a report of paraplegia after the use of endovascular stent grafts in the acute treatment of BAI.59 Early mortality may also be lower, with rates being between 0% and 16%.57–60 However, it should be noted that long-term data do not exist. With regard to complications, sometimes it may be necessary to cover the left subclavian artery, which may cause left arm ischemia.57 In this event, an extraanatomic bypass (such as a carotid–subclavian bypass) can be performed. In summary, stent grafting is currently not the standard of care for all patients, but it clearly has a role for patients who are not stable enough to undergo a thoracotomy. However, it is entirely conceivable that this will surpass open repair as the standard of care for all patients in the future, given all of its advantages. One issue that should be of concern with this patient population is blood pressure. High blood pressure increases the risk for rupture and should be avoided. Reduction of the change in pressure over the change in time reduces wall stress significantly and has been shown to reduce the in-hospital aortic rupture rates. Pain and blood pressure should be controlled to a target systolic pressure of approximately 110 mm Hg, starting with morphine and an intravenous beta-blocker such as esmolol. If target pressures cannot be achieved with these interventions, sodium nitroprusside should be added. The advantage of using esmolol and sodium nitroprusside is that they have a relatively short half life.


Operative Technique Before the operation starts, the patient should undergo a complete set of laboratory studies, should be typed and crossed for at least 2 U, and other blood products such as platelets, cryoprecipitate, and fresh-frozen plasma should be readily available. A cell saver should be employed as well. The cardiologists should be alerted, as they will be needed for intraoperative TEE, which should be considered for all patients unless contraindicated. A doublelumen tube or single-lumen tube with left bronchial blocker should be used, as single right lung ventilation allows optimal exposure of the aorta. Throughout the preoperative workup, as well as during the operation, blood pressure control should be paramount, as a hypertensive episode could result in free rupture before the repair begins. Right femoral and right radial arterial lines should be obtained for monitoring both upper and lower extremity perfusion. The left groin should be prepped and prepared for possible left heart bypass. Large-bore intravenous access and a pulmonary artery catheter should be placed. Temperature, electrocardiogram, and oxygen saturation should all be continuously monitored. A nasogastric tube should be placed and the stomach emptied, followed by the removal of the nasogastric tube so that a TEE probe can be placed.The patient should then be placed in a right lateral decubitus position with the table flexed. A standard fourth interspace posterolateral thoracotomy offers good exposure to the aortic isthmus and proximal descending aorta. Heparinization is relatively contraindicated for intracranial hemorrhage and lung injury. Some sort of lower extremity perfusion should probably be employed when performing this repair. Historically, patients undergoing this procedure could expect about a 10% chance of permanent lower extremity paralysis after repair of BAI.2,26,30,31,38,61 For years surgeons have used a “clamp and sew” technique for repair of these injuries, and it is thought that the lack of oxygenated blood to the distal aorta during a clamp and sew repair was one of the factors that led to this rather high level of paralysis. Many surgeons have adopted some sort of lower extremity perfusion method. There is good evidence to suggest this technique, particularly when clamp times are greater than 30 minutes, leads to lower rates of paralysis.2,62 Moreover, combined short cross-clamp times with lower body perfusion can significantly decrease the incidence of paralysis.2,61,62 Thus, in most medical centers, the clamp and sew technique has fallen by the wayside in favor of lower extremity bypass. However, it should be noted that some have also had low paraplegia rates using simple cross-clamping techniques,26,27 and that simple aortic cross-clamping is warranted in a few discrete circumstances. Any patient who is actively bleeding and there is no time to employ lower body perfusion will

26. Thoracic Aorta

require simple aortic cross clamping. Additionally, in some circumstances, such as lack of training or hardware to employ lower body perfusion methods, simple aortic cross-clamping may be the only option. Again, if clamp times are kept to less than 30 minutes the risk of paraplegia is relatively low. Partial left heart bypass shunts blood from the left atrium to the lower body via the distal thoracic aorta or left femoral artery.64,65 This method has been demonstrated to be very effective, as one review of five published series demonstrated no paraplegia in 58 patients.66 We prefer to use this technique. It is achieved by placing a 16- to 20-F cannula in the left atrium through the left inferior pulmonary vein to provide inflow into a pump, which in turn pumps to the distal aorta—preferably as proximal as possible or in the femoral artery. The technique serves a number of purposes: it unloads the left heart and allows better control of proximal blood pressure at the time of cross clamping, it maintains lower body perfusion, and it gives the surgeon good control of the intravascular volume. Ventricular arrhythmias are problematic given that the heart still perfuses the upper body and brain. Right atrial to femoral artery partial bypass is another method that can be employed. This system is done essentially entirely from the groin. A long venous catheter is passed via the left common femoral vein into the right atrium using a guidewire technique. The femoral artery is also cannulated for the perfusion of blood from the pump, which can be used with or without an oxygenator. The distinct advantage to this modality is that it gives the surgeon the opportunity to go on full bypass, which is relevant in the case of arch injury or ventricular arrhythmias. Moreover, if there are issues with the ability of the patient to oxygenate well on the right lung because of injury or intrinsic disease, this is advantageous. Once the chest is opened, single lung ventilation should be employed. If the patient cannot be adequately ventilated on the right lung alone, then cardiopulmonary bypass should be instituted. The mediastinal pleura should be incised along the anterior surface of the proximal left subclavian artery. The left subclavian should then be encircled with a tape. Dissection should be carried out on the aortic arch, starting lateral to the vagus nerve and carried out proximal to the left common carotid, as this is usually the point needed for proximal aortic control in most cases. Great care should be taken during this dissection to avoid injury or excessive stretching of the phrenic or vagus nerves. The aortic arch between the left common carotid and the left subclavian artery is then encircled with tape. The distal aorta is controlled by dissection of the overlying pleura and encircling it with a tape (Figure 26.4). If left heart bypass is to be employed, it is done at this point. The left inferior pulmonary vein is dissected ante-

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Figure 26.4. The surgeon’s view (left thoracotomy). After the left lung is deflated and retracted anteriorly, the plane is developed between the left carotid and left subclavian arteries and is encircled with a vessel loop. There is also a vessel loop passed around the distal aorta. A Rommel tourniquet is also placed on the left subclavian artery for control. (Reprinted with permission from Miller OL, Calhoon JH. Acute traumatic aortic transection. In Kaiser LR, Kron IL, Spray TL, eds. Mastery of Cardiothoracic Surgery. Philadelphia: Lippincott-Raven Publishers, 1998.)

riorly, and a purse string suture is placed. Arterial cannulation is performed through the distal aorta (by direct cannulation through a purse string suture) or femoral artery (by Seldinger technique). The inferior pulmonary vein is then cannulated, and bypass is instituted. Once the blood pressure is stable, the left subclavian, proximal, and distal aortas are clamped in respective succession. At this point the periaortic hematoma is entered, and the extent of the injury is identified (Figure 26.5). Although it is sometimes possible to primarily repair the aorta, it is usually best to debride the torn edges and place a short interposition graft (we prefer to use Dacron).2,26–28,30,67–70 The graft is sewn using a running 3-0 or 4-0 polypropylene suture with the proximal anastomosis performed first, followed by the distal anastomosis (Figure 26.6). After completion of the anastomosis, the distal clamp should be removed, followed by the proximal aortic and then the left subclavian. The patient should then be weaned off of bypass and heparin reversed. Double lung ventilation should be reinstituted, the chest closed, and the patient taken back to the cardiac intensive care unit.

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Figure 26.5. The hematoma is opened, and the edges of the aorta are debrided. (Reprinted with permission from Miller OL, Calhoon JH. Acute traumatic aortic transection. In Kaiser LR, Kron IL, Spray TL, eds. Mastery of Cardiothoracic Surgery. Philadelphia: Lippincott-Raven Publishers, 1998.)

Complications and Outcomes For patients who arrive alive at the hospital with traumatic rupture of the aorta, there is still approximately a 30% mortality rate.2,31 It should be noted, however, that those who are hemodynamically stable and can undergo a planned repair will have about a 14% mortality rate.2

Figure 26.6. After completing the proximal anastomosis, the graft is trimmed to an appropriate length, and the distal anastomosis is performed. De-airing and back bleeding through the distal anastomosis should be done after releasing the proximal clamps and before releasing the distal clamp to avoid embolization. (Reprinted with permission from Miller OL, Calhoon JH. Acute traumatic aortic transection. In Kaiser LR, Kron IL, Spray TL, eds. Mastery of Cardiothoracic Surgery. Philadelphia: Lippincott-Raven Publishers, 1998.)


Those patients who are in extremis or who have ruptured aortas will have mortality rates that approach 100%.2 One third of all patients will die before repair can be performed, and, of the remaining two thirds of patients who die, about one half will die during the repair and one half after the repair. Paralysis in patients who have open repairs occurs approximately 10% of the time.31 However, the institution of lower extremity perfusion appears to be lowering the rates of paraplegia when cross-clamp times exceed 30 to 35 minutes.2,31,62,71 There are no reports thus far of any patients who have suffered paralysis after endovascular stent grafting. Complications that are directly caused by the operation itself in addition to paraplegia include recurrent laryngeal nerve injury and suture line aneurysms; these occur relatively infrequently. Such patients often have multiple injuries, and thus there are a number of complications that may not be directly caused by the aortic repair of itself. Thus the postoperative care of these patients will often be complex, because the trauma of the operation itself will be superimposed on the rest of the injuries the patient has sustained. Pneumonia is the most common complication and occurs at a rate of 20% to 30%.2,30,33,72,73 This is due in large part to the thoracic injuries often sustained, such as pulmonary contusions, broken ribs, and hemothoraces, as well as prolonged time spent on a ventilator in the intensive care unit. Other complications include renal failure, sepsis, empyema, and abdominal abscess.2,30,33,73 To summarize, BAI is a postindustrial age phenomenon. With increases in population and the use of motor vehicles, the incidence will only increase over time. Most people who suffer from BAI will not live to make the trip to the hospital. Those patients who do make it to the hospital, on the other hand, will now have good odds of having their aorta repaired with ever-decreasing chances of suffering any long-term sequelae from the operation. The standard of care in most hospitals today is open repair with some form of lower extremity perfusion, given the increased risk of paralysis with clamp and sew techniques for operations greater than 30 minutes. It is likely that the use of endovascular stent grafts will continue to increase over the next decade, as early results suggest that this is potentially a better alternative to open repair because of the ability to obviate a thoracotomy and decrease the risk of paralysis. Long-term data are necessary to establish whether or not it is indeed better than open repair.

Aortic Dissection History and Incidence Sennertus74 is generally given credit for being the first to describe the dissection process, which he did in the mid-

26. Thoracic Aorta

seventeenth century. Approximately 100 years later, Morgani75 described a number of cases in which blood penetrated the layers of the aortic wall. In 1802, Maunoir76 provided a more detailed description of the process and is credited with giving the process the name “dissection.” The first surgical attempts to intervene in this process were performed by Gurin77 in 1935, when he performed a fenestration procedure to alleviate ischemia caused by malperfusion. About 20 years later DeBakey78 was the first to repair a type B aortic dissection, which he repaired by excising the diseased portion of the descending aorta and anastomosing the ends primarily. The first reported repairs of type A dissection were done by Hufnagel and Conrad79 by means of excising the torn aorta, reuniting the proximal and distal ends, and primarily anastomosing the vessel in an end-to-end fashion.79 However, this method was replaced by the use of a prosthetic graft, which was introduced by Cooley and DeBakey and is still used today. Aortic dissection is the most frequently diagnosed lethal condition of the aorta.80–82 Interestingly, it occurs nearly three times as frequently in the United States as does rupture of an abdominal aortic aneurysm.83 The incidence is about 5 to 30 cases per 1 million people per year.84 More than 60% are Stanford type A dissections.85 Men are more frequently affected, with the ratio ranging from 2 : 1 to 5 : 1, depending on the series.86–88 The incidence, however, is related to the prevalence of risk factors (Table 26.2), with hypertension being the most common factor among patients.85,89

Table 26.2. Risk factors for thoracic aortic dissection. Genetic/congenital • Connective tissue disorders • Ehlers-Danlos syndrome • Marfan syndrome • Turner syndrome • Anatomic abnormalities • Bicuspid aortic valve • Congenital aortic stenosis • Polycystic kidney disease • Coarctation of the aorta Acquired • Hypertension • Smoking, dislipidemia, cocaine/crack • Aortitis • Cystic medial disease of the aorta • Iatrogenic • Atherosclerosis • Thoracic aortic aneurysm • Trauma • Pharmacologic • Hypervolemia (pregnancy) • Pheochromocytoma • Sheehan syndrome • Cushing syndrome

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Etiology and Pathogenesis Aortic dissection by definition is the development of a false lumen between the layers of the media. Because a number of pathologic processes lead to dissection, it is unlikely that a single disease process explains the phenomenon. It is probably best to think of the etiologies of aortic dissection as those that are genetic connective tissue disorders and those that are acquired. Marfan syndrome, Ehlers-Danlos syndrome, and familial forms of thoracic aneurysm and dissection are the three major forms of inherited connective tissue disorders known to affect the arterial walls and are associated with aortic dissection. Marfan syndrome is the most prevalent connective tissue disorder, inherited in an autosomal dominant pattern of inheritance with an incidence of approximately 1 in 7,000. The genetic defect results in defective fibrillin in the extracellular matrix, and this can have protean manifestations in multiple organ systems. Over 100 mutations in the fibrillin-1 gene have been identified in people with this disorder, and the penetrance of the disease is variable; there are therefore many different phenotypic variations. However, one thing that is thought to be common among people with aortic wall involvement is the dedifferentiation of vascular smooth muscle cells. This is thought to be caused by enhanced elastolysis of aortic wall components given the defective fibrillin in the extracellular matrix.90 It is also thought that the enhanced expression of metalloproteinases in vascular smooth muscle cells of patients with Marfan syndrome promotes fragmentation and elastolysis.91 Like Marfan syndrome, annuloaortic ectasia and familial aortic dissection also have mutations in the fibrillin gene. Bicuspid and unicommisural aortic valves are also risk factors for development of aortic dissection.92 Ehlers-Danlos syndrome (EDS), like Marfan syndrome, has a number of genetic abnormalities that are manifest in a number of different phenotypes.The disease is a result of a defect in collagen, like Marfan syndrome, a crucial element in the extracellular matrix, and is manifest by skin extensibility, joint hypermobility, and tissue fragility.93 It is estimated to occur in approximately 1 in 10,000 births. There are six major types, but aortic involvement is seen primarily in autosomal dominant EDS type IV, also known as “vascular EDS.”93 The disorder is caused by both quantitative and qualitative defects in type III collagen. Interestingly, patients with vascular EDS often have little skin hyperextensibility; however, the skin is thin, translucent, and feels soft. These patients can exhibit poor wound healing and bruisabilty, and patients with vascular EDS are at risk for vascular complications manifest by arterial rupture, tears, or dissection in arteries throughout the body. Arteries in the thorax and abdomen are involved approximately 50% of the time, and extremities are involved 25% of the

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time.93–98 Because arteriography can lead to complications in this population, noninvasive means should be used in the diagnosis of dissection. With regard to acquired conditions, chronic hypertension is the most common condition associated with aortic dissection. Of note, hypertension is found in more than 75% of cases. It is thought that hypertension causes intimal thickening, fibrosis, and fatty acid deposition, and the extracellular matrix undergoes degradation, apoptosis, and elastolysis. Both of these mechanisms can lead to an intimal disruption, usually at the edge of plaques.99 Moreover, the resultant necrosis of smooth muscle cells and fibrosis of the elastic structures of the vessel wall decrease the compliance of the aortic wall to pulsatile forces, making it more vulnerable for the development of dissection.100 Iatrogenic dissection can be caused by a number of procedures involving the aorta, such as any catheterization procedure, aortic root, and/or cannulation for cardiopulmonary bypass, aortic cross clamping, as well as any surgical procedure performed on the aorta.92,101–103 Thus, surgeons must always have dissection in the backs of their minds when complications of unknown etiology arise after these procedures. Another theory is that aortic dissections are the result of the creation of an intramural hematoma caused by bleeding from vasa vasorum. This has been put forth because about 20% of patients with acute aortic dissection are found to have an intramural hematoma.1,104–106 Intramural hematomas rarely regress, and involvement in the ascending aorta is an indication for acute surgery because there is a significant risk of rupture as well as propagation and involvement of the coronary ostia.104,107

Clinical Presentation The diagnosis of acute aortic dissection requires a high level of clinical suspicion. It should be considered in the setting of severe unrelenting chest pain that comes on suddenly. This pain is present in most patients, and this is usually the first time they have experienced such pain. The pain is usually in the midsternum for ascending aortic dissection and in the interscapular region for descending aortic dissection. Classically, the pain is described as “ripping” or “tearing,” and it is constant. In the largest prospective study performed to date on patients with aortic dissection, severe chest pain of abrupt onset was the most common complaint, occurring in 73% of patients.85 Patients may also present with syncope alone, with no other signs of symptoms.108–112 Patients may also have signs or symptoms related to malperfusion of limbs, brain, or other organs. Abdominal pain and an increase in lactate may indicate involvement of the celiac trunk or the mesenteric artery. Oliguria or anuria may indicate involvement of the renal arteries. Risk factors include


primary hypertension, the presence of aneurysmal disease of the aorta, and, less commonly, a genetic connective tissue disorder. Patients can present in any number of ways, from stable with a tachycardia to severe hypotension. Pulse deficits can be present in up to 40% of patients and are associated with higher morbidity and mortality rates and poorer outcomes.113 Abnormal perfusion of the upper extremities can indicate that there is ascending aortic involvement, whereas abnormal perfusion of the lower extremities suggests distal involvement. It is also crucial at the time of presentation to obtain a thorough neurologic examination, as abnormalities are present in up to 35% of acute type A dissections.113 Hypotension may be due to aortic rupture, acute aortic regurgitation, pericardial tamponade, or myocardial infarction.85,110,111 On physical examination, a diastolic murmur or muffled heart sound may be heard.With tamponade, jugular venous distension and pulsus paradoxus may be present. Loss of breath sounds, particularly on the left side, can be indicative of left-side hemothorax. Stroke may occur but is infrequent, occurring in less than 5% of patients with acute type A dissection. Loss of perfusion to lumbar or intercostal arteries may result in spinal cord ischemia and paraplegia.

Diagnostic Studies At the time of presentation, along with the stabilization of the patient, blood tests, electrocardiogram, and chest x-ray should be obtained. Complete blood count, serum electrolytes, myocardial enzymes, blood type and screen, liver function tests, myoglobin, lactic acid, and coagulation studies should be obtained. The electrocardiogram will reveal ischemic changes in approximately 17% of acute type A dissections and in 13% of type B dissections, as well as left ventricular hypertrophy in people with long-standing hypertension.85 Myocardial infarction is relatively rare, occurring approximately 3% of the time.85 The chest x-ray will be abnormal in up to 90% of patients with acute dissection, although a normal x-ray cannot rule out dissection. Classic features include a widened mediastinum, rightward tracheal displacement, irregular aortic contour with loss of the aortic knob, an indistinct aortopulmonary window, and a left pleural effusion. If there is a high clinical suspicion of dissection at this point based on the presentation, the physical examination, and the chest x-ray, care should be expedited to verify that dissection has occurred. The primary modalities used now are CT and echocardiography. These modalities are fast and accurate, which gives them the advantage over magnetic resonance imaging and aortography. It is common to require the use of two imaging modalities to diagnose aortic dissection.85,114

26. Thoracic Aorta

409

Helical CT is now the most frequently utilized first test to diagnose acute aortic dissection, comprising approximately 61% of all first studies.85,114 It has high sensitivity and specificity for the detection of all types of aortic dissection, approaching an accuracy of 100%.115,116 When performed as CT angiogram, arch vessel involvement can be identified with a greater than 95% accuracy rate.115 Diagnosis requires two or more channels separated by an intimal dissection flap. Other findings that can be diagnostic include a hyperattenuating intima, delayed enhancement of a false lumen, and hematomas in the mediastinum, pericardium, or pleura. Transesophageal echocardiography is the second most frequently used study for diagnosing acute aortic dissection, being used approximately 33% of the time.85,114 It is the most commonly used secondary study, comprising approximately 56% of secondary studies done. Transesophageal echocardiography may be a more appropriate imaging modality for patients who are unstable and cannot be brought safely to the CT scanner. Patients can be brought to the operating room, sedated, and have TEE. The sensitivity, specificity, and positive and negative predictive values all approach 100% in experienced hands.117 This study is more operator dependent than CT, although there is a slight risk of causing aortic rupture when doing the study. Making the diagnosis requires visualization of an echogenic surface separating two distinct lumens, repeatedly, in more than one view, and differentiated from normal surrounding cardiac structures. The true lumen is identified by expansion during systole and collapse in diastole. Color Doppler can also aid in distinguishing flow in the false lumen from thrombosis.

Stable – study

Aortography traditionally has been held as the gold standard for the diagnosis of aortic dissection; however, this has been supplanted by CT and echocardiography. The International Registry of Acute Aortic Dissection (IRAD) found that aortography comprised only 4% of the first studies performed, but comprised 17% of the secondary confirmatory studies.85,114 The need for skilled personnel and the fact that it is an invasive test make it less advantageous than CT or echocardiography. The advantages of aortography include the ability to perform catheter-based interventions in the setting of acute type B dissections with evidence of mesenteric ischemia. However, the use of stent grafts is not yet the standard of care, but they are increasingly being used in this patient population. In our medical center, aortography is used only in the setting of equivocal findings of CT scan or echocardiography. Magnetic resonance imaging is extremely accurate in the diagnosis of aortic dissection, as the images obtained can yield details of the aorta, pericardium, and surrounding structures. It has not yet become widely available, and in the emergent setting it is not yet a highly used modality.

Classification and Management Decisions Patients with acute aortic dissection will essentially fall into one of two categories: those who need an urgent operation and those who do not (Figure 26.7). The decision to operate is largely based on the anatomic portion of the aorta that has undergone dissection. These anatomic areas can best be described by either the

Possible Dissection • High index of suspicion • Clinical presneation • Chest Xray • Wide mediastinum • Loss of aortic knob

Unstable

• Intraoperative TEE • Aortogram if TEE contraindicated

Helical CT scan + for Dissection

No further studies

Equivocal

TEE or Aortography

– for dissection Type A

To Operating room for definitive repair • Supportive care if operation is not performed

Figure 26.7. An algorithm for the management of aortic dissection. CT, computed tomography; ICU, intensive care unit; TEE, transesophageal echocardiography.

Unstable • Malperfusion issues

Type B

Unstable • Malperfusion issues

Attempt to treat malperfusion issues by endovascular means if possible. Otherwise pt needs operation.

No further studies

Stable

Treat in ICU • Blood pressure control

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DeBakey or the Stanford classification system. The DeBakey system classifies patients into four types. Type I includes dissections that involve the proximal aorta, the aortic arch, and the descending thoracic aorta. Type II involves only the ascending aorta. Type IIIa involves the descending thoracic aorta, and type IIIb involves the descending thoracic as well as the abdominal aorta (Figure 26.8A). The Stanford system only has two classified types of dissection: A and B. Stanford type A involves the ascending aorta, and type B involves only the descending aorta (Figure 26.8B). This classification system is helpful to the surgeon in that type A dissections should receive an operation, whereas type B dissections can usually be medically managed. Because of this practicality, the Stanford classification system is the one most often used by practicing cardiac surgeons when describing aortic dissections. The natural history of acute type A aortic dissection carries with it high morbidity and mortality rates, as approximately 50% will be dead within 48 hours.118 Moreover, after the onset of symptoms, there is a 1% to 2% rise in mortality rate per hour.85 The most common causes of death are aortic rupture, stroke, visceral ischemia, and cardiac tamponade.110,119 Thus, the primary goal of surgery is to avoid aortic rupture into the pericardium or pleural space. Although the presence of a type A dissection alone is an indication for surgery, there are a number of contraindications to surgery. Age over 80 years is a relative contraindication, as there are few reported survivors in this age group. Neurologic sequelae are a relative contraindication to surgery. Patients who are comatose or obtunded will most likely not improve with surgery. However, stroke and paraplegia are not absolute contraindications. It should be noted that although the dissection may extend into the descending aorta (DeBakey type I), the replacement of the ascending aorta can result in the correction of any malperfusion issues that were caused by dissection. Interestingly less than 10% will have obliteration of the false lumen, although most malperfusion deficits will be corrected after repair. If the repair of the ascending aorta does not result in a correction of malperfusion deficits, other interventions are necessary. Although type B dissection is less lethal than type A dissection, it can still be associated with a 30-day mortality rate of 10%.85 Moreover, patients who have evidence of malperfusion manifested by ischemic lower extremities, renal failure, or visceral ischemia may have mortality rates as high as 25% at 30 days. Uncomplicated type B dissection should be treated medically, as approximately 75% of patients with acute type B dissection can be effectively treated in this fashion. More than one half can be managed medically for the rest of their lives.120 There are, however a number of indications for operat-

P.I. Ellman and I.L. Kron I

II

IIIa

IIIb

A Intimal tear

Intimal tear

B Figure 26.8. (A) The DeBakey classification system. Type I involves the proximal aorta, arch, and descending aorta. Type II involves the ascending aorta exclusively. Type IIIa involves only the thoracic aorta distal to the left subclavian artery, and type IIIb involves the abdominal aorta as well. (Reprinted with permission of The McGraw Hill Companies from Green R, Kron IL. Aortic dissection. In Cohn LH, Edmunds LH, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003.). (B) The Stanford classification system. (Reprinted with permission from Gardner TJ. Acute aortic dissection. In Kaiser LR, Kron IL, Spray TL, eds. Mastery of Cardiothoracic Surgery. Philadelphia: Lippincott-Raven Publishers, 1998.)

26. Thoracic Aorta

ing on type B dissections, namely, rupture, visceral or limb malperfusion, dissection expansion, and failure of medical management. Factors that may favor early operation include the presence of Marfan syndrome, a large false aneurysm, arch involvement, and presumed medical compliance issues.121 The acute care and stabilization of these patients should be maximized. Thus, it is extremely important to diagnose the dissection early as well as its type. Cardiac and vascular surgeons as well as interventional radiologists have developed, and continue to develop, techniques that are useful for patients with descending aortic involvement with both type A and type B dissections.Although type A dissections can only be definitively treated by open cardiac surgery, peripheral vascular malperfusion can occur, and these complications can be dealt with by interventional techniques. Type B malperfusion issues or dissection propagation can be treated definitively by interventional techniques. Slonim et al.122 have published one of the larger retrospective studies of endovascular techniques at Stanford for patients suffering from ischemic complications with acute aortic dissection. Over a 6-year period, 40 patients (32 male and 8 female) underwent percutaneous treatment for peripheral ischemic complications of 10 type A and 30 type B acute aortic dissections. All type A dissections that were surgically repaired (9/10) were repaired before the interventional procedure was performed. Thirty of these patients had renal, 22 had leg, 18 had mesenteric, and 1 had arm ischemic complications. Fourteen patients were treated with stenting of either the true or the false lumen combined with balloon fenestration of the intimal flap, 24 with stenting alone and 2 with fenestration alone. They were able to successfully revascularize 93% of these patients. There were nine procedure-related complications. Because ischemic complications are associated with a high mortality rate, they had a 30-day mortality rate of approximately 25%. There were 5 late deaths (17%) in the remaining 30 patients.Techniques can range from fenestration of a false lumen to create a communication with the true lumen to the use of covered stents to enter to a false lumen or the use of noncovered stent grafts to enlarge a compressed true lumen. The use of stent grafts as definitive therapy for a type B dissection is growing in acceptance, and early results are encouraging.123 Flow can be restored in up to 90% of vessels obstructed by aortic dissection.124–126 Many medical centers are now utilizing these strategies in the setting of both complicated and uncomplicated descending aorta dissection. It is conceivable that over time interventional techniques will replace open techniques for the treatment of type B dissections, as well as malperfusion complications with type A and type B dissections. The initial medical management will be guided by the stability of the patient. The unstable patient belongs in

411

the operating room. In the operating room stabilization, resuscitation, or acute care surgery can take place with echocardiography occurring concurrently to aid in the diagnosis. Any procedure should preferentially be done on an anesthetized patient, as hypertension due to stress can cause rupture or propagation of the dissection. If the patient is stable, blood pressure control should be measured in both arms and kept with a systolic pressure between 90 and 110 mm Hg. The avoidance of hypertension is predicated on two issues: first, shear stress on the aorta is decreased by minimizing the rate of rise of aortic pressure to decrease the dissection propagation. Second, aortic wall stress is lowered by decreasing systolic blood pressure. If a patient is in pain, analgesics should be used first. After that, nitroprusside will help to get the pressure down quickly, and the addition of esmolol will decrease pulse pressure.

Operative Technique for Type A Dissection The only curative therapy that currently exists for type A dissection is open surgery. However, only 72% of patients presenting with type A aortic dissection will undergo surgery.85 Age (>80 years old is generally considered the relative number, although a fit 80-year-old person could conceivably tolerate the operation), other comorbidities, death, or refusal to undergo surgery are the main reasons why people do not have the operation who have a type A dissection. Approximately 15% of patients will have concomitant coronary artery bypass surgery, 9% will require a total arch replacement, 10% a partial arch replacement and 15% will need valve repair or replacement.85 Preparation should include the single endotracheal tube for operations through a median sternotomy and double-lumen tubes if the procedure is to be performed through a left thoracotomy. The patient should have central venous access with a pulmonary artery catheter, as well as radial arterial lines and a femoral arterial line to continually assess peripheral perfusion. Anesthesia cardiology should be employed to help with transeophageal echocardiography. Temperature can be measured through a Foley catheter and a nasopharyngeal probe. The skin should be widely prepped, including the axillary and femoral arteries to allow for all cannulation options. A cell saver should be employed, as blood loss can be substantial in these procedures. The patient should be typed and crossed for at least 2 U of blood, and preparations should be made to have fresh-frozen plasma, platelets, and cryoprecipitate available. There are a number of options for arterial and venous cannulation for cardiopulmonary bypass. The choice will depend on a number of issues. There is still controversy regarding which femoral artery to cannulate, but we prefer the right because it usually supplies the true

412

lumen.Alternatively, the axillary artery can be used effectively after a graft is anastomosed to it.127 Venous cannulation is usually through the right atrium using a two-stage venous cannula. A left ventricular vent is necessary in the setting of aortic valve incompetence and should be placed through the right superior pulmonary vein or rarely through the left ventricular apex wall. For type B dissections, partial left heart bypass, as in the case of acute aortic disruption, has replaced the clamp and sew technique. During the repair of a type A dissection, one must decide on the manner in which the brain will be protected. This can be achieved by deep hypothermia or continued perfusion, be it antegrade or retrograde. If deep hypothermia is to be used, it is thought that up to 14 minutes of circulatory arrest is acceptable at a temperature of 25°C and up to 31 minutes at 15°C.128 However, for longer periods of time at 15°C, one sees a higher incidence of neurologic sequelae, being as high as 60% at 60 minutes.Thus, for complex repairs that will require longer than 30 minutes, cerebral perfusion should probably be used. Retrograde cerebral perfusion can be done through a bicaval cannula, with reversal of flow occurring through the superior vena cava cannula. It can also be done in a dual-stage manner, with the placement of a retrograde coronary sinus catheter into the superior vena cava through a purse string suture. Selective antegrade perfusion can be accomplished by placing cannulae in the innominate and the left common carotids through the ostia from the inside of the aorta once it is open. The left subclavian should be occluded to avoid back flow, and pressure should be approximately 50 to 70 mm Hg. The cannulae are removed just before completing the anastomosis of the brachiocephalic vessels to the vascular graft, at which time cardiopulmonary bypass may be reinstituted. After sternotomy, other modifications of the incision can be performed such as a supraclavicular, cervical, or trapdoor incision to gain exposure to the brachiocephalic vessels or the descending thoracic aorta if need be. The dissection should be carried out first on the distal arch, taking care not to injure the left vagus nerve with its recurrent branch and the left phrenic nerve. An open distal repair is the procedure of choice (Figure 26.9). After placing a clamp on the mid ascending aorta and cardiac arrest is achieved, the aorta proximal to the clamp is opened. At this point, the aortic valve should be evaluated as systemic cooling occurs. The valve usually can be resuspended. If the sinuses are not dilated, then the aorta is transected 5 to 10 mm distal to the sinotubular ridge. If there is a dissection that involves the root the intima of the coronary, ostia may or may not be involved. If they are not involved, a repair of the sinotubular junction can be performed, reuniting the dissected aortic layers


Figure 26.9. In most cases an open distal repair is performed. The native aortic valve can usually be repaired and resuspended. The layers of the aorta are repaired with a piece of felt placed in between (both proximally and distally). An interposition graft is then used to complete the repair. (Reprinted with permission from Gardner TJ. Acute aortic dissection. In Kaiser LR, Kron IL, Spray TL, eds. Mastery of Cardiothoracic Surgery. Philadelphia: Lippincott-Raven Publishers, 1988.)

between one or two strips of Teflon felt using 3-0 or 4-0 Prolene suture. A minimal disruption of the coronary ostia can be repaired primarily using a 5-0 or 6-0 suture. If the coronary ostium is circumferentially dissected and aortic root replacement is necessary, an aortic button should be excised and the layers reunited. The coronary button should then be reimplanted into the vascular graft. Aortocoronary bypass should be performed only when the coronary ostium is not reconstructable. Aortic valve insufficiency is common in these patients, but the valve can be preserved in most patients.85 The mechanism is usually caused by the loss of commissural support of the valve leaflets. This is repaired first by placing pledgeted 4-0 Prolene sutures to reposition each of the commisures at the sinotubular ridge, followed by a layer of Teflon felt placed circumferentially to reunite the dissected aortic root layers. Some have used Bioglue between the layers of the aorta prior to suture repair of the sinotubular ridge. If the valve cannot be spared, a formal replacement of the valve and the ascending aorta

26. Thoracic Aorta

should be performed using a composite valve graft or homograft. The valve is implanted using horizontal mattress 2-0 Tycron sutures. The left coronary button should be implanted into the graft first, and then the right coronary button implanted after the graft is clamped and placed under pressure to allow for the proper anatomic position of the right coronary button. Once the core temperature reaches approximately 20°C, perfusion is discontinued for a brief period of circulatory arrest. The aortic clamp on the mid ascending aorta is released, and the intima of the aortic arch is inspected and then repaired. If the intima is intact, the distal anastomosis is performed; the graft is then cannulated, de-aired, and clamped for resumption of cardiopulmonary bypass. If the intima is not intact, a hemiarch reconstruction should be performed. The integrity of the brachiocephalic vessel intima and ostia should be inspected from the inside of the aorta. If they are intact, they can be implanted as a Carrel patch into a vascular graft after repair (Figure 26.10). If, however, the dissection involves individual vessels, repair will be needed for the individual vessels, and then they will be implanted into the graft or to short interposition grafts if the dissection extends past the origin of the arteries. If the ascending aorta cannot be cross clamped because of fear of rupture, the patient is cooled to 20°C and circulatory arrest should be employed. The aorta should be opened, and the distal anastomosis performed. As before, the graft should be cannulated, de-aired, and proximally clamped and cardiopulmonary bypass reinstituted. Because a cross clamp is not applied, the left ventricle must be decompressed once fibrillation starts during systemic cooling to prevent distension and irreversible myocardial injury. During the rewarming period, the proximal ascending aortic repair should be completed. If the dissection is limited to the ascending aorta or to the proximal arch away from the origin of the brachio-

Figure 26.10. If the dissection involves the arch vessels, an arch repair is needed. This can be performed by Carrel patch or by anastomosing each vessel to the graft individually. If the dissection involves the origins of the vessels, then short interposition grafts can be utilized in the repair. (Reprinted with permission of The McGraw Hill Companies from Green R, Kron IL. Aortic dissection. In Cohn LH, Edmunds LH, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003.)

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cephalic vessels, an alternative repair can be performed. This entire procedure can be done without requiring deep hypothermia and circulatory arrest. Antegrade perfusion can be performed through the distal arch or the right subclavian artery, or retrograde perfusion through the femoral artery is another alternative. After an aortic cross clamp is applied just proximal to the innominate artery, the ascending aorta is resected to include the inferior aspect of the arch. The layers of the dissected aorta proximal to the clamp are then reunited if necessary. The proximal reconstruction is then performed.

Technique for Type B Dissection The ideal position for the repair of a type B dissection is right lateral decubitus position. The pelvis should be positioned in such a way that the femoral vessels are accessible. A double-lumen endotracheal tube should be employed. A posterolateral thoracotomy through the fourth intercostal space will allow for good access to the aorta. If, however, there is extension of the dissection into the abdomen with resultant visceral malperfusion, a thoracoabdominal incision should be employed. Repair of a type B dissection has many similarities to an open repair for BAI. Given the relatively high rates of paralysis reported (about 20%129), there are a few strategies that should be employed when performing this operation. The same tenets discussed with regard to lower extremity perfusion in the repair of BAI hold true here as well. Also, given the possibility that disruption of the intercostal arteries can be a contributing factor to paralysis, one should try to replace as little of the descending aorta as possible. Once the aorta has been exposed, the repair of a descending aortic dissection is similar to that discussed for repair of an aortic disruption. A plane should be developed between the left subclavian and left common carotid arteries and the left subclavian encircled with umbilical tape and Rommell tourniquet. As before, the left vagus and recurrent laryngeal nerves should be identified and preserved during the course of the dissection. The descending aorta should be dissected, and, if left heart bypass is to be employed via the left inferior pulmonary vein, a 4–0 Prolene purse string should be placed posteriorly. After the patient is heparinized a 14-F cannula should be placed into the left inferior pulmonary vein and another cannula placed in the femoral artery. Left heart bypass should then be instituted at flow rates between 1 and 2 L/min. The left subclavian artery is controlled by the Rommell tourniquet, and clamps are placed on the aorta between the left subclavian artery and left common carotid as well as distally. Arterial pressures should be between 100 and 140 mm Hg by right radial artery and greater than 60 mm Hg by the femoral artery. The aorta should then be opened longitudinally,

414


and bleeding from intercostal arteries can be controlled by figure of 8 suture ligation. The aorta should be transected just distal to the origin of the left subclavian artery and the proximal anastomosis of the graft performed using a 3-0 Prolene suture with or without Teflon felt strips. Once the proximal anastomosis is complete the proximal clamp is released and repositioned on the graft. The integrity of the anastomosis should then be inspected. The distal aorta should now be inspected and repaired, with either Teflon felt or glue. The distal anastomosis should then be performed, clamps released, and left heart bypass terminated. We recommend directly repairing anything larger than a 14-F hole left in the femoral artery from cannulation.

Outcomes and Complications Acute aortic dissection is associated with an in-hospital mortality rate of approximately 27%.85 However, there are a number of important factors that play into the outcomes of patients who have acute aortic dissection. Patients with type A dissection who do not undergo surgery have the highest mortality rates (58%), followed by type B patients who had surgery (31%), type A patients who had surgery (26%), and type B patients who were treated medically (11%) (Figure 26.11). The higher rate of mortality for patients with type B dissection who undergo surgery versus those with type A is most likely because the patients who undergo surgery for type B dissection often are sicker with malperfusion or rupture. Age also is a risk factor for both types A and B dissection.109,111,130 Patients older than 70 years with type A A/Medical (n = 81) B/Surgical (n = 35) All Patients (N = 464)

A/Surgical (n = 208) B/Medical (n = 140)

60

Cumulative Mortality, %

50 40 30 20 10

30

28

26

24

22

20

18

16

14

12

8

10

6

h

4

4

200 cc for 3 hrs)

ATLS Protocol

Indication for immediate laparotomy (hemodynamically unstable, evisceration) To OR for open exploration

Observe

mortality included blood transfusions of greater than 10 U, revised trauma score, and need for thoracotomy. Therefore, they emphasized early identification of associated injuries and control of bleeding to improve survival. Accurate mortality rates are difficult to assess for chronic disruption of the diaphragm. First, most of the missed injuries are secondary to a blunt cause, and, second, they may not be identified as directly resulting in death. In a small series of 10 patients with both blunt and penetrating trauma with delayed diagnosis of their injury, there was a 10% mortality rate.95 In a larger series of 50 patients of whom 27 suffered a penetrating trauma, there was a 2% mortality rate.98 In this study, two patients had a perforated viscus at the time of repair, and one of the deaths was secondary to postoperative perforation. Clearly, it is beneficial to identify these injuries at the time of the trauma to prevent such complications.

Conclusions Given this review, it seems prudent to consider a diaphragm injury for any patients with penetrating thoracoabdominal wounds because the incidence can be quite high. History and physical examination alone are inadequate to make this diagnosis, and current radiographic techniques are too inaccurate to be relied on safely to exclude this diagnosis. For patients without another indication for exploration, thoracoscopy is a reasonable option when the injury is higher in the chest and from a low-velocity mechanism or when intraabdominal injuries are thought unlikely. Laparoscopy is a better

High velocity weapon and/or high index of suspicion for intraperitoneal penetration No

Thoracoscopy based on surgeon’s preference

–

No indication for immediate operation

+

Yes

Or Laparoscopy +

If no indication for open exploration then open or closed diaphragm repair based on surgical skill. Otherwise open exploration

–

Observe

choice when one has a high index of suspicion for an intraperitoneal injury and can be done safely with the elimination of a large number of laparotomies. These diagnostic and therapeutic considerations were recently summarized.99 Treatment is dependent on surgical skill. Closed and open repairs are equivalent in their strengths and outcomes. Therefore, if a patient does not require an open exploration for other reasons, then repair via a scope is a good option. Despite the animal data suggesting that most of these will heal, such has not been shown in humans, and the complications from missed injuries should prompt repair when these injuries are identified. Morbidity and mortality rates are closely related to the associated injuries. Standard trauma protocols should be followed to care for these victims so that all injuries can be adequately addressed. With aggressive early intervention these patients can expect good outcomes with minimal complications. Figure 27.6 provides an algorithm for the approach to these patients.

Surgical Emergencies Related to Hiatal Hernia Hiatal hernia is defined as herniation of part or whole of the stomach into the chest through the esophageal hiatus. It is classified into three types depending on the position of the gastroesophageal (GE) junction. The most common (80%) is type I, also called sliding hiatal hernia. In this type, the GE junction rises into the chest to varying heights, dragging the proximal parts of greater and lesser curvatures. The next most common (15%) is

430

M.B. Aboutanos, T.M. Duane, A.K. Malhotra, and R.R. Ivatury

Table 27.3. Surgical emergencies associated with hiatal hernias.

Following cessation of the hemorrhage, aggressive medical therapy with endoscopic surveillance to ensure healing is recommended. When the cause is an ulcer within the hiatal hernia, efforts to exclude malignancy and appropriate therapy for the Barrett’s epithelium should be undertaken after the acute hemorrhage has been controlled. In the extremely rare situation when the bleeding cannot be controlled by endoscopic means, emergent surgery is indicated. Surgery in such situations is fairly difficult because of the relative inaccessibility of the lesion and the severe inflammation and dense adhesions that maybe present. When planning for the surgery, it is important to consider the site of the ulcer, as an ulcer high up in the chest may prove to be inaccessible through a laparotomy. If it is known that the ulcer is fairly high, consideration should be given to approach the lesion through a left posterolateral thoracotomy. Even when the lesion is accessible from the abdomen, the patient should be draped in a fashion that a thoracotomy can rapidly be performed either separately or by converting the laparotomy incision into a thoracoabdominal incision. Once the bleeding lesion is located, the actual procedure will depend on the hemodynamic status of the patient, the degree of concern for malignancy, and the presence or absence of Barrett’s esophagus. In the ideal situation with a patient relatively stable, patient dissection to release all adhesions and to free the distal esophagus should be performed. Once the esophagus and the herniated stomach are freed, if there is significant concern for malignancy or advanced Barrett’s disease, appropriate resection should be performed. If the concern for malignancy is low, and no Barrett’s changes are known to be present, oversewing of the bleeding ulcer followed by an appropriate antireflux procedure should be performed. In the latter situation, if dissection is extremely difficult, an acceptable method is to cut around the deeply adherent ulcer and exclude the ulcer by closing the esophagus or stomach as the case maybe and completing the procedure with an appropriate antireflux procedure. The wrap of the antireflux procedure can be utilized to buttress the suture line of the hollow viscus closure.102 When the patient is hemodynamically unstable, the least surgery to control the bleeding should be performed. This usually consists of opening the organ and oversewing the bleeding lesion. In some cases it maybe necessary to return in 24 to 48 hours and perform a resection or antireflux procedure.

Emergencies associated with complications of acid reflux Hemorrhage caused by erosive esophagitis and/or ulceration Hiatal hernia ulcer perforation Esophageal stricture with esophageal dilatation and atony Emergencies associated with mechanical complication Acute gastric volvulus

type II, also called rolling or paraesophageal hiatal hernia. In this type, the position of the GE junction remains intraabdominal, while parts or all of the fundus and body herniate into the chest through the esophageal hiatus to lie adjacent to the distal esophagus. The least common (5%) is the mixed type, or type III, and has elements of both type I (herniation upward of the GE junction with parts of the stomach) and type II (herniation of parts of the fundus and body to lie adjacent to the esophagus within the chest). The fundamental pathophysiology involved in the formation of hiatal hernia is the structural weakness of the phrenoesophageal membrane. The complications associated with hiatal hernia, which may present as an emergency requiring intervention, can broadly be divided into two categories (Table 27.3). First are complications arising from interference with the lower esophageal sphincteric mechanism allowing reflux of stomach acid into the lower esophagus. These are more common with type I hernias and include esophagitis and ulceration, which can cause upper gastrointestinal hemorrhage, ulcer perforation with resultant mediastinitis with or without peritonitis, and stricture formation with dilatation and atony of the proximal esophagus. Second are complications related to the abnormal mobility of the stomach making it prone to volvulus. These mechanical complications are more often associated with type II hernias.

Upper Gastrointestinal Hemorrhage The presentation and management of upper gastrointestinal hemorrhage have been dealt with elsewhere in this book. The specific problems associated with bleeding caused by severe reflux esophagitis, or from a peptic ulcer situated within the herniated stomach, are presented here. Approximately 3% of all upper gastrointestinal hemorrhages are caused by either severe erosive esophagitis or a deeply penetrating esophageal ulcer.100 Ulcers are most often found in association with Barrett’s epithelium and are typically located at the junction of gastric columnar and esophageal squamous epithelium. Hemorrhage due to either of these causes is rarely massive and usually self-limiting. In the rare event that the bleeding fails to stop spontaneously, endoscopic therapy is the initial treatment of choice and has a fairly high success rate.101

Hiatal Hernia Ulcer Perforation Peptic ulcers associated with a hiatal hernia may be found within the herniated stomach or at the part of the stomach that traverses the hiatus. The latter ulcer is thought to occur because of ischemia produced at this

27. Diaphragm

spot by the displacement of the stomach. Perforation of such ulcers is an exceedingly rare event, with only case reports found in the literature.103 Such perforations through the wall of the viscus may occur insidiously, with the ulcer first becoming adherent to and then penetrating into adjacent mediastinal organs of the cardiovascular or respiratory systems.104,105 These may give rise to findings such as spontaneous pneumopericardium.106 Less often reported are free perforations resulting in mediastinitis and/or peritonitis.103 For patients with peritonitis, the diagnosis will usually be made at the time of surgery. In the absence of peritonitis, the patients usually present with features of an intrathoracic catastrophe and are often treated for medical conditions. Whether the diagnosis is made at the time of surgery or preoperatively, the principles of management are similar to those outlined earlier for bleeding ulcer within a hiatal hernia. However, the adhesions in cases of acute or chronic perforation may be even more dense and hence surgery more difficult. Morbidity and mortality rates of such an event are very high because of the diagnostic delay and technical difficulty.

Acute Gastric Volvulus The normal stomach is held in position by attachments at the cardia and pylorus and peritoneal folds, with the vessels traversing them, over both curvatures. The normal stomach cannot be made to rotate through 180° unless these attachments are either stretched or absent. The most common acquired defect that results in the lengthening of these attachments and hence makes the stomach prone to volvulus is hiatal hernia, especially type II. Most cases of volvulus associated with hiatal hernia are of the organoaxial type where the axis of rotation runs from the cardia to the pylorus, and most cases are anterior. Although most cases of volvulus associated with a hiatal hernia are chronic, acute volvulus can occur, usually after a large meal. The presentation of an acute volvulus can be fairly dramatic. Borchardt,107 who first described the condition in 1904, emphasized three principal features: (1) severe pain in the epigastrium associated with distension, (2) vomiting followed by inability to vomit and continued retching, and (3) inability to pass a nasogastric tube. It is thought that the process is initiated by pyloric occlusion resulting in violent vomiting typical of a high occlusion. As the stomach rotates, the cardia too gets occluded, which causes the later retching and inability to vomit and retch. As both ends of the stomach are occluded, the patient develops a closed-loop obstruction, which can cause massive distension and interference with the vascular supply of the organ. Three additional features were later added to this classic description: (1) minimal abdominal signs if most of the stomach is in the thorax,

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(2) abdominal and/or chest radiograph showing a gasfilled organ in the lower chest, and (3) obstruction of the stomach on contrast radiography. In a series of 25 patients with acute volvulus, gangrene of the stomach was found in 7 (28%). Gangrene was heralded by bleeding, cardiorespiratory distress, and shock.108 Acute volvulus can at times be reduced by simple passage of a nasogastric tube, although in most cases, as noted above, nonpassage of the tube is one of the presenting features. In such situations urgent operation is essential to prevent the disastrous complication of strangulation and gangrene. At the time of surgery, in the absence of strangulation and if the patient is stable, the volvulus should be reduced, and a definitive procedure for the hiatal hernia, usually including an antireflux procedure, should be carried out. If the patient’s condition is deemed unstable, the reduced stomach should be held in place by some form of gastropexy, the simplest of these being a gastrostomy. When gastric necrosis has taken place, resection will have to be performed, the extent of which is dictated by the extensiveness of the necrosis. Because acute gastric surgery for gangrene carries high morbidity and mortality rates, the traditional recommendation has been that elective corrective surgery for type II hernias should be performed to prevent this complication from occurring, even if the hiatal hernia itself is causing minimal or no symptoms. However, this view has recently been challenged. In a study presented to the American Surgical Association, Stylopoulos and associates109 pointed out that the available surgical literature and the Nationwide Inpatient Sample Database do not support routine elective repair of asymptomatic paraesophageal hernias. Their analysis suggested that prophylactic surgery would be more beneficial than “watchful waiting” for only one of five 65-year-old patients. In summary, both traumatic and nontraumatic conditions of the diaphragm present challenges to the acute care surgeon. A well-informed surgeon will utilize the various diagnostic and therapeutic options to reduce their associated morbidity and mortality rates.

Critique With documentation of a diaphragmatic hernia and the fact that it is the delayed (3 years) sequela of a previous injury (left thoracoabdominal penetrating wound), definitive management is now required. This is obviously a missed diaphragmatic injury that should have been found and repaired, and the abdominal cavity should have been thoroughly explored at the time of the original injury. The thoracoabdominal area (from the nipples to the costal margins) has been

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called the “ultimate blind spot,” because no conventional diagnostic study (helical CT scan, ultrasound, MRI, or diagnostic peritoneal lavage) can reliably rule out a diaphragmatic injury. Therefore, celiotomy was the preferred management for these injuries, particularly on the left side. However, Ivatury and others highlighted the advantage of laparoscopy in diagnosing the penetrating diaphragmatic injuries. If a diaphragmatic injury is discovered, then the patient undergoes a celiotomy for a formal abdominal exploration. (It is not recommended that such an exploration be done laparoscopically for fear of missing an intraabdominal injury.) Because it is 3 years after the index injury, a thoracostomy would be the best approach to repair this diaphragmatic hernia because of better exposure and ease of repair compared with a transabdominal approach. In the acute care setting, a transabdominal approach should be the preferred choice because full abdominal exploration would be required. After 3 years, there should be no clinically significant intraabdominal injury. Answer (D)

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433 56. Hirsch EF. Repair of an abdominal wall defect after a salvage laparotomy for sepsis. J Am Coll Surg 2004; 198(2):324–328. 57. Bender JS, Lucas CE. Management of close-range shotgun injuries to the chest by diaphragmatic transposition: case reports. J Trauma 1990; 30:1581–1584. 58. Zantut L, Ivatury R, Smith S, et al. Diagnostic and therapeutic laparoscopy for penetrating abdominal trauma: a multicenter experience. J Trauma 1997; 42(5):825–831. 59. Leppaniemi A, Haapiainen R. Occult diaphragmatic injuries caused by stab wounds. J Trauma 2003; 55:646–650. 60. Martinez M, Briz JE, Carillo EH. Video thoracoscopy expedites the diagnosis and treatment of penetrating diaphragmatic injuries. Surg Endosc 2001; 15:28– 33. 61. Murray JA, Demetriades D, Cornwell EE 3rd, et al. Penetrating left thoracoabdominal trauma: the incidence and clinical presentation of diaphragm injuries. J Trauma 1997; 43:624–626. 62. Chen JC, Wilson SE. Diaphragmatic injuries: recognition and management in sixty-two patients. Am Surg 1991; 57:810–815. 63. Stylianos S, King TC. Occult diaphragm injuries at celiotomy for left chest stab wounds. Am Surg 1992; 58:364–368. 64. Symbas PN, Vlasis SE, Hatcher C Jr. Blunt and penetrating diaphragmatic injuries with or without herniation of organs into the chest. Ann Thorac Surg 1986; 42(2):158. 65. Wiencek RG Jr, Wilson RF, Steiger Z. Acute injuries of the diaphragm. An analysis of 165 cases. J Thorac Cardiovasc Surg 1986; 92(6):989–993. 66. Shackleton KL, Stewart ET, Taylor AJ. Traumatic diaphragmatic injuries: spectrum of radiographic findings. Radiographics 1998; 18:49–59. 67. Adegboye VO, Ladipo JK, Adebo OA, et al. Diaphragmatic injuries. Afr J Med Med Sci 2002; 31:149–153. 68. Karmy-Jones R, Carter Y, Stern E. The impact of positive pressure ventilation on the diagnosis of traumatic diaphragmatic injury. Am Surg 2002; 68:167–172. 69. Udobi KF, Rodriguez A, Chiu WC, Scalea TM. Role of ultrasonography in penetrating abdominal trauma: a prospective clinical study. J Trauma 2001; 50:475–479. 70. Chiu WC, Shanmuganathan K, Mirvis SE, et al. Determining the need for laparotomy in penetrating torso trauma: a prospective study using triple-contrast enhanced abdominopelvic tomography. J Trauma 2001; 51:860– 869. 71. Mirvis SE, Shanmuganathan K. MR imaging of thoracic trauma. Magn Reson Imaging Clin North Am 2000; 8:91–104. 72. Ochsner MG, Rozycki GS, Lucente F, et al. Prospective evaluation of thoracoscopy for diagnosing diaphragmatic injury in thoracoabdominal trauma: a preliminary report. J Trauma 1993; 34:704–710. 73. Smith RS, Fry WR, Tsoi EK, et al. Preliminary report on videothoracoscopy in the evaluation and treatment of thoracic injury. Am J Surg 1993; 166:690–695. 74. Uribe RA, Pachon CE, Frame SB, et al. A prospective evaluation of thoracoscopy for the diagnosis of penetrat-

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28 Abdominal Wall Jeffrey A. Claridge and Martin A. Croce

Case Scenario An 82-year-old nursing home patient undergoes emergency intervention for an acute abdomen. Patient stated that the only thing that relieved the pain was flexion of her right thigh. Exploration confirmed strangulate bowel resulting from intestinal herniation. Which abdominal wall/pelvic hernia usually presents as an intestinal obstruction of unknown origin? (A) (B) (C) (D) (E)

Femoral hernia Lumbar hernia Umbilical hernia Spigelian hernia Obturator hernia

Anatomy In-depth knowledge of the anatomy and innervation of the abdominal wall is crucial to all facets of abdominal surgery. The emergency surgeon must have a thorough knowledge of abdominal wall anatomy. The abdomen is the portion of the body bounded above by the diaphragm and continuing into the pelvis below the plane of the pelvic inlet. A trauma surgeon defines the abdominal cavity as beginning below the level of the nipples because a penetrating injury here can violate the diaphragm and injure intraabdominal organs, which can be seen as high as the fifth intercostal space. The abdominal wall is bordered above by the cartilages of the seventh to twelfth ribs and by the xiphoid process of the sternum. Inferiorly, the abdominal wall boundaries are the bones of the pelvis and the inguinal ligament. The prominent iliac crest forms the upper limit of the region of the hip; the curve of the crest ends ventrally in the anterior superior spine of the ileum, which is an important anatomic landmark that can be easily palpated. The

inguinal ligament stretches between the pubic tubercle and the anterior superior iliac. This ligament is the rolledunder inferior margin of the aponeurosis of the external abdominal oblique muscle. In the groin, this is the anatomic separation between the abdominal wall and the lower extremity. Three vertical lines are visible on the anterior abdominal wall and extend from the pubic tubercles to the costal margin.The linea alba is the central line that marks the aponeurotic junction between the two rectus muscles. Two linea semilunares define the lateral margins of the rectus muscles. For simplicity and localization of pain the division of the abdomen into quadrants provides a convenient reference. Such quadrants are defined in relation to the vertical line of the linea alba and to an imaginary transverse plane through the umbilicus. The abdominal wall is made up of many layers of skin, fat, fascia, and muscle. A scalpel blade or bullet must penetrate multiple layers to enter the innermost layer of the peritoneum. These layers are illustrated in Figure 28.1 and are slightly different depending on the location of the abdomen and relation to the arcuate line (Table 28.1). Being able to identify the layers is crucial to reapproximation of tissue edges and healing of wounds. Furthermore, knowledge of the different layers allows for the creation of complex closures and reconstruction. The understanding of tissue planes and the different physiologic properties of the layers allows for the understanding of many infectious processes. The skin is the outermost layer followed by subcutaneous fat, followed by Scarpa’s and then Camper’s fascia. These layers may be involved in some types of necrotizing soft tissue infections and allow for rapid spread of organisms. The next layers are muscle and aponeurotic sheaths. The muscles of the abdominal wall comprise two groups, anterolateral and posterior. The posterior muscle is the quadratus lumborum. The anterolateral muscles include two vertical muscles, rectus abdominus and pyramidalis, and three thin muscular layers, which alternate in their fiber

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TUS

REC

T1 T2

Peritoneum Obliquus externus Transversalis fascia Obliquus internus Linea alba Transversus

T3 T4 C5

T5

Figure igure 28 28.1. 1 Layers of the abdominal wall on cross section. section (Adapted from Townsend C. Beauchamp RD, Evers BM, Mattox K. Sabiston Textbook of Surgery, 17th ed. Philadelphia: WB Saunders, 2004, with permission from Elsevier.)

T6 T7 T8 T9

direction. These are the external abdominal oblique, internal abdominal oblique, and transversus abdominus muscles, which have extensive aponeurotic insertions. Their aponeuroses form a sheath for the rectus abdominus and pyramidalis muscles. The alternation in the direction of their muscles and aponeuroses adds strength to the abdominal wall. This also allows for muscle-splitting techniques to be used to enter the abdomen, avoiding transecting muscle and minimizing tissue damage. A muscle-splitting technique versus a muscle-dividing technique has been shown to decrease postoperative pain and increase patient mobility.1 Knowledge of the muscular anatomy of the abdominal wall and use of muscle-splitting techniques can be useful for emergent surgeries, including appendectomy, open cholecystectomy, and hernia repairs. The innermost layer is the peritoneum, which is separated from the innermost muscle layer of the transversus abdominus. In between these two layers is the preperitoneal space, and it has varying amounts of fat within. Anatomic recognition and knowledge of this

Table 28.1. Layers of the abdominal wall from superficial to deep. Location in relation to arcuate line Cranial to arcuate line

Caudal to arcuate line

Layers from superficial to deep Skin, Camper’s fascia (fatty layer of superficial fascia), Scarpa’s fascia (membranous layer of superficial fascia), deep fascia, external abdominal oblique aponeurosis, anterior layer of internal abdominal oblique aponeurosis, rectus abdominus, posterior layer of internal abdominal oblique aponeurosis, transversus abdominus aponeurosis, transversalis fascia, extraperitoneal fat, parietal peritoneum Skin, Camper’s fascia (fatty layer of superficial fascia), Scarpa’s fascia (membranous layer of superficial fascia), deep fascia, external abdominal oblique aponeurosis, internal abdominal oblique aponeurosis, transversus abdominus aponeurosis, rectus abdominus, transversalis fascia, extraperitoneal fat, parietal peritoneum

T10 T11 T12 L1

Figure 28.2. Segmental innervation of the anterior chest and abdominal wall.

space is crucial to many hernia repairs, which are discussed later in this chapter. The innervation of the muscles of the abdominal wall is by ventral rami of spinal nerves thoracic seven through lumbar four. This is the same segmental sequence that provides the cutaneous nerves in the region (Figure 28.2). The nerves of the anterior abdominal wall muscles are the intercostal nerves seven through eleven and the subcostal, iliohypogastric, and ilioinguinal nerves. The innermost layer of the abdominal wall, the parietal peritoneum, is richly innervated and very sensitive. Unlike the visceral peritoneum the parietal peritoneal surfaces sharply localize painful stimuli to the site of its origin.

Evaluation of Abdominal Wall A large number of patients will require evaluation of the abdomen secondary to abdominal pain or traumatic injury. It has been estimated that 5% to 10% of all emergency department visits, or 5 to 10 million patients, with abdominal symptoms present to emergency departments yearly.2 Another study demonstrated that up to 25% of patients in the emergency room have abdominal pain.3 Physical examination of the abdomen always begins with inspection. Specific attention should be paid to scars, hernias, masses, abdominal wall defects, and location of

28. Abdominal Wall

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injuries. Traditionally, palpation of the abdomen is the next phase of the abdominal examination. Following inspection is auscultation, especially for a patient with acute abdominal pain. The examiner can gently listen to the abdomen without causing any discomfort. This may gain the patient’s trust and give him or her more time to relax to allow for further evaluation and palpation. Auscultation of the abdomen gives information about the presence and quality of bowel sounds. A quiet abdomen generally indicates an ileus, whereas hyperactive bowel sounds with high-pitched rushes and tinkles are more characteristic of a mechanical bowel obstruction. One should also listen for the presence of bruits as a marker of vascular disease. Gentle palpation with the stethoscope at the end of the auscultatory phase of the physical examination may elicit information regarding tenderness of the patient’s abdominal wall. This portion of the examination is the point at which the examiner can transition into the palpation phase of the abdominal examination. Palpation should begin with gentle pressure away from the point of abdominal discomfort. The examiner should observe the patient’s facial expression for signs of pain or discomfort. The detection of increased muscle tone during palpation is referred to as “guarding,” which may be voluntary or involuntary. Involuntary guarding is more concerning for peritonitis. The guarding may also be generalized or it may be localized. The location of pain on the abdominal wall can aid the clinician in making the diagnosis (Figure 28.3). Another sign of peritonitis is rebound tenderness.The last step of the abdominal exam-

Stomach Gallbladder

Pancreas

Small Intestine

Colon

Figure 28.3. Location of pain from abdominal viscera. (Adapted from Townsend C. C Beauchamp RD, RD Evers BM, BM Mattox K. Sabiston Textbook of Surgery, 17th ed. Philadelphia: WB Saunders, 2004, with permission from Elsevier.)

ination is percussion. When gentle percussion elicits tenderness, it indicates inflammation and has the same implication as rebound tenderness. Percussion of the abdominal wall may demonstrate tympani as found in bowel obstruction, or it may demonstrate percussive dullness and evidence of fluid in ascites.

Hernias Simply put, a defect in the normal anatomy of the abdominal wall is the cause of a hernia. The decision to operate emergently or urgently on a patient with a hernia depends on the presentation of the patient. A call to the emergency room or medical intensive care unit to evaluate a patient who is septic and has a large scrotal hernia that worries the nonsurgical colleagues should not immediately prompt operative intervention. The physician should be able to elicit hernias by palpation as well as by asking the patient to perform maneuvers to increase intraabdominal pressure. A valsalva maneuver, or asking the patient to stand if able, is often sufficient. There are many types of hernias, some of which are discussed later in this chapter, and recognition of which hernias need to be fixed acutely is critical. In general, a hernia that cannot be reduced is termed an “incarcerated hernia” and should be repaired immediately. The concern is that bowel is being strangulated within the incarcerated hernia. Signs that make this more ominous are tenderness during palpation of the hernia, redness around the hernia, fever, tachycardia, and leukocytosis. Furthermore, the signs of a bowel obstruction in the presence of an incarcerated hernia warrant acute surgical intervention. Waiting to operate in this scenario adds morbidity to the procedure. Kulah et al.4 evaluated 385 consecutive acute care surgeries for incarcerated external hernia. They demonstrated that inguinal and umbilical hernias were most common, at 75% and 13%, respectively. Additionally, they reported that older age, presence of coexisting diseases, and duration of symptoms were associated with negative outcomes. There are also hernias that are difficult to reduce and may take effort or require sedation to be reduced. If these patients do not have signs of bowel obstruction, fever, elevated white blood count, tachycardia, or evidence of local inflammation, an emergent operation is not generally indicated. However, this is a hernia that is clearly symptomatic and in our opinion should be operated at the next convenient opportunity. The timing of this is usually the next working day during the elective schedule.

Groin Hernias Groin hernias are the most common of all abdominal wall hernias. Their exact prevalence is unknown. However,

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studies have estimated that the lifetime risk of inguinal hernia repairs is 27% for men and 3% for women.5 Groin hernias have been classically described and classified on the basis of the clinical presentation of the hernia sac. Thus, they were described as a direct inguinal hernia, an indirect inguinal hernia, both direct and indirect hernia (pantaloon hernia), or femoral hernia. Now that hernias are often repaired from a posterior approach this classification is less relevant, because only the neck of the hernia sac and the parietal defect can be seen. Fruchaud6 introduced the concept that groin hernias all share the common feature of emerging or beginning in a single weak area he termed the “myopectineal orifice” (MPO). The MPO is a bony muscular framework that is bridged and bisected by the inguinal ligament. The inguinal ligament serves as the dividing line separating inguinal from femoral hernias and defines the medial border of the orifice of the femoral canal. The femoral vessels and the spermatic cord transverse the MPO. The integrity of the MPO depends on the strength of the transverse fascia, which is the innermost muscle layer. Failure of the transverse fascia to retain the peritoneum is the fundamental cause of all hernias of the groin. Operating in an acute setting on a hernia is generally more difficult and has been shown to have higher complications rates.5,7 Arenal et al.8 demonstrated that both increased age and need for acute care surgery were associated with increased mortality. Patients who present with incarcerated groin hernias have been shown in studies9,10 to be older, have higher American Society of Anesthesiologists scores, and have a high incidence of femoral hernias. Furthermore, inguinal hernia incarceration was shown to be associated with increased morbidity and mortality. If the patient has an incarcerated hernia, the surgeon must evaluate the contents to ensure its viability. Thus, this needs to be kept in mind if the hernia is either intentionally or spontaneously reduced after anesthesia and muscle relaxants. The decision about which type of operation to perform depends on many factors. There are several options for approaching and repairing a groin hernia. In general, there are two established approaches for repairing a groin hernia. There is an anterior and a posterior approach. There are multiple techniques to each approach. The anterior approach was traditionally used to repair without prosthetic material. The four most popular repairs are the Marcy hernioplasty, the Bassini hernioplasty, the Shouldice hernioplasty, and the Cooper’s ligament hernioplasty. With the Marcy hernioplasty, the deep inguinal ring is tightened and returned to normal size by the placement of one or two permanent monofilament sutures. These sutures are placed medially in the transverse aponeurotic arch and laterally in the iliopubic tract or femoral sheath.

J.A. Claridge and M.A. Croce

For the Bassini hernioplasty, Bassini divided the floor of the inguinal canal, which is a step that is omitted by some surgeons. This is a three-layer repair that consists of approximating the internal oblique abdominal muscle, the transverse abdominal muscle, and the transverse fascia to the inguinal ligament and iliopubic tract. With the Shouldice hernioplasty, the floor of the inguinal canal is repaired by imbrication of the innermost fascial layer of the abdominal wall. Suturing begins at the pubic tubercle. The iliopubic tract is fastened to the undersurface of the transverse aponeurotic arch, with a single running suture that is run to the deep internal ring and then run back to approximate the free edge of the transversalis to the shelving edge of the inguinal ligament. The internal oblique abdominal muscle being sutured to the inguinal ligament is described in Shouldice’s repair, but is a step that is not uniformly done. With the Cooper’s ligament hernioplasty (McVayLotheissen repair), the repair consists of attaching the transverse aponeurotic arch to Cooper’s ligament, the medial side of the femoral sheath, and the anterior femoral sheath with interrupted sutures. This repair addresses the three areas that are most vulnerable for herniation in the MPO, the deep inguinal ring, Hesselbach’s triangle, and the femoral canal. Therefore, the Cooper’s ligament repair is used to manage femoral hernias and large indirect and direct inguinal hernias. The suture affixing the transverse aponeurotic arch to the medial edge of the femoral sheath is called the “transition suture.” Relaxing incisions along the rectus sheath are mandatory. Anterior prosthetic hernioplasty has become increasingly popular. The reason for the increase in popularity is in part because of some of the criticisms of the classic repairs. It is well accepted that considerable experience is required to obtain excellent results using the classic repairs. A classic repair is also thought to be inadequate for recurrent hernias, especially if it was repaired with a classically described technique initially. The largest criticism is that these classic repairs produce tension, and the problems of continued tissue deterioration and strain are not addressed. The most popular version of the anterior prosthetic hernioplasty is the Lichtenstein’s tension-free hernioplasty. The repair consists of a polypropylene patch laid over the posterior wall of the inguinal canal. The patch is tailored with a slit or keyhole for the spermatic cord. The prosthesis should extend 1.5 to 2.0 cm medial to the pubic tubercle and well lateral to the deep inguinal ring. The patch is sutured securely medially to the pubic tubercle and to the inferior shelving edge of the inguinal ligament inferiorly. It is then sutured superiorly to the underside of the rectus sheath and conjoint tendon. Another type of repair using mesh involves using a mesh plug, which is placed in the hernia defect.

28. Abdominal Wall

These mesh techniques can also be modified for a posterior preperitoneal approach. This preperitoneal space is a logical site in which to implant a prosthesis. The prosthetic material is held in place by intraabdominal pressure. The preperitoneal space for repair of groin hernia is best approached with an abdominal incision. This allows for excellent exposure without the dissection of the inguinal canal. Over the past decade there has been an increase in the use of laparoscopic techniques for groin hernia repairs. The two most common techniques for laparoscopic inguinal hernia repair both involve the insertion of mesh into the preperitoneal space. One is referred to as the “transabdominal preperitoneal” approach and the other is referred to as the “totally extraperitoneal” approach. It is important to understand the different types of hernia repairs; however, for the emergency surgeon, it is more important to identify patients who need emergent operations. Although most hernia repairs are performed electively,5 there are certainly times when groin hernias need emergent/urgent repair. The indication for emergent/urgent repair of groin hernia is mainly incarceration of the hernia. A nonreducible groin hernia needs to be operated on as soon as possible. The findings at the time of the operation will dictate the type of repair that can and should be performed. Thus, knowledge of various types of procedures is crucial to emergency general surgeons. At this time our opinion is that an incarcerated hernia is a relative contraindication to a laparoscopic approach. Without advanced laparoscopic skills, laparoscopic techniques are contraindicated if the patient exhibits any signs of bowel obstruction or strangulation with an incarcerated hernia. The main rationale for this is as follows. A systematic review (McCormick Cochrane Database) demonstrated that laparoscopic repair techniques have similar recurrence rates in elective cases and may have minimal improvements in return to function and less pain. The Veterans Administration study,11 however, demonstrated a higher percentage of recurrence and an increase in complications with laparoscopic inguinal hernia repair. Additionally, laparoscopic surgery requires that all patients get general anesthesia. For patients who are acutely ill, as is often the case in dealing with acute care surgical situations, the option of local or regional anesthetic technique is attractive. Furthermore, if the patient has distended loops of bowel, visualization may be difficult and pneumoperitoneum may be dangerous in an acutely ill patient. Finally, if there is a high suspicion of strangulation and a question of bowel viability, gross contamination with perforation or bowel resection would make the use of prosthetic mesh unwise. One may, however, consider using the laparoscope in the event of the bowel being reduced without it being evaluated

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during open repairs. This is only practical if there are no signs of bowel distention. When the surgical team has deemed that the patient has an incarcerated groin hernia, it should be treated promptly. Kurt et al.12 demonstrated that although men may have a higher incidence of groin hernia incarceration, women have a higher incidence of bowel compromise requiring resection. Additional risk factors for patients needing bowel resection were patients with femoral hernias and age older than 65 years. Fluid resuscitation should begin immediately if the patient shows signs of dehydration and/or illness from prolonged bowel obstruction. Intravenous access and resuscitation should take no more than a couple of hours. The operating room is also a great place to continue resuscitation. A delay in repairing/correcting the underlying etiology of the illness will likely harm the patient. We favor either a preperitoneal approach using a lower transverse abdominal incision or a classic anterior inguinal incision. When operating, one must make a diligent effort to assess the contents of the hernia sac. The difficulty in this is getting control of the neck of the hernia before reducing it. Evaluation of the contents for necrosis is crucial. If necrosis is discovered or bowel is determined to be not viable, it should be resected.There may already be perforation and local inflammation/infection. In any of these later cases synthetic mesh is not indicated. We would recommend primary repair. If a defect was extremely large and it could not be closed, there are options of using other materials. Vicryl mesh is one option. This will reabsorb and may lead to recurrence, but in the face of infection it is a better option than placing synthetic permanent mesh. Other options are discussed later in this chapter and include biomaterials such as Surgisis (Cook Inc.) and acellular cadaveric dermis (AlloDerm, LifeCell Corporation, Branchburg, NJ).

Other Abdominal Wall Hernias Ventral Hernias “Ventral hernias” in this chapter refer to umbilical, periumbilical, parastomal, Spigelian, epigastric, and incisional hernias. The large incisional hernia or planned ventral hernia is discussed later in this chapter. True umbilical hernias are rare in adults. They are common in infants and usually close without surgical treatment. However, repair is indicated in infants if the hernia is greater than 2 cm in diameter and in all children whose umbilical hernia is still present at 3 to 4 years of age. These seldom need emergent repair and can be dealt with electively. However, adults with periumbilical hernias require repair. Strangulation of the colon, small bowel, and especially omentum is not uncommon. Epigastric hernias occur between the decussating fibers of

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the linea alba above the umbilicus. Spigelian hernias are relatively rare ventral hernias that occur along the semilunar lines lateral to the rectus abdominal muscle and usually below the umbilicus. Incisional hernias are defects secondary to breakdown along a previous fascial closure. These can be midline or anywhere an abdominal incision can be. A parastomal hernia is a hernia near an ostomy. Regardless of the type of hernia, all but parastomal hernias of the aforementioned hernias can be approached with a similar thought process. Parastomal hernias are discussed separately. The indication to operate on ventral hernias in a nonelective setting is incarceration. If the patient has a nonreducible mass, he or she should be scheduled for repair. For the same reasons as mentioned earlier, we recommend open repair for symptomatic incarcerated hernias. However, if the patient has no evidence of bowel obstruction or the hernia contents were reduced, laparoscopy is a viable option. At the time of operation, the contents of the hernia sac need to be evaluated for ischemic changes. Often the omentum is incarcerated, and it can be reduced during the procedure when the sac is opened. If bowel is in the hernia sac, it must be carefully inspected for evidence of ischemia or necrosis. Often it may have some venous congestion and show signs of inflammation. If it is viable it should “pink up” after it is reduced. If it has clear areas of necrosis or perforation, it should be resected. A Richter’s hernia is a hernia that may have a partial segment of incarcerated bowel. This may create a small area of necrosis without signs of obstruction. Likewise, ischemic or necrotic omentum needs to be resected.After the contents of the hernia sac are reduced, the hernia sac should be excised and the fascial edges should be identified and dissected free from sac, surrounding connective tissues, or other adhesions. It is important to debride the fascial edges to healthy tissue, because reapproximation of scar will lead to a recurrent hernia. Clearly identifying and visualizing 1 cm of fascia circumferentially around the defect is crucial to properly repairing these hernias. If the hernia is small and not a recurrent hernia, it can be closed with nonabsorbable sutures. Larger hernias are best treated with a prosthetic closure. There are many techniques used to describe the closures of small primary defects (vest over pants imbrication, interrupted simple sutures, multiple figure-of-eight sutures, and continuous suture closures). The key concept is tension-free reapproximation of healthy fascia. Thus, sutures should be placed and tied to reapproximate and not strangulate the tissues. Arroyo et al.13 demonstrated that the use of prosthetic closure was superior to primary closure for umbilical defects.They demonstrated a recurrence rate of 11% with suture closure versus a 1% recurrence with mesh (p =


0.0015). A contraindication to the placement of synthetic mesh is exposure of bowel contents. When resection is needed, primary repair can be performed if there is little to no tension. An attractive alternative is the use of biologic mesh material. There are numerous reports in the literature advocating the utility of these products.14,15 There are multiple methods for securing the mesh, including overlay, underlay, and sandwich-type techniques. If laparoscopy is the method of surgery, the mesh underlay technique is the method to be used for repair.

Parastomal Hernias A parastomal hernia is a hernia that occurs in proximity to an ostomy. Paracolostomy hernias are more common than paraileostomy stomas. This is likely because of the size of the defect created at the time of the initial surgery. In addition, these hernias are more likely to occur when the stoma emerges through the semilunar lines rather than through the center of the rectus abdominal muscle. Thus, most fascial defects and hernias are lateral to the ostomy. However, they can occur anywhere in relation to the ostomy. In our experience, parastomal hernias seldom need emergent repair. However, there are several reasons to include them in this text. One, like all hernias, they can cause bowel obstruction secondary to incarceration of bowel. A second reason, and perhaps the more important reason, is that emergent general surgeons and trauma surgeons may see a higher proportion of these hernias. Trauma situations and emergent general situations increase the frequency of ostomies. Additionally, the ostomies are created at the end of a long case and may need to be performed rapidly. Hernias have also been demonstrated to be more common after acute care surgery.16 Often these patients are critically ill and have prolonged recovery times and likely poor wound healing. Thus, besides taking care to create the ostomy correctly, knowledge of how to address the complications of them is important to emergency general surgeons. The decision of when to operate on a parastomal hernia depends on the symptoms and the type of patient presenting. If the patient is presenting with symptomatic incarceration and/or complete bowel obstruction, emergent surgical intervention is needed. Parastomal hernias may also cause chronic problems with maintenance of the ostomy. Patients may have a change in bowel habits and have intermittent obstruction requiring dilation and/or frequent irrigation of the ostomy. More commonly, correct seating and fit of the appliance may be difficult. These more chronic problems can be dealt with on an elective basis. The second issue of deciding when to address the parastomal hernia depends on the type of

28. Abdominal Wall

patient. For the patient with a temporary ostomy it seems wise to wait for the resolution of the initial etiology before it is repaired. The patient with a permanent ostomy can be repaired electively. There are a variety of methods to repair parastomal hernias. The best method is clearly either moving the ostomy to a different site or taking the ostomy down and returning the continuity of the gastrointestinal tract. If the ostomy is temporary, it is likely that the ostomy was present for only a short time and the defect is small. Thus, this can often be repaired with simple sutures and reapproximation of superior fascial edges to inferior fascial edges. If the ostomy is permanent and can be moved to a second site, this is advised. The site should be marked preoperatively with the patient wearing normal clothes. The site should be within the center of the rectus muscle and not in a skin crease. Observe the patients’ abdomen when they stand and sit. Also observe where the patients wear their pants, as they may have a preference on the location based on how they wear their clothes. Again, marking preoperatively is very important. Abdominal exploration via a midline incision before taking the ostomy down is advisable as this will allow for reduction of the hernia and facilitate freeing the ostomy from the abdominal wall. At this time we recommend repairing the defect. If it is small and it can be closed with minimal tension, consider primary repair. Otherwise, mesh may be needed to reinforce the closure. Synthetic material is not recommended if bowel contents were spilled. Biologic material is an attractive alternative to synthetic mesh, especially in the face of contamination. After the hernia defect is closed the new ostomy can be created in the preoperatively marked position. The skin at the previous ostomy site should be left partially open to allow adequate wound care. When moving the ostomy is not an option, there are techniques for hernia repair. Two techniques are described in the literature. One is described by Leslie17 in which the incision is made away from the stoma. The skin and subcutaneous tissue are dissected from the abdominal wall and reflected to expose the bowel and fascial defect. The defect is closed with sutures and a piece of mesh is placed anteriorly over the repair with a slit in it to be positioned around the bowel. If a large amount of undermining a dead space occurred during dissection, a closed suction drain is recommended. Sugarbaker18 described a technique that repairs the hernia from within the abdomen and also uses mesh. The availability of biologic mesh products now allows the surgeon to consider using them in the repair of parastomal hernias. The advantage of biologic meshes is that they are not permanent, minimizing the chances of bowel erosion. Their collagen matrices allow for ingrowth of tissue, and they appear to be relatively resistant to infection.

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Abdominal Wall Trauma Blunt abdominal wall trauma seldom causes injury to the abdominal wall that requires surgical intervention. However, the presence of obvious abdominal wall trauma needs to trigger concern of internal injuries. A welldescribed injury pattern is that caused by a rapid deacceleration injury while wearing a lapbelt. A red or line abrasion may be seen across the lower abdomen, and the patient may have a lumbar Chance fracture. In this situation the clinician needs to have a high clinical suspicion for intraabdominal injury—especially bowel or mesenteric tears. Wotherspoon et al.19 demonstrated a higher risk of intestinal injury in patients with an abdominal seatbelt sign. These injuries can also cause a large amount of shearing injury leading to a large soft tissue injury. These injuries can be difficult to manage and may involve multiple trips to the operating room for debridement. Penetrating abdominal wall trauma is a very common problem faced by the emergency trauma surgeon. As mentioned earlier, the abdominal cavity can begin just below the nipples. Thus patients with lower penetrating chest wounds must have their abdomen evaluated for intraabdominal injury. If the pleura cavity has been violated, the diaphragm must be evaluated. The two main groups of penetrating injuries are stab and gunshot wounds. Patients with gunshot wounds to the abdomen require emergent laparotomy with few exceptions. Their incidence of significant abdominal injury is approximately 80%. On the other hand, patients with stab wounds have a lower abdominal injury rate (about 33%) when a mandatory laparotomy policy is employed. Thus, gunshot and stab wounds necessitate different management schemes. Evaluation of anterior stab wounds is straightforward and illustrated in Figure 28.4. If the anterior fascia is violated, further inspection is needed. The wound should be locally explored, unless intraabdominal injury is obvious. Lidocaine should be injected for local exploration. The entire wound tract must be evaluated. If there is anterior fascia violation or the wound cannot be locally explored fully, the patient needs further intraoperative exploration. Diagnostic peritoneal lavage is not indicated and in this scenario has been shown to be unreliable for penetrating trauma. If there is violation of the fascia but no clear evidence of intraabdominal injury, the surgeon may either observe the patient or perform laparoscopy. If the peritoneum is intact, the laparoscope can be withdrawn and the procedure ended. If there are no other injuries the patient can be safely discharged to home. Our practice is to convert to an open exploration if the laparoscope demonstrates peritoneal violation. If laparoscopy is not available a small midline incision can be made to evaluate for peritoneal violation. The incision can be extended for further exploration if necessary.

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J.A. Claridge and M.A. Croce Hemodynamically stable, nontender abdominal exam

Yes

No

Local wound exploration

To OR

Violation of anterior fascia

Definitely no violation of anterior fascia

Equivocal violation of anterior fascia

To OR for laparoscopy/ laparotomy

Discharge

To OR for laparoscopy/ laparotomy

Figure 28.4. Algorithm of treatment for penetrating abdominal wound.

Some centers have advocated observation and serial examinations for knife stab wounds. A delay in diagnosis of bowel injuries has been demonstrated to increase morbidity. Another diagnosis that will confront the emergency surgeon is a rectus sheath hematoma. Patients with rectus sheath hematomas are more commonly women. Patients complain of abdominal pain and may have anemia. Causes include local trauma, straining associated with defecation, coughing, sneezing, and spontaneous. Often patients are receiving anticoagulation therapy. In the literature there are numerous reports of rectus sheath hematoma presenting or masquerading as numerous other conditions, including abruptio placenta,20 sigmoid diverticulitis,21 and appendicitis.22,23 Ultrasound has been advocated by some as a procedure to assist in the diagnosis of rectus sheath hematoma.24,25 A method of classification using computed tomography (CT) scan was proposed by Berna et al.26 and demonstrated three types of hematomas. Type I was a minimal hematoma. Types II and III were moderate and severe hematomas, respectively, and required hospitalization. Anticoagulation is associated with larger hematomas. Patients with larger hematomas likely need transfusion of packed red blood cells and coagulation factors. These patients may present with signs and symptoms similar to patients with an acute abdomen. Both CT scan and ultrasound may be able to assist in the diagnosis. However, it is likely that CT scan is more readily available has fewer user errors. A CT scan may also offer more information about a patient with abdominal pain.

However, the advantage of ultrasound is that it is less costly and is very appropriate, especially for women. Most rectus sheath hematomas do not require surgery. If there is evidence of ongoing bleeding after correction of a patient’s coagulopathy, surgery is indicated. Free fluid in the abdomen is also a sign that the hematoma has ruptured and thus less likely to tamponade. The surgery involves an incision over the hematoma and evacuation of the hematoma. Often the bleeding vessel cannot be identified. We recommend dissecting more inferiorly and ligating the inferior epigastric artery. Although not a common diagnosis, rectus sheath hematomas should be considered in the differential diagnosis for a patient with acute lower abdominal pain. This is especially important if the patient is receiving anticoagulation therapy, as there have been fatalities reported secondary to rectus sheath hematomas.27 Judicious use of laparotomy is prudent.

Abdominal Compartment Syndrome Definition Abdominal compartment syndrome (ACS) is caused by increased intraabdominal pressure that results in pathologic changes. Normal intraabdominal pressure is typically less than 15 mm Hg. The technique to measure intraabdominal pressure with intravesicular pressure monitoring was well described by Kron et al.28 The cardiovascular, pulmonary, and renal systems appear to be the most sensitive to the changes in abdominal compartment pressure. The cardiovascular system is affected mainly by reduction in venous return. Thus, decreasing both preload and cardiac output will further exacerbate the shock condition. The pulmonary system is affected secondary to the increase in intraabdominal pressure, causing elevation of the diaphragms. This transmits into higher intrathoracic pressures and subsequent alveolar hypoventilation, leading to subsequent increase in carbon dioxide and acidosis. Hypoxia may also be present, as there is collapse of more alveolar tissue and interparenchymal edema. The renal system is also affected by the increase in intraabdominal pressure. Studies have demonstrated direct effects of increased pressure on the kidney parenchyma and subsequent decrease in glomerular filtration rate.29 Furthermore, the decrease in cardiac output further leads to a decrease in glomerular filtration rate and low urine output. Patients with closed head injuries also suffer from increased abdominal pressure with increased intracranial pressures. This increase in intracranial pressures is often exacerbated by hypoxia, hypercapnia, decreased venous return, and hypotension. There is no absolute number at which a patient has ACS; however, an intraabdominal pressure greater than

28. Abdominal Wall

25 mm Hg measured via bladder pressures is considered elevated. Thus an intraabdominal pressure >25 mm Hg with presence of the above-mentioned pathophysiology defines ACS. Primary ACS has been well recognized by trauma surgeons for many years. Primary ACS is seen often after damage-control operations and occurs in patients with intraabdominal and pelvic pathologies. Secondary ACS is a syndrome now recognized to be caused by conditions outside the abdominal and/or pelvic cavity. Secondary ACS is seen in patients with severe shock needing massive resuscitation.

Etiology There are many causes of ACS. All patients with ACS are critically ill and carry a significant mortality risk. Abdominal compartment syndrome is most often described in patients with massive abdominal or pelvic hemorrhage. It typically occurs after laparotomy when the fascia is closed and the patient has ongoing blood loss and edema. Other conditions that can lead to ACS are pancreatitis, abdominal burns, and ischemia/reperfusion injury to the bowels. The term “secondary ACS” has been coined to refer to ACS in the absence of abdominal or pelvic pathology and caused by edema and ascites in the presence of shock. This can occur septic shock as patients need large volumes of fluid and develop leaky capillaries that cause massive bowel edema. This can be seen as shock bowel on CT scan (Figure 28.5). Whatever the etiology, the common factor is the abdominal wall and mainly the more restrictive fascia, except in burn where the skin plays a large restrictive role. Like other areas of the body such as extremities, heart within the pericardium, and brain within the cranial vault, the abdomen is enveloped within a closed space. An increase in volume in a closed space leads to an increase in pressure and subsequent pathology.

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Treatment Once the diagnosis is made the decision to intervene should be immediate. Depending on the physical set up of the intensive care unit and operating room the abdomen may be opened at bedside. A midline laparotomy should be performed as soon as possible. The patient’s physiologic disarray should begin to correct itself immediately. The most immediate physiologic change that is noticed is a rapid decrease in peak airway pressures. The fascia should be opened from approximately 3 to 4 cm below the xiphoid to a couple of centimeters above the pubic symphysis. If the patient already has a midline incision, simple opening of the incision is usually all that is required. Again, the results of releasing the tension of the abdomen are immediate and often impressive. Fluid and intestines will spring from the wound; thus our bias is to perform this procedure in the operating room. If bleeding or hemorrhage is the etiology, good illumination is paramount. A scrub nurse and access to vascular instruments are also important. After the abdomen has been opened and hemostasis is ensured, quick exploration for injuries is warranted. The amount of irrigation is one of personal choice. There are multiple methods to “close” the abdomen to prevent evisceration and control fluid loss. These methods are discussed next. Being able to identify patients at risk for developing ACS would be beneficial, because the mortality of ACS is reported to be between 25% and 75 %.30 Additionally, an open abdomen is clearly associated with increased morbidity, longer hospital stays, and increased health care costs.

Closure of the Abdominal Wall and/or Skin In this section we discuss three areas. The first is the decision to close skin. The second is the decision to close fascia and how to manage an open abdomen. The third is the long-term management of the open abdomen and the resultant ventral hernia.

Skin Closure

Figure 28.5. Computed tomography scan showing evidence of shock bowel.

There are generally three types of closure, which are primary closure, secondary closure, and tertiary closure. Primary or first-intention closure is the most common and can be used for clean wounds. These wounds are immediately closed and usually with the most simple sutures. They can also be closed immediately with skin grafts or flap closures. Secondary closure involves no active intent to seal the wound. These wounds are left open and allowed to heal via contraction and

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Table 28.2. Surgical wound classification.

Wound class I, Clean

II, Clean contaminated

III, Contaminated

IV, dirty infected

Accepted range of infection

Definition Uninfected operative wound in which no inflammation is encountered and the respiratory, alimentary, genital, or urinary tract is not entered. In addition, clean wounds are primarily closed and, if necessary, drained with closed drainage. Operative incisional wounds that follow blunt trauma should be included in this category if they meet criteria An operative wound in which the respiratory, alimentary, genital, or urinary tracts are entered under controlled conditions and without unusual contamination. Specifically, operations involving the biliary tract, appendix, vagina, and oropharynx are included in this category, provided no evidence of infection or major break in technique is encountered Open, fresh, accidental wounds. In addition, operations with major breaks in sterile technique or gross spillage from the gastrointestinal tract and incisions in which acute, nonpurulent inflammation is encountered are included in this category Old traumatic wounds with retained devitalized tissue and those that involve existing clinical infection or perforated viscera. This definition suggests that the organisms causing postoperative infection were present in the operative field before the operation

reepithelialization. These wounds are seen most commonly when there is a high level of bacterial contamination. Tertiary closure is also commonly referred to as “delayed primary closure.” Generally this involves closing an open wound after several days when the tissue bed is clean and the bacterial counts are low. Additionally there is an increase in phagocytes in the wound over the next several days. Thus, it is thought that these wounds can be best closed at around days four to six postoperatively. If this is done, the wound must be watched carefully and should be closed loosely. The emergent surgeon needs to determine which wounds to close. The risk of closing all wounds is of course infection. An infection of the wound can lead to fascial breakdown and wound dehiscence. Likewise, all wounds should not be left open, as dressing changes lead to discomfort and increased resource utilization. Thus, one needs to have a logical approach to deciding how and when to close the skin. The core issue deals with determining the risk of developing a surgical site infection (SSI). Classically, four types of wounds have been described.31 These are clean, clean contaminated, contaminated, and dirty. A description of each and the accepted infection rates are given in Table 28.2. The National Nosocomial Infection Surveillance System (NNIS) has modified this system to include evaluation of the risk factors of long procedure time (>75th percentile), the presence of a contaminated or dirty wound, and an American Society of Anesthesia (ASA) score of 3or higher. The number of risk factors is associated with a percent risk of SSI (Table 28.3).32 Although these numbers are important for determining overall risk factors for developing SSI, they do not necessary apply to emergent surgery. By definition an emergent surgery increases the ASA score and also an E

1%–5%

3%–11%

10%–17%

>27%

is added (for emergency), thus increasing the risk of worse outcomes for such patients. Additionally, patients requiring emergent surgery are more likely to have addition risk factors, including need for blood transfusions and poor glucose control, and are more likely critical care patients. These factors all increase the risk of SSI. In general, our recommendation is to err on keeping the skin open and reduce the morbidity of a SSI. An SSI in a critically ill patient can be a devastating complication. Open skin wounds usually heal quickly and can be closed by delayed primary closure. All clean and clean contaminated wounds should be able to be closed. The skin wounds that are contaminated or dirty are routinely left open. There are a variety of techniques described to minimize the wound size and hopefully speed the healing process of secondary intention. Sections of the wound can be closed or reapproximated with staples and wicks left in for 2 to 3 days after which they can be removed. If the wound looks clean at that time, some advocate using steristrips to close the small defects, and others let these areas heal by secondary intention. If the wound looks like it is draining or infected, the staples can be removed. Others

Table 28.3. National Nosocomial Infection Surveillance System score and risk for surgical site infections (SSIs). No. of risk factors

Risk of SSIs

0 1 2 3 Risk factors

1.5 2.9 6.8 13.0 Procedure time >75th percentile, contaminated or dirty wound, ASA >3

ASA, American Society of Anesthesia.

28. Abdominal Wall

advocate leaving the entire wound open and beginning frequent dressing changes the following day. The decision of which technique is best to use is not addressed in the literature and largely depends on personal experience and preference. The key principles to remember are that the wound that is at higher risk for SSI needs to have the skin left widely open to allow for drainage and that midline abdominal wounds mainly heal from side to side, not vertically. Cosmesis, although important, is not the critical issue for the emergent surgical patient. A wound that has to be reopened or dehisces will also result in worse cosmesis than a wound that heals well with secondary intention. There is minimal to no cosmetic difference in abdominal wounds that are closed with delayed primary closure and primary closure.

The Decision to Close Fascia and Subsequent Management of the Open Abdomen The decision to close fascia in our opinion is very straightforward. The fascia should be left open in all patients with ACS. Patients who will need reexploration within the next 24 to 48 hours should also have their fascia left open. These patients may be coagulopathic and require packing or have had damage-control surgery and need to have their gastrointestinal continuity returned. The last major reason not to close patients is when there is concern of developing ACS. Numerous studies have been performed to identify patients at risk for developing ACS.30,33–36 The risk factors that have been identified in trauma patients have been high injury severity scores, increased serum lactate levels, increased base deficits, and blood transfusions.34 Raeburn et al.36 demonstrated that increased peak airway pressures were predictive of developing ACS for patients who have had a damage-control operation. If the abdomen is tight it should not be closed, especially in patients who have required a large amount of fluid resuscitation and/or who need ongoing resuscitation. Similar to closing the skin, we recommend erring on the side of keeping the abdomen fascia open. Any fascial closure under tension is a recipe for disaster. There are a variety of methods used to cover the intestines and manage the open abdominal wound. One technique of closure involves applying numerous towel clips to the skin to reapproximate the skin edges. It is very quick and requires about two towel clips for each 3 cm of incision. There are several situations when doing this may be advantageous. If the patient is extremely ill and needs to be taken off the operating table, quick application of numerous towel clips to the skin is an excellent choice. This may be appropriate for patients who are becoming extremely coagulopathic and cold. If all surgical bleeding

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Figure 28.6. Use of radiograph cassette to temporarily cover the abdomen.

has been addressed, it is crucial to get such patients to the intensive care unit for continued resuscitation with products and warming. This technique allows for easy abdominal packing as well. Towel clipping is also useful for patients with pelvic bleeding or other indications for an arteriogram. The disadvantage of the technique is that abdominal fluid may leak from the abdomen and be challenging for nursing. Another potential disadvantage is that it may not open the abdomen enough to prevent ACS. Another technique involves suturing a clear drape or covering to the skin. This drape may be a split open 3-L intravenous bag or a sterile cassette cover (for radiographs) (Figure 28.6). We recommend not suturing the material to the fascia to minimize ischemia and injury to the abdominal fascia.This method can be employed when the abdominal fascia needs to remain open and the patient needs a planned return to the operating room in the next 24 to 48 hours. The advantage of this technique is that it allows for inspection of the abdominal contents and it can be done relatively quickly. The disadvantage is that material needs to be sewn to the skin and fluid may leak around it. This leakage is problematic for fluid balance and can increase skin irritation. Yet another technique involves creating a vacuum covering over the intestines. We simply use a nonadhesive plastic drape (10-10 3M drape) with fenestrations cut in them, two blue towels sandwiched with two large, flat closed-suction drains, and an adhesive bio dressing on top (Figure 28.7). The drains then need to be hooked up to low continuous suction. Concerns with this technique include the application of suction and the risk of fistula caused by an improperly placed nonadhesive drape. Another disadvantage is that the dressing needs to be changed at least every 3 days in the operating room. The advantages of this technique are

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A

B

C

D

E

F

Figure 28.7. (A) Materials needed to create a vacuum dressing (VAD): two JP drains, a 10-10 drape (sterile nonadhesive plastic drape), two sterile blue towels, and adhesive bio-occlusive drape. (B) Fenestrations are cut into the 10-10 drape. (C) The fenestrated 10-10 drape is then place over the bowels and

tucked under the abdomen. (D) This process is then repeated with a blue towel over the 10-10 drape. (E) Two large flat JP drains are placed. (F) A sterile blue towel is then place over the wound and an adhesive dressing is placed. The JP drains are then hooked to low continuous suction.

28. Abdominal Wall

that it is quick and inexpensive, especially by avoiding commercially made products. Fluid management is generally good. The active suction and removal of fluid may allow for possible closure of the fascia. We advocate bringing the patient to the operating room every 3 days to change the dressing, wash out the abdomen, and assess for possible closure. If a feeding tube has not already been placed, it can be at any time pending surgeon preference. Care should be taken to place the feeding tube lateral from the midline to facilitate occlusive vacuum dressing (VAD) changes. At the time of the VAD change we opt to place Vicryl mesh to the fascia if the wound can still not be closed with minimal tension. The last technique involves sewing Vicryl mesh to the fascia. This contains the abdominal organs while relieving the intraabdominal pressure. We recommend using woven Vicryl sewn 360° around the abdominal defect. The sutures should be placed directly to the fascia with healthy bites approximately 1 cm apart. The mesh acts to contain the abdominal contents while holding some of the integrity of the fascia. Over the following days attention should be paid to pulling the fascia back together, which can be done by suturing the center of the mesh together. After the edema has improved, some patients can be brought back to the operating room for formal fascial closure. In the event that the patient needs followup surgery or a second look, the mesh can be cut in the midline, especially if primary closure is still not an option at the time of surgery. After a period of time, usually 2 to 3 weeks, the patient can be returned to the operating room. We have previously demonstrated that the fistula rate is higher in patients who are grafted after 3 weeks.37 At that time the patient should have a healthy bed of granulation under the fascia. The mesh should be removed and the abdomen irrigated gently off and then covered with a split-thickness skin graft. We typically harvest from the anterior thigh and mesh the skin 2 : 1 or 3 : 1 for large defects. Both of the techniques of VAD and utilizing Vicryl mesh have utility and have some success of being able to close the fascia primarily. Unfortunately, a large number of patients will leave with a planned ventral hernia. This can be very large and will likely get larger with time.

The Planned Ventral Hernia As mentioned, planned ventral hernias can be large and can be associated with a hostile abdomen. Additionally, these patients have recovered from a severe illness. The timing of definitive reconstruction needs to be based on these issues. The patient should have had time for convalescence to allow for an increase in endurance, muscle strength, and nutrition. This process for seriously ill patients often takes several months. Furthermore, time is needed for healing within the abdominal cavity and

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for remodeling of scar tissue and adhesions. However, waiting too long is fraught with complications as well. These hernias will enlarge, and often the patient will gain further weight, thus leading to further separation of fascia and loss of abdominal domain. The grafted skin over the abdomen should be soft and separate from the underlying viscera. Our recommendation is to ideally perform the surgery between 6 and 12 months. These defects can be closed with placement of permanent synthetic mesh, placement of a newer biologic mesh, component separation, or a combination of these techniques. Our preference is to do a modified components separation; hernias have been demonstrated to recur in 5% of patients with this technique.37 The technique is described in Figure 28.8. In summary, patients with open abdomens have a high incidence of morbidity and mortality. Recognizing ACS and knowledge of the management options for these patients combined with diligent care can clearly save lives and return people to a normal functional status.

Figure 28.8. Modified components separation technique for abdominal wall reconstruction. The top panel shows the normal anatomy above the arcuate line. The posterior rectus sheath is mobilized from the rectus muscle, and the external oblique fascia is divided. The internal oblique component of the anterior rectus sheath is divided down to the arcuate line. The repair is completed by suturing the medial border of the posterior sheath (B) to the lateral border of the anterior sheath, (B′) with approximation of the medial portion of the anterior sheath (A to A′) in the midline. (Reprinted with permission from Jernigan et al.37 Copyright © Lippincott Williams & Wilkins.)

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Critique The obturator hernia tends to occur in thin, frail elderly women. The preoperative diagnosis is usually an intestinal obstruction of unknown origin. The obturator foramen is the largest foramen in the body. It is formed by the ischial and pubic rami. The foramen is located in the anterolateral pelvic wall. With the exception of a small area, it is closed by the obturator membrane. The obturator canal, a 3-cm tunnel, begins in the pelvis at the defect in the obturator membrane. It passes obliquely downward and ends in the obturator region of the thigh. Usually, preperitoneal connective tissue and fat enters the pelvic orifice of the obturator canal—the prehernia stage. The final stage occurs when there is entrance of an organ, usually the ileum. Pain extending down the inner surface of the thigh to the knee is not uncommon. This pain is often relieved by flexion of the ipsilateral thigh (HowshipRomberg sign). For acute care intervention, a midline vertical abdominal incision is usually the approach made for definitive management. Answer (E)

References 1. Baguley PE, de Gara CJ, Gagic N. Open cholecystectomy: muscle splitting versus muscle dividing incision: a randomized study. J R Coll Surg Edinb 1995; 40(4):230–232. 2. Graff LGT, Robinson D. Abdominal pain and emergency department evaluation. Emerg Med Clin North Am 2001; 19(1):123–136. 3. Cordell WH, et al. The high prevalence of pain in emergency medical care. Am J Emerg Med 2002; 20(3):16165–9. 4. Kulah B, et al. Emergency hernia repairs in elderly patients. Am J Surg 2001; 182(5):455–459. 5. Primatesta P, Goldacre MJ. Inguinal hernia repair: incidence of elective and emergency surgery, readmission and mortality. Int J Epidemiol 1996; 25(4):835–839. 6. Fruchaud H. Le Traitement Chirurgical des Hernies de L’Aine Chez L’Adulte. 1956. 7. Richards SK, Vipond MN, Earnshaw JJ. Review of the management of recurrent inguinal hernia. Hernia 2004; 8(2):144–148. 8. Arenal JJ, et al. Hernias of the abdominal wall in patients over the age of 70 years. Eur J Surg 2002; 168(8/9):460–463. 9. Alvarez C. Open mesh versus laparoscopic mesh hernia repair. N Engl J Med 2004; 351(14):1463–1465. 10. Alvarez Perez JA, et al. Emergency hernia repairs in elderly patients. Int Surg 2003; 88(4):231–237. 11. Neumayer L, et al. Open mesh versus laparoscopic mesh repair of inguinal hernia. N Engl J Med 2004; 350(18):1819– 1827.

12. Kurt N, et al. Risk and outcome of bowel resection in patients with incarcerated groin hernias: retrospective study. World J Surg 2003; 27(6):741–743. 13. Arroyo A, et al. Randomized clinical trial comparing suture and mesh repair of umbilical hernia in adults. Br J Surg 2001; 88(10):1321–1323. 14. Buinewicz B, Rosen B. Acellular cadaveric dermis (AlloDerm): a new alternative for abdominal hernia repair. Ann Plast Surg 2004; 52(2):188–194. 15. Hirsch EF. Repair of an abdominal wall defect after a salvage laparotomy for sepsis. J Am Coll Surg 2004; 198(2): 324–328. 16. Mingoli A, et al. Incidence of incisional hernia following emergency abdominal surgery. Ital J Gastroenterol Hepatol 1999; 31(6):449–453. 17. Leslie D. The parastomal hernia. Surg Clin North Am 1984; 64(2):407–415. 18. Sugarbaker PH. Prosthetic mesh repair of large hernias at the site of colonic stomas. Surg Gynecol Obstet 1980; 150(4):576–578. 19. Wotherspoon S, Chu K, Brown AF. Abdominal injury and the seat-belt sign. Emerg Med (Fremantle) 2001; 13(1):61– 65. 20. Ramirez MM, Burkhead JM 3rd, Turrentine MA. Spontaneous rectus sheath hematoma during pregnancy mimicking abruptio placenta. Am J Perinatol 1997; 14(6):321–323. 21. Klingler PJ, et al. Rectus sheath hematoma clinically masquerading as sigmoid diverticulitis. Am J Gastroenterol 2000; 95(2):555–556. 22. Lohle PN, et al. Nonpalpable rectus sheath hematoma clinically masquerading as appendicitis: US and CT diagnosis. Abdom Imaging 1995; 20(2):152–154. 23. Bober SE, et al. Rectus sheath hematoma simulating appendiceal abscess. J Ultrasound Med 1992; 11(4):179– 180. 24. Cervantes J, et al. Ultrasound diagnosis of rectus sheath hematoma. Am Surg 1983; 49(10):542–545. 25. Klingler PJ, et al. The use of ultrasound to differentiate rectus sheath hematoma from other acute abdominal disorders. Surg Endosc 1999; 13(11):1129–1134. 26. Berna JD, et al. Rectus sheath hematoma: diagnostic classification by CT. Abdom Imaging 1996; 21(1):62–64. 27. Ducatman BS, Ludwig J, Hurt RD. Fatal rectus sheath hematoma. JAMA 1983; 249(7):924–925. 28. Kron IL, Harman PK, Nolan SP. The measurement of intra-abdominal pressure as a criterion for abdominal reexploration. Ann Surg 1984; 199(1):28–30. 29. Doty JM, et al, Effects of increased renal parenchymal pressure on renal function. J Trauma Inj Infect Crit Care 2000; 48(5):874–877. 30. Balogh Z, et al. Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma Inj Infect Crit Care 2003; 54(5):848–861. 31. Mangram AJ, et al. Guideline for prevention of surgical site infection, 1999. Hospital Infection Control Practices Advisory Committee. Infect Control Hosp Epidemiol 1999; 20(4):250–280. 32. Culver DH, et al. Surgical wound infection rates by wound class, operative procedure, and patient risk index. National

28. Abdominal Wall Nosocomial Infections Surveillance System. Am J Med 1991; 91(3B):152S–157S. 33. Balogh Z, et al. Supranormal trauma resuscitation causes more cases of abdominal compartment syndrome. Arch Surg 2003; 138(6):637–643. 34. Ivatury RR, et al. Intra-abdominal hypertension after lifethreatening penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal compartment syndrome. J Trauma Inj Infect Crit Care 1998; 44(6):1016–1023.

449 35. McNelis J, Marini CP, Simms HH. Abdominal compartment syndrome: clinical manifestations and predictive factors. Curr Opin Crit Care 2003; 9(2):133–136. 36. Raeburn CD, et al. The abdominal compartment syndrome is a morbid complication of postinjury damage control surgery. Am J Surg 2001; 182(6):542–546. 37. Jernigan TW, et al. Staged management of giant abdominal wall defects: acute and long-term results. Ann Surg 2003; 238(3):349–357.

29 Foregut Philip E. Donahue

Case Scenario A 45-year-old international business man is taken emergently to the operating room because of an acute abdomen and demonstration of free air under the diaphragm on chest x-ray. Surgical exploration reveals a perforated proximal body gastric ulcer. This patient has had no history of peptic ulcer disease and has been, essentially, free of health-related problems. Which of the following should be the operative plan of choice? (A) (B) (C) (D) (E)

Truncal vagotomy and pyloroplasty Truncal vagotomy and antrectomy Highly selective vagotomy Omental buttress repair (Graham patch) Subtotal gastrectomy

Urgent and emergent foregut problems pose unique challenges for patients, physicians, and surgeons in every community on a daily basis. As portrayed on weekly television, the action-hero doctors and nurses become larger than life in their assumed roles, combining accurate diagnosis with an efficient remedy or operation, all packaged into 60 minutes of advertisements and intense activity. Television outcomes, of course, are usually very, very palatable and acceptable to all participants, in contrast to real-life situations where many things are unclear and many outcomes less than perfect. In the real world of surgical practice, everyone’s complaints must be evaluated cautiously while initiating stabilization and treatment maneuvers. The initial responders and emergency facility staff, most of whom are nonsurgeons, must make sophisticated judgments about the type of problem as well as the focus and sequence of investigations; surgeons, by virtue of training and experience, are expected to have an answer to the following questions: Does this problem, with or

450

without a diagnosis, require surgical intervention? Which operation should be performed? What will happen after the operation? Emergency room personnel and surgeons evaluate and treat urgent and emergent conditions; their decisions are made in prospect, with incomplete datasets, attempting to achieve the best possible outcomes with patients presenting in whatever condition exists. This chapter is dedicated to these heroes of the sick and needy. The physician, the ultimate historian, provides insights that make an individual patient’s complaints understandable (whether in prospect or retrospect).1 This chapter’s goal is to assist focused investigation and interventions for diseases affecting the hollow organs just above or beneath the diaphragm, collectively referred to as the “foregut.” As there is no consensus about the “best” and most cost-effective approach to testing for many of these conditions, the views expressed are quite subjective, reflecting the view of an experienced surgeon with a lifetime of direct experience with the worst of these conditions. Experience suggests that failure to intervene often leads to death, whereas an urgent intervention can sustain life and function. The surgeon, by virtue of his or her knowledge of the natural history of disease entities, is expected to recommend the most appropriate intervention in an individual circumstance. Furthermore, in dire circumstances, the general surgeon is the only one who can best estimate the overall risks and benefits of aggressive interventions. If the material in this chapter is helpful to either patients or treating physicians, then a useful purpose will have been served in its preparation. This has been my hope in preparing this chapter.

Foregut Symptoms The foregut structures have a limited capacity for demonstrating that they are not well and few ways of showing their loss of normal function. Stimuli from an individual

29. Foregut

visceral structure (e.g., stomach) travel to and are interpreted by the brain, a remote central processing unit (CPU) that interprets stimuli with reference to previous life events as it determines the relevance of the current condition. Because most of us have limited experience with serious emergencies, our CPU often cannot identify the source or magnitude of the problem. The general symptoms of nausea, vomiting, pain, and discomfort in the abdomen are typical complaints caused by increased pressure within hollow organs; these symptoms are mediated through a combination of afferent vagus nerve pathways that traverse the brain stem nuclei and nerve impulses from the thoracolumbar autonomic nervous system. When bleeding, obstruction, or perforation is present, any observer can recognize the need for immediate attention. Other foregut symptoms are unpredictable and nonspecific, leading experienced examiners to avoid conclusions about the etiology or prognosis of specific events until all possible information is available. The overlapping patterns of signs and symptoms are completely consistent with the innervation of these organs, whose central connections are clustered within a few millimeters of the brain stem.2,3

Esophagus, Esophagogastric Junction, Stomach, Duodenum The swallowing tube is the site of intense activity during a 24-hour cycle of activities, conducting saliva and swallowed materials through its 10-inch length. Although many of the problems that present for evaluation seem to be acute, the retrospective analysis often suggests otherwise because patients do not present themselves (as a rule) for the evaluation of possible problems or vague symptoms and because some symptoms, such as those associated with obstruction, may not become apparent until the process is quite advanced. Urgent signs or symptoms, therefore, often indicate an advanced state in the natural history of the disease process.4,5 Overt signs and symptoms of esophageal disease may include pain, odynophagia (painful swallowing), dysphagia, and drooling and are readily linked to the swallowing tube. Similarly, prompt regurgitation of swallowed food or liquid has an obvious relation to an abnormality in the swallowing process. In contrast, more subtle symptoms such as solid food intolerance, altered sleeping position, or retrosternal discomfort may occur as a result of many possible disorders, several of which will be investigated before inflammation, ulceration, or obstruction of the esophagus comes to the fore in the differential diagnosis. Often, the physician as well as the patient is so relieved that cardiac disease appears unlikely that the investigation of other possible causes is postponed indefinitely. As

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it happens, that may be a big mistake, which is often abundantly clear in retrospect.

Evaluation The initial evaluation and sequence of testing are determined by the particular complaints and condition of the patient. For example, if dysphagia includes symptoms such as choking and immediate return of swallowed material, an oropharyngeal lesion may be responsible, as opposed to dysphagia with substernal or subxiphoid discomfort, which is more typical of distal esophageal problems such as gastroesophageal reflux.4 In contrast to obstructive lesions, which often have characteristic features, the source of perforation or bleeding is usually not apparent before the initiation of treatment. When bleeding or perforation is suspected, the acute physiologic response can be dramatic, and supportive measures are initiated before the diagnostic process begins.6,7 Proximal esophageal lesions, including cricopharyngeal achalasia and ingested foreign bodies, cause difficulty swallowing immediately, with prompt choking and/or regurgitation. Distal esophageal conditions, including tumors, diverticula, and esophageal achalasia, cause dysphagia within minutes of swallowing, with or without regurgitation. Regurgitation, the aborad transit of swallowed esophageal content, is characterized by bland taste and substantial saliva admixture and occurs at unpredictable intervals after swallowing. If the normal esophagus is acutely occluded, a relatively small volume (50 to 100 cc) will cause immediate regurgitation promptly after swallowing; a distended esophagus, in contrast, may contain several hundred cc of semisolid content, without a definite pattern of regurgitation after ingestion of food or liquid. Any patient with dilated esophagus is prone to regurgitate from time to time, because any abrupt change in intrathoracic pressure results in a similar change in intraluminal content. Weight loss in conjunction with complaints of regurgitation reinforces the serious nature of the complaint, is not an early symptom as a rule, and does not of itself predict whether the underlying cause is malignant or benign. Chest pain, when present, is categorized according to its nature as sharp, dull, heavy, crushing, or burning; because of the possible causes, chest pain demands cautious evaluation. Some descriptions of chest pain are incredibly unique, depending on the individual’s command of language and expression. Pains that radiate to the neck, jaw, or left arm may be angina pectoris; those that are aggravated by deep breath may be due to the pleural inflammation associated with pneumonia or to perioperative inflammation in postoperative patients.

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Unfortunately for the patient, all of these may be caused by esophageal perforation as well; elimination of the first three possibilities, or wrongful interpretation of the source of pleural effusion, may have fatal consequences if an esophageal perforation is present.8 Burning pain with or without accompanying regurgitation is suggestive of gastroesophageal reflux (GER); when this symptom is relieved by antisecretory medications, an inferential diagnosis of GER is suggested. Pain that is sharp, radiating to the back, or with a marked crescendo–decrescendo pattern is not typical of GER, suggesting increased pressure within a hollow viscus. When chest pains or discomfort are caused by GER, the term “atypical” reflux is used to highlight this etiologic mechanism for a problem that is quite severe at times, mimicking acute coronary occlusion. Another variety of pain may be caused by trapped gas and liquid content in an incarcerated segment and is relieved by spontaneous (or induced) vomiting or by gastric intubation; if accompanied by symptoms of GER, the diagnosis of paraesophageal hernia or gastric volvulus is suggested. Severe and unrelenting pain, especially back pain, is a serious concern that demands investigation. Just as constant headache demands a computed tomography (CT) scan of the head, continuous and severe back pain demands a CT scan to rule out aortic aneurysm, dissection, or perforation. Previous operations such as fundoplication may cause deep subxiphoid pain as well as shoulder pain presumably due to the stout sutures placed in the diaphragm for repair of the hiatus hernia.Although the foregoing statements are true, the observer relies on the combination of prior experience and instinct in evaluating the causality; the choice of observation, invasive testing, or intervention is a matter of judgment, and the consequences of missed perforation can be catastrophic.9,10 Because the foregut is composed of hollow organs with an inner mucosa and outer muscular layers, the diseases that occur are limited to a relatively small group of signs and symptoms related to erosion or inflammation of the lining mucosa, increased intraluminal pressure, or obstruction of aborad flow of intestinal contents. Tables 29.1 through 29.4 highlight the classes of disease that affect the foregut organs, arranged according to the presenting symptom. The illustrations of the surgical procedures were chosen to illustrate the breadth of surgical techniques employed to treat these foregut diseases. Although more complete and comprehensive illustrations can be found in specialty textbooks of surgery, there is a new alternative for viewing images of these surgical conditions: web-based search engines such as Google Image and Web-Medicine for immediate access to images for each condition. The world of medical education continues to show dramatic change.

P.E. Donahue

Obstruction Obstruction of the swallowing tube is a result of inflammatory, neoplastic, degenerative, and acquired conditions (Table 29.1). Whatever the cause, whether a foreign body, inflammatory stricture, mucosal outpouching, or neoplastic growth, the patient requires prompt attention because dehydration, pulmonary aspiration, or other consequences will undoubtedly follow. When a foreign body such as a piece of meat is responsible, the condition is both obvious and identifiable as acutely related to swallowed material; a synonym of this condition (“steakhouse syndrome”) is both accurate and descriptive. If the patient is a child, there may be other dramatic overtones related to the terror and uncertainty that accompany difficulty swallowing, with intermittent choking and gasping for breath. At times, the onset of obstruction creeps to “center stage” inapparently, because symptoms do not occur until 90% of the esophageal lumen is blocked. Whatever the cause, esophageal obstruction from intrinsic or extrinsic disease is a serious problem that requires prompt evaluation and treatment. The source of the pain is always at the heart of the interaction with the patient, and this is quite true of the patient with an obstruction of the esophagus. At the

Table 29.1. Causes of foregut obstruction. Intrinsic disease, congenital or acquired Achalasia Pylorospasm Antral web Annular pancreas Benign and malignant tumors Leiomyoma Gastrointestinal stromal tumor Duplication cyst

Types II and III hiatus hernia Gastric volvulus Diverticulum Epiphrenic Intraluminal (duodenal)

Carcinoma Squamous cell (esophagus) Adenocarcinoma (cardia, stomach, duodenum) Peptic ulcer/stricture Gastroesophageal junction Gastric outlet Blunt trauma Intramural hematoma of duodenum

Extrinsic disease Bone diseases Osteophyte Disk space abscess Foreign body Peach pits (esophagus) Dentures Toys, coins Swallowed meat, hair, vegetables Bezoar, trichobezoar, phytobezoar Pericardial cyst Vascular lesions Dissecting aneurysm Aortic aneurysm Mesenteric artery syndrome Pancreatic disease Pseudocyst Abscess Annular pancreas

29. Foregut

beginning of the interaction, there is no guarantee that the complaint is due to an esophageal source, and the practitioner must always consider the heart and major vessels as possible sources of the problem; for this reason every patient requires a complete physical examination, with special attention to the cardiovascular and pulmonary systems.A rapid pulse, abnormal pulse amplitude in upper extremities, enlarged heart, or other abnormalities should be sought and may have a direct bearing on the final diagnosis. For most adults an electrocardiogram (ECG) and chest x-ray are the first studies performed, and these studies provide extremely useful information for the practitioner. If the ECG does not reveal an acute myocardial problem (ST-T segment changes typical of severe ischemia, acute myocardial infarction, or unusual findings such as peaked T waves, which require immediate attention), the source of the pain can be sought beginning with an oral contrast examination. The findings may include complete obstruction without passage of contrast and prompt regurgitation of swallowed material; this is typical of a high obstruction at the level of the cricopharyngeus muscle. Other findings include restricted passage of contrast with deformity of the esophageal wall or distortion of the normal contour of the esophagus by a mass such as a tumor, enlarged lymph node, or extrinsic mass. The x-ray findings will determine the next step in diagnosis, with specific approaches chosen on an ad hoc basis.11,12

Differential Diagnosis Swallowed objects are the most commonly encountered obstructions, including pieces of meat, toys, dentures, and fruits. The patient complains of dysphagia, drooling, and inability to swallow and usually relates a gradual progression of symptoms. The progression from first symptoms to near-complete obstruction may be relatively short, whereas the natural history of the lesion, which includes the asymptomatic period, is much longer. The severity of the complaint can be assessed directly by evaluating the response to questions about weight loss, presence and frequency of regurgitation, and other symptoms such as choking, coughing, and episodes of aspiration. The patient with drooling (difficulty tolerating saliva) or who cannot tolerate liquids has a high-grade obstruction and requires urgent evaluation. Although underlying intrinsic diseases such as stricture, carcinoma, anatomic abnormalities (whether congenital or acquired) may ultimately be responsible for the patient’s condition, foodstuffs that become impacted in a narrowed swallowing tube are often the cause of an immediate and dramatic increase in the patient’s degree of discomfort and distress. Needless to say, investigation of the difficulty must proceed without delay.6,13–15 The spectrum of possible findings and sometimes bizarre situations that physi-

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cians, radiologists, endoscopists, and surgeons encounter is limitless and truly amazing.

Physical Examination When obstruction is suspected, the clinician will examine the head and neck for obvious abnormalities, especially edema, enlarged lymph nodes, or signs of distended neck veins. The status of the esophageal lumen can be evaluated only indirectly by physical examination (auscultation), and other diagnostic tests such as x-rays and endoscopic examinations are usually required to achieve a diagnosis. Auscultation of a normal swallowing “gurgle” in the subxiphoid location can occasionally avoid a hurried transfer to a diagnostic facility for a patient who claims to be in terrible straits, because a typical sound in the subxiphoid space 12 to 15 seconds after swallowing virtually excludes severe obstruction, favoring hysteria or emotional distress as the explanation for the symptoms. Most patients will require a more sensitive study, such as barium meal or endoscopic examination with biopsy, to reach a diagnosis, and either can be performed with a reasonable expectation of success in diagnosis. The choice of diagnostic procedure is purely a matter of judgment and resource availability.16

Endoscopic Examinations Flexible endoscopic examination allows simultaneous diagnosis and treatment and is an ideal approach for acutely symptomatic patients who have just eaten a meal. Often the limiting factor in performing endoscopy is the ability of the patient to relax and cooperate; for most adults conscious sedation will suffice for the performance of the procedure, whereas for infants a general anesthetic may be necessary. The endoscopic appearance of foreign bodies is usually readily apparent to a trained endoscopist, and there are several ways of dealing with specific items. A piece of meat or steak impacted at the gastroesophageal junction can be fragmented piecemeal or sometimes pushed into the gastric cavity; dentures, sharp objects, coins, and thermometers are removed with the assistance of overtubes, pouches, or other devices as the situation demands. Sharp objects pose particular problems when they have eroded into contiguous structures, and a sharp piece of metal impinging on a large vascular structure in the thorax can pose serious potential problems. Surgical procedures, however, are employed only for those patients with a specific remediable problem and are not indicated in all cases. That having been said, it is not at all rare for an experienced surgeon to decide that acute care surgical intervention is necessary if specific indicators are present; nonsurgeons sometimes misinterpret the definitive approach of experience and judgment for

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hyperaggressive treatment, which does not allow time for conservative measures. In this modern world of practice, all possible issues must be addressed, and all possible participants in decisions must be kept informed as to the why and how of decision making. Because serious medical and surgical problems usually have a definite risk of death and disability, none of us takes these matters lightly; however, we are surgeons, and we are the ones who know that even radical procedures can be done with a reasonable expectation of a good outcome.17 Often, the best outcome is available only to the patient operated before developing complications related to hospital care. The endoscopist often discovers unusual pathology that has been surprisingly silent before the current disease episode, including far advanced benign or malignant conditions such as advanced adenocarcinoma. A near-complete obstruction, interestingly, does not imply the presence of cancer; for example, if the stomach can be entered with only mild to moderate resistance, achalasia of the esophagus might be present and can be confirmed by postoperative esophageal manometry. If the stomach cannot be entered with the endoscope, the next step will be performance of a contrast study (esophagram) as well as a CT scan; occasionally, a distended stomach that cannot be entered via endoscopic routes must be decompressed by other means.12 As shown in Table 29.1, there are several possible findings, ranging from foreign body (dentures, foodstuffs, bezoars) to far-advanced malignancy, whether the lumen being visualized is in the esophagus, stomach, or duodenum.As a rule, a specific therapeutic maneuver is not performed at the initial endoscopic procedure unless there is additional information available to the endoscopist; for example, for a patient with previously diagnosed esophageal cancer, the endoscopist might insert a stent to facilitate swallowing. Alternatively, if the patient has had previous treatment for ulcer disease, and narrowing of the gastric outlet is observed, balloon dilation of the pyloric channel might be performed. Endoscopic techniques are very attractive and have profound utility for specific patients and compare favorably with traditional surgical approaches in some cases. When endoscopy reveals a tapering stricture without mucosal deformity, inflammation, or obvious tumor, the stomach either can or cannot be intubated and the undersurface of the stricture examined. Is this typical achalasia, pseudoachalasia, stricture, or incarcerated paraesophageal hernia (type I or type II)? The endoscopist will perform biopsies of the mucosa in or near the strictured or narrowed segment. The esophagram may show a “bird’s beak” deformity, suggestive of achalasia of the esophagus, whereas the CAT scan will demonstrate enlarged periesophageal lymph nodes if present, with or without massive deformity of the wall of the esophagus or stomach, or a mass lesion involving the retroperitoneal

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aorta and diaphragm. These typical findings of advanced carcinoma do not change the need for an intervention but must be considered in the construction of a treatment plan; at all times, keep the patient’s family informed of the possible outcomes.

Radiographic Studies Many patients present via the emergency room and often have x-rays performed as part of the initial examination. When an obstruction is present, there are a number of possible findings, depending on the site of the obstruction, including air–fluid levels in the chest, mediastinum, or abdomen, or other abnormalities such as absence of the usual air–fluid level beneath the diaphragm. Other possible x-ray findings are case specific, for example a retroanastomotic (Peterson) hernia causing gaseous distention of the afferent limb following Billroth II gastrectomy, can be evaluated on an ad hoc basis by the surgeon. Similarly, other CT scan findings can trigger additional diagnostic steps on the one hand or obviate further procrastination in others.18 Compared with the uncertainties and deliberations of the preoperative period, including the agonizing uncertainties attendant to decisions to proceed with surgery, the conduct of the surgical procedure is relatively uncomplicated.The incision is selected with respect to the target organ and the anticipated operation.

Diverticula Hypopharyngeal Diverticulum (Zenker’s Diverticulum) The outpouching of mucosa occurs through a potential weak spot in the posterior wall of the hypopharynx as a result of poorly coordinated swallowing between the hypopharynx and the cricopharyngeus muscle. The true incidence of hypopharyngeal diverticula is unknown, but they can become quite large without causing symptoms. The corrective procedure is most often performed via an anterior neck incision parallel to the anterior border of the left sternocleidomastoid muscle; if the diverticulum presents on the right side, a right-sided incision is made along the sternocleidomastoid muscle. The surgical procedure must include myotomy of the cricopharyngeus muscle, because the clinical syndrome is caused by dysfunction (relaxation abnormality) of this muscle; the diverticulum itself is either ignored (when very small, ∼1 to 2 cm in greatest dimension), inverted and suspended from the anterior cervical fascia (moderate sized, ∼2 to 4 cm), or excised (large, >4 cm in greatest dimension). Myotomy is performed in a similar fashion as myotomies elsewhere, as described (vide infra) regarding achalasia of the esophagus.

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Epiphrenic Diverticulum Epiphrenic diverticula occasionally present with complete obstruction of the esophagus, and operation is performed in an urgent fashion. More often, the presenting complaints are less dramatic, consisting of dysphagia, weight loss, or regurgitation. For at least 50 years, surgeons have recognized that diverticula can develop as a consequence of motility disorders (viz., achalasia and others) and that the myotomy distal to the neck of the diverticulum is at least as important as treatment of the diverticulum itself. The approach to the diverticulum is dictated by the experience and judgment of the surgeon; 10 years ago most surgeons utilized a thoracotomy performed via the seventh or eighth left interspace. Presently, the success of transabdominal laparoscopic diverticulectomy and myotomy has become apparent, and this approach will eventually be practiced in most cases. In contrast to the hypopharyngeal diverticula, sac excision is necessary in all cases; surgical staplers are extremely useful in the mediastinum with either a transthoracic or transabdominal approach. Intraoperative endoscopy is occasionally very useful for determining the precise location of the neck of the diverticulum and to verify that sufficient dissection has been performed. The dissection of the diverticulum aims to allow division of the neck of the diverticulum without any narrowing of the esophageal lumen; stapling devices can be applied with a large bougie within the esophagus (50 F–tapered tip) to avoid constriction of the lumen. The same bougie can be used to distend the lumen of the esophagus during myotomy.

Intraluminal Duodenal Diverticulum (Recanalization Failure in the Duodenum) Intraluminal duodenal diverticula can be observed in infants, children, or adults and occur in the juxtaampullary duodenum. Diagnosis is the major hurdle for this condition, and surgical removal of the diverticulum is the appropriate treatment. Whether an endoscopic, laparoscopic transabdominal approach, or traditional open surgical procedure is chosen, the end result will be satisfactory as long as duodenal narrowing is not created and the biliary and pancreatic ducts traversing ampulla of Vater are not injured. In such cases, a catheter placed into the gallbladder for pre- and postexcision cholangiograms can provide immediate confirmation regarding the presence or absence of unimpeded flow of contrast through the ampulla and into the duodenal lumen.

Achalasia of the Esophagus The diagnosis of achalasia is usually but not always well established when the patient comes to the attention of the surgeon. Younger patients are sometimes not recog-

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nized for years because the esophagram may not be typical of achalasia or because the physician in charge does not think of performing a simple esophageal motility test. Occasionally a motility examination cannot be completed, and the surgeon must operate on the patient without a preoperative motility test; in such cases the typical history, x-ray, or combination of circumstances suffice to justify the performance of an operation. Of course, patient and family (as well as the medical chart) must have been informed and the reasons for performing an operation without a complete workup documented. Most surgeons utilize the transabdominal approach for myotomy. The abdominal approach allows extension of the myotomy onto the anterior wall of the stomach for 1.5 to 2.0 cm; this approach results in a more effective myotomy, because some of the gastric muscle (gastric sling fibers) are affected similarly as the lower esophageal sphincter muscles in achalasia. In addition, most surgeons perform a limited antireflux operation after a complete esophageal myotomy to mitigate the symptomatic effects of gastroesophageal reflux should it occur postoperatively.19,20 The myotomy is performed with a hook cautery device, cold knife, or other means such as bipolar shears or harmonic scalpel. The aim is to divide the various muscle layers that prevent the passing of esophageal contents toward the stomach. After first gaining access to the submucosa, the surgeon patiently dissects the muscles away from the submucosa, attempting to avoid entering the lumen of the esophagus. If mucosal perforation does occur, it is important that it be recognized at the time, because repair can be conveniently performed without side effects; unrecognized perforation, on the other hand, can lead to mediastinitis or peritonitis with its attendant serious risks (Figures 29.1 through 29.3).21

Hiatus Hernia Large hiatus hernias can obstruct the esophagus and/or stomach at times, especially when portions of the stomach have herniated through the esophageal hiatus to reside in the mediastinum. The type II and type III hiatus hernia can be complicated by incarceration and strangulation of the stomach, although the precise incidence of this complication is not known and a subject of debate. Often the initial problem noted is an abnormal air–fluid level on a chest x-ray, a finding that leads quickly to other diagnostic tests or to urgent surgery depending on the condition of the patient. If the patient is asymptomatic, then an endoscopic examination might provide definitive evidence of the presence of the hernia by demonstrating the orifice of the herniated portion of stomach adjacent to the esophagogastric junction. Usually the location of the diaphragm and the diaphragmatic hiatus can be established during endoscopy, and any rugal folds extending

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Transdiaphragmatic Approach to the Distal Esophagus The division of the diaphragm from the hiatus toward the xiphoid process, popularized by Pinotti et al., has simplified the exploration of the lower mediastinum at open surgery. Entry into the mediastinum along the right or left crus is often a gateway to the mediastinal esophagus during reoperative surgery that can help avoid injury to the esophageal wall and allow direct visualization of the esophagus above the points of fixation from previous operations. Laparoscopic surgeons have demonstrated the feasibility of the transabdominal approach and have reported success in well over 90% of the cases. There is still no consensus about the incidence of “short” esophagus and, by extension, the need for esophageal lengthening procedures. Also, there is debate about the necessity of a routine antireflux operation and the role of prosthetic mesh for reinforcement of the hiatus repair or bridging

Figure 29.1. Modified Heller myotomy. The esophagocardiomyotomy extends for 6 cm on the esophagus and 1–2 cm on the cardia of the stomach, including the sling fibers of the proximal stomach. The proximal extent of the myotomy is several centimeters above the crural sling of the esophageal hiatus. (Reprinted from Donahue PE, Horgan S, Liu Katherine J-M, Madura JA, Floppy Dor fundoplication after esophagocardiomyotomy for achalasia. Surgery 2002; 132:712–723, with permission from Elsevier.)

above the diaphragm are evidence of a paraesophageal hernia. Although large hernias are very obvious, it is sometimes difficult to identify small hernias endoscopically. Esophageal motility studies and prolonged esophageal pH monitoring are not routinely necessary because they are unreliable when the stomach is displaced into the thorax. The basic principles of operative technique are hernia sac excision, reduction of the incarcerated organs, and repair of the diaphragmatic defect.22

Minimally Invasive Surgery The initial surgical approach for all hiatus hernias is by minimally invasive means when possible. Surgeons have debated the merits of transthoracic versus transabdominal surgical approaches for years, but most modern surgeons prefer the transabdominal route, which provides better exposure and allows a more precise reduction of the hernia and repair of the esophageal hiatus.

Figure 29.2. Fixation of Dor fundopexy. The gastric fundus is folded over the site of the myotomy and anchored to the right and left crus and to the edges of the myotomy at fixation points (numbers 1–6). (Reprinted from Donahue PE, Horgan S, Liu Katherine J-M, Madura JA, Floppy Dor fundoplication after esophagocardiomyotomy for achalasia. Surgery 2002; 132:712–723, with permission from Elsevier.)

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is employed if the esophagus is so short that it still resides intrathoracically despite wide mobilization and can be performed by either approach. There are several technical ways of creating the Collis gastroplasty, including ingenious combinations of stapling devices such as a transgastric end-to-end anastomosis followed by a GIA stapler placed parallel to the lesser curve, intersecting the anastomosis donut hole to create a “neoesophagus.” These have been supplanted by the simpler wedge resection of the gastric fundus followed by placation of residual stomach, performed with intraluminal bougie via laparoscopy.24 Esophageal shortening is rarely encountered, partially because of the use of more effective antacid medications that avoid or reduce the incidence of transmural inflammation leading to stricture and shortening; in our clinic in Chicago the need for esophageal lengthening is unusual, perhaps because we have learned that the issue of shortening cannot be assessed until mediastinal dissection and sac reduction from mediastinum has been completed.

The Role of Fundoplication

Figure 29.3. Completed Dor fundoplication. The fundus is sutured to the arch of the esophageal hiatus to prevent later herniation of the fundus into the thorax. (Reprinted from Donahue PE, Horgan S, Liu Katherine J-M, Madura JA, Floppy Dor fundoplication after esophagocardiomyotomy for achalasia. Surgery 2002; 132:712–723, with permission from Elsevier.)

of diaphragmatic defects. Since most hiatus hernias can be repaired without mesh, and, because there are occasional complications caused by mesh erosion or infection, experienced surgeons utilize mesh selectively.23,24

Transthoracic Versus Transabdominal Approach Surgeons have usually debated the relative merits of transthoracic versus transabdominal surgical approaches from the biased approach of their trade guild, with thoracic surgeons favoring the former and general surgeons reporting success with the latter. Lately, the availability of the laparoscopic tools has made this discussion moot, because almost all surgeons employ the laparoscopic approach. The transabdominal approach allows more precise reduction of the stomach and more accurate reconstruction of the esophageal hiatus; the transthoracic approach does allow complete esophageal mobilization and removal of the hernia sac but sacrifices the precise reconstruction of the hiatus. Gastroplasty, a technique for allowing fundoplication to reside beneath the diaphragm,

The role of routine fundoplication after reduction of paraesophageal hernia remains controversial. Most patients with paraesophageal hiatal hernias do not have reflux symptoms preoperatively; furthermore, patients repaired with reduction of the hernia, sac excision, and reconstruction of the esophageal hiatus do not have gastroesophageal reflux postoperatively, as a rule. On the other hand, because patients with the esophagus trapped above the diaphragm will have abnormal pH studies, younger surgeons are apt to recommend fundoplication as a routine maneuver; in addition, partial or total fundoplication may reduce the chance of postoperative recurrence of hernia. Whether routine use of mesh reinforcement of the esophageal hiatus repair is indicated remains controversial; with or without reinforcement, some of the repairs will recur, and, depending on the method of categorizing severity or extent of recurrence, the incidence of recurrence may be quite high.

Peptic Stricture of the Esophagus Esophageal strictures are most often caused by gastroesophageal reflux disease (GERD) and are often symptomatic only in reference to the reflux component. The patient often compensates for the presence of stricture by avoiding those foods that characteristically cause a swallowing problem. The incidence of dense stricture at the gastroesophageal junction has diminished dramatically in the 25 years following the introduction of the first effective histamine receptor antagonists (H2RBs) and proton pump inhibiting agents (PPIs). Because the

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aggressive effects of acid and pepsin on the gut mucosa have been greatly ameliorated by effective treatments, the complication of stricture is seen only when a patient cannot take medicine for one of several reasons or when the patient has surfaced from an underserved medical area where drugs were unavailable. Optimal treatment of peptic stenosis is debated by physicians and surgeons. Surgeons know that fundoplication performed before stricture formation has better results and that long-standing inflammation can lead to failure of esophageal propulsion (motor failure) and the need for esophageal resection.

Nissen Fundoplication The completed wrap must be at least 1.0 cm long, and at least two sutures (2–0 silk or nylon) are required. Sutures include the anterior and posterior shoulders of the fundic wrap, resulting in a 360° wrapping of the distal esophagus; an intraluminal bougie (50 to 60 F) is placed to prevent a too-tight fundoplication as we described 28 years ago.25 Fundoplication works to prevent reflux by the mass effect of the plicated fundus, as opposed to active squeezing or augmentation of the lower esophageal sphincter. To achieve a tension-free (floppy) fundoplication in Chicago, furthermore, it is often necessary to divide the short gastric vessels.

Closure of Esophageal Hiatus Permanent sutures (2–0 silk or nylon) are used for hiatus closure. Figures-of-eight or Teflon-pledgeted sutures are often used, with or without mesh reinforcement according to the surgeon’s preference.23

Obstructing Mass Lesions: Esophagus, Stomach, and Duodenum In the presence of Foregut obstruction the timing and specific nature of the intervention are always a matter of judgment which depends upon a host of specific factors. The patient’s condition and comorbidities, as well as the availability of specific diagnostic and therapeutic alternatives, are among the important considerations. Most of the benign conditions that afflict patients can be dealt with effectively at the first operation; when a malignant lesion has been identified, the usual goal of complete excision and reconstruction may be modified according to individual circumstances, including the site, size, and extent of the primary lesion. For bulky tumors at the gastroesophageal junction or the body of the stomach, the resection is sometimes postponed until neoadjuvant therapy can be performed, because dramatic changes in the extent of tumor are sometimes observed.26 At present, the first operation performed might be incisional

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biopsy of the mass followed by a feeding jejunostomy, providing an avenue for nutritional support until the most appropriate treatment can be chosen. There is still a role, however, for radical resection of large tumors of the proximal stomach that encroach on the gastroesophageal junction, arising from either the gastric wall or retroperitoneum. The operation of total gastrectomy is usually performed, with reconstruction by means of a Roux-en-Y jejunal loop, with or without a pouch at the esophagojejunal anastomosis. The use of stapling devices (viz., CEEA stapler, United States Surgical Corporation) has simplified the performance of the esophageal anastomosis, which can be accomplished much more rapidly than the conventional hand-sewn anastomosis.

Obstructing Duodenal Ulcer (Peptic Stricture of Gastric Outlet) For adult patients, the onset of episodic vomiting, especially after solid food intake, and other signs of gastric outlet obstruction can be insidious. There is a normal tendency to minimize symptoms at times, especially by those adults dealing with other responsibilities who have little time to think about their own situation in an objective fashion. When a person has a history of peptic ulcer disease, the possibility of pyloric channel ulcer or stenosis of a fibrotic pyloric ring must be considered, and appropriate tests to establish the diagnosis are performed. Radiographic studies are often the first test obtained and reveal a large stomach with or without large amounts of residual undigested food; if a CT scan has been obtained, the absence of enlarged lymph nodes suggests but does not guarantee a benign cause of obstruction. Endoscopic biopsy has a 95% sensitivity for discovery of adenocarcinoma and should be performed preoperatively whenever possible.

Gastric Resection Versus Pyloroplasty? Open Surgery Versus Laparoscopic Exploration? The abdomen is explored by laparoscopic means or via a midline incision and the site of obstruction directly inspected. If the surgeon can identify carcinomatosis or other signs of unresectable cancer, then formal laparotomy can often be avoided in favor of a laparoscopic palliative procedure; when the laparoscopic examination does not reveal the source of obstruction, the next operative maneuver is conversion to laparotomy, because surgeons’ hands and fingers can identify induration and inapparent palpable thickening in areas not directly accessible with the laparoscope. If an obstructing duodenal ulcer is seen, the operation of choice is a matter of preference, with experienced surgeons preferring one of the following approaches:

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which were substantially changed in the same period, are now rarely necessary as a result of the discovery of effective antisecretory medications. In our own medical center the incidence of advanced ulcer has decreased dramatically, as it has elsewhere; previously, there were 200 to 300 ulcer operations per year, and at present there are less than 25; our fathers in surgery, students of the antrectomy and vagotomy, would be amazed at the current statistics after the introduction of antibiotic treatments for Helicobacter species.29–31 I believe, and most of my colleagues believe, that a vagotomy of some type still has a role for patients with severe ulcer disease; of course, the unstable patient is another matter. Occasionally, a partial gastrectomy without vagotomy will be performed, depending on the situation; a type IV gastric ulcer, rarely encountered in the modern world of digestive surgery, for example, is an ideal candidate for the Pauchet gastrectomy (Figures 29.5 and 29.6), which incorporates the ulcer in the tongue of

Figure 29.4. Areas of vagotomy. These seven sites or “areas” contain preganglionic vagus nerves that innervate the stomach. The original highly selective vagotomy included sites 1–3, whereas the extended highly selective vagotomy also included sites 4, 6, and 7. (Reprinted from Skandalakis LJ, Donahue PE, Skandalakis JE. The vagus nerve and its vagaries. Surg Clin North Am 1993; 73(4):769–784, with permission from Elsevier.)

subtotal gastrectomy, vagotomy (truncal or highly selective) with antrectomy or pyloroplasty (Heineke Mikulicz, Finney, or Jaboulay), or gastroenterostomy. (Highly selective vagotomy with pyloroplasty or gastroenterostomy is a highly effective operation for pyloric stenosis caused by ulcer, with a very low incidence of sequelae such as postvagotomy gastric atony or alkaline gastritis observed with other procedures.) The type of vagotomy is a matter of choice, but my favorite remains the highly selective vagotomy, with or without a drainage procedure depending on the presenting problem; with modern techniques, this procedure (when performed with the assistance of harmonic scalpel dissection) adds 15 minutes to the operation and achieves the goal of permanently reducing acid output (Figure 29.4; see also Figures 29.11 through 29.14).27,28 Techniques of gastrectomy have not changed much in the past 50 years. Vagotomy techniques (see Figure 29.4),

Figure 29.5. Rotation gastrectomy, 1. Gastric ulcers near the gastroesophageal junction cannot be included in a conventional gastrectomy but can be included with a free-hand technique that spares uninvolved portions of the stomach (anterior gastric wall in this case). The resulting lesser curve suture line “rotates” posteriorly as the clamps are removed, making the term “rotation gastrectomy” literally correct. (Reprinted with permission from Donahue PE, Nyhus LM. Surgical excision of gastric ulcers near the gastroesophageal junction. Surg Gynecol Obstet 1982; 155:85–88.)

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Figure 29.7. Schoemaker approach—complete antrectomy.The removal of 25% to 40% of the distal stomach includes a portion of the lesser curvature shown to include gastrinproducing tissue; this maneuver, once thought physiologically important, is really most useful in facilitating tubularization of the gastric remnant. (Reprinted with permission from Wastell C, Corliss D, Nyhus LM. Gastric ulcer. In Wastell C, Donahue PE, Nyhus LM, eds. Surgery of the Esophagus, Stomach, and Small Intestine, 5th ed. Boston: Little Brown & Co., 1995, pp 469–483.)

Pyloric Stenosis (Neonates) Figure 29.6. Rotation gastrectomy, 2. As the dissection proceeds, clamps on the cut edges of the stomach control bleeding, and a stout suture (2–0 Vicryl, general closure needle) allows approximation of tissues, which often have substantial inflammation and edema. (Reprinted with permission from Donahue PE, Nyhus LM. Surgical excision of gastric ulcers near the gastroesophageal junction. Surg Gynecol Obstet 1982; 155:85–88.)

lesser curvature. Although the indications for resections are limited, there are still patients who require traditional and extensive surgical resections. My only concern at present is that there is insufficient time and opportunity to train the next generation of surgeons regarding these matters. When a possible cancer is present, resection is planned with a goal of a 5 cm margin from the tumor. Whether the reconstruction is performed ad modem Billroth I or Billroth II, antecolic versus retrocolic, isoperistaltic versus retroperistaltic, with inverting or everting suture lines, is of no import in a modern world; all of the techniques work as long as a leak is avoided (Figures 29.7 through 29.10). The “angle of sorrows” suture of the threecornered junction of the anterior and posterior gastric wall and the duodenum/jejunum is still an important one, because it inverts the tissues prone to ischemic necrosis postoperatively. Although it may not be physiologically necessary to effect complete removal of gastric antral tissue along the lesser curve in this era of modern pharmacotherapy, a tubular gastric remnant is still required for subsequent anastomosis.31–33

Gastric outlet obstruction in neonates may be a result of pyloric stenosis, a disease of unknown etiology occurring mostly in males less than 6 months of age. The specific physical findings of a palpable lump in the right subcostal

Figure 29.8. Planning the extent of gastric resection. The positions of the clamps can be placed according to the surgeon’s plan of operation and can be shifted several centimeters in either direction without substantial effects on outcome. (Reprinted with permission from Wastell C, Corliss D, Nyhus LM. Gastric ulcer. In Wastell C, Donahue PE, Nyhus LM, eds. Surgery of the Esophagus, Stomach, and Small Intestine, 5th ed. Boston: Little Brown & Co., 1995, pp 469–483.)

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A C

B

Figure 29.9. Penetrating ulcers—Suture technique. Gastroduodenostomy occasionally provides a challenge in the presence of scarified posterior duodenal wall, or disparity in size between the stomach and duodenum. (Reprinted with permission from Wastell C, Corliss D, Nyhus LM. Gastric ulcer. In Wastell C, Donahue PE, Nyhus LM, eds. Surgery of the Esophagus, Stomach, and Small Intestine, 5th ed. Boston: Little Brown & Co., 1995, 469–483.)

discovered, and wide resection of the duodenum is the usual remedy. Intramural hematoma after blunt injury occurs in younger adults and children as a result of blunt injuries to the duodenal wall sustained during trauma, athletic events, or other activities. The disease is a curiosity that is amenable to a relatively minor surgical procedure, incision of the wall of the duodenum (near the ligament of Treitz) and evacuation of the submucosal hematoma. Superior mesenteric artery syndrome is an acquired condition that occurs after rapid weight loss and is not unusual in patients who are immobilized after trauma or various orthopedic procedures that require long immobilization. Several recent cases reported after laparoscopic gastric bypass illuminate yet another possible cause of this condition.

Internal Hernia One of the common occurrences after gastric bypass is the internal hernia of a loop of jejunum utilized to drain the gastric segment. The end result is an internal hernia that causes obstruction to flow, and, because it occurs in the morbidly obese, the ordinarily vague signs and symptoms of compromised intestinal viability are magnified. The CT scan provides a means of making the diagnosis but can usually be employed only for those weighing less than 350 pounds.

margin area may be subtle, but the sonographic demonstration of a typical thickened muscle segment at the distal stomach is sometimes diagnostic. Surgical treatment of this disorder is aimed at dividing the thickened muscle that surrounds the gastric outlet; medical treatment with per-mouth or intravenous atropine sulfate given before meals is also effective. Pyloromyotomy (Ramstedt procedure) can be performed surgically or via laparoscopic incision and is dramatically effective in relieving the gastric outlet obstruction. Because the underlying mucosa is normal, there is no need to enter the lumen of the gastrointestinal tract when performing pyloromyotomy; inadvertent entry is repaired with suture closure, similar to mucosal perforations performed during esophageal myotomy.

Duodenal Obstruction Nonpeptic stenosis of the duodenum occurs in adults as a result of neoplasm or other conditions ranging from superior mesenteric artery syndrome to pancreatic pseudocyst. The most common of these is pancreatic cancer, which leads to obstruction of the second or third part of the duodenum, leading to vomiting and inability to eat solid foodstuffs. In contrast, adenocarcinoma of the duodenum is often discovered in the investigation of a patient with anemia or occult gastrointestinal bleeding. In either circumstance, the disease is far advanced when

Figure 29 29.10. 10 Gastroduodenostomy. Gastroduodenostomy The gastroduodenostomy is performed with two layers, with special attention at the threecorner junction at the lesser curve of the stomach and the duodenum. This “angle of sorrows” is at particular risk for leaks because of its vascularization. (Reprinted with permission from Wastell C, Corliss D, Nyhus LM. Gastric ulcer. In Wastell C, Donahue PE, Nyhus LM, eds. Surgery of the Esophagus, Stomach, and Small Intestine, 5th ed. Boston: Little Brown & Co., 1995, 469–483.)

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Perforation

Table 29.3. Causes of perforation: esophagus, stomach, and duodenum.

Perforation of the foregut has great potential for serious morbidity (Tables 29.2 and 29.3). Failure to diagnose and treat perforation can lead to death or profound morbidity, and all practitioners will be challenged with this problem during their career. The sequelae of perforation vary according to the site and to the acuity of symptoms that ensue; as in all matters pertaining to the human body, there is great variation among individuals and their reactions to a given stimulus, and no two perforations are alike. Free perforation, contained perforation, formefruste perforation, microscopic perforation: all of these terms describe details that affect the severity of the presentation. As surgeons we are called on to have a higher level of excellence than physicians in providing definitive treatment for this condition; as a result, the recommendations we make for care in a given situation must be heavily weighted with the issue of patient safety. Therefore, surgical procedures, often the safest approach, are frequently part of our recommendation. When nonoperative treatment has an approximate 50% chance of success, the chance for successful operative procedure may be substantially diminished by the “watchful waiting.” One circumstance in which watchful waiting can be considered is in the individual with pneumoperitoneum or pneumomediastinum following upper gastrointestinal endoscopy, with or without biopsy, who has no evidence of peritoneal irritation, fever, or physical distress. Knowing that gaseous insufflation of air is sometimes followed by a dissection of air into the retroperitoneum, abdomen, or mediastinum without morbid sequelae, the clinician may adopt a waiting attitude for 12 to 24 hours only if a contrast study of esophagus, stomach, and duodenum does not show extravasation of contrast.

Intrinsic disease

Table 29.2. Sources of foregut bleeding. Intrinsic disease Mucosal inflammation Reflux esophagitis Gastritis Duodenitis Hiatus hernia strangulation Diverticulum Carcinoma Squamous cell Adenocarcinoma Intramural tumor Leiomyoma Gastrointestinal stromal tumor

Extrinsic disease Portal hypertension Splenic vein thrombosis Cirrhosis of liver

Disk space infection Dissecting aneurysm Aortoenteric fistula Graft infection Mycotic aneurysm Pancreatic disease Pseudocyst Abscess/splenic aneurysm Splenic vein thrombosis

Esophagitis Gastroesophageal reflux disease Peptic ulcer Hiatus hernia Incarcerated Morgagni hernia Gastric volvulus Epiphrenic diverticulum Hypopharyngeal diverticulum Boerhaave syndrome

Extrinsic disease Iatrogenic perforation Endoscopy (rigid/flexible) Dislocated gastrostomy tube Stent insertion Foreign bodies (dentures) Orthopedic hardware Missiles/gunshot wounds Dissecting aneurysm Pseudoaneurysm Graft infection Mycotic aneurysm

Diagnosis and Management The diagnosis of perforation is made when a patient has one or more symptoms associated with pain, distress, or altered consciousness and is found to have physical signs or findings consistent with perforation of a hollow viscus. In practical terms, the spectrum of complaints is quite wide, ranging from minimal discomfort in the neck, chest, back, or abdomen to those of excruciating discomfort involving the entire peritoneal cavity. Physical signs of perforation are nonspecific, consisting of primary or secondary signs of peritonitis or infection if these conditions are present. Primary signs of peritonitis such as involuntary muscle guarding and peritoneal irritation might be diffuse or localized depending on the site of the perforation and whether or not the perforation has been contained or “walled off” by contiguous organs resulting in a “forme-fruste” perforation. When inflammation of the neck or abdominal wall is seen, with or without subcutaneous crepitation caused by air or gases, the condition of advanced sepsis is usually present except if the cause is endoscopic insufflation. The interpretation of abnormal signs and symptoms, as usual, requires sophisticated judgment and interpretation. Radiographic signs of perforation include the presence of extraluminal air, as seen in the upright chest x-ray or CT scan or extravasation of oral contrast material during a CT scan of the chest or abdomen or during an upper gastrointestinal contrast study. Extraluminal gas or contrast material is never normal, and every instance requires cautious interpretation; however, every instance does not mandate surgical intervention.

Esophagus Almost every case of esophageal perforation can lead to a fatal outcome if not recognized and treated appropriately. The most common types of perforation are caused by diagnostic or therapeutic maneuvers, and endoscopic procedures account for the majority of these. Stenting of

29. Foregut

esophageal malignancy, submucosal resection of highgrade dysplasia or early esophageal cancer, and pneumatic dilation of esophageal achalasia are the most common endoscopic procedures, although sclerotherapy of bleeding esophageal varices, snare excision of esophageal tumors, and others have also been reported. The proximal esophagus is at risk during endotracheal intubation, when the stylus or the endotracheal tube itself can enter the wall of the esophagus. The patient with unrecognized perforation might have swelling or subcutaneous emphysema in the neck (or supraclavicular fossa), fever, pain, or other evidence of cervicofacial inflammation. Once subcutaneous crepitations have been recognized, the onus is on the practitioner to respond in an appropriate way. Perforation in mid or distal esophagus occurs most commonly after dilation of a benign or malignant stricture or after pneumatic dilation (disruption) of the lower esophageal sphincter in achalasia of the esophagus. With the advent of self-expanding stents to maintain the esophageal lumen patency, the incidence of perforation is less than the 5% to10% incidence reported with rigid stents that required extensive dilation before insertion. Pneumatic dilation in patients with achalasia has a 3% to 5% incidence of perforation, which can convert a simple outpatient procedure into a lifethreatening medical and surgical emergency. Spontaneous perforation of the esophagus, the Boerhaave syndrome, is the prototype of the unrecognized esophageal leak, which was described over 200 years ago. Despite awareness of the syndrome, individuals with “emetogenic vomiting” still pose serious diagnostic challenges for clinicians; up to 50% of patients forget or deny that they vomited, and affected individuals are often in desperate straits, thought to have aspiration pneumonia or cardiac disease because of substantial pleural effusions, obliterated costophrenic angles, and other nonspecific signs of disease. Remember: No patient is too sick to have an esophagram. (This single sentence can help every young reader of this chapter to save at least one of his or her patients’ lives over the course of a medical career.) Patients with large pleural effusions may have an unrecognized esophageal perforation, and liberal use of oral contrast material can help the clinician to make a diagnosis of an occult esophageal perforation, which cannot be treated successfully without control of the esophageal leak by resection, repair, exclusion, or diversion.10 The surgical treatment of perforation depends on the clinical condition of the patient and all pertinent findings related to the illness. When pneumatic dilation of the esophagus is the cause, some physicians recommend conservative treatment; on balance, however, trained surgeons know that a precise Heller myotomy can be done simultaneously with closure of an iatrogenic perforation and will perform it in the acute setting when possible. The use of nonoperative treatment for pneumatic

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dilator–induced perforation is potentially dangerous, possibly leading to fatal sepsis; if the patient is encouraged to use this “wishful” treatment, then the hour of opportunity for definitive surgery might be lost.

Gastric and Duodenal Perforation Gastric perforation occurs because of ulceration of the mucosal and muscular lining of the stomach and was frequently caused by peptic ulcer disease before the advent of modern antibiotic treatments versus Helicobacter species and proton pump inhibitors. At present, most perforations are related to injudicious ingestion of nonsteroidal antiinflammatory agents as a remedy for arthritis or other rheumatoid conditions. Other causes are foreign bodies, caustic agents, erosion by contiguous organs (such as edge of diaphragm), or ischemic necrosis resulting from incarceration or strangulation of the gastric wall. The forme-fruste perforation is one in which surrounding tissues “wall off” the site of the impending perforation, providing protection from diffuse peritonitis; in contrast, a perforation that liberates acid and pepsin into the peritoneal cavity quickly elicits the typical response of a perforated ulcer: peritonitis, involuntary guarding of the abdominal wall, and prostration. Treatment of free perforation consists of lavage of the peritoneal cavity, removing all digestive ferments from contact with the abdominal contents. The hole in the stomach must be closed either by direct suture or by omental patch. Alternatively, gastric resection is performed for some large/chronic gastric ulcers, depending on the circumstances at the time of perforation. When cancer of the stomach or duodenum is suspected as a cause of the perforation, a frozen section diagnosis can be very useful in establishing the need for a resection versus simple patch closure of the perforation site. If the perforation is within 1.0 cm of the pylorus (either proximal or distal), the causal factor(s) may include acid hypersecretion, analgesic-associated injury, or ischemia related to drug ingestion. The specific treatment of such lesions may include closure alone and/or closure with pyloroplasty if pyloric stenosis is present. Vagotomy of truncal or highly selective type is sometimes indicated, depending on the operating surgeon and the specific patient’s conditions. My choice is the highly selective vagotomy with pyloric reconstruction (vide supra). Because proton pump inhibitors and antibiotics effective against Helicobacter pylori are widely available, the optimistic view of best possible treatment is sometimes stated as “closure of the perforation followed by long-term antibiotic treatment and antisecretory medications.” This simplistic view, however, does not address the issues surrounding Helicobacter species–negative ulcerations of the stomach and duodenum or provide satisfactory longterm management for those whose ulcers recur during

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treatment. Because the numbers in both categories are up to 50% of the patients seen, there is a rationale for a “definitive” procedure at the first operation, especially if that operation can be performed with minimal morbidity. Many of the patients we see with acute perforations have had ulcer disease for years and present with a relatively short history of abdominal pain; because the bacterial species associated with gastric perforations are largely not as pathogenic as those associated with colonic perforations, a pyloric reconstruction with highly selective vagotomy can be easily performed with reasonable expectation of quick recovery and minimal morbidity. When patients are moribund or have extensive comorbidities, a simple omental patch is performed, with full realization that sometimes a pyloric stenosis will remain in the postoperative period. If a foreign body perforation (e.g., chicken bone, sewing needle) is observed, simple closure of the perforation is employed.

Bleeding Upper gastrointestinal hemorrhage (UGIH) occurs with regularity in all clinical settings; the death rate and the incidence of problems caused by ulcer increase with each decade in the population at large.34 Endoscopic diagnosis and management (Table 29.4) are the keystone of effective care, because 90% of bleeding sites can be identified and more than 70% managed successfully. Surgery, often considered the intervention of last resort, can be

life saving when other alternatives have been unsuccessful; surgeons must recognize those situations when urgent surgery is necessary. Experienced surgeons are vital participants in the multidisciplinary team of caregivers for patients with gastrointestinal bleeding.

Sentinel Bleeding When major blood vessels such as the aorta and named major branches erode into the intestine, they do so with a characteristic pattern in which the first bleeding episode is of a limited nature, allowing the medical team to organize its resources before performing corrective surgery. The common sources for sentinel bleeding are aneurysms of the aorta or major visceral structures; pseudoaneurysms related to infection of an aortic graft; or garden-variety mycotic aneurysms of the aorta or its branches. Extraintestinal bleeding sources, including vascular malformations, pseudoaneurysms of the splanchnic circulation including late sequelae of pancreatic necrosis and infections of vascular prostheses, or coagulopathic states are of great interest and are managed individually and are not further mentioned herein. Other lesions that cause massive bleeding infrequently, such as submucosal tumors, are generally not life threatening and are managed according to the same treatment strategy.

Mallory-Weiss Tears Mallory-Weiss lesions contribute to nearly 10% of all upper gastrointestinal bleeding episodes and are still

Table 29.4. Control of Hemorrhage from Esophagus, Stomach, and Duodenum. Bleeding Site Esophageal ulcer GERD Tear—Mallory Weiss Esophageal varices Gastric ulcer, Types I–IV require individual assessment Acute Gastric Ulcers Gastric Cancer Gastric Varices Anastomotic Bleeding Duodenal Ulcer

Endoscopic Rx Coagulation, Injection Coagulation, Injection Sclerosis, banding Coagulation Injection (vessels 16,000/μL >11 mmol/L >350 IU/L >250 IU/L

During initial 48 hours Hematocrit Blood urea nitrogen Calcium PaO2 Base deficit Fluid sequestration

Decrease of more than 0.10 Increase of more than 5 mg/dL 6 L

Table 31.3. Balthazar computed tomography (CT) grading system for acute pancreatitis. Grade A B C D E

CT finding Normal pancreas Pancreatic enlargement Pancreatic and/or peripancreatic fat inflammation Single peripancreatic fluid collection Two or more fluid collections and/or retroperitoneal air

creatitis present (Table 31.3). If the CT scan fails to reveal radiographic evidence of severe pancreatitis (Balthazar grade B or less) laparoscopic cholecystectomy and intraoperative cholangiography can safely be performed at any time.71–73 On the hand, if severe pancreatitis is noted (Balthazar grade C or higher), surgical intervention should be deferred and a conservative approach with bowel rest and total parenteral nutrition begun.74,75 For patients with gallstone pancreatitis who present with persistent abdominal pain and abnormal liver function tests, an emergency ERCP, sphincterotomy, and stone extraction should be performed as soon as possible.66,76,77 What appears less clear is the appropriateness of ERCP for the patient with mild to moderate pancreatitis. Sharma’s metaanalysis of randomized controlled trials examining the role ERCP and sphincterotomy in acute biliary pancreatitis revealed that morbidity and mortality were reduced by this approach. Ricci et al.,78 reflecting the European approach, believe that regardless of the severity of pancreatitis, ERCP and sphincterotomy should initially be performed in all instances and then followed by laparoscopic cholecystectomy. This approach has not uniformly been accepted because of the risk of exacerbating acute pancreatitis by injecting a high-volume bolus of contrast material into the pancreatic duct.

Gallstone Ileus Gallstone ileus, an uncommon complication of chronic cholecystitis, results in mechanical small bowel obstruction. With multiple bouts of acute and chronic cholecystitis and the ensuing inflammatory process, the gallbladder becomes walled off by the duodenum. As the process repeats itself, fistulization between these two hollow viscous organs occurs, providing a pathway for the migration of gallstones into the intestinal tract. Gallstones are usually trapped in the distal ileum or at the ileocecal valve, resulting in a mechanical small bowel obstruction (rather than the misnomer “ileus”). A plain abdominal x-ray may classically demonstrate dilated small bowel loops with air–fluid levels in addition to pneumobilia, air in the biliary tree (Figure 31.3). Appropriate management dictates prompt surgical intervention to relieve the small bowel obstruction.79 At laparotomy,

31. Liver and Biliary Tract

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Figure 31.3. (A) Plain abdominal radiographs demonstrating small bowel dilatation, pneumobilia, and a radiopaque stone in the pelvis of a patient with gallstone ileus. (B) Computed tomography scans from the same patient clearly demonstrates pneumobilia and localizes the stone in the small bowel lumen.

A

B

the point of obstruction is readily apparent, but multiple, often nonobstructing stones may have entered the gastrointestinal tract in up to 30% of patients. A complete and thorough evaluation of the entire small bowel becomes mandatory. Calculi found proximal to the area of obstruction should be milked upward into an area of normal bowel and extracted via a small longitudinal enterotomy that can be closed transversely. Bowel resection is seldom necessary and is reserved only for patients with coexisting ischemia of the small bowel. Cholecystectomy and repair of the cholecystoduodenal fistula should usually be discouraged at the initial operation.80–82

Neoplasms Surgical emergencies related to underlying neoplasms most commonly include tumor rupture with free hemorrhage into the greater peritoneal cavity, central tumor necrosis with abscess formation, and biliary obstruction secondary to invasion or extrinsic compression of major biliary ducts. Tumor rupture can occur in patients with either benign or malignant lesions, but abscesses and biliary obstruction are usually sequelae of malignant tumors. Each of these difficult problems requires multidisciplinary expertise for appropriate management.

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S.P. Hiotis and H.L. Pachter

Tumor Rupture Free rupture of hepatic tumors into the peritoneal cavity can result in life-threatening hemorrhage and can pose complex and difficult management issues. Although relatively uncommon, patients with any underlying solid liver mass of significant size (>5 cm) are at risk for rupture, hemorrhage, and subsequent shock. Some benign tumors are also associated with an increased risk of rupture, and, along with their counterpart malignant lesions, tumor size is considered to be a significant risk factor. Hepatic adenoma, for example, often develops in women taking oral contraceptive pills and carries a higher risk for rupture than other benign liver lesions; the pathophysiology behind the propensity for hepatic adenomas to rupture is presently unknown (Figure 31.4).83 Giant hepatic hemangiomas also carry an elevated risk for

A

tumor rupture. Hemangiomas are classified as giant when their greatest diameter exceeds 5 cm. Risk for rupture and other symptoms in patients with these highly vascular tumors is thought to increase proportionally with tumor diameter.84 Any large malignant lesion can similarly rupture into the peritoneal cavity. Hepatocellular carcinoma is the most common hepatic malignancy associated with hemoperitoneum, but other malignancies, including intrahepatic Cholangiocarcinoma, metastatic adenocarcinoma, and metastatic carcinoid tumor have also been known to rupture into the peritoneal cavity.85–87 The clinical presentation in patients with tumor rupture is always intimately associated with abdominal pain, tachycardia, a dropping hemoglobin level, and eventual hypotension. A history of blunt trauma to the abdomen followed by the onset of symptoms is usually noted. Some patients describe very subtle blunt injury

B

C

Figure 31.4. Noncontrast computed tomography scan (A) from a young woman taking oral contraceptive pills. Highdensity fluid (arrow) in noncontrast image suggests the presence of blood. (B) Computed tomography scan with intravenous contrast from the same patient clearly demonstrates a hemorrhagic adenoma (arrow). (C) CT scan with contrast demonstrating a right-sided giant hepatic hemangioma in a different patient.


before symptoms; for example, a patient whose automobile hits a bump in the road suddenly develops abdominal pain and comes directly to the emergency room.83 Evaluation with complete blood count often reveals a severe normocytic anemia. Ultrasonography reveals free peritoneal fluid and usually confirms the presence of a liver mass. Computed tomography scanning with intravenous contrast is the preferred diagnostic modality for assessment of patients with suspected rupture of a hepatic tumor. A CT scan with contrast (1) demonstrates the extent of subcapsular hematoma; (2) allows for the distinction between ascites and free blood in the peritoneal cavity by assessing the Hownsfeld units of the fluid (>25 Hownsfeld units usually indicates the presence of blood); (3) determines the presence or absence of a “contrast blush,” the hallmark of active hemorrhage; (4) identifies the exact point of hemorrhage and its relationship to major vascular and biliary structures; and (5) provides the means by which definitive control of the bleeding can be achieved through angioembolization. The initial management of the patient with a ruptured liver tumor should include resuscitation with intravenous fluids and transfusion of blood products when necessary through large-bore intravenous catheters, followed by prompt transport of the patient (accompanied by a physician) to the angiography suite.88 Hepatic angiography, in this instance, has a dual purpose: (1) to determine the presence of ongoing hepatic arterial or portal venous bleeding and its precise location and (2) to provide the necessary access by which selective angioembolization can arrest bleeding. Several appropriate materials are available to interrupt arterial inflow, including metallic coils, Avitene, Gelfoam, polyvinyl alcohol (PVA) beads, autologous clot, and Bioglue (Figure 31.5).

Figure 31.5. Postembolization angiogram of a patient with right-sided hepatocellular carcinoma. Metallic coils were used to occlude arterial inflow into this large hypervascular tumor.

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Angioembolization is not always effective in controlling hemorrhage, and in such instances operative intervention may be unavoidable.89 The most common indication for surgical management is hemodynamic instability despite all available nonoperative strategies. To achieve optimal results it would be prudent, when feasible, to have an experienced hepatobiliary surgeon present, as a rapid hepatic resection may become necessary. Emergency resection in the face of ruptured liver tumors is a highly complex and difficult procedure and is often associated with inordinately high morbidity and mortality rates. Operative intervention, if necessary, should not be approached laparoscopically. An open surgical approach is preferred, as it affords maximal exposure of the liver and represents the safest method with which to promptly control the ongoing hemorrhage. Complete resection with negative margins is not necessarily an appropriate goal in an acute care situation. For critically ill patients who are exsanguinating, the immediate objective must always be to promptly gain control of hemorrhage and then rapidly terminate any further surgery. If indicated, temporary packing, rapid towel clip closure, and planned reexploration or transfer to a facility with greater expertise in this area may be life-saving.

Abscess Hepatic tumors that have grown to a significantly large size can go on to develop central necrosis. This feature is essentially a unique characteristic of malignancies and is almost never observed in benign neoplasms.90 Even highly vascular malignancies such hepatocellular carcinomas can outgrow their arterial inflow, resulting in areas of necrosis. Tumor necrosis is best delineated by radiographic imaging studies that include intravenous contrast. Both CT and MRI with intravenous contrast can readily demonstrate the presence of necrosis within otherwise viable hepatic neoplasms. On rare occasion, necrotic tumors can become secondarily infected and undergo abscess formation. Once an abscess has formed, therapeutic intervention is always necessary. Abscesses associated with liver cancers may warrant treatment plans that differ from management of their counterparts not associated with cancer. For patients with otherwise resectable tumors who exhibit mild signs of sepsis, giving intravenous antibiotics to sterilize the bloodstream followed by complete resection seems to be a reasonable approach. For patients with severe infections, not controllable with antibiotics alone, percutaneous drainage of the abscess may become necessary to achieve resolution of the infection before resection. Important considerations in formulating an individualized treatment plan include the risk of seeding the extrahepatic space with tumor cells along the percutaneous drainage route. A second consideration is the juxtaposed

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risk of proceeding with a formal liver resection for a patient with an unresolved infection.91–93 This situation can pose difficult management dilemmas, and definitive decisions regarding treatment are often best made after an informed and detailed discussion with the patient.

Biliary Obstruction Obstruction of biliary outflow secondary to hepatic, biliary, or periampullary malignancies is a commonly seen problem. The etiology of malignant biliary obstruction mimics the incidence of each tumor within a particular geographic region. In the United States and western European countries, adenocarcinoma of the pancreas is the most common cause of malignant biliary obstruction. In East Asian countries with endemic hepatitis B– positive populations, hepatocellular carcinoma is a more likely cause. Malignant biliary obstructions can be classified according to their anatomic location in either the proximal biliary tree or distal bile duct. Although the clinical presentation may be similar in both instances, definitive treatment varies greatly. Distal biliary tract obstruction secondary to an underlying malignancy is likely to be caused by one of four common primary periampullary tumors: (1) pancreatic adenocarcinoma, (2) distal bile duct cholangiocarcinoma, (3) periampullary carcinoma, and (4) duodenal adenocarcinoma. Other less likely possibilities include locally advanced gastric and colon cancer and a variety of metastatic carcinomas invading the porta hepatis. Classically the patient presents with painless jaundice, although in reality many patients actually present with upper abdominal or back pain. Patients also frequently describe weight loss, decreased appetite, and fatigue. Jaundiced patients are commonly evaluated initially with basic blood tests, including liver function tests and transabdominal ultrasound. All patients found to have a dilated common bile duct and a suspected periampullary mass on ultrasound must next be evaluated with CT scan with intravenous contrast or MRCP (Figure 31.6). Axial imaging studies are essential in delineating the relationship between the tumor, the common bile duct, and the surrounding blood vessels 94,95 The proximity to an underlying neoplasm and patency of the portal vein and its branches, superior mesenteric artery, and common hepatic artery are crucial variables in determining potential resectability. Axial imaging studies are also very helpful in determining the presence of distant disease or lymphatic involvement, which usually precludes resection for cure. Patients who present with malignant distal biliary obstruction and a resectable tumor without metastases should not be immediately referred for endoscopic or percutaneous biliary drainage procedures unless the

A

B Figure 31.6. 31 6 (A) Magnetic resonance image with intravenous contrast demonstrating a mass in the head of the pancreas (arrow) with decreased signal intensity, suggestive of neoplasm. (B) Magnetic resonance image with emphasis on cholangiopancreatography demonstrating a double duct sign in a patient with biliary obstruction secondary to a malignant neoplasm in the head of the pancreas.

predominant clinical picture is consistent with cholangitis and ongoing sepsis. When definitive resection can be offered within a reasonable period of time (1 week), there is justification in allowing biliary obstruction to continue until resection and a surgical biliary–enteric


reconstruction can be accomplished. This approach is strengthened by the following theoretical advantages: (1) the cost and risks of a potentially unnecessary procedure are avoided; (2) indwelling biliary stents produce periampullary inflammatory changes that may increase the difficulty of resection; and (3) a foreign body in the biliary tree can lead to contamination of a previously sterile compartment.96 Patients for whom complete resection cannot be offered within a reasonable period of time should be managed with early ERCP and stent placement or PTC.97 Operative biliary bypass procedures for patients who are not candidates for complete resection are currently discouraged. Avoidance of surgical biliary bypass procedures has been extensively documented in the literature. Several retrospective studies on this topic have definitively demonstrated that patients with unresectable periampullary malignancies have a median survival time of less than 12 months and thus will subsequently require only a minimal number of stent changes during that period of time. Moreover, only a fraction of patients managed with nonoperative biliary drainage will fail and ultimately require a surgical bypass.98–100 An exception to this approach is the patient who presents with an unresectable periampullary malignancy along with biliary and gastric outlet obstruction. For such patients prompt operative intervention is justified to reconstruct both gastric and biliary drainage. Patients with proximal biliary obstruction often pose a more difficult problem than those with distal obstruction. Common etiologies for proximal biliary obstruction include proximal cholangiocarcinoma and hepatocellular carcinoma. Evaluation with liver function tests and ultrasound is appropriate in the initial period. Computed tomography with contrast or MRI is essential in the diagnostic work up of these patients. Most hepatobiliary surgeons would not advocate prompt surgical management without anatomic delineation of the proximal biliary tree and its relationship to the area of obstruction. Although often helpful for diagnostic purposes, ERCP is of limited therapeutic value in cases of high malignant biliary strictures because of the technical difficulty involved in advancing stents across a high stricture via an endoscopic approach. Percutaneous transhepatic cholangiography is more likely to provide both important diagnostic information and a portal for further therapeutic maneuvers. Technical challenges in performing adequate PTC in these patients relate to the involvement of the right, left, or bilateral biliary trees. Protection from cholangitis and sepsis is relatively straightforward by the placement of an external drain above the level of obstruction. In some instances both right and left catheter placement may be necessary to achieve complete decompression for lesions situated at the bifurcation of the main hepatic ducts. After an initial period of decompression with external

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drainage, the drainage stent can then be internalized, allowing for free flow of bile into the duodenum. Resectability is ultimately determined by several factors: (1) the absence of extrahepatic disease, (2) the relationship of the tumor to major surrounding vascular structures, (3) the ability to spare an adequate amount of functional hepatic parenchyma, and (4) the technical feasibility of constructing a biliary enteric anastomosis.

Portal Hypertension Cirrhosis of the liver secondary to any underlying etiology results in increased pressure within the portal venous system. The pathophysiology responsible for portal hypertension is related to increased resistance in small central veins that results from parenchymal fibrosis.101,102 Similar changes also occur in patients with major hepatic venous outflow obstruction, such as those with BuddChiari syndrome. The common sequelae of portal hypertension are numerous and include varices, hypersplenism, and thrombocytopenia. Variceal hemorrhage is the most life-threatening complication in the acute setting, and it can lead to extraordinarily difficult management issues. Although varices can develop in a number of anatomic locations, esophageal and gastric varices are most common. Esophageal variceal hemorrhage manifests initially as hematemesis, and patients with bleeding esophageal varices can lose massive quantities of blood in a very brief period of time. Prompt diagnosis and treatment are essential. Several diagnostic modalities such as CT and angiography are useful in detecting the presence of esophageal varices in the elective setting.103 Upper endoscopy, however, remains the most useful diagnostic tool in both the elective and acute setting. Endoscopy with direct visualization of varices is highly accurate and also provides the opportunity for treatment of bleeding varices by banding or direct injection of sclerosing agents.104,105 Endoscopy in patients with bleeding esophageal varices must be approached with extreme caution as hemorrhage can be exacerbated by the mechanical stress on the wall of the esophagus during the procedure. Although endoscopic therapy is effective in the setting of minimal or no hemorrhage, it is marginally useful as a therapeutic maneuver in the patient with massive hemorrhage. Treatment of the patient with significant acute variceal hemorrhage must be aggressive and rapidly implemented. Resuscitation with intravenous fluid, transfusion of blood products, and correction of underlying coagulopathy are obvious initial measures. These patients may deteriorate rapidly with the sudden onset of hemodynamic collapse, often with little warning. The unpredictable nature of the patient with active esophageal

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variceal bleeding would mandate that they be monitored in a critical care unit. In addition to giving a somatostatin analog (octreotide), once the diagnosis of esophageal variceal hemorrhage is definitively established, placement of a Sengstaken-Blakemore (SB) tube can be life saving.106 Proper placement of an SB tube requires some familiarity with the device.107 These tubes are modified nasogastric tubes that contain two separate balloons: a long esophageal balloon along its shaft and a spherical gastric balloon at its end. Each of these balloons is insufflated separately, and balloon pressure must be measured carefully during insufflation. The underlying design of the SB tube is based on insufflation of the esophageal balloon to a pressure high enough to occlude variceal blood flow but low enough to avoid pressure necrosis of the esophagus (24 to 45 mm Hg). The gastric balloon is insufflated before the esophageal balloon, and it serves to facilitate gentle traction along the gastric cardia, which is held with a counterweight at the patient’s bedside. Extreme care must be taken to avoid inadvertent insufflation of the gastric balloon within the esophagus, as a catastrophic esophageal blowout can result. The tubes are uncomfortable, and adequate sedation of the unobtunded patient is necessary. It has been our practice to intubate all patients requiring the insertion of an SB tube to prevent aspiration. Sengstaken-Blakemore tube placement in addition to other effective nonoperative measures such as beta blockade and intravenous pitressin serve only as temporizing measures for patients with portal hypertension.108,109 Definitive long-term treatment requires reduction of portal venous hypertension via a portalsystemic shunt. Two successful approaches may be employed, depending on institutional expertise: (1) surgical portal-caval shunt and (2) interventional transjugular portal-systemic shunt (TIPSS).110 Despite the controversy regarding which of the two methods is superior overall, both have proven highly effective at controlling hemorrhage in the setting of acute variceal bleeding. Many surgical variations for portal-caval shunting, including an end-to-side portal-caval shunt, side-to-side portal-caval shunt, or the prosthetic interposition H-graft technique, have been used with success. The latter surgical approach is the only one to have been compared with TIPSS in a randomized prospective study. Rosemurgy and colleagues111–113 have reported on their extensive experience with both surgical H-graft shunts and TIPSS. In their prospective experience, results with surgical portal-caval shunting were slightly superior than those with TIPSS. The data provided by Rosemurgy notwithstanding, most tertiary care centers perform far more TIPSS procedures than surgically created portal-caval shunts. As expertise, ease, and success by interventional radiologists in TIPSS insertion increase, this approach


would seem to outweigh the marginal benefits and the associated morbidity of an operative portal-caval shunt.114,115

Hemobilia Hemobilia is rare condition that most commonly occurs as a result of either trauma to the liver or iatrogenic injury. Other less likely etiologies include rupture of neoplasm or arterial-venous malformation with hemorrhage into the biliary tree. Endoscopy may play a useful role in establishing the correct diagnosis if blood is seen coming from the ampulla of Vater. In most instances, further diagnosis and management should be made with angiography and angioembolization when feasible. Angiography provides essential diagnostic information by localizing the source of hemorrhage. Following localization, selective hepatic arterial embolization is usually highly effective in controlling hemorrhage.116,117 Operative intervention, however, may be necessary for patients with hemodynamic instability secondary to ongoing hemorrhage not controlled by embolization. Surgery is predicated upon suture ligation of bleeding vessels within the hepatic parenchyma or resection of the segment(s) within which hemorrhage has been localized. These procedures are difficult and require an intimate familiarity with complex hepatobiliary surgical techniques.

Critique The constellation of symptoms and findings is strongly suggestive of a suppurative cholangitis. Further diagnostic screening would probably confirm a dilated and blocked distal common bile duct (choledocholithiasis). The intervention that this critically ill patient should undergo, at this time, is an endoscopic retrograde cholangiography, with removal of a lodged stone in the common bile duct. A cholecystectomy and further evaluation of the biliary radicals can be performed at another time when the patient has recovered from this acute problem. Answer (D)

References 1. Couinaud C. Liver anatomy: portal (and suprahepatic) or biliary segmentation. Dig Surg 1999; 16:459–467. 2. Botero AC, Strasberg SM. Division of the left hemiliver in man—segments, sectors, or sections. Liver Transplant Surg 1998; 4:226–231.

31. Liver and Biliary Tract 3. Strasberg SM. Terminology of liver anatomy and liver resections: coming to grips with hepatic Babel. J Am Coll Surg 1997; 184:413–434. 4. Jung G, Krahe T, Krug B, Hahn U, Raab M. Delineation of segmental liver anatomy. Comparison of ultrasonography, spiral CT and MR imaging for preoperative localization of focal liver lesions to specific hepatic segments. Acta Radiol 1996; 37:691–695. 5. Amitrano L, Guardascione MA, Brancaccio V, Balzano A. Coagulation disorders in liver disease. Semin Liver Dis 2002; 22:83–96. 6. Roe PG. Liver function tests in the critically ill patient. Clin Intensive Care 1993; 4:174–182. 7. Moseley RH. Evaluation of abnormal liver function tests. Med Clin North Am 1996; 80:887–906. 8. Lauterburg BH. Assessment of liver function prior to hepatic resection. Swiss Surg 1999; 5:92–96. 9. Shaked A, Nunes FA, Olthoff KM, Lucey MR. Assessment of liver function: pre- and peritransplant evaluation. Clin Chem 1997; 43:1539–1545. 10. Blendis L, Wong F. The hyperdynamic circulation in cirrhosis: an overview. Pharmacol Ther 2001; 89:221– 231. 11. Fenchel S, Fleiter TR, Merkle EM. Multislice helical CT of the abdomen. Eur Radiol 2002; 12(Suppl 2):S5–S10. 12. Delgado Millan MA, Deballon PO. Computed tomography, angiography, and endoscopic retrograde cholangiopancreatography in the nonoperative management of hepatic and splenic trauma. World J Surg 2001; 25:1397– 1402. 13. Brink JA. Contrast optimization and scan timing for single and multidetector-row computed tomography. J Comput Assist Tomogr 2003; 27(Suppl 1):S3–S8. 14. Mortele KJ, McTavish J, Ros PR. Current techniques of computed tomography. Helical CT, multidetector CT, and 3D reconstruction. Clin Liver Dis 2002; 6:29–52. 15. Nelson RC, Spielmann AL. Liver imaging with multidetector helical computed tomography. J Comput Assist Tomogr 2003; 27(Suppl 1):S9–S16. 16. Reddy SI, Grace ND. Liver imaging. A hepatologist’s perspective. Clin Liver Dis 2002; 6:297–310, ix. 17. Ros PR, Mortele KJ. Hepatic imaging. An overview. Clin Liver Dis 2002; 6:1–16. 18. Vauthey JN, Rousseau DL Jr. Liver imaging. A surgeon’s perspective. Clin Liver Dis 2002; 6:271–295. 19. Shankar S, van Sonnenberg E, Silverman SG, Tuncali K. Interventional radiology procedures in the liver. Biopsy, drainage, and ablation. Clin Liver Dis 2002; 6:91–118. 20. Huang CJ, Pitt HA, Lipsett PA, et al. Pyogenic hepatic abscess. Changing trends over 42 years. Ann Surg 1996; 223:600–609. 21. Pereira FE, Musso C, Castelo JS. Pathology of pyogenic liver abscess in children. Pediatr Dev Pathol 1999; 2:537– 543. 22. Barakate MS, Stephen MS, Waugh RC, et al. Pyogenic liver abscess: a review of 10 years’ experience in management. Aust N Z J Surg 1999; 69:205–209. 23. Moore SW, Millar AJ, Cywes S. Conservative initial treatment for liver abscesses in children. Br J Surg 1994; 81: 872–874.

493 24. Brolin RE, Nosher JL, Leiman S, Lee WS, Greco RS. Percutaneous catheter versus open surgical drainage in the treatment of abdominal abscesses. Am Surg 1984; 50:102– 108. 25. Lang EK, Springer RM, Glorioso LW III, et al. Abdominal abscess drainage under radiology guidance: causes of failure. Radiology 1986; 159:329–336. 26. van Sonnenberg E, Wittich GR, Casola G, et al. Percutaneous drainage of infected and noninfected pancreatic pseudocysts: experience in 101 cases. Radiology 1989; 170:757–761. 27. Goletti O, Lippolis PV, Chiarugi M, et al. Percutaneous ultrasound-guided drainage of intra-abdominal abscesses. Br J Surg 1993; 80:336–339. 28. Voros D, Gouliamos A, Kotoulas G, Kouloheri D, Saloum G, Kalovidouris A. Percutaneous drainage of intra-abdominal abscesses using large lumen tubes under computed tomographic control. Eur J Surg 1996; 162:895–898. 29. Ch Yu S, Hg Lo R, Kan PS, Metreweli C. Pyogenic liver abscess: treatment with needle aspiration. Clin Radiol 1997; 52:912–916. 30. Gerzof SG, Johnson WC, Robbins AH, et al. Expanded criteria for percutaneous abscess drainage. Arch Surg 1985; 120:227–232. 31. Sharma MP, Dasarathy S, Sushma S, Verma N. Long term follow-up of amebic liver abscess: clinical and ultrasound patterns of resolution. Trop Gastroenterol 1995; 16:24–28. 32. Carpenter HA. Bacterial and parasitic cholangitis. Mayo Clin Proc 1998; 73:473–478. 33. Sinanan MN. Acute cholangitis. Infect Dis Clin North Am 1992; 6:571–599. 34. Nahrwold DL. Acute cholangitis. Surgery 1992; 112:487– 488. 35. Kimmings AN, van Deventer SJ, Rauws EAJ, Huibregtse K, Gouma DJ. Systemic inflammatory response in acute cholangitis and after subsequent treatment. Eur J Surg 2000; 166:700–705. 36. Rerknimitr R, Fogel EL, Kalayci C, Esber E, Lehman GA, Sherman S. Microbiology of bile in patients with cholangitis or cholestasis with and without plastic biliary endoprosthesis. Gastrointest Endosc 2002; 56:885–889. 37. Sheen-Chen S, Chen W, Eng H, et al. Bacteriology and antimicrobial choice in hepatolithiasis. Am J Infect Control 2000; 28:298–301. 38. Karachalios GN, Zografos G, Patrikakos V, Nassopoulou D, Kehagioglou K. Biliary tract infections treated with ciprofloxacin. Infection 1993; 21:262–264. 39. Gumaste VV. Antibiotics and cholangitis. Gastroenterology 1995; 109:323–325. 40. Sung JJ, Lyon DJ, Suen R, et al. Intravenous ciprofloxacin as treatment for patients with acute suppurative cholangitis: a randomized, controlled clinical trial. J Antimicrob Chemother 1995; 35:855–864. 41. Siegel JH, Rodriquez R, Cohen SA, Kasmin FE, Cooperman AM. Endoscopic management of cholangitis: critical review of an alternative technique and report of a large series. Am J Gastroenterol 1994; 89:1142–1146. 42. Lee WJ, Chang KJ, Lee CS, Chen KM. Surgery in cholangitis: bacteriology and choice of antibiotic. Hepatogastroenterology 1992; 39:347–349.

494 43. Balci NC, Sirvanci M. MR imaging of infective liver lesions. Magn Reson Imaging Clin North Am 2002; 10:121–135, vii. 44. Barreda R, Ros PR. Diagnostic imaging of liver abscess. Crit Rev Diagn Imaging 1992; 33:29–58. 45. Fujihara T, Nagai Y, Kubo T, Seki S, Satake K. Amebic liver abscess. J Gastroenterol 1996; 31:659–663. 46. Hughes MA, Petri WA Jr. Amebic liver abscess. Infect Dis Clin North Am 2000; 14:565–582, viii. 47. Sharma MP, Dasarathy S. Amoebic liver abscess. Trop Gastroenterol 1993; 14:3–9. 48. Pedrosa I, Saiz A, Arrazola J, Ferreiros J, Pedrosa CS. Hydatid disease: radiologic and pathologic features and complications. Radiographics 2000; 20:795–817. 49. Gunay K, Taviloglu K, Berber E, Ertekin C. Traumatic rupture of hydatid cysts: a 12-year experience from an endemic region. J Trauma 1999; 46:164–167. 50. Bartoloni C, Tricerri A, Guidi L, Gambassi G. The efficacy of chemotherapy with mebendazole in human cystic echinococcosis: long-term follow-up of 52 patients. Ann Trop Med Parasitol 1992; 86:249–256. 51. De Rosa F, Teggi A. Treatment of Echinococcus granulosus hydatid disease with albendazole. Ann Trop Med Parasitol 1990; 84:467–872. 52. Sakai Y. Images in clinical medicine. Emphysematous cholecystitis. N Engl J Med 2003; 348:2329. 53. Yusoff IF, Barkun JS, Barkun AN. Diagnosis and management of cholecystitis and cholangitis. Gastroenterol Clin North Am 2003; 32:1145–1168. 54. Fayad LM, Holland GA, Bergin D, et al. Functional magnetic resonance cholangiography (fMRC) of the gallbladder and biliary tree with contrast-enhanced magnetic resonance cholangiography. J Magn Reson Imaging 2003; 18:449–460. 55. Gore RM, Yaghmai V, Newmark GM, Berlin JW, Miller FH. Imaging benign and malignant disease of the gallbladder. Radiol Clin North Am 2002; 40:1307–1323, vi. 56. Johansson M, Thune A, Blomqvist A, Nelvin L, Lundell L. Management of acute cholecystitis in the laparoscopic era: results of a prospective, randomized clinical trial. J Gastrointest Surg 2003; 7:642–645. 57. Kitano S, Matsumoto T, Aramaki M, Kawano K. Laparoscopic cholecystectomy for acute cholecystitis. J Hepatobiliary Pancreat Surg 2002; 9:534–537. 58. Bhattacharya D, Senapati PS, Hurle R,Ammori BJ. Urgent versus interval laparoscopic cholecystectomy for acute cholecystitis: a comparative study. J Hepatobiliary Pancreat Surg 2002; 9:538–542. 59. Papi C, Catarci M, D’Ambrosio L, et al. Timing of cholecystectomy for acute calculous cholecystitis: a metaanalysis. Am J Gastroenterol 2004; 99:147–155. 60. Senapati PS, Bhattarcharya D, Harinath G, Ammori BJ. A survey of the timing and approach to the surgical management of cholelithiasis in patients with acute biliary pancreatitis and acute cholecystitis in the UK. Ann R Coll Surg Engl 2003; 85:306–312. 61. Serralta AS, Bueno JL, Planells MR, Rodero DR. Prospective evaluation of emergency versus delayed laparoscopic cholecystectomy for early cholecystitis. Surg Laparosc Endosc Percutan Tech 2003; 13:71–75.

S.P. Hiotis and H.L. Pachter 62. Byrne MF, Suhocki P, Mitchell RM, et al. Percutaneous cholecystostomy in patients with acute cholecystitis: experience of 45 patients at a US referral center. J Am Coll Surg 2003; 197:206–211. 63. Haroun A, Hadidi A, Tarawneh E, Shennak M. Magnetic resonance cholangiopancreatography in patients with upper abdominal pain: a prospective study. Hepatogastroenterology 2003; 50:1236–1241. 64. Raraty MG, Finch M, Neoptolemos JP. Acute cholangitis and pancreatitis secondary to common duct stones: management update. World J Surg 1998; 22:1155– 1161. 65. Himal HS. Common bile duct stones: the role of preoperative, intraoperative, and postoperative ERCP. Semin Laparosc Surg 2000; 7:237–245. 66. Hammarstrom LE, Andersson R, Stridbeck H, Ihse I. Influence of bile duct stones on patient features and effect of endoscopic sphincterotomy on early outcome of edematous gallstone pancreatitis. World J Surg 1999; 23:12– 17. 67. Yao LQ, Zhang YQ, Zhou PH, Gao WD, He GJ, Xu MD. Endoscopic sphincterotomy or papillary balloon dilatation for choledocholithiasis. Hepatobiliary Pancreat Dis Int 2002; 1:101–105. 68. Brooks AD, Mallis MJ, Brennan MF, Conlon KC. The value of laparoscopy in the management of ampullary, duodenal, and distal bile duct tumors. J Gastrointest Surg 2002; 6:139–146. 69. Cohen ME, Slezak L, Wells CK, Andersen DK, Topazian M. Prediction of bile duct stones and complications in gallstone pancreatitis using early laboratory trends. Am J Gastroenterol 2001; 96:3305–3311. 70. Meek K, de Virgilio C, Murrell Z, et al. Correlation between admission laboratory values, early abdominal computed tomography, and severe complications of gallstone pancreatitis. Am J Surg 2000; 180:556–560. 71. Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: value of CT in establishing prognosis. Radiology 1990; 174:331–336. 72. Balthazar EJ. Complications of acute pancreatitis: clinical and CT evaluation. Radiol Clin North Am 2002; 40:1211– 1227. 73. Balthazar EJ. Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology 2002; 223:603– 613. 74. Pisters PW, Ranson JH. Nutritional support for acute pancreatitis. Surg Gynecol Obstet 1992; 175:275–284. 75. Ranson JH, Rifkind KM, Roses DF, Fink SD, Eng K, Spencer FC. Prognostic signs and the role of operative management in acute pancreatitis. Surg Gynecol Obstet 1974; 139:69–81. 76. Barkun AN. Early endoscopic management of acute gallstone pancreatitis—an evidence-based review. J Gastrointest Surg 2001; 5:243–250. 77. Kaw M, Al-Antably Y, Kaw P. Management of gallstone pancreatitis: cholecystectomy or ERCP and endoscopic sphincterotomy. Gastrointest Endosc 2002; 56:61–65. 78. Ricci F, Castaldini G, de Manzoni G, et al. Treatment of gallstone pancreatitis: six-year experience in a single center. World J Surg 2002; 26:85–90.

31. Liver and Biliary Tract 79. Lobo DN, Jobling JC, Balfour TW. Gallstone ileus: diagnostic pitfalls and therapeutic successes. J Clin Gastroenterol 2000; 30:72–76. 80. Doko M, Zovak M, Kopljar M, Glavan E, Ljubicic N, Hochstadter H. Comparison of surgical treatments of gallstone ileus: preliminary report. World J Surg 2003; 27:400– 404. 81. Reisner RM, Cohen JR. Gallstone ileus: a review of 1001 reported cases. Am Surg 1994; 60:441–446. 82. Zuegel N, Hehl A, Lindemann F, Witte J. Advantages of one-stage repair in case of gallstone ileus. Hepatogastroenterology 1997; 44:59–62. 83. Suarez-Penaranda JM, de la Calle MC, Rodriguez-Calvo MS, Munoz JI, Concheiro L. Rupture of liver cell adenoma with fatal massive hemoperitoneum resulting from minor road accident. Am J Forensic Med Pathol 2001; 22:275– 277. 84. Hotokezaka M, Kojima M, Nakamura K, et al. Traumatic rupture of hepatic hemangioma. J Clin Gastroenterol 1996; 23:69–71. 85. Yoshida H, Onda M, Tajiri T, et al. Treatment of spontaneous ruptured hepatocellular carcinoma. Hepatogastroenterology 1999; 46:2451–2453. 86. Sonoda T, Kanematsu T, Takenaka K, Sugimachi K. Ruptured hepatocellular carcinoma evokes risk of implanted metastases. J Surg Oncol 1989; 41:183–186. 87. Vergara V, Muratore A, Bouzari H, et al. Spontaneous rupture of hepatocellular carcinoma: surgical resection and long-term survival. Eur J Surg Oncol 2000; 26:770– 772. 88. Sato Y, Fujiwara K, Furui S, et al. Benefit of transcatheter arterial embolization for ruptured hepatocellular carcinoma complicating liver cirrhosis. Gastroenterology 1985; 89:157–159. 89. Shimada R, Imamura H, Makuuchi M, et al. Staged hepatectomy after emergency transcatheter arterial embolization for ruptured hepatocellular carcinoma. Surgery 1998; 124:526–535. 90. Sarmiento JM, Sarr MG. Necrotic infected liver metastasis from colon cancer. Surgery 2002; 132:110–111. 91. Huang SF, Ko CW, Chang CS, Chen GH. Liver abscess formation after transarterial chemoembolization for malignant hepatic tumor. Hepatogastroenterology 2003; 50:1115–1118. 92. Kim W, Clark TW, Baum RA, Soulen MC. Risk factors for liver abscess formation after hepatic chemoembolization. J Vasc Intervent Radiol 2001; 12:965–968. 93. Song SY, Chung JW, Han JK, et al. Liver abscess after transcatheter oily chemoembolization for hepatic tumors: incidence, predisposing factors, and clinical outcome. J Vasc Intervent Radiol 2001; 12:313–320. 94. Yeh TS, Jan YY, Tseng JH, et al. Malignant perihilar biliary obstruction: magnetic resonance cholangiopancreatographic findings. Am J Gastroenterol 2000; 95:432–440. 95. Georgopoulos SK, Schwartz LH, Jarnagin WR, et al. Comparison of magnetic resonance and endoscopic retrograde cholangiopancreatography in malignant pancreaticobiliary obstruction. Arch Surg 1999; 134:1002–1007. 96. Marcus SG, Dobryansky M, Shamamian P, et al. Endoscopic biliary drainage before pancreaticoduodenectomy

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for periampullary malignancies. J Clin Gastroenterol 1998; 26:125–129. Lai EC, Lo CM, Liu CL. Endoscopic stenting for malignant biliary obstruction. World J Surg 2001; 25:1289–1295. Espat NJ, Brennan MF, Conlon KC. Patients with laparoscopically staged unresectable pancreatic adenocarcinoma do not require subsequent surgical biliary or gastric bypass. J Am Coll Surg 1999; 188:649–657. Lillemoe KD, Cameron JL, Hardacre JM, et al. Is prophylactic gastrojejunostomy indicated for unresectable periampullary cancer? A prospective randomized trial. Ann Surg 1999; 230:322–330. Sohn TA, Lillemoe KD. Surgical palliation of pancreatic cancer. Adv Surg 2000; 34:249–271. MacMathuna P, Vlavianos P, Westaby D, Williams R. Pathophysiology of portal hypertension. Dig Dis 1992; 10(Suppl 1):3–15. McCormick PA, Jenkins SA, McIntyre N, Burroughs AK. Why portal hypertensive varices bleed and bleed: a hypothesis. Gut 1995; 36:100–103. Hoefs JC, Jonas GM, Sarfeh IJ. Diagnosis and hemodynamic assessment of portal hypertension. Surg Clin North Am 1990; 70:267–289. Celinska-Cedro D, Teisseyre M, Woynarowski M, Socha P, Socha J, Ryzko J. Endoscopic ligation of esophageal varices for prophylaxis of first bleeding in children and adolescents with portal hypertension: preliminary results of a prospective study. J Pediatr Surg 2003; 38:1008–1011. Yoshikawa I, Murata I, Nakano S, Otsuki M. Effects of endoscopic variceal ligation on portal hypertensive gastropathy and gastric mucosal blood flow. Am J Gastroenterol 1998; 93:71–74. Teres J, Cecilia A, Bordas JM, Rimola A, Bru C, Rodes J. Esophageal tamponade for bleeding varices. Controlled trial between the Sengstaken-Blakemore tube and the Linton-Nachlas tube. Gastroenterology 1978; 75:566– 569. McCormick PA, Burroughs AK, McIntyre N. How to insert a Sengstaken-Blakemore tube. Br J Hosp Med 1990; 43: 274–277. Sokucu S, Suoglu OD, Elkabes B, Saner G. Long-term outcome after sclerotherapy with or without a betablocker for variceal bleeding in children. Pediatr Int 2003; 45:388–394. Schiedermaier P, Koch L, Stoffel-Wagner B, Layer G, Sauerbruch T. Effect of propranolol and depot lanreotide SR on postprandial and circadian portal haemodynamics in cirrhosis. Aliment Pharmacol Ther 2003; 18:777– 784. Gusberg RJ. Distal splenorenal shunt—premise, perspective, practice. Dig Dis 1992; 10(Suppl 1):84–93. Rosemurgy AS 2nd, Bloomston M, Zervos EE, et al. Transjugular intrahepatic portosystemic shunt versus Hgraft portacaval shunt in the management of bleeding varices: a cost-benefit analysis. Surgery 1997; 122:794– 800. Serafini FM, Zwiebel B, Black TJ, Carey LC, Rosemurgy AS 2nd. Transjugular intrahepatic portasystemic stent shunt in the treatment of variceal bleeding in hepatocellular cancer. Dig Dis Sci 1997; 42:59–65.

496 113. Rosemurgy AS, Serafini FM, Zweibel BR, et al. Transjugular intrahepatic portosystemic shunt vs. smalldiameter prosthetic H-graft portacaval shunt: extended follow-up of an expanded randomized prospective trial. J Gastrointest Surg 2000; 4:589–97. 114. McCormick PA, Dick R, Chin J, et al. Transjugular intrahepatic portosystemic stent-shunt. Br J Hosp Med 1993; 49:791–797.

S.P. Hiotis and H.L. Pachter 115. Boyer TD. Transjugular intrahepatic portosystemic shunt: current status. Gastroenterology 2003; 124:1700– 1710. 116. Pachter HL, Hofstetter SR. The current status of nonoperative management of adult blunt hepatic injuries. Am J Surg 1995; 169:442–454. 117. Pachter HL. Is a conservative approach justified in penetrating liver injury? HPB Surg 1995; 8:205–208.

32 Pancreas Juan A. Asensio, Patrizio Petrone, and L.D. Britt

Case Scenario You are asked to evaluate a patient who was admitted for alcohol-induced pancreatitis. The patient has had a smoldering course despite aggressive resuscitation and is, currently, febrile and toxic while receiving broad-spectrum antimicrobial therapy. Physical examination demonstrates midepigastric tenderness on moderate palpation. Computed tomography scan findings are consistent for necrotizing pancreatitis. The white blood cell count has increased from 12,000 to 16,000 over the past 48 hours. Which of the following is the most prudent management plan at this time? (A) Continued medical management (B) Peritoneal lavage (C) Computed tomography—directed biopsy of the necrotic tissue for confirmation of infectious etiology (D) Celiotomy (E) Administration of octreotide

The pancreas is a classic example of an organ poorly designed to withstand the ravages of trauma. Located in the inaccessible and dark reaches of the retroperitoneum, injuries to the pancreas are infrequently suspected and often diagnosed late while more apparent injuries to other organs are addressed. Furthermore, as if to add an insult to injury, pancreatic injuries can be missed, even by experienced trauma surgeons. The soft consistency of this organ and its marginal blood supply, which is shared with the duodenum, are not amenable to sound, leak-proof repairs that heal uneventfully. Pancreatic resections, particularly those involving the head, are extremely difficult procedures, especially when performed under the adverse physiologic conditions of shock or exsanguination.

Because it lies against a most unyielding neighbor, the spinal column, the pancreas is extremely susceptible to crush injury. The pancreas, when injured, can be quite an unforgiving organ. Its myriad of enzymatic byproducts, used for digestion, can also cause injury to the host by digesting suture lines used to repair hollow viscera or vascular structures. Repairing or resecting the pancreas is technically challenging, especially at the time of suturing. Its soft consistency is often not amenable to the placement of sutures. Any less than delicate moves during repair or any undue application of force during its mobilization will be met with tearing or bleeding from the gland that can be quite difficult to control.

Pertinent Anatomy for Trauma Surgeons The pancreas lies transversally in the retroperitoneum across the upper abdomen. It measures between 15 and 20 cm in length, approximately 3 cm in width, and 1 to 1.5 cm in thickness. Its average weight is approximately 90 g, with a normal weight ranging from 40 to 180 g. It is almost triangular in shape and is related to the omental bursa above, the transverse mesocolon anteriorly, and the greater abdominal cavity below. Its motion is relatively limited; therefore, for all practical purposes, it is considered a fixed organ. The pancreas is anteriorly related to the liver, duodenum, pylorus, stomach, and spleen above; the duodenum, jejunum, transverse colon, and spleen below; and at the same level as the transverse colon, mesocolon, and spleen. Posterior to the pancreas and sharing an anatomically intimate relationship are the aorta, inferior vena cava, both right and left renal veins, and right renal artery. The pancreas is also in close proximity to the hilum of the right kidney. The superior mesenteric artery and vein course posterior to the neck of the pancreas, in their groove, and are closely attached

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to the uncinate process, with the uncinate wrapping around the posterolateral aspect of the vein. The head of the pancreas lies within the concave sweep of the duodenum, with the body directly crossing the spine and angularly directed superiorly and toward the left shoulder, with the tail in close communication with the hilum of the spleen. The pancreas is arbitrarily divided into five parts: the head, the uncinate process, the neck, the body, and the tail. Although variations in the shape of the pancreas are known, they are of little surgical importance. The head of the pancreas is defined as the portion lying to the right of the superior mesenteric artery and vein. It is located at the level of the second lumbar vertebra in the midline or slightly to the right of it. The head of the pancreas is located to the left of the spinal column in approximately 5% of individuals.1 It lies nestled in the C-loop of the duodenum and, in conjunction with it, is suspended from the liver by the hepatoduodenal ligament; thus it is firmly fixed to the medial aspect of the second and third portions of the duodenum. The divisory line between the head and the neck is marked anteriorly by a line originating from the portal vein superiorly to the superior mesenteric vein inferiorly. The head of the pancreas is flattened. Its anterior surface is related to the pylorus and transverse colon. The anterior pancreaticoduodenal arcade parallels the duodenal curvature but is related to the anterior pancreatic surface rather than to the duodenum. Similarly, the posterior surface of the head of the pancreas is related to the hilum and medial border of the right kidney, the right renovascular pedicle, the inferior vena cava and ostia of the left renal vein as it drains into the inferior vena cava, the right crus of the diaphragm, the posterior pancreaticoduodenal arcade, and the right gonadal vein. The distal portion of the common bile duct is usually totally or partially embedded in the pancreatic substance in 85% or lies in a groove behind the pancreatic head in 15% of the cases. An abnormal hepatic or middle colic artery may lie within or behind the head.2 The uncinate process of the pancreas is an extension of the lower left part of the posterior surface of the head, usually passing behind the portal vein and the superior mesenteric vessels just anteriorly to the aorta and inferior vena cava. The presence of the uncinate process is variable. It may be absent, or it may completely encircle the superior mesenteric vessels. Knowledge of its presence should always be taken into consideration when planning distal pancreatectomy. The neck of the pancreas measures approximately 1.5 to 2 cm in length and lies at the level of the first lumbar vertebra. It is fixed between the celiac trunk superiorly and the superior mesenteric vessels inferiorly. It is defined as that portion that overlies the superior mesen-

J.A. Asensio, P. Petrone, and L.D. Britt

teric vessels. Anteriorly, the neck is partially covered by the pylorus. To the right, the gastroduodenal artery gives off the superior pancreaticoduodenal artery. Posteriorly the union of the superior mesenteric and splenic veins forms the portal vein. In general, there are no anterior tributaries to this vessel. However, one or two small veins may enter directly the portal vein, and four to five may enter the superior mesenteric vein. Making contributions to the portal vein from the right are a few short lateral veins, whereas entering the portal vein from the left are both the left gastric and splenic veins and rarely the inferior mesenteric vein. The body of the pancreas lies at the level of the first lumbar vertebra and is technically defined as that portion of the pancreas that lies to the left of the superior mesenteric vessels. It is triangularly shaped and is related to the fourth portion to the duodenum and the ligament of Treitz. Both superior mesenteric vessels emerge from under the inferior border of the body and pass over the uncinate process of the head of the pancreas. The crossing over of these vessels divides the third and the fourth portions of the duodenum. The superior border of the body of the pancreas is related to the celiac axis and hepatic artery on the right and to the splenic vessels on the left. The splenic artery and vein course along its superior border. The anterior surface of the body of the pancreas is covered by the posterior wall of the omental bursa that separates the pancreas from the stomach. It is also related to the transverse mesocolon that separates into two layers, one leaf covering its anterior and one leaf covering its inferior surface. The middle colic artery emerges from beneath the inferior border of the pancreas to course through the leaves of the mesocolon. The inferior mesenteric vein is close to the distal portion of the inferior border of the body. The posterior surface is in close proximity to the origin of the superior mesenteric artery, left crus of the diaphragm, the left renovascular pedicle, left kidney, and adrenal gland. The tail of the pancreas rises to the level of the twelfth thoracic vertebra. It is quite mobile. This lends for easy mobilization while its tip is closely related to the hilum of the spleen. Along with the splenic vessels, it is covered by the two layers of the splenorenal ligament. There is no true anatomic landmark dividing the body and the tail, nor is there any anatomically defined dividing line as in the case of the head and neck. The main pancreatic duct of Wirsung originates at the tail of the pancreas at the level of twelfth thoracic vertebra.3 Throughout its course in the tail and body, the duct lies midway between the superior and inferior margins and slightly more posterior than anterior. The duct of Wirsung and the accessory duct of Santorini lie anterior to the major pancreatic vessels. In the body and tail, 15 to 20 short tributaries enter the duct at almost right

32. Pancreas

angles.4,5 The superior and inferior tributaries tend to alternate with one another. In addition, the duct of Wirsung may receive a longer tributary draining the uncinate process. In some patients, the duct of Santorini in the head empties directly into the main duct. Upon reaching the head of the pancreas, the duct of Wirsung may or may not join the duct of Santorini. It turns in a caudal and slightly posterior direction before the entrance at the level of the ampulla of Vater, where the duct turns horizontally to join the caudal surface of the common bile duct to enter the wall of the duodenum, usually at the level of the second lumbar vertebra.6 The duct of Santorini may drain the anterior superior portion of the head of the pancreas by entering either directly into the duodenum at the minor papilla or into the duct of Wirsung. In 60% of the patients, both ducts open into the duodenum, whereas in 30%, the duct of Wirsung carries the entire secretion of the gland, and the duct of Santorini ends blindly. In 10% the duct of Santorini carries the entire secretion of the gland. In this case the duct of Wirsung is small or totally absent.7 The arterial blood supply of the pancreas originates from both the celiac trunk and the superior mesenteric artery. The pancreaticoduodenal arterial arcades are constant. They are formed by a pair of superior and inferior pancreaticoduodenal arteries, each bifurcating into anterior and posterior branches to form these arcades. These arcades lie within the pancreas and also supply the duodenum.The gastroduodenal artery arises as the first major branch from the common hepatic artery approximately 1 cm after the common hepatic artery originates from the celiac trunk.8 It also gives off the right gastroepiploic and subsequently the superior pancreaticoduodenal artery, which bifurcates into both anterior superior and posterior superior pancreaticoduodenal arteries.The anterior superior pancreaticoduodenal artery lies on the anterior surface of the pancreas and gives off 8 to 10 branches to the anterior surface of the duodenum and numerous branches to the pancreas. On the anterior superior surface, it joins the anterior inferior pancreaticoduodenal artery, a branch from the inferior pancreaticoduodenal artery coming from the superior mesenteric artery to form the anterior arcade. The posterior superior pancreaticoduodenal artery can only be seen when the pancreas is mobilized in a cephalad direction to expose its posterior surface. The posterior superior pancreaticoduodenal artery then joins the posterior inferior pancreaticoduodenal artery to form the posterior arcade. Another very important blood vessel supplying the pancreas is the dorsal pancreatic artery, known by several names, such as the great superior pancreatic artery of Haller, the superior pancreatic artery of Testut, or the supreme pancreatic artery of Kirk (magna pancreatica). It lies posterior to the neck of the pancreas, and its most

499

common origin is from the proximal splenic artery in 39% of the cases. However, it may arise from the celiac trunk, from the hepatic artery, and least frequently from the superior mesenteric artery. The splenic artery is located on the posterior aspect of the body and tail of the pancreas, and it follows a tortuous course above or below the superior margin of the pancreas, giving off many branches. There are from 2 to 10 branches of the splenic artery that supply the body and tail of the pancreas; many of these branches anastomose with the transverse pancreatic artery. The venous drainage of the pancreas in general parallels the arteries and lies superficial to them. Venous drainage of the pancreas is to the portal vein, the splenic vein, and the superior and inferior mesenteric veins. The portal vein arises from the confluence of the superior mesenteric and splenic veins behind the neck of the pancreas. The portal vein lies behind the pancreas and in front of the inferior vena cava. It can easily be separated from the posterior surface of the pancreas. As a result, the pancreatic neck can be separated from the portal vein with a small risk of bleeding when transecting the neck of the pancreas either to perform a distal pancreatectomy or to gain exposure to the confluence of the portal and superior mesenteric veins, or to either vessels, in an effort to control massive retropancreatic bleeding.9,10

Anatomic Location of Injury An extensive review of the literature to identify the anatomic location of pancreatic injuries yielded 1,024 injuries (Table 32.1). In this review, the most frequent sites of pancreatic injury included a combination of the head and neck, with 378 injuries (37%), and the body, which sustained 352 (34%). The least frequently injured Table 32.1. Anatomic location of injury. First author (year)

Head and neck 11

Body

Tail

Baker (1963) Culotta (1956)12 Jones (1965)13 Anane-Sefah (1975)14 Babb (1976)15 Campbell (1980)16 Nilsson (1986)17 Feliciano (1987)18 Leppaniemi (1988)19 Lewis (1991)20 Gentilello (1991)21 Madiba (1995)22 Asensio (2004)23

13 8 25 20

27 5 37 9

16 8 13 15

26 13 6 101 17

28 21 6 21 20

30

131 11 43 82

50

Total

378 (37%)

Multiple

6

11 7 6

2 63 65 352 (34%)

38 79 294 (29%)

23 (3%)

500


portion of the pancreas was the tail, accounting for 294 injuries (29%). Multiple sites of injury occurred in 23 patients (3%). An anatomic combination of injuries to the head and neck is the most frequent site for both penetrating and blunt trauma. However, with penetrating trauma, injuries are generally distributed throughout the anatomic course of the pancreas. In blunt trauma most injuries occur at the neck of the gland.

Associated Injuries The pancreas is rarely injured alone. In fact, multiple associated injuries are the rule rather than the exception. This situation is particularly true for both mechanisms of

injuries. Isolated pancreatic injuries are usually seen in the form of blunt pancreatic transections. An extensive review of the literature, including a total of 3,679 patients who sustained 8,480 associated injuries, demonstrates that the liver is the most frequently associated organ injured, with a frequency of 19% of the cases. Other commonly associated injured organs include the stomach (15%), spleen (10.5%), colon (8%), and duodenum (8%). Major abdominal venous injuries, to the inferior vena cava and the portal and superior mesenteric veins, were present in 5.5% of the cases. Arterial injuries, to the aorta and superior mesenteric artery, were present in 4.5% of the patients. Thus vascular injuries represent the third most frequent injury seen in association with pancreatic injuries (Tables 32.2 through 32.4).

Table 32.2. Associated injuries (n = 8,480). First author (year)

No. of patients

Associated injuries

First author (year) 46

24

62

153

Gorenstein (1987)

Baker (1963)11

82

116

Leppaniemi (1988)19

Stone (1962)

13

Jones (1965)

77

25

Salyer (1967)

Werschky (1968) Foley (1969)27 Sheldon (1970)

28

Bach (1971)

140

109

49

3

3

44

98 45

30

63

123

Salam (1972)31

4

2

White (1972)

Yellin (1972)

32

60

Anderson (1974)

33

70 14

48

Fabian (1990)

59

29

Pachter (1989)

1

1 26

204

43 16

47

Flynn (1990)

Ivatury (1990)50 20

Lewis (1991)

Gentilello (1991)

1,215 2

Stone (1981) Berni (1982)

38

283

39

Cogbill (1982)

54 40

Fitzgibbons (1982)41 Oreskovich (1984) Sims (1984)

43

Wynn (1985)

44

Nowak (1986)45

42

63

63

80

55

5

30

152

237

Craig (1995)56

13

27

Degiannis (1995)

57

57

164

Degiannis (1996)

58

48

161

1

5

Smith (1996)59 60

961

Akhrass (1997)

72

230

89

61

51

96

62

154

46

39

81

62

196

214

720

3,679

8,480

Farrell (1996)

116

Patton (1997)

56

116

Timberlake (1997)63

44

220

38

Rosen (1994)

44

117

143

57

54

25

1

11 103

17

Buck (1992)

6

448

85

280

53

Lowe (1977)34

Majeski (1980)37

65

175

Madiba (1995)22

Graham (1979)

7

74

Delcore (1994)

608

9

131

174

300

89

Voeller (1991)52

Cogbill (1991)

366

36

27

43

48

76

Jones (1978)

21

10

50

35

Associated injuries

51

Babb (1976)15

Anane-Sefah (1975)

21

No. of patients

117 43

40

72

42

116

64

Young (1998)

Asensio (2004) Total

23

32. Pancreas

501

Table 32.3. Associated injuries (n = 8,480) per organ. First author (year) Stone (1962)24 Baker (1963)11 Jones (1965)13 Salyer (1967)25 Werschky (1968)26 Foley (1969)27 Sheldon (1970)28 Bach (1971)29 White (1972)30 Salam (1972)31 Yellin (1972)32 Anderson (1974)33 Anane-Sefah (1975)14 Babb (1976)15 Lowe (1979)34 Jones (1978)35 Graham (1978)36 Majeski (1980)37 Stone (1981)38 Berni (1982)39 Cogbill (1982)40 Fitzgibbons (1982)41 Oreskovich (1984)42 Sims (1984)43 Wynn (1985)44 Nowak (1986)45 Gorenstein (1987)46 Leppaniemi (1988)19 Pachter (1989)47 Fabian (1990)48 Eastlick (1990)65 Flynn (1990)49 Ivatury (1990)50 Lewis (1991)20 Gentilello (1991)21 Cogbill (1991)51 Voeller (1991)52 Buck (1992)53 Rosen (1994)54 Delcore (1994)55 Madiba (1995)22 Craig (1995)56 Degiannis (1995)57 Degiannis (1996)58 Smith (1996)59 Akhrass (1997)60 Farrell (1996)61 Patton (1997)62 Timberlake (1997)63 Young (1998)64 Asensio (2004)23 Total

Major vessel

Stom

BT

10 8 41

35 24 40

3

24

26

8 1

7 2 11

2

61 2 16 8 18

21 5 99 23 3 149 184

5 2 28 20 1 37 55

6

59

7 22

150 28 17 23 7 23 14 20 3 18 1 19 1 26 37 26 6 26 68 10 14 2 59 5 19 21 1 39 5

23 82

9 33 100

379

1,536

16 25 87 18

29

11 9

3

10

37

Liver

SB

Colon

Major veins

32 24 47

7 16

8 9 12

63

21

27 7 22

8 5 9 12 8 3 1 6 1 12 4

28 11 1 56 73 46 3 13 11 4 8 17

6 4

4 43 98 56 12

4

1 7 1

Major arteries 8 3 6 29 3 4

21 5 41 35 4 117 206

2 5 18 5 4 20

113 10 18 23 3

26

65 65 1 35 2

4

Duod

Sp

GU

13 12 16 1 31 2 8 7 14

18 10 13

19 10 16

29

29

19 7 18

10 4

7

7 6 38 21 1 53 122

16 38 5 56 88 56 10 17 7

1 14

10 8 2

12 26

1 9

2 21

22 25

21 42 17 1 22 58 9 14

23

3

1 11 1 8 4 3 6

5 7 29 5 10 2 14 2 32 32

6 16 34 6 5 1 21

2 4

12 12

8 5

17 5

3 8 49

14 14 24 4 21 74

3 13 1 2 22 1 9 54

1 28 105

7 18

540

671

479

1,300

158

8

9 2 1

26 18

6

3

5

8

8

1 11 1

58 24 17

8 7 3 2

9 1 5 6 13 4

12 18 19 12

19 15 4

39 34

18 30

14

15

22 4 16 6

7

15 4

1

28

22 4 22 78

22 13 53

13 19 69

374

653

886

651

3 12 7

BT, biliary tree; Duod, duodenum; GU, genitourinary; SB, small bowel; Sp, spleen; Stom, stomach.

68 5 10 15

3

1

5

13 3

88 22 1 67 136 1 70 19 9 9 2 10 13 12 3

7 21 1 15

2

502


Table 32.4. Associated injuries (n = 8,480). Organ

No. of injuries

Percentage (%)

Liver Stomach Major vessels Spleen Colon Duodenum Genitourinary Small bowel Major veins Major arteries Biliary tree/gallbladder

1,536 1,300 1,232 886 671 653 651 540 479 374 158

18.0 15.0 14.5 10.5 8.0 8.0 8.0 6.0 5.5 4.5 2.0

Total

8,480

100

Surgical Techniques Intraoperative Evaluation and Exposures Proven or suspected pancreatic injury, coupled with the classic findings of intraabdominal injury, mandates immediate exploratory laparotomy. Abdominal injuries should be explored through a midline incision extending from xiphoid to pubis, followed by a thorough exploration of the entire abdominal cavity. The pancreas should be thoroughly explored. The head, neck, body, and tail should be visualized directly. Intraoperative findings that alert the trauma surgeon to the presence of a pancreatic injury include central retroperitoneal hematoma, proximity injuries, bile staining noted in the retroperitoneum, and edema surrounding the pancreas and lesser sac.66,67 The goal of a thorough exploration of all pancreatic injuries is to include or exclude the presence of a major pancreatic ductal injury. There are three basic maneuvers to achieve this goal. A Kocher maneuver is first performed by sharply incising the lateral peritoneal attachments of the duodenum and sweeping the second and third portions medially, utilizing a meticulous combination of sharp and blunt dissection. In the presence of a large retroperitoneal hematoma we recommend that the nasogastric tube be advanced through the pylorus to serve as a guide and thus avoid iatrogenic lacerations of the duodenal wall during dissection. Duodenal mobilization should be extensive to allow for palpation of the head of the pancreas to the level of the superior mesenteric vessels. This maneuver will allow the surgeon to visualize the anterior and posterior aspects of the second and third portions of the duodenum and will also permit exposure of the head and uncinate process of the pancreas and inferior vena cava. If the pericaval tissues are dissected cephalad, the inferior vena cava can also be exposed at its suprarenal location. The trauma surgeon must determine if the patient possesses an uncinate process. This is absent in approximately 15% of patients. This becomes an important

consideration if the trauma surgeon entertains performing a distal pancreatectomy to the left of the superior mesenteric vessels, as, normally, a resection to the left of the superior mesenteric vessels extirpates approximately 65% of the gland. Although this is an extensive resection, it is not associated with the development of pancreatic exocrine or endocrine insufficiency. However, if the uncinate process is absent, resection to the left of the superior mesenteric vessels will result in extirpation of 80% of the pancreatic mass. Resections of this magnitude have been associated with the development of pancreatic insufficiency and the need for insulin replacement. The next maneuver to expose the pancreas consists of transection of the gastrohepatic ligament to gain access to the lesser sac. This facilitates inspection of the superior border of the pancreas, including the head and body, as well as the splenic artery and vein as they course along the superior border of the pancreas. Transection of the gastrocolic ligament permits full inspection of the anterior aspect and inferior borders of the gland inclusive of the head, body, and tail. Complex maneuvers for pancreatic exposure include the Aird maneuver, which exposes the posterior aspect of the tail by mobilizing the splenic flexure of the colon and lienosplenic, splenocolic, and splenorenal ligaments. This mobilizes the spleen from a lateral to medial position.When an injury is detected penetrating the anterior surface of the pancreas, the trauma surgeon must evaluate the integrity of the main pancreatic duct, as this is the “sine qua non” of major pancreatic injury. This requires exposure of the posterior aspect of the body and tail of the pancreas. This complex maneuver may be accomplished by sharply transecting the retroperitoneal attachments of the inferior border of the pancreas while elevating the organ cephalad to allow for inspection of the posterior surface, followed by careful bimanual palpation. This maneuver is technically challenging and should be performed with meticulous precision to prevent iatrogenic injury to the superior mesenteric vessels. All of these maneuvers can provide accurate intraoperative assessment of both glandular and ductal integrity.66–68

Intraoperative Adjunct Techniques The use of clinical intraoperative observations such as direct visualization of ductal violations, complete transection of the pancreas, laceration of more than one half of the diameter of the gland, central perforations, and severe lacerations with or without massive tissue disruption can predict the presence of a major ductal injury with a high degree of accuracy. However, there are circumstances in which assessment of the ductal integrity cannot be made. In these cases, intraoperative pancreatography has been recommended as a technique for visualization of the main pancreatic duct.69,70

32. Pancreas

503

The technique of intraoperative pancreatography consists of intubating the ampulla of Vater through an open duodenotomy and cannulating the main pancreatic duct. Alternatively, but not recommended, the tail of the pancreas can be amputated and the main duct also cannulated via the amputated tail of the pancreas. The duct is then cannulated with a 5-F pediatric feeding tube followed by gentle instillation of 1 to 5 mL of contrast material to radiographically visualize the pancreatic duct and detect any escape of contrast.71 Intubating the ampulla of Vater requires the creation of a duodenotomy, unless there is an associated duodenal injury present. Location of the ampulla of Vater may also be very difficult even with an open duodenum. In extreme and rare cases when pancreatography is imperative, a choledochotomy may be performed with passage of biliary probes or Bakes dilators to identify the ampulla. This also carries the risk of iatrogenic injury to the common bile duct and ampulla, as well as the need for placement of a T tube in a generally small common bile duct that can result in biliary leaks and/or fistulas. Similarly, closure of the duodenotomy may predispose the patient to the development of a duodenal leak and/or fistula. An alternative method to intraoperative pancreatography is a cholangiography using a small butterfly needle. This has a very limited but valuable role and should be reserved to assess ductal integrity when injuries have occurred at the head of the pancreas. This adjunct procedure may yield trauma surgeons vital information to determine whether extensive damage exists to the major duct in the head as a criterion for selection of a complex procedure such as pancreaticoduodenectomy.

Injury Classification All pancreatic injuries must be classified utilizing the American Association for the Surgery of Trauma—Organ Injury Score (AAST-OIS)72 (Table 32.5). Simpler surgiTable 32.5. American Association for the Surgery of Trauma— Organ Injury Score (AAST-OIS) for pancreatic injuries. Grade I II

Injury Hematoma Laceration Hematoma Laceration

III

Laceration

IV

Laceration

V

Laceration

Description Minor contusion without duct injury Superficial laceration without duct injury Major contusion without duct injury or tissue loss Major laceration without duct injury or tissue loss Distal transection or parenchymal injury with duct injury Proximal* transection or parenchymal injury involving ampulla Massive disruption of pancreatic head

* Proximal pancreas is to the patient’s right of the superior mesenteric vein. Source: Reprinted with permission from Moore et al.72

Table 32.6. Surgical techniques and procedures for pancreatic and pancreaticoduodenal injuries. Simple drainage Simple pancreatorraphy Complex pancreatorraphy Distal pancreatectomy (to the left of the superior mesenteric vessels) Distal pancreatectomy (to the left of the superior mesenteric vessels) with splenic preservation Extended distal pancreatectomy (to the right of the superior mesenteric vessels) Extended distal pancreatectomy (to the right of the superior mesenteric vessels) with distal pancreaticojejunostomy Duodenal diverticularization (vagotomy and antrectomy, gastrojejunostomy, duodenorraphy, T-tube drainage, and external drainage) Pyloric exclusion Pancreatoduodenectomy (Whipple’s procedure)

cal techniques should be selected for management of the lesser grade injuries while reserving the most complex techniques for the more challenging and severe injuries.

Principles of Injury Management A large number of surgical techniques have been described (Table 32.6). Approximately 60% of all pancreatic injuries can be treated by external drainage alone. Approximately 70% can be treated by simple pancreatorraphy plus drainage. Basic surgical principles, such as debridement to viable tissue, closure of the transected pancreas with staples and/or nonabsorbable sutures, and ligation of the transected pancreatic duct if identified, are the mainstays of successful management of pancreatic injuries. We strongly recommend that all pancreatic contusions, as well as any capsular lacerations, be managed by simple external drainage with closed suction systems. The capsule of the pancreas should not be closed by itself, as this has been known to lead to the formation of pancreatic pseudocysts. Any injury that lacerates the pancreatic parenchyma should be gently examined to determine whether there is major versus minor ductal involvement. Having excluded this type of injury, we recommend performing simple pancreatorraphy utilizing nonabsorbable sutures in order to approximate the edges of the lacerated parenchyma. Pancreatorraphy decreases the incidence of leak from pancreatic exocrine secretions and thus the inflammatory process in surrounding tissues. At times, it may be quite difficult for the trauma surgeon to determine the involvement of the major ductal system. Performing a pancreatorraphy in this scenario will not only miss but also undertreat a major ductal injury, increasing the possibility for development of severe postoperative complications. In this scenario, it is necessary to upgrade the injury in order to select more

504

appropriate treatment, which in this case would be pancreatic resection. This decision is simplified if the injury lies to the left of the superior mesenteric vessels, where distal resection, although technically challenging, does not approach the degree of complexity of a resection to the right of the superior mesenteric vessels. If this injury were to lie to the right of the superior mesenteric vessels, the surgeon must consider either draining extensively and accepting the development of a pancreatic fistula with all of the associated complications or performing an extended resection to the right of the superior mesenteric vessels. The other alternative is performing a segmental pancreatic resection followed by pancreaticojejunostomy, which implies accepting the risk of an anastomotic leak. This procedure is problematic and not recommended. All pancreatic injuries should be drained. Closed suction systems are employed to establish wide pancreatic drainage. External drainage serves to evacuate pancreatic exocrine secretions and to control a pancreatic fistula, should it develop. The placement of closed suction systems decreases the rate of intraabdominal abscess formation as pancreatic secretions are more reliably collected, and excoriation of the skin is thus avoided. Although there is no uniformity as to the length of time that drains must remain in place, we recommend leaving the drains for 7 to 10 days, as any fistulization process should be evident by that time. Drainage should be maintained while the patient resumes oral intake, as it is well known that pancreatic drainage may decrease after 7 days. However, a significant increase in drainage will often occur subsequently after oral intake has been resumed and should alert the trauma surgeon to the possibility of impending complications. The trauma surgeon must possess a vast of armamentarium of surgical procedures to manage pancreatic injuries. Grade I and grade II injuries occur with a frequency of 60% and 20%, respectively. Grade III injuries represent 15% of all pancreatic injuries, whereas grade IV injuries are uncommon, occurring with a frequency of 5%. It is for these higher grade injuries that the broader armamentarium of complex surgical techniques should be reserved. The conservative approach with adherence to injury grade and management guidelines will produce better results; this includes selecting the least complex surgical procedure to manage the pancreatic injury, conservative but judicious resection, and debridement and control of pancreatic secretions via external drainage.

Special Situations Pancreaticoduodenal Injuries Pancreaticoduodenal injuries are fortunately rare. These injuries are most commonly caused by penetrating injury


and are frequently associated with multiple concomitant injuries. Patients with higher pancreatic injury severity and associated duodenal injuries of a significant grade should be considered as candidates for more complex pancreaticoduodenal repairs, such as duodenal diverticulization or pyloric exclusion. Pancreatic injuries of grade II or above in association with duodenal injuries caused by severe blunt trauma or missiles, those involving more than 75% of the duodenal wall, those involving the first and second portions of the duodenum or common bile duct, and those associated with delay in repair of more than 24 hours are also candidates. Other criteria that may lead the surgeon to strongly consider diverticulization or pyloric exclusion include compromised blood supply to the duodenum and associated injury to the head of the pancreas without disruption of the main pancreatic duct or any pancreatic injury associated with a duodenal injury involving more than 50% of the circumference of the duodenum. The main purpose of this procedure is to exclude the duodenum from the passage of gastric contents, thus allowing for a suitable period of time for the duodenal repair to heal, which can be severely threatened by the presence of pancreatic secretions that promote suture line dehiscence. Pancreaticoduodenectomy was first reported by Whipple et al.73 in 1935 as a staged procedure. Modifications were subsequently added to refine the procedure now performed rourinely. In 1961, Howell and colleagues74 first performed pancreaticoduodenectomy for penetrating trauma. In 1964, Thal and Wilson75 first performed pancreaticoduodenectomy as a treatment for patients sustaining severe blunt trauma to the head of the pancreas. These authors reported three patients who underwent pancreaticoduodenectomy and recommended limiting the use of this procedure for patients incurring massive pancreaticoduodenal injuries involving the head of the pancreas. In 1969, Halgrimson and colleagues76 reported their experience from Vietnam with two patients, operated on a delayed basis, who survived. Foley and colleagues,27 also in 1969 and based on three blunt trauma patients, described the following indications for pancreaticoduodenectomy: • Massive uncontrollable bleeding from the head of the pancreas, adjacent vascular structures, or both • Massive and unreconstructable ductal injury in the head of the pancreas • Combined unreconstructable injuries of the following: ⴰ Duodenum and head of the pancreas ⴰ Duodenum, head of the pancreas, and common bile duct Before considering pancreaticoduodenectomy, the trauma surgeon must thoroughly assess the extent of injury; we recommend good exposure of both pancreas

32. Pancreas

and duodenum by an initial extensive Kocher maneuver. This should be extensive enough so that the surgeon can palpate the entire head of the pancreas to the level of the superior mesenteric vessels. This allows the surgeon to visualize both anterior and posterior aspects of the second and third portions of the duodenum and will also permit exposure of the head and uncinate process of the pancreas and inferior vena cava. Intraoperative inspection for ductal violation of the main pancreatic duct, complete transection of the head of the pancreas, pancreatic fluid leak, central perforations, and severe lacerations with or without massive tissue disruption can predict the presence of a major pancreatic ductal injury with a high degree of accuracy. Similarly, meticulous and gentle exploration of the injured head of the pancreas utilizing the finest of malleable retractors will often expose an injured main pancreatic duct. Assessment of the viability of the duodenum is also quite important. Frequently, injuries in the medial aspect of the first and second portions of the duodenum within the C-loop are deemed unreconstructable upon preliminary inspection. However, with further meticulous dissection, utilizing a Kittner dissector and with the help of fine malleable retractors, some are amenable to primary repair. These maneuvers must be carried out systematically to avoid devascularization of both duodenum and head of the pancreas. If the criteria originally described by Foley and later validated by Asensio are met, the trauma surgeon must proceed to pancreaticoduodenectomy. Pancreaticoduodenectomy is clearly a formidable procedure in critically ill patients. A review of 64 series reported in the literature from 1964 to 2003 yielded 253 patients who underwent pancreaticoduodenectomy (Table 32.7). Subsequently, 75 of these patients died. The tabulated mortality rate for all series reviewed was 30%, which is not at variance with the range of 30% to 40% reported in the literature. Asensio and colleagues,111 with the largest series of the literature, reported the use of pancreaticoduodenectomy for severe pancreaticoduodenal injuries. In this series they reported 18 patients with severe and unreconstructable injuries of the head of the pancreas and the first or second portion of the duodenum. In addition, these patients also sustained injuries involving the main pancreatic duct, the intrapancreatic portion of the distal common bile duct, and the ampulla of Vater, with devitalization and destruction of the blood supply. Twelve patients lived, for an overall survival rate of 67%. This compares very favorably with the survival rate reported in the literature, which ranges from 64% to 69%, given the severity of the injuries, large blood losses, and largest number of associated abdominal injuries reported to date. However, much remains to be done to improve the high mortality rates for these rare but highly challenging patients.

505 Table 32.7. Experience with pancreaticoduodenectomy in trauma patients. First author 75

Thal Walter77 Thompson78 Salyer25 Sawyers79 Wilson80 Brawley81 Werschky26 Pantazelos82 Halgrimson76 Foley27 Gibbs83 Bach29 Nance84 Jones85 Smith86 Salam31 Anderson87 White30 Owens88 Steele89 Sturm90 Anderson33 Yellin91 Anane-Sefah14 Chamber92 Balasegaram93 Heitsch94 Lowe34 Karl95 Hagan96 Graham36 Stone97 Majeski37 Cogbill40 Levinson98 Berni39 Henarejos99 Oreskovich42 Adkins100 Moore101 Fabian102 Sims43 Donahue103 Jones (1971–1978)104 Ivatury105 Smego106 Wynn44 Nowak45 Walker107 Feliciano18 Melissas108 Leppaniemi19 McKone109 Eastlick65 Gentilello21 Heimansohn110 Ivatury50 Delcore55 Degiannis58 Smith59 Young64 Asensio111 Total

Year 1964 1966 1966 1967 1967 1967 1968 1968 1969 1969 1969 1970 1971 1971 1971 1971 1972 1973 1972 1973 1973 1973 1974 1975 1975 1975 1976 1976 1977 1977 1978 1979 1979 1980 1982 1982 1982 1983 1984 1984 1984 1984 1984 1985 1985 1985 1985 1985 1986 1986 1987 1987 1988 1988 1990 1991 1990 1990 1994 1996 1996 1998 2003

No. of patients

No. of deaths

2 1 2 1 1 2 3 1 1 3 3 1 3 5

1 0 1 0 0 0 0 1 1 0 0 0 0 2

5 4 2 5 3 3 5 2 10 6 1 8 2 6 1 2 6 3 1 1 1 8 1 10 5 1 1 2 1 12 7 1 3 1 1 13 1 3 5 1 3 6 6 4 3 1 2 18

2 1 1 0 1 3 2 1 6 0 0 5 2 0 1 2 3 3 0 0 1 0 0 0 1 0 1 0 1 7 3 0 2 1 0 6 0 1 0 0 1 0 2 0 2 1 0 6

253

75 (30%)

506

Mortality Pancreatic injuries, as a whole, carry a significant mortality rate. A review of 44 series in the literature dating from 1956 to 1998 reveals rates of 5% to 54%. A total of 4,134 patients were analyzed of which 790 died for a mean mortality rate of 19%. The lowest rate was reported by Babb and Harmon15 in 1976. Of their 76 patients, 4 died, yielding a mortality rate of 5%. Fifty-five patients (72%) sustained penetrating abdominal injuries of which 28 were gunshot wounds, 4 were shotgun wounds, and 23 were stab wounds. Remarkably, the head of the pancreas was injured in 26 (34% of the patients). There were 180 associated injuries of which 18 (10%) were to major abdominal blood vessels. Seventy-two of the 76 patients survived, and there were 71 major complications. Although this figure is quite remarkable, it is at variance with most other mortality rates reported in the literature and definitely at variance with the literature. The highest mortality rate was reported by Gentilello et al.21 in a series of 13 patients of whom 7 died, for a mortality rate of 54%.This series is unique because it includes only patients who experienced severe combined pancreaticoduodenal injuries. In addition, 9 of the 13 patients sustained additional ampullary or distal common bile duct injuries, as well as a significant number of other associated injuries. Only two (15%) sustained major venous injuries, and no major arterial injuries were reported. All 13 patients underwent pancreaticoduodenectomy, including a formal gastrojejunostomy with common bile duct implantation in the jejunal loop and pancreatic duct ligation with no reconstructive pancreaticojejunostomy. Consequently, this series deals with a very critically injured patient population, and its resultant high mortality rate is also at variance with the literature. Several authors have reported their overall mortality rates separately from the mortality rates caused exclusively by pancreatic injuries. Associated injuries are responsible for the majority of deaths of patients sustaining pancreatic injuries. Five studies that distinguished mortality from associated injuries versus the pancreatic injury itself revealed that out of 586 patients, 134 died, yielding a mortality rate of 23%. Ninety-nine (74%) died of associated injuries, whereas 35 (26%) succumbed secondary to their pancreatic injury. This yields a ratio of associated injuries to pancreatic mortality of 3.5 to 1. These figures were confirmed in an excellent review of pancreatic injuries by Glancy.112 Mortality can be analyzed based on several variables. It can be reviewed on a temporal basis and subdivided into early and late mortality. Most early deaths with pancreatic injuries are caused by exsanguination, usually secondary to major associated vascular injuries. In our own review, associated major vascular injuries were the third most common associated injury and certainly the most lethal. These findings are repeatedly born out in the literature.


Graham et al.113 reported 73 patients who died out of 448 patients, for a 16% mortality rate. Of the 73 deaths, 47 patients (64%) died during the first 24 hours secondary to hemorrhagic shock, prolonged bleeding, hypothermia, coagulopathy, and the sequelae of massive blood replacement. Similarly, Jones, in his first series,35 consisting of 300 patients, reported 59 deaths of which 26 (44%) occurred within 24 hours. In Jones’s subsequent series,104 consisting of 500 patients, shock was present in 48% of the patients, and their mortality rate was 40% compared with the 4% mortality rate for normotensive patients. Of the 104 patients who died, 89% had experienced a significant period of shock. Fifty died intraoperatively, secondary to uncontrolled hemorrhage.In the series of Patton et al.,62 17 of 134 patients (13%) died from massive hemorrhage. Mechanism of injury is an important determinant of mortality. In 14 series, the mortality rate secondary to shotgun wounds was 51%, whereas injuries from other types of penetrating and blunt trauma incurred mortality rates ranging from 7% to 23%. Similarly, associated injuries and their numbers are also important determinants of mortality rate. It is well known that patients sustaining penetrating trauma are much more likely to have associated injuries. Howell et al.74 and Stone et al.38 correlated the presence or absence of one or more associated injuries in patients sustaining pancreatic injuries caused by either mechanism. They noted a significant difference in 297 of 298 patients (99.7%) with penetrating trauma versus only 62 of 70 patients (88.6%) sustaining blunt trauma. The number of associated injuries clearly affected mortality. Graham et al.,113 Howell et al.,74 Balasegaram,114 and Werschky and Jordan26 in their series totaling 712 patients, reported the mortality rate for patients with zero to one, two to three, and four or more associated injuries as 2.5%, 13.6% and 29.6%, respectively. According to Asensio,71 factors known to increase mortality rates include associated duodenal and common bile duct injuries. Proximal pancreatic injuries are also related to increases in mortality. The type of operative intervention employed to manage these patients can also be correlated with mortality. Glancy112 reviewed eight studies encompassing 1,407 patients in which mortality was correlated with the type of operative procedure. The overall mortality rate in this group of patients was 16.8%. Patients undergoing total pancreatectomy and pancreatic ductal reanastomosis had consistently higher mortality rates: 100% and 50%, respectively. However, this subset of patients was too small to reach any meaningful conclusions. In 214 patients, Asensio and colleagues23 reported a mortality rate of 31%. In this series, 20 patients required emergency department thoracotomy. Patients sustaining penetrating injuries incurred a greater period of intraoperative hypotension than those who sustained blunt injury—124 minutes vs. 16 minutes (p < 0.005)—and required a larger number of units of blood transfused—

32. Pancreas

penetrating 11.3 ± 0.9 units vs. blunt 8.5 ± 1.5 units (p > 0.005). Mortality correlated well with the AAST-OIS for pancreatic injuries: grade I, 4%; grade II, 15%; grade III, 37%; grade IV, 66%; and grade V, 82%.

Morbidity Pancreatic injuries are associated with very high rates of morbidity. Forty series in the literature encompassing 3,898 patients were selected and reviewed because they clearly outlined morbidity figures. Overall, morbidity rates ranged from 11% to 62%, with an average rate of 36.6%.The lowest morbidity rate was reported by Voeller et al.52 The highest morbidity rate was reported by Campbell and Kennedy.16 Pancreatic morbidity is represented primarily by fistulas. The literature shows no uniformity in the definition of a pancreatic fistula. As a matter of fact, prolonged pancreatic drainage is considered as “a way of life” with these injuries. Another conclusion expressed in the literature is that fistula formation may not be a true complication but simply a result of appropriate therapy. Because fistula formation is usually associated with external drainage and the reason for draining is to avoid collection of pancreatic secretions, the presence of a fistula may signify the prevention of a more serious complication such as a pseudocyst. Therefore, does constitute a fistula? In our opinion, any drainage of more than 50 mL that persists longer than 2 weeks with elevated amylase and lipase levels should be considered a fistula. In our review of the literature, fistulas were identified with an incidence of 14%; pancreatic abscess was the second most frequent complication (8%), and posttraumatic pancreatitis occurred in 4% of the cases. Pseudocysts were identified in 3% of the patients, whereas late hemorrhage occurred with an incidence of 1%. Lumped into the category of “other complications” is exocrine and endocrine insufficiency (4%). It is hard to determine from the literature the true incidence of this complication. Cogbill et al.,51 in a retrospective multiinstitutional 5year study of 74 patients, reported 10 fistulas, for an incidence of 14% in 71 survivors of the initial operation. This figure falls within the range of 3% to 24% reported in the literature. In this series, the maximum daily fistula output ranged from 70 to 1,000 mL. Spontaneous closure of fistulas occurred in 8 (89%) of 9 survivors in a period of time ranging from 6 to 54 days after discovery. Only one patient required surgical reintervention for completion pancreatectomy of the distal remnant 154 days after the initial operation. Fistulas result in mortality if associated with pancreatic abscesses. The management of pancreatic fistulas consists of careful monitoring of fluid and electrolyte status concomitant with fluid replacement. Protection of the skin at the fistula site is critical in avoiding significant ulceration of

507

the skin secondary to the corrosive effect of the pancreatic enzymes. We recommend the performance of endoscopic retrograde cholangiopancreatography (ERCP) for confirmation and delineation of the fistulous tract, which is most helpful in establishing the cause of the persistent fistula and in formulating the plan for further therapy. Aggressive parenteral nutrition with absolute gastrointestinal tract rest is the time-tested method to manage these fistulas, along with maintenance of adequate drainage. This represents the gold standard. One alternative tried was enteral nutrition with an elemental diet provided via distal feeding jejunostomy; however, the authors observed in some cases that the fistula output increased significantly in some patients whereas others tolerated enteral nutrition well and without a concomitant increase in the output. Similarly, the authors noted that a very small group of patients can tolerate a low-fat elemental diet orally without an increase in output; this group remains a very small minority of patients.There are certainly no known explanations as to why this small and selected group of patients does well with this management. This is indicative of our lack of knowledge of the many feedback loops at work between both the proximal and distal small bowel and the pancreas. The long-acting somatostatin analog octreotide acetate has also been used to inhibit pancreatic exocrine secretion.115 This was originally reported as a helpful adjunct in the management of complications following elective pancreatic procedures. Good results were noticed, with decreasing times to closure of the postoperative fistula. The use of this synthetic analog has been extrapolated as an adjunct in the management of posttraumatic pancreatic fistulas; however, few data exist in the literature documenting its efficacy. We use it consistently and have noted good results in terms of hastening the closure of fistulas. Pancreatic abscess as a specific infectious complication of pancreatic injury is difficult to define given the large number of associated injuries in pancreatic trauma. The association with either a colon or a duodenal injury results in a 60% rate of abscess formation versus a much lower rate of 10% to 15% for patients without colonic or duodenal injuries. Similarly, Jones104 reported that 60% of patients with colon injuries in his series developed intraabdominal abscess, but few were related to the pancreatic injury. Graham et al.36 reported an 8% incidence of abscess formation in his series generally associated with hepatic and colonic injuries but only a 2% incidence of pancreatic-specific abscesses. Cogbill et al.51 reported intraabdominal abscess formation in 24 of 71 surviving patients, an incidence of 34%. Left upper quadrant abscesses are much more common after distal pancreatectomy than after distal pancreatectomy with splenic preservation. The mainstay of management consists of percutaneous CT-guided drainage. Cogbill et al.51 reported a 79% success rate with this approach.

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Posttraumatic pancreatitis has been defined by Cogbill et al.51 as an elevated serum amylase level persisting for more than 3 days. The vast majority of posttraumatic pancreatitis results from blunt abdominal trauma. It is treated with nasogastric decompression, bowel rest, and aggressive nutritional support and usually resolves spontaneously. A highly lethal complication of posttraumatic pancreatitis is its evolution into hemorrhagic pancreatitis. This is usually manifested by bloody pancreatic drainage. It carries an extremely high mortality rate, because there is no effective treatment known.The usual scenario demands the return of the patient to the operating room with the hope of controlling the bleeding by either debridement or pancreatectomy; however, this is usually futile. We have tried interventional angiography with mixed results. Pancreatic pseudocysts generally result from overlooked blunt pancreatic injuries treated nonoperatively. Kudsk et al.116 documented 22 pseudocysts in 42 patients with blunt pancreatic injuries managed nonoperatively in seven series reported between 1952 and 1983. Graham et al.36 reported a 2% incidence of pseudocyst formation after penetrating injury. Cogbill et al.51 reported a 3% incidence of posttraumatic pseudocyst formation. Pseudocyst formation is usually regarded as failure to establish adequate postoperative drainage to manage pancreatic secretions. The presence of a pseudocyst should be considered if there is prolonged elevation of the serum amylase level postoperatively, and it should be aggressively pursued. All posttraumatic pseudocysts should be investigated with ERCP, which will delineate the status of the duct. This is important in selecting the method of management. If the ductal system is found to be intact, the pseudocyst can be managed with percutaneous drainage. If the pseudocyst has resulted secondary to a missed ductal injury, percutaneous drainage will not provide definitive therapy, and these patients are best managed by reexploration and pancreatectomy or by internal drainage via a Roux-en-Y jejunal limb. On rare occasions endoscopic transpancreatic stenting of the pancreatic duct has been tried successfully. Posttraumatic hemorrhage can be quite a lethal complication. Both Jones35 and Graham et al.36 describe erosion of vessels surrounding the pancreas. This may occur when there has been an inadequate debridement or external drainage and is totally unpredictable. The management consists of returning the patient to the operating room, but this carries a very high mortality rate. We have tried angiographic embolization as a temporizing means before returning the patient to the operating room, as well as for definitive control, with mixed results. Either exocrine or endocrine insufficiency is unusual after pancreatic injuries. Distal pancreatectomy to the left of the superior mesenteric vessels should leave adequate functioning pancreatic tissue. Jones,104 in a series of 500


patients, reported 11 patients who had 11.5 to 14 cm of the pancreas resected, or 80% or more of the pancreas, as measured by pathologic examination. Three of these patients subsequently developed pancreatic insufficiency requiring hormonal replacement for life. Balasegaram93 reported no pancreatic insufficiency after resections of up to 90% of the pancreas. No case of pancreatic insufficiency was reported by Graham et al.,36 whereas Cogbill et al.40 reported only one patient who required insulin following an 80% resection.

Pancreatic Emergencies (Nontrauma)* Complications of acute pancreatitis are the most common problems that an acute care surgeon will encounter. Such complications include biliary pancreatitis, infected or hemorrhagic pseudocyst, necrotizing pancreatitis, and pancreatic abscess. The definitions of term describing pancreatitis are highlighted in Table 32.8. Table 32.8. Definitions of terminology in pancreatitis. Acute interstitial pancreatitis: A mild, self-limited form of pancreatitis characterized by interstitial edema and an acute inflammatory response without necrosis, local complications, or systemic manifestations such as organ failure Necrotizing pancreatitis: A severe form of acute pancreatitis characterized by locoregional tissue necrosis and systemic manifestations such as pulmonary, renal, or cardiac failure Sterile necrosis: Acute pancreatitis leading to tissue necrosis without supervening infection Infected necrosis: Acute pancreatitis with locoregional tissue necrosis complicated by bacterial or fungal infection Acute fluid collections: A fluid collection occurring early in the course of acute pancreatitis, located in or near the pancreas, and lacking an epithelial lining or a defined wall of granulation or fibrous tissue Pancreatic pseudocyst: A pancreatic or peripancreatic fluid collection with a well-defined wall of granulation tissue and fibrosis, absence of an epithelial lining. Pancreatic pseudocysts can arise in the setting of chronic pancreatitis, without the sequela of an episode of necrotizing pancreatitis. One of the common complications of pseudocyst is the development of infection Pancreatic cysts: A fluid-filled pancreatic mass with an epithelial lining. These may be neoplastic lesions, such as serous cystadenomas or mucinous cystic tumors, or congenital cysts Pancreatic abscess: A circumscribed intraabdominal collection of pus, usually in proximity to the pancreas, containing little or no pancreatic necrosis, arising as a consequence of necrotizing pancreatitis or pancreatic trauma Suppurative cholangitis: Bacterial infection within the biliary tree, associated with ductal obstruction, usually from a stone or stricture Source: Adapted with permission from Bradley E and members of the Atlanta International Symposium. A clinically based classification system for acute pancreatitis. Arch Surg 1993; 128(5):586–590.

* This section is reprinted with the kind permission of Springer Science and Business Media from Mulvihill SJ. Pancreas. In Norton JA, Barie PS, Bollinger RR, Chang AE, Lowry SF, Mulvihill SJ, Pass HI,Thompson RW, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer, 2001: 523–526.

32. Pancreas

509

Table 32.9. Ranson criteria for assessing severity of acute pancreatitis. At admission

Within the first 48 hr

Age >55 years White blood cell count >16,000/μL Serum glucose >200 mg/dL (11 mmol/L) Serum lactate dehydrogenase >400 IU/L Serum aspartate aminotransferase >250 IU/L

Drop in hematocrit >10% Fluid deficit >4,000 mL Serum calcium 55years of age) had a higher rate of failure than those patients 10%) with pelvic trauma.11 Any blood at the urethral meatus or expression of blood with Foley catheterization is a warning sign of a concomitant genitourinary injury. A rectal examination may reveal a high-riding or “floating” prostate. Concomitant head and intraabdominal injuries are not uncommon with highenergy pelvic trauma and are frequently the cause of death in such patients. Dalal et al.12 reviewed 343 multitrauma patients with pelvic ring disruptions and found a significant difference between the causes of death in people with pelvic injuries caused by lateral-compression forces (brain injury) and those caused by anteriorposterior compression forces (visceral organ injury).

Radiographic Evaluation Before instituting measures to reduce pelvic volume (at least the more invasive ones), it is helpful to know whether the pelvic fracture sustained by the patient has resulted in an increase in pelvic potential space. For example, placing a pelvic C-clamp on the hemodynamically unstable trauma patient with a Tile A or Tile B lateral-compression type injury, in which the pelvis is already imploded onto itself, not only will be ineffective

37. Pelvis

but also may delay the diagnosis of the true source of bleeding. Thus, understanding plain radiographs of the pelvis and their implication for potential pelvic volume and stability is critical. The standard trauma radiographs include an anteriorposterior chest, a cervical spine film (with an adequate lateral image often viewed as the most important), and an anterior-posterior view of the pelvis. The anterior-posterior pelvis radiograph provides the clinician with an overall sense of the “personality” of the injury: whether it is low or high energy, whether the hemipelvis is internally rotated or externally rotated, and whether there are any stigmata of translational vertical instability. Although anterior lesions, such as a pubic rami fracture or symphyseal displacement, are often obvious, posterior lesions, such as subtle SI joint widening, sacral fractures, iliac fractures, or L5 transverse process fractures, can be more subtle. An avulsion fracture of the transverse process of L5 is especially worrisome as it may indicate an antecedent vertical shearing mechanism producing posterior instability. Avulsion fractures of the sacrum or ischial spine may indicate disruption of the sacrospinous ligament. To better characterize the nature of the injury, socalled inlet and outlet views should be obtained in every case of pelvic ring trauma. An inlet view is taken with the patient in a supine position and the beam tilted 60° caudally (Figure 37.4A). This view gives a true axial view of

A

B Figure 37.4. (A) An inlet view of the pelvic ring taken with the patient in a supine position and the beam tilted 60° caudally, giving a true axial view of the sacrum. (B) An outlet view is also obtained with the patient supine but with the beam directed 45° cephalad, giving a true anterior-posterior view of the sacrum. (Reprinted with permission from Rockwood CA Jr, Green DP, Bucholz RW, Heckman JD, eds. Rockwood and Green’s Fractures in Adults, 4th ed, vol 2. Philadelphia: Lippincott-Raven, 1996: 1599.)

595

the sacrum and is ideal for looking at anterior to posterior displacement of the hemipelvis through the SI joint, the sacrum, or the iliac wing. An outlet view is also taken with the patient supine but with the beam directed 45° cephalad (Figure 37.4B). This gives a true anteriorposterior view of the sacrum and is therefore well suited to detect vertical displacement or rotatatory abnormalities of the hemipelvis. Dynamic stress push–pull films can also be helpful in evaluating patients with pelvic ring fractures. The most accurate results of such films require general anesthesia and can be useful in determining whether there is truly a component of translational instability in a pelvic ring injury that may appear like a Tile B on nonstress images. Tile5 defined vertical instability as hemipelvis displacement greater than or equal to 1 cm. Although acetabular fractures should really be thought of as separate entities from pelvic ring disruptions, these two injuries may be confused by trauma personnel. It is important for trauma teams to recognize that isolated acetabular fractures, while technically pelvic fractures, do not have the same potential for pelvic bleeding that pelvic ring disruptions do. Unless they are associated with an open-book pelvic ring injury, acetabular fractures do not benefit from external stabilization. Nonetheless, it is prudent to discuss the radiographic evaluation of acetabular fractures in this context such that their differences from pelvic ring disruptions can be delineated. Understanding fracture lines in and around the acetabulum requires not only an anterior-posterior view of the pelvis but also oblique images. These images, often referred to as “Judet views,” are composed of two 45° oblique views of the hemipelvis: one with the obturator foramen en face (the so-called obturator oblique view) and one with the iliac wing en face (the iliac oblique). Note that an obturator oblique image of one hemipelvis reveals the iliac oblique of the contralateral side. In evaluating the anterior-posterior pelvis film for an acetabular fracture, one should look at any discontinuities in the iliopectineal line (the inferior three fourths of which marks the anterior column) and the ilioischial line (posterior column). The obturator oblique view brings the anterior column into profile, and the posterior wall of the acetabulum is seen en face. In contrast, the iliac oblique shows the posterior column en face and the anterior wall in profile. Note that in most isolated acetabular fractures, the ligaments of the pubic symphysis, pelvic floor, and SI complex are completely uninvolved, and the pelvic ring remains stable. Computed tomography (CT) has revolutionized imaging of pelvic ring injuries and offers outstanding visualization of SI widening and subtle fractures of the sacrum. Figure 37.5 illustrates the added fracture detail an axial CT scan image provides compared with plain film. Although performing CT scanning of pelvic ring disruptions has become commonplace and is currently the

596

C.M. Rodner and B.D. Browner

A

B

C

Fig gure 37.5. Ms. C.B. is a pedestrian struck by a motor vehicle. (A) An nterior-posterior plain film demonstrates bilateral rami fractures and d a right-sided posterior fracture in the sacroiliac (SI) region. (B) Axxial computed tomography scan more clearly delineates the posterior fracture fragments and degree of SI displacement. (C) Angiograp phy demonstrated a right-sided internal iliac artery hemorrhage.

standard of care, obtaining three-dimensional reconstruction images has become possible at many medical centers and provides extraordinary visualization of the pelvis in space (Figure 37.6).

Hemodynamic Status and Emergent Stabilization It cannot be emphasized enough that as the physical examination is occurring the patient’s hemodynamic status must continuously be carefully monitored. Establishing two 14- to 16-gauge intravenous lines in the upper extremity is a good idea to allow for appropriate fluid resuscitation. Avoiding lower extremity access sites is probably wise in the setting of a pelvic ring fracture

because of the possibility of damaged venous circulation in that region. If the patient remains hemodynamically unstable, and in the absence of obvious external hemorrhage, internal bleeding must of course be suspected. From a general surgical perspective, the presence of intraabdominal bleeding can be ruled out with either a deep peritoneal lavage (DPL) or, less invasively, an abdominal ultrasound examination at the bedside or a CT scan. In the presence of a disrupted pelvic ring, particularly in those force patterns that produce an external rotation open-book deformity of one or both sides of the pelvis, retroperitoneal hemorrhage must be suspected as well. Retroperitoneal hemorrhage can be associated with massive loss of a patient’s intravascular volume, as the retroperitoneal space can hold up to 4 L of blood volume.

37. Pelvis

A

B Figure 37.6. Three-dimensional reconstruction images of a normal pelvis, with (A) inlet and (B) outlet projections.

The most common cause of such hemorrhage in the setting of pelvic trauma is a disruption of the venous plexus in the posterior pelvis. Less commonly, but possible, is injury to larger vessels, such as the external or internal iliac. Arterial injury is much less common, and only a small percentage of patients with pelvic fractures require embolization. In a 5-year review of 800 patients admitted to a Level I trauma center with pelvic fractures, Agolini et al.13 found that only 1.9% required embolization. Unless the potential space is decreased with external stabilization, venous bleeding in the presence of an openbook type of pelvis injury may continue undeterred until the patient is in shock. Thus, the chief determination that the trauma surgeon, in conjunction with the orthopedist,

597

must make in this context is whether stabilizing the pelvis is appropriate. There are several different options for decreasing retroperitoneal volume emergently, thus helping to tamponade venous bleeding. As mentioned previously, one well-described way to do this is before the patient even arrives in the hospital with the application of MAST. Such pneumatic trousers work by increasing peripheral vascular resistance as well as by physically splinting previously moving fracture fragments. After they are applied en route, MAST should not be removed until intravenous access is established and the patient is in a controlled environment, such as an operating room. Military antishock trousers are not intended for indefinite use, as skin problems and compartment syndromes have been well described with prolonged use. Often, of course, patients with pelvic ring injuries are not diagnosed in the field, and they arrive in the trauma room without MAST applied. In a hemodynamically unstable patient with an open-book pelvic ring injury, emergent pelvic stabilization can be a matter of life or death. It is important to reiterate that not all pelvic ring fractures will benefit from pelvic stabilization. It makes sense that only lesions that increase the potential space in the pelvis for hemorrhage, such as partially stable open-book fractures (i.e., a Tile B-1 injury) and all completely unstable (Tile C) injuries, would benefit from interventions aimed at reducing pelvic volume. There are several reasonable means to achieve this end, such as wrapping a sheet or placing a compressive strap circumferentially around the pelvis or applying a pelvic clamp or a more traditional anterior external fixator. Noninvasive pelvic stabilization with a circumferential compression strap has been shown in a biomechanical cadaveric study to be an effective means to achieve reduction of external-rotation type pelvic fractures.14 Wrapping a sheet around the pelvis can also be effective in closing down anterior symphyseal diastasis. A “bean bag” positioning device can be applied to the flanks of the patient to help reduce pelvic volume as well.15 Using skeletal traction through the injured femoral supracondylar region is helpful as an adjunctive measure by pulling the displaced hemipelvis into a more reduced position, helping to tamponade venous bleeding. Tile recommends using 30 pounds of traction through skeletal pins in the distal femur to help maintain pelvic ring disruptions in the reduced position. By hanging weight off the injured extremity, the hemipelvis is given an internal rotation force, thereby closing down anterior diastasis. This is of course most effective in achieving stability if there is integrity to the posterior ligaments. The added benefit of skeletal traction is that it prevents shortening of the hemipelvis in the indefinite period of time between injury and definitive operative stabilization. Another way to emergently stabilize the pelvis is by applying a pelvic clamp in the emergency room to the

598


A B Figure 37.7. (A) An example of a particular pelvic C-clamp model developed by Dr. Dr Bruce Browner. Browner (B) It is easy to access the abdomen or the perineum, depending on which way the clamp is swung.

posterior aspect of the pelvis.16,17 Application of a pelvic C-clamp is appealing because it can be applied relatively quickly in the emergency room while allowing the trauma surgeon adequate access to the abdomen (Figure 37.7). Pohlemann et al.18 have described a safe anatomic landmark for pin placement as the region on the lateral aspect of the iliac wing where a palpable “groove” is formed by angulations of the lateral cortex. In general, pin insertion should be in the cancellous bone superior to the acetabulum in the posterior aspect of the pelvis. Although pelvic C-clamps are in use at many medical centers, the more standard method for controlling unstable pelvic ring injuries remains the application of an anterior external fixator with two or three pins placed in the anterior iliac crest and joined by an anterior frame.19,20 Although they can conceivably be applied in the emergency room like pelvic C-clamps, anterior fixators are more commonly placed in the operating room. When laparotomies are necessary, the application of these fixators may unfortunately be further delayed. During the evaluation and resuscitation of the pelvicfractured patient, the timing of placement of the pelvic stabilization device is sometimes debated. At our trauma center, it is thought that a pelvic C-clamp should be applied initially in all hemodynamically unstable patients with unstable pelvic fractures. Delaying pelvic stabilization to the operating room may allow retroperitoneal hemorrhaging to continue in the interim and puts the patient at unnecessary risk as the trauma room’s “golden hour” of resuscitative opportunity elapses. If the patient becomes stable with this simple orthopedic intervention, the need for a laparotomy may be precluded. Trauma surgeons in Europe, who take care of both orthopedic and intraabdominal injuries, also proceed in this fashion, with the application of a pelvic stabilizer being seen as a top priority in the emergency room.21,22

Whether the pelvis is stabilized with a C-clamp or an anterior frame, external fixators exert their effectiveness not only by reducing pelvic volume but also by preventing disruption of blood clots. However, such fixators alone do not provide sufficient posterior stabilization if the posterior pelvic ligaments are disrupted. Both pelvic clamps, as well as more traditional external frames, have been shown to restore adequate stability to Tile B, but not Tile C, fractures.17,23 Using pelvic external fixation in conjunction with skeletal traction through the involved leg may help control vertical instability more effectively, although not completely. Only if the patient remains hemodynamically unstable despite adequately stabilizing the pelvis and findings on DPL (or abdominal ultrasound or CT scan) are negative should arterial bleeding be assumed and angiography performed. This is a critical point for the trauma team to understand. Because the vast majority of pelvic bleeding originates from venous sources,24 patients with openbook pelvic ring injuries should be sent to the angiography suite only after the application of a pelvic stabilization device has failed to provide hemodynamic stability. In contrast, patients who are hemodynamically unstable with closed-book pelves could be considered for earlier angiography (albeit still after intraabdominal sources of hemorrhage are ruled out). In order to clearly delineate this point, consider the following contrasting cases of Ms. C.B. and Mr. J.W. Ms. C.B. is a 54-year-old female pedestrian struck by a motor vehicle. She came to the trauma room hemodynamically unstable, despite plain films that showed a relatively closed-book pelvic ring injury (see Figure 37.5A). Not surprisingly, given the nature of her pelvic fractures, Ms. C.B. remained hemodynamically unstable despite emergent application of a compressive pelvic sheet in the trauma room. After abdominal ultrasound was performed and showed no intraabdominal bleeding, the

37. Pelvis

599

A

C

Figure 37.8. Mr. J.W. was involved in a head-on motor vehicle accident. (A) Anterior-posterior plain film demonstrates approximately 4 cm of symphyseal diastasis, suggesting injury to the ligaments of the pubic symphysis and pelvic floor. The right sacroiliac (SI) joint is widened, implicating injury to the anterior SI ligaments on this side. This characteristic open-book hemipelvis is consistent with a Young-Burgess AP-II or Tile B1 pelvic ring disruption. (B) Axial computed tomography scan lends support to this being a Tile B (and not a Tile C) injury, because, although there is right-sided anterior SI widening, the posterior SI joint spaces are symmetric. Therefore, although the pelvic ring is rotationally unstable, its intact posterior SI ligaments confer to it vertical and translational stability. (C–E). Emergent application of a pelvic C-clamp effectively “closed” the pelvic ring, as demonstrated by anterior-posterior (C), inlet (D), and outlet (E) images.

patient was taken urgently to angiography where a rightsided internal iliac artery hemorrhage was identified and successfully embolized (see Figure 37.5C). Mr. J.W. is a 52-year-old male driver of an automobile involved in a high-speed head-on collision. He too came

B

D

E

to the trauma room hemodynamically unstable, but (unlike Ms. C.B.) with radiographic findings of an openbook pelvic ring injury (Figure 37.8A). Rather than rush this patient off to the angiography suite or to the operating room, the traumatologist reviewed his plain films

600

and astutely identified an unstable pelvic ring injury consistent with an AP-type mechanism producing an external-rotation deformity of the hemipelvis. As a result, the orthopedic surgeon was consulted, and a C-clamp was applied to Mr. J.W.’s pelvis within 30 minutes of his arrival to the trauma room. Moments after application of the Cclamp, presumably because of the dramatic reduction of his pelvic volume (Figure 37.8C–E) and subsequent tamponade of venous hemorrhage, J.W.’s heart rate and blood pressure normalized. It is critically important to recognize the folly in taking a patient such as Mr. J.W. to angiography before applying simple pelvic stabilization measures in the trauma room. Once a patient becomes hemodynamically stable, an additional treatment question must be asked: Does the pelvic ring need to be fixed? To answer this question, the orthopedic surgeon should be consulted—if he or she is not already involved in the case. Through orthopedic consultation, the need for further imaging studies or surgery can be determined. The orthopedist may choose to fix certain fractures in the first day or two, whereas in other instances waiting a couple of weeks may be deemed preferable. Although discussing techniques for definitive fixation of the pelvis is beyond the scope of this chapter, it is important to realize that the orthopedic surgeon has two goals when dealing with unstable pelvic ring injuries. The first goal, to reduce pelvic volume when appropriate, is immediate and can be a matter of life or death. The second goal is to restore the integrity of the pelvic ring and to give the patient the best chance to avoid long-term dysfunction from his or her injury. This involves preventing malunion and nonunion and restoring leg lengths as best as possible. The timing of surgery is dictated by the patient’s stability and the condition of the surrounding soft tissues. The specific surgical approach used depends on both the integrity of the skin and the specific fracture pattern needing to be fixed. It is important that traumatologists and orthopedists communicate with each other so that the placement of suprapubic tubes or colostomy pouches, if possible, are not in line with the preferred orthopedic incision. No discussion of pelvic fractures is complete without mentioning the complications that can result from both the injury itself and the operative treatment. Nerve injury can of course result from either the initial injury or the surgical manipulation. The overall prevalence of nerve injury in patients with pelvic fractures is approximately 10% to 15%.25 Deep venous thromboses are common after pelvic trauma, in the range of 35% to 50%, and antithrombotic prophylaxis is warranted.26,27 The incidence of symptomatic pulmonary embolism (PE) is in the range of 2% to 10% and that of fatal PE lower, from 0.5% to 2%. Infection is of course a serious complication, and great care should be taken to avoid operating through damaged skin and subcutaneous tissues. Even in


the best of circumstances, severe pelvic ring disruptions have a profound effect on future quality of life. Although appropriate emergent care may be life saving, lingering pain from more severe fractures is unfortunately quite common.28 In summary,unlike most other orthopedic injuries,highenergy trauma to the pelvic ring has the potential to be life threatening. Although it is obvious that the orthopedic surgeon should be well versed in the diagnosis and management of pelvic ring injuries, it is important to recognize the key role that all caregivers have in successfully managing these fractures. All trauma personnel, from the onthe-scene paramedic, to the emergency room physician, to the trauma team leader, must have a high clinical suspicion for these injuries in patients who have been involved in high-energy falls or motor vehicle accidents. Recognizing patients at risk for unstable pelvic fractures, vigilantly monitoring their response to resuscitation, and applying acute pelvic stabilization when it is both appropriate clinically (i.e., in the setting of hemodynamic instability) and radiographically (i.e., in open-book type ring disruptions) can indeed be the difference between life and death.

Critique Hemorrhage is the leading cause of death directly related to pelvic fractures. Sepsis is the second leading cause of death directly related to a pelvic fracture. Proctoscopy is an essential component in the evaluation of this patient to rule out an associated rectal injury. On occasion, a rectal injury is obvious when digital rectal examination determines that there is a spicule or an edge of fragmented bone penetrating the rectum. If there is evidence of an associated rectal injury, the patient should undergo a colostomy to divert the fecal stream. Answer (E)

References 1. Vrahas M, Hearn TC, Diangelo D, Kellam J, Tile M. Ligamentous contributors to pelvis stability. Orthopedics 1995; 18:271–274. 2. Tile M, Hearn T. Biomechanics. In Tile M, ed. Fractures of the Pelvis and Acetabulum, 2nd ed. Baltimore: Williams & Wilkins, 1995; 22–36. 3. Tile M. Pelvic ring fractures: should they be fixed? J Bone Joint Surg Br 1988; 70:1–12. 4. Tile M. Classification. In Tile M, ed. Fractures of the Pelvis and Acetabulum, 2nd ed. Baltimore: Williams & Wilkins, 1995; 66–101. 5. Tile M. Acute pelvic fractures I: causation and classification. J Am Acad Orthop Surg 1996; 4:143–151. 6. Tile M. Acute pelvic fractures II: principles of management. J Am Acad Orthop Surg 1996; 4:152–161.

37. Pelvis 7. Young JW, Burgess AR, Brumback RJ, et al. Pelvic fractures: value of plain radiography in early assessment and management. Radiology 1986; 160:445–451. 8. Gansslen A, Pohlemann T, Paul CH, et al. Epidemiology of pelvic ring injuries. Injury 1996; 27(Suppl 1):S-A13–20. 9. McMurtry RY, Walton D, Dickinson D, et al. Pelvic disruption in the polytraumatized patient. A management protocol. Clin Orthop 1980; 151:22–30. 10. Slatis P, Huittinen VM. Double vertical fractures of the pelvis: a report on 163 patients. Acta Chir Scand 1972; 138:799–807. 11. Colapinto V. Trauma to the pelvis: urethral injury. Clin Orthop 1980; 151:46–55. 12. Dalal S, Burgess AR, Siegel J, et al. Pelvic fracture in multiple trauma: classification by mechanism is key to pattern of organ injury, resuscitative requirements, and outcome. J Trauma 1989; 29:1000–1002. 13. Agolini SF, Shah K, Jaffe J, et al. Arterial embolization is a rapid and effective technique for controlling pelvic fracture hemorrhage. J Trauma 1997; 43:395–399. 14. Bottlang M, Simpson T, Sigg J, et al. Noninvasive reduction of open-book pelvic fractures by circumferential compression. J Orthop Trauma 2002; 16:367–373. 15. Falcone RE, Thomas BW. “Bean bag” pelvic stabilization. Ann Emerg Med 1996; 28:458. 16. Buckle R, Browner BD, Morandi M. A new external fixation device for emergent reduction and stabilization of displaced pelvic fractures associated with massive hemorrhage. J Orthop Trauma 1993; 7:177–178. 17. Ganz R, Krushell RJ, Jakob RP, et al. The antishock pelvic clamp. Clin Orthop 1991; 267:71–78.

601 18. Pohlemann T, Braune C, Gansslen A, et al. The pelvic emergency clamps: anatomic landmarks for a safe primary application. J Orthop Trauma 2004; 18:102–105. 19. Kellam JF. The role of external fixation in pelvic disruptions. Clin Orthop 1989; 241:66–82. 20. Riemer BL, Butterfield SL, Diamond DL, et al. Acute mortality associated with injuries to the pelvic ring: the role of early patient mobilization and external fixation. J Trauma 1993; 35:671–677. 21. Nerlich M, Maghsudi M. Algorithms for early management of pelvic fractures. Injury 1996; 27(Suppl 1):S-A29–37. 22. Pohlemann T, Bosch U, Gansslen A, et al. The Hannover experience in management of pelvic fractures. Clin Orthop 1994; 305:69–80. 23. Witschger P, Heini P, Ganz R. Pelvic clamps for controlling shock in posterior pelvic ring injuries: application, biomechanical aspects and initial clinical results. Orthopade 1992; 21:393–399. 24. Mucha P Jr, Welch TJ. Hemorrhage in pelvic fractures. Surg Clin North Am 1988; 68:757–773. 25. Weis EB. Subtle neurological injuries in pelvic fractures. J Trauma 1984; 24:983–985. 26. Geertz WH, Code KI, Jay RM, et al. A prospective study of venous thromboembolism after major trauma. N Engl J Med 1994; 331:1601–1606. 27. Buerger PM, Peoples JB, Lemmon GW, et al. Risk of pulmonary emboli in patients with pelvic fractures. Am Surg 1993; 59:505–508. 28. Draijer F, Egbers HJ, Havemann D. Quality of life after pelvic ring injuries: follow-up results of a prospective study. Arch Orthop Trauma Surg 1997; 116:22–26.

38 Lower Extremities Tina A. Maxian and Michael J. Bosse

Case Scenario A 28-year-old motorcyclist, who lost control of his bike, is brought to the trauma bay by the emergency medical technicians for evaluation and definitive management of multiple injuries. The patient has been hemodynamically stable throughout his transport and upon arrival. He is alert, oriented, and complaining only of left lower extremity pain. Advanced Trauma Life Support protocol was initiated. In addition to scattered torso abrasions and superficial lacerations of bilateral lower extremities, the patient was found to have an unstable left knee. The involved extremity has no palpable dorsalis pedis and posterior tibial pulses. Plain radiography of the neck and chest demonstrated no obvious injuries. Focused abdominal sonography revealed no fluid accumulation. After life-threatening injuries were ruled out, the knee dislocation was reduced with no return of pulses. What is the most appropriate management plan at this time? (A) (B) (C) (D) (E)

Operative exploration Expectant (observation) management Traction application and admission Arthroscopy Arteriography

Surgery may be deemed urgent in order to save an extremity or to save the patient’s life. Although this chapter deals with treatment of a variety of lower extremity conditions, in all cases, the overall condition of the patient must be kept in mind. In some clinical scenarios, a compromised limb that may be salvageable when occurring in isolation may need to be amputated from a patient in extremis in order to save the patient’s life. Always, preservation of the patient’s life supercedes preservation of the limb. Additionally, should a patient become unsta-

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ble, the surgeon must be prepared to abandon complex procedures and resort to simpler ones, coming back later for staged procedures once the patient is more stable. Foremost, the surgeon must have a plan before embarking on an emergent procedure, and the goals of that plan should be kept in mind in the operating room. Patients who require emergent surgery may be extremely ill and may not tolerate prolonged procedures. The temptation to do “just a little more” should be resisted, as a short procedure can insidiously, and unintentionally, become a long one if the surgeon is distracted from the goals, resulting in additional and unnecessary physiologic stress on an already sick patient.

Infections Necrotizing Soft Tissue Infections The challenge with necrotizing soft tissue infections is in making the diagnosis. For the septic patient with an obviously infected and necrotic limb, the diagnosis is straightforward. The difficulty is identifying the patient with a necrotizing soft tissue infection before it progresses to overwhelming sepsis.1–4 Necrotizing soft tissue infections destroy fat, fascia, and even muscle.2,4,5 They can occur at any age and tend to occur in those who are immunocompromised through advanced or extremely young age, diabetes, or chronic renal failure or in the extremities with local compromise because of peripheral vascular disease or lymphadema.6,7 Patients may or may not have previous trauma. If present, often the trauma is trivial. Patients may have cellulitis with pain out of proportion to the apparent involvement. They may or may not have systemic signs or symptoms.1 Crepitus on examination or subcutaneous air on plain radiographs is virtually pathognomonic.4 As the infection progresses, the skin involvement changes from a cellulitic appearance to a more

38. Lower Extremities

necrotic one, with bullae and violaceous skin color changes.2 The most common cause of single microbe infection is group A Streptococcus; however, necrotizing soft tissue infections may be polymicrobial or may be caused by a myriad of Gram-positive and Gram-negative organisms acting alone.1–3 Initial treatment is broad-spectrum antibiotics, resuscitation, and support for those patients who are systemically ill and surgical debridement. Once in the operating room, all signs of infection in the skin, soft tissues, and muscles should be debrided. If the entire extremity is compromised, then a guillotine amputation should be performed at the level that will provide clean margins. The wounds should not be closed. Serial debridements at 24 to 48 hours are required until viable margins are obtained. With massive debridements, early plastic surgery consultation may be advisable in order to obtain appropriate soft tissue coverage. Hyperbaric oxygen therapy has been reported to improve outcome in some small patient series2,3,8; however, there are no randomized trials that clearly demonstrate any improved efficacy with its use in necrotizing soft tissue infections. Vacuum-assisted dressings have been of some use in the management of soft tissue infections in limited clinical studies.9

Septic Joints Typically, a septic joint has a painful range of motion, with overlying warmth and erythema. The patient may or may not have systemic symptoms of fever and malaise and an elevated peripheral white blood cell count.10 Usually, the C-reactive protein and erythrocyte sedimentation rates are elevated.10–12 The diagnosis of septic arthritis, however, is made through aspiration of the joint fluid, which is then sent for Gram stain, cell count, differential, and crystal analysis (to rule out crystalline arthropathy).10 An emergent washout of the joint is usually performed when organisms are seen on the Gram stain, for white cell counts >50,000, and for neutrophil counts >90% of the joint fluid total white blood cell count.10 Joint irrigation and debridement should be performed emergently to minimize articular cartilage destruction. In children, growth disturbances,13 such as premature physeal closure or, conversely, complete physeal separations,14 may result if the joint is not washed out expeditiously. The washout may be arthroscopic or open; there are no clinical data supporting the superior efficacy (or lack thereof) of arthroscopic washout over open arthrotomy. For infected total joint replacements, the urgency is usually not as great as when a native joint is at risk unless the patient is septic. Infections that occur within the first 2 weeks of joint replacement may be treated with an irrigation and debridement with polyethylene liner exchange, so the surgeon proceeding with such a washout

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should be sure that the correct components are available.15,16 For infections occurring after the first 2 weeks, eradication of the infection is better accomplished with a twostage procedure consisting of removal of the components and placement of an antibiotic spacer, followed by later reimplantation of new components once the infection has been cleared.15,16 If the entire prosthesis must be removed, any surgeon entertaining removal of an infected total joint should have all the necessary removal equipment available and should be able to construct an antibiotic spacer with the appropriate levels of antibiotics.17 For patients who are truly septic and in extremis due to an infected total knee or infected antibiotic spacer, serious consideration should be given to emergent guillotine above the knee amputation.18,19 An emergent hip disarticulation or resection arthroplasty would be the equivalent procedure at the hip, but this has been infrequently reported.20

The Nontraumatic Ischemic Extremity The patient with acute limb ischemia will present with some or all of the classic “P’s” for ischemia: pain, pulselessness, pallor, poikilothermia, paralysis, and paresthesias. Because this patient group tends to have a history of peripheral vascular disease,21 handheld Doppler devices should be used to evaluate for pulses when none are palpable. Preoperatively, one needs to consider the cause and duration of the ischemia, as both play roles in determining the type of surgery required. Embolic events tend to have sudden onset of symptoms, occur in patients with a recent cardiac event (myocardial infarction, new-onset arrhythmia), and may have a minimal history of claudication. Thrombotic events tend to have a vague onset in patients with a history of claudication. The Society for Vascular Surgery–International Society for Cardiovascular Surgery (SVS-ISCVS) has classified acute limb ischemia to facilitate communication and aid with clinical decision making (Table 38.1) for both nontraumatic and traumatic ischemia.22 Surgical decision making for this patient population must also take into account the patients’ frequent significant comorbidities, especially diabetes mellitus and cardiac and pulmonary conditions.23,24 If no allergies or other contraindications are present, all patients should be given aspirin and started on a heparin protocol.21 Basic laboratory tests to evaluate renal function and to determine if acidosis or hyperkalemia are present should be performed.21 An electrocardiogram to evaluate for arrythmias or myocardial infarction should be obtained, as most embolic phenomena tend to be cardiac in origin.21,25 The patient should be hydrated.26 For those facing surgery and with a significant cardiac history, a

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Table 38.1. SVS-ISCVS clinical categories of acute limb ischemia. Doppler signals Category I.

Viable

II. Threatened a.

Marginally

b.

Immediately

III. Irreversible

Description

Capillary return

Not immediately threatened

Intact

Reversible if relieved quickly Salvageable if promptly treated Salvageable with immediate revascularization

Slow

Amputation required

Absent (marbling)

Muscle weakness None

None Mild, moderate

Profound (rigor)

Sensory loss None

Arterial

Venous

Audible, pulsatile flow

Audible

No pulsatile flow, inaudible

Audible

Inaudible

Inaudible

Minimal (toes or none) More than toes, associated with rest pain Profound (anesthetic)

Source: Adapted from Rutherford RB, Baker D, Ernst C, et al. Recommended standards for reports dealing with lower extremity ischemia: revised version. J Vasc Surg 1997; 26:517–538, with permission from Elsevier.

Swan-Ganz catheter may be necessary for fluid management.21,26 The level of demarcation on the lower extremity, as well as any neurologic deficits, may give an indication as to the level of obstruction. For patients with Level I or IIa ischemia with less severe symptoms of a more chronic duration,24 an attempt at endovascular revascularization may be a reasonable choice. For those with Level III symptoms, prompt amputation may be life saving, with any attempt at revascularization placing the patient at risk from reperfusion injury with renal dysfunction, pulmonary insufficiency, and/or cardiovascular collapse.27 For an amputation, the level at which to perform the amputation and whether or not to close the wound become the primary concerns. For an extremely sick patient or when the margins of necrosis are unclear, a guillotine amputation may be best done emergently, with a plan to perform a second look and revision with closure at a later time. If, however, clean, viable flaps are available and the patient is stable, the surgeon may proceed with immediate closure. For those with Level II ischemia caused by an embolism or thrombus in situ, an open catheter thromboembolectomy is warranted.21 The femoral artery is exposed and a thromboembolectomy performed taking care not to injure or dissect the vessel. In some cases, exposure below the knee may be performed to gain access to a vessel. After removing the embolus or thrombus, angiography is used to verify patency of the vascular system. If an occlusion persists, a bypass, or even amputation, may be required.23,28 Distal fasciotomies should be performed for all Level IIb revascularizations.21

Compartment Syndrome A compartment syndrome occurs in an osseofascial compartment when either the volume of the compartment is decreased (as with occlusive dressings or a cast) or the

contents of the compartment increase (e.g., postperfusion swelling, hemorrhage). In either scenario, the intracompartmental pressure increases and, if not relieved, eventually exceeds the capillary perfusion pressure, causing ischemia.29 A compartment syndrome can occur with crush injuries, burns, and fractures or after revascularization with reperfusion. Compartment syndromes may also occur with open fractures,30 because, although traumatic wounds may cause tears in the fascia, these tears by no means ensure decompression of the compartments. Compartment syndromes do not have to have a traumatic etiology. Certain drugs (statins) or nutritional supplements (creatine) have also been associated with compartment syndromes.31 Clotting abnormalities (anticoagulants, hemophilia) may cause excessive bleeding after seemingly innocuous trauma and result in a compartment syndrome.32,33 The classic signs and symptoms of a compartment syndrome include pain out of proportion to the injury and uncontrollable pain in a patient who previously was relatively comfortable.34 Pain may also occur with passive range of motion of the ankle and toes. Compartments are tense on examination. Paresthesias and pulselessness usually occur late and are of no use in early diagnosis.34,35 In an unconscious patient or a patient with a spinal cord injury, the patient may not be able to communicate or to sense that he or she is in pain. Pain may also be absent in patients with spinal or epidural anesthesia.36–39 These confounding factors have led to the use of compartment pressure measurements to assist with the diagnosis. Compartment syndrome is generally taken to exist when compartment pressures are within 30 mm Hg of the diastolic pressure.34,35 A compartment syndrome may exist with lower pressures in a hypotensive patient,34 as the hypotension contributes to ischemia. Undoubtedly, patients may have compartment pressures within 30 mm Hg of the diastolic pressure who do not have clinically


605

Peroneus longus m. Extensor digitorum longus m. Tibialis anterior m. Soleus m.

Peroneus brevis m.

taking care to protect the superficial peroneal nerve in the lateral compartment (Figure 38.1B). The medial incision is made posteromedially (Figure 38.2A), taking care to identify and protect the saphenous vein if encountered. The superficial posterior compartment fascia is released; then the muscles are pealed off the posterior aspect of the tibia until the deep posterior compartment is encountered and its fascia released (Figure 38.2B). To release the compartments of the thigh,43 a lateral incision is made. The tensor fascia lata is incised (Figure 38.3A). Next, the intermuscular septum between the lateral and posterior compartments is identified and released in order to decompress the posterior compartment (Figure 38.3B). At this point, the medial compartment is reassessed. If it is still tense on clinical examination, or if repeated pressure measurements still indicate elevated pressures, then a separate medial incision is made to release the medial compartment.

A Extensor digitorum longus m. Tibialis anterior m. Extensor hallucis longus m. Deep peroneal n. bundle Saphenous n. bundle Superficial peroneal n. Peroneus longus m. Flexor digitorum longus m. Tibial n. bundle

B

Flexor hallucis longus m. Tibialis posterior m. Soleus m. Sural n. bundle

igure 38.1. Lateral fasciotomyy incision of the leg. g (A) Incision after compartment release. (B) Path of the surgical release in the transverse plane.

apparent compartment syndromes.40 The diagnosis needs to be bolstered by clinical examination. Once the diagnosis of a compartment syndrome is made, the patient should be taken emergently for fasciotomies. The fasciotomies should release the skin and fascia over the muscle. For a two-incision approach in the leg, the lateral incision does not need to be taken proximal to the fibular head or distal to the lateral malleolus: this is a tendonous region, and, consequently, there is no muscle tissue to be decompressed here (Figure 38.1A). Conversely, the fasciotomy incisions should not be minimal dermatomies with subcutaneous release of the fascia. The skin itself may act as a constrictive barrier if not released adequately.41 For a two-incision technique in the leg,42 the lateral incision is centered over the approximate fascial plane between the anterior and lateral compartments, although this may be difficult to identify in obese patients or in a markedly swollen limb. Once the skin is incised, the fascia over the anterior and lateral compartments is released,

Gastrocnemius m. Tibia Soleus m.

Flexor digitorum longus m.

A Tibialis anterior m. Extensor hallucis longus m. Deep peroneal n. bundle Saphenous n. bundle

Extensor digitorum longus m. Superficial peroneal n. Peroneus longus m.

Flexor digitorum longus m.

B

Tibial n. bundle Sural n. bundle

Flexor hallucis longus m. Tibialis posterior m. Soleus m.

Figure 38.2. Medial fasciotomy incision of the leg. (A) Incision after compartment release. (B) Path of the surgical release in the transverse plane.

606


Iliotibial tract

Vastus lateralis m.

medial side of the calcaneus.29 Opinions differ, however, on the need to decompress foot compartment syndromes, as the residual deformity associated with the fasciotomies may exceed that of the intrinsic foot contractures. In all cases, obviously necrotic muscle should be debrided. If the muscle in all compartments is dead, then an amputation to a viable level should be performed. There are extremely limited data demonstrating the efficacy of hyperbaric oxygen therapy in the treatment of compartment syndromes.47 Vacuum-assisted dressings to fasciotomies have been shown to decrease serum myoglobin levels in a rabbit model of compartment syndrome,48 but no similar clinical studies with humans have been published to date.

Biceps femoris m. (short)

Trauma Irreducible Dislocations

A Rectus femoris m. Vastus lateralis m. Perforating a. and v.

Vastus medialis m. Sartorius m.

Saphenous n. bundle

Irreducible dislocations of the lower extremity are those in which a closed manipulation does not result in joint reduction. The reduction may be blocked by interposed soft tissues or incarcerated fracture fragments. The surgical goals are to remove the blocks to reduction, by open means when necessary, to repair any vascular problems that remain after reduction, and to provide fixation when necessary to keep the joint reduced.

Iliotibial tract Biceps femoris m. (short)

Adductor longus m. Gracilis m.

Biceps femoris m. (long) Sciatic n. bundle Semitendinosus m. Semimembranosus m.

Adductor magnus m.

Hip Irreducible dislocations of the hip can be caused by acetabular fracture dislocations with the head “button holed” through the capsule, large incarcerated fragments contained in the joint (Figure 38.4), or acetabular

B igure 38.3. Lateral fasciotomy incision of the thigh. (A) Incision after compartment release. (B) Path of the surgical release in the transverse plane.

Gluteal compartment syndrome, although rare, does occur and is released through an incision similar to a posterior approach to the hip.36,44 The fascia of the gluteus maximus, gluteus medias, and tensor fascia lata must be released while protecting the neurovascular structures. Like compartment syndromes of the leg or thigh, those of the foot are characterized by pain, swelling, and elevated intracompartmental pressures,29,45,46 Generally, to adequately release the interossei and adductor compartments, dorsal incisions are made medial to the second metatarsal and lateral to the fourth metatarsal.29 Care must be taken to make these incisions in the appropriate locations to avoid necrosis of the skin bridge that can occur if the incisions are made too close together. The medial, superficial, calcaneal, and lateral compartments are decompressed through a medial incision over the

Figure 38.4. A radiograph of a hip fracture dislocation with an incarcerated fragment. The fragment is blocking concentric reduction of the right hip.


fracture dislocations accompanied by femoral head fracture. Overall, outcomes for patients with irreducible hip dislocations tend to be poor.49 Additionally, outcomes related to the hip are worse with longer times to reduction.50,51 A surgeon faced with an irreducible dislocation of the hip should be comfortable with complex acetabular surgery before proceeding; otherwise, the patient should be transferred to a surgeon who regularly deals with such surgery. However, if faced with a progressive neurologic deficit or vascular injury, or should a neurovascular deficit occur after a successful, closed reduction, the patient needs emergent open reduction or transfer to a facility with staff capable of performing one.52–54

Knee The irreducible dislocation of the knee is characterized by a skin pucker, representing the medial femoral condyle “button holed” through the capsule.55–57 Patients with this injury need emergent reduction to avoid skin necrosis, which can cause disastrous long-term results.57 Open reduction is required if the knee cannot be reduced with closed manipulation under general anesthesia. If a vascular injury is also present, the patient requires emergent repair, as with any vascular injury. For knee dislocations with a normal vascular examination before and after reduction, arteriography does not need to be performed, and the patient may be monitored with serial examinations for the first 48 hours.58,59 Emergent ligamentous repair is not recommended,60–62 and the patient may need to be placed in knee-spanning external fixation if the knee is unstable after reduction or if large areas of soft tissue compromise are present that require management and would be inappropriate for treatment in a splint or knee immobilizer.

Ankle and Foot Irreducible ankle and foot dislocations are most commonly seen in ankle fracture dislocations or in subtalar dislocations. Such injuries require open reductions emergently to reduce tenting on soft tissue or if a vascular injury is present that does not improve with closed manipulation. Irreducible subtalar dislocations tend to occur with higher energy mechanisms. In one series,63 one third of subtalar dislocations required open reductions. The key to an open reduction is to identify the direction of the dislocation in order to decide on the surgical approach that will gain access to the structures most likely responsible for blocking the reduction. Soft tissue entrapment blocks reduction in 50% of irreducible reductions. For lateral dislocations, the posterior tibialis, flexor hallucis, or flexor digitalis longus tendons tend to be the blocking

607

structures.63 For medial dislocations, the blocking structures tend again to be the tibialis posterior and the flexor digitalis longus or the talar head button holed through the capsules.63 Bony blocks or capsular incarcerations may also occur in either dislocation direction.

Femoral Neck Fractures in the Young “Young” is generally defined as less than 50 years of age, although for certain individuals the age to consider urgent reduction of a femoral neck fracture may be extended to 65 years or older. Femoral neck fractures in young patients usually result from high-energy trauma. Fractures resulting from a fall or from minimal trauma (other than displaced stress fractures) occur because the bone is compromised by some metabolic process (e.g., osteoporosis or chronic renal disease). In these cases, fixation may be inadequate, or the patient’s condition may be such that definitive treatment is hemiarthroplasty. The femoral head receives its blood supply through retinacular vessels within the capsule, the metaphyseal bone, and the artery of the ligamentum teres, with the most important contribution coming from the superior retinacular and lateral epiphyseal vessels.64 In a femoral neck fracture, especially a displaced one, the superior reticular vessels may be disrupted, leaving only the inferior ones. Should these vessels be disrupted as well, the head becomes entirely dependent on the artery of the ligamentum teres, which generally provides only a small contribution in the adult. Accurate, prompt fracture reduction is thought to “unkink” these vessels if they are not torn. When the femoral neck fracture in a young patient results from high-energy trauma, any life-threatening or limb-threatening injuries should be addressed first. The femoral neck fracture should then be treated, if possible, without compromising the patient’s resuscitation, as soon as possible65 in order to reduce the incidence of avascular necrosis of the head and fracture nonunion. An attempt at closed reduction may be performed first on a fracture table. Any reduction maneuvers should be gentle so as not to traumatize further the already tenuous blood supply to the femoral head.66–68 External rotation may tear any remaining inferior retinacular vessels.64 Gentle traction is applied to the leg. The hip is internally rotated and then abducted.69,70 The reduction is assessed in two views using fluoroscopy. If the reduction is anatomic, the surgeon may proceed with fixation, preferably with three, percutaneously placed, cannulated screws. All starting portals should be above the level of the lesser trochanter71 to avoid stress risers that can lead to iatrogenic subtrochanteric fractures. The screw threads should not cross the fracture site to allow for compression.70 The screws should be tightened simultaneously to avoid a malreduction. Because posterior comminution tends to be present in most

608

displaced fractures,72 tightening screws that are more posteriorly located first will cause the fracture to fall into retroversion. For basicervical femoral neck fractures that would require starting portals very close to the lesser trochanter and also cause a relatively large lever arm on the smaller screws, a compression hip screw with a derotation screw should be used for fixation.73 Controversy exists as to whether capsulotomy should be performed. Two very small clinical studies showed that if the hip capsule was intact, then intracapsular pressures were elevated.74,75 In another small study involving human patients,76 blood flow was shown to be decreased in the femoral head with an intact capsule and elevated capsular pressures. When capsulotomy was performed, the capsular pressure decreased.76 However, there are no clinical studies that demonstrate that capsulotomy has any effect on patient outcome. If the reduction is not anatomic after an attempt at closed reduction, then preparation for an open reduction should be made rather than remanipulating the hip and traumatizing its vasculature further.69 If the surgeon is comfortable with an anterior approach on the fracture table, the patient can be prepped out with attention made to prepping the leg out more anteriorly than is usual when using a fracture table. Otherwise, the patient should be transferred to a radiolucent table. The anterolateral approach to the hip is used to perform an open reduction.65,69 The capsulotomy is performed anteriorly and in line with the femoral neck to minimize dissection. The reduction is made and fixation obtained with cannulated screws in the same manner as with closed reduction. If a femoral shaft fracture complicates the femoral neck fracture, several fixation options have been described: cannulated screws and a retrograde nail, screws with plating, a reconstruction nail, or cannulated screws with an antegrade nail. The reconstruction nail has proved to have the most complications of the device combinations.77 In general, the femoral neck fracture should take precedence and be fixed first should the patient decompensate and the surgery need to be stopped.78 The femur fracture can then be treated in traction or with an external fixation until the patient’s condition allows definitive fixation.

Vascular Injury The most important goals in vascular injury management are gaining control of bleeding and maintaining limb viability.79 When external hemorrhage is present, control of bleeding is initially attempted with direct pressure and packing. In some cases, direct pressure may have to be maintained until operative exposure and control is obtained. Tourniquet use is discouraged, as it causes additionally ischemia and tissue compromise in an already


compromised extremity. In a worst case scenario, for an extremely sick patient whose mangled, ischemic limb is only one of multiple traumatic injuries, proceeding with an amputation may be in the best interest of the patient, even though vascular reconstruction may be possible, as a manner of controlling bleeding and avoiding a revascularization insult to the patient. When amputation of a mangled extremity is the obvious surgical option, application of a tourniquet above the injury level can be employed to limit blood loss as the patient is evaluated and prepared for the operating room. The diagnosis of vascular injury must also be made correctly. Fractures and dislocations should be reduced and splinted and the vascular examination repeated. If the “hard signs” of vascular injury remain, then the patient requires operative treatment80: pulselessness, pallor, paresthesia, pain, paralysis, poikilothermia; obvious active arterial hemorrhage; a rapidly expanding, large, or pulsatile hematoma; a palpable thrill or audible bruit; or absent pulses and distal ischemia. In contrast, the “soft signs” of vascular injury can be managed expectantly,80,81 which include history of active bleeding at the injury scene; a penetrating wound or blunt trauma in close proximity to a major artery; a small, nonpulsatile hematoma; unexplained neurologic deficit in an extremity; or unexplained shock. Arteriography should also be used when the patient’s injuries are such that it is difficult to discern if the ischemia or lack of motion is caused by a soft tissue, vascular, or nerve injury, especially with fractures, dislocations, or shotgun injuries.80,82,83 Gunshot wound proximity is not a sensitive indicator of vascular injury in a patient with a normal examination.84 For older patients with chronic vascular insufficiency and trauma, angiography may need to be used more liberally to rule out vascular injury because of the confusing picture of symptoms.85 Compartment syndromes can also cause abnormalities on angiograms.86 Consequently, when a compartment syndrome is present, fasciotomies should be performed before any vascular exploration is performed and the vascular status reassessed after the fasciotomies are completed. The fasciotomies also decompress the collaterals and venous system, which permits some flow to occur while the repair is being carried out.83 Some injuries may be treated within the angiography suite, and, as interventional radiographic techniques improve, the list of treatable conditions continues to expand. Currently, low-flow arteriovenous fistulas, false aneurysms, or branches of larger arteries or vessels in anatomic regions that are difficult to reach surgically can be embolized with coils or balloons.80 If radiographically diagnosed uncontrollable bleeding is amenable to surgical repair, a balloon may be placed in the angiography suite to control bleeding, with subsequent repair in the operating room.80 At all times, the team treating a trauma


patient in the angiography suite must remain cognizant that the patient is a trauma patient: the patient must be kept warm, procedures must be expedited, and the patient must be closely monitored for declines in hemodynamic or respiratory status. The Doppler index is of assistance in determining if a vascular injury is present. The distal systolic blood pressure of the injured extremity is divided by the systolic blood pressure in an uninjured extremity. A value less than 0.9 is a significant predictor of an arterial injury80,82; however, such measurements may be difficult to make in a multitrauma patient who may not have an uninjured upper extremity or whose fractures or splints in the involved lower extremity may make pressure measurements difficult if not impossible.87 Duplex ultrasound may also be used to assess the vessels, although this technique requires specialized equipment and personnel that may not be available at all times. When available, imaging of the vessels with this modality in patients with soft signs should be considered. Systemic or local heparin may be helpful for combined or crush injuries or when a long delay is possible between injury and revascularization.88 If systemic heparinization is contraindicated because of other injuries, intermittent intraarterial irrigation may be used during revascularization.88 Evidence clearly shows that muscle necrosis is present after even as short a time as 3 hours of ischemia.27 After 6 hours of total ischemia, muscle necrosis is nearly complete.27 The degree of ischemia that occurs in an injured extremity is not necessarily total, however, and depends on the level of injury, the presence of functioning collaterals, and the degree and duration of shock in which the patient has been.89 Reperfusion of a cadaveric extremity, however, may very well kill a patient, especially if an entire extremity is reperfused.27 Temporary intraluminal shunting should be used when faced with an ischemic limb that requires fracture fixation, extensive soft tissue debridement, or treatment of a life-threatening emergency that will cause delay until the definitive revascularization surgery can be performed.80,82,90 The priority should be to restore blood flow within 3 to 6 hours; however, such shunts have successfully been left in place up to 52 hours without systemic anticoagulation in damage-control situations.91 Once in the operating room, the entire lower extremity to be revascularized should be prepped, as well as the contralateral lower extremity or upper extremity, if grafting is anticipated or a possibility. If extraanatomic grafting is a possibility, the patient should be prepped to the axillae. Any foreign bodies, especially penetrating ones, should not be removed until proximal vascular control has been obtained.82 The repairs vary as necessary, with extraanatomic grafts usually reserved for repairs in beds with significant mounts of soft tissue injury or infection.80

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Autogenous grafts are preferred80,86; however, synthetic grafts may be used in sites above the knee when no autogenous grafts are available or a large-sized discrepancy may result with an autogenous graft.80 Synthetic grafts may also be used for an unstable patient who requires a rapid repair to avoid graft harvest.80,92 In this scenario, however, consideration should be given to temporary shunting followed by definitive repair once the patient is stable. All repairs should be without tension and covered with adequate soft tissue in order to prevent dessication followed by rupture of the graft. Several small studies have documented that vascular repair followed by fracture fixation can be performed in this order with no subsequent disruption or compromise of the vascular repair.92–94 Obviously necrotic muscle should be debrided; however, it is important to note that perfused, dead muscle will readily bleed if partially debrided and may lead to significant blood loss, especially if the patient is anticoagulated or coagulopathic. Muscle viability is determined most reliably by contractility, which is tested by lightly touching the muscle with the electrocautery or by briskly striking the muscle. Of note, muscle necrosis of all four compartments of the lower leg should prompt the surgeon to proceed with an amputation. Once repairs are complete, postrepair arteriography or duplex examination is performed in the operating room, if the patient can tolerate the additional contrast load. In this manner, thrombi or stenosed repairs may be identified and corrected before leaving the operating room. The remaining subsections cover aspects of revascularization unique to each anatomic region of the lower extremity.

Femoral Artery Injuries For femoral injuries, the incision is made over the femoral triangle.80 If proximal access is needed to control bleeding, a second incision may be made in the superior to the inguinal ligament in order to gain proximal control via the external iliac artery.88 A Fogarty catheter is used to remove clot or thrombus in the vessel before repair, and, ideally, retrograde bleeding is present.88 If a graft interposition is required for repair, autologous saphenous vein is harvested. However, in this anatomic region, synthetic grafts may be used. For grossly contaminated wounds or wounds with extensive soft tissue injuries, an extraanatomic repair can be performed, through the posterior soft tissue planes.88 Intravascular shunts may also be used as a temporizing measure in this anatomic region.88,92 In a damage-control scenario, with an exsanguinating, dying patient, the femoral artery may be ligated with the knowledge that such a maneuver results in a 50% amputation rate.88 The proximal

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profunda femoris may also be ligated if faced with exsanguination.80 Intimal flaps, focal narrowing, small, false aneurysm, and arteriovenous fistulas may all be observed and repaired electively if signs of ischemia occur or worsen.88 Vein repair should also be performed, if possible, as such repairs have been shown to improve the patency of arterial repairs.Also, a more normal distal vascular bed resistance is maintained, and a reduced incidence of chronic venous insufficiency and associated postphlebitic syndrome occurs.88,95

Popliteal Artery Of the arterial injuries to the leg, those to the popliteal artery are the most limb threatening because of the limited collaterals to the foot and leg.85,86 The popliteal artery divides into the anterior tibial artery and the tibioperoneal trunk, which exists for several millimeters before dividing into the peroneal and posterior tibial arteries. The vein travels close to the artery in this region, which explains the frequency of simultaneous injury to both. The popliteal vein should be repaired at the same sitting as the artery, if possible, to reduce outflow obstruction and to improve limb salvage.83 Shunts may be difficult to use distal to the knee because of the decreasing size of the vessels.83 The patient is placed supine on the operating room table with the hip flexed and abducted. A medial approach is used to the vessels,83,96 although a posterior approach may be used when a penetrating wound occurs directly posterior.85 The artery should be debrided to healthy tissue, with an end-to-end repair the most desired result.85 If more than 2 cm is debrided, then a graft is required. The geniculates should not be divided to mobilize the vessels.85 Prosthetic grafts should be avoided in this anatomic region, if possible.86 If an extraanatomic bypass is required, it should be placed out through lateral tissues.80 If a repair is performed after knee dislocation, the knee may be stabilized with knee-spanning external fixation.

Infrapopliteal Arteries Three main arteries supply the leg and foot: the anterior and posterior tibial arteries and the peroneal artery. These vessels have a good collateral supply, so, if one vessel is injured, no repair needs to be performed. Should an injured vessel actively continue to bleed, either ligation or embolization may be performed.80,83 If, however, two of the vessels are injured or the tibioperoneal trunk is injured, then a vascular repair should be performed. Venous injuries in this anatomic region are rarely repaired.80,83


A longitudinal incision is used to gain access to the vessel of interest and a Fogarty catheter used to remove any thrombus.83 These vessels can rarely be repaired primarily and generally require an autogenous saphenous vein graft because of their small size.83 Shunts are also difficult to use in this region because of the small size of the vessels.83

Open Fractures and Open Joints The classic teaching is that open fractures need to be debrided within 6 to 8 hours as this is thought to be the time it takes for bacteria to multiply to the critical infecting innoculum of 105 organisms.97 The early work determining this was done before antibiotics were used regularly. With the use of antibiotics, the window for washout may be expanded, although there are no randomized, clinical trials proving any of these practices.98–101 The key is to diagnose an open fracture correctly and to start the appropriate antibiotics. Our protocol is to use a broad-spectrum cephalosporin to provide antibiotic coverage for Gustilo type I through type IIIB open fractures, with the addition of an aminoglycoside reserved for type IIIC open fractures. For wounds contaminated with soil, fresh water, or “farm wounds,” penicillin coverage is added. Wounds are washed out using 1 L of normal saline in the emergency room, a sterile dressing is applied, and the fracture is splinted.This dressing is not removed again until the patient is in the operating room for definitive washout, as such repeat looks increase the infection rate.102 With the advent of digital photography, consideration should be given to obtaining quick digital photos of wounds in the emergency room to show to team members who arrive later, rather than disturbing the dressings. The current literature supports washout of an open fracture as soon as is possible, given operating room availability and the patient’s condition.98 For a multiple trauma patient, this may mean going to the intensive care unit for several hours for warming and resuscitation before proceeding to the operating room. One retrospective review of multiple types of open fractures at multiple sites showed no increase in infection or nonunion rates with times up to 13 hours to definitive irrigation and debridement.99 Data from the Lower Extremity Assessment Project (LEAP) corroborated this result, with the patient’s time from injury to admission at the trauma center being the only factor predictive of infection.100 Another study retrospectively examined lowenergy type I open fractures in over 91 patients who received intravenous antibiotics, but only one patient had a formal washout within 12 hours. Some patients received no formal irrigation and debridement, yet no infections were observed in the study.103 Once in the operating room, the open fracture must be explored. Dead or heavily damaged skin, especially the


traumatic wound edges, should be excised. Nonviable muscle should be excised. The fracture itself should be stabilized with appropriate fixation. If the wound can be closed, there is no hard evidence indicating that it should not be.101 Currently, a randomized study is underway to determine if closable wounds associated with tibia fractures may be closed primarily versus brought back to the operating room for a repeat washout with secondary closure. Of course, if any tissue, especially muscle, is of questionable viability at the time of the original surgery, or if the wound is extremely contaminated, the patient should be brought back to the operating room in 24 to 48 hours for a second-look procedure.101 At present, there exist only small clinical studies that suggest vacuumassisted dressings may be of benefit with traumatic wounds.104

The Mangled Extremity In the emergency room, grossly contaminated wounds should be washed out, wounds packed with sterile dressings, and the extremity splinted. As long as bleeding in the extremity is controlled in this manner, the patient may remain in the splint while being resuscitated in the intensive care unit or while undergoing other life-saving procedures. Temporary intravascular shunts may be placed and left in while the patient undergoes resuscitation or other procedures.91 For the patient in extremis, a guillotine amputation with control of bleeding may be the best course of action, especially for an ischemic mangled extremity. For the “less ill” patient, vascular repair (if necessary), irrigation and debridement, and skeletal stabilization should be the course of action. The vascular repair should take precedence over skeletal stabilization as discussed in the section on vascular injuries.92–94 External fixation is typically the form of stabilization used initially in the management of mangled extremities. External fixators can be rapidly applied and then converted to other forms of fixation once the degree of soft tissue injury becomes fully known. Fixators may be placed in the operating room or the intensive care unit. For fixator placement in the intensive care unit, spot radiographs may be used to determine the approximate levels for pin placement with skin stab incisions made accordingly. This can be especially useful for fixation of the femur where the thigh musculature obscures bony landmarks. Ideally, the external fixation pins should go through regions where open reduction is not planned later to avoid potential contamination of the tissues and interference with flap placement. Fixators on the femur may be anterior or lateral. Unfortunately, anterior pins violate the quadriceps mechanism but are often the easiest to place, especially in the intensive care unit. Ideally, spanning fix-

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ators should have pins into segmental fracture fragments, as the segments will sag otherwise and the entire construct will shorten. One rapid form of spanning fixator that can be applied to the leg uses tibial and calcaneal traction pins that are then connected with a unilateral frame. In extremely ill patients, traction pins alone may be placed. For entire leg involvement, a calcaneal traction pin may be used to provide traction to the lower extremity. Vacuum-assisted dressings may be useful in the management of the soft tissue injuries encountered in mangled extremities104; however, there are currently few published data from randomized clinical trials to show improvement in patient outcome with these dressings.104,105 The multicenter LEAP study comparing the results of amputation with limb salvage for mangled extremities showed that patient outcome was no different whether limb salvage or amputation was performed.106 However, the outcomes for patients with early amputations was better than for those whose amputations were performed later.107 The LEAP study did show, however, that none of the current mangled extremity scoring systems was clinically useful in determining whether a limb should be amputated.108

Critique With there being no immediate life-threatening injuries, the management priority for this patient, at this time, is addressing the obvious acute arterial insufficiency of the involved extremity. This patient should undergo acute care exploration of the popliteal artery, with repair of bypass being the likely surgical option. With there not being multiple levels of injury, arteriography is not essential for this particular patient, and such an intervention would delay definitive management and possibly result in irreparable damage. This patient has a popliteal artery injury and needs operative intervention by both vascular and orthopedic surgeons. Answer (A)

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614 82. Bandyk DF. Vascular injury associated with extremity trauma. Clin Orthop 1995; 318:117–124. 83. Keeley SB, Snyder WH,Weigelt JA.Arterial injuries below the knee: fifty-one patients with 82 injuries. J Trauma 1983; 23:285–292. 84. Francis H, Thal ER, Weigelt JA, Redman HC. Vascular proximity: is it a valid indication for arteriography in asymptomatic patients? J Trauma 1991; 31:512–514. 85. Frykberg ER. Popliteal vascular injuries. Surg Clin North Am 2002; 82:67–89. 86. Feliciano DV, Herskowitz K, O’Gorman RB, et al. Management of vascular injuries in the lower extremities. J Trauma 1988; 28:319–328. 87. Johansen K, Lynch K, Paun M, Copass M. Non-invasive vascular test reliably exclude occult arterial trauma in injured extremities. J Trauma 1991; 31:515–522. 88. Carrillo EH, Spain DA, Miller FB, Richardson JD. Femoral vessel injuries. Surg Clin North Am 2002; 82:49–65. 89. Reber PU, Patel AG, Sapio NLD, Ris H-B, Beck M, Kniemeyer HW. Selective use of temporary intravascular shunts in coincident vascular and orthopedic upper and lower limb trauma. J Trauma 1999; 47:72–76. 90. Wolf YG, Rivkind A. Vascular trauma in high-velocity gunshot wounds and shrapnel-blast injuries in Israel. Surg Clin North Am 2002; 82:237–244. 91. Granchi T, Schmittling Z, Vasquez J, Schreiber M, Wall M. Prolonged use of intraluminal arterial shunts without systemic anticoagulation. Am J Surg 2000; 180:493–497. 92. Starr AJ, Hunt JL, Reinert CM. Treatment of femur fracture with associated vascular injury. J Trauma 1996; 40:17–21. 93. Drost TF, Rosemurgy AS, Proctor D, Kearney RE. Outcome of treatment of combined orthopedic and arterial trauma to the lower extremity. J Trauma 1989; 29:1331– 1334. 94. McHenry TP, Holcomb JB, Lindsey RW. Fractures with major vascular injuries from gunshot wounds: implications of surgical sequence. J Trauma 2002; 53:717–721. 95. Ashworth EM, Dalsing M, Glover JL, Reilly MK. Lower extremity vascular trauma: a comprehensive, aggressive approach. J Trauma 1988; 28:329–336. 96. Muscat JO, Rogers W, Cruz AB, Schenck RC. Arterial injuries in orthopaedics: the posteromedial approach for vascular control about the knee. J Orthop Trauma 1996; 10:476–480.

T.A. Maxian and M.J. Bosse 97. Elek SD. Experimental staphylococcal infections in the skin of man. Ann NY Acad Sci 1957; 65:85–90. 98. Khatod M, Botte MJ, Hoyt DB, Meyer RS, Smith JM, Akeson WH. Outcomes in open tibia fractures: relationship between delay in treatment and infection. J Trauma 2003; 55:949–954. 99. Harley BJ, Beaupre LA, Jones CA, Dulai SK, Weber DW. The effect of time to definitive treatment on the rate of nonunion and infection in open fractures. J Orthop Trauma 2002; 16:484–490. 100. Pollak AN, Castillo RC, Jones AL, Bosse MJ, MacKenzie EJ, Group LS. Time to definitive treatment significantly influences incidence of infection after open high-energy lower-extremity trauma. In Orthopaedic Trauma Association 19th Annual Meeting, Salt Lake City, UT, 2003: 98–100. 101. Weitz-Marshall AD, Bosse MJ. Timing of closure of open fractures. J Am Acad Orthop Surg 2002; 10:379–384. 102. Olson SA, Schemitsch EH. Open fractures of the tibial shaft: an update. Instr Course Lect 2003; 52:623– 631. 103. Yang EC, Eisler J. Treatment of isolated type I open fractures: is emergent operative debridement necessary? Clin Orthop 2003; 410:289–294. 104. Webb LX. New techniques in wound management: vacuum-assisted wound closure. J Am Acad Orthop Surg 2002; 10:303–311. 105. Hercovici D, Sanders RW, Scaduto JM, Infante A, Dipasquale T. Vacuum-assisted wound closure (VAC therapy) for the management of patients with highenergy soft tissue injuries. J Orthop Trauma 2003; 17:683– 687. 106. Bosse MJ, MacKenzie EJ, Kellam JF, et al. An analysis of outcomes of reconstruction or amputation of leg-threatening injuries. N Engl J Med 2002; 347:1924–1931. 107. Smith DG, Castillo RC, MacKenzie EJ, Bosse MJ, Group LS. Functional outcome of patients who have late amputation after trauma is significantly worse than for those who have early amputation. In Orthopaedic Trauma Association 19th Annual Meeting, Salt Lake City, UT, 2003: 101–102. 108. Bosse MJ, MacKenzie EJ, Kellam JF, et al. A prospective evaluation of the clinical utility of the lower-extremity injury-severity scores. J Bone Joint Surg Am 2001; 83A: 3–14.

39 Hand and Upper Extremities David T. Netscher and Idris Gharbaoui

Case Scenario A motorcyclist is brought to the trauma bay after crashing into a parked pick-up truck. He is alert, oriented, and hemodynamically stable. The patient has no intrathoracic or abdominal injuries. He does have extensive abrasions and bruises of his upper extremities, although radiologic evaluation demonstrates no skeletal fractures or dislocation. However, over of the course of 3 hours, the patient complains of increasing numbness and paresthesia of the left forearm. On physical examination, the involved extremity is swollen and very tense, with tenderness over the forearm musculature and paresthesia confirmed over the distribution of the median and ulnar nerves. The patient has a very strongly palpable radial pulse. Which of the following should be the management at this time? (A) Application of a sequential compression garment (B) Elevation of the involved extremity and artenography (C) Three-compartment fasciotomy (D) Venous Doppler studies (E) Repeated extremity x-rays

Principles Treatment Planning Acute care surgery to the upper extremity may be secondary to trauma or may be from nontraumatic causes such as infections, compartment syndrome, and vascular emergencies. Treatment must be directed at the specific structures damaged—skeletal, tendon, nerve, vessels, and integument.1 Goals of management in acute care situations are to obtain a healed wound, to preserve motion, and to retain distal sensation. Stable skeletal architecture

is essential for effective motion and function of the extremity, and this is established in the primary phase of care. It also results in reestablishing skeletal length, straightening deformities, and correcting compression or kinking of nerves and vessels. Arteries should also be repaired in the acute phase of treatment to maintain distal tissue viability. Similarly, extrinsic compression on arteries must be released emergently such as in compartment pressure problems. In clean-cut type injuries, tendons should be repaired primarily. In situations where there is a chance that tendon adhesions may form, such as with associated fractures, it is often better nonetheless to repair the tendons with preservation of their length and if necessary to perform tenolysis later. However, in open, contaminated, and severe crushing injuries, it is prudent to delay repair of both tendon and nerve injuries. In sharp, clean-cut wounds primary nerve repair lessens the possibility of nerve end retraction and therefore the need for later nerve graft. Primary repair of nerves should not be performed in situations in which contusion-causing forces have been directed to the nerve (gunshot wounds, power saw injuries, blunt crushing), since the extent of the proximal axonal injury may not be immediately evident. Nerve repair before this is apparent may result in abnormal nerve ends being reattached, negating the chance for return of function. In severe soft tissue injuries, wound closure may not be immediately possible. However, initial open treatment is directed at preventing infection and protecting critical deep structures by proper dressing and wound management. Adequate debridement is essential, but thereafter appropriate soft tissue coverage must be achieved as soon as possible. The sooner the soft tissue coverage can be achieved, the less likely there will be secondary deformity due to fibrosis and joint contractures.The more rapidly one can start hand therapy, the better the chances of maximizing return of function. The treatment regimen consists of debridement, rigid skeletal fixation, and early soft tissue resurfacing followed by protected range of

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motion exercises as soon as possible. Early soft tissue reconstruction results in improved function, decreased morbidity, and shortened hospital stay. Appropriate treatment of acute care situations involving the upper extremity requires knowledge of local and regional anesthesia, use of a tourniquet to provide a bloodless field, correct placement of incisions to minimize later scar contractures, appropriate use of dressings and splints to reduce edema and maintain functional position, and above all a clear knowledge of the unique anatomy of the hand and upper extremity that will not only aide in accurate clinical diagnosis but also enable surgery to be performed safely.

Anesthesia The choice of general, regional (such as intravenous Bier block or brachial plexus block that includes either supraclavicular or axillary block) or local anesthesia is gov-

A

erned by the extent and length of the operation.2,3 An upper arm tourniquet can be used on the unanesthetized extremity with only local anesthetic field infiltration or wrist or digital block for as long as 30 minutes in the relaxed cooperative patient provided the arm is well exsanguinated. After this time tourniquet pain will not permit more extensive local anesthetic procedures. The need to operate in other areas, such as for the harvesting of bone, nerve, tendon, or skin graft, and more extensive surgical procedures will require general anesthesia. Digital blocks and median, ulnar, and radial wrist nerve blocks are very useful especially for more limited emergency room procedures (Figure 39.1). Digital nerve blocks as a rule should not include epinephrine, which could lead to vasospasm, ischemia, and necrosis, although recent evidence implies the safety of distal blocks using an epinephrine solution. The maximum safe dose of lidocaine is 4 mg/kg.

C

B Figure 39 39.1. 1 Median M di anesthetic th ti block bl k is i done d by b locating l ti the th interspace between the palmaris longus and flexor carpi radialis tendons in the distal forearm just proximal to the carpal tunnel. (A) Ulnar nerve block is performed by inserting the injecting needle just proximal to the pisiform and passing deep

D

E t the to th flexor fl carpii ulnaris l i ttendon. d (B D) A wheal (B–D) h l off llocall anesthetic raised across the dorsum of the wrist will anesthetize the branches of the superficial radial nerve and also the dorsal cutaneous branch of the ulnar nerve. (E) A method of injecting to achieve a digital nerve block.

39. Hand and Upper Extremities

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Tourniquet Application Clear visualization of all structures in the operative field depends on tourniquet use.1 Penrose drains, rolled rubber glove fingers, or commercially available tourniquets can be used on digits. Great care is taken in using any constrictive device on digits as narrow bands can cause direct injury to underlying nerves and digital vessels. With use of upper arm tourniquets, the skin beneath the cuff should be protected by several wraps of cast padding. During skin preparation this area must be kept dry in order to prevent blistering of the skin by an inflated cuff over moist padding. The cuff selected should be as wide as the diameter of the arm. Standard pressures used are 250 to 280 mm Hg in adults and 150 to 200 mm Hg in children. As a rule, the cuff should be deflated every 2 hours for 15 to 20 minutes to revascularize distal tissue and to relieve pressure on the nerves locally before reinflating the cuff for more extensive procedures. Exsanguination is performed by wrapping the extremity with a Martin’s bandage in all cases except those involving infection or tumors. In these cases, there is a possibility of embolization by mechanical pressure, and so exsanguination should be avoided. Merely elevating the extremity for a few minutes before tourniquet inflation suffices.

Incisions Incisions should be of the Bruner zigzag or midaxial type or combinations of these in order to avoid motionrestricting scars (Figure 39.2).1 Any scar dorsal or palmar to the flexion axis of a joint or crossing its axis at 90° can cause contracture across that joint. The juncture of a skin graft and healthy skin is also a potential scar line, and so

Figure 39.2. Placement of incisions for palmar exposure of structures (longitudinal midaxial digital incisions must not be placed volar to joint flexion creases).

Figure 39.3. Edema and swelling tend to accumulate dorsally (cross-hatching), drawing the fingers into extension at the metacarpophalangeal joints.

the design for a margin of the graft should also be planned on the same lines as the incision so as to prevent contractures, even if on occasion this requires removal of small areas of healthy skin. Palmar incisions follow the pattern of the skin creases. Dorsal incisions of the fingers and wrists and also incisions on the forearm may follow longitudinal straight lines.

Dressings and Splints The purposes of dressings are to protect wounds, absorb drainage, and help splint repaired structures.4 The first layer should be nonadherent and may contain an antibiotic. The next layer should be soft and bulky and is usually followed by a firmer external wrap. Conforming compression is useful, but constriction is harmful. Splints should be made to protect only the part necessary and should not prevent motion in the remainder of the extremity. Frequently patients will keep the injured, operated, or infected hand in a flexed wrist position, and this automatically causes the metacarpophalangeal joints to extend, thereby placing the collateral ligaments in their shortest length. Edema fluid is deposited dorsally, and the resulting tightness causes stiff joints (Figure 39.3); thus, a splint that keeps the hand in the “protected” position should extend the wrist 40° to 50°, maintain the metacarpophalangeal joints at 70° of flexion, and maintain the interphalangeal joints in a neutral position (Figure 39.4). Postoperative hand elevation is essential to reduce edema.

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Neurovascular Examination

Figure 39.4. The “safe” position or “protected” position of the hand (below) differs from the “resting” position of the hand (above). The former is the preferred manner of splinting the injured hand, as it preserves the maximum length of collateral ligaments and minimizes the risk of developing postoperative extension contractures at the metacarpophalangeal joints and flexion contractures at the interphalangeal joints.

An Allen test confirms the patency of the ulnar and radial arteries. Moving two-point discrimination is the most sensitive method of testing for sensory loss and is easily done by using a bent paperclip (Figure 39.7).5,6 The ends of the paperclip are set 5 to 8 mm apart for fingertip pulp testing. Points are aligned along the axis of the finger and moved transversely across the axis. If the test is not reproducible, because the patient is uncooperative, suspicion of nerve injury is simply confirmed by the tactile adherence test in which a plastic pin is passed back and forth gently across the pulp on either side of each finger. Adhesion, caused by sweat, is shown by slight but definite movement of the finger being examined (an anesthetic finger pulp will not sweat). A knowledge of surface anatomy of nerves helps in the evaluation of a specific lacerating injury (Figure 39.8).7 The ulnar attachment of the flexor retinaculum is to the pisiform and hook of hamate, and radial attachment is to the scaphoid and ridge of trapezium. The median nerve passes through the carpal tunnel between these landmarks. It provides sensation to the thumb, index finger, middle finger, and radial half of the ring finger. The palmar cutaneous branch of the median nerve arises from its radial aspect 5 to 6 cm proximal to the wrist and provides sensation to the palmar triangle. The ulnar nerve is on the radial side of the pisiform and passes to the ulnar side of the hook of the hamate in its passage through Guyon’s canal. It provides sensation to the little finger and ulnar half of the ring finger, while the dorsal branch of the ulnar nerve (arising proximal to the wrist and curving dorsally around the head of the ulna) supplies the same digits on their dorsal aspect. The superficial radial sensory nerve emerges from under the brachioradialis in the distal forearm and divides into two or three branches

Examination and Diagnosis Observation Inspection of the resting posture of the hand provides valuable information. A severed flexor tendon is readily diagnosed by the fact that the affected finger does not assume its normal resting position in line with the natural flexion cascade of the adjacent digits (Figure 39.5).5,6 Extensor tendon injuries might be indicated by a droop at the affected joint. On the other hand, a clawed posture of the little and ring fingers is characteristic of an ulnar nerve injury. Absence of sweating at the fingertips may also imply a nerve injury in that particular distribution. Swelling and erythema may be indicative of a hand infection, and a purulent flexor tenosynovitis will always result in a flexed position of the finger. Rotational and angular deformities of the digits will occur when there are underlying fractures (Figure 39.6).

Figure 39.5. Flexor tendon injury to the middle finger is readily diagnosed by the resting posture of that digit, which does not assume the natural resting flexion “cascade” of the adjacent fingers.


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Figure 39.6. (Left to right) Rotational deformity is seen with the fingers flexed. This is secondary to a spiral fracture of the middle finger metacarpal. Closed reduction of the fracture and

percutaneous pinning show restoration to normality of the previous deformity.

proximal to the radial styloid, which proceed in a subcutaneous course across the “anatomic snuffbox” to innervate the skin of the dorsum of the first web space. The number of fingers served by each nerve may vary. As an absolute rule, however, the palmar surfaces of the index and little fingers are always served by the median and ulnar nerves, respectively (Figure 39.9). With regard to the motor supply of the nerves,7 the ulnar nerve serves the hypothenar muscles, interossei, ulnar two lumbricals, adductor pollicis, and deep head of the flexor pollicis brevis. The median nerve serves abductor pollicis brevis, opponens pollicis, radial two lumbricals, and superficial head of the flexor pollicis brevis. In summary, the median nerve supplies all of the extrinsic digit flexors and wrist flexors (except the flexor digitorum profundus to the ring and little fingers and the flexor

carpi ulnaris, which are supplied by the ulnar nerve) and all the thumb intrinsic muscles (except the adductor pollicis, supplied by the ulnar nerve). The ulnar nerve innervates all the interossei, all the lumbricals (except the radial two, supplied by the median nerve), and the adductor of the thumb.The radial nerve supplies all of the wrist, finger, and thumb long extensors. There are two muscle tests that may provide one with an absolute diagnosis of median and ulnar nerve injury. The motor function of the abductor pollicis brevis tests the median nerve. With the hand flat and facing palm up, the patient is asked to touch with the thumb the examiner’s fingers held directly over the thenar eminence (Figure 39.10A). The flexor digiti minimi muscle function tests the motor supply of the ulnar nerve: In the same hand position, the patient is asked to raise the little finger vertically, flexing the metacarpophalangeal joint to a 90° angle with the interphalangeal joints straight (Figure 39.10B).

Musculoskeletal Examination

Figure 39.7. Testing of two-point sensory discrimination. (This test can also be simply done by bending up the ends of a paperclip.)

Tendons are individually tested for integrity.7 Flexion at the distal joints of the thumb and fingers (Figure 39.11A,B) respectively confirms integrity of the flexor pollicis longus and flexor digitorum profundus. Testing of flexor digitorum superficialis tendons is more complex (Figure 39.11C). It is not possible to flex the ulnar three distal interphalangeal (DIP) joints independently of one another because of the common origin of the profundus tendons; therefore, two of the three are fixed in extension by the examiner, and the patient is asked to bend the third. This movement will be produced by the flexor digitorum superficialis and occurs at the proximal interphalangeal (PIP) joint. In one third of normal patients, the superficialis cannot produce little finger flexion. In half of these, there is a common origin with the ring finger, and

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A

B

Figure 39.8. (A) Surface landmarks of the superficial radial nerve as it crosses the “anatomic snuffbox.” (B) The ulnar nerve passes through Guyon’s canal between the pisiform (P) and hook of hamate (H) bone landmarks. (C)The transverse carpal ligament forms the roof of a carpal tunnel and spans between the scaphoid (S) and trapezium (T) on the radial side and between the pisiform (P) and hook of hamate (H) on the ulnar side. The median nerve travels through the carpal canal before dividing into the digital branches and the recurrent motor branch to the thenar muscles.

C

Figure 39.9. Sensory distribution of the ulnar nerve (×), radial nerve (−), and median nerve (•) to the hand.

A

B

Figure 39.10. (A) Palmar abduction of the thumb tests the median muscle innervation. (B) Flexion of the little finger at the metacarpophalangeal joint is performed by innervation of the hypothenar muscles (flexor digiti minimi) by the ulnar nerve.


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Figure 39.11. (A) Flexor pollicis longus is tested by thumb intraphalangeal joint flexion. (B) Flexor digitorum profundus flexes the distal intraphalangeal joint while the rest of the finger is stabilized and prevented from flexing. (C) Testing of the flexor digitorum superficialis to the middle finger is done by holding the other three fingers out in extension and the middle finger flexes at the proximal interphalangeal joint. (D) Long extensors of the fingers are tested by placing the hand flat on an examining surface and then elevating the specific finger from that surface.

so flexion will occur if the ring finger is permitted to flex simultaneously. More infrequently, there is no profundus tendon to the little finger, and the superficialis inserts into both the middle and distal phalanges. The long and short extensors and long abductor of the thumb can be tested by asking the patient to extend the thumb against gentle resistance while the tendons are individually palpated. The long extensors of the fingers are tested by asking the patient to extend against gentle resistance applied to the dorsum of each proximal phalanx (Figure 39.11D).

Special Investigations

A 8

Radiographs are obtained in almost every case. These will help in diagnosis and evaluation of fractures and also in investigation of foreign bodies (Figure 39.12). Multiple

䉴 Figure 39.12. This patient had a seemingly innocuous dorsal hand laceration and refused to offer any potentially incriminating history about the mechanism of injury. (A) A radiograph showed a radiodense foreign object directly overlying the metacarpophalangeal joint (arrow). (B) Upon surgical exploration of that joint, an assailant’s broken off tooth (arrow) was found imbedded in the articular cartilage of the distal metacarpal.

B

A

B

C

D

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radiographic views of the affected part are frequently required to define the pathology. Glass is frequently visualized on plain radiographs and if not seen but suspected, is clearly visualized by computed tomography (CT) or magnetic resonance imaging (MRI).9,10 If plastic is painted, it may be seen on routine radiographs; otherwise, it is only poorly visualized on CT scan but clearly seen with MRI. Wood foreign bodies are detected by CT or MRI but not by routine radiography.9,10. Various stress radiographic views and cineradiography are useful for demonstrating dynamic wrist instability patterns (particularly scapholunate separation).8 Arthrography detects ligamentous tears by extravasation of contrast material between the radiocarpal, distal radioulnar, and midcarpal joints. Magnetic resonance imaging may detect triangular fibrocartilage tears. Radionuclide bone scanning may be helpful, and focal uptake may be seen in phase III in osteomyelitis, but for the hand false-positive scans are seen because of close proximity of soft tissue infections to the bones. “Occult” wrist fractures may be localized by increased radionuclide uptake, but a false-positive test may occur with ligamentous injuries.8 Computed tomography may be the best modality for diagnosing suspected carpal fractures that are not seen on routine radiographs. Wrist arthroscopy is a recently introduced diagnostic and therapeutic modality for a number of wrist problems, particularly for disorders of the triangular fibrocartilage. Minimally invasive surgery with arthroscopic guidance has added a new dimension to the treatment of acute wrist disorders, including scaphoid and distal radius intraarticular fractures. Patients with ischemic problems usually require noninvasive vascular studies. Doppler pressure measurements help to localize the site of the lesion. Angiography should be done in the presence of a vasodilator (such as Priscoline or nitroglycerin) or axillary block in order to differentiate apparent vessel occlusion from vasospasm. Subtraction radiographs with magnification help to improve the detail and definition of the vascular study (particularly in the distal forearm and hands).6,8

Fingertip and Nailbed Injuries All patients presenting with nailbed injuries must have radiograms.11 An underlying distal phalangeal fracture must have appropriate protective splinting, reduction to improve alignment if necessary, and occasional internal fixation if the fracture is unstable. Internal fixation is most frequently provided by simply placing a longitudinal 0.028-inch Kirschner wire. Appropriate antibiotics are administered, as technically the fractures are open. The least severe injury of the dorsum of the fingertip is a nailbed hematoma. If seen early, the hematoma can


be decompressed by perforating the nail plate after administration of a digital local anesthetic block.11 Most fingertip and nailbed injuries can be managed with digital block anesthesia and placement of a Penrose drain at the base of the finger as a tourniquet. If the nail plate is split, the nail should be gently removed to examine the underlying nailbed. Suture repair of the nailbed is done by using loupe magnification and a 6-0 catgut suture. Stellate nailbed injuries must be meticulously repaired after appropriate wound irrigation and cleansing. Once the nailbed has been repaired, it is best to place the thoroughly cleaned nail back into the nail fold where it both serves as a rigid splint for an underlying distal phalangeal fracture and prevents adhesions from forming between the adjacent surfaces of the nail fold, which might lead to an unsightly “split” nail deformity. If a piece of nailbed is missing, the undersurface of the avulsed nail plate should be examined. The missing piece may still be adherent to the nail, and it can be gently removed and replaced as a nailbed graft. If the missing piece of nailbed cannot be retrieved, the defect may be treated by obtaining a split nailbed graft from an adjacent nail or from a toenail bed. More severe dorsal fingertip injuries can be resurfaced by using a reverse cross-finger subcutaneous flap as described by Atasoy. Some injuries may be so severe that amputation revision may be the most sensible and functional solution. Volar fingertip injuries also range from the simple to the more complex. These often involve multiple digits such as with lawnmower accidents. If bone is not exposed and the soft tissue defect is less than 1 cm in an adult, the wound is best left open and managed with soaks and dressings.11 Such injuries heal with surprisingly good functional and cosmetic results. Larger soft tissue defects of the fingertip pulp may be more appropriately treated with a small split-thickness skin graft. On the other hand, if bone is exposed, one should consider either flap coverage or revision of amputation by trimming back exposed bone to obtain soft tissue coverage. If the loss is dorsally angulated, an advancement flap is indicated. A neurovascular V-Y advancement flap is classically described for this type of defect.12 More extensive neurovascular island advancement flaps such as that represented by the step advancement flap described by Evans may be considered (Figure 39.13).13 If the soft tissue loss is angulated in a more volar direction, a cross-finger flap (Figure 39.14),14 or even an adjacent finger digital island flap or a homodigital flap, may be considered (Figures 39.15 and 39.16).13,15 The latter requires microvascular tissue handling techniques. If an amputated fingertip is retained, reimplantation may be considered. This will give an aesthetic nail reconstruction; however, more important, reimplantation of avulsed tissue containing either thumb pulp or index finger pulp should always be considered in view of the


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Figure 39.13. (A) V-Y step advancement flap is reconstructed as an island based on the digital neurovascular structures. (B) This is advanced to the fingertip (as much as 2 cm advancement may be achieved) to cover a soft tissue defect that is dorsally angulated and so helps maintain the skeletal length of the finger.

A

A

Figure 39.14. (A,B) A cross-finger pedicle flap from the dorsum of the ring finger covers exposed bone and a volar soft tissue fingertip wound. The dorsal donor site of the ring finger must be skin grafted, and the fingers must be kept joined together for 11 to 14 days before separating the two digits. (C) Long-term result shows a pleasing aesthetic reconstruction with preservation of digital length. Protective sensation at the fingertips is generally restored in time.

B

C

B

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A B

C

A

C

Figure 39.15. (A) A large volar avulsing wound has both bone and tendon sheath exposed on the little finger. (B) An arterialized flap based on the ulnar digital vessels of the ring finger (leaving the digital nerve intact to that ring finger) is transposed to the little finger soft tissue wound with skin grafting done to the donor defect. (C) Long-term functional recovery is seen.

B

Figure 39.16. (A) A less extensive volar angulated pulp injury of the finger is seen. (B,C) A homodigital reverse pattern arterialized flap is transposed to the fingertip to avoid having to tether adjacent fingers together as would otherwise be the case with a cross-finger flap.


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A

B

C

Figure 39 39.17. 17 Microvascular Mi l reattachment tt h t off a traumatically t ti ll avulsed l d th thumb b pulp. l

functional importance of good sensation in these two digits (Figure 39.17).11 When the amputated part has been too severely crushed, the thumb pulp may be reconstructed by a neurovascular island sensate flap (“kite

flap”) based on the vascular branches of the first dorsal metacarpal artery from the dorsoradial aspect of the proximal phalanx of the index finger and transposed to reconstruct the thumb pulp (Figure 39.18).13

B A

Figure 39.18. (A) Thumb pulp avulsion injury with the amputated part could not be salvaged. (B,C) A “kite” flap was used for reconstruction. This flap is subtended on the first dorsal metacarpal artery and is transposed from the dorsum of the index finger. Skin grafting is necessary for the donor site.

C

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Open Soft Tissue Injuries and Complex Wounds Before adequate tissue coverage can be safely provided, satisfactory wound debridement must be done.16 Modern day debridement is much more aggressive than before, because in this era of microvascular tissue transfer we no longer fear being unable to cover exposed vital structures. Another basic tenet of wound management has in the past been the principle of delayed wound closure; however, with regard to upper extremity injuries, this concept is now being challenged. Functional outcome is of paramount importance in upper extremity injuries, and the more rapidly one can start hand therapy the better the chances of maximizing return of function. Treatment consisting of radical debridement, rigid fixation, immediate soft tissue resurfacing, and even immediate reconstruction of segmental bone defects and tendon loss, followed by early protective range of motion exercises, has been shown in some reports to result in excellent functional outcome.16 All evidence is yet to be gathered to determine if the potentially increased risk of infection has outweighed improved function, decreased morbidity, and shortened hospital stay that might result from immediate soft tissue coverage and reconstruction. Adequate debridement and wound irrigation are key. Irrigation under a pressure of at least 7 psi has been shown to be effective but must be combined with the judicious use of parenteral antibiotics. Once a wound has satisfied the requirements of closure, the reconstructive options must be considered. Each wound should be approached with the reconstructive ladder (Figure 39.19) in mind, and the simplest option that is best suited to both the general condition of the patient and the local requirements of the specific

Reconstructive Ladder

Secondary Healing

Skin Graft

Local Pedicle Flap

Intrinsic Local Island Flap

Regional Flap

Figure 39.19. The h reconstructive i lladder. dd

Free Flap

wound should be selected. Skin graft is suitable for wounds of large surface area that do not expose important structures, such as burn injuries; however, in the hand and upper extremity, a more durable wound coverage is often required. Skin grafts may be applied directly over tendons (if paratenon is intact), but they may not be very suitable because tendons adhere to overlying grafts, causing a deformity with tendon motion. More important, however, is the frequent secondary need for tenolysis and hence the requirement for coverage that is more durable than a skin graft. A skin graft may, on the other hand, provide useful temporary coverage when the severe nature of the patient’s injuries precludes more elaborate immediate wound closure. Our understanding of soft tissue coverage was clarified when McGregor popularized the concept of axial—and random—pattern flaps.17 The former is a single pedicled flap with an anatomically recognized arteriovenous system running along its access. The groin flap, based on the superficial circumflex iliac artery, was one of the earliest axial pattern flaps described and is still frequently used for resurfacing of the upper extremity. A groin flap may be used for preliminary soft tissue coverage to conserve recipient vessels prior to needed further microvascular surgery such as a planned subsequent toe transfer. A groin flap may also have a role for soft tissue coverage of the hand where recipient arteries and veins are unavailable for free flap reconstruction. This occurs particularly in a patient with peripheral vascular disease, or one who has recovered from a significant soft tissue infection and cellulitis, or in a drug abuser or with extravasation injuries where recipient arteries, and in particular veins, may be unavailable (Figure 39.20). In contrast, a random pattern flap is one that lacks any significant bias in its vascular pattern. Such flaps were classically thought to need a length-base ratio of 1 : 1 to avoid distal tip necrosis; however, Milton showed that absolute flap length, not width, is crucial. We now know that absolute survival flap length of random pattern flaps is determined by the axiality of the flap: that is, a longer flap can be obtained by orienting it along the longitudinal rather than the transverse axis of an extremity. This is because the predominant direction of the vessels is longitudinal, and so by random chance more vessels will run along the length of the flap. Increased flap length (that is, improved reliability) is also obtained by including fascia (so-called fasciocutaneous flaps) or by tissue expansion. The fascia carries with it its own inherent blood supply, while the capsule produced around the silicone tissue expander is also very vascular and so imparts viability to the overlying skin. Local and regional flaps are described by the way in which they are moved. There are two types: flaps that rotate about a pivot point (rotation and transposition flaps) and


A

B

C Figure 39.20. 39 20 (A) An extravasation injury from a chemotherchemother apy solution requires debridement. (B,C) Groin pedicle flap keeps the hand initially attached to the body, and the pedicle is separated after 3 weeks. (Courtesy of Melvin Spira, MD.)

advancement flaps.17 Axial flaps may consist of skin only (e.g., groin flap), fascia and fasciocutaneous tissue (e.g., radial forearm, lateral arm, temporoparietal flaps), or muscle and musculocutaneous tissue (e.g., latissimus dorsi, rectus abdominis, and gracilis). Radial forearm flap

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and posterior interosseus flap may be pedicled on the distal blood supply so that the venous flow is retrograde (Figure 39.21).18 Flaps offer a number of advantages over skin grafts.17 They avoid contraction, fill dead space, cover important structures (vessels, bone, tendons, nerves), help clean up infection, enhance vascularity, and provide specific functions (e.g., latissimus muscle transfer to restore biceps function). Since Ger’s use of muscle flaps for osteomyelitis in the 1960s,“antiinfection” has been attributed to muscle. Mathes has provided scientific data to support this premise. We believe it is the good blood supply of an axial pattern flap that provides the ability to “clean up” infection in a contaminated but nonetheless adequately debrided wound. Reconstructive requirements of the upper extremity may be summarized as follows: 1. Replace the missing tissue type with a similar type. In the hand and fingers, thin and pliable soft tissue coverage is required. 2. There may be a subsequent or simultaneous need for secondary reconstruction of bone, tendon, and nerve in addition to the soft tissue requirements. Under these circumstances, skin grafts would be inadequate soft tissue coverage. 3. Flap reconstructions may need to be sensate, especially at the fingertips.19 4. The size of the defect needs to be reconstructed three dimensionally. A deep volume of soft tissue may be required as well as a large surface area in certain injuries. 5. Flap reconstruction may need to be functional and provide motion. Injuries in the shoulder girdle region and upper arm can be covered by a wealth of potential pedicle muscle and cutaneous flaps. An example is a patient who had a gunshot wound to the lateral aspect of the deltoid region where a latissimus dorsi musculocutaneous flap not only helped provide soft tissue contour wound coverage but also augmented missing muscle function (Figure 39.22). Closure of elbow wounds has been described by a number of elaborate means; however, a large posterior arm rotation flap often readily covers the extensor aspect of the olecranon (Figure 39.23), and a transposition flap (with the donor site skin grafted) will cover vital exposed structures in the antecubital fossa. On the dorsum of the hand, a local random pattern flap provides thin and pliable soft tissue coverage. A transposition flap (Figure 39.24) shifted radially covered the exposed basilar thumb joint and allowed the metacarpal base and shattered trapezium to be reconstructed by soft tissue tendon interposition and immediate bone grafting.

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A

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D

E

F

A

B

Figure 39.21. (A) A wound involving the web space and adjacent surfaces of the index and middle fingers. (B–D) A reverse flow radial forearm fasciocutaneous flap is transposed from the ipsilateral forearm distally to the traumatic defect. (E,F) Functional outcome.

C

Figure 39 39.22. 22 A wound of the deltoid area resulting from a shotgun blast is successfully covered with a latissimus dorsi muscumuscu locutaneous flap.


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Figure 39.23. A rotation flap (arrow) designed on the posterior aspect of the upper arm readily covers an olecranon wound.

A

B

C

D

Figure 39.24. 39 24 (A) A bl blastt iinjury j to t the th base b off the th thumb th b resulted in a shattered thumb metacarpal and trapezium and substantial soft tissue wound. (B) A transpositional flap pro-

vides id stable t bl wound d coverage (arrow). ( ) (C) IImmediate di t b bone reconstruction was undertaken. (D) Final reconstruction has restored thumb prehension.

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A

C

B

D

Figure 39.25. (A,B) A blast injury to the radial side of the distal forearm and hand. (C) Soft tissue coverage over the reconstructed bone with latissimus dorsi microvascular muscle

transfer and a skin graft. (D) With time the muscle atrophies, and well-contoured reconstruction is restored.

Free vascularized tissue transfers are specifically indicated where there is a need to cover sites that ordinarily cannot be reached by pedicle flaps or to meet specific reconstructive requirements.20 All areas of the upper extremity, unlike the distal third of the leg, can be reached by pedicle flaps. However, some defects may be so large as to make pedicle flaps impractical. A gunshot wound to the dorsoradial aspect of the wrist resulted in a very large soft tissue wound, tendon injuries, and comminuted fractures to the first metacarpal base and radial side of the wrist (Figure 39.25). Free bone graft reconstruction at the base of the thumb metacarpal with flexor carpi radialis tendon interposition and volar oblique ligament reconstruction to restore the anatomic configuration of the thumb basilar articulation with a traumatically destroyed trapezium was performed. This reconstruction was covered with well-vascularized soft tissue using latissimus dorsi muscle free flap covered by a skin graft. The transformed muscle will generally atrophy with time, and this will generally result in a good contour and

is preferred over the more bulky musculocutaneous flap. A microvascular free flap is clearly required where certain reconstructive goals must be met, as in cases of segmental bone loss in the arm.20 In this large soft tissue wound to the forearm from a shotgun injury with associated segmental bone defect, a reconstruction was performed with a composite myo-osseus flap using latissimus dorsi muscle and a serratus muscle with vascularized rib, all on a single thoracodorsal vascular pedicle (Figure 39.26). The muscle was covered with a split-thickness skin graft. Finally, microvascular reconstruction enables singlestage reconstruction of bone and soft tissue and avoids hand dependency that would occur with a groin flap and enables motion at the earliest possible time when combined with rigid bone fixation. Early motion, wellvascularized soft tissue of adequate bulk, and extremity elevation reduce the risk of hand stiffness and contractures.


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A

B

C

D

E

F

Figure 39.26. (A,B) Shotgun injury to the mid forearm with both significant soft tissue loss and segmental bone loss. (C,D) Composite microvascular transfer using the latissimus dorsi, ser-

ratus anterior, and a rib all on a single thoracodorsal vascular pedicle enables a single-stage reconstruction of the soft tissue and bone defect. (E,F) Final outcome of the reconstruction.

Replantations and Amputations of the Upper Extremity

exists because, in the case of major replantations, ischemic time is crucial to viability of muscle and functional outcome. Ischemic muscle may result in myonecrosis, myoglobinemia, and infection that may threaten the patient’s life as well as limb. Amputations can be classified into three types21:

Replantation is the reattachment of a part that has been completely amputated. Revascularization requires reconstruction of vessels in a limb that has been severely injured or incompletely severed in such a way that vascular repair is necessary to prevent distal necrosis but some soft tissue (skin, tendon, nerves) is intact.21 Revascularization generally has a better success rate than replantation, because venous and lymphatic drainage may be intact. Minor replantation is a reattachment at the wrist, hand, or digital level, whereas major replantation is that performed proximal to the wrist.21 This clinical distinction

1. Guillotine amputation: This is used for tissue that is cut by a sharp object and is minimally damaged. 2. Crush amputations: A local crush injury can be converted into a guillotine injury simply by debriding back edges, but this may not be practically feasible for a more diffusely crushing injury. 3. Avulsion amputations: These are the most unfavorable type for replanting, because structures are injured at different levels. This may occur, for example, with a

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so-called ring avulsion injury. Extensor tendons are shredded, flexor tendons are often avulsed at the musculotendinous junctions, and nerves are stretched and may be ripped from end organs. Viability alone of a replantation is not construed as a measure of its success; useful function must be achieved. Replantation has both absolute and relative contraindications. It is strongly contraindicated at any level of amputation if there is significant concomitant life-threatening injury; severe chronic illness that precludes transportation or prolonged surgery; or extensive injury to the affected limb or amputated part. The following factors must also be considered when planning for potential replantation of amputated parts22: 1. Ischemia time: For amputated digits, more than 12 hours of warm ischemia is a relative contraindication. Promptly cooling the part to 4° to 10°C dramatically alters the ischemia factor, but even ischemia exceeding 24 hours does not preclude successful replantation. Ischemia time is more crucial for replants above the proximal forearm, and these should not be considered after more than 6 to 10 hours of warm ischemia time. 2. Affected parts: Good candidates for replantation are those who have amputations of the thumb or multiple digits or through the palm, wrist, and individual fingers distal to the insertion of the flexor digitorum superficialis tendon. Single digit injuries other than the thumb, in zone II, are generally not reattached because of the unfavorable functional outcome and the consequent adverse overall functional result on the hand with a single stiff finger. Because the function of the thumb accounts for 40% of total hand function, almost all amputated thumbs should be replanted with care taken to preserve the length of the thumb. 3. Patient considerations:A decision to replant a single digit proximal to the insertion of the flexor digitorum superficialis tendon is influenced by special circumstances, such as a patient who is a young woman or a professional musician or a child. Not only are sex, occupation, and age important considerations, but also mental health. For a child, an attempt should be made to replant almost any amputated part, because useful function can usually be anticipated and also because the child’s eventual vocation is unknown. Old age is usually not a barrier to replantation provided that the vessels are not seen to be atherosclerotic when examined under the microscope. Mental stability is frequently difficult to assess in the limited time available for preoperative evaluation in the emergency room. Amputation should not be considered an outmoded operation; rather, it is necessary when replantation might not be indicated.22 When primary amputation is performed, the stump should be preserved with as much length as possible. An exception might be made if there


is only a very short segment of proximal phalanx. If a ring or middle finger is involved, the short stump might have little value to the hand, in as much as small objects will fall through the gap. A short proximal phalangeal remnant at the index finger position may serve as an impediment to thumb to middle finger prehension. In all of these situations one might consider formal ray amputations to improve overall hand function. The ends of the cut nerve should be allowed to retract or should be buried in muscle in order to minimize the occurrence of painful neuromas after amputation. Tendons should also be divided sharply and allowed to retract. The practice of suturing the flexor and extensor tendons over the end of the middle, ring, or small finger stump seriously impairs the motion of the uninjured fingers owing to the common origin of these flexors. There is an active flexion deficit in the uninjured digits, which nonetheless have a normal passive range. This is called the quadriga syndrome and is corrected by release of the flexor tendon remnant of the injured digit.

Operative Procedure for Replantation Before transportation, the amputated part is placed in a clean, dry, plastic bag that is sealed and placed on top of ice in a Styrofoam container. This keeps the part sufficiently cool at 4° to 10°C without freezing.21 Bone shortening allows skin to be debrided back to where it is free of contusion and where direct tensionfree closure can be achieved. In the thumb, bone shortening should be minimized to less than 10 mm. Bruner incisions may be used for exposure. The order of repair is usually bone, tendons, muscle units, arteries, nerves, and finally veins.21 In replanting the proximal portion of the digit, preplacing the sutures to the proximal and distal tendon ends enables the digit to be held in extension to expose microvascular structures on the volar surface. Once neurovascular repairs are completed, tendon ends are then simply coapted. Establishment of arterial flow before venous flow clears lactic acid from the replanted part.The functional veins can now also be detected by spurting bleeding. However, blood loss must be closely monitored. For major replantations, reestablishing arterial circulation as rapidly as possible is crucial to limiting the ischemia time period.21 A dialysis shunt or carotid shunt may be placed between the arterial ends. Intermittent clamping of the shunt may be necessary to restrict blood loss. In the upper extremity, bone shortening can be aggressive to achieve primary skin closure and primary nerve repair. Preparatory exploration of the distal amputated part under the microscope by an initial surgical team not only determines whether or not a replantation is technically feasible but also can be started while the patient is being prepared for the operating room. Judicious use of anticoagulants may enhance the success of


the replantation. Topical application of 2% lidocaine or papaverine may help to relieve vasospasm. Postoperative dressings consist of longitudinal strips of nonadherent mesh gauze, loose fluff gauze, and a plaster splint, and postoperative elevation minimizes edema and venous congestion. The patient’s room must be kept warm, and smoking is forbidden postoperatively. Aside from antibiotics and analgesics, one aspirin tablet a day for its retarding effect on platelet aggregation is suggested. Postoperative monitoring is done hourly for color, pulp turgor, capillary refill, and digital temperature.

Tendon Injuries Flexor Tendons For better understanding and treatment of tendon injuries, the international agreement on anatomic nomenclature for the flexor and extensor zones of the hand was reached at the First Congress of the International Federation for Surgery of the Hand in Rotterdam in June 1980. Flexor tendon injuries are divided into five zones (Figure 39.27).23 In zones I, II, and IV, each tendon is surrounded by a synovial sheath and is contained within a semirigid fibro-osseus canal. The synovial membrane has both parietal and visceral (epitenon) layers. In the other zones, the tendons are surrounded by loose areolar (paratenon) tissue. Healing in those parts devoid of a fibrous sheath is usually excellent because of the good blood supply from the paratenon. In addition, the profundus tendons in zone III have a segmental blood supply via the lumbrical muscles. Tendons in the carpal tunnel (zone IV) have a rich blood supply provided by the mesotenon; however, zone II and zone I have a precarious blood supply.23 It is thought that complimentary

Figure 39.27. Flexor tendon zones of injury.

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Figure 39.28. Vascular supply of flexor tendons in the digital flexor tendon sheath is derived through the vincula. Nutritional support of the synovium in this region is thus essential for tendon healing where blood supply is relatively tenuous.

nutritional support is provided by the synovial fluid. In order for tendon gliding to occur, the mesotenon has disappeared in the digital flexor sheaths except at the sites of the vincula that carry the vessels from the periosteum (Figure 39.28). They supply the longitudinal intrinsic vascular system, which runs through the tendons and is located chiefly in their dorsal and lateral aspects. The complimentary role of blood and synovial circulation can be extended to the understanding of tendon healing. Opposing but not mutually exclusive theories have been proposed to explain normal tendon healing. According to one theory, healing depends on blood supplied by adhesions formed from the sheath and surrounding tissues beginning a few days after injury. Tendon motion speeds regression of adhesions and strengthens the repair. A newer theory proposes that tendons completely devoid of blood supply will heal if bathed in synovial fluid. A primary tendon repair is undertaken within a few hours of injury and is generally reserved for cleanly cut tendons.24 Delayed primary repair may be performed from several hours up to 10 days after injury and is indicated for tidy but potentially contaminated wounds to allow for prophylaxis against infection before tendon repair. Relative contraindications to immediate tendon repair are (1) injuries more than 12 hours old; (2) crush wounds with poor skin coverage; (3) contaminated wounds, especially human bites; (4) tendon loss greater than 1 cm; (5) injury at multiple sites along with tendons; and (6) destruction of the pulley system. After 4 weeks, secondary repair is generally not possible because of retraction of the musculotendinous units so that reapproximation of the tendon ends produces undesirable joint flexion. Additionally, after 4 weeks the proximal tendon may coil and thicken, becoming too large to pass under the pulley into the flexor tendon sheath. The surgeon’s endeavors are directed to avoiding the four major complications that interfere with the smooth gliding and integrated action of tendons: adhesions, attenuation, rupture, and joint and soft tissue contractures.23,24 Prerequisites for tendon repair are aseptic conditions in an operating room with good lighting, good instruments, adequate anesthesia (axillary block or general anesthesia), and loupe magnification.

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Figure 39.29. Access to lacerated tendons within the flexor tendon sheath is facilitated by enlarging the existing laceration in the sheath. However, avoid excising A2 or A4 pulleys.

Partial tendon injuries must be treated appropriately in order to produce a smooth juncture at the site of injury.23 Prevention of complications rests with exploration of all wounds likely to cause partial flexor tendon lacerations. Partial lacerations of 50% or less are treated simply by trimming the lacerated portion and do not need to be sutured. Those partial injuries greater than 50% should be repaired. Nonrepaired, less than 50% partial lacerations have a significantly higher ultimate load and stiffness than those that are repaired. Failure to diagnosis a partial flexor tendon laceration at the time of primary repair may lead to delayed tendon rupture, entrapment between the tendon laceration and a laceration in the flexor sheath, or trigger finger. Zone II tendon injuries merit special attention.25 This zone is called the “no-man’s land” of Bunnell. Three tendons (profundus and two slips of superficialis) traverse zone II, and they constantly interchange their mutual spatial relationships. Tendon injury in this region necessitates enlarging the sheath opening in order to gain access to sufficient tendon length for repair. The existing laceration in the sheath is used in making a longitudinal trap door incision so that a flap of sheath can be lifted up (Figure 39.29). Enough room is left for subsequent sheath closure if technically possible. Care should be taken to avoid excising the annular pulleys, especially A2 and A4, although it has been shown that as much as 50% of either of these two pulleys can be excised for on the flexor tendon sheath without any significant biomechanical consequences. Flaps can be raised on either side of these pulleys and repair performed by working on each side. It is difficult to repair both profundus and superficialis tendons if they are injured. Nonetheless, both should be repaired as resection of the superficialis reduces overall grip strength, predisposes to recurvatum and swan neck deformity at the PIP joint, and damages the vincula supply to the profundus. Usually skin wounds have to be extended to display the divided tendon ends. The Bruner zigzag exposure is preferred. The tendons are handled with fine-toothed forceps only at their cut ends; their surface is never touched. The wrist is flexed, and a small Keith needle is passed transversely through the proximal tendon about


2 cm from its end, transfixing it to the skin and sheath but avoiding the neurovascular bundle. Immobilization of the tendon in this way facilitates tension-free repair. The ragged tendon ends may be squared off, but no more than a total of 1 cm should be resected, or some permanent contracture will result. The tendon ends are brought together by a single tension-holding “core suture.” (A modified Kessler suture is preferred.) The transverse limb of the suture is placed volar to the longitudinal limbs and nearer to the tendon ends so as to “lasso” the lateral tendon fibers caught in the loops (Figure 39.30). Such locking loops increase by 10% to 50% the ultimate tensile strength of the repair. If this is not done, and a grasping loop rather than a locking loop is placed, tension on the suture line can open up the loop, increasing the propensity for gapping at the repair site. The ideal suture material for tendon repair has not been found. A 4-0 coated polyester or braided nylon is the best material for the core stitch. Based on data from a number of studies and adjusting for friction, edema, and the effect of early repair stress,

Figure 39.30. Locking core suture and running epitenon peripheral suture enable a strong, smoothly gliding flexor tendon repair to be achieved. Most would now add at least a second core suture or employ a double-stranded suture material because it has been shown that at least four strands crossing the repair site are optimum.


rough estimates allow for preparation of a strength versus force graph. The safety of any four-strand core suture repair can then be appreciated.24 Some achieve a four-stranded core repair by using a double-stranded type of suture material. Others place a second core suture with a single-stranded material. Such a four-stranded core repair should permit light composite grip during the entire healing period. Additionally, a running circumferential peripheral epitendon suture repair is also placed. This not only helps to smooth the surface of the repair site but adds to the ultimate tensile strength of the repair and reduces gap formation. A peripheral 6-0 nylon coapting suture serves the purpose. Thus, the characteristics of the ideal primary flexor tendon repair are (1) sutures easily placed in the tendon, (2) secure suture knots, (3) smooth junction of tendon ends, (4) minimal gapping at the repair site, (5) minimal interference with tendon vascularity, and (6) sufficient strength throughout healing to permit the application of early motion stress. Zone I injury may be caused by a penetrating injury. However, closed traction injury may cause profundus tendon avulsion most frequently involving the ring or middle finger. For repair of zone I injuries a pull-out suture is necessary if distal tendon length is insufficient to repair the tendon securely (Figure 39.31), although suture bone anchors have now facilitated this mode of tendon repair into bone at the base of the distal phalanx.

Figure 39.31. Method of performing a zone I tendon repair when there is inadequate distal tendon stump for a secure tendon-to-tendon junction repair. DIPJ, distal interphalangeal joint; PIPJ, proximal interphalangeal joint.

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A 4-0 monofilament suture is placed transversely through the tendon 1 cm proximal to the cut end and is woven distally along each side of the tendon. A distally based periosteal flap is raised from the volar surface of the distal phalanx. The suture is passed under the flap and around the distal phalanx or through two drill holes and out through the nail over a button.The periosteal flap and distal tendon stump is secured over the repair. The pullout suture is retained for 6 weeks. Postoperatively, hand elevation is important to reduce edema. The wrist is placed in about 20° of flexion and the metacarpophalangeal joints at about 40° to 60° of flexion. The splint is molded against the fingers with the interphalangeal joints fully extended. A system of rubberband dynamic traction may be used as described by Kleinert following repair of flexor tendons in zone II, with good results obtained in over 80% of cases.25 An alternative regimen for postoperative care has been described by Duran in which a similar protective splint is used, but controlled passive mobilization is performed. Most recent hand surgery literature is replete with confirmation of the beneficial effects of applying early controlled forces to healing tissues.26 Advocates of controlled active digital motion believe that this technique generates greater gliding of the healing tendon, fewer adhesions, and the ability to more rapidly achieve tendon strength than passive motion protocols.25–27 Improved excursion of flexor tendons can be obtained by addition of a palmar bar to the Kleinert dynamic rubber-band protocol, and even greater excursion can be expected if wrist extension is added. Differential excursion between the two digital flexors is dramatically increased by a synergistic splint that allows for wrist extension and finger flexion. This position of wrist extension and metacarpophalangeal joint flexion produces the least tension on a repaired flexor tendon during active digital flexion; thus, we have come to adapt the hinged brace technique advocated by Strickland and the so-called place and hold protocol.23 A tenodesis splint with a wrist hinge is fabricated to allow for full wrist flexion, wrist extension of 30°, and maintenance of metacarpophalangeal flexion of at least 60°. Following composite passive digital flexion, the wrist is extended, and passive flexion is maintained. The patient actively maintains digital flexion and holds that position for approximately 5 seconds. The patient is instructed to use the lightest muscle power necessary to maintain digital flexion. This type of protected motion postoperative protocol extends for 6 weeks.

Extensor Tendons Proper diagnosis and treatment of extensor tendon injuries requires quite a bit of knowledge of the relatively complex anatomy of the extensor mechanism of the

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D.T. Netscher and I. Gharbaoui Extensor apparatus

Transverse fibers

Oblique fibers Central extensor tendon

DIPJ

PIPJ Lateral band Lumbrical muscle

Interosseous muscle

Figure 39.32. Anatomy of the extensor mechanism over the dorsum off the d h fi finger.

dorsum of the finger (Figure 39.32).28,29 The common extensor tendon, through the sagittal bands, extends the metacarpophalangeal joint by lifting the volar plate at the base of the proximal phalanx (there is no bony attachment per se of the extensor tendon to the proximal phalanx itself). The central slip of the common extensor extends the PIP joint, and the conjoined tendon extends the DIP joint. Injuries to these structures can result from open lacerations or closed avulsions of the distal insertions. All lacerations should be repaired if 50% or more of the width of the tendon is divided. Extensor tendon avulsions are most likely to occur at the DIP joint from a “jamming” type of injury that results in a mallet finger deformity (Figure 39.33).30 If a bone fragment representing 50% or more of the articular surface is involved or if there is a volar subluxation of the DIP joint, an open reduction with internal fixation should be per-

Mallet Finger

Boutonniere

Drop Finger

Figure 39.33. Depending on the location, extensor tendon injuries will result in mallet finger, boutonniere deformity, or a “dropped” fingertip.

Figure 39.34. A mallet fracture from a closed injury requires open reduction and internal fixation such as this case with a large avulsion bone fragment and volar subluxation of the distal phalanx.

formed (Figure 39.34). If there is a tendon rupture or only a small piece of bone avulsed, good results can be obtained by 6 weeks of continuous splinting with the DIP joint in extension (Figure 39.35B). Subsequent to this splinting, the DIP joint should be further protected during sleeping hours for 2 more weeks. Closed tears through the triangular ligament may be caused by joint subluxation or a jamming type of injury and result in a boutonniere deformity (see Figure 39.33).31 The central slip attachment at the base of the middle phalanx is disrupted so that extension of that joint is altered. The lateral bands lose their support dorsal to the PIP joint axis and slip volar to it, becoming flexors of the PIP joint and extensors of the DIP joint. Within 6 weeks of injury these can be treated satisfactorily by extension splinting at the PIP joint but maintaining the DIP joint free for active flexion and extension (Figure 39.35A). If there is an open laceration to the central slip mechanism and adjacent triangular ligament, direct suture repair or reinsertion into bone by means of minibone anchor sutures should be performed followed by the same postoperative protocol as for a closed avulsion injury. Extensor tendon injuries proximal to the PIP joint result in a drop finger (see Figure 39.33). They should be repaired and splinted for 4 weeks with the metacarpophalangeal joint at neutral. Common extensor tendon injuries over the dorsum of the hand and at the wrist must be repaired and then treated postoperatively by one of a number of different controlled motion protocols, one of which such schemes is a dynamic rubber-band extension outrigger brace or use of a relative motion splint as described by Merritt in which the affected digit is kept at a more dorsal pitch to the adjacent fingers, thus relaxing the repaired tendon.28 This latter splint causes minimal interference with day-to-day activities during the rehabilitation period.


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A

B Figure 39.35. (A) Closed boutonniere proximal interphalangeal injury is treated by continuous finger splinting that immobilizes the joint but allows active flexion of the distal interphalangeal joint. (B) Closed mallet injury without a significant bone fracture is treated by continuous finger splinting for 6 weeks and immobilizes the distal interphalangeal joint.

Nerve Injuries Severance of a peripheral nerve involves an acute loss of sensory, motor, and sympathetic functions. Knowledge of the motor and sensory distributions of the nerve allows for a clinical evaluation of the injury32; however, associated injuries such as fractures and muscle and tendon lacerations may complicate the evaluation. Loss of pseudomotor activity occurs within 30 minutes of the nerve injury; a loss of sweating can be demonstrated with a ninhydrin test. Nerve conduction studies, on the other hand, are not helpful immediately following the injury. They become useful 3 weeks after the injury. They demonstrate fibrillation and denervation potentials in muscles that are completely denervated so that in a closed injury they may differentiate between a neuropraxia and a neurotmeses. Later, nerve conduction studies may help monitor nerve regeneration after repair.33

From 25% to 75% of the nerve consists of connective tissue; thus, nerves heal by scarring, and the aim of surgical repair of a severed nerve is to minimize the degree of the scarring.33,34 The epineurium completely surrounds the nerve and also binds groups of fascicles loosely together. Each fascicle is surrounded by a thin sheath of connective tissue called the perineurium that functions as a diffusion barrier. Rupture of the perineurial sheath results in loss of the conduction properties of the enclosed nerve fibers. Endoneurium provides the connective tissue packing between individual nerve fibers. During limb movement a peripheral nerve undergoes longitudinal excursion within its bed.The greatest excursion of peripheral nerves occurs at the wrist proximal to the carpal tunnel where the median nerve has 15.5 mm of gliding when the wrist ranges through a full arch of flexion and extension. Longitudinal excursion of the nerve during limb movement must be added to the normal retraction of the divided nerve when considering a repair. Primary nerve repair is done within 72 hours of injury, delayed primary repair from 72 hours to 14 days, and secondary nerve repair in 14 or more days following injury. Factors that might influence the timing of nerve repair are the following: 1. Metabolic changes within the nerve: Peak metabolic activity in the nerve occurs within 4 to 20 days following injury, and it has been postulated that nerve repairs might optimally be performed in the second or third week postinjury. There are no clinical studies to support this hypothesis. 2. Muscle cell changes: Muscle spindles start to atrophy at 3 to 4 months. There is no hope of motor function return after 18 months. 3. Sensory end-organs: Sensory end-organs survive without nerve innervation, but the quality of sensation depends on the ability of the brain to decode messages received from the end-organs. Young patients accomplish better sensory recovery after a long delay (even more than a year) than can be achieved with adults. Fibrosis of the distal nerve channels may block axonal growth after a prolonged delay following injury, and this may also limit the degree of sensory recovery. 4. Wound condition: Treatment of skin loss, vascular insufficiency, and skeletal instability all take precedence over nerve repair. In the presence of a severely crushed or avulsed nerve or after a gunshot blast, secondary nerve repair is better at which time the proximal and distal extents of the nerve injury from the site of division can be better appreciated. Nonetheless, at the time of acute management of the wound, identification of cut ends and temporary approximation to maintain elastic length are helpful. 5. Patient condition: Nerve repair is an exacting operation and must be delayed until the patient’s condition permits suitable circumstances.

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Thus, primary neurorrhaphy is recommended when (1) the nerve is sharply incised, (2) there is minimal wound contamination, (3) there are no injuries that preclude obtaining skeletal stability or adequate skin cover, (4) the patient is sufficiently stable to undergo an operation, and (5) appropriate magnification and instrumentation are available. Within a nerve, fascicles are not separate cables running in parallel throughout the length of the nerve. There are multiple interconnections between them resulting in an intraneural plexus.32,34,35 This explains the difficulty of nerve reconstruction in cases of segmental loss and the often suboptimal clinical results following repair of even a sharply incised nerve laceration. Within hours of the nerve injury, the nerve cell body in the anterior horn of the spinal cord undergoes metabolic changes, and transected axons begin to sprout. Wallerian degeneration occurs in the entire segment distal to the injury and 1 to 2 cm proximal to it.The endoneurial tubes during this process are cleared of debris from axons and myelin, allowing a path for axonal regeneration. Subsequent axonal regeneration occurs at a maximum rate of 1 to 2 mm per day. In closed injuries, when the severity of a nerve injury is unknown, repeated clinical evaluations and electrical studies every 3 to 6 weeks will help distinguish between neuropraxia and axial axonal injury. In most cases, surgical exploration with repair is indicated after 3 months if no clinical recovery is detected. Nerve repair is performed with magnification using microsurgical techniques and either epineurial or group fascicular suture placement. The repair should be tension free. Fibrin glue can be used in combination with a limited number of sutures. With sharp nerve lacerations, an epineurial repair provides as good a functional recovery as fascicular repair provided that anatomic landmarks such as vasa nervorum allow an accurate and precise matching of the cut nerve ends. Current investigation suggests that optimum nerve regeneration and matching of proximal and distal axons occur by a combination of neurotropism and contact guidance. A critical distance must exist between proximal and distal nerve segments to obtain the maximum benefit of neurotropism. With standard nerve grafting it is the surgeon who determines the topography of the proximal and distal fascicles. The fascicular alignment chosen may not always be appropriate. For small gaps, probably up to 3 cm in humans, experimental evidence suggests it might be more appropriate to place a polyglycolic acid tube to bridge the gap rather than to perform nerve grafting. If a nerve gap exists, it may be overcome by proximal and distal mobilization or, in the case of the ulnar nerve, anterior nerve transposition; however, excessive mobilization of the nerve ends must be avoided as this impairs the vascularity of the nerve. If there is judged to be too much tension on the nerve repair (it cannot be held


together with 8-0 nylon sutures), nerve grafting (or in some instances placement of a nerve tube) must be done.35 Donor sources are most frequently from the posterior interosseus nerve or the median antebrachial cutaneous nerve for small digital nerves and the sural nerve for nerve gaps of larger nerves. Following repair, the affected part is splinted for 3 weeks to protect the anastomosis in a position of least tension. Secondary deformity for motor nerve injuries may be prevented by appropriate splinting (such as an anti-claw brace for ulnar palsy) until motor recovery occurs. After nerve repair, Tinel’s sign is monitored as an index of progressive recovery.

Fractures and Dislocations Pain, swelling, limited motion, and deformity suggest the presence of fracture or dislocation. Standard anteroposterior (AP) and lateral x-rays may miss some fractures and dislocations, and multiple x-ray views are frequently necessary to establish the exact diagnosis. Posteroanterior (PA), oblique, carpal tunnel, and stress views are often useful as are ancillary studies such as arthrography, bone scan, CT scan, and MRI. Fractures may be rotated, angulated, telescoped, or displaced. Angulation is described by the direction in which the apex of the fracture points, and displacement is described by the direction of the distal fragment.36,37 Fractures may be closed or open depending on whether or not a wound is involved; they may be complete, incomplete, or comminuted (more than two pieces); and they may be transverse, longitudinal, oblique, or spiral. Dislocation of joints may be complete or incomplete (subluxed) depending on the severity of the capsular injury. Displaced fractures or dislocations should be repositioned as soon as possible. This decreases soft tissue injury, decompresses nerves that might be stretched, and relieves kinking of blood vessels. Good bony contact and stability are essential for fractures to heal. Some fractures are stable and require only external support in a splint or cast, whereas others are unstable and require internal support, which can be provided by Kirschner wires, internal wire sutures through drill holes in the fracture fragments, screws, or plates, or even external fixation devices. The more complicated the fixation, the more dissection is required to apply that fixation and therefore the greater is the potential for scarring about adjacent tendons and consequential stiffness; however, screws and plates can nonetheless establish a degree of rigid synostosis that will allow for early motion of the part and so potentially reduce the risk of cicatricial stiffness. Intraarticular fractures require accurate reduction in order to preserve motion. Significant step-off on the articular surface may alter motion and lead to later develop-


ment of arthrosis. Persistent rotational deformity and significant lateral angular deformity will generally not remodel with time, and this can be avoided by observing the alignment of the injured fingers as compared with adjacent digits while passively gently flexing them into a fist after reduction is obtained. If they do not fit comfortably adjacent to each other and do not point toward the distal pole of the scaphoid, a fresh attempt at reduction should be performed; thus, clinical observation of good anatomic alignment of fractures is important in assessing the final result. A thorough neurovascular examination should always be performed both before and after fracture reduction has been completed. Most common fractures and dislocations are discussed below.

Clavicle Fractures Clavicle fractures represent one of the most common bone injuries (5% to 10% of all bone fractures). The mechanism of injury can be direct or indirect, such as falling on an outstretched hand. Clavicle fractures are classified into three groups: I (middle third), representing 80% of clavicle fractures; II (lateral third); and III (medial third). Diagnosis is usually easy, and complications are rare. However, high-velocity injuries may have multiple associated injuries such as a fracture to the ipsilateral scapula and upper ribs, pneumothorax, and neurovascular injuries. Most middle third clavicular fractures heal uneventfully with nonoperative immobilization for 4 to 6 weeks, such as with the use of a sling.38 A variety of slings, straps, and braces have not been shown to necessarily be superior to the others in the treatment of these fractures. Surgical treatment with open reduction and internal fixation is indicated in cases of open injury or pending skin disruption, neurovascular compromise, unstable floating shoulder (an associated fracture of the surgical neck of the scapula), or wide separation of the clavicular ends with soft tissue interposition. With lateral third fractures, the coracoclavicular ligament provides stability in most cases, allowing also for nonoperative treatment to be successful.

Proximal Humerus Fractures Proximal humerus fractures make up 2% to 3% of upper extremity fractures and occur more frequently in elderly people, especially with associated osteoporosis. These are fractures proximal to the insertion of the pectoralis major and involve the proximal humeral shaft, head of the humerus, or anatomic neck or surgical neck of the humerus.38 A fracture is considered nondisplaced, regardless of the number of fragments if translation is less than

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1 cm and angulation is less than 45°. The blood supply of the humeral head is at risk in all fractures involving the anatomic neck. Associated injuries are relatively frequent, including glenohumeral dislocation, injuries to the brachial plexus, axillary nerve, and also vascular injuries. Most cases result from indirect trauma (fall on the outstretched arm). Radiographic evaluation requires at least AP, lateral, and axillary views, and a CT scan may be helpful for the more complex cases. Most cases are only mildly displaced and can be treated nonoperatively with a comfort sling or splint. Early range of motion is essential and may be started as soon as the second week after injury. With displaced fractures, closed or open reduction followed by percutaneous pinning or internal fixation is necessary. If the humeral head is devascularized, especially in elderly patients, the fracture may be more reliably treated with a hemiarthroplasty.

Humeral Shaft Fractures Humeral shaft fractures extend from the insertion of the pectoralis major proximally to the supracondylar ridge distally. The level of the fracture relative to muscle insertions determines the deforming forces and angulation of the fracture. Above the deltoid insertion, the proximal fragment is pulled into adduction by the pectoralis major, and the distal fragment under the influence of the deltoid is displaced into adduction. Below the deltoid, the proximal fragment is abducted. The radial nerve is in close contact with the posterior aspect of the humerus, particularly in fractures involving the middle third of the shaft, and so it is potentially at risk for injury. Other potential associated injuries may include the brachial artery and the median and ulnar nerves. The mechanism of injury can be indirect by fall on an outstretched upper extremity but is more often through a direct injury. The vast majority of these fractures can be treated nonoperatively such as using a hanging cast. Close follow up with x-rays every 4 to 6 weeks is necessary. Deformities of up to 20° to 30° of angulation or 2 to 3 cm of shortening are usually accepted. As soon as the fracture seems stable, functional bracing enables humerus immobilization so that shoulder and elbow rehabilitation can begin. Indications for surgery include open fractures, polytrauma, bilateral humerus fractures, floating elbow, segmental fracture, and vascular injuries, as well as obese and uncooperative patients. Radial nerve paralysis usually recovers spontaneously and in most cases therefore is usually not a surgical indication; however, if open reduction is indicated for other reasons, the radial nerve should be explored if the patient has a preexisting radial palsy. Open reduction and internal fixation is achieved by means of compression plate and screw fixation or by means of intramedullary nailing.

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Fractures of the Distal Humerus Fractures of the distal humerus may be intraarticular or extraarticular, and treatment is very challenging, often surgical, necessitating solid anatomic reduction that allows for early range of motion. Complications are frequent, including compartment syndrome, loss of fixation, nonunion, heterotopic calcification, and stiffness. The mechanism of injury is usually an indirect trauma, with the deforming forces transmitted with the elbow in either flexion or extension, or a varus or valgus deformity resulting in a variety of different fracture patterns. Neurovascular injuries may involve the brachial artery, median, ulna, or radial nerve around the elbow area. Except for some nondisplaced stable fractures, there is generally no place for nonoperative treatment or percutaneous pinning of these fractures in adults. Surgical treatment in most cases requires anatomic reduction and fixation with lag screws or plates and screws, depending on the complexity of the fracture. Fixation should be solid enough to allow immediate range of motion to the elbow. Indomethacin may be helpful in reducing the incidence of subsequent heterotopic ossification. In children, supracondylar fractures are usually treated with closed reduction and percutaneous pinning.

Olecranon Fractures If the fracture is thought to be nondisplaced, it should be checked radiographically with the elbow at 90° of flexion. If there is no separation with this increased flexion, immobilization for 3 weeks followed by sling and rehabilitation under supervision can then be undertaken. However, in all other cases open reduction and internal fixation are required for olecranon fractures. This is followed by early protected range of motion for these intraarticular fractures.39

Radial Head Fractures Radial head fractures are usually caused by axial loading from a fall on an outstretched hand, and the radial head is impacted against the capitellum.39 Mason classifies four types: type I, undisplaced fracture; type II, displaced fracture that involves only part of the radial head; type III, comminuted fracture; and type IV, fracture associated with elbow dislocation. Clinical examination should carefully rule out a distal radioulnar dissociation (EssexLopresti lesion).40 Quality x-rays should rule out any other associated fractures such as to the coronoid, olecranon, and capitellum. Nonoperative management is indicated for type I and type II fractures with less than 2 mm of displacement. Immobilization in a sling is necessary for 2 to 3 weeks followed by early active supervised range of motion. For all fractures with severe radial head displacement, surgical


treatment is indicated. Once surgical exposure has been achieved, evaluation of the degree of comminution and of elbow stability is required. The radial head can then be fixed or replaced. Radial head excision is not recommended, as it may result in instability.

Forearm Fractures Forearm fractures might involve isolated fractures of the radius or ulna, or both bones may be fractured together. A Monteggia fracture is described as the association of an ulnar fracture and radial head dislocation. Galeazzi fractures are the association of a radius fracture and distal ulnar dislocation. More than for any other fractures, the radiographic examination should focus on the joints above and below the fractures. Examination evaluates the neurovascular integrity of the distal extremity. Compartment syndrome may also be associated. For adults, isolated fractures of the ulna that are only mildly displaced can be treated with cast immobilization. All other fractures should generally be treated surgically. Bone fixation is achieved with either plate and screws or flexible intramedullary nails. In most cases, anatomic reduction of the forearm fracture will generally result in a spontaneous reduction of the radial head or the distal radioulnar joint when there is an associated proximal or distal dislocation. Finally, open fractures, especially when associated with a severe soft tissue injury, are often treated with external fixation.

Distal Radius Fractures Fractures of the distal radius represent the most common that involve the upper extremity. Therapeutic modalities have evolved considerably over the past few years, but many controversies still persist. These injuries occur to different age population groups, elderly and young patients. In older patients these fractures are typically extraarticular and often follow a less severe trauma. Because the bone is osteoporotic, there is a relatively frequent need for supportive bone grafting. Immobilization should be as short as possible to prevent stiffness. In contrast, in young adult patients there is usually a highenergy trauma that results in intraarticular and comminuted distal radius fractures. Possible associated injuries include carpal or distal radioulnar instability and triangular fibrocartilage injury, and for these reasons the tendency is to more aggressively treat these patients surgically. Colles and Smith fractures represent extraarticular fractures with, respectively, dorsal and volar displacement. A Barton’s fracture is a marginal articular fracture involving the rim of the distal radius in a coronal plane. These fractures can be either anterior or posterior. Fractures in the sagittal plane may involve the radial styloid and are also known as “chauffeur’s fractures.” Fractures


involving the lunate fossa of the distal radius are known as die-punch fractures. Scapholunate disassociations are often associated with fractures of the radial styloid. Rupture of the extensor pollicis longus tendon can occur as an early complication of even mildly displaced distal radius fractures. Treatment may be closed for stable fractures that are not excessively displaced. For displaced fractures, a closed reduction may first be attempted. The criteria for an acceptable reduction include restoration of radial length, volar tilt, and radial inclination. Unstable fractures, or unacceptable reduction, need surgical management, and multiple described procedures include percutaneous pin fixation, open reduction with internal fixation, and external fixation.41

Scaphoid Fractures Scaphoid is by far the most common carpal bone fracture. The scaphoid waste comes into contact in hyperextension with the dorsal rim of the radius when falling on an outstretched hand. Understanding blood supply to the scaphoid is important.42 The proximal pole of the scaphoid is poorly vascularized, and all of its blood supply comes in a retrograde fashion from distal to proximal. For this reason, avascular necrosis and nonunion are frequent complications of proximal pole scaphoid fractures. Fractures of the scaphoid are suspected in patients with pain and tenderness in the anatomic “snuffbox” or with tenderness elicited by pressure on the scaphoid tubercle.43 Diagnosis is usually confirmed by AP, lateral, and oblique wrist x-rays, although an additional specific scaphoid radiographic view with the resting ulnar deviation may be helpful (Figure 39.36). If x-rays are negative with a strong clinical suspicion of a scaphoid fracture, a

Figure 39.36. (A) Displaced scaphoid fracture (arrow). (B,C) This fracture has been treated with a cannulated screw.

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thumb spica cast should be applied with repeated x-rays performed within 10 to 15 days. An immediate bone scan or preferably a CT scan is another option when there is doubt about a potential scaphoid fracture. Early diagnosis is essential so that appropriate treatment can be instituted to reduce the risk of complications. Closed treatment consists of 8 to 12 weeks of immobilization starting initially with a long arm and a thumb spica cast followed then with a short arm thumb spica cast. Unstable fractures with displacement more than 1 mm and an intrascaphoid angle of greater than 45° and associated ligamentous injuries and vertical pattern fractures that tend to be of a more unstable configuration should generally be treated surgically (see Figure 39.36). Modern cannulated screws or intraoperative fluoroscopy and arthroscopy may even allow a minimally invasive percutaneous fixation of some of these scaphoid fractures.

Metacarpal Fractures Stable metacarpal fractures may be treated with splinting alone. Those with dorsal or volar angulation can be stabilized by percutaneous insertion of intramedullary fixation pins. If they are displaced or unstable, such as long oblique or spiral fractures, or multiple metacarpal fractures, open reduction and internal fixation should be performed.36,37 The internal fixation can be achieved with Kirschner wires, lag screws, or plate and screws depending on the fracture pattern configuration.44,45 Dorsally angulated fractures at the neck of the little finger metacarpal, the so-called boxer’s fracture, do not require reduction if the dorsal angulation is less than 30°. Mobility of the carpometacarpal joint will compensate for this degree of angulation. If the angulation is greater than 30°,

A

B

C

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the fracture should be reduced and if necessary maintained with internal fixation. Occasionally these fractures need to be opened in order to obtain satisfactory reduction and stability. Oblique fractures at the base of the thumb metacarpal (Bennett’s fracture) result in the small proximal fragment being held in position by the volar oblique ligament to the trapezium. The entire remaining portion of the thumb metacarpal is displaced dorsally and radially because of the pull of the abductor pollicis longus tendon. These structures should be properly reduced and secured with internal fixation. Comminuted fractures at the base of the thumb metacarpal (Rolando’s fracture) are frequently treated by closed reduction. Accurate reduction is important to the ultimate function of the thumb, and, therefore, if the fragments are large and badly displaced, an open reduction is indicated. Fractures of the shaft of the thumb metacarpal tend to become displaced by the opposing muscle forces of the abductor and the adductor on the proximal and distal fragments, respectively; thus, even undisplaced fractures may with time become progressively more displaced and angulated, necessitating an internal fixation.


A

B

C

D

Phalangeal Fractures In some cases, such as for irreducibility, malrotation, intraarticular fractures,46 open fractures, segmental bone loss, and multiple fractures involving the hand, operative fixation is required (Figure 39.37). Overzealous treatment by open reduction and internal fixation can lead to excessive scarring, tendon adhesions, and stiffness.44,45 In proximal phalangeal fractures, the interossei tend to flex the proximal fragment while the extensor mechanism extends the distal fragment, resulting in a volar angulation. In middle phalangeal fractures, the displacement depends on the level of the fracture relative to the insertion of the central slip. Displacement is dorsal in proximal fractures and volar in distal fractures. Stable fractures can be treated by initial immobilization followed by buddy taping and progressive mobilization. It is important to note that there is little correlation between clinical and radiographic bone healing. Mobilization is usually started after about 4 weeks based on clinical improvement. When operative treatment has secured solid rigid bony fixation, earlier range of motion may be instituted. Fractures of the distal phalanx are very frequent. They represent half of all hand fractures. Most of them result from crush injuries with associated nailbed injuries. Precise reduction is generally not required; hence, treatment generally consists of splinting alone. Unstable shaft fractures, with overriding of the fragments, are indications for reduction and longitudinal Kirschner wire fixation.

Figure 39.37. (A,B) A displaced proximal phalangeal fracture at the base of the little finger. (C,D) This was treated by closed manipulation of the fracture and percutaneous pinning to maintain stability.

Carpal Dislocations The lunate and perilunate dislocations represent the most common form of wrist dislocation. They result from hyperextension of the wrist on an outstretched hand. The radiologic diagnosis may sometimes be difficult, and up to 25% of these injuries are still missed in the emergency room. They can be a pure lunate dislocation with rupture of the scapholunate (Figure 39.38) and lunotriquetral ligaments or a fracture-dislocation involving a transscaphoid perilunate dislocation or with a fracture involving the radial styloid, capitate, hemate, and triquetrum. Median nerve compression is frequently associated. Even though reduction can often be achieved by closed manipulation and distraction; surgical repair of the scapholunate and lunotriquetral ligaments are necessary with K-wire protection and splinting for 6 weeks.


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between the metacarpal head and the base of the proximal phalanx. Attempts at closed reduction are fruitless because of the entrapment phenomenon resulting from this arrangement. Open reduction may be approached through either the dorsum or the palm. In the latter approach, caution must be used to avoid injury to the digital nerves stretched over the metacarpal head. In either approach, the trapped volar plate must be released. Metacarpophalangeal joint dislocation of the thumb often results from jamming it in a radial direction, thus tearing the ulnar collateral ligament. In about 75% of complete tears, the ulnar collateral ligament pulls proximally and comes to rest dorsal to the extensor hood (a Stener lesion) (Figure 39.40). These lesions cannot heal spontaneously, because the ulnar collateral ligament is prevented from reattaching to bone. They require operative repair. Radial deviation of the joint by 40° degrees or more or volar subluxation of the joint suggests a complete tear, and ligament repair should be performed. Stress radiographs (sometimes enabled only after the digit is anesthetized with a metacarpal block) may be required

Figure 39.38. Scapholunate ligament disruption is indicated by a widened gap between the scaphoid and lunate bones (arrow).

Dislocations Involving the Hand Closed dislocation of the PIP or DIP joints can frequently be managed by closed reduction and splinting. If the joint is unstable after reduction, it needs exploration for ligament repair.46 A PIP joint volar dislocation is frequently associated with a tear in the triangular ligament of the extensor mechanism through which the head of the proximal phalanx protrudes and becomes trapped. Attempts at closed reduction fail, because they further tighten the fibers of the lateral bands and the central slip around each side of the protruding neck of the proximal phalanx. These injuries require open reduction with repair of the tear. Dorsal dislocations of the PIP joint involve the volar plate. Instability of the joint after reduction signifies that at least one collateral ligament is also involved, and open reduction and repair are required. If there is an avulsion from the volar base of the middle phalanx of a bone fragment representing one third or more of the articular surface, this may also require open reduction and internal fixation. Palmar dislocations of the head of the index finger metacarpal often require metacarpal open reduction (Figure 39.39). The head of the metacarpal becomes trapped between the superficial, transverse palmar ligament, the flexor tendons and lumbrical muscles, and the natatory ligament, while the volar plate becomes trapped

A

B

C

Figure 39.39. (A) Palmar dislocation at the head of the index finger metacarpal (arrow) was “irreducible” by closed technique. (B,C) A more unusual “irreducible” desiccation of the head of the little finger metacarpal is seen (arrows). The digital nerves are often stretched over the volar surface of the head of the metacarpal.

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A

B Figure 39.40. (A) Closed injury of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb showing marked joint instability. (B) A classic Stener lesion is seen intraoperatively with a disrupted ulnar collateral ligament (arrow) tracking proximally and resting dorsal to the extensor hood.

to facilitate diagnosis of a complete ulnar collateral ligament injury of the thumb metacarpophalangeal joint.

Vascular Emergencies Acute vascular injuries may follow closed or penetrating extremity trauma or may occur after iatrogenic injury. Fractures or dislocations may be causes of vascular injury. Onset of symptoms may be delayed, as the culmination of swelling, hypotension, and intimal injury all combine to result in late thrombosis and vascular insufficiency. Following the acute arterial injury, symptoms result from a combination of the adequacy of collateral circulation, posttraumatic sympathetic tone, and vasomotor control mechanisms. Patients with an upper extremity arterial injury who have adequate collateral circulation and normal vasomotor control may have minimal symptoms, and vascular reconstruction is not necessarily mandatory; however, adequate anatomic vasculature may be com-


promised by inappropriate distal functional control with consequent vasospasm and arteriovenous shunting.47,48 For patients who have inadequate collateral circulation, the distal ischemia will further increase sympathetic tone and produce additional arterial spasm and induce more ischemia; thus, the effects of arterial injury in the upper extremity may be magnified by the additional presence of a concomitant nerve injury.47,48 If there is a noncritical arterial injury, reconstruction may be advocated to restore parallel flow in case of future injury, to enhance nerve recovery, to facilitate healing, and to prevent cold intolerance. However, reported patency rates even with microvascular techniques for single vessel repairs vary from 47% to 82%.49 The following injuries, however, are optimally managed by vascular repair/reconstruction: axillary or brachial artery injury, combined radial and ulnar artery injury, and radial or ulnar artery injury associated with poor collateral circulation. The following are relative indications for repair: extensive distal soft tissue injury, technical ability to achieve repair without compromising patient wellbeing, and combined vascular and neural injury.49 Need for arterial reconstruction requires assessment of adequacy of collateral circulation, and this is based primarily on initial clinical judgment to include assessment of color, capillary refill, turgor, and temperature; however, the final decision regarding arterial reconstruction is often made in the operating room after exploration. Once the injured structures have been isolated, potential bleeding sites controlled, and the hematoma evacuated, the distal extremity can be more adequately assessed.47 At this time, the lacerated vessel ends are controlled by atraumatic vascular clamps, and the tourniquet is released. Capillary refill and turgor of the distal extremity is then assessed as is the backflow from the distal lacerated vessel ends. Digital blood pressure can be quantified with a sterile Doppler probe and cuff, and a digital brachial index of 0.7 or greater suggests adequate perfusion.50 If there is poor collateral flow, then arterial reconstruction should be performed. At this time, the standard of care does not require arterial repair of isolated noncritical vessels. Brachial artery lacerations, particularly those injuries occurring above the origin of the profunda brachii, are reconstructed unless there are clinical contraindications. In combined radial and ulnar artery injuries, one or both vessels should be reconstructed. If possible, both vessels are repaired. Preoperative evaluation, particularly for closed injuries, may be facilitated by special investigations; however, important details of the patient’s history are also the presence of previous injury, particularly repetitive insults, blood dyscrasias, drug exposure, tobacco use, and factors that might be associated with connective tissue disorders. Physical examination for a vascular disorder of the upper extremity must include a thorough evaluation of the entire upper extremity, the neck, careful


auscultation of the heart for heart murmurs, and auscultation for bruits in the neck or thoracic outlet region that might be supportive of embolic phenomena or might be an irregular rhythm from atrial fibrillation. A radial brachial index (RBI) and a digital brachial index (DBI) can be calculated. A DBI or RBI of less than 0.7 indicates inadequate arterial flow to a hand or digit and necessitates either medical or surgical intervention.50 Differences of 15 mm Hg between fingers or a wrist-to-finger difference of 30 mm Hg is thought to indicate occlusion at the level of or distal to the palmar arch. A pressure difference greater than 20 mm Hg at the same level between the affected and contralateral extremity may also indicate arterial stenosis or occlusion. Noninvasive vascular studies by pulse volume recordings and Doppler evaluations provide a wealth of information. Contrast arteriography provides the best anatomic structural information of the upper extremity vasculature but is nonetheless a static evaluation of the extremity. Information is optimized by using intraarterial vasodilators (such as Priscoline) to identify stenoses that might be secondary to vasospasm and substraction techniques that minimize background interference. The potential problems of arteriography include catheterinduced vasospasm with possible failure to observe distal arterial reconstitution because of vasospasm. Consider regional anesthetic block, such a stellate ganglion block, if vasospasm prevents adequate visualization. Acute arterial occlusion can also occur from nonlacerating arterial injuries such as cannulation injuries, whereas acute occlusion in the upper extremity arteries may occur as the result of repetitive frequent trauma (hypothenar hammer syndrome), atherosclerosis, proximal embolic event, and systemic disease with or without a hypercoagulable state. Significant arterial occlusion produces ischemia and vasospasm. The prognosis may be related to etiology; for example, posttraumatic ulnar artery thrombosis has a much better prognosis than Buerger’s disease. Repetitive trauma may produce localized thrombosis resulting from periadventitial scarring. The trauma may also potentially cause intima damage to the media, disruption of the internal elastic lamina, and exposure of endothelial collagen leading to aneurysmal dilatation and/or thrombosis. As with acute arterial lacerations, arterial thrombosis or embolism may have adverse distal deleterious effects based on the extent of the occlusion, the adequacy of the collateral flow, and the sympathetic tone. Cannulation injuries most frequently involve the brachial or radial arteries such as following arterial blood studies, indwelling arterial catheters, and cardiac catheterization.51 Surgical repair of the brachial artery is necessary in the presence of distal ischemia, active bleeding, or aneurysm. Surgical options may include resection and ligation, arterial reconstruction, and/or thrombectomy with embolectomy. The loss of a radial pulse

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without ischemic symptoms distally is not an indication for acute care surgery. The extremity may be observed clinically in an awake and alert patient. In an unconscious patient, a Doppler probe and distal pressure measurements are helpful to evaluate the affected extremity. Arterial injection injuries may occur during medical procedures or may be self-inflicted during drug abuse and occasionally a consequence of workplace exposure. Distal ischemia may occur following inadvertent or inappropriate injection of pharmaceutical products such as barbiturates, propoxyphene, and nonparenteral narcotics. Severe vascular events may occur following workplace injury involving solvents, paint products, and lubricants; however, intraarterial injection is infrequent in such workplace injuries. These injection injuries result in severe acute extremity ischemia on the basis of secondary vasospasm, chemical endarteritis, and arterial blockage with activation of the clotting cascade. There are generally acute symptoms of arterial insufficiency with diffuse hand swelling, numbness, and discoloration. The injection wounds often appear innocuous. There may be rapid development of skin and soft tissue necrosis. Diagnostic modalities are aimed at determining if there is segmental and reconstructible occlusive arterial disease. Unfortunately, end artery occlusion within the microvascular beds is common, and systemic anticoagulation with systemic support remains the only treatment option. Management of ischemic symptoms secondary to a dialysis arteriovenous fistula includes ligation or banding.52 Ligation may be required for recurrent thrombosis and resultant distal embolization. Documentation of a “steal” phenomenon requires recording of digital pressure before and after occlusion of the radial artery below the fistula. A DBI of less than 0.64 is significant. Banding or takedown of the shunt will then be required. Acute arterial thrombosis that is secondary to either closed external posttraumatic occlusive disease or primary vascular occlusive disease is treated based on the severity of the distal ischemia, collateral circulation, and the vascular sympathetic tone. Treatment options are increased collateral blood flow through elimination of tobacco products, increased nutritional tissue blood flow with the use of calcium channel blockers, possibly a sympathectomy, either chemical or surgical (such as resection of the thrombosed segment and ligation as in the Leriche type sympathectomy), and surgical restoration of the circulation (through thrombectomy, resection and vein graft, arterial bypass), and/or thrombolytic therapy.53,54

High-Pressure Injuries Pressure injection injuries to the hand are relatively uncommon, but the consequences of a missed diagnosis

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are very serious.55,56 The severity of these injuries requires prompt response and urgent disposition. High-pressure injection guns are found in the industrial setting and are used for painting, lubricating, cleaning, and mass farm animal vaccinations. Materials that may be injected with these devices include paint, paint thinners, oil, grease, water, plastic, vaccines, and cement. A pressure of 100 psi can penetrate through skin. These high-pressure injection guns generate pressures ranging between 3,000 and 12,000 psi. Injection injuries can also be caused by other sources, such as defective lines and valves. Pneumatic hoses, grease boxes, and hydraulic lines can all cause a high-pressure injection injury. Several factors affect the extent of tissue injury, including the type of material, amount of material, anatomic location of the injection, and velocity of the injected material, but the type of material injected is the most important prognostic factor. Oil-based paints and paint thinners can generate significant early inflammation leading to severe fibrosis. Because tendon sheaths of the index, middle, and ring fingers end at the level of the metacarpophalangeal joints, material injected at either the DIP or PIP flexion creases will remain within those digits; however, the tendon sheaths of the thumb and little finger extend all the way into the radial and ulnar bursae; thus, material injected at either the DIP or PIP of the little finger or at the interphalangeal flexion crease of the thumb has the potential for extension into the forearm and could even cause a compartment syndrome, carpal tunnel syndrome, or ulnar nerve compression in Guyon’s canal. Initial presentation of the patient with a high-pressure injection injury may be benign and subtle. This can result in mismanagement and in minimizing the patient’s complaints. The break in the skin may be a very benignlooking pinhole-sized puncture site; however, several hours later the digit becomes increasingly more painful, swollen, and pale. Prompt recognition and realization of the severity of the injury is key. Antibiotic prophylaxis is started. Radiographs will help determine the extent of dispersion of the injected material. Nonlead-based paints may appear as subcutaneous emphysema, and grease may appear lucent on radiographs. On the other hand, leadbased paints may be seen as radiopaque soft tissue densities. Incisions are made to decompress the affected tissue and then perform an extensive exploration of all areas infiltrated by the injected material. Foreign material and all necrotic tissue must be debrided. Appropriate irrigation is performed to help reduce fibrosis and scarring. The wounds are then closed loosely over Penrose drains, left open to heal by secondary intention, or closed in a delayed manner. Despite prompt recognition and treatment, many can result in surgical amputation of the digits.


Frostbite and Chemical and Extravasation Injuries Frostbite Treatment of frostbite consists of restoring core body heat and rapidly rewarming the frozen extremity with a 44°C water bath until a digital flush appears. Active hand therapy must be instituted. The place of regional sympathectomy or possibly chemical sympathetic block in acute management of frostbite injuries is controversial; however, if disabling vasospastic syndrome persists as a chronic sequela to occult injury, digital sympathectomy is helpful.57 Avoidance of premature amputation is important. Demarcation and mummification of digits may take as long as 2 to 3 months.

Chemical Burns Chemical burn injuries may affect the hands in industrial environments. Water lavage is the most important part of treatment and should be started at the scene of the accident. Its continuation for 1 to 2 hours for acid burns and longer for alkali burns is important. After lavage, treatment follows the same principles as those for thermal burns, although some chemicals require specific therapeutic antidotes.58 Reducing agents such as hydrochloric acid are merely diluted if only small amounts of water are available and therefore must be neutralized with soap or soda lime if massive water lavage is not available. Hydrofluoric acid is common in rust removers and degreasers. Hypocalcemia and hypomagnesemia have been reported with burns over more than 5% of the body surface area. Treatment requires immediate water lavage followed by subdermal injection of 10% calcium gluconate (painful if not combined with local or regional anesthesia). Calcium carbonate gel has more recently been used for topical application instead of the injection therapy. Injuries caused by phenol (not water soluble) require specific treatment with topical polyethylene glycol (PEG 400) followed by water lavage. Treatment of white phosphorous burns involves principally water lavage followed by identification and excision of the remaining phosphorous particles. Irrigation with dilute 1% copper sulfate solution helps identify the phosphorous particles.This is followed immediately by water lavage to avoid the toxic effects of the copper sulfate. Sterile debridement and delayed closure of phosphorous burns is then performed as necessary.

Extravasation Injuries Injuries from extravasation of chemotherapeutic agents used to frequently affect the upper extremity; however,


the use of more permanent subcutaneously tunneled central lines has reduced the incidence of these injuries. A number of specific antidotes have been recommended in the past. The treatment of these injuries has now been simplified. If extravasation is expected, the infusion must be stopped immediately. Cold packs are applied for 15 minutes four times a day for 58 hours and the extremity elevated. This regimen is effective for most injuries. If blistering, ulceration, and pain occur in the damaged tissue, however, progressive necrosis to the limits of the extravasation will then follow, and a surgical excision of all of the damaged tissue is necessary. The option for wound coverage following debridement will then depend on the extent of the debridement that was required and on the various tissues that might be exposed, but most such injuries can generally be treated with delayed splitthickness skin grafting.59

Compartment Syndrome Compartment syndrome results in symptoms and signs occurring from increased pressure within a limited space that compromises the circulation and function of the tissues in that space.60–62 High pressure in a closed space reduces capillary perfusion below a level necessary for tissue viability. Volkmann’s ischemic contracture is the sequela of compartment syndrome. This results in fibrosed, contracted, and functionless muscle and in insensible nerves. The relationship between local blood flow (LBF) and the arteriovenous (AV) gradient can be expressed by the following formula: LBF = PA − Pv Local blood flow in a compartment equals local arterial pressure (PA) minus local venous pressure (Pv) divided by the local vascular resistance (R). With the lowering of the local AV gradient, oxygen perfusion of the muscles and nerves decreases, function ceases, and muscle ischemia progresses to the death of that muscle and its subsequent replacement by fibrous tissue. Muscle ischemia that lasts for over 4 hours can also give rise to significant myoglobinuria, which may reach a maximum up to 3 hours after the circulation is restored. Significant myoglobinuria may produce renal failure, and, therefore, in the presence of myoglobinuria one must retain a high urinary output and an alkaline urine. A forced Mannitolalkaline diuresis may be required. A variety of injuries are known to cause compartment syndrome: • Decreased compartment volume ⴰ Closure of fascial defects ⴰ Application of extensive traction to fractured limbs

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ⴰ

Externally applied pressure (tight casts or dressings, lying on the limb) • Increased compartment content ⴰ Bleeding ⴰ Increased capillary permeability (embolectomy, reperfusion after injury) ⴰ Trauma (fracture, contusion, wringer injuries) ⴰ Burns (thermal and especially electrical) • Other injuries ⴰ Intraarterial drug injection ⴰ Cold exposure ⴰ Snake bite ⴰ Injection ⴰ High-pressure injection injuries ⴰ Increased capillary pressure ⴰ Venous obstruction or venous ligation ⴰ Diminished serum osmolarity such as nephrotic syndrome The diagnosis of compartment syndrome must be based primarily on clinical evaluation of muscle and nerve ischemia (Figure 39.41). Although it is possible to measure intracompartment pressures, a decision to perform a fasciotomy must be based on a high degree of suspicion.61,62 All too often attention is focused on the peripheral circulation, but compartment ischemia may be severe and still not affect color or temperature of the fingers, and distal pulses are rarely obliterated by compartment swelling; however, the circulation in the muscle and the nerve may be greatly reduced. Peripheral nerves will conduct impulses for 1 hour following ischemia and can survive for 4 hours with only neuropraxic damage. After 8 hours of total ischemia, irreversible nerve changes are complete. Ischemic skeletal muscle remains electrically responsive up to 3 hours following ischemia and may survive as long as 4 hours without irreversible damage, but at 8 hours complete irreversible damage has occurred.

Figure 39.41. Patient with compartment syndrome has marked swelling of the hand and skin blistering. Clinical signs may not always be as florid as this.

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The hallmark of muscle and nerve ischemia is pain. Pain is persistent, progressive, and unrelieved by immobilization. The pain is accentuated by passive muscle stretching, and this is the most reliable clinical test for making the diagnosis of compartment syndrome. The next most important clinical finding is diminished sensation, and this indicates ischemia of that nerve as it passes through the affected compartment.The third most important finding is weakness of the affected muscle. Finally, the closed compartments in the forearm and hand are palpated and are found to be tense and tender, confirming the diagnosis of compartment syndrome. When performing a passive muscle stretch test, the examiner needs to keep in mind that there are 3 separate compartments in the forearm and 10 compartments in the hand. The muscles in the volar compartment of the forearm include the flexors of the finger, thumb, and wrist, and these muscles are tested by passive extension of the fingers, thumb, and wrist. The dorsal forearm compartment includes the finger, thumb, and ulnar wrist extensors and the long thumb abductor, and this compartment is therefore tested by passive finger and thumb and wrist flexion. The intrinsic compartments of the hand are tested by passively abducting and adducting the fingers while the metacarpophalangeal joints are maintained at full extension and the PIP joints in flexion. The adductor compartment of the thumb is tested by simply pulling the thumb into palmar abduction, and the thenar muscles can be tested by radial abduction of the thumb and the hypothenar muscles by extending and adducting the little finger. Treated in the differential diagnosis of compartment syndrome are nerve injury and arterial injury. These diagnoses are differentiated as shown in Table 39.1. When the clinical diagnosis is difficult because, either through inebriation or unconsciousness, the patient cannot cooperate, compartment pressure can be measured. The Whitesides technique62 is simply performed by setting up an arterial line transducer system and connecting this to an 18-gauge needle. After the equipment is zeroed to atmospheric pressure, the needle is plunged into the compartment where pressure is to be measured. Such equipment is readily available in most acute care Table 39.1. Differential diagnoses of compartment syndrome as applied to nerve injury and arterial injury.

Pressure increased in the compartment Pain with stretch Paresthesia or anesthesia Paresis or paralysis Pulses intact +, Present; −, absent.

Compartment syndrome

Arterial occlusion

Neuropraxia

+

−

−

+ +

+ +

− +

+ +

+ −

+ +

A

B Figure 39.42. (A) A commercially available handheld device for measuring compartment pressure. (Courtesy of the Stryker Corporation.) (B) Tip of the indwelling slit catheter (enlarged).

settings in the intensive care unit, emergency room, and operating room. A commercially available intracompartment pressure monitoring system is made by the Stryker Corporation (Figure 39.42). This consists of a handheld monitor that is connected to a disposable indwelling slit catheter. The pressure threshold for fasciotomy remains controversial. However, Mubarak has recommended that fasciotomy be performed in patients with an intracompartment pressure greater than 30 mm Hg. Others have recommended that a pressure that is 20 mm Hg below diastolic should be the indicator. If compartment syndrome is suspected, external compressive dressings and splints should be fully released immediately. If pain and clinical signs persist, then a fasciotomy is done.60 Important principles with regard to performing a forearm fasciotomy are that damage to cutaneous nerves must be avoided; skin flaps are created to cover the median nerve at the wrist and flexor tendons in the distal forearm and the ulnar nerve at the elbow while awaiting secondary closure or skin grafting; the median or ulnar nerves can be released as they pass through the carpal tunnel and Guyon’s canal; the brachial artery may be explored in conjunction with compartment


Figure 39.43. Proposed incisions for performing forearm and hand fasciotomies.

release; and straight line incisions across the wrist and elbow joint must be avoided to reduce the risk of subsequent contracture formation. The palmar incision starts in the valley between the thenar and hypothenar muscles to release the carpal tunnel, and the incision then curves transversely across the flexion crease of the wrist to the ulnar border of the wrist (Figure 39.43). This incision thus avoids the palmar cutaneous branch of the median nerve and prevents flexion contracture across the wrist crease. It also provides an opportunity to release Guyon’s canal as well. The incision then extends at least 5 cm in length proximally up the forearm before curving back in a radial direction so as to have a large skin flap that will cover the median nerve and distal forearm tendons. At the elbow the apex of the flap must be just radial to the medial epicondyle, and this flap then prevents linear contracture across the antecubital fossa and provides a cover for the brachial artery and the median nerve when the wound is left open. The incision can then readily be extended proximally up the arm without difficulty following the course of the brachial artery as necessary. The dorsal and “mobile wad” compartments of the forearm are readily released through a straight incision as needed. When performing a forearm fasciotomy, the decompression should be carried out along the entire volar compartment and always decompresses the carpal tunnel and is carried up proximally to the forearm to at least where the lacertus fibrosus (the bicipital aponeurosis) is released. On the hand, the dorsal and volar interosseous muscle compartments and the adductor compartment to the thumb can be released through two parallel longitudinal incisions on the dorsum of the hand positioned over the second and fourth metacarpals. The thenar compartment and hypothenar compartments may be opened by longitudinal incisions along the radial side of the first metacarpal and the ulnar side of the fifth metacarpal, respectively. Fasciotomies to the digits are based on the degree of swelling present.

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Postoperative splinting in an appropriate “safe” position and conforming dressings are essential. The wrist is kept in comfortable dorsiflexion, and the thumb is held in palmar abduction. Elevation of an extremity in a nondecompressed compartment problem does decrease tissue perfusion; however, once fasciotomy has been performed, postoperative elevation is recommended to promote venous drainage and reduce swelling. Most of the wounds can be partially closed at 5 days. If the skin cannot be closed secondarily within 10 days, a splitthickness skin graft can be applied to prevent excessive granulation tissue and lessen exposure of muscles and tendons to resulting fibrosis and scarring. Skin closure should not be done over questionably necrotic tissue or with excessive skin tension.

Acute Upper Extremity Infections Kanavel63 clarified the anatomy of the hand as it related to infection and applied this knowledge to the principles of surgical drainage. He injected the various spaces of the hand with plaster of Paris to delineate the anatomic boundaries and then by slowly increasing the injection pressure determined the manner of extension of simulated infectious processes when the spatial boundaries were breached. A hand infection may involve skin, subcutaneous tissue, tendon sheaths, joints, bone, and the deep spaces of the hand and forearm.64 Acute infections are caused by a wide variety of pathogens but particularly the pyogenic bacteria and also on occasion by viruses.

Routes of Infection and Infecting Organisms Septic thrombophlebitis affecting the hand or upper extremity is a complication related to the presence of an indwelling venous catheter. Such infections are managed by catheter removal and antibiotic therapy. Intravenous abscess may occasionally develop, extending along the venous system with systemic bacterial seeding, septicemia, and even death. Delaying vein excision can result in significant morbidity and death. A variety of microorganisms have been cultured, including Streptococcus faecalis, Pseudomonas aeruginosa, Bacteroides fragilis, other staphylococcal and streptococcal species, Candida species, and Enterobacteriaceae. Toxic shock syndrome (TSS), a toxemia rather than a septicemia, has been reported following hand surgical procedures.64 Although TSS usually presents with a benign-appearing local wound infection, the systemic symptoms include a desquamating rash, fever, hypotension, and multiple organ failure. Most surgical cases of TSS are associated with Staphylococcus aureus toxin-1 (TSST-1). The presence is confirmed in the patient’s serum by a reverse passive latex agglutination test. A patient with TSS is transferred to intensive care

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monitoring. The wound is debrided, and any implants or drains are removed. The antibiotic choice is clindamycin, which is bacteriostatic and inhibits TSST-1 production. The herpetic whitlow is caused by type I or II herpes simplex virus and may be confused with paronychia.64 The infection begins with the appearance of small clear vesicles with localized swelling, erythema, and intense burning pain. The vesicles may appear turbid and then coalesce over the next 10 to 14 days before ulcerating. Tender lymphadenopathy and lymphangitis may be present. Diagnosis is confirmed by culturing the virus from the vesicular fluid, assessing immunofluorescent serum antibody titers, or performing a Tzanck smear. These measures are rarely required, because clinical diagnosis is usually sufficient. Treatment is nonoperative, because this infection is usually self-limiting. Vesicle unroofing for pain relief has been advocated. Antibiotic therapy and drainage may be indicated with bacterial superinfection. These infections occur particularly in patients whose fingers might be contaminated by oral flora, such as dental hygienists. Despite these less usual routes of infection, most portals of entry to the hand by infecting microorganisms are by direct penetration, and most sites are involved by direct inoculation or by contiguous spread into adjacent sites; however, gonococcal infection may be a rare cause of tenosynovitis or septic joint by hematogenous spread. Infections may thus affect fingertips, tendon sheaths, and deep spaces of the hand, joints, and bone. Approximately 65% of hand infections are caused by aerobic organisms, with S. aureus isolated in about 35% of infections, the most common organism. Other commonly found aerobic organisms are alpha-hemolytic streptococci and group A beta-hemolytic streptococci. Gram-negative bacilli are uncommon but may occur from contaminated wounds or from wounds in patients who are drug abusers or have an altered immune status. The most striking difference in the microbial flora of human and animal bite wounds is the higher number of mean isolates per wound in human bites, the difference being mostly because of the presence of anaerobic bacteria.65 Human bites can occasionally transmit other infectious diseases, such as hepatitis B, tuberculosis, syphilis, and actinomycosis. The incidence of Eikenella corrodens in human bite infections of the hand has been reported to vary between 7% and 29%. The most commonly isolated organisms from infected human bite wounds are, as in animal bites, alpha-hemolytic streptococci and S. aureus, beta-lactamase–producing strains of S. aureus, and Bacteroides species. Anaerobic bacteria are more prevalent in human bite infections than previously recognized and include Bacteroides, Clostridium, Fusobacterium, Peptococcus, and Veillonella species. Most studies of animal bite wounds are focused on the isolation of Pasteurella multocida, disregarding the role of anaerobes. Recent studies, however, of gingival canine


flora and of dog bite wounds point toward an oral flora of multiple organisms; Pasteurella multocida has been isolated from only 26% of dog bite wounds in adults. Most animal bites cause mixed infections of both aerobic and anaerobic bacteria. Cat-scratch disease may follow a bite or a scratch from a cat, dog, or monkey and is caused by a recently named motile Gram-negative bacterium, Afipia felis. The cutaneous lesion develops into a red nodule; chills, fever, malaise, and tender regional axillary lymphadenopathy follow. The organism can be identified in both the primary lesion and in the draining nodes by the WarthinStarry silver impregnation stain. A diagnostic skin test with a specific cat-scratch disease antigen is available. Cat-scratch disease has no specific treatment, but recovery is general complete in 2 to 5 months.

Anatomy of Hand Infections Any hand infection, even on the volar surface, will include dorsal swelling because of the looser fascia on the dorsum of the hand and the paucity of fascial septa to the skin combined with the fact that the hand’s lymphatic drainage runs palmar to dorsal. Dorsal swelling alone should not be mistaken for a dorsal hand infection. If a true dorsal infection is present, that aspect of the hand will be warm to the touch and painful to palpation. A hand infection may include signs of lymphatic spread and ascending lymphangitis. The three primary lymph drainage sites for the hand are the epitrochlear nodes for the ring and little fingers, the axillary nodes for the thumb and index finger, and the deltopectoral nodes for the middle finger. Figure 39.44 shows common sites of finger infections and depicts the route of spreading. Dorsal subcutaneous abscesses and peronychia occur commonly. A vesicle or pustule may be indicative of a felon beneath. Abscesses in the volar fat pad may point in a palmar direction or track to the dorsum before pointing; flexion creases often act as barriers to proximal or distal spread. An abscess in

D

A C B

E

Figure 39.44. Common sites of hand infections and routes of spread of infections. (A) Paronychia. (B) Felon. (C) Volar middle phalangeal pulp abscess. (D) Dorsal finger abscess. (E) Volar infection may spread dorsally, proximally in subcutaneous layers, or through the lumbrical canal to deep palmar spaces.


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the palmar (proximal) fat pad may spread either by tracking dorsally, passing the flexion crease barrier proximally, and entering the subcutaneous tissue of the palm or by the lumbrical canal to the deep palmar space. A collarbutton abscess is an advanced lesion that usually arises at the metacarpophalangeal joint with abscess cavities on both the palmar and dorsal aspects of the hand. Such advanced lesions are rarely seen today with modern antibiotics and early surgical treatment of septic foci.

Types of Infections Superficial Paronychial Infections Paronychia is the most common infection of the hand and usually results from trauma to the eponychial or paronychial region.66 Infection localizes around the nail base, advances around the nail fold, and burrows beneath the base of the nail. Swelling and erythema are present at the base of the nail and may extend up each paronychial side. If pus is trapped beneath the nail, pressure on the nail will evoke exquisite pain. Treatment incisions may not be necessary. A Freer elevator is used to lift approximately one fourth of the nail adjacent to the infected paronychium extending proximally to the edge of the nail. This portion of the nail is transected and gauze packing inserted beneath the nail fold. In runaround infections, an incision involving the junction of the eponychial fold with the paronychium may be required.

Infections at Intermediate Depths Infections at intermediate depths are pulp space infections (felons) and also deep web space infections.66 The former may involve the terminal pulp or the middle or proximal volar pulp spaces and may result from direct

implantation or may represent spread from a more superficial subcutaneous infection. The pulp of the distal digital segment is a fascial space closed proximally by a septum joining the distal flexion crease to the periosteum where the long flexor tendon is inserted. This space is also partitioned by fibrous septa. Tension in the distal digital segment can become so great that the arteries to the bone are compressed, resulting in gangrene and necrosis of the distal three fourths of the terminal phalanx. The base of the terminal phalanx receives its blood supply from vessels that do not traverse this dense tissue. Spread from a pulp space infection may move into a joint space, to the underlying bone, or burst through the septum proximally to involve the rest of the finger. With infection of the distal digital pulp space, one must not wait for fluctuance before making the decision for surgery because of the danger of ischemic necrosis of the skin and bone. Clinical diagnosis is made by rapid onset of throbbing pain, swelling, and exquisite tenderness of the affected pulp space. Surgical draining is required. The two preferred possible incisions are either a single volar longitudinal incision or a unilateral longitudinal incision. The longitudinal incision must not cross the DIP joint flexion crease. Web space abscesses result from either direct implantation or spread from a pulp space. A red and tender mass in the web space separates the fingers. Spread from this location may go proximally through the lumbrical canal to involve the deep spaces of the hand. Clinically there is loss of the normal palmar concavity with a widened space between the fingers. Dorsal swelling will be present, and it should not be mistaken for the infection site. A surgical incision is placed transversely across the web space. A counter longitudinal incision made be placed dorsally between the bases of the proximal phalanges, and generous communication is established between the two incisions (Figure 39.45).

A

D

D C

E B

C E

A

Figure 39.45. Surgical approaches to hand infections. (A) Web space (palmar and dorsal). (B) Midpalmar space. (C) Thenar space (palmar and dorsal). (D) Open drainage of finger (index).

(E) Through-and-through irrigation of tendon sheath (middle finger).

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Deep Infections Deep Palmar Space Infections Deep palmar space infections are localized to the deep spaces of the hand between the metacarpals and the palmar aponeurosis.67 A transverse septum to the metacarpal of the middle finger divides the deep space into an ulnar midpalmar space and a radial thenar space. The transverse head of the adductor pollicis partitions the thenar space from the retroadductor space. Ballooning of the palm, thenar eminence, and posterior aspect of the web between the thumb and index finger is characteristic depending on which of the affected spaces is involved. The dorsal subaponeurotic space of the hand deep to the extensor tendons may also be affected by isolated infection, generally as a result of direct implantation. Dorsal hand swelling is accompanied by erythema and tenderness. Appropriate surgical incisions are illustrated in Figure 39.45. For midpalmar space infections, a longitudinal curvilinear incision is the preferred approach. The preferred approach to surgical drainage of thenar space abscesses is a dual volar and dorsal incision. On the volar side the incision is made adjacent and parallel to the thenar crease. Great care is taken to avoid injury to the palmar cutaneous branch of the median nerve that is in the subcutaneous plane in the proximal part of the incision and to the motor branch of the median nerve that is in a deeper plane. The deeper dissection is carried bluntly toward the adductor pollicis and extended over the distal edge of the adductor. A second slightly curved longitudinal incision is made over the dorsum of the first web space. A Penrose drain is placed in each incision following thorough drainage of the respective spaces. A dorsal subaponeurotic space infection is sometimes difficult to differentiate from a simple cellulitis. A longitudinal incision is made directly over the abscess.67 Pyogenic Flexor Tenosynovitis Kanavel’s cardinal signs include the following: The finger is held flexed, as this position allows the synovial sheath its maximum volume and eases pain; symmetric swelling of the entire finger is present with edema of the back of the hand; the slightest attempt at passive extension of the affected digit produces exquisite pain; and the site of maximum tenderness is at the proximal cul-de-sac of the index, middle, and ring finger synovial sheaths in the distal palm or in the case of infection of the sheaths of the thumb and middle finger more proximally in the palm.The radial and ulnar bursae communicate in approximately 80% of cases and may simultaneously be infected. If they are both infected, the site of maximum tenderness is proximal to the flexor retinaculum at the wrist.Infections from the synovial spaces may spread into the deep palmar spaces by rupturing the proximal cul-de-sac in the palm. Bursal


infections may spread into the forearm space of Parona, deep to the flexor tendons in the distal part of the forearm, and create a horseshoe-shaped abscess. Pyogenic flexor tenosynovitis may be aborted with parenteral antibiotics, extremity elevation, and hand immobilization if the patient is seen within the first 24 to 48 hours of onset of infection. If the course is unsuccessful within 48 hours, or if the patient is seen more than 48 hours after onset of infection, surgical drainage must be undertaken. The preferred surgical approach is through two separate incisions.68 A midaxial incision is made in the finger, usually on the ulnar side (on the radial side of the thumb and little finger). The digital artery and nerve remain with the volar flap, and the dissection proceeds to the tendon sheath. The synovium between A3 and A4 pulleys is incised. Cloudy fluid is encountered. A second incision is made in the palm over the tendon to drain the cul-de-sac. A 16-guage polyethylene catheter is inserted beneath the A1 pulley into the sheath.The sheath is flushed manually with sterile saline every 2 hours. After surgery, a bulky hand dressing absorbs the drainage. Infections of the ulnar and radial bursae are the proximal extensions of the tendon sheath of, respectively, the flexor digitorum profundus of the little finger and the flexor pollicis longus of the thumb. Each may be opened and irrigated in a similar manner if involved.

Acute Fulminant Infections Necrotizing Fasciitis Necrotizing fasciitis is divided into two types based on bacteriology.69 Type I consists of a combination of anaerobic bacteria and facultative aerobic bacteria, such as the Enterobacteriaceae, Escherichia coli, Serratia marcescens, Klebsiella pneumoniae, and streptococci other than group A. Type II consists of cases in which group A streptococci are isolated alone or in combination with Staphylococcus aureus or Staphylococcus epidermidis. Vibrio vulnificus from seawater may also result in a rapidly progressing necrotizing fasciitis. Predisposing factors, especially to the polymicrobial form of necrotizing fasciitis, are diabetes mellitus, alcoholism, vascular disease, and intravenous drug abuse. Infection may first appear benign with a low-grade cellulitis; the progression is then rapid with development of moderate to severe pain. Lymphangitis is rare. Nonpitting edema, which can sometimes be massive, spreads beyond the erythematous area. Skin develops a patchy, dusky discoloration, and bullae are noted. Soft tissue crepitus is uncommon, but gas can often be demonstrated radiographically. Vascular thromboses in the subcutaneous plane result in skin necrosis. Infection dissects along fascial planes with necrosis of fascia and superficial fat. The fascia turns gray and liquefies, producing a watery exudate,“dishwater pus,” in the fascial plane. Only radical surgical debridement can control the infection. All


necrotic skin, fat, fascia, and muscle must be debrided, with fasciotomies extended well beyond the area of cellulitis, and even re-debridement performed within 24 hours should be considered. Clostridial Myonecrosis (Gas Gangrene) Clostridial myonecrosis is a rare anaerobic infection resulting from proliferation of Gram-positive rods. Gas gangrene infections may involve nonclostridial organisms. Exotoxins cause necrosis of muscle and subcutaneous tissue and in fact produce hydrogen sulfide and carbon monoxide and dissect along soft tissue planes. Early aggressive surgical debridement is essential, and intravenous penicillin is started immediately. The Gram stain reveals Gram-positive rods. Hyperbaric oxygen therapy is recommended as a treatment adjunct. Diabetic Gangrene Diabetic gangrene is usually seen in diabetic patients with peripheral vascular disease. Gram-negative and Grampositive infections occur. Prompt aggressive debridement is important with use of broad-spectrum antibiotics. Nondiabetic Gangrene Nondiabetic gangrene is caused by mixed anaerobic and nonanaerobic organisms. Myonecrosis and soft tissue gas may be similar to those of clostridial infection. Aeromonas hydrophila from freshwater contamination can cause gangrene indistinguishable from a clostridial infection. Aggressive debridement and intravenous antibiotics are required.

Critique Urgent intervention is needed for this upper extremity compartment syndrome. A complete fasciotomy is required, which necessitates opening three fascial compartments (volar, dorsal, and the mobile wad).The volar compartment encompasses the flexors of the wrist and fingers, along with the median and ulnar nerves. The posterior interosseous nerve and the extensors for the wrist and fingers are located in the dorsal compartment. The extensor carpi radialis longus and brevis, along with the brachioradialis, are found in the mobile wad. The incision for this fasciotomy starts proximal to the antecubital fossa and is extended distal to the midpalm, which will include releasing the carpal tunnel. The symptomatology and physical findings are too advanced for arm elevation. Also, a compartment syndrome can exist in the presence of palpable pulses. Answer (C)

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References 1. Green DP. General principles. In Green DP, Hotchkiss RN, Pederson WC, eds. Green’s Operative Hand Surg, 4th ed. New York: Churchill Livingstone, 1999; 1–21. 2. Ramamurthy S, Hickey R. Anesthesia. In Green DP, Hotchkiss RN, Pederson WC, eds. Green’s Operative Hand Surg, 4th ed. New York: Churchill Livingstone, 1999; 22–47. 3. Seiler JG. Anesthesia for hand surgery. In Essentials of Hand Surgery. Philadelphia: Lippincott Williams & Wilkins, 2002; 57–64. 4. Seiler JG. Casting and splinting. In Essentials of Hand Surgery. Philadelphia: Lippincott Williams & Wilkins, 2002; 57–64. 5. Seiler JG. Physical examination of the hand. In Essentials of Hand Surgery. Philadelphia: Lippincott Williams & Wilkins, 2002; 23–48. 6. Smith P. Injury. In Smith P, ed. Lister’s The Hand: Diagnosis and Indications. 4th ed. London: Churchill Livingstone, 2002; 1–140. 7. Seiler JG. Anatomy. In Essentials of Hand Surgery. Philadelphia: Lippincott Williams & Wilkins, 2002; 4– 22. 8. Metz VM, Wunderbaldinger P, Gilula LA. Update on imaging techniques of the wrist and hand. Clin Plast Surg 1996; 23:369–384. 9. Magid D, Thompson JS, Fishman EK. Computed tomography of the hand and wrist. Hand Clin 1991; 7:219–233. 10. Russell RC, Williamson DA, Sullivan JW, et al. Detection of foreign bodies in the hand. J Hand Surg 1991; 16A:2– 11. 11. Brown RE. Fingertip and nailbed injuries in hand surgery. In Light TR, ed. Update II: American Society for Surgery of the Hand. Rosemont, IL: American Academy of Orthopedic Surgeons, 1999; 257–261. 12. Atasoy E, Loakimidis E, Kasdan ML, et al. Reconstruction of the amputated fingertip with a triangular volar flap. J Bone Joint Surg 1970; 52A:921–926. 13. Foucher G, Khouri RK. Digital reconstruction with island flaps. Clin Plast Surg 1997; 24:1–32. 14. Atasoy E. Reversed cross-finger subcutaneous flap. J Hand Surg 1982; 7:481–483. 15. Germann G, Rutschler S, Kania N, Raff T. The reverse pedicle heterodigital cross-finger flap. J Hand Surg 1997; 22B:25–29. 16. Breidenbach WC. Emergency free tissue transfer for reconstruction of acute upper extremity wounds. Clin Plast Surg 1989; 16:505–514. 17. Lister GD, Pederson WC. Skin flaps. In Green DP, Hotchkiss RN, Pederson WC, eds. Green’s Operative Hand Surgery, 4th ed. New York: Churchill Livingstone, 1999; 1783. 18. Martin D, Dakhach J, Casoli V, Pellisier P, Ciria-Lorens G, Khouri RK, Beaudet J. Reconstruction of the hand with forearm island flaps. Clin Plast Surg 1997; 24:33–48. 19. Venkataswami R, Subramanian N. Oblique triangular flap: a new method of repair for oblique amputations of the fingertip and thumb. Plast Reconstr Surg 1980; 66:296– 300. 20. Brown DN, Upton J, Khouri RK. Free flap coverage of the hand. Clin Plast Surg 1997; 24:57–62.

654 21. Scheker LR, Netscher DT. Replantations and amputations of the upper extremity. In Kasdan ML, ed. Occupational Hand and Upper Extremity Injuries and Diseases. Philadelphia: Hanley & Belfus, 1991; 215–231. 22. Zhong-Wei C, Meyer VE, Kleinert HE, et al. Present indications and contraindications for replantation as reflected by long-term functional results. Orthop Clin North Am 1981; 12:849–870. 23. Strickland JW. Development of flexor tendon surgery: twenty-five years of progress. J Hand Surg 2000; 25A:215– 235. 24. Strickland JW. Flexor tendon injuries: II. Operative technique. J Am Acad Orthop Surg 1995; 3:55–62. 25. Lister GD, Kleinert HE, Kutz JE, Atasoy E. Primary flexor tendon repair followed by immediate controlled mobilization. J Hand Surg 1977; 2:441–451. 26. Gelberman RH, et al. Influences of the protected passive mobilization interval on flexor tendon healing. A prospective randomized clinical study. Clin Orthop 1991; 264:189– 196. 27. Hung LK, Chan A, Chang J, Tsang A, Leung PC. Early controlled active mobilization with dynamic splintage for treatment of extensor tendon injuries. J Hand Surg 1990; 15A:251–257. 28. Aulicino DL. Extensor tendon injuries. In Light TR, ed. Hand Surgery Update II: American Society for Surgery of the Hand. Rosemont, IL: American Academy of Orthopedic Surgeons, 1999; 149–158. 29. Netscher DT. Extensor tendon injuries. In Goldwyn R, Cohen M, eds. The Unfavorable Result in Plastic Surgery: Avoidance and Treatment, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2001; 751–770. 30. Brzezienski MA, Schneider LH. Extensor tendon injuries at the distal interphalangeal joint. Hand Clin 1995; 11:373–386. 31. Massengill JB. The boutonniere deformity. Hand Clin 1992; 8:787–801. 32. Sunderland S. The anatomic foundation of peripheral nerve repair techniques. Orthop Clin North Am 1981; 12:245–266. 33. Watchmaker GP, MacKinnon SE. Advances in peripheral nerve repair. Clin Plast Surg 1997; 24:63–73. 34. Jabaley ME, Wallace WH, Heckler FR. Internal topography of major nerves of the forearm and hand. J Hand Surg 1980; 5A:1–18. 35. Millesi H, Meissl G, Berger A. Interfascicular nerve grafting. Orthop Clin North Am 1981; 12:287–301. 36. Seiler JT. Fractures and dislocations of the metacarpals and phalanges. In Essentials of Hand Surgery. Philadelphia: Lippincott Williams & Wilkins, 2002; 91–113. 37. Stern PJ. Fractures of the metacarpals and phalanges. In Green DP, Hotchkiss RN, Pederson WC, ed. Green’s Operative Hand Surgery, 4th ed. New York: Churchill Livingstone, 1999; 711–771. 38. Blake ER, Hoffman J. Emergency department evaluation and treatment of the shoulder and humerus. Emerg Med Clin North Am 1999; 17:859–876. 39. Ring D, Jupiter JB. Fracture-dislocation of the elbow. Hand Clin 2002; 18:55–63. 40. Stabile KJ, Pfaeffle HJ, Tomaino MM. The Essex-Lopresti fracture-dislocation factors in early management and salvage alternatives. Hand Clin 2002; 18:195–204.

D.T. Netscher and I. Gharbaoui 41. Abboudi J, Kulp RW. Treating fractures of the distal radius with arthroscopic assistance. Orthop Clin North Am 2001; 32:307–315. 42. Amadio PC. Scaphoid fractures. Orthop Clin North Am 1992; 23:7–17. 43. Barton NJ. Twenty questions about scaphoid fractures. J Hand Surg 1992; 17B:289–310. 44. Kozin SH, Thoder JJ, Lieberman G. Operative treatment of metacarpal and phalangeal shaft fractures. J Am Acad Orthop Surg 2000; 8:111–121. 45. Stern PJ. Management of fractures of the hand over the last 25 years. J Hand Surg 2000; 25A:817–823. 46. Kiefhaver TR, Stern PJ. Fractures and dislocations of the proximal interphalangeal joint. J Hand Surg 1998; 23A: 368–380. 47. Koman LA, Ruch DS, Patterson-Smith B, et al. Vascular disorders. In Green DP, Hotchkiss RN, Pederson WC, eds. Green’s Operative Hand Surgery, 4th ed. New York: Churchill Livingstone, 1999; 2254–2302. 48. Koman LA, Smith BP, Pollock FE Jr, et al. The microcirculatory effects of peripheral synthectomy. J Hand Surg 1995; 20A:709–717. 49. Gelberman RH, Nunley JA, Koman LA, et al. The results of radial and ulnar arterial repair in the forearm. Experience in three medical centers. J Bone Joint Surg 1982; 64A:383–387. 50. Sumner DS. Noninvasive assessment of the upper extremity and hand ischemia. J Vasc Surg 1986; 3:560–564. 51. Lee KL, Miller JG, Laitung P. Hand ischemia following radial artery cannulation. J Hand Surg 1995; 20B:493–495. 52. Redfern AV, Zimmerman NB. Neurologic and ischemic complications of upper extremity vascular access for dialysis. J Hand Surg 1995; 20A:199–204. 53. Freidman J, Fabre J, Netscher D, et al. Treatment of acute neonatal vascular injuries: the utility of multiple interventions. J Pediatr Surg 1999; 34:940–945. 54. Wheatley MJ, Marx MP. The use of the intra-arterial urokinase in the management of hand ischemia secondary to palmar and digital arterial occlusion. Ann Plast Surg 1996; 37:356–363. 55. Christodoulou L, Melikyan EY, Woodbridge S, et al. Functional outcome of high-pressure injection injuries of the hand. J Trauma 2001; 50:717–720. 56. Schnall SB, Mirzayan R. High-pressure injection injuries to the hand. Hand Clin 1999; 15:245–248. 57. Vogel JE, Dellon AL. Frost bite injuries of the hand. Clin Plast Surg 1989; 16:565–576. 58. Bentivdena PE, Deane LM. Chemical burns of the upper extremity. Hand Clin 1990; 6:253–259. 59. Larson DL. What is the appropriate management of tissue extravasation by anti-tumor agents? Plast Reconstr Surg 1985; 75:397–405. 60. Gelberman RH, Zikaib GS, Mubarak SJ, et al. Decompression of forearm compartment syndromes. Clin Orthop 1978; 134:225–229. 61. Mubarak SJ, Hargens AR. Acute compartment syndromes. Surg Clin North Am 1983; 63:539–565. 62. Whitesides TE, Haney TC, Morimoto K, et al. Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop 1975; 113:43–51.

39. Hand and Upper Extremities 63. Kanavel AB. An anatomical, experimental, and clinical study of acute phlegmons of the hand. Surg Gynecol Obstet 1905; 1:221–260. 64. Ouellett EA. Infections. In Light TR, ed. Hand Surgery Update II: American Society for Surgery of the Hand. Rosemont, IL: American Academy of Orthopedic Surgeons, 1999; 411–421. 65. Mennen U, Howells CJ. Human fight-bite injuries to the hand: a study of 100 cases within 18 months. J Hand Surg 1991; 16A:431–435.

655 66. Jebson PJL. Infections of the fingertip: paronychias and felons. Hand Clin 1998; 14:547–555. 67. Jebson PJL. Deep subfascial space infections. Hand Clin 1998; 14:557–566. 68. Neviaser RJ. Closed tendon sheath irrigation for pyogenic flexor tenosynovitis. J Hand Surg 1978; 3:462– 466. 69. Gonzalez MH, Kay T, Weinzweig N, Brown A, et al. Necrotizing fasciitis of the upper extremity. J Hand Surg 1996; 21A:689–692.

40 Peripheral Vasculature David V. Feliciano

Case Scenario A high school cheerleader sustains a right supracondylar fracture (radiographic confirmation) after tripping and falling on her outstretched arm. There is evidence of a slight neurologic deficit and vascular insufficiency with diminished distal pulses. The patient has no other injuries and is hemodynamically stable. Which of the following is the most appropriate definitive management approach for the injury? (A) Immobilization of the elbow flexed to 90° (B) Immobilization of the elbow flexed at 45° (C) Traction of the forearm, with countertraction proximally (C) Open exploration and reduction (E) Traction applied to the hyperextended elbow

Upper Extremity Upper Extremity Highlights 1. At least 10% of arterial emboli from cardiac or proximal arterial sources occur in the upper extremities. 2. The rare patient with ischemia in the hand after removal of an arterial line should first receive an intraarterial infusion of a thrombolytic agent. 3. Recently occluded prosthetic grafts used for angioaccess should have the venous end opened to allow for thrombectomy and verification of patency of the arterial and venous anastomoses. 4. Actively bleeding injuries in the second portion of the axillary artery are best exposed by division of the tendon of the pectoralis minor muscle at the coracoid process.

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5. Extraanatomic bypass grafts are indicated when there is loss of soft tissue over an extensive arterial injury or when there is simultaneous infection in soft tissue and underlying artery or arterial repair. 6. The three musculofascial compartments of the forearm are the volar, dorsal, and “mobile wad.”

Embolic Occlusion of the Brachial Artery Although arterial emboli from a cardiac or proximal arterial source most commonly lodge at or below the bifurcation of the abdominal aorta, at least 10% occur in the upper extremities.

Diagnosis Arterial emboli from a cardiac source such as atrial fibrillation, atherosclerotic cardiac disease, or a cardiomyopathy may lodge in the proximal brachial artery at the origin of the profunda brachii (deep brachial) artery. Because of the extensive collateral flow to the forearm through the profunda brachii artery, there may be a delay in presentation of the patient if the embolus lodges distal to its origin. The patient will complain of paresthesias in the fingers and pain in the forearm. Physical examination will confirm pale fingers, the absence of palpable radial and ulnar pulses, and a brachial–brachial index less than 0.4 to 0.5. When the diagnosis is strongly suspected and there is no obvious contraindication (i.e., recent cerebrovascular accident), a bolus of intravenous heparin sodium at a dose of 10,000 U should be administered. As further workup proceeds, heparin is administered at 500 to 1,500 U/hr to maintain the partial thromboplastin time at 2 to 2.5 times normal. In thin patients with an acute presentation, it may be possible to localize the site of the embolic occlusion by careful palpation of brachial pulsations on the medial arm. When the patient has presented

40. Peripheral Vasculature

in a delayed fashion or the size of the arm precludes palpation of brachial pulsations, a diagnostic arteriogram is indicated to localize the embolus. This study can be helpful for all patients, however, to document a high bifurcation of the brachial artery and the presence of further clot at the origin of either the radial or the ulnar artery.

Treatment Because the operative approach is simple, direct thrombolytic therapy is not indicated. A preoperative partial thromboplastin time should be measured as the patient has been heparinized as noted above, and a dose of an intravenous cephalosporin antibiotic should be administered. Before operation, the patient is positioned with the trunk on the side of the occlusion at the very side edge of the operating table and the upper extremity abducted 90o on an armboard. Some surgeons choose to place a 2inch diameter rolled sheet longitudinally under the ipsilateral trunk and shoulder to further elevate the axilla for ease of proximal exposure, should this be needed. Skin preparation includes the ipsilateral neck, chest, axilla, and entire upper extremity to the fingertips. A sterile plastic bag can be used to cover the hand in light-skinned patients to allow for visualization of color changes after the embolectomy has been completed. Another option is to cover the hand, forearm, and distal arm in an orthopedic stockinette. A 7- to 8-cm longitudinal incision overlying the area of the embolus is made on the medial arm in the biceps–triceps groove, the deep fascia is incised over the neurovascular bundle, and its surrounding sheath is incised. It is often possible to expose the proximal brachial artery with only minimal dissection of the medially placed median nerve. The two brachial veins surrounding the artery will have to be dissected away before proximal and distal control of the brachial artery can be obtained with 360o vascular loops (Dev-O-Loops, The Ludlow Co., Chicopee, MA). The area of isolation is ideally at the site of the embolus where distal arterial pulsations disappear. A transverse arteriotomy is made at the site of occlusion using a No. 11 or 15 blade, and the embolus is extracted by manual compression of the now-collapsed arterial segment. A No. 4 balloon embolectomy catheter is then passed retrograde for 15 to 20 cm under proximal vascular control. The inflated balloon is withdrawn and, if no proximal embolus is retrieved after two passes, 10 to 15 mL of a solution of 50 U heparin/mL of saline is injected before the proximal vessel loop is tightened. A No. 3 balloon embolectomy catheter is then passed distally for 30 to 40 cm.To clear the orifices of both the radial and ulnar arteries distally, it is worthwhile to rotate the balloon catheter on second and third passes as it

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approaches the presumed or known site of the bifurcation of the brachial artery. Vigorous backbleeding without clot is reassuring, and 10 to 15 mL of heparinized saline solution is injected distally before the distal vessel loop is tightened. The arteriotomy is closed with interrupted sutures of 6–0 polypropylene. Proximal and distal flushing is completed before the last three sutures are tied down. The distal vessel loop is removed to allow for evacuation of intraluminal air as the last sutures are tied down. After removal of the proximal vessel loop, the return of palpable radial and ulnar pulses at the wrist obviates the need for a completion arteriogram. Postoperative screening to determine the source of the embolus is mandatory. The primary diagnostic test is transesophageal echocardiography, as 75% to 80% of peripheral emboli have a cardiac source (atrial or ventricular thrombus, subacute bacterial endocarditis, Libman-Sacks endocarditis, atrial myxoma, paradoxical embolus). Screening for a proximal source in the ascending or transverse thoracic aorta or proximal innominate or subclavian artery is accomplished using thoracic computed tomography (CT), CT arteriography, or a standard arch aortogram. Even when the source of the embolus cannot be detected by the screening methods listed, long-term anticoagulation with daily warfarin sodium is mandatory.

Arterial Thrombosis Secondary to a Monitoring Device Short- or long-term cannulation of either the radial or brachial artery is commonly used in critically ill patients. Before insertion of a cannula in either artery, it is appropriate to perform the modified Allen test described in 1966.1,2 Although the sensitivity of this test is not 100%, a positive result should preclude cannulation of the artery in question. Once an arterial cannula is inserted in any extremity, continuous or intermittent flushing with heparinized saline solution is routine and should lower the incidence of thrombosis. Unfortunately, partial or complete thrombosis, particularly after the insertion of a radial artery line, occurs in up to 20% to 30% of patients if the cannula is left in place for more than 3 days.3,4 Ischemic complications in the hand or fingers remain rare, however, in the absence of hypotension or need for drugs that cause vasoconstriction.5

Diagnosis The ipsilateral hand and fingers should be inspected on a regular basis by the surgical team and nursing personnel once an arterial cannula has been inserted in an intubated patient. Evaluation on an hourly basis as part of the assessment of vital signs is appropriate when the patient

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is septic, hypotensive, and/or being administered drugs that cause vasoconstriction. Should the fingers or hand become cool, blanched, or mottled, the cannula is removed immediately. Failure of the local circulation to improve is strongly suggestive that local thrombosis or distal embolization has occurred.

Treatment It has long been recognized that the three options for treatment of these patients include a cervicothoracic sympathetic block (stellate ganglion block) by an anesthesiologist, infusion of a thrombolytic agent, or a direct surgical approach. These can obviously be used in combination, but it is appropriate to obtain consultation from anesthesiology for the stellate ganglion block as a decision on a thrombolytic agent versus surgery is being considered. In most situations, definitive therapy is best accomplished using an intraarterial infusion of a thrombolytic agent such as urokinase or tissue plasminogen activator (tPA). With either agent the infusion catheter should be placed within the thrombus by the interventional radiologist and periodic arteriograms performed to assess the therapeutic response. With successful resolution of the thrombus, the catheter is removed when the fibrinogen level is more than 100 mg/dl.6 Failure of infusion of a thrombolytic agent or early rethrombosis after cessation of a thrombolytic agent and administration of an anticoagulant should prompt a surgical attempt at salvage if the fingers or hand remain ischemic after cannulation of the radial artery. After preparation of the arm and forearm in the operating room, a 2.5-cm longitudinal incision is made in the distal volar forearm directly over the radial artery. Once proximal and distal arterial control has been obtained with vessel loops, a transverse arteriotomy is performed. Local thrombus is extracted; a No. 3 Fogarty balloon catheter is then passed into the distal radial artery and deep palmar arch and retrieved in a gentle fashion. After the infusion of 10 to 15 mL of heparinized saline distally, the transverse arteriotomy is closed with interrupted 7–0 polypropylene sutures using the flushing sequence described previously. Early rethrombosis suggests the need for a segmental resection of the area of the radial artery injured by the catheter and insertion of a cephalic vein interposition graft. Postoperative infusion of a low dose of thrombolytic agent may be a useful adjunct.

D.V. Feliciano

anastomoses; (2) kinking or twisting of the prosthetic graft; (3) inadequate flushing of the graft before releasing vascular clamps; or (4) failure to recognize upstream venous narrowing or occlusion. After the administration of intravenous heparin at a dose of 1 mg/kg and a cephalosporin antibiotic, proximal and distal vascular control of the recipient vein and the prosthetic graft is obtained. The prosthetic graft proximal to the venous anastomosis is opened in a transverse manner. Retrograde passage of a No. 4 or 5 Fogarty balloon catheter should remove any thrombus, verify patency of the proximal (arterial) anastomosis, and rule out kinking or twisting of the prosthetic graft. Successful prograde passage of a No. 6 or 7 Fogarty balloon catheter should rule out narrowing of the distal (venous) anastomosis or upstream venous narrowing or occlusion. If there is still concern about the latter problem because of “catching” of the balloon catheter as it is withdrawn, an intraoperative venogram is performed through the graftotomy. A tapered infusion catheter is first inserted through the graftotomy and held in place by a tight vessel loop. Either a fluoroscopic image or a hard-copy upstream venogram is obtained after injecting 35 mL of a 60% iodine-based contrast agent. Upstream venous narrowing will mandate extension of the angioaccess graft above this point or an attempt at balloon dilatation. A marked narrowing in a more proximal vein will need to be treated by balloon dilatation and insertion of an endovascular stent in an interventional radiology suite. Infection of a prosthetic angioaccess graft may present as a false aneurysm along the body of the graft, erosion of the graft through the patient’s skin with or without hemorrhage, or pus draining from one or both anastomotic sites (Figure 40.1). As with other infected prostheses, the graft will almost always have to be removed to

Occlusion or Infection of an Angioaccess Graft Early occlusion of a prosthetic looped graft in the volar forearm or straight graft in the arm is caused by one of the following: (1) technical problems with one of the

Figure 40.1. Infected forearm prosthetic angioaccess graft with multiple pseudoaneurysms.


clear the infection. Also, removal of a thrombosed graft is significantly easier than one that is still patent. In the hands of the occasional angioaccess surgeon, it is best to obtain control of the brachial artery with a vessel loop proximal to the old arterial anastomosis before it is exposed. After the administration of 1 mg/kg of intravenous heparin, the proximal (arterial) anastomosis is exposed and the presence of infection verified. The proximal brachial artery is occluded, and a decision is reached on whether a 1.5 to 2.0 mm cuff of graft can be left to allow for easy closure of the arterial end with a continuous 6–0 polypropylene suture after removal of the remainder of the graft. The absence of pus at this location makes this an acceptable option, whereas the presence of pus around the proximal anastomosis would generally rule out this option. In the latter instance, complete removal of the arterial end of the graft will force the use of one of several unpleasant options. These would include primary closure of a rigid arteriotomy site, the insertion of a small cephalic vein patch as an arterioplasty, or segmental resection of the brachial artery with an end-to-end anastomosis. The same principles can be applied to the venous anastomotic site, although the risk of a postoperative blowout of the repair caused by residual infection is significantly less.

Traumatic Injuries to Arteries Injuries to the axillary, brachial, radial, or ulnar arteries account for approximately 45% to 52% of peripheral arterial injuries treated in civilian trauma centers.7,8 Because of its length and exposed position in the upper extremity, injuries to the brachial artery are 3 to 3.5 times more common than those to the axillary artery.

Diagnosis Traumatic occlusion or transection of the axillary or brachial artery without a subsequent repair does not always result in loss of the upper extremity because of the extensive collateral flow in this area. In DeBakey and Simeone’s review of 2,471 arterial injuries in American military personnel in World War II, injuries to the axillary artery (n = 74), most of which were treated by ligation, resulted in an amputation rate of 43.2%.9 In similar fashion, injuries to the brachial artery below the origin of the profunda brachii artery (n = 209) that were treated by ligation resulted in an amputation rate of 25.8%.9 Therefore, a major injury to the axillary or brachial artery may be more subtle than one to the superficial femoral artery; that is, a wavering pulse (intermittently palpable) or audible Doppler pulse may be present, even with a proximal occlusion or major injury. A patient with “hard” signs of an arterial injury (external hemorrhage, pulsatile hematoma, decrease in or loss

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of pulse and distal ischemic signs, or palpable thrill/ audible bruit) after a penetrating injury should be moved to the operating room immediately with few exceptions. Diagnostic studies as previously described are not indicated, although an on-table surgeon-performed preoperative retrograde or antegrade brachial arteriogram may help determine the extent of injuries after a shotgun wound from a distance. For the patient with “hard” signs of an arterial injury after blunt trauma, there is often a need to rule out life-threatening injuries to the brain, thorax, or abdomen using CT before moving the patient to the operating room. It is appropriate, however, to realign any displaced fracture with traction or a splint or to reduce any dislocated joint as soon as possible to see if distal pulses return. A patient with “soft” signs of an arterial injury (history of arterial bleeding, proximity of extremity injury to artery, nonpulsatile hematoma, or injury to adjacent nerve) needs further diagnostic evaluation. Diagnostic options include formal arteriography in an interventional radiology suite, surgeon-performed arteriography in the emergency center or operating room, or observation only. There are not enough data to justify the use of CT arteriography or magnetic resonance imaging (MRI) arteriography in evaluating possible peripheral vascular injuries at this time. The major disadvantage to formal arteriography in an interventional radiology suite is the associated time delay. Even during daylight hours, a minimum delay of 60 minutes is expected by the time the study is scheduled, the patient is transferred to the radiology suite, and the study is completed. When the delay is likely to be even longer, a surgeonperformed arteriogram in the emergency center is appropriate.10 Possible injuries to the proximal brachial and axillary arteries are evaluated by a retrograde brachial–axillary technique. An 18-gauge, 5.23-cm disposable catheter over needle is inserted into the distal brachial artery toward the shoulder by immobilizing the vessel against the humerus. A blood pressure cuff is then placed on the distal arm below the catheter in the brachial artery, and the arm is abducted to 90% and externally rotated. As the patient’s head is turned away from the side of the injection, the blood pressure cuff is inflated to 300 mm Hg, and 50 mL of 60% meglumine diatrizoate dye is rapidly injected.A properly performed retrograde one-shot arteriogram will visualize the ipsilateral brachial, axillary, subclavian, and carotid arteries (Figure 40.2). With a possible injury to the distal brachial artery, the catheter over needle is inserted into the proximal brachial artery toward the hand. The distal arteriogram is performed with the arm once again abducted on an armboard. When the “one-shot” hard-copy arteriogram does not clearly visualize the area in question, a repeat injection can be performed depending on the patient’s renal status.

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Figure 40.2. Retrograde brachial-axillary-subclavian arteriogram performed in the emergency center.

Treatment When an arteriogram documents an abnormality in the wall of the vessel (intimal flap or irregularity, subintimal hematoma, spasm, or small pseudoaneurysm) but intact flow to the hand, there are three options. These include continued observation (“nonoperative management”) with a repeated arteriogram in 3 to 7 days; insertion of an endovascular stent or stent graft; or operation. Nonoperative management is 87% to 95% successful when chosen for the appropriate lesions listed earlier.11,12 If the patient refuses a follow-up arteriogram, careful education regarding acute and chronic signs of arterial occlusion is imperative. Also, the patient should have scheduled follow-up visits to the office or clinic for the next 2 months to detect signs of ischemia, expansion of a pseudoaneurysm, or delayed development of an arteriovenous fistula. Endovascular stenting is rarely considered for modest injuries to the axillary, brachial, or forearm arteries, as operation is so easily performed and does not usually threaten the life of even the multiplyinjured patient. Operation, of course, is difficult to justify when there is not a significant pseudoaneurysm or arteriovenous fistula, and pulses at the wrist are still present despite a proximal arteriographic abnormality. For the patient who presents with hard signs of an injury to the axillary or brachial artery, immediate operation is indicated as previously mentioned. Because

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occlusion of the radial or ulnar artery leads to loss of the hand only 1% to 5% of the time, this particular lesion may be treated nonoperatively. In the operating room, skin preparation includes the entire anterior and lateral neck and chest and entire upper extremity to the fingertips as previously described. One lower extremity from the umbilicus to the toenails should be prepped, as well, to allow for retrieval of the greater saphenous vein from the groin or ankle area. It is helpful to cover the entire upper extremity in an orthopedic stockinette and place it at the side of the patient if an injury to the first or second portion of the axillary artery is suspected. This will allow more room for the operating team as well as relax the muscles around the shoulder girdle as dissection proceeds. With a suspected injury to the third portion of the axillary artery, the upper extremity is abducted at 90o and placed on an armboard. The axillary artery starts at the lateral border of the first rib and becomes the brachial artery at the lateral border of the teres major muscle.12 The operative approach varies depending on whether the arterial injury is located in the first portion (lateral border of the first rib to medial border of the pectoralis minor muscle), second portion (behind the pectoralis minor muscle), or third portion (lateral border of the pectoralis minor muscle to lateral border of teres major muscle). Injuries to the first or second portions that are not actively hemorrhaging are most commonly approached through an infraclavicular incision centered on the midclavicle.14 After splitting the upper fibers of the pectoralis major muscle in a transverse fashion, the clavipectoral fascia is divided. Proximal arterial control is obtained by retracting the anteriorly positioned axillary vein in an inferior fashion and placing a vessel loop around the axillary artery just inferior to the clavicle. Distal control is obtained, as needed, by extending the infraclavicular incision into an incision in the deltopectoral groove (Figure 40.3). Should active hemorrhage from the second portion of the artery occur during dissection or the tamponaded injury is in the second portion, lateral retraction of the tendon of the pectoralis minor tendon is necessary. Persistent inadequate exposure of this arterial location mandates division of the tendon of the pectoralis minor muscle near the coracoid process to preserve the medial pectoral nerve. An injury in the third portion can be approached through the aforementioned incision in the deltopectoral groove. An alternate, but uncommonly utilized, approach involves a lateral pectoral incision along the edge of the pectoralis major muscle. Injuries to the axillary artery, particularly those that are bleeding actively, are challenging because of the adjacent cords of the brachial plexus. The blind application of angled vascular clamps often entraps portions of the cords, leading to a partial brachial plexopathy for 12 to 24 months. Therefore, elevation of the injured artery


Figure 40.3. Standard incision for exposure of entire axillary and proximal brachial arteries.

proximally and distally with vessel loops is mandatory before vascular clamps are applied. The second problem in dealing with injuries at this location is the somewhat fragile nature of the axillary artery. This artery is rarely involved with significant atherosclerosis and is extraordinarily soft with a consistency that sometimes approaches that of the subclavian artery. Lateral repairs performed with suture bites that are too thin or end-to-end repairs performed under tension will lead to sutures tearing through when vascular clamps are released. The brachial artery starts at the lateral border of the teres major muscle, courses through the medial arm, and bifurcates at the radial tuberosity of the forearm. The operative approach in the arm has been described previously. When an injury occurs near the elbow, the standard S-shaped incision extending from the medial biceps–triceps groove is used. This incision crosses the antecubital fossa and then turns longitudinally beyond the midaspect of the volar side of the forearm. The fascia overlying the neurovascular bundle medially and the bicipital aponeurosis beneath the antecubital fossa are divided to allow for complete exposure of the brachial artery proximal to its bifurcation. There is a logical sequence for performing a complex repair (end-to-end anastomosis or insertion of a graft) of the axillary or brachial artery after proximal and distal arterial control has been obtained with vessel loops. When an end-to-end anastomosis is to be performed, a posterior knot is usually placed at 6 o’clock. If exposure is limited, as in an end-to-end anastomosis performed near the clavicle, it is helpful to perform the first one third of the posterior anastomosis in an open fashion (no pos-

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terior knot) in both directions to allow for complete visualization of all suture bites.15 After this portion of the anastomosis is complete, the ends of the artery are pushed together as both sutures are pulled tight. Because both ends of the artery are now stabilized, a No. 5 or 6 Fogarty embolectomy catheter is passed proximally and distally to remove any thrombolic or embolic material. Approximately 10 to 15 mL of heparinized saline solution (50 U/mL of solution) is then injected into each end of the artery, and the vascular clamps are reapplied. The remaining two thirds of the anastomosis is completed by running one end of the continuous suture along one side and the other end along the other side. The last few loops of suture, however, are left loose to allow for flushing before the anterior knot is tied. The proximal vascular clamp is removed for flushing and then reapplied. The distal vascular clamp is removed to allow for flushing, as well. As air is evacuated by the distal flushing, the two suture ends are pulled up tight and tied. Once the first knot has been tied, the proximal arterial clamp is released. Bleeding from suture holes is controlled by the application of oxidized regenerated cellulose (Surgicel, Johnson & Johnson Medical, Inc., Arlington, TX) or Avitene (Med Chem Products, Inc., Woburn, MA). Because distal in situ thrombosis is very unusual during proximal arterial repairs in the upper extremity, the return of palpable pulses at the ipsilateral wrist obviates the need for a completion arteriogram. When distal pulsations are diminished or absent after removal of the vascular clamps, a completion arteriogram is mandatory. When an interposition graft will be necessary to restore arterial continuity in the upper extremity, a reversed autogenous saphenous vein graft from the thigh of an uninjured lower extremity is the first choice. In the 15% to 20% of young male patients with saphenous veins that are too small for replacement of a major vessel such as the axillary artery, a ringed polytetrafluoroethylene synthetic graft is an acceptable alternative. The operative technique for each anastomosis may be as described above, or a more traditional approach may be used. The triangulation approach described by Carrel16 involves placing stay sutures at 120o intervals on the circumference of the graft and on the recipient vessel. After these are tied and the ends of the graft and recipient vessel are in apposition, each 120o segment of the anastomosis may be readily approximated by a continuous suture technique. A related approach that is pertinent to the use of a rigid polytetrafluoroethylene interposition graft is to place only two stay sutures 180o apart to appose the ends of the graft and recipient vessel. When an interposition graft has been inserted, the terminal flushing maneuvers and evacuation of air are performed as described previously as the second anastomosis is completed.

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When an interposition graft has been inserted to complete an arterial repair in the upper extremity, it is the practice of the author to place all adult patients on an intravenous drip of 10% dextran 40 in 5% dextrose (10% Gentran 40, Baxter Healthcare Corp., Deerfield, IL) at a dose of 40 mL/hr × 3 days. This agent can prevent or reverse cellular aggregation and will prolong the bleeding time. In addition, adult patients are started on 81-gr aspirin tablets once a day by rectal suppository or orally starting in the recovery room and maintained on this medication for the next 3 months.17 There are two other innovative operative techniques that may be helpful in trauma and infection problems involving the arteries of the upper extremity. The first is the use of extraanatomic bypass grafting. The indications for this technique include (1) loss of soft tissue over injured artery or vein; (2) postoperative wound infection with blowout of underlying arterial repair; or (3) simultaneous infections in soft tissue and underlying artery secondary to injection of illicit drugs.18 In each of these situations, the arterial bypass graft is placed in a separate subcutaneous tunnel from the area of missing or infected soft tissue. The operative technique involves longitudinal extension of the operative incision or soft tissue defect to expose healthy proximal and distal artery. The extensions are usually 4 to 6 cm long to allow for transection of the healthy portion of the proximal artery followed by the performance of an end-to-end anastomosis to a reversed saphenous vein graft from an uninjured lower extremity. The proximal graft is then tunneled at an angle away from the soft tissue defect or infection through healthy soft tissue. The anastomosis of the extraanatomic bypass graft to distal healthy artery is once again performed beyond the soft tissue defect or infection. As a final step, both proximal and distal anastomoses and the ends of the extraanatomic bypass graft are covered by suture closure of the healthy soft tissue at the previously described extensions (Figure 40.4). The other innovative operative technique is the use of temporary intraluminal shunts in arteries and/or veins of both the upper and lower extremities. The indications for this technique include (1) Gustilo IIIC combined orthopedic-vascular injuries, including mangled extremities or near amputations; (2) preservation of an amputated upper extremity at the arm, forearm, or wrist level before replantation; or (3) rapid restoration of arterial inflow or venous outflow, or both, as part of a peripheral vascular damage-control operation in the patient near death.19 With the Gustilo IIIC fractures or partial/complete amputations of the upper extremity, the first operative priority is insertion of a temporary intraarterial plastic shunt by the general/trauma/vascular surgeon. This allows for appropriate orthopedic stabilization, reconstruction, or debridement before formal revascularization with interposition grafts. Of course, definitive repair

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Figure 40.4. Infected pseudoaneurysm of the distal right brachial and proximal radial and ulnar arteries underlying severe cellulitis was replaced by an extraanatomic saphenous vein bypass graft from the distal brachial artery (end-to-end) to the midulnar artery (end-to-side). The path of the graft is marked on the skin. (Reprinted from Feliciano DV. Heroic procedures in vascular injury managment. The role of extraanatomic bypasses. Surg Clin North Am 2002; 82:115–124, with permission from Elsevier.)

with such grafts may be performed at a second operation depending on the patient’s other injuries and metabolic state. For patients with prehospital near-exsanguination and a need for a damage-control operation, the rapid insertion of a temporary intraarterial plastic shunt preserves the injured extremity in the patient with “metabolic failure” from hemorrhage. Such patients have a body temperature less than 35°C, an arterial base deficit less than −10 to −15, and/or an intraoperative coagulopathy.20 A prolonged arterial repair under these circumstances will endanger the patient’s life, and damage-control principles mandate a short first operation to control hemorrhage and restore arterial inflow (or venous outflow). The operative technique involves obtaining proximal and distal control around the injured portion of the artery (or vein). After debridement of the injured section, a Fogarty balloon catheter is passed into the proximal and distal artery. The usual injection of 10 to 15 mL of heparinized saline (50 U/mL) into each end is deferred for coagulopathic patients. The largest plastic shunt that will fit into both ends of the transected artery is chosen. The most commonly utilized shunt is an Argyle Carotid Artery Shunt (Sherwood Medical, St. Louis, MO) ranging in size from 8 to 14 Fr. A hemostat is placed at the midaspect of the shunt, and the shunt is inserted into the proximal artery for 8 to 10 mm. A 2–0 silk tie is tightened down near the end of the artery to hold the shunt in place. The hemostat is removed to verify flow through the shunt and then reapplied. The distal end of the shunt is then inserted into the distal end of the artery for 8 to 10 mm


and fixed in place with another 2–0 silk tie, and the hemostat is removed to restore arterial flow. With larger intraluminal shunts and adequate venous outflow from the upper extremity, anticoagulation will not be necessary. After orthopedic procedures have been completed or when the patient undergoing damage-control shunting has been stabilized in the intensive care unit, the shunts can be removed. Before removal, however, an assessment is made of the distance between the two ends of the shunted artery. As the injured artery has already been debrided and further debridement at the sites of the 2–0 silk sutures will be necessary, most patients will require insertion of a saphenous vein interposition graft. The graft is retrieved from the thigh of an uninjured lower extremity in the usual fashion. A decision on anticoagulation is made depending on the extent of the patient’s injuries and current coagulation tests. In the absence of injuries to the brain, intraabdominal solid organs, or soft tissues of the injured extremity, a 1 mg/kg loading dose of intravenous heparin is administered before the ends of the artery around the intraluminal shunt are clamped. The 2–0 silk sutures are cut, the crushed ends of the artery are removed, a Fogarty balloon catheter is passed proximally and distally, and the saphenous vein interposition graft is sewn in place as described earlier.

Traumatic Injuries to Veins Diagnosis Injuries to veins in the upper extremities are infrequently discussed. Diagnostic tests such as venograms are not employed to document the presence of a peripheral venous injury as the consequences of missing such an injury are so modest; that is, pressure dressings usually control venous hemorrhage from small injuries, and late venous pseudoaneurysms are extraordinarily rare. The only indications for operation are venous bleeding not controlled by a pressure dressing or the suspected or known presence of an associated arterial injury.

Treatment The incisions previously described for arterial injuries in the upper extremities are the same ones used for possible venous injuries. Proximal and distal control around a major venous injury, however, can be awkward because of multiple venous branches. As the venous system is characterized by low pressure, the use of small, medium, and large metal clips for ligation followed by division of venous branches is appropriate as exposure and control are obtained. Proximal and distal control around an area of injury can usually be maintained with use of vessel loops under tension rather than with angled vascular clamps.

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Because of the presence of valves in the venous system, injection of heparinized saline toward the hand after distal venous control has been obtained is not performed. For the same reason, passage of a Fogarty balloon catheter toward the hand or toward the heart is inappropriate. Essentially all major injuries to the brachial or axillary venae comitantes or veins can be ligated as there are extensive venous collaterals throughout the upper extremity. On rare occasions in stable patients with an isolated major injury to the axillary vein, resection and an end-to-end anastomosis or insertion of a saphenous vein interposition graft has been performed. Lateral venorrhaphies for lesser injuries are performed with interrupted or continuous sutures of 7–0 polypropylene. With a meticulous suture technique, peripheral venous repairs (most studied in the lower extremities) have been documented to have short-term patencies exceeding 75% in several reports.21,22

Compartment Syndromes and Fasciotomies Diagnosis A compartment syndrome is defined as increased pressure within a closed fascial space that reduces capillary perfusion to a level less than that required for the viability of tissues.23 Most compartment syndromes result from an increase in content of the compartment as caused by edema or hemorrhage or, on rare occasions, by chronic overexertion of muscles. Trauma and/or ischemia to the extremity remain the most common causes. A history of a delay in presentation when ischemia in an extremity is present should make the attending physician suspicious that a compartment syndrome is present or is likely to develop. The patient will often complain of pain out of proportion to the extent of an injury, as well. General findings on physical examination that increase the likelihood of a compartment syndrome occurring include systemic shock in combination with an ischemic extremity, evidence of a crush injury, and marked swelling of the extremity. The presence of a tender or tight musculofascial compartment does not, however, precisely correlate with the presence of a compartment syndrome. Rather, pain on passive stretch of muscles in the compartment is strongly suggestive. Other neurologic findings that often suggest the presence of an established compartment syndrome include hypesthesia in the sensory distribution of a nerve that courses through the compartment in question or weakness of the involved muscles. Finally, restoration of arterial inflow after a greater than 4- to 6-hour delay, the need to clamp arterial inflow and venous outflow vessels at the time of vascular repair, and ligation of a major outflow vein are procedures at operation that make a compartment

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syndrome more likely to develop. Also, it is important to note that distal pulses in an extremity are often still palpable or audible by a Doppler device after a revascularization procedure even though a compartment syndrome is present. One approach in vascular or trauma surgery services has been to perform a fasciotomy to relieve a suspected compartment syndrome whenever any of the historical, physical, or operative factors described earlier are present. An aggressive approach such as this will avoid missing a compartment syndrome, but will surely result in some unnecessary or “prophylactic” fasciotomies. Another approach is to measure the intracompartmental pressure (normal, 4 to 8 mm Hg) and only perform fasciotomy when a certain elevated pressure has been reached. A large number of techniques for measurement of intracompartmental pressure have been described. including (1) needle injection, (2) wick catheter, (3) slit catheter, (4) arterial transducer, and (5) the STIC device (Solid-State Transducer IntraCompartmental Monitor System, Stryker Surgical, Kalamazoo, MI).23–25 Unfortunately, there is little consensus in the literature about the absolute intracompartmental pressure that mandates a fasciotomy to avoid permanent muscular or neural damage. A rising pressure more than 30 mm Hg,24,26 a pressure more than 45 mm Hg23 or a less than 20 mm,27 or a 30 mm Hg28 difference between diastolic blood pressure and the intracompartmental pressure have all been suggested over the past 25 years. In a somewhat ecumenical approach, the American College of Surgeons Committee on Trauma poster entitled “Management of Peripheral Vascular Trauma” (2002) suggests that fasciotomy be performed for pressures “>30–35 mm Hg.”29

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and flexor carpi ulnaris muscles is divided from the aponeurosis of the elbow down to the carpal tunnel at the wrist (decompression of superficial flexor compartment). These two muscles are separated with retractors, the ulnar nerve and artery are identified overlying the flexor digitorum profundus, and the fascia overlying this muscle and the flexor pollicis longus is divided as well (decompression of deep flexor compartment). After complete decompression of the volar compartment, it is worthwhile to remeasure the intracompartmental pressure in the dorsal (extensor) and mobile wad compartments. Should these pressures still be elevated, the dorsal compartment is approached through a skin incision in the pronated forearm from the lateral epicondyle of the humerus to the midline of the wrist. The fasciotomy is performed in the interval between the extensor digitorum communis and extensor carpi radialis brevis muscles toward the radial side of the forearm. The role of epimysiotomy of decompressed muscles is unclear, and a carpal tunnel release at the wrist is often added if the wrist and hand are swollen. Any pale forearm muscle that still contracts with stimulation from the electrocautery device should be left in place at the first operation. The entire forearm is then covered with a bulky dressing and elevated by attaching a forearm stockinette to an intravenous pole. After 3 to 7 days of elevation in patients with obviously viable forearm muscles, the patient is returned to the operating room. Closure of the skin incision is best accomplished by undermining the subcutaneous tissues and placing multiple interrupted vertical mattress skin-only sutures of 2–0 nylon. When the tension is too great to complete the skin closure with sutures, a split-thickness skin graft harvested from the anterolateral thigh is applied.

Treatment Fasciotomies to relieve compartment syndromes in the upper extremities account for only 20% of all fasciotomies performed after trauma and even less after nontrauma vascular occlusions.Therefore, many surgeons are not familiar with the operative techniques that are utilized. The forearm is divided into three musculofascial compartments, including volar, dorsal, and the “mobile wad.”27 Other authors describe superficial flexor, deep flexor, and extensor compartments.24 The volar compartment (flexion, pronation, supination) is opened first using the “ulnar approach.” The incision begins on the lateral (radial side) of the forearm distal to the antecubital fossa, proceeds transversely across the forearm parallel to the arm–forearm fold, and then makes a right angle turn down the ulnar volar aspect of the forearm. At the wrist, the ulnar incision curves toward the radial side until it crosses the carpal tunnel along the thenar crease of the palm. The fascia overlying the flexor digitorum sublimis

Lower Extremity Lower Extremity Highlights 1. Catheterization injuries to the femoral artery include retroperitoneal and intraperitoneal hemorrhage, acute thrombosis, and acute pulsatile hematomas in the groin. 2. Approximately 45% of arterial emboli from cardiac or proximal arterial sources lodge at the bifurcation of the common femoral artery. 3. Failure of a transfemoral balloon catheter embolectomy is usually the result of simultaneous embolism to the popliteal or trifurcation vessels or to atherosclerotic disease locally or at Hunter’s canal. 4. An infected femoral artery pseudoaneurysm in the drug addict must be completely excised; fortunately, the need for revascularization is uncommon.


5. Embolic occlusion of the “trifurcation” vessels mandates below-knee exposure of the anterior tibial, posterior tibial, and peroneal arteries, which usually requires division of the anterior tibial vein. 6. Temporary intraluminal plastic arterial (and venous) shunts in the extremities are indicated for patients with Gustilo IIIC combined orthopedic–vascular injuries or as part of peripheral vascular damage control for patients with near exsanguination. 7. A below-knee two-incision four-compartment fasciotomy is advised when the measured intracompartmental pressure is more than 30 to 35 mm Hg.

Catheterization Injuries of the Femoral Artery Diagnosis Catheterization of the common femoral artery is generally utilized for truncal or peripheral angiography or angioplasty, cardiac catheterization, coronary angioplasty or insertion of stents, and insertion of intraaortic balloons. Complications that occur include intraperitoneal and retroperitoneal hemorrhage, thrombosis of the common femoral or external iliac artery, and the development of a pseudoaneurysm or arteriovenous fistula in the groin.30,31 In one review, the need for surgical intervention ranged from 0.6% after diagnostic cardiac catheterization to 11.5% after insertion of an intraaortic balloon.30 Intraperitoneal hemorrhage from perforation of the distal external iliac artery will often lead to an initial episode of hypotension during the catheterization procedure. Changes on the cardiac monitor suggestive of ischemia are usually absent at this point. After a response to the infusion of fluids, hypotension will recur, and the catheterization procedure may have to be terminated. The general or vascular surgeon notified at this point should confirm the diagnosis by physical examination of the abdomen supplemented by a surgeon-performed ultrasound. Using a 3.5 MHz probe (3.5 × 106 cycles/sec), the presence of anechoic (black) fluid in Morison’s pouch, the splenorenal area, or the pelvis on the abdominopelvic ultrasound confirms the diagnosis of intraabdominal hemorrhage. The patient with retroperitoneal hemorrhage may develop hypotension hours after the catheterization procedure has been completed. The hypotension that develops will usually respond to the infusion of fluids, and emergency laboratory studies will confirm new-onset anemia. An abdominopelvic CT is often performed before the surgeon is called if the patient is reasonably stable. A CT performed with intravenous

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contrast that does not demonstrate extravasation into the distal retroperitoneum suggests that the injury has been tamponaded by surrounding clot. Extravasation of contrast into the retroperitoneal hematoma confirms continued bleeding and mandates operation if coagulation studies are normal. Acute thrombosis of the common femoral or external iliac artery secondary to dissection during the catheterization procedure or compression of the arterial entrance site at the completion of the procedure will cause immediate symptoms. The patient will complain of pain or numbness in the ipsilateral foot. The femoral artery pulse in the groin may be diminished or absent along with popliteal and pedal pulses. A temperature change in the skin will be present in the distal thigh and below. In the absence of preexisting symptoms, such as ipsilateral decreased pedal pulses, claudication, rest pain, or distal arterial ulcers, the diagnosis of thrombosis secondary to the catheterization procedure is most likely. A palpable pulsatile mass that develops in the groin after a catheterization procedure is an acute pulsatile hematoma. Such lesions are commonly, but incorrectly, described as “pseudoaneurysms.” The diagnosis is made on physical examination and confirmed with a surgeonperformed ultrasound using a 7.5 MHz linear probe. The rare arteriovenous fistula that develops after a catheterization procedure is detected by the presence of a palpable thrill/audible bruit on physical examination. The diagnosis is confirmed using duplex ultrasonography, a combination of real-time B-mode imaging and pulsedwave Doppler, or color duplex imaging (“triple imaging”) in a vascular laboratory.

Treatment The operative approach to intraperitoneal or retroperitoneal hemorrhage from a catheterization injury may vary according to the training of the surgeon. A general surgeon consulted for such a patient may feel more comfortable approaching a distal injury to the external iliac artery through a lower midline laparotomy. This is especially true with hypotensive or obese patients or with those who have had previous surgery in the same groin.32 After evacuation of intraperitoneal blood, the small bowel is eviscerated to the right and the sigmoid colon to the left. In the profoundly hypotensive patient, the midline retroperitoneum is opened and a DeBakey aortic clamp is used to cross-clamp the infrarenal abdominal aorta. As the patient is resuscitated, the distal retroperitoneum 2 to 3 inches proximal to the inguinal ligament is opened over the external iliac vessels as they come out of the pelvis. The external iliac artery is encircled with a vessel loop that allows for the vessel to be pulled proximally and elevated away from the adjacent external iliac vein. Further sharp dissection directly on the artery

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should demonstrate the area of perforation, which is then oversewn with interrupted 6–0 polypropylene sutures. Should the distal external iliac artery not be injured, the adjacent vein is dissected toward the inguinal ligament. A vessel loop that encircles the external iliac vein will increase hemorrhage from a more distal perforation and should be avoided. Other general or vascular surgeons will approach presumed distal injuries to the external iliac artery (or vein) by dividing several centimeters of the inguinal ligament over the vessels. Another approach is to perform release of the inguinal ligament.33 When the vascular injury is approached through the groin, a small Cooley C-shaped vascular clamp may be used to obtain proximal arterial control in the retroperitoneum. A vascular clamp applied to the common femoral vein in the groin may cause a modest decrease in hemorrhage from the distal external iliac vein as dissection proceeds superiorly to the area of the perforation. Acute thrombosis of the common femoral or external iliac artery is approached through a longitudinal incision overlying the femoral vessels in the groin. The longitudinal incision allows for complete exposure of the distal external iliac artery by partial division of the inguinal ligament. Also, as many patients undergoing catheterization of the femoral artery have underlying atherosclerosis, complete dissection of the origins of the superficial femoral and profunda femoris arteries can be accomplished as well. After the administration of a 1-mg/kg loading dose of intravenous heparin and with vessel loops placed around the distal external iliac artery or the proximal common femoral artery, the superficial femoral artery, and the profunda femoris artery, an angled vascular clamp is applied to the external iliac or common femoral artery. Distal control on the branch vessels can often be accomplished by placing the vessel loops on traction. A 12-mm longitudinal arteriotomy is made over the site where the arterial pulse was noted to disappear prior to placing the proximal vascular clamp. After 6–0 polypropylene stay sutures are placed on either side of the arteriotomy to enhance exposure, local thrombus is manually extracted. The lumen is washed clean with heparinized saline solution and inspected carefully for size, presence of an elevated plaque, or an injury to the posterior wall. When none of these is present, a No. 5 to No. 7 Fogarty embolectomy catheter is passed retrograde through the arteriotomy under manual or vessel loop control for a distance of 10 to 15 cm. The balloon on the catheter is inflated to the listed size using a tuberculin syringe and withdrawn gently. When two consecutive passes of the balloon catheter proximally yield no thrombus and free flow of pulsatile arterial blood is noted, 10 to 15 mL of heparinized saline (50 U/mL) are injected before the proximal arterial clamp is reapplied. The vessel loops on the superficial femoral and profunda femoris arteries are released one at a time to confirm that

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vigorous backbleeding is present. If this does not occur, No. 3 to No. 5 Fogarty embolectomy catheters are passed distally as described above. Should severe local atherosclerosis be present when the arteriotomy is first made and the thrombus has been extracted, an endarterectomy through the media of the common femoral artery may be necessary. The arteriotomy is then closed with a saphenous vein or thin-walled polytetrafluoroethylene patch angioplasty. For the past 10 to 15 years, ultrasound-guided compression of postcatheterization “pseudoaneurysms” in the groin has been the standard of care.34 In general, 15minute periods of compression are followed by ultrasound examination using a 7.5 MHz linear probe of the pseudoaneurysm to confirm thrombosis of the extraluminal blood. The technique is successful because of the small perforations that standard catheterizations create. In most patients, an acute arteriovenous fistula in the common or superficial femoral artery is approached through the longitudinal groin incision described above. Proximal and distal arterial control is obtained using vascular clamps or vessel loops. The area of adherence is separated, a finger is used to control hemorrhage from the small venotomy, and the arterial and venous perforations are closed with interrupted 6–0 polypropylene sutures.

Embolic or Thrombotic Occlusion of the Femoral Artery Diagnosis In patients with peripheral arterial emboli originating from atrial fibrillation, atherosclerotic cardiac disease, cardiomyopathy, or proximal atherosclerosis (rare), approximately 45% lodge at the bifurcation of the common femoral artery.35 The sudden signs of acute femoral artery embolic occlusion are well known and have been described previously for patients with catheterization-induced thrombosis of the common femoral artery. In the absence of atrial fibrillation, atherosclerotic cardiac disease, or a cardiomyopathy, an acute thrombotic occlusion of the common femoral artery may be present. As noted previously, this is more likely to be present when there is a history of ipsilateral decreased pedal pulses, claudication, rest pain, or distal arterial ulcers.

Treatment Some elderly patients will present in a delayed fashion after an embolism to or thrombosis of the femoral artery and have advanced ischemic changes of the foot or leg. Such changes include a cold insensate foot or leg without movement or even early manifestations of gangrene. As


resuscitation is initiated, it is important to measure serum potassium, creatinine, arterial blood gases, and urine myogloblin in these patients even if revascularization is not planned. The presence of hyperkalemia, an elevated creatinine level, metabolic acidosis, and myoglobinuria are strongly suggestive of rhabdomyolysis.36 Although an early amputation would theoretically correct these metabolic problems, they already increase the risk of any type of anesthesia in the elderly patient. The hyperkalemia and metabolic acidosis are treated in the standard fashion, and a Swan-Ganz catheter is used to direct needed fluid resuscitation to correct the elevated creatinine level and clear myoglobin from the urine. In addition, the urine is alkalinized by the administration of intravenous bicarbonate. When the patient’s hyperkalemia and acidosis are corrected and clearing of urine is noted, the patient is taken to the operating room. The level of amputation, the management of the stump, and the need for a femoral embolectomy or thrombectomy to aid healing of the stump are based on the patient’s condition and on the local physical findings at the time of amputation. There are patients in whom the viability of the extremity is unclear at the time of presentation or even after resuscitation. In some there may be a concern that a compartment syndrome secondary to prolonged ischemia followed by vigorous resuscitation may be compromising the physical examination of the leg and foot. It is appropriate for such patients to initiate the operative procedure with a short incision in the position of a normal below-knee anterior/peroneal compartment fasciotomy at the mid-leg (to be described). A 3- to 4-inch fasciotomy over the anterior compartment of the leg will allow for confirmation of dead versus viable muscle that bulges through the incision. Amputation followed by an embolectomy or thrombectomy in the common femoral artery is appropriate in the first instance. With bulging viable muscle, a below-knee four-compartment fasciotomy (to be described) is performed followed by the embolectomy or thrombectomy. Based on the paper by Blaisdell et al.37 in 1978, some surgeons choose to treat patients with a viable extremity and a period of ischemia in the lower extremity exceeding 10 to 12 hours with high-dose heparin rather than an acute care embolectomy or thrombectomy. The 20,000 units of heparin recommended as an initial bolus is followed by a continuous infusion of 2,000 to 4,000 units per hour.37 The preferred approach for other patients with acute embolic occlusion of the common femoral artery is to administer a 10,000-unit intravenous bolus of heparin as the patient is prepared for an acute care operation. When thrombotic occlusion is strongly suspected, an abdominal aortogram with bilateral femoral arterial runoff studies is often performed before heparin is administered. After a

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partial thromboplastin time is checked and a dose of an intravenous cephalosporin antibiotic is administered, a longitudinal incision is made over the common femoral artery. Once the common femoral, superficial femoral, and profunda femoris arteries have been encircled with vessel loops, the common femoral artery is clamped and traction or bulldog vascular clamps are applied to the branch vessels. A transverse arteriotomy just proximal to the bifurcation is made in patients with a probable diagnosis of embolic occlusion. If the common femoral artery has an extensive amount of plaque on palpation and the history is supportive of thrombotic occlusion, some surgeons choose to make a longitudinal arteriotomy just proximal to the bifurcation. The embolus is extracted from the common femoral artery by manual compression of the now-collapsed arterial segment. Much as with embolic occlusion of the proximal brachial artery, a No. 4 or No. 5 balloon embolectomy catheter is passed retrograde for 15 to 20 cm under proximal vascular control. If no proximal embolus is retrieved after two passes, 10 to 15 mL of a solution of 50 units of heparin/mL of saline is injected. A No. 4 balloon embolectomy catheter is then passed distally for its entire length down the superficial femoral artery. Very gentle traction is placed on the inflated balloon as it is withdrawn, and the balloon is partially deflated each time resistance is encountered. This is necessary to avoid stripping diseased intima from such a commonly diseased artery in adults. It is unlikely that all infrapopliteal “trifurcation” vessels will be cleared of embolic material, if present, by distal passage of a balloon catheter from the common femoral artery. In one study performed in cadavers, embolectomy catheters passed from the groin entered the peroneal artery in 90% of instances.38 After the injection of 10 to 15 mL of heparinized saline into the superficial femoral artery, a No. 3 balloon embolectomy catheter is passed for 15 cm into the profunda femoris artery. It may be useful to dissect out the first bifurcation of this vessel if extensive embolic material is present to allow for passage of the catheter into separate branches. Once again, great care is taken not to disrupt atherosclerotic plaque as the balloon catheter is withdrawn from this often fragile vessel. After the injection of heparinized saline, the common femoral arteriotomy is closed with interrupted 6–0 polypropylene sutures and terminal flushing as previously described. As a completion arteriogram is mandatory after embolectomies performed in the lower extremity, one option is to pass a 20-gauge short plastic catheter over metal needle through the last gap in the arteriotomy site before the final one or two 6–0 polypropylene sutures are placed. A completion femoropopliteal–tibioperoneal arteriogram can be performed by injecting 35 mL of 60% meglumine diatrizoate dye and counting “1,000, 2,000,” up to “5,000” before the hard-copy x-ray film is shot. The x-ray cassette

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patients with infected limbs of aortobifemoral bypass grafts. Others occur in drug addicts who have inadvertently injected contaminated material into the wall of an artery adjacent to the intended vein. The “traumatic infected pseudoaneurysm” that results can present as a pulsatile mass in the groin or as an arterial hemorrhage from the apex of the mass.39 In the former instance, a surgeon-performed ultrasound using a 7.5 MHz linear probe will confirm the presence of a fluid-filled cavity outside the common femoral artery. When bleeding is present, a presumptive diagnosis is made based on the patient’s history of self-administered needle injections into vessels in the groin.

Treatment

Figure 40.5. An intraoperative transfemoral postembolectomy arteriogram-documented spasm in the distal popliteal artery as the cause of diminished pedal pulses.

is placed to encompass the distal superficial femoral artery, popliteal artery, and the proximal one third to one half of the shank vessels (Figure 40.5). Another approach is to visualize the same area using fluoroscopic imaging. The management of thrombotic occlusion of the common femoral artery is somewhat beyond the focus of this chapter. After removal of local thrombus, attempted passage of a balloon catheter will document whether proximal, local, and/or distal atherosclerotic narrowing or occlusive disease is present. Therapeutic options vary depending on the location and extent of disease. They include local endarterectomy/patch angioplasty, insertion of a crossover femorofemoral bypass graft, or, on occasion, the insertion of an aortobifemoral bypass graft. When associated occlusion of the superficial femoral artery at Hunter’s canal is present, an acute care femoropopliteal bypass may have to be performed.

Ruptured Femoral Artery Pseudoaneurysm Secondary to Inadvertent Injection of Illicit Drugs Diagnosis There are few peripheral vascular surgical emergencies more dramatic than the rupture of an infected femoral artery pseudoaneurysm. These may occur rarely in

For the bleeding patient, immediate pressure is applied as standard resuscitation is performed. Aspiration of the infected pseudoaneurysm with a small needle at another site will allow for appropriate culture and sensitivity studies. Once hemorrhage has stopped, a bulky pressure dressing similar to that used after arteriograms performed through the common femoral artery is applied. Intravenous antibiotics, particularly those with antistaphylococcal coverage, are started immediately. The presence of methicillin-resistant Staphylococcus aureus in community-acquired infections is now well documented and should be considered when choosing an antibiotic. After 18 to 24 hours of intravenous antibiotics, the patient is taken to the operating room for complete excision of all infected segments of the femoral artery. When a large infected pseudoaneurysm of the common femoral artery is present, proximal arterial control is obtained via a lower abdominal quadrant extraperitoneal approach (to be described). Also, the longitudinal groin incision may have to be extended distally in order to allow for complete excision of infection in the proximal superficial femoral artery. All infected arterial segments are excised, including the proximal profunda femoris artery, if necessary. The arterial ends are suture ligated with polypropylene suture, covered with a transposition muscle flap if soft tissue coverage is inadequate, and the remainder of the infected area is packed open.40 It is common knowledge in public hospitals that a surprising number of patients with excision of the common femoral artery and its bifurcation vessels continue to have a viable lower extremity. This has been confirmed in a large published series.41 A lower extremity that is ischemic preoperatively or in the early postoperative period will have to be revascularized. One option is the insertion of an extraanatomic prosthetic graft from the ipsilateral external iliac artery through the obturator foramen to a segment of the superficial femoral artery distal to the infected cavity in the groin.42,43 Another is


the insertion of an interposition autogenous superficial femoral vein graft retrieved from the contralateral thigh.44

Embolic Occlusion of the Popliteal “Trifurcation” Vessels Diagnosis In patients with arterial emboli in the lower extremity originating from the previously described sources, transfemoral embolectomy may fail to reestablish blood flow to the foot. One reason may be associated atherosclerotic disease in the superficial femoral artery at Hunter’s canal that is noted on a completion arteriogram. Another may be an embolus to the popliteal artery or to the “trifurcation” vessels of the shank, the particular focus of this section.

Treatment The appearance of an embolus in the popliteal artery on a postfemoral embolectomy arteriogram mandates reopening of this vessel. Repeated distal passage of the No. 4 balloon embolectomy catheter is performed until the embolus is retrieved. Failure of retrieval suggests that a chronic thrombus or underlying atherosclerosis is present. One option is to perform a distal medial thigh incision along the anterior border of the sartorius muscle. After the fascia is incised, the sartorius muscle is retracted posteriorly and the vastus medialis muscle anteriorly. The popliteal vessels are exposed, and chronic disease is confirmed by palpation. If a softer segment of popliteal artery can be palpated beyond this point, a popliteal-shank intraoperative arteriogram can be performed. This will allow for proper selection of a site for distal anastomosis of a salvage femoropopliteal or femorotibial bypass graft. Should the completion arteriogram document likely embolic occlusion of two or more “trifurcation” vessels, a local embolectomy is indicated. An 8-cm longitudinal incision beginning at the posterior edge of the condyle of the tibia is made in the medial infrapopliteal area, approximately 1 cm below the posterior edge of the tibia. It is imperative to avoid injury to the greater saphenous vein, which usually lies posterior to the incision described. After the fascia is incised posterior to the edge of the tibia and inferior to the overlying tendons of the sartorius, gracilis, and semitendinosus muscles, the medial head of the gastrocnemius muscle is retracted posteriorly. To obtain appropriate exposure in large patients, the electrocautery may be used to separate the medial attachments of the soleus muscle to the tibia as well. A proper “trifurcation” embolectomy mandates the placing of vessel loops around the distal popliteal, anterior tibial,

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posterior tibial, and peroneal arteries. This dissection is somewhat tedious, especially if there is associated atherosclerosis at this location. Proper exposure of all vessels will usually involve careful ligation and division of the anterior tibial vein and separation of the posterior tibial and peroneal arteries from their associated veins. Once complete exposure and arterial control have been obtained, a 1-mg/kg loading dose of intravenous heparin is administered. The direction of incision in the distal popliteal artery is the surgeon’s choice. Using both hands, a No. 3 balloon embolectomy catheter is first directed down the oblique course of the anterior tibial artery to the ankle. If no distal embolus is retrieved after two passes, 10 to 15 mL of a solution of 50 U heparin/mL of saline is injected before tightening the loop on this vessel is tightened. Subsequent passes of the balloon embolectomy catheter down the posterior tibial and peroneal arteries are performed, as well, followed by the injection of regional heparinized saline as described. A diseased distal popliteal artery at the site of the arteriotomy is managed with a small vein patch angioplasty using a continuous 6–0 or 7–0 polypropylene suture. Once again, a completion arteriogram is appropriate to confirm the restoration of arterial inflow to the foot.

Traumatic Injuries to Arteries Injuries to the femoral, popliteal, or shank arteries account for approximately 48% to 55% of peripheral arterial injuries treated in civilian trauma centers.7,8 Because of its length and exposed position in the lower extremity, injuries to the common or superficial femoral artery are 2 to 2.5 times more common than those to the popliteal and shank arteries.

Diagnosis Traumatic occlusion or transection of the common or superficial femoral or the popliteal artery without a subsequent repair results in a much higher loss of the lower extremity as compared to analogous injuries in the upper extremity as previously described. The lack of collateral vessels in otherwise healthy young injured patients mandates early diagnosis and treatment for the main “end” arteries listed. In DeBakey and Simeone’s review9 of 2,471 arterial injuries in American military personnel in World War II, injuries to the common femoral or superficial arteries, most of which were treated by ligation, resulted in amputation rates of 81.1% and 54.8%, respectively. In similar fashion, injuries to the popliteal artery treated by ligation resulted in an amputation rate of 72.5%.9 Much as with arterial injuries in the upper extremity, patients with injuries in the lower extremity are separated into those with “hard” or “soft” signs of an arterial injury. Once again, the only patient with hard signs who may

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benefit from an on-table surgeon-performed preoperative femoral arteriogram is one with a shotgun wound and pellets covering a wide area of the thigh. For the patient with soft signs and likely delays before a formal arteriogram can be performed, a surgeon-performed femoral arteriogram in the emergency center is appropriate if the surgeon is uncomfortable with observation.10 The 18-gauge, 5.23-cm disposable catheter over needle is inserted into the common femoral artery toward the head just inferior to the inguinal ligament. To evaluate the common or superficial femoral artery, 25 to 30 mL of 60% meglumine diatrizoate dye is injected rapidly. As the injection is completed, a one-shot hard-copy arteriogram or a fluoroscopic image is obtained of the common and superficial femoral arteries.10 Excellent images of the popliteal and shank arteries can be obtained by injecting 35 mL of contrast, counting “1,000, 2,000, 3,000, 4,000, 5000,” and then performing the one-shot exposure or the fluoroscopy.10 When the area of the vessel in question is not visualized, the timing of a second shot or fluoroscopic image is adjusted, as needed.

Treatment Arterial wall abnormalities documented on formal or surgeon-performed arteriograms associated with intact pedal pulses are managed with observation, insertion of an endovascular stent or stent graft, or operation. Much as with such limited injuries documented in the major arteries of the upper extremity, careful follow-up of nonoperated patients is necessary to document progression rather than healing of the lesion. Skin preparation of patients with hard signs should extend from the nipples to the toenails bilaterally and encompass the entire circumference of both lower extremities. Once again, a sterile plastic bag can be used to cover the foot of light-skinned patients. Another option is to cover the foot, leg, and thigh in an orthopedic stockinette. Injuries to the common femoral, proximal superficial femoral, or profunda femoris arteries are approached through the previously described longitudinal groin incision inferior to the inguinal ligament. An injury right at the inguinal ligament or the presence of a large pulsatile hematoma overlying the groin and inguinal ligament will mandate obtaining more proximal arterial control. An ipsilateral oblique anterior flank incision is made 3 cm above the inguinal ligament. Successive muscle and aponeurotic layers including the transversus abdominis muscle and transversalis fascia laterally are divided. The peritoneum is pushed medially using spongesticks to enter the retroperitoneal space and expose the psoas muscle. After the ureter is elevated with the peritoneum, the external iliac artery is encircled with a vessel loop and clamped for proximal arterial control.

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Once proximal and distal control has been obtained around arterial injuries in the groin, certain principles should be kept in mind. One is that the profunda femoris artery should not be sacrificed for reasons of exposure. Even if an end-to-end anastomosis or insertion of an interposition graft into the common femoral artery has been necessary, it is not difficult to reimplant the end of the profunda femoris artery into this reconstructed segment. This involves rotating the vascular clamps on the common femoral artery 90o toward the midline. A small posterolateral arteriotomy in the common femoral artery or graft replacement will then allow for an end-toside anastomosis to the profunda femoris artery using 6–0 polypropylene suture. Another principle is that the greater saphenous vein from an uninjured thigh remains the interposition arterial conduit of choice. Therefore, one should always avoid the temptation to retrieve the adjacent greater saphenous vein as an interposition conduit to replace an injured common or superficial femoral artery in the groin or thigh. This is inappropriate, especially in a patient with an associated injury to the ipsilateral common or superficial femoral vein that may thrombose after even a meticulous repair. Two of the operative techniques mentioned previously have particular applicability with arterial injuries in the lower extremities. An extraanatomic bypass graft should always be considered when a close-range shotgun blast causes an extensive arterial injury associated with a large defect in soft tissue of the groin or thigh. Because such a wound will require extensive debridement and repeated open packing for weeks, any arterial repair with a saphenous vein graft should be routed well around the defect through healthy soft tissue. Also, the use of a temporary intraarterial luminal shunt should always be considered in near-exsanguinated patients with the sequelae of shock (Figure 40.6). This approach obviates the need for a deci-

Figure 40.6. A 14-F “carotid artery” shunt in the popliteal artery and a 24-F thoracostomy tube shunt in the popliteal vein in a railroad worker with a crush injury to the distal thigh.


sion on life versus limb as it allows for salvage of both in properly selected patients. Injuries to arteries below the groin are approached through longitudinal incisions as well. The superficial femoral artery in the proximal three fourths of the thigh lies posterior to the inferior edge of the sartorius muscle. With anterior mobilization of this muscle and division of the surrounding sheath, the superficial femoral artery (and vein) are easily exposed. In the distal one fourth of the thigh, exposure of the proximal popliteal artery involves mobilizing the sartorius muscle posteriorly and the vastus medialis muscle anteriorly. Occasionally, the adductor magnus tendon comprising the edge of the adductor hiatus may have to be divided as well.45 The entire popliteal artery system is exposed by extending the medial distal thigh incision into an incision 1 cm posterior to the edge of the tibia. The tendons of the sartorius, gracilis, and semitendinosus muscles will often require division 1 to 2 cm away from their insertions on the tibia for complete exposure. Each tendon should be divided between two colored sutures, with different colors used for each of the three tendons. This will allow for accurate reapproximation of the tendons following the arterial repair. The principles of arterial repair are the same in the lower extremity as previously described for the upper extremity (Figure 40.7). In medical centers that care for large numbers of penetrating arterial wounds in the lower extremities, only one third can be repaired with simple lateral sutures. Over two thirds will require segmental resection, and the majority of these (55% to 60%) will have an interposition graft inserted.46

Figure 40.7. Fine points in peripheral arterial repair include use of small vascular clamps or Silastic vessel loops, open anastomosis technique, regional heparinization, passage of a Fogarty catheter proximally and distally, and arteriography on completion. (Courtesy of Baylor College of Medicine, Houston, Texas, ©1981.)

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One area in which the repair of arteries in the lower extremity differs from that in the upper extremity is in the management of extensive distal injuries. Although loss or ligation of the radial or ulnar artery will rarely result in loss of the hand, the loss of two shank arteries from an extensive blunt injury will often lead to a belowor above-knee amputation. Certain patients with these injuries have true mangled extremities and will be served best by an immediate amputation. Others will have disruption or thrombosis of the tibioperoneal trunk or of the anterior tibial artery and one of the branches of the tibioperoneal trunk. The combination of a crushing or shearing injury and loss of two main arteries will often leave one or more muscle compartments of the leg and/or the foot ischemic. In such patients innovative bypasses originating in the distal popliteal artery and crossing over a fracture site may be necessary to restore adequate arterial flow to the leg and foot.

Traumatic Injuries to Veins Diagnosis As with venous injuries in the upper extremities, the only indications for operation are venous bleeding not controlled by a pressure dressing or the suspected or known presence of an arterial injury.

Treatment Venous injuries in the lower extremities are approached through the usual longitudinal incisions and managed as previously described. The one unique aspect of management is the much stronger emphasis on repair rather than ligation. The popliteal vein and superficial femoral vein inferior to its junction with the profunda femoris vein are true end veins draining the leg. Ligation of either of these veins has some theoretical disadvantages. There is always the concern that a below-knee compartment syndrome will develop in the early postoperative period, that there will be an acute adverse impact on arterial inflow into the shank, and that chronic edema of the leg will occur.46–50 Several civilian series have documented that venous ligation in the popliteal and superficial femoral veins is surprisingly well-tolerated in young trauma patients.46–49 This is particularly true if absolute bed rest and elevation of the injured lower extremity for the first 5 to 7 days after ligation are mandatory.50 There is not a clear-cut increase in the need for postligation fasciotomy, amputations are rare, and edema of the leg often resolves over time.46–49 This is in marked contrast to the 50% edema reported after ligation of the popliteal vein during the Vietnam War.51 Nonetheless, in the absence of near exsanguination and sequelae of shock such as severe hypothermia, profound metabolic acidosis, and an intraoperative coagulopathy,

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Figure 40.8. A 10-mm ringed polytetrafluoroethylene graft in the distal superficial femoral vein.

the superficial femoral and popliteal veins should be repaired. Options for repair include lateral venorrhaphy with 6–0 polypropylene suture, vein patch venoplasty using the greater saphenous vein from the contralateral ankle, or insertion of an autogenous saphenous vein graft or externally supported polytetrafluoroethylene graft (Figure 40.8)22,46–49,52,53 Because of the time needed to make spiral and panel vein grafts and the mixed patency rates reported, these are rarely performed in American trauma centers.53,54 When damage-control venous surgery is necessary because of near exsanguination, thoracostomy tubes in sizes of No. 20 to No. 24 French are used as intraluminal shunts. These large tubes fit the veins of the thigh and groin and rarely thrombose in the absence of postoperative hypotension. After any type of complex venous repair in the lower extremity, it is the practice of the author to wrap the entire lower extremity with an elastic bandage at modest tension to avoid causing a compartment syndrome. The lower extremity is elevated on three to four pillows for 5 to 7 days, and strict bed rest is mandatory as previously described. Dextran 40 is administered intravenously at 40 mL/hr × 3 days, and an 81-gr aspirin tablet is administered once a day by rectal suppository or orally starting in the recovery room. The aspirin is continued for 3 months. A duplex venous study is performed before discharge.

Compartment Syndromes and Fasciotomies Diagnosis Palpation of the muscle compartments of the leg is very inaccurate in diagnosing a compartment syndrome. Therefore, compartment pressures are measured using one of the devices previously described. Because the anterior compartment of the leg is prone to developing a

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compartment syndrome in high-risk patients, the pressure is always measured first in this compartment. If the pressures in this compartment and in the deep posterior compartment immediately posterior to the tibia are greater than 30 to35 mm Hg, a below-knee two-incision four-compartment fasciotomy is performed. A compartment syndrome of the thigh is uncommon, but it has occurred in patients with severe pelvic fractures, ligation of the common or external iliac vein or common femoral vein, or, on rare occasions, with severe fractures of the femur. This entity will be present in many patients with the secondary extremity compartment syndrome following resuscitation from near exsanguination as well.55 A compartment pressure greater than 30 to 35 mm Hg in either the anterior or posterior compartment is an indication to perform a thigh two-incision three-compartment fasciotomy.

Treatment The leg is divided into four musculofascial compartments, including anterior, peroneal, superficial posterior, and deep posterior. The anterior and peroneal compartments are approached through a 25- to 30-cm longitudinal incision 2 cm anterior to the upper edge of the fibula. The subcutaneous tissue and skin of both flaps are mobilized using traction with rake retractors and manual pressure with a laparotomy pad over fingers. Perforating vessels are divided and ligated with 3–0 silk ties to eliminate postoperative oozing in coagulopathic patients. When the intermuscular septum is clearly visualized or palpated, separate longitudinal fasciotomies approximately 4 cm apart are made over the entire anterior and peroneal compartments. The superficial and deep posterior compartments are approached through a 25- to 30-cm longitudinal incision 2 cm posterior to the lower edge of the tibia. Care should be taken to avoid injury to the greater saphenous vein and nerve. The subcutaneous tissue and skin of both flaps are mobilized as above. The superficial posterior compartment is visualized by further traction on the posterior skin flap and opened over its entire length with a longitudinal incision. The deep posterior compartment may often be visualized in the distal aspect of the calf through the standard skin incision. Complete decompression of this musculofascial compartment posterior to the tibia and medial to the fibula will, however, require detachment of the soleus muscle from the back of the tibia.56 The thigh is divided into three musculofascial compartments, including the quadriceps (anterior), hamstrings (posterior), and adductors (medial). The quadriceps compartment is approached through a 30-cm longitudinal anterolateral incision along the iliotibial tract from the intertrochanteric space to the lateral epicondyle of the distal femur. A longitudinal fasciotomy is


made, and the fascia can be lifted off the rectus femoris muscle anteriorly as well. Access to the hamstrings compartment is obtained by mobilizing the vastus lateralis muscle anteriorly. The thick intermuscular septum medial to this muscle is then opened with a longitudinal incision to decompress the hamstrings compartment. If pressure in the adductor compartment is still elevated after the other two compartments of the thigh have been opened, the adductor compartment is approached through a 30cm medial and longitudinal skin incision posterior to the sartorius muscle. After minimal mobilization of the skin and subcutaneous flaps, a longitudinal fasciotomy incision is made over the adductor muscles.

Critique A supracondylar fracture with an associated neurologic deficit or vascular insufficiency dictates an open reduction that will allow exploration of the involved structures. Traction applied to the hyperextended elbow is contraindicated, for such a maneuver could cause further compression and injury of the neurovascular structure. Unfortunately, this injury could lead to a Volkmann’s ischemic contracture. Answer (D)

References 1. Allen EV. Thromboangiitis obliterans: methods of diagnosis of chronic occlusive arterial lesions distal to the wrist with illustrative cases.Am J Medical Sci 1929; 1–78:234–244. 2. Ejrup B, Fischer B, Wright IS. Clinical evaluation of blood flow to the hand: the false-positive Allen test. Circulation 1966; 33:778–780. 3. Gardner RM, Schwartz R, Wong HC, et al. Percutaneous indwelling radial-artery catheters for monitoring cardiovascular function. Prospective study of the risk of thrombosis and infection. N Engl J Med 1974; 290:1227–1231. 4. Bedford RF. Long-term radial artery cannulation: effects on subsequent vessel function. Crit Care Med 1978; 6:64–67. 5. Johnson FE, Sumner DS, Strandness DE Jr. Extremity necrosis caused by indwelling arterial catheters. Am J Surg 1976; 131:375–379. 6. Comerota AJ, Malone MD. Simplified approach to thrombolytic therapy of arterial and graft occlusion. In Yao JST, Pearce WH, eds. Practical Vascular Surgery. Stamford, CT: Appleton & Lange, 1999: 321–334. 7. Mattox KL, Feliciano DV, Burch J, et al. Five thousand seven hundred sixty cardiovascular injuries in 4459 patients. Epidemiologic evolution 1958 to 1987. Ann Surg 1989; 209:698–707. 8. Frykberg ER, Schinco MA. Peripheral vascular injury. In Moore EE, Feliciano DV, Mattox KL, eds. Trauma, 5th ed. New York: McGraw-Hill, 2004: 969–1003.

673 9. DeBakey ME, Simeone FA. Battle injuries of the arteries in World War II. An analysis of 2,471 cases. Ann Surg 1946; 123:534–579. 10. O’Gorman RB, Feliciano DV. Arteriography performed in the emergency center. Am J Surg 1986; 152:323–325. 11. Frykberg ER, Vines FS, Alexander RH. The natural history of clinically occult arterial injuries: a prospective evaluation. J Trauma 1989; 29:577–583. 12. Stain SC, Yellin AE, Weaver FA, et al. Selective management of nonocclusive arterial injuries. Arch Surg 1989; 124:1136–1141. 13. Wind GG, Valentine RJ. Axillary artery. In Wind GG, Valentine RJ, eds. Anatomic Exposures in Vascular Surgery. Baltimore: William & Wilkins, 1991: 138–157. 14. Graham JM, Mattox KL, Feliciano DV, et al. Vascular injuries of the axilla. Ann Surg 1982; 195:232–238. 15. Feliciano DV. Managing peripheral vascular trauma. Infect Surg 1986; 5:659–669, 682. 16. Carrell A. The surgery of blood vessels. Johns Hopkins Hosp Bull 1907; 18:18–28. 17. The Dutch Bypass Oral Anticoagulants or Aspirin Study Group. Efficacy of oral anticoagulants compared with aspirin after infrainguinal bypass surgery. The Dutch Bypass Oral Anticoagulants or Aspirin (BOA) Study: a randomized trial. Lancet 2000; 355:346–351. 18. Feliciano DV. Heroic procedures in vascular injury management. The role of extra-anatomic bypasses. Surg Clin North Am 2002; 82:115–124. 19. Feliciano DV. Evaluation and treatment of vascular injuries. In Browner BD, Jupiter JB, Levine AM, Trafton PG, eds. Skeletal Trauma: Basic Science, Management, and Reconstruction. Philadelphia: W.B. Saunders, 2003: 250–267. 20. Feliciano DV, Moore EE, Mattox KL. Trauma damage control. In Moore EE, Feliciano DV, Mattox KL, eds. Trauma, 5th ed. New York: McGraw-Hill, 2004: 877– 900. 21. Sharma PVP, Shah PM, Vinzons AT, et al. Meticulously restored lumina of injured veins remain patent. Surgery 1992; 112:928–932. 22. Parry NG, Feliciano DV, Burke RM, et al. Management and short-term patency of lower extremity venous injuries with various repairs. Am J Surg 2003; 186:631–635. 23. Matsen FA III. Compartmental Syndromes. New York: Grune & Stratton, 1980. 24. Amendola A, Twaddle BC. Compartment syndromes. In Browner BD, Jupiter JB, Levine AM, Trafton PG, eds. Skeletal Trauma:. Basic Science, Management, and Reconstruction. Philadelphia: W.B. Saunders, 2003: 268–292. 25. Feliciano DV, Cruse PA, Spjut-Patrinely V, et al. Fasciotomy after trauma to the extremities. Am J Surg 1988; 156:533– 536. 26. Mubarak SJ, Hargens AR. Compartment syndromes and Volkmann’s contracture. Philadelphia: W.B. Saunders, 1981: 117. 27. Whitesides TE Jr, Heckman MM. Acute compartment syndrome: update on diagnosis and treatment. J Am Acad Orthop Surg 1996; 4:209–218. 28. McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures. The pressure threshold for decompression. J Bone Joint Surg Br 1996; 78:99–104.

674 29. Feliciano DV. Management of peripheral vascular trauma (Poster). American College of Surgeons Committee on Trauma/Subcommittee on Publications. Chicago: American College of Surgeons, 2002. 30. Skillman JJ, Kim D, Baim DS. Vascular complications of percutaneous femoral cardiac interventions. Incidence and operative repair. Arch Surg 1988; 123:1207–1212. 31. Cutler BS, Okike ON, Vander Salm TJ. Surgical versus percutaneous removal of the intra-aortic balloon. J Thorac Cardiovasc Surg 1983; 86:907–911. 32. Franco CD, Goldsmith J, Ohki T, et al. Iatrogenic vascular injury. In Hobson RW II, Wilson SE, Veith FJ, eds. Vascular Surgery: Principles and Practice, 3rd ed, revised and expanded. New York: Marcel Dekker, 2004: 1098. 33. Franco CD, Goldsmith J, Veith FJ, et al. Management of arterial injury produced by percutaneous femoral procedures. Surgery 1993; 113:419–425. 34. Hajarizadeh H, LaRosa CR, Cardullo P, et al. Ultrasoundguided compression of iatrogenic femoral pseudoaneurysm. Failure, recurrence, and long-term results. J Vasc Surg 1995; 22:425–433. 35. Mills JL, Porter JM. Basic data related to clinical decisionmaking in acute limb ischemia.Ann Vasc Surg 1991; 5:96–98. 36. Sharp LS, Rozycki GS, Feliciano DV. Rhabdomyolysis and secondary renal failure in critically ill surgical patients. Am J Surg 2004; 188:801–806. 37. Blaisdell FW, Steele M, Allen RE. Management of acute lower extremity arterial ischemia due to embolism and thrombosis. Surgery 1978; 84:822–831. 38. Short D, Vaughn GD III, Jachimczyk J, et al. The anatomic basis for the occasional failure of transfemoral balloon catheter thromboembolectomy.Ann Surg 1979;190:555–556. 39. Wilson SE, Van Wagenen P, Passaro E Jr. Arterial infection. Curr Probl Surg 1978; 15:1–89. 40. Strinden WD, Dibbell DG Sr, Turnipseed WD, et al. Coverage of acute vascular injuries of the axilla and groin with transposition muscle flaps: case reports. J Trauma 1989; 29:512–516. 41. Ting AC, Cheng SW. Femoral pseudoaneurysms in drug addicts. World J Surg 1997; 21:783–787. 42. DePalma RG, Hubay CA. Arterial bypass via the obturator foramen. An alternative in complicated vascular problems. Am J Surg 1968; 115:323–328.

D.V. Feliciano 43. Fromm SH, Lucas CE. Obturator bypass for mycotic aneurysm in the drug addict. Arch Surg 1970; 100:82– 83. 44. Valentine RJ, Clagett GP. Aortic graft infections: replacement with autogenous vein. Cardiovasc Surg 2001; 9:419– 425. 45. Wind GG, Valentine RJ. Axillary artery. In Wind GG, Valentine RJ, eds. Anatomic Exposures in Vascular Surgery. Baltimore: William & Wilkins, 1991: 384–388. 46. Feliciano DV, Herskowitz K, O’Gorman RB, et al. Management of vascular injuries in the lower extremities. J Trauma 1988; 28:319–328. 47. Bermudez KM, Knudson MM, Nelken NA, et al. Long-term results of lower-extremity venous injuries. Arch Surg 1997; 132:963–968. 48. Yelon JA, Scalea TM. Venous injuries of the lower extremities and pelvis: repair versus ligation. J Trauma 1992; 33:532–536. 49. Timberlake GA, O’Connell RC, Kerstein MD. Venous injury: to repair or ligate—the dilemma. J Vasc Surg 1986; 4:553–558. 50. Mullins RJ, Lucas CE, Ledgerwood AM.The natural history following venous ligation for civilian injuries. J Trauma 1980; 20:737–743. 51. Rich NM, Hobson RW, Collins GJ Jr, et al. The effect of acute popliteal venous interruption. Ann Surg 1976; 183:365–368. 52. Feliciano DV, Mattox KL, Graham JM, et al. Five-year experience with PTFE grafts in vascular wounds. J Trauma 1985; 25:71–82. 53. Pappas PJ, Haser PB, Teehan EP, et al. Outcome of complex venous reconstructions in patients with trauma. J Vasc Surg 1997; 25:398–404. 54. Zamir G, Berlatzky Y, Rivkind A, et al. Results of reconstruction in major pelvic and extremity venous injuries. J Vasc Surg 1998; 28:901–908. 55. Tremblay LN, Feliciano DV, Rozycki GS. Secondary extremity compartment syndrome. J Trauma 2002; 53:833– 837. 56. Amendola A, Twaddle BC. Compartment syndromes. In Browner BD, Jupiter JB, Levine AM, Trafton PG, eds. Skeletal Trauma: Basic Science, Management and Reconstruction. Philadelphia: W.B. Saunders, 2003: 268–292.

Part III Administration, Ethics, and Law

41 Understanding the Latest Changes in EMTALA: Our Country’s Emergency Care Safety Net Thomas R. Russell

On April 7, 1986, President Ronald Reagan signed into law the Consolidated Omnibus Budget Reconciliation Act of 1985, which incorporated legislation known as the Emergency Medical Treatment and Labor Act (EMTALA) to address the problem of “patient dumping” by hospital emergency departments. Although originally designed to serve as a safety net for emergency patients, the statute grew in both scope and complexity during the following two decades, wreaking widespread confusion within the physician and hospital communities regarding their respective responsibilities under the law. During the 1990s,this confusion,particularly over physician on-call requirements, grew to such mammoth proportions that the involved players in the health care delivery system began petitioning Congress and the Health Care Financing Administration (now known as the Centers for Medicare and Medicaid Services [CMS]) in earnest for clear and understandable guidance about EMTALA mandates. As part of this effort, physician and hospital groups also urged Congress and the agency to revise the regulations to better reflect the original intent of the statute. Thankfully, these efforts paid off when CMS finally issued new EMTALA regulations that went into effect November 10, 2003, providing guidance that better clarifies physician and Medicare-participating hospital responsibilities under the law. This chapter examines the main tenets of the revised EMTALA regulations and their positive impact on the future of surgical practice and emergency surgical care, as well as highlight lingering issues that need to be addressed. Finally, new trends in the delivery of care that are influencing acute care are discussed.

Understanding the Basics for Hospitals: Obligation to Examine, Treat, and Stabilize In January 1985, San Francisco General Hospital became the final destination for the triage and treatment of

Eugene “Red” Barnes, a 32-year-old unemployed mechanic who had been fatally wounded when he was stabbed in an altercation outside an abandoned hotel in Richmond, California. An investigation into the emergency care that Mr. Barnes received before arriving at San Francisco General revealed a number of weaknesses in our country’s emergency care safety net for the uninsured, primarily the lack of a federally mandated obligation for hospitals to examine, treat, and stabilize all patients with an emergency condition regardless of the patient’s insurance coverage. Under EMTALA, this obligation is triggered when an individual comes to a hospital’s dedicated emergency department or presents on hospital property and requests an examination or treatment of a medical condition or a request is made on the individual’s behalf. In the absence of such a request, EMTALA would also apply if a prudent layperson observer believes that an individual needs examination or treatment for a medical condition. This main tenet of EMTALA has expanded and contracted over the years based on the interpretation of what constitutes a “hospital emergency department.” The current regulations state that a dedicated emergency department is defined as any department of the hospital (located on or off the main hospital campus) that is licensed by the state as an emergency department; held out to the public as providing emergency services; or has provided at least one-third of its outpatient visits for treatment on an urgent basis during the previous year.1 Exceptions to this rule are individuals who come to offcampus outpatient clinics that do not routinely provide emergency services or patients who have begun to receive scheduled, nonemergency outpatient services at the main campus of the hospital. Once the hospital determines that the individual does indeed have an emergency medical condition, that hospital must stabilize the emergency condition or, if it is unable to stabilize the patient, must transfer the patient to a hospital that is capable of providing such treatment.

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The latter aspect of this requirement was included to ensure that patients with severe injuries or very complex medical conditions are examined and triaged to the appropriate acute care facility as quickly as possible.

Penalties, Enforcement, and Resolution of EMTALA Violations When CMS receives a report of an alleged EMTALA violation, the agency’s regional office sends state surveyors to conduct an investigation. Generally, in determining ETMALA compliance, CMS will consider all relevant factors and look for specific patterns of care that could point to EMTALA infractions. Hospitals that fail to comply with EMTALAmandated responsibilities can have their Medicare participation terminated and can be subject to civil monetary penalties of up to $50,000 per violation. If a physician serving as “an agent of the hospital” on its on-call panel is called by the hospital to provide acute care screening or treatment and either fails or refuses to appear within a reasonable period of time, that physician may be in violation of EMTALA and could also face fines of up to $50,000 per violation. Patients who have suffered physical harm and hospitals that believe they have incurred a financial loss as a result of an inappropriate transfer also have a private right of action against hospitals that violate EMTALA. In its January 2001 report entitled “The Emergency Medical Treatment and Labor Act: The Enforcement Process,” the Department of Health and Human Services’ Office of Inspector General recommended that CMS make certain that providers will not be terminated from the Medicare program for an EMTALA violation without peer review. Congress implemented that recommendation in the Medicare Prescription Drug, Improvement, and Modernization Act by requiring HHS to request a quality improvement organization review before making a compliance determination that would terminate a hospital’s Medicare privileges. An exception to this rule would be in the case when a delay would jeopardize the health and safety of the individual. Also, in response to complaints from hospitals and physicians that they are kept in the dark as to whether an EMTALA investigation, once opened, is ongoing or has been resolved, the act also requires that a procedure be established to notify hospitals and physicians when an EMTALA investigation is closed.

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Physician Obligations Under EMTALA Many surgeons complain about the numerous EMTALA obligations that the federal government has imposed on the physician community. In truth, the statute does not place any direct obligations or liabilities on physicians. EMTALA focuses its mandates on hospitals or “agents of the hospital,” for example, hospital medical staff or oncall physicians. It is when they fall into the latter group that physicians come under the scrutiny of the law. If one examines EMTALA, he or she will realize that the statute maintains that the hospital, and not its medical staff or individual physicians, is responsible for maintaining an on-call roster for the emergency department. However, when physicians join the medical staff of a hospital or agree to take a call, they become a “responsible physician” under EMTALA by virtue of entering into a contract with the hospital to examine, treat, and/or transfer individuals who are covered by the law.2 In doing so, they are now acting as agents of the hospital and therefore share responsibility and liability with the hospital for providing EMTALA-related services. This is true regardless of whether or not the contract references EMTALA responsibilities. Because the final responsibility for maintaining on-call coverage falls on the hospitals, the medical staff bylaws for these institutions usually include language that requires physicians to comply with hospital policies and procedures as a condition of maintaining their clinical privileges at the hospital. This language, which is congruent with standards issued in the Joint Commission on Accreditation of Healthcare Organizations’ manual, encompasses the hospital’s policy for on-call coverage. Although surgeons “voluntarily” accept their role as agents of the hospital when they secure privileges, many of them receive little training regarding the EMTALA guidelines and, thus, are often unsure of their responsibilities under the statute. This fact was illustrated in a past survey of hospital emergency departments conducted by the Department of Health and Human Services (DHHS) Office of Inspector General (OIG). In a 2001 report, OIG found that “training increases EMTALA awareness, and nearly two-thirds of emergency physicians, nurses, and registration staff receive training. However, only onequarter of on-call specialists are trained on EMTALA guidelines.”4 Since the inception of EMTALA, surgeons have found it difficult to distinguish between their responsibilities under the law versus “policy” developed by hospitals to comply with EMTALA. The following sections of this chapter examine the various issues that surgeons should be aware of when serving as an agent of the hospital, either on its medical staff or on an on-call panel.

41. The Latest Changes in EMTALA

EMTALA On-Call Requirements Continuous Call EMTALA requires that Medicare-participating hospitals maintain an on-call list of physicians to provide services to patients who seek care in hospital emergency departments. The CMS has provided several memoranda and guidance documents since the original EMTALA regulations were released to help clarify various provisions of the act, including the on-call provisions. Despite the agency’s attempts to clear up ambiguity, it has remained a challenge for physicians to know what EMTALA mandates; whether hospital bylaws relating to emergency care are actually required by EMTALA; and how the law should be interpreted in specific circumstances. The most onerous, and perhaps most confusing, aspect of EMTALA for surgeons and other physicians is the on-call requirements. Hospitals, often out of fear of EMTALA violations, impose unrealistic on-call requirements on their physicians. It is not uncommon for a single specialist who covers multiple hospitals to be required, as a condition for joining a hospital’s staff, to be on-call 24 hours a day, 7 days a week. In some cases, surgeons have been expected to leave their office practice activities, or even an operation, in order to respond to emergency department calls at the hospitals for which they have privileges. A “24–7” demand for on-call services creates such unrealistic schedules and unreasonable demands for surgeons and other specialists that a number of these practitioners have altered their practices, often dropping privileges at a number of hospitals, in an effort to maintain viable practices and some semblance of quality of life. Many areas of the country have an insufficient population base to support a large number of specialists in certain fields, such as neurosurgery, cardiovascular services, pediatric surgery, obstetrics/gynecology, and orthopedics. This situation is especially true in rural areas and in areas that have small hospitals providing care to populations spread out over a great distance. Being selective about the day or circumstance for providing on-call services in these areas is usually not an option for these high-risk specialties. Recognizing this burden, CMS revised the on-call language to state that a hospital’s on-call list must be maintained in a manner that best meets the needs of the hospital’s patients who are receiving services required under EMTALA in accordance with the capability of the hospital, including the availability of on-call physicians. The CMS intended this modification to provide more flexibility for hospitals and their medical staffs to determine how best to provide emergency medical care and respond to on-call needs. The agency states that these decisions can be made reasonably only at the individual hospital level through coordination between the hospitals and their staff of physicians.4

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The CMS issued this clarification in the latest regulations because of confusion over one of the most perpetuated myths of EMTALA—the existence of the “rule of three,” which states that if a hospital has more than three physicians within a specialty, it must provide continuous emergency department coverage for that specialty. The CMS makes it clear that no such rule exists; however, many hospitals have developed policies based on this principle, and physicians historically have been led to believe that it is mandated by EMTALA. Some people have argued that EMTALA should require a minimum number of hours for individual physicians to be on call, the times for which physicians should be on call, or the number of physicians needed to fulfill on-call responsibilities at particular hospitals. The CMS has rejected these proposals from a practical standpoint. The agency maintains that the wide variations with regard to medical staff size, specialty mix, and general capabilities that exist among institutions that participate in the Medicare program make it infeasible to mandate a particular minimum level of on-call coverage that must be maintained by all hospitals. The latest changes to EMTALA provide other specific clarifications regarding on-call requirements that are aimed at allowing hospitals and their medical staffs to develop more realistic policies and procedures to achieve the goals of EMTALA and to address critical issues that have long concerned surgeons and other physicians with regard to the regulations.

Simultaneous Call Many surgeons hold privileges at several hospitals, particularly in areas where shortages of certain specialties exist. The CMS has only recently established that it is critically important for the interests of patients and hospital emergency departments that physicians be permitted to be on-call at more than one hospital simultaneously.6 In updating its policy, the agency recommends to hospitals that they notify each other when a physician is on-call at more than one hospital simultaneously and that each hospital involved be made aware of the physician’s on-call schedule. Furthermore, hospitals are required to have in place written policies and procedures to follow in situations when a physician is on-call at another hospital and is unable to respond. Such policies and procedures could include arranging for a back-up on-call physician or executing an appropriate transfer.7

Scheduling Elective Surgery While On-Call Performing elective surgery while on call has become an issue that surgeons struggle with in an effort to maintain their regular busy practice while fulfilling EMTALA requirements. In the past, the CMS has made conflicting statements in guidelines regarding whether physicians

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who cannot respond to an emergency call because they are performing elective surgery have violated EMTALA. To clarify this issue, the agency now emphatically states in the current regulations that EMTALA does not prohibit surgeons from performing elective surgery while on call. This is welcome news to many surgeons who are on call for days or weeks at a time.

Scope of Privileges “Many physicians limit their scope of practice to welldefined subspecialty areas, even though they are often credentialed by their hospitals to perform all surgery for the broader specialty for which they are board-certified.” For example, a neurosurgeon, with limited privileges for spine surgery, would argue that he or she is not required to take call for head trauma. Surgeons should be aware that the CMS addresses this issue in the current regulations, and hospitals may soon begin to move toward defining core privileges for a number of specialties. The CMS states that “a physician who is in a narrow specialty may, in fact, be medically competent in his or her general specialty and in particular may be able to promptly contribute to the individual’s care by bringing to bear skills and expertise that are not available to the emergency physician or other qualified medical personnel at the hospital.” CMS also stresses that although the emergency physician and the on-call specialist may need to discuss the best way to meet the individual’s medical needs, the agency believes any disagreement between the two regarding the need for the on-call physician to come to the hospital and examine the individual must be resolved by deferring to the medical judgment of the emergency physician or other practitioner who has personally examined the individual.8 Although the new EMTALA regulations clarify that on-call coverage determinations are to be made jointly by the hospital and the physicians on its on-call roster, it is the hospitals that are put in the position of ensuring that policies and procedures are in place to provide coverage of emergency department services. In turn, physicians practice at hospitals under privileges extended to them by those hospitals. If a physician refuses to assume on-call responsibilities or to carry out the responsibilities he or she has assumed, the hospital could suspend, curtail, or even revoke the offending physician’s privileges. Thus, hospitals will still maintain a tremendous amount of leverage in the development of on-call policies and schedules. Despite this fact, surgeons should take solace in knowing that they now have more concrete knowledge of what EMTALA requires, an invaluable asset when negotiating privileges with hospitals, working to maintain a viable practice, and striving to provide comprehensive emergency care in their communities.

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Some individuals may argue that the CMS’s most recent actions “relax” EMTALA standards and will endanger the safety net established by the law. Physicians believe that the clarifications made to EMTALA hold promise to have a positive impact on a situation that has been, up to the present time, increasingly unsustainable.

EMTALA Reforms Included in Medicare Prescription Drug Law Managed Care Reimbursement for EMTALA-Related Services Managed care plans often require preauthorization for services delivered in the emergency room. Under EMTALA, though, Medicare-participating hospitals or physicians are barred from seeking preauthorization before providing medical treatment unless such activities do not delay required screening and stabilization services. Thus, hospitals and physicians often wind up in a financial quandary when treating managed care patients in the emergency room—either foregoing payment or risking the imposition of EMTALA fines. A key provision in the new Medicare Prescription Drug, Improvement, and Modernization Act (MPDIMA), which was signed into law December 8, 2003, addresses the issue of managed care plans making retrospective denials for emergency screening and stabilization services. Under MPDIMA, medical necessity determinations for EMTALA services must be made “on the basis of the information available to the treating physician or practitioner (including the patient’s presenting symptoms or complaint) at the time the item or service was ordered or furnished by the physician or practitioner (and not on the patient’s principal diagnosis).” Many experts in the medical community and in Congress have long advocated that managed care plans be required to pay for justifiable screening and treatment services provided under EMTALA. Hopefully, this key reform in the Medicare prescription drug law will resolve many of the disputes that hospitals and physicians often encounter with the managed care community’s approach to reimbursement for emergency care services.

EMTALA Technical Advisory Group Another key provision of MPDIMA establishes a new EMTALA Technical Advisory Group “to review issues related to EMTALA and its implementation.” Table 41.1 lists its responsibilities. Membership in the advisory group will consist of 19 individuals, including the administrator of the CMS and the OIG of the Department of Health and Human Services. Seven slots on the advisory group are reserved for representatives from the

41. The Latest Changes in EMTALA Table 41.1. General responsibilities of the EMTALA technical advisory group. 1. Shall review EMTALA regulations 2. May provide advice and recommendations to the Secretary of DHHS with respect to those regulations and their application to hospitals and physicians 3. Shall solicit comments and recommendations from hospitals, physicians, and the public regarding the implementation of such regulations 4. May disseminate information on the application of such regulations to hospitals, physicians, and the public.

physician’s community in the areas of emergency medicine, cardiology or cardiothoracic surgery, orthopedic surgery, neurosurgery, pediatrics or a pediatric subspecialty, obstetrics/gynecology, and psychiatry. The physician and hospital communities are optimistic that this new group will help CMS in its future deliberations on implementing changes in EMTALA regulations.

Issues Remaining Although the federal government has come a long way in addressing the concerns of the medical community regarding the scope of EMTALA, a number of issues remain that will continue to impact access to emergency surgical care. These issues include managed care reimbursement policies and emergency room overcrowding; proliferation of single-specialty hospitals; lack of liability protections for EMTALA-related services; and growing burdens on trauma centers and community hospitals.

Managed Care Pressures I have discussed how Congress has now addressed the issue of managed care reimbursement for EMTALArelated services, but there are a number of other practices used by this industry that continue to place stress on the emergency care safety net. One such pressure revolves around patients’ inability to receive timely access to specialty care in the nonhospital setting. More often than not, managed care plan enrollees, some knowledgeable about EMTALA requirements, may use the emergency room when they cannot get an appointment with their regular specialist or primary care physician. Add to this number the more than 40 million uninsured who view the emergency room as their primary source of health care and the result is massive overcrowding. This kind of nonemergent saturation of emergency room departments across the country, particularly in urban areas, is resulting in numerous injured patients being unnecessarily diverted—causing critical delays for individuals requiring acute care.

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Impact on Trauma Centers and Community Hospitals Although many physicians are heralding the recent changes in EMTALA’s on-call requirements, others, particularly in the trauma community, are worried that these changes will further exacerbate the financial difficulties facing trauma centers and community hospitals. Under EMTALA, hospitals are now only required to maintain an on-call list “in a manner that best meets the needs of the hospital’s patients in accordance with the capability of the hospital, including the availability of on-call physicians.”9 Many trauma professionals believe that this change in the regulation will provide hospitals, particularly forprofit entities, with the ability to shield themselves from caring for severely injured patients by limiting on-call schedules. For example, some hospitals may only provide on-call coverage until 9:00 p.m. every night, leaving the local trauma center as the provider of last resort. One trend that will likely grow as a result of this change will be increased demands by specialists for hospitals to provide on-call compensation or stipends for emergency room coverage. The trauma community views this as yet another financial burden that trauma centers and community hospitals will have to bear in order to maintain their trauma designation or to keep the doors of their emergency room open. Some other old and new factors that will likely influence the viability of trauma centers in the future include lack of medical liability protections for EMTALArelated services and the exploding growth of specialty hospitals in areas such as cardiac and orthopedic care. At the federal level, Congress is examining both of these issues. In terms of medical liability protection, some legislators are calling for a narrow approach to medical liability reform that would focus solely on providing caps on noneconomic damages for EMTALA and OB-GYN services. With regard to the growth of specialty hospitals, Congress has imposed an 18-month moratorium on physician investments in specialty hospitals through mid 2005 in order to study the impact of this growing trend in care delivery on patient access to specialty services, particularly in the emergency room environment.

Suggestions from the Surgical Community for Solidifying the Safety Net over the Next Decade In pulling together this chapter, I reached out to a broad array of surgeons from all parts of the country, physicians who are on the front lines of providing emergency surgical care. Without exception, all of these individuals applauded the recent changes in EMTALA. Some of them also had very good suggestions regarding aspects of

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the law that should be addressed to better enhance timely patient access to specialized emergency care. These suggestions include better hospital triage and transfer policies; more flexibility regarding on-call response time; and evaluation of hospital staff cutbacks and recent implementation of the 80-hour resident work week on hospital capacity. Although greatly abbreviated here, the preceding comments were all presented to me with one goal in mind— improving care for the emergency patient. Surgical schedules and caseloads are increasing, reimbursement is declining, and liability insurance premiums are skyrocketing. In the twenty-first century, these trends have led many surgeons to alter their practices in ways that would have seemed unimaginable a decade ago: limiting scope of privileges, dropping participation in hospital medical staffs, and requesting stipends for providing oncall coverage. Many individuals outside the profession mistakenly view these changes in surgical practice as selfish and selfserving, but surgeons know that these modifications have often become necessary in order to maintain a viable practice so that they may continue treating patients, albeit for a reduced range of services. Despite this fact, surgeons whom I have spoken to about the EMTALA issue tell me that they still view the ability to provide charity care as an integral part of why they became a physician and that hopefully they will be able to continue to provide services to the local community in this regard. It is a shame that the last 20 years of government involvement in strengthening the emergency care safety net may have inadvertently weakened it to the breaking point. Surgeons, in general, state that, to mend this safety

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net, our country and government must recognize the public good that emergency medical and trauma systems provide to Americans every day. As such, legitimate EMTALA services would then become a mandated covered benefit under both Medicare and private health insurance plans; hospitals and physicians would receive reasonable liability protections for treating emergency and severely injured patients; and funding would be increased to help properly staff emergency rooms so that patients are evaluated and triaged quickly and appropriately.

References 1. Federal Register, Vol. 68, No. 174, Part II. Medicare Program; Clarifying Policies Related to the Responsibilities of Medicare-Participating Hospitals in Treating Emergency Medical Conditions; Final Rule. DHHS, CMS. September 9, 2003: 53263. 2. Bitterman R. Overview of Hospital and Physician Responsibilities Mandated by EMTALA. Foster. Providing Emergency Care under Federal Law: EMTALA. Dallas: The American College of Emergency Physicians, 2000: 21. 3. Joint Commission on Accreditation of Healthcare Organizations. Manual, 1999, Medical Staff Standard 1.1.3. 4. DHHS Office of Inspector General Report OEI-090-9800220. The Emergency Medical Treatment and Labor Act: Survey of Hospital Emergency. January 2001: 2. 5. 68 Federal Register. September 9, 2003: 53264. 6. Department of Health and Human Services, Centers for Medicare and Medicaid Services Survey and Certification Letter No. S&C-02-34, June 13, 2003. 7. 68 Federal Register. September 9, 2003: 53254. 8. 68 Federal Register. September 9, 2003: 53255. 9. 68 Federal Register. September 9, 2003: 53264.

42 Informed Surgical Consent Linda S. Laibstain and Robert C. Nusbaum

General Rule Informed surgical consent is a legal doctrine in force throughout each of the 50 United States, and it is governed by statute or by case law, or both, in every state. There is uniformity in principle, but sufficient variation exists to require the surgeon to be familiar with the specific statutes, where they exist, and the applicable case law, of the state in which he or she practices. The basic rationale for informed consent was stated by Justice Cardozo in a 1914 decision in the Superior Court of New York: “Every human being of adult years and sound mind has a right to determine what shall be done with his own body; and a surgeon who performs an operation without his patient’s consent commits an assault, for which he is liable in damages.”1 Subsequent case law makes clear that a patient’s agreement to a proposed course of treatment is legally effective only to the extent that he or she has been informed as to (1) what the diagnosis or problem is, (2) what is to be done, (3) the risks involved, and (4) the alternatives to the contemplated treatment—hence the term “informed consent.” Failure to obtain informed surgical consent can expose the surgeon to liability for damages for assault and battery, or negligence, or both, unless the failure is excused by justifiable exceptions, such as medical emergency or other situations discussed in this chapter.

and cannot safely rely upon a recitation to that effect at the foot of the signed document. Supplementary oral explanation by the surgeon or a qualified assistant is good practice and should be the rule rather than the exception. Such explanations should be documented at the time in the patient’s record. In the case of a language barrier, an interpreter may be needed to ensure that the patient understands what is being explained and what consent is being given. If the patient cannot read, the medical record should contain a notation that the document has been read or explained to the patient. Most hospitals will supply one or more required forms designed to obtain informed consent for surgery and related procedures, including such matters as administration of anesthesia, consent for students to be present to observe, and consent for preservation of removed organs and tissue for use in the advancement of medical science and education. In most situations, patients have the right to cross out provisions of the consent form to which they object, for example, use of their organs or tissue for research or education or the presence of student observers. The surgeon should become familiar with these forms, and keep them readily available. In the final analysis, it is the surgeon’s responsibility to see that the consent form used in a given case adequately describes the contemplated treatment, the risks, and the alternatives. The Hospital Law Manual published by Aspen Publishers, Inc., contains an excellent chapter on consents and a comprehensive appendix of useful forms.2

Evidence of Consent Informed surgical consent is best evidenced by a document signed by the patient and covering, among other desirable subjects, the elements set forth above, namely, a description of the diagnosis and proposed treatment, the risks, and the alternatives. It is important that the contents of the document be understandable by people of ordinary intelligence. The surgeon should make certain that the patient has read and understood the document

What Constitutes a Medical Emergency It is well settled in the law and the practice of medicine that there is an exception to the informed consent doctrine for cases of medical emergency. Many states have enacted laws and many courts have rendered decisions as to what elements are necessary to constitute an emergency, justifying the performing of medical or surgical procedures in the absence of informed consent. Surgeons

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should rely on the “medical emergency” exception only when a real medical emergency exists, “requiring immediate action for the preservation of the life or health of the patient under circumstances in which it is impossible or impracticable to obtain the patient’s consent or consent by anyone authorized to assume such responsibility.”3 A “medical emergency” is a condition that endangers the life or health of a patient.4 It must be a condition for which immediate surgery is required to save the life of a patient, to preserve a patient’s organs or limbs, or to alleviate a patient’s suffering and pain.5 One state statute defines a medical emergency as a situation in which (1) in competent medical judgment, the proposed surgical or medical treatment or procedures are reasonably necessary; and (2) a person authorized to consent (for the patient) is not readily available and any delay in treatment could reasonably be expected to jeopardize the life or health of the person affected or could reasonably result in disfigurement or impaired faculties.6

Exceptions to Informed Consent It is generally recognized that “a patient’s consent is limited to those procedures made known and contemplated at the time consent is given.”7 Some courts have carved out limited exceptions for situations in which unexpected or acute care conditions or problems arise during the course of an authorized procedure. While performing surgery for which there is an authorized consent, a surgeon may face an unanticipated emergency. Courts have permitted exceptions to the informed consent requirement in situations where it could be shown that there was an immediate threat to the patient’s life or health without time to awaken the patient from anesthesia or obtain a family member’s consent. In the absence of consent, courts are particularly hesitant to sanction the removal of a patient’s organs or limbs without compelling reasons, especially so in situations involving the removal of reproductive organs. The case of Barnett v. Bacharch provides guidance for the surgeon who encounters an unanticipated emergency during the course of surgery. In Barnett, the patient, who was pregnant and complaining of pain in her lower abdomen, was diagnosed as having a tubal pregnancy. While the patient was under anesthesia, the surgeon found she had an acute appendix and, without consulting the patient’s husband, removed the appendix. The court held that an acute appendix, with potentially dangerous consequences if not removed immediately, created a medical emergency sufficient to justify its removal without additional consent.8 In the Louisiana case of Douget v. Touro Infirmary, a patient with a lengthy history of surgeries and extensive adhesions underwent an anterior lumbar fusion operation by a physician experienced in this type of procedure.

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During the surgery, the physician encountered hundreds of adhesions and other unanticipated complications, including serious hemorrhaging. As a result of these complications, the surgeon determined that one of the patient’s kidneys had only a slight chance of survival and, if not removed, might result in severe sepsis. In addition, the surgeon removed the patient’s spleen, believing it was impossible to save. The court, in the Douget case, affirmed the jury’s decision that an acute care situation existed, requiring immediate action by the surgeon. The court held that prolonging the anterior fusion operation for the surgeon to leave the operating room to explain the situation to the patient’s husband and request his informed consent could have resulted in jeopardizing the life or health of the patient’s wife.9 An example of a court reaching a different decision is Tabor v. Scobee, a case in which a 20-year-old patient consented to an operation for appendicitis. During the procedure, the surgeon determined that the patient’s fallopian tubes were infected, swollen, and sealed off at both ends. The surgeon proceeded to remove them, believing that failure to do so within the next several months could result in serious harm or death. He was unable to obtain the patient’s consent because she was under anesthesia and did not attempt to obtain the consent of the patient’s stepmother, apparently in the hospital at the time. The court held that the patient’s medical condition did not constitute a “medical emergency,” because there would be an opportunity for the patient to make an informed decision without immediate jeopardy to her life or health.10 A similar situation occurred in the Louisiana case of Rogers v. Lumbermens, in which the surgeon, engaged to perform a simple appendectomy, also performed a hysterectomy as a precautionary measure, without the knowledge or consent of the patient or her husband. The court found that no emergency existed to justify the surgery under the circumstances.3 Surgeons must recognize that procedures otherwise considered emergencies may not justify surgery without consent if there is a reasonable opportunity to obtain consent.

The Unconscious Patient An exception to the informed consent doctrine is generally recognized for treatment of an unconscious patient in need of acute care surgery. This is based on the proposition that “when the patient is unconscious and in immediate need of acute care medical attention, the duties of disclosure imposed by the doctrine of informed consent are excused because irreparable harm and even death may result from the physician’s hesitation to provide treatment.11

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This proposition is illustrated by the often-cited case of Jackovach v. Yocom, decided by the Supreme Court of Iowa in 1931. Albert Jackovach, a 17-year-old boy, was injured while trying to jump off a moving train. After being dragged along the tracks, he was taken to the local hospital, where he was found to have a serious scalp wound, which was bleeding profusely, and a severely mangled and crushed elbow joint and arm. Before taking the patient to the operating room, efforts were made to reach his parents, who lived in a town approximately 8 miles away and who did not have a telephone. Neither of his parents was located until some time after the operation was completed. Evidence at trial showed that the patient initially was taken to the operating room, where he was put under anesthesia for treatment of his head wound to stop the flow of blood and to save his life. The surgeon, assisted by two other physicians, determined that the crushed and mangled condition of the patient’s arm was a “menace” to his life and that it was necessary to amputate the arm. Despite the subsequent argument of the patient and his parents that x-rays should have been taken and consent obtained before the patient’s arm was amputated, the court held that consent was implied by the circumstances of the situation. The court made a key finding, in the ensuing 70 years frequently referred to by those in the medical and legal professions: “If a surgeon is confronted with an emergency which endangers the life or health of the patient, it is his duty to do that which the occasion demands within the usual and customary practice among physicians and surgeons in the same or similar localities, without consent of the patient.”12 The Iowa court also noted the futility and potential dangers to the patient if his physicians were to release him from the anesthesia for the sole purpose of ascertaining whether the patient and his parents would consent to the amputation.

Capacity to Consent In addition to making a medical diagnosis, a surgeon may need to make a determination of a patient’s capacity to provide informed consent. This determination is to establish whether the patient is capable of understanding his or her medical condition, the nature and effect of the proposed treatment, and the risks involved in proceeding both with and without such treatment, including alternatives, if any.13 Although it is clear that a patient who is unconscious does not have the capacity to consent, the issue is not always clear in situations involving patients with diminished capacity resulting from trauma, head injuries, intoxication, or other impairments that can affect the patient’s ability to understand the elements described above.

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When a physician determines that a patient is incapable of providing consent for an acute care procedure, the physician should attempt to locate and obtain the consent of a family member, if at all practicable.13 If a family member cannot be located and if in the physician’s judgment the patient will suffer harm as a result of the delay, the surgeon should proceed with appropriate treatment or surgery.14*

Intoxicated Patients The issue of capacity frequently arises in the treatment of intoxicated patients who refuse to authorize recommended procedures. Although each patient must be evaluated individually for ability to give informed consent, courts generally give deference to the practice of good medicine. Illustrative of this proposition is the case of Miller v. Rhode Island Hospital, in which a patient was admitted to the hospital’s trauma service following a vehicular accident, resulting in injuries to his head, face, and ribs. He was evaluated by three trauma team physicians and underwent a number of diagnostic tests. The patient, found to have the equivalent of 16 alcoholic drinks in his blood, objected to the physician’s plan to perform a diagnostic peritoneal lavage, which was established hospital protocol for a patient with his injuries. The patient later sued the hospital, complaining that anesthesia was administered and the procedure performed over his vehement objection. The Supreme Court of Rhode Island, in a detailed analysis, agreed with the surgeon’s decision and the hospital’s policy to perform a nonconsensual peritoneal lavage if the patient suffered an injury likely to cause internal injuries and if the “patient’s mental status was impaired by drugs, alcohol or an injury to the head, such that the patient cannot sense or report symptoms of internal bleeding.”15 The court noted that the treatment was consistent with the standards established by the American College of Surgeons and that the surgeon’s decision to perform the procedure was supported by his findings and by other physicians present at the time.

Minors As a general rule, the medical emergency exception to the informed consent doctrine also applies to minors.

* As technology advances and methods and speed of electronic communication (cellular telephones, fax machines, etc.) evolve, there are more options available to reach family members, if they can be identified and located. The practicality of using these communications should be balanced against the patient’s medical needs, based on the best judgment of the surgeon.

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Although a parent or guardian’s consent is normally required to treat a minor, it is generally not required if the delay would likely result in immediate injury or death.16 Most states have statutes that deal with consent for acute care medical treatment of minors. For example, Massachusetts statute law provides: No physician, dentist or hospital shall be held liable for damages for failure to obtain consent of a parent, legal guardian or other person having custody or control of a minor child . . . to emergency examination or treatment, including blood transfusions, when delay in treatment will endanger the life, limb or mental well-being of the patient.17

Surgeons should be familiar with their hospitals’ procedures for providing emergency medical care to minors when parents cannot be located, including how to get in touch with designated hospital administrators/personnel to implement the procedures. This is especially important in situations involving life-threatening conditions that, although serious, allow time for obtaining a court order in the absence of consent of a parent or legal guardian. Courts are inconsistent in their application of the emergency exception with respect to minors in cases where neither consent nor a court order was obtained before acute care surgery.16 Hospital attorneys often have standing arrangements to obtain an expedited hearing for court approval of acute care surgery or related treatment in cases where voluntary consent is unavailable and dire consequences may result if surgery is too long delayed. Some courts recognize an exception for the mature minor. This exception allows a minor to give informed consent “if it is determined that the patient has the ability and maturity to understand and comprehend the nature of his or her condition, proposed treatment, the associated risks and potential results in view of the surrounding circumstances.”16 Although court decisions vary depending on the specific facts, the Jackovach case described above, in which physicians amputated the patient’s arm, while the patient was under anesthesia for life-threatening head injury, and the Luka case that follows, are examples of judicial deference to the decisions of surgeons practicing good medicine with respect to minors in acute care situations. In Luka v. Lowrie, a 15-year-old boy was brought to the hospital with a mangled and crushed foot. Shortly after giving his name and the street where he lived, he lapsed into unconsciousness. The surgeon, after learning that the patient’s parents were not in the hospital and upon consultation with four other physicians, agreed that an immediate amputation of the patient’s foot was necessary to save the patient’s life. The court ruled that the surgeon’s decision to operate, in the absence of consent, was appropriate given the condition of the patient and the potential consequences if surgery was not performed.18

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Patient’s Refusal to Consent It is a well-established principle in law and medicine that a competent person may refuse to consent to medical treatment and that a physician must respect a competent person’s refusal of treatment, even in an emergency. The right to refuse medical treatment applies to all forms of medical treatment, including life-saving and lifesustaining procedures. It also includes refusal of blood transfusions, an issue that frequently arises in the context of an emergency as well as during the course of nonemergency medical treatment.19 Because issues involving patients’ refusal of treatment, including refusal of blood transfusions, frequently arise in life-threatening situations, physicians and hospitals are sometimes unwilling to proceed with what they consider unsound medical practice—hence the large number of these types of cases that are brought before the courts for resolution.20 Courts often reach different decisions on these issues, based in large part on the specific factual situations and the level of the patient’s competency to make an informed decision. A Florida court has held that a patient with kidney disease, who was likely to die within a few hours without a blood transfusion, had the right to refuse the transfusion. The court found that the patient was competent and mentally alert, and there was no overriding reason to require a transfusion that would violate the patient’s religious beliefs. The court made it clear that the patient had the right to refuse a transfusion for himself as a matter of self-determination but stated that its conclusion was limited to the facts before it and that the outcome might be different for a parent or guardian refusing treatment for another person.21 In re Quackenbush deals with a 72-year-old competent patient who refused to consent to amputation of his legs, despite likely death from gangrene in a matter of weeks without the surgery. The patient had declined medical treatment for 40 years and described himself as a “conscientious objector” to medical care. The New Jersey court upheld the patient’s right to refuse treatment and declined a petition by the hospital to order surgery.22 An unusual case from the Supreme Judicial Court of Massachusetts illustrates the type of dilemma that can be faced by emergency personnel. This case was brought by the parents of a young woman, Catherine Shine, an asthmatic, who presented to the emergency room with a severe asthma attack. Having suffered from this condition all her life, and knowledgeable about various treatments, she made it known to hospital personnel (and they agreed) that only oxygen would be administered. After the patient removed the oxygen mask because it gave her a headache, the emergency room attending physician determined that she required intubation. The patient was restrained and intubated, contrary to her stated

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instructions. The patient, having been traumatized by these events, vowed never to go to a hospital again. Two years later, while suffering an asthma attack, she adamantly refused to go to a hospital. She was finally taken by ambulance to a hospital, where she died 2 days later, despite medical treatment. The court declined to dismiss the case, ruling that a jury could consider whether the treating physician took all steps necessary to obtain the patient’s consent or the consent of a family member for treatment.23 Issues involving refusal to give consent, particularly for blood transfusions, can be problematic with an unconscious patient, a patient with limited capacity, or a minor. They sometimes arise when family members voice the patient’s objection, religious or otherwise, contrary to the physician’s recommendation. When confronted with a parent’s or representative’s refusal to consent to treatment, the physician should seek the assistance of designated hospital personnel (on-call administrator, legal counsel, etc.) to obtain guidance or to petition the courts, if necessary. Courts generally analyze these matters on a case by case basis, depending, in part, on whether the patient has previously expressed instructions, the patient’s condition, and, in some circumstances, whether there is a compelling state interest in the preservation of life that outweighs the patient’s religious tenets expressed by family members.20

Documentation When treating a patient over his or her objection, or when there are issues as to the patient’s capacity to give informed consent, the physician should (1) document objective findings, for example, blood alcohol levels and Glasgow Coma Scores; (2) document in the patient’s record the subjective findings forming the basis for the decision; (3) consult with other physicians or health care providers, if feasible; (4) document efforts to reach family members or otherwise obtain consent; and (5) document the need for the immediacy of the procedure. It is obligatory that surgeons be familiar with their own state statutes, leading cases, and hospital policies and regulations concerning informed consent in order to make sound decisions. Some states provide detailed requirements for informed consent and specific exemptions for acute care procedures, but others provide little or no guidance. Most hospitals have regulations for performing surgery when the patient’s consent is not available, including protocols for notification of “on-call administrators.” These individuals are usually well informed and very helpful. Adhering to hospital guidelines, as well as thorough documentation of the physician’s reasons for performing acute care surgical procedures without the

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consent of the patient or a representative are essential for all concerned. In conclusion, it is impossible to anticipate the variety of situations that may present themselves to the emergency physicians, often requiring quick decisions. However, there are certain steps the surgeon and other medical personnel can and should take to ensure good medicine while limiting exposure to liability for performing medical procedures to which the patient or his family express objections or may object in the future. The following guidelines are suggested: 1. Be familiar with the laws in the state where you operate with respect to informed consent, refusal of treatment, treatment of incapacitated patients, minors, and so forth. 2. Know your hospital’s policies for treatment in emergency situations—know the hospital administrator or designated person to contact when emergency/consent issues arise and know how to get in touch with that person. 3. Have available informed consent forms for surgical procedures, ancillary procedures (e.g., anesthesia), and other treatment. Use the forms! 4. Consult with other physicians and health care providers on difficult issues, time permitting. This includes involvement of others in decisions to operate, administer anesthesia, and order transfusions. 5. Discuss with the patient, and/or his or her designated representative, the diagnosis and nature of the patient’s condition, the proposed treatment and material risks, and alternatives to that treatment. 6. Document your findings, diagnosis, and treatment. 7. Document discussions with patient and representative concerning consent issues. 8. Practice good medicine!

References 1. Schloendorff v. Society of New York Hospital, 211 N. Y. 125, 129–130, 105 N. E. 92, 93 (1914). 2. Hospital Law Manual. New York: Aspen Publishers, Inc., 2006. 3. Rogers v. Lumbermen’s Mutual Casualty Company, 119 So. 2d 649, 650 (1960). 4. Jackovach v. Yocom, 212 Iowa 914, 237 N.W. 444, 449 (1931). 5. Sullivan v. Montgomery, 155 Misc. 448, 279 N.Y.S. 575 (1935). 6. Louisiana Revised Statutes 40:1299.54 (2006). 7. Consent to medical and surgical procedures by Arnold J. Rosoff. In Hospital Law Manual. New York: Aspen Publishers, Inc., 2006: 1–252. 8. Barnett v. Bacharch, 34 A. 2d 626 (1943). 9. Douget v. Touro Infirmary, 537 So. 2d 251, 260 (1988). 10. Tabor v. Scobee, 254 S. W. 2d 474 (1951). 11. Hartman K, Liang B: Exceptions to informed consent in emergency medicine. Hosp Physician 1999; 35:53–59. 12. Jackovach v. Yocom, 212 Iowa 914, 237 N. W. 444, 449 (1931).

688 13. Miller v. Rhode Island Hospital, 625 A. 2d 778, 785 (1993). 14. Canterbury v. Spence, 464 F. 2d 772, 788, 789 (1972). 15. Miller v. Rhode Island Hospital, 625 A. 2d 778, 781 (1993). 16. Veilleux D. Medical practitioner’s liability for treatment given child without parent’s consent, 67 A.L.R. 4th 511, The Lawyers Co-operative Publishing Company, 2004. 17. Mass. Gen. Laws Ann. Ch. 12 §12F (2006). 18. Luka v. Lowrie, 171 Mich. 122, 136 N. W. 1106 (1912).

L.S. Laibstain and R.C. Nusbaum 19. In re Brown, 294 Ill. App. 3d 159, 689 N. E. 2d 397, 228 Ill. Dec. 525 (1997); appeal denied, 177 Ill. 2d 570, 698 N. E. 2d 543 232 Ill. Dec. 452 (1998). 20. Karnezis K. Patient’s right to refuse treatment allegedly necessary to sustain life, 93 A.L.R. 3d 67, The Lawyers Cooperative Publishing Company, 2004. 21. St. Mary’s Hosp. v. Ramsey, 465 So. 2d 666 (Fla. Dist. Ct. App. 4th Dist. 1985). 22. In re Quackenbush, 156 N. J. Super. 382, 283 A. 2d 785 (1978). 23. Shine v. Vega, 429 Mass. 456, 709 N. E. 2d 58 (1999).

43 Advance Directives David G. Jacobs

These are the duties of a physician—to cure sometimes, to relieve often, to comfort always Anonymous1

This chapter discusses the issues surrounding advance directives, focusing specifically on the impact these documents may have on the care of the acute care surgical patient.At first, it may seem somewhat unusual to include a chapter on this topic in a text devoted to the care of the acute care surgical patient. However, it is important to remember that acute surgical illness, whether from injury, sepsis, or shock, may render the patient incapable of participating in decision making at the time of presentation. Furthermore, the nature of acute surgical illness not infrequently results in postoperative complications, organ failure, and prolonged intensive care unit stays, requiring invasive and expensive treatment modalities that, for some patients, may be life saving but, for others, may simply be death delaying. Thus, some understanding of the history of advance directives, the types of documents that currently exist, and their relative advantages and disadvantages is necessary to ensure optimal outcomes for this patient population. In this regard, the word “outcomes” is used in its broadest sense, as the treatment goals from the patient’s perspective may be radically different from those of the treating surgeon. Advance care planning in general, and advance directives in particular, refers to a process whereby a patient rendered temporarily or permanently incapable of participating in treatment decisions can exert his or her right to autonomy, thus ensuring a favorable outcome from the patient’s perspective.

History of the Development of Advance Directives Ethical Foundation The principle of autonomy, the right of each person to determine what will or will not be done to his or her body,

is one of the guiding bioethical principles of our time. So basic and fundamental is this right that most courts now appear to recognize it as the first principle of medical ethics.2 This principle provides the ethical foundation for the “Patient’s Bill of Rights” approved by the American Hospital Association in 1973, in which the express right of a competent patient to refuse treatment was supported.3 In the same year, the American Medical Association recognized the reciprocal rights of both patient and physician to determine appropriate end-of-life treatments.4 Current opinion suggests that patient autonomy is so fundamental to medical decision making that it should be extended even to individuals who, because of acute or chronic illness, are no longer able to direct their own medical care. This, in turn, mandates the creation of some means of exerting this autonomy after medical decision-making capacity has been lost, that is, advance directives. Two other principles of modern medical ethics are important to consider when discussing advance care planning—beneficence and social justice. Beneficence declares that whatever is best for each person should be accomplished, whereas social justice holds that resources, particularly scarce ones, should be allocated fairly. As will be discussed later, both of these principles, along with autonomy, strongly influence end-of-life care and thus impact advance care planning as well. In most cases, medical care can delivered in such a way as to be consistent with all three of these principles. However, under certain circumstances, particularly in end-of-life situations, it may not be possible to satisfy all principles simultaneously. When this occurs, the relative primacy of autonomy as an ethical principle will generally direct the decision making.

Legal Foundation Advance directives have existed, in one fashion or another, for more than 30 years, as evidenced by Kutner’s proposal of a “living will” in 1969 as a way for a patient

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with terminal illness to specify the nature of future medical care.5 However, it was not until the well-publicized case of Karen Ann Quinlan in 1976 that a patient’s right to refuse medical care in certain “terminal” situations gained the public’s attention and support. In this case, the State Supreme Court of New Jersey authorized the discontinuance of ventilatory support from Ms. Quinlan (thus effectively allowing her death) on the basis of a patient’s right to privacy. Just as important, however, was the Court’s recognition that this authority extended to Ms. Quinlan’s parents, without whom the patient’s right to privacy would have been lost.6 Advance care planning, however, was still virtually nonexistent until two significant developments, both of which occurred in the early 1990s. The first was the case of Cruzan vs. Director, Missouri Department of Health.7 This case involved a young woman who was rendered severely and permanently mentally incapacitated as a result of a motor vehicle crash. There was universal agreement among her physicians that she was indeed in a “persistent vegetative state” from which she would not recover. She was successfully weaned from mechanical ventilation, but continued to receive enteral nutrition via a surgically placed gastrostomy tube. Her parents petitioned the Court to force termination of her nutritional support, citing their daughter’s statement that she would not want to continue to live if she could not be “at least halfway normal.” Their request was granted, only to be overturned on appeal by the Missouri State Supreme Court on the grounds that the parents had not supplied “clear and convincing” evidence that Ms. Cruzan would have rejected such treatment. This decision was then further appealed to the United States Supreme Court that, in a split decision (5–4), upheld the State Supreme Court’s decision to refuse termination of nutritional support. Although the majority opinion of the Supreme Court recognized the patient’s right to autonomy, it also recognized the right of every state to determine criteria by which the authenticity of the patient’s end-of-life wishes could be deduced. Despite siding with the majority, Justice O’Connor appeared to strongly support the right of a previously competent, now incompetent patient to direct his or her own end-of-life care when she wrote the following: Few individuals provide explicit oral or written instructions regarding their intent to refuse medical treatment should they become incompetent. States which decline to consider any evidence other than such instructions may frequently fail to honor a patient’s intent. Such failures might be avoided if the State considered an equally probative source of evidence: the patient’s appointment of a proxy to make health care decisions on her behalf. . . . Today’s decision, holding only that the Constitution permits a State to require clear and convincing evidence of Nancy Cruzan’s desire to have artificial hydration and nutrition withdrawn, does not preclude a future determination

D.G. Jacobs that the Constitution requires the States to implement the decisions of a patient’s duly appointed surrogate.8

This statement by Justice O’Connor, suggesting a possible role of the federal government in mandating compliance with a surrogate’s medical decisions, provided significant impetus to the adoption of advance directive legislation. Two additional lessons from the Cruzan decision are germane to this discussion. First, there is no distinction made among the various forms of life-sustaining treatment; nutrition and hydration are no different from mechanical ventilation and other more invasive therapies when considering “life-support” strategies. Second, there is no ethical or legal difference between withholding and withdrawing treatment from a patient. Thus, the physician need not be concerned that initiating a particular “life-support” therapy will preclude him or her from withdrawing that therapy on the patient’s behalf in the future.9

The Patient Self-Determination Act The second event that was critical in fostering the development of advance directives was the Patient SelfDetermination Act (PSDA) of 1990.10 This federal legislation required that all health care institutions (hospitals, nursing homes, health maintenance organizations, etc.) that received federal funding provide written information to each adult patient regarding that patient’s legal right to make decisions concerning medical care, to refuse treatment, and to formulate advance directives. In addition, the institution was required to document advance directives in the patient’s medical record, ensure compliance with state law regarding advance directives, and avoid making care conditional on completion of such directives. The purpose of the PSDA was a good one—to encourage discussions between patients and physicians regarding end-of-life care preferences, thus facilitating patient autonomy. Some, however, have suggested a more jaded and sinister rationale behind this legislation, a financial motive. The PSDA as passed was a part of the Omnibus Reconciliation Act of 1990 that, among other things, provided for an overall net reduction in Medicare payments to health care institutions. This raises an intriguing question: Does more widespread use of advance directives have any impact on health care expenditures? Chambers et al.,11 in a study of nearly 500 Medicare patient deaths, documented a mean inpatient charge of $30,478 for patients with advance directives compared with $95,305 for those without directives, even after controlling for severity of disease, use of an intensive care unit, and number of procedures. Similar findings have been noted by Weeks et al.12 Thus, the use of advance directives, by limiting presumably unwanted expensive

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end-of-life care, resulted in the potential of significant cost savings. Other authors have examined this issue and have found no decrease in health care expenditures for patients with advance directives.13,14 Some of the discrepancy between these findings may be due to the relatively large number of patients in some of these studies whose advance directives were not followed, resulting in comparable charges for both groups. Future studies comparing patients whose directives were actually followed with those whose directives were ignored will be necessary to determine whether advance directive use reduces health care costs. The larger ethical issues raised here—the societal value of end-of-life care and who should pay for it—relate directly to the third ethical principle described earlier— social justice, the equitable allocation of scarce resources. Whether the impetus for creation of the PSDA was autonomy, beneficence, social justice, or some combination of these principles, will probably never be known. The immediate impact of the Cruzan decision and the PSDA was the rapid development and dissemination of legislation regarding advance directives. All 50 states have enacted advance directive legislation of one type or another, and all of these laws provide immunity to physicians and other health professionals who follow the patient’s wishes as expressed in a living will. However, there is a great deal of variability from state to state regarding the form, function, and authority ascribed to these documents.15 This lack of uniformity has weakened the overall effectiveness of advance directive legislation and has created obstacles to both patients and physicians in terms of completing these documents. Advance directive laws vary significantly among states in such areas as who can be designated as a proxy, the conditions under which these directives can be activated, and even the process by which these documents can be revoked. Some states restrict their living will laws to directives that limit resuscitative efforts in end-of-life care, whereas others allow their documents to specify “aggressive” care. Most states authorize both living wills and the appointment of a health care power of attorney. However, three states, Massachusetts, Michigan, and New York, authorize only the appointment of a health care agent, while one state, Alaska, authorizes only the use of living wills.16 Therefore, it is incumbent on the patient and physician to be familiar with the limitations and restrictions set forth by their particular state as well as to recognize that an advance directive drawn up in accordance with one state’s regulations may not be recognized in a different state. It has been recommended that patients have advance directives drawn up for each state in which they may find themselves requiring this sort of “protection.” In an attempt to reduce confusion and to provide for some consistency across the states regarding advance

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directives, the National Conference of Commissioners on Uniform State Laws proposed the Uniform Health-Care Decisions Act in 1993 that provides for a uniform, consistent approach to advance directive implementation, management, and enforcement within and between state jurisdictions.17 Unfortunately, to date this legislation has been adopted by less than 10 states. Sadly, the PSDA does not seem to have had much impact on advance care planning in the United States. Today it is estimated that only 10% to 15% of patients have actually signed advance health care directives.18–23 The reasons behind this apparent lack of interest in completing advance directives are many, varied, and not well understood.24,25 Perhaps the most comprehensive study to examine the impact of advance health care decision making in the post-PSDA era is the SUPPORT study, in which 9,105 seriously ill patients in five teaching hospitals participated in an intervention in which a nurse facilitated communication among the patient, family, physicians, and hospital staff to improve understanding of outcomes and promote advance care planning. Only 20% of these patients had an advance directive prior to the study, and the intervention did nothing to improve this rate. The study also documented poor physician–patient communication regarding cardiopulmonary resuscitation preferences and other endof-life issues, even for those few patients who had completed advance directives.26–28 Despite the fact that the PSDA mandates that patients admitted to health care institutions be given the opportunity to complete these documents, there is essentially uniform agreement that this is not the optimal time, from either a patient or physician perspective, to enter into these types of discussions.29–31 Many patients, because of the illnesses that have prompted hospital admission, may not be in a position to discuss advance directives. Furthermore, it seems intuitive that many of the patients who are able to discuss advance directives may not be willing to do so, as these discussions may perhaps heighten fears and suspicions. This perception is corroborated in the SUPPORT study, in which more than 50% of patients refused to discuss end-of-life management when they were seriously ill.26 Other authors have reached similar conclusions,32,33 but work by Reilly et al.34 suggests that in excess of 80% of hospitalized patients are willing to undertake such discussions with their physicians. Importantly, only 47% of patients actually had these discussions, highlighting the reluctance that physicians have in initiating these conversations. The health care facility, therefore, caught between legislation requiring them to provide patients with this opportunity and physicians reluctant if not unwilling to engage patients in these discussions, has relegated the responsibility of providing information regarding advance directives to hospital admissions personnel who, in many cases, distribute this information in

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a perfunctory fashion along with a myriad of other required patient notifications, including forms for authorization for treatment, release of information, and authorization for assignment of benefits. Thus the potential impact of the PSDA has been significantly hampered.20,35 One potential solution would be to distribute advance directive information to patients prior to hospital admission. Cugliari et al.36 documented a significantly higher rate of advance directive completion (40% vs. 4%) by simply distributing information about directives one day before admission as opposed to at the time of admission. Although this represents a marked improvement in document execution, it does not provide for physician involvement, nor does it address the needs of patients admitted under nonelective circumstances. For these and other reasons, it is generally acknowledged that discussions regarding advance directives should occur between a patient and his or her primary care physician in the outpatient setting, well in advance of the need for implementation of such directives.18,29 Evidence, however, suggests that these outpatient discussions are not occurring.37,38 Why not? When polled, the majority of patients favor hearing about their illnesses and their health care options but believe that these discussion should be initiated by the physician.19,39–42 Multiple studies have documented the extent of, and reasons for, physician reluctance to initiate discussion about advance directives.18,39,43,44 Some physicians perceive that their patients will respond negatively to a discussion on advance directives, particularly at the time of hospital admission. However, this concern is not born out in the published literature.18,19,45 Furthermore, many physicians have not been provided the training necessary to undertake these types of discussions,46,47 nor are they compensated for the time that would be required to adequately discuss the issues.38 For example, advocates of the Values History, one particular directive, estimate that it might take five patient visits or 1 year to complete this document. Another recent study noted that physicians with expertise in the area of advance directives spend, on average, 15 minutes per office visit in discussions about these issues with their patients.48 Given the time and financial constraints imposed upon modern-day medical practices, extensive patient–physician discussions about advance directives may not be an option.49 Some have recommended the use of financial incentives to hospitals or physicians to encourage patient–physician discussion,50,51 but, to date, no legislative provisions have been made to support this. Finally, for both the physician and the patient, ethnicity and sociocultural norms seem to play a role in advance directive discussions and decision making.52–56 Clearly, greater effort needs to be expended in identifying the causes for the underutilization of these documents and in finding solutions for them.

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Types of Advance Directives Advance directives may be classified in several ways and, as a result, describing the various types of documents can be confusing. Most commonly, advance directives refers to any document in which a competent patient makes known his or her wishes regarding the nature and extent of medical care desired should he or she lose decisional capacity in the future. Others use the term to specifically refer to those directives that are “advisory” in nature. The American Medical Association describes two categories of advance directives, advisory and statutory.57 Advisory documents attempt to accurately represent a patient’s wishes and might include such things as a worksheet containing potential end-of-life scenarios with choices indicating the patient’s preferred mode of treatment. Alternatively, they might include a statement of values that could provide a framework on which the physician and the family could base their subsequent decisions. Other examples include notes written by a physician in the medical record reflecting discussions that he or she has had with the patient, as well as written documentation of conversations between the patient and family members. Regardless of their form, these documents are legally binding under the law. Statutory documents give physicians immunity from malpractice for following a patient’s wishes. Examples of these documents include living wills and durable power of attorney for health care designations. Importantly, the degree of flexibility and options accorded the patient by these documents varies significantly from state to state and, as a result, may not provide the desired amount of “protection” required by the patient, as one state’s document may not be recognized as valid in another state. Regardless of how these documents are classified, the two documents with which both patients and physicians should be most familiar are the living will and the durable health care power of attorney.

Living Wills Living wills represent the earliest form of advance directive, dating back to 1969.5 In general, living wills are documents that instruct physicians on the type of medical care the patient would like to receive in the event he or she loses decision-making capacity. The language in these documents is generally broad and conceptual rather than specific, although many living will forms do enable patients to add specific requests. Advantages of the living will include the fact that these documents allow the patient the opportunity to specify both the conditions under which certain treatments should be provided or withheld (qualifying statements) as well as the nature of


those treatments (directive statements). Thus, for example, a patient may specify that endotracheal intubation may be carried out as part of an operative procedure but not in the event of cardiopulmonary arrest. Living wills have generally been used to limit interventions provided to the patient at the end of life, but this is by no means the only type of medical directive provided for by living wills. Some patients have used living wills to indicate their desire to have all treatment options and resuscitative measures provided to them, irrespective of clinical circumstances.58 Others have used living wills to designate that medical care be carried out according to specific religious customs or traditions,59–61 whereas others have used these documents to indicate their desire to donate their organs upon their deaths.49,50 Clearly, however, the most common purpose for the completion of living wills is to limit the use of certain medical interventions perceived by the patient to be unnecessary or unwarranted in end-of-life situations. Unfortunately, the language used in most living wills is sufficiently vague and ambiguous so as to render their interpretation meaningless in many clinical situations. Use of words such as “terminal condition,” “extraordinary means,” “imminent death,” and others have introduced an unwanted degree of subjectivity into the interpretation of these documents by both physicians and family members.62 Some authors (and states) have attempted to reduce this ambiguity by attaching either to the living will itself or to another form of advisory document either a scenario-based or value-based assessment to give the patient the opportunity to make clear under what specific conditions and circumstances “aggressive” end-of-life care would be provided.49,50 Others have argued, however, that inclusion of these additional documents does nothing to ensure that the intent of the patient will be sustained when required and that these “enhancements” may actually restrict patient autonomy.63,64 Ethical arguments have, as well, been raised against the use of living wills on the basis of the concept of “personhood.”65 This point of view holds that it is inappropriate to bind individuals to a decision that they made when they possessed perhaps a completely different set of values and interests. For example, should a pleasantly demented, but functional, individual be denied “aggressive” end-of-life care simply because he or she, 20 years previously, believed that “dementia” would represent an unacceptable quality of life? Despite these concerns, living wills have been demonstrated to increase the accuracy of substituted judgments by hospital-based physicians in contrast to primary care physicians or family surrogates.66 Thus, determining the presence of completed advance directives may be of value to the “emergency” physician or surgeon, where prior knowledge of the patient’s wishes may influence care.

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Durable Health Care Power of Attorney The other common form of advance directive is the durable health care power of attorney (DHPA) in which a competent patient identifies an individual who will act as that patient’s surrogate under those circumstances in which the patient loses decision-making capacity. This individual could be a family member, friend, or even physician, and, in most states, the DHPA requires the signature of the named surrogate or “proxy.” This form of advance directive has the advantage of preserving the patient’s right to informed consent in that, under conditions of lost decision-making capacity, the surrogate would be informed of the risks and benefits of proposed treatment strategies and then would make decisions on behalf of the patient using the “substituted judgment” standard—that is, making the decision that the patient would make were the patient capable. When a proxy does not possess sufficient information to use the substituted judgment standard, a decision would be made using the “best interests” standard in which the proxy makes decisions that maximize patient benefit, consistent with the ethical principle of beneficence. The DHPA, unlike the living will, therefore, provides the patient with an opportunity for decision-making under conditions that may not have been anticipated at the time that the directive was executed and therefore not specifically addressed within the living will. In this fashion, a DHPA adheres more faithfully to the doctrine of informed consent, which requires that a decision be made after the diagnosis has been established and all available treatment options with the attendant risks and benefits have been considered. For these reasons, most authorities recommend completion of a DHPA at a minimum, along with a living will if desired.64 So important is the presence of a proxy under these circumstances that some states have enacted legislation providing for designation of a surrogate decision maker (in order of priority: guardian, spouse, adult children, parent, sibling, adult grandchild, friend, estate guardian) who would be empowered to make health care decisions for the incompetent patient based on the “substituted judgment” or “best interests” principle in the event that an advance directive has not been completed.67 A brief discussion of the concepts of “competence” and “capacity” is necessary here as DHPAs only become effective when the patient loses decision-making capacity or competence. Hence, the assessment of capacity is integral to establishing and preserving patient autonomy. The task of determining who is competent and who has lost medical decision-making capacity can be challenging at times, but typically the process is straightforward and can (and should) be completed by the physician primarily responsible for the patient’s care. It should not usually be necessary to involve psychiatrists in these

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D.G. Jacobs igure 43.1. Decision making in emergency surgery. (Reprinted with permission from Yamani et al.74)

Emergency Surgical Patient

Does the patient have decisional capacity? Yes No

No

Does the patient have an advance directive?

Discuss treatment options with the patient

Yes

Does the patient have an advance directive?

What type of directive does the patient have? No

Yes

Review the directive with the patient

Determine the patient’s wishes; encourage him to write an advance directive

Living Will

Yes

Health Care Power of Attorney

Does the directive contain specific instructions No

Are the instructions No applicable to the situation?

Are the patient’s wishes known? Yes

Yes

Follow the patient’s instructions

Does the evidence of the patient’s wishes satisfy state requirements? Yes

No

No

Seek ethical/legal guidance if time permits; Otherwise proceed according to “Best Interests” standard

Follow the patient’s wishes and/or the agent’s instructions

determinations. Also, it should be emphasized that, although the terms “capacity” and “competence” are frequently used interchangeably, there are some important differences. “Competence” is a legal term and refers to an individual’s ability to make rational, informed decisions about one’s life and property.68 Individuals over the age of 18 years are presumed to be competent unless declared otherwise by a court of law. Capacity is a medical term, is very much related to the concept of autonomy and informed consent, and can be defined as the “ability to understand the significant benefits, risks, and alternatives to proposed health care, and to make and communicate a health care decision.”17 Unlike competence, capacity is not absolute and must always be interpreted in a temporal and situational context. Therefore, a particular patient may possess the capacity for certain medical decisions, but not others, or at one point in time, but not another. For example, a postoperative acute care surgical patient may lack the capacity to make decisions regarding the appropriateness of

instituting dialysis or mechanical ventilation, but the capacity to choose an appropriate DHPA may well be preserved. Similarly, this patient’s capacity for medical decision making may fluctuate over time, depending upon clinical status, medications administered, and the nature and extent of medical procedures to which the patient has been subjected. The approach to determining loss of decisional capacity should be orderly and systematic. A standard minimental status examination involving an assessment of alertness, attention, memory, and reasoning will identify the majority of patients lacking decisional capacity. On occasion, these more basic functions will be preserved, necessitating a specific assessment of the patient’s capacity relative to the specific medical issue in question. Although many criteria have been proposed, and several evaluation tools exist to aid in the determination of decisional capacity, none has been proven to be superior to another.69–72 In its simplest terms, the capacity assessment need only address the two questions contained in the


earlier definition of capacity: (1) Does the patient understand the significant benefits, risks and alternatives to the proposed plan of care? (2) Can the patient make and communicate a health care decision? In order to give patients the very best chance to establish their decisional capacity (and thereby retain their autonomy), they must be provided with a thorough explanation of the risks and benefits of, and alternatives to, the proposed intervention. This is why the physician responsible for the patient’s care is likely to be in a better position to judge the patient’s decisional capacity than is the psychiatric specialist. Once the question of decisional capacity has been determined, medical decision making can then proceed, guided by the physician, the patient (if not incapacitated), the advance directive (if present), and other patient advocates (decisionally incapacitated patient, no advance directive). The American Medical Association’s Policy Statement E-2.20, Withholding or Withdrawing LifeSustaining Medical Treatment, nicely summarizes this approach to decision making.73 An algorithm showing how this process might occur is given in Figure 43.1.74

Advance Directives: Unfulfilled Potential The potential of advance directives to significantly alter end-of-life care in the United States has never been realized for two major reasons.The first, the overall small percentage of Americans who have actually completed advance directives, was discussed earlier. Second, even for patients who have completed these directives, there is little evidence that they actually alter end-of-life care.75,76 In one study of the impact of advance directives on hospital and skilled nursing facility care, care was consistent with the directive in only 75% of cases. Interestingly, of those cases when care was inconsistent with the directive, 75% actually received less aggressive care than specified in the directive.76 It is obvious that possession of an advance directive does not guarantee that the patient’s intent will be achieved. Why are these documents not effective? There appear to be several reasons. First, it is important to recognize that the advance directive may not actually reflect the patient’s wishes or intent. There may be several reasons for this, including limitations placed on these documents by the states in which they are drafted. For example, some states have no provisions in their living wills for a patient to refuse artificial nutrition and water should they desire. Furthermore, many patients are not receiving any education about, or help with completion of, these documents, including guidance from physicians. Although the intent of the PSDA was to encourage patient–physician interaction regarding this issue, there is little evidence that

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meaningful discussion is occurring from either a quantitative standpoint (percentage of patients who have had any discussion about the content of their advance directives with their physicians)77 or a qualitative one (percentage of patients who have a good understanding of the content of their advance directives).78 Not infrequently, the physician is unaware of the existence of advance directives.28,79 In one recent study of seriously ill intensive care unit patients, only 5% of patients had completed advance directives at the time of admission. Of those with advance directives who subsequently died, 11% underwent “unwanted” cardiopulmonary resuscitation because of lack of awareness of the advance directive on the part of the physician.80 Many patients have completed advance directives and have not informed either their physician or their family.81 The Internet has provided easy access to a myriad of advance directive products, and many patients are completing these without the knowledge or assistance of their physicians. Hence, when the patient loses decisional capacity, no one is aware of the existence of directives that might aid in decision making. One possible solution would be a requirement that these documents be co-signed by both the physician and the proxy, if one has been selected.81 Even if an advance directive is known to exist, it may not be readily available to the health care team at the time of presentation. These documents may be in the possession of family members, surrogates, or in the office chart of the primary care physician. Morrison et al.,82 in a study of 114 geriatric patients with previously executed advance directives, noted that only 26% of patients had these directives recognized during their hospitalizations. More importantly, of the subgroup of patients judged not to have decisional capacity during these hospitalizations, only 26% had their directives recognized.82 Some have recommended the actual appending of the advance directive to the Medicare card such that its contents would be immediately available to health care providers.83 Others have called for the creation of a central repository that would contain not only a patient’s advance directive but also the names and contact information of the primary care physician and any surrogates named by the patient.57 An additional shortcoming of advance directives, already alluded to, is the vague and imprecise language employed in many of these documents, found both in the qualifying statements within the document (“if my condition is __”), as well as in the directive statements (“then I do not wish __”). This, in turn, allows for significant differences in interpretation of the patient’s actual intent among the various health care providers and patient surrogates. Many qualifying statements specify conditions such as “terminal,” “incurable,” and “no reasonable expectation of recovery” that defy strict definition, thus potentially allowing unwanted aggressive care to proceed

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on purely subjective grounds. It has been well documented that many physicians choose not to adhere to advance directives because they believe that the patient’s condition does not meet the criteria outlined in the qualifying statements.24,64,65,75 Even when there is universal agreement that the criteria set forth in the qualifying statement have been met, the intent of the advance directive may be subverted, intentionally or unintentionally, through the physician’s interpretation of the terms “extraordinary means,” “heroic measures,” or “life-prolonging procedures” employed in the directive statements. For example, a blood transfusion and therapeutic endoscopy for a bleeding duodenal ulcer may seem extraordinary to the patient, but may be entirely reasonable in the physician’s mind, given the high likelihood of short-term “cure.” This highlights the shortcomings of the living will compared with the DHPA in that, under this specific scenario, the risks and benefits of blood transfusion and endoscopy could be discussed with the patient’s proxy, allowing authentic decision-making consistent with the patient’s values and beliefs to occur in real time. The DHPA, however, may not be the ultimate answer either. Not infrequently, the DHPA is unaware that he or she has been chosen to serve in this capacity and, when presented with this information, may be unwilling or unable to serve. Furthermore, the chosen proxy, even if willing to serve, may have ideological differences with the course of action dictated by the advance directive and therefore is unable to carry out the directive. Under these circumstances, a family member or some other surrogate will need to be identified who can fulfill this role. Finally, it is not at all clear that proxies can reliably make health care decisions for the patient using the “substituted judgment” standard.84–90 This once again highlights the need for thorough discussion among the patient, surrogate, and physician in order that the patient’s preferences and wishes be carried out.

Advance Directives: Relevance to the Acute Care Surgeon The principle of patient autonomy, although difficult to achieve, must still be preserved in the acute care setting. Thus, informed consent, either implicit or explicit, is necessary for all procedures, diagnostic tests, or treatments to be instituted. Frequently, however, the patient requiring acute care surgery lacks the requisite decision-making capacity to provide informed consent. Under these circumstances, a physician may render treatment without the patient’s informed consent. The underlying legal principle for this is termed implied or presumed consent, and it applies when the patient is deemed to be “incompetent.”91

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Ethically speaking, the principle of patient autonomy no longer prevails because preservation of autonomy under these circumstances would require the identification of a surrogate decision maker, thus delaying potentially life-saving medical therapy. Instead, beneficence becomes the dominant ethical principle, directing that treatment be provided according to what a “reasonable” person would want, for example, resuscitation. If, however, an authentic and relevant advance directive is immediately available, an unlikely event, then autonomy once again prevails, and care consistent with the directive should be provided. Here, the determination of “authenticity” and “relevance” is critical. In order to be judged to be authentic, the directive must have been appropriately and officially executed, with the necessary signatures and co-signatures. Advance directive identification bracelets and wallet cards present greater challenges in establishing authenticity, not to mention patient intent, and these should probably be ignored in the acute care setting unless their intent is clearly unambiguous.91 “Relevance” is the second test to which the advance directive must be subjected. The responsible physician must ensure that the qualifying and directive statements set forth in the patient’s advance directive apply to the clinical scenario at hand. Thus, the elderly patient with acute cholecystitis should not be denied cholecystectomy when the directive specifies “no heroic measures in the event of terminal illness.” Certainly the ambiguity of this statement precludes an unambiguous interpretation of the patient’s intent, but it is probably wiser to proceed with cholecystectomy, and then reevaluate, with any available surrogates, the intent of the directive in the early postoperative period, remembering that there is no difference, from an ethical standpoint, between withholding an intervention, and withdrawing it. An advance directive may also lead to a situation wherein the surgeon finds himself or herself ethically in disagreement with the care parameters outlined in the directive. This may be due to a directive that specifies aggressive care in circumstances that the surgeon believes represent medical futility, or, conversely, where the surgeon believes that care prohibited by the directive will be of benefit to the patient. Under this circumstance, the physician is under no obligation to passively adhere to the dictates of the directive. The physician, however, does have a responsibility to not abandon the patient and therefore is charged with the responsibility of finding a physician who can, in good conscience, carry out the dictates of the patient’s advance directive. Occasionally, input from an institutional ethics committee can help to resolve differences between the health care team and the advance directive (or the proxy) and thereby avoid the necessity of identifying alternate health care providers. As a last resort, some states have enacted binding legis-


lation that provides for a legal solution to these conflicts.92 All other reasonable efforts should be exhausted before resorting to this form of “mediation.” One circumstance that is perhaps unique to the emergency surgeon is that of the patient with a do-not-resuscitate (DNR) type of advance directive that sustains cardiopulmonary arrest in the course of an operative procedure. Ideally, this eventuality will have been discussed with the competent patient (or the proxy) prior to undertaking the operative procedure and clear agreement reached on the course of action to be followed under this circumstance.93 The emergent nature of the procedure does not release the surgeon from the obligation of exploring these difficult types of issues with the patient and/or proxy and documenting the results of these discussions in the medical record. In the event that intraoperative cardiac arrest does occur without some mutual understanding having been reached regarding the role of cardiopulmonary resuscitation, arguments have been made for both suspension of and adherence to the DNR order. Proponents of withholding cardiopulmonary resuscitation emphasize the right of the patient to expire peacefully while under anesthesia and, just as importantly, avoiding the possibility of condemning the patient to continuing to endure the unacceptable existence that prompted the DNR order in the first place.94 Reasons cited for utilizing cardiopulmonary resuscitation include the view that resuscitation is, in fact, part of, indeed inseparable from, the operative procedure itself and that the decision to proceed with surgery carries with it an obligation to employ all available methods to achieve patient survival. Furthermore, given the readily available resources in the operating room and the many potentially reversible causes of intraoperative cardiac arrest that occur there, the outcomes following intraoperative cardiac arrest are far better than cardiac arrest that occurs anywhere else. Thus, the overall poor postcardiac arrest outcomes that may have prompted the DNR order may not pertain under these circumstances.95 A middle-of-the-road approach takes into consideration the cause of the cardiac arrest, recommending cardiopulmonary resuscitation if the etiology of the arrest is easily correctable or iatrogenic in nature and withholding cardiopulmonary resuscitation if the patient’s underlying process has precipitated the arrest. Such distinctions are not always possible, and so, if there is any doubt about the exact etiology of the arrest, resuscitative efforts should be undertaken, recognizing that support can always be withdrawn at some future point should the patient’s clinical condition so warrant. The American College of Surgeons’ Statement on Advance Directives by Patients: “Do Not Resuscitate in the Operating Room” discourages both the automatic enforcement or cancellation of DNR orders and instead advocates a policy of “required reconsideration” of previous advance

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directives whereby the patient (or proxy) and responsible physician reach consensus regarding the approach to be taken in the event of intraoperative cardiac arrest based on perceived risks and benefits.96

Recommendations Although advance care planning offers patients the opportunity to preserve autonomy in end-of-life decision making, many are not taking advantage of the benefits these documents provide. Furthermore, the potential impact of advance directives on end-of-life care is substantially reduced by the vague and ambiguous language contained in these documents, the lack of uniformity and portability across state lines, and the physician’s lack of awareness of, and access to, these directives in critical situations. If advance care planning is ever to achieve the potential that was intended for it, then change, both legislative and behavioral, is needed. Some potential solutions include the following: • Institute widespread educational programs for patients regarding the importance of advance care planning. • Create educational and financial incentives for physicians to initiate and maintain end-of-life discussions with patients. • Mandate that all advance directives be discussed with and co-signed by the patient’s physician. • Create federal legislation that mandates the use of uniform language and medical care options in advance directives and that provides for reciprocity in directive recognition across all 50 states. The Uniform Health Care Decisions Act of 1993 represents a good example of such legislation and should be widely adopted.17 • Establish a central repository for advance directives. This would provide for consistent access to these documents when the primary care physician or surrogate is not available to guide treatment. Finally, it must be reemphasized that advance care planning involves much more than completion of an advance directive. Rather, it is the patient–physician communication that occurs in the process of completing the directives that is critical. Through these discussions, both patient and physician gain greater insight into those values that will guide end-of-life care, the patient understands and appreciates more fully what medical options exist for end-of-life care, the development of patient–physician trust is enhanced, and patient autonomy is reinforced. In the acute care setting, it is the surgeon’s responsibility to seek the presence of these directives, verify their authenticity, and honor them unless doing so would create an ethical conflict for the surgeon. Furthermore, the emergency surgeon, when clinical circumstances permit, should take advantage of any

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and all opportunities to initiate thoughtful and careful discussions with patients and/or their surrogates regarding end-of-life treatment preferences. This in turn ensures that autonomy is preserved, beneficence is maximized, and social justice is facilitated.

References 1. Strauss M, ed. Familiar Medical Quotations. Boston: Little, Brown and Company, 1968. 2. Furrow BR GT, Johnson SH, et al. Bioethics: Health Care Law and Ethics, 3rd ed. St. Paul: West Group, 1997. 3. American Hospital Association: A Patient’s Bill of Rights. Chicago: AHA, 1973. 4. Judicial Council of the American Medical Association: Report on Physician and the Dying Patient. Chicago: AMA, 1973. 5. Kutner L. Due process of euthanasia: The living will, a proposal. Ind Law J 1969; 44:539–554. 6. In re Quinlan. Vol 10: 70 NJ; 1976:355 A.352d647. 7. Cruzan v Director, Missouri Department of Health: 497 U.S. 261, 110 S. Ct. 2841, 111 L.Ed.2d 224; 1990. 8. O’Connor S. 881503 Concur v. Director, Missouri Dept. of Health. 497 US 261 1990. Available at: http://supct. law.cornell.edu/supct/html/88-1503.ZC1.html. Accessed January 9, 2004. 9. Fairman RP.Withdrawing life-sustaining treatment. Lessons from Nancy Cruzan. Arch Intern Med 1992; 152(1):25–27. 10. Omnibus Reconciliation Act of 1990. Public Law No. 101– 508. 1990; Sec. 4206. 11. Chambers CV, Diamond JJ, Perkel RL, Lasch LA. Relationship of advance directives to hospital charges in a Medicare population. Arch Intern Med 1994; 154(5):541– 547. 12. Weeks WB, Kofoed LL, Wallace AE, Welch HG. Advance directives and the cost of terminal hospitalization. Arch Intern Med 1994; 154(18):2077–2083. 13. Schneiderman LJ, Kronick R, Kaplan RM, Anderson JP, Langer RD. Effects of offering advance directives on medical treatments and costs. Ann Intern Med 1992; 117(7): 599–606. 14. Teno J, Lynn J, Connors AF Jr, et al. The illusion of end-oflife resource savings with advance directives. SUPPORT Investigators. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatment. J Am Geriatr Soc 1997; 45(4):513–518. 15. Gillick MR. Advance care planning. N Engl J Med 2004; 350(1):7–8. 16. Source: Partnership for Caring, Inc; March 2000 Data. Available at: http://www.partnershipforcaring.org/Resources/developments_set.html. Accessed January 26, 2004. 17. National Conference of Commissioners on Uniform State Laws. Uniform Health-Care Decisions Act. Available at: www.law.upenn.edu/bll/ulc/fnact99/1990s/uhcda93.pdf. Accessed January 26, 2004. 18. Gamble ER, McDonald PJ, Lichstein PR. Knowledge, attitudes, and behavior of elderly persons regarding living wills. Arch Intern Med 1991; 151(2):277–280.

D.G. Jacobs 19. Emanuel LL, Barry MJ, Stoeckle JD, Ettelson LM, Emanuel EJ. Advance directives for medical care—a case for greater use. N Engl J Med 1991; 324(13):889–895. 20. La Puma J, Orentlicher D, Moss RJ. Advance directives on admission. Clinical implications and analysis of the Patient Self-Determination Act of 1990. JAMA 1991; 266(3):402– 405. 21. Johnson RF Jr, Baranowski-Birkmeier T, O’Donnell JB. Advance directives in the medical intensive care unit of a community teaching hospital. Chest 1995; 107(3):752– 756. 22. Gross MD. What do patients express as their preferences in advance directives? Arch Intern Med 1998; 158(4):363–365. 23. Hanson LC, Rodgman E. The use of living wills at the end of life. A national study. Arch Intern Med 1996; 156(9): 1018–1022. 24. Wolf SM, Boyle P, Callahan D, et al. Sources of concern about the Patient Self-Determination Act. N Engl J Med 1991; 325(23):1666–1671. 25. Llovera I, Ward MF, Ryan JG, et al. Why don’t emergency department patients have advance directives? Acad Emerg Med 1999; 6(10):1054–1060. 26. Teno J, Lynn J, Wenger N, et al. Advance directives for seriously ill hospitalized patients: effectiveness with the patient self-determination act and the SUPPORT intervention. SUPPORT Investigators. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatment. J Am Geriatr Soc 1997; 45(4):500–507. 27. Teno JM, Licks S, Lynn J, et al. Do advance directives provide instructions that direct care? SUPPORT Investigators. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatment. J Am Geriatr Soc 1997; 45(4):508–512. 28. The SUPPORT Principal Investigators. A controlled trial to improve care for seriously ill hospitalized patients. The study to understand prognoses and preferences for outcomes and risks of treatments (SUPPORT). JAMA 1995; 274(20):1591–1598. 29. Loewy EH, Carlson RW. Talking, advance directives, and medical practice. Arch Intern Med 1994; 154(20):2265– 2267. 30. White ML, Fletcher JC. The Patient Self-Determination Act. On balance, more help than hindrance. JAMA 1991; 266(3):410–412. 31. Doukas DJ. Competency and the routine discussion of advance directives. Am Fam Physician 1992; 45(2):473–474. 32. Frankl D, Oye RK, Bellamy PE. Attitudes of hospitalized patients toward life support: a survey of 200 medical inpatients. Am J Med 1989; 86(6):645–648. 33. Singer PA, Martin DK, Lavery JV, Thiel EC, Kelner M, Mendelssohn DC. Reconceptualizing advance care planning from the patient’s perspective. Arch Intern Med 1998; 158(8):879–884. 34. Reilly BM, Magnussen CR, Ross J, Ash J, Papa L, Wagner M. Can we talk? Inpatient discussions about advance directives in a community hospital. Attending physicians’ attitudes, their inpatients’ wishes, and reported experience. Arch Intern Med 1994; 154(20):2299–2308. 35. Annas GJ. The health care proxy and the living will. N Engl J Med 1991; 324(17):1210–1213.

43. Advance Directives 36. Cugliari AM, Miller T, Sobal J. Factors promoting completion of advance directives in the hospital. Arch Intern Med 1995; 155(17):1893–1898. 37. Markson LJ, Fanale J, Steel K, Kern D, Annas G. Implementing advance directives in the primary care setting. Arch Intern Med 1994; 154(20):2321–2327. 38. Morrison RS, Morrison EW, Glickman DF. Physician reluctance to discuss advance directives. An empiric investigation of potential barriers. Arch Intern Med 1994; 154(20): 2311–2318. 39. Shmerling RH, Bedell SE, Lilienfeld A, Delbanco TL. Discussing cardiopulmonary resuscitation: a study of elderly outpatients. J Gen Intern Med 1988; 3(4):317–321. 40. Havlir D, Brown L, Rousseau GK. Do not resuscitate discussions in a hospital-based home care program. J Am Geriatr Soc 1989; 37(1):52–54. 41. Joos SK, Reuler JB, Powell JL, Hickam DH. Outpatients’ attitudes and understanding regarding living wills. J Gen Intern Med 1993; 8(5):259–263. 42. Johnston SC, Pfeifer MP, McNutt R. The discussion about advance directives. Patient and physician opinions regarding when and how it should be conducted. End of Life Study Group. Arch Intern Med 1995; 155(10):1025– 1030. 43. Kohn M, Menon G. Life prolongation: views of elderly outpatients and health care professionals. J Am Geriatr Soc 1988; 36(9):840–844. 44. McCrary SV, Botkin JR. Hospital policy on advance directives. Do institutions ask patients about living wills? JAMA 1989; 262(17):2411–2414. 45. Lo B, McLeod GA, Saika G. Patient attitudes to discussing life-sustaining treatment. Arch Intern Med 1986; 146(8): 1613–1615. 46. Tulsky JA, Fischer GS, Rose MR, Arnold RM. Opening the black box: how do physicians communicate about advance directives? Ann Intern Med 1998; 129(6):441–449. 47. Tulsky JA, Chesney MA, Lo B. How do medical residents discuss resuscitation with patients? J Gen Intern Med 1995; 10(8):436–442. 48. Roter DL, Larson S, Fischer GS, Arnold RM, Tulsky JA. Experts practice what they preach: a descriptive study of best and normative practices in end-of-life discussions.Arch Intern Med 2000; 160(22):3477–3485. 49. Doukas DJ, McCullough LB. The values history. The evaluation of the patient’s values and advance directives. J Fam Pract 1991; 32(2):145–153. 50. Emanuel LL, Emanuel EJ. The Medical Directive. A new comprehensive advance care document. JAMA 1989; 261(22):3288–3293. 51. Hickey DP. The disutility of advance directives: we know the problems, but are there solutions? J Health Law 2003; 36(3):455–473. 52. Romero LJ, Lindeman RD, Koehler KM, Allen A. Influence of ethnicity on advance directives and end-of-life decisions. JAMA 1997; 277(4):298–299. 53. Blackhall LJ, Murphy ST, Frank G, Michel V, Azen S. Ethnicity and attitudes toward patient autonomy. JAMA 1995; 274(10):820–825. 54. Caralis PV, Davis B, Wright K, Marcial E. The influence of ethnicity and race on attitudes toward advance directives,

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life-prolonging treatments, and euthanasia. J Clin Ethics 1993; 4(2):155–165. Eleazer GP, Hornung CA, Egbert CB, et al. The relationship between ethnicity and advance directives in a frail older population. J Am Geriatr Soc 1996; 44(8):938–943. Mebane EW, Oman RF, Kroonen LT, Goldstein MK. The influence of physician race, age, and gender on physician attitudes toward advance care directives and preferences for end-of-life decision-making. J Am Geriatr Soc 1999; 47(5):579–591. American Medical Association. E-2.225: Optimal Use of Orders—Not-To-Intervene and Advance Directives. April 17, 2003. Available at: http://www.ama-assn.org/ama/pub/ category/print/8462.html. Accessed January 22, 2004. Kapp MB. Response to the living will furor: directives for maximum care. Am J Med 1982; 72(6):855–859. Grodin MA. Religious advance directives: the convergence of law, religion, medicine, and public health. Am J Public Health 1993; 83(6):899–903. Ridley DT. Honoring Jehovah’s Witnesses’ advance directives in emergencies: a response to Drs. Migden and Braen. Acad Emerg Med 1998; 5(8):824–835. Kleinman I. Written advance directives refusing blood transfusion: ethical and legal considerations. Am J Med 1994; 96(6):563–567. Thompson T, Barbour R, Schwartz L. Adherence to advance directives in critical care decision making: vignette study. BMJ 2003; 327(7422):1011. Brett AS. Limitations of listing specific medical interventions in advance directives. JAMA 1991; 266(6):825– 828. Silverman HJ, Vinicky JK, Gasner MR. Advance directives: implications for critical care. Crit Care Med 1992; 20(7): 1027–1031. Tonelli MR. Pulling the plug on living wills. A critical analysis of advance directives. Chest 1996; 110(3):816– 822. Coppola KM, Ditto PH, Danks JH, Smucker WD. Accuracy of primary care and hospital-based physicians’ predictions of elderly outpatients’ treatment preferences with and without advance directives. Arch Intern Med 2001; 161(3): 431–440. Menikoff JA, Sachs GA, Siegler M. Beyond advance directives–health care surrogate laws. N Engl J Med 1992; 327(16):1165–1169. Grisso T. Evaluating Competence. New York: Plenium Press, 1986. Appelbaum PS, Grisso T. Assessing patients’ capacities to consent to treatment. N Engl J Med 1988; 319(25):1635– 1638. Drane JF. Competency to give an informed consent. A model for making clinical assessments. JAMA 1984; 252(7): 925–927. Grisso T, Appelbaum PS, Hill-Fotouhi C. The MacCAT-T: a clinical tool to assess patients’ capacities to make treatment decisions. Psychiatr Serv 1997; 48(11):1415–1419. Tunzi M. Can the patient decide? Evaluating patient capacity in practice. Am Fam Physician 2001; 64(2):299–306. American Medical Association. E-2.20: Withholding or Withdrawing Life-Sustaining Medical Treatment. July 22,

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D.G. Jacobs 2002. Available at: http://www.ama-assn.org/ama/pub/ category/print/8457.html. Accessed January 9, 2004. Yamani M, Fleming C, Brensilver JM, Brandstetter RD. Using advance directives effectively in the intensive care unit. Terminating care in the presence—or absence—of directives. J Crit Illn 1995; 10(7):465–467, 471–473. Teno JM, Stevens M, Spernak S, Lynn J. Role of written advance directives in decision making: insights from qualitative and quantitative data. J Gen Intern Med 1998; 13(7): 439–446. Danis M, Southerland LI, Garrett JM, et al. A prospective study of advance directives for life-sustaining care. N Engl J Med 1991; 324(13):882–888. Virmani J, Schneiderman LJ, Kaplan RM. Relationship of advance directives to physician-patient communication. Arch Intern Med 1994; 154(8):909–913. Fischer GS, Tulsky JA, Rose MR, Siminoff LA, Arnold RM. Patient knowledge and physician predictions of treatment preferences after discussion of advance directives. J Gen Intern Med 1998; 13(7):447–454. Teno JM, Lynn J, Phillips RS, et al. Do formal advance directives affect resuscitation decisions and the use of resources for seriously ill patients? SUPPORT Investigators. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments. J Clin Ethics 1994; 5(1):23–30. Goodman MD, Tarnoff M, Slotman GJ. Effect of advance directives on the management of elderly critically ill patients. Crit Care Med 1998; 26(4):701–704. Emanuel EJ, Emanuel LL, Orentlicher D. Advance directives. JAMA 1991; 266(18):2563. Morrison RS, Olson E, Mertz KR, Meier DE. The inaccessibility of advance directives on transfer from ambulatory to acute care settings. JAMA 1995; 274(6):478–482. Pollack S. A new approach to advance directives. Crit Care Med 2000; 28(9):3146–3148.

84. Seckler AB, Meier DE, Mulvihill M, Paris BE. Substituted judgment: how accurate are proxy predictions? Ann Intern Med 1991; 115(2):92–98. 85. Suhl J, Simons P, Reedy T, Garrick T. Myth of substituted judgment. Surrogate decision making regarding life support is unreliable. Arch Intern Med 1994; 154(1):90–96. 86. Hare J, Pratt C, Nelson C. Agreement between patients and their self-selected surrogates on difficult medical decisions. Arch Intern Med 1992; 152(5):1049–1054. 87. Ouslander JG, Tymchuk AJ, Rahbar B. Health care decisions among elderly long-term care residents and their potential proxies. Arch Intern Med 1989; 149(6):1367–1372. 88. Zweibel NR, Cassel CK. Treatment choices at the end of life: a comparison of decisions by older patients and their physician-selected proxies. Gerontologist 1989; 29(5):615– 621. 89. Tomlinson T, Howe K, Notman M, Rossmiller D. An empirical study of proxy consent for elderly persons. Gerontologist 1990; 30(1):54–64. 90. Uhlmann RF, Pearlman RA, Cain KC. Physicians’ and spouses’ predictions of elderly patients’ resuscitation preferences. J Gerontol 1988; 43(5):M115–121. 91. Iserson KV. Nonstandard advance directives: a pseudoethical dilemma. J Trauma 1998; 44(1):139–142. 92. Fine RL, Mayo TW. Resolution of futility by due process: early experience with the Texas Advance Directives Act. Ann Intern Med 2003; 138(9):743–746. 93. Peterson LM. Advance directives, proxies, and the practice of surgery. Am J Surg 1992; 163(3):277–282. 94. Walker RM. DNR in the OR. Resuscitation as an operative risk. JAMA 1991; 266(17):2407–2412. 95. Cohen CB, Cohen PJ. Do-not-resuscitate orders in the operating room. N Engl J Med 1991; 325(26):1879–1882. 96. Statement of the American College of Surgeons on Advance Directives by Patients. “Do Not Resuscitate” in the operating room. Bull Am Coll Surg 1994; 79(9):29.

44 The Nonviable Patient and Organ Procurement Frederic J. Cole, Jr., Jay N. Collins, and Leonard J. Weireter, Jr.

The current state of medical technology and critical care support is such that people who never had a chance of survival a generation ago routinely leave the hospital and return to productive lives. The unfortunate side effect of this remarkable advance is that not all patients fare so well. The patient rapidly delivered to tertiary care for resuscitation only to be found to have a lethal central nervous system disease is a common occurrence on trauma and critical care services. The concept of the nonsalvageable patient and the role of futile care has become a regular part of conversations among medical staff at all levels—physician, nursing, resident, medical student, and allied health professional. Recognition of this patient is not always simple. We will argue these issues among ourselves. Who is nonsalvageable? What care is futile? How do we broach this with the families of these patients? The evolution of solid organ transplantation needed the recognition of cerebral death criteria as a method to identify potential viable organ donors. How one determines cerebral death is unfortunately not uniform as it exists at the law—medicine interface. Criteria are agreed on, but application of the criteria is variable. Then there is the issue of how does one care for the potential donor in the workup phase of transplantation. This requires as much if not more critical care resources than the care of the original insult that culminated in cerebral death in the first place. This chapter attempts to put these issues into perspective and to offer a methodology to deal with the questions raised.

Defining the Problem Consider two cases, which are common in the practice of emergency surgery: 1. A previously vigorous 74-year-old woman in the intensive care unit following sigmoid colectomy, end colostomy, and Hartmann’s pouch for perforated diverti-

culitis with peritonitis is receiving aggressive ventilator therapy for respiratory insufficiency, fluids, and low-dose vasoactive agents for distributive shock. She has mild renal insufficiency but is not requiring dialysis. She is receiving enteral nutritional support and broad-spectrum antibiotics for generalized peritonitis and returns to the operating room several times for repeated peritoneal irrigation and debridements and drainage of interloop abscesses. Gradually her sepsis resolves, the vasopressors are weaned off, her renal function improves, her respiratory function improves, and she is weaned successfully from the ventilator. She transfers to the floor and eventually goes to the acute rehabilitation unit. 2. A 68-year-old man sustains a fall from a ladder while cleaning out the gutters. He suffers a right flail chest with fractures of ribs 3 to 8, right hemopneumothorax treated by right tube thoracostomy, and a closed midshaft tibia fracture. He undergoes intramedullary nailing of the tibia fracture the day of injury and is admitted to the intensive care unit postoperatively for monitoring. He has a history significant only for mild hypertension and diabetes. Despite aggressive pain control measures, his pulmonary toilet is poor. He develops progressive respiratory dysfunction, culminating in intubation and mechanical ventilation. He develops a Gram-negative ventilator-associated pneumonia requiring broadspectrum antibiotic therapy. Despite appropriate stress ulcer prophylaxis, he suffers a hemodynamically significant upper gastrointestinal bleed requiring endoscopic intervention. He develops acute renal failure related to his hemorrhage and requires dialysis. Over the ensuing weeks, his condition waxes and wanes with rallying periods during which he seems to clear his infections and begins to make progress in being weaned from the ventilator. Such a rally is then followed by another fever spike, leukocytosis, positive culture, drop in blood pressure, and intolerance of work of breathing and enteral feeding. Support is increased; another rally ensues, followed by deterioration.

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Surgeons are trained and comfortable with the first scenario. They expect to intervene surgically in the diseases of critically ill patients and then support them as they recover. They are comfortable employing the variety of advanced technologies, therapies, medicines, and surgical techniques common in the modern intensive care unit to return their critically ill patients to their previous state of health. This is, after all, why we admit our patients to intensive care units: to employ technology in the form of monitoring devices, ventilators and respiratory care, dialysis machines, and medicines such as antibiotics, sedatives, analgesics and vasoactive agents to support their vital functions and physiology as they recover from their primary disease processes. Surgeons are much less comfortable with the second scenario, which is all too familiar despite all of the advanced technologies and therapies available in the modern intensive care unit. Up to 40% of intensive care unit patients do not survive to leave the hospital.1–3 As the scenario implies, the physiology and vital functions of such patients can be maintained for quite some time before an irreversible terminal event occurs. Such maintenance does not come without cost. There is an obvious monetary cost to continuing to provide aggressive intensive care. The rising percentage of the Gross Domestic Product that the cost of medical care represents in our country has led to pressure from employers, the federal government, and third-party payers on doctors and hospitals to keep costs down. A significant portion of this money is spent in the last weeks of life in intensive care units.4 There is also a cost in terms of resources. Hospital beds in general and intensive care beds in particular are at a premium as hospitals struggle with staffing shortages and need for efficiency. It is all too common for the emergency departments of our hospitals to be boarding a number of critically ill patients waiting for an intensive care unit bed. There are human costs to providing this support as well. The patient is frequently in pain and fearful or anxious.1 There is an emotional toll on families and caregivers as repeated efforts fail to restore health.5 Inevitably, someone begins to question whether aggressive care with curative intent should continue. This may be a family member or one of the critical care team.

The Problem with Futility There has been a change in the last 40 years in how such issues are addressed and managed.6 This change parallels a shift in the ethical imperative in the doctor–patient relationship from the historical norm of benign paternalism to one of primacy of patient autonomy.6–8 Whereas there was little room for discussion in the past when the physician, the subject matter expert, recommended a course of

F.J. Cole, Jr., J.N. Collins, and L.J. Weireter, Jr.

treatment, today we place a great deal of emphasis on the need for the patient (or the patient’s surrogate) to actively participate in selecting the appropriate course of action. Thus any unilateral decision on the part of the physician to continue curative care or to withdraw lifesustaining therapies is today viewed with disdain.9 Interestingly, this emphasis on patient autonomy has emerged even as physicians have become more willing to limit and/or withdraw aggressive life-sustaining therapy. In contrast to the Karen Quinlan case in which conflict between Ms. Quinlan’s physicians and family arose over the wish of the family to have potentially life-sustaining therapy (the ventilator) discontinued and the doctors’ refusal, today the conflict is more likely to be over the insistence of the family that some life-sustaining therapy be continued after the critical care team believes that there is no hope of any long-term benefit from continuation of the therapy.8,10 This leads inevitably to a discussion of medical futility. There are legal and ethical precedents that physicians need not provide futile care.6,8,11,12 From a physician’s perspective, this concept is at first deceivingly simple. The historical goal after all is to return the patient to his or her premorbid state of health, and, failing that, returning them to an acceptable state of health with minimal morbidity. Being able to function independently, or with some assistance, but, at a minimum, being able to interact with one’s environment in a meaningful manner are laudable goals, and physicians quickly point them out. Some have advocated that determination of futility is purely a function of the medical staff assessing the patient, determining that there is no realistic hope for meaningful recovery, and making the “diagnosis” of futility.8–11 There are a number of problems with physiciandefined futility. First, determining which patients cannot achieve meaningful survival is less than an exact science. Physicians are certainly subject matter experts with respect to disease, options for treatment, and prognosis, but they are not able to accurately predict who will survive and who will not.1 There are a number of severity of illness scores: Simplified Acute Physiology Score (SAPS), Injury Severity Score (ISS), Mortality Prediction Model (MPM), Therapeutic Intervention Scoring System (TISS), and the various versions of Acute Physiology and Chronic Health Evaluation (APACHE), among others. None has reliably been demonstrated to accurately predict mortality for individual patients10,13 Any physician who has cared for critically ill patients for any length of time can relate stories of patients who all thought were hopeless only to see them walk back into the unit months later to thank the staff. Second is the matter of defining meaningful survival. Differing life experiences, religious traditions, and education will lead to different definitions. For some, any life is God-given and therefore inviolable. For others, the

44. Organ Procurement

absence of higher cortical function (persistent vegetative state) is synonymous with an unacceptable existence, making efforts to maintain vital functions futile. In the final analysis, determination of futility always involves a value judgment. Physicians are not subject matter experts in this arena. A third problem with physician-determined futility has already been suggested. The rising cost of medical care has put pressure on hospitals and doctors to be cost effective. Thus there is an implicit conflict of interest for the physician who is tasked with managing hospital and societal resources at the same time that one is providing optimum care for individual patients. The patient then is left with the task of determining what futility is.10 The physician serves to inform the patient regarding reasonable expectations for what may transpire with various courses of action.14 Unlike the situation of a patient with a progressing malignancy, patients in the intensive care unit for whom these discussions become pertinent are rarely able to participate in them at the time that they become pertinent.1 The decision then falls to the patient’s surrogate, usually the next of kin, but potentially a court-appointed guardian when there is no next of kin.8,10,14

Communication Is the Key One result of the shift to an emphasis on patient autonomy in the patient—physician relationship is that many patients will have executed “living wills,” or medical powers of attorney, which may provide insight into what the patient’s wishes might be in the event of catastrophic illness. Hospitals are now required to inquire and document patients’ preferences with respect to resuscitation.15 There is an increased awareness of these issues by the lay public through television programs and other media, and families are more likely to have discussed these issues than in the past. Nevertheless, there is some reluctance to engage patients or their families in discussion of these issues. Some providers fear that they will unnecessarily alarm the patient and family or that such conversation will give a false sense that the team is abandoning the patient.1,13,16,17 Indeed, abruptly engaging in a discussion regarding withdrawal of care after weeks of aggressive curative care can be confusing to the family as well as the critical care team. A better approach is one of continuing conversations in which current condition, planned interventions, and expectations are honestly discussed.1,13,17–19 Such discussions should involve all available stakeholders: patient/family/surrogate, physicians, nurses, therapists, clergy, and social workers. There has been little formal training in how to conduct such conversations in the past. Inadequate training can also lead to inhibition in addressing end of life issues.

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There are a number of models for these discussions. The most familiar is the “family conference” in which a formal meeting is arranged involving all of the parties mentioned above. Frequently such meetings are called to ask “the question” of the family when the physicians believe that further curative efforts are not of benefit. These then become high-stakes discussions with a significant amount of tension. There are less formal “daily updates,” which generally involve physicians, nurses, or other members of the critical care team transmitting information regarding the patient’s condition to the family in a more informal setting, often at the bedside. Unfortunately, these conversations do not always address what the patient’s wishes may or may not have been.They tend to be focused on where the patient is on the road to recovery and what the next therapeutic or diagnostic steps may be. A new innovation in transmitting information to families is the practice in many intensive care units of having family members attend and participate in daily rounds. This provides the family with medical information and with an opportunity for discussions regarding the patient’s previously stated goals and wishes. Whatever method is utilized, the crucial element is that there is an ongoing dialogue between the critical care team and the decision makers. Early discussion of what the patient’s values and goals are regarding their health and life combined with realistic assessment of the patient’s risk of death and impairment are critical to forging a mutually supportive relationship between the family and the health care team. Such a relationship allows the family and the providers to work together continuously to meet the patient’s goals rather than coming together for high-stakes decision making regarding discontinuation of life-sustaining therapy at the end of the patient’s illness without a solid basis for working together. There can be a continuum from curative to palliative care using this approach.20 There is emphasis on relief of symptoms and patient autonomy throughout the episode of care. When possible, conversations before illness or surgery among family, patient, and physician can lay the groundwork by establishing the patient’s values, goals, and expectations for treatment. Decisions can be made regarding limitations and end points of therapy that the patient finds appropriate. In the world of acute care surgery, such discussions can rarely occur as the acute treatment plan is developed and implemented. Early and ongoing discussions with the family can be utilized to learn what may have been discussed earlier in the nonacute setting among the patient, the family, and/or the primary care physician. There may be a living will, which should be sought for inclusion in the medical record. As treatment proceeds and milestones are either met or missed, reassessment of the consistency of the current plan with the patient’s goals can be determined. Each therapy can be evaluated with respect to its ability to help the

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patient achieve the goal of therapy.Treatments that do not further the patient’s goals may be withdrawn.1,4,13,18 As “cure” is increasingly recognized to not be a realistic goal, the focus changes and palliative therapies, instituted at the outset, are the only ones left in place. The importance of involvement of the entire health care team cannot be overemphasized. All stakeholders must possess the same objective data and subjective evaluations of those data to formulate a coherent and cohesive plan of care. Once the decision is made to change the focus of care from cure to palliation, it is important to understand how such care is most effectively delivered. There is an abundance of evidence that patients and their families have not been satisfied with the end-of-life care being provided in intensive care units.1,19,21 Consistent areas of concern are communication and symptom relief. Both of these components must be adequately addressed for effective end-of-life care to be rendered.1,18,19,21,22

End-of-Life Care The importance of effective communication has already been emphasized with respect to including all stakeholders in the conversation and sharing all relevant data, opinions, and thoughts. How the communication occurs is at least as important as the information being exchanged. Surgeons, physicians, and nurses are busy people. There is never enough time in the day to accomplish all that lies before us. Nevertheless, it is imperative that the health care workers be invested in these conversations leading to and following a decision to cease seeking cure. It is important that the family know that the surgeon is committed to the process and is not “squeezing them in” between cases.22 These discussions must not be rushed. The family needs the opportunity to work through the issues and to express their opinions, beliefs, and concerns. This cannot be done effectively on the fly in the hallway. A comfortable room apart from the intensive care unit needs to be available for such conversations to occur in private without interruption.19,22 Although autonomy dictates that the ultimate decision regarding cessation of curative care lies with the family, the primary physician must take an active role in the decision to pursue palliative end-of-life care. The physician must lend medical expertise to the process as well as shepherding the family through its steps: not deciding for them, but facilitating their decision. This may involve sharing their opinions, feelings, and doubts in a genuine and honest manner. Such interactions may require clinicians to expose their own vulnerabilities and preclude them from maintaining a safe emotional distance. Thus clinicians must have come to terms with their own thoughts about death and dying and be comfortable sharing them.22


There are a number of issues to be addressed in providing effective end-of-life care. Communication has been emphasized and cannot be overemphasized. The surgeon, nurses, and other professionals who were involved in the process of shifting focus to palliation must continue to be attentive to the patient and the family.1,18,19,22 Assurances to this effect must be given and realized. Some of the dissatisfaction families have reported in recent years has to do with the sense of abandonment caused by infrequent assessments by and interactions with the staff once the decision to abandon seeking cure is made. Effective care mandates frequent assessments of the efficacy of prescribed therapies and emergence of new symptoms.1 Realistic information regarding the anticipated course needs to be communicated to the family, updated, and changed as the clinical situation changes.22 The focus of end-of-life care is symptom relief for the patient. Further details regarding specific strategies are outlined below. Frequent assessment of symptoms and therapies should be undertaken as noted earlier. The family should be involved in this evaluation as well. Pain relief tends to be the primary end point. Evidence of pain may include restlessness, agitation, tachycardia, hypertension, and tachypnea. Other concerns may include anxiety, dyspnea, abdominal distension or pain, and nausea. There may be a trade-off between alertness and symptom relief. Which gets preference is determined through ongoing discussions with the family and patient if he or she are able to participate. The family must also be included in the care. It is a tremendously stressful time as they anticipate the loss of their loved one. Ideally they should have access to a waiting room in proximity to the intensive care unit. It should be comfortable with telephone access to an outside line and a television. Some intensive care units make Internet access available to patients’ families, and post updates on patient condition to the unit Web page. The family should have ready if not immediate access to nourishment and refreshments. There should be nearby accommodations (within the hospital) for them to sleep as well.23 Access to the patient should be liberal. If the intensive care unit has restricted visiting hours, they should be opened up for the family, allowing them to spend as much time as possible and desired with their loved one. Restrictions on personal items should be liberalized as well as restrictions on the number of visitors to the extent possible. The family may also be allowed and encouraged to participate in personal care of the patient if desired.1,17,23 To some extent this re-creates the situation in the past when people died at home with their families attending to them. Being able to provide hands-on comfort care to their loved one can greatly assist some family members in coming to acceptance and work through their grief.


All therapies must be evaluated for their contribution to the goal of symptom relief. Many routine interventions such as daily laboratory tests will be discontinued on this basis to prevent the pain of venipuncture. Agents for oral thrush may be continued as providing treatment for the symptoms related to the infection, whereas systemic antibiotics for other infections may be discontinued, especially if the agents require intravenous access. Fevers are treated with antipyretics, but ice packs and other topical coolants are avoided as being productive of discomfort.18 Symptoms of pain and distress are well treated with narcotics, such as morphine, and benzodiazepines. Transdermal narcotic administration systems are particularly useful if intravenous access is a problem. Respiratory depression is rarely observed in this patient population despite significant doses. One series demonstrated no difference in time to death for patients who received narcotics and those who did not. The implication is that it is the disease process that determines time of death.18,24 Haloperidol can be of use if there is also delirium present. Doses of all agents must be titrated to effect. Use of pain and sedation scales may be very useful.

Withdrawal of Life-Sustaining Treatment All of the foregoing processes described as being optimal palliation are appropriate for both curative care and endof-life care. The area of removing therapies that are deemed inconsistent with the goals of palliation when the decision has been made that cure is no longer a reasonable end point is a frequent concern for many practitioners. While no provider is interested in continuing modalities that are frequently painful or at least uncomfortable, may interfere with interaction with family members, or create other problems when they are no longer deemed capable of returning the patient to health, neither are they interested in causing pain, distress, or being accused of assisting suicide or killing the patient. With respect to the last point first, it is appropriate to recall that discontinuation of an unwanted therapy is equivalent ethically and legally to withholding the therapy in the first place. The principle of autonomy allows patients to choose what therapies they will and will not accept. This is different from the situation in which a patient requests an intervention that has no purpose other than to hasten or cause death—so-called physicianassisted suicide. This last remains illegal in most places in the United States. Legitimate therapies or treatments have as their goal restoration of health. When this is no longer possible, or when the burden of the treatment is too great in the opinion of the patient or the surrogate, the treatment may be foregone.

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The interventions most likely to be considered for withdrawal in the intensive care environment are mechanical ventilation, administration of vasopressors and inotropes, hemodialysis, antibiotics, enteral/ parenteral nutrition, and intravenous fluids.18 The last to be withdrawn is likely to be mechanical ventilation because of concerns regarding airway maintenance and symptoms of respiratory insufficiency. Some practitioners will remove the interventions sequentially, saving ventilation for last in the hope that the patient will expire without needing to have the ventilator removed.13,18 The areas of nutrition and hydration are the others most likely to be problematic for clinicians and families to remove.18,23 Concerns regarding both of these actions can be addressed through consideration of symptoms likely to result and how to treat those symptoms. Removal of vasopressors and inotropes will likely result in hypotension, and frequently death rapidly ensues. There may rarely be agitation, but this is well treated with sequential doses of a benzodiazepine.23 The consequences of discontinuing hemodialysis—acidosis, fluid overload, uremia, and electrolyte imbalance—for the most part require no intervention.18 Uremia may result in gastritis that can be managed with antacids or acid-secretion suppression. Dyspnea from hypervolemia or uremic pericardial or pleural effusions may be relieved by administration of oxygen, morphine, benzodiazepines, and fluid restriction.18 Discontinuation of antibiotics rarely causes symptoms. If fever is present and causing the patient discomfort, it can be treated with antipyretics, alternating acetaminophen with nonsteroidal antiinflammatory agents.18 Those who are dying typically do not experience hunger. In fact, administration of feedings may cause abdominal distention and distress.18,23 Knowledge of these facts goes a long way in eliminating concern about “withholding food” from the patient and allowing them to “starve.” The dying similarly do not often complain of thirst but do commonly complain of dry mouth. Sips of liquids, ice chips, and use of glycerin swabs, lip balm, and petroleum jelly can all be useful in relieving this symptom. Continued provision of adequate oral hygiene is also important. Thrush should be treated with antimonilial agents. Nausea when it occurs can be treated with a number of antiemetics. There are different approaches to discontinuation of mechanical ventilation: immediate extubation, terminal weaning with or without extubation, discontinuation of the ventilator without weaning, and continuation of intubation. There are proponents of each method who typically justify their approach as being more comfortable for the patient. Regardless of which approach is selected, appropriate preparation is necessary. The degree of respiratory insufficiency should be assessed so that the family can be properly counseled as to what to expect:

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rapid demise or independent ventilation for some time. The family must also understand that independent ventilation may continue for days or weeks or even become permanent (e.g., in the case of the persistently vegetative patient with no other significant organ dysfunction). The family and the caregivers should all understand what symptoms are likely to occur and what treatments to relieve the symptoms will be administered.1,13,18,22,23 Before mechanical ventilation is discontinued, administration of an anxiolytic such as midazolam is appropriate. If the ventilator support is to be gradually decreased to off (terminal wean), distress in the form of tachypnea, tachycardia, and restlessness may occur. These symptoms may be effectively treated with bolus doses of morphine, additional doses of midazolam, and/or a morphine infusion. Titration of the medications may be necessary to keep symptoms in check. Good tracheal toilet before extubation and an antisecretory agent (glycopyrrolate) may reduce problems with secretions (although creating dry mouth). In contrast to the controlled discontinuation of life support that follows discussions about the futility of further care and what the patient would desire, families are often thrown into chaos when their loved one has suffered a rapid-onset devastating cerebral event. Subarachnoid hemorrhage from a ruptured aneurysm, blunt cerebral injury from a motor vehicle crash or assault, or a gunshot wound to the head renders the victim almost but not quite dead. Worse yet, while the brain has been devastated the remainder of cardiopulmonary function continues almost as if nothing has happened. The deterioration of cerebral function can be tracked as the brain stem reflexes are lost from cephalad to caudad. Eventually the lowest lying reflexes, those controlling spontaneous respiratory drive and heart rate control, are lost. Unfortunately, the patient still exhibits a blood pressure, heart rate, and body temperature because of our intensive interventions. We tell families that their loved one is dead. They ask how, the monitor shows a blood pressure and heart rate. Now begins a potentially tedious and uncomfortable discussion about how people can die because their brain is dead. Lifenet, our organ procurement organization, has developed a program utilizing specially trained chaplains to facilitate this discussion with families of a potential organ donor. After the family has been informed that cerebral death criteria have been met, this chaplain approaches the family regarding organ donation. It is clear that this chaplain is separate from the team caring for the patient before the declaration of cerebral death. They are there to discuss organ donation, inquire as to the wishes of the patient regarding donation, if known, and answer questions that guide the family through the process of considering donation.


The Determination of Brain Death The brain is the organ most sensitive to loss of oxygen and perfusion. Its function may be irreversibly lost despite preservation of other organ functions. However, the advances in intensive care units over the years have allowed many patients who would have died to now survive for days or weeks without evidence of neurologic activity or hope for recovery. This progress in health care identified a major problem: What should be done for patients with no chance of recovery of neurologic function? In 1968, an ad hoc committee at Harvard University defined irreversible coma, or brain death, as a persistent comatose state of a known etiology with the absence of movement, brain stem reflexes, and breathing.25 Based on this information, the American Bar Association, American Medical Association, and the National Conference of Commissioners on Uniform State Laws developed the Uniform Determination of Death Act in 1980.26 In it, death has occurred in “an individual who has sustained either (1) irreversible cessation of circulatory and respiratory functions, or (2) irreversible cessation of all functions of the entire brain, including the brain stem. A determination of death must be in accordance with accepted medical standards.” This declaration is accepted as law in all 50 states. However, there is no one defined method to determine brain death. The criteria for the declaration of brain death are established by the individual states and vary from state to state. In some states, state law outlines the procedure for the determination of brain death. In others, the individual hospital facilities have the authority to enact a policy that describes the procedure for the determination of brain death. Written documentation of loss of all neurologic activity by either one or two licensed physicians is usually all that is required. In some states, one of the physicians is required to be a neurospecialist, but this may not always be possible, especially in smaller hospitals. In some states there must be an interval of 6 hours between the times of examinations, whereas in others no time interval is required.27 The determination of brain death does need to be in accordance with acceptable medical standards. In general, brain death is demonstrated by the complete loss of activity of the cerebral cortex with the absence of function of the midbrain, pons, and medulla. This is clinically demonstrated by the persistence of a comatose state, loss of all brain stem reflexes, and loss of spontaneous respirations. These guidelines were published by the American Academy of Neurology in 1995.27 The declaration of brain death requires a thorough neurologic examination, certainty about the etiology of the patient’s comatose state, and exclusion of contributing factors.28 Severe hypothermia, locked-in syndrome, drug intoxication, and Guillan-Barre syndrome with


cranial nerve involvement are all examples of conditions that may mimic a state of persistent coma.29 The certainty of irreversibility of the comatose state must be established as well as the etiology. In adults brain death is most often a result of cerebrovascular disease or traumatic brain injury.29 A computed tomographic (CT) scan of the brain is essential in determining the etiology of coma. This may reveal a mass effect, herniation of the brain stem, infarction, hemorrhage, or edema. At times the early CT findings after cardiopulmonary arrest, hypoperfusion, or central nervous system (CNS) infections may be normal, and follow-up CT scans are warranted. If the head CT is normal and suspicion of CNS infections is high, a diagnostic lumbar puncture is indicated. Before brain death is considered, the individual must be as physiologically normal as possible. Severe electrolyte, acid–base, or endocrine abnormalities must be corrected and excluded as causes of the coma. Patients must be free of all toxins, sedatives, narcotics, neuromuscular blockers, and other mind-altering drugs. This may require a period of observation to ensure that all drugs have been metabolized and eliminated. Patients must be normotensive and normothermic. Patients may be receiving vasopressors as needed to maintain a normal blood pressure (a mean arterial pressure of 60 mm Hg or greater). Coma from hypothermia must be excluded. Rewarming measures may be required until the core temperature is at least 32°C.27 Once a patient is thought to have sustained an irreversible brain injury and is metabolically normal, a thorough neurologic examination needs to be performed. The diagnosis of brain death requires documentation of a coma, absence of brain stem reflexes, and apnea. A persistent comatose state is one in which there is no response to any type of external stimuli. Patients do not spontaneously open their eyes or respond to verbal commands. Painful stimulation such as supraorbital or nail bed pressure does not result in movement or withdrawal of any extremity. However, spinal reflexes remain intact in a brain dead patient. This may result in spontaneous movements of the arms and legs or flexion at the waist. Although these movements can be shocking, this does not contradict the diagnosis of brain death if all other criteria are met. Decorticate or decerebrate posturing and seizure activity imply cortical activity and are not consistent with brain death. An examination of brain stem reflexes reflective of cranial nerve (CN) function needs to be completed next.27 Pupillary response to light measures the activity of CNs II and III. Fixed and dilated pupils unresponsive to light suggest loss of midbrain function. Gentle touching of the cornea with a cotton tip swab normally results in blinking of the eye. Loss of this corneal reflex (CNs V and VII) suggests loss of mid pons activity. If the eyes remain fixed forward with rapid rotation of the head, loss

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of the oculocephalic reflex (CNs VIII, III, and VI) has occurred. Loss of the oculovestibular reflex (CNs VIII, III, and VI) implies loss of lower pons activity. This occurs when ice-cold water is instilled in the ear canal and the eyes do not move. Pharyngeal (gag) and tracheal (cough) reflexes (CNs IX and X) are best tested by irritating the hypopharynx with a tongue depressor or the trachea with a suction catheter through the endotracheal tube. Absence of all of these central reflexes demonstrates loss of function of the midbrain and pons. After the loss of brain stem reflexes has been documented, the presence of apnea must be demonstrated. While keeping the patient well oxygenated, one looks for the absence of respirations in response to an elevated partial pressure of carbon dioxide (pCO2). The patient is initially preoxygenated with 100% oxygen.29 Arterial blood gas (ABG) is then measured to document a normal pCO2 (38 to 42 mm Hg). The ventilator is turned off and a catheter is placed through the endotracheal tube to the level of the carina. Oxygen is delivered at 6 to 10 L/min. Oxygen saturation is continuously measured by a pulse oximeter. During the apnea test the physician must remain at the bedside for the entire test period to watch for the absence of respiratory efforts. Any attempt at respiration shows the patient to have some function of the medulla oblongata, and the test is negative. Without respirations, the pCO2 usually rises 3 to 5 mm Hg/min. After 5 to 8 minutes an ABG sample is drawn. If the pCO2 is greater than 60 mm Hg or has risen more than 20 mm Hg from baseline and the patient has demonstrated no efforts at respiration, the apnea test is positive and supports the diagnosis of brain death. If these tests cannot be reliably performed or are indeterminate, other confirmatory tests may need to be performed. It may be difficult to do cranial nerve testing in patients with facial trauma or previous ocular abnormalities. Patients with severe drug intoxication may require an extended period of time to clear their system of the drugs. It may not be possible to do an apnea test on a patient with chronic obstructive pulmonary disease, severe retention of CO2, or severe hypoxemia. These confirmatory tests are also recommended for children under 1 year of age.30 The absence of blood flow to the brain is diagnostic of brain death. No visualization of the intracranial arteries on cerebral angiography results when intracranial pressure is greater than systemic arterial pressure. The external carotid artery may fill, but there is no visualization of flow at the circle of Willis or at the base of the skull. A nuclear brain scan with technetium has good correlation with angiography and will show no intracranial uptake of the radionucleotide. This results in the “hollow skull” sign and is diagnostic of brain death. Transcranial Doppler ultrasonography can also demonstrate lack of blood flow to the brain. Small systolic peaks in early systole without

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diastolic flow or reverberating flow indicate a very high vascular resistance and elevated intracranial pressure.31 Finally, absent electrical activity for at least 30 minutes on electroencephalography supports the diagnosis of brain death. Once an individual has been declared brain dead, that person is legally dead and all artificial means of support, including the ventilator, may be discontinued. However, it is appropriate to discuss this diagnosis with the family before removing support. Ideally the family is aware of the severity of the situation and the diagnosis of brain death is not a surprise. The option of organ donation may be considered at this time but is best approached from someone outside the primary health care team.

Care of the Potential Organ Donor Once patients are determined to be brain dead and potential organ donors, they are at risk for a number of adverse events unless fastidious attention is directed to their care. Complicating factors include the disease processes that lead to cerebral death and the subsequent deterioration as CNS regulation of vital physiologic functions is lost. Trauma with its soft tissue injury, hemorrhage-related shock, and preexisting coronary artery disease become important contributors to the physiologic demise of the potential donor. The time constraints imposed are variable, ranging from very short for a hemodynamically unstable patient to almost as long as 18 to 24 hours. Adequate tissue perfusion is essential to maintaining satisfactory end-organ function for transplantation. The end points of resuscitation include normalizing hemodynamics and maintaining acid–base balance, normal coagulation function, and temperature control. A urine output of 0.5 to 1.0 mL/kg/hr is a common surrogate of adequate perfusion. Care of the potential donor can be a challenge as the mechanisms of dying clash with the need to maintain physiologic viability. This section addresses care of the potential donor in the time interval during which tissue typing and donor evaluation occurs before harvesting and transplantation. The focus is on common conditions encountered and their treatment.

Cardiovascular System Issues Cardiovascular integrity is required to maintain an adequate donor for organ transplantation. A minimum mean arterial pressure of 60 to 70 mm Hg should be the goal as this will ensure adequate organ perfusion. Pressure measurement devices include automated cuff measurements, depending on auscultatory technology and arterial lines. Although both methodologies have advantages and disadvantages, the ability to sample blood via the arterial


line makes that the preferable method for measuring blood pressure. Location of the arterial line is at the discretion of the practitioner, and common practice favors the radial or brachial position. Femoral arterial catheterization for pressure monitoring carries an increased infection risk and is discouraged, although there are circumstances in which that route should be used. Fastidious attention to detail to minimize infection and other risks is necessary to preserve optimal end-organ function. Shock, the inability to meet the oxygen needs of the tissue beds, is a common problem and will interfere with transplantation success unless dealt with rapidly and correctly. Shock can be the result of the injury or disease state that preceded cerebral death but can also arise from the treatment of that injury or disease. Hypotension, usually as a manifestation of hypovolemic shock, is common. This may occur when hemorrhage has been inadequately treated. Overly aggressive diuretic therapy directed at intracranial pressure may also decrease blood pressure. Diabetes insipidus with inadequate fluid replacement will also decrease blood pressure. Alternatively, hypotension may result from vasodilation as occurs in severe infection. The intrinsic pumping function of the heart may be so compromised that the cardiac output fails to increase blood pressure appropriately to meet end-organ needs. Regardless of etiology, rapid determination of cause and institution of treatment are essential if organ function suitable for transplantation is to be achieved. The parties responsible for maintaining the potential donor need a thorough understanding of the events leading to cerebral death determination. Detailed conversation with the team treating the patient before cerebral death declaration will help clarify many of these details. Not uncommonly, the Organ Procurement Agency has a long-standing relationship with the intensive care practitioners and is in close communication with them leading up to the declaration of cerebral death. The family, once consent for donation has occurred, may be a good source for background medical information that might not be related to the events leading to cerebral death. A thorough medical history is part of the Organ Procurement Agency representatives’ requirements, but instability in the potential donor and the urgency to treat may preclude that discussion from occurring in a timely fashion. The etiology of hypotension may be multifactorial. Hemorrhage control needs to be ensured. Replacement of intravascular volume should readily correct the pressure if hypovolemia is the issue. Central venous pressure determination is an adjunct to shock therapy in that determination of the filling pressures of the right heart can be used as a surrogate for left ventricular end diastolic volume determination. Ideally, central venous pressure should be maintained in the range of 8 to 12 mm Hg.


More specific information can be determined with a flowdirected pulmonary artery catheter. This allows measurement of the pulmonary artery pressure at occlusion of the pulmonary artery, the “wedge” pressure, which in the absence of mitral valve pathology looks directly into the left atrium and ventricle during diastole. Normal pressures range from 12 to 15 mm Hg. Cardiac output can be determined with a pulmonary artery catheter and a variety of physiologic variables calculated from the data determined. Central venous oxygen saturation measured from the pulmonary artery is available and is used to determine if whole-body oxygen utilization is appropriate. The decision to use one device versus another is dictated by the stability of the patient, the preceding clinical course, and the need for greater information to help elucidate the reasons for ongoing hemodynamic instability. The risks of both devices are low in experienced hands. Pneumothorax with subsequent pulmonary complications occurs in approximately 2% of central venous line placements. The pulmonary artery catheter has a risk of cardiac valvular damage or of inciting arrhythmias in certain populations. As with any invasive device, it is the responsibility of the health care professional to balance the risk of the device with the benefit derived from the information the device provides. Once the type of central pressure monitoring has been decided, the practitioner needs to be attentive to the data derived. Fluid administration may take the form of crystalloid or colloid. The argument here is beyond the scope of this discussion and is frequently left to a given protocol employed by the treating institution. It is important to realize that dogmatic adherence to any given position may be detrimental, and fluid administered should reflect the needs of the patient. Packed red blood cell transfusion for ongoing hemorrhage or significant anemia, freshfrozen plasma or platelets for specific coagulopathy defects, and crystalloid fluids for dehydration replacement as commonly seen with the development of diabetes insipidus represent appropriate utilization of these substances. The balance between over- and underhydration underscores the crystalloid colloid controversy. Ideally, one would like to construct a Starling curve with optimal cardiac output response to ensure end-organ perfusion. Failing that, one needs to be suspicious that specific diseases such as pneumothorax, tension pneumothorax, cardiac tamponade, or cardiogenic shock may be present. Identification and treatment of a specific condition should lead to resolution and return to stable, normal hemodynamics. Associated with brain injury is a release of catecholamines, epinephrine, norepinephrine, and dopamine. Cerebral herniation is accompanied by a profound coronary vasospasm that may induce significant myocardial

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ischemia with decreases in cardiac contractility that occur over minutes to hours. As cerebral death is completed and neural control lost, there will be a profound vasodilation with further drop in blood pressure as a relative hypovolemia is induced.32–35 Aggressive use of echocardiography to evaluate contractile function and measure ejection fraction may be the best way to track this development and monitor therapy. Pharmacologic support of the failing heart and circulation requires judicious use of alpha- and beta-agonists to provide inotropic support for contractility while controlling heart rate so as not to further exacerbate myocardial ischemia.36 If adequate preload has been obtained, as measured by central filling pressures, and mean arterial pressure is still less than 60 mm Hg, cardiac contractility may be augmented with inotropic agents such as dopamine. Dosing can begin between 5 and 10 mg/kg/min. The point is that hypotension with mean arterial pressure less than 60 mm Hg needs rapid treatment. Fluids plus inotropic agents to increase the mean arterial pressure are essential. Maintaining this pressure between 80 and 90 mm Hg is a reasonable goal. Alternatively, the systolic blood pressure needs to be maintained greater than 100 mm Hg. A more aggressive inotropic agent use should be discussed with the transplant surgeons. Use of such agents may be part of a predetermined resuscitation protocol. The inability to keep the mean arterial pressure above 60 mm Hg will compromise donor organ function and threaten the viability of the donor. The role of thyroid hormone replacement therapy in this situation is controversial. Triiodothyronine infusion is associated with increased myocardial contractility independent of beta-receptors, possibly because of calciumdependent cardiac contractile proteins.37–39 The decision to use or not to use such replacement should be the result of specific protocol development by the treating team. A typical dosing regimen is levothyroxine 200 μg/250 mL normal saline (NS) and begun at 20 μg/hr and 25 mL/hr, with a maximum dose of 30 μg/hour to keep systolic blood pressure above 100 mm Hg. Alternative etiologies of hypotension include specific medication effects during support of the patient in the time leading up to cerebral death declaration. Aggressive diuretic therapy leading to hypovolemia should be detected and volume status restored. The use of barbiturate coma can result in a negative inotropic effect on the heart. This should be resolved before the declaration of cerebral death but may have residual effects that need to be addressed independently. A specific cause of hypovolemia with cardiac consequences is the development of diabetes insipidus. The loss of hypothalamic–pituitary function with decreased release of posterior pituitary hormones, especially vasopressin, results in an unchecked urinary output as the antidiuretic effect is lost. Volume-for-volume fluid

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replacement is necessary, and intravenous vasopressin may be needed to ameliorate the condition. The diagnosis of diabetes insipidus is made by the production of large volumes, often several hundred milliliters per hour, of dilute urine as characterized by a specific gravity less than 1.005. Hypertension, a mean arterial pressure consistently above 100 mm Hg, can cause adverse cardiac effects if left untreated. Hypertension and bradycardia are the cardiovascular hallmarks that accompany brain stem herniation and require no particular treatment other than that directed at the CNS pathology. Long-standing hypertension increases the stress on the myocardium, and the degree of injury is a function of the degree and duration of the hypertension. Short-acting beta-blockers or carefully titrated vasodilating agents can be used intravenously to obtain the blood pressure control necessary. Sodium nitroprusside in doses of 0.3 μg/kg/min up to 10 μg/kg/min may be used to control severe hypertension. Rapid vasodilatation with sudden drops in mean arterial pressure can occur with nitroprusside use, so fastidious titration is essential. Frequently, hypertension requires no specific therapy other than awareness of its presence.

Fluid and Electrolyte Issues Fluid and electrolyte disturbances are commonly seen in the potential organ donor. They, like the cardiovascular abnormalities, result from the disease process leading to cerebral death or from the therapy preceding cerebral death declaration, or they are sequelae of the loss of neurologic control that accompanies death. Vasopressin is elaborated by the posterior pituitary and acts as a potent antidiuretic agent under normal conditions. With the development of cerebral demise the pituitary no longer elaborates vasopressin with the resultant loss of regulation of renal tubule function.40–42 Urine output consists of dramatic volumes of dilute urine, as no concentrating or resorptive ability exists. A urine specific gravity less than or equal to 1.005 in the face of no diuretic therapy and urine output frequently in excess of hundreds of milliters hourly supports the diagnosis. Therapy is directed at reestablishing the hormonal control of fluid resorption in the kidney. Vasopressin administered as an intravenous bolus dose of 5–10 units followed by a titratable infusion in conjunction with volume-for-volume replacement of urinary loss with 0.25 NS can readily correct the problem. Alternatively, intermittent doses of intravenous desmopressin, 1–2 μg every 2 hours, until urine output is in the range of 200 mL/hr, can be used. Pros and cons of vasopressin and desmopressin center on the vasoconstrictive effects of vasopressin on donor organs and potential detrimental effects of desmopressin on the transplanted kidney.43–45


The free water deficit induced by such diuresis can be substantial and requires aggressive correction.The hypernatremia that accompanies diabetes insipidus is a reflection of water loss far in excess of any sodium loss and can be used to determine the volume deficit in liters that results. The free water deficit is calculated as follows: Free water deficit (liters) = 140 (0.6 × weight in kg)/measured Na+ Replacement should proceed with 0.25 NS administered to meet 50% of the deficit over 3 to 4 hours and the remainder as reassessment of the sodium and fluid status dictates.46 Inadequate glucose control can produce an osmotic diuresis. Serum glucose in excess of 300 mg/dL in conjunction with marked glucosuria should prompt aggressive glycemic control with intravenous insulin and water replacement as outlined above. Glycemic control with blood glucose less than or equal to 250 mg/dL with normalization of intravascular volume should be rapidly obtained. Hyponatremia is far less common. It is of little concern until sodium drops below 125 mg/dL. One confounding variable is the fact that pseudohyponatremia results from elevation of serum glucose that artificially lowers measured sodium. To correct for the sodium, 3 mg/dL should be added to the measured sodium for every 100 g/dL of glucose elevation over 300 mg/dL. Abnormalities of potassium and magnesium require correction as the potential for cardiac arrhythmia increases with marked increased or decreased levels of these electrolytes. Most intensive care units have potassium replacement protocols to maintain potassium levels in the normal range. Hyperkalemia may require more aggressive methods to bring the levels into the normal range. Glucose and insulin shift potassium into the intracellular space and allow rapid albeit short-term control. Binding resins and dialysis, although commonly used in critical care, may not be appropriate for the donor population. Specific protocols for replacement and control of potassium, magnesium, and calcium should be developed and utilized by the care team in conjunction with the transplant surgeons.

Acid–Base Balance Issues Acid–base disturbances reflect underlying pathophysiology and need to be addressed quickly.Acidosis, pH < 7.20, carries a risk of decreasing cardiac contractility and inducing cardiac arrhythmia. Renal blood flow decreases and serum potassium level increases as acidosis worsens. There is also a diminished responsiveness to catecholamines. Alkalosis induces coronary vasospasm and is also associated with arrhythmia risk. Potassium and magnesium are shifted intracellularly, which may have a role


in cardiac irritability. Hemoglobin–oxygen binding intensifies in alkalosis making peripheral offloading at the tissue interface more difficult, leading to microcirculatory hypoxia. Acidosis is probably a more commonly encountered problem. Respiratory causes are amenable to correction of minute ventilation. Respiratory alkalosis is seen if hyperventilation has been utilized to control intracranial hypertension before cerebral death declaration or if severe volume contraction has been protracted and untreated. Metabolic acidosis can arise for a number of reasons many of which should have been clarified before declaration of death. The anion gap is an easy method to stratify etiologies. The anion gap represents the difference between the cation and anion species present in plasma: AG = (Na+ + K+) − (Cl− − HCO3−) A normal anion gap is 8 to 12. A normal anion gap acidosis results from early renal failure, prolonged total parenteral nutrition use, prolonged hyperventilation, or the use of acetazolamide as a diuretic.47–49 An increased anion gap acidosis commonly reflects inadequately resuscitated shock. Elevation of the base deficit and serum lactate level will corroborate shock as the likely etiology. Alternatively, established renal failure may be an etiology. Other common causes such as diabetic ketoacidosis, toxin ingestion, and hyperosmolar nonketotic states should have been identified and rectified before the declaration of cerebral death. Correction of the acidosis is directed at the primary cause. Shock needs to be resuscitated and ketoacidosis corrected with insulin and intravenous fluid. Occasionally bicarbonate will need to be administered to mitigate the effects of the acidosis before correction of the underlying pathology is complete. The HCO3 deficit can be calculated as follows: mEq HCO3 = 24 − [measured HCO3 × 0.4 (patient weight in kg)] This will determine the HCO3 quantity to be replaced and avoid overzealous administration with overshooting the target pH and subsequently inducing alkalosis.

Coagulation System Issues Coagulation defects may arise as a consequence of medications used by the patient before the events leading to cerebral death or as part of the recent disease and treatment. Coagulation is a temperature-dependent series of reactions. Body temperatures less that 92°F are associated with shutdown of the coagulation cascade as platelet function virtually stops. Temperature control becomes essential to minimize this risk. Coumadin, aspirin, clopidogrel, and ticlopidine are commonly used outpatient anticoagulants. Heparin is

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routinely used in the hospital therapeutically or to help maintain indwelling arterial lines as a flush solution. The use of these agents needs to be specifically sought and appropriate measures taken to counter their effects as necessary. Consumptive coagulopathy frequently accompanies severe trauma with massive hemorrhage. Replacement of lost blood with component therapy from the blood bank frequently underestimates the need for specific coagulation components. Replacement of platelets and use of fresh-frozen plasma or cryoprecipitate, alone or in combination, will be dictated by the clinical situation and the laboratory data obtained. A specific coagulation defect known as disseminated intravascular coagulation represents a breakdown in the balance between clot formation and lysis, with the scales tilted in favor of clot lysis. In the scenario of the cerebral death patient, overwhelming sepsis can be an etiology of disseminated intravascular coagulation, but more commonly it is severe cerebral injury. The brain is a tremendous tissue thromboplastin reservoir. The injured brain releases large quantities of tissue thromboplastin. The result is an augmented coagulation system. The response to this abnormal clot formation is an upregulation of plasmin activity and increased clot lysis. The key to the diagnosis of disseminated intravascular coagulation is the knowledge of the pathophysiology. Prolongation of the protime (PT) and partial thromboplastin time (aPTT) and a decrease in the platelet count and fibrinogen levels demonstrate consumption of the coagulation cascade elements. Detection of fibrin degradation products and D-dimer species reflect the increased lytic activity. Classically therapy is directed at the inciting cause with support of the coagulation system with factor replacement as indicated. Systemic heparization as a way to stop the coagulation and thus interrupt the process is advocated as an adjunct. Unfortunately in the cerebral death patient the head injury is not treatable. Heparin probably has no role here either. Therapy is directed at specific factor replacement to help control the coagulation abnormality in the short term. Regular determination of the hospital disseminated intravascular coagulation screening panel will detect all the components of the coagulation system and allow appropriate correction. Overwhelming infection, a common disseminated intravascular coagulation initiator and usually precluded organ donation, is not usually a consideration in care of the donor. Obstetric causes of disseminated intravascular coagulation, such as amniotic fluid embolus, are distinctly unusual in this situation.50

Temperature Regulation Issues The center of temperature regulation resides in the hypothalamus. With cerebral death, temperature regulatory function is lost. Patients may demonstrate hyper- or

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hypothermia. Hyperthermia reflects inflammatory drivers from the cytokine cascade as a response to injury or infection. The increased cellular metabolic rate with increased oxygen consumption can be detrimental to end-organ function. The possible role of infection driving such fever response needs to be considered and sources of infection sought. The inability to respond to environmental cooling commonly accompanies cerebral death. Therapy of the injury or disease preceding death uses medications and fluid administration none of which is at body temperature. Intensive care unit rooms are kept at temperatures comfortable for the medical staff rather than the patients’ needs. As in the discussion of coagulation, temperature protection is a critical factor to be concerned about, as it is far easier to maintain body temperature that it is to recoup it. The goal should be as normal a body temperature as possible, with temperatures 9 over the study period (1989–2000) was 6.2%. There is also variation in outcomes among hospitals. The top 10% of hospitals deliver a statistically significant improvement in mortality rate.87

Present Arrangements There is still no nationally coordinated policy for the care of the severely injured. There are 32 ambulance services operating as independent NHS trusts. Individual hospitals are often served by more than one ambulance agency. In all but a few areas, seriously injured patients are still taken to the nearest hospital rather than to a designated hospital with appropriate resources and experienced staff. An exception is the Helicopter Emergency Medical Service, established in 1988 in London and partly funded by the NHS and charitable organizations. Operating during daylight hours, an experienced trauma physician is flown to the scene of accidents within the Greater London area, where life-saving intervention and stabi-

B.F. Ribeiro et al.

lization may be performed at the scene of the accident. The patient is then transferred to the most appropriate hospital, either by air or by land ambulance, where an awaiting trauma team has been activated. There are approximately 240 acute care hospitals in England, Wales, and Northern Ireland with emergency departments, but only 22 of these have neurosurgery departments on site. Five hospitals have the full range of surgical services (general surgery [including vascular and paediatric], orthopedics, cardiothoracics, neurosurgery, maxillofacial, and plastics). However, there are wellestablished systems of referral for head, spine, and burn injuries and an increased willingness to transfer such patients.85

Incidence and Costs of Severe Injury The incidence of severe trauma (ISS >15) in the United Kingdom is estimated to be 4 per 1 million per week. The average acute care hospital is not likely to be called on to treat more than one severely injured patient each week, which suggests that some hospitals may have too little experience to give these patients their best chance of an optimum outcome. It is estimated that on average 1 per 1,000 acute care cases admitted to the hospital are multiply injured patients. Without centralization to larger acute care hospitals, adequate experience in the definitive management of such patients is hard to acquire.85 In 1997, a fatal injury was estimated to cost the nation $1.7 million, a major injury $190,000, and a minor injury $15,000. These costs included direct medical expenditures, loss of economic activity, and the human aspects of grief, suffering, and pain. Annual hospital costs for road trauma alone are about $1 billion and ambulance costs are $38 million more.85

The Future The Royal College of Surgeons of England, along with the British Orthopaedic Association, in 2000 published a follow up to their 1988 report titled “Better Care for the Severely Injured.” There were several key recommendations in the following areas85: 1. A national trauma service:This should be developed based on a “hub and spoke” arrangement among hospitals within a defined geographic area or system. Each system would serve a population of up to 3 million, with a single integrated emergency ambulance service. There would be one major acute care hospital (Level I) in each system with all specialities on site. This would be supported by acute care general hospitals (Level II) acting in partnership with the major acute care hospital and would be able to resuscitate the severely injured and treat most injuries. Some acute care general hospitals would be

49. United Kingdom

designated as Level III, as they may not receive sufficient numbers of major trauma patients to retain the skills of staff or justify the expense required for the reception and resuscitation of major injuries. 2. Prehospital care: Emergency ambulances attending major trauma should have a paramedic trained to the Prehospital Trauma Life Support standard. The paramedic will select the most appropriate receiving hospital and radio ahead to activate the trauma team. Patients with life-threatening trauma or multiple injuries should never be taken to the Level III hospital. The use of helicopter retrieval may be beneficial in isolated locations, especially where distances from the Level I hospital may be great. 3. Interhospital transfer: Protocols for secondary transfers from Level II to Level I hospitals must be in place, with targets for transfer time. 4. Audit and research: A National Trauma Audit Committee should set standards and develop realistic outcome indicators. A National Trauma Audit Research Network should collect data from all hospital trusts receiving severely injured patients, ensuring development, improvement, and monitoring of standards of care. In addition to these nationwide recommendations, a working party has been set up to develop practical proposals to optimize care, treatment, and transfer of severely injured patients within London. There are approximately 1,400 severely injured patients treated in London per year, with two thirds requiring transfer for specialist care. As in many other parts of the country, current services in the capital are neither well located nor well coordinated. The London Severe Injury Working Group has built on the recommendations of the Royal College of Surgeons of England specifically for the city of London, and suggests the following88: 1. Improved patient pathways: faster prehospital response and treatment, optimal prehospital routing (including bypass to specialist centers), and criteria for automatic transfer to specialist care 2. A London-wide trauma system: establishment of networks, clinical governance and auditing, and a systemwide coordination center 3. Pediatric trauma: multispecialist units with a network of approved pediatric trauma admitting hospitals and approved pediatric trauma receiving hospitals around each unit, allowing prompt treatment and transfer of pediatric trauma patients to the most appropriate center Despite the recommendations, trauma care in the United Kingdom has seen little progress. There is still little prospect of a national trauma service being established, and, to date, only 50% of receiving hospitals provide data to a national trauma audit research network. The nearest the United Kingdom has to a designated trauma center is likely to be the Royal London

781

Hospital. The Helicopter Emergency Medical Service is based on the helipad on top of the hospital, and, through the efforts of individuals over the last 10 or so years, the hospital has developed toward being a specialist trauma center. There is certainly a degree of a “hub and spoke” model within the local acute care hospitals in terms of secondary transfer, and the Helicopter Emergency Medical Service has the ability to take the severely injured directly to the most appropriate hospital, which is not always the Royal London Hospital. To improve trauma care in the United Kingdom, a national policy is required with a strong commitment by the government to maintain and increase the current level of consultants involved in major trauma. One hundred percent participation in national auditing is a must to providing quality observational evidence valuable insight into both good and bad practices.86 Without facing up to such challenges, trauma care in the United Kingdom may continue to plateau. There is some hope for progress in the near future given the changes in other fields, most notably cancer services. The NHS has embarked on an ambitious plan to improve cancer services nationally with the development of a network of cancer units and cancer centers. Minimum standards of care, multidisciplinary teams, management protocols, and referral patterns have been established for specific malignancies. Cancer units will provide care for most patients with the common malignancies,for example, breast and colorectal. Cancer centers will provide the leadership for the units within their network, monitor standards, and provide treatment for the less common tumors or where data have demonstrated that high volume surgery leads to better outcome, for example, pancreatic, esophageal, and hepatic malignancies.89,90 This pattern of care could be adapted to the advantage of injured patients: a trauma system consisting of trauma units providing care for the majority of injured patients and trauma centers providing care for the most seriously injured and leadership within their local network.Trauma systems could then work within a framework of agreed on protocols, referral patterns, and standards of care. The idea of a trauma system for the United Kingdom has been proposed several times to date, but no action has been taken. With the development and acceptance of national standards and programs in other specialities in the NHS, the time for a UK national trauma system may be approaching.

The Emergency Department (Acute Care Facility) of the Future The emergency department of the future will need more front-line specialists of sufficient seniority to assess new emergency admissions and to make decisions about the

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B.F. Ribeiro et al. Figure 49.2. Proposed integrated pathway for access to emergency care. MAU, medical assessment unit; SAU, surgical assessment unit. (Source: http:// uktransplant.org.uk/statistics.)

Patient

Ambulance Service

General Practitioner (GP)

Self Referral

Discharge

Patient Triage Area (Accident & Emergency Dept.)

Resuscitation & Major Trauma

Rapid Assessment MAU/SAU*

Minor Injuries Unit

Appropriate Specialist Care

GP Unit

Patient’s GP

Outpatient Department

need for surgery without delay. To achieve this, new integrated pathways of care will be required. The role of nurses, physiotherapists, and radiographers will need to change as they take on a more therapeutic role.91 To improve patient flow, an effective triage of patients must be established to identify patients who are the most at risk (Figure 49.2). The Medical Royal Colleges and the Department of Health have agreed to proposals to aid the development of the new emergency departments within the NHS.92 Only time will tell if this succeeds where others have failed. The implementation of the EWTD in August 2004 has ensured that most trainees do not remain resident on call.93 New ways of working are requiring separate day and night shifts, and, in order to maximize teaching and training, as much emergency work as possible will be moved from evening and night-time to occur between 9 am and 9 pm. Several initiatives have been considered. The Out of Hours Medical Team (OoHMT) will provide a mixed team of physicians, anesthetists, surgeons, and nurses to manage the acutely ill patient at night. Consultant surgeons will be available on call, from home, to deal with emergencies requiring urgent surgery at night. Health care in the United Kingdom is changing rapidly. The reduction in trainee hours, the introduction of independent treatment centers (staffed by overseas doctors), the inclusion of 10 new member states into the European Union, and providing free access for specialists to work in the United Kingdom will all have a significant impact on health care delivery. The NHS has received a substantial boost in funding in the past 2 years, under the current Labour Government. More will be required if services are to be maintained and emergency care given the priority it deserves.

Social Services

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49. United Kingdom 13. Calman K. Hospital Doctors: Training for the Future. The Report of The Working Group on Specialist Medical Training. London: HMSO, 1993. 14. Beecham L. New Scottish CMO criticises training reforms. BMJ 1996; 313:947. 15. Addison PDR, Getgood A, Paterson-Brown S. Separating elective and emergency surgical care (the 50 emergency team). Scot Med J 2001; 46:48. 16. Thomson HJ, Jones PF. Active observation in acute abdominal pain. Am J Surg 1986; 152:522–525. 17. Cochrane RA, Edwards AT, Crosby DL, Roberts CJ, Lewis PA, McGee S, et al. Senior surgeons and radiologists should assess emergency patients on presentation: a prospective randomised controlled trial. J R Coll Surg Edinb 1998; 43:324–327. 18. Gray DWR, Collin J. Non-specific abdominal pain as a cause of acute admission to hospital. Br J Surg 1987; 74:239– 242. 19. Paterson-Brown S. The acute abdomen: the role of laparoscopy. In: Williamson RCN, Thompson JN, eds. Bailliere’s Clinical Gastroenterology: Gastrointestinal Emergencies, Part 1, London: Bailliere Tindall, 1991:691–703. 20. Decadt B, Sussman L, Lewis MPN, et al. Randomised clinical trial of early laparoscopy in the management of acute non-specific abdominal pain. Br J Surg 1999; 86:1383–1386. 21. Clavien PA, Burgan S, Moossa AR. Serum enzymes and other laboratory tests in acute pancreatitis. Br J Surg 1989; 76:1234–1243. 22. Kylanpaa-Back M-L, Kemppainen E, Puolakkainen P, et al. Reliable screening for acute pancreatitis with rapid urine trypsinogen-2 test strip. Br J Surg 2000; 87:49–52. 23. Thompson MM, Underwood MJ, Dookeran, KA, Lloyd DM, Bell PRF. Role of sequential leucocyte counts and Creactive protein measurements in acute appendicitis. Br J Surg 1992; 79:822–824. 24. Davies AH, Bernau F, Salisbury A, Souter RG. C-reactive protein in right iliac fossa pain. J R Coll Surg Edinb 1991; 36:242–244. 25. Middleton SB, Whitbread T, Morgans BT, Mason PF. Combination of skin temperature and a single white cell count does not improve diagnostic accuracy in acute appendicitis. Br J Surg 1996; 83:499. 26. Gronroos JM, Gronroos P. Leucocyte and C-reactive protein in the diagnosis of acute appendicitis. Br J Surg 1999; 86:501–504. 27. Dunlop MG, King PM, Gunn AA. Acute abdominal pain: the value of liver function tests in suspected cholelithiasis. J R Coll Surg Edinb 1989; 34:124–127. 28. Stower MJ, Hardcastle JD. Is it acute cholecystitis? Ann R Coll Surg Engl 1986; 68:234. 29. Ogata M, Mateer JR, Condon RE. Prospective evaluation of abdominal sonography for the diagnosis of bowel obstruction. Ann Surg 1996; 223:237–241. 30. Gallego MG, Fadrique B, Nieto MA, et al. Evaluation of ultrasonography and clinical diagnostic scoring in suspected appendicitis. Br J Surg 1998; 85:37–40. 31. Chen S-C, Yen Z-S, Wang H-P, Lin F-Y, Hsu C-Y, Chen WJ. Ultrasonography is superior to plain radiology in the diagnosis of pneumoperitoneum. Br J Surg 2002; 89:351– 354.

783 32. Stengel D, Bauwens K, Sehouli J, et al. Systematic review and meta-analysis of emergency ultrasonography for blunt abdominal trauma. Br J Surg 2001; 88:901–912. 33. Williams RJLI, Windsor ACJ, Rosin RD, Mann DV, Crofton M. Ultrasound scanning of the acute abdomen by surgeons in training. Ann R Coll Surg Engl 1994; 76:228–233. 34. Wellwood JM, Wilson AN, Hopkinson BR. Gastrografin as an aid to the diagnosis of perforated peptic ulcer. Br J Surg 1971; 58:245–249. 35. Fraser GM, Fraser ID. Gastrografin in perforated duodenal ulcer and acute pancreatitis. Clin Radiol 1974; 25:397–402. 36. Donovan AJ, Vinson TL, Maulsby GO, Gewin JR. Selective treatment of duodenal ulcer with perforation. Ann Surg 1979; 189:627–636. 37. Crofts TJ, Park KGM, Steele RJC, Chung SS, Li AKC. A randomized trial of non-operative treatment for perforated peptic ulcer. N Engl J Med 1989; 320:970–973. 38. Stewardson RH, Bombeck CT, Nvhus LM. Critical operative management of small bowel obstruction. Ann Surg 1978; 187:189–193. 39. Dunn JT, Halls JM, Berne TV. Roentgenographic contrast studies in acute small bowel obstruction. Arch Surg 1984; 119:1305–1308. 40. Riveron FA, Obeid FN, Horst HM, Sorensen VJ, Bivins BA. The role of contrast radiography in presumed bowel obstruction. Surgery 1989; 106:496–501. 41. Chung CC, Meng WC, Yu SC, Leung KL, Lau WY, Li AK. A prospective study on the use of water-soluble contrast follow-through radiology in the management of small bowel obstruction. Austr and NZJ Surg 1996; 66:598–601. 42. MJ Brochwocz, S Paterson-Brown, JT Murchison. Small bowel obstruction—the water-soluble follow-through revisited. Clin Radiol 2003; 58:393–397. 43. Chen S-C, Lin F-Y, Lee P-H, YU S-C, Wang S-M, Chang JJ. Water soluble contrast study predicts the need for early surgery in adhesive small bowel obstruction. Br J Surg 1999; 86:1692–1698. 44. Stewart J, Finan BJ, Courtney DF, Brennan TG. Does a water soluble contrast enema assist in the management of acute large bowel obstruction: a prospective study of 117 cases. Br J Surg 1984; 71:799–801. 45. Koruth NM, Koruth A, Matheson NA. The place of contrast enema in the management of large bowel obstruction. J R Coll Surg Edinb 1985; 30(4):258–260. 46. Shrier D, Skucas J, Weiss S. Diverticulitis: an evaluation by computer tomography and contrast enema. Am Coll of Gastroenterol 1991; 86:1466–1471. 47. McKee RF, Deignan RW, Krukowski ZH. Radiological investigation in acute diverticulitis. Br J Surg 1993; 80:560– 565. 48. Ng CS, Watson CJE, Palmer CR, et al. Evaluation of early abdominopelvic computer tomography in patients with acute abdominal pain of unknown cause: prospective randomised study. BMJ 2002; 325:1387–1389. 49. Rao PM, Rhea JT, Novelline RA, Mostafavi AA, McCabe CJ. Effect of computed tomography of the appendix on treatment of patients and use of hospital resources. N Engl J Med 1998; 338:141–146. 50. McColl I. More precision in diagnosing appendicitis. N Engl J Med. 1998; 338:190–191.

784 51. Calder FR, Jadhav V, Hale JE. The effect of a dedicated emergency theatre facility on emergency operating patterns. J R Coll Surg Edinb 1998; 43:17–19. 52. Dawson EJ, Paterson-Brown S. Emergency general surgery and the implications for specialisation. Surgeon. Surg JR Coll Surg Edinb Irel 2004; 165–170. 53. Darby CR, Berry AR, Mortensen N. Management variability in surgery for colorectal emergencies. Br J Surg 1992; 79:206–210. 54. Mercer SJ, Knight JS, Toh SKC, Walters AM, Sadek, Somers SS. Implementation of a specialist-led service for the management of acute gallstone disease. Br J Surg 2004; 91: 504–508. 55. Elson DW, Sa’adedin F, Partridge R, et al. The separation of upper and lower emergency surgery: implications for emergency specialisation. Br J Surg 2004; 91(Suppl 1):62. 56. Anakwe REB, Collie MHS, Bradnock T, Zorcolo L, Bartolo DCCB. A study to assess the impact of a new specialist colorectal unit. Br J Surg 2004; 91(Suppl 1):iv–v. 57. Organ donation and transplant activity per million population (PMP) in Europe 2002. http://www.uktransplant.org. uk/statistics. 58. New W, Solomon M, Dingwall R, McHale J. A Question of Give and Take: Improving the Supply of Donor Organs for Transplantation. Research Report 18. London: King’s Fund Institute, 1994. 59. Nicholson M. Kidney Transplantation from Non-Heart Beating Donors. Position paper prepared by the National Kidney Research Fund. Peterborough: NKRF, 2002. 60. Conference of Medical Royal Colleges and Their Faculties in the UK. Diagnosis of brain death. BMJ 1976; 12:1187– 1188. 61. Conference of Medical Royal Colleges and Their Faculties in the UK. Diagnosis of death—memorandum issued by the honorary secretary of the Conference of Medical Royal Colleges and their Faculties in the UK. BMJ 1979; i:332. 62. Wijnen RMH, Booster MH, Stubenitsky BM, de Boer J, Heineman E, Kootstra G. Outcome of transplantation of non-heart beating donor kidneys. Lancet 1995; 345:1067– 1070. 63. Collins GM, Bravo-Suarman M, Terasaki PI. Kidney preservation for transplantation. Lancet 1969; ii:1219–1222. 64. O’Grady JG, Alexander GJM, Hayllar KM, Williams R. Early indicators of prognosis in fulminant hepatic failure. Gastroenterology 1989; 97:439–445. 65. Department of Health. Hospital Episode Statistics England: Financial Year 2001–02. London: Department of Health, 2002. 66. The Vascular Surgical Society of Great Britain and Ireland. The Provision of Vascular Services 2004. London: The Vascular Surgical Society, 2004. 67. Michaels JA, Browse DJ, McWhinnie DL, Galland RB, Morris PJ. Provision of vascular surgical services in the Oxford Region. Br J Surg 1994; 81:377–381. 68. Samy AK, MacBain G. Abdominal aortic aneurysm: ten year’s hospital population study in the city of Glasgow. Eur J Vasc Surg 1993; 7:561–566. 69. The Vascular Surgical Society of Great Britain and Ireland. The Provision of Emergency Vascular Services. London: The Vascular Surgical Society, 2001.

B.F. Ribeiro et al. 70. Dawson K, McFarland R, Halliday A, Thomas, M. Shared emergency vascular cover between two district general hospitals: implications for a consultant service. Br J Surg 1998; 85:564. 71. Cook SJ, Rocker MD, Jarvis MR, Whiteley MS. Patient outcome alone does not justify the centralisation of vascular services. Ann R Coll Surg Engl 2000; 82:268– 271. 72. The Vascular Surgical Society of Great Britain and Ireland. The Provision of Vascular Services. London 1998. 73. The Vascular Surgical Society of Great Britain and Ireland. Training in Vascular Surgery. London: The Vascular Surgical Society, 2001. 74. The Royal College of Radiologists and the Vascular Surgical Society of Great Britain and Ireland. Provision of Vascular Radiology Services. London: The Vascular Surgical Society, 2003. 75. Surgery in Hospitals Serving Isolated Communities. Report by the Working Party of the Royal College of Surgeons of Edinburgh, July 1998. 76. Ritchie WP, Rhodes RS, Biester TW. Workloads and practice patterns of General Surgeons in the United States 1995–1997 Ann Surg 1999; 4:533–543. 77. Birks DM, Gunn IF, Birks RG, Strasser RP. Colorectal surgery in rural Australia: SCARS, a surgeon based audit of workload standards. ANZ J Surg 2001; 71:154– 158. 78. Carter YH, Jones PW. Mortality Trends in UK 1979–1997. London: Child Accident Prevention Trust, 2002. 79. Our Healthier Nation—A Contract for Health. London: Department of Health, 1998. 80. Earlam R. Trauma centres: a British perspective. Br J Surg 1999; 86:723–724. 81. Trunkey DD. A time for decisions. Br J Surg 1988; 75:937– 939. 82. Commission on the Provision of Surgical Services. The Management of Patients with Major Injuries. London: The Royal College of Surgeons of England, 1988. 83. Nicholl J, Turner J. Effectiveness of a regional trauma system in reducing mortality from major trauma: before and after study. BMJ 1997; 315:1349–1354. 84. Lecky F, Woodfrord M, Yates DW. Trends in trauma care in England and Wales 1989–1997. Lancet 2000; 335:1771–1775. 85. Yates DW, Woodford M, Hollis S. Preliminary analysis of the care of injured patients in 33 British hospitals: first report of the United Kingdom major trauma outcome study. BMJ 1992; 305:737–740. 86. Lecky FE. Trauma care in England and Wales: Is this as good as it gets? Emerg Med J 2002; 19:488–489. 87. Lecky FE, Woodford M, Bouramra O, Yates DW. Lack of change in trauma care in England and Wales since 1994. Emerg Med J 2002; 19:520–523. 88. London Severe Injury Working Group. Modernising Trauma Services in London. Report and recommendations. Unpublished. 89. Begg CB, Cramer LD, Hoskins WJ, Brennan MF. Impact of hospital volume and operative mortality of major cancer surgery. JAMA 1998; 280:1747–1751. 90. Birkmeyer JD, Siewers AE, Finlayson EV, Stukel TA, Lucas FL, Batista I, et al. Hospital volume and surgical

49. United Kingdom mortality in the United States. N Engl J Med 2002; 346: 1128–1137. 91. The Royal College of Surgeons of England. The Provision of Emergency Surgical Services—An Organisational Framework. London: The Royal College of Surgeons, 1997.

785 92. Reforming Emergency Care—The Emergency Department. http://www.doh.gov.uk/capacityplanning, 2004. 93. Clarke MD, Anderson ADG, Mackie J. Training the higher surgical trainee within the framework of the European Working Directive (EWTD). Ann R Coll Surg Eng (Suppl) 2004; 86:82–84.

50 Acute Care Surgery: Australia Thomas Kossmann and Ilan S. Freedman

The ways in which acute care surgical services across the world have developed and are currently delivered vary greatly from one country to another. The evolution of these services is particularly influenced by the interplay of unique geographic and demographic factors in each individual country and is ultimately determined by resources and demand.1 The mechanisms by which trauma and other emergency surgical care is provided in Australia differ substantially from those in the United States and Europe. This chapter outlines the provision of acute care surgery in Australia as well as Australia’s contribution to acute care surgery in the neighboring Pacific Island countries. Australia is one of the largest countries in the world and has a landmass comparable with the United States or Europe.2 Much of the land is,however,barren,inhospitable desert (the so-called outback) and is sparsely populated. Australia’s population of approximately 20 million people is highly urbanized, with almost 90% of Australians living in several large cities along the coastlines.1,2 However, despite increasing urbanization, a substantial population continues to live in smaller regional, isolated communities in what is broadly defined as “rural Australia.”3 Many of these people live there permanently,whereas others reside temporarily for purposes of work, holiday, or travel. The towns in these regional areas of Australia generally decrease in size and are further apart as one travels inland. Many of the larger regional towns support well-equipped health care services, but the more remote communities are often situated great distances from medical facilities.Many small rural towns are geographically and socially isolated, but all Australians nevertheless expect equitable access to high-quality health care. Various management systems have been developed to meet the challenge of providing a sustainable, achievable, and high quality of surgical care to those living in these vast and isolated regions and across the continent of Australia. Optimal care of major trauma injuries entails a multidisciplinary treatment approach and the availability

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of specialist facilities such as neurosurgery, thoracic surgery, and modern intensive care units that often cannot be provided or are not sustainable in smaller rural hospitals. In Australia, there has consequently been an emphasis in developing mechanisms to rapidly retrieve major trauma patients from rural areas and to deliver them efficiently to the larger metropolitan centers. In contrast, the treatment of nontraumatic general surgical emergencies requires the availability of skillful surgeons and good operative facilities, but transfer of the patient to a major city hospital is seldom necessary. Australia has a proud tradition of training and providing highly skilled and versatile general surgeons who manage the majority of the general surgical emergencies in rural Australia. To enhance the services provided to remote regions, outreach services such as the Royal Flying Doctor Service have been developed.1 These services have the capability to fly surgical teams to remote rural areas and transfer patients to the larger regional hospitals. To place Australia’s metropolitan and rural acute care surgical services in context, this chapter reviews the geography of the continent of Australia and outlines factors that affect the demographics of the country. The workings of Australia’s health care system are explored, and the system of surgical training in Australia is outlined. Important factors that affect the medical workforce and the distribution and provision of surgical services are also considered. Trauma and nontrauma acute care surgery in Australia are considered separately. The supporting role that Australia provides to the health care facilities in its broader region, in particular to the Pacific Island countries, is also described.

Geography and Demography Australia is the smallest continent and largest island in the world and is situated in the southern hemisphere between the Indian Ocean and the South Pacific. The

50. Australia

country is comparable in size to the United States and covers a landmass of approximately 7,682,300 square kilometers.2 Australia is, however, the world’s driest continent and consequently has a much smaller population. The center of the country receives particularly little rainfall and is consequently a vast stretch of sparsely populated desert or semidesert. Australia’s population of approximately 20 million people is consequently distributed unevenly across the continent. The majority of the population is highly urbanized, and most Australians live in the capital cities of the states and territories.1 These cities have developed in close proximity to reliable water supplies or along the coasts around safe harbors, particularly along the fertile southeast coastal strip of Australia. In this region, the cities of Melbourne, Sydney, and Brisbane contain more than half of the entire country’s population. A substantial number of people do, however, live in remote regional or rural areas of the country. The larger regional towns serve as industrial centers and provide a wide range of social and medical facilities. Smaller rural towns may, however, contain less than 1,000 people and are frequently surrounded by vast farming or cattle grazing regions. These communities are often geographically isolated from one another and may often be situated hundreds of kilometers from a major city. The further one moves from the coast, the more widespread the rural population centers tend to become. The population of Australia has increased greatly since the end of World War II and has more than doubled in the past 50 years. This is due in large part to extensive government-supported migration programs and to a lesser extent to an increase in the national birth rate. The majority of the population remains of European extraction, and English is the national language. However, in recent years, migration, particularly from Asia, has increased substantially, and Australia is now a profoundly multiethnic and multicultural society.1

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provide a full range of specialist acute care surgical services, including cardiothoracic and neurosurgery. Most Australians requiring either elective or acute care surgery are treated in public hospitals, which involves no direct cost to the patient. Patients with private medical insurance have the option of being treated either in a private hospital or as private patients in public hospitals (semiprivate). This entitles them to minor perks such as choice of individual medical practitioners, but the standard of care provided to private versus nonpaying patients in the public hospitals is equal. The Australian health care system also provides rebates for medical treatment administered outside the hospitals by general practitioners (primary care physicians), specialist physicians, and surgeons who set their own fees.4 Most choose a fee that relates to the rebate so that patients pay only marginal out-of-pocket fees for services provided outside the hospital. The federal government also operates a Pharmaceutical Benefits Scheme, which makes approved medications available at substantially subsidized cost. A patient’s attendance for medical treatment in Australia and compliance with prescribed treatment is thus generally independent of their financial status.1 Australia’s health care system is by no means flawless in that patients without private medical insurance are sometimes made to endure lengthy waiting periods for elective procedures at the public hospitals. However, patients with conditions requiring urgent treatment generally have no waiting period and enjoy a high standard of service.1 The Australian health system successfully allows all the country’s inhabitants, regardless of financial status, to have fast access to acute care services and any required acute care surgical treatment. The system also ensures that Australians have equitable and affordable access to general practitioners.

The Australian Medical System

Distribution and Provision of Surgical Services

Australia operates a universal national health care system that aims to enable all citizens to enjoy an affordable high standard of health care.1 The system is partially funded by a flat-percentage special income tax levy and is largely supplemented by federal government resources.4 The major trauma centers, the vast majority of the tertiary teaching hospitals, and most of the small metropolitan and district hospitals are publicly funded. Australia also provides an optional second tier of private hospitals, many of which were originally established by religious or nonprofit organizations. The smaller private hospitals cater predominantly to elective medical and surgical admissions. The major private centers do, however, operate large emergency departments and

The uneven distribution of Australia’s population has led to a markedly skewed distribution of the country’s surgeons, with the majority of surgical specialists tending to practice in metropolitan areas of the country. Australia’s acute care surgical services were designed with the ramifications of this in mind.1 Australia’s major cities offer the full range of surgical subspecialties with surgeon-to-patient ratios similar to those in major cities in the United States and the United Kingdom. Modern operating and perioperative facilities, well-equipped intensive care units, and world-class anesthetic services are generally widely available. There is long tradition among Australian doctors for clinical excellence and high standards of technical skills, and the

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quality of care provided in Australia’s major hospitals is comparable to that of most “first world” centers.1 In the larger regional towns, with populations of 25,000 to 250,000 people, a wide range of local specialists, such as orthopedic surgeons, urologists, and otolaryngologists, are usually available. Towns with populations between 10,000 and 25,000 people are often situated far from the major cities and are usually too small and too isolated to sustain the services of resident specialist surgeons. These towns instead have several general surgeons who provide a wide range of surgical services. Depending on the size and needs of the local population, specialist surgeons from either the larger regional centers or major cities visit these towns at regular intervals to supplement the services provided by the resident general surgeons. In true rural or remote areas, defined as more than a few hundred kilometers from a major urban area and where the population served is less than 10,000 people, limited surgical services are often provided by general practitioners who have a particular interest in surgery.5 Some small communities may also enjoy the services of a single resident general surgeon. Local services provide backup and relief when required. Anesthetic services in regional Australia tend to run in parallel with the general surgical services. General practitioner anesthetists usually service small towns with populations up to 25,000 people, and progressive input from specialist anesthetists is usually provided above that population level.

Acute Care Trauma Surgery in Australia Australia has a long and successful history of reducing morbidity and mortality from trauma through the aggressive implementation of primary prevention strategies that seek to reduce the environmental and behavioral factors that contribute to major injuries. For example, the state of Victoria led the world in introducing legislation for compulsory wearing of motor vehicle seatbelts and later in the introduction of random breath testing, speed detection, and red-light traffic cameras.1 These measures had a dramatic effect, and by 1992 the death rate due to road trauma in Victoria was 1.6 per 10,000 vehicles, the lowest for any major developed country in the world. Despite maximal public prevention measures, some people will inevitably continue to sustain major traumatic injuries. These injuries are often “time critical” in that prompt, appropriate care reduces morbidity and mortality. The literature has increasingly supported the concept that severely injured patients achieve optimal outcomes when treated in major trauma centers that consistently manage large trauma volumes. Most of Australia’s states

T. Kossmann and I.S. Freedman

and territories provide modern, well-equipped tertiary hospitals, but in many states a high percentage of major trauma patients have traditionally been delivered to the nearest emergency department and not necessarily admitted directly to the major trauma centers. To improve the streamlining of major trauma patients to designated trauma centers and to improve the standard of care in the prehospital setting, Australia’s states have begun to embrace the concept of integrated trauma systems. To illustrate the development of such a trauma system and the impact of the system on management of major trauma patients, the Victorian State Trauma System is described. The state of Victoria occupies the southeastern portion of Australia and covers an area of 227,590 square kilometers. It has a population of 4.9 million people, 3.5 million of whom live in Melbourne, the capital city. Several Victorian studies in the 1990s evaluated the management of road traffic fatalities involving people who were alive when the ambulance services arrived and indicated that a significant proportion of deaths may have been potentially preventable.6–8 Organizational, prehospital, and hospital management and system problems, which included prolonged accident scene times, inadequate prehospital and emergency department life support skills, and the triage of patients to hospitals with inadequate resources were identified.6–8 The Victorian State Government responded by implementing an advanced and integrated statewide trauma system that aims to provide optimal care from the injury scene through rehabilitation.9

Prehospital Care In remote parts of Australia, injuries are sustained significant distances from a medical facility. Paramedic response times and the standard of prehospital and in-transit care provided can consequently significantly impact a trauma patient’s outcome from injury. Integrated, prehospital care is a vital step in the sequence of comprehensive trauma management. In the 1980s, Victoria’s metropolitan ambulance services were consolidated into a single prehospital provider for the greater metropolitan area, and in 1992 the state’s five rural services were integrated into a single rural ambulance service. All Victorian ambulance services now share common training, dispatch, and clinical practice protocols. A third ambulance division, Air Ambulance Victoria, coordinates a rotary wing service staffed by Mobile Intensive Care Ambulance (MICA) personnel and also operates fixed wing aircraft out of the state capital, Melbourne, to rural centers. The use of transport helicopters facilitates the rapid transfer of seriously injured patients from nearby rural areas to the metropolitan major trauma services. Fixed wing aircraft are utilized for transfers from more

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distant sites. Transport from remote regions is often coordinated with the Royal Flying Doctor Service.

CONSCIOUS STATE RESPIRATORY RATE HYPOTENSION CYANOSIS

Designation of Hospitals to Receive Trauma Patients

Primary Injury Services

Regional Victoria

Metropolitan Mebourne

Increasing resources for trauma care

Urgent Care Services Primary lnjury Services

CHILD (20% (adults or children) or suspected respiratory tract major compound fraure fracture to two or more of the following: femur/tibia/humerus fractured pelvis serious crush injury

IF ANY OF THE ABOVE ARE PRESENT

IF NONE OF THE ABOVE ARE PRESENT

THESE PATIENTS ARE AT HIGH RISK OF HAVING MAJOR TRAUMA Ejection from vehicle Motor/cyclist impact (>30 km/h) High Speed MVA (>60 km/h) Vehicle rollover Fatality in the same vehicle Fall from height (>5 m) Explosion Pedestrian impact (>30 km/h) Prolonged extrication (>30 min)

CONSIDER CO-MORBIDITIES Age 50 years Significant underlying medical condition Pregnancy

MAJOR TRAUMA

AT RISK OF HAVING MAJOR TRAUMA

Figure 50 50.2. 2 Prehospital P h it l major j trauma t criteria. it i (Courtesy (C t off The Victorian Department of Human Services, Victoria, Australia, with permission.)

Regional Consultative Committees

Regional Trauma Services

Metropolitan Trauma Services

ADULT GCS 30 min) Age 55 Pregnancy Significant underlying medical condition

Deterioration of GCS, vital signs, or patient’s condition and/or significant findings on further evaluation

YES Liaison with Major Trauma Services

NO

Consider discharge or admission after appropriate evaluation and observation

lintiate trauma treatment protocol Prepare for rapid and early transport to appropriate MAJOR TRAUMA SERVICE

and transfer protocols were consequently formulated, and a rapid response retrieval system was designed.9 Prehospital major trauma criteria were developed using specific physiologic, anatomic, and mechanistic indicators to identify major trauma patients (see Figure 50.2). A 30minute major trauma bypass protocol was also developed in which patients who fulfill the triage criteria for major trauma and who are within 30 minutes of an MTS are delivered directly to the MTS with the ambulance bypassing nearer non-MTS hospitals (Figure 50.4). This time period was selected so that most patients given average system activation and injury scene times would reach a hospital well within the “golden hour” of trauma care. Communication processes were also streamlined to provide seamless information transfer, and wider application of mobile systems for early prehospital to hospital communications was instituted. Regional retrieval services coordinate retrieval missions that require treatment at a regional hospital level, but timely liaison with the statewide retrieval system occurs for situations possibly requiring tertiary level care. Simultaneous dispatch of regional and statewide retrieval services is sometimes activated to minimize time transport delays or to provide support to the regional ambulance services or local hospitals. Regular audits of the triage and transfer system’s efficacy are performed to verify that the triage and transfer protocols operate as intended. A meticulous trauma registry has been established to record details pertaining to all phases of care for each trauma patient. Regular audits of each component of the system are performed, and system enhancements continue to be made as required.9

igure 50.3. Major trauma interhospital guidelines. (Courtesy of The Victorian Department of Human Services, Victoria, Australia, with permission.)

MAJOR TRAUMA 2 cm); (6)

Figure 51.8. Laparoscopic closure of a perforated duodenal ulcer.

adhesions caused by the disseminated gastric content are too severe; (7) gastric cancer is suspected; or (8) the surgeon in charge is not used to laparoscopic procedures. Infection of H. pylori and high salt intake are the risk factors of gastric cancer,19 and gastric cancer is the second leading cause of cancer death in Japan. Patients with early gastric cancer (i.e., carcinoma confined to the mucosa and submucosal layer) are treated with endoscopic mucosal resection (EMR),20,21 laparoscopy-assisted gastrectomy,22 or conventional open gastrectomy, depending on the size, depth, degree of histologic differentiation, and other factors. Iatrogenic perforation of the stomach occurs in about 5% of the patients who undergo EMR.23 In some cases, the perforation can be closed by endoscopic clipping and treated with intubation of a nasogastric tube and systemic administration of antibiotics.23 However, when there are signs of peritoneal sepsis, acute care surgery is indicated preferably by laparoscopic approach. Closure of the perforation site and intraperitoneal lavage are generally performed. If there is a possibility that carcinoma cells remain at the margin of EMR, a local resection encompassing the possible residual lesion around the site of perforation is indicated. When spontaneous or iatrogenic perforation of advanced gastric cancer necessitates acute care surgery, a laparoscopic procedure is contraindicated because pneumoperitoneum with carbon dioxide may exacerbate peritoneal dissemination of neoplastic cells.

Fulminant Hepatic Failure One of the most disastrous of the nontrauma emergencies is fulminant hepatic failure (FHF), a severe liver dysfunction caused by sudden loss of hepatocyte function

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characterized by hepatic encephalopathy and coagulopathy. In Japan, FHF is estimated to affect over 1,000 individuals annually. Whereas drug-induced acute liver failure plays a large role in FHF in the United States, about 90% of FHF cases in Japan are associated with hepatitis A, hepatitis B, non-A, non-B, and non-C hepatitis, and other viral infections. The treatment for FHF consists of plasmapheresis in combination with continuous hemodialysis and filtration in an intensive care unit. When the conventional medical treatments fail to restore the liver function, a living-donor liver transplantation (LDLT) is the choice of treatment in Japan because cadaver donors

K. Takaori and N. Tanigawa

are rarely available. Over 400 LDLTs are performed each year for various diseases, such as biliary atresia (Figure 51.9), and about 50 LDLTs are estimated to be carried out for FHF with satisfactory outcome in Japan. A lateral segment or left lobe is usually used for FHF in pediatric recipients, and left plus caudate lobes or the right lobe of the donor liver are used for FHF in adult patients.24 Auxiliary partial orthotopic liver transplantation from living donors has been successful in only a limited number of cases.24,25 Survival rate after LDLT for FHF ranges from 60% to 100%, comparable to the survival rate after cadaver donor transplantation in the United

A

B

Figure 51.9. The ZEUS robotics system. A cholecystectomy was carried out in a teleconference including the European Institute of Telesurgery, University of Strasbourg, France, and the operating theater of Osaka Medical College, Japan. (A) The operator and a manipulator (a master robot). (B) The patient and robotics arms (a slave robot).

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States. A hybrid artificial liver support system utilizing hepatocytes remains an experimental therapy at the present time.26,27

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necrosis because most of these cases can be treated by the CRAI therapy or conventional treatments.34

Acute Care Surgery in the Future Acute Pancreatitis Approximately 20,000 patients per year suffer from acute pancreatitis in Japan, and 7.2% of the patients died of the disease in 1999. The mortality rate in Japan is comparable to that in the West, at between 7.5% and 17.0%. The etiology of acute pancreatitis includes alcohol abuse (30.1%), gallstones (23.9%), idiopathic (22.7%), exaggeration of chronic pancreatitis (5.6%), endoscopic retrograde cholangiopancreatography (3.9%), surgery (2.6%), endoscopic sphincterotomy (1.7%), drugs (1.2%), and hyperlipidemia (1.2%). The Japanese Society for Abdominal Emergency Medicine and the Japan Pancreas Society, in collaboration with an investigation team sponsored by Ministry of Health, Welfare, and Labor, established a guideline for the clinical management of acute pancreatitis in 2003.28,29 Based on reports from both the English and the Japanese literature, the guideline recommends mostly similar practices as those currently used in the United States and other countries.30–32 However, some intensive treatments such as continuous regional arterial infusion (CRAI) of protease inhibitor and antibiotics are practiced almost exclusively in Japan. According to the original method by Takeda et al.33, nafamostat mesylate, a potent protease inhibitor, and imipenem, an antibiotic with good penetration into pancreatic tissue, are continuously infused into the celiac artery. They reported that the CRAI treatment significantly reduced the mortality rate compared with systemic infusion of the same drugs33 and that the CRAI therapy was effective when initiated within 72 hours after the onset of acute necrotizing pancreatitis.34,35 Their results had been confirmed by other institutions in Japan.36 In a rat model of necrotizing pancreatitis, it was shown that nafamostat has maximal effects on the pancreas and peritoneal capillary leakage when delivered by way of local intraarterial infusion and that nafamostat shows a greater reduction of lung leukocyte infiltration and capillary leakage when delivered by intravenous route.37 In the United States, however, the beneficial effects of the CRAI therapy are not approved clinically. Computed tomography–guided or ultrasound-guided fine-needle aspiration is recommended to confirm pancreatic infection, and a necrosectomy should be indicated in case of infected pancreatic necrosis. Following necrosectomy, continuous closed lavage or open drainage is recommended while conventional drainage with simple drainage tube(s) is not.There is some controversy regarding surgical intervention for noninfected pancreatic

Several practical highlights of acute care surgery in developing countries were mentioned in the first section of this chapter. In reality, however, the demand for acute care surgery is hardly met in the majority of these countries. Even in industrial nations, accessibility to acute care surgery varies from community to community, and the management of acute care surgery is not consistent among centers. It is imperative to obtain harmonization in education, research, and practice in acute care surgery in the future international communities. The following are possibilities for establishing global standards for acute care surgery in the future: the realization of routine tele-surgery in association with education of doctors and medical personnel by telecommunication technologies; international collaboration for application of regenerative medicine to surgical therapeutics; and introduction of a global health care system into the setting of acute care surgery.

Tele-Surgery Tele-surgery is defined as a surgical procedure carried out from a distance.38 Advances in telecommunication technologies and application of robotics to surgery have enabled even intercontinental tele-surgery.38–40 Teleconference, tele-consultation, tele-mentoring, and other tele-medicine systems can be used in combination with tele-surgery (Figure 51.9).41–43 Tele-surgery provides opportunities to share experiences and expertise of surgery among physicians beyond the barriers of geography, nations, and politics. In the near future, it will become a reality that surgery requiring special techniques and expertise for patients in remote locations or inaccessible circumstances will be tele-manipulated by specialists and that tele-surgery will benefit acute care surgery in the rural areas, remote islands, war zones,44 and ultimately in space.

Regenerative Medicine Application of regenerative medicine to acute care surgery is most promising. The initial step has been the topical use of growth factors. It is already well known that growth factors accelerate the healing processes of wounds and burns,45 and growth factors are now commercially prepared for topical administration. For patients with spinal cord injury, topical administration of neurotrophin 3 may help regenerate the spinal cord.46 With the development of tissue engineering, cultured

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Table 51.1. Recommendations of the G8 Global Healthcare Applications Sub-Project (SP)-4. Standards, Network Reliability, Security, and Application 1. Tele-health applications and networks should adopt as many standards as possible and be harmonized with recommendations of the International Standard Organisation working groups. 2. There is a need to develop a process model for each health care/medical discipline with technical needs defined in terms of quality of service, security, and application interoperability; they should remain understandable to the clinical user. 3. Existing tele-health infrastructures need to be compatible and interoperable with digital dial-up and/or TCP/IP protocols; they should adopt emerging technologies, which have been demonstrated and the least expensive. 4. Tele health systems should receive bandwidth on demand, as appropriate for the application. Organizational Issues 1. National governments should recognize both health and economic benefits of interoperable tele-health and make health a strategic argument for interoperable tele-health. 2. National governments should create and promote working models toward interoperability and promote industry and health sector partnerships. 3. National governments should implement national and international strategies resolving the issues of licensures, credentialing, and health care provider reimbursement. 4. National governments should recognize the need for national leadership to promulgate consensus building and a vision for a future health care system that fully integrates and benefits from tele-health and tele-medicine. Human Factors 1. National governments should financially support training and education of health professionals and students in using tele-health instruments. 2. National governments should provide incentives to established health professionals to learn, acquire, and use tele-health and telemedicinebased systems. 3. National governments should provide funding to evaluate key human factors and systems in tele-health. 4. National governments should ensure adequate access to technical expertise among the user community. 5. National governments should support the development of multilingual health information and tele-health systems. Evaluation of tele-medicine and tele-health 1. Evaluation should be an integral part of all tele-health deployed with the aim to assess whether its application was effective in improving health outcome, appropriate for the needs of the population, reliable, and cost effective compared with other instruments to achieve the same goal. 2. It should assess the systemic aspects and interactions with other instruments, programs, policies, and effects of conditions (e.g., government frameworks). 3. It should measure impacts on the acceptability, workforce distribution, and competence of health personnel. 4. Evaluation should aim at development of evidence-based tele-medicine through good practice documentation, thus improving the key management issues and dissemination. Medicolegal aspects 1. As infrastructures for the use of PKI evolve, governments must ensure that there is an appropriate legal framework for its use in the health care sector and that dialogue takes place at an international level to ensure interoperability of its use among countries. 2. Patients must give fully informed consent for the use of their personal medical information for health care, evaluation, or research, even if data are anonymous; their use for commercial purposes should be restricted to informed and ethically approved uses. Professional and patient organizations should work together to promote better understanding of privacy and confidentiality. 3. An international group of national representatives must develop ethical and medicolegal guidelines for the practice of tele-medicine; formal work conducted by various groups such as the Einbeck group should be considered as a starting model. 4. The major barrier of health care professional licensing should be resolved by deciding that the tele-medicine activity is occurring at the site of the consultant; the patient should agree that he or she will follow the legal rules at the site of the consultant, as is done currently when the patient travels physically to that site. Continued work of the G8 SP-4 Working Group 1. The G8 GHAP SP-4 participants wish to pursue their common efforts in international collaboration. 2. Additional forums are required to formulate recommendations on the evaluation and implementation of medical, ethical, legal, and technical aspects of tele-medicine services, including aspects of cross-border services. 3. G8 and other participating countries should provide sufficient funding to their national representatives, experts, and expert centers to pursue their work and disseminate their conclusions and recommendations. 4. The former G8 SP-4 Working Group should collaborate with other international health care organizations, such as the World Health Organization, to facilitate the integration of health tele-matics to health care strategies worldwide. 5. This new international body of experts should report annually on its progress and activities to national health authorities and to citizens through an active Web site. Source: Reprinted with permission from Nerlich et al.56

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epithelia became available, and allogenic skin grafts have been employed as scaffolds of epithelial growth after trauma, burn injury, venous ulcers, or bacterial dermatitis.47,48 Establishment of embryonic stem cell lines from human blastocytes49 has led to enthusiasm for therapeutic use of stem cells. Embryonic stem cells are derived from multipotent cells of the early mammalian embryo and characterized by prolonged undifferentiated proliferation and developmental potential to form derivatives of all three embryonic germ layers. However, the investigation of embryonic stem cells is restricted to various extents for ethical reasons in Germany, United States, Japan, and some other nations. Another cell source for regeneration of tissues and organs has been found in tissue-derived somatic stem cells. It was originally believed that somatic stem cells can differentiate into the tissue or germ layer from which they are derived. However, it has also become apparent that some tissue-derived somatic stem cells can differentiate outside the tissue of their origin.50,51 Bone-marrow derived stem cells, neural stem cells, umbilical cord cells, and placenta are now considered potential sources of somatic stem cells for regenerative medicine. Expectations are particularly high for bone marrow–derived mesenchymal stem cells because they can differentiate into skin,52 bone, cartilage, fat (adipocyte), muscle (myocyte), nerve (astrocytes, oligodendrocytes, neurons),53 blood vessel (endothelium),54 heart (myocardium), lung (bronchial epithelium, pneumocytes), esophagus (squamous epithelium), stomach (gastric mucosa), intestine (endothelium), liver (hepatocyte, cholangiocytes), and kidney (renal tubules).55 Furthermore, there is no need to immunosuppress patients treated with autologous bone marrow–derived stem cells. In the future, lost or damaged organs or body parts will be replaced by new tissues regenerated from the stem cells, and acute care surgery will undergo a Copernican revolution.

Global Health Care The twenty-first century is bringing a borderless world and presenting new challenges in all facets of medical care. Frequent travels abroad and increased migrations of the population require practitioners, including those who engage in acute care surgery, to be more knowledgeable of diseases with specific geographic distributions. The current consensus is that international collaboration is needed to improve the quality and cost efficiency of each field of health care through tele-medicine, tele-health, and health tele-matics. To establish an international concerted collaboration in this regard, national representatives of G7, joined by Russia later on, have organized

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the G8 Global Healthcare Applications (GHAP) SubProject (SP)-4.56 The GHAP SP-4 first focused on the use of telemedicine tools in acute care medicine. The objective of this first project was to establish a transnational and multilingual acute care system. The study concluded that, from a technological viewpoint, a worldwide telemedicine network is feasible and can be implemented gradually and in steps. Application of global health care to acute care surgery will improve the quality of the practice in not only industrial nations but also in developing countries and may be further enhanced by a series of recommendations by G8 GHAP SP-4 (Table 51.1). Despite the fluidity of borders between nations, inequalities of economy, of welfare, and of health are further expanding in the world at the present time. It is imperative for a healthier world in the future that global health care systems be applied to all fields of medicine, including acute care surgery beyond the barriers of economics, politics, language, religion, and culture.

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Index

A ABCs (airway, breathing, and circulation) of acute care surgery, 43–44 of initial assessment of patients, 4–7 of prehospital care, 215, 216–218 of preoperative care, 72–73 Abdomen acute, 754, 771 anatomic definition of, 435 anatomic zones of, 52–53 injuries to as abdominal compartment syndrome cause, 10–11 electrical trauma-related, 163 explosions-related, 243, 244 motor vehicle accidents-related, 209 nonhemorrhagic, 37 types of, 37, 38 vascular, 61, 538–542 intrathoracic, 420, 421 pain in. See Pain, abdominal Abdominal acute care surgery, 52–61 anesthesia management in, 37–38 bedside, 115–118 morbidity and mortality rates in, 17 open abdomen in, 70, 757 adverse health effects of, 443 bedside management in, 118 component separation of, 183–184 damage-control approach to, 176–177, 181 delayed primary closure of, 182–184 fascial layer management of, 118 indications for, 176–177 long-term management of, 445–447 management of, 176–186 temporary wound management of, 177–181 timing of reconstruction of, 181–182 as percentage of all acute care surgery, 44 subspecialization within, 771

surgical exploration techniques in, 52–61 wound closure in, 61 Abdominal cavity, anatomic definition of, 435 Abdominal compartment syndrome, 10–11, 38, 61, 115, 118, 134, 176–177 damage-control approach to, 176 definition of, 10, 442–443 etiology of, 443 fascial closure in, 445 laparotomy treatment for, 118 primary, 176 resuscitation-related, 8, 134 secondary, 176, 178, 182, 443 Abdominal pressure. See also Abdominal compartment syndrome inspiration-related increase in, 421 Abdominal wall anatomy/layers of, 435–436 closure of, 443–447 evaluation of, 436–437 hernia of, 439–441 innervation of, 436 reconstruction of, 447 trauma to, 441–442 Abdominal washouts, 118 Abortion, 717, 718, 735 Abscess abdominal packing-related, 181 anorectal, 549–550 “collar-button,” 651 colonic, 554 deep cervical, 293 epidural, 333, 343, 344 in the hand, 650–651 hepatic, 481–482, 487, 489–490 amebic, 798 intracerebral, 343–344 lateral pharyngeal, in pediatric patients, 309–310

mediastinal, 112 pancreatic, 507, 508 parotid, 293 peritonsillar, 288, 376 in pediatric patients, 308 prostatic, 565 pulmonary, 367, 373–374 renal and perirenal, 562–564 retropharyngeal, 288 in pediatric patients, 308–309 subdural, 333, 343, 344 subscapular, 562 Accessory duct of Santorini, 498–499 Achalasia, 188, 320, 321, 323, 451, 452, 454, 462–463 Acid-base disorders. See also specific acid-base disorders in potential organ donors, 710–711 Acidemia, lactic, 70 Acidosis as “dark angel” of death, 44, 176, 177, 184 metabolic, 12, 472 in potential organ donors, 711 resuscitative treatment for, 44 Acid-related injuries, 126, 147, 323 Acquired immunodeficiency syndrome (AIDS), esophagitis associated with, 327 Acrocyanosis, 70 Acute care surgery. See also specific surgical procedures timing of, 771 Acute Physiology and Chronic Health Evaluation (APACHE) II scores, 9 Acute radiation syndrome, 241 Acute respiratory distress syndrome (ARDS), 114, 366, 370–371 Adenocarcinoma, 458, 490 Adenoidectomy, as hemorrhage cause, 291–292 Adenoma, hepatic, 488

809

810 Adolescents involvement in motor vehicle accidents, 251, 259 suicide by, 255 Adrenal insufficiency, 15, 79–80 Advanced Burn Life Support (ABLS), 131 Advanced Cardiac Life Support (ACLS), 269, 401 Advance directives, 69, 191, 689–700, 727–729, 731 Advanced Trauma Life Support (ATLS), 3, 4, 6, 141, 195–196, 197, 199, 214, 234, 269–270, 333, 351 Advanced Trauma Operative Management (ATOM) course, 271–273 Aging. See also Elderly patients normal physiologic changes associated with, 187–188 Airbags, 206, 250, 350 Aird maneuver, 502 Air embolism, 49, 52, 301 Air leaks, 364, 365, 367, 370–371 Air transport, of patients, 154–155, 195–196, 757–758, 788–789, 791, 793 Airway, difficult, 297, 298 Airway compromise, etiology of, 300 Airway injuries, lethal/potentially lethal, 6 Airway management, 4–7, 297–301. See also Endotracheal intubation; Intubation in burn patients, 136–137 in laryngotracheal trauma patients, 277, 304 in neck trauma patients, 45, 47 prehospital, 216–217, 222–224 in pulmonary emergency patients, 362–363 in tracheobronchial trauma patients, 364 transtracheal, 223, 224 untimely, 296 Airway obstruction burn injury-related, 134 head and neck emergencies-related, 279, 288, 289 hemostasis after, 301–303 management of, 5 pharyngeal/laryngeal emergencyrelated, 277 signs and symptoms of, 297 supraglottis-related, 305, 306 Albumin, liver disease-related increase in, 480 Albumin solutions, 8, 9 Alcohol use as drowning risk factor, 255

Index as injury risk factor, 258–259 as motor vehicle accident risk factor, 250, 252 as necrotizing gangrene risk factor, 567 as peptic ulcer disease risk factor, 474 preoperative assessment of, 69 Alcohol withdrawal syndrome, 69 Alimentary tract acute care surgery, 44 Alkaline agents-related injuries, 126, 147, 323 Alkalosis, in potential organ donors, 710–711 Allen test, 618 AlloDerm®, 182 Altered mental status in burn injury patients, 138 in elderly patients, 188–189 in neurologic emergency patients, 334 postoperative, 77 Alzheimer’s disease, 333, 727 Ambient temperature, effect on energy expenditure, 96 Amebiasis, 484, 798 American Association for the Surgery of Trauma, 394 Organ Injury Score (AAST-OSI), 503 American Association of Anesthesiology, 32, 444 American Association of Orthopedic Surgery, 202 American Bar Association, 706 American Board of Surgery, 43 American Burn Association, 125, 153–154 American College of Cardiology/American Heart Association (ACC/AHA), cardiac risk stratification guidelines, 189–190 American College of Surgeons, 153–154, 155, 197, 269–270, 685, 697, 748, 749, 750, 755 American Medical Association, 706 American Society of Anesthesiologists, 187 American Spinal Injury Association, 335, 339 Ampulla of Vater, intubation of, in pancreatography, 503 Amputations surgical of burned extremities, 142–143 of cold-injured tissue, 148 for limb ischemia management, 604 lower extremity, 603, 604, 611 for necrotizing soft tissue infection management, 173 of septic joints, 603 upper extremity, 632, 662

traumatic explosions-related, 243, 244 of the fingertips, 622, 625 types of, 631–632 Amyloid angiopathy, 342 Anabolic agents, 101–102 Anal fissures, 551 Analgesia in chest wall trauma patients, 6–7 epidural thoracic, 6–7 patient-controlled, 6 use in intensive care units, 109, 111 Anatomic divisions, interfaces between, 44, 45 “Anatomic snuffbox,” 618–619, 620, 641 Anemia, 130, 221 Anesthesia, 30–42 intraoperative management of, 33–34 postoperative management of, 34 preoperative management of, 31–32 use in Australia, 788 use in hand and upper extremity acute care, 616 use in rural hospitals, 198 use in the intensive care unit, 109, 111 Anesthesia Crisis Resource Management (ACRM), 264, 270 Aneurysmectomy, as splenic trauma cause, 515 Aneurysms aortic abdominal, rupture of, 10, 407, 534–537 dissecting, 345 as sentinel bleeding source, 464 thoracic, 327–328, 400, 407 cerebral, rupture of, 341 of renal artery, rupture of, 537–538 of splenic artery, 517, 524, 542 visceral, rupture of, 537–538 Angioaccess grafts, occlusion or infection of, 658–659 Angioembolization, of massive hemoptysis, 381 Angiography of arteriovenous malformations, 569–570 computed tomography of pulmonary embolism, 369 of superior vena cava occlusion, 384 of massive hemoptysis, 381 Angiography suite, lower-extremity trauma treatment in, 608–609 AngioJet®, 528 Angiomyolipoma, renal, 568–570 Anhydrous ammonia-related injuries, 126, 147 Anion gap, 711 Anisakiasis, 800–801

Index Ankle, irreducible dislocations of, 607 Anorectal disease and trauma, 549–551 as necrotizing gangrene cause, 567 Anthrax, as biological weapon, 240 Antibiotic-resistant bacteria, 114, 171 Anticoagulation therapy during extracorporeal membrane oxygenation, 86 in limb ischemia patients, 603 in upper-extremity replantation patients, 632–633 in vascular emergency patients, 37 Antioxidants, 101 Antrectomy, 458–459 Anxiety, alcohol as self-treatment for, 69 Aorta abdominal, injuries to, 540 infrarenal, exposure of, 58, 59 injuries to gunshot wound-related, 317 pancreatic trauma-associated, 500 penetrating trauma, 390 occlusion of, 530–533 repair of, 52 suprarenal, surgical exposure of, 54, 55 thoracic, 400–419 blunt trauma to, 400–406 descending, exposure of, 51 dissection of, 406–415 tears of, 209, 210, 422 Aortic bifurcation, surgical exposure of, 58, 59 Aortic dissection, 406–415 ischemia associated with, 528–530 surgical repair of, 528–530 thoracic, 406–415 type A, 528, 530 type B, 528–530 Aortic valve insufficiency, 412–413 Aortography of aortic dissection, 409 of blunt aortic trauma, 401, 402 Apnea, ventilatory management of, 67, 81 Apoplexy, pituitary, 343 Appendicitis diagnosis of, 769, 770, 771 diverticulitis as mimic of, 555 in the elderly, 190 Arginine vasopressin, as shock treatment, 84 Argon Beam Coagulator, 519 Aristotle, 513 Arrhythmias, cardiac blunt coronary artery trauma-related, 396 electrical injuries-related, 163

811 penetrating cardiac trauma-related, 393 Arterial blood gases, 77 Arterial blood oxygen saturation, 76 Arterial insufficiency, 602, 611 Arterial monitoring, intraoperative, 75 Arterial occlusion, 524, 525–533 Arterial oxygen hemoglobin saturation, 4 Arteries. See also specific arteries injuries to abdominal, 61 compartment syndrome-related, 648 pancreatic trauma-associated, 500, 501, 502 in upper extremity, 659–663 Arteriography of abdominal and pelvic vascular trauma, 539 contraindication to, 408 of lower extremity, 608 of mesenteric arterial occlusion, 526 Arteriosclerosis, cerebral, 342 Arteriovenous malformations, 342, 345, 570 Arthritis, in the elderly, 189 Arthrocentesis, bedside, 119 Arthroscopy, of the wrist, 622 Arytenoid dislocation, 312 Ascariasis, 798–799 Ascites, 115–116, 437, 798 Aspergillosis, 170, 171 Asphyxia, traumatic, 384 Asphyxiants, 135–136 Aspiration airway placement-related, 300 in the elderly, 188 endotracheal intubation-related, 6 of foreign bodies, 290, 291 intragastric feeding-related, 100 pulmonary abscess-related, 374 Atelectasis, 7, 76–77, 290 Atracurium, 109 Atria, penetrating trauma to, 390 Atrial fibrillation, 75 Auscultation abdominal, 437 esophageal, 453 during head and neck examinations, 279, 280 Australia, acute care surgery in, 786–795 Autonomy, of patients, 689, 696, 702, 704, 705, 717, 718, 719, 721 double effect doctrine and, 734 of elderly patients, 191 informed consent and, 725–726 limitations to, 727 organ donation and, 732, 733 treatment withdrawal and, 731

Autotransplants, ureteral, 579–580 Axillary artery anatomy and exposure of, 62, 661 injuries to, 659, 660–661 Axillary veins, injuries to, 663 B Backboards, 225–226. See also Cervical spine, immobilization of Back pain, 452 Banks, Sam, 202 Barnes, Eugene “Red,” 677 Barotrauma, 161 Barrett’s esophagus, 323, 325, 328, 430 Basal energy expenditure (BEE), 95, 96 Base deficit (BD), 11–12 Beck’s triad, 390 Bedside procedures, 106–124, 757 Beecher, Henry, 724 Beneficence, 717, 719, 721 toward suicidal patients, 727 Benign prostatic hyperplasia (BPH), 572–573 Bernoulli principle, 220, 221–222 Beta-blockers, 74–75, 102 use in elderly patients, 189–190, 191 Bicycle helmets, 253 removal of, 226 Biliary tract anatomy and physiology of, 479–480 disease and disorders of, 482–487 calculus disease, 484–487 liver function tests in, 769 obstruction, 483, 490–491 pancreatic trauma-associated, 501, 502 Bilirubin, total, 480 Bilobectomy, of pulmonary gangrene, 375 Bioethics, 715–739 Biomedical industry, as research funding source, 724–725 Bioterrorism, 239–240, 243 “Bird’s beak” deformity, 454 Bite wounds animal, 650 human, 621, 633, 650 Bitumen-related burns, 147 Bladder injuries to, 60, 594 intraoperative iatrogenic, 580–581 rupture of, 581 Bladder cancer, as hematuria cause, 572 Bladder pressure. See Abdominal compartment syndrome Blast trauma, 230–231. See also Bombings to chest wall, 350 electrical trauma-associated, 161, 164 explosions-related, 242–244

812 Blast trauma (cont.) physics and pathophysiology of, 212, 242–243 pulmonary parenchymal, 365 thoracic aortic, 401 to thumb, 629 Blood alcohol level (BAL), 258, 259 Blood-borne disease transmission, prevention of, 43, 108, 110 Blood flow assessment of, 7 cerebral, brain death-related absence of, 707–708 Blood loss. See also Hemorrhage debridement-related, 609 fluid and blood requirements in, 7 Blood pressure. See also Hypertension; Hypotension perioperative monitoring of, 75 in potential organ donors, 708–709 in septic patients, 172 during shock, 222 Blood products, availability for ICU patients, 71 Blood transfusions, 9–10 adverse effects of, 9–10 availability in rural and remote areas, 196–197 in burn patients, 150 as gastrointestinal hemorrhage treatment, 475 indications for, 10 in mass casualty victims, 234 in pancreatic trauma patients, 506–507 patient’s refusal of, 686, 687, 726 restrictive use of, 9 in soft-tissue surgery patients, 38–39 Blood urea nitrogen (BUN), 10, 78 “Bloody vicious cycle,” 44 Blunt trauma abdominal, 441 as hepatic tumor rupture cause, 488–489 nonoperative management of, 755 vascular, 538, 539, 540–541 blast-related, 243 cardiac, 389, 394–397 cervical spine immobilization in, 225 to the chest wall, 348, 352 diaphragmatic, 421–424 esophageal, 315 to the head, 336–338 mechanisms of injury in, 206–212 motor vehicle accidents-related, 206–212 pancreatic, 500, 506–507 pelvic vascular, 538, 539 pulmonary parenchymal, 365 thoracic aortic, 400–406 tracheobronchial, 363

Index Body temperature. See also Fever; Hyperthermia; Hypothermia; Thermal regulation; Thermogenesis measurement of, 80 Boerhaave’s syndrome, 314, 321, 328, 463 Bogotá bag, 178 Bombings, as trauma cause, 231, 240, 241, 242–244, 750 “second-hit” phenomenon in, 232, 244 Botulinum toxin, as biological weapon, 240 Boutonnière deformity, 636, 637 Boyle’s law, 208 Brachial artery injuries to, 644, 645, 659, 660, 661 occlusion/thrombosis of, 656–658, 667 pseudoaneurysm of, 662 surgical exposure of, 62, 661 Brachial veins, injuries to, 663 Brain, oxygen consumption in, 77 Brain death, 706, 732 determination of, 701, 706–708, 773 head trauma-related, prevention of, 773 thermoregulation loss during, 712 Brain injuries. See also Head injuries falls-related, 253 implication for fracture fixation, 39 mechanisms of injury in, 206–207, 208 motorcycle accidents-related, 253 motor vehicle accidents-related, 207, 208 pelvic ring fractures-related, 594 Brain stem reflexes, brain death-related absence of, 707 Brain Trauma Foundation, 35 Brain tumors, 332, 334, 343 Bronchial arteries hemorrhage from, 378 in inhalation injuries, 135 Bronchial blocker systems, 362–363 Bronchiectasis, 367 Bronchography, computed tomography, 364 Bronchoscopy of massive hemoptysis, 379–380 of tracheobronchial trauma, 364 of tracheoinnominate artery fistula, 382 Bronchoscopy simulation, 268 Bronchus, foreign bodies in, 294–296 Bruce, John, 767 Bubonic plague, as biological weapon, 240 Budd-Chiari syndrome, 491 Bundle branch block, 390 Burn centers, necrotizing soft tissue infection treatment in, 173

Burn patients, 125–160, 254–255 airway management in, 136–137 anabolic steroid therapy for, 102 burn wound excision and grafting in, 142–145, 151 metabolic and nutritional support for, 97, 100, 151–153 organ system support for, 137–139 pain control in, 137–138 resuscitative priorities for, 130–134 survival of, 155 topical antibiotic therapy for, 139–142 transportation and transfer of, 126, 153–155 ventilatory support for, 135, 137 wound care for, 139–146 Burns, 125–160, 254–255 bitumen-related, 147 carbon monoxide poisoning associated with, 135 caustic ingestion-related, 289 chemicals-related, 146–147, 646 as compartment syndrome cause, 120, 604 cyanide poisoning associated with, 136 disaster and mass casualty-related, 230–231 electrical, 126, 161, 162, 163, 164 epidemiology of, 125–127 explosions-related, 243 first-degree, 128 inhalation injuries associated with, 129, 134–137 as intraabdominal hypertension cause, 11 mechanical injuries associated with, 150–151 organ system response to, 126, 128–130 pathophysiology of, 127–130 prevention of, 254–255 second-degree, 128 third-degree, 120, 128 total body surface area of, 131, 132, 133, 154–155 C Calculi biliary, 484, 485–486 renal, 570, 571, 572 Caloric requirements, calculation of, 95–96 Camper’s fascia, 435, 436 Cancer. See also specific types of cancer in the elderly, 189 as mortality cause, 731–732 Candidiasis, 140, 171 Cannulae, vascular as arterial injury cause, 645 replacement of, 71

Index Capillary refilling time, in shock, 222 Capnography, 77, 217 Capnometry, 12 Capsulotomy, with femoral neck fracture reduction, 608 Caput medusae, 115–116 Carbohydrates, as nutritional support component, 94, 96 Carbon dioxide, end-tidal, 73, 77 Carbon monoxide poisoning, 135 Carboxyhemoglobin, 76, 135 Cardiac arrest. See Cardiopulmonary arrest Cardiac enzymes, as cardiac trauma markers, 393, 396, 397 Cardiac monitoring and care perioperative, 74–76 prehospital, 218 Cardiac risk stratification, in surgical patients, 189–190 Cardiac surgery, reoperative, 115 Cardiac trauma, 389–399 blunt, 389, 394–397 cardiopulmonary bypass in, 398 iatrogenic endovascular, 397 penetrating, 389–394 transmediastinal gunshot wounds, 397 Cardiopulmonary arrest lightning strike-related, 229, 246 resuscitative thoracotomy for, 48–49 Cardiopulmonary bypass cannulation for, 411–412 for cardiac trauma repair, 398 extracorporeal membrane oxygenation use in, 86–87 in pulmonary embolism patients, 368 Cardiopulmonary resuscitation (CPR) of electrical injury patients, 163 prehospital, 218 Cardiovascular disease, in the elderly, 189 Cardiovascular system aging-related changes in, 187–188 components of, 221 trauma-related failure of, 221 Cardioversion, direct current, 75 Carotid arteries injuries to, 302, 337 internal, titanium clipping of, 291, 292 ligation of, in dying patients, 52 proximal, in neck exposure, 46 surgical exposure of, 45–46 Carotid (blow) catastrophe, 301–302 Carotid pulse, in shock, 222 Carotid-subclavian bypass, 404 Carpal dislocations, 642 Carpal tunnel syndrome, 646 Car safety seats, for children, 250 Case analysis/management, 721–722, 736–739

813 Catecholamines in hypermetabolic response, 92 in stress response, 68 as vasodilatory shock treatment, 84 Catheters/catheterization arterial, 75 central venous, 75–76 as cardiac trauma cause, 397 as femoral artery injury cause, 664, 665–666 Foley, 60, 268, 303, 559 indwelling contamination of, 71 urinary, 10 venous, as thrombophlebitis cause, 649 nasal gastric, 70 for optimal intravenous access, 7 for peritoneal dialysis, 116 pulmonary artery (Swan-Ganz), 76 in high-risk surgical patients, 190 in limb ischemia patients, 603–604 as pulmonary artery rupture cause, 383–384 urethral, 572 Cat-scratch disease, 650 Causa equina syndrome, 345 Caustic inhalation/ingestion, 277, 289, 305, 313, 323–324 Cavitation, 205–206 Celiac artery, 525 ligation of, 542 Celiotomy, 43, 66, 70 Cellulitis, 602–603 anorectal, 549 differentiated from lateral pharyngeal abscess, 309 pelvic, 551 Central cord syndrome, 345 Central venous oxygen saturation (ScvO2), 11 Central venous pressure (CVP), 75–76 in potential organ donors, 708–709 Cerebritis, 343, 344 Cerebrovascular accidents. See Stroke Cervical artery, transverse, injuries to, 302 Cervical spine immobilization of, 215, 216–217, 218, 220, 224–226, 339 injuries to, 207–208, 339 anesthesia management of, 36–37 electrical injuries-related, 163 motor vehicle accidents-related, 207–208, 208 nasotracheal intubation in, 298 prehospital assessment and management of, 215 Cesarean section, 198, 578 Chagas’ disease, 315

Chemical injuries, 146–147 as mass casualties, 230–231, 240–241, 243 Chest, anterior, innervation of, 436 Chest wall trauma, 348–361. See also Thoracic trauma analgesia for, 6–7 biomechanics of, 349–350 categories of, 351–356 initial evaluation of, 350 injuries associated with, 349 mortality rate in, 349 pain management for, 356–357 prevention of, 350 Child abuse/maltreatment burn injuries as, 126–127, 141 as chest wall injury cause, 348 mandated reporting of, 729 prevention of, 256 types of, 256 Children. See also Infants; Neonates adenoidectomy-related hemorrhage in, 291 anesthesia management in, 40–41 for bedside procedures, 111 bicycle-related injuries in, 253 burn injuries in, 155, 254–255 enteral nutritional support for, 97 fluid therapy for, 130–131 growth hormone therapy for, 153 hypocalcemia associated with, 133–134 propranolol therapy for, 102 wound care for, 139 caustic ingestion in, 323 cervical spine immobilization in, 226 chest wall trauma in, 348 drownings in, 255 electrical injuries in, 126 esophageal foreign body impaction in, 326 foreign body aspiration/ingestion in, 294–296, 452 head and neck emergencies in, 305–313 injury-related mortality rates in, 779 intrahospital transport of, 107 intussusception in, 473 mortality causes in, 258 motor vehicle-related injuries in, 250, 251–253 neurologic emergencies in, 334 overwhelming postsplenectomy sepsis in, 521 potassium iodide use in, 242 rib fractures in, 349, 357 spine injury imaging in, 339 splenic anatomy in, 515 upper airway manipulation in, 297–298 urogenital emergencies in, 581–585

814 Chin lift maneuver, 5 Chlorine-related injuries, 146 Cholangiocarcinoma, of distal bile ducts, 490 Cholangiography, transhepatic, 480, 483 Cholangiopancreatography, 480 endoscopic retrograde, 483, 485–486, 491, 507, 508 magnetic resonance, 480, 485, 490 Cholangitis, 482–484 suppurative, 482–483 Cholecystectomy, 190, 484, 485, 486, 771 robotics-assisted, 802 Cholecystitis, 484–485 acalculous, 116, 484 suppurative, 190 Cholecystostomy, 116, 485 Choledocholithiasis, 485–486 Choledochotomy, 503 Cholelithiasis, 190, 484 Chromium, 101 Chronic critical illness, 80–81 Chronic disease in the elderly, 189–190, 191 as mortality cause, 731–732 Chronic health status, of preoperative patients, 69, 72 Chronic obstructive pulmonary disease, 534, 731–732 Circumcision, complications of, 581–582 Cirrhosis, as bleeding varices cause, 465 Claudication, 603 Clavicle, fractures of, 355, 639 Clinical Ethics (Jobsen, Siegler, and Winslade), 721 Clostridial infections, 14, 16, 153, 567 Coagulation factor therapy, 12 Coagulopathy as compartment syndrome cause, 604 as “dark angel” of death, 44, 176, 177, 184 head trauma-related, 338 lactated Ringer’s solution-related, 9 nutritionally-related, 153 posttraumatic, 12, 338 in potential organ donors, 711 resuscitative treatment for, 44 Cold injuries, 147–148 Colectomy, 515, 552–553 Colitis amebic, 798 clostridial, 14, 16 indeterminate, 557 ischemic, 558–559 pseudomembranous, 556 ulcerative, 555–556 Colloid solutions, 78 contraindication to, 171 as shock treatment, 8–9 Colocolostomy, 555

Index Colon injuries to electrical injury-related, 163 pancreatic injury-associated, 500, 501, 502 obstruction of, cancer-related, 552 perforation of, 552, 554, 556, 557 sigmoid, mobilization of, 58 Colonoscopy simulation, 268, 269 Coloproctostomy, 555 Colorectal cancer, 552–553 Colorectal disease and trauma, 552–559 Colorectal surgery, 190, 771, 779 Colorimetry, indirect, 95 Colostomy, 173 Coma glucose therapy for, 334 myxedema, 80 pentobarbital, 338 Combat situations, cervical spine immobilization in, 224 Comitubes, 224 Commotio cordis, 395 Compartment pressure, 604–605 measurement of, 118–120, 647, 648 Compartment syndromes abdominal. See Abdominal compartment syndrome burn injuries-related, 134 electrical injuries-related, 163, 164 of the extremities, 118, 119–120 lower extremity, 604–606, 608, 672–673 upper extremity, 615, 647–649, 653, 663–664 fasciotomy treatment for. See Fasciotomy injection injury-related, 646 Competency, of patients, for informed consent, 685, 725–726 Complete blood count (CBC), 79 Computed tomography (CT) for abdominal pain evaluation, 16 of angiomyolipoma, 569 of aortic dissection, 408, 409, 415 of aortoenteric fistula, 537 of blunt aortic trauma, 401, 402, 403 of blunt cardiac trauma, 395, 397 of blunt diaphragmatic trauma, 422, 423 for brain death determination, 707 of cerebritis, 344 of cerebrovascular accidents, 341 of descending necrotizing mediastinitis, 376, 377, 378 of diverticulitis, 770–771 of emphysematous pyelonephritis, 561, 562 of esophageal trauma, 316, 317 for flank pain assessment, 571

of gallstone ileus, 487 of genital necrotizing gangrene, 568 of hand and wrist trauma, 622 of the head and neck, 187, 191, 282, 336, 337–338 of hepatic pyogenic abscess, 482 of intraparenchymal hematoma, 342 for ischemic stroke evaluation, 342 of the liver and biliary system, 480 of necrotizing pneumonia, 373, 374 of neurologic emergencies, 335 of pancreatitis, 486 of pelvic ring fractures, 595–596 of penetrating cardiac trauma, 391 of penetrating diaphragmatic trauma, 425 of prostatic abscess, 565 of pyonephrosis, 564 of rectus sheath hematomas, 442 of renal abscess, 563 of ruptured abdominal aortic aneurysm, 535 of shock bowel, 443 of sinuses, 290 of small bowel obstruction, 472, 473 of spinal injuries, 339–340 splenic, 513–514, 516, 517 of transmediastinal gunshot trauma, 397 of urinary tract obstruction, 571 Confidentiality, 716–717, 729 Conflict of interest, 724–725 Congenital abnormalities, as neurologic emergency cause, 332 Congenital adrenal hyperplasia, 582, 583 Congestive heart failure, 75, 731–732 Consent, to treatment, 717. See also Informed consent Consolidated Omnibus Budget Reconciliation Act, 677, 720 Consultations, ethical and legal, 733 Contractures, Volkmann’s ischemic, 647 Contrast agents, as nephropathy cause, 78 Controlled Substances Act, 735 Contusions cerebral, 335, 337 myocardial, 394, 395–396 pancreatic, 503 pulmonary, 6, 208, 217, 349 Cope’s Early Diagnosis of the Acute Abdomen, 15 Copper, 101 Core body temperature, 80 Cori cycle, 92 Cornea, electrical injuries to, 163–164 Coronary arteries, injuries to blunt trauma-related, 395, 396 iatrogenic trauma-related, 397

Index penetrating trauma-related, 390, 392–393 Coronary artery bypass grafting, 392–393 Coronary artery disease, 531–532 Corticotropin stimulation test, 79, 80 Cortisol, 67, 68, 80 Cough, foreign body aspiration-related, 294–296 Cranial nerves, functional assessment of, 335 C-reactive protein, 769 Creatine, as compartment syndrome cause, 604 Creatinine, 10, 78 Crepitus, 395, 602 Cricoarytenoid joints, 286 Cricoid cartilage, 286 Cricoid pressure, 5 Cricothyroidectomy, 5, 6, 36 Cricothyroidotomy, 223, 299, 364 contraindications to, 45 Crisis management, 245 Critical illness, sustained and chronic, 80–81 Critical incident management (CISM), 232 Crohn’s disease, 474, 549, 557 Croup, 288, 289, 305, 306–308 Crush injuries blunt diaphragmatic, 422 as compartment syndrome cause, 604 explosions-related, 243 pancreatic, 497 thoracic aortic, 401 vascular injuries associated with, 609 Cruzan vs. Director, Missouri Department of Health, 690, 691, 726, 731 Crystalloid solutions, 7, 8–9, 78 Cutaneous injuries, as necrotizing gangrene cause, 567 Cyanide poisoning, 136 Cystography, of bladder rupture, 581 Cystourethrography, voiding, 584 Cysts, hydatid, 484 Cytomegalovirus, 327 D Damage-control procedures, 43–44 for esophageal emergencies, 52 for hypothermia, coagulopathy, and acidosis, 12 for mass casualties, 234 for open abdomen, 176–177, 181 Death. See also Brain death; Patients, deceased determination of, 732 physicians’ hastening of, 734–735 preventable, 743, 744

815 pronouncement of, 10 “three dark angels” of, 44, 176, 177, 184 Debridement, 38, 39 of cold injuries, 148 of compartment syndrome, 606 of electrical injuries, 162, 164 of hand and upper extremity injuries, 626 of necrotic muscle, as blood loss cause, 609 of necrotizing fasciitis, 119, 652–653 of necrotizing soft tissue infections, 166, 171–173, 603 Decannulation, 300–301 Decision-making capacity, of patients, 722 determination of, 716–717, 726 of elderly patients, 191 impaired, 723, 726, 727 for informed consent, 723, 725–726 Definitive care, 747–748 Degenerative diseases, as neurologic emergency cause, 332, 333 Dehydration, 221, 472 Demyelinating diseases, as neurologic emergency cause, 332, 333 Denver Health Medical Center, 43, 44 Depression alcohol as self-treatment for, 69 undiagnosed, 727 Developing countries, acute care surgery in, 794–795, 796–799 Dextrose, 77–78 Diabetes insipidus, in potential organ donors, 709–710 Diabetes mellitus in elderly patients, 142–143, 189–190 as gangrene risk factor, 653 as limb ischemia risk factor, 603 as mucormycosis risk factor, 290, 291 as necrotizing gangrene risk factor, 567 as necrotizing soft tissue infections risk factor, 167, 169, 170 as renal abscess risk factor, 562 as urogenital prostheses infection risk factor, 566 Diaphragm anatomy and function of, 420–421 injuries to, 420–434 anatomic and physiologic considerations in, 420–421 blunt trauma/rupture, 421–424, 428, 429 outcomes in, 428–429 penetrating trauma/rupture, 421, 425–428, 429

Diaphragmatic transposition, 356 Diarrhea starvation-related, 99 total parenteral nutrition-related, 99 Diazepam, 109 Die-punch fractures, 640–641 Dieulafoy’s lesions, 475 Digital brachial index (DBI), 645 Digoxin, as mesenteric ischemia cause, 525 Disaster and mass casualty management, 229–248, 750 after terrorism attacks, 230, 232, 236, 237, 239–244 disaster planning and reporting in, 244–245 incident command in, 238–239, 245 medical care of casualties in, 233–235 phases of disaster response in, 231–233 search and rescue effects in, 232–233 triage in, 233, 234–238, 241, 243–244 Disk herniation, 340, 345 Dislocations electrical trauma-related, 163 of hand and upper extremity, 638, 642–644 of hip, 206, 606–607 irreducible lower extremity, 606–607 Distal interphalangeal joints (DIP) dislocation of, 643 extensor tendon injuries to, 636 injection injuries to, 646 Diverticula, 451, 454–455, 553–555 duodenal, 455, 464 epiphrenic, 455 as foregut obstruction cause, 452 Meckel’s, 474, 475 Zenker’s (hypopharyngeal), 454, 465 Diverticulectomy, transabdominal laparoscopic, 455 Diverticulitis, 770–771 cecal, 555 in the elderly, 190 malignant, 554–555 Dobutamine, 15 Domestic violence. See Intimate partner violence Do-not-resuscitate (DNR) orders, 697, 727, 728, 731 Doppler index, of lower extremity vascular trauma, 609 Dorsal pancreatic artery, location of, 499 Driving while intoxicated (DWI), 250, 258–259 Droperidol, 110 Drownings, 255 Duct of Wirsung, 498–499 Duodenal diverticulization, 504

816 Duodenal ulcers as gastrointestinal hemorrhage cause, 464, 465, 475 obstructing, 458–460 perforated, 801 visualization of, 474 Duodenotomy, 467 Duodenum. See also Gastroduodenal trauma; Pancreaticoduodenal trauma diverticula of, 455, 464 as hemorrhage site, 464 injuries to iatrogenic injuries, 537 pancreatic trauma-associated, 500, 501, 502 obstruction of, 461, 471 perforation of, 462, 463 surgical exposure of, 55–56 surgical mobilization of, 502 Durable health care power of attorney, 693–695, 696, 703, 718 Duty to warn, 716–717 Dysphagia, 188, 277, 278, 279, 451, 453 Dysphoria, 279 Dyspnea, 279 E Ear, nose, throat emergencies, 277–304. See also Larynx; Pharynx Ears, examination of, 279 Eastern Association for the Surgery of Trauma (EAST), 39, 516 Echocardiography of aortic dissection, 408 of penetrating cardiac trauma, 390, 391, 393 transesophageal, 32, 40 of aortic dissection, 409 of blunt aortic trauma, 401, 402–403, 404 contraindications to, 403 intraoperative, 36, 37 of pulmonary embolism, 369 Ectasia, annuloaortic, 407 Edema of abdominal organs, 10 of burn-injured tissues, 127, 128, 132, 133, 134 cerebral, 34–35, 134, 336, 337, 384 cervical, 384 pulmonary, 134 retropharyngeal, 309 tracheal, 136 vasogenic, 336 Edrophonium, 110 Education and training in acute care surgery, 467–469, 743, 755 in Australia, 791–792

Index curriculum in, 752–753 in developing countries, 794, 795 in Japan, 799–800 for rural surgeons, 199–200, 792 surgical simulation use in, 263–274 in vascular surgery, 776 in injury prevention and control, 259 “Eggplant deformity,” 575, 576 Ehlers-Danos syndrome, 407–408 Elbow, wound closure in, 627, 629 Elder abuse, 127, 729 Elderly, definition of, 187 Elderly patients, 187–193 abdominal surgery in, 17 aortic dissection in, 410, 414 burn injuries in, 142–143, 254 clinical presentation of, 188–189 ethical and end-of-life issues regarding, 191 femoral artery occlusion in, 666–667 hemodynamic instability in, 84 lower-extremity vascular trauma in, 608 morbidity and mortality rates in, 187, 189 chest wall trauma-related, 349 pedestrian injuries in, 252 perioperative management of, 189–190 postoperative management of, 34 preference for local hospitals, 779 preoperative assessment of, 189 rib fractures in, 357 sigmoid volvulus in, 557 specific considerations for, 190–191 suicide in, 255 Elderly persons, as drivers, 250–251 Elderly population, 743, 744 Electrical injuries, 126, 161–165 Electrocardiography (ECG) for cardiac trauma evaluation, 390, 396 for chest pain evaluation, 453 perioperative, 74, 75 Electrolyte disorders. See also specific electrolyte disorders burn injuries-related, 133–134, 152–153 in potential organ donors, 710 Embolism air, 49, 52, 301 aortic, 530–531 mesenteric, 525 pulmonary, 75 massive, 13, 368–370 pelvic ring fracture-related, 600 prophylaxis against, 79 Embolization, of massive hemoptysis, 381 Emergency, definition of, 195

Emergency, medical definition of, 683–684 informed consent and, 683–684 Emergency departments in Australia, 787 definition of, 677 as emergency general surgery access site, 756 future developments in, 781–782 Emergency general surgery (EGS) services, Vanderbilt Model of, 754–763 Emergency medical services systems, 202–205 Emergency medical technicians (EMTs) interaction with acute care surgeons, 202 training levels of, 203 Emergency Medical Treatment and Labor Act (EMTALA), 677–682, 720 Emphysema as air leak cause, 370 subcutaneous, 312, 315, 321, 364, 567 Empyema parapneumonic, 371 postoperative, 375 pulmonary gangrene-related, 375 retained hemothorax-related, 368 retained parenchymal missilesrelated, 367 subdural, 112 surgical management of, 371–373 thoracic, 114 Encephalopathy, Wernicke’s, 334 Endobronchial blockers, 380 Endocrine monitoring and care, postoperative, 79–80 Endocrine system, aging-related changes in, 188 End-of-life care advance directives for, 69, 191, 689–700, 727–729, 731 pain management in, 716–717 palliative, 703, 704–705, 731–732 physician-patient-family communication in, 703–704 withdrawal of treatment in, 705–706, 731–732, 735 withholding of treatment in, 729–731 Endometriosis, as hemoptysis cause, 378–379 Endophthalmos, 278, 279 Endoscopy bedside, 117–118 esophageal, 325, 326–327, 453–454, 462–463 of gastrointestinal hemorrhage, 475 oropharyngeal, 465–466

Index use in rural and remote areas, 198–199 Endotoxemia, as hypermetabolic response cause, 92 Endotracheal intubation, 298 alternatives to, 6 of bleeding ulcer patients, 465 complications of, 298, 299 decannulation of, 300–301 as esophageal perforation cause, 321, 463 failure of, 6 indications for, 5 of neck trauma patients, 47 pediatric, of laryngotracheobronchitis patients, 307 prehospital, 216, 223 technique, 5–6 training in, 723 Endovascular management. See also Stents of abdominal and pelvic vascular trauma, 539, 540 of acute mesenteric ischemia, 527–528 of aortic dissection, 529–530, 531 of aortic thrombosis, 533 as cardiac trauma cause, 397 of hemorrhage, 524 of renal arterial occlusion, 530, 531, 532 of renal vein thrombosis, 534 of ruptured abdominal aortic aneurysm, 536 of ruptured visceral/renal arteries, 538 as vascular injury cause, 538, 541 Energy expenditure basal energy expenditure (BEE), 95, 96 factors affecting, 96 total energy expenditure (TEE), 95 Energy production, 220–221 Enteral nutrition, 78–79 administration route for, 100, 116–117 for burn injury patients, 97, 138, 151–153 contraindication to, 84, 103 early, 78 effect on energy expenditure, 96 effect on intestinal barrier function, 92, 96, 98 formulas, 79, 99, 100 immune-enhanced, 79, 97, 98–99 nutrient composition of, 94–95, 97, 99 operative preparation for, 70 parenteral nutrition versus, 97–98 preoperative, 108 timing of, 99–100 Enteritis, bacterial, 799 Enterotomy, small bowel, 472–473, 474

817 Epididymitis, 577 Epididymo-orchitis, 576, 577 Epiglottitis, 288–289, 297–298 Epistaxis, 277, 302–303 Errors, medical, disclosure of, 726–727 Erythema, 603 Erythropoietin, 130 Escharotomy, 119, 120, 132, 133, 161, 165 Eschars avascularity of, 139 edema formation beneath, 132, 133 Esmolol, 75 Esophageal cancer, 325–326, 328, 452, 462–463 Esophageal Doppler monitor (EDM), 76 Esophageal emergencies, 314–331 anatomic considerations in, 314–315 bacteriology of, 315 bleeding varices/hemorrhage, 462–463, 464, 465, 491–492 damage-control approach to, 52 esophageal strictures, 322–323, 324, 454, 457–458 general considerations in, 314 nontraumatic, 314, 320–328 perforation, 320–323, 452, 462–463 spontaneous. See Boerhaave’s syndrome strictures, 457–458 surgical exposure in, 51, 54–55 traumatic, 314, 315–320 Esophageal obturator airway (EOA), 223–224 Esophagectomy, transhiatal, 323, 324 Esophagitis, 327, 430 Esophagography, 316–317, 321–322, 463 Esophagoscopy, 317 Esophagostomy, 52 Essex-Lopresti lesions, 640 Ethics. See also Bioethics definition of, 715 Etomidate, 109 Eustachian tube, 284 Euthanasia, voluntary, 735 Evidence-based medicine, 748, 760 Exophthalmos, 278, 279 Explosion disasters. See Bombings Exsanguination, 38, 210, 403, 609–610 Extensor tendons, injuries to, 618, 635–636 Extracorporeal membrane oxygenation (ECMO), 85–87, 366, 371, 397 Extravasation, 627, 646–647 Extremities. See also Hand and upper extremity; Lower extremity bedside surgery in, 118–119 cadaveric, reperfusion of, 609 failed revascularization in, 62 injuries to, 44

damage-control procedures for, 64–65, 126, 229, 246 electrical and lightning injuries, 161–165 prehospital management of, 226–227 vascular, exposure techniques for, 61–63 Extubation, 34, 36–37, 300–301 Eyes, examination of, 278, 279 F Face examination of, 279 fractures of, 5, 310–311 Facet dislocations, cervical, 340 Facial nerve, in neck exposure, 45–46 Facial palsy, 278 Falls as blunt trauma cause, 395, 422 in the elderly, 253–254 electrical injuries-related, 161 mechanisms of injury in, 211 as thoracic aortic trauma cause, 400, 401 Farrington, J.D. “Deke,” 202 Fasciitis, necrotizing, 38, 118, 119, 166, 169, 170, 652–653. See also Necrotizing soft tissue infections Fasciotomy, 118–119 of electrical injuries, 162, 164 lateral, 605 lower extremity, 63–64, 605–606, 608, 672–673 upper extremity, 664 forearm, 63, 64, 647, 648–649 Fat embolism syndrome, 40 Fatty acid deficiency, in burn patients, 152 Fecoliths, 571 Feeding tubes. See also Nutritional support placement of, 116–117 Felons, 650, 651 Femoral arteries. See also Gastric feedinty tubes; Gastrostomy; Jejunostomy injuries to, 609–610, 669–671 catheterization-related, 664, 665–666 ligation of, 609 occlusion of, 666–668 profunda, location of, 62, 64 pseudoaneurysm of, 666, 668–669 surgical exposure of, 62 Femoral neck fractures, in young patients, 607–608 Femoral shaft fractures, 608 Femoral veins, injuries to, 671–672

818 Femur, injuries to fractures, 211, 227, 607–608 motor vehicle accidents-related, 206, 207 Fenestration, endovascular, 529 Fever, 72 beneficial effects of, 96 effect on metabolic rate, 96 head trauma-related, 344 hypermetabolic response-related, 91 postoperative, 90 stress-related decrease in, 68 Fibrothorax, 367 Fick principle, 220 Fight-or-flight response, 130 Fingers. See also Thumb extensor tendon repair in, 635–637 flap coverage for, 627, 628, 629 flexor tendon repair in, 633–635 infections of, 649 innervation of, 618–619 surgical amputation of, 632 Fingertip pulp testing, 618 Fingertips “dropped,” 636 injuries to, 622–625 Firearms-related injuries. See Gunshot trauma Fire-related injuries, 125, 126. See also Burn patients; Burns Fireworks-related injuries, 126 Fistulas aortoenteric, 465, 537 aortoesophageal, 327–328 arteriovenous, 608 dialysis, 645 bronchopleural, 367, 371, 372, 373–374, 375 cholecystoduodenal, 486, 487 enteral, 177, 178 pancreatic, 507 sigmoid, 555, 556 sigmoidovaginal, 555 tracheoesophageal, 328 of tracheoinnominate artery, 378, 380, 381–382 Fistulotomy, primary, 549–550 Flail chest, 6, 217, 348, 349, 352, 353 Flaps Boari, 579 for electrical injury closure, 164–165 for hand and upper-extremity injury closure, 626–631 for open abdomen closure, 183 Flexor tendons anatomic zones of, 633, 634, 635 examination of, 618 injuries to, 618, 633–635 integrity testing of, 619, 621

Index Fluid resuscitation/therapy, 8–9 for burn injury patients, 125, 130–134, 155 for electrical injury patients, 163 for necrotizing soft tissue infection patients, 170–171 Parkland formula for, 125, 155 physiology of, 221 postoperative, 77–78 for potential organ donors, 709, 710 prehospital, 218, 220–222 volume-restricted, 221–222 Flumazenil, 110, 334 Flynn, John, 793 Focused systems review, 69 Food aspirated, 290 esophageal impaction of, 324–326, 453 Foot compartment syndromes of, 606 irreducible dislocations of, 607 Football helmets, removal of, 226 Forearm blast trauma to, 630 fasciotomy of, 63, 64, 647, 648–649 fractures of, 640 Foregut trauma. See Gastroduodenal trauma Foreign bodies as airway obstruction cause, 5 aspirated, 290, 291 colorectal, 559 as gastric perforation cause, 464 gastroesophageal impaction of, 324–327, 453–454 in the hand, 621–622 in the head, 343–344 ingested, 288, 289–290, 294–296, 305, 313, 451, 452, 473 in lower extremity, 609 phargyngeal/laryngeal, 277 retained pulmonary parenchymal, 367 as urogenital prostheses infection risk factor, 566 Fractures as abdominal compartment syndrome cause, 10–11 Bennett’s, 642 boxer’s, 641 in burn injury patients, 150 Chance, 441 chauffeur’s, 640 of the clavicle, 355, 639 Colles’, 640 damage-control principles for, 64 electrical injuries-related, 163 falls-related, 211 femoral, 211, 227, 607–608 fixation of, anesthesia management during, 39–40

of hand and upper extremity, 638–642, 640 hangman’s, 340 of hip, 253 humoral, 639, 640 immobilization of, 227 Jefferson’s, 340 of long bones, 64, 150, 422, 594 of lower extremity, 610–611 metacarpal, 619 Monteggia, 640 olecranon, 640 open, 604, 610–611 pelvic ring, 589–601 penile, 575–576 phalangeal, 622, 642 radial, 640–641 Rolando’s, 642 scaphoid, 641 of the scapula, 355–356 spinal, 339–340 of the sternum, 354–355, 395, 401, 402 of the tibia, 211, 611 vertebral, 335 Free water deficit, 710 Free water replacement, in burn injury patients, 152–153 Fresh-frozen plasma, 12 Frostbite, 147–148, 230–231, 646 “Full code,” 735 Functional status assessment, 69 Fundopexy, Dor, 456, 457 Fundoplication after paraesophageal hernia reduction, 457 Nissen, 321, 325, 458 as pain cause, 452 Futile medical care, 701–704, 716–717, 730–731 voluntary euthanasia during, 735 G Gag reflex, 289, 465–466 Galen, 227, 513 Gallbladder, injuries to, 163, 502 Gallstone ileus, 473, 486–487 Gallstones, 19, 484, 485–486 Gangrene biliary stasis-related, 484 diabetic, 653 Fournier’s, 38, 550 gas, 168, 653 gastric, 431 necrotizing, 169, 567–568 nondiabetic, 653 pulmonary, 374–375 Gas, in renal and perinephric tissues, 561, 562 Gastrectomy, 458–460, 466–467 Gastric artery, left, 525

Index Gastric bypass, as internal hernia cause, 461 Gastric feeding tubes, 70, 117 Gastric outlet obstruction, 458–461, 460–461 Gastric procedures, as splenic trauma cause, 515 Gastric ulcers bleeding, 465–467 perforated, 450, 463–464, 469, 801 surgical treatment for, 466–467 Gastrinoma, 474 Gastritis, 466 Gastrocolic ligament, 56, 502 Gastroduodenal artery, 57, 499 Gastroduodenal trauma, 450–470 evaluation of, 451–452 foregut obstruction, 452–461 foregut perforation, 462–464 upper gastrointestinal hemorrhage, 464–469 Gastroduodenostomy, 461 Gastroenterostomy, 458–459 Gastroepiploic nerves, 468 Gastroesophageal junction tumors, 458 Gastroesophageal reflux disease (GERD), 188, 327, 451, 452, 457 Gastrohepatic ligament, dissection of, 61 Gastrointestinal monitoring, postoperative, 78–79 Gastrointestinal motility, burn-related changes in, 129–130, 138–139 Gastrointestinal surgery, in the elderly, 190 Gastrointestinal tract aging-related changes in, 188 perforation of, 60–61 Gastropancreatic fold, 467 Gastroplasty, Collis, 457 Gastrosplenic ligament, anatomy and location of, 514 Gastrostomy, 100, 117 G8 Global Healthcare Applications (GHAP) Sub-Project (SP)-4, 804, 805 Genitalia ambiguous, 582–584 necrotizing gangrene of, 567–568 Genitourinary emergencies. See Urogenital emergencies Gissane, William, 767 Glasgow Coma Scale, 5, 218, 336, 337, 338, 345, 394, 687 Glass, embedded in the hand, 622 Global health care, 804, 805 Glossopharyngeal nerve, in neck exposure, 46 Glucagon, 92, 527 Gluconeogenesis, in hypermetabolic response, 92–93

819 Glucose, as nutritional support component, 94 Glucose administration, in comatose patients, 334 Goiter, substernal, 384 “Golden hour,” of trauma care, 598 Gonadal dysgenesis, 582 Good Samaritan acts, 716–717, 733–734 Grafts angioaccess, occlusion or infection of, 658–659 for burn injuries, 142, 143, 144–145, 151 for hand and upper extremity injuries, 626 Granulocyte colony-stimulating factor, 130 Greater saphenous vein, in groin arterial injuries, 670 Great vessels, exposure and repair of, 50–51, 52 Growth hormone, 81, 100, 101–102, 153 “Guarding,” 437 Gunshot trauma abdominal, 441, 506, 538 cardiac, 389–391, 393–394, 397 to chest wall, 356 diaphragmatic, 425 esophageal, 316, 317, 318 to head, 338, 339 to lower extremity, 608 mechanisms of injury in, 212–214 pharyngoesophageal, 318 prevention of, 249, 258 pulmonary parenchymal, 365, 367 transmediastinal, 317 to upper extremity, 627, 628 to wrist, 630, 631 H Haloperidol, 110 Hand and upper extremity, 615–655 amputations/replantation of, 631–633, 662 compartment syndrome of, 615, 647–649, 653, 663–664 infections of, 649–653 injuries to chemical burns, 646 complex wounds, 626–631 examination and diagnosis of, 618–622 extravasation injuries, 646–647 fingertip and nailbed injuries, 622–625 fractures and dislocations, 638–644 frostbite, 646 high-pressure injuries, 645–646 nerve injuries, 615, 637–638 open soft tissue injuries, 626–631

radiographic assessment of, 621–622 soft tissue coverage for, 615–616 tendon injuries, 618, 633–637 vascular injuries, 615, 644–645 innervation of, 618–619, 620 lymph drainage sites of, 650 reconstructive requirements for, 627 treatment principles for, 615–618 vascular exposure techniques for, 62 Harris-Benedict equation, 95–96 Hartmann procedure, 554 Hayward, Richard, 739 Head and neck. See also Head injuries; Neck imaging of, 281, 282 surgical emergencies in, 288–296 bedside surgical interventions for, 112 in pediatric patients, 305–313 as percentage of all acute care surgery, 44 Head and neck examination, 278–281 Head injuries blunt trauma-related, 336–338 brain death prevention in, 773 explosions-related, 243, 244 fever associated with, 344 injuries associated with blunt diaphragmatic trauma, 422 rib fractures, 352 secondary brain injuries, 7 motor vehicle accidents-related, 207, 208, 210, 211 penetrating trauma-related, 338–339 Head tilt-chin thrust maneuvers, 5 Head tilt maneuver, 298 Health Insurance Portability and Accountability Act (HIPAA), 720–721, 729 Heart/lung transplantation, 772, 774 Heart rate. See also Tachycardia aging-related decrease in, 188 in pulseless patients, 10 Heart transplantation, 772, 774 Heart transplant candidates, ventricular assist device use in, 88–89 Heimlich maneuver, 324 Helicobacter pylori, 459, 463–464, 474, 800, 801 Helmets, 253 removal of, 226 Hemangioma, giant hepatic, 488 Hematocrit, perioperative, 79 Hematologic monitoring, 79 Hematoma cervical, 112 of chest wall, 351 epidural, 336, 338 intramural, 408, 461 intraparenchymal, 342

820 Hematoma (cont.) mediastinal, 395 pancreatic, 503 periaortic, in thoracic aorta repair, 405, 406 peritoneal, 539–540 rectus sheath, 442 retrohepatic, 541 retroperitoneal, 561, 585 splenic, 516, 517, 518, 519 subdiaphragmatic, 516 subdural, 112, 336–337, 338 Hematuria, 570, 572, 573 Hemobilia, 492 Hemodynamic instability, 4, 84–90 circulatory support in, 84–89 as contraindication to enteral feeding, 84, 103 prehospital assessment and management of, 215 Hemodynamic monitoring, perioperative, 190 Hemoglobin-based oxygen carriers (HBCOs), 10 Hemogram, preoperative, 70 Hemopericardium, 391 Hemoperitoneum, 488 Hemoptysis catamenial (endometrosis), 378–379 massive, 378–382 pulmonary artery catheter-related, 383–384 pulmonary gangrene-related, 375 retained parenchymal missilesrelated, 367 tracheobronchial trauma-related, 364 tracheoinnominate artery fistularelated, 382–383 Hemorrhage airway. See Hemoptysis blunt aortic trauma-related, 403, 404–405 burn injuries-related, 143–144 cervical, 47 compression dressing-based management of, 222 controlled, 221 detection of source of, 7 diverticulosis-related, 553–554 effect on oxygen delivery, 221 endovascular management of, 524 esophageal, 327–328, 462–463, 464, 491–492 evaluation of, 7 foregut, 462 gastrointestinal, 16–17, 327, 430, 451, 464–469, 466 bedside endoscopic evaluation of, 117–118 as sentinel bleeding, 464–465

Index small bowel obstruction-related, 471, 474–475 hemorrhoids-related, 551 hepatic trauma-related, 59–60 “hypertensive,” 342, 443 as hypotension cause, 7, 8 intraabdominal, 222, 443 in lower extremity, 608 mediastinal, 115 open abdomen-related, 177 pancreatic trauma-related, 506, 508 pelvic, 443, 600 pericardial, 397 pharyngeal/laryngeal, 277, 288, 289, 301–303 in pituitary fossa, 343 prehospital management of, 226–227 pulmonary parenchymal, 365, 366 renal, 60, 568–570 retroperitoneal, 222, 596–597, 665 ruptured abdominal aorta-related, 535 in soft tissue surgery patients, 38, 39 splenic, 60 stress-related mucosal (SRGMH), 117 subarachnoid, 341–342 uncontrolled, 221 vascular trauma-related, 524, 525 Hemorrhoidectomy, bleeding after, 551 Hemorrhoids, 550–551, 555–557 Hemothorax, 217, 218 contaminated, 371 massive, 6 as mortality risk, 349 penetrating cardiac trauma-related, 390 pulmonary artery catheter tearrelated, 383–384 retained, 362, 367–368, 371, 385 Heparin, 61–62, 79, 86, 609 Hepatic arteries, 525 blood flow in, 525 ligation of, 60 location of, 57 surgical repair of, 542 thrombosis of, in hepatic allografts, 775 Hepatitis, as liver failure cause, 802 Hepatobiliary acute care surgery, 479–496 Hepatocellular carcinoma, 488, 489 Hermaphroditism, 582, 584 Hernia abdominal, 190–191, 435, 437–441, 471–472 diaphragmatic, 322, 420, 431–432 direct, 438 in elderly patients, 190–191 femoral, 435, 438 groin, 190–191 hiatal, 325, 429–431, 455–457

incarcerated, 437, 438, 439 indirect (pantaloon hernia), 438 inguinal, 438 intercostal pulmonary, 356 internal, 461 obturator, 435, 448 open abdomen-related, 118 paraesophageal, 190 planned ventral, 178, 447 retroanastomic (Peterson), 454 as small bowel obstruction cause, 473 visceral, 422, 423, 428 Hernioplasty, 438, 515 Herpes simplex virus infections, 650 High-pressure injuries, 645–646 Hip dislocations of, 206, 606–607 fractures of, 253 Hippocrates, 227 Histamine, 127 Histamine-2 blockers, 78 Hoarseness, 278, 279 Hodgkin’s lymphoma, 384 Holt, Walter, 202 Homicidal patients, 729 Homicide, 257, 258 Hormones. See also specific hormones in hypermetabolic response, 92 therapeutic applications of, 100–101 wound healing-enhancing effects of, 100 Horner’s syndrome, 293 Hospital Emergency Incident Command System (HEICS), 238 Hospital ethics committees, 733 Host defense mechanisms, 97, 130 Human acellular dermis (AlloDerm®), 182 Human immunodeficiency virus (HIV) infection, 565 Humeral shaft fractures, 639 Humerus fractures, 639, 640 Hunt-Hess Scale, 341 Hydatid disease, 484 Hydration, 307, 709 Hydrocephalus, 341, 344, 345 Hydrochloric acid burns, 646 Hydrofluoric acid burns, 146–147 Hydromorphone, 109 Hydronephrosis, 571 Hydroxyethyl starch (HES), 9 21α-Hydroxylase deficiency, 582, 583 Hyperbaric oxygen therapy, 173, 653 Hyperbilirubinemia, 480 Hypercholesterolemia, in elderly patients, 189–190 Hypercoagulopathy, 533 Hyperemia, 127, 128 Hyperglycemia chromium deficiency-related, 101

Index in elderly patients, 189, 191 in intensive care unit patients, 94 postoperative, 79 preoperative, 70 in surgical patients, 189 Hyperkalemia, 133, 710 Hyperlactacidemia, 11 Hypermetabolic state, 72, 80, 91–93, 94, 96 Hypernatremia, in burn injury patients, 152–153 Hypersplenism, 515 Hypertension as abdominal aortic aneurysm rupture cause, 534 as aortic dissection cause, 408 in blunt aortic trauma patients, 404 in elderly patients, 189–190 intraabdominal, 10–11, 134. See also Abdominal compartment syndrome poorly-controlled, 69 portal, 465, 480, 491–492 in potential organ donors, 710 pulmonary artery, 383 Hyperthermia, 333 malignant, 30, 41, 106–107 perioperative, 80 in potential organ donors, 711–712 Hyperventilation, in neurologic emergency patients, 35 Hypocalcemia, burn injuries-related, 133–134 Hypoglossal nerve, 46, 47 Hypokalemia, burn injuries-related, 133 Hyponatremia, 153, 710 Hypoparathyroidism, burn injuriesrelated, 133–134 Hypoperfusion, 7, 8, 10, 11–12, 13, 221 Hypopharynx, 281, 282, 284, 318 Hypotension aortic dissection-related, 408, 411 blunt cardiac trauma-related, 396 compartment pressure in, 604–605 differential diagnosis of, 13 head trauma-related, 7 neurologic emergency-related, 334 penetrating cardiac trauma-related, 394 in potential organ donors, 708–709 pulse pressure in, 13 retroperitoneal hemorrhage-related, 665 small bowel perforation-related, 473 spinal cord injury-related, 339 Hypothalamic-pituitary-adrenal axis, in chronic critical illness, 81 Hypothenar hammer syndrome, 645 Hypothermia, 230–231, 333 aging-related susceptibility to, 188

821 in burn injury patients, 155 as “dark angel” of death, 44, 176, 177, 184 as head trauma treatment, 338 perioperative, 80 posttraumatic coagulopathy-related, 12 in potential organ donors, 711–712 profound accidental, 799 resuscitative treatment for, 44 systemic, 147–148 Hypothyroidism, 80, 188 Hypovolemia, 221. See also Shock, hypovolemic compensatory mechanisms in, 221–222 postoperative, 78 as tachycardia cause, 75 Hypoxemia, postoperative, 76–77 Hypoxia head trauma-related, 7 myocardial, 221 neurologic emergency-related, 334 Hysterectomy, as ureteral injury cause, 578 I Icterus, scleral, 70 Ileum, terminal, intussusception of, 471, 477 Ileus, gallstone, 486–487 Iliac blood vessels hemorrhage from, 596 injuries to, 537, 541 surgical exposure of, 58, 59 thrombosis of, 666 Iliac crest, 435 Iliocaval confluence, 58, 59 Iliofemoral vein, thrombosis of, 368 Immersion injuries, as child abuse, 126–127 Immobilization, of spinal trauma patients, 215, 216–217, 218, 220, 224–226, 339, 340 Immunosuppressed patients. See also Acquired immunodeficiency syndrome (AIDS); Human immunodeficiency virus (HIV) infection mucormycosis in, 291 necrotizing soft tissue infections in, 167, 169, 170, 602 Incompetence, 726 Induction agents, 6, 33, 39 Infants. See also Neonates parotid/parapharyngeal inflammation in, 293–294 renal vein thrombosis in, 533 urine output in, 10

Infection. See also specific types of infection electrical injuries-related, 164 in the extremities, 118–119, 649–653 hepatic, 481–484 in intracranial space, 343–344 as neurologic emergency cause, 332, 333 nutritional support and, 93, 97–98 pharyngeal/laryngeal, 288–289 postsplenectomy, 513, 515, 520 as splenic rupture cause, 515 Infection control, 93 for burn injuries, 139–141 in the intensive care unit, 110–111 Infectious diseases in developing countries, 797–799 postoperative monitoring and care for, 80 Inferior mesenteric artery, 525 iatrogenic injuries to, 537 location of, 499 surgical repair of, 542 Inferior mesenteric vein, anatomic relationship to pancreas, 498 Inferior vena cava blood flow in, 420–421 injuries to, 500, 541 suprahepatic, exposure of, 55 suprahepatic, surgical exposure of, 55 surgical exposure of, 58 thrombosis of, 534 Inferior vena cava filters, 79, 118–119, 120–121 Inflammatory bowel disease, 473, 555–557 Influenza viruses, 306 Informed consent, 683–688, 696, 716–717, 718, 722–724 advance directives and, 727 autonomy in, 725–726 exceptions to/waivers of, 683–686, 723, 734–735 for ICU-based procedures, 108 implied, for Good Samaritan acts, 734 for organ donation, 732–733 patient’s capacity to provide, 685, 725–726 patient’s refusal to provide, 686–678 Infrapopliteal artery, injuries to, 610 Inguinal ligament, anatomy of, 435 Inhalation injuries, 5, 129, 134–137, 243 Initial assessment, of acute care surgery/trauma patients, 3–23 Injection injuries, 645–646 Injuries. See also specific types of injuries economic cost of, 780 mechanisms of, 205–214 as mortality cause, 249, 250, 779 prevention and control of, 110–111, 249–262

822 Injury severity scores (ISSs) as aggressive resuscitation indicator, 11 of burn/multitrauma patients, 150 of cardiac trauma patients, 394–395 of elderly patients, 191 in futile medical care, 702 of mass casualty victims, 235 mortality rates associated with, 780 Inspiration, vena cava blood flow during, 420–421 Insulin, anabolic effects of, 102 Insulin-like growth factor-1, 100, 101–102 Insulin resistance, aging-related increase in, 188 Intensive care, postoperative, 72–80 Intensive care unit (ICU), 71–80 bedside procedures in, 106–124, 757 infection control in, 110–111 postoperative care in, 72–80 preparation of, 71 in rural and remote areas, 197 transfer of surgical patients to, 70 Intensive care unit patients, mortality rate in, 702 Intensive care unit teams, 756–757 Intercostal nerve block, 356 Interleukins, in hypermetabolic response, 92 International Registry of Acute Aortic Dissection (IRAD), 409 Intestines. See also Large intestine; Small intestine arterial anatomy of, 525 barrier function of, 92, 96, 98 obstruction of, 437 pelvic ring fracture-related injuries to, 594 Intimate partner violence, 256–257 mandated reporting of, 729 Intoxicated patients. See also Alcohol use waiver of informed consent for, 685 Intraabdominal pressure, elevated, abdominal compartment syndrome-related, 10, 11, 442–443 Intraabdominal trauma, pancreatic trauma associated with, 502 Intraaortic balloon pumps (IABPs), 87 Intracranial pressure elevated abdominal compartment syndromerelated, 442 bedside management of, 111–112 head injury-related, 336, 338 neurosurgical trauma-related, 34–35 subarachnoid hemorrhage-related, 341 monitoring of, 345

Index Intravenous drug abuse, 167, 169–170, 562, 668–669 Intravenous immunoglobulins, 171 Intubating laryngeal mask airway (ILMA), 224, 300 Intubation, 298–301. See also Endotracheal intubation face-to-face, 223 post-anesthesia, 34 prehospital, 216–217, 223 in pulmonary emergency patients, 362–363 Intussusception, bacterial enteritisrelated, 799 Ipecac, syrup of, 323 Iron replacement therapy, 101 Irrigation of empyema, 372 ocular, 147 of open fractures, 39 of soft tissue wounds, 38 Ischemia aortic dissection-related, 410, 411, 528–530 cerebral, 35 colitis-related, 558–559 end organ tolerance to, 533 in lower extremity, 603–604 mesenteric, 176, 184, 525–529 small bowel obstruction-related, 471, 472, 476–477 as small bowel perforation cause, 474 neural, 647, 648 renal, 530, 533, 541–542 six “P’s” of, 603, 608 in small bowel, 100, 471, 472, 474, 476–477, 558 Ischemia time, for replantation of amputated parts, 632 J Japan, acute care surgery in, 799–805 Jaundice, 70, 465, 485, 490 Jaw lift maneuver, 222, 298 Jaw thrust maneuver, 5, 222, 298 Jehovah’s Witnesses, 726 Jejunostomy, 99–100 Joint Commission on Accreditation of Healthcare Organizations (JCAHO), 678 Joints open, of lower extremity, 610–611 septic, 603 total replacement of, 603 Jones, Robert, 767 Justice (fairness) principle, 718–719, 72 K Kanavel’s cardinal signs, 652 Karyotyping, 582–583, 584

Kehr’s incision, 517 Kehr’s sign, 516 Ketamine, 109, 111 Ketoacidosis, diabetic, in potential organ donors, 711 Ketorolac, 110 Kidney injuries to blunt diaphragmatic traumaassociated, 422 vascular, 541–542 ischemic, 530 Kidney transplantation, 772, 774 Knee arthrocentesis of, 119 dislocations of, 602, 607, 611 Kocher maneuver, 55, 57, 58, 502, 504–505, 541 Kwashiorkor, 796 L Lacerations to the bladder, 580 diaphragmatic, 424 to the hand, 618 hepatic, 60 pancreatic, 502, 503 splenic, 517, 519, 520 Lactate, blood levels of, 11 Laparoscopy bedside, 118 of diaphragmatic trauma, 423, 426, 427–428, 429 of esophageal trauma, 322–323 in hernia repair, 439 simulation education in, 270 splenic, 520 Laparotomy bedside, 118 of penetrating diaphragmatic trauma, 425, 426–427 Laplace’s law, 534 Large intestine. See also Colon obstruction of, 770 Larrey, Dominique Jean, 235 Laryngeal arteries, 286–287 Laryngeal mask airway (LMA), 224, 300 Laryngeal nerves, 287 in aortic trauma repair, 406 Laryngoscopes, 280 Laryngotracheobronchitis, 305, 306–307, 308 Larynx anatomy and function of, 286–287 examination of, 281 foreign bodies in, 294–296 imaging of, 282 injuries to, 288 esophageal trauma-associated, 315 inhalation injuries, 135

Index in pediatric patients, 306, 312–313 lymphatics of, 287, 288 physiology of, 287 sagittal view of, 278 in untimely airway management, 296 Lavage of chemical injuries, 146 diagnostic peritoneal, 517 bladder injury during, 580 in burn patients, 150 of diaphragmatic trauma, 422, 426–427 of hemorrhage, 7 of pelvic ring fractures, 596 Lean body mass, 95 Left heart bypass, 405, 406 Left ventricular hypertrophy, agingrelated, 188 Legal principles, affecting acute care surgery, 719–721 Lienorenal ligament, 514 Life expectancy, increase in, 187 Life-sustaining treatment patient’s refusal of, 686, 716–717, 726, 730 withdrawal of, 702, 705–706, 717, 729–730, 731 withholding of, 729–731, 735 without consent, 717 Ligament of Treitz, 55, 56, 58 Lightning-related injuries, 126, 161–165, 229, 246 Limb salvage, 611 Lipids, as nutritional support component, 94–95 Lipolysis, in hypermetabolic response, 92–93 Lithotripsy, 571, 572 Little, Miles, 716 Liver anatomy and physiology of, 479–480 arterial anatomy of, 525 injuries to blunt diaphragmatic traumaassociated, 422 chest wall trauma-related, 349 damage-control maneuvers for, 59–60 as hemorrhage cause, 59–60 pancreatic trauma-associated, 500, 501, 502 in rural and remote populations, 198 pyogenic abscesses of, 481–482 surgical exposure of, 57 Liver allografts, hepatic artery thrombosis in, 775 Liver failure, fulminant, 774, 801–803 Liver fluke disease, 484 Liver function test, 769

823 Liver transplantation, 774, 775, 802–803 Liver tumors, rupture of, 487–489 Living wills, 689–690, 692–693, 703, 718 Lobar torsion, 378 Lobectomy, 365, 366, 367, 375 London, Peter, 767 Long-bone fractures, 64, 150, 422, 594 Long-term acute care centers, 760 Lorazepam, 109 Lower extremity, 602–614. See also Ankle; Foot beside acute care for, 118 compartment syndrome of, 604–606 infections of, 602–604 injuries to, 606–611 motor vehicle accidents-related, 206–207 open fractures, 610–611 vascular injuries, 608–610 mangled, 608, 611 open joints of, 610–611 vascular exposure techniques for, 62–63 Lower Extremity Assessment Project (LEAP), 610, 611 Lumbosacral plexus trauma, 594 Lunate bone, dislocations of, 642 Lung, aging-related changes in, 188 Lung cancer, as superior vena cava syndrome cause, 384 Lung isolation, 362–363 Lung transplantation, 772, 774 Luteinizing hormone, in chronic critical illness, 81 Lye-related injuries, 146 Lymphoma, mediastinal, 384 M Magnetic resonance imaging (MRI) of angiomyolipoma, 569 of aortic dissection, 408, 409 of diaphragmatic trauma, 422, 423, 425 of electrical injuries, 163 of genital necrotizing gangrene, 568 of the hand and wrist, 622 of the head and neck, 282 of the liver and biliary system, 480 for neurologic emergency evaluation, 335–336 of spinal trauma, 340 Maimonides, 513 Malabsorption, 99 Malaria, 513, 521, 797 Malignant hyperthermia syndrome, 30, 41, 106–107 Mallet finger deformity, 636, 637 Mallory-Weiss tears, 327, 464–465, 466 Malnutrition, 70, 91, 796–797

Malpractice, 468, 715, 719, 720 Good Samaritan acts and, 734 Managed care, 680, 681 Mandible examination of, 279 fractures of, as airway obstruction cause, 5 Marasmus, 796 Marfan syndrome, 407, 411 Maryland Institute for Emergency Medical Services System (MIEMSS), 24 Mayo, William, 513 McVay-Lotheissen repair, 438 Mechanical ventilation after airway placement, 301 in burn injury patients, 137 capnography and, 77 effect on energy expenditure, 96 in flail chest patients, 352, 353 in necrotizing soft tissue infection patients, 171 postoperative, 78 prolonged, 70 withdrawal of, 705–706 Meckel’s diverticulum, 474, 475 Median nerve, anatomy and function of, 618, 619, 620 Median nerve blocks, 616 Mediastinitis, 47, 318, 375–378, 384 Mediastinum descending necrotizing infection of, 376–378 gunshot trauma to, 317, 397 penetrating trauma to, 317–318, 390 Medicare, 690 Medicare Prescription Drug, Improvement, and Modernization Act, 678, 680–681 Medication history, 68 Megacolon, toxic, 549, 555, 556, 559 Meningitis, 333, 343, 344 Mental status examination prehospital, 218 preoperative, 69 Meperidine, 77, 109 Mesenteric arteries. See also Inferior mesenteric artery; Superior mesenteric artery ischemia of, 525–529 Mesenteric bypass, 526–527 Mesenteric veins. See also Inferior mesenteric vein; Superior mesenteric vein thrombosis of, 533 Mesh as burn injury dressing, 140, 141 use in hernia repair, 439 use in open abdomen management, 118, 178, 183

824 Mesh (cont.) use in splenic trauma repair, 519–520 use in splenorrhaphy, 60 Metabolic equivalents (METs), 189 Metabolic rate, in burn injury patients, 151 Metabolism aerobic and anaerobic, 220–221 in critical illness, 76 Metacarpal fractures, 619, 641–642 Methemoglobinemia, 76 Metoclopramide, 152 Midazolam, 109, 111 Middle colic artery, anatomic relationship to pancreas, 498 Military antishock trousers (MAST). See Pneumatic military antishock trousers (MAST) Mineral supplementation, 101 Minors. See also Children; Infants; Neonates informed consent for, 685–686, 687 Miranda warning, 717 Mivacurium, 109 Morals, definition of, 715 Morphine, 77, 109 Mortality, prediction of, 702 Motorcycle accidents, mechanism of injury in, 211–212 Motorcycle helmets, 253 removal of, 226 Motor vehicle accidents alcohol use-related, 250, 252, 258–259 as blunt abdominal vascular trauma cause, 538 as blunt aortic trauma cause, 400, 401, 406 as blunt cardiac trauma cause, 394 as blunt diaphragmatic trauma cause, 421 as chest wall trauma cause, 348, 349–350 economic cost of, 780 as esophageal trauma cause, 315 extrication of victims from, 218, 219 fatal, in Australia, 788 injury prevention in, 250–251 mechanisms of injury in, 205–212 as pelvic ring fracture cause, 596, 598–600 in rural and remote areas, 196, 198 as tracheobronchial trauma cause, 363 in the United Kingdom, 780 Mucormycosis, 290–291 Multiple organ failure, 8, 11, 171 Murphy’s sign, 485 Muscle relaxants, 35–36, 38. See also Paralytic agents Muscle wasting, 91, 100, 101–102

Index Musculoskeletal trauma, prehospital management of, 226–227 Mustard gas-related injuries, 126, 146 Myocardial infarction aortic dissection-related, 408 coronary artery trauma-related, 396 intraaortic balloon pump use in, 87 as mortality cause, 731–732 penetrating cardiac trauma-related, 393 perioperative, 37, 74 as shock cause, 84, 87, 89 Myocardial ischemia, 37, 74, 221, 393, 528 Myocardium, injuries to blunt trauma-related, 7, 394, 395–396 penetrating trauma-related, 390, 392, 393 repair of, 52 Myonecrosis, clostridial, 653 Myopectineal orifice, 438 Myotomy, 454, 455, 463 N Nailbed injuries, 622 Naloxone, 110, 334 Narcotics. See also Opiates as postoperative analgesia, 34 use in anesthesia maintenance, 33 use in palliative care, 705 Nasal airway, 222–223 Nasal intubation, 298 Nasogastric intubation, 100 in blunt aortic trauma patients, 404 as diaphragmatic rupture cause, 422, 423 as gastric volvulus treatment, 431 for gastrointestinal hemorrhage localization, 474 as small bowel obstruction treatment, 472, 473 as small bowel perforation treatment, 473–474 Nasojejunal intubation, 100 Nasolaryngoscopy, 280–281 Nasopharyngoscopes, 280 Nasopharynx anatomy of, 283 examination of, 280–281 National Nosocomial Infection Surveillance System, 444 National Trauma Data Bank, 748, 749 National Violent Injury Surveillance System, 258 Neck anatomic zones of, 311–312, 314 auscultation and palpation of, 280 examination of, 279–280, 282 fluid drainage in, 112 injuries to, 45–47

airway management of, 45, 47 anesthesia management of, 36–37 “bubbling,” 364 burn injuries, 133 damage-control approach to, 47 emergent exploration of, 36 in pediatric patients, 311–312 penetrating trauma, 317–318 as percentage of all acute care surgery, 44 surgical exposure techniques for, 45–47 vital structures of, 45–47 Neck masses, 278 Neck rigidity, ruptured cerebral aneurysm-related, 341 Necrosis liver tumor-related, 489 muscle, 609 toxic epidermal, 149–150 Necrotizing soft tissue infections (NSTI), 38, 166–175, 602–603 Neonates patent ductus arteriosus ligation in, 115 pyloric stenosis in, 460–461 urine output in, 10 Neostigmine, in combination with glycopyrrolate, 110 Nephrectomy, 60, 515, 561 Nephropathy, contrast agent-related, 78 Nephrostomy tubes, percutaneous, 571, 572 Nerve blocks, in hand and upper extremity acute care, 616 Nerve injuries electrical trauma-related, 163–164 to the hand and upper extremity, 617, 637–638 pelvic ring fracture-related, 600 Neurologic emergencies, 332–347 aging-related, 188 anesthesia management of, 34–36 bedside surgical interventions for, 111–112 burn injuries-related, 138 electrical trauma-related, 163–164 as elevated intracranial pressure cause, 34–35 initial treatment for, 334–335 nontraumatic emergencies, 341–345 operative decision making for, 336 pathology of, 332–334 in rural and remote areas, 198 secondary survey of, 335–336 traumatic emergencies, 336–340 Neurologic examination, 77 for brain death determination, 706–707 focused, 335

Index Neurologic monitoring, perioperative, 77 Neurolsurgical emergencies. See Neurologic emergencies Neuromuscular blocking agents, 77, 109–110 Neuropraxia, 648 Neurorrhaphy, primary, 638 Neurovascular examination, of the hand and upper extremity, 618–619 Nitric oxide synthase, enzyme-inducible, 14–15 Nitrogen wasting, perioperative, 72, 80 “No code,” 735 “No-man’s land of Bunnell,” 634 Nonmalficence, 718, 719, 721 Nonsteroidal anti-inflammatory drugs (NSAIDs) adverse effects of, 170, 327, 473, 474 as chest wall trauma-related pain treatment, 357 Nonviable patients, organ procurement and, 701–714 Nose examination of, 279, 280 fractures of, in pediatric patients, 310, 311 Nosebleed. See Epistaxis Nosocomial infections, blood transfusion-related, 9 Nuclear/radiologic agents-related injuries, 241–242, 243 Nurse practitioners, 776–777 Nutritional status assessment, 93–94 Nutritional support. See also Enteral nutrition; Parenteral nutrition; Total parenteral nutrition anabolic agents in, 101–102 for burn injury patients, 151–152 calculation of nutritional requirements in, 95–97 effect on intestinal barrier function, 92, 96, 98 for electrical injury patients, 163 goals of, 93–94 immune system-enhancing, 79, 97, 98–99 for infection prevention and control, 93 for necrotizing soft tissue infection patients, 173 operative preparation for, 70 overfeeding or underfeeding in, 94, 96 for pancreatic trauma patients, 507 pharmacology of, 100–101 postoperative, 77–78 principles and practices of, 91–103 route and timing of, 97–100

825 O Obstetric/gynecological surgery, in rural and remote areas, 198, 199 “Occult hyperfusion syndrome,” 34 Octreotide acetate, 507 Ocular injuries, acidic or alkaline agentrelated, 147 Odynophagia, 305, 315 Ogilvie’s syndrome, 556, 558 Oliguria, 10, 11, 12–13, 78 Omohyoid muscle, in neck exposure, 45 Operating rooms, for acute care surgery, 24–29, 756 in Japan, 800 for mass causality management, 234 Operative approaches, in acute care surgery, 43–66 Opiates, tissue accumulation of, 77 Opioid overdose, 334 Oral airways, 222–223 Oral cavity, examination of, 280 Oral contraceptives, as hepatic adenoma risk factor, 488 Oral intubation, 298 Orchidopexy, 576 Oregon Death with Dignity Act, 735 Organ donors, care for, 708–712 Organophosphate poisoning, 334 Organ procurement, 706–712 Organ transplantation, 772–775 Oropharynx anatomy of, 283–284 examination of, 280 Orthopedic emergencies. See also Fractures anesthesia management of, 39–40 in rural and remote areas, 198, 199 Osteomyelitis, 39, 352, 627 Ostomy, hernias in proximity to, 440–441 Otalgia, 278, 279 Otitis media, 279 Otoscopy, 279 Overdose, as neurologic emergency cause, 334 Oxandralone, 102 Oxygen, supplemental, 4 Oxygenation, 76 cerebral, 35 extracorporeal membrane (ECMO), 85–87 perioperative monitoring of, 77 preoperative, 108 Oxygen delivery, 221 P Packed red blood cell transfusions, 9 Packing abdominal, 10–11, 176, 181 nasal, 302–303

perihepatic, 59, 60 perirenal, 60 Pain abdominal, 436, 437 acute, 15–17 laparoscopic evaluation of, 769 nonspecific, 769–770 ultrasonographic evaluation of, 770 chest aortic dissection-related, 408 differential diagnosis of, 451–452, 451–453 esophageal perforation-related, 452 compartment syndrome-related, 604 effect on metabolic rate, 96 flank, 571 following initial resuscitation, 68 ischemia-related, 603, 608 postoperative, 76–77 as tachycardia cause, 75 Pain management in burn injury patients, 137–138 in chest wall trauma patients, 6–7, 353, 356–357 double effect principle and, 734, 735 during end-of-life care, 716–717 Palliative care, 703, 704–705, 731–732 Pallor, ischemia-related, 603, 608 Palpation, abdominal, 437 Pancreas anatomy of, 497–499 injuries to, 497–512 blunt diaphragmatic traumaassociated, 422 classification of, 503, 504 injuries associated with, 422, 500–502, 506 location of, 499–500 morbidity/mortality rates of, 506–508 in pancreatic head, 61 as pancreaticoduodenal trauma cause, 504–505 pertinent surgical anatomy in, 497–500 surgical techniques for, 497, 502–505 surgical exposure of, 55–57 Pancreas transplantation, 774 Pancreatectomy, distal, 502, 507, 508 Pancreatic cancer, 461 Pancreatic emergencies (nontrauma), 508–509 Pancreatic insufficiency, 508 Pancreaticoduodenal artery, anatomy of, 499 Pancreaticoduodenal trauma, 504–505, 506 Pancreaticoduodenectomy, 61, 504–505 Pancreaticojejunostomy, 504

826 Pancreatitis, 800 alcohol use-related, 497 biliary, 508 complications of, 508–509 diagnostic tests for, 769 gallstone, 486 grading of, 486 hemorrhagic, 466, 508 necrotizing, 508 posttraumatic, 507, 508 Ranson’s prognostic criteria for, 486 severity assessment of, 509 treatment for, 796, 803 Pancreatography, intraoperative, 502–503 Pancreatorraphy, 503 Pancuronium, 109 Pantridge, J.F., 202–203 Paracentesis, bedside, 115–116 Parainfluenza virus, 306 Paralysis, 531, 603, 608 Paralytic agents, 5–6, 77 Parapharyngeal space mass, 292–293 Paraplegia, 142, 345 Parasitic diseases, 484, 797–799 Paré, Ambroise, 421 Parenteral nutrition, 78–79 effect on intestinal barrier function, 92, 96, 98 enteral nutrition versus, 97–98 fat component of, 94 Paresthesias, 161, 165, 603, 608 Paronychia, 650, 651 Parotid gland abscess of, 293 in neck exposure, 45–46 Passive muscle stretch test, 648 Patent ductus arteriosus, ligation of, 115 “Patient dumping,” 677 Patients deceased in mass casualty triage, 236, 237 use in medical teaching situations, 723 difficult, 717 homicidal, 729 indigent, 717, 720 suicidal, 727 unconscious, informed consent for, 684–685 Patient Self-Determination Act, 690–692, 695, 727 Pedestrian injuries, 251–252, 253 Pellagra, infantile, 796 Pellegrino, Edmund, 735 Pelvic ring fractures, 589–601 Pelvic surgery, as percentage of all acute care surgery, 44

Index Pelvis injuries to fractures, 10, 64, 421, 422, 540, 541, 589–601 vascular, 538–542 normal, 597 stabilization of, 597–598 surgical exposure of, 58–59 Penetrating abdominal trauma index (PATI), 559 Penetrating trauma abdominal, 10, 441–442, 559 vascular, 538–539, 540–541 blast-related, 243 cardiac, 389–394 cervical, 317–318 diaphragmatic, 421, 425–428 esophageal, 315, 317–318 to the head, 338–339 mechanisms of injury in, 212–214 mediastinal, 317–318 pancreatic, 500, 506–507 pelvic vascular, 538–539 pharyngoesophageal, 318–319 pulmonary parenchymal, 365 simulation education in, 271–273 spinal, 340 thoracic, 10 tracheobronchial, 364 Penicillin, bacterial resistance to, 373 Penile prostheses, infections of, 566–567 Penis acute scrotum and, 576–577 “buried,” 582 burn injuries to, 133 circumcision complications of, 581–582 fractures of, 575–576 priapism of, 573–575 Peptic ulcers, 78 as foregut obstruction cause, 452 hemorrhagic, 327, 430, 466, 474–475 hiatal hernia-associated, 430–431 perforated, 473–474, 770 Periampullary carcinoma, 490 Pericardial fluid, in penetrating cardiac trauma, 390, 391 Pericardial window, subxiphoid, 391 Pericardiocentesis, 13, 391 Pericarditis, inflammatory postoperative, 393 Pericardium blood in, 391 operative access to, 391, 392 Perilunate dislocations, 642 Perineum, necrotizing gangrene of, 567–568 Perioperative management, of acute care surgery patients, 67–83 actions in the operating room, 70–71 preoperative care, 68–70

stress response and, 67–68, 72–80 Peripheral nerve injuries, 340 Peripheral vascular conditions, 656–674 of lower extremity, 664–673 of upper extremity, 656–664 Peritoneal dialysis, catheter placement in, 116 Peritoneoscopy, 118 Peritonitis diverticulitis-related, 770 in elderly patients, 190 esophageal trauma-related, 318, 324 mesenteric ischemia-related, 475 open-abdomen management of, 181–182 primary bacterial, 115 purulent or fecal, 176, 554 signs and symptoms of, 437 small bowel obstruction-related, 471–472, 473 tertiary, 118 Peritonostomy, retroperitoneal, 57 Peroneal artery, injuries to, 610 Petroleum distillate-related injuries, 126, 146 Phalangeal fractures, 622, 642 Pharmaceutical industry, as research funding source, 724–725 Pharmacology, nutrient, 100–101 Pharyngeal muscles, 284, 285 Pharyngoesophageal trauma, operative management of, 318–319 Pharynx anatomy and physiology of, 283–285 general conditions of, 285–286 inhalation injuries to, 135 sagittal view of, 278 surgical emergencies involving, 288–294, 296 Phenol-related injuries, 126, 147 Phenytoin, 334–335 Phleboliths, imaging of, 571 Phrenic nerve in blunt aortic trauma repair, 405 location of, 52 in neck exposure, 46, 47 in proximal right subclavian artery dissection, 52 in resuscitative thoracotomy, 48 Phrenic nerve stimulation, inferior vena cava blood flow during, 421 Physicians on-call schedules of, 768–769, 771 religious beliefs of, 717, 719 shortage of, 743 Pilonidal cyst-abscess, 551 Pituitary apoplexy, 343 Platelet count, 108 Platelet transfusions, preoperative, 108 Pleural effusions, 114, 321, 463

Index Pneumatic compression devices, 79 Pneumatic military antishock trousers (MAST), 218, 222, 594, 597 prolonged use of, 119 Pneumobilia, 487 Pneumomediastinum, 314, 328, 364, 462 Pneumonectomy, 366–367, 373, 375 Pneumonia, 7, 76–77, 135, 373–374, 375, 406 Pneumonitis, 364, 374 Pneumopericardium, 395 Pneumoperitoneum, 462 Pneumothorax loculated, 114–115 mortality risk associated with, 349 motor vehicle accidents-related, 208 open, 6 penetrating cardiac trauma-related, 390 persistent, 364 spontaneous, as air leak cause, 370 tension, 6, 7, 13, 423 Poikilothermia, ischemia-related, 603, 608 Poiseuille’s law, 7 Poisoning, as neurologic emergency cause, 334 Polyneuropathy, of critical illness, 77 Polyps, nasal, 290–291 Popliteal artery anatomy and surgical exposure of, 63, 64 embolic occlusion of, 669 injuries to, 602, 610, 611, 669–671 Popliteal veins, injuries to, 671–672 Porta hepatis, exposure of, 57 Portal vein isolation of, 57 ligation of, 61 location of, 499 pancreatic trauma-associated injuries to, 500 surgical repair of, 542 thrombosis of, 533 Positive end-expiratory pressure (PEEP), 35, 137 Postanesthesia care units (PACUs), 34 Potassium supplementation, in burn injury patients, 153 Potassium wasting, perioperative, 72, 80 Prehospital care, 202–228 assessment and management in, 214–220 in Australia, 788–789, 793 emergency medical services and, 202–205 regional trauma systems and, 747 in rural and remote areas, 195 special field skills for, 222–227 Pressure injection injuries, 645–646

827 Priapism, 573–575 Pringle maneuver, 59–60, 61, 541 Prioritizing, surgical, 30–31 Procidentia, rectal, 551–552 Proctocolectomy specimens, in ulcerative colitis, 556 Proctoscopy, 589, 600 Profunda femoris artery, in groin arterial injuries, 670 Prolactin, 81 Propofol, 109, 111 Propranolol, anabolic effect of, 102 Proptosis, 278, 279 Prostaglandins, 127 Prostate cancer, 572 Prostate gland “floating,” 594 normal, 572 Prostatitis, 565–566, 572 Prosthetics, urinary and genital, infections of, 566–567 Protein, as nutritional support component, 94, 97 Protein C deficiency, septic shockrelated, 15 Proteolysis, in hypermetabolic response, 92–93 Prothrombin time, 480 Protocols, versus standing orders, 204 Proton pump inhibitors, 78, 117, 457–458, 463, 474 Proximal interphalangeal joints (PIP) dislocation of, 643 extensor tendon injuries to, 636 injection injuries to, 646 Pseudoachalasia, 454 Pseudoaneurysms of brachial artery, 662 catheterization-related, 665 of prosthetic angioaccess graft, 658–659 of radial artery, 662 thoracic aortic, 209, 210 of ulnar artery, 662 Pseudocysts, pancreatic, 461, 503, 507, 508 Pseudoeschars, 128 Pseudohermaphroditism, 582, 584 Ptosis, 278, 279 Pulmonary arteries pulmonary artery catheter-related rupture of, 383–384 right, location of, 51 Pulmonary emergencies airway management in, 362–363 hemoptysis massive, 378–382 pulmonary artery catheter-related, 383–384 infections, 371–378 injuries, 362–368, 362–388

blast-related, 243 burn injuries, 129 damage-control approach to, 52 motor vehicle accidents-related, 208–209 parenchymal, 208–209, 365–367 retained parenchymal missiles, 367 lobar torsion, 378 massive pulmonary embolism, 368–370 persistent air leak, 364, 370–371 retained hemothorax, 367–368 superior vena cava syndrome, 384 thoracoscopy of, 363 thoracotomy of, 363 tracheoinnominate artery fistula, 382–383 Pulmonary hilum surgical exposure of, 51–52 trauma to, as hemorrhage cause, 49 Pulmonary monitoring and care, perioperative, 76–77 Pulmonary veins, location of, 51 Pulse as circulation adequacy indicator, 7 in shock, 222 Pulselessness, ischemia-related, 603, 608 Pulseless patients, pronouncement of death in, 10 Pulse oximetry, 4, 73, 76, 77, 217, 298, 465 inaccurate readings on, 76 Pulsus paradoxus, 408 Pupils, fixed and dilated, 338 Pus, “dishwater,” 172, 652 Pyelonephritis, 561–562, 570 Pyloric exclusion, 504 Pyloric stenosis, in neonates, 460–461 Pyloromyotomy, 461 Pyloroplasty, 458–459, 467 Pyonephrosis, 564–565 Q Quinlan, Karen Ann, 690, 702, 731 R Radial artery injuries to, 644, 645, 659 occlusion or thrombosis of, 657–658, 660 pseudoaneurysm of, 662 Radial brachial index (RBI), 645 Radial fractures, distal, 640–641 Radial head fractures, 640 Radial nerve anatomy and function of, 618–619, 620 superficial, anatomic course of, 618–619 Radial nerve blocks, 616 Radial pulse, in shock, 222

828 Radial styloid fractures, 640 Radiation injuries, 148–149, 230–231, 241–242, 243 Radiology, interventional, 756, 776 Rally packs, 334 Rapid-sequence intubation, 6 Reagan, Ronald, 677 Rectal prolapse, 551–552 Rectum, mobilization of, 58 Recurrent laryngeal nerve, location of, 47 Red blood cell scans, tagged, 553 Refractory period spectral analysis, 164 Regenerative medicine, 803, 805 Registries, trauma, 748, 749 Regurgitation, 451, 452 Rehabilitation services, 165, 750, 760 Religion, relationship to bioethics, 717, 719 Religious history, 719 Renal arteries aneurysm of, 537–538 inadequate perfusion of, 10 injuries to, 542 occlusion of, 530, 531, 541 Renal cancer, as hematuria cause, 572 Renal cell carcinoma, 570 Renal failure, 77, 78, 134, 153 Renal monitoring, 77–78 Renal system, aging-related changes in, 188 Renal veins iatrogenic injuries to, 537 thrombosis of, 533–534 Replantation, of amputated parts, 631–633 Research, conflict of interest in, 724–725 Research participation, informed consent for, 724 Respiratory syncytial virus, 306 Respiratory system, aging-related changes in, 188 Respiratory tract infections, in pediatric patients, 305 Resting energy expenditure (REE), 92, 151 Resuscitation, 218, 220. See also Fluid resuscitation/therapy assessment of, 10–12 in burn patients, 130–134 definition of, 3 ethics of, 717 initial, preoperative care following, 68 prehospital, flowchart for, 225 supranormal, 8 Resuscitative surgery, 43–44 Retractors, self-retaining, 44 Revascularization, of the extremities, 609, 631 Rhabdomyolysis, 667

Index Rhinitis, 277 Rhinorrhea, 277 Rhinoscopy, 279 Rib blocks, 356–357 Rib fractures, 208–209, 348, 349, 351–352, 353–354 biomechanics of, 349–350 blunt aortic trauma-associated, 401 of floating ribs, 351, 352 multiple, 217, 357 prevention of, 350 repair of, 353–354 Right atrial-to-femoral artery bypass, 405 Ringer’s ethyl pyruvate solution (REPS), 9 Ringer’s lactated solution, 8, 9, 78, 221 “Ring sign,” 563 Robotics technology, 28, 793 Rocuronium, 110 Royal College of Surgeons, trauma services recommendations of, 779, 780–781 Rural and remote areas, 194–201 blunt abdominal vascular trauma in, 538 on-call physician services in, 679 poisoning treatment in, 334 prehospital care in, 195 in the United Kingdom, 776–779 S Saline solutions, 8 San Diego Trauma Registry, 743, 744 San Francisco General Hospital, 677 Scald burns, 125, 126–127, 254–255 Scalene muscles, in neck exposure, 46, 47 Scandinavia, organ transplantation procedures in, 772 Scaphoid fractures, 641 Scapholunate ligament disruptions, 642, 643 Scapula fractures, 355–356 Scapulothoracic dissection, 356 Scarpa’s fascia, 435, 436 Schistosomiasis, 797, 798 Scrotum, acute, 576–577 Search and rescue, 232–233 Seat belts, 206, 250, 350 Secondary effects, 718 Sedation/sedatives administration during endotracheal intubation, 5–6 postoperative administration of, 77 tissue accumulation of, 77 use in intensive care unit patients, 109, 111 Seizures, neurologic emergency-related, 334–335

Self-inflicted injuries, burns as, 125 Sellick maneuver, 5 Sengstaken-Blakemore tubes, 492 Sensory deficits, aging-related, 188 Sepsis. See also Shock, septic biliary, 483–484 blood pressure levels in, 172 enteral nutrition in, 99 as infection risk factor, 513 intraabdominal, 179 necrotizing soft tissue infectionsrelated, 169 postsplenectomy, 513, 515, 521 preoperative assessment and treatment of, 69, 70 severe, 14 Serotonin, 127 Serroraphy, 468 Sexual abuse, of children, 256 Shadow-Line, The (Conrad), 739 Shank artery, traumatic injuries to, 669 Sharps-related injuries, prevention of, 108, 110 Shock, 12–15 assessment of, 222 burn injury-related, 130 cardiogenic, 13, 84, 86–87, 89 definition of, 8 in hemodynamically-instable patients, 4 hemorrhagic, 3, 7, 8–9, 12–13, 17, 366 hypovolemic, 12–13, 75 intravenous access in, 7 neurogenic, 7 obstructive, 13 in potential organ donors, 708, 711 prehospital management of, 220 septic, 14–15, 39, 84 severe, 218 traumatic, 13 uncompensated, 221, 222 vasodilatory, 14–15, 84–85 Shock bowel, 443 Shoulder “floating,” 356 fractures of, 355–356 Shoulder girdle trauma, flap coverage for, 627, 628 Shunts intrapulmonary, 7 temporary intraluminal, 44, 662–663, 670–671 transjugular portal-systemic, 492 ventriculoperitoneal, failure of, 344–345 Sickle cell anemia, as priapism cause, 574, 575 Siegler, Mark, 721 Silver nitrate, 140 Silver sulfadiazine, 140

Index Simulation education, in acute care surgery, 263–274 Sinuses computed tomography of, 290 examination of, 279 pyriform, 284 Sinusitis, 277 Skin color, in shock, 222 Skin examination, in head and neck emergency patients, 279 Skin substitutes, 145–146, 150 Skin temperature, in shock, 222 Skull fractures, 207, 208 “Slow code,” 735 Small intestine, 471–478 hemorrhage from, 471, 474–475 injuries to, 422, 501, 502 ischemia in, 100, 471, 476–477, 558 Meckel’s diverticulum of, 474, 475 obstruction of, 471–473, 770 perforation of, 471, 472, 473–474 strangulated, 770 Small intestine submucosa (SIS®), 182 Smith fractures, 640 Smoke, toxic components of, 135, 136 Social history, 69 Soft tissue emergencies anesthesia management of, 38–39 hand and upper extremity trauma, 626–631 Soft tissue infections, necrotizing (NSTI), 38, 166–175, 602–603 Specialists, in urban versus rural areas, 194, 197–198 Sphincterotomy, 549–550 Spinal cord injuries to, 339 in burn injury patients, 150 hypopharyngeal trauma associated with, 318 as shock cause, 7 as urogenital prostheses infection risk factor, 566 nontraumatic pathology of, 345 Spine degenerative disease of, 332, 333 fractures of, 339–340 immobilization of, 215, 216–217, 218, 220, 224–226, 339 injuries to anesthesia management in, 36 traumatic, 339–340 Spiritual history, 719 Spleen accessory, 514 clinical anatomy of, 514–515 in exposure of the pancreas, 56 function of, 513, 515 injuries to, 513–522 blunt aortic trauma-related, 401

829 chest wall trauma-related, 349 as hemorrhage cause, 60 iatrogenic injuries, 515, 537 nonoperative management of, 513–514, 515–516 operative management of, 516–521 pancreatic trauma-associated, 502 severity grading of, 516, 517, 519 splenic clinical anatomy in, 514–515 mobilization of in pancreatic trauma repair, 502 in splenic trauma repair, 517–518 rupture of, 513, 515, 521 Splenectomy, 60, 515, 516, 521 complications of, 513–514, 515, 520, 521 laparoscopic, 520 partial, 516, 518 Splenic arteries, 525 anatomy and location of, 498, 499, 514 aneurysms of, 517 distal, in exposure of the pancreas, 56 Splenic salvage, 516, 521 Splenic tissue, autotransplantation of, 520 Splenic veins, 56–57, 498, 514 Splenorrhaphy, 60, 518 Spondylolisthesis, 340 Sports-related trauma, 351–352 Stabilization, of surgical patients, errors in, 197 Stab wounds abdominal, 441–442, 506, 538 cardiac, 389, 390, 393–394 diaphragmatic, 425 esophageal, 316 to the head, 338 pharyngoesophageal, 318, 319 thoracic, 202, 227 Standing orders, versus protocols, 204 Staphylococcal scalded skin syndrome (SSS), 149 Starch solutions, 9 Starvation, as diarrhea cause, 99 Statins, as compartment syndrome cause, 604 Status epilepticus, 334 “Steakhouse syndrome,” 324, 452 Stem cells, 805 Stener lesions, 643, 644 Stents as aortic trauma treatment, 404, 406, 409 esophageal, 328, 462–463 J ureteral, 580 Sternal fractures, 354–355, 395, 401, 402 Sternocleidomastoid muscle, exposure of, 45, 46

Sternotomy, 364, 365, 391, 392, 412 median, 50, 51, 55, 61 postoperative reopening of, 115 Stevens-Johnson syndrome, 149 Stomach gangrene of, 431 as hemorrhage site, 464 pancreatic trauma-associated injuries to, 500, 501, 502 perforation of, 462, 463–464 volvulus of, 191, 431 Stomach cancer, risk factors for, 801 Stomach tumors, 458 Streptokinase, 368, 370 Stress, physiologic response to, in chronic critical illness, 67–68, 72–81 Stridor, 279 “String sign,” carotid, 343 Stroke, 341–343 aortic dissection-related, 408, 410 in elderly patients, 189 hemorrhagic, 333, 334, 335, 341–342 ischemic, 333–334, 335, 342–343 as mortality cause, 731–732 “Stroke in progress,” 342–343 Subarachnoid space, infection in, 343 Subclavian arteries injuries to, 46, 49, 302, 352 ligation of, in dying patients, 52 in neck exposure, 46, 47 Subclavian vein, as central venous pressure catheter site, 75–76 Subglottis, postintubation stenosis of, 294 Subspecialties, 744 Subspecialties, surgical, 744, 754, 771, 787 Subspecialty consultants, 758 Succinylcholine, 109 Sucralfate, 78 Sudden death, 74, 395, 731–732 Suicidal patients, 727 Suicide, 255, 258, 731–732 by caustic ingestion, 323 by foreign body ingestion, 326 physician-assisted, 705, 718, 719, 720, 735 prevention of, 255, 726 as rational choice, 727 Sulfa allergies, 141 Superficial radial nerve, anatomy and function of, 618–619, 620 Superior mesenteric artery blood flow in, 525 embolism of, 476 exposure of, 58 iatrogenic injuries to, 537 ischemia of. See Ischemia, mesenteric location of, 58, 497–498, 499 surgical repair of, 542

830 Superior mesenteric artery syndrome, 461 Superior mesenteric vein in exposure of the pancreas, 56–57 ligation of, 61 location of, 497–498 as pancreatic blood supply source, 499 pancreatic trauma-associated injuries to, 500 Superior vena cava, blood flow in, 420–421 Superior vena cava syndrome, 384 Supraglottis, disorders of, 287, 305–306 Surgical site infections (SSIs), 444–445 Swallowing, 284–285 Syncope, aortic dissection-related, 408 Systemic inflammatory response syndrome (SIRS), 14, 17, 84–85, 92, 151 Systemic vascular resistance, 13 T Tachycardia, 74–75 Tachypnea, 69–70 Tamponade, cardiac aortic dissection-related, 408, 410 cardiac trauma-related, 390, 391, 394–395 central vascular catheters-related, 397 endobronchial, 380 as obstructive shock cause, 13 pericardial, 13, 221, 390, 391 postoperative, 115 solid-organ, 44 of venous hemorrhage, 525 Tar injuries, 126, 147 Taste, 285 Telemedicine, 199, 802, 803 Tenolysis, 626 Tenosynovitis, flexor, 618, 652 Terrorist attacks, 230, 232, 236, 237, 239–244, 750 Testicles, during perianal debridement, 173 Testicular torsion, 576 Testosterone, in chronic critical illness, 81 Tetanus immunization/prophylaxis, 81, 155 Therapeutic Intensity Scoring System (TISS), 107 Thermal regulation during anesthesia maintenance, 33 disorders of, in tropical populations, 799 in potential organ donors, 711–712 Thermogenesis, effect on energy expenditure, 96 Thigh, anatomy of, 672 Thiopental, 109

Index Thomas, Oliver, 227 Thoracentesis, 114 Thoracic surgery, as percentage of all acute care surgery, 44 Thoracic trauma, 48–52 bedside surgical interventions for, 114–115 as blunt cardiac trauma cause, 395 as blunt diaphragmatic trauma cause, 422 damage-control approach to, 52 motor vehicle accidents-related, 207 ventilation in, 217 Thoracoscopy of air leaks, 367 of blunt diaphragmatic trauma, 423 of empyema, 372 of penetrating cardiac trauma, 391 of penetrating diaphragmatic trauma, 428, 429 of retained hemothorax, 368 Thoracostomy, 367 bedside, 114 Thoracotomy, 363 of air leaks, 370 anterior, 52 anterolateral, 49, 50–51 of aortic dissection, 413 of blunt aortic trauma, 403, 404, 405 of empyema, 372–373 left book (trap door), 49 lung resection with, 365 posterolateral, 50, 364, 365, 377 of pulmonary abscess, 374 resuscitative, 10, 48–49, 52 of retained hemothorax, 368 Thorascopy, 363 Thromboembolectomy, open catheter, 604 Thrombolytic therapy, 368, 369–370, 527–528 Thrombosis acute mesenteric, 525–526 aortic, 530–533 deep venous, 76, 79, 368 pathophysiology of, 524 venous, 533 Thumb blast injuries to, 629 metacarpophalangeal joint dislocation of, 643, 644 palmar abduction of, 620 pulp avulsion injuries to, 625 Thyroid cartilage, 286 Thyroid disorders, 80 Thyroid hormone replacement therapy, for potential organ donors, 709 Thyroid hormones, in chronic critical illness, 81

Tibia fractures of, 211, 611 motor vehicle accident-related injuries to, 207 Tibial arteries, injuries to, 610 Tissue expander devices, 182–183 Tissue plasminogen activator, 528 Tissue transfers, upper-extremity, 630 Tonometry, 76 Tonsillectomy, 288, 292, 308 Tonsillitis, 288 Total energy expenditure (TEE), 95 Total parenteral nutrition (TPN) adverse effects of, 97–98, 99, 101, 573 for burn injury patients, 151 enteral nutrition versus, 97 Tourniquets, 227, 608, 616, 617 adverse effects of, 608 Toxic epidermal necrolysis (TEN), 149–150 Toxic exposure, burn injury-related, 135–136 Toxic shock syndrome (TSS), 168, 649–650 Toxins, as neurologic emergency cause, 332 Trachea burn injury-related edema of, 136 esophageal trauma-associated injuries to, 315 foreign bodies in, 290 stenosis of, 294 Tracheitis, in pediatric patients, 305, 308 Tracheobronchial trauma, 363–365 Tracheoinnominate artery, fistulas of, 378, 380, 381–382 Tracheolaryngeal fractures, 5 Tracheostomy, 6, 45, 70, 299–300, 301, 364 bedside, 112–114 infection rate after, 110–111 as mediastinal abscess cause, 112 as tracheoinnominate artery fistula cause, 382 in tracheopharyngeal trauma, 6 Tracheotomy. See Tracheostomy, 299 Tractotomy, 52, 365, 366 Transfer, of patients in Australia, 790 of burn injury patients, 153–155 of nontraumatic surgical emergency victims, 748 in rural and remote areas, 197, 778–779, 780 Transport, of patients. See also Air transport, of patients of burn injury patients, 153–155 intrahospital, 107 of nontraumatic surgical emergency victims, 746

Index patient instability during, 71–72 in rural and remote areas, 195–196, 197, 777–778, 780, 781, 786 Transureteroneocystostomy, 579 Trauma, morbidity and mortality rates in, 731–732, 754 Trauma centers, 754–755 in Australia, 787, 788, 789–790 definition of, 754 nontraumatic surgical emergency patients at, 747 Trauma services, in the United Kingdom, 779–781 Trauma systems regional system for surgical emergencies (RSSE), 743–751 in rural and remote areas, 195 Traumatic brain injuries. See Brain injuries Treatment, life-sustaining. See Lifesustaining treatment Treatment planning, simulation education in, 269 Triage, 3, 24, 29, 215 accuracy of, 236–237 in Australia, 788, 790 categories of, 235–236 in disaster and mass casualty management, 233, 234–238, 241, 243–244 of nontraumatic surgical emergency victims, 746 in rural emergent surgery, 196 Troponins, 393, 396, 397 Trunkey, D. D., 779 Tuberous sclerosis syndrome (TSS), 568 Tularemia, as biological weapon, 240 Tumor necrosis factor, in hypermetabolic response, 92 Two-point discrimination test, 618, 619 Tympanic membrane examination of, 279 rupture of, 164, 243 U Ulcers. See also Duodenal ulcers; Gastric ulcers; Peptic ulcers esophageal, 328 Ulnar artery injuries to, 644, 659 location of, 62 occlusion of, 660 pseudoaneurysm of, 662 Ulnar nerve, anatomy and function of, 618–620 Ulnar nerve blocks, 616 Ultrasonography, 111 abdominal, 770 of abdominal aortic aneurysm rupture, 535

831 of acute bacterial prostatitis, 565–566 focused assessment with sonography for trauma (FAST), 7, 13, 234, 390–391, 425 of prostatic abscess, 565 of pyonephrosis, 564 of renal abscess, 563 splenic, 517 Unconscious patients, informed consent for, 684–685 Uniform Determination of Death Act, 706 United Kingdom, acute care surgery in, 767–785 United States Department of Transportation, 203 Universal precautions, 43 University of Pennsylvania, 747 Upper extremity. See Hand and upper extremity Ureteroneocystostomy, 579, 580 Ureteroscopic procedures, as ureteral injury cause, 577–578 Ureteroureterostomy, 578–579 Ureters anatomy of, 577, 578 ileal, 579 injuries to, 577–581 Urethra, injuries to, 575, 581 Urethral valves, posterior, 572, 584–585 Urinary sphincters, artificial, infections of, 566 Urinary tract, obstruction of, 570–573 Urine output, 7, 10 hypovolemia-related decrease in, 78 in potential organ donors, 710 as renal perfusion indicator, 10 Urogenital emergencies, 561–588 acute scrotum, 576–577 hemorrhage, 568–570 iatrogenic complications, 577–581 infections, 561–568 pancreatic trauma-associated, 501, 502 pediatric emergencies, 581–585 pelvic ring fracture-related, 594 penile emergencies, 573–576 urinary tract obstruction, 570–573 Urogenital surgery, as percentage of all acute care surgery, 44 Urokinase, 368, 370 Uvulopharyngopalatoplasty, 291 V Vacuum-assisted closure (VAC), for large wounds, 178, 179–181 Vagotomy, 458–460, 463, 466, 467, 468 Vagus nerve in blunt aortic trauma repair, 405 in neck exposure, 46 Valvular lesions, 390

Valvular trauma, blunt cardiac, 396 Vanderbilt University Medical Center, emergency general surgery (EGS) model of, 754–763 Van Rehn, Ludwig, 389 Varices, bleeding esophageal, 462–463, 464, 465, 491–492 gastric, 465 Vascular emergencies, 524–548 abdominal, 61 abdominal and pelvic trauma-related, 538–542 abdominal aortic aneurysm rupture, 534–537 acute mesenteric ischemia, 176, 184, 471, 472, 474, 476–477, 525–529 anesthesia management of, 37 aortic occlusion, 530–533 arterial occlusion, 525–533 blunt head trauma-related, 337 blunt trauma-related, 37 in the extremities, 61–63 of the hand and upper extremity, 615, 644–645 to hand and upper extremity, 644–645 ischemia, 525–530 lower-extremity, 608–610 as neurologic emergency cause, 332, 333 penetrating trauma-related, 37 ruptured visceral or renal artery aneurysms, 537–538 in rural and remote areas, 195, 198 in the United Kingdom, 775–776 venous occlusion, 533–534 Vascular surgery, as percentage of all acute care surgery, 44 Vasopressin, as vasodilatory shock treatment, 84–85 Vasospasm, subarachnoid hemorrhagerelated, 341–342 Vecuronium, 110 Veins. See also specific veins injuries to abdominal, 61 in lower extremity, 671–672 pancreatic trauma-associated, 500, 501, 502 in upper extremity, 663 Vena cava. See also Inferior vena cava; Superior vena cava iatrogenic injuries to, 537 infrarenal, ligation of, 61 retrohepatic, surgical exposure of, 57 Vena cava filters. See also Inferior vena cava filters as cardiac trauma cause, 397 Venoarterial bypass, extracorporeal membrane oxygenation use in, 86

832 Venous occlusion, 524–525, 533–534 Ventilation. See also Mechanical ventilation bag-valve-mask, 5, 217 percutaneous transtracheal, 45 prehospital, 217–218, 222–224 in preoperative patients, 72 tympanomastoid, 284 Ventilation perfusion scintigraphy, of pulmonary embolism, 369 Ventilator management, in potential organ donors, 712 Ventricles, penetrating trauma to, 390 Ventricular assist devices (VADs), 87–89 Ventricular preload, 11 Ventricular septal defects, 390 Ventriculitis, 343 Ventriculostomy, bedside, 111 Vertebral arteries injuries to, 337 in neck exposure, 46 Vertebral body tumors, 345 Vertebral fractures, 335 Vesalius, Andreas, 400 Victoria, Queen (of England), 767 Video-assisted thorascopic surgery (VATS), 362, 363, 372, 385, 426 Violence. See also Child maltreatment/abuse; Intimate partner violence; Gunshot trauma; Stab wounds toward youth, 257 Virtual reality education, in surgery, 270 Viscous criterion (VC), 350

Index Viscous response, 350 Vital signs, 10 Vitamin supplementation, in burn patients, 101, 153 Vocal cord paralysis, 287, 288, 293 Volume status, assessment of, 7, 75–76, 78 Volvulus, 190, 431, 473, 557–558, 799 Vomiting/nausea duodenal ulcers-related, 458 emetogenic, 463 as gastric volvulus cause, 431 gastroduodenal trauma-related, 451 small bowel obstruction-related, 471–472 W Water-related injuries, 255 Weapons of mass destruction (WMDs), 239–244 Weight loss, hypermetabolic responserelated, 91 Wheezing, subglottic/tracheal stenosisrelated, 294 White cell count, in abdominal pain patients, 769 White phosphorus-related burns, 146, 147, 646 Whitlows, herpetic, 650 Wittman patch, 179, 181 World Health Organization, 797 World Trade Center, terrorist attacks on, 240, 244

Wound healing hypermetabolic response during, 92–93 nutrition-based enhancement of, 100–101 Wounds, surgical classification of, 444 infections of, 444–445 Wrist injuries to, 622, 630, 631, 642 instability testing of, 622 X X-rays chest of aortic dissection, 408 of blunt aortic trauma, 401, 402 of blunt diaphragmatic trauma, 422–423 for chest pain evaluation, 453 of penetrating cardiac trauma, 390 of penetrating diaphragmatic trauma, 425 for perforated peptic ulcer evaluation, 770 of pelvic ring fractures, 594–595 Y Youth violence, 257 Z ZestrilTM, 296 Zinc, 101

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