Surgical Pitfalls: Prevention and Management

Steven K. Libutti, Section Editors: A. Alfred Chahine, MD, FACS Associate Professor of Surgery and Pediatrics The Ge...

Author: Stephen R. T. Evans MD FACS

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Steven K. Libutti,

Section Editors: A. Alfred Chahine,

MD, FACS

Associate Professor of Surgery and Pediatrics The George Washington University School of Medicine Program Director General Surgery Residency Georgetown University Medical Center Washington, DC

Edward E. Cornwell III,

MD, FACS, FCCM

LaSalle D. Leffall Jr Professor Chairman of Surgery Howard University Hospital Washington, DC

Gerard M. Doherty,

MD, FACS

Chief Tumor Angiogenesis Section Surgery Branch, National Cancer Institute Professor of Surgery Uniformed Services University of the Health Sciences Bethesda, Maryland

M. Blair Marshall,

MD

NW Thompson Professor of Surgery University of Michigan Head Section of General Surgery University of Michigan Health System Ann Arbor, Michigan

Leigh A. Neumayer,

MD

Professor of Surgery Section of Colon and Rectal Surgery Department of Surgery University of Wisconsin School of Medicine and Public Health Madison, Wisconsin MD, MBA

Professor Georgetown University Chief of Transplantation Surgery Vice-Chairman Department of Surgery Georgetown University Hospital Washington, DC

MD

Chief Division of Vascular Surgery Medical Director Non-invasive Vascular Lab Georgetown University Hospital Washington, DC

Shawna C. Willey, Lynt B. Johnson,

MD, MS

Professor of Surgery University of Utah School of Medicine Huntsman Cancer Institute Salt Lake City, Utah

Richard F. Neville, Eugene F. Foley,

MD, FACS

Associate Professor of Surgery Georgetown University School of Medicine Chief Division of Thoracic Surgery Department of Surgery Georgetown University Medical Center Washington, DC

MD, FACS

Associate Professor Georgetown University Director Betty Lou Ourisman Breast Health Center Lombardi Comprehensive Cancer Center Washington, DC

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

Surgical pitfalls: prevention and management

ISBN: 978-1-4160-2951-9

Copyright © 2009 by Saunders, an imprint of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s Health Sciences Rights Department in Philadelphia, PA, USA: phone: (+1) 215 239 3804, fax: (+1) 215 239 3805, e-mail: [email protected]. You may also complete your request on-line via the Elsevier homepage (http://www.elsevier.com), by selecting ‘Customer Support’ and then ‘Obtaining Permissions’.

Notice Knowledge and best practice in this ﬁeld are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editors assumes any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. The Publisher Library of Congress Cataloging-in-Publication Data Surgical pitfalls : an evidence-based approach to prevention and management / [edited by] Stephen R.T. Evans ; section editors, A. Alfred Chahine . . . [et al.].—1st ed. p. ; cm. Includes bibliographical references. ISBN 978-1-4160-2951-9 1. Surgical errors. I. Evans, Stephen R. T. II. Chahine, A. Alfred. [DNLM: 1. Intraoperative Complications—prevention & control. 2. Evidence-Based Medicine. 3. Medical Errors—prevention & control. 4. Risk Factors. 5. Risk Management. 6. Surgical Procedures, Operative—adverse effects. WO 181 S961 2009] RD27.85.S87 2009 617′.9—dc22 2008034840

Publishing Director: Judith Fletcher Acquisitions Editor: Scott Scheidt Developmental Editor: Sarah A. Myer Project Manager: Mary B. Stermel Design Direction: Steven Stave Marketing Manager: Brenna Christensen

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Printed in China Last digit is the print number:

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To my loving wife Karen, who every day fuels the ﬁre of love in my heart and makes every moment together pure joy. Stephen Evans,

MD

Contributors Christopher J. Abularrage, MD Fellow in Vascular Surgery, Massachusetts General Hospital, Boston, Massachusetts Infrainguinal Revascularization

Sara A. Bloom, MD Chief Resident, Department of Surgery, Georgetown University Hospital, Washington, DC Axillary Surgery

Reid B. Adams, MD Professor of Surgery, Division Chief, Surgical Oncology, and Chief, Hepatobiliary and Pancreatic Surgery, University of Virginia Health System, Charlottesville, Virginia Enterectomy

Benjamin Braslow, MD Assistant Professor of Surgery, University of Pennsylvania School of Medicine; Director of Emergency Surgical Service, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania Damage Control: Abdominal Closures

Mark S. Allen, MD Professor and Chair, Division of General Thoracic Surgery; Consultant, Division of General Thoracic Surgery, Mayo Clinic, Rochester, Minnesota Pneumonectomy

David A. Bruno, MD Chief Resident, Department of Surgery, Georgetown University, Washington, DC Resection and Reconstruction of the Biliary Tract

Stephen L. Altman, Esq, JD Partner, Hamilton Altman Canale & Dillon, LLC, Fairfax, Virginia Legal Considerations

Joseph F. Buell, MD, FACS Professor of Surgery and Director of Transplantation, University of Louisville, Louisville, Kentucky Laparoscopic Liver Resection

Rupen Amin, MD Research Fellow, Georgetown University School of Medicine, Washington, DC Pancreaticoduodenectomy

John Byrne, MB, BCh, BAO, MCh, FRCSI(Gen) Attending, Albany Medical Center Hospital, Albany, New York Aortic Surgery

Andrea Badillo, MD Resident in General Surgery, The George Washington University, Washington, DC Graham Patch Repair

A. Alfred Chahine, MD, FACS Associate Professor of Surgery and Pediatrics, The George Washington University School of Medicine; Program Director, General Surgery Residency, Georgetown University Medical Center, Washington, DC Imperforate Anus and Hirschsprung’s Disease; Congenital Diaphragmatic Hernia

Catherine Bertram, JD Partner, Regan Zambri & Long, PLLC, Washington, DC Legal Considerations Parag Bhanot, MD Assistant Professor of Surgery, Georgetown University Hospital, Washington, DC Open Inguinal Hernia Repair with Plug and Patch Technique; Laparoscopic Incisional Hernia Repair

David C. Chang, PhD, MPH, MBA Assistant Professor of Surgery, Department of Surgery, Johns Hopkins School of Medicine, Baltimore, Maryland Evaluating Trauma Literature

Joseph A. Blansﬁeld, MD Clinical Assistant Professor of Surgery, Temple University School of Medicine, Philadelphia; Associate, Department of Surgical Oncology, Geisinger Medical Center, Danville, Pennsylvania Isolated Limb Perfusions and Extremity Amputations

Zandra Cheng, MD Breast Surgeon, Anne Arundel Medical Center Breast Center, Annapolis, Maryland Breast Biopsy and Breast-Conserving Surgical Techniques

Kenneth J. Bloom, MD Clinical Professor of Pathology, Keck School of Medicine; Chief Medical Ofﬁcer, Clarient, Inc., Aliso Viejo, California Image-Guided Breast Biopsy

Mark D. Cipolle, MD, PhD, FACS Medical Director, Trauma Program, and Member of Staff, General Surgery, Christiana Care Health System, Wilmington, Delaware Central Vein Catheterization

viii

CONTRIBUTORS

Bryan M. Clary, MD Associate Professor of Surgery, and Chief, Hepatobiliary Surgery, Duke University Medical Center, Durham, North Carolina Trisectionectomy Edward E. Cornwell III, MD, FACS, FCCM LaSalle D. Leffall Jr Professor and Chairman of Surgery, Howard University Hospital, Washington, DC Management of Thoracic Trauma; Management of Pancreatic and Duodenal Injuries; Traumatic Brain Injury; Managing Injuries to the Spleen Derrick D. Cox, MD Chief Resident, General Surgery, Georgetown University Hospital, Washington, DC Open Inguinal Hernia Repair with Plug and Patch Technique Aimee M. Crago, MD, PhD Fellow, Surgical Oncology, Memorial Sloan Kettering Cancer Center, New York, New York Preoperative Pitfalls; Gastrectomy with Reconstruction Dale A. Dangleben, MD Assistant Program Director, General Surgery Residency, and Member of Staff, General Surgery, and Trauma/ Surgical Critical Care, Lehigh Valley Hospital, Allentown, Pennsylvania Central Vein Catheterization R. Clement Darling III, MD Professor of Surgery, Albany Medical College; Chief, Division of Vascular Surgery, Albany Medical Center Hospital, Albany, New York Aortic Surgery Elizabeth A. David, MD Resident, General Surgery, Georgetown University Hospital, Washington, DC Arterial Catheterization; Laparoscopic Nissen Fundoplication James E. Davies, MD Assistant Professor, Department of Cardiothoracic Surgery, University of Iowa, Iowa City, Iowa Pneumonectomy David Deaton, MD Assistant Professor, Georgetown University; Chief of Endovascular Surgery, Division of Vascular Surgery, Department of Surgery, Georgetown University Hospital, Washington, DC Endovascular Interventions Demetrios Demetriades, MD, PhD Professor of Surgery, University of Southern California School of Medicine; Director of Trauma and Critical Care, Los Angeles County and University of Southern California Medical Center, Los Angeles, California Management of Penetrating Neck Injury

Kiran K. Dhanireddy, MD Transplant Fellow, UCLA Medical Center, Los Angeles, California Distal Pancreatectomy Gerard M. Doherty, MD NW Thompson Professor of Surgery, University of Michigan; Head, Section of General Surgery, University of Michigan Health System, Ann Arbor, Michigan Thyroid Surgery Jessica S. Donington, MD Assistant Professor, Department of Cardiothoracic Surgery, New York University, New York, New York Chest Wall Resections Brian J. Duffy, MD The George Washington University; Research Fellow, Children’s National Medical Center, Washington, DC Pectus Excavatum Quan-Yang Duh, MD Professor of Surgery, University of California, San Francisco; Attending Surgeon, Veterans Affairs Medical Center, San Francisco, California Laparoscopic Inguinal Hernia Repair David T. Efron, MD Assistant Professor of Surgery, Johns Hopkins School of Medicine; Director of Trauma, Division of Acute Care Surgery: Trauma, Critical Care, Emergency and General Surgery, The Johns Hopkins Hospital, Baltimore, Maryland Management of Thoracic Trauma; Management of Pancreatic and Duodenal Injuries Martin R. Eichelberger, MD Professor of Surgery and Pediatrics, The George Washington University; Attending Surgeon, Children’s National Medical Center, Washington, DC Pectus Excavatum Rebecca Evangelista, MD Assistant Professor of Surgery, Georgetown University Medical Center; Staff Surgeon, Veterans Affairs Medical Center, Washington, DC Open Gastrostomy Feeding Tube Placement and Percutaneous Endoscopic Gastrostomy Tube Placement; Open Jejunostomy Tube Placement Stephen R. T. Evans, MD, FACS Robert J. Coffey Professor and Chairman, Department of Surgery, Georgetown University Medical Center, Washington, DC From Error to Perfection: The Process of Surgical Maturation; Teaching Technical Skills—Errors in the Process; Preoperative Pitfalls; Arterial Catheterization; Chest Tube Insertion; Paracentesis; Laparoscopic Nissen Fundoplication; Laparoscopic Esophagomyotomy with Dor Fundoplication; Gastrectomy with Reconstruction

CONTRIBUTORS

Eleanor Faherty, MD Staff Surgeon, and Captain, United States Air Force, Malcolm Grow Medical Center, Andrews Air Force Base, Maryland Open Gastrostomy Feeding Tube Placement and Percutaneous Endoscopic Gastrostomy Tube Placement; Open Jejunostomy Tube Placement; Lateral Pancreaticojejunostomy (Puestow) Procedure; Supraclavicular Lymph Node Biopsy Elizabeth D. Feldman, MD Assistant Professor, Georgetown University, Washington, DC Mastectomy Felix G. Fernandez, MD Cardiothoracic Fellow, Barnes-Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri Thymectomy and Resection of Mediastinal Masses Richard E. Fine, MD Clinical Associate Professor, Department of Surgery, University of Tennessee College of Medicine— Chattanooga Unit, Chattanooga, Tennessee; Director, Breast Care Continuum Program, Wellstar Kennestone Hospital, Marietta, Georgia Image-Guided Breast Biopsy Thomas M. Fishbein, MD Professor, Department of Surgery, Georgetown University; Director of Small Bowel and Pediatric Liver Transplant Program, Georgetown University Hospital, Washington, DC Distal Pancreatectomy; Resection and Reconstruction of the Biliary Tract James FitzGerald, MD Attending Surgeon, Washington Hospital Center, Washington, DC Ileostomy Eugene F. Foley, MD Professor of Surgery, Section of Colon and Rectal Surgery, Department of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin Hemorrhoidectomy; Anal Fistulotomy Hugh M. Foy, MD Professor of Surgery, and Head, Wind River College, University of Washington School of Medicine; Attending Surgeon, Harborview Medical Center, Seattle, Washington Teaching Technical Skills—Errors in the Process Charles M. Friel, MD Associate Professor of Surgery, and Chief, Section of Colon and Rectal Surgery, University of Virginia, Charlottesville, Virginia Low Anterior Resection; Abdominal Perineal Resection with Colostomy

ix

Kelly Garrett, MD Chief Resident, Albany Medical College, Albany, New York Left Colectomy: Open and Laparoscopic Ankur Gosalia, MD Assistant Professor of Anesthesiology, Temple University, Philadelphia; Attending Anesthesiologist, Western Pennsylvania Hospital, Pittsburgh, Pennsylvania Anesthesia for the Surgeon Vicente H. Gracias, MD Associate Professor of Surgery, and Chief, Surgical Critical Care, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania Damage Control: Abdominal Closures Jay A. Graham, MD Resident, Department of Surgery, Georgetown University, Washington, DC Laparoscopic Surgery; Right Hepatectomy; Left Hepatectomy Philip C. Guzzetta, Jr., MD Professor of Surgery and Pediatrics, The George Washington University; Pediatric Surgery Chief Resident Program Director, Children’s National Medical Center, Washington, DC Malrotation, Volvulus, and Bowel Obstruction Adil H. Haider, MD, MPH Assistant Professor of Surgery, Division of Trauma/ Critical Care, Johns Hopkins School of Medicine, Baltimore, Maryland Traumatic Brain Injury; Managing Injuries to the Spleen Elliott R. Haut, MD, FACS Assistant Professor of Surgery and Anesthesiology and Critical Care Medicine, Division of Acute Care Surgery: Trauma, Critical Care, Emergency and General Surgery, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins School of Medicine; Director, Trauma / Acute Care Surgery Fellowship, The Johns Hopkins Hospital, Baltimore, Maryland Evaluation and Acute Resuscitation of the Trauma Patient Mary Hawn, MD, MPH Associate Professor of Surgery, and Chief, Section of Gastrointestinal Surgery, University of Alabama at Birmingham, Birmingham, Alabama Open Primary and Mesh Repairs Richard F. Heitmiller, MD Associate Professor of Surgery, Johns Hopkins Medical Institutions; J.M.T. Finney Chairman of Surgery, Union Memorial Hospital, Baltimore, Maryland Esophageal Surgery Earl Hodin, MD Attending Surgeon, Children’s National Medical Center, Washington, DC, and Inova Fairfax Hospital, Falls Church, Virginia Inguinal and Umbilical Hernias

x

CONTRIBUTORS

Arsalla Islam, MD Assistant Instructor, GI Endocrine Surgery Division, Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas Adrenal Surgery

James Laredo, MD Assistant Professor, Division of Vascular Surgery, Department of Surgery, Georgetown University; Georgetown University Hospital, Washington, DC Venous Surgical Pitfalls

Kamal M. F. Itani, MD Professor of Surgery, Boston University School of Medicine; Chief of Surgery, Veterans Affairs Boston Healthcare System, Boston, Massachusetts Umbilical and Epigastric Hernias

David W. Larson, MD Consultant in Surgery and Assistant Professor of Surgery, Mayo Clinic, Mayo Medical School, Rochester, Minnesota Right Colectomy: Open and Laparoscopic

Patrick G. Jackson, MD Associate Residency Program Director, Georgetown University; Assistant Professor of Surgery, Georgetown University Hospital, Washington, DC Laparoscopic Surgery; Vagotomy and Pyloroplasty; Lateral Pancreaticojejunostomy (Puestow) Procedure; Pancreatic Cyst/Debridement

Edward C. Lee, MD, FACS, FASCRS Associate Professor of Surgery, Chief, Section of GI/ Surgical Oncology, and Vice Chairman for Clinical Affairs, Albany Medical College, Albany, New York Left Colectomy: Open and Laparoscopic

Lynt B. Johnson, MD, MBA Professor, Georgetown University; Chief of Transplantation Surgery, and Vice-Chairman, Department of Surgery, Georgetown University Hospital, Washington, DC Right Hepatectomy; Left Hepatectomy; Pancreaticoduodenectomy; Pancreatic Cyst/Debridement Benjamin Kim, MD Staff Physician, Kaiser Permanente West Los Angeles Medical Center, Los Angeles, California Laparoscopic Inguinal Hernia Repair Lawrence T. Kim, MD, FACS Professor, Department of Surgery, University of Arkansas for Medical Sciences; Chief, Surgical Service, Central Arkansas Veterans Healthcare System, Little Rock, Arkansas Parathyroid Surgery Daniel Kreisel, MD, PhD Assistant Professor of Surgery, Pathology and Immunology, Washington University in St. Louis, St. Louis, Missouri Thymectomy and Resection of Mediastinal Masses John C. Kucharczuk, MD Assistant Professor of Surgery, University of Pennsylvania School of Medicine; Division of Thoracic Surgery, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania Bronchoscopy: Flexible and Rigid; Esophagoscopy: Flexible and Rigid; Mediastinoscopy; and Anterior Mediastinotomy Paul C. Kuo, MD, MBA Professor of Surgery, and Chief, Division of General Surgery, Duke University Medical Center, Durham, North Carolina Trisectionectomy

Stacy Loeb, MD Resident in Training (Urology), Johns Hopkins Medical Institutions, Baltimore, Maryland Paracentesis Amy D. Lu, MD, MPH, MBA Associate Professor of Surgery, Albert Einstein College of Medicine; Director, Renal Transplant Program, Monteﬁore Medical Center, Bronx, New York Gallbladder: Cholecystectomy (Laparoscopic vs. Open) Jeffrey Lukish, MD Associate Professor of Surgery and Pediatrics, and Chief, Division of Pediatric Surgery, Uniformed Services University of the Health Sciences, Bethesda, Maryland Tracheoesophageal Fistula and Esophageal Atresia Repair Robyn A. Macsata, MD Chief, Vascular Surgery, Veterans Affairs Medical Center, Washington, DC Arteriovenous Hemodialysis Access Donna-Marie Manasseh, MD Co-Director of the Women’s Breast Health Center, Stamford Hospital Foundation, New Haven, Connecticut Axillary Surgery Carlos E. Marroquin, MD Assistant Professor of Surgery, Duke University Medical Center, Durham, North Carolina Trisectionectomy M. Blair Marshall, MD, FACS Associate Professor of Surgery, Georgetown University School of Medicine; Chief, Division of Thoracic Surgery, Department of Surgery, Georgetown University Medical Center, Washington, DC Bronchial and Vascular Sleeve Lobectomy

CONTRIBUTORS

Marga F. Massey, MD, FACS Associate, Center for Microsurgical Breast Reconstruction, Charleston/Chicago/Salt Lake City, Charleston, South Carolina Component Separation for Complex Abdominal Wall Reconstruction and Recurrent Ventral Hernia Repair Aarti Mathur, MD Resident in Surgery, Georgetown University, Washington, DC Chest Tube Insertion; Laparoscopic Splenectomy Fabio May da Silva, MD Professor of Clinical Surgery, Universidade do Sul de Santa Catarina; Thoracic Surgeon, Secretaria do Estado de Santa Catarina, Florianopolis, Santa Catarina, Brazil Bronchial and Vascular Sleeve Lobectomy Michael McLeod, MD Associate Professor, Michigan State University, Kalamazoo, Michigan Thyroid Surgery Aziz Merchant, MD Fellow, Minimally Invasive Surgery, Emory University, Atlanta, Georgia Pyloromyotomy Angela M. Mislowsky, MD Chief Resident—Surgery, Union Memorial Hospital, Baltimore, Maryland Esophageal Surgery Bruno Molino, MD Director, Division of Trauma, Liberty Health—Jersey City Medical Center, Jersey City, New Jersey Damage Control: Abdominal Closures Gitonga Munene, MD Chief Resident Physician, Georgetown University Hospital, Washington, DC Gastrectomy with Reconstruction Russell J. Nauta, MD, FACS Professor of Surgery, Harvard Medical School; ViceChairman, Surgery, Beth Israel-Deaconess Medical Center; Chairman of Surgery, Mount Auburn Hospital and Harvard Health Services, Cambridge, Massachusetts General Laparotomy Edward W. Nelson, MD Professor of Surgery and Division Chief of General Surgery, University of Utah School of Medicine, Salt Lake City, Utah Prolene Hernia System—Hernia Repair Richard F. Neville, MD Chief, Division of Vascular Surgery, and Medical Director, Non-invasive Vascular Lab, Georgetown University Hospital, Washington, DC Carotid Endarterectomy; Infrainguinal Revascularization

xi

Kurt D. Newman, MD Professor of Surgery and Pediatrics, The George Washington University School of Medicine; Surgeon in Chief, and Executive Director, Joseph E. Robert, Jr. Center for Surgical Care, Children’s National Medical Center, Washington, DC Pyloromyotomy C. Joe Northup, MD, FACS Assistant Professor, University of Virginia Health System, Charlottesville, Virginia Laparoscopic Appendectomy Fiemu Nwariaku, MD, FACS, FWACS Malcolm O. Perry MD Professor, and Associate Professor and Vice Chair, Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas Adrenal Surgery Michael D. Pasquale, MD, FACS, FCCM Associate Professor of Surgery, Penn State College of Medicine, Penn State University, Hershey; Senior Vice Chair, Department of Surgery, Chief, Division of Trauma/Surgical Critical Care, and Member of Staff, General Surgery, and Trauma/Surgical Critical Care, Lehigh Valley Hospital, Allentown, Pennsylvania Central Vein Catheterization; Pulmonary Artery Catheterization James F. Pingpank, Jr., MD Head, Surgical Metabolism Section, Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland Isolated Limb Perfusions and Extremity Amputations Dahlia Plummer, MD Vascular Fellow, Georgetown University, Washington, DC Carotid Endarterectomy Todd A. Ponsky, MD Assistant Professor of Surgery, Case Western Reserve University; Assistant Professor of Surgery, Division of Pediatric Surgery, Rainbow Babies and Children’s Hospital, Cleveland, Ohio Wilms’ Tumor and Neuroblastoma David M. Powell, MD Associate Professor of Surgery and Pediatrics, The George Washington University; Attending Surgeon, Children’s National Medical Center, Washington, DC Pectus Excavatum Brian Reuben, MD Chief Resident, General Surgery, University of Utah, Salt Lake City, Utah Component Separation for Complex Abdominal Wall Reconstruction and Recurrent Ventral Hernia Repair T. A. Rothenbach, MD Staff Surgeon, Pediatric Surgery Inc., The Children’s Hospital at Saint Francis, Tulsa, Oklahoma Congenital Diaphragmatic Hernia

xii

CONTRIBUTORS

Shawn D. Safford, MD Assistant Professor of Surgery, Uniformed Services University of the Health Sciences, Bethesda, Maryland Tracheoesophageal Fistula and Esophageal Atresia Repair Ali Salim, MD Program Director, General Surgery Residency, CedarsSinai Medical Center, Los Angeles, California Management of Penetrating Neck Injury Rovinder S. Sandhu, MD, FACS Clinical Assistant Professor of Surgery, Penn State College of Medicine, Penn State University, Hershey; Medical Director, Adult Transitional Trauma Unit, and Member of Staff, General Surgery, and Trauma/Surgical Critical Care, Lehigh Valley Hospital, Allentown, Pennsylvania Central Vein Catheterization; Pulmonary Artery Catheterization Babak Sarani, MD Assistant Professor of Surgery, University of Pennsylvania; Attending Surgeon, Division of Traumatology, Emergency Surgery, and Surgical Critical Care, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania Anesthesia for the Surgeon; Graham Patch Repair John E. Scarborough, MD Assistant Professor of Surgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina Trisectionectomy Bruce Schirmer, MD Stephen H. Watts Professor of Surgery, University of Virginia Health System, Charlottesville, Virginia Laparoscopic Gastric Bypass Joseph B. Shrager, MD Professor of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford; Chief, Division of Thoracic Surgery, Stanford University Hospital, Stanford; Staff Surgeon, Palo Alto Veterans Affairs Health Care System, Palo Alto, California Cervical Tracheal Resection and Reconstruction

Scott J. Swanson, MD The Eugene W. Friedman Professor of Surgical Oncology, Mount Sinai School of Medicine; Chief, Division of Thoracic Surgery, Mount Sinai Medical Center, New York, New York Lobar Resections Lorraine Tafra, MD Director, The Breast Center, Anne Arundel Medical Center, Annapolis, Maryland Breast Biopsy and Breast-Conserving Surgical Techniques Amit D. Tevar, MD, FACS Assistant Professor, University of Cincinnati, Cincinnati, Ohio Laparoscopic Liver Resection Mark J. Thomas, MD Assistant Professor, University of Cincinnati, Cincinnati, Ohio Laparoscopic Liver Resection Trevor Upham, MD Surgical Resident, Department of Surgery, Georgetown University Hospital, Washington, DC Pancreatic Cyst/Debridement Daniel Vargo, MD Associate Professor of Surgery, Division of General Surgery, Department of Surgery, University of Utah, Salt Lake City, Utah Component Separation for Complex Abdominal Wall Reconstruction and Recurrent Ventral Hernia Repair Diana M. Weber, MD Surgeon, Presbyterian Hospital, Albuquerque, New Mexico Laparoscopic Splenectomy; Supraclavicular Lymph Node Biopsy Todd S. Weiser, MD Assistant Professor, Mount Sinai School of Medicine; Attending, Mount Sinai Medical Center, New York, New York Lobar Resections Tamica White, MD Thoracic Surgeon, Surgical Specialists of North Jersey, Englewood, New Jersey Vagotomy and Pyloroplasty

Anton N. Sidawy, MD, MPH Professor of Surgery, Georgetown and George Washington University Schools of Medicine; Chief, Surgical Service, Veterans Affairs Medical Center, Washington, DC Arteriovenous Hemodialysis Access

Shawna C. Willey, MD, FACS Associate Professor, Georgetown University; Director, Betty Lou Ourisman Breast Health Center, Lombardi Comprehensive Cancer Center, Washington, DC Mastectomy

Niten Singh, MD Assistant Professor of Surgery, Uniformed Services University of the Health Sciences, Bethesda, Maryland; Chief, Endovascular Surgery, Madigan Army Medical Center, Tacoma, Washington Venous Surgical Pitfalls; Endovascular Interventions

Alexander Wohler, MD Fellow in Cardiothoracic Surgery, Mount Sinai Medical Center, New York, New York Laparoscopic Esophagomyotomy with Dor Fundoplication

William H. Snyder, MD Professor of Surgery, Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas Adrenal Surgery

James C. Yang, MD Assistant Professor, Uniformed Services University of the Health Sciences; Senior Investigator, Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland Management of Soft Tissue Sarcoma

Preface

It is on our failures that we base a new and different and better success. —Havelock Ellis As a profession, surgeons are exceedingly reluctant to publicize our errors. Whether they are errors in judgment or intraoperative technical errors, they are usually kept to ourselves or become semi-public when presented formally at the usual Morbidity and Mortality conferences held weekly at all hospitals by surgeons throughout the country. It is quite clear, however, that the Morbidity and Mortality conference proves to be the most educationally productive conference for all surgeons because of how much we learn from our own errors as well as the errors of others. Surgical Pitfalls has been a work in progress for many years and is targeted not just at surgeons in training but at surgeons of all levels of expertise. Our hope is that this will lead to signiﬁcant error prevention and improve and enhance error training through surgical residencies. We have therefore constructed this book to include all of the major specialties in surgery. This book is unique in its intent to identify intraoperative errors that occur at speciﬁc steps during both simple and complex operations, but more importantly identifying how to prevent the error, the consequences of the error if they occur, and lastly, how to repair or correct the error once it has happened. The book covers over 80 major operative procedures in addition to discussing common errors, especially errors in preoperative decision making based upon individual organ systems and risk stratiﬁcation that should be considered in preoperative assessment and evaluation of all patients. Additionally, errors made in teaching technical skills are reviewed, errors in communication that lead to medical legal issues, and lastly an over-

view in the introductory section on the process of surgical maturation. During this ﬁrst edition we have attempted to be as comprehensive as possible in describing all major published intraoperative complications and intraoperative errors that are made in our decision making. As previously stated, however, surgeons are reluctant not just to talk about our mistakes, but certainly loathe publishing them. In preparation for our second edition we are actively soliciting cases with substantial intraoperative or radiographic conﬁrmation and documentation of the speciﬁc errors and complications that have occurred with the intent of making the second edition even more comprehensive and truly an “Encyclopedia of Error” or the “Textbook of Morbidity and Mortality.” I would like to thank all of our extremely talented contributing authors for their tremendous time and effort put in to this ﬁrst edition. It is certainly much easier to write an operative procedures textbook on how to do an operation; it is far more difﬁcult to write a procedures manual on how NOT to do an operation. I greatly thank our contributors for their patience as we moved through this sometimes arduous process. We have adhered to a template which we hope that the reader will ﬁnd exceedingly useful and user-friendly. In addition to our contributing authors I would like to extend a heartfelt thanks to our staff at Elsevier, including Scott Scheidt, Sarah Myer, and our publishing director, Judy Fletcher. They have shared the passion, excitement and energy that we all have for this ﬁrst edition and have made the job all that much easier. Stephen R. T. Evans,

MD, FACS

Introduction

Although the hospital course of a patient is affected profoundly by what happens inside the operating room, many complications can be prevented by adequate preoperative preparation. Rates of postoperative myocardial infarction, congestive heart failure, pneumonia, bleeding, and infection are all affected by identiﬁcation of a patient’s individual risk factors and medical optimization of the patient’s condition prior to surgery. A clear history and physical examination, reconciliation of a patient’s medication list, and consultation with appropriate specialists are the ﬁrst steps in ensuring that an operation will go as smoothly as possible, and that hospital length of stay and preoperative morbidity and mortality rates are maintained at a minimum.

Complications The grade of Complications is: Grade 1—Requires medical treatment only, i.e., antibiotics for a urinary tract infection

Grade 2—Requires a procedural intervention, i.e., percutaneous drainage of a pelvic abscess Grade 3—Requires reoperation, but without permanent disability or removal of an organ Grade 4—Leads to a permanent disability, i.e., renal failure requiring dialysis; or reoperation with organ removal Grade 5—Death

Indications The surgeon should complete a mental, if not physical, checklist of preoperative risk factors and appropriate interventions for each patient who is scheduled for the operating room. There are no exceptions to this dictum. Even in emergent situations, knowledge of the patient’s comorbidities should be elucidated as soon as possible to aid in intraoperative and postoperative care.

Section I

GENERAL CONSIDERATIONS Stephen R. T. Evans, MD An error the breadth of a single hair can lead one a thousand miles astray. —Chinese proverb

1

From Error to Perfection: The Process of Surgical Maturation Stephen R. T. Evans, MD Mishaps are like knives that either serve us or cut us, as we grasp them by the blade or the handle.—James Russell Lowell

SURGICAL ERRORS Who Is to Blame? The landmark report, To Err Is Human, from the Institute of Medicine (IOM) published in 19991 spurred enormous attention and focus on patient safety. Initiatives to reduce the number of preventable deaths from medical errors have received widespread awareness, both in the medical literature and in the lay press.1 Five years after the IOM report, Leape and Berwick published a grim account on the lack of progress that the medical community has made in enhancing patient safety.2 These authors urged the medical community to take ownership in the matter and said, “We will not become safe until we chose to become safe.”2 Despite this pessimistic view, a few reports of improvement have been published over the last several years. Brennen3 demonstrated this more optimistic viewpoint. He showed that the rate of injury in medical care in the 1970s was 4.6% in the state of California, but by 1984, New York’s rate declined to 3.7%, and by 1992, Colorado’s and Utah’s rates fell to 2.9%. In addition, he reiterated what has long been known: that major

2

SECTION I: GENERAL CONSIDERATIONS

operative procedures in cardiac surgery and neurosurgery have shown signiﬁcant reductions in complication rates and overall mortality over the last several decades.3 Although at times met by some degree of animosity, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) and the Agency for Health Care Research and Quality have certainly taken ownership in developing policies to reduce medical errors on a national level. They have mandated error reduction policies in the operating room such as preoperative checklists, surgical marking for “correct side and correct patient,” and the obligatory “timeout” to enhance communication in the operating room. These JCAHO policies are touted to minimize errors by enhancing communication between anesthesia, nursing, and surgical staff.

Taking Ownership At the individual practitioner level, signiﬁcant room for improvement still exists because we have not uniformly “chosen to become safe.” This is because the surgical approach has historically been more reactive than proactive. Although we, as surgeons, have a strong history of dissecting our own craft, evaluating successes and reviewing ﬂaws in forums such as morbidity and mortality (M&M) conferences, we have not acted cohesively. We all know that the surgical M&M conference—in which surgeons tend to be honest and open about mistakes and propose to learn from those mistakes—has been hailed as the best educational experience for all trainees. However, this forum can be disorganized and happenstance and could become more word of mouth than anything reportable. Indeed, many other ﬁelds of medicine do not even participate in a weekly M&M conference. Moreover, even when we know that errors are deﬁnable and predictable in given operations, our ability to educate and train in error reduction has fallen short. Passionate discussions that may surface in each hospital’s lecture hall are often forgotten by the next week. Why have we not developed a national registry to report errors that are discovered in these surgical think tanks? Why do we not have a monthly journal dedicated solely to exploring these mistakes to better our ﬁeld? Many barriers exist to open discussion of surgical errors at a national level, not the least of which is the medicolegal climate. Whereas a uniﬁed approach at error reduction seems insurmountable, the current intense focus on patient safety should drive this initiative. We cannot accept anything less than the effort toward perfection. As Deming stated, “if we had to live with 99.9%, we would have: two unsafe plane landings per day at O’Hare, 16,000 pieces of lost mail every hour, 32,000 bank checks deducted from the wrong bank account every hour” (Deming, personal communication, November 1987). Our sophisticated culture demands this effort. It is time for the individual surgeon to take ownership in this matter. This textbook focuses exclusively upon the

individual in an attempt to improve error reduction at both the cognitive and the technical levels. We also hope to affect the future of surgical education by exposing practical ways to teach not just the surgical resident but also more experienced surgeons on the approach to error reduction on a daily basis. We hope that by looking carefully at ﬂaws in cognitive thought processes or technical errors that are preventable, the opportunities for improvement at the practicing physician level will become obvious.

The Paralysis of Fear Leape4 talked about the powerful fear of error (Fig. 1–1). This trilogy is encompassed by (1) the fear of embarrassment by colleagues, (2) the fear of patient reaction to errors, and (3) the fear of litigation. It has seemingly paralyzed our ability to proactively approach error reduction. Moreover, these collective fears are certainly the reasons why we have not uniformly shared and/or published our complications. First, we loathe exposing our ignorance or technical failures to our fellow surgeons and medical colleagues. To become the talk of the surgeon’s lounge over a recent operative failure is our worst nightmare. Second, we face the fear of patient reaction to the mistake we made. It is natural to be uncomfortable talking to patients after mistakes and errors have occurred. Even more distressing is working in an academic health center where resident training is conducted and a mistake occurs. Patients may commonly ask, “What is the resident’s role in my operation and in my care?” And if a mistake occurs, the patient may ask, “Is this is an error caused by the resident?” or “Is this a training error?” Lastly, the prevailing fear of litigation may have become the most dominant stagnating force we face. The

Figure 1–1 Lucian Leape. (Courtesy of Lucian L. Leape, MD.)

1 FROM ERROR TO PERFECTION: THE PROCESS OF SURGICAL MATURATION “MALPRACTICE MACHINE” is on our radar screen daily and has certainly been popularized on the Internet at such sites as “ﬁghtingforyou.com.” One can ﬁnd common headlines such as “Surgical errors are among the most carefully regarded secrets in the medical industry.”

The Paradox Although it is a formidable, some say impossible, task, we cannot be frozen by inaction in an attempt to strive for perfection. Leape described this complex conﬂict: “the paradox . . . that although the standard of medical practice is perfection—error-free patient care—all physicians recognize that mistakes are inevitable.”2 We know we are all human, but this is not an explanation accepted by the media, the public, the insurance companies, or malpractice lawyers.

THEORIES OF HUMAN PERFORMANCE Knowledge-, Rule-, and Skill-Based Performances To understand how human errors occur, we must ﬁrst understand the theories behind human performance. Rasmussen and Jensen5 have written extensively on the concepts of human performance, which they divide into three types: (1) knowledge-based, (2) rule-based, and (3) skill-based.5 First, knowledge-based performance occurs when we act on novel thought during new situations (e.g., this is the intern’s life—all operations are new to them and all patient scenarios on the wards are unique to them). Second, ruled-based performance happens when we develop solutions to problems dictated by stored rules—patterns of behavior that occur based upon speciﬁc situations (e.g., when we are presented with the unmistakable, discreet areolar plane while mobilizing a right colon, we know our dissection can proceed expediently and safely). Third, skilled-based performance refers to patterns of thought and action that are unconscious or preprogrammed. These are certainly the most common, routine performances that we carry on a daily basis (e.g., driving a car on the same roads daily to work or an experienced surgeon performing his or her 500th inguinal hernia repair).

Errors in Human Performance Reason6 and Rasmussen and Jensen5 have classiﬁed errors that can occur in each of these performance categories. Knowledge-based errors happen when there is simply a lack of experience or knowledge or a misinterpretation of the problem. These commonly occur to either the inexperienced surgeon or trainee who is on the steep end of the learning curve and who encounters a novel clinical

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situation. It is these knowledge-based errors that we hope this book will clearly illuminate so that we can all avoid them. Rule-based errors are categorized as misapplied expertise. The wrong rule is chosen during problem solving. This is commonly related to a misperception of the situation or misapplication of a “rule” that is understood but not used correctly. Lastly, skill-based errors are referred to as “slips.” They occur when there is an unusual break in the routine or lack of an additional check (or “time out”) so that we, for example, operate on the wrong leg or on the wrong patient or leave a malleable in the patient after laparotomy. Interestingly, these are more likely to occur with physiologic conditions such as fatigue and psychological interferences such as boredom or frustration. Which errors are the most common? Actually, slips, the skill-based errors, are the most common because most of our daily mental functioning is automatic. However, the rate of error is higher with knowledge-based errors because these typically occur on the steep part of the learning curve.6 This book’s aim is to illuminate and expose pitfalls and errors at all three levels and to change our performance in surgery by focusing training and policy on error reduction.

Perceptual Errors in the Operating Room: Heuristics Understanding the etiology and mechanism for technical errors that occur in operative procedures is a generalized theme throughout this textbook. In a highly referenced and quoted article, Way and coworkers7 studied patients with major bile duct injuries during laparoscopic cholecystectomy in order to determine the cause of the errors. They classiﬁed each injury into three different groups: (1) knowledge and decision making errors, (2) a lack of technical skills, and (3) errors of perceptual input or a misperception of the anatomy. The majority of the injuries were of the third type. This variety of error mechanism is based on the principle of heuristics. Heuristics are normal, rapid, subconscious responses that work based upon subjective or illusory contours or shapes. If you look at an example such as the Kanizsa triangle (Fig. 1–2), you may think you are seeing a white triangle surrounded by dark circles. However, a white triangle is NOT actually present, your mind merely constructs it from the backdrop of the circles. The white triangle also appears to be brighter than the surrounding area, but in fact, it is not. As surgeons, we have all encountered heuristics in some way or another. Interestingly, it is inherent in the way our brain functions. Our brain is wired to use the ﬁrst information that comes to mind in order to understand or comprehend the world. Heuristics are important to recognize, especially in the setting of the operating room. As we proceed through a common operation and visualize globally what the

4

SECTION I: GENERAL CONSIDERATIONS HEURISTICS

• Imagery • The tendency to use the first information that comes to mind • “Fooling” the mind

Figure 1–2 Kanizsa triangle. (From Way LW, Stewart L, Gantert W, et al. Causes and prevention of laparoscopic bile duct injuries. Ann Surg 2003;237:460–469.)

operative ﬁeld looks like, we may have a tendency to become complacent about what we see. Humans prefer common patterns and familiarity, especially in the operating room. Therefore, we seek out what we already know from memory. Making a rapid decision based only on misrepresented visual input could get us in trouble. This book will hopefully open our minds to the hidden anatomy that we must all be cognizant of to prevent technical errors. As Reason6 described, “the price we pay for this automatic processing of information is that perceptions, memories, thoughts, and actions have a tendency to err in the direction of the familiar and the expected.”

THE IMPORTANCE OF ERROR RESPONSE So, I Made a Mistake . . . Although it does seem that “to err is human” and much of our abilities to make errors is a constant experience throughout existence, our responses to mistakes are quite individual. First, some of us simply deny that the error even occurred by constantly deﬂecting the situation and taking no ownership of the error itself. Second, others may be overcome with fear after making an error such that subsequent similar operations are performed with the sole focus on not making a mistake instead of performing the operation correctly. This is a disaster in the setting of oncologic surgery, in which inadequate resections are performed overshadowed by the constant fear of trying to avoid ureteral or vascular injuries. Third, some of us are overcome with passive acceptance. This is the surgeon who believes that mistakes will always occur no matter what we do, and therefore, there is no necessity for change or intervention. Finally, there are those who are deeply analytical. After we make a mistake, we are self-critical, analyze the literature, review videos, and channel all of our energy into self-improvement to minimize the chances of that error occurring again. It turns out that our response to making an error is one of the most important reactions we make in our career.

In residency, we may remember those residents who did not succeed. What was it about them that made them fail? Bosk at the University of Pennsylvania studied this and discovered that failure is related to these responses to making mistakes. Bosk studied the University of Pennsylvania neurosurgery program and found that the failures were residents with passive acceptance, who believe that mistakes will rarely occur or that “bad outcomes [have occurred] due to things outside my control.”8 Conversely, the successful neurosurgery resident was the analytical surgeon who admits that she or he makes terrible mistakes, “plenty of mistakes,” and “is driven to eliminate failure.”

The Resident’s Response to Error Paralleling Bosk’s study, Wu and colleagues9 asked 114 internal medicine residents: How did they handle the most signiﬁcant mistake they made while training? Ninetynine percent of the mistakes were serious; in fact, 31% of these resulted in death. The mistakes included diagnostic errors (33%), prescribing errors (29%), evaluation errors (21%), and procedural errors (11%). Amazingly enough, only 54% of the residents discussed the mistake with the attending! This remarkably low percentage could be related to a lack of comfort and/or a power imbalance between resident and attending to discuss errors. We argue that there is not an adequate medical culture established to allow a healthy, free-ﬂowing discussion about errors. Interestingly, 88% of the residents discussed the mistake with another physician who was not a supervisor. And only 24% of the residents reported the mistake to the patient or the families—again, the lack of comfort and uneasiness with the young trainee in the position of making an error. Although this chapter does elucidate the true lack of error reporting in residency, it also proves that constructive changes can occur after residents accept responsibility for the mistake and discuss it with the attending physician—not, however, in forums such as M&M. Indeed, 50% of the residents stated that the real issues were never discussed at M&M! As stated by Greenberg and associates,10 “According to both attending and resident surgeons, the most important personality trait for success in a surgical residency is the ability to admit error.” As Hilﬁker11 stated, “We see the horror of our own mistakes, yet we are given no permission to deal with their enormous emotional impact. The medical profession simply has no place for its mistakes.”

Is Morbidity and Mortality Conference Enough? It seems obvious that if the most important component of a successful surgeon is, ﬁrst, the ability to admit error and, second, to deeply ponder the issues surrounding the error, then the M&M conference should be one of the most critical aspects of residency training. Unfortunately, this may not be so.

1 FROM ERROR TO PERFECTION: THE PROCESS OF SURGICAL MATURATION When looking at error response at M&M conferences, a prospective review of 332 M&M conferences in internal medicine (n = 232) and surgery (n = 100) was conducted at an academic medical center.12 Piernissi and coworkers12 showed that M&M conferences may have considerable room for improvement. Only 38% of the errors in medicine and 79% of the errors in surgery were attributed to a particular cause, even though cases were discussed longer in medicine (34.1 min) than in surgery (11.7 min). In addition, fewer internal medicine cases (37%) versus surgical cases (72%) included adverse events. In both medicine and surgery, when errors were discussed speciﬁcally as errors, only 40% were discussed explicitly. So what exactly is happening at these conferences? As surgical educators, we are aware of the Accreditation Council for Graduate Medical Education (ACGME) requirements that “All deaths and complications that occur on a weekly basis should be discussed.” Interestingly, not all specialties mandate a weekly complications conference.

HOW DO WE ACHIEVE PERFECTION? THE GIFTED AND TALENTED The Gifted Response to Error Clearly, the success of any surgeon is related to how he or she will respond to errors that will inevitably occur. Going beyond surgery, many believe success in life is linked to our responses to error. Gladwell8 was interested in studying those special people that ultimately achieve colossal success in life (Fig. 1–3). His article, entitled “The Physical Genius,”8 discussed characteristics that link Wayne Gretzky, the brilliant hockey player, YoYo Ma, the gifted

Figure 1–3 Malcolm Gladwell. (Courtesy of www.gladwell.com, Brooke Williams photographer.)

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cellist, and Charlie Wilson, a brilliant neurosurgeon at the University of California at San Francisco (UCSF). Gladwell discovered that one of the most important traits these people all shared was their drive for ﬂawless, error-free performances. Gladwell described the inherent traits of Don Quest, a neurosurgeon at Columbia Presbyterian Hospital in New York, and what makes him so successful. Yes, Quest believes that ﬁne motor skills and swift decision making are important, but are of little value without the right sort of personality. After studying the successful and failing neurosurgery residents, Bosk8 described the “Quest” personality as those with “a practical-minded obsession with the possibility and consequences of failure.” “Physical geniuses are driven to greatness because they have found something so compelling that they cannot put it aside.”8

The Power of Visualization and “Chunking” Not only do these gifted individuals deliberate on the mishaps, but they all have a keen sense of visualization and are able to live in what is almost an extra dimension of reality as well. Gretzky has the capacity to pick up on subtle patterns in the hockey game that others generally miss; he commonly says that he sees the entire rink, not where the puck is, but in fact—where the puck will be. Brilliant surgeons can simultaneously look at tissue planes and look beyond the recognized anatomy to what lies behind the operative ﬁeld. As Charlie Wilson described in Gladwell’s article,8 “an ability to calculate the diversions and to factor in the interruptions when faced with an internally confusing mass of ‘blood and tissue’ ” is the true description of the gifted and talented surgeon. The ability to visualize has been described in detail by Stephen Kosslyn, who discussed four separate human capacities working in combination.8 The ﬁrst ability is to generate an image, that is, take something out of longterm memory and reconstruct it. Second, visualization requires image inspection. Take the mental image and draw inferences from it. This clearly requires moving from that image with visualization and making it real and applicable to wherever you are currently working, whether on an operating ﬁeld, a basketball court, or a hockey rink. Third is image maintenance, the ability to hold the picture steady so that you can actually make real time and actually utilize that visualization for practical purposes doing what you are currently doing right now. Lastly is image transformation, the ability to take the image and manipulate it. This means to look at it from multiple views, rotate it 45°, 90°, or 180°, so that these views will allow you better capacity to utilize it again during your immediate need. Many gifted athletes have discovered that these processes can be learned and practiced during mental training exercises. In addition, the process of visualization in the gifted mind occurs through patternized thought. The concept that enables the mastermind to achieve success

6

SECTION I: GENERAL CONSIDERATIONS

is called “chunking.” Chunking describes how our mind stores familiar sequences. Bobby Fischer, the brilliant grand master chess player talked about seeing patterns, not individual pieces on the board. Michael Jordan practiced visualization regularly. He would see the basketball court and see multiple patterns of defenses that could be thrown up against him in any given game. He chunked these typical patterns together and would be able to respond to these typical patterns quickly. Master surgeons also chunk together the sequences in operations that they have performed so many times—they can see where they will be in the operation in 10-, 20-, and 30-minute intervals. Chunking patterns together enables these brilliant individuals to respond quickly to error . . . and prevent the mistake before it happens because they have been in this situation so many times before.

THE FUTURE . . . A MEDICAL CULTURAL UPHEAVAL Should We Teach the Reproducible and Predictable Errors We Make? Training must include . . . a consideration of safety issues. These issues include understanding . . . how errors can occur at various stages . . . and instruction in methods for avoidance of errors.4 Our interest in error training arose from an article on a step-by-step approach to the laparoscopic Nissen fundoplication.13 With each deﬁned step, we identiﬁed speciﬁc pitfalls that could potentially occur at each step. After this article was published, our residents clamored for similar articles or modules for every operative procedure in general surgery, and we began to ask the question, should this be the way we teach surgery: how to, but also how NOT to?

THEORIES OF HOW WE ACQUIRE TECHNICAL SKILLS The Fitts and Posner Model In order to understand the processes and bases of teaching technical skills, we must comprehend, on a theoretical level, how we acquire skills. The concept of skill acquisition is surprisingly constant throughout human experience. Although Reason6 and Rasmussen and Jensen5 set the foundation for understanding these processes, the eloquent and notable treatise, Human Performance, by Fitts and Posner14 outlined the three fundamental phases for acquiring “performance-based skills” (Fig. 1–4). The ﬁrst is the cognitive phase. During this cerebral phase, we actively intellectualize the skill or procedure. For example, we may outline the speciﬁc, detailed steps of an individual procedure and analyze the reasons and rationale for it.

THE FITTS AND POSNER MODEL* Cognitive phase

Autonomous phase

Associative phase

*Human performance, 1969.

Figure 1–4 Fitts and Posner model. (From Fitts P, Posner MI. Human Performance. Belmont, CA: Brooks/Cole Publishing, 1969.)

The second, more active, phase of skill acquisition is the intermediate or associative phase. During this phase, our “old habits which have been learned as individual units during the early phase of skill learning are tried out and new patterns begin to emerge.”14 We link our thought process with action: in our case, utilizing eye-hand coordination. This phase can last for a very short or a very long time, depending on the complexity of the procedure. The associative phase is interesting because here we develop “subroutines” that make up parts of the whole skill. We integrate and compile these subroutines in order to learn the entirety of the skill. In addition, repetition of each subroutine and each skill is important during this phase. Fitts and Posner14 actually studied modes of repetition and showed that too-frequent repetition within a short period of time will “result in a greater depression in performance than the same amount of repetition with more frequent rest” (p. 13). Moreover, if there are components of the skill that are completely independent of each other (e.g., typing different passages with separate hands), it is actually better to practice each component separately (p. 14). The third and ﬁnal phase of skill acquisition is the autonomous phase. The autonomous phase occurs when we feel we have intrinsically “learned” a task or procedure. The individual processes and subroutines become autonomous, less subject to any cognitive control or any outside interference or environmental distraction. The individual practitioner has become unconsciously competent in performing the task. To reach the autonomous phase requires extensive practice such that the motor skills reach the unconscious mode or become automatic. Much has been written about what are optimal practice patterns, but probably no one has written more than Ericsson15 at Florida State University. Ericsson’s writing on deliberate practice is broad based and covers a variety of ﬁelds including sports, music and the arts, and also medicine and surgery. He deﬁned three components of deliberate practice: (1) focus on a deﬁned task to improve a particular aspect of performance (which is measurable), (2) repeated practice, and (3) immediate coaching and feedback in performance.15 Whereas most young trainees hope to achieve

1 FROM ERROR TO PERFECTION: THE PROCESS OF SURGICAL MATURATION the autonomous phase in their growth and development such that they are able to perform what is perceived as a high performance level, there is an interesting twist to automaticity in any deﬁned skill. By Ericsson’s perspective, automaticity actually leads to an arrested phase of growth in one’s personal development of her or his own skills. As an example in the practice of surgery, residents and young surgeons after multiple repetitive operations in the same area ﬁnally achieve a phase at which they are comfortable with the operation and are able to, for the most part, perform in an unconsciously competent fashion, meeting the deﬁnition of automaticity (or the autonomous phase in the Fitts and Posner model14). This level of competency is the point at which they have reduced most of their obvious gross errors such that they are perceived by their peers as being “an excellent practitioner” and may in fact, in their own mind, now have reached expert status. Again, as Ericsson15 deﬁned it, the failure to attain expert status comes because of complacency with competency. As Ericsson views it, “for aspiring expert performers . . . they must avoid the arrested development associated with automaticity and to acquire cognitive skills to support their continued learning and environment.”15 Or, to restate it more bluntly, “Although everyone in a given domain tends to improve with experience initially, some develop faster than others and continue to improve during ensuing years. These individuals are eventually recognized as experts and masters.” “In contrast, most professionals reach a stable average level of performance within a relatively short timeframe and maintain this mediocre status for the rest of their careers.” This quote from Ericsson is not to suggest that the majority of surgeons practicing are “mediocre” in their practice, but it does emphasize and elucidate the point that reaching a level of competency may work against achieving expert status because of the complacent nature that the individual practitioner views his or her capacity to perform.

Error Training and Cognitive Remodeling in the Fitts and Posner Model Somewhere along the learning curve of any given skill, errors are made and learned. By understanding how we acquire skills and where we learn errors, we can hope not only to unlearn the errors but also to prevent them from being learned. Fitts and Posner14 made a brief reference to the concept of errors when they mentioned where mistakes can occur during skill acquisition, but certainly no attention was given to the process of preventing mistakes during skill acquisition. Thus, we propose an extension to the Fitts and Posner model14 with an interval phase of error training, which enters the three-phase model after the cognitive phase (Fig. 1–5). Introducing error training during skills acquisition allows us to emphasize the errors we inherently

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THE FITTS AND POSNER MODEL* Cognitive phase Cognitive remodeling phase

Autonomous phase

Error training phase

Associative phase

*Human performance, 1969.

Figure 1–5 Fitts and Posner model of error training and cognitive remodeling. (From Fitts P, Posner MI. Human Performance. Belmont, CA: Brooks/Cole Publishing, 1969.)

make while gaining skills. These errors are commonly predictable and, unfortunately, durable. Conversely, while we learn a given skill set, we can preemptively recognize the common errors that will occur for the given skill set so as to NOT learn them. It is crucial that error training occurs prior to the intermediate or associative phase when actions become more innate and intuitive. We may all know that the worst error made is one that is not recognized. In addition, we propose that there is a cyclical way that we learn and perform skills so that cognitive remodeling occurs as we become more knowledgeable and more experienced in the procedure. After a prolonged period of time performing the same procedure, we begin to rethink the procedure and how we carry out the task. We recognize where we can move quickly and where we must move slowly in an operation, we eliminate wasteful movements, and so on. This cognitive remodeling is a desired process as surgeons mature in their approach to a speciﬁc procedure. It is this dimension of “error training” that we hope to emphasize in this book. It should be central to how we learn skills and, moreover, is crucial to understand as we train residents and young surgeons in our craft. By recognizing pitfalls while we train, and focusing on the ways to eliminate them, we start to look at the procedure differently, from a more careful perspective. We think about how we do the operation, how to reﬁne it and to establish more efﬁcient and effective steps in the ultimate polished and perfect result. It may not be too far-fetched to argue that a focus on error training may prove to be an extremely useful part not only of the medical educational processes of performance-based skills, but also of the global patient safety initiatives that we hope may change the way we practice medicine. To help answer this question, Rogers and colleagues16 at Southern Illinois University published an elegant but quite simple study to show the impact of error training. Thirty senior medical students were assigned to one of four different training groups to learn two-handed knot tying. The groups included (1) no training, (2) error training only, (3) correct training only, and then (4) error training plus correct training. They then compared all four

8

SECTION I: GENERAL CONSIDERATIONS

groups. Overall, 11 errors were identiﬁed; the 4 most common accounted for 75% of the total errors. Too much right-handed motion accounted for 38% of the errors; failure to maintain consistent tension, 17%; hands too close to the knot, 17%; and failure to cross the hands, 7%. Rogers and colleagues16 showed that common and even predictable error training coupled with correct skills training clearly leads to superior skills acquisition. One could extrapolate from this that, in fact, predictable errors can be identiﬁed and delineated from virtually any operation and utilized in global skills training. In Way and coworkers’ article7 outlining common bile duct injuries in laparoscopic cholecystectomies, the errors were not only predictable but in fact also reproducible. Would it improve national outcomes if the resident and practicing surgeon learning the basics of the laparoscopic cholecystectomy also learned the steps that lead to prevention of these described errors? Let us look at this a little differently. Can the ability to detect errors during an operation when observing someone or observing videos have any correlation to skill level? Bann and associates17 took 38 volunteer surgeons and recruited them to undertake three exercises. Two of these were bench-top tasks that were scored using Objective Structural Assessment of Technical Skills (OSATS) global rating techniques. The third was the ability to detect simple errors in 22 synthetic models of common surgical procedures. Those volunteers who were able to detect errors clearly performed with a higher technical ability than those who could not (P < .5). Does this simply mean that those individuals who can detect errors as an external observer are more sophisticated in their ability to carry out the procedure? This study would certainly make that argument, and in fact, understanding errors in skills acquisition is probably an additional level above and beyond what individuals are currently trained to do.

Information Overload The downside of error training is information overload. Just learning how to do a procedure, on both a cognitive and a technical level, can be overwhelming for trainees and young surgeons. The vast majority of textbooks and analysis in surgery are geared toward how to do the operation, not how NOT to do the operation. We may think that we all respond differently to information overload, but Miller18 in the 1960s studied the human response to this excessive input and discovered three broad responses. First, we may work faster and faster, trying to somewhat battle the input, and continue to let errors occur, just hoping to ﬁnish the learned task. The second response is to disregard or ﬁlter out part of the information that we are trying to learn so as to learn only a part of the whole. The third response to information overload is called queuing, in which our brain places the input messages on hold and asks them to wait in line. The information becomes backed up and then one by one ﬁlters back in slowly but methodically.

Unfortunately, in the process of learning a complex operation and simultaneously learning how not to do the operation could lead to a complete disregard or foraging out of part of the information. But we do not think this warning should inhibit us from focusing on teaching technical errors. E. F. Schumacher, a Nobel laureate who wrote Small Is Beautiful and also A Guide for the Perplexed, is quoted in the latter book on how we should approach an issue that is as complex as the issues centered around patient safety, medical mistakes, and resident error training: “Can we rely on it that a ‘turning around’ will be accomplished by enough people quickly enough to save the modern world?” This question is often asked, but whatever answer is given to it will mislead. The answer “yes” would lead to complacency, the answer “no” to despair. It is desirable to leave these perplexities behind us and get down to work.

Error Training The most fruitful lesson is the conquest of one’s own error. Whoever refuses to admit error may be a great scholar but he is not a great learner. Whoever is ashamed of error will struggle against recognizing and admitting it, which means that he struggles against his greatest inward gain.—Johann Wolfgang von Goethe (1749–1832), Maxims and Reﬂections As we began studying human performance, technical skills acquisition, the gifted and the talented, resident training, and medical mistakes, we realized that we may need a novel approach to how we think about surgery. More importantly for the future, a novel approach to how we teach our craft. We cannot expect that we will all study the Fitts and Posner model14 with error training and cognitive remodeling and hope that this will be a basis to enhance skills performance and to, ultimately, minimize technical errors. Little has been published on surgical errors and error prevention. Anatomic Complications of General Surgery, Skandalakis and coworkers’19 beautiful book published in 1983 (currently no longer in press), is a staple and mainstay for many surgeon’s libraries. Greenﬁeld published his book, Complications in Surgery and Trauma, in 1984.20 It was updated by Mulholland and Doherty as Complications in Surgery in 2006.21 However, the focus has not been on purely cognitive or technical errors. However, something still seems to be missing because we continue to see the same mistakes over and over again. It is quite clear that errors will always occur from the level of the intern all the way to that of the gifted surgeon. The mechanisms of errors are slowly being understood, both from a theoretical perspective and also from an extremely practical perspective. The common mistakes that are made technically and cognitively for each disease and for each operation are now becoming more clearly

1 FROM ERROR TO PERFECTION: THE PROCESS OF SURGICAL MATURATION understood, and these common repetitive errors are predictable and allow an excellent opportunity for error training that is individualized for each procedure and each diagnosis. In addition, responses to error are poorly developed, poorly role-modeled, and poorly implemented— making it difﬁcult for surgical trainees, young surgeons, and experienced surgeons alike. The concept of error training may clearly play an important and signiﬁcant role in error reduction. This textbook attempts to deﬁne speciﬁc technical and cognitive errors for a large breadth and depth of operations in surgery with the hope and intent of establishing a comprehensive encyclopedia of pitfalls that can occur in surgery that can be utilized by both young and old surgeons for years to come. Nothing stands out so conspicuously, or remains so ﬁrmly ﬁxed in our memory, as something in which we have blundered.—Cicero, De Oratore, I, 129

REFERENCES 1. Institute of Medicine. To Err Is Human. Washington, DC: National Academies Press, 2000. 2. Leape L, Berwick D. Five years after To Err Is Human— what have we learned? JAMA 2005;293:2384–2390. 3. Brennan TA. The Institute of Medicine report on medical errors—could it do harm? N Engl J Med 2000;342:1123– 1125. 4. Leape L. Error in Medicine. JAMA 1994;272:1851–1857. 5. Rasmussen J, Jensen A. Mental procedures in real-life tasks: a case-study of electronic trouble shooting. Ergonomics 1974;17:293–307. 6. Reason J. Human Error. Cambridge, MA: Cambridge University Press, 1992. 7. Way LW, Stewart L, Gantert W, et al. Causes and prevention of laparoscopic bile duct injuries. Ann Surg 2003;237:460–469.

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8. Gladwell M. The physical genius. The New Yorker, August 2, 1999; pp 57–65. 9. Wu AW, Folkman S, McPhee SJ, Lo B. Do house ofﬁcers learn from their mistakes? JAMA 1991;265:2089–2094. 10. Greenburg A, McClure D, Penn N. Personality traits of surgical house ofﬁcers. Surgery 1982;98:368–372. 11. Hilﬁker D. Facing our mistakes. N Engl J Med 1984;310: 118–122. 12. Piernissi E, Fischer MA, Campbell AR, Landefeld CS. Discussion of medical errors in morbidity and mortality conferences. JAMA 2003;209:2838–2842. 13. Evans SRT, Jackson P, Czerniach D, et al. A stepwise approach to laparoscopic Nissen fundoplication: avoiding technical pitfalls. Arch Surg 2000;135:723–728. 14. Fitts P, Posner MI. Human Performance. Belmont, CA: Brooks/Cole Publishing, 1969. 15. Ericcson KA. Deliberate practice and the acquisition and maintenance of expert performance in medicine and related domains. Acad Med 2004;79(suppl 10):570– 581. 16. Rogers DA, Regehr G, MacDonald J. A role for error training in surgical technical skill instruction and evaluation. Am J Surg 2002;183:242–245. 17. Bann S, Khan M, Datta V, Darzi A. Surgical skill is predicted by the ability to detect errors. Am J Surg 2005;189:412–415. 18. Miller JG. Adjusting to overloads of information. In. Rioch DM, Weinstein EA (eds): Disorders of Communication. Research Publications, Vol 42. New York: Association for Research in Nervous and Mental Diseases, 1964; pp 87–100. 19. Skandalakis JE, Gray SW, Rowe JS. Anatomic Complications in General Surgery. New York: McGraw-Hill, 1983. 20. Greenﬁeld LJ. Complications in Surgery and Trauma. Philadelphia: JB Lippincott, 1984. 21. Mulholland M, Doherty G. Complications in Surgery. Philadelphia: Lippincott Williams & Wilkins, 2006.

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Teaching Technical Skills—Errors in the Process Hugh M. Foy, MD and Stephen R. T. Evans, MD INTRODUCTION The primary duty of a surgical educator is to help instill the knowledge, skill, and attitudes that will help develop the trainee into the very best surgeon possible. Experience tells us that the success of an operation depends on innumerable factors, some controllable, others not. A successful operative procedure is the cumulative sum of thousands of perfectly done steps. It follows logically that our primary responsibility as surgeons is to ensure that our technical input is as perfect as possible, given that much else is subject to chaos, chance, and the attention of others. When teaching surgical technique, it becomes even more important to ensure the quality of our craft by our precise and professional instruction of our residents, while at the same time allowing the necessary “graduated responsibility” that is important for the professional development and maturation of a surgeon.1a Our technical input is, in fact, the only factor that is in our direct control. The other external factors—the patient’s premorbid state, anesthetic care, alteration in normal physiology and unanticipated physiologic deterioration—are far less controllable. All of these conditions continually threaten the surgeon’s best intentions and technical skill. A surgeon’s technique must, therefore, be as perfect as possible in order to tip this precarious balance in the favor of the restoration of the patient’s health. As Bosk remarked in his wellknown sociologic study of surgery training, Forgive and Remember, “Every time a surgeon operates, he is making book on himself. Besides the enormous amount of theoretic and technical expertise that is his cognitive capital, the surgeon carries in his head an odds-book for each procedure.”1 Much attention had been focused on how the principles of aviation safety and training might apply to the practice of medicine in general and, speciﬁcally, the training of surgeons.2 Training strategy in both aviation and surgery share some important similarities: (1) They require a body of prerequisite knowledge; (2) They are highly technical; (3) They are done in the setting of unforgiving circumstances; (4) They require quick, precise decision making;

and (5) They require a sequence of subroutines and graduated responsibility. The fundamental inescapable fact in both activities is that human life is held in a precarious position: Our patient’s life is suspended by general anesthesia as the plane and its pilot are suspended in the air by aeronautical engineering. Both medicine and aeronautical engineering are constantly defying unforgivable laws of nature. Ignore either of these basic supports during the endeavor and death is imminent. Both activities are pressed by time, are charged with intensity, and occur in a variable physical environment in which errors can quickly result in morbidity and mortality. Both require training, skill, practice, and quick decisions that are often made with limited data. However, important differences between training surgeons and training pilots limit the application of the aviation model to surgery. Recently, a consulting ﬁrm has even proposed to help apply the principles of the highly technical training of ﬁghter pilots to surgical programs and to our professional organizations that seek to improve the training of surgeons. The differences are notably in the setting, engineering parameters, and the resultant simulation equipment. Pilot training in the last several decades has occurred in a very controlled setting. Candidates are selected after extensive examination with batteries of tests grading their intellectual, physical, psychomotor, and emotional abilities. Before any actual ﬂight training begins, they attend months of didactic lectures in “ground school,” learning the principles of aeronautic engineering, meteorology, and ﬁnally, the engineering speciﬁcs of generic and individual aircraft. The previously described process sounds fairly similar to our medical schools’ curriculum in the basic sciences and clinical clerkships in the various medical specialties. Aviation, however, is much more focused and, by its very nature, precisely deﬁned, described, and quantiﬁed by the principles of aeronautical engineering. As a consequence, simulation techniques have been somewhat easier to develop. Equally signiﬁcant, the threat of war and a substantial military budget helped catapult the ﬁeld of ﬂight simulation in its inception during the days leading up to World War II.

12

SECTION I: GENERAL CONSIDERATIONS

Actual ﬂight training begins in a simulator, safe from the unforgiving reality of gravity. When the student proves proﬁcient, she or he takes to the air in a real plane with an instructor. Obviously, pilots must learn to ﬂy in less threatening, noncombat conditions before they learn the more complicated and dangerous skills of air-to-air combat. Further screening and selection ﬁnally distills the pool of aviators to the select group of highly skilled ﬁghter pilots. Here, too, however, training is done in the absence of “live ﬁre” from a real enemy. Ironically, military aviation has not been faced with a real-life, direct lethal threat from a capable enemy force for more than 50 years, other than occasional ﬁre from surface-to-air defensive missiles. The enemy is usually a colleague who chases the trainee through the air or a computerized threat in a highly developed virtual environment. Following the live ﬂight exercise, the scenario is reviewed and dissected in a lengthy “debrieﬁng” often lasting many hours. In stark contrast, surgery training has traditionally been conducted under the live ﬁre of a real patient who may suffer dire consequences from our mistakes. In decades past, the instructor was often a senior resident, with barely more experience than the learner. In addition, a very large portion of surgical education occurs in our large, mostly public-sector, “safety-net” hospitals and trauma centers in which logistic challenges heighten the high stakes of a real-live patient. Ironically, all too often, the number of patients and the serious degree of their illness are inversely proportional to the logistic support and supervision provided to the trainee. Our trauma centers often serve as our major training centers in which precious little time is available to methodically train residents in the aviation paradigm. Fortunately (and ironically), supervision by attendings has improved as a result of considerable pressure and actual laws enacted and strictly enforced by the federal government that require the attending to be physically present in the operating room in order to be paid. Unfortunately, a frequent occurrence in this resourceconstrained environment is for the attending to ﬁnd himself or herself trying to juggle several overlapping cases with trainees who have little prior experience. It is exactly these constrained resources and variable experience of trainees that may make aviation-based models all the more important and potentially helpful adjuncts to our classic training model of “see one; do one; teach one.” The knowledge of such approaches can help make the surgical instructor more efﬁcient and the resident better educated. Often, the “teaching moment” is effectively the only opportunity for the teacher to cover the various tenets of surgical and technical training, from the assessment of the resident’s prior experience to the review after the case of “what might we have done differently.” Surgical educators, lacking the luxury of hours to accomplish activities like their counterparts in aviation training, must recognize and make effective use of these ﬂeeting “teaching moments” to ensure the safe conduct of the patient’s surgical care.

Our primary objective as surgical educators should be to present to the trainee the most basic, conservative, reliable, and safe techniques. Short cuts that require advanced clinical judgment can be saved for later as the resident matures. First and foremost, the trainer must emphasize attention to detail, adherence to Hallstead’s principles of surgery, and consideration of the emotional needs of the patient and staff. It all boils down to what they know, what they can do with their hands, and what they do with their hearts—otherwise known as the cognitive, psychomotor, and affective domains of learning.

BASIC PRINCIPLES OF SURGICAL TECHNICAL INSTRUCTION AND LEARNING Until recently, little has been written regarding the theory and tenets of teaching and learning in the operating room (OR). The advent of minimally invasive or videoendoscopic surgery heralded by the development of laparoscopic cholecystectomy in the late 1980s and its unforgiving two-dimensional perspective stimulated a renaissance in surgical technical training. From the days of Halstead, certain fundamentals have been espoused but rarely written. Recently, hundreds of articles have been published as attention to skills training has virtually exploded. Consistent with Halstead’s reclusive nature, his principles remain more the oral, rather than the written, tradition of surgery. During the development of the ﬁrst formal training program for surgeons in this country, Halstead would admonish his trainees to carefully consider the root cause of any technical complication. These principles are best remembered in the order in which they are applied during the normal course of an operation: 1. 2. 3. 4. 5. 6. 7. 8. 9.

Aseptic technique. Adequate exposure. Cutting under tension and countertension. Adequate hemostasis. Gentle handling of tissues. Débridement of devitalized tissue. Obliteration of dead space. Assurance of adequate blood supply. Avoidance of excess tension on the suture line.

The speciﬁc conditions and psychomotor training principles have been outlined in various resources and can be helpful in discussing complications that may result from a lack of appreciation and application by the surgical instructor. Learning any motor skill is distinctly different from learning verbal or intellectual skills. Motor skill learning requires application of a “chain of responses,” or ordered, linked tasks, that cannot be accomplished until the preceding task is ﬁnished. Like the sign above the confused cartoon character’s bed: “pants ﬁrst, then shoes.” The precise incision cannot be made until the right amount

2 TEACHING TECHNICAL SKILLS—ERRORS IN THE PROCESS of tension and countertension is applied to the skin. The suture cannot be tied until it is precisely placed in the bowel wall. The artery should not be incised before proximal and distal control are obtained. This succession of tasks has also been described as the “organization of subroutines.”3 Certain conditions make learning a technical skill more likely. Contiguity, or the repeated attempts in close chronological sequence under similar but slightly different conditions, will greatly enhance learning. One cannot learn to ride a bike by trying once today and repeatedly at monthly intervals. Repeated attempts allows for repeated corrective actions. Corrections in one’s technique on repeated trials will oscillate about the mean, which is the desired behavior. Learning a very complex skill like slalom water-skiing is extremely difﬁcult and can be accomplished only by repeated corrections in which the novice ﬁrst leans too far forward, then too far back, incrementally making smaller adjustments, and ﬁnally, on the 10th or 12th attempt stands up, propelled by perfect tension on the rope that transfers the force and speed of the boat. Neither learning to ride a bike nor learning slalom skiing can be achieved while standing still. Both require movement, momentum, and real-time feedback by an instructor. The same is true of operative skill. Analysis of common bile duct injuries in the early years of laparoscopic cholecystectomy revealed that most injuries occurred in the ﬁrst 12 to 20 attempts at the procedure, implying that a plateau of initial competence was more likely after a dozen or so attempts.4 The intern will never learn more about inguinal herniorrhaphy than when she or he performs three such cases in a single morning. Here, they can ﬁnally appreciate the subtle differences in the variable muscular and aponeurotic contributions of the internal oblique muscle, the variance in the size and shape of the hernia sac, and other inherent differences in anatomy and pathology, while the basic steps and repair technique remain constant.

THE OPERATIVE PROCEDURE: SETTING, LOCATION, AND PITFALLS Much attention has been given to the technical or the psychomotor aspect of performing an operation: the actual cutting and sewing of tissues during the procedure. All domains of learning are important contributions to the learning of the trainees and the successful outcome of their patients. Learning theorists maintain that there are three classic domains of learning: cognitive, psychomotor, and affective. Chronologically, the operative learning experience can be said to have three periods: preoperative, intraoperative, and postoperative. In each period, all three domains of learning are important, but one may often predominate. In the preoperative phase, the cognitive domain is predominant. A careful interview of the patient, applying the skills ﬁrst introduced in medical school, is

13

vital to extracting important information regarding the unfolding of the symptom complex in a pattern from which a provisional, clinical diagnosis is made. Inattention to detail, either in the patient’s history or in the review of his or her previous records and diagnostic studies, can have signiﬁcant deleterious effects on intraoperative decision making and postoperative management. Lack of psychomotor skill in performing a physical examination can also be problematic. Obtaining an informed consent from the patient is one of the most demanding of all affective tasks facing the surgeon. Informed consent is much more than merely having the patient or their representative sign a form. Unfortunately, all too often this task is delegated to a more junior team member, sometimes one not even involved in the actual operation. A properly done informed consent involves several steps: Step 1 Step 2

Step 3 Step 4

Step 5

Step 6

Education of the patient. Description of the differential diagnosis and relative degree of certainty of the working diagnosis based on available information and tests. Explanation of the indications and steps of the proposed procedure. Mention of alternative forms of treatment, their relative success rates and why the proposed procedure is, in the judgment of the surgeon, the preferred alternative. A description of the possible complications, both generic (such as bleeding, infection, and the risk of anesthesia) and also ones more speciﬁc to the particular operation. The expected postoperative course and eventual outcome.

PREOPERATIVE PITFALLS— COGNITIVE PHASE OF SKILLS ACQUISITION Most of the work of the preoperative phase involves the cognitive realm of learning and the cognitive phase of skills acquisition. The indications of the operation should be clear, and the intellectual preparation should be accomplished through studying the appropriate educational materials and thoroughly reviewing the patient’s history, examination, and diagnostic studies. However, more subtle tasks need to be attended to: (1) performing a “learning needs assessment (LNA),” (2) deﬁning goals and objectives, and (3) familiarizing oneself with the necessary equipment to be used.

Learning Needs Assessment LNA is the process of determining the previous experience of a learner so that the teacher can better tailor the instructional focus to the individual resident or student. Failure to accurately inquire and appreciate the prior experience

14

SECTION I: GENERAL CONSIDERATIONS

and knowledge can result in inefﬁcient and unnecessary frustration for both the attending and the resident and affect patient outcome. Underappreciation of a learner’s capabilities may result in hovering unnecessarily, teaching skills she or he has already mastered, and wasting the time of all involved. This is more likely to be the case early in the academic year. As the year progresses, it is more likely to occur at the beginning of a rotation in a larger program in which the attending may have little or no prior experience or knowledge of the newly arrived resident on the service.

Basic Principle Prior to beginning the procedure, the attendings must obtain knowledge of the operating residents’ prior experience. They must “ask the learner.” The teaching assistant must not assume but must ask the resident what his or her prior experience has been, including (1) factual or cognitive knowledge of the case, (2) prior operative experience, and (3) awareness of common pitfalls and complications. It is critical that the attending establish the level of instruction necessary to avoid either overestimating or underestimating the resident’s ability. Overestimating a resident’s abilities can have disastrous consequences. Conversely, underestimation of technical ability carries the risk of insulting the trainee and wasting precious time. In smaller programs, this is less likely a problem because attendings and residents often spend more time together in longer rotations characterized by more intimate contact in the OR. In larger programs spread across several integrated institutions, this is less likely and a careful LNA is of critical importance. In addition, attendings may overestimate residents’ abilities based on their own prior experience delving into their memory of decades long passed. Often, one hears the admonition, “Why a chief resident should be very capable of doing a routine colectomy with a junior resident.” Such an assumption may be based on the attendings’ memory of their training program in decades past in which direct attending supervision was sparse as best, particularly on emergency cases at night. Surgery has changed dramatically in the last several decades. Most notably, attending presence in the OR has signiﬁcantly increased. More recently, the 80-hour work week restriction has compounded the insidiously diminished independent responsibility of the resident. We can no longer make assumptions based on the past. Sound practice is to include the LNA in the preoperative checklist in order to avoid potential disastrous complications based on false assumptions, as illustrated in the following scenario. Example: Overestimating a Resident’s Capability A patient is brought to the emergency room with a stab wound in the left third intercostal space in the midclavicular line. The patient is hypotensive with signs of cardiac tamponade. The chief resident, now halfway through her or his ﬁnal year, is known to be one of the best in the

program, seasoned with 2 extra years in the laboratory and accepted as a good team leader. The attending assumes that she or he has the prerequisite knowledge of cardiac repair and stands by ready to help. After the resident deftly performs an anterolateral thoracotomy, incises the pericardium, and relieves the tamponade, the patient improves. A 1-cm, nonbleeding laceration in the right ventricle is noted and repair is attempted with a running suture using a monoﬁlament suture, which tears the ventricle and results in massive hemorrhage. Fortunately, the attending looking over the resident’s shoulder is ﬁnally able to repair the enlarged wound with a generous supply of pledgets and appropriately placed horizontal mattress sutures. If only one could live the last few moments over again and simply ask the resident, “Have you ever sewn a laceration in a beating heart before?” Grade 4 complication Alternative Scenario

Before beginning the thoracotomy, the attending turns to the chief resident and asks if she or he had ever sewn a traumatic laceration in a beating ventricle, making sure to distinguish the technique as uniquely different from closure of the atrium. The resident remarks that she or he has not, and the attending describes the appropriate technique of using horizontal mattress sutures over pledgets to help distribute the tension and avoid further injury. Discussion: Particularly in emergent cases, failure to accomplish an LNA in a timely, precise manner can have dire consequences. A precise and speciﬁc inquiry must be made of the learner, because transference from one technique in one anatomic structure cannot necessarily be made to another. As the example illustrates, the technique for closure of the atrium, commonly done in elective surgery after decannulation, is distinctly different from closure of a laceration in a beating ventricle.

Example: Underestimation of a Resident’s Experience On a busy Monday morning, the OR schedule is full. It is the beginning of the year, and the ﬁrst case is a recurrent inguinal hernia in an obese patient. The chief resident hastily assigns residents to cases. Much to the attending’s chagrin, an intern reports to the OR to scrub on the case. The attending, faced with a busy schedule full of overlapping commitments, is disappointed and visibly agitated, complaining that a more experienced resident has not been assigned to this case, which will require skills in reoperative surgery far beyond the ability of an intern. Irate and upset, the attending lets his or her disappointment show, alienating not only the intern but also the circulating nurse, scrub technician, and anesthesiologist. The air in the room is icy cold, and tension runs high. Halfway through the case, a trauma code is called and the attending becomes further agitated as he or she realizes that the case cannot be left for the intern alone to proceed, even with the more mundane aspects.

2 TEACHING TECHNICAL SKILLS—ERRORS IN THE PROCESS Alternative Scenario

The attending takes a deep breath, holds his or her words of disappointment and gathers the best equanimity he or she can muster, reminding himself or herself that he or she is here, at this hospital, to teach and to teach all, regardless of ability. A ﬂexible approach with the attending doing the more difﬁcult part of the case is outlined as the case is brieﬂy discussed with the resident at the scrub sink. As the case proceeds, the attending is surprised at the technical facility of the intern, particularly with dissection through the scarred tissue. Remarking at the intern’s skill, he or she is reminded that the intern is a transfer to the program, having recently immigrated to the United States after completing 4 years of training in the home country. When the trauma code is announced, the attending pages his or her partner to cover. Discussion: Performing an LNA is accomplished by simply asking the resident about prior experience with any particular procedure. It is best done early, before the procedure begins. A brief inquiry into the resident’s prior knowledge and experience in general and in a particular case helps better set the stage and adjust the attending’s expectations appropriately. Nothing can be more disappointing than false expectations unmet. Emotional control and attitude can prevent a chilling, negative atmosphere in the OR that affects all personnel. Done properly, an LNA sets the stage with realistic expectations and will more likely result in an educational activity characterized by the appropriate and productive levels of anxiety, preparation, and care.

Deﬁned Goals and Objectives Basic Principle Before beginning any operation, it is important to precisely deﬁne the goals and objectives of the operation. Much attention has been paid to goals and objectives in clinical education, and most accrediting bodies require that these be put in writing for all rotations, programs, and even individual lectures. Simply stated, goals are what one wishes to accomplish and objectives are the means by which the goal is to be reached. Goals can be multiple, and if so, they must be prioritized. Objectives are the “how and what” of an operation. They can be both assigning appropriate roles for different members of the team and determining strategy for the operation. Sometimes, the goal of the operation is obvious: “Remove the gallbladder” is the goal in an elective cholecystectomy. In an exploratory laparotomy for an unstable trauma patient, the goals may be multiple and more obscure, particularly for the neophyte resident. Restatement of the priorities involved in more complex operations is important; otherwise, trainees may be distracted by less critical tasks at hand. When faced with multiple procedures in a single operation, it is helpful to lead the resident through the list of procedures necessary and assign their relative priority,

15

keeping in mind that the most critical procedures must be done ﬁrst in the event the patient becomes unstable and the operation is aborted or curtailed. In an exploratory laparotomy for trauma, the priorities are assigned along lines akin to the basic principles of resuscitation: (1) stop the bleeding, (2) control contamination, and (3) repair and reconstruct damaged structures if not deemed unwise and unsafe because of the dangerous triad of hypothermia, coagulopathy, and acidosis. In an otherwise stable patient in whom many different reconstructive or reparative procedures are needed, it is important not to burn any bridges nor to perform irreversible steps before other, less deﬁnitive intermediate steps are accomplished. The most important task should be accomplished ﬁrst, such as performing the descending colostomy before reanastamosing the terminal ileum so as to not leave the patient with a blind loop obstruction of the ascending colon with no route of decompression if the case needs to be terminated early. Similarly in any individual procedure, one should not divide the colon before the mesentery is ﬁrst mobilized and taken down and the vessels ligated. Assigning the precise roles of the members of the surgery team before the operation begins is critical so that each individual’s expectations are clear and appropriate and confusion is subsequently minimized. Typically, only one person can direct the operation as the teaching ﬁrst assistant, whether it is the attending or the chief resident. If both the attending and the senior resident are scrubbed in to help a junior through the case, then the roles should be deﬁned ahead of time. Often, the attending will act as second assistant, chiming in with tips to help the case move along more smoothly.

Example: Unclear Assignment of Operative Roles An unstable patient is brought expediently to the OR after an ultrasound revealed a large amount of blood in the peritoneal cavity. The 3rd-year resident rotating on the service from another afﬁliated program missed the orientation session the day before and arrived in the OR eager to do the laparotomy, “get the numbers,” and fulﬁll her or his operative trauma experience required for completion of residency. She or he was unaware that the trauma service policy was for all unstable patients’ cases to be done by the chief resident until hemorrhage control is established and the case is deemed appropriate for a less experienced resident to be the “primary surgeon”. She or he steps up to the patient’s right side and helps drape the patient, eager to accept the scalpel and begin. The attending arrives, asks her or him to step back so that the chief resident can begin. The visiting resident, visibly disappointed and upset, reluctantly agrees. Over the course of the next several days, she or he is sullen, argumentative, and uncooperative. She or he complains to her or his home program director who calls the chief of trauma to complain.

16

SECTION I: GENERAL CONSIDERATIONS

Alternative Scenario

Unable to either turn back the clock or completely orient the visiting 3rd-year resident before the emergent case, the chief resident informs her or him of the policy for the chief resident to perform the case with the attending until the patient’s stability is ensured. The chief resident apologizes and refers the 3rd-year resident to the section in the orientation packet that states the policy and where in the coordinator’s ofﬁce a copy can be picked up. The chief resident asks that the 3rd-year resident assist if the attending is delayed in arriving to the OR.

Example: Lack of Prioritization of Multiple Operative Tasks The same trauma patient, when explored, is found to have ruptured spleen, extensive mesenteric lacerations, and multiple bowel perforations. All four quadrants are packed off, which appears to control the hemorrhage from the left upper quadrant. The bleeding mesentery is examined and the vessels ligated. The sigmoid colon has deep, fullthickness injuries through the wall with fecal spillage. The residents débride the edges and close the sigmoid injury in two layers. Suddenly, the anesthesiologist announces that the patients’ blood pressure is 50 mm Hg, and the laboratory panel returns with evidence of worsening acidosis and coagulopathy. Still, little or no blood seems to be coming from the left upper quadrant. The patient develops high inspiratory pressures and nearly arrests. The packs are removed from the splenic fossa to reveal that the ruptured spleen has been bleeding into the chest through a 6-cm-long posteromedial tear in the diaphragm. Alternative Scenario

The teaching assistant calmly reiterated the principles and priorities as the abdomen was being opened, helping all involved to understand the priorities involved. After ligation of the bleeding mesentery, the colon injury is quickly stapled off, leaving the repair or diversion for later. The left upper quadrant is reexplored, the spleen mobilized and removed, the diaphragm repaired, and a left chest tube placed. Discussion: Goals and objectives for any learning opportunity need to be clearly stated to all members of the team before proceeding. Preferably, this can be accomplished before the operation: in a preoperative planning conference or at the scrub sink after LNA has been done. In emergency cases, it should occur as the team is assembled and the surgeons are gowning, draping, and making the incision. It takes only a minute. If neglected or omitted, it can have catastrophic results. The teaching moment is often just that long, and the opportunity can be lost just as quickly.

Equipment Familiarization Basic Principle For many generations, most surgical procedures were fairly constant in their design, conduction and equipment.

Since the late 1980s there has been an explosion in the approach, technology, and innovation spurred on by minimally invasive surgery. In the early years of laparoscopic cholecystectomy, many complications occurred owing to lack of appreciation of the lack of depth perception in this new two-dimensional environment, unfamiliarity with newly developed equipment, and hidden liabilities of certain, seemingly innocuous aspects like CO2 insufﬂation. Technical adaptations of the procedure, anticipation of potential complications, and improvements in instrumentation have overcome many of these challenges. Regardless of these advances, it remains critical for the surgeon to be familiar with whatever equipment may be needed. As new and better instruments are developed, prior familiarization with equipment is ever more important.

Example: Unfamiliarity with Equipment A senior resident is assigned to help a new attending with a laparoscopic colon resection. The attending assumes that the resident has completed the endoscopic stapled anastomosis exercise in the technical skills laboratory. Unfortunately, she or he is in the half of her or his class that was to receive the training in the latter half of the year. The resident rushes to the OR to ﬁnd that the case has been started with the fellow. The resident scrubs in and, as the case proceeds, is asked to step forward to perform the anastomosis. She or he is given the endoscopic stapler as the attending lines up the bowel for a side-to-side anastomosis. The stapler is threaded into the bowel and the resident attempts to ﬁre it, not realizing that the scrub techncian has failed to remove the safety tab that blocks the instrument’s ﬁring. Not wanting to be seen as incompetent, the resident forcefully closes and ﬁres the stapler, breaking the handle. No other stapler is available that is suitable for the case, and the case requires conversion to an open procedure to complete the anastomosis. Alternative Scenario

A new stapler is proposed to be added to the general surgery inventory. Prior to approval, the manufacturer’s representative demonstrated the device at a regular faculty meeting and the following week to the residents in their weekly technical skills laboratory. Before using it in the OR, the attending asked the resident if she or he was familiar with the instrument and had attended the demonstration session. The resident carefully inserted the stapler into the lumen of the bowel, realized that the safety tab was still in place, removed it, and ﬁred it as she or he announced the speciﬁc steps in the procedure out loud to the attending and the rest of the team. Discussion: In an ever-changing surgical environment characterized by constant innovation, it is imperative that new instruments are formally introduced and that all surgeons, trainees, and attendings alike be instructed in their proper use before they are to be utilized in the OR on a live patient. Deﬁned curricula and technical skills laboratories have sprung up in training institutions around the

2 TEACHING TECHNICAL SKILLS—ERRORS IN THE PROCESS country, and formal accreditation protocols have been established to ensure a safe venue for familiarization and practice before the trainee is expected to use new instruments and techniques in the OR. Accreditation of residents in many procedures, both old and new, such as central line insertion, is advocated to make sure that the residents have been properly instructed and proctored through their initial attempts and that their competence is certiﬁed before they are allowed to perform the procedures independently.5

INTRAOPERATIVE PITFALLS—THE FIXATIVE AND AUTONOMOUS PHASES OF SKILLS ACQUISITION Basic Principle Technical proﬁciency in the OR is a continuous process of improvement. Stages of achieving mastery have been described by Dreyfus and Dreyfus,6 proceeding through a logical process of acquiring both awareness and skill: ● ● ● ●

Unconsciously incompetent Consciously incompetent Consciously competent Unconsciously competent

The logical school of epistemology distinguishes between awareness and knowledge. The learner begins both unaware and ignorant. Awareness (consciousness) and competence (technical proﬁciency) are distinct phenomenon and can be analyzed in a 2 × 2 matrix (Fig. 2–1) or as a linear progression leading to mastery, as listed previously. Regardless of the task, the naïve learner initially has no idea of the complexity of the task, because it looks relatively easy when demonstrated by a master. All

Figure 2–1 The progression to mastery is a logical transition involving both awareness and competence. In order to effectively teach surgical skills, the expert must regress to the “consciously competent” stage.

17

of us remember our ﬁrst attempt at sewing the skin and our nearly ballistic trajectory of the needle once freed from the resistance of the skin. Our lack of appreciation of how to brace our hand and check the movement of the needle quickly converted our naïve conﬁdence and helped take us to the next and essential step of “consciously incompetent” when we realized that sewing the skin was much harder than it looked. With practice, the learner becomes consciously competent. He or she can perform the task but must focus, concentrate, and pay careful attention. After years of experience and hundreds of repetitions, the surgeon may become “unconsciously competent” as her or his body becomes one with the surgical instruments and he or she reaches what has been described as the “autonomous phase” of skills acquisition—like the experienced driver who gets in the car and drives to work, hardly conscious of the thousands of steps taken en route and taken for granted.

Practice Practice, practice, practice is an essential element of achieving mastery. However, practice alone is not enough as espoused by the great football coach Vince Lombardi who stated, “practice does not make perfect. Perfect practice does.”6a Implied in that wisdom is the essence of coaching and teaching. A good instructor not only must be a master but also must appreciate the method and the steps in helping the learner achieve proﬁciency. The operative teacher must guide the initial attempts, providing feedback in real time to the learner. Often, words cannot describe the exact movement desired. To do so involves a considerable transference of motor knowledge to verbal instructions in terms that the learner can understand. Often, a demonstration is necessary, even at the risk of alienating an overcautious resident who fears he or she will “lose the case.” Done with political sensitivity, a demonstration can be very effective. If “a picture is worth a thousand words,” a demonstration is worth a million. Independent practice is essential in helping the learner progress toward unconscious competence. The repeated practice of a technique in a relatively nonthreatening environment is as important as the real-time feedback that guides the initial attempts of the learner in the consciously incompetent stage. But to progress to a consciously competent level, the trainee must have the opportunity to practice in an environment devoid of the discerning eye and constant critique of the well-meaning but often overvigilant attending, which often results in an excess degree of performance anxiety. Inherently entangled in this quest is the dilemma of how one can achieve a “system of graduated responsibility” and, at the same time, ensure the competence of the learner. The increased presence of attendings required by modern reimbursement and supervision policies creates a constant threat to this critical facet of the surgeon’s training. The challenge requires a very

18

SECTION I: GENERAL CONSIDERATIONS

intimate relationship between the teacher and the learner so that direct, observational instruction can gradually fade as the resident becomes more adept. The titration of the teaching surgeon’s involvement is surely a delicate balance that requires careful assessment of not only the learners’ technical ability and judgment but, equally important, their honest self-awareness of their limitations. It is critical that they recognize when they need help and to call for it in a timely fashion. If medicine is indeed an art, then surgical instruction is the distillation of medical education to its absolute essence.

Example: Lack of Autonomous Awareness The chief resident is left in the OR to close with the junior resident after completion of the procedure. The attending goes out to talk with the family. When coming back in, the “counts are correct”: Two days later the patient is found to have vague abdominal pain and a plain X-ray shows a malleable retractor left in the abdominal cavity. Although the chief resident is felt to be “unconsciously competent” at this stage of training, even minor distractions can lead to signiﬁcant errors. Alternative Scenario

The resident, in accord with hospital policy, requests that an x-ray of the operative ﬁeld be done before the patient is undraped and awakened. The retractor is recognized. Several fascial sutures are removed and the retractor retrieved. The attending waits until the resident notiﬁes her or him before visiting with the patient’s family in the waiting room. Discussion: Many safeguards have been employed to ensure that the operation is as safe as possible and that such unexplainable misadventures like retained instruments, wrong-side surgery, and transfusion reactions are avoided. Simple methods such as marking the patient’s surgery site with an indelible marker in the preoperative holding area, “time-out” recitation of the operative consent, and positive identiﬁcation of the patient are simple and effective ways of ensuring that the operation is as safe as possible. New technologic innovations such as radiofrequency chips on laparotomy sponges and routine postoperative x-ray examination of the operative ﬁeld have become commonplace in many hospitals. Notiﬁcation of the patients’ family after the operation is extremely important, but this should not be done until one is absolutely sure that the operation is indeed over and the patient is doing well.7–9

usually later in their career, from the overanxious and impatient younger attendings? The masters were able to do anything and they could teach you in a manner that was calm, effective, and enjoyable. They could see things from your perspective. They could appreciate when you could run free and when careful attention was needed. They appreciated parallax, deﬁned as the difference in the appearance of an object when seen from two different vantage points not on a straight line. When operating on many midline structures, the resident surgeon and the attending/instructor typically stand on opposite sides of the table, with the surgical site between. Their vantage points are often 90° different. As a consequence, they often see very different ﬁelds. During an open cholecystectomy, the gallbladder, when viewed from the right side of the table, is partially hidden from the resident’s view under the edge of the liver but is in plain view of the teaching assistant on the patient’s left. Failure to appreciate this difference can lead to catastrophic technical errors. Similarly, exposure and retraction must be presented to the resident’s view from the opposite side of the table (Figs. 2–2 and 2–3). Correctly done, this often negates the clear view of the teaching assistant who must have the insight and conﬁdence to allow the resident’s dissection. Failure to show and expose the ﬁeld adequately and accurately can lead to trouble.

Example: Lack of Appreciation of Parallax A particularly difﬁcult laparoscopic cholecystectomy is converted to an open procedure. The triangle of Calot is densely adherent to the infundibulum of the gallbladder. The resident’s view of the base of the gallbladder is difﬁcult because the patient is obese, the wound is deep, and the distended gallbladder and liver edge partially obstruct the view of the cystic duct. The attending’s view, in contrast, is clearer and affords the view of a thin but discernable plane between the infundibulum and the

TECHNICAL TIPS: BECOMING AN AWARE INSTRUCTOR Parallax We all remember our favorite instructors in the OR and we will never forget those who could turn a simple procedure into a nightmare. What distinguished these masters,

Figure 2–2 Resident’s view of the gallbladder from the patient’s right side. The gallbladder is barely visible and obscured by the wound edge, retractor, and lap pad.

2 TEACHING TECHNICAL SKILLS—ERRORS IN THE PROCESS

Figure 2–3 The attending’s view from the patient’s left side. The gallbladder is obvious and in plain view.

immediately adjacent common duct. Frustrated with the resident’s hesitancy and faint-hearted attempts at dissection, the attending urges the resident to “cut, cut.” Unsure but willing to please, the resident’s Metzenbaum scissors skate off the distended gallbladder and lacerate the common duct. Discussion: The resident’s view of the operative ﬁeld (see Fig. 2–2) can be drastically different from that of the attending across the table (see Fig. 2–3). Because more biliary surgery is done in the two-dimensional view afforded by a video screen, familiarity with open procedures is rare. In addition, only the most difﬁcult cases default to the open method. Dissection in difﬁcult, deep, and challenging cases can be treacherous, not only for the resident but also for the recently trained attending who likely has minimal experience with open biliary surgery. Anatomic structures in the surgical ﬁeld that lie underneath the incision and in close proximity to critical structures are particularly dangerous: for example, the common bile duct in cholecystectomy for cholecystitis and the ureter in colon resection in diverticulitis. Appreciation of the principle of parallax and patience with the less experienced resident is of critical importance in achieving a safe outcome.

Bracing Basic Principle Bracing is one of the simplest techniques to help the neophyte achieve a greater deal of proﬁciency. It is based on the physics of a lever that consists of a long, rigid structure resting on a fulcrum. The lever has two components: the level arm and the moment arm. The placement of the fulcrum, or brace point, close to the object to be dissected helps amplify the strength of the lever and dampen the effects of the movement of the lever arm. The longer the moment arm, the more ampliﬁcation of the movement of the lever arm. Moving the brace point closer to the target minimizes the moment arm, dampens the

19

natural tremor that we all have, and increases the power and control of the instrument. Several trips to the dentist for teeth cleaning can help one better understand the importance of bracing. Dentists and dental hygienists know that a typical molar has 32 different and distinct surfaces. The cleaning, drilling, and ﬁlling of a tooth demands precision in fractions of a millimeter. An inexperienced hygienist will typically “skate” off the surface of the tooth and impale the patient’s gums with the instrument. In contrast, the experienced hygienist or dentist never takes the heel (or hypothenar eminence) off the patients chin, carefully bracing and checking each stroke of the instrument. Movements are careful, controlled, and precise because of the focused attention to bracing. In surgery, bracing has both a micro and a macro application. Microbracing is an essential skill in microsurgery, dentistry, and vascular surgery in which the ﬁeld is small and the tolerances measured in fractions of millimeters. Microbracing requires moving the fulcrum closer to the point of action, minimizing tremor, and affording precise control of the instrument. It helps avoid “past pointing” once the resistance of the tissue is passed. Bracing is facilitated by having the OR table at the correct height, which in most cases should be at the surgeon’s elbow. Adjusted so, it will allow the surgeon to rest the forearm on the patient or the heel of the hand on the edge of the wound. With the wrist locked and a predictable angle of the needle on the needle holder, one simply supinates the forearm to scribe the needle in a controlled, smooth arc through the tissue. The nondominant forearm is held at a right angle to the other, and the forceps is ready to assist the manipulation of the tissue or accept the needle when appropriate (Figs. 2–4 and 2–5). Macrobracing is critical in those maneuvers that take considerable strength to penetrate tissue with marked resistance such as the chest wall when placing a chest tube or the placing of wire sutures through the sternum. The surgeon’s legs are slightly bent at the knees, the upper body is locked in place, “engaging the core,” the elbows are tucked against the torso and/or on the iliac crest, and both hands are held ﬁrmly on the instrument. One hand (the dominant) provides the necessary forward force while the other checks the movement of the instrument after the resistance of the tissue is overcome. “One hand is the gas, the other is the brakes.”

Example: Failure to Brace and Control Movement An intern is asked to place a chest tube in a victim of a motorcycle collision, a 250-pound man in acute distress. The chest wall is thick and muscular, making the dissection difﬁcult. Having placed a tube only in a simulator, the intern is unaware of the great degree of force necessary to penetrate the dense intercostal muscles. As the Pean clamp ﬁnally penetrates the chest wall, the intern is equally unprepared for checking its forward motion. The clamp continues through the diaphragm and into the spleen.

20

SECTION I: GENERAL CONSIDERATIONS

Simplifying Movement Simplifying movement, like bracing, is mostly a matter of physics. In performing a controlled and repetitive movement, the fewer muscles and fewer joints that are utilized, the better the control and the less fatigue due to use and overuse of unnecessary muscles. When sewing, the wrist is locked and the only movement necessary is supination of the forearm. The needle scribes a smooth, atraumatic, and predictable arc through the tissue. The needle should remain in place when released as no additional strain or torque is applied during its placement. As a result, the needle’s location, even when obscured by a bloody ﬁeld, should be predictable and easily retrieved by merely repeating a similar movement aimed just beyond the ﬁrst.

Figure 2–4 Lack of bracing. The resident’s fulcrum, or brace point, is the scapulothoracic junction.

Example: Lack of Simplifying Movement The morning after a challenging Whipple procedure for severe chronic pancreatitis of the head and uncinate process in a patient with pancreas divisum, your chief resident is unable to open the jar of ointment to apply to the clinic patient’s burn wound owing to extreme soreness and spasm of his or her neck and upper back muscles. The cumulative effect of the repeated movement and static posture of the challenging 10-hour operation have taken their toll owing to their lack of bracing and simpliﬁcation of movement.

Visualization Visualization, or seeing with the mind’s eye, further facilitates the smooth, careful application of the instrument on the patient’s tissues. Used by athletes who rehearse their complex routines in their mind at the top of the slalom skiing course or at the edge of the gymnastic apparatus, it helps set a mind map of the complex movements to follow. Visualization also helps the surgical trainee develop an awareness of the underlying anatomic structures to be either incorporated (like the submucosa in a Lembert stitch of the bowel) or avoided (like the parotid duct when suturing a facial laceration). A favorite senior resident, who was also a student of martial arts, once remarked: “It is a very Zen thing. Your whole consciousness should ride the tip of the needle as it arcs through the tissue.” Or as Yoda, in the Star Wars trilogy, admonished his student: “See with your mind, Luke, not with your eyes.” Figure 2–5 Maximal bracing. Forearms and hands resting on the ﬁeld and held at 90°.

Example: Lack of Visualization During a laparoscopic cholecystectomy, the resident fails to appreciate the proximity of the right hepatic duct posterior to the cystic duct/infundibular junction owing to their overlapping nature. Unfamiliar with how movement of the gallbladder with the opposite hand and turning of the 30°-angled scope can help reconstruct a

2 TEACHING TECHNICAL SKILLS—ERRORS IN THE PROCESS

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three-dimensional image, the resident’s attempts to dissect the triangle of Calot results in injury to the right hepatic duct, which lies immediately posterior to the cystic duct.

should always be speciﬁc: a particular technical maneuver, action, or omission. It should precisely deﬁne your expectations and the manner in which you expect the learner to change.

POSTOPERATIVE PITFALLS—THE AFFECTIVE DOMAIN OF LEARNING

Technical Feedback

Basic Principles Feedback has been described as the “currency” of adult learning. Without providing learners incremental guidance to improve their skill, their practice may result only in the perpetuation of bad habits or the extinction of good ones. It is only with feedback that we can most efﬁciently guide initial attempts and add encouragement as they demonstrate progress. The basic principles of feedback can be easily remembers with the pneumonic, “TENDS to be both positive and negative”: T E N D S

timing environment nonjudgmental based on direct observation speciﬁc information should be both positive and negative

Entire books have been written on how to provide feedback in any educational or supervisory setting. There are many barriers to doing it well. We all want to be liked and are typically uncomfortable in confronting and correcting others. Leveling harsh criticism (often confused with negative feedback) may seem inappropriate at the time because of the presence of others. However, feedback must be given in a timely fashion to be effective. Barring other obstacles, sooner is better than later. Serious negative feedback is best given in private. The OR is always staffed with an entire team, and extremely harsh words can negatively affect all within earshot. One effective technique useful in giving timely but important negative feedback in the OR is to quietly invite a particularly surly or uncooperative resident over to the x-ray board and, while feigning explanation of the ﬁlm, speak in a very quiet, but ﬁrm, unmistakable manner. You can then relate your displeasure with their attitude, lack of skill, or preparation and set deﬁnite guidelines for their continued participation in the case. Feedback should be nonjudgmental. It should be about objective behaviors, not based on your opinion of why something was done or character ﬂaws suspected in the learner. It is much better to state that “I am disappointed in your lack of preparation for the case,” rather than calling the resident “lazy.” Likewise, it is best to limit your feedback to those behaviors or actions that you yourself witness rather than relying on hearsay or rumor. As a program director or administrator, it is critical to have on hand any written documentation previously submitted by others during a feedback session. In such formal sessions and in other ad hoc sessions in real time, the feedback

Technical feedback is a bit easier and less emotional in nature and, consequently, easier to impart. As Bosk, in his famous treatise on surgery training, Forgive and Remember1 observed, “technical errors due to lack of experience are the most forgivable of all errors.” In the OR, a little humor to lessen the blow on the resident’s ego can sometimes go a long way. One of my most effective attendings once described my feeble attempts to incise the linea alba as the “Cuisinart technique.” The message was clear, but kind and in good faith. In order to provide effective technical feedback, it is critical for the instructor to be able to “see” the procedure from the learner’s perspective and relate in words the exact movement or technique desired. It is often extremely difﬁcult to describe in precise words our intent. Transference of our motor memory into words that can be understood by the learner can often fall short of its mark and be confusing and subsequently frustrating for both the instructor and the learner. When faced with that frustrating conundrum, we often resort to a demonstration. To be an effective learner and recipient of feedback, residents must be conﬁdent enough to receive the help rendered by the demonstration and not fear they are “losing the case.” Such fears are heightened if the demonstration is excessively long. Used sparingly, demonstration of a technique can be extremely helpful. Again, if a picture is worth a thousand words, a demonstration can be worth millions. Feedback on technique must be done in real time and done almost continuously during the conduct of the operation as each movement is performed. A summative or global critique after the operation should emphasize general trends or tendencies that are both positive and negative. The attending should discuss not only areas for improvement but also things that the resident did particularly well. The well-known “sandwich technique,” espoused by Blanchard in his classic primer, The One Minute Manager, is a helpful strategy. The feedback session should begin with a positive comment such as acknowledging the resident’s persistence, followed by citing speciﬁc examples of where improvement is needed. Finally, it is best to end with the other “bread of the sandwich,” a positive acknowledgment and encouraging remark to help motivate the resident to persist in her or his efforts to improve. Feedback and Acknowledgment of the Operative Team

Surgery is a team sport that has many members. Most of this discussion has centered on a teaching environment, but regardless of the setting, either in a teaching hospital or in private practice, the other players on the team should be acknowledged. First and foremost is the patient. It is

22

SECTION I: GENERAL CONSIDERATIONS

often helpful to stand by and reassure, as much as possible, the patient as he or she emerges from anesthesia. It is important to thank the rest of the team, the anesthesiologist, nurses, and technicians, for their help. Any problems that arose should be addressed in a kind and objective but clear manner. If necessary, more serious matters requiring negative feedback can be discussed in private. Feedback is typically sparse in the immediate postoperative period because the patient in the recovery room is affected by the amnesic properties of many of the anesthetic agents and other medications. Writing of the orders and dictation of the operative note are also important to accomplish promptly. As soon as possible, one member of the team, typically the most senior, should speak with the patient’s family. The hours spent in the waiting room while a loved one is undergoing an operation are some of the longest in one’s life. The ﬁrst words that should come out of your mouth is that the patient is ﬁne or, less frequently, they are in some degree of danger. Until family members hear that the patient is well, they assume the worse. The referring physician or primary care provider should also be promptly notiﬁed, updated, and advised of any condition that might complicate the recovery period and should be graciously thanked for allowing you to participate in the care of their patient. Attention to all involved in the operation will help build a sense of teamwork and camaraderie with your colleagues both in and out of the OR and ensure that your next operation will more than likely be as successful as possible.

REFERENCES 1. Bosk CJ. Forgive and Remember: Managing Medical Failure, 2nd ed. Chicago: University of Chicago Press, 2003. 1a. Accreditation Council for Graduate Medical Education (ACGME). Program requirements for graduate medical education in surgery, January 1, 2008. Available at http:// www.acgme.org/acWebsite/downloads/RRC_progReq/ 440_general_surgery_01012008.pdf 2. McGreevy JM. The aviation paradigm and surgical education. J Am Coll Surg 2005;201:110–117. 3. Romfh RF, Cramer FS. Technique in the Use of Surgical Tools, 2nd ed. Norwalk, CT: Appleton & Lange, 1992. 4. The Southern Surgeons Club. A prospective analysis of 1518 laparoscopic cholecystectomies. N Engl J Med 1991;324:1073–1078 [published correction appears in N Engl J Med 1991;325:1517–1518]. 5. Bell RH. Surgical Council on Resident Education: a new organization devoted to graduate surgical education. J Am Coll Surg 2007;204:341–346. 6. Dreyfus HE, Dreyfus SE. Mind Over Machine. New York: New York Free Press, 1982. 6a. Phillips DT. Run to Win. New York: Macmillan, 2002; p 95. 7. Gibbs VC. Patient safety practices in the operating room: correct-site surgery and nothing left behind. Surg Clin North Am 2005;85:1307–1319. 8. Dagi TF, Berguer R, Moore S, Reines HD. Preventable errors in the operating room—part 2: retained foreign objects, sharps injuries, and wrong site surgery. Curr Probl Surg 2007;44:352–381. 9. Blanchard K, Johnson S. The One-Minute Manager. New York: Harper Collins, 1982.

3

Legal Considerations Catherine Bertram, JD and Stephen L. Altman, MD INTRODUCTION As trial lawyers with over 50 years of combined experience we urge you to invest the time it takes to read this chapter. Then, make a commitment to change your practice to consent patients correctly. Top surgeons understand that effective communication with their patients is a skill that needs to be updated and reﬁned over time just like surgical technique. Proper consent does not require more time when you understand the true nature of an adequate consent.

LEGAL PITFALLS IN SURGICAL CARE BEFORE ENTERING THE OPERATING ROOM Let us start by emphasizing the key point of this chapter— informed consent is a process. It is not a hospitalgenerated form. Surgeons make a critical error when they assume that getting a patient to sign the hospital’s consent forms means that they have complied with the requirements of informed consent. This error can be quite costly to your practice and to your reputation. Consent is a process that requires communication between the surgeon and the patient. Usually, it is a twostep process that starts during the ofﬁce visit and continues at the hospital before surgery. The ofﬁce visit is your opportunity to take the time to explain the proposed surgery, the risks and alternatives, and the consequences of not proceeding. Thus, patients have time to reﬂect on all the information you have given them and can really make an informed decision to proceed with the surgery you suggest. The time for having that discussion is not in the hallway of the same-day surgery unit while you are trying to get in the ﬁrst case of the day. That is not fair to you or to the patient and is certainly not the best use of your time. Patients can feel pressured to agree and will often say they were so worried about the surgery that they did not even listen or that they signed the forms just to get things moving without having time to ask questions or to reﬂect on the complex decision they were asked to make. In most hospitals, the surgical consent form is executed right before surgery. This is a good practice because it

provides some evidence that the patient consented to surgery. However, in most states, that form alone is not sufﬁcient to establish that you met your duty to your patient. We have both seen surgeons mismanage their relationship with their patient and their family in ways that have led to medical errors, an omission through miscommunication, or claims from patients that the surgeon failed to provide them with sufﬁcient information to make an informed decision about surgery: Here are three ways we have observed: (1) the surgeon acted as an all-knowing being; (2) no ofﬁce notes were kept about the consent discussion or the refusal of care; (3) the surgeon did not tell the patients about who would assist with their surgery.

Surgeon as All-Knowing Being If you have this aura and express it to your patients, then this is what they will expect. If you tell the patients

what surgery they need and just assure them that “everything will be ﬁne,” then you have taken complete responsibility for the decision making as well as the outcome. No wonder the patient (and the jury) will want to hold you 100% responsible for any negative outcome. Practice Pointer. Communication and decision making are a two-way street. Patients have responsibilities along with their rights. Share these responsibilities with the patient. Make the patient part of your health care team. Here are some ways to do that: ● Have brochures in your ofﬁce that explain ofﬁce hours,

after-hours call procedures, what to do in an emergency, and who to call in your ofﬁce if they are having problems after surgery. Tell them whether they are responsible for bringing their ﬁlms to the hospital. Also, the brochure can outline their role in follow-up after getting laboratory tests, diagnostic tests, especially from outside providers. Make sure they understand how to get to you if they think they are having a complication and need to be seen. If others will take calls for you, explain how that works. ●

Use American College of Surgeons or other specialized brochures, videos, and computer-

24

SECTION I: GENERAL CONSIDERATIONS

generated educational materials to supplement your discussion with patients regarding the alternatives, risks, and beneﬁts of the surgery you propose. Also direct them to websites that you think are accurate for basic information, if appropriate. You can provide a fact sheet that explains in detail why the surgery is performed, the alternatives, the risks, and what to expect after surgery. This can be handed out, not as a substitute for discussion, but as a supplement. Your staff can use a checklist to conﬁrm that the patient received the materials. Whereas this is not a substitute for discussion, it certainly helps support your argument that the patient was thoroughly informed about the surgery before the big day! ● If you send a patient for a magnetic resonance imaging (MRI) scan at an outside facility and they need to come back to discuss results, the order for the MRI should include a section that reminds them that it is their responsibility to obtain the ﬁlm and obtain a follow-up appointment. Many surgeons have the patient sign this acknowledgment. That is a good way to communicate that the patient is sharing responsibility for the implementation of the plan of care.

No Ofﬁce Notes about the Consent Discussion or the Refusal of Care A surgeon’s note, timed and dated contemporaneously with the event, is the best way to avoid subsequent allegations regarding lack of informed consent. Surgeons often fail to document the most important part of a discussion when a patient refuses care. The key part to document is that you told them the potential consequences of their refusal. A patient cannot make an informed decision about whether to have a surgery or a major diagnostic test without weighing what might happen if they do not have it. Example: “Told the patient that the lump was probably just a cyst but told her to go and have a mammogram.” It is easy to understand if the patient later says, “I trusted Dr. Smith when she said it was just a cyst, so it didn’t seem necessary to have the mammogram.” Practice Pointers. Make sure that you document not only the fact that you had a discussion about the surgery but also that you reviewed the risks, alternatives, and likely outcome if nothing was done. The note should state that the patient understood your explanations and that all questions were answered. ● If the patient has any additional risks or conditions that

make the surgery more risky, you need to document that portion of the discussion more extensively. ● When the patient refuses or seems like she or he is not going to have the surgery, you need to add details about your explanations of the risks of delay and the consequences of no treatment. This is often a good

time for a follow-up letter to the patient, sent by certiﬁed mail.

Not Telling Patients about Who Will Assist You with Their Surgery In general, patients will appreciate and understand that you cannot perform the surgery by yourself, but in most circumstances, you have a duty to explain who will be involved and what the assistants will be doing. Patients will also understand that sometimes others, including vendors and technical people, need to be present to assist with device placement. It is your job to make sure the patient agrees to that. Failing to explain these facts can result in claims for fraud or battery. You may also get testimony in a malpractice case that the patient never consented to having a resident do certain portions of the surgery. Practice Pointers ● If you are in a teaching hospital, you must explain what

the resident’s role will be and document that you had this discussion with the patient. ● If you are in a community hospital, you must explain who will be assisting you with surgery and what they will be doing. Document that discussion. ● If vendors or others will be present, the patient has a right to know and needs to consent. ● Some hospital consent forms include general language regarding assistants and others in the operating room, but you are the person that the patient agreed could perform the surgery, not others, so make sure the patient is clear about the role of others. These are fairly simple, straightforward concepts that need to be incorporated into your practice to make certain the patient is provided with all the facts before he or she consents to surgery.

LEGAL PITFALLS IN SURGICAL CARE AFTER THE OPERATING ROOM Murphy’s Law: If anything can go wrong, it will. When Murphy developed his law, he must have been partially thinking about health care providers. What else could explain why doctors and other health care personnel spend countless hours talking with patients about things that might go wrong during treatments and procedures? Why else are entire books like this written about surgical pitfalls if adverse outcomes do not actually occur? Whether a doctor is just ﬁnishing a residency program or is getting ready to retire, every doctor should know that you do not need to commit medical malpractice to get sued, you just have to have an unhappy patient—and nothing, we repeat, nothing, can make a patient or family more unhappy than an unexpected surgical complication.

3 LEGAL CONSIDERATIONS Part of the problem and shock can be ameliorated with a good, complete, preprocedure informed-consent discussion. That topic has already been dealt with in this chapter. Unfortunately, even the best informed-consent conversation or document, by itself, may not be enough to prevent a malpractice suit from being ﬁled. You are lucky, however, because when an adverse outcome occurs, you have a second chance to prevent a lawsuit from being ﬁled or, if it is destined to be ﬁled, to improve your chances of prevailing. Although most of these are common sense suggestions, in 30 years of litigating hundreds of medical negligence cases, we have both come to appreciate that common sense does not always rule when a serious injury or death occurs. Thus, a bit of repetition may prove helpful.

DOS AND DON’TS ● Don’t stop seeing or decrease the frequency of visits

with your patient or your patient’s family. When problems occur, this is the time for you to be the most visible. We cannot begin to tell you the number of

depositions we have taken in which the patient or the family complains that Dr. X “never seemed to be around to answer our questions after the surgery” or “I never saw Dr. X for the several days between the surgery and the death of my husband.” Rather than making the heart grow fonder, absence will make the patient or the family think that you do not want to face them and explain what occurred. We have known doctors who have called subsequent treating physicians to simply inquire about how the patient is doing and made note of those conversations in their ofﬁce charts. ● Do make sure that the family of the patient knows of your concern over what occurred. It is not an admission of liability to express condolences over death or to let a patient know that you are sorry they have suffered a complication. We have even known of surgeons who attended funerals of patients who died after a surgery. To ignore a problem leads the patient or the family to think you do not care. If a patient thinks you do not care about her or his welfare, you are much more likely to be included in any litigation. Remember, the general rule is that people do not sue people they like. The authors are frequently amazed at the number of times potential defendants in malpractice litigation are not sued even though a real question exists about whether their actions were a deviation from the standard of care. This topic is usually explored at deposition only to learn that the patient simply did not want to sue Dr. X because the patient liked him or her. ●

Don’t try to explain what occurred until you are sure of your facts and until your conclusion can be corroborated. Obviously, you are going to be ques-

25

tioned immediately by the patient or the family about what occurred. You will need to describe to them, from a factual standpoint, what you know up to that point. Just refrain from making conclusions as to the cause of problems. In most instances, you would not try to make a diagnosis without adequate data. Why do it now? The admonition not only applies to direct conversations with patients but also to documention. In a recent obstetric case, a baby was transferred to the neonatal intensive care unit (NICU) for a brachial plexus injury postdelivery. The neonatologist, who should have known better, reported that he was dealing with a newborn with an obvious brachial plexus injury caused by excessive traction. Not only was that conclusion shared with the parents in the following days, it was repeated during the pendency of the litigation. In fact, the defendant doctor vigorously denied that excessive traction was used, and had evidence to support that defense. The family and their attorney kept arguing that even the neonatologist concurred that negligence had caused the injuries at birth. It would have been a simple matter for the neonatologist to write “obvious brachial plexus injury, cause unknown at this time.” Similarly, in a recent laparoscopic appendectomy case on a 20-weeks’ pregnant patient, a general surgeon wrote, in a nonperforated appendix procedure, “that upon entering the abdomen, I saw purulent ﬂuid around the appendix.” What he really saw was a whitish exudate and not purulent ﬂuid because there was no source for the purulence in this nonperforated appendix simulation. Weeks later, the patient developed an infection after a spontaneous abortion, and the surgeon was sued for not starting antibiotics in the presence of purulence. The entire lawsuit, over 7 trial days, could possibly have been averted had he simply written that he visualized a white substance around the appendix rather than calling it purulence, especially because he had no information that it was. ● Do make complete records whenever an adverse outcome occurs including as much factual information as you can recall. The plaintiff’s attorney may argue that you are attempting to create a defense, your attorney will counter by arguing that you were attempting to facilitate the investigation or understanding of what occurred by providing the most detail possible. Any entry along these lines should be correctly dated and timed, so that there is no argument that someone was attempting to “alter” their records. ● Don’t ever, ever, alter your records. Even if your alteration, deletion, or addition is perfectly innocent, it will never appear that way. If, after an adverse outcome, you are found to have made a change to an existing record, that patient, their family, and most important, the jury will automatically assume you were attempting to delete a harmful notation and will not believe a word you say. Statistics tell us that approximately 70%

of all medical malpractice cases that go to trial

26

SECTION I: GENERAL CONSIDERATIONS

end up favorably for the health care provider. Clearly, that means that cases are won even in cases in which signiﬁcant injuries or death occurs. You can talk your way out of a bad outcome. You can never talk your way out of a lie. ● Do carefully read chart entries after an adverse outcome occurs and be sure to properly and timely note any disagreements you might have with the charted information. We know what you are thinking right now. You simply do not have time to read entries that should have been accurately charted by residents, colleagues, or consultants. Take the time. If you make your disagreement known contemporaneously with your review of the note, you can argue that there was a legitimate disagreement. Many of you sign off on notes written by others. A smart plaintiff’s attorney will start by getting you to agree that your countersignature on a note is your statement that you agreed with what was written. As you can see, making your disagreement known 2 years later, when you are in the midst of a malpractice case, will cause you to look like you are manufacturing a defense because you have already agreed that your signature is your statement that you agreed with the note. It will be further argued by your opponent that you now recognize how harmful that fact or comment is to your defense and that any reasonable doctor would have corrected that mistake earlier if, in fact, a disagreement really existed. ● Don’t ignore legitimate requests for medical records by a patient, a family member, or an attorney representing the patient. In many states, the time to respond to

these requests and the amount that can be charged are governed by statute. To ignore this type of request or to take too long to respond will cause the person making the request to question why the records were not sent and will again raise the specter that you are attempting to hide something. The records, in their entirety, should be timely copied and mailed, along with an appropriate letter, inquiring as to whether there is any other way you might be of assistance and again inquiring into the health of the patient or to pass along your sympathies. In another recent general surgery matter involving a failure to timely diagnose and treat a breast mass, the surgeon was accused of withholding information and falsifying his records when his ofﬁce took months to send out records, did so in a piecemeal fashion, and never sent out all the records. The case, ultimately won by the surgeon, could have been tried in a few days with the central issued being standard of care. Instead, the surgeon’s credibility became the central issue, and days were wasted calling present and past employees about record keeping and responding to record requests. The lists of Dos and Don’ts goes on forever and is far too numerous to cite, in its entirety, here. When you are faced with that inevitable, adverse outcome and you are questioning how you should be handling a particular situation, always ask yourself this question: How would my patient or a jury view my actions? Your choice might just be the thing to keep you from being sued or the exact thing that helps you win.

4

Preoperative Pitfalls Aimee M. Crago, MD, PhD and Stephen R. T. Evans, MD INTRODUCTION Although the hospital course of a patient is affected profoundly by what happens inside the operating room, many complications can be prevented by adequate preoperative preparation. Rates of postoperative myocardial infarction, decomposition of congestive heart failure, pneumonia, bleeding, and infection are all affected by identiﬁcation of a patient’s individual risk factors and medical optimization of the patient’s condition prior to surgery. A clear history and physical examination, reconciliation of a patient’s medication list, and consultation with appropriate specialists are the ﬁrst steps in ensuring that an operation will go as smoothly as possible, and that hospital length of stay and preoperative morbidity and mortality rates are maintained at a minimum.

INDICATIONS The surgeon should complete a mental, if not physical, checklist of preoperative risk factors and appropriate interventions for each patient who is scheduled for the operating room. There are no exceptions to this dictum. Even in emergent situations, knowledge of the patient’s comorbidities should be elucidated as soon as possible to aid in intraoperative and postoperative care.

PREOPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7

Neurologic evaluation and assessment of pain susceptibility Cardiac risk assessment and preoperative optimization Pulmonary risk assessment and preoperative optimization Screening for advanced liver disease Assessment of renal function Assessment of infection risk and wound healing ability Assessment of nutritional status

Assessment of bleeding risk and identiﬁcation of the hypercoagulable patient Step 9 Identiﬁcation of endocrine dysfunction Step 10 Documentation of the family history Step 8

PREOPERATIVE EVALUATION Neurologic Evaluation and Assessment of Pain Susceptibility Failure to Recognize Carotid Disease ● Consequence The incidence of ischemic stroke ranges from less than 1% for elective surgery procedures to as much as 10% in post–coronary artery bypass graft (CABG) patients with concurrent carotid disease.1 Grade 4/5 complication ● Intervention Therapy for patients after cerebrovascular accident (CVA) is mainly supportive, centering on blood pressure control and rehabilitation to maximize functional outcomes. More aggressive therapy in the form of intra-arterial thrombolysis may be considered only in the ﬁrst hours after stroke. Functional outcomes with thrombolysis appear similar to those seen in nonoperative stroke victims. Retrospective studies do, however, show a 25% chance of surgical site bleeding. Mortal complications have been reported with thrombolysis after craniotomy, so this treatment should not be employed in this population.2 ● Prevention The low incidence of stroke in postoperative patients without history of transient ischemic attack (TIA) or CVA means that preoperative screening of the asymptomatic patient is likely unwarranted. However, rates of CVA increase in the general surgery population with symptoms and are noted to range from 3% to 4% in those with a known carotid stenosis or positive history. Similar outcomes are seen in patients undergoing major

28

SECTION I: GENERAL CONSIDERATIONS Table 4–1 Alternative to Intravenous Narcotics in the Postoperative Patient

Prior stroke? Yes

Carotid ultrasound

No

Yes

Symptoms of carotid disease?

Greater than 60% stenosis? Yes

Carotid endarterectomy

Drug

Contraindications/Side Effects

Nonsteroidal anti-inﬂammatory drugs (e.g., ketorolac)

Renal dysfunction/acute renal failure

Dextromethorphan

Seizure, arrhythmia, brain damage

Cyclo-oxygenase 2 inhibitors

Cardiovascular disease, renal dysfunction/acute renal failure, gastrointestinal bleeding

Acetaminophen

Hepatic dysfunction

Neurontin

Somnolence, dizziness, fatigue

Local anesthetic

Seizure, arrhythmia

Ketamine

Psychotropic effects

Peripheral nerve block • Axillary nerve block • Supraclavicular nerve block • Interscalene nerve block • Paravertebral nerve block • Lumbar plexus block • Femoral nerve block • Sciatic nerve block

Seizure, arrhythmia

Epidural anesthesia

Seizure, arrhythmia, hypotension

No No

OR

Figure 4–1 Algorithm for preoperative evaluation for carotid disease.

vascular surgery.3 It seems prudent, therefore, that carotid endarterectomy (CEA) should, where possible, precede elective general or vascular surgery procedures in patients with known cerebrovascular disease (Fig. 4–1). This recommendation would be concordant with that applied to patients with carotid disease and requiring coronary artery revascularization (CABG). Debate still exists as to the timing of CEA versus CABG, but in the setting of asymptomatic coronary artery disease (CAD), the carotid is addressed ﬁrst to decrease the rate of CVA at the time of CABG (10%–5.3%). Conversely, risks of comorbid cardiac disease must be considered in the context of asymptomatic carotid disease, because delay of coronary revascularization to allow recovery from CEA leads to an increase in overall mortality (9.4%) despite low rates of stroke.4 The possibility of concurrent CEA and CABG has been explored, but its role is controversial.

Failure to Recognize Low Pain Threshold ● Consequence Tachycardia, pneumonia, and opioid withdrawal are consequences of failure to recognize low pain threshold. Chronic pain patients are often recognized at presentation for elective general surgery procedures. These patients develop tolerance to opioids, and hyperalgesia manifests as increased sensitivity to pain and high analgesia requirements compared with those in opioidnaïve patients. Excessive pain increases the risk of both postoperative pulmonary (owing to splinting and poor mobilization) and cardiac complications. Patients inadequately treated may develop symptoms of nausea, vomiting, and hemodynamic instability consistent with narcotic withdrawal. Grade 1 complication

● Intervention Opioid dosing remains the mainstay of postoperative pain control. However, the use of adjuvant therapies, such as those presented in Table 4–1, has been shown to reduce opioid requirements and may aid in treatment of postoperative pain in patients with chronic pain. Intravenous (IV) narcotics should be used to treat symptoms of opioid withdrawal.5 ● Prevention A patient’s daily dosage of narcotics as well as expectations for postoperative pain should be discussed prior to surgery, and a perioperative pain regimen should be planned between patient, surgeon, and anesthesiologist. Standing doses of preoperative pain regimens should not be stopped pre- or perioperatively. In the case of gastrointestinal (GI) surgeries, oral medications should be substituted with IV equivalents after surgery to prevent withdrawal.5 In addition, patients will require supplemental narcotics, two to four times the doses required by opioid-naïve patients, for adequate pain control.6,7 Narcotics can, in part, be effectively administered by continuous infusion through patientcontrolled analgesia (PCA), which will also provide an efﬁcient means for delivery of supplemental drugs.5 Adjuvant therapies such as those outlined in Table 4–1 have been shown to reduce postoperative opioid requirements in patients with chronic pain. Of note, epidurals should utilize lipophilic narcotics because these are more effective in patients with chronic pain and should not replace IV narcotics because such management could

4 PREOPERATIVE PITFALLS Table 4–2 Commonly Used Narcotics and Their Approximate Conversion Drug

Oral Dose

Intravenous Dose

Hydrocodone

30 mg q3h

—

Hydromorphone

7.5 mg q3h

1.5 mg q3h

Fentanyl

—

0.1 mg q1h

Meperidine

300 mg q3h

100 mg q3h

Morphine

30 mg q3h

10 mg q3h

Oxycodone

30 mg q3h

—

Box 4–1

Sedation Scales

Ramsey Sedation Scale 1 2 3 4 5 6

Anxious, agitated, restless Cooperative, oriented, and tranquil Sedated but responds to commands Asleep; brisk response to glabellar tap or loud auditory stimulus Asleep; sluggish response to light glabellar tap or loud auditory stimulus Asleep; no response to deep painful stimulus

Richmond Agitation-Sedation Scale (RASS) +4 Combative

result in withdrawal. Partial opioid agonists such as buprenorphine or nalbuphine should also be avoided because they too may cause withdrawal.5 Transition to an oral regimen provides another challenge for patient and clinician. The equivalent to the daily postoperative narcotic requirement can be calculated (Table 4–2) and prescribed in part (generally one half the requirement) as long-acting oral opioids such as oxycodone or methadone. Intermittent breakthrough doses of short-acting medications can be prescribed to fulﬁll the remainder of the daily requirement and can be slowly tapered to return the patient to his or her baseline narcotic regimen over a 2- to 4-week period.5

Failure to Recognize Alcohol Dependence ● Consequence Alcohol withdrawal syndrome (characterized by tremor, insomnia, agitation, hypertension, diaphoresis, fever, nausea, vomiting, and hallucinations) may precede delirium tremens (DT) and result in cognitive change, hallucination, and seizure. Alcohol dependence is common in surgical patients. Patients with cancers of the oropharynx and GI tract often have comorbid alcohol dependence, and more than one third of trauma patients may be alcohol dependent. Less than one quarter of these patients are recognized preoperatively or on admission, resulting in high rates of withdrawal symptoms and requiring admission to the intensive care unit (ICU) for hemodynamic and neurologic monitoring as well as aggressive medical intervention.8 Grade 1/4/5 complication ● Intervention Multiple meta-analyses have looked at the treatment of patients with alcohol withdrawal and DT. Sedativehypnotic drugs, generally benzodiazepenes, appear to be the most effective medications for preventing alcohol withdrawal seizures and related mortality once symptoms of withdrawal occur. The choice of benzodiazepene is based on desired onset and duration of action, with IV dosing providing the most rapid effect, and long-acting medications being associated with fewer breakthrough symptoms but higher rates of oversedation. Intermittent doses of diazepam or lorazepam can

29

+3 Very agitated +2 Agitated +1 Restless

0 Alert and calm −1 Drowsy −2 Light sedation −3 Moderate sedation −4 Deep sedation −5 Unarousable

Overtly combative or violent, immediate danger to staff Pulls on or removes tubes or catheters, aggressive behavior toward staff Frequent nonpurposeful movement or patient-ventilator dyssynchrony Anxious or apprehensive but movements not aggressive or vigorous Not fully alert, sustained (>10 sec) awakening, eye contact to voice Brieﬂy (<10 sec) awakens with eye contact to voice Any movement (but no eye contact) to voice No response to voice, any movement to physical stimulation No response to voice or physical stimulation

Adapted from Ramsey MAE, Savege TM, Simpson BRJ, et al. Controlled sedation with alphaxalanoe-alphadolone. BMJ 1974;2:656– 659; and from Sessler C, Gosnell M, Grap MJ, et al. The Richmond agitation-sedation scale. Validity and reliability in adult intensive care patients. Am J Respir Crit Care Med 2002;166:1338.

be repeated until sedation is achieved and then administered hourly to maintain sedation.9 Affects of benzodiazepine and adjuvant medications should be titrated for light sedation (patient is easily aroused from sleep) against an objective sedation scale such as the Ramsey Sedation Score10 or the Richmond Agitation-Sedation Scale11 (Box 4–1). Patients can be weaned from treatment medications by titrating for symptoms evaluated in relation to these tools. Prescription of clonidine, haldol, or propofol for persistant symptoms can be beneﬁcial as an adjunct to benzodiazepenes, but these drugs have not been shown to prevent seizure when given as monotherapy.8,9 Supplementation of IV ﬂuids with magnesium, thiamine, and folate can correct deﬁciencies seen in many patients with alcohol dependence. ● Prevention (Fig. 4–2) A thorough history will elicit a history of alcohol use in many patients with symptoms of liver disease.

30

SECTION I: GENERAL CONSIDERATIONS

Trauma? Yes

Blood alcohol level elevated? Yes

No

Pre-op evaluation with greater than 3 CAGE questions answered affirmatively? No

Prophylaxis with benzodiazepenes to maintain Ramsey score 2–4

Any CAGE questions answered ‘yes’ or abnormal labs?

Yes

Repeat history and physical, consider post-operative prophylaxis

Yes

Prophlaxis with benzodiazepenes to maintain Ramsey score 2–4

No

Post-operative symptoms of withdrawal (tachycardia, agitation, etc.)? Yes

Intravenous benzodiazepenes with intermittent doses of these and adjunct medications (clonidine, haldol, etc) for symptoms

Box 4–2 ● ● ● ●

CAGE Questions

Have you ever felt you should cut down on your drinking? Have other people annoyed you by criticizing your drinking? Have you ever felt guilty about drinking? Have you ever taken a drink in the morning to steady your nerves or get rid of a hangover (eye opener)?

Adapted from Ewing JA. Detecting alcoholism: the CAGE Questionnaire. JAMA 1984;252:1905–1907. Copyright © 1984, American Medical Association. All rights reserved.

Laborotory values may be helpful in that elevated liver function tests and γ-glutamyltransferase (GGT) may conﬁrm suspected alcohol use. Alcoholic patients may be anemic with a high mean corpuscular volume (MCV). The CAGE questionnaire (Box 4–2) is commonly applied to identify those patients with suspected alcohol dependence.12 Answering yes to three of the CAGE questions is strongly correlated with alcohol dependence, and patients who do so should be placed on perioperative DT prophylaxis. Afﬁrmative answers to any of the CAGE questions or laboratory values suggestive of alcohol dependence should prompt consideration of postoperative prophylaxis, as should an elevated blood alcohol level measured on admission of a trauma patient.8 Standard dosing regimens for prophylaxis include regular administration of diazepam or lorazepam. Again,

Figure 4–2 Algorithm for prevention and management of alcohol withdrawal in the surgical patient.

haldol and clonidine can be employed for breakthrough symptoms, and patients should be monitored for signs of psychomotor agitation, hemodynamic instability, and cognitive changes.8

Cardiac Risk Assessment and Preoperative Optimization Failure to Recognize or Medically Optimize the Patient with Ischemic Heart Disease or Congestive Heart Failure ● Consequence Myocardial infarction (MI) and congestive heart failure (CHF) seen as consequences of subsequent left ventricular dysfunction. Physiologic stress related to operative procedures and altered rapid eye movement (REM) sleep secondary to anesthesia are known to be associated with postoperative MI. In high-risk populations, rates of postoperative MI have historically approached 50%. Risk factors for a postoperative cardiac event were ﬁrst described by Goldman and colleagues in 1977,13 but these have been reﬁned in numerous studies, as described later. Grade 1/4/5 complication ● Intervention Treatment for patients with postoperative MI centers on reduction of oxygen demand and decrease in after-

4 PREOPERATIVE PITFALLS load. β-Blockers reduce heart rate and have been shown to have a positive effect on mortality after MI. Nitroglycerin dilates coronary arteries and improves oxygen delivery to the myocardium in patients with ongoing discomfort. This drug also treats CHF and hypertension. Aspirin is indicated in the setting of acute MI, and supplemental oxygen should be prescribed. Patients with ongoing chest pain or hemodynamic instability should be evaluated for emergent cardiac catheterization.14 The risk of bleeding associated with ﬁbrinolytic therapy makes this option less feasible in the postsurgical patient than in the general population of cardiac patients. Patients with symptoms of ﬂuid overload and CHF may require ionotropic agents such as dopamine or placement of an intra-aortic balloon pump. Diuretics are appropriate for preventing pulmonary edema. These drugs should also be administered to patients with CHF recognized preoperatively and who are experiencing episodes of postoperative decompensation. ● Prevention Patients should undergo a complete preoperative history and physical examination. Those with cardiac symptoms or over age 40 require a baseline echocardiogram. This evaluation is aimed at identifying factors

31

contributing to perioperative cardiac risk and was published in the American College of Cardiology/ American Heart Association Guidelines for Perioperative Cardiac Evaluation for Noncardiac Surgery (Tables 4–3 and 4–4). Based on this risk stratiﬁcation and the risk of the planned procedure (see Table 4–3), indications for further preoperative testing can be easily identiﬁed (see Table 4–4). With few exceptions, patients with only minor risk factors can generally undergo surgery without further testing whereas those with major risk factors may require preoperative coronary angiography and medical optimization. Patients at intermediate risk for surgery have traditionally been advised to undergo noninvasive testing in the form of exercise or chemical stress tests to further stratify their perioperative risk of MI. If reversible perfusion defects are observed on stress testing, coronary angiography before intermediate or high-risk procedures is advisable.15,16 β-Blockade has become the mainstay of pharmacotherapy for prevention of postoperative MI. In randomized, prospective studies, patients at risk for cardiac events were given β-blockers in the perioperative period and had reduced incidences of ischemic events and mortality.17–19 This has been borne out in a recent meta-analysis.20 When patients are stratiﬁed according to the Revised Cardiac

Table 4–3 Preoperative Cardiac Risk Stratiﬁcation

Adapted from recommendations in Eagle KA, Berger PB, Calkins H, et al. ACC/AHA Guideline Update for Perioperative Cardiovascular Evaluation for Noncardiac Surgery—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Circulation 2002;105:1257–1267.

32

SECTION I: GENERAL CONSIDERATIONS

Table 4–4 Preoperative Evaluation for Ischemic Heart Disease

Adapted from recommendations in Eagle KA, Berger PB, Calkins H, et al. ACC/AHA Guideline Update for Perioperative Cardiovascular Evaluation for Noncardiac Surgery—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Circulation 2002;105:1257–1267.

Box 4–3 Revised Cardiac Risk Index (Indications for Preoperative b-Blockers)

Adapted from Lee TH, Marcantanio ER, Mangione CM, et al. Derivations and prospective validation of a simple index for prediction of cardiac risk of major non-cardiac surgery. Circulation 1999;100:1043–1049.

Risk Index (Box 4–3), those with three risk factors clearly beneﬁt from preoperative β-blockade in conjunction with high-risk procedures; those with no risk factors do not require the drug.21,22 Intermediate-risk patients are likely helped and, in the absence of clear contraindications, should be prescribed the drugs. In the context of widespread prescription of β-blockers, risks of perioperative cardiac complications have signiﬁcantly decreased. In fact, a contemporary study suggested that preoperative stress tests may no longer beneﬁt patients at intermediate risk because revascularization does not improve outcomes after high-risk surgery in certain populations but simply delays the timing of the procedure.23 In a manner similar to that of β-blockers, recent evaluation of α2-agonists suggests that these medications may prevent perioperative cardiac events.20 Special attention should be paid to patients with a preoperative diagnosis of CHF. These patients should have a preoperative echocardiogram to delineate function of the ventricles. Fluid resuscitation should be carefully monitored and diuretics used to increase urine production during remobilization (postoperative day 2–3). Stopping these medications postoperatively when patients take them on a regular basis can result in oliguria because renal function is often dependent on loop diuretics after longterm use.

Failure to Recognize Risk of Atrial Fibrillation ● Consequence A rapid ventricular response to atrial ﬁbrillation can lead to hemodynamic instability; intraventricular clots can cause thromboembolic events. Risk factors for development of postoperative atrial ﬁbrillation include type of procedure (cardiac and thoracic surgery), prior history of arrhythmia, and age over 60. Grade 1/4/5 complication ● Intervention Rate control is known to produce improvement in blood pressure, allowing for adequate preload. Boluses of drugs such as calcium channel blockers (e.g., diltiazem) or β-blockers (e.g., lopressor, esmolol, or labetolol) can rapidly improve rate. These drugs should not be used in tandem because together they can cause fatal bradyarrhythmias. Cardioversion is more often accomplished using antiarrhythmics such as amiodorone. Electrical cardioversion may be necessary in the hemodynamically unstable patient. No clear difference in long-term outcomes has been demonstrated between rate control and antiarrhythmic therapies.24 However, contraindications to the drugs may dictate therapy. β-Blockers are inappropriate in advanced chronic obstructive pulmonary disease (COPD), and amiodorone can cause severe pulmonary toxicity when administered intravenously after lung resection.25 Additional roles have been identiﬁed for drugs such as adenosine that can slow the heart rate, at least transiently, to deﬁne the underlying rhythm. Potassium and magnesium should be administered to maintain serum levels greater than 4 mEq/L and 2 mEq/L, respectively, stabilizing myocardial muscle ﬁbers. Anticoagulation should be considered after 48 hours of atrial ﬁbrillation to reduce the risk of thromboembolic events.25 ● Prevention Recent meta-analyses have examined the role for preoperative pharmacologic treatment to reduce rates of

4 PREOPERATIVE PITFALLS postoperative atrial tachyarrhythmias in cardiac and thoracic patients. Those patients with risk factors such as age and requirement for pneumonectomy have been prescribed preoperative β-blockers. This reduces the incidence of postoperative atrial ﬁbrillation by more than one half. Calcium channel blockers have similar effects in patients undergoing noncardiac thoracic surgery, and atrial pacing can improve outcomes in CABG patients. Preventive treatment with magnesium, amiodarone, or ﬂecanide may prove beneﬁcial, but in this context, the actions of these drugs are incompletely described.26,27

Pulmonary Risk Assessment and Preoperative Optimization Failure to Recognize Obstructive Sleep Apnea ● Consequence Obstructive sleep apnea (OSA) affects 2% to 5% of the population. It results from failure to protect the oropharyngeal airway during periods of REM sleep. In the healthy patient, this results in arousal and resetting of the respiratory drive. However, the addition of sedation and alterations in sleep rhythm associated with postoperative pain control and anesthesia can produce multiple OSA-related complications, including hypertension, MI, and death.28 Grade 1/4/5 complication ● Intervention Initiation of continuous positive airway pressure (CPAP) should be considered when patients have observable apnea, although no controlled studies have proved its efﬁcacy. Treatment of hypertension may require invasive monitoring and IV antihypertensive medications including α- and β-blockers. Arrhythmias and myocardial ischemia are treated with rate control and supportive care, as described in prior sections. Narcotics should be limited and supplemented with alternative drugs. Benzodiazepenes should be strictly avoided. ● Prevention As with many preoperative pitfalls, preventing the complications of OSA begins with recognition of the patient with the disorder. A thorough history and physical examination should seek to identify those patients with a known history of OSA and those with witnessed snoring and apneic episodes at night. A thick neck and obesity are both associated with OSA. Although sleep testing (polysomnography) remains the “gold standard” for identifying OSA patients, it may not be feasible, owing to lack of access, to preoperatively test all patients with risk factors.28 Patients with OSA should not be prescribed benzodiazepenes because resultant muscle relaxation further compromises the airway. Opioids blunt patient response to

33

hypercarbia and hypoxia, resulting in a tendency toward apnea, and their use should be minimized. Those adjuvant drugs listed in Table 4–1 can be used to decrease narcotic requirements. Continuous pulse oximetry sufﬁces for monitoring OSA patients in cases in which multiple comorbidities, high narcotic requirements, or hypertensive volatility are not noted. If these issues are of concern, ICU monitoring may be warranted in the OSA patient (Fig. 4–3). As noted previously, patients with known or suspected diagnosis of sleep apnea should be prescribed CPAP in the pre- and postoperative periods. Patients with observed episodes of apnea should also be considered for treatment. No level-one data have shown clear beneﬁt with use of short-term CPAP, although small studies suggest that patients with OSA on preoperative CPAP may have better blood pressure control and fewer postoperative complications.29

Failure to Recognize and Treat Chronic Pulmonary Disease ● Consequence Postoperative pulmonary complications are common with prevalences ranging from 6% to 76% based on the type of procedure and the deﬁnition of complications. Pneumonia, respiratory failure, bronchopleural ﬁstula, atelectasis, and pneumothorax all contribute to postoperative morbidity and mortality. American Society of Anesthesia (ASA) Preoperative Assessment score and COPD are both major risk factors for the development of postoperative pulmonary complications. Special attention should be paid to patients undergoing open thoracic and upper abdominal surgeries, those receiving general anesthesia, the elderly, the obese, known smokers, and the malnourished.30 Grade 1–5 complication ● Intervention Treatment of postoperative pulmonary complications is mainly supportive. Pneumonia mandates antibiotic therapy; chest tube insertion will improve function for patients with pneumothorax; and mechanical ventilation can improve oxygenation and acid-base disturbances in patients with respiratory failure. Respiratory therapy including bronchodilators and chest therapy can balance the effects of underlying lung disease and should be routinely prescribed. Incentive spirometry and CPAP can be considered as means to increase both forced vital capacity (FVC) and functional residual capacity (FRC) in patients with postoperative atelectasis. ● Prevention Adequate patient selection and preparation as well as preoperative planning have been the primary means of preventing postoperative pulmonary complications. In patients undergoing low-risk surgery, history and

34

SECTION I: GENERAL CONSIDERATIONS

Pre-op diagnosis of sleep apnea? Yes

No

Risk factors for OSA (thick neck, apneic episodes, heavy snoring)? Yes

Pre and post-op CPAP

Positive

Consider sleep study.

No

OR

Post-operative apnea Post-operative hypertensive crises, high narcotic requirements Yes

Consider ICU

No

Continuous pulse oximetry, minimize narcotics and benzodiazepenes.

physical examination can generally identify those at risk. Complaints of dyspnea or unexplained fevers or a history of extensive cigarette smoking necessitates further evaluation by spirometry. In these patients and those with active pulmonary symptoms, a period of pulmonary rehabilitation, including intense bronchodilator therapy and respiratory exercises, may improve surgical outcomes. When possible, incentive spirometry training should be initiated prior to elective surgery. Baseline chest radiographs should be documented in patients of advanced age or with any risk factors for pulmonary complications.30 Special consideration must be made in patients undergoing thoractomy, esophagectomy, open heart surgery, and upper abdominal surgeries. Signiﬁcant changes in postoperative lung volumes, pain associated with operative incisions, and temporary paralysis of the phrenic nerve contribute to higher rates of postoperative pulmonary complications. Spirometry is recommended before these procedures to deﬁne the degree of underlying lung disease and is essential in patients undergoing pulmonary resection. A forced expiratory volume measured over 1 second (FEV1) of greater than 2.0 has traditionally indicated that a patient is able to undergo pneumonectomy, whereas an FEV1 greater than 1 to 1.5 L is essential for lobectomy. In instances in which these volumes are not noted, a patient may undergo split lung function studies. A postoperative predictive value of 40% normal is generally indicative of a candidate with acceptable risk for surgery. In cases of patients with borderline function, risk stratiﬁca-

Yes

Consider post-op CPAP, continuous pulse oximetry, minimize narcotics and benzodiazepenes.

Figure 4–3 Algorithm for perioperative management of patients with known or suspected sleep apnea.

tion can be further deﬁned by exercise tolerance testing30,31 (Fig. 4–4). In addition to preoperative pulmonary rehabilitation to improve lung function, several other options have been addressed to aid in prevention of pulmonary complications. Epidural anesthesia has been suggested as a means to minimize pulmonary complications, although studies differ on the actual beneﬁt associated with this therapy. Laparoscopic surgery appears to reduce the postoperative pulmonary risk over those of comparable open procedures though this may not be a viable option in COPD patients.32 Smoking cessation for greater than 8 weeks preoperatively decreases pulmonary morbidity, as discussed later.

Screening for Advanced Liver Disease Failure to Recognize Advanced Liver Disease ● Consequence Surgery in patients with either acute or chronic liver disease can result in decompensation. Patients are noted to have worsening coagulopathy with ascites, encephalopathy, hemodynamic instability, and renal failure. Death can result. Grade 1/4/5 complication ● Intervention Care of the postoperative patient with liver disease is supportive. Bleeding must be treated with transfusion of fresh frozen plasma and platelets to correct elevated

4 PREOPERATIVE PITFALLS

• Esophagectomy • Cardiac surgery • Abdominal surgery

• Lobectomy

• Pneumonectomy

FEV1 >1 to 1.5L

FEV1 >2L

Yes

FEV1 >40% predicted on split-lung function studies

Yes

Figure 4–4 Algorithm for preoperative pulmonary evaluation in patients with lung disease.

prothrombin time and thrombocytopenia, respectively. Ascites may respond to diuretics. Therapeutic paracentesis provides temporary relief to patient with restrictive lung physiology secondary to ascites. Hyponatremia is treated with free water restriction. Encephalopathy requires prescription of lactulose with or without enteral antibiotics such as neomycin. Hemodynamic instability may require pressor support. Patients with hepatorenal syndrome may be initially treated with ﬂuid resuscitation, although hemodialysis is eventually required in many instances. ● Prevention Initial screening for liver disease comprises a thorough history and physical examination. Risk factors for cirrhosis including infection with hepatitis B or C, history of alcohol abuse, or less commonly genetic diseases such as Wilson’s disease and hematochromatosis should be elucidated. Physical stigmata of cirrhosis include spider angiomata, caput medusa, ﬂuid wave on abdominal examination, palmar erythema, gynecomastia, and jaundice. In the case of risk factors or suspected liver disease, liver function tests (LFTs) and coagulation studies should be ordered. Traditionally, risk stratiﬁcation in the cirrhotic patient has been assessed using the Child-Pugh classiﬁcation33 (Table 4–5). Although patients with class A cirrhosis can generally undergo surgery with relative few complications, those with more advanced disease have high rates of complications and death (see Table 4–5). Careful weighing of the beneﬁts of surgery should be made before counseling the patient, and symptoms of liver disease should be controlled by optimal medical management (e.g., cor-

Yes

No

Pre-operative bronchodilators, pulmonary exercise, smoking cessation

Pre-operative bronchodilators, pulmonary exercise, smoking cessation

No Consider exercise tolerance testing versus non-operative management

• OR • Consider local anesthesia (vs. general) and minimally invasive surgical approaches

35

• OR • Consider local anesthesia (vs. general) and minimally invasive surgical approaches

Table 4–5 Child-Pugh Class System Assignment of Points Points

1

2

3

Albumin (g/dl)

>3.5

2.8–3.5

<2.8

Bilirubin (mg/dl)

<2

2–3

>3

Prothrombin time (sec prolonged)

1–3

4–6

>6

Encephalopathy

None

Controlled

Dense

Ascites

None

Controlled

Refractory

Calculation of Class (sum points for individual values) Total Points

Child’s Class

Mortality Rate after Open Abdominal Surgery (%)

5–6

A

10

7–9

B

30

>9

C

80

rection of coagulopathy, treatment of encephalopathy with lactulose) before proceeding to the operating room. More recently, several small series assessed the role of the model for end-stage liver disease (MELD) score in preoperative work-up34 (Eq. 1). The MELD score has the beneﬁt of requiring no objective interpretation by the clinician. MELD score and Child-Pugh class appear to correlate well. To date, speciﬁc recommendations regarding risk versus MELD score have been incompletely deﬁned, although a score greater than 15 appears to

36

SECTION I: GENERAL CONSIDERATIONS

predict mortality above 15%, MELD greater than 25 predicts mortality above 25%, and MELD greater than 35 predicts mortality above 50%.35

(Eq. 1)

3.8 × ln(bilirubin [mg/dl]) + 11.2 × ln(International Normalized Ratio [INR]) + 9.6 ln(creatinine [mg/dl])

In patients with an acute abdomen and signs of liver disease, care should be taken to avoid misdiagnosis of spontaneous bacterial peritonitis (SBP). The physical examination in patients with SBP and acute inﬂammatory processes can be similar, but exploratory laparotomy runs the risk of patient decompensation if the true diagnosis is SBP.

Assessment of Renal Function Failure to Recognize Renal Dysfunction ● Consequence Acute renal failure (ARF) may occur in 4% to 8% of critically ill patients in the ICU, and a signiﬁcant proportion of these patients will require hemodialysis. The most common causes of ARF in postsurgical patients are prerenal azotemia and acute tubular necrosis (ATN) related to administration of IV contrast or other nephrotoxic agents (Box 4–4). Postrenal causes of ARF are often related to malfunction of indwelling catheters and prostatic hypertrophy.36,37 Grade 1/4/5 complication

Box 4–4 Commonly Used and Encountered Nephrotoxic Agents ● ●

● ● ● ●

● ● ● ● ● ● ●

Iodinated contrast dye Antibiotics ● Vancomycin ● Aminoglycosides ● Rifampin ● Cephalosporins ● Penicillins ● Amphotericin B Furosemide Angiotensin-converting enzyme inhibitors Angiotensin II receptor antagonists Chemotherapeutics ● Cisplatin ● Cyclosporine ● Tacrolimus ● Allopurinol ● Mitomycin Cocaine H2 receptor antagonists Phenytoin Volatile hydrocarbons Myoglobin Calcium Endotoxin

● Intervention Treatment of ARF begins with ﬂuid resuscitation. A central venous pressure of 10 to 12 mm Hg (in the absence of signiﬁcant cardiac dysfunction) can conﬁrm that intravascular volume is sufﬁcient. A Swan-Ganz catheter may be required for more invasive monitoring if additional clariﬁcation about cardiac contribution to renal perfusion is needed. Nephrotoxic agents such as those listed in Box 4–4 should not be prescribed. Supportive care with hemodialysis should not be taken lightly because ﬂuid shifts related to this treatment may induce further damage to the kidney. Unremitting acidosis, hyperkalemia, or uremia in the context of renal failure cannot be deﬁnitively treated in any other manner, however. Recent studies examined the role of fenoldopam in preventing progression in patients with early ATN. These studies did not show a consistent improvement in patients receiving the drug, but some subgroups of patients may beneﬁt from its administration. Dopamine has no role in the treatment of ATN.36 ● Prevention Prevention of ARF begins with recognizing the patient at risk for ARF (Box 4–5). Fluid hydration is essential for those receiving nephrotoxic agents.38 N-Acetyl cysteine can improve outcomes in patients with chronic renal insufﬁciency (CRI) requiring IV contrast agents.39 Bicarbonate given in conjunction with IV contrast agents is believed to act as a scavenger for free radicals related to these agents and appears to provide some degree of renal protection.40 Serum levels of nephrotoxic agents should be routinely measured to prevent supratherapeutic dosing whenever possible (e.g., IV administration of vancomycin, gentamicin, and tobramycin). In all other instances, pharmacologic agents should be prescribed after calculation of the patient’s creatinine clearance as described by Cockroft and Gault41 (Eq. 2). This value is adjusted by a factor of 0.85 in females.

Box 4–5 Risks for Acute Renal Failure in the Surgical Patient ●

Surgical procedure Cardiac surgery ● Aortic cross-clamping ● Liver or renal transplantation Diabetes/preoperative chronic renal failure Underresuscitation Sepsis Burn injury Liver disease Cardiac failure Ureteral injury Nonfunctioning indwelling catheter ●

● ● ● ● ● ● ● ●

4 PREOPERATIVE PITFALLS (Eq. 2) (140 − age [in yr]) × (weight [in kg]/0.81) × (serum creatinine [in μmol/L])

Assessment of Infection Risk and Wound Healing Ability Failure to Administer Preoperative Antibiotics ● Consequence Rates of wound infection are related to the type of procedure and range from 1.5% in clean cases (those in which there is no associated inﬂammation and no entry into the alimentary, respiratory, or genitourinary tracts during surgery) to 40% in dirty cases (those with frank contamination related to infection or foreign body). Risk factors for development of wound infection include the length of procedure (>75th percentile compared with similar cases), age, diabetes, poor nutritional status, obesity, and an ASA score of 3, 4, or 5. Immunosuppresive medications including steroids can further increase rates of poor wound healing and surgical site infection.42 Grade 1–5 complication ● Intervention Treatment of surgical infections revolves around drainage of abscess collection. This can be accomplished by opening the skin incision when infections involve the subcutaneous tissues. Abscess cavities within the surgical site may require reoperation for drainage or the placement of a percutaneous drain. Cultures should be obtained, and antibiotics started empirically at the time of diagnosis should be tailored based on culture results. For superﬁcial infections with likely pathogens being Staphylococcus and Streptococcus, ﬁrst-generation cephalosporins or penicillin derivatives are adequate coverage except when methicillin-resistant Staphlyococcus aureus (MRSA) is suspected, necessitating treatment with linezolid or vancomycin. For infections related to pathogens of the respiratory or alimentary tract, combination therapy aimed at anaerobic organisms and

37

gram-negative bacteria should be employed. Metronidazole with ﬂuoroquinolones, piperacillin-tazobactam combinations, second-generation cephalosporins, and carbepenams are frequently used combinations. ● Prevention Prevention of wound infection relies on the administration of preoperative antibiotics (Table 4–6). Studies indicate that the proper timing of antibiotic administration is half an hour before incision, corresponding with induction of anesthesia. If surgery lasts longer than 2 half-lives of an antibiotic, additional dosing should be considered. Dilution related to high-volume transfusion should also prompt readministration.42 Although clean cases were historically not believed to warrant preoperative antibiotics, this is still debated; beneﬁts have been suggested in numerous studies, especially in instances in which clean cases involve placement of a prosthetic mesh as in herniorrhaphy.43,44 Antimicrobials acting against staphylococcal and streptococcal species should be administered preoperatively in these instances. Broader-spectrum drugs or combination regimens such as those discussed previously are more appropriate as prophylaxis for surgeries involving the bowel and the respiratory and genitourinary tracts. A signiﬁcant decrease in rates of infection after surgery on the bowel was initially reported when a preoperative bowel regimen with both mechanical and antimicrobial preparations was used to decrease the quantity of intraluminal bacteria. Although several randomized trials questioned this practice,45 the standard of care among surgeons remains mechanical bowel preparation with or without oral neomycin and erythromycin prior to elective procedures.46

Incomplete Tobacco Use History ● Consequence Complications related to an incomplete tobacco use history include poor wound healing, dehiscence, wound

Table 4–6 Perioperative Wound Infections and Prevention Rate of Infection (%)

Deﬁnition

Preoperative Antibiotics

Clean

1.5

• No inﬂammation • No entry into GI, GU, or respiratory tract

• First-generation cephalosporin • Vancomycin

Clean-contaminated

7.7

• Minor break in technique • Entry into GI, GU, or respiratory tract with no spillage

• Metronidazole with ﬂuoroquinolones • Piperacillin-tazobactam • Second-generation cephalosporins • Carbepenams

Contaminated

15.2

• Major break in technique • Entry into GI, GU, or respiratory tract with spillage • Traumatic wound

Dirty

40

• Gross purulence • Fecal contamination • Traumatic wound with delay in treatment

GI, gastrointestinal; GU, genitourinary.

38

SECTION I: GENERAL CONSIDERATIONS

infection, pneumonia, failed vascular reconstruction, increased ventilator dependence, anastomotic leaks, and death.47 Grade 1–5 complication ● Intervention Treatment of smoking-related complications is mainly supportive. Aggressive pulmonary toilet including incentive spirometry, early ambulation, and suctioning may aid in recovery from pneumonia and improve respiratory function. Wound infections should be treated with antibiotics and drainage and dehiscence with operative repair. ● Prevention Although aggressive pulmonary toilet may help to prevent pneumonia and respiratory failure in smokers postoperatively, an overall reduction in surgery-related complications may be improved by smoking cessation before surgery.47 An 8-week window is believed to improve pulmonary function and decrease pulmonary secretions that predispose patients to pneumonia and COPD exacerbation.48 Recent studies suggest that patients who enter a preoperative smoking-cessation program may reduce rates of wound as well as pulmonary complications. These reports vary in their degree of signiﬁcance, and no clear duration of abstinence has been deﬁned to be required for observations of these beneﬁts.49,50

Patient with pre-operative weight loss or albumin ⬍2.5

Enteral supplementation failed? Yes

One week parenteral nutrition for supplementation • OR • Consider placement of enteral feeding tube if anticipate persistant failure to feed orally or anticipate prolonged postoperative fast.

Pre-operative TPN? No

Failed enteral feeding anticipated to continue to two weeks?

Assessment of Nutritional Status Failure to Assess Patient Nutritional Status Many patients referred for surgery have chronic GI dysfunction or anorexia related to cytokine production and associated with malignancy. Severely malnourished patients are generally deﬁned as those with albumin levels less than 2.5 g/dl and those with preoperative weight loss greater than 20%.51 ● Consequence Common consequences of failure to assess a patient’s nutritional status include dehiscence of the surgical wound and anastomotic breakdown. Wound healing is more signiﬁcantly compromised in those defects that are not treated by primary reanastomosis, but instead heal by secondary intention. Infection may progress to multiple organ system failure (MOSF) and death.52 Grade 1–5 complication ● Repair Repair is directed toward treatment of associated complications. Wound dehiscence requires reoperation. Anastomotic breakdown dictates prolonged fasting with total parenteral nutrition (TPN) for nutritional support. Antibiotics should be prescribed for associated infections and ICU support prescribed for MOSF.

No

Yes

Yes

Continue parenteral supplementation until enteral feedings adequate to meeting nutritional requirements

Initiate TPN

Figure 4–5 Management of the malnourished surgical patient.

● Intervention A protocol for identifying and treating the malnourished surgical patient is presented in Figure 4–5. History or laboratory values consistent with severe malnutrition are an indication for preoperative TPN. Calculation of nitrogen balance, as described in Eqs. 3, 4, and 5, can conﬁrm whether a patient is catabolic (negative balance) or anabolic (positive balance). (Eq. 3)

Nitrogenin = protein (in g/day)/6.25

(Eq. 4)

Nitrogenout = urinary nitrogen (in g/day) + insensible losses (2–8 g/day)

(Eq. 5)

Nitrogen balance = nitrogenin − nitrogenout

The Veterans Administration Total Parenteral Nutrition Cooperation study53 stratiﬁed patients according to degree of malnutrition as evidenced by preoperative weight loss and hypoalbuminemia and randomized patients to treat-

4 PREOPERATIVE PITFALLS ment with preoperative TPN or to a control group. In severely malnourished patients, the risk of noninfectious complications (e.g., anastomotic leaks, bronchopleural ﬁstulae, MOSF) with a 7-day course of preoperative TPN was reduced from 43% to 5%. Increased rates of infectious complications did not appear to justify the use of TPN in mild to moderately malnourished populations, however. These ﬁndings have been borne out by multiple subsequent trials and have resulted in the adoption of preoperative TPN as the standard of care in severely malnourished patients. Treatment appears to be of no beneﬁt when prescribed for less than 1 week. Postoperatively, patients should continue TPN started preoperatively until enteral feeds can be initiated. The question of postoperative TPN in patients without indications for preoperative therapy was addressed by a randomized study published by Sandstrom and associates,54 which noted increased rates of postoperative complications in those patients unable to tolerate oral feeds after GI surgery and receiving only IV ﬂuids for longer than 14 days. In patients without contraindications, early enteral feedings (administered as early as 6 hours postoperatively in some series of esophagectomy patients) are clearly superior to postoperative TPN, reducing rates of postoperative infectious complications and length of ICU and hospital stays.55,56 No clear evidence relating mortality to mode of feeding has been published.

Assessment of Bleeding Risk and Identiﬁcation of the Hypercoagulable Patient Failure to Identify the Patient at Risk of Bleeding ● Consequence Inherited and acquired coagulopathies place patients at risk for surgical bleeding. Special attention should also be placed on the signiﬁcant proportion of older surgical patients who are maintained on antiplatelet and anticoagulant medications for treatment and prevention of cardiovascular conditions. End-stage renal disease (ESRD) and liver disease (ESLD) are comorbid conditions associated with signiﬁcant risk of bleeding diathesis. Grade 1–5 complication ● Intervention Platelet dysfunction as seen in renal disease can be treated with 1-deamino(8-D-arginine) vasopressin (DDAVP) and platelet transfusion should excessive bleeding occur. Transfusion of platelets alone should be used for treatment of thrombocytopenia and consumptive coagulopathies and in patients receiving massive transfusion of packed red blood cells. Fresh frozen plasma can be used for treatment of bleeding associated with deﬁciency of most factors in the clotting cascade, and transfusion with concentrated recombinant factors can be used for von Willebrand disease, as well as for factor VIII and IX deﬁciencies. Local

39

control can be achieved with ﬁbrin sealants or collagenenriched matrices. Activated factor VII can be administered in patients with ongoing bleeding in whom standard transfusion therapies have failed to improve the clinical condition.57 ● Prevention Coagulation disorders can be elucidated on history by inquiring about previous episodes of unusual bleeding. Recurrent GI bleeding, epistaxis, hematuria, menorrhagia, or hemarthroses suggest a bleeding disorder. History of ESRD is associated with platelet dysfunction, and stigmata of ESLD are worrying for coagulopathy and thrombocytopenia. Collagen vascular diseases including lupus and Ehlers-Danlos are risks for intraoperative bleeding. Poor diet is associated with vitamin K deﬁciency and deﬁcits in clotting factors. Organomegaly warrants further work-up to rule out liver or hematologic disorders.58 In the absence of any of the previously cited risk factors, no evidence has been found to indicate that further work-up is necessary before elective surgery to exclude bleeding disorders. In fact, in a population of low-risk patients, the partial thromboplastin time (PTT) was found to have no predictive value as related to postoperative hemorrhage.59 Preoperative preparation with known coagulation defects are described in Table 4–7.60 Patients on oral anticoagulation or antiplatelet regimens require special care. Recovery of adequate platelet function requires at least 2 to 4 days after stopping aspirin. Similar results affect management of patients on clopidogrel and ticlopidine, irreversible inhibitors of platelet function. Complete recovery of platelet function takes 7 days, and patients should be instructed to cease taking antiplatelet agents 5 to 7 days before elective surgery. If the risk of acute thrombus is high as in patients with recently placed coronary artery stents, elective surgery should be postponed. Emergent surgery can be performed on patients taking aspirin or novel antiplatelet drugs because postoperative bleeding risk is generally limited to wound hematoma. More severe bleeding risk is present, however, when patients are on both aspirin and clopidogrel because these drugs act synergistically and perioperative morbidity is great in this population.61 Management of coumadin in the perioperative setting is based on the indication for which it is prescribed (Fig. 4–6). The complications of thromboembolic events require perioperative bridging with unfractionated heparin or low-molecular-weight heparin in patients with mechanical heart valves. Recent venous embolic disease (within 1 mo) similarly indicates the need for perioperative heparin derivatives.62–64

Failure to Treat for Hypercoagulable State ● Consequence The incidence of deep venous thrombosis (DVT) was historically quoted as ranging from 15% to 30% in

40

SECTION I: GENERAL CONSIDERATIONS

Table 4–7 Treatment of Coagulation Factor Disorders Bleeding Disorder

Target Factor Level

Plasma Product

Hemophilia A Minor surgery

>30% for 3–4 days

Major surgery

>80%–100% for 4 days, then >50% for 3–7 days

Cardiovascular, prostate, and neurosurgery

>100% for 3 days, then 80%–100% for 7–10 days

Recombinant or plasma-derived monoclonal factor VIII concentrates

Hemophilia B Minor surgery

>30% for 3–4 days

Major surgery

>80%–100% for 4 days, then >50% for 3–7 days

Cardiovascular, prostate, and neurosurgery

>100% for 3 days, then 80%–100% for 7–10 days

Recombinant or monoclonal plasmaderived factor IX concentrates

von Willebrand Disease Minor surgery

>50% for 1–3 days

Major surgery

Keep 50%–100% for 7–10 days

DDAVP or vWF-containing factor VIII concentrates

Factor XI Deﬁciency Minor surgery

>30% for 3–4 days

Major surgery

>45% for 7–10 days

FFP

Factor VII Deﬁciency Minor surgery

>15%

Major surgery

>25%

FFP or recombinant human factor VIIa

Factor X Deﬁciency Minor surgery

>15%

Major surgery

>50% perioperatively, then >30%

FFP or prothrombin complex concentrates

Factor V Deﬁciency Minor surgery

>25%

Major surgery

>50% perioperatively, then >25%

FFP

Minor surgery

20%–40%

FFP or prothrombin complex concentrates

Major surgery

20%–40%

Prothrombin Deﬁciency

A- or Hypoﬁbrinogenemia Minor surgery

>50–100 mg/dl for 1–3 days

Major surgery

>50–100 mg/dl for 2–3 wk

Cryoprecipitate

Factor XIII Deﬁciency Minor surgery

>5%

Major surgery

>5%

FFP or cryoprecipitate

DDAVP, 1-Desamino-8-D-arginine vasopressin; FFP, fresh frozen plasma; vWF, von Willebrand factor. From Streiff MB. Abnormal operative and postoperative bleeding. In Cameron J (ed): Current Surgical Therapy, 8th ed. Philadelphia: Elsevier Mosby, 2001; p 1124, Table 4.

4 PREOPERATIVE PITFALLS

41

Stop coumadin 4 days pre-operative

Low risk for thromboembolism (atrial fibrillation or DVT ⬎3 months before procedure)

Post-operative DVT prophylaxis with LMWH or heparin

Restart coumadin on POD 0

Figure 4–6 Perioperative management of the patient on coumadin. LMWH, low molecular weight heparin.

postsurgical patients before the institution of prophylactic measures. Pulmonary embolism caused death in 0.2% to 0.9% of patients.65,66 In fact, as many as 29% of postoperative deaths occurring in the ﬁrst 30 days after a procedure and in prophylaxis may have resulted from pulmonary embolism (PE) according to some autopsy studies.67 Grade 1/4/5 complication ● Intervention Although surveillance for postoperative DVT is rarely indicated, symptoms of unilateral lower extremity pain, color change, or edema should prompt emergent imaging, duplex ultrasonography (DUS), of the deep veins. In cases in which a high clinical suspicion for DVT is present, yet DUS is negative, pelvic computed tomography (CT) or venography may be useful to delineate the presence of a pelvic clot. Unexplained respiratory distress and an elevated arterial-alveolar gradient requires spiral CT scan of the chest, ventilation˙ ) scanning, or pulmonary angiography perfusion (V˙/Q to rule out PE. After diagnosis of a DVT or PE, patients should be immediately started on therapeutic anticoagulation. A high index of suspicion and respiratory distress is indicated for empirical treatment. High-dose unfractionated heparin should be administered intravenously to obtain an activated PTT between 60 and 80 seconds. Recently, lowmolecular-weight heparins such as enoxaparin have been employed, and this drug, given subcutaneously in doses of 1 mg/kg twice daily (once daily in renal failure patients), has been shown to be equally effective in preventing clin-

Intermediate risk

Prophylactic heparin or LMWH starting two days pre-operatively, continuing postoperatively

Resume coumadin on POD 0

High risk (mechanical valve, DVT within 1 month)

Admit for therapeuticic heparin 2 days pre-operatively

Therapeutic LMWH starting 2 days pre-operatively

D/C 4–6 hours pre-operatively and restart 12 hours post-op

D/C 12 hours preoperatively and restart 12 hours post-op

Resume coumadin on POD 0, stop heparin or LMWH after therapeutic INR

ical sequelae of DVT and PE.68 In the case of severely compromised oxygenation ability, thrombolysis may be essential, but the risk of postoperative bleeding should be recognized. In patients at risk for bleeding and who have a contraindication to anticoagulation, or in those who develop DVT or PE despite medical therapy, an inferior vena cava (IVC) ﬁlter can be placed in the setting of DVT to prevent migration of the clot to the lungs.69 Long-term consequences of DVT including venous stasis are not addressed by this mode of therapy; however, and multiple complications are associated with IVC ﬁlter placement including recurrent DVT, ﬁlter migration, insertion site injury, and IVC occlusion. Recently, removable IVC ﬁlters have been approved for use in the U.S. market, aiming to prevent these complications by ﬁlter retrieval after the risk of PE decreases.70 Results related to these ﬁlters are incompletely characterized. They do appear to prevent PE, but almost 50% are unable to be removed owing to ongoing contraindications to anticoagulation or to large emboli wedged in the ﬁlter.71 ● Prevention Surgery itself is a risk factor for development of DVT and PE, but as in the prevention of most postoperative complications, a thorough history and physical examination should be completed to assess a patient’s risk for coagulation disorders. The conditions most commonly associated with elevated risk of postoperative DVT and PE are age, obesity, previous DVT or PE, genetic predisposition, and cancer.70 It should be noted that orthopedic procedures (major joint surgery) and

42

SECTION I: GENERAL CONSIDERATIONS

Table 4–8 Thromboembolism Risk in Surgical Patients DVT (%) Level of Risk

Calf

PE (%)

Proximal

Clinical

0.4

0.2

Low risk Minor surgery in patients <40 yr with no additional risk factors

2

Moderate risk Minor surgery in patients with additional risk factors Surgery in patients aged 40–60 yr with no additional risk factors

10–20

2–4

High risk Surgery in patients >60 yr, or age 40–60 with additional risk factors (prior VTE, cancer, molecular hypercoagulability)

20–40

4–8

Highest risk Surgery in patients with multiple risk factors (age >40 yr, cancer, prior VTE) Hip or knee arthroplasty, HFS Major trauma; SCI

40–80

10–20

Fatal

Successful Prevention Strategies

<0.01

No speciﬁc prophylaxis; early and “aggressive” mobilization

1–2

0.1–0.4

LDUH (q12h), LMWH (≤3400 U daily), GCS, or IPC

2–4

0.4–1.0

LDUH (q8h), LMWH (>3400 U daily), or IPC

0.2–5

LMWH (>3400 U daily), fondaparinux, oral VKAs (INR, 2– 3), or IPC/GCS + LDUH/LMWH

4–10

GCS, glucocorticosteroid; INR, International Normalized Ratio; IPC, intermittant pneumatic compression; LDUH, low dose unfractionated heparin; LMWH, low-molecular-weight heparin; SCI, spinal cord injury; VKAs, vitamin K antagonists; VTE, venous thromboembolism. From Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism—the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126(suppl):338–400, Table 5.

therapy for trauma carry high risks of venous thromboembolic disease (VTED). Risks after colorectal surgery are somewhat higher than those following other general surgery procedures. Recommendations for prevention of postoperative VTED are based on a consensus statement by the American College of Chest Physicians Conference on Antithrombotic and Thrombolytic Therapy.72 Prescription of postoperative graded compression stockings, low-dose unfractionated heparin, low-molecular-weight heparin, or vitamin K inhibitors (e.g., coumadin) is based on the type of surgery the patient has undergone and the number of risk factors a patient is known to have. Table 4–8 summarizes these recommendations, which are based on currently available randomized, controlled trials and meta-analyses.72 The role of IVC ﬁlters in the prevention of PE in surgical patients is poorly deﬁned. Although clinicians have resisted this indication in an attempt to prevent long-term complications of the ﬁlters, the possibility of removable ﬁlters has encouraged reexamination of this therapy. Obesity and trauma surgery are the ﬁrst ﬁelds likely to adopt routine prophylactic IVC ﬁlter placement owing to the high rate of VTED in respective patient populations.70 Patients with known DVT and surgical disease are also considered for prophylactic IVC ﬁlter placement.

Identiﬁcation of Endocrine Dysfunction Failure to Treat and Prevent Hyperglycemia ● Consequence Multiple studies have demonstrated that patients with poor blood sugar control have higher rates of wound

infections.73–75 ICU patients with hyperglycemia are prone to septicemia and resultant MSOF.76 Complications of diabetes such as gastroparesis and neuropathy place patients at risk of aspiration and autonomic instability, respectively, and indicate that both anesthesiologists and surgeons must be aware not only of the immediate effect of hyperglycemia on postoperative healing but also of the derangements associated with chronic physiologic changes related to diabetes.77,78 Grade 1/4/5 complication ● Intervention In patients with persistent hyperglycemia, aggressive control to maintain blood sugar below 120, as discussed later, is essential. Treatment of infections is mainly supportive, with IV antibiotics tailored to the microorganism, débridement or drainage as necessary, and ventilatory or dialysis support as required for MSOF. ● Prevention Preventing the postoperative complications related to diabetes begins before the induction of anesthesia (Box 4–6). Patients should be directed to stop taking oral antihyperglycemics the day before surgery to prevent interactions with anesthesia that may result in lactic acidosis and arrhythmia. Long-acting insulin medications should be taken through the day of surgery, but after initiation of the fast, injection with short-acting analogues should stop to prevent hypoglycemic reactions. The fast should be broken before the start of surgery by administration of IV dextrose. This appears to minimize the insulin resistance observed postoperatively. When possible, epidural anesthesia should be

4 PREOPERATIVE PITFALLS

Box 4–6 ● ● ● ● ● ●

Perioperative Management of Diabetes

Hold short-acting insulin and oral medications with onset of fast. Continue long-acting insulin analogues (L-glargine) on day of surgery Break fast immediately preoperatively with dextrosecontaining IV ﬂuid Low threshold for insulin drip intra- and postoperatively Floor patients with goal blood sugar <150 Intensive care unit patients with goal blood sugar <120

considered because this blunts the physiologic stress response related to surgery and the related insulin resistance and hyperglycemia. Nasogastric tubes should be inserted liberally, and erythromycin should be considered to prevent aspiration related to poor gastric motility. The beneﬁt of tight blood glucose control using insulin has recently been shown via a large randomized, controlled study of ICU patients treated with IV insulin infusion to maintain blood glucose levels of 80 to 110 versus 180 to 200. A signiﬁcant proportion of the patients in this study were surgical patients. Tight control was related to a decrease in mortality from 8% to 4.6%. Decreased requirements for ventilatory support and renal replacement therapy were observed in the aggressively treated patient population, and rates of septicemia were reduced from 67% to 25%.76 Although it remains to be deﬁned whether blood sugars must be maintained as low as the aggressively treated group in this study, it is obvious that hyperglycemia must be constantly evaluated and treated.

Failure to Recognize Adrenal Insufﬁciency ● Consequence Hypotension and shock are consequences of failure to recognize adrenal insufﬁciency. Glucocorticoids perpetuate the actions of catecholamines, supporting blood pressure and potentiating their ionotropic effects. Postoperative patients with unrecognized adrenal insufﬁciency may initially complain of abdominal pain with nausea, vomiting, and diarrhea and progress to a shock state requiring vasopressors for blood pressure support. In primary adrenal insufﬁciency (diseases affecting the adrenal gland itself and not regulation via pituitary or hypothalamic regulatory pathways), mineralocorticoid deﬁcits may manifest as persistent hyponatremia and hyperkalemia. Grade 1 complication ● Intervention Stress dose steroids can improve hemodynamic stability, allowing patients to wean from pressor support. ● Prevention The most common form of adrenal insufﬁciency encountered by the surgeon is tertiary adrenal insufﬁ-

43

ciency, which is seen in patients treated with steroids for comorbid conditions such as inﬂammatory bowel disease, COPD, collagen vascular diseases, rheumatoid arthritis, or central nervous system tumors. Patients receiving more than 5 days of methylprednisolone dosed at 20 mg or greater each day are likely to have suppression of the adrenal axis.79 The adrenal axis does not fully recover for over 9 months, suggesting that anyone who has received high-dose steroids during the year before surgery should be evaluated for adrenal insufﬁciency.80 Low-dose steroids (5 mg daily of methylprednisolone or its equivalent) do not generally result in adrenal insufﬁciency, and these patients should not require stress doses of steroids preoperatively.81 Patients with a history or risk factors for tuberculosis, advanced human immunodeﬁciency syndrome, or autoimmune diseases should be screened with laboratory testing for signs of primary adrenal insufﬁciency. Physical signs include hyperpigmentation, chronic fatigue, weight loss, diarrhea, abdominal pain, and emesis. Hyponatremia or hyperkalemia may be present, representing mineralocorticoid deﬁciencies. Patients using chronic topical or inhaled steroids may develop tertiary adrenal insufﬁciency. Pituitary tumors may compromise the production of adrenocorticotropic hormone (ACTH), resulting in secondary adrenal insufﬁciency.82 If risk factors for adrenal insufﬁciency are identiﬁed, patients without a clear need for steroids can be evaluated using a corsyntropin stimulatory test, which evaluates the effect of exogenous stimulation on cortisol production. Failure to respond adequately deﬁnes a subset of patients who will require stress dose steroids. Dosing of stress dose steroids and requirement for postoperative tapering are based on the extent of the surgical procedure.81 Special note should be made of the risk for poor wound healing in patients on chronic steroids. This is related to increased risk of wound dehiscence, anastomotic leak, and stump breakdown. High doses of vitamin A and vitamin C can potentially improve outcomes, and reinforcement of the surgical site with retention sutures or tissue ﬂaps should be considered when tissues are noted to be friable and weak.

Documentation of the Family History Failure to Take an Adequate Family History ● Consequence Metachronous cancers, missed synchronous cancers, and recurrent vascular disease are consequences of failure to take an adequate family history. The advent of genetic testing and the description of familial cancer syndromes have resulted in a need for carefully considering a patient’s family and personal medical histories to identify those with cancer syndromes and those with advanced vascular disease owing to metabolic aberrations. Grade 1–5 complication

44

SECTION I: GENERAL CONSIDERATIONS

Table 4–9 Genetic Syndromes Commonly Encountered by the Surgeon Syndrome

Genetic Defect

Associated Cancers

Diagnosis

Treatment and Screening

FAP

APC

• Colorectal cancer in 4th decade • Duodenal adenocarcinoma • Rarely pancreatic, biliary, ileal pouch adenoma, gastric adenoma, papillary thyroid cancer, hepatoblastoma

• Family history • Endoscopic identiﬁcation of 100s to 1000s of colorectal polyps • Genetic testing

• Colonoscopy beginning between ages 10 and 20 • Upper tract endoscopy every 2–5 yr • Annual physical examination for thyroid nodules • Consider AFP and abdominal US until age 6 yr to identify hepatoblastoma • Prophylactic colectomy in 2nd decade

Attenuated FAP

APC

• Right-sided polyps more common • Variable incidence of colon cancer

• As in FAP

• Prophylactic colectomy vs. endoscopic polypectomies • EGD, thyroid, and hepatoblastoma screening as in FAP

Gardner syndrome

APC

• Variable incidence of colon cancer • Osteosarcoma, lipoma, sebaceous cyst neoplasms, dental abnormalities

• As in FAP

• As noted earlier in attenuated FAP

Turcot syndrome

APC or microsatellite instability

• Variable incidence of colon cancer • Medulloblastoma and glioblastoma multiforme

• As in FAP

• As noted earlier in attenuated FAP

HNPCC (Lynch 1)

hmL1, hmSH2, hmsH6, PMS2 (microsatellite instability)

• Early-onset colon cancer • Right-sided colorectal cancer • Histology signiﬁcant for microsatellite instability, signet ring cells, mucinous neoplasms, lymphocytic inﬁltrate • Metachronous cancers • Endometrial cancer • Small bowel cancer • Transitional cell carcinoma • Café-au-lait spots • Gastric cancer in certain pedigrees

• Amsterdam criteria for diagnosis • Three affected family members • One is the ﬁrst-degree relative of the other two • One is diagnosed before age 50 • Disease affects two successive generations • Genetic testing

• Colonoscopy starting 10 yr before the earliest colorectal cancer in the pedigree • Local resection with annual to biennial colonoscopy or subtotal colectomy • Annual urinalysis and urine cytology • Annual endometrial aspiration biopsy or transvaginal ultrasound; consider postmenopausal hysterectomy • Gastroscopy in families with affected pedigree

Peutz-Jeghers

STK 11 (LKB 1), a serinethreonine kinase

• Mucocutaneous hyperpigmentation • Intestinal hamartomas • Gastrointestinal cancers • Rarer breast, endometrial, pancreatic, lung, cervical, testicular cancers

• Family history • Histologic examination of small intestine hamartomas • Mucocutaneous hyperpigmentation • Genetic testing

• Biennial EGD and upper GI with small bowel follow-through starting at age 10 • Biannual colonoscopy starting in early adulthood

JPS

PTEN, SMAD4, BMPR1A

• Colorectal cancer • Digital clubbing • Gastric polyposis and cancer

• Family history with JPS polyps • >5 juvenile polyps with conﬁrmed histology • JPS polyps throughout intestinal tract

• Annual colonoscopy with polypectomy starting in teens • Biennial EGD • Consider prophylactic subtotal colectomy

Cowden disease

PTEN

• • • • •

• As in JPS with additional characteristics noted in previous column • Difﬁcult to distinguish from JPS and may be subset

• As noted earlier in JPS • Mammography starting at age 30 • Thyroid screening beginning in teens

As in JPS Breast cancer Thyroid cancer Multinodular goiter Facial tricholemmas

4 PREOPERATIVE PITFALLS

45

Table 4–9 Genetic Syndromes Commonly Encountered by the Surgeon—cont’d Syndrome

Genetic Defect

Associated Cancers

Diagnosis

Treatment and Screening

BRCA mutation carrier

BRCA

• • • • •

• Family history (premenopausal breast cancer, male breast cancer, ovarian cancer, multiple affected members of family) • Genetic testing of affected individuals if possible, otherwise related members

• Breast conserving therapy vs. mastectomy (therapeutic or prophylactic) • Annual mammogram, consider alternating every 6 mo with annual MRI • Consider postmenopausal bilateral salpingoopherectomy • Tamoxifen for 5 yr • Consider aromastat inhibitors after tamoxifen course

MEN 1

Menin

• Parathyroid hyperplasia • Pancreatic neoplasms (predominantly neuroendocrine) • Anterior pituitary gland neoplasms • Rarely lipoma, adrenal/thyroid adenomas, cutaneous angioﬁbromas, bronchial/thymic carcinoids

• Family history • Genetic testing

• Annual screening for hormones related to functioning neuroendocrine tumors of the pancreas • Consider additional work-up with CT, somatostatin-receptor scintography, MRI for symptoms • Annual calcium, PTH, screen for symptoms of prolactinoma, acromegaly

MEN 2

Ret

• Medullary thyroid cancer • Pheochromocytoma • Mucosal neuromas (MEN 2B only) • Neuroﬁbromatosis (MEN 2B only) • Marfanoid habitus (MEN 2B only) • Hyperparathyroid (MEN 2A only)

• Family history • Genetic testing

• Prophylactic thyroidectomy • Screening for symptoms of pheochromocytoma by history and measurement of urinary catecholamines, serum metanephrines • Resect pheochromocytoma before thyroid cancer • Unilateral (consider bilateral) adrenalectomy for pheochromocytoma

Breast Ovarian Colon Prostate Pancreatic

AFP, α-fetoprotein; CT, computed tomography; EGD, esophagogastroduodenoscopy; FAP, familial adenomatous polyposis; GI, gastrointestinal; HNPCC, hereditary nonpolyposis colorectal cancer; JPS, juvenile polyposis syndrome; MEN, multiple endocrine neoplasia; MRI, magnetic resonance imaging; PTH, parathyroid hormone; US, ultrasound.

● Intervention Patients will require additional surgeries or develop progressive disease. ● Prevention Hyperhomocystinemia is an important consideration in the vasculopath. These patients develop early-onset cardiac and peripheral vascular symptoms, a history often seen in other family members as well. Treatment with vitamin supplementation may blunt progression of atherosclerotic changes. Cancers that develop in the context of germline mutations require special cancer screening protocols, preoperative planning, and extensive discussion with patients regarding genetic testing of themselves and their families. Table 4–9 summarizes the best characterized of these syndromes and protocols, their recognition, diagnosis, and appropriate treatment strategies for these patients.83–89

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SECTION I: GENERAL CONSIDERATIONS

6. Rapp SE, Ready LB, Nessly ML. Acute pain management in patients with prior opioid consumption: a casecontrolled retrospective review. Pain 1995;61:195–201. 7. Peacock JE, Wright BM, Whithers MR, et al. Evaluation of a pilot regimen for postoperative pain control in patients receiving oral morphing pre-operatively. Anesthesia 2000;55:1208–1212. 8. Spies CD, Rommelspacher H. Alcohol withdrawal in the surgical patient: prevention and treatment. Anesth Analg 1999;88:946–954. 9. Mayo-Smith MF, Beecher LH, Fischer TL, et al. Management of alcohol withdrawal delirium: an evidence-based practice guideline. Arch Intern Med 2004;164:1405– 1412. 10. Ramsey MAE, Savege TM, Simpson BRJ, et al. Controlled sedation with alphaxalanoe-alphadolone. BMJ 1974;2:656–659. 11. Sessler C, Gosnell M, Grap MJ, et al. The Richmond agitation-sedation scale. Validity and reliability in adult intensive care patients. Am J Respir Crit Care Med 2002; 166:1338. 12. Ewing JA. Detecting alcoholism: the CAGE questionnaire. JAMA 1984;252:1905–1907. 13. Goldman L, Caldera DL, Nussbaum SR, et al. Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med 1977;297:845–850. 14. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for management of patients with ST-elevation myocardial infarction—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for Management of Patients with Acute Myocardial Infarction). Circulation 2004;110:588–636. 15. Eagle KA, Singer DE, Brewster DC, et al. Dipyridamolethallium scanning in patients undergoing vascular surgery. JAMA 1987;256:2185–2188. 16. Eagle KA, Berger PB, Calkins H, et al. ACC/AHA guideline update for perioperative cardiovascular evaluation for noncardiac surgery—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Circulation 2002;105:1257–1267. 17. Mandango DT, Layug EL, Wallace A, et al. Effect of atenolol on mortality and cardiovascular morbidity after noncardiac surgery. N Engl J Med 1996;335:1713– 1720. 18. Polderman D, Boersma E, Bax JJ, et al. The effect of bisoproprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular surgery. Dutch Echo-cardiographic Cardiac Risk Evaluation Applying Stress Echocardiography Study Group. N Engl J Med 1999;341:1789–1794. 19. Maggio PM, Taheri PA. Perioperative issues: myocardial ischemia and protection—beta-blockade. Surg Clin North Am 2005;85:1091–1102. 20. Stevens RD, Burri H, Tramer MR. Pharmacologic myocardial protection in patients undergoing noncardiac surgery: a quantitative systematic review. Anesth Analg 2003;97:623–633.

21. Lee TH, Marcantanio ER, Mangione CM, et al. Derivations and prospective validation of a simple index for prediction of cardiac risk of major non-cardiac surgery. Circulation 1999;100:1043–1049. 22. Boersma E, Poldermans D, Bax JJ, et al. Predictors for cardiac events after major vascular surgery: role of clinical characteristics, dobutamine echocardiography, and betablocker therapy. JAMA 2001;285:1865–1873. 23. McFalls EO, Ward HB, Moritz TE, et al. Coronary-artery revascularization before elective major vascular surgery. N Engl J Med 2004;351:2795–2804. 24. Lee JK, Klein GJ, Krahn AD, et al. Rate control versus conversion strategy in post-operative atrial ﬁbrillation: a prospective, randomized pilot study. Am Heart J 2000; 140:871–877. 25. Amar D. Strategies for peri-operative arrhythmias. Best Pract Res Clin Anesth 2004;18:565–577. 26. Sedrakyan A, Treasure T, Browne J, et al. Pharmacologic prophylaxis for postoperative atrial tachyarrhythmias in general thoracic surgery. Evidence from randomized clinical trials. J Thorac Cardiovasc Surg 2005;129:997– 1005. 27. Crystel E, Connolly SJ, Sleik K, et al. Interventions on prevention of postoperative atrial ﬁbrillation in patients undergoing heart surgery: a meta-analysis. Circulation 2002;106:75–80. 28. Goolish J, Kaw R, Michota F, et al. Unrecognized sleep apnea in the surgical patient: implications for the perioperative setting. Chest 2006;129:198–205. 29. Gupta R, Parvizzi J, Hanssen A, et al. Post-operative complications in patients with obstructive sleep apnea syndrome undergoing hip or knee replacement: a case control study. Mayo Clin Proc 2001;76:897–905. 30. Powel CA, Caplan CE. Pulmonary function tests in preoperative pulmonary evaluation. Clin Chest Med 2001; 22:703–714. 31. Reilly JJ. Evidence-based preoperative evaluation of candidates for thoracotomy. Chest 1999;116S:474S– 476S. 32. Chumillas MS, Ponce JL, Delgado F, et al. Pulmonary function and complications after laparoscopic cholecystectomy. Eur J Surg 1998;164:433–437. 33. Pugh RNH, Murray-Lyon IM, Dawson JL, et al. Transection of the oesophagus for bleeding oesophageal varices. Br J Surg 1973;60:646–649. 34. Kamath PS, Wiesner RH, Malinchoc M, et al. A model to predict survival in patients with end-stage liver disease. Hepatology 2001;33:464–470. 35. Nothup PG, Wanamaker RC, Lee VD, et al. Model for end-stage liver disease predicts nontransplant surgical mortality in patients with cirrhosis. Ann Surg 2005;242:244–251. 36. Tang IY, Murray PT. Prevention of perioperative acute renal failure: what works. Best Pract Res Clin Anesthesiol 2004;18:91–111. 37. Jarnberg P-O. Renal protection strategies in the perioperative period. Best Pract Res Clin Anesthesiol 2004;18:645– 660. 38. Solomon R, Werner C, Mann D, et al. Effects of saline, mannitol, and furosemide on acute decrease in renal function induced by radiocontrast agents. N Engl J Med 1994;331:1416–1420.

4 PREOPERATIVE PITFALLS 39. Buck R, Krzossok S, Morkowetz F, et al. Acetylcysteine for prevention of contrast nephropathy: a meta-analysis. Lancet 2003;362:598–603. 40. Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized, controlled trial. JAMA 2004;291:2328– 2334. 41. Cockroft DW, Gault MH. Prediction of creatinine clearance from serum creatinine. Nephron 1976;16: 31–41. 42. Solomkin J. Perioperative antimicrobial prophylaxis. In Fischer JE (ed): Mastery of Surgery. Philadelphia: Lippincott Williams & Wilkins, 2007; pp 101–109. 43. Platt R, Zaleznik DF, Hopkins CC, et al. Perioperative antibiotic prophylaxis for herniorrhaphy and breast surgery. N Engl J Med 1990;322:153–160. 44. Aufenacker TJ, van Geldere D, van Mesday T, et al. The role of antibiotic prophylaxis in prevention of wound infection after Lichenstein open mesh repair of primary inguinal hernia: a multi-center, double-blind, randomized control trial. Ann Surg 2004;240:955–960. 45. Zmorao O, Mahajna A, Bar-Zakai B, et al. Colon and rectal surgery without mechanical bowel preparations: a randomized prospective trial. Ann Surg 2003;237:363– 367. 46. Nichol RL, Choe EU, Weldon CB. Mechanical and antibacterial bowel preparation in colon and rectal surgery. Chemotherapy 2005;51(suppl 1):S115–S121. 47. Moller A, Villebro N. Interventions for preoperative smoking cessation. Cochrane Database Syst Rev 2006;1. 48. Warner MA, Offord KP, Warner ME, et al. Role of preoperative cessation of smoking and other factors in post-operative pulmonary complications: a blinded, prospective study of coronary artery bypass patients. Mayo Clin Proc 1989;64:609–616. 49. Moller AM, Villebro N, Pedersen T, et al. Effect of preoperative smoking intervention on post-operative complications: a randomized clinical trial. Lancet 2002;359: 114–117. 50. Sorenson LT, Jorgenson T. Short-term pre-operative smoking cessation intervention does not affect post-operative complications in colorectal surgery: a randomized clinical trial. Colorectal Dis 2003;5:347– 352. 51. Howard L, Ashley C. Nutrition in the perioperative patients. Annu Rev Nutr 2003;23:263–282. 52. Daley J, Khuri SF, Henderson W, et al. Risk adjustment of the postoperative morbidity rate for the comparative assessment of the quality of surgical care: results of the National Veterans Affairs Surgical Risk Study. J Am Coll Surg 1997;185:328–340. 53. Veterans Affairs Total Parenteral Nutrition Cooperative Study. Perioperative total parenteral nutrition in surgical patients. N Engl J Med 1991;325:525–532. 54. Sandstrom R, Drott C, Hylanter A, et al. The effect of postoperative intravenous feeding (TPN) on outcome following major surgery in a randomized study. Ann Surg 1993;217:185–195. 55. Bozzetti F, Brage M, Gianotti L, et al. Postoperative enteral versus parenteral nutrition in malnourished patients with gastrointestinial cancer: a randomized multicentre trial. Lancet 2001;358:1487–1492.

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56. Gabor S, Renner H, Matzi V, et al. Early enteral feeding compared to parenteral nutrition after oesophageal and oesophagogastric resection and reconstruction. Br J Nutr 2005;93:509–513. 57. Grounds M. Recombinant factor VIIa and its use in severe bleeding in surgery and trauma: a review. Blood Rev 2003;17(suppl 1):S11–S21. 58. Cobas M. Preoperative assessment of coagulation disorders. Int Anesthesiol Clin 2001;39:1–15. 59. Suchman AL, Mushlin AI. How well does the activated partial thromboplastin time predict postoperative hemorrhage? JAMA 1986;256:750–758. 60. Streiff MB. Abnormal operative and postoperative bleeding. In Cameron J (ed): Current Surgical Therapy, 7th ed. Philadelphia: Elsevier Mosby, 2001; p 1124. 61. Harder S, Klunkhardt U, Alvarez JM. Avoidance of bleeding during surgery in patients receiving anticoagulant and/or antiplatelet therapy. Clin Pharmokinet 2004;43: 963–981. 62. Jafri SM, Mehta TP. Periprocedural management of anticoagulation in patients on extended warfarin therapy. Semin Thromb Hemost 2004;30:657–664. 63. Spyropoulos AC, Turpie AGG. Perioperative bridging interruption with heparin for the patient receiving longterm anticoagulation. Curr Opin Pulm Med 2005;1:373– 379. 64. Ansell J, Dalen J, Bussey J, et al. Managing oral anticoagulant therapy. Chest 2001;119(suppl):22S–38S. 65. Mismetti P, Laporte S, Darmon JY, et al. Meta-analysis of low molecular weight heparin in the prevention of venous thromboembolism in general surgery. Br J Surg 2001;88: 913–930. 66. Clagett GP, Reisch JS. Prevention of venous thromboembolism in general surgery patients: results of meta-analysis. Ann Surg 2003;208:227–240. 67. Lindbland B, Erikssoon A, Bergqvist D. Autopsy-veriﬁed pulmonary embolism in the surgical department: analysis of the period from 1951 to 1968. Br J Surg 1991;78: 849–852. 68. Pezzuoli G, Neri Serneri GG, Settembrini P, et al. Prophylaxis of fatal pulmonary embolism in general surgery using low-molecular-weight heparin Cy 216: a multicentre, double-blind, randomized controlled trial versus placebo (STEP). Int Surg 1973;74:205– 210. 69. Becker DM, Philbrich JT, Selby JB. Inferior vena cava ﬁlters. Indications, safety, effectiveness. Arch Intern Med 1992;152:1985–1994. 70. Sarani B, Chun A, Venbrux A. Role of optional (retrievable) IVC ﬁlters in surgical patients at risk for venous thromboembolic disease. J Am Coll Surg 2005;201:957– 964. 71. Millward SF, Oliva VL, Bell SD, et al. Gunther retrievable vena cava ﬁlter: results from the Registry of the Canadian Interventional Radiology Association. J Vasc Interv Radiol 2001;12:1053–1058. 72. Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism: the seventh ACCP Conference on antithrombotic and thrombolytic therapy. Chest 2004; 126(suppl):338–400. 73. Guvener M, Pasaoglu I, Demircin M, et al. Perioperative hyperglycaemia is a strong correlate of postoperative

48

74.

75.

76.

77.

78.

79.

80.

SECTION I: GENERAL CONSIDERATIONS

infection in type II diabetic patients after coronary artery bypass grafting. Endocrine J 2002;49:531–537. Pomposelli JJ, Baxter JK III, Babineau TJ, et al. Early postoperative glucose control predicts nosocomial infection rate in diabetic patients. J Parenter Enteral Nutr 1998;22:77–81. Golden SH, Peart-Vigilance C, Kao WH, et al. Perioperative glycemic control and the risk of infectious complications in a cohort of adults with diabetes. Diabetes Care 1999;22:1408–1414. 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. Robertshaw HJ, McAnulty GR, Hall GM. Strategies for managing the diabetic patient. Best Pract Res Clin Anaesthesiol 2004;18:631–643. Ljungqvist O, Nygren J, Soop M, et al. Metabolic perioperative management: novel concepts. Curr Opin Crit Care 2005;11:295–299. Zora JA, Zimmerman D, Carey TL, et al. Hypothalamicpituitary adrenal axis suppression after short-term, highdose glucocorticoid therapy in children with asthma. J Allergy Clin Immunol 1986;77:9–13. Graber AL, Ney RL, Nicholson WE, et al. Natural history of pituitary-adrenal recovery following long-term suppression with corticosteroids. J Clin Endocrinol Metab 1965; 25:11–16.

81. Axelrod L. Perioperative managements of patients treated with glucocorticoids. Endocrinol Metab Clin North Am 2003;32:367–383. 82. Connery LE, Coursin DB. Assessment and therapy of selected endocrine disorders. Anesthesiology Clin North Am 2003;22:93–123. 83. Boardman LA. Heritable colorectal cancer syndromes: recognition and preventive management. Gastroenterol Clin North Am 2002;31:1107–1131. 84. Vasen HF, Mecklin JP, Khan PM, et al. The International Collaborative Group on Hereditary Non-Polyposis Colorectal Cancer (ICG-HNPCC). Dis Colon Rectum 1991;34:424–425. 85. Ford D, Easton DF, Bishop D, et al. Risks of cancer in BRCA1 mutation carriers. Lancet 1994;343:692–695. 86. Lastumbo L, Carbine N, Wallace J, et al. Prophylactic mastectomy for the prevention of breast cancer. Cochrane Database Syst Rev 2004;Oct 18(3):CD002748. 87. Calderon-Margalit R, Paltier O. Prevention of breast cancer in woman who carry BRCA1 and BRCA2 mutations: a critical review of the literature. Int J Cancer 2003;112:357–364. 88. Doherty GM. Multiple endocrine neoplasia type I. J Surg Oncol 2005;89:143–150. 89. Lee NC, Norton JA. Multiple endocrine neoplasia type 2B—genetic basis and clinical expression. Surg Oncol 2000;9:111–118.

5

Anesthesia for the Surgeon Ankur Gosalia, MD and Babak Sarani, MD INTRODUCTION Perioperative management has changed signiﬁcantly since the early 1980s. Speciﬁcally, many operations that historically required preoperative hospitalization are now performed as same-day admission, outpatient, or ofﬁcebased procedures. An estimated 400,000 outpatient surgical procedures were performed in 1984, compared with 8.3 million procedures in 2000.1 Because of this, surgeons must be familiar with anesthesia techniques, risks, and pitfalls. Persons older than age 65 make up the fastest-growing segment of the population in the United States and are expected to account for 20% of the population by 2025.2 As expected, this segment of the population has many comorbidites that must be accounted for when evaluating perioperative risk and the safety of outpatient procedures requiring conscious sedation. Familiarity with methods used to assess operative risk can make preoperative evaluation and preparation smooth and cost effective. Utilizing an organ system–based approach, this chapter discusses anesthetic pitfalls with which the surgeon should be familiar. The chapter is further divided into issues related to surgery in the outpatient/ofﬁce-based setting and those related to more invasive inpatient procedures. For the latter, an organ system–based discussion is used to discuss pitfalls in the preoperative, intraoperative, and postoperative settings.

OUTPATIENT AND OFFICE-BASED ANESTHETIC PITFALLS Neurologic System Tables 5–1 and 5–2 list many of the commonly used analgesic and amnestic/anxiolytic agents, their doses, and reversal agents.

Meperidine-Related Seizure Meperidine (Demerol) has a unique proﬁle in that it has a toxic metabolite, normeperidine, that has a longer halflife than the parent drug but no analgesic effects. Normeperidine can accumulate to toxic levels in patients with hepatic or renal dysfunction.

● Consequence Persistent dosing of meperidine can cause accumulation of normeperidine to toxic levels that can lead to life-threatening seizures. These seizures are extremely difﬁcult to control. Grade 4/5 complication ● Repair Seizures related to the use of meperidine should be treated immediately with benzodiazepines (preferably midazolam [Versed] or lorazepam [Ativan]). Sodium thiopental or propofol can also be used, but these agents are more likely to cause severe hypotension. Phenytoin (Dilantin) is not effective in stopping or preventing seizures due to normeperidine. Patients may require intubation to control the airway if the seizures do not stop. ● Prevention The use of meperidine for analgesia should be avoided entirely or minimized in all patients because this agent does not have a favorable analgesic proﬁle in comparison with morphine, hydromorphone (Dilaudid), or fentanyl and has the potential to cause seizures in those patients with renal and hepatic impairment. If meperidine must be used, only small, incremental doses should be administered, especially in the outpatient setting. This agent is contraindicated in those with signiﬁcant renal or hepatic dysfunction.

Local Anesthetic–Related Seizure ● Consequence Intravascular administration of local anesthetic or overdose into the interstitium can cause life-threatening seizures.3 Bier blocks are whole extremity blocks performed by intravenous injection of high doses of local anesthetic in an extremity that has been isolated via a tourniquet. Such blocks can cause seizures if the tourniquet is released before the injected anesthetic has dissipated to nontoxic levels or is not sufﬁciently tight to prevent systemic exposure. Table 5–3 lists the commonly used local anesthetics, doses, and duration of effect. Grade 4/5 complication

50

SECTION I: GENERAL CONSIDERATIONS

Table 5–1 Commonly Used Analgesics Agent

Dose

Duration

Pitfalls and Side Effects

0.02–0.08 mg/kg IV (2–6 mg IV)

2–6 hr

Respiratory depression,* hypotension,* itching

Meperidine (Demerol)

0.2–0.75 mg/kg IV (25–50 mg IV)

2–4 hr

Seizure,‡ respiratory depression*

Fentanyl

0.5–1 mcg/kg IV (25–100 mcg IV)

30 min–1 hr

Respiratory depression,* depot effect when used chronically§

Hydromorphone (Dilaudid)

0.001–0.02 mg/kg IV (0.1–2 mg IV)

2–6 hr

Respiratory depression*

Ketorolac (Toradol)

15–30 mg IV or PO

4–6 hr

Nephrotoxic,储 ulcerogenic, platelet dysfunction

Naloxone¶

40–400 mcg

5–10 min

Seizure, acute pain

Ketamine

0.5–1 mg/kg IV

30 min

Hallucination

Morphine †

*Dose dependent. † Not recommended for chronic pain owing to accumulation of toxic metabolite. ‡ Use with extreme caution in patients with renal or liver insufﬁciency. § Continuous or frequent dosing can cause signiﬁcant build-up in fat stores owing to lipophilic proﬁle. 储 Limit continuous intravenous dosing to 4–6 days. ¶ Reversal agent for all opioids. Can induce withdrawal if administered quickly. IV, intravenously; PO, orally. From Rutter T, Tremper K. Anesthesiology and pain management. In Greenﬁeld L, Mulholland M, Oldham K, et al (eds): Surgery: Scientiﬁc Principles and Practice, 2nd ed. Philadelphia: Lippincott-Raven, 1997; pp 438–454.

Table 5–2 Commonly Used Amnestic/Anxiolytic Agents Agent

Dose

Duration

Time to Onset (min)

Pitfalls and Side Effects

Midazolam (Versed)

2–4 mg IV

30 min

1 min

Respiratory depression, hypotension*

Lorazepam (Ativan)

2–4 mg IV

4–6 hr

5 min†

Respiratory depression, hypotension*

Diazepam (Valium)

0.5–1 mg IV

1 hr

1–2 min

Respiratory depression, hypotension*

Flumazenil‡ (Romazicon)

0.2 mg IV (max dose 3 mg)

30–60 min

2 min

Seizures

*Dose dependent when administered alone but synergistic when combined with narcotic medications. † Beware of iatrogenic overdose owing to recurrent dosing as a result of the long onset of action. ‡ Reversal agent for benzodiazepines. Can cause seizures if administered quickly. IV, intravenously. From Rutter T, Tremper K. Anesthesiology and pain management. In Greenﬁeld L, Mulholland M, Oldham K, et al (eds): Surgery: Scientiﬁc Principles and Practice, 2nd ed. Philadelphia: Lippincott-Raven, 1997; pp 438–454.

Table 5–3 Commonly Used Local Anesthetics Agent

Max Dose (Interstitial)

Duration

Lidocaine (plain)

5 mg/kg

30–60 min

Lidocaine with 100 mcg epinephrine*

7 mg/kg

1.5–2 hr

Bupivacaine (Marcaine/Sensorcaine)

3 mg/kg

3–4 hr

Chloroprocaine

15 mg/kg

30–60 min

Tetracaine†

2 mg/kg

3 hr

†

*Contraindicated in organs supplied by end-arterioles. † Ester class agent that can cause allergic reaction in patients allergic to para-aminobenzoic acid (PABA). From Rutter T, Tremper K. Anesthesiology and pain management. In Greenﬁeld L, Mulholland M, Oldham K, et al (eds): Surgery: Scientiﬁc Principles and Practice, 2nd ed. Philadelphia: Lippincott-Raven, 1997; pp 438–454; and Salam GA. Regional anesthesia for ofﬁce procedures: part I: head and neck surgeries. Am Fam Physician 2004;69:585–590.

● Repair Local anesthetic–related seizures should be treated immediately with barbiturates. Generally, phenytoin is not required for long-term prophylaxis or treatment, but all patients require intensive care unit admission for observation and treatment of recurrent seizures. No speciﬁc reversal agents are available for local anesthetic seizures. ● Prevention Surgeons must be familiar with the particular local anesthetic used, its toxic proﬁle, and dosing limitations. Needle aspiration should be performed prior to injecting the local anesthetic to ensure interstitial (as opposed to intravascular) injection. Finally, bier blocks are best performed under the direction of a trained anesthesiologist.

5 ANESTHESIA FOR THE SURGEON

Inadequate Analgesia ● Consequence Aside from the emotional discomfort of pain, inadequate analgesia induces the stress response and causes an increase in catecholamine release. This results in a signiﬁcant increase in cardiac work that can result in myocardial ischemia in patients with coronary artery disease. Grade 1 complication ● Repair Both local and systemic modalities of analgesia can be used to manage pain. ● Prevention Pain is best prevented by administration of local anesthetic prior to any skin incision. Signs such as hypertension, tachycardia, and tachypnea should be monitored as indices of pain in patients who are unable to communicate. Furthermore, administration of long-acting local anesthetic at the completion of the procedure can provide comfort in the immediate postoperative period while waiting for long-acting systemic analgesics (such as oxycodone) to take effect.

Inadequate Amnesia/Anxiolysis ● Consequence As with inadequate analgesia, inadequate anxiolysis and amnesia cause an increase in catecholamine release and cardiac work. Grade 1 complication ● Repair Although high doses of narcotic can cause anxiolysis, this feeling is best controlled with benzodiazepines or propofol. Of note, both agents can cause signiﬁcant dose-related respiratory depression and hypotension, as discussed later. ● Prevention Although small doses of benzodiazepines can be used to provide both anxiolysis and amnesia before and during the start of a procedure, propofol is now the preferred agent owing to its rapid onset/offset proﬁle.4 Increasingly, automated infusion of propofol or other sedatives is being used to ensure a constant blood concentration of agent. Studies have shown that patients prefer such dosing regimens and require less total drug than regimens utilizing bolus doses.5–7

Respiratory System One of the most common serious adverse events associated with surgeon-delivered anesthesia is airway compromise.8 This is most commonly seen in patients receiving conscious sedation.

51

Delay in Control of the Airway and Failure to Recognize Respiratory Compromise ● Consequence Inability to recognize oversedation, hypoxemia, or hypercapnea causes a delay in obtaining expedient control of the airway. This can result in aspiration, altered blood gases, hypoxic brain injury, or cardiac failure. Furthermore, persistent bag-valve ventilation and inability to quickly intubate patients increase the risk of vomiting and aspiration. Respiratory depression can result in impaired oxygenation and/or ventilation. Either of these results can lead to depressed mental status and inability to protect the airway. Furthermore, circulatory derangement (hypotension, bradycardia) can occur if carbon dioxide levels increase or oxygen levels decrease rapidly. Grade 4/5 complication ● Repair All surgeons administering conscious sedation should be trained and comfortable with orotracheal intubation and must have all necessary equipment and medications readily available. At a minimum, all surgeons must have a bag-mask and either oropharyngeal or nasopharyngeal airway immediately available to temporarily control ventilation while arrangements are made for more deﬁnitive airway management. ● Prevention Both the surgeon and the staff should be trained in recognizing signs of inadequate ventilation. These signs may include increased work of breathing, which often manifests as paradoxical movement of the chest and abdomen or use of accessory muscles; agitation or confusion; and decreased sensorium. The surgeon should not wait for hypoxemia (desaturation) to develop before intervening and should be familiar with the dose and duration of effect of reversal agents (see Tables 5–1 and 5–2). Ultimately, it is critical to remember that the decision to intubate a sedated patient is a clinical one and the surgeon should not wait for conﬁrmatory tests or maneuvers prior to intervening if she or he feels that the airway or respiratory system is compromised. It is important for the surgeon to assess the adequacy of the patient’s airway and pulmonary reserve prior to administering a sedative or analgesic agent. Assessment of the airway should include the Mallampati score (ability to visualize the tonsillar pillars), ability to open the mouth fully, submental distance, degree of neck mobility, and presence of facial hair. It has been shown that increasing Mallampati score, inability to open the mouth more than two ﬁnger widths, and submental distance less than three ﬁnger widths are associated with difﬁculty with orotracheal intubation.9 Furthermore, facial hair can make bagmask ventilation difﬁcult by preventing the mask from sealing around the mouth adequately.

52

SECTION I: GENERAL CONSIDERATIONS

Medication-Related Respiratory Depression ● Consequence As noted previously, respiratory depression can result in impaired oxygenation and/or ventilation with resultant circulatory collapse and altered mental status. Grade 1/4 complication ● Repair The narcotic antagonist naloxone can be used to reverse the respiratory effects of narcotics, and ﬂumazenil (Romazicon) can be used to reverse the effects of benzodiazepines. However, the half-life of either agent is much shorter than the drug against which it is directed. Therefore, patients need to be monitored very carefully for recurrence of the side effects. Also, rapid administration of either reversal agent can induce withdrawal and, in the case of ﬂumazenil, seizures. Patients who continue to require reversal agent owing to signiﬁcant overdose should be intubated and mechanically ventilated until the respiratory depressive effects of the medication(s) have fully resolved. ● Prevention Most medications used for analgesia and amnesia/ anxiolysis can cause respiratory depression. This lifethreatening complication can be prevented most effectively by using only small, incremental dose of medications and being mindful of the synergistic (not additive) effects of opioids and benzodiazepines.

Cardiovascular System Hypotension Opioid medications provide mainly analgesia with little to no cardiac depression. However, they cause varying degrees of histamine release. Histamine release is primarily caused by morphine, followed by hydromorphone, and is least likely to occur with fentanyl. Other commonly used sedatives, such as propofol and benzodiazepines, have a direct vasodilatory effect. ● Consequence Histamine release can result in peripheral vasodilatation and hypotension in the preload-dependent (hypovolemic) patient. Similarly, benzodiazepines and propofol can cause hypotension if given quickly or in high doses, especially in volume-depleted patients. Grade 1 complication ● Repair Medication-related hypotension can be treated in almost all cases with intravenous ﬂuids alone. Rarely, a small dose of an α1-receptor agonist (e.g., phenylephrine) may be needed to temporarily control the blood pressure while ﬂuid resuscitation is continued.

● Prevention The vasodilatory effects of medications can be minimized by slow administration of small doses. Furthermore, adequate hydration prior to administration of moderate to high doses will further decrease the hypotensive effects of the medication(s), although this scenario is most often addressed in the inpatient setting, in which deeper sedation is often required.

End-Organ Ischemia ● Consequence Use of local anesthetics containing epinephrine in endorgans can cause ischemia owing to vasospasm. Although rare, ischemia can threaten end-organ viability. Grade 4 complication ● Repair No speciﬁc therapy exists to reverse the vasoconstrictive effects of epinephrine on terminal arterioles. The patient should be kept well hydrated to maximize perfusion until the effects of epinephrine wear off. ● Prevention Epinephrine-containing local anesthetics should not be used near organs supplied by a terminal arteriole. Such organs include ﬁngers, toes, ears, tip of the nose, and penis.

Bupivacaine-Induced Arrhythmia ● Consequence Intravascular injection of bupivacaine or toxic doses of bupivacaine can induce potentially lethal ventricular dysrhythmias. Such dysrhythmias are characteristically nonreversible and, thus, frequently fatal. Grade 5 complication ● Repair Standard advanced cardiac life support measures should be instituted. However, patients are rarely resuscitated from a dysrhythmia related to an intravascular injection of bupivacaine or overdose. ● Prevention As noted previously, needle aspiration should be performed prior to injecting the local anesthetic to ensure interstitial injection, and the surgeon must be familiar with the dosing regimen for bupivacaine. Table 5–3 contains the dosing and pharmacologic proﬁle of bupivacaine and other commonly used local anesthetics.

Hematologic System Methemoglobinemia A common anesthetic pitfall that can acutely affect the surgical patient hematologically is methemoglobinemia resulting from aerosolized anesthetic used for endoscopic

5 ANESTHESIA FOR THE SURGEON procedures. Lidocaine; benzocaine, tetracaine, and butamben (Cetacaine); have been associated with methemoglobinemia, with Cetacaine implicated most often.10,11 ● Consequence Because methemoglobin cannot transport oxygen, peripheral tissues are rendered ischemic, and profound acidosis with cardiovascular collapse can occur quickly.12 Patients will become cyanotic, and the pulse oximeter will show low-normal oxygen saturation despite the ﬁnding of high dissolved oxygen on an arterial blood gas sample. Grade 1/2 complication ● Repair The most effective treatment for methemoglobinemia is intravenous methylene blue (1–2 mg/kg; maximal dose is 7 mg/kg). This reduces the iron in the heme molecule back into a state at which it can once again transport oxygen. Reversal of cyanosis and recovery of cardiovascular instability should be noted in 20 to 40 minutes. Of note, intubation and mechanical ventilation with high inspired oxygen levels will not be of assistance. ● Prevention The most effective way to prevent this occurrence is to use as little topical anesthetic as possible. Although the exact mechanism underlying this disorder is not known, most reports suggest it is a dose-dependent phenomenon.

PITFALLS FOR SPECIFIC BLOCKS 13 The landmarks for each of the blocks discussed later are summarized in Table 5–4. In addition, Figures 5–1 to 5–4 depict the anatomic location for each injection.

53

Ilioinguinal Nerve Block The addition of ilioinguinal nerve block to the anesthetic regimen used for inguinal herniorrhaphy is associated with a lower cost and higher patient satisfaction score than those of general anesthesia or systemic sedation with local anesthesia alone.14,15 A 10- to 20-ml mixture of 0.25% bupivacaine and 1% lidocaine is injected through all layers of the anterior abdominal wall approximately 1.5 cm medial to the anterior superior iliac spine (see Fig. 5–1). This block is not intended to be used as the sole modality for analgesia during inguinal herniorrhaphy; rather, it is meant to supplement an overall regimen so as to provide better postoperative pain control and facilitate discharge from the recovery area. ● Consequence Failure to anesthetize the ilioinguinal nerve can result from poor injection technique. This can be due to failure to inject deep to the oblique muscles of the anterior abdominal wall or to failure to inject a sufﬁcient amount of agent. Although it is possible to injure the cecum or sigmoid colon during this procedure, there are no reports of bowel injury resulting from this injection—most likely because a small-bore needle is used, and unintentional injection into the bowel is innocuous. The consequence of such an injection will be inadequate analgesia and postoperative pain. Grade 1 complication ● Repair and Prevention Because the purpose of this block is postoperative pain control, it is very difﬁcult to assess whether proper technique has been used intraoperatively. Deep inﬁltration with 20 ml of local anesthetic injected along the needle tract during needle withdrawal is the best method to try to ensure adequate neural blockade.

Table 5–4 Landmarks for Regional Blocks Type of Block

Landmarks

Comments

Finger

1 cm distal to the webspace, along the radial and ulnar sides of the ﬁnger

Epinephrine-containing anesthetics are contraindicated

Median nerve

Deep to the ﬂexor retinaculum, between the tendons of the ﬂexor carpi radialis and the palmaris longus or just lateral to the tendon of the ﬂexor carpi radialis

Aspirate prior to injection to avoid inadvertent arterial injection

Ulnar nerve

Deep to the ﬂexor retinaculum, medial to the tendon ﬂexor carpi ulnaris tendon, and also along the styloid process of the ulna

Usually requires two separate injections to anesthetize the dorsal and volar branches

Radial nerve

Wide area extending from the snuff box toward the ulnar aspect of the wrist

Posterior ankle

1 cm above the posterior aspect of the medial and lateral malleoli, deep to the ﬂexor retinaculum

Anesthetizes sole of foot. Aspirate prior to injection to avoid injection into the posterior tibial artery/vein

Anterior ankle

1 cm above the anterior aspect of the medial and lateral malleoli

Anesthetizes the dorsum of the foot

From Salam GA. Regional anesthesia for ofﬁce procedures: part II: extremity and inguinal area surgeries. Am Fam Physician 2004;69:896–900.

54

SECTION I: GENERAL CONSIDERATIONS Iliohypogastric n. Ilioinguinal n.

Transvers abdominus m.

Quadratus lumborum m.

Internal Oblique m.

External Oblique m.

Psoas major m. Genitofemoral n.

Lateral cutaneous branch of subcostal n. Femoral br. Genital br.

2

1 Genital br. Anterior scrotal ilioinguinal n.

Figure 5–1 Ilioinguinal nerve block. Excessive injection of anesthetic can result in femoral nerve palsy, whereas inappropriately placed injectate will manifest as ineffectual analgesia postoperatively.

Inadvertent Femoral Nerve Block ● Consequence Injection of an excessive amount of local anesthetic or injection in the incorrect plane at the time of attempted placement of ilioinguinal nerve block can result in transient femoral nerve palsy. This complication has been reported in 5% of adults and 10% of children undergoing elective inguinal herniorrhaphy.16,17 Until the block resolves, patients will complain of signiﬁcant weakness or inability to bear weight on the affected extremity. Grade 1 complication ● Repair This block is most often detected in the recovery room after the patient attempts to ambulate, and it cannot be reversed once it occurs. The duration of the block depends on the type and amount of anesthetic administered. ● Prevention The plane between the transversus abdominis and the transversalis fascia fuses laterally with the iliacus fascia, which contains the femoral nerve.18 It is not possible to avoid injection between these muscles because the

surgeon cannot discriminate between them during a percutaneous injection. However, this complication can be avoided by limiting the volume of injectate and thus limiting the amount of anesthetic that can pool around the femoral nerve.

Finger Block Two nerves travel on each side of each ﬁnger. The needle is inserted 1 cm distal to the webspace at the medial and radial sides of the digit (see Fig. 5–2). One milliliter to 2 ml of 1% lidocaine or 0.25% to 0.5% bupivacaine is injected.

Intravascular or Intraneural Injection ● Consequence Intravascular or intraneural injection of local anesthetic can have local and/or systemic manifestations. Locally, a hematoma may cause short- to moderate-term neuropraxia and/or pain or ischemia. As discussed previously, systemic manifestations can range from hypotension to seizures, depending on the agent(s) injected. As noted in the section on “end-organ ischemia,” epinephrine-containing anesthetics are absolutely contraindicated for this particular block and should not be used. Grade 4/5 complication

5 ANESTHESIA FOR THE SURGEON

55

● Repair The landmarks at the wrist should be identiﬁed, as instructed later, and a new attempt should be made to anesthetize the hand. Three milliliters to 5 ml of anesthetic are usually sufﬁcient to adequately anesthetize the hand.

Needle entry sites Dorsal digital n.

Dorsal digital n.

Proper palmar digital n.

Figure 5–2 Digital block. Note the proximity of the vessels to the digital nerves. Epinephrine-containing solutions are absolutely contraindicated because they can result in profound arteriole spasm and digital ischemia. Furthermore, the volume of injectate should be limited to minimize compression of the vessels.

● Prevention As depicted in Figure 5–3, the median nerve travels deep to the ﬂexor retinaculum at the wrist, medial to the ulnar aspect of the ﬂexor carpi radialis (FCR). The tendon of this muscle can be noted by asking the patient to ﬂex the wrist. Anesthetic is then injected just medial to the medial border of the FCR tendon. Also, anesthetic can be injected in the space between the tendons of the FCR and the palmaris longus. This space is identiﬁed by asking the patient to ﬂex the wrist and oppose the thumb and ﬁfth digit. The correct depth for injection is felt as a loss of resistance as the needle passes through the ﬂexor retinaculum. As with ﬁnger blocks, care must be taken to ensure that neither vascular or intraneural injection takes place.

Ulnar Nerve Block ● Repair Little treatment—other than elevation, warm compresses, and hydration to optimize blood ﬂow to the affected extremity—is possible for local complications. The treatment of systemic toxicity is discussed previously. ● Prevention The best way to prevent such complications is to aspirate prior to injecting the anesthetic to ensure interstitial inﬁltration as opposed to intravascular injection. Furthermore, anesthetic should not be injected if the patient complains of “shooting” or “electric” pain on needle entry. Such symptoms suggest intraneural placement of the needle. The needle should be removed and reinserted. As already mentioned, epinephrinecontaining anesthetics should not be used for digital blocks.

The ulnar nerve provides sensation to the surfaces of the palm and ﬁngers not covered by the median nerve and also to the dorsal surface of the hand. Inappropriate needle placement has the same consequences and repair as those discussed previously regarding median nerve blocks. The ulnar nerve divides in the area of the wrist to innervate the volar and dorsal aspects of the hand. The volar branch is anesthetized by injecting lateral to the tendon of the ﬂexor carpi ulnaris, taking care to ensure that intravascular injection into the ulnar artery does not occur. The dorsal branch is anesthetized by placing the anesthetic along the styloid process of the ulna (see Fig. 5–3).

Radial Nerve Block

The median nerve provides sensation to the radial aspect of the palm, the volar surface of the ﬁrst three digits (thumb, index, and middle ﬁnger), and the radial half of the ring ﬁnger.

The radial nerve provides sensation to the dorsum of the hand and the ﬁrst three ﬁngers proximal to the distal interphalangeal joint. A broad area along the dorsal aspect of the wrist must be inﬁltrated to anesthetize this area. Injection is begun in the area of the snuffbox and extended to the ulnar side of the wrist along the dorsal aspect of the hand. Because this injection is not near major blood vessels, the chance of inadvertent intravascular injection is lessened.

Incorrect Positioning of the Needle for Injection

Ankle Block

● Consequence Incorrect identiﬁcation of the necessary landmarks for injection will result in ability to adequately anesthetize the hand. Grade 1 complication

Local anesthetic cannot be used to anesthetize only a portion of the sole of the foot owing to marked pain associated with the procedure. As such, a regional (ankle) block is needed. The sole of the foot is anesthetized utilizing a posterior ankle block, whereas the dorsum

Median Nerve Block

56

SECTION I: GENERAL CONSIDERATIONS

Ulnar styloid process

Median n. Distal radial prominence

Ulnar n. Ulnar artery

A

Radial artery

Flexor carpi radialis tendon

Flexor carpi radialis tendon Palmaris longus tendon

B of the foot is made insensate using an anterior ankle block.

Incorrect Positioning of the Needle for Injection ● Consequence As with the blocks noted previously, incorrect identiﬁcation of the necessary landmarks for injection will result in nonsatisfactory anesthesia. Grade 1 complication ● Repair The landmarks at the ankle should be identiﬁed, as instructed later, and a new attempt should be made to anesthetize the foot. Ten milliliters of anesthetic is usually sufﬁcient to adequately anesthetize each aspect of the foot. ● Prevention As seen in Figure 5–4, the nerves that have to be anesthetized for a posterior ankle block are the sural nerve and tibial nerve. The sural nerve is best accessed 1 cm above and posterior to the lateral malleolus. The tibial nerve is located posterior to the posterior tibial artery

Figure 5–3 Median and ulnar nerve blocks. Care must be taken to prevent either intraneural or intra-arterial injection.

and deep to the ﬂexor retinaculum. It is best anesthetized by inserting the needle 1 cm above and posterior to the medial malleolus, taking care to aspirate prior to injection to avoid intra-arterial injection. As with inﬁltration of the median and ulnar nerves, loss of resistance indicates that the needle has passed through the ﬂexor retinaculum and is at the proper depth for injection. An anterior ankle block is done by anesthetizing the superﬁcial peroneal and saphenous nerves. The superﬁcial peroneal nerve is blocked by injecting just above and anterior to the lateral malleolus. The saphenous nerve is blocked by injecting just above and anterior to the medial malleolus.

INPATIENT ANESTHETIC PITFALLS FOR THE SURGEON Preoperative Medications In general, all preoperative medications that do not interfere with the planned procedure (such as anticoagulants) should be continued the day of surgery—this is especially

5 ANESTHESIA FOR THE SURGEON

57

Ankle Section

A

2

1 Tibialis anterior tendon

Superficial peroneal n.

Deep peronal n. Saphenous v. Saphenous n. Tibialis posterior tendon

Tibia

Posterior tibial a.

Fib

Posterior tibial n. Fibular brevis m. Calc Sural n.

B

Figure 5–4 Ankle block.

true of antihypertensive medications, most notably βblocking agents. Current literature suggests that appropriately administered β-blockade started weeks prior to surgery reduces perioperative ischemia and may reduce the risk of myocardial infarction (MI) and death in high-risk patients.19–22 Perioperative α2-agonists may have similar effects.23,24 ● Consequence Stopping medications acutely can result in impaired homeostasis. This is classically noted when clonidine is stopped. A severe rebound tachycardia can occur. Similarly, serum levels of most antiseizure medications can drop precipitously if more than one dose is omitted from the daily regimen. Steroids should be continued perioperatively, although there are neither level I nor II data to guide management of patients who are on chronic steroids. Although many surgeons and anesthesiologists also give at least one “stress” dose of steroid (100 mg hydrocortisone intravenously) at the time of induction to possibly prevent addi-

1

2

sonian crisis, little evidence supports this practice, and the decision to administer steroids must take into account the anticipated surgical stress and probability of adrenal insufﬁciency. In a review article, Salem and colleagues25 summarized the current role of perioperative steroids and offered guidelines to the need for supplemental perioperative dosing. Grade 1/2 complication ● Repair and Prevention Patients should be instructed to stop preoperative medications only when absolutely necessary. Most frequently, this involves stopping anticoagulants. In this situation, the time that the patient’s coagulation parameters are normalized should be kept to a minimum, depending on the reason underlying the need for anticoagulation. When possible, aspirin and/or clopidrogrel should be continued. ● Patients on chronic β-blocking agents should be

given an intravenous β-blocker until they are able to

58

SECTION I: GENERAL CONSIDERATIONS

take oral medications postoperatively. This is a core measure monitored by the Centers for Medicare and Medicaid Services.26 ● Postoperative dosing of pain medication should be adjusted to accommodate the tolerance that patients on chronic opioids develop. It is common for patients with chronic pain to require dosages up to 10 times higher than that required to obtain analgesia in a patient who is opioid naïve.27 ● Patients with diabetes should be instructed to take half of their normal dose of short-acting insulin on the morning of surgery. Their procedures should be scheduled as morning cases to minimize their nothingby-mouth (NPO) time. Patients should be instructed to refrain from taking any long-acting insulin or oral hypoglycemic drug on the day of surgery.28

Neurologic Pitfalls Exacerbation of Cervical Spine Injury during Intubation Cervical spine injuries may easily be worsened with neck ﬂexion or extension during intubation. The majority of injuries are due to fracture and dislocation of the vertebral column.

● Repair and Prevention The anesthesiologist must be notiﬁed preoperatively of the level and timing of the injury in order to be prepared for this hyperreﬂexic state. Pharmacologic intervention may be needed to restore homeostasis intraoperatively with the use of potent arterial and vasodilators such as sodium nitroprusside, nitroglycerin, and/or nicardipine.

Patients with Peripheral Motor Neuropathy or History of Stroke Patients presenting with a history of stroke, spinal cord injury, or peripheral motor neuropathy (secondary to Guillain-Barré, polio, amyotrophic lateral sclerosis, myasthenia gravis, musculodystrophy) have a potentially unique muscle physiology that warrants further examination to plan the proper anesthetic regimen. The time since infarct or onset of disease is very important to the anesthesiologist, who may be required to administer a depolarizing muscle relaxant (succinylcholine) to facilitate intubation.

● Consequence Exacerbation of a cervical spine injury can result in signiﬁcant (and possibly permanent) neurologic dysfunction, including high spinal paralysis. Grade 4 complication

● Consequence Patients with neuromuscular disorders are prone to severe hyperkalemia after administration of succinylcholine, a depolarizing muscle relaxant. The hyperkalemic response is directly related to the amount of paralyzed muscle mass and the time lapse since insult owing to up-regulation of the acetylcholine receptor in paralyzed muscle.33 Severe hyperkalemia can result in a fatal cardiac dysrhythmia. Grade 5 complication

● Repair and Prevention Although it is controversial whether a rigid cervical collar must be kept in place during direct laryngoscopy, it is essential to maintain in-line cervical traction throughout the intubation process. Furthermore, a ﬁberoptic bronchoscope may be used instead of direct laryngoscopy to secure the airway in patients with a known or suspected unstable cervical spine injury.29–31

● Repair Patients with sudden cardiac dysrhythmia after administration of succinylcholine should be suspected of having severe hyperkalemia (Box 5–1). In addition to standard advanced cardiac life support, measures directed at acutely lowering the serum potassium level should be instituted immediately. Such measures include the judicious use of calcium gluconate or chlo-

Paralyzed Patients The level of injury or lesion and time since injury of patients with known spinal cord disease presenting for elective or semielective surgery are of critical importance. Overactivity of the sympathetic nervous system is common with transactions at T5 or above but is unusual with injuries below T10 and usually presents days to weeks after injury.32 ● Consequence Transection of descending inhibitory neurons leaves the spinal cord with innate excitatory reﬂexes. These reﬂexes can potentially lead to autonomic hyperreﬂexia with minimal surgical stimulation. Such stimulation may lead to intense uninhibited sympathetic discharge and profound tachycardia and hypertension. Grade 1 complication

Box 5–1 Conditions Causing Susceptibility to Hyperkalemia after Succinylcholine Administration ● ● ● ● ● ● ● ● ● ● ● ● ● ●

Extensive burn injury (>24 hr old) Massive trauma Spinal cord transection (>48 hr) Acute renal failure Stroke Massive trauma/crush injury Prolonged immobility (>7 days) Guillain-Barré syndrome Severe Parkinson disease Acute tetanus exacerbation Acidosis with hypovolemia Profound sepsis Severe intra-abdominal sepsis Congenital muscle diseases

5 ANESTHESIA FOR THE SURGEON Table 5–5 Complications of Malignant Hyperthermia Sign

Physiologic Effect

Muscle rigidity/spasm

Inability to ventilate, hyperkalemia

Hyperkalemia

Cardiac dysrhythmia

Rhabdomyolysis, myoglobinuria

Renal failure

Increase metabolism, acidosis

Cardiovascular collapse due to extreme tachycardia or severe acidosis, hypoxemia

Fever (late sign)

Seizures, cerebral edema, brain anoxia

59

hypovolemia resulting from severe pyrexia. Severe hyperkalemia should be treated with insulin/glucose, bicarbonate, ﬂuid resuscitation, and/or dialysis as indicated by the patient’s electrocardiogram and hemodynamic status.35

● Prevention Nondepolarizing muscle relaxants should be used in this patient population to avoid potential hyperkalemia.

● Prevention The most effective way to prevent MH is to recognize its risk factors, most notably family history, and avoid the use of volatile anesthetics and succinylcholine in these patients. The syndrome is inherited as an autosomal dominant trait. Furthermore, the surgeon and anesthesia provider must be familiar with signs of MH. Of note, fever is a very late sign. The earliest sign of MH is a sudden increase in the partial pressure of exhaled carbon dioxide and masseter muscle spasm. Patients who may have experienced MH should be referred to the national registry for MH (1-800-MHHYPER) for proper evaluation and counseling.

Malignant Hyperthermia Patients with musculodystrophy, central cord disease, osteogenesis imperfecta, and those with a family history of malignant hyperthermia (MH) are at risk for developing this syndrome.

Patients with Parkinson Disease Patients with Parkinson disease must continue their medications throughout the perioperative period. Furthermore, speciﬁc medications may worsen muscle rigidity and should be avoided.

● Consequence MH is a rare (1 : 15,000) life-threatening condition that can develop as a result of volatile anesthetic or succinylcholine administration. It is characterized by an acute hypermetabolic state occurring up to 24 hours after administration of a volatile general anesthetic or succinylcholine. The consequences of this syndrome are listed in Table 5–5. Life-threatening complications can include muscle rigidity, which can prevent adequate ventilation; severe hyperkalemia and cardiac dysrhythmia; myoglobinuria and acute renal failure; severe hyperthermia, leading to seizures and brain anoxia or cerebral edema; and metabolic acidosis and cardiovascular collapse.34,35 Grade 1/4/5 complication

● Consequence Patients with Parkinson disease should continue their medications because abrupt withdrawal may lead to difﬁculty with intubation and ventilation owing to worsened muscle rigidity. Grade 1 complication

ride, intravenous insulin and dextrose 50%, sodium bicarbonate, and hyperventilation.

● Repair If MH occurs intraoperatively, then surgery must be aborted as expediently as possible. Dantrolene is the only approved medication for the treatment of MH. Its mechanism of action involves stabilization of the sarcoplasmic reticulum to prevent further release of calcium from the skeletal muscle stores and ongoing muscle contraction. The dose is 2.5 mg/kg every 5 minutes until symptoms abate or until a maximum dosage of 10 mg/kg is reached, and then 1 mg/kg every 6 hours for 24 to 48 hours. All patients should be cooled aggressively with ice packs and intubated with 100% oxygen with hyperventilation to meet their high oxygen and metabolic demands during the crisis phase. Massive ﬂuid resuscitation may be needed to prevent renal failure owing to myoglobinuria and

● Repair and Prevention Phenothiazines, butyrophenones, and metoclopramide should not be given to patients with Parkinson disease because these agents can exacerbate symptoms as a consequence of their antidopaminergic activity.36

Cardiovascular Pitfalls Preoperative Evaluation and Clearance The most common reason for delay in elective surgery is inadequate cardiac work-up and optimization of medical therapy in the setting of ischemic heart disease. Speciﬁc criteria related to preoperative evaluation and medical clearance for surgery are discussed elsewhere. Patients with Aortic and Mitral Stenosis ● Consequence Severe aortic stenosis poses a great perioperative risk for noncardiac surgery. If stenosis is moderate (aortic valve oriﬁce area of 0.7–0.9 cm2 and aortic valve index of 0.5 cm2/m2) with symptomatic impairment or stenosis is critical (aortic valve oriﬁce area of <0.7 cm2 with an aortic valve index of <0.5 cm2/m2), then elective surgery should be postponed until after aortic valve replacement. Mortality risk approaches 10% in

60

SECTION I: GENERAL CONSIDERATIONS

certain patient populations (age >70, those with chronic renal insufﬁciency or with insulin-dependent diabetes mellitus) undergoing noncardiac surgery with critical aortic stenosis.23,37 Grade 5 complication ● Repair and Prevention Because aortic and mitral stenoses demand a long diastolic ﬁlling period, adequate β-blockade should be started preoperatively to avoid symptoms of heart failure and pulmonary edema. Sinus rhythm should be maintained with antiarrhythmic medications as needed, and these should be continued perioperatively. Furthermore, afterload-reducing agents (e.g., hydralazine or calcium channel blocker) should not be used in patients with aortic stenosis to maximize forward ﬂow and prevent heart failure. Instead, the primary goals of hemodynamic management should focus on preservation of diastolic blood pressure and coronary perfusion pressure at all costs to avoid hypoperfusion of the endocardium.38

Hypotension on Induction Many anesthetics (inhalational and intravenous) possess potent vasodilatory and/or cardiodepressant properties. Thus, patients frequently become hypotensive during induction and require aggressive therapies for rapid stabilization. ● Consequence Signiﬁcant, prolonged hypotension that lowers mean arterial blood pressure to less than 25% of preinduction levels can lead to end-organ dysfunction, including possibly stroke, MI, acute liver injury, acute tubular necrosis of the kidney, retinal artery hypoperfusion leading to optic nerve ischemia and postoperative blurred vision or blindness, and spinal cord malperfusion. Grade 4 complication ● Repair Treatment includes the use of volume loading and small doses of a vasopressor such as ephedrine or phenylephrine. On rare occasions, hypoperfusion of the brainstem and coronary arteries may necessitate the use of small bolus doses of epinephrine to regain sympathetic tone and cardiac output. ● Prevention Hypertensive patients are frequently intravascularly volume depleted, and adequate intravenous ﬂuids should be given prior to induction of anesthesia. This is especially true if patients are acutely ill and require hospitalization prior to surgery. Propofol, midazolam, and sodium thiopental are commonly used drugs for induction of anesthesia, but all possess signiﬁcant potential for reducing systemic vascular

resistance. In patients who will not tolerate even minimal hypotension, drugs such as etomidate or ketamine may be more appropriate. Etomidate, a GABAnergic agent, has minimal effects on the cardiovascular system and does not release histamine. A mild reduction in peripheral vascular resistance may lead to a slight decline in mean arterial blood pressure, but myocardial contractility, cardiac output, and cerebral perfusion pressure are unchanged. Of note, etomidate has a side effect proﬁle that includes short-term myoclonus in 30% of individuals. Furthermore, multiple doses of etomidate and infusions of etomidate can dramatically suppress adrenal function, which can result in refractory hypotension requiring steroid supplementation. Etomidate has also been linked to increased levels of postoperative nausea when used as an induction agent.39–44 Ketamine affects multiple sites throughout the central nervous system and acts as an N-methyl-D-aspartate (NMDA) antagonist. Its effects are to functionally and temporarily dissociate conduction from the thalamus to the cortical system and to the limbic system. Ketamine’s effects on the cardiovascular system are primarily stimulatory in nature, causing an increase in arterial blood pressure, heart rate, cardiac output, and systemic vascular resistance. For this reason, it has become a successful induction agent in the setting of profound hypovolemia and is not recommended in the setting of coronary artery disease, uncontrolled hypertension, congestive heart failure, or aortic aneurysm or dissection. It is also a profound bronchodilator and a salivary stimulant as well. Ketamine’s side effect proﬁle includes increased intracranial pressure and cerebral metabolism. It is also an intense dissociative amnestic agent that can cause unwanted hallucinations.45

Perioperative Pacemaker and Implantable Cardioverter-Deﬁbrillator Management Patients with pacemaker or implantable cardioverterdeﬁbrillators (ICDs) should have their device evaluated immediately prior to the start of the operation and immediately afterward. The deﬁbrillator function should be turned off, and the pacemaker should be in a default “demand-only” mode with a set minimum ventricular rate to avoid asystole or “R-on-T” phenomena during the procedure. ● Consequence Electrocautery may generate current in the vicinity of the device. The following may occur in response to the extra electrical current: ● Temporary or permanent resetting to a backup, reset,

or noise-reversion pacing mode is of little consequence because the backup rate is usually sufﬁcient to maintain adequate cardiac output. ● Temporary or permanent inhibition of pacemaker output can cause prolonged periods of bradycar-

5 ANESTHESIA FOR THE SURGEON dia, depending on the patient’s endogenous heart rate. ● An increase in pacing rate owing to activation of the rate-responsive sensor can cause erratic changes in heart rate and cardiac output. ● ICD ﬁring due to activation by electrical noise will result in unnecessary deﬁbrillation that may result in myocardial injury. ● Myocardial injury at the lead tip that may cause failure to sense and/or capture. Grade 1/2 complication ● Repair If a hemodynamically unstable rhythm becomes present during surgery then immediate external cardioversion is warranted and paddles should be placed as far from the implanted device as possible to minimize myocardial injury at the tips of the leads. In emergent cases, when there is insufﬁcient time or lack of proper equipment to reprogram the ICD, a magnet can be placed over the device intraoperatively. This reverts the pacemaker to its backup demand-only setting and deactivates the deﬁbrillation function in most (but not all) devices. ● Prevention As noted previously, the deﬁbrillation function of the ICD should be turned off and the pacer be placed in a demand mode at a ﬁxed rate prior to the start of operation, and the use of monopolar cautery should be minimized. Adverse interactions are more likely if the electrocautery is unipolar and return lead placement leads the current through the axis of the pacemaker/ ICD. Finally, the anesthesiologist should know the patient’s underlying rhythm and the settings of the pacemaker and be prepared to intervene appropriately if the cardiac rhythm changes. All ICDs should be interrogated postoperatively and restored to their preoperative settings.23,46,47

Pulmonary Pitfalls Optimization of Asthma Regimen ● Consequence Failure to optimally control asthma preoperatively can lead to difﬁculty ventilating the patient intraoperatively or inability to extubate postoperatively. Grade 1 complication ● Repair The inciting cause for the bronchospasm should ﬁrst be established and disease-speciﬁc treatment should be initiated. Intraoperative or postoperative asthma exacerbation can be treated with oxygen, aggressive bronchodilator therapy with β2-agonists, and inhaled anticholinergics and/or inhaled or intravenous epinephrine. The bronchial effects of intravenous steroids

61

are not immediate and may take effect after 4 to 6 hours; therefore, steroids should be given early if the patient does not respond to initial treatment. General anesthesia with endotracheal intubation facilitates the use of inhalational anesthetic agents, which are profound bronchodilators and may serve as last-line treatment of severe bronchospasm. Of note, inadequate anesthesia is the most common cause of an asthmatic attack during surgery. ● Prevention Preoperative wheezing or dyspnea suggests poorly controlled disease. Respiratory tract infections are common stimuli that evoke acute exacerbations of asthma; therefore, delaying surgery 2 to 3 weeks after clinical recovery from an upper respiratory tract infection in patients with asthma is recommended. Reﬂex-induced laryngospasm and bronchospasm may be prevented with 1 mg/kg lidocaine given intravenously 2 minutes prior to airway manipulation. Finally, an adequate depth of anesthesia should be maintained throughout the period of surgical stimulation. β-Blocker–induced wheezing in patients with reactive airway disease is better treated with inhaled anticholinergic agents (e.g., ipratroprium) than with β2-agonists.48–51

Improving Outcomes in Patients with Obstructive Sleep Apnea ● Consequence Patients with obstructive sleep apnea (OSA) are becoming increasingly more common and now approach 5% to 9% in the general U.S. population. OSA is commonly found in obese, middle-aged men. OSA is now considered a perioperative outcomes risk factor for morbidity and mortality. The risk of postoperative episodic hypoxemia, acute hypercapnia, reintubation, delirium, MI, unplanned postoperative intensive care unit admission, and death is signiﬁcantly increased in patients with OSA undergoing surgery. The need for postoperative analgesia with narcotics places these patients at signiﬁcantly more risk for respiratory failure, hypoxia, and death in the immediate postoperative period owing to their extreme sensitivity to changes in the CO2 respiratory response curve. Grade 2/5 complication ● Repair Supplemental oxygen and utilization of continuous positive airway pressure (CPAP) or bilateral positive airway pressure (BiPAP) immediately after extubation will decrease the risk of transient hypoxia and hypercapnia, especially in those patients who required CPAP at home prior to surgery. The judicious use of naloxone to treat opioid-induced respiratory depression is acceptable, but small doses should be given initially (40 mcg every 2 min) until effect so as not to fully reverse the analgesia provided.

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SECTION I: GENERAL CONSIDERATIONS

● Prevention CPAP training should be instituted prior to date of surgery, and plans should be made in advance for its use in the immediate postoperative period. The use of CPAP immediately after extubation has been shown to clearly decrease the development of hypoventilatory atelectasis and hypoxemia and to improve outcomes. Assessment of neck circumference and obtaining sleep studies preoperatively may be beneﬁcial in the setting of OSA to determine the amount of hypopnea, hypoxia, and apnea experienced during sleep. Planned use of regional anesthesia or local anesthesia infusions in wound sites will decrease the systemic opioid pain requirements and decrease the risk of respiratory depression leading to hypoxia and death.28,50,52,53

The Pregnant Patient Approximately 1% to 2% of pregnant patients require nonobstetric surgery during their pregnancy. The most common procedures are appendectomy, cholecystectomy, and diagnostic laparoscopy for abdominal pain. In general, anesthesia poses a risk to the fetus throughout the gestational period, although the risk is highest during the ﬁrst trimester and decreases thereafter. Conversely, the risk of anesthesia to the mother is lowest during the ﬁrst trimester of pregnancy and increases thereafter. Thus, only urgent or emergent operations should be performed during the pregnant state and for 6 weeks postpartum.54

Maternal Bleeding ● Consequence The pregnant patient has a high resting cardiac output and expanded blood volume, which results in a relative dilutional anemia. This means that the patient is able to withstand bleeding without manifesting many of the signs associated with impending cardiac collapse, but she has a decreased ability to augment oxygen delivery once a critically low hemoglobin level is reached. Failure to appreciate subtle changes in blood pressure or heart rate may result in shunting of blood away from the placenta and fetal hypoxemia. The fetus cannot tolerate a state of low oxygen delivery because it is in a relatively hypoxic environment at baseline. Grade 4 complication ● Repair and Prevention Bleeding must be minimized and intravenous volume status maintained closely in the pregnant patient. Patients beyond 16 weeks’ gestation should be positioned 20° to 30° left lateral decubitus to move the gravid uterus away from the vena cava and optimize venous return to the heart. Blood transfusion is recommended early in pregnant patients whose bleeding is not readily controlled intraoperatively. The surgeon must keep the anesthesia provider aware of excessive

bleeding. Use of exogenous vasopressors must be avoided because these medications also cause shunting of blood away from the placenta and fetal hypoxemia.54,55

Hypoxemia during Intubation ● Consequence Maternal functional residual capacity decreases markedly as the uterus distends during fetal growth. Furthermore, maternal and fetal metabolism cause a net increase in maternal minute ventilation (to remove excess CO2) and oxygen consumption. Combined, these effects render the mother susceptible to rapid desaturation during periods of apnea. Hypoxic episodes are not tolerated by the fetus, which lives in a relative hypoxic environment. Progesterone, the dominant hormone of pregnancy, relaxes all smooth muscle. This causes the stomach to lose motility, and so all pregnant patients should be assumed to have a full stomach. Failure to intubate the patient quickly using rapid-sequence methods and the Sellick maneuver (compression of the trachea onto the esophagus) can result in aspiration during induction and is one of the leading causes of maternal death during anesthesia.54 Grade 4/5 complication ● Repair In situations in which the patient desaturates or aspirates during induction, the patient should be immediately intubated and placed on high-ﬂow oxygen to minimize the hypoxic period. Failure to intubate in the setting of full-term pregnancy warrants immediate rescue maneuvers (as discussed later) and possible emergency tracheostomy. Decisions regarding subsequent extubation must be tailored to the patient’s clinical condition once it is stabilized. ● Prevention The patient should be preoxygenated while awake and spontaneously breathing prior to induction, and only physicians who are facile and well-versed in intubation should attempt to intubate a patient who is pregnant. Rapid-sequence techniques, utilizing little or no bag ventilation and the Sellick maneuver, should be used to reduce the likelihood of aspiration during induction. Emergency airway equipment, including laryngeal mask airways, oral and nasal airways, and ﬁberoptic bronchoscopes, should be available for immediate use in the setting of failed orotracheal intubation. These advanced interventions are best performed by a trained anesthesiologist.

Spontaneous Abortion and Fetal Malformation All surgical procedures requiring more than local anesthesia are associated with up to a ﬁvefold increase in the risk

5 ANESTHESIA FOR THE SURGEON of spontaneous abortion. The risk is highest during the ﬁrst trimester and decreases thereafter. Organogenesis takes place from the 3rd to the 8th week of gestation. ● Consequence All volatile anesthetics are presumed to be teratogenic during the ﬁrst trimester, and all opioids and sedatives freely cross the placental barrier. The fetus has a markedly decreased ability to metabolize medications because its liver has not fully developed. Therefore, all medications have much more lasting effects on the fetus than on the mother. Because of this, elective procedures requiring more than local anesthetic or neuroaxial blockade (e.g., spinal or epidural anesthesia) must be avoided during the ﬁrst trimester. Grade 4/5 complication ● Prevention Although there are no clear studies evaluating the effects of neuroaxial blockade on the fetus during the ﬁrst trimester, it has been shown that neuroaxial blockade increases uterine and placental blood ﬂow. However, such blockade is also more difﬁcult to titrate and can result in maternal hypotension. The surgeon, obstetrician, and anesthesia provider must communicate to identify patients who can be managed with neuroaxial blockade and possibly spared the effects of general anesthesia.55,56

The Pediatric Patient Failure to Recognize Difﬁcult Intubation ● Consequence Pediatric patients have a large head and tongue, an anterior airway, and a long and “ﬂoppy” epiglottis. These factors make intubation in all pediatric patients more challenging than in adults. Furthermore, an upper respiratory tract infection within the last 2 to 4 weeks has been shown to increase the incidence of laryngospasm 5 times and postoperative bronchospasm and the need for reintubation 10 times. As with pregnant patients, pediatric patients have a higher oxygen consumption and lower functional residual capacity than adults. This means that they do not tolerate prolonged periods of apnea and can desaturate quickly during induction. Grade 1 complication ● Prevention As with treating pregnant patients, only physicians familiar with the anatomy of the pediatric airway and well-versed in pediatric intubation should attempt this procedure. Emergency airway equipment, including laryngeal mask airways, oral and nasal airways, and ﬁberoptic bronchoscopes, should be available for immediate use in the setting of failed intubation.

63

Aspiration during Induction ● Consequence Aspiration during induction can lead to respiratory failure and the need for prolonged mechanical support, pneumonia, or death. Grade 2 complication ● Prevention Pediatric and adult NPO guidelines state that patients who are eating solids or formula should be NPO 4 to 8 hours prior to induction and intubation, and patients who are drinking clear liquids should be NPO 2 to 4 hours prior to induction and intubation, with longer ﬂuid and solid fasts not decreasing aspiration risks. These guidelines vary from institution to institution. In patients with aspiration risks (i.e., status post– cerebrovascular accident, full stomach, small bowel obstruction, hiatal hernia, diabetic with gastroparesis, trauma, pregnancy, pain/stress, esophageal disease, poor level of consciousness and motor control), rapidsequence induction with Sellick maneuver should be performed and the patient should be NPO from all oral intake for at least 8 hours prior.53,57 The current evidence shows that most healthy ambulatory patients have a very low incidence of clinically signiﬁcant aspiration during general anesthesia. The best preventive strategy involves making sure solids, especially fatty foods, are prohibited.

Preoperative Evaluation for Postoperative Nausea and Vomiting Postoperative nausea and vomiting (PONV) remains a common complication after general and regional anesthesia, with 25% of patients who undergo general anesthesia experiencing PONV within 24 hours of surgery in the United States.58,59 It is a leading cause of unanticipated hospital admission and a limiting factor in early discharge after ambulatory surgery. Some studies suggest that patients are more concerned with avoiding PONV than with avoiding postoperative pain.58,60 ● Consequence Vomiting and retching can lead to potential aspiration, increased myocardial oxygen demand, and demandrelated ischemia and can weaken or disrupt fascial closure. Grade 1/3 complication ● Repair PONV should be treated immediately and aggressively. Table 5–6 lists some of the common drugs used in treatment, but knowledge of their side effect proﬁles and contraindications should be noted before administration. Although nonpharmacological techniques such as acupuncture, transcutaneous electrical nerve stimulation (TENS), and hypnosis have been shown to be

64

SECTION I: GENERAL CONSIDERATIONS

Table 5–6 Antiemetics, Mechanism of Action, and Timing in Adults Drug

Mechanism

Appropriate Timing

Pitfalls and Side Effects

Ondansetron

5-HT3 Antagonist

End of surgery

No adverse events related to recurrent or high dosing

Dexamethasone

Anti-inﬂammatory

Beginning of surgery

No adverse effects related to single pre-/intraoperative dose No effect on PONV if given late after induction

Droperidol

Dopaminergic antagonist/ GABAnergic

End or beginning of surgery

Extreme sedation and dystonia, EPS at high doses, prolonged QT syndrome and torsades de pointes

Ephedrine

Indirect sympathomimetic

Unknown

Severe hypertension and tachycardia in high doses

Promethazine

H1 Antagonist, Dopaminergic antagonist

End of surgery

Extreme sedation, confusion, EPS, respiratory depression at high doses

Scopolamine patch

Anticholinergic

Night before surgery

Sedation, confusion

EPS, extrapyramidal symptoms; 5-HT3, serotonin; PONV, postoperative nausea and vomiting. From Gan T, Meyer T, Apfel C. Consensus guidelines for managing postoperative nausea and vomiting. Anesth Analg 2003;97:62–71.

Box 5–2 Risk Factors for Postoperative Nausea and Vomiting

Box 5–3 Strategies to Reduce Baseline Risk of Postoperative Nausea and Vomiting

High Risk

●

●

●

● ● ●

Female Sex History of PONV or motion sickness Nonsmoking status Use of intraoperative or postoperative opioids

● ● ● ●

Medium Risk ● ● ● ●

Use of volatile anesthetics within 0–2 hr of emergence Nitrous oxide Duration of surgery Type of surgery: laparoscopy, orthopedic, ENT, strabismus, neurosurgery, plastic, and breast surgery

ENT, ear, nose, and throat; PONV, postoperative nausea and vomiting. From Gan T, Meyer T, Apfel C. Consensus guidelines for managing postoperative nausea and vomiting. Anesth Analg 2003;97:62–71.

effective in preventing PONV in some patients when performed before surgery, current recommendations do not support their use in the acute setting of PONV.58 ● Prevention Proper treatment and prophylaxis against PONV remain controversial, but it is clear that universal prophylaxis against PONV with current modes of therapy is not cost effective.58 Low-risk patients may require no prophylactic therapy, but high-risk patients should be pretreated aggressively with “triple therapy” because PONV can be as frequent as 70% to 80% after surgery in this group. Triple therapy includes, but is not limited to, any three of the medications listed in Table 5–6 given in appropriate dosing and properly timed. The ﬁrst steps in the prevention of PONV are to identify those patients at highest risk and to reduce baseline risk factors. Box 5–2 lists the risk factors for PONV. The incidence of PONV increases with increasing number of risk factors, with the greatest risk factors being (1) female

● ●

Regional anesthesia Propofol for induction and maintenance of anesthesia Supplemental oxygen Avoidance of dehydration Avoidance of nitrous oxide Avoidance of inhalational volatile anesthetics Minimization of perioperative opioids Avoidance of neostigmine

From Gan T, Meyer T, Apfel C. Consensus guidelines for managing postoperative nausea and vomiting. Anesth Analg 2003;97:62–71.

gender, (2) history of PONV or motion sickness, (3) nonsmoking status, and (4) the use of intraoperative and postoperative opioids.61,62 The risk of PONV approaches 80% if all four of these factors are present. Strategies for reducing these risks are listed in Box 5–3. General anesthesia is associated with an 11-fold increased risk for PONV over that of regional anesthesia. Propofol is far superior to any other induction drug in preventing postoperative nausea. Oxygen supplementation, adequate hydration, avoidance of nitrous oxide and volatile anesthetics (e.g., isoﬂurane, desﬂurane), and minimizing opioid use are all recommended strategies for reducing risk and should be incorporated in a multimodal approach.62

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52. Brooks-Brunn JA. Predictors of postoperative pulmonary complications following abdominal surgery. Chest 1997; 111:564–571. 53. Gupta R, Parvizi J, Hanssen A, Gay P. Postoperative complications in patients with obstructive sleep apnea syndrome undergoing hip or knee replacement: a casecontrol study. Mayo Clin Proc 2001;76:897–905. 54. Cooper GM, McClure JH. Maternal deaths from anaesthesia. An extract from Why Mothers Die 2000–2002, the Conﬁdential Enquiries into Maternal Deaths in the United Kingdom, Chapter 9: Anaesthesia. Br J Anaesth 2005;94: 417–423. 55. Leicht C. Anesthesia for the pregnant patient undergoing non-obstetric surgery. Anesthesiol Clin North Am 1990;8: 131. 56. Brodsky JB, Cohen EN, Brown BW Jr, et al. Surgery during pregnancy and fetal outcome. Am J Obstet Gynecol 1980;138:1165–1167. 57. Goresky G, Maltby J. Fasting guidelines for elective surgical patients. Can J Anaesth 1990;37:493. 58. Gan T, Meyer T, Apfel C. Consensus guidelines for managing postoperative nausea and vomiting. Anesth Analg 2003;97:62–71. 59. Sinclair D, Chung F, Mezei G. Can postoperative nausea and vomiting be predicted? Anesthesiology 1999;91:109– 118. 60. Mascario A, Weinger M, Carney S, Kim A. Which clinical anesthesia outcomes are important to avoid? Anesth Analg 1999;89:652–658. 61. Apfel C, Laara E, Koivuranta M, et al. A simpliﬁed risk score for predicting postoperative nausea and vomiting. Anesthesiology 1999;91:693–700. 62. Scuderi P, James R, Harris L, Mims G. Multimodal antiemetic management prevents early postoperative vomiting after outpatient laparoscopy. Anesth Analg 2000;91:1408–1414. 63. Rutter T, Tremper K. Anesthesiology and pain management. In Greenﬁeld L, Mulholland M, Oldham K, et al (eds): Surgery: Scientiﬁc Principles and Practice, 2nd ed. Philadelphia: Lippincott-Raven, 1997; pp 438–454. 64. Salam GA. Regional anesthesia for ofﬁce procedures: part I. Head and neck surgeries. Am Fam Physician 2004;69: 585–590.

6

General Laparotomy Russell J. Nauta, MD INTRODUCTION Conviction that one should undertake only an invasive procedure whose complications one can manage is a fastfading tenet as increasing numbers of nonsurgical specialists attempt invasive procedures. The granting of privileges in abdominal surgery, however, still assumes that the individual so honored will be able to plan an approach, accommodate to the sequelae of previous abdominal surgery, enter the abdomen, accomplish the intended task, repair or otherwise manage injuries created while doing so, deal with the sequelae of inﬂammation, treat infection, and deliver postoperative care with minimal assistance. No amount of technical expertise trumps careful preoperative planning. Strategies to avoid traumatic entry into the peritoneal cavity, preoperative determination of the need for mechanical and antibiotic bowel preparation, choice of incision, and planning optimal exposure are as important as intra-operative technical judgment and facility with the instruments. In some cases, the surgeon may have weeks to contemplate these issues, whereas in more urgent situations, such as frank peritonitis, ruptured viscus, leaking aneurysm, or trauma, the planning stage is signiﬁcantly truncated. Patients who have had prior abdominal surgery or exposure to radiation, in particular, require extensive contingency planning by the operating surgeon. Previously radiated patients may be particularly unforgiving of operative misadventure because radiation may impede repair mechanisms and both the cellular and the vascular phases of wound healing.1 Unlike laparoscopic surgery, in which incision choice is often dictated by optical considerations, instrument trajectory, and vantage point, the surgeon performing open surgery can select from several standard incisions. However, not all incisions adapt well to unexpected operative ﬁndings. Traditionally, operations in which the exact source or extent of acute intra-abdominal pathology is not known are approached through an abdominal midline incision, which can be readily extended in either direction, as dictated by operative ﬁndings. In the case of patients with a previous midline incision, the incision at reoperation is often begun well above or below the previous laparotomy scar to permit atraumatic entry into the peritoneum. Pragmatically, the midline incision is also useful for operations

on large abdominal tumors or spleens, which, because of their size, may not be able to be delivered through a transverse incision. Caudad extension of a midline incision allows improved exposure of pelvic tumors, whereas cephalad extension facilitates release of the colonic ﬂexures. Detailed knowledge of embryology and anatomy begets well-vascularized incisions and tension-free, well-perfused anastomoses. For example, a surgeon familiar with the trajectory of counterclockwise midgut rotation about the superior mesenteric vessels during the second trimester of gestation2 can draw on the knowledge to reverse the process at operation to facilitate tension-free low pelvic anastomosis of the colon (Fig. 6–1) or to expose the lateral retroperitoneum in the avascular planes described by Cattell, Braasch, and Maddox and associates (Figs. 6–2 and 6–3).3,4 Some have advocated avoidance of midline incisions because of controversial concerns related to structural weakness and attenuated blood supply. Evidence supporting these misgivings is not convincing in studies in animals or humans, but transverse incisions may have other advantages. Sometimes, selecting a low transverse incision over a midline incision extending more cephalad will favorably affect pulmonary toilet and maintain functional reserve capacity without compromising intra-abdominal exposure. The right lower quadrant (RLQ) transverse incision, for example, both allows for optimal operative exposure and facilitates pulmonary toilet in resection of cecal cancers. In the upper abdomen, transverse incisions can facilitate open packing or repetitive entry, as when multiple sequential laparotomies are required for the débridement of pancreatic necrosis. A once-common belief that muscle-dividing transverse incisions or muscle-reﬂecting paramedian incisions convey additional strength solely because of their multiple separately closed fascial layers or superior blood supply is also unsupported by experimental or clinical evidence. Indeed, a contradicting body of evidence supports the superiority of mass closure over layered closure even in areas off the midline, where multiple fascial layers exist (Fig. 6–4).5 In circumstances in which the pathology is conﬁdently delineated by a preoperative history, physical examination, and/or preoperative imaging studies, it may be preferable to use one of a number of anatomically deﬁned “specialty”

68

SECTION I: GENERAL CONSIDERATIONS

Superior mesenteric artery

A

Superior mesenteric artery

B Figure 6–1 A, In the second trimester of embryologic life, the cecal bud migrates 270° counterclockwise from a position in the left lower quadrant to ultimately assume its characteristic anatomic position in the right lower quadrant. The superior mesenteric artery serves as the axis of this rotation. Because the aortic blood supply from which the colonic vessels ramify is in the midline, the rotation leaves the gutters themselves avascular. The white line of Toldt represents the avascular plane for incision and is the anterior conﬂuence of the colonic visceral peritoneum with the parietal peritoneum of the lateral abdominal wall. B, When a segment of the left colon is removed, embryologic rotation is reversed to allow the proximal end to be brought into tension-free apposition to the distal end for anastomosis.

6 GENERAL LAPAROTOMY

Cattell and Braasch maneuver

Duodenum

Figure 6–2 The maneuver developed by Cattell and Braasch for right medial visceral rotation takes advantage of the avascular right colonic gutter in mobilizing the colon so that the surgeon might inspect the retroperitoneal structures behind it.

Inferior vena cava Abdominal aorta

Maddox maneuver

Figure 6–3 The Maddox maneuver takes advantage of the avascularity of the left colonic gutter to rotate the left colon medially to allow inspection of the retroperitoneum on the left side of the abdomen.

Figure 6–4 The difference in suture placement between individual closure of the fascial layers and mass closure in a midline incision.

Stomach Spleen

69

70

SECTION I: GENERAL CONSIDERATIONS

incisions. Examples are the right subcostal (Kocher) incision for open cholecystectomy and duodenal exploration, the muscle-splitting RLQ incision for appendectomy, and the Pfannenstiel incision for nonmalignant gynecologic pathology.

Incorrect Choice of the Kocher Incision ● Consequence In some circumstances, the right subcostal incision is insufﬁcient to complete a gastrectomy, to adequately explore the duodenum, or to evaluate unsuspected pelvic pathology. ● Repair The Kocher incision is the easiest of the three specialty incisions to modify, in that it can be easily extended transversely in either direction because fascia and muscle have been divided in the same direction as the skin. ● Prevention Choose a midline incision if pelvic pathology is expected. Upper abdominal pathology can usually be exposed after extension of a Kocher incision.

Incorrect Choice of the Muscle-Splitting Appendectomy Incision ● Consequence If the diagnosis of appendicitis is incorrect or if the appendix cannot be delivered through an RLQ musclesplitting incision, that incision cannot be extended in its original form because it is made by separating the ﬁbers of the external oblique, internal oblique, and transversalis muscles in three different directions. Because of the orientation of these muscles, their separation forms a “keyhole” incision with limited exposure beyond McBurney’s point. ● Repair Extension of the muscle-splitting appendectomy incision to permit additional exploration requires the medial end of the incisions in the two oblique muscles to change direction slightly as the extension is developed transversely across the rectus sheaths. In some instances, it is possible to spare the rectus muscle itself when extending the incision in this manner (Fig. 6–5). However, if more incision is required, the incision may be extended as far to the left as is necessary, thereby permitting access to the entire abdomen. ● Prevention Whereas exploration for pathologically normal appendices still occurs, the limitations to further exploration that this incision imposes should be able to be mitigated by heavier reliance on preoperative imaging. In equivocal cases, a laparoscopic approach or midline

incision should be chosen over the muscle-splitting RLQ incision.

Incorrect Choice of the Pfannenstiel Incision ● Consequence Use of the Pfannenstiel incision, which marries a cosmetically acceptable low transverse abdominal incision with a vertical midline fascial incision, also presumes that the scope of the pathology has been accurately assessed prior to surgery. If more exposure is required because this is not so, the surgeon’s ability to make the incision larger is limited. Even extensive extension of both skin and fascial incisions in their original directions does not achieve more exposure because the incisions are made at 90° to each other (Fig. 6–6). ● Repair Extend the transverse skin incision ﬁrst, and in both directions. Should this not afford the opportunity to extend the fascial incision in a cephalad direction, an inverted T skin incision will have to be accepted, as the midline fascia and its overlying skin are incised cephalad to accommodate the exposure. ● Prevention Abdominal imaging or laparoscopic evaluation may help decide whether a Pfannenstiel, a midline laparotomy, or a laparoscopic/laparoscopy-assisted approach is most appropriate.

Failure to Consider the Consequences of an Incision’s Innervation and Blood Supply ● Consequence When making a new incision parallel to another recent laparotomy incision, the surgeon should consider the possibilities that the intervening abdominal wall’s vasculature will be compromised or that denervation injury will result. This is less true if the second incision is made many years after the ﬁrst. Even without prior incision, subcostal or chevron incisions, which divide the obliquely coursing intercostal nerve branches, may result not only in sensory deprivation to the area inferior to the scar but in postoperative lower abdominal denervation atrophy and laxity as well. The problem is worse when such incisions are bilateral (Fig. 6–7). ● Repair Denervated muscle atrophies. Attention to the bulk and the bleeding from the musculature at the time of the second incision may dictate the width of fascial closure bites, particularly when a midline incision follows a paramedian incision. In most other circumstances, choice of a midline incision for a second operation is safe. Denervation laxity from subcostal or chevron incisions occurs sporadically and cannot be repaired. The

6 GENERAL LAPAROTOMY

71

External oblique incision

Internal oblique incision

Original Rectusincisions sparing extension

Transversus abdominis incision

Original Rectusincisions sparing extension

Figure 6–5 The muscle-splitting appendectomy incision is notoriously strong and seldom develops a hernia because the three lateral muscles—external oblique, internal oblique, and transversalis—are opened in different directions. When operative ﬁndings dictate that this incision be enlarged, however, the direction of the muscular incision in the external oblique and internal oblique musculatures must be altered slightly as the incision is extended medially across the rectus sheaths. If only a small extension is required, the rectus muscle itself may be able to be spared and retracted medially as the anterior and posterior sheaths are incised. Full-thickness retraction of the three muscle layers with vectors of force at 90° to the axis of intended extension will facilitate the alignment of the three layers as medial extension proceeds.

best the surgeon can do is not to mistake the laxity for an abdominal wall hernia, which it is not. ● Prevention Attention should be paid to previous abdominal incisions and to a contemplated incision’s direction, position, vasculature, and innervation before the incision is made.

Failure to Anticipate Malignant or Nonmalignant Adhesions when Making the Abdominal Incision An abdominal scar should alert the surgeon to the potential for intra-abdominal adhesions caused iatrogenically or in response to the original pathology. The abdominal surgeon should be aware of any existing muscular defect in an area of intended incision as well as whether prosthetic mesh has been previously placed to repair a defect of the abdominal wall. Adhesion of the viscera to the

abdominal wall in these circumstances, and in the case of tumors close to the anterior abdominal wall, should be presumed. ● Consequence Visceral injury or compromise of en-bloc resection of tumor may occur if the surgeon does not correctly anticipate the position of the viscera, the adhesions, and the tumor. ● Repair See the section on “Injury to the Intestine,” below. ● Prevention An unrepaired hernia increases the likelihood of visceral injury as the abdominal incision is developed beneath the dermis, whereas the presence of prosthetic mesh in an operative ﬁeld substantially increases the likelihood

72

SECTION I: GENERAL CONSIDERATIONS

External oblique m. Rectus sheath

Skin and fascial incision

Rectus sheath

Rectus abdominis

Vertical incision

Extension of skin and anterior sheath incision

Figure 6–6 In the case of the Pfannenstiel incision, the cosmetically desirable low transverse skin incision is placed at right angles to the midline fascial incision. Whereas the skin incision may be lengthened to accommodate upward extension of the fascial incision, at some point, it may have to be abandoned or converted to an inverted T incision to accommodate the disparity in directions. For this reason, “specialty” incisions should be selected only when the pathology is well-deﬁned preoperatively.

Superior epigastric a.

Rectus abdominis m.

Inferior epigastric a.

that the abdominal viscera will be adherent to the anterior abdominal wall in the region of the repair. In the case of suspected matting of the intestine due to inﬂammation, tumor, or previous abdominal surgery, an effort should be made to enter the peritoneal cavity well away from the site of the pathology. Incision selection and the choice to lengthen a previous incision have as their goal exposure of a previously inviolate area of fascia and peritoneum for atraumatic entry into the abdomen. As with reuse of a previous laparotomy incision, in hernia patients, the initiation of a subsequent incision well away from the visceral bulge or the original repair will often permit entry into the abdomen through an unscarred region and allow identiﬁcation of structures to be preserved. Thus, beyond the goal of

Subcostal incision Anterior cutaneous nerve of subcostal nerves

Figure 6–7 The intercostal nerves course obliquely in the abdominal wall, as shown. Thus, upper abdominal incisions traversing multiple nerve levels cause sensory and motor deprivation to the skin and muscles inferior to the incision. When the incision is bilateral, the denervation atrophy of the lower abdominal musculature may result in an undesirable loss of muscle tone. A bulge may occur without overt herniation.

optimal exposure of the intra-abdominal pathology, incisional planning seeks to ensure that surgical entry is volitionally made into the peritoneal cavity itself rather than erroneously made into the lumen of a hollow viscus or the capsule of a solid organ. Small incisions reduce, and may compromise, exposure. In the case of malignancy, a longer incision may preserve the opportunity for en-bloc resection. Incisional planning for removal of large tumors or the extirpation of pathologically enlarged organs can be facilitated by abdominal palpation after anesthetic agents have relaxed the abdominal wall, thereby avoiding incision directly into the tumor or its parietal peritoneal attachments. The surgeon should not forego this one last opportunity for the physical examination to inform incisional planning.

6 GENERAL LAPAROTOMY

Failure to Identify the Peritoneal Cavity ● Consequence Mistaking the wall of a viscus for a point at which the peritoneum permits atraumatic entry may result in visceral injury. ● Repair See the section on “Injury to the Intestine,” below. ● Prevention Unless a hernia is present, the muscular fascia of the abdominal wall is seen before the peritoneum, thereby ensuring that the peritoneal cavity will be prospectively identiﬁed and opened in a controlled fashion. Although identifying the abdominal midline may seem an intuitive quest, incisions intended for the linea alba are often made off midline, causing the surgeon to unnecessarily enter the rectus sheath and compromise bloodless entry into the peritoneal cavity. The surgeon knows that the anterior rectus sheath has been mistaken for the linea alba when the rectus muscle and its sheaths are visible as separate layers, because true midline incisions do not expose the red muscle bellies of the rectus abdominis muscles before encountering properitoneal fat. The midline may be identiﬁed in obese patients by basing one end of a midline incision at the umbilicus or xiphoid or by having both operator and ﬁrst assistant simultaneously apply lateral traction after the skin incision is made. The subcutaneous tissue will “part” and identify the abdominal midline by exposing the cross-hatching of the subcutaneous fat (Fig. 6–8). In more lateral inci-

Subcutaneous fat

“Crosshatching” of subcutaneous fat overlies linea alba

Figure 6–8 Lateral traction of the divided skin and superﬁcial subcutaneous fat in obese subjects allows identiﬁcation of the midline through observation of the midline subcutaneous fat, whose cross-hatching strands identify the linea alba.

73

sions, the rectus, oblique, and transversalis muscles and their fasciae are sequentially and identiﬁably divided before the peritoneum is exposed. Independent of the choice or direction of incision, the anterior surface of the parietal peritoneum is often fused to the deepest layer of fascia. Thus, the safest entry into the peritoneal cavity is with a knife. The surgeon and ﬁrst assistant should elevate the peritoneum with toothed forceps; peritoneal entry is made with the belly of a No. 10 blade. Although compelling reasons of hemostasis, economy of time, and surgeon experience might suggest division of the muscle layers with the electrocautery, with rare exception, the initial entry into the peritoneal cavity should be made with cold steel. Even the unfortunate surgeon who ﬁnds that an incision intended only for the peritoneum has also entered a loop of intestine will be gratiﬁed at the time of repair that she or he has cleanly incised, rather than burned or spread, her or his way into the intestine. Once a small entry has been made into the peritoneal cavity, the operating surgeon should insert his or her ﬁnger and palpate the parietal peritoneum in the direction of intended incisional extension, in order to see whether the incision may be atraumatically developed in that direction. If free of adhesions, the incision can then be enlarged with the electrocautery, dividing all layers of the abdominal wall simultaneously rather than in sequence. In the case of previous laparotomy, hernia, inﬂamed abdominal viscera, enterocutaneous ﬁstula, or adherent tumor, the laparotomy incision should be developed under direct vision and only as far as the ﬁrst intraperitoneal adhesion. At this point, Kocher clamps should be placed to elevate the fascial edges of both sides of the incision so that loops of bowel adherent to it might be visualized. For initial dissection, after careful fascial division, an area is typically chosen in which the adhesions are translucent because a pocket of air or ﬂuid has collected beneath them and their associated loops of intestine, signaling the absence of other viscera at risk beyond them. Translucent adhesions may be taken down sharply, and the free abdominal cavity may be thus visualized and entered (Fig. 6–9). For the same reason that spreading with the scissors is not desirable in entering the peritoneal cavity, minimal spreading is often best in the early development of the laparotomy. With traction provided by Kocher clamps in the vertical direction, the operating surgeon can often, with the aid of a Mikulicz pad held by the “clawed” nondominant hand, apply atraumatic tangential traction to the adhered loop of bowel, thereby permitting identiﬁcation of interloop adhesions or adhesions of bowel to abdominal wall. The adhesions are maximally exposed and lengthened by this maneuver, and lysis can occur with sharp dissection as the ﬁngers of the surgeon’s nondominant hand subsequently shift into the free space thus created (Fig. 6–10). Lysis of adhesions is a shared and dynamic responsibility between the operating surgeon (often positioned on

74

SECTION I: GENERAL CONSIDERATIONS

90°

0°

45°

ﬁrst assistant is optimally positioned to lyse adhesions in the pelvis. For this reason, in pelvic operations, the surgeon stands on the patient’s left side. Although it is tempting to identify and “chase” interloop adhesions deep into the peritoneal cavity, a focused determination and a synergistic cooperative strategy should be formulated between ﬁrst assistant and operating surgeon to ﬁrst identify and free the entire underside of the parietal peritoneum and to develop the entire length of the contemplated abdominal wall incision before deeper intra-abdominal pathology is addressed.

Injury to the Intestine

Figure 6–9 Kocher clamps applied to the divided fascia of a wound should be retracted at 90° to the body; the nondominant hand of the operating surgeon should be fanned over a Mikulicz pad; and gentle traction should be applied tangentially. The adhesions will thus be maximally lengthened and exposed under controlled tension, with less likelihood of traumatizing the bowel.

Figure 6–10 The ﬁrst assistant presents adhesions to the operating surgeon in such a way that there is a “curtain” rather than a “tent” of bowel as the operating surgeon applies tension. In this manner, avoidance of a traction tear on the apex of the tent or accidental amputation of the bowel when lysing pointed adhesions will not occur.

the patient’s right and lysing adhesions to the left of midline) and the ﬁrst assistant (often positioned on the patient’s left and lysing adhesions to the right of midline). Assuming right-handed dominance and these positions at the operating table, the operating surgeon is best positioned to lyse adhesions in the epigastric midline and the

● Consequence Visceral leak, abscess, ﬁstula, sepsis, shock, or death may occur, depending on the time of discovery of the visceral injury, the amount of soilage incurred, the resistance of the host, and the success of the repair. ● Repair Injury to the intestine usually occurs while freeing it from either the abdominal wall or an adjacent viscus. Management of an iatrogenic injury depends on operative circumstances, whether the injury is to the large or the small intestine, whether a bowel preparation has preceded surgery, and whether the injury is full thickness or partial thickness. Partial-thickness injuries usually need not be repaired. However, in the presence of severe adhesive disease, prior radiation, hematoma, or other comorbidity compromising repair, the relative paucity of a normal blood supply may cause a partial-thickness injury to evolve to a full-thickness injury in the postoperative period. When a loop of bowel is injured, it is tempting to react immediately by attempting to place sutures or Babcock or Allis clamps to stem the ﬂow of enteric contents. However, even atraumatic clamping of a partially deﬁned enterotomy often helps very little and sometimes induces further trauma. Rather than close the enterotomy in an adhered loop of bowel in situ, the loop should be freed from adjacent structures, mobilized for complete inspection, and assessed for its salvage potential. Mobilization may demonstrate signiﬁcant bowel injury or devascularization. A temporizing “damage control” approach, with temporary suture or stapling of the bowel, or division of the bowel with subsequent reassessment, may well be appropriate, but only after mobilization. To commit to deﬁnitive repair, resection, and/or anastomosis at the time of injury, before mobilization, or before the goals of the operation have been achieved has the potential to waste time; the initial closure may be inadequate or multiple injuries in the same short segment of bowel may be identiﬁed and need to be handled by incorporation of several injuries into a single resection. Full-thickness small bowel injuries are handled differently than full-thickness large bowel injuries. In general, independent of whether the bowel has had mechanical or

6 GENERAL LAPAROTOMY antibiotic preparation, most small bowel injuries may be handled with simple repair or resection and repair with anastomosis; uncomplicated full-thickness large bowel injuries in unprepared intestine should, generally, be handled with simple repair if they are solitary and if minimal fecal contamination has occurred. When possible, intestinal injuries should be closed transversely to minimize the likelihood that the repair would “hourglass” or narrow the caliber of the involved viscus. The HeinekeMikulicz pyloroplasty6 gives good evidence that even when a rent is absolutely and deliberately longitudinal, most enterotomies can be closed transversely. If resection is required for extensive large bowel injury in circumstances in which there has been no bowel preparation, consideration should be given to exteriorizing the ends of the bowel, with reanastomosis at a subsequent surgery. Primary closure of a large bowel injury becomes more and more indefensible when the patient is ill; the operation is extensive; the injuries are unexpected, multiple, or substantial; or compromise of a prosthetic device by failed closure is possible. Permanent prosthetic devices such as nonabsorbable mesh should generally not be electively placed in the setting of enteric injury. Whereas patient, unhurried dissection along the antimesenteric surface of the small intestine is often successful in freeing even the densest of adhesions, in some circumstances, it becomes abundantly clear that a loop of small intestine diving into the pelvis will not be able to be freed under direct visualization. In operations for intestinal obstruction, this situation is heralded by a dilated loop diving into the pelvis adjacent to an unobstructed loop coming out of the pelvis. When this circumstance exists, and when injury to such bowel in freeing it is judged to be inevitable, the appropriate goal is to expeditiously resect as short a segment of intestine as is possible, while preserving and minimizing injury to the structures to which the involved loop is adhered. To commit to the tedious freeing of such a loop in the hope of salvaging it is a fool’s errand; it often proves to not be possible, and the futile attempt wastes a signiﬁcant amount of operating time. When small bowel resection is judged to be inevitable in adhesive disease, the afﬂicted loop should be delivered into the upper abdomen by the least traumatic means possible, and an assessment should then be made as to whether repair or resection with anastomosis is most appropriate. When the afﬂicted loop is attached to tumor and en-bloc resection is contemplated, the loop adherent to the tumor is isolated and left in situ for future mobilization with the specimen, and fecal continuity is restored by anastomosis of the two functioning ends of the bowel thus freed from the tumor. ● Prevention Only after the incision has been extended to the desired length is a directed approach to the pathology undertaken with adhesiolysis. In so doing, the bowel should be minimally instrumented with grasping forceps or

75

Figure 6–11 Once a translucent area in the adhesive curtain is identiﬁed and developed, the index ﬁnger of the nondominant hand can be “hooked” around the remaining adherent loops of bowel, and they can be freed. The operator’s nondominant index behind the bowel both provides traction and ensures the operating surgeon that additional loops of bowel are not adherent.

other traumatic instruments, as tangential traction with cotton pads or presentation of the bowel by elevating it manually often provides sufﬁcient retraction to allow visualization of intervisceral adhesions. As lysis progresses, an effort should be made to repetitively identify and selectively work at the antimesenteric surface of adhesions to minimize the chance of compromising the bowel’s blood supply. The assistant should present adhesions as a broad band attaching bowel to adjacent viscus or abdominal wall, rather than tenting them in a manner that invites enterotomy (Figs. 6–10 and 6– 11). Use of the electrocautery should be avoided, as should large spreads of the scissors or grasping of the intestine with surgical instruments. Most adhesions can be progressively exposed and lysed as small incisions are made with the scissors without spreading. The site chosen for incision develops dynamically as exposure unfolds; in lieu of scissor use, some prefer sharp adhesiolysis with the No. 10 blade. Adhesiolysis with the No. 10 blade should not be attempted by the novice surgeon because it requires a delicate touch and considerable experience with the texture and spectrum of abdominal adhesions. Frequent blade changes are necessary for effective use of the technique because it is the knife’s tip, rather than its belly, that incises the adhesion. The tip of the blade should be placed at the position of intended initiation of the adhesiolysis and rotated counterclockwise to form a large acute angle with the intended direction of incision. The knife should then be dragged to the right, maintaining this acute angle as the adhesion is lysed. The largest acute angle of blade

76

SECTION I: GENERAL CONSIDERATIONS ● Repair Injury to bowel may preclude prosthetic repair, necessitating primary closure or abandonment of repair altogether.

A

B

C Figure 6–12 A and B, In lysis of adhesions using a scalpel, the tip of the No. 10 blade engages the adhesion. The largest acute angle that will allow the knife to cut while being dragged in the intended direction of the lysis is chosen. C, Smaller acute angles risk injury to the bowel.

with trajectory permitting the knife to be moved in the intended direction should be chosen and maintained as the blade is moved (Fig. 6–12). Smaller angles will increase the likelihood of bowel injury. Lysis of adhesions is among the most sophisticated tasks performed by the abdominal surgeon, and no preconceived time should be allotted for its completion. Extensive adhesions demand extensive patience and meticulous dissection. When dense adhesions are anticipated, no competing commitments on the surgeon’s time should be made. When adhesions are encountered unexpectedly in the course of dissection, arrangements should be made for all competing commitments to be rescheduled to minimize the risk of bowel injury. The ﬁrst assistant should provide the operating surgeon with as panoramic a view as the anatomic situation permits. Success is often less the result of heroic traction than of an assessment as to how the bowel can be manipulated to best display the desired incisional plane.

Visceral Injury during Exposure of a Ventral Hernia Defect ● Consequence The operative plan for elective repair of ventral hernia often presupposes the placement of prosthetic mesh under aseptic conditions. Visceral injury compromises the bacteriologic environment of the wound.

● Prevention Even in the setting of previous laparotomy, in patients with an intact abdominal wall, the surgeon’s potential to injure the abdominal viscera is at least theoretically limited by the necessity to traverse the fascia before the viscera are encountered. When those viscera lie in the subcutaneous tissue, as is the case with ventral hernia or previous stomal creation, the potential for visceral injury is enhanced. The techniques for safe subsequent laparotomy, as described previously, may be adapted to permit deﬁnition and exposure of ventral hernias. An incision is begun at some distance from the palpable hernia sac in order to avoid entry into a peritoneal sac apposed to the skin. As the hernia occupies space in the subcutaneous tissue that is vacated after repair, incorporating an overlying ellipse of skin at the beginning of the operation serves three useful purposes. The maneuver minimizes the timeconsuming need for dissection of the sac from the overlying and often attenuated skin, which is often subsequently discarded. Improved visibility created by wider exposure enhances the surgeon’s ability to deﬁne the sac’s interface with the fascia and to avoid visceral injury. Finally, resection of redundant skin and subcutaneous tissue acknowledges the new geometry of the wound and the absence of a visceral bulge after fascial repair, thereby minimizing the magnitude of the skin ﬂaps and making seroma formation less likely. In either mobilizing a hernia sac or identifying the serosal surface of an externalized viscus during stomal reversal, blunt dissection is the surgeon’s friend. For ventral hernias, the sac is exposed after careful incision of the skin and subcutaneous tissue. The gloved hand invaginated into a Mikulicz pad strips the subcutaneous fat away from the sac to allow visualization of the sac’s origin at the disrupted fascia of the abdominal wall. Three approaches to safe repair are possible. For hernias in which incarceration is not suspected, some surgeons prefer to bluntly develop the plane between the abdominal wall’s musculature and the sac’s parietal peritoneum without ever entering the peritoneal cavity. They then close the muscular wall extraperitoneally. Other surgeons prefer to identify a point in the sac at which the viscera are not believed to be adherent to the peritoneum. They open the sac in that region, dissect the omentum or hollow viscus away from the parietal peritoneum, resect the sac, and then close the defect. A third option is to open the peritoneum only after circumferential identiﬁcation of the sac’s interface with the fascial ring is complete (Fig. 6–13). In the latter two instances, safe entry into the peritoneal cavity is pursued with adhesiolysis as described previously for recurrent laparotomy.

6 GENERAL LAPAROTOMY

Muscle

Skin

77

Peritoneum

Subfascial plane

or

A

B

C

Subfascial plane

Peritoneum

Prosthetic mesh

D

Fat

Skin

or

E

Subfascial plane

Peritoneum

Prosthetic mesh

Figure 6–13 A, After skin incision and exposure of the fascia of the abdominal wall, deﬁnition of the ventral hernia sac is achieved by blunt dissection in the subcutaneous space with a Mikulicz pad. B, Keeping the peritoneum of a broad-based hernia sac intact, a subfascial plane is developed to allow primary closure of the musculofascial defect or the attachment of prosthetic mesh. This technique is not suitable for situations in which incarceration is suspected or for narrow-necked hernia sacs. C, Some surgeons enter the sac in an area where the viscera are not believed to be adherent before the sac is fully exposed to the level of its interface with the fascia of the abdominal wall. D, Alternatively, the sac is completely exposed, and the surgeon enters at its interface with the fascial ring. E, Repair of the fascia is accomplished with either primary closure or subfascial implantation of prosthetic mesh circumferentially anchored to healthy fascia.

Visceral Injury during Dissection of an Intestinal Stoma ● Consequence Often, stomal closures can be effected without opening the counterincision made to create them by dissecting circumferentially about the stoma itself and preserving as much of the functioning intestine as possible. Injury

to the bowel, compromise of its blood supply, or incorporation of an unrecognized bowel injury into a stomal closure can result in enteric leak and the failure of stomal closure. Recognized injury may require extension of the laparotomy to resect or expose more intestine to ensure that two viable ends of bowel are available for reanastomosis.

78

SECTION I: GENERAL CONSIDERATIONS

● Repair Once the bowel is injured during dissection of a stoma, repair is ill advised; exposure and mobilization of an undamaged segment of intestine are preferable. ● Prevention A blunt dissection technique speciﬁc to separation of the subcutaneous tissue from the serosa of a stoma was ﬁrst demonstrated to me by Hechtman (personal communication, Brigham & Women’s Hospital, Boston, 1983). The stoma is sharply circumscribed with a fullthickness scalpel incision made at a distance of no more than 1 mm from the mucocutaneous junction. This peristomal incision is then developed sharply into the subcutaneous tissue circumferentially until fat is exposed. Then, using the heel of the knife handle typi-cally used to carry a No. 10 blade, the serosal surface of the viscus is gently stroked in the direction of the fascia. This maneuver allows for identiﬁcation and sharp lysis of any remaining dermal adhesions and clear visualization of the subcutaneous viscus and its interface with fascia. As the maneuver is circumferentially pursued, it is usually possible to identify a point at which the externalized viscus can be readily separated from the abdominal wall musculature and from which the circumferential separation of stoma from abdominal wall can proceed without either enterotomy or loss of bowel length. As with hernia repair or the identiﬁcation of the distal end of a Hartmann colostomy, the maneuver may be coupled with enlargement of the original stomal incision, abdominal counterincision, or both. Loop stomas may often be fully dissected without a counterincision when dissection is performed with the knife handle as described (Fig. 6–14). The millimeter of circumferential skin is easily removed from the bowel’s serosal surface once the stoma has been mobilized.

Liver Injury ● Consequence Unexpected injury to the liver at laparotomy most often occurs because of failure to appreciate an attachment of its capsular surface to the anterior abdominal wall. Under such circumstances, retraction of the abdominal wall avulses the capsule, thereby stripping it and inciting bleeding. ● Repair Iatrogenic rents are usually less than 1 cm in depth and are often insufﬁcient to produce life-threatening hepatic hemorrhage. However, such injuries can be an annoying source of constant oozing during the operation and may compromise exposure of the intended operative ﬁeld. Should the liver be injured over its dome, the combination of pressure and electrocautery or use of the Argon beam device is often sufﬁcient to obtain

Figure 6–14 Hechtman’s technique for separation of the subcutaneous tissue from the serosa of an externalized loop of intestine. The stoma is circumscribed a millimeter away from the mucocutaneous junction. The heel of the knife blade is utilized to bring the adherent subcutaneous fat away from the serosal surface of the bowel, leading the surgeon to the fascial ring. A point of the fascial ring usually becomes apparent where the bowel can readily be freed from it. This point is utilized as the entrance point for circumscription of the bowel, freeing it from fascia without enterotomy and without loss of length.

hemostasis. However, if the injury is near a hollow viscus, use of the electrocautery is unsafe because of energy scatter; the hollow organ in jeopardy should be sharply dissected free of the liver before the electrocautery is used near it. Rarely, mattress sutures are needed to obtain hemostasis of an avulsed liver edge. ● Prevention Injury can be avoided by a diligent focus of both surgeon and assistants on the parietal peritoneal surface as laparotomy is extended over the capsular surface of the liver. Properly managed, sharp dissection allows the liver to drop away as the parietal peritoneum overlying it is separated from Glisson’s capsule.

Splenic Injury and Avoidance of Misadventure in the Lesser Sac ● Consequence Bleeding, splenic repair or removal, pancreatic injury, and pancreatic ﬁstula may occur as short-term conse-

6 GENERAL LAPAROTOMY quences. Immunocompromise and increased susceptibility to infection with encapsulated bacteria may subsequently result in splenectomized patients. ● Repair Should the spleen be damaged because of excess traction on the stomach or colon, the injury often responds to packing. As with the liver, electrocautery may be selectively used if all hollow viscera are free of the spleen. Mattress sutures are less successful in securing hemostasis in splenic injury than in controlling superﬁcial hepatic bleeding. The spleen should be delivered into the midline for such repairs, following lysis of its diaphragmatic attachments. Excessive trauma to the convexity of the splenic capsule in doing so can be avoided by dissecting the diaphragm free of the spleen as the latter is gently retracted medially. When splenic injury is combined with bowel injury or results in hemorrhage that is difﬁcult to control, splenectomy is often the best choice. If splenectomy is chosen, care should be taken on ligature of the hilar vessels to avoid injury to the pancreatic tail, which resides in the splenic hilum. Should injury to the tail be noted, suture repair of the pancreas should occur. A drain should be placed in the area to facilitate the management of enzyme-rich pancreatic drainage should the repair fail. Uncomplicated splenectomies or splenic injuries that are repaired without pancreatic injury, however, should not be drained.7 As the need to remove spleens for trauma or hematologic disease has diminished, iatrogenic injury has become the chief reason for splenectomy. Splenic injury most often occurs in elective surgery by triangulation of its diaphragmatic attachments and the application of excessive traction to either the stomach or the splenic ﬂexure of the colon as these are manipulated for left upper quadrant surgeries (Fig. 6–15). ● Prevention Incision planning for safe entry into both the abdomen and the lesser sac has a role in avoiding splenic injury. When the greater curvature of the stomach is mobilized for gastric operations or elective splenectomy, the laparotomy incision should be made in either the left subcostal or the midline position in a way that allows gastric retraction and facilitates visualization of the spleen and its hilum. The surgeon should recognize that the middle colic artery and right gastroepiploic artery are closest to each other in the abdominal midline and that a residual veil of embryologic mesogastrium puts both vessels at risk for unintended injury in the approach to either. To avoid the injury, initial entry into the lesser sac should be near the midportion of the stomach’s greater curvature, where the right gastroepiploic artery becomes attenuated and the gastrocolic omentum can be readily traversed quite far to the left of midline and well away from the origin of the middle

79

Stomach

GSL SRL PSL SCL Phrenocolic lig. Pancreas

Diaphragm

Colon

Figure 6–15 The tethering of the spleen to the diaphragm, stomach, and splenic ﬂexure of the colon in the left upper quadrant is the anatomic determinant for splenic injury with traction on the colon or stomach.

colic artery. Gentle caudal traction of the transverse colon by the assistant, combined with anterior traction of the stomach by the surgeon, will often identify a translucent area in this region of the gastrocolonic omentum into which atraumatic entry into the lesser sac can be made without vascular injury (Fig. 6–16). Anesthesia personnel should assist the surgeon. A surprising number place the nasogastric tube as an ornamental device only; judicious suction on a well-placed tube facilitates the surgeon’s atraumatic traction on the stomach and facilitates lesser sac entry and visualization of the splenic hilum. For elective gastric surgery or splenectomy, there is no need to mobilize or deliver the diaphragmatic (convex) surface of the spleen early in the dissection. Rather, the short gastric vessels should be identiﬁed and ligated in situ and under direct vision, with purchases of sufﬁcient size to allow vascular pedicle ligation well away from the gastric wall. Postoperative necrotic perforations of the gastric wall, as reported in the older gastrectomy literature, are more likely full-thickness clamp or ligature injuries than devascularization associated with vessels ligated at appropriate distances along the greater curvature. The process of freeing the stomach from the spleen is facilitated not only by suction on the nasogastric tube but also by the gentle lateral pressure of the extensor surface of the ﬁrst assistant’s cupped left hand exerted against the gastric remnant as the operating surgeon places the deep ties. The linear stapling device used for laparoscopic surgery allows the uppermost short gastric vessels to be identiﬁed and secured with good visualization and minimal gastric retrac-

80

SECTION I: GENERAL CONSIDERATIONS

R. gastroepiploic artery

Enter lesser sac through mesocolon (lesser sac)

LATERAL Anterior

LATERAL Posterior

Anterior

Posterior Stomach

Transverse colon

rs se Les

Middle colic artery

Gastro-colic omentum Transverse colon

Greater omentum

tion, avoiding undue tension and avulsion of the diaphragmatic aspect of the spleen’s capsule (Fig. 6–17). The inferior pole of the spleen is often injured with excessive medial retraction of the splenic ﬂexure of the colon during its mobilization for colonic resection or leftsided retroperitoneal exposure. Two maneuvers decrease the likelihood of this event. The lower pole of the spleen can be exposed in a controlled manner, and injury to it avoided, if the colon dissection is begun by entering the lesser sac through the gastrocolic omentum at the midportion of the greater curvature and proceeding to the patient’s left to join a separate incision made along the white line of Toldt. This second incision, in turn, is initiated at a convenient spot lateral to the descending colon

Aorta

sa c

Gastro-colic omentum

Right gastroepiploic artery

Duodenum

ac

Right gastroepiploic artery

r se Les

Transverse mesocolon

Small intestine

Figure 6–16 Entry into the lesser sac near the midportion of the greater curvature to the left of midline places the surgeon well away from the origins of the right gastroepiploic and middle colic arteries, thereby avoiding vascular injury to the transverse mesocolon.

and is developed superiorly under direct vision until the operator approaches the lower pole of the spleen. By periodically and gently lifting the omentum in the region of the splenic ﬂexure, and concurrently following the colon retrograde from the point of incisional initiation in the white line of Toldt, the course of the colon at the ﬂexure and the position of the spleen can be inferred and the two incisions can be joined. This joining of the lateral aspect of the incision in the gastrocolic omentum with the superior aspect of the incision in the white line of Toldt allows for mobilization of the splenic ﬂexure under direct vision in a way that does not put tension on the splenic capsule or cause its avulsion. A common error made in making or connecting these incisions is to impatiently and

6 GENERAL LAPAROTOMY

81

Nasogastric tube Spleen Stomach

Lesser sac

Endoscopic GIA

Figure 6–17 Utilizing the exposure provided by the combination of a functioning nasogastric tube and extension of the ﬁrst assistant’s wrist. The cupped left hand of the assistant against the stomach wall allows working space for the surgeon if a cupped hand exerts gentle pressure. The endoscopic linear stapler is shown securing the superiormost short gastric vascular pedicle.

imprudently lift up on the splenic ﬂexure during the dissection, thereby bringing the colon and its lienocolic ligaments forward, but leaving the spleen itself attached posteriorally to the diaphragm. This erroneous maneuver seldom improves visibility, and it is often difﬁcult to judge and ﬁnely control the tension placed on the spleen when pulling on the colon in this way. The splenic capsule, as the entity least able to resist these forces, tears. The preferred alternative is for the operator to push down on the splenic ﬂexure with a laparotomy pad as the ﬂexure is approached, to gently ﬂex the ﬁngers of the nondominant hand, and to exert tangential traction medially (not anteriorally) as the incision in the line of Toldt is joined to the one dividing the gastrocolic omentum and exposing the lesser sac (Fig. 6–18). Sometimes, the lienocolic adhesions are exceptionally robust and need to be divided between clamps or clips. Under most circumstances, however, they can be simply divided with the electrocautery or the scissors under direct vision.

Injury to the Esophagus ● Consequence Sepsis, intra-abdominal contamination, subsequent operation, shock, or death may occur, depending on the time of recognition of the injury and the success of the repair.

● Repair Should the esophagus be erroneously entered while encircling it bluntly, the organ can usually be rotated to allow the placement of interrupted nonabsorbable sutures. Most authors would reinforce such a closure with a fundoplication, performed in much the same manner as an elective Nissen for reﬂux disease (Fig. 6–19).8 ● Prevention Injury to the esophagus most often occurs when a welldescribed and crucial ﬁrst step in its mobilization is omitted. After the peritoneal and diaphragmatic attachments of the left lobe of the liver have been divided to expose the esophageal hiatus, this ﬁrst maneuver is to sharply and transversely incise the peritoneum overlying the distal esophagus from the angle of His on the patient’s left side to the junction of the stomach’s lesser curvature with the esophagus on the patient’s right. It is only then that the esophagus can be properly mobilized and atraumatically encircled. The right index ﬁnger of the operating surgeon is inserted into the mediastinum superior to the angle of His and encircles the esophagus, with great care taken to appreciate the full circumference of the esophagus and the easily palpable groove between this organ and the aorta. Bleeding from high lesser curvature vessels occurs with a transverse trajectory of the circumscribing ﬁnger and is

82

SECTION I: GENERAL CONSIDERATIONS

Spleen

Incision in gastrocolic omentum

Incision in line of Toldt

Colon

avoided when the circumscribing ﬁnger makes an obtuse angle pointing from the angle of His to the patient’s right shoulder.

Injury to the Ureter ● Consequence Urinoma may accumulate and subsequent surgery may be necessary if an injury is not recognized or if adequate repair of a ureteral injury is not achieved. ● Repair The blood supply to a ureter ramiﬁes proximally from branches of its ipsilateral hypogastric artery. If the proximal ureter is injured and not devascularized and the remaining ureter can be readily identiﬁed, the injury can often be repaired over a stent placed either cystoscopically or through a cystotomy. In the latter case, the bladder should be closed in multiple absorbable layers and decompressed postoperatively with a Foley catheter. All repairs of ureters or bladder should be drained. Extensive injuries or injuries associated with devascularization of the ureter demand urologic consultation because they may require mobilization of the kidney, interposition of a loop of bowel, “hitch” mobilization of the bladder, or all three. Suspected ureteral injuries may be conﬁrmed with an intravenous methylene blue injection, the persence of dye in the operative ﬁeld conﬁrming injury. ● Prevention Injury to the ureter is often a complication of hysterectomy or the mobilization of the colon for its resec-

Figure 6–18 An incision in the white line of Toldt on the left side is connected to a surgically created opening in the gastrocolonic omentum by a maneuver that pushes down upon the colon’s splenic ﬂexure and then retracts it tangentially in a coronal plane under direct vision and controlled tension. The lienocolic ligaments thus exposed may be lysed using cautery or sharp dissection, as dictated by their size and vascularity.

tion or for retroperitoneal exposure. For pelvic conditions known to be inﬂammatory, careful tracing of the ureter from a proximal identiﬁcation point can usually avoid injury. Avoidance of ureteral injury in the pelvis can best be accomplished by proximal identiﬁcation after complete division of the ipsilateral white line of Toldt. Few ureters identiﬁed close to the renal pelvis are injured while being exposed in antegrade dissection. The ureter enjoys a relatively constant relationship to the bifurcation of the common iliac artery, which represents an additional anatomic landmark. Involvement of a ureter by an obstructing pelvic cancer is heralded by proximal ureteral dilatation; in this circumstance, the ureter cannot be freed externally, and— depending on the likelihood of cure—the ureter will have to be stented or its proximal segment diverted to preserve excretion. Operations done on the uterine cervix should proceed in close proximity to it if ureteral injury is to be avoided. Whether use of preoperatively placed ureteral stents avoids ureteral injury in abdominal and pelvic surgery is controversial and a matter of individual surgeon choice. Gittes (personal communication, Peter Bent Brigham Hospital, Boston, 1978) observed that placement of a ureteral stent does not preclude injury to the ureter in a scarred, inﬂamed, ﬁbrosed, or tumor-laden retroperitoneum—“it just makes the injury crunchy.”

Bladder Injury ● Consequence Urine leak or the need for subsequent surgery may occur if bladder injuries are not recognized or are inadequately repaired.

6 GENERAL LAPAROTOMY Incision in peritoneum

83

Angle of His

Esophagus

Stomach

A

Figure 6–19 A, The peritoneum overlying the gastroesophageal junction is incised transversely from the gastroesophageal junction on the patient’s right side to the angle of His. B and C, The ﬁnger encircling the esophagus in the mediastinum points toward the right shoulder, and not transversely, thereby precluding entry into the well-vascularized region of the high lesser curvature of the stomach. D, The suture line for repair of a distal esophageal injury is encompassed within a Nissen fundoplication performed for that purpose.

B

C

D

● Repair Injury to the intraperitoneal urinary bladder is readily identiﬁed at laparotomy either by visualization of the Foley catheter balloon or by the presence of urine in the operative ﬁeld. As with suspected ureteral injuries, methylene blue dye may be intravenously injected, its presence noted in the operative ﬁeld conﬁrming injury.

If the bladder injury is incisional or otherwise selflimiting, the edges of the defect should be identiﬁed and the injury should be closed with a two-layer closure. The inner layer is full thickness and the outer layer is an imbrication. Injuries to the posterior wall of the bladder are approached transvesically and occur more often with

84

SECTION I: GENERAL CONSIDERATIONS

vaginal surgery than during laparotomy. The transvesical approach allows for trigonal visualization during repair.9,10 Injection of pigmented intravenous dyes may facilitate the delineation of the injury. A repaired bladder is typically decompressed for 10 days to 2 weeks with a Foley catheter after repair, whether the injury to the bladder is volitional (as for primary repair, ureteral stent placement, or colovesical ﬁstula repair) or accidental. An additional drain is placed near the repair and brought out through the anterior abdominal wall. If the extravesical drain has been dry, some surgeons discontinue the Foley without obtaining a radiologic study; others perform a cystogram on all patients. ● Prevention Prevention of bladder injuries is best afforded by preoperative decompression with a Foley catheter for pelvic surgeries, awareness of the position of the bladder and the Foley balloon during dissection, and a method of dissection of adhered visceral loops that stays close to their antimesenteric surface and does not stray into the retroperitoneal fat.

Vascular Injuries ● Consequence Bleeding may continue from unsecured vessels. Visceral ischemia may result from occlusion of vessels essential to organ perfusion. ● Repair Vascular injuries should be initially managed by an attempt to obtain control proximal and distal to the injury. As an injured vessel is isolated, one should be able to tell whether it is a tributary of a major vessel that can be sacriﬁced or whether it is an essential vessel. The injured portion of essential arteries should be mobilized as much as is practical, isolated with vascular clamps if possible, and repaired with nonabsorbable monoﬁlament sutures. Rarely, the avulsion or damage to an essential vessel will be sufﬁciently great that completion of the transection with end-to-end anastomosis or vascular graft placement is required. Because all such repairs of transections carry the potential for thrombosis as the task is being completed, some have suggested that a ﬂush of heparinized saline solution distal to the repair helps to avoid thrombosis during occlusion for repair. Because the reports of such repairs are as uncontrolled as their precipitating bleeds, the advantages of this approach are unknown, and heparinization is usually far from the surgeon’s thoughts on the occasion of just having controlled an exsanguinating bleed. Although textbook achievement of proximal and distal control is optimal, signiﬁcant vascular injuries occur precisely because the three-dimensional preinjury mobilization is insufﬁcient to allow the controlled isolation and clamping routine that characterizes elective vascular

surgery. Mannick (personal communication, Brigham & Women’s Hospital, Boston, 1982) stated that one question is diagnostic of whether a queried physician is a surgeon or not—whether she or he is more respectful of arterial or venous bleeding. The surgeon always chooses venous. Venous injuries do not often allow the ease of dissection of arterial injuries because the thin vein wall predisposes repairs to further tearing with ongoing and potentially exsanguinating hemorrhage. Accordingly, particularly with venous injuries, a temporary solution is required in order to be able to see to complete the dissection. Three maneuvers may be used: application of Allis clamps to the venotomy to further characterize the injury and obtain exposure, application of a side-biting clamp to the injury, or proximal and distal compression with sponge sticks employed as surrogates for clamps and thereby facilitating further dissection and control (Fig. 6–20). The portal vein is constituted of the conﬂuence of the superior mesenteric vein, inferior mesenteric vein, and splenic vein. Injury to it is most often made in its exposure during pancreaticoduodenectomy. The superior mesenteric tributary of the portal vein may be identiﬁed by an extended Kocher maneuver, which reﬂects the hepatic ﬂexure of the colon and identiﬁes the mesenteric vein’s course beneath the surgical neck of the pancreas, as described by Cameron.11 Alternatively, after opening the lesser sac through the gastrocolic omentum, the surgeon may identify and follow the middle colic vein onto the superior mesenteric vein’s anterior surface. The atraumatic separation of the anterior surface of the conﬂuence from the pancreas is testament that the disease has not involved the vein’s wall; that the vein’s adventitial, but not endothelial, surface has been exposed; and that a tunnel can be developed between the anterior surface of the vein and the surgical neck of the pancreas by the judicious use of gentle cephalad blunt dissection (Fig. 6–21). If hemorrhage from venous injury occurs because the diagnosis of inseparability of vein from tumor was made by blunt digital venotomy in this subpancreatic tunnel, the injury should be initially addressed by packing the tunnel. Cellulose or crystallized collagen products will usually secure hemostasis in small tears or avulsion of small branches. Larger rents represent one of the most unforgiving and poorly salvaged injuries in all elective surgery. The best treatment is avoidance. Second best is to proceed to rapid and complete exposure of the injury before extensive blood loss—in all but an exsanguinating situation. If the patient is resectable or if preliminary maneuvers do not stop the bleeding, efforts at more complete exposure of the injury, including expeditious division of pancreatic parenchyma, should rapidly follow the injury to facilitate exposure. Injury to the portal conﬂuence during pancreaticoduodenectomy can also occur during the delivery and passage of the proximal jejunum under the root of the mesentery and into the subhepatic space or during the subsequent dissection of the vein from the uncinate process of the

6 GENERAL LAPAROTOMY

Figure 6–20 Methods of controlling venous hemorrhage. A, Allis clamps are sequentially applied to the venotomy to close it.The clamps are adjusted to produce minimal encroachment on the venous lumen and then undersewn to complete the lateral venorrhaphy. B, A side-biting (Satinsky) clamp is applied to the vein, excluding the injured portion. This maneuver requires that at least 50% of the vessel be able to be clamped, which is not possible in all circumstances. Venotomy is closed under direct vision with a running suture, and the clamp is released. C, “Sponge sticks”—small gauze pads loaded on ringed forceps—are used as surrogates for vascular clamps in an attempt to slow or stop bleeding and to facilitate visualization of the injury. This may facilitate direct repair, application of Allis clamps, or further dissection to enable a side-biting clamp to be placed.

85

A

B

pancreas. In both cases, the culprit is likely the avulsion of side branches of the portal vein, which can be exposed, closed with Allis clamps and undersewn. Exposure of the injury and salvage of the patient with such an injury may demand the presence of several experienced vascular surgeons. Packing of the injury should occur until they are available. ● Prevention As with all injuries, knowledge of the normal anatomy and its variants as well as unhurried dissection facilitates avoidance of injury.

Problems of Fascial Closure: Wound Infection, Wound Dehiscence, Evisceration, and Incisional Hernias ● Consequence The surgical literature has historically and repetitively warned of the ﬁscal and physiologic cost of abdominal

C wound disruption. Contemporary surgeons who protest that such costs are exaggerated on the grounds that few additional hospital days are now required to care for patients with wound infections often have not included the cost of dressings, outpatient nurse visits, and subsequent surgeries in their calculations. ● Repair Fascial closures may fail subtly or dramatically, early or late. Wounds may have disrupted subclinically at the fascial level in the immediate postoperative period only to present with an incisional hernia much later on or may herald early dehiscence by a disproportionate discharge of serosanguinous ﬂuid through the skin in the immediate postoperative period. Evisceration is the extrusion of bowel through fascia and skin disrupted in the immediate postoperative period. Whereas the latter condition is clearly the most urgent and psychologically distressing, as the patient is beside himself or herself both ﬁguratively and literally, both dehiscence and evis-

86

SECTION I: GENERAL CONSIDERATIONS

Portal vein

Superior mesenteric vein

Figure 6–21 Insertion of the index ﬁnger beneath the surgical neck of the pancreas to verify that a dissection plane exists at the origin of the portal vein beneath the pancreas. The surgeon follows the anterior surface of the superior mesenteric vein as it courses beneath the pancreas to join the splenic and inferior mesenteric veins at the portal conﬂuence.

ceration are signiﬁcantly morbid events in an already compromised patient. Whereas a small dehiscence in a densely adhered abdomen may be able to be managed nonoperatively, it will virtually always eventually result in a signiﬁcant ventral hernia. The greater concern is that, if ignored, a serosanguineous herald discharge may foreshadow evisceration. In this situation, consideration should be given to returning the vast majority of dehisced patients to the operating room for exploration and assessment of the potential for reclosure. No two such patients are alike, making the examination of the merits of the competing remedies difﬁcult. In patients with fascial disruption attributable to simple failure to secure the knot or to inadequate placement of sutures, reclosure may be attempted with more attention to detail. Patients who have either necrotizing infection or extensive disruption of the fascial edges by infection or sutures cutting through the closure may require a different approach. Mass closure of the wound with retention sutures placed through all layers of the abdominal wall has been advocated as either a primary or a secondary approach to closure in hopes of minimizing evisceration. Its success in secondary closure probably relates to its ability to obtain wider fascial purchase and to gather and appose musculofascial tissue to bring together and buttress the wound edges. ● Prevention Only some of the determinants of wound healing are under the surgeon’s direct control. Others are the

products of comorbid metabolic or hematologic disease; and still others are byproducts of the patient’s body habitus. The surgeon who performs emergent or urgent laparotomy is often asked to accept some determinants of deﬁciencies in wound healing in exchange for the need to urgently address the presenting complaint. When possible, the postponement of elective surgery until adverse comorbid conditions can be corrected or optimized is a basic tenet of surgery. Intuitive measures include the treatment of comorbid infectious disease when a clean case or prosthetic implant is anticipated, the optimization of glucose control in the perioperative period as a means of demonstrably decreasing wound complications, the maintenance of tissue oxygen tension and the correction of nutritional deﬁciencies. Although it makes intuitive sense that a patient depleted of carbohydrate and fat reserves would metabolize muscle protein and have teleologically diminished incentives to synthesize the protein modulators of the immune response (thereby fostering impaired wound healing), it is difﬁcult to demonstrate that restoration of a normal albumin or weeks of preoperative hyperalimentation create demonstrable survival beneﬁt in the recovery of large cohorts of hospitalized postoperative patients. Wound strength is conferred by the dermal and fascial layers only. However, heroic hyperpronative contortional efforts to avoid incorporation of muscle into a fascial closure often paradoxically result in a suboptimal purchase of the fascia itself, thereby facilitating postoperative wound disruptions. The surgeon’s attention to detail, technique,

6 GENERAL LAPAROTOMY and choice of suture material are important. However, as with all aspects of surgery, the quality of the surgical closure is determined more by the caliber of the surgeon than by the caliber of her or his suture material. Kocher clamps or intra-abdominal retractors should allow the operating surgeon the opportunity to visualize the closure needle as it traverses the parietal peritoneum as she or he protects the underlying abdominal viscera. The ideal assistant to the surgeon performing abdominal closure will retract the skin and subcutaneous tissues to allow optimal visualization of the fascial layer. Care should be taken not to catch the dermis in the fascial closure, which causes a painful dimpling of the skin immediately adjacent to the wound. Either such a stitch must be redone or the dermis must be released prior to skin closure. Most abdominal wounds in adults should be closed with monoﬁlament fascial suture material of zero caliber or larger. Smaller-caliber material may fracture as the abdominal wound elongates during muscular loading and as the intra-abdominal pressure increases after closure. Increasing tension on the wound has been demonstrated to approach perfusion pressure in some animal models of wound failure, yet no reliable bedside tool exists for the calibration of tension on fascial sutures during wound closure. Advocates of interrupted closure decry the “Lindbergh principle,” whereby, like Charles Lindbergh’s reliance on the reduced weight of the one-engine plane for his successful transatlantic ﬂight, the integrity of fascial closure resides with the one terminal knot securing the running closure. They also cite potential strangulation of the suture line as the running suture tightens perioperatively. However, discounting rare circumstances in which the terminal knot of a running closure unties, the theoretical advantages of intersutural perfusion to the wound edge have not produced a superior rate of intact fascial closure for surgeons using the interrupted technique. A likely explanation for this is that the tissue tension from adjacent sutures creates equivalent ischemia to that imposed by a running stitch. Meta-analyses and prospective randomized studies attempting to identify comparable patients and closing them with interrupted or running closures have produced similar results; a slight advantage shown in some randomized studies favors the running suture group. Assuming that an adequate caliber suture is chosen and that the knot(s) remains secure, a continuous suture providing a suture length–to–wound length ratio of 4 : 1 is most often advocated, based on clinical experience and burst-strength experiments in laboratory animals (Fig. 6–22). These data argue that even the hypothetical relative weakness of the midline wound to its transverse counterpart are eliminated by the placement of sutures at least 1 cm from the wound edge, incorporating all layers of fascia and muscle, and progressing no more than 1 cm with serial bites.12 A normal inﬂammatory response in a well-nourished host with intact cellular, vascular, and chemical mediators

87

1 cm 1 cm 1 cm

Figure 6–22 Optimal fascial closure provides a suture length– to–wound length ratio of 4 :1.

is optimal for normal wound healing. The link between wound infection and development of a subsequent ventral hernia is well established, as is the reduction in tensile strength of wounds closed by secondary intention compared with those closed primarily. The hope that a wound might heal with primary closure should not override reasoning developed through evidence-based imperatives that suggest secondary closure. The National Nosocomial Infections Study (NNIS) classiﬁcation of wounds as clean, clean contaminated, or grossly infected is intended to stimulate the surgeon to choose proper closure material and to decide whether to leave the skin open based on risk factor assessment once fascial closure has been effected.13 Sutures with interstices and whose constitution incites an inﬂammatory response have generally been abandoned in favor of monoﬁlament synthetic sutures, in the hope that the latter would minimize the chances for wound infection. Among monoﬁlaments, suture material has been developed that absorbs at a time when inherent tensile strength of the wound would be presumed to have developed. With the liability that they remain as a foreign body indeﬁnitely and are often the source of patient’s pain or other local difﬁculties, nonabsorbable monoﬁlament sutures for patients at high risk of wound disruption nonetheless remain the choice of many surgeons. Avoidance of wound infection and its sequelae is facilitated by skin preparation, by instrument sterilization, and by the sterile environment created in the operating room. Skin preparation has historically been accomplished with a bacterial desiccant such as povidone-iodine (Betadine), but chlorhexidine and its analogues have recently been advocated as preparations whose toxicity to bacteria is longer lasting. Some have suggested that overzealous use of the cautery and fat necrosis predispose to wound infection. Others have claimed that wound protector devices minimize inoculation of the subcutaneous tissue during laparotomy in clean-contaminated cases. As treatment for wound infection involves removal of the skin closure and drainage of the extrafascial subcutaneous space, it makes sense to eliminate the skin closure completely in grossly contaminated wounds or in wounds in which the subcutaneous tissue has the potential to have received a sufﬁcient inoculum to make wound infection likely. Logarithmic reductions in bacterial counts have been shown to be able to be effected with serial dressing

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changes.14 When bacterial inoculation is combined with ischemic or bacterial compromise of the subcutaneous tissues, some have advocated the use of enzymatic débridement agents. Once the wound’s bacterial counts have been judged to be decreased on clinical or quantitative determination, a decision can be made as to whether to secondarily tape it shut or close it with sutures or whether to apply a vacuum sponge to the subcutaneous tissue, achieving both wound contraction and contaminant evacuation.15 How to best avoid visceral injury during abdominal wall closure is a matter of personal choice by the operating surgeon. Malleable retractors—either unsheathed or augmented by rubber extensions as exempliﬁed by the “ﬁsh” retractor—or subfascial layering of Mikulicz pads are used by some surgeons to keep the abdominal viscera away from the parietal peritoneum during closure. However, nothing focuses the surgeon’s attention on the safety of

A

B

Fascial needle Dermis

C

the process like the presence of his or her own hand in the wound as the fascial closure proceeds. What should be in the nondominant hand of the surgeon is a matter of controversy (G. Steele, personal communication, Brigham & Women’s Hospital, Boston, 1983). Steele advocated that the fascial closure stitch enter the abdomen into a space created by the unadorned cupped nondominant hand. This technique shields the viscera so that they intrude no further than that hand’s dorsal surface. Hooking the nondominant hand’s index and third ﬁngers on the other side of the incision allows visualization of the parietal peritoneum as the fascial stitch leaving the abdomen is placed. This maneuver requires that the surgeon’s two ﬁngers bring the abdominal wall forward as the assistant retracts skin and subcutaneous tissue. Advocates of this technique note that absence of an instrument in the surgeon’s left hand facilitates its use for retraction and frees it for the tying function (Fig. 6–23). Other surgeons insist

Figure 6–23 A, Closure of the abdominal wall with no instrument in the nondominant hand. The nondominant (left) hand is inserted into a midline wound. B, Elbow extension as the wrist is positioned at 180° elevates the abdominal wall as the cupped hand protects the bowel during fascial suture placement. C, Twoﬁngered “hooking” of the other side of the abdominal wall facilitates safe placement of sutures by allowing the curved portion of the needle to clear the abdominal viscera before it engages the fascia. The assistant pulls the skin and subcutaneous fat away from the closure so that it is not retracted downward, which produces pain.

6 GENERAL LAPAROTOMY

89

Figure 6–24 The sheathed SuturTek needle application device. The ﬁrst squeeze of the device permits the needle to engage the tissue and resheaths it. The second squeeze permits disengagement and movement of the device to engage the sewed side of the incision while simultaneously resheathing the needle.

that the surgeon should always have two instruments in hand and that an instrument such as a forceps be utilized in addition to the retraction provided by the assistant’s Kocher clamp. If an instrument is to be used by the surgeon to grasp fascia, it should be a sturdy toothed forceps or Kocher clamp capable of exerting substantial anterior traction on the fascia. Even with a focused team, optimal retraction, and deﬁnitive exposure of the fascial layers, closure of the abdominal wall is a common place for the surgeon or her or his assistants to incur needlestick injuries. The substitution of blunt needles for sharp needles to close fascia has been advocated by the American College of Surgeons in hopes of addressing this problem.16 In addition, sheathed needle devices, such as that developed by SuturTek, Incorporated, have sought to provide protection, automate the pronation necessary to achieve adequate fascial purchase (Fig. 6–24), provide equivalent purchase without hypersupination or hyperpronation, and protect the operating surgeon and her or his assistants.17 Whether the use of blunt needles and such devices will, in fact, favorably affect the incidence of needlestick injury remains to be seen. Overzealous attempts by anesthesia personnel to coordinate abdominal wall closure with emergence from anesthesia occasionally produce a patient emerging from anesthesia near the end of the operation, but before the ﬁnal fascial suture has been placed. This practice places the patient at extraordinary risk for injury to the underlying viscera as the patient strains and pushes these viscera against the anterior abdominal wall, compromising visu-

alization, placement, and tying of the fascial stitch. Remarkably, the reﬂex response to the surgeon’s observation that relaxation is inadequate is more often a report of how many “twitches” are evident on a neuromuscular blockade monitor rather than deepening of the anesthetic, as if a monitor’s output should trump the experiential data being reported by the surgeon from the operative ﬁeld. It is better for the patient to spend a few more moments under an appropriate level of anesthesia than to compromise fascial closure or risk injury to intestine. If the bowel is accidentally or otherwise impaled or distorted during fascial closure, the needle should be backed out and the injury to the bowel wall assessed. It is better to acknowledge the presence of signiﬁcant tethering of the bowel to an abdominal wall adhesion with release of the intestine or to take the time for visceral repair after signiﬁcant tearing than to incur an unnecessary postoperative obstruction or intestinal ﬁstula.

When the Fascia Should Not Be Closed: The Abdominal Compartment Syndrome ● Consequence Tight abdominal closures have been implicated in visceral hypoperfusion and decreased respiratory excursion. Extrapolating from the physiologic compromise witnessed by pediatric surgeons in their care of patients with gastroschisis and omphalocele closure, adult surgeons caring for massively resuscitated trauma victims have described a syndrome of restrictive small volume ventilation, visceral hypoperfusion, and oliguria known

SECTION I: GENERAL CONSIDERATIONS

90

30 25 20 15 10

40 50

5 0

60

Water manometer or transduced equivalent

Foley catheter with balloon inflated

3-way Foley stopcock catheter (for flushing)

Figure 6–25 Method of measuring intraabdominal pressure using a Foley catheter. The bladder is transduced to either a monitor screen or a water manometer.

as the abdominal compartment syndrome.18 Investigated by Harmann in a dog model of increased intraabdominal pressure19 and subsequently in humans using manometrically measured bladder pressures as surrogates for intra-abdominal pressures, the evolving literature suggests leaving the skin and fascia open after acute interventions in which closure of the abdomen would create such elevated pressures and opening the abdomen (and leaving it open) when such parameters exist in an acutely ill, but unoperated, patient.20 The abdominal compartment syndrome is suspected based on the clinical circumstances of tight abdominal closure or massive abdominal distention and conﬁrmed by manometric pressure measurements of ﬂuid within the urinary bladder (Fig. 6–25). Measurements of 22 mm H2O or greater are believed to represent elevations that compromise glomerular ﬁltration and perfusion pressure in the clinical setting of oliguria, increased peak ventilatory pressures, and shock. ● Repair Postponing deﬁnitive closure until such time as the abdominal wall has accommodated and the interstitial ﬂuid has been dispersed allows for delayed primary closure of the fascia. However, unlike the situation in neonates, in which the operation is often classiﬁed as a clean case and staged closure is anticipated with several intervening months permitting accommodation, adults suffering abdominal compartment syndrome have often been acutely injured exogenously or iatrogenically, with a contaminated wound and ongoing concern for the integrity of the intra-abdominal viscera. Under such circumstances, temporary containment of the abdominal viscera without beneﬁt of fascial, skin, or prosthetic

closure of the abdominal wall must be effected because deﬁnitive closure would produce intra-abdominal pressures high enough to compromise perfusion pressure and a prosthetic mesh augmenting the abdominal wall would likely become infected. To allow the abdomen to remain open during a period of known collagen deposition and adhesion formation, and to enable its subsequent closure without adhesiolysis, strategies have been developed for short-term prevention of adhesions of viscera to the anterior abdominal wall at the incision’s edge. Originally, the Bogota Bag, a resterilized silicone bag recycled after use for storage of sterile irrigant or intravenous ﬂuid, was adapted for use as an intravenous visceral bag similar to the Schuster silo used in infants for treatment of omphalocele and gastroschisis.21,22 The bag is sutured to the wound edges. A modiﬁcation of the Bogota bag can be constructed in any operating room by apposing the sticky sides of two plastic surgical drapes. Trimmed to a size larger than the fascial defect, the large, double-thickness plastic sheet is then placed into the peritoneal cavity between the viscera and the anterior abdominal wall in a way that precludes contact of the visceral peritoneum with the parietal peritoneum at the wound’s edges. Moist towels, subcutaneous suction drains, and a large plastic drape placed over the entire apparatus preclude both the accumulation of additional ﬂuid under the dressing and the leakage of interstitial ﬂuid into the bed, thereby facilitating nursing care (Fig. 6–26). Interval returns to the operating room as the interstitial ﬂuid recedes permit sequential assessment of the potential for deﬁnitive closure. Other circumstances, such as objective loss of the anterior abdominal wall because of blast or bullet injury, preclude primary closure of the abdominal wall. Compartment

6 GENERAL LAPAROTOMY Suction drain

91

Plastic sheet

Towels

Muscle/fascia

Small intestine

Plastic sheets

Figure 6–26 Creation of a modiﬁed “Bogota bag” for the management of the open abdomen. The sticky sides of two plastic surgical drapes are apposed and then tucked under all corners of the abdominal wound to preclude adhesion of visceral peritoneum to parietal peritoneum. Moist towels and suction drains are then placed. A third plastic drape completes the closure. Interstitial ﬂuid is collected by suction applied to the suction drains.

release, tissue transfer, absorbable meshes, intestinal submucosal xenografts, and autogenous split-thickness skin grafts applied after the establishment of a base of granulation in such wounds have been utilized as late-closure measures. Wound management when the skin, the fascia, or both cannot be closed is facilitated by nutritional supplementation and supportive care directed at the establishment of a granulating base and the avoidance of intestinal ﬁstula formation. When bacterial counts in the wound are demonstrably low as determined by either quantitative wound culture or qualitative examination of wound drainage, ambulatory wound care may be facilitated by the application of a negative-pressure vacuum assisted closure (VAC) device.23 This delivers negative pressure to wounds, evacuates accumulating ﬂuid, and has been applied either to the subcutaneous space or onto a granulating bed when the fascia is not intact. Application of negative pressure to the wound removes transudate and light exudative material and promotes wound contraction and patient mobility. The VAC device may be applied whether or not the fascia is present once a granulating base has been established. It may be used in either hospitalized patients or outpatients. Recently, some have advocated a modiﬁcation of the VAC system to treat complex wounds where a granulating base and an intestinal ﬁstula coexist (Fig. 6–27).24 This modiﬁcation pouches the ﬁstula, which is excluded from the VAC dressing when possible, while the VAC exerts negative pressure on the granulations. In preliminary reports, such patients are said to have increased mobility and decreased length of stay. ● Prevention Abdominal compartment syndrome occurs in the setting of increased intestinal ﬂuid due to massive resuscitation and multisystem failure. The surgeon is usually not able to affect the cause. Prevention is directed at the limitation of iatrogenic contributions to multisystem organ failure.

Normal abdominal wall

VAC device Intestinal fascia and pouch Sponge

Nonadherent gauze Plastic sheet

Granulation tissue

Figure 6–27 Modiﬁcation of the vacuum assisted closure (VAC) device to accommodate an intestinal ﬁstula within a granulating base. The ﬁstula is pouched, and the granulating base is protected with nonadherent gauze to permit the application of negative pressure on the VAC sponge.

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Infectious Complications of Laparotomy: Postoperative Intra-Abdominal Abscess and Postoperative Enterocutaneous Fistula ● Consequence Sepsis, shock, multiple subsequent surgeries, and death may occur if the infectious problem is not approached systematically. ● Repair Infection may be the reason for laparotomy or it may develop insidiously as a complication in the postoperative period, masked by the paralytic ileus that accompanies most intra-abdominal surgeries. Postoperative ileus is believed to be a vestigial, primitive, and teleologic reﬂex aimed at limiting peristalsis and resultant peritoneal soilage through enterotomies of animals wounded in the wild. In patients, an ileus may allow 3 to 7 days to elapse before the symptoms of anastomotic failure, neglected perforation, or unnoticed enterotomy become manifest with resumption of peristalsis. Therefore, any hyperdynamic, febrile postoperative abdominal surgical patient should have these diagnoses considered. Infected ﬂuid collections in the abdomen are classiﬁed as either communicating or not communicating with the intestine. Noncommunicating collections (pure abscesses) are typically the sequelae of inoculation of a portion of the peritoneal cavity with visceral contents or external contaminants as part of either the primary pathology or its treatment. Their presence implies lack of evacuation at the ﬁrst procedure or a small visceral leak that rapidly sealed after inoculation. They are more often discovered by abdominal imaging done as part of an evaluation for fever than by history or physical examination, although some pelvic collections may be felt on rectal or pelvic examination and subphrenic collections may be suspected by the presence of ipsilateral shoulder pain. Noncommunicating abscesses can almost always be treated with catheter drainage by an experienced interventional radiologist, who also plans the trajectory of the drainage approach. Ultrasonography has yielded to computed tomography scan in the diagnoses of most intra-abdominal abscesses. Both modalities are used by interventional radiologists to accurately and safely approach and drain the collections they discover. Only rarely must a subphrenic abscess be approached surgically through the bed of a resected lower thoracic rib (Fig. 6–28) because the radiologists are not able to identify a safe trajectory for percutaneous puncture. Enterocutaneous ﬁstulas may occur spontaneously in parasitic disease and in Crohn’s disease or as the result of anastomotic failure or iatrogenic injury. The latter typically manifests in one of three ways: 1. The “communicating abscess.” In this circumstance, an intra-abdominal ﬂuid collection identiﬁed radiographi-

cally is initially believed to be a noncommunicating abscess, but the initial drainage of purulent material is eventually followed and supplanted by ongoing drainage of enteric material. Percutaneous drainage thus converts the intra-abdominal collection to an enterocutaneous ﬁstula. Collections with this potential usually contain air as well as ﬂuid. 2. Spontaneous drainage of enteric contents occurs through the original laparotomy incision or a drain site, usually related to anastomotic failure, unrecognized pathology, enterotomy unrecognized at the ﬁrst operation, or visceral incorporation into fascial closure. 3. “Slow dehiscence.” In this circumstance, a single loop of bowel is adhered to both sides of an abdominal wound. As the fascial closure disrupts, adhesion of the loop to both sides persists, resulting in intestinal wall disruption and ﬁstulization into the wound (Fig. 6–29). Berry and Fischer25 identiﬁed ﬁve phases of management of a ﬁstula: recognition/stabilization, investigation, decision making, implementation of deﬁnitive therapy, and healing. Sequential attention is paid to ﬂuid and electrolyte repletion, drainage of sepsis, control of ﬁstula drainage, and local skin care. Nutritional support is then instituted, and upon stabilization, typically 7 to 10 days after presentation, a ﬁstulogram, upper or lower gastrointestinal contrast study, or other advanced radiographic study is performed. Many ﬁstulas will close in the absence of conditions ﬁrst described by Welch and coworkers26—distal obstruction, cancer, foreign body, inﬂammatory bowel disease, or ongoing associated infection. It is reasonable to persist with supportive measures for ﬁstula care only if progress is being made and if the determinants of persistent ﬁstulization are absent. The additive psychological distress of patient and surgeon and the desire of both to see the problem “ﬁxed” should not push the surgeon to early laparotomy, given that ﬁstulas often declare themselves precisely at the time when inﬂammatory conditions from the ﬁrst surgery make the abdomen most hostile to a subsequent surgical approach. Although well intentioned, the surgeon seduced to operate for anything other than uncontrolled sepsis or intestinal necrosis during this early period will often ﬁnd that he or she has increased, rather than reduced, the number of intestinal ﬁstulas. One important exception to this admonition is the desirability of proximal diversion as an adjunct to ﬁstula control in the case of large bowel ﬁstulas or when such diversion can stop ongoing soilage, can be readily accomplished in an area remote from the epicenter of the reparative process and facilitates efﬂuent control. Whereas a direct operative approach to a leaking sigmoid colon anastomosis through the original operative ﬁeld, for example, might be difﬁcult, proximal diversion with either ileostomy or transverse loop colostomy outside the original operative ﬁeld (and therefore distant from the attendant adhesions) may greatly facilitate attempts at catheter drainage of the

6 GENERAL LAPAROTOMY

12th rib

A

B

Periosteum

93

Latissimus dorsi muscle

Liver Perirenal fat

Diaphragm

Diaphragm

Bed of 12th rib

D

C

Right subphrenic space

Ribs

Liver

Abscesses

Right post. subhepatic

Right ant. subhepatic

Figure 6–28 A, Technique of drainage of subphrenic abscess by posterior resection of a ﬂoating rib. B, The rib is exposed along its course and amputated. C–E, The subhepatic space is entered caudal to the visualized pleura, and the suction drains are placed.

Kidney

E

leaking ﬂuid and control of sepsis. Deﬁnitive operation to address the site of the colonic abnormality may be conducted in a minimally contaminated environment at a subsequent time. The protecting stoma may be either left in place as the distal defect is repaired in anticipation of closure at a third operation or taken down at the second surgery. Usually, repairs distal to a diversion in this setting are radiologically veriﬁed to be intact before the stoma is

closed. In general, stoma closures are elective operations; a distal radiographic study is universally useful both as a preoperative planning tool and to identify persistent, synchronous, or clinically occult pathology. ● Prevention Identiﬁcation of visceral injury, whether endemic to the pathology or iatrogenically created at the time of

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SECTION I: GENERAL CONSIDERATIONS Thinning of viscus as wound dehisces

Viscus tethered to both sides of incision

Division and exterioralization of lumen of bowel as fixed tethering points follow fascial edges during dehiscence.

Granulation tissue overlying exposed viscera Fascia Skin

Figure 6–29 Enterocutaneous ﬁstula development by slow dehiscence. As a single loop of bowel is tethered between separating fascial edges, enterotomy and ﬁstula develop.

operation, allows repair, externalization, or drainage as appropriate.

Intestinal Obstruction after Laparotomy ● Consequence Hospitalization for nasogastric decompression and reoperation for intestinal obstruction are common occurrences after an initial abdominal operation. ● Repair Unless it is believed to be the result of direct injury, tethering, occlusion of the bowel during fascial closure, or irreversible twisting of the bowel’s mesentery on its replacement into the abdomen, most obstructions occurring during the immediate postoperative period can be managed with nasogastric suction rather than a second operation. The diagnosis of early postoperative obstruction is made on clinical grounds after careful inspection of the abdominal wall of a recently operated patient for hernia or fascial defect. Typical symptoms of abdominal pain and vomiting, with or without leukocytosis and fever, lend support to the diagnosis but also occur with normal postoperative ileus. When a persistent postoperative ileus should be reclassiﬁed as a small bowel obstruction is a highly subjective determination awaiting a universally accepted deﬁnition of postoperative obstruction. Because the presence or absence of bowel sounds is increasingly denigrated as an important physical distinction, and as third-party payors push for early discharge and “fast-tracking” of patients, the early feeding of patients with physiologic intestinal atony have resulted in patients being classiﬁed as having early postoperative obstruction when they were simply fed too early in their postoperative course and then became distended or vomited as a result.

Plain ﬁlms of the abdomen, as with patients developing obstructive symptoms remote from surgery, show dilated loops of small bowel. Air-ﬂuid levels may be present in both circumstances, with variable amounts of gas present in the colon. The absolute absence of gas in the colon, when seen in any intestinal obstruction, is concerning but does not portend intestinal ischemia with the same frequency in the immediate postoperative period as the same ﬁndings occurring at a time remote from the ﬁrst surgery. The bowel must truly be suspected to be threatened to warrant operation during the acute phases of ﬁbrinous inﬂammation. The vast majority of immediate postoperative obstructions can be managed nonoperatively with nasogastric suction, judicious ﬂuid management, and repletion of electrolytes, whereas such a strategy of nearuniversal nonoperative management would likely endanger substantial numbers of patients developing obstruction long after their ﬁrst operation.27 ● Prevention Prevention of intestinal obstruction has interested surgeons because they themselves create adhesions after all types of abdominal surgery and are thus aware of the morbidity of both iatrogenic and naturally occurring obstruction. Various mechanical and chemical means have been used in attempts to prevent postoperative small bowel obstructions, particularly by obstetricians and gynecologists who are concerned not only with intestinal dysfunction but also with infertility. Noble28 incorrectly proposed that orderly arrangement of small bowel loops within the abdomen, facilitated by seromuscular tacking sutures, would reduce the incidence of recurrent obstruction. Others advocated the use of long intestinal tubes, introduced as preformed stents into the small intestine, to serve the same function. Neither tech-

6 GENERAL LAPAROTOMY nique has affected the incidence of recurrent obstruction durably enough to be widely utilized.29 Dextran, steroids, antibiotic irrigation solutions, and limitation of radiation ﬁelds during radiation therapy have been utilized in attempts to minimize postoperative small bowel obstruction, particularly in patients undergoing radiation to the pelvis after gynecologic or related operation. The latest and most promising topical product used for prevention is sodium hyaluronate carboxymethylcellulose (Sephraﬁlm). Becker and associates30 sought to standardize a clinical model by wrapping the Sephraﬁlm around the peristomal parietal peritoneum of freshly created stomas. Sephraﬁlm appeared to reduce adhesions around the stoma when it was inspected on reversal, but critics of the model protested that peristomal adhesions are not a common, reproducible, or signiﬁcant clinical problem. Thus, it was unclear whether the relative absence of adhesions around some stomas at the time of reversal was good chemistry or good luck. A more recent large, multiinstitutional prospective, randomized study purported to vindicate the use of the compound in demonstrating fewer reoperations and hospitalizations for small bowel obstruction in patients treated with Sephraﬁlm and followed for 5 years.31 However, the study did not control for the threshold of surgeons to operate nor for the lack of uniform approach from surgeon to surgeon. Unfortunately, such lack of controls is pervasive in the small bowel obstruction literature, making any assessment of an intervention’s impact difﬁcult. Indeed, the ability to assess the efﬁcacy of any intervention for small bowel obstruction is hampered by the heterogeneous nature of intestinal obstructions, the threshold for subsequent operation for obstruction, the universal proclamation of adhesions as the cause by the biased operating surgeon, the ﬁnancial rewards of operating, and the industrial funding of many studies.32 Conversely, a study requiring demonstrably dead bowel as an endpoint because of its deﬁnitiveness would be correctly judged unethical. As a result, whether any preventive strategy affects adhesion formation remains controversial.

CONCLUSION Those privileged to enter the abdomen surgically should be aware of the spectrum of disease they might encounter or create and be globally capable of managing the patients in and out of the operating room. The decision to cross the threshold from nonoperative to operative intervention for abdominal pathology carries with it the responsibility to carry the patient through all events presented by both the disease and the intervention and directs whether an open or a laparoscopic approach is chosen. Abdominal interventions are grounded in well-established principles of nutrition, infection control, dissection, abdominal wall

95

repair, visceral repair, and surgical principles developed by surgeons for surgeons. In stark contrast to those who would attribute complications to systems failure or fatigue, surgeons attribute complications in abdominal surgery to disease processes or to themselves.

REFERENCES 1. Bristow RG, Hill RP. Molecular and cellular basis of radiotherapy. In Tannock IF, Hill RB (eds): The Basic Science of Oncology, 3rd ed. New York: McGraw-Hill, 1998; pp 295–321. 2. Thorek P. Anatomy in Surgery. Philadelphia: JB Lippincott, 1951; pp 413–418. 3. Sheldon GF, Lim RC, Yee ES, Petersen SR. Management of injuries to the porta hepatis. Ann Surg 1985;202: 539. 4. Mattox KL, McCollum WB, Beall AC Jr, et al. Management of penetrating injuries of the suprarenal aorta. J Trauma 1975;15:808. 5. Tera H, Aberg C. Tissue strength of structures involved in musculo-aponeurotic layer sutures in laparotomy incision. Acta Chir Scand 1976;142:349. 6. Martin CJ, Kennedy T. Reconstitution of the pylorus. World J Surg 1982;6:221–225. 7. Cohn LH. Local infections after splenectomy: relationship of drainage. Arch Surg 1965;90:230. 8. Glatterer MS, Toon RS, Ellestad C, et al. Management of blunt and penetrating external esophageal trauma. J Trauma 1985;25:784–792. 9. Cetin S, Yazicioglu A, Ozgur S, et al. Vesicovaginal ﬁstula repair: a simple suprapubic transvesical approach. Int Urol Nephrol 1988;20:265–268. 10. Leng WW, Amundsen CL, McGuire EJ. Management of female GU ﬁstulas: transvesical or transvaginal approach 1985–1988. J Urol 1998;160(6-1):1995–1999. 11. Cameron JL. Rapid exposure of the portal and superior mesenteric veins. Surg Gynecol Obstet 1995;176:395. 12. Israelsson LA, Johnson T, Knutsson A. Suture technique and wound healing in midline laparotomy incisions. Eur J Surg 1996;162:605–609. 13. Culver DH, Horan TC, Gaynes RP, et al. Surgical wound infection rates by wound class, operative procedure and patient risk index. Am J Med 1991;91(Suppl 3B):1535. 14. Pollock AV. The treatment of infected wounds. Acta Chir Scand 1990;156:505–513. 15. Morykwas M, Argenta L, Touchard R. Use of negative pressure to promote healing of pressure sores and chronic wounds. Proceedings of the Annual Conferences of Wound, Ostomy, and Continence Nurses Association, July 10, 1993, San Antonio, TX. 16. Committee on Perioperative Care. American College of Surgeons. Statement on blunt suture needles. Bull Am Coll Surg 2005;90:11. 17. Davis M. Advances in engineered sharps injury prevention technology: suturing. In Davis M (ed): Advanced Precautions for Today’s OR: The Operating Room Professional’s Handbook for the Prevention of Sharps Injuries and Bloodborne Exposures, 2nd ed. Atlanta: Sweinbinder, 2001.

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18. Burch JM, Moore EE, Franciose R, et al. The abdominal compartment. Surg Clin North Am 1996;76:833. 19. Kaufman CR, Cooper GL, Barcia PJ. Polyvinyl chloride membrane as temporary fascial substitute. Curr Surg 1987;44:31–34. 20. Balogh Z, McKinley BA, Holcomb JB, et al. Both primary and secondary abdominal compartment syndromes can be predicted early and are harbingers of multiple organ failure. J Trauma 2003;54:848. 21. Burch JM, Ortiz VB, Richardson RJ, et al. Abbreviated laparotomy and planned reoperation for critically injured patients. Ann Surg 1992;215:476–484. 22. Schuster SRA. New method for the staged repair of large omphaloceles. Surg Gynecol Obstet 1967;123:837–850. 23. Brock WB, Barker DE, Burns RP. Temporary closure of open abdominal wounds: the vacuum pack. Am Surg 1995;61:30. 24. Goverman J, Yelon J, Platz JJ, et al. The “ﬁstula vac,” a technique for management of enterocutaneous ﬁstula arising within the open abdomen. Report of 5 cases. J Trauma 2006;60:428–431. 25. Berry SM, Fischer JE. Enterocutaneous ﬁstulas. Curr Probl Surg 1994;31:469–576.

26. Edmunds LH, Williams GH, Welch CE. External ﬁstulas arising from the gastrointestinal tract. Ann Surg 1960;152:445–471. 27. Pickelman J, Lee RM. The management of patients with suspected early post-operative small bowel obstruction. Am Surg 1989;210:216. 28. Noble TG. Treatment of Peritonitis and Its Aftermath. Indianapolis, IN: AV Grindle, 1945. 29. Sprouse LR II, Arnold CL, Thow GB, Burns RP. Twelve year experience with the Thow long intestinal tube: a means of preventing post-operative bowel obstruction. Am Surg 2001;67:357–360. 30. Becker JM, Dayton MT, Fazio VW, et al. Prevention of post-operative abdominal adhesions by a sodium hyaluronidate–based bioresorbable membrane: a prospective, randomized, double-blind multicenter study. J Am Chem Soc 1996;183:406–407. 31. Fazio VW, Cohen Z, Fleshman JW, et al. Dis Colon Rectum 2006;49:1–161. 32. Nauta RJ. Advanced abdominal imaging is not required to exclude strangulation if complete small bowel obstructions undergo prompt laparotomy. J Am Coll Surg 2005;200: 904–911.

7

Laparoscopic Surgery Jay A. Graham, MD and Patrick G. Jackson, MD INTRODUCTION Laparoscopy was ﬁrst introduced at the beginning of the 19th century. In 1901, George Kelling was the ﬁrst to endoscopically examine the peritoneal cavity, and he called the procedure koelioscopie.1 In the 1940s, French gynecologist Raoul Palmer used laparoscopy for preoperative diagnosis and tissue biopsy.2 Throughout the better part of the 20th century, laparoscopy remained in the hands of gynecologists. In 1985, Dr. Erich Muhe quietly performed a rudimentary laparoscopic cholecystectomy that largely went unnoticed. It was not until Dr. Phillipe Mouret performed what is widely considered to be the ﬁrst laparoscopic cholecystectomy that the surgical community heralded this procedure.3 The advent of the laparoscopic cholecystectomy opened the door for modern-day laparoscopic surgery and a revolution soon followed. Over 750,000 laparoscopic cholecystectomies are performed each year in the United States.4 Whereas this operation has proved to be the “gold standard” for gallbladder disease, the complexity of operations done laparoscopically continues to be advanced. Although minimally invasive surgery offers new and often less morbid options to patients, these procedures can pose signiﬁcant risks. This chapter seeks to outline the major complications in this burgeoning ﬁeld.

INDICATIONS Need to perform intra-abdominal procedure

OPERATIVE STEPS Step 1 Induction of general anesthesia Step 2 Access to peritoneal cavity insufﬂation with CO2

ADVERSE OUTCOMES FOR ABDOMINAL ACCESS Initial Abdominal Entry Although laparoscopic surgery is an exciting mode of managing surgical problems because it minimizes the

morbidities associated with traditional open approaches, it can be associated with a higher incidence of intraabdominal injury. Three basic modes of abdominal entry in laparoscopic surgery are (1) blind insertion of a primary trocar without creation of a pneumoperitoneum, (2) insertion of the Veress needle with subsequent establishment of the pneumoperitoneum, (3) Hasson technique5; open cutdown and direct visualization while placing the primary trocar. All of these techniques are associated with varying degrees of complications. Veress needle and trocar injuries account for many of the injuries seen in laparoscopic surgery. Minor complications occur during 1.58% of cases, whereas major complications—including bowel perforation, bladder injury, vascular injury, and abdominal wall hematoma—occur in 0.41% of cases (Figs. 7–1 to 7–3).6 Vascular and gastrointestinal injuries are the most troubling aspects of laparoscopic surgery. Although they occur infrequently, their occurrence can result in signiﬁcant morbidity and even death. Retrospective studies suggest that major vascular and bowel injuries occur in 0.04% to 0.18% of cases. The Swiss Association for Laparoscopic and Thoracoscopic Surgery published its ﬁnding of an 0.18% incidence after a prospective study of 14,243 patients.7 The initial entry into the abdomen to create the pneumoperitoneum is a major cause of bowel injury during laparoscopic surgery. A review of 40 litigated laparoscopic cases that resulted in bowel injury demonstrated that many of these injuries are insidious.8 This delayed recognition is problematic for both the patient and the physician.

Bowel Injury ● Consequence Trocar injuries are responsible for most of the malpractice claims associated with laparoscopic surgery.9 The U.S. Food and Drug Administration (FDA) through its Manufacturer and User Facility Device Experience (MAUDE) database identiﬁed 31 fatal and 1353 nonfatal injuries associated with trocar insertion from 1997 to 2002. The literature is replete with case reports detailing solid and hollow viscus organ injuries from trocars (see Fig. 7–3).

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SECTION I: GENERAL CONSIDERATIONS Veress needle

Abdominal wall

Intestines

Figure 7–1

Gastrointestinal injury from Veress needle.

Veress needle

Liver

Aorta Spinal column

Figure 7–2 Vascular or gastrointestinal injury from Veress needle.

Figure 7–3

Gastrointestinal injury from trocar placement.

Most injuries are presumed to stem from the primary trocar placement, usually in the umbilical region. This initial placement is virtually blind, whereas the subsequent trocar insertions can be done under direct visualization. Optical-access visual obturator trocars were supposed to provide a safer alternative for primary trocar placement. These devices are made of clear plastic and allow visualization of the separation of the abdominal wall layers as they are inserted. However, even with these instruments, there have been documented injuries.10 A study that included 1283 patients showed a 0.31% incidence rate of injury when using these devices.11 The use of the Veress needle is an alternative to direct or open trocar insertion. Invented by Dr. Janos Veress in the 1930s, it was originally used to treat tuberculosis by creating a pneumothorax, which was the mainstay of treatment during this time. A dual needle consisting of a spring-loaded blunt inner core and a sharp outer sheath was created because it offered fewer risks of trauma to the lung. As the Veress needle is placed through soft tissue, the blunt inner needle is displaced and the sharp outer sheath can cut through tissue. Once the needle is inside a hollow cavity, the blunt needle springs back into position to guard the sharp outer sheath. In the 1970s, the Veress needle became popular as the ﬁeld of laparoscopic surgery expanded.12 The Veress needle can be used as a substitute for other methods of establishing a pneumoperitoneum. However, many studies have shown that its use may yield higher complication rates. Published studies demonstrate that the Veress needle is more likely to cause minor complications such as subcutaneous emphysema and extraperitoneal insufﬂation.13,14 These studies are in line with older studies that concluded that Veress needle use results in a signiﬁcantly higher incidence of minor complications.15,16 However, a great deal of debate exists in the literature with many reviews concluding that the Veress needle is a safe alternative to the other entry techniques. A retrospective review of 2126 laparoscopic operations, in which the Veress needle was exclusively used, yielded no complications.17 Grade 2/3/4 complication ● Repair A study that analyzed laparoscopic injuries that were reported to the FDA and Physician Insurers Association of America (PIAA) found that the organ most commonly injured is the small bowel. The study also showed that small and large bowel injuries were the most likely to go unrecognized in a 24-hour period. Because delay in recognition can lead to signiﬁcant morbidity, the surgeon’s suspicions should be heightened if the clinical course deviates from the norm. Moreover, this delay in treatment has been shown to cause a 26% rate of mortality.18

7 LAPAROSCOPIC SURGERY Although vascular injuries occur with less frequency than bowel injuries, the odds of mortality are very high. The aorta, inferior vena cava, portal vein, and iliac vessels are all prone to injury from initial trocar placement. In some thin individuals, the aorta can lie within 5 cm of the anterior abdominal wall. This underscores a critical element of laparoscopic surgery in that every attempt should be made against pushing trocars all the way into the abdomen. Trocars that are fully advanced to the external cannula are prone to diving into the retroperitoneum, causing signiﬁcant vascular injury.19 As common sense dictates, recognized injury repair should be completed during the original operation. Laparoscopic repair should be attempted unless delay, as with hemorrhage, may adversely affect the patient’s outcome. ● Prevention Although there is no true consensus on the safest technique for initial abdominal entry, many believe that open laparoscopic access, as described by Hasson, is the safest. A retrospective analysis of 5284 patients who underwent open laparoscopy discovered that only 1 patient suffered a bowel injury.20 In patients with presumed umbilical adhesive disease from prior abdominal surgery, alternative techniques for abdominal insufﬂation and entry have been described. Insufﬂating with a Veress needle placed in the left ninth intercostal space and primary trocar placement in the left upper quadrant has been used with low injury rates.21 Placing the initial trocar in this region, speciﬁcally in the left midclavicular line 3 cm below the costal margin, has been advocated by many surgeons as a safe alternative when umbilical adhesions are suspected.22 Veress needle insufﬂation should be guided by initial intra-abominal pressure. In a study of 259 women, initial pressures lower than 8 mm Hg at 1 L/min ﬂow of CO2 demonstrated correct position; pressures greater than 8 mm Hg correlated with interstitial placement.23 Abdominal wall lifting has been advocated when placing a Veress needle to avoid potential complications. In theory, this technique allows for lifting the abdominal wall away from bowel and vasculature. However, this method is associated with an increased number of insertion attempts, which may increase the likelihood of organ perforation. The most consistent means of prevention of trocar placement injuries requires macrobracing (Figs. 7–4 and 7–5). As the trocar is placed in the abdominal wall, the tip will separate the layers of the abdominal wall. Eventually, the tip will penetrate the peritoneal cavity, with the resultant loss of resistance on the trocar. Without bracing by the nondominant hand, the trocar can damage nearby structures such as the intestines or retroperitoneal tissues. By bracing with the nondominant hand, the loss of resistance does not result in distribution of force to unwanted structures.

Figure 7–4

Inadequate macrobracing.

Figure 7–5

Correct macrobracing.

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Retroperitoneal Hematoma The literature offers sparse details on the prevalence of retroperitoneal hematomas caused during abdominal laparoscopic procedures. However, one can extrapolate from the penetrating trauma guidelines to help foster decision making because inadvertent trocar insertion can mimic stab wounds (Figs. 7–6 and 7–7). ● Consequence The mortality associated with retroperitoneal hematomas deserves notice. The trauma literature reports a mortality of 13%.24 Superior mesenteric artery (SMA) injuries are particularly dangerous to the patient, with mortality rates approaching 54%.25 Grade 2/3/4 complication ● Repair The abdomen is divided into three zones with respect to retroperitoneal hematomas. Zone I is the centromedial aspect of the retroperitoneum, lying between the kidneys and extending from the diaphragmatic hiatus

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SECTION I: GENERAL CONSIDERATIONS Veress needle

lead to signiﬁcant morbidity and mortality. Therefore, trocars must be placed under direct vision whenever possible, and the retroperitoneum should be visualized prior to exsufﬂation.

Port Site Bleeding Liver

Aorta Spinal column

Figure 7–6 Retroperitoneal vascular injury from Veress needle.

● Consequence Port site bleeding is believed to occur when placement of a trocar through the abdominal wall lacerates a branch of the epigastric vessels. Intraoperatively, the port site bleeding can often be appreciated and controlled. If unrecognized, these bleeds are usually manifested as a hematoma a few days postoperatively. The incidence of port site hematomas is approximately 6.25%.27 Grade 2/3/4 complication ● Repair Bleeding can be controlled using a variety of methods. Direct pressure can be placed on the area of concern using an instrument inserted into another port. Pressure can also be applied using a Foley catheter and tenting it against the abdominal wall.28 The bleeding vessel can be cauterized using an instrument that carries current from the Bovie device. The port site can also be enlarged to gain control of the bleeding vessel. Alternatively, by cantilevering the trocar in four directions, the surgeon can determine in what area the vessel injury lies and a bolster suture can be placed.29 Lastly, Surgicel can be pulled through the bleeding port site to help tamponade the vessel.30

Figure 7–7 Abdominal wall hematoma from trocar placement (arrow).

to the inferior vena cava (IVC) bifurcation. Zone II extends laterally from the kidneys to the paracolic gutters, and zone III comprises the pelvic region. Penetrating trauma to zone I should always be explored because injury in this area can involve major vessels.26 These guidelines should be followed during laparoscopic surgery. The most likely scenario involves a trocar injury to the major vessels that course in zone I. If an injury to a major vessel is found, the surgeon must decide whether to proceed with ligation, primary repair, or interposition graft placement. Penetrating trauma to zones II and III can be managed without exploration if the patient is stable. A computed tomography (CT) scan should be obtained to identify the site of injury. An angiogram may be used to further characterize the hematoma and for therapeutic embolization. ● Prevention Retroperitoneal vascular injury can have devastating consequences for the patient. Delay in diagnosis can

● Prevention All trocars should be pulled out of the body using direct vision to inspect for bleeding. If bleeding is encountered, it can be controlled using one of the methods previously discussed.

PHYSIOLOGIC CONSEQUENCES As laparoscopic surgery has become more prevalent in the ﬁeld of surgery, it is increasingly important to understand the challenges of this mode of access to the peritoneal cavity. In general, the relative contraindications for laparoscopic surgery are related to the physiologic changes from pneumoperitoneum. For example, patients with increased intracranial pressure, ventriculoperitoneal shunts, hypovolemia, and congestive heart failure are ill advised to have laparoscopic surgery.

Cardiovascular Complications Laparoscopic surgery performed on patients with cardiovascular morbidity should be undertaken with heightened awareness of the associated risks. Anesthesia as well

7 LAPAROSCOPIC SURGERY has well-documented, potentially deleterious effects on the cardiovascular system. Thus, in patients who have signiﬁcant cardiovascular morbidity, laparoscopic surgery can be a relative contraindication owing to stresses of anesthesia. The cardiovascular changes that occur during laparoscopic surgery are well established, but these rarely have deleterious effects because of advanced monitoring techniques. Patient positioning and the establishment of the pneumoperitoneum are the two factors that may cause signiﬁcant cardiovascular strain. Cardiac output is particularly susceptible to the pressures of laparoscopic surgery. Since the early 1990s, many studies showed that there is a decrease in cardiac output during various laparoscopic procedures.31 For example, a 20% to 59% decrease in cardiac index was detected in 15 nonobese patients during laparoscopic cholecystectomies.32

Cardiac Output Patient positions in combination with a pneumoperitoneum can have detrimental effects because they alter the normal physiology of venous return. ● Consequence Reverse Trendelenburg positioning and pneumoperitoneum can limit venous return, which can lead to decreased preload and subsequent changes in cardiac output.33 This decrease in cardiac output following insufﬂation and reverse Trendelenburg has been well documented.34,35 One study showed a 20% reduction in cardiac output with 12 mm Hg pneumoperitoneum and reverse Trendelenburg of 30°.36 Grade 1/2 complication ● Repair Laparoscopy requires a multidisciplinary approach owing to the added physiologic burdens that may occur during surgery. Feedback from anesthesia is important and underscores the need for open communication throughout a case. Cardiopulmonary problems should prompt the surgeon to level the table and decrease the pneumoperitoneum until all physiologic issues are addressed. ● Prevention The role for invasive versus noninvasive cardiac monitoring is controversial, and thus, the case is often left up to clinician judgment. Although there is no clear consensus regarding placement of these devices, in patients with cardiac disease, monitoring should strongly be considered. Increasing the intravascular volume can help mitigate the effects of reverse Trendelenburg and intra-abdominal pressure.37 Insufﬂating the abdomen with the patient in the horizontal position is also recommended to guard against a synergistic decrease in cardiac output.38 Lastly,

101

sequential pneumatic devices have been shown to counteract these hemodynamic changes, and they should be placed on the patient prior to insufﬂation.39

Cardiac Arrhythmias The preponderance of cardiac arrhythmias during laparoscopic surgery has been described in the literature. It is generally believed that these arrhythmias occur as a result of peritoneal stretch receptor mediation via the vagus nerve during insufﬂation.40 CO2 is also believed to be proarrhythmic because it can irritate cardiac muscle and alter conduction pathways.41 ● Consequence Bradyarrhythmias and atrioventricular dissociation during laparoscopic surgery are just some of the more common arrhythmias described in the literature.42,43 However, during abdominal insufﬂation, the patient is prone to any type of arrhythmia and must be monitored closely. Grade 1/2 complication ● Repair Benign arrhythmias such as sinus tachycardia can be medically managed during surgery. However, more lethal arrhythmias should be managed expediently using advanced cardiac life support (ACLS) protocols. ● Prevention Recent studies show that using sequential compression devices on the lower extremities can decrease the sympathetic response. Also, helium has been proposed as an alternative to CO2 because it may cause fewer arrhythmias. As of now, further studies are needed to ascertain which gas is better for laparoscopy.

Pulmonary Complications Pneumothorax ● Consequence Pneumothoraces are well-described complications of laparoscopic surgery.44,45 However, the deﬁnitive etiology is unclear. A CO2 pneumothorax, sometimes referred to as a capnothorax, can arise if the peritoneopleural surfaces are violated, allowing CO2 to pass through the esophageal and aortic hiatuses or through any diaphragmatic defects. CO2 diffusion into the pleural space has also been described as a potential mechanism for the formation of a capnothorax. Barotrauma from increased airway pressures following insufﬂation can lead to a bronchopleural conduit that allows air to enter the pleural space, causing the classic pneumothorax. Signs that facilitate the diagnosis of a pneumothorax or capnothorax are a decrease in the partial pressure of oxygen in arterial blood (PaO2), with an increase in both the partial pressure of CO2 in arterial

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SECTION I: GENERAL CONSIDERATIONS

blood (PaCO2) and the end-tidal carbon CO2 concentration ETCO2, increased airway pressure, and decreased or absent breath sounds. A radiograph conﬁrms the suspected diagnosis. Grade 2/3 complication

Gas Embolism The literature is replete with incidents of CO2 gas embolism during laparoscopic surgery.49–51 This complication is usually manifested by an abrupt decrease in ETCO2 and cardiopulmonary collapse.52

● Repair The difference between a pneumothorax and a capnothorax is that the latter resolves in a short time following exsufﬂation. The high solubility coefﬁcient of CO2 allows for the rapid absorption of CO2 into systemic circulation. Therefore, follow-up radiographs should be taken to ascertain whether the lung is expanded. If the pneumothorax has not resolved and the clinical situation warrants, a thoracostomy tube should be placed.

● Consequence Even though venous gas embolism has been extensively reported during laparoscopic hepatic resection, it can occur during any pneumoperitoneum-based procedure. Whereas the incidence has been estimated at 15 per 100,000 patients, gas embolism is most likely a common occurrence that is unrecognized.53,54 This phenomenon is not usually associated with cardiopulmonary instability because CO2 is much more soluble than O2 in blood. Grade 1/2 complication

● Prevention Pneumoperitoneum pressures lower than 15 mm Hg and smaller tidal volumes with positive-pressure ventilation should be used during laparoscopy to guard against pneumothorax in patients at risk, such as those with chronic obstructive pulmonary disease (COPD).

˙ Q ˙ Mismatch and Shunting V/ It has been shown that insufﬂation transiently decreases the pulmonary shunt and increases the PaO2.46 However, this change is eliminated with the continued pneumoperitoneum. Insufﬂation of the abdomen elevates the diaphragm and decreases the functional residual capacity (FRC) of the lung.47 This decrease in the FRC can sig˙ Q ˙ pulmonary relationships. niﬁcantly alter V/ ETCO2 is found to rise with creation of CO2 pneumoperitoneum, reaching a plateau level at 30 minutes if insufﬂation is kept constant. ● Consequence In theory, a decrease in FRC will have a more profound effect on patients with signiﬁcant pulmonary morbidities than on healthy subjects. Patients with less pulmonary reserve are less able to cope with atelectatic lung and the resultant shunt. Grade 1/2 complication ● Repair Positive-pressure ventilation can reverse the decreased oxygen tension and hypercapnia caused by elevation of the diaphragm.48 Positive-pressure ventilation decreases the shunt by increasing the FRC. ● Prevention Increases in the partial pressure of CO2 in alveolar gas (PACO2) are manifested by hypercapnia and acidosis. To offset this rise in PACO2, the patient must be hyperventilated to avoid academia. Arterial blood gases should be assessed as clinically indicated.

● Repair Cardiovascular resuscitative efforts must begin immediately after the recognition of gas embolism. Evacuation of the pneumoperitoneum should occur ﬁrst, and if at all possible, the patient should be placed in left lateral decubitus position. If a central line is present, a syringe may be used to aspirate the gas embolism. ● Prevention In theory, any venous injury in which the central venous pressure is lower than the pneumoperitoneum can allow CO2 gas to enter the circulation. Therefore, central venous pressure should be maintained at an adequate level and the pneumoperitoneum kept at minimal settings. The patient should also be hyperventilated to blow off CO2, thereby allowing for rapid absorption of CO2 into the blood.

Renal Complications Rhabdomyolysis Rhabdomyolysis can occur in any postoperative patient after prolonged operative times. A literature review reveals that with respect to laparoscopy, this complication is mainly associated with laparoscopic nephrectomies. However, one article detailed a 1.4% incidence in gastric bypass procedures.55 ● Consequence Rhabdomyolysis is a well-known phenomenon that usually occurs in crush injuries and can lead to acute renal failure because myoglobin precipitates in urine, leading to nephron injury. Grade 1/2 complication ● Repair The hallmark of treatment of rhabdomyolysis is intravenous hydration and alkalization of the urine

7 LAPAROSCOPIC SURGERY to prevent crystallization of myoglobin. The most common intravenous solution used is 5% dextrose in water with 3 amps of sodium bicarbonate. Serial creatinine and urine output should be measured to trend the curves. ● Prevention Every attempt should be made to pad to patient on the operative bed so as to displace the pressure points. Also, the use of kidney bumps should be minimized becausse they may cause muscle ischemia in the ﬂank.56 Postoperatively, clinical suspicion for rhabdomyolysis should be raised in any patient who complains of ﬂank and gluteal pain. Delay in diagnosis heightens the chance of the patient developing acute renal failure; therefore, a creatinine phosphokinase (CPK) level should be checked immediately. If the CPK is elevated, treatment should commence immediately.

Hemodynamic Complications Deep Vein Thrombosis Changes in venous ﬂow during laparoscopic surgery have been postulated to contribute an increased incidence of deep vein thrombosis (DVT). ● Consequence A low-ﬂow venous state in the femoral vein has been demonstrated during abdominal insufﬂation.57 This decrease in femoral vein ﬂow may increase the risk for DVT in the lower extremities. Grade 1/2 complication ● Repair A patient with a DVT is treated with anticoagulation therapy to prevent pulmonary embolism. ● Prevention Although there is no clear consensus on the risk of DVT during laparoscopic surgery, most surgeons place sequential compression devices on their patients prior to abdominal insufﬂation. These devices can reverse venous stasis in the lower extremities and should be used in patients before establishment of the pneumoperitoneum.58

Splanchnic Circulation ● Consequence Increased intra-abdominal pressure caused by insufﬂation can have profound effects on the splanchnic vasculature.59 The splanchnic circulation includes vessels that supply and drain the abdominal organs. Pneumoperitoneum pressures can decrease visceral organ blood ﬂow through vessel compression. Grade 1/2 complication

103

● Repair Patients with laboratory evidence of ischemia or venous congestion after laparoscopic surgery can be managed with supportive care. ● Prevention To counterbalance impaired visceral ﬂow caused by pneumoperitoneum, the intravascular volume should be optimized to ensure better ﬂow with increased intraabominal pressures.

REFERENCES 1. Spaner SJ, Warnock GL. A brief history of endoscopy, laparoscopy, and laparoscopic surgery. J Laparoendosc Adv Surg Tech A 1997;7:369–373. 2. Schlogel G. Raoul Palmer and the coelio-surgical adventure from 1940 to 1995. Hist Sci Med 1996;30:281–287. 3. Vecchio R, MacFayden BV, Palazzo F. History of laparoscopic surgery. Panminerva Med 2000;42:87–90. 4. Nakeeb A, Comuzzie AG, Martin L, et al. Gallstones: genetics versus environment. Ann Surg 2002;235:842– 849. 5. Hasson HM. A modiﬁed instrument and method for laparoscopy. Am J Obstet Gynecol 1971;110:886–887. 6. Orlando R, Palatini P, Lirussi F. Needle and trocar injuries in diagnostic laparoscopy under local anesthesia: what is the true incidence of these complications? J Laparoendosc Adv Surg Tech A 2003;13:181–184. 7. Schafer M, Lauper M, Krahenbuhl L. Trocar and Veres needle injuries during laparoscopy. Surg Endosc 2001;15: 275–280. Epub 2000;December 12. 8. Vilos GA. Laparoscopic bowel injuries: forty litigated gynaecological cases in Canada. J Obstet Gynaecol Can 2002;24:224–230. 9. Fuller J, Ashar BS, Carey-Corrado J. Trocar-associated injuries and fatalities: an analysis of 1399 reports to the FDA. J Minim Invasive Gynecol 2005;12:302–307. 10. Brown JA, Canal D, Sundaram CP. Optical-access visual obturator trocar entry into desufﬂated abdomen during laparoscopy: assessment after 96 cases. J Endourol 2005; 19:853–855. 11. Thomas MA, Rha KH, Ong AM, et al. Optical access trocar injuries in urological laparoscopic surgery. J Urol 2003;170:61–63. 12. Szabó I. Veres needle: in memoriam of the 100th birthday anniversary of Dr János Veres, the inventor. Am J Obstet Gynecol 2004;191:352–353. 13. Agresta F, De Simone P, Ciardo LF, Bedin N. Direct trocar insertion vs Veres needle in nonobese patients undergoing laparoscopic procedures: a randomized prospective single-center study. Surg Endosc 2004;18: 1778–1781. Epub 2004;October 13. 14. Gunenc MZ, Yesildaglar N, Bingol B, et al. The safety and efﬁcacy of direct trocar insertion with elevation of the rectus sheath instead of the skin for pneumoperitoneum. Surg Laparosc Endosc Percutan Tech 2005;15:80–81. 15. Bryon JW, Markenson G, Miyazawa K. A randomized comparison of Veres needle and direct trocar insertion for laparoscopy. Surg Gynecol Obstet 1993;177:259–262

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16. Yerdel MA, Karayalcin K, Koyuncu A, et al. Direct trocar insertion versus Veres needle insertion in laparoscopic cholecystectomy. Am J Surg 1999;177:247–249. 17. Florio G, Silvestro C, Polito DS. Periumbilical Veres needle pneumoperitoneum: technique and results in 2,126 cases. Chir Ital 2003;55:51–54. 18. Chandler JG, Corson SL, Way LW. Three spectra of laparoscopic entry access injuries. J Am Coll Surg 2001; 192:478–491. 19. Voitk A, Rizoli S. Blunt Hasson trocar injury: long intraabdominal trocar and lean patient—a dangerous combination. J Laparoendosc Adv Surg Tech A 2001;11:259– 262. 20. Hasson HM, Rotman C, Rana N, Kumari NA. Open laparoscopy: 29-year experience. Obstet Gynecol 2000; 96(5 pt 1):763–766. 21. Agarwala N, Liu CY. Safe entry techniques during laparoscopy: left upper quadrant entry using the ninth intercostal space—a review of 918 procedures. J Minim Invasive Gynecol 2005;12:55–61. 22. Audebert AJM, Gomel V. Role of microlaparoscopy in the diagnosis of peritoneal and visceral adhesions and in the prevention of bowel injury associated with blind trocar insertion. Fertil Steril 2000;73:631–635. 23. Vilos GA, Vilos AG. Safe laparoscopic entry guided by Veres needle CO2 insufﬂation pressure. J Am Assoc Gynecol Laparosc 2003;10:415–420. 24. Selivanov V, Chi HS, Alverdy JC, et al. Mortality in retroperitoneal hematoma. J Trauma 1984;24:1022– 1027. 25. Asensio JA, Berne JD, Chahwan S, et al. Traumatic injury to the superior mesenteric artery. Am J Surg 1999;178: 235–239. 26. Bageacu S, Kaczmarek D, Bageacu S, et al. Management of traumatic retroperitoneal hematoma. Review. French. J Chir (Paris) 2004;141:243–249. 27. Bhattacharya S, Tate JJ, Davidson BR, et al. Abdominal wall haemotoma complicating laparoscopic cholecystectomy. HPB Surg 1994;7:291–296. 28. Boswell WC, Odom JW, Rudolf R, et al. A method for controlling bleeding from abdominal wall puncture sites after laparoscopic surgery. Surg Laparosc Endosc 1993;3: 47–48. 29. Soper NJ. Access to abdomen. In Scott-Conner C (ed): The SAGES Manual: Fundamentals of Laparoscopy and GI Endoscopy. New York: Springer, 1999; pp 22–36. 30. Rastogi V, Dy V. Control of port site bleeding from smaller incisions after laparoscopic cholecystectomy surgery. Surg Laparosc Endocsc Percutan Tech 2002;12: 4:224–226. 31. O’Malley C, Cunningham AJ. Anesthesia for minimally invasive surgery: laparoscopy, thoracoscopy, hysteroscopy. Anesthesiol Clin North Am 2001;19:1. 32. Joris JL, Noirot DP, Legrand MJ, et al. Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg 1996;76:1067–1071. 33. Wahba RWM, Beique F, Kleiman SJ. Cardiopulmonary function and laparoscopic cholecystectomy. Can J Anaesth 1995;42:51–63. 34. Bannenberg JJ, Rademaker BM, Froeling FM, et al. Hemodynamics during laparoscopic extra- and intraperito-

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7 LAPAROSCOPIC SURGERY 52. Beck DH, McQuillan PJ. Fatal carbon dioxide embolism and severe haemorrhage during laparoscopic salpingectomy. Br J Anaesth 1994;72:243. 53. Orebaugh SL. Venous air embolism: clinical and experimental observations. Crit Care Med 1992;20:1169–1177. 54. Schmandra TC, Mierdl S, Bauer H, et al. Transoesophageal echocardiography shows high risk of gas embolism during laparoscopic hepatic resection under carbon dioxide pneumoperitonem. Br J Surg 2002;89:870–876. 55. Khurana RN, Baudendistel TE, Morgan EF, et al. Postoperative rhabdomyolysis following laparoscopic gastric bypass in the morbidly obese. Arch Surg 2004; 139:73–76. 56. Reisiger KE, Landman J, Kibel A, Clayman RV. Laparoscopic renal surgery and the risk of rhabdomyolysis:

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Section II

BEDSIDE PROCEDURES Stephen R. T. Evans, MD All human errors are impatience, a premature breaking off of methodical procedure, an apparent fencing-in of what is apparently at issue.—Franz Kafka

8

Central Vein Catheterization Michael D. Pasquale, MD, Rovinder S. Sandhu, MD, Mark D. Cipolle, MD, PhD, and Dale A. Dangleben, MD INTRODUCTION In the United States, more than 5 million central vein catheters are inserted every year, making it one of the most commonly performed bedside procedures.1

INDICATIONS ● Unobtainable peripheral venous access or to avoid repeated peripheral “sticks” ● Need to deliver high ﬂows of crystalloid, colloid, or blood products ● Central venous pressure measurement or access for placement of a pulmonary arterial catheter ● Administration of sclerosing agents such as chemotherapeutic agents or hyperalimentation ● Placement of transvenous pacemakers ● Performance of hemodialysis or plasmapheresis Central vein access can be obtained via the jugular, subclavian, or femoral vein, and site selection will vary depending on why access is being obtained, ease of placement, and associated risks. As with any invasive procedure, risks are associated with central vein catheterization that are both hazardous to patients and costly to treat.2–4 The overall complication rate for central vein catheterization

is approximately 15%,5 and as with other technical tasks, this risk tends to decrease with operator experience.6 Mechanical complications have been reported to occur in 5% to 19% of patients, infectious complications in 5% to 26%, and thrombotic complications in 2% to 26%.5–9 The objective of this chapter is to discuss, in detail, the complications associated with central vein access in the hope that a thorough knowledge of the potential problems will result in a decrease in the actual occurrences.

OPERATIVE STEPS Step 1 Step 2

Step 3 Step 4 Step 5 Step 6

Assess patient’s need for central venous catheterization Review patient’s chart, particularly checking for history of coagulation abnormalities and history of deep venous thrombosis Choose appropriate site for placement (i.e., internal jugular, subclavian, or femoral vein) Obtain consent Gather supplies Perform a “time out” between the physician and bedside nurse

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Step 7

Prep the patient—including correct patient positioning for particular site Cannulate the vein Place guidewire Place the catheter over the guidewire Remove the guidewire Aspirate all ports of the catheter Flush all ports with saline solution Secure catheter in place Place sterile dressing Conﬁrm placement with radiography if appropriate

Step Step Step Step Step Step Step Step Step

8 9 10 11 12 13 14 15 16

INDICATION: PROCEDURE: CATHETER: SITE: RIGHT LEFT RECIDENCY: PGY:

CENTRAL VEIN ACCESS: SETUP Prior to the procedure, a number of “checks” should be performed to ensure that the procedure is completed in the safest and most efﬁcient way. At our institution, a Central Line Checklist has been created to ensure that the appropriate measures for the procedure are considered (Fig. 8–1). This checklist accounts for preprocedure, procedure, and postprocedure issues and serves as a performance improvement tool as well. The ﬁrst step in central line placement is to assemble all of the necessary materials needed to perform the procedure and complete

Medical Surgical/trauma Elective Emergent/code TLC SGC Cortis Infuser Internal jugular Subclavian Femoral Internal jugular Subclavian Femoral EM FM IM Surgery OB/GYN 1 2 3 4 5 6 Other: Procedural checklist

YES

Pre-procedure Consent obtained (for elective procedures)? If no, give reason: Confirm landmarks, position patient correctly for procedure? Assemble equipment/verify supplies? TIME OUT (check patient ID, announce procedure, including site)? Abnormal labs checked? (i.e., INR, platelets, etc.) Sedation used? List meds Procedure Cleanse hands Sterile set up and prep (mask, gown, cap, drape, sterile site) Inadequate prep due to clinical urgency If inadequate prep, line placed later Vein cannulated – attempt #1 Vein cannulated – attempt #2 Unsuccessful (state reason:

)

Assistance called after unsuccessful attempts Guidewire removed All ports flushed after good blood draw Sutured/stapled in place Use ultrasound/Sonasite Assisting physician followed same precautions All staff in room and patient wear masks Pre-empted by clinical urgency Aseptic technique maintained throughout procedure Post-procedure CXR ordered, reviewed Complications

If yes:

Arterial cannulation

Air embolus

Cardiac dysrhythmias

Catheter malposition

Hematoma

Pneumothorax

Uncontrolled bleeding

Other:

Attending notified of complications Previous number of successful central lines by operator User ID number:

Figure 8–1 Central venous line procedural checklist.

Date:

NO

8 CENTRAL VEIN CATHETERIZATION the tasks outlined in the preprocedure portion of the checklist. 1. Consent should be obtained after describing the procedure and the potential complications to the patient and/or patient’s guardian. In situations in which consent cannot be obtained, the reason must be clearly documented. 2. Conﬁrmation of landmarks and proper positioning of the patient for the procedure should be done. Depending on the patient’s underlying medical condition, one may consider cardiac and oxygen saturation monitoring. 3. All necessary equipment and supplies should be veriﬁed. Maximal sterile-barrier precautions, including mask, cap, gown, sterile gloves, and a large sterile drape should be used because these precautions have been shown to reduce the rate of catheter-related bloodstream infections.10 4. Prior to initiating the procedure, a “time out” should be performed between the physician and the bedside nurse. The time out should include verbalizing the patient’s name and the procedure to be performed, including the site of procedure. It should be ensured that this is the procedure/patient listed on the consent form. It is recommended that the performance of the time out be documented. 5. Prior to placement, the chart should be reviewed to ensure that there are no contraindications to using the speciﬁc site for the central line—for example, if the patient is coagulopathic, placement in an easily compressible location (e.g., femoral vein) may be chosen to avoid potential bleeding complications associated with inadvertent arterial puncture. 6. Consideration should be given for conscious sedation. If it is deemed necessary, appropriate monitoring should be utilized and medications documented. Some institutions will require conscious sedation privileges for the operator, and this should be investigated prior to using sedative agents. Preparation is key to the successful completion of central line placement in a safe and efﬁcient manner.

Internal Jugular Vein Catheterization In the central approach for internal jugular vein (IJV) catheterization, the apex of the triangle formed by the two heads of the sternocleidomastoid muscle and the clavicle serves as a landmark. The IJV runs deep to the sternocleidomastoid muscle and then through this triangle before it joins the subclavian vein (SV) to become the brachiocephalic vein. Right-sided access is typically preferred because the apical pleura do not rise as high on the right and one can avoid the thoracic duct. After the landmarks have been identiﬁed, sterile preparation with either chlorhexidine or povidone-iodine (Betadine) has been accomplished, and full-barrier precautions have been uti-

109

lized, local anesthesia (1% lidocaine) is administered and the patient is placed in head-down 15° Trendelenburg position with the head rotated 45° away from the side of cannulation. This position provides for easy landmark identiﬁcation and needle insertion as well as allowing for distention of the vein and prevention of air embolism during line placement. It is important to remember that in patients with suspected neck injury, an alternative approach should be considered to prevent turning of the patient’s neck. The patient’s arm should be straight down at the side of the body. The physician typically stands at the head of the bed and places his or her index and middle ﬁnger (of the nondominant hand) on the carotid pulse and inserts a 22-gauge “ﬁnder” needle through the skin, immediately lateral to the carotid pulse and slightly superior to the apex of the triangle. The needle is advanced past the apex of the triangle, in the sagittal plane 30° posterior and caudad toward the ipsilateral nipple, at an approximate 50° angle above the frontal plane of the skin. The needle should be advanced and gently aspirated until there is free return of venous blood. The IJV is usually located near the surface of the skin and should be encountered at or before 3 cm of the needle has been inserted. If the ﬁrst pass is unsuccessful, the needle should be directed slightly more medially on the next insertion attempt. With the ﬁnder needle in place, an 18-gauge introducer needle is inserted alongside it and into the vein. If the ﬁnder needle is removed prior to placement of the introducer needle, care should be taken to ensure the same course.

Subclavian Vein Catheterization When utilizing the infraclavicular approach for SV catheterization, note that the SV arises from the axillary vein at the point where it crosses the lateral border of the ﬁrst rib. The SV is usually 1 to 2 cm in diameter and ﬁxed in position directly beneath the clavicle. It is separated from the subclavian artery by the anterior scalene muscle. For catheterization, the patient is placed in 15° to 30° Trendelenburg position, and the shoulders are maintained in neutral or slightly extended position by a small towel roll placed between the shoulder blades. After identiﬁcation of the landmarks (sternal notch, clavicle, deltopectoral groove), sterile preparation (chlorhexidine or povidineiodine), and administration of local anesthesia (1% lidocaine), the skin is punctured 2 to 3 cm caudal to the midpoint of the clavicle just lateral to the deltopectoral groove with an 18-gauge, 2.5-inch introducer needle. A guide to the puncture site can be created by having the operator place her or his index ﬁnger in the sternal notch and the thumb of the same hand at the junction of the medial and middle third of the clavicle, which is typically in the deltopectoral groove. The needle can be inserted just lateral and caudal to the operator’s thumb. The needle should not be bent and should be advanced parallel to the clavicle, aiming toward the sternal notch until the tip of the needle abuts the clavicle at the junction of its medial

110

SECTION II: BEDSIDE PROCEDURES

and middle thirds. The needle is then passed beneath the clavicle, with the needle hugging the inferior surface of the clavicle. During insertion of the needle, slight negative pressure should be held on the syringe until a ﬂash of blood is seen. If no blood returns with passage of the needle, the needle is withdrawn past the clavicle while gentle suction is applied. Blood return may be achieved during withdrawal of the needle. If the ﬁrst pass is unsuccessful, the needle should be angled in a slightly more cephalad direction on the next attempt. The right SV approach is generally preferred because the dome of the pleura of the right lung is usually lower than the left, and the thoracic duct is avoided. The left SV has a sweeping curve to the apex of the right ventricle and is the preferred approach when placing a temporary transvenous pacing device.

Femoral Vein Catheterization When the femoral vein is used for access, the patient should be positioned supine with the ipsilateral hip slightly externally rotated. The landmarks that should be identiﬁed prior to beginning include the anterior superior iliac spine, the pubic tubercle, and the femoral artery. The femoral arterial pulse will generally be palpated at the midpoint between the anterior superior iliac spine and the pubic tubercle. The femoral vein is located medial to the femoral artery and parallels its course. If the femoral pulse cannot be palpated, the location of the vein can be approximated by going two ﬁngerbreadths lateral and two ﬁngerbreadths caudal to the pubic tubercle. After identiﬁcation of the landmarks, sterile preparation with chlorhexidine or povidone-iodine, and administration of local anesthesia (1% lidocaine), the skin is punctured below the inguinal crease at a 45° angle aiming cranially and medial to the femoral pulse. Staying below the inguinal crease allows for direct compression should an inadvertent arterial stick occur. An inadvertent arterial stick above the inguinal ligament can result in retroperitoneal hemorrhage that may require operative intervention to control. Typically, the vein should be encountered by 5 cm of insertion; if it is not, the needle should be withdrawn slightly while aspirating and redirected laterally, taking care to avoid puncturing the femoral artery. The femoral site is the safest site for the inexperienced user. In a patient requiring emergent resuscitation, the femoral approach generally allows swift access while avoiding crowding at the head of the bed.

Seldinger Technique Once the vein has been accessed, the Seldinger technique should be utilized to place the catheter. This technique involves the passage of a soft-tipped guidewire through the needle and subsequent removal of the needle. After making a small nick in the skin with a no. 11 scalpel blade, a dilator is passed over the guidewire, the dilator is

removed, the catheter is passed over the wire, and the wire is removed. During the passing of the guidewire, the operator should have the monitor facing him or her. A common mistake is to pass the wire too far, into the atrium or ventricle, resulting in arrhythmia.11 Close atten-

tion to patient hemodynamics and oxygen saturation during the procedure is mandatory. If the vein cannot be accessed after multiple attempts, stop, reassess, and consult with an experienced operator. When attempting an internal jugular or subclavian approach, prior to moving to the contralateral side, a chest x-ray should be performed to ensure that there is no evidence of injury, that is, pneumo/hemothorax. One of the more common complications is failure to cannulate the central vein. This tends to be a more frequent occurrence in the internal jugular and subclavian routes. This is due, in part, to the fact that central access is “blind” and guided by the use of anatomic landmarks, which may not correlate with vessel location.12 It has been argued that ultrasound guidance may be useful in situations in which difﬁcult access is anticipated. Such situations would include obese patients or those with swollen neck/upper extremity that would make landmarks difﬁcult to identify, those who have had multiple central venous catheters placed and had distorted or thrombosed veins, those requiring repeated access via the central vein, and those with coagulopathy.13

Ultrasound Guidance Techniques Traditionally, the site of initial needle insertion during central line placement is determined by using palpable or visible anatomic structures with known relationships to the desired vein as landmarks.13 However, ultrasound is increasingly being used to identify vessels and guide needle insertion when placing central lines. The ﬁrst reported use of Doppler ultrasound to assist with catheter placement was by Legler and Nugent in 1984.14 Since then, multiple studies have reported on this technique.12,15–20 Several meta-analyses that reviewed landmark versus ultrasoundguided IJV central line placement demonstrated signiﬁcant relative risk reductions in complications, mean insertion attempts, and failed catheter insertions when ultrasound was employed.21–23 The results of ultrasoundguided SV central line placement are not as uniform in documenting an advantage over landmark techniques. However, most randomized studies suggest that there is beneﬁt in utilization of ultrasound guidance for the placement of SV catheters.7,12,15–20,23 It should be emphasized that this technique is operator-dependent, and it is recommended that prior to utilizing this technique, operators undergo both didactic and “hands-on” training. During the technique, the ultrasound transducer is the component of the ultrasound system that contacts the patient and is held by the sonographer. To ensure appropriate imaging and ultrasound resolution, the highest frequency should be selected to

8 CENTRAL VEIN CATHETERIZATION maximize deﬁnition of the vessel image while maintaining adequate depth of penetration of the ultrasound signal (typically 7.5 MHz). Moreover, the ultrasound beam should be directed essentially perpendicular to the vessel. In order to cannulate, the vein must ﬁrst be visualized appropriately. With the transducer centered over the vein, the midpoint should be used for introduction of the access needle. The needle will appear hyperechoic (white) when viewed sonographically. Once the vessel has been accessed, the central line is placed as described previously. For IJV access, the transducer should be placed just cephalad to the clavicle at the insertion of the two heads of the sternocleidomastoid muscle. For femoral vein access, the transducer is placed a few centimeters distal to the inguinal ligament; for SV access, holding the transducer below the clavicle allows for adequate visualization.

111

Sternal notch

Clavicle

Mastoid

Sternocleidomastoid muscle

Figure 8–2 Internal jugular vein anatomy.

PATIENT CHARACTERISTICS There are multiple approaches for obtaining central venous access; however, successful catheterization by any approach is dependent on a thorough understanding of the anatomy (Figs. 8–2 to 8–4). Whenever the landmarks cannot be identiﬁed for one route of access, another route should be considered. If central access is needed for resuscitation from shock, the femoral approach should be considered because of the speed and safety with which it can be performed, particularly if the neck landmarks are difﬁcult to identify or if access to the neck is precluded by other care providers during the resuscitation.1 Subsequent to the resuscitation, consideration should be given to changing the line site because femoral cannulation has been associated with greater risk of infectious and thrombotic complications.1,5–8 Obtaining a past medical history is very important prior to line insertion. Patients who have had multiple access procedures performed in the past (e.g., chronic renal failure, chemotherapy, intravenous antibiotics), a history of failed catheterization attempts, the need for catheterization at a site of previous surgery, skeletal deformity, or scarring secondary to radiation therapy pose a greater challenge and patient safety dictates that the procedure be performed or supervised by an experienced physician.1,7 In addition, multiple catheterizations can lead to venous stenosis/thrombosis, resulting in difﬁculty accessing the vein and placing the catheter successfully.24 When such a situation is encountered, the physician should consider using ﬂuoroscopy and/or ultrasound to aid in the central line insertion. Special consideration should be given to patients who have undergone previous thoracic surgery (e.g., lobectomy) because compromise of the good lung (e.g., pneumo/hemothorax) may have devastating consequences, whereas placement of a chest tube (if needed secondary to iatrogenic pneumo/hemothorax) on the side of previous thoracic surgery can be difﬁcult owing to the

Sternal notch

Clavicle

Sternocleidomastoid muscle

* Note position of index finger at sternal notch.

Figure 8–3 Subclavian vein anatomy.

Nerve and artery Inguinal ligament

Anterior superior iliac spine Femoral vein

Pubic symphysis

Figure 8–4 Femoral vein anatomy.

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SECTION II: BEDSIDE PROCEDURES

presence of intrathoracic adhesions. Patients who have indwelling central venous devices (e.g., pacemaker, deﬁbrillator) are unique in that placement of a central line could disrupt the device and thereby jeopardize the function. It is imperative that an ample history be taken prior to performing a central line insertion. Like prior catheterization attempts and prior surgery/ scarring, patients with low or high body mass index pose a signiﬁcant challenge to central line insertion.24–26 Excessive soft tissue, particularly in the supine position, distorts the usual landmarks and spatial relationships in the neck. This is most marked when trying to approach the SV because breast tissue frequently falls toward the clavicle and should prompt one to consider an alternative approach or utilize ultrasound for vessel identiﬁcation.27 In such cases, it may be necessary to align the puncture site closer to the sternal notch and more inferior to the clavicle. This medial approach shortens the distance to the vein and allows one to ensure that the tip of the needle runs on the underside of the clavicle. Manual downward traction on the breast or taping the breasts out of the ﬁeld should also be considered because this will allow for better identiﬁcation of landmarks. A lack of soft tissue such as that seen in cachectic patients may also contribute to higher morbidity. In these patients, there tends to be a decreased amount of space between the clavicle and the ﬁrst rib, thus increasing the risk of pneumothorax.28 Care must be taken during needle insertion, staying directly on the clavicle, aiming toward the sternal notch without directing the needle downward toward the cupula of the lung. The contracted patient poses a similar challenge when obtaining central venous access, and it is vitally important to attempt to get the patient’s shoulders into a neutral position. If this cannot be achieved, an alternative site should be considered. A good technique is to always keep the needle and syringe parallel to the clavicle and remember that a failed catheter placement attempt is one of the strongest predictors of subsequent complication.7 Another alternative for SV cannulation is the supraclavicular approach,26,28 but this should be performed only by an experienced operator familiar with the anatomy and the technique. Brieﬂy, the needle is introduced above the clavicle at the midpoint of the triangle formed by the sternal and clavicular heads of the sternocleidomastoid muscle. The needle should be advanced at a 30° angle slowly aiming toward the sternum until a ﬂash of venous blood is obtained. The Seldinger technique is used to complete the procedure. This approach has been reported to be safe, with a low complication rate.29 Patients with a history of bleeding disorders or those on anticoagulants should have a coagulation proﬁle obtained prior to insertion of a central line. Anticoagulation places the patient at higher risk for hematoma formation, especially if the subclavian artery is punctured. In addition, the anatomic location of this vessel—posterior and inferior to the clavicle—makes it difﬁcult to control

bleeding by use of external compression. Therefore, if placement is not urgent, anticoagulation should be corrected prior to inserting the line or an alternative site should be utilized. In emergent situations, our personal preference is to utilize the femoral (ﬁrst choice) or internal jugular approach in anticoagulated patients. Both of these sites allow for better external compression should bleeding or inadvertent arterial puncture occur. It is important to realize that there is no uniform agreement on site selection in these cases; however, it is also important to understand the problems that may occur when one does not have access for compression should bleeding occur.30 Coagulopathy is not an absolute contraindication to SV catheterization; experience and adherence to safe technical principles are key.

MECHANICAL TECHNICAL COMPLICATIONS Mechanical complications are important because their effects are usually immediate and contribute to increased hospital length of stay, increased hospital costs, need for subsequent interventions, and an increased mortality rate.24 The most common mechanical complications associated with central line catheterization include arterial puncture, hematoma, hemothorax, and pneumothorax.1,24 Other mechanical complications include catheter malposition and failure to place the catheter, which has been discussed previously. As shown by McGee and Gould1 and Eisen and coworkers,24 the incidence of these complications varies according to the site utilized for catheterization. Femoral catheterization is reported to have a higher incidence of mechanical complications than those of subclavian or internal jugular placement.5

Arterial Puncture Inadvertent arterial puncture during subclavian line placement is a common occurrence, with an overall reported incidence in the range of 1% to 13% with 2% to 5% being typical. This incidence increases to about 40% if multiple attempts are made. ● Consequence Arterial puncture can lead to hematoma and/or pseudoaneurysm formation17 (Fig. 8–5). The consequences of subclavian arterial puncture are not as potentially serious as the consequences of inadvertent internal carotid artery puncture (e.g., cerebral thromboembolic event, airway compromise). However, bleeding from the subclavian artery is much more difﬁcult to control. In addition, such bleeding may be more easily missed because the blood may track into the pleural cavity. For this reason, the subclavian route is generally believed to be the least suitable approach to the central circulation in the anticoagulated patient. Inadvertent arterial

8 CENTRAL VEIN CATHETERIZATION

113

resultant expanding hematoma should have their airway secured and plans should be made for operative intervention. Although percutaneous closure devices have been successfully used to control bleeding from the subclavian and femoral vessels, their use in the carotid artery is not recommended. In a few circumstances, the blood may track into the pleural cavity, resulting in the formation of a hemothorax. After ensuring that the bleeding from the artery has stopped, any signiﬁcant hemothorax should be treated by placement of a chest tube. If the needle goes through the vein and the artery, there is long-term risk of developing an arteriovenous ﬁstula or aneurysm. If it is determined that the line is in the artery, the line should be removed and pressure applied to the affected artery for approximately 5 minutes. If the patient is anticoagulated, the coagulopathy should be corrected prior to removing the line. At times, this may be done in the operating room or the interventional radiology suite using a percutaneous closure device. If the International Normalized Ratio/ partial thromboplastin time (INR/PTT) is normal, the line can simply be removed at the bedside with appropriate observation for continued bleeding and/or hematoma development.

A

B Figure 8–5 Mediastinal hematoma post line.

puncture is the reason that all attempts at femoral central line placement should be done below the level of the inguinal ligament. This will allow for compression and prevent retroperitoneal hemorrhage from inadvertent puncture of the external iliac artery. The true incidence of subclavian hematoma from catheter placement has not been reported owing to the difﬁculty in assessing the location and depth of the vessel in relation to the clavicle and overlying soft tissue. There are a few case reports of extrapleural, mediastinal, or soft tissue hematomas after subclavian line placement; however, these usually occur in the face of coagulopathy. In addition, both subclavian arteriovenous ﬁstula31 and aneurysm32 formation after inadvertent subclavian arterial puncture have been described. Grade 1/2 complication ● Repair Fortunately, if the patient is not anticoagulated and the artery is not dilated, the needle can be removed and gentle, steady pressure held on the vessel. Patients having an inadvertent carotid arterial puncture with

● Prevention The most important means of prevention is careful cannulation of the vein. If one cannot distinguish venous from arterial blood, a blood gas can be sent and/or the line can be transduced at the time of cannulation.33 It is imperative to know the patient’s coagulation factors and platelets prior to beginning and to choose the appropriate puncture site accordingly. The internal mammary artery arises from the ﬁrst part of the subclavian artery, close to the medial margin of the scalenus anterior. Thus, it can be argued that an ipsilateral subclavian approach to the central circulation is contraindicated in patients undergoing internal mammary artery grafting in case the origin of the internal mammary artery is damaged. In practice, this does not appear to be the case, and there are few reports of internal mammary artery damage complicating subclavian venipuncture.34,35

Pneumothorax Pneumothorax is one of the most common technical complications of SV and/or IJV catheterization (Fig. 8–6). The overall incidence is typically quoted at between 1% and 2%,36,37 but this increases to about 10% if multiple attempts at venipuncture are made.38 ● Consequence This complication leads to pneumothorax, with the possibility of impaired respiratory status, or hemodynamic collapse if a tension pneumothorax develops. There are frequent reports of delays in the appearance of a pneumothorax for up to 96 hours after venipuncture,39–41 and a meta-analysis by Plewa and Ledrick42

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Air Embolism Air embolism is a very rare complication of IJV or SV catheterization. It has been shown that as little as 20 cc of air can harm a critically ill patient, but the reported lethal dose in humans is 100 cc.44,45 ● Consequnce Air embolism can lead to difﬁcult oxygenation or hemodynamic collapse. This complication tends to occur during insertion of the line when the patient is in the head-up position and there is negative pressure in the thoracic cavity (during inspiration). Grade 1/2/5 complication

Figure 8–6

Hinmon pneumothorax.

suggested that delayed pneumothorax complicated approximately 0.4% of all central venous access attempts, was much more common after SV than IJV approaches, was asymptomatic in about 22% of cases, and resulted in a tension pneumothorax in a similar proportion of patients. Although rare, in patients with emphysematous disease and multiple blebs, pneumothorax may result in a large, difﬁcult to control, and life-threatening air leak. Grade 1/2/3 complication ● Repair Depending on the size of the pneumothorax, treatment may range from the administration of oxygen (to enhance resolution) to formal chest drainage. In the case of a tension pneumothorax, one must be prepared to perform needle thoracostomy prior to the tube thoracostomy in the presence of hemodynamic collapse. If concern exists for a bleb puncture and a resultant large air leak and pneumothorax, the patient should be prepared for emergent thoracotomy. ● Prevention Pnemothorax occurs more commonly in thin patients and in those with hyperexpanded chests, and it is more likely if a lateral or supraclavicular approach to the SV is used, or if the Seldinger needle is allowed to stray posteriorly during venipuncture. For these reasons, it is important to obtain a chest x-ray immediately after placement of an SV or IJV line and to monitor these patients for possible delayed pneumothorax over the subsequent 3 to 4 days. Debate continues as to whether the IJV or SV site has a higher incidence of pneumothorax, but currently, there appears to be no clear difference.43

● Repair If an air embolism occurs or is suspected, the patient should be placed in the left lateral decubitus position while maintaining the head down.46 By doing this, the air is prevented from ﬂowing out of the right ventricle into the pulmonary artery and can thereby be slowly reabsorbed or, if deemed necessary, gently aspirated with a pulmonary artery catheter. Also, patients should be placed on 100% oxygen; if the previously discussed methods do not help, hyperbaric oxygen treatment could be considered.47 ● Prevention This complication can be prevented by following the prescribed technique mentioned earlier in this chapter. In addition, once the needle is in the vein, the hub should be occluded at all times to prevent air from entering the vein. When the catheter is placed, attention should be directed to each port to conﬁrm that these are also closed off to the atmosphere. One must also be wary of this complication during removal of catheters because air embolism may be more common during this time.48

Thoracic Duct Injury Thoracic duct injury is a very rare complication of leftsided IJV or SV catheterization. ● Consequence It presents either as a chylous leak at the puncture site along the catheter or as a chylothorax.49,50 The thoracic duct ends by draining into the posterolateral junction of the left IJV and SV. The anatomy can be variable and the duct may enter anterolaterally and therefore be more prone to injury. The diagnosis is conﬁrmed by sending the ﬂuid for triglyceride analysis and lymphocyte count.49,50 Grade 1/2/3 complication ● Repair Most of these injuries will respond to conservative management such as chest tube placement and hyperalimentation.50 If the patient fails conservative therapy, thoracic duct ligation may be required.49

8 CENTRAL VEIN CATHETERIZATION ● Prevention Avoidence of left SV or left IJV approach. However, the incidence of this complication is rare, so left-sided central venous cannulization is not contraindicated.

Arrythmia Close attention to patient hemodynamics and oxygen saturation during the procedure is mandatory. One small prospective study showed 41% of central vein catheterizations resulted in atrial arrhythmias and 25% produced some degree of ventricular ectopy.11 ● Consequence This is generally transient and resolves once the wire is slowly withdrawn. If the patient is not monitored, this could go unnoticed and result in a potentially fatal arrhythmia. Grade 1 complication ● Repair Treatment is to slowly withdraw the guidewire. No long-standing morbidity or mortality resulted from these arrhythmias.11 Rarely, one must consider administering antiarrhythmic agents. ● Prevention Arrhythmias are difﬁcult to prevent; however, close monitoring of the patient will keep this complication relatively benign.

Guidewire Loss One hand should be kept on the guidewire at all times to prevent inadvertent loss of the wire into the central vein. Loss of the guidewire (Fig. 8–7) usually happens in an unsupervised situation when the operator does not advance the guidewire the whole way through the catheter prior to placing the catheter through the skin and thus advances the catheter with the wire in it into the central vein.

Figure 8–7 Chest x-ray shows guidewire loss and migration after placement of femoral central venous line.

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● Consequence The guidewire could migrate into the heart or the IVC. There have been a few case reports of the guidewire getting caught in an IVC ﬁlter.51–53 Grade 1/2 complication ● Repair If this complication occurs, the patient should be taken immediately to interventional radiology and the wire removed under direct ﬂuoroscopy. If the guidewire becomes caught in the IVC ﬁlter, a hemostat should be placed on the guidewire at the skin level and the patient should be taken to the interventional radiology suite. Under ﬂuoroscopy, the guidewire can be carefully released and pulled out and an alternative site planned for placement of the central line. ● Prevention Proper technique and supervision should prevent most guidewire losses. If a patient is known to have an IVC ﬁlter, central line placement should be performed under ﬂuoroscopy to avoid the wire being caught in the ﬁlter and damaging or malpositioning the ﬁlter.

Cardiac Perforation Cardiac perforation with associated pericardial tamponade during central vein catheterization has been reported (Fig. 8–8) but is extremely rare thanks to efforts put forth by the U.S. Food and Drug Administration and the catheter companies. ● Consequence It is important that physicians be aware of this complication as well as the potential for catheter erosion and subsequent development of pericardial tamponade because the condition is often lethal.52 In a 1998 retrospective review of 25 cases of cardiac tamponade from central venous catheterization, it was noted that all postinsertion chest radiographs showed the tip of the catheter to be within the pericardial silhouette, and all patients developed unexplained hypotension from hours to 1 week after central line placement. Other associated signs included chest tightness (8 patients), shortness of breath (12 patients), air hunger (15 patients), and inferior wall injury shown by electrocardiogram (7 patients).54 This and several other articles suggest that this complication can be prevented and the outcome improved if the signs previously discussed are investigated promptly.54–57 Grade 3/4/5 complication ● Repair If patient develops a pericardial tamponade, the best chance of survival is early recognition and surgical repair. Unfortunately, it is often not discovered in time and the outcome is often poor.

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SECTION II: BEDSIDE PROCEDURES line infection to line sepsis increases morbidity and mortality.63 A central line can become infected at the puncture site via migration of the pathogen along the catheter and also by hematogenous seeding of the catheter.1 The most common way that catheters become infected is migration of skin organisms at the puncture site into the catheter tract, resulting in the colonization of the tip of the catheter.64 Grade 1 complication

A

B Figure 8–8 A, Cardiac tamponade resulting from perforation of the right ventricle with central line guidewire. B, Postmortem view of perforation of right ventricle secondary to central line guidewire.

● Prevention Always use the J-wire provided in most commercially available central access kits. Avoid using stiffer guidewires without the assistance of ﬂuoroscopy. Place the catheter in the proximal superior vena cava, avoiding placement within the cardiac silhouette.

Other Interestingly, there have been case reports of spinal accessory nerve injury as a complication of IJV cannulation.58 Injuries to the brachial plexus and vagus and phrenic nerves have also been documented.59–62 These nerve injuries are very rare, and a better understanding of neck anatomy will reduce their incidence.

● Treatment Treatment of catheter-associated infection involves removing the catheter and administering antibiotics. The prevalent organism is coagulase-negative staphylococcus, which has a high rate of resistance to methicillin. One must keep this in mind prior to beginning antimicrobial agents for presumed line infections and line sepsis. ● Prevention Although emergency situations exist in which central venous catheterization is done under substerile conditions, it cannot be overemphasized how important maximal barrier precautions and technique are to preventing catheter site infection and catheter-related sepsis.10 It is recommended that there be institutional tracking of central line–associated infections using the Centers for Disease Control and Prevention deﬁnitions of bloodstream infection, catheter infection, and colonization. In the setting of strict sterile technique with insertion by experienced operators, a prospective, observational study showed that SV, IJV, and femoral catheter sites have similar risks of catheter infection.65 Other studies, however, suggest that femoral vein and IJV catheterization are associated with a higher infection rate.5,66,67 As mentioned previously, the best way to reduce infection risk with central line placement is strict adherence to sterile protocol, placement by experienced operators, and catheter maintenance by trained nurses.65 Antibiotic administration prior to central line insertion is not recommended and should be discouraged because of the increased risk of developing antibiotic resistance.68 In immunocompromised patients, however, several studies have shown that antibiotic use decreased catheter-related infection.69,70 The use of antimicrobial-impregnated catheters has been studied, but to date, the results are conﬂicting and there is no general consensus as to whether they should be used on a routine basis.8,71

Catheter-Related Venous Thrombosis

CATHETER PROBLEMS Catheter Infection ● Consequence Catheter infection is the most common complication related to central line insertion, and the progression of

● Consequence Catheter-related venous thrombosis is related to both venous injury caused by line placement and the presence of a foreign body within the vein. The presence of a central vein catheter is the greatest independent predictor of upper extremity deep vein throm-

8 CENTRAL VEIN CATHETERIZATION bosis, increasing the risk sevenfold.72 Central venous thrombosis may result in swelling of the ipsilateral extremity, clot embolization, and infection. The reported rates of catheter-related central venous thrombosis varies (≤33% in one series) and may differ by site selection.5,72–74 However, the overall incidence of symptomatic catheter-related thrombosis ranges from 0% to 4%.75 Grade 1/2 complication ● Treatment If there are any clinical signs or symptoms of central vein thrombosis such as ipsilateral swelling and pain, a venous duplex should be performed. After the central line is removed, anticoagulation remains the mainstay for central vein thrombosis to prevent clot propagation. The risk of clinically signiﬁcant pulmonary embolism related to central vein catheter thrombosis is approximately 5%.76 ● Prevention Although little can be done to prevent catheter-related thrombosis, vigilance in inspecting the site and extremity may lead to earlier diagnosis and treatment.

Other There have been a few case reports of catheter embolization (grade 2/3/4), which generally result from a distal fracture in a long-term catheter.77–79 Although this is rare, it should be recognized as life-threatening and addressed immediately. Radiographic localization and interventional radiographic extraction techniques are generally required for retrieval. Catheter occlusion (grade 1) is another common complication of central venous access. There are many ways in which a central catheter may become occluded including occlusion by the ﬁbrin sheath that forms around the catheter, intraluminal or mural thrombus formation, and injury to the venous endothelium. If the catheter becomes occluded, patency can be restored at times by use of a ﬁbrinolytic agent. These agents act by activating plasminogen to form plasmin, which degrades ﬁbrin. Alteplase (tissue plasminogen activator [t-PA], 0.5–2 mg) is the approved agent/dose for clearing a clotted catheter.

SUMMARY In summary, complications of central venous access can be minimized by 1. Performance of an ample history. 2. Acquiring a detailed knowledge of central venous anatomy and the anatomy of surrounding structures. 3. Adherence to maximal barrier precautions and sterile technique. 4. Knowledge of potential complications. 5. Development of a procedural protocol.

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REFERENCES 1. McGee DC, Gould MK. Preventing complications of central venous catheterization. N Engl J Med 2003;348: 1123–1133. 2. Pittet D, Tarara D, Wensel RP. Nosocomial bloodstream infection in critical ill patients: excess length of stay, extra costs, and attributable mortality. JAMA 1994;271:1598– 1601. 3. Arnow PM, Quimosing EM, Beach M. Consequences of intravascular catheter sepsis. Clin Infect Dis 1993;16:778– 784. 4. Richards MJ, Edwards JR, Culver DH, Gaynes RP. Nosocomial infections in medical intensive care units in the United States. Crit Care Med 1999;27:887–892. 5. Merrer J, De Jonghe B, Golliot F, et al. Complications of femoral and subclavian venous catheterization in critically ill patients: a randomized controlled trial. JAMA 2001; 286:700–707. 6. Sznajder JI, Zveibil FR, Bitterman H, et al. Central vein catheterization: failure and complication rates by three percutaneous approaches. Arch Intern Med 1986;146: 259–261. 7. Mansﬁeld PF, Hohn DC, Fornage BD, et al. Complications and failures of subclavian-vein catheterization. N Engl J Med 1994;331:1735–1738. 8. Raad I, Darouiche R, Dupuis J, et al. Central venous catheters coated with minocycline and rifampin for the prevention of catheter-related colonization and bloodstream infections. A randomized, double-blind trial. The Texas Medical Center Catheter Study Group. Ann Intern Med 1997;127:267–274. 9. Veenstra DL, Saint S, Saha S, et al. Efﬁcacy of antisepticimpregnated central venous catheters in preventing catheter-related bloodstream infection: a meta-analysis. JAMA 1999;281:261–267. 10. Raad II, Hohn DC, Gilbreath J, et al. Prevention of central venous catheter–related infections by using maximal sterile barrier precautions during insertion. Infect Control Hosp Epidemiol 1994;15:231–238. 11. Stuart RK, Shikora SA, Akerman P, et al. Incidence of arrhythmia with central venous catheter insertion and exchange. J Parenteral Enteral Nutr 1990;14:152–155. 12. Skolnick ML. The role of sonography in the placement and management of jugular and subclavian central venous catheters. AJR Am J Roentgenol 1994;163:291–295. 13. Gibbs FJ, Murphy MC. Ultrasound guidance for central venous catheter placement. Hosp Physician 2006;42:23– 31. 14. Legler D, Nugent M. Doppler localization of the internal jugular vein facilitates central venous cannulation. Anesthesiology 1984;60:481–482. 15. Bold RJ, Winchester DJ, Madary AR, et al. Prospective, randomized trial of Doppler-assisted subclavian vein catheterization. Arch Surg 1998;133:1089–1093. 16. Hind D, Calvert N, McWilliams R, et al. Ultrasonic locating devices for central venous cannulation: meta analysis. BMJ 2003;327:361. 17. Lefrant J-Y, Cuvillon P, Benezet J-F, et al. Pulsed Doppler ultrasonography guidance for catheterization of the subclavian vein: a randomized study. Anesthesiology 1998;88:1195–1201.

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18. Miller AH, Rith BA, Mills TJ, et al. Ultrasound guidance versus the landmark technique for the placement of central venous catheters in the emergency department. Acad Emerg Med 2002;9:800–805. 19. Randolph AG, Cook DJ, Gonzalez CA, Pribble CG. Ultrasound guidance for placement of central venous catheters: a meta-analysis of the literature. Crit Care Med 1996;24:2053–2058. 20. Teichgraber UKM, Benter T, Gebel M, Manns MP. A sonographically guided technique for central venous access. AJR Am J Roentgenol 1997;169:731–733. 21. National Institute for Clinical Excellence, National Health Service. Final appraisal determination: ultrasound locating devices for placing central venous catheters. Available at www.nice.org.uk/page.aspx?o=35419 (accessed October 4, 2006). 22. Rothschild JM. Ultrasound guidance of central vein catheterization. Agency for Healthcare Research and Quality. Available at www.ahrq.gov/clinic/ptsafety/pdf/ chap21.pdf (accessed October 4, 2006). 23. Verghese ST, McGill WA, Patel RI, et al. Ultrasoundguided internal jugular venous cannulation in infants: a prospective comparison with the traditional palpation method. Anesthesiology 1999;91:71–77. 24. Eisen LA, Narasimhan M, Berger JS, et al. Mechanical complications of central venous catheters. J Intensive Care Med 2006;21:40–46. 25. Lefrant J, Muller L, De La Coussaye M, et al. Risk factors and immediate complication of subclavian vein catheterization in critically ill patients. Intensive Care Med 2002;28:1036–1041. 26. Nevarre DR, Domingo OH. Supraclavicular approach to subclavian catheterization: review of the literature and results of 178 attempts by the same operator. J Trauma 1997;42:305–309. 27. Haire WP, Lieberman RP. Deﬁning the risks of subclavian-vein catheterization. N Engl J Med 1994;331:1769– 1770. 28. Helmkamp BF, Sanko SR. Supraclavicular central venous catheterization. Am J Obstet Gynecol 1985;153:751–754. 29. Muhm M, Sunder-Plassmann G, Apsner R, et al. Supraclavicular approach to the subclavian/innominate vein for large-bore central venous catheters. Am J Kidney Dis 1997;30:802–808. 30. Foster PF, Moore LR, Sankary HN, et al. Central venous catheterization in patients with coagulopathy. Arch Surg 1992;127:273–275. 31. Ricolﬁ F, Valiente E, Bodson F, et al. Arteriovenous ﬁstulae complicating central venous catheterization: value of endovascular treatment based on a series of seven cases. Intensive Care Med 1995;21:1043–1047. 32. Huddy SPJ, McEwan A, Sabbat J, Parker DJ. Giant false aneurysm of the subclavian artery. Anaesthesia 1989;44: 588–589. 33. Oliver WC Jr, Nuttall GA, Beynen FM, et al. The incidence of artery puncture with central venous cannulation using a modiﬁed technique for detection and prevention of arterial cannulation. J Cardiothorac Vasc Anesth 1997;11:851–855. 34. Kulkarni R, Moreyra AE. Left internal mammary artery perforation during Swan-Ganz catheter insertion. Cathet Cardiovasc Diagn 1994;4:317–319.

35. Morand P, Masson D, Charbonnier B, et al. Iatrogenic arteriovenous ﬁstula from the internal mammary artery. Arch Mal Coeur Vaiss 1981;74:105–110. 36. Sise MJ, Hollingsworth P, Brimm JE, et al. Complications of the ﬂow-directed pulmonary artery catheter: a prospective analysis in 219 patients. Crit Care Med 1981;9:315– 318. 37. Patel C, Laboy V, Venus B, et al. Acute complications of pulmonary artery catheter insertion in critically ill patients. Crit Care Med 1986;14:195–197. 38. Lefrant JY, Muller L, Nouveoon E, et al. When subclavian vein cannulation attempts must be stopped? Presented at the American Society of Critical Care Anesthesiologists (ASCCA), Orlando, October 16, 1998. Anesthesiology Suppl B, Abstract B11, September 1998. 39. Plaus WJ. Delayed pneumothorax after subclavian vein catheterization. J Parenter Enteral Nutr 1990;14:414– 415. 40. Sivak SL. Late appearance of pneumothorax after subclavian venipuncture. Am J Med 1986;80:323–324. 41. Spiliotis J, Kordossis T, Kalfarentzos F. The incidence of delayed pneumothorax as a complication of subclavian vein catheterisation. Br J Clin Pract 1992;46:171–172. 42. Plewa MC, Ledrick D. Delayed tension pneumothorax complicating central venous catheterization and positive pressure ventilation. Am J Emerg Med 1995;13:532– 535. 43. Ruesch S, Walder B, Tramèr MR. Complications of central venous catheters: internal jugular versus subclavian access—a systematic review. Crit Care Med 2002;30:454– 460. 44. Kashuk JL, Penn I. Air embolism after central venous catheterization. Surg Gyn Obstet 1984;159:249–252. 45. Ordway CB. Air embolus via CVP catheter without positive pressure: presentation of case and review. Ann Surg 1974;179:479–481. 46. Flanagan JP, Gradisar IA, Gross RJ, Kelly TR. Air embolus—a lethal complication of subclavian venipuncture. N Engl J Med 1969;281:488–489. 47. Blanc P, Boussuges A, Henriette K, et al. Iatrogenic cerebral air embolism: importance of an early hyperbaric oxygenation. Intensive Care Med 2002;28:559–563. 48. Heckmann JG, Lang CJ, Kindler K, et al. Neurologic manifestations of cerebral air embolism as a complication of central venous catheterization. Crit Care Med 2000;28: 1621–1625. 49. Khalil KG, Parker FB Jr, Mukherjee N, Webb WR. Thoracic duct injury. A complication of jugular vein catheterization. JAMA 1972;221:908–909. 50. Ruggiero RP, Caruso G. Chylothorax—a complication of subclavian vein catheterization. J Parenter Enteral Nutr 1985;9:750–753. 51. Chattar-Cora D, Tutela RR Jr, Tulsyan N, et al. Inferior vena cava ﬁlter ensnarement by central line guidewires: a report of 4 cases and brief review. Angiology 2004;55: 463–468. 52. Duong MH, Jensen WA, Kirsch CM, et al. An unusual complication during central venous catheter placement. J Clin Anesth 2001;13:131–132. 53. Yengul TN, Bonilla SM, Goodwin SC, et al. Retrieval of a Greenﬁeld IVC ﬁlter displaced to the right brachiocephalic vein. Cardiovasc Intervent Radiol 2000;23:403–405.

8 CENTRAL VEIN CATHETERIZATION 54. Collier PE, Blocker SH, Graff DM, Doyle P. Cardiac tamponade from central venous catheters. Am J Surg 1998;176:212–214. 55. Collier PE, Goodman GB. Cardiac tamponade caused by central venous catheter perforation of the heart: a preventable complication. J Am Coll Surg 1995;181:459– 463. 56. Collier PE, Ryan JJ, Diamond DL. Cardiac tamponade from central venous catheters. Report of a case and review of the English literature. Angiology 1984;35: 595– 600. 57. Burns S, Herbison GJ. Spinal accessory nerve injury as a complication of internal jugular vein cannulation. Ann Intern Med 1996;125:700. 58. Chabanier A, Dany F, Brutus P, Vergnoux H. Iatrogenic cardiac tamponade after central venous catheter. Clin Cardiol 1988;11:91–99. 59. Depierraz B, Essinger A, Morin D, et al. Isolated phrenic nerve injury after apparently atraumatic puncture of the internal jugular vein. Intensive Care Med 1989;15:132– 134. 60. Paschall RM, Mandel S. Brachial plexus injury from percutaneous cannulation of the internal jugular vein. Ann Emerg Med 1983;12:58–60. 61. Sylvestre DL, Sandson TA, Nachmanoff DB. Transient brachial plexopathy as a complication of internal jugular vein cannulation. Neurology 1991;41:760. 62. Vest JV, Pereira MB, Senior RM. Phrenic nerve injury associated with venipuncture of the internal jugular vein. Chest 1980;78:777–779. 63. Pittet D, Wenzel RP. Nosocomial bloodstream infections. Secular trends in rates, mortality, and contribution to total hospital deaths. Arch Intern Med 1995;155:1177– 1184. 64. Mermel LA, McCormick RD, Springman SR, Maki DG. The pathogenesis and epidemiology of catheter-related infection with pulmonary artery Swan-Ganz catheters: a prospective study utilizing molecular subtyping. Am J Med 1991;91(suppl):S197–S205. 65. Deshpande KS, Hatem C, Ulrich HL, et al. The incidence of infectious complications of central venous catheters at the subclavian, internal jugular, and femoral sites in an intensive care unit population. Crit Care Med 2005;33: 13–20; discussion 234–235. 66. Norwood S, Wilkins HE III, Vallina Van L, et al. The safety of prolonging the use of central venous catheters: a prospective analysis of the effects of using antisepticbonded catheters with daily site care. Crit Care Med 2000;28:1376–1382. 67. Richet H, Hubert B, Nitemberg G, et al. Prospective multicenter study of vascular-catheter–related complications and risk factors for positive central-catheter cultures in

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intensive care unit patients. J Clin Microbiol 1990;28: 2520–2525. Hospital Infection Control Practices Advisory Committee (HICPAC). Recommendations for preventing the spread of vancomycin resistance. Infect Control Hosp Epidemiol 1995;16:105–113. Bock SN, Lee RE, Fisher B, et al. A prospective randomized trial evaluating prophylactic antibiotics to prevent triple-lumen catheter-related sepsis in patients treated with immunotherapy. J Clin Oncol 1990;8:161–169. Henrickson KJ, Axtell RA, Hoover SM, et al. Prevention of central venous catheter–related infections and thrombotic events in immunocompromised children by the use of vancomycin/ciproﬂoxacin/heparin ﬂush solution: a randomized, multicenter, double-blind trial. J Clin Oncol 2000;18:1269–1278. Dunser MW, Mayr AJ, Hinterberger G, et al. Central venous catheter colonization in critically ill patients: a prospective, randomized, controlled study comparing standard with two antiseptic-impregnated catheters. Anesth Analg 2005;101:1778–1784. Joffe HV, Kucher N, Tapson VF, Goldhaber SZ. Upper extremity deep vein thrombosis: a prospective registry of 592 patients. Circulation 2004;110:1605–1611. Epub 2004;September 7. Durbec O, Viviand X, Potie F, et al. Lower extremity deep vein thrombosis: a prospective, randomized, controlled trial in comatose or sedated patients undergoing femoral vein catheterization. Crit Care Med 1997;25: 1982–1985. Timsit JF, Farkas JC, Boyer JM, et al. Central vein catheter–related thrombosis in intensive care patients: incidence, risk factors, and relationship with catheterrelated sepsis. Chest 1998;114:207–213. Lowell JA, Bothe A Jr. Venous access. Preoperative, operative, and postoperative dilemmas. Surg Clin North Am 1991;71:1231–1246. Hingorani A, Ascher E, Markevich N, et al. Risk factors for mortality in patients with upper extremity and internal jugular deep venous thrombosis. J Vasc Surg 2005;41: 476–478. Nazareno J, Elliott JA, Finnie KJC. Cardiac arrhythmia due to subclavian catheter fracture and embolization. Can J Cardiol 2005;21:791–792. Peskin B, Soudack M, Ben-Nun A. Hickman catheter rupture and embolization—a life-threatening complication. Isr Med Assoc J 1999;1:289. Roggla G, Linkesch M, Roggla M, et al. A rare complication of a central venous catheter system (Port-a-Cath). A case report of a catheter embolization after catheter fracture during power training. Int J Sports Med 1993;14: 345–346.

9

Pulmonary Artery Catheterization Rovinder S. Sandhu, MD and Michael D. Pasquale, MD INTRODUCTION

● Management of multiorgan system failure and/or

Pulmonary artery catheterization (PAC) has been the subject of enormous controversy regarding its utility since its introduction by Swan and Ganz and coworkers in 1970.1 Detailed discussion regarding this controversy is beyond the scope of this chapter. However, a study performed by Connors and colleagues in 19962 comparing outcomes of critically ill patients managed with or without a PAC within the ﬁrst 24 hours after admission to an intensive care unit (ICU) revealed an association between PAC and an increased relative risk of hospital mortality and increased utilization of resources. This paper reignited the controversy and made clinicians reevaluate the efﬁcacy and safety of the pulmonary artery (PA) catheter. Many studies show no beneﬁt or harm from PAC3–5; others show decreased mortality.6,7 Amid the controversy, physicians continue to use PAC in critically ill patients, although no validated indications exist for its use. PA catheters are used to provide various hemodynamic parameters. Directly measured data include heart rate, waveforms, cardiac output, pulmonary artery pressures, right atrial pressure (central venous pressure [CVP]), pulmonary arterial occlusion pressure (PAOP; wedge), and mixed venous oxygen saturation. In addition, using these parameters, many other values—including mean arterial blood pressure, body surface area, stroke volume, systemic and pulmonary vascular resistance, ventricular stroke work, and oxygen delivery and consumption—can be calculated.8

● Management of hemodynamic instability after cardiac

severe burns surgery ● Assessment of response to treatment in patients with

primary pulmonary hypertension ● Aspiration of air emboli

In addition, PAC may be useful in perioperative monitoring of high-risk patients undergoing high-risk procedures. As with any other invasive procedure, PAC has its own inherent technical complications during insertion. The overall risks of complications have been reported to be anywhere from 5% to 15%. These include complications related to venous access and to right heart catheterization and PAC as well as infectious and thrombotic complications.10

OPERATIVE STEPS Step 1 Step 2

Step 3 Step 4 Step 5 Step 6

INDICATIONS 9 Step 7 ● Diagnosis of shock states ● Differentiation of high- versus low-pressure pulmonary ● ● ● ●

edema Diagnosis of primary pulmonary hypertension Diagnosis of valvular disease, intracardiac shunts, cardiac tamponade, and pulmonary embolus Monitoring and management of complicated acute myocardial infarction Assessment of hemodynamic response to therapies

Step Step Step Step Step Step Step

8 9 10 11 12 13 14

Assess patient’s need for pulmonary artery catheterization Review patient’s chart—particularly checking for history of coagulation abnormalities and history of deep venous thrombosis Choose appropriate site for placement (i.e., internal jugular or subclavian) Obtain consent Gather supplies Perform a “time out” between the physician and bedside nurse Prep the patient—including correct patient positioning for particular site Cannulate the vein Place guidewire Place the cordis over the guidewire Remove the guidewire Aspirate blood from the cordis Flush the cordis Flush the ports of the pulmonary artery catheter

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Step 15 Attach catheter to transducer and check frequency response Step 16 Place pulmonary artery catheter through the cordis to 20 cm Step 17 Inﬂate balloon and follow until a pulmonary artery occlusion tracing is identiﬁed Step 18 Deﬂate balloon and identify pulmonary artery tracing Step 19 Secure catheter Step 20 Place sterile dressing Step 21 Check placement with chest x-ray

OPERATIVE PROCEDURE Prior to placing a PA catheter, one must obtain all necessary equipment and review the patient’s chart. 1. Informed consent should be obtained from the patient or power of attorney. 2. Review the patient’s chart to make certain no contraindications exist (e.g., coagulopathy, tricuspid or pulmonary valve mechanical prosthetics, right heart mass, tricuspid or pulmonary valve endocarditis, history of heparin-induced thrombocytopenia [many PA catheters are heparin-coated; non-coated ones are available], and history of left bundle branch block). 3. An experienced nurse should be available and in the room to assist with the procedure, along with a physician experienced in PAC and waveform analysis. 4. All necessary equipment should be gathered including introducer sheath, PA catheter, transducers, and ﬂushes. In addition, as in central vein catheterization, maximal sterile-barrier precautions should be used (mask, cap, gown, sterile gloves, and a large sterile drape). 5. Although most patients are critically ill or in the operating room while having a PA catheter placed, appropriate sedation and local anesthetic should be used.

2. Subclavian vein a. Higher risk of pneumothorax. b. Usually high rate of successful PAC in right- or leftsided placements. c. Subclavian arterial puncture may be more difﬁcult to control, especially in coagulopathic patients, and may lead to hemothorax. 3. Femoral vein a. No risk of pneumothorax. b. Arterial puncture is easier to control with pressure, although peripheral embolization is of concern. c. Difﬁcult PAC; ﬂuoroscopy may be useful. d. History of internal jugular vein catheterization ﬁlter is an absolute contraindication. 4. External jugular and antecubital approaches a. Usually require ﬂuoroscopy. b. Difﬁcult for PAC, although published rates of success are in excess of 75%.11,12 c. Higher rates of thrombosis in peripheral veins. Complications of central vein catheterization are discussed in Chapter 8, Central Vein Catheterization. These include pneumothorax, hemothorax (grade 2), thoracic duct injury (grade 2/3), arterial puncture, possible pseudoaneurysm formation or arteriovenous ﬁstula formation (grade 1/2/3), air embolism (grade 2/5), cardiac perforation with associated cardiac tamponade (grade 3/4/5), thrombus (grade 1/2/5), and infections (grade 1). Once central vein catheterization is achieved, one can prepare for PAC. Many different PA catheters exist; they all have some similarities (Fig. 9–1): 1. 2. 3. 4. 5.

Yellow port—PA port Blue port—CVP port Pink port—1.5-cc balloon port Clear port—infusion port (if available) PA catheter marked at 10-cc intervals for monitoring placement

The ﬁrst step in PAC is to obtain venous access. A PA catheter can be introduced most commonly through internal jugular, subclavian, and femoral sheath introducers. If needed, the external jugular vein or antecubital fossa can be used. Each site has speciﬁc risks. Review Chapter 8, Central Vein Catheterization, for insertion of introducer sheaths and complications in accessing these sites. Each site has its own advantages and disadvantages for subsequently placing a PA catheter. 1. Internal jugular vein a. Lower risk of pneumothorax. b. Right-sided offers the most direct approach to the heart. c. Left-sided offers a less direct approach to the heart and may make achieving a PAC more difﬁcult. d. Risk of carotid puncture and dilation with a largebore sheath introducer may lead to cardiovascular accident or neck hematoma and loss of airway.

Figure 9–1

Pulmonary artery catheter.

9 PULMONARY ARTERY CATHETERIZATION

123

In addition to these general guidelines, specialized catheters are increasingly available. These include pacing PA catheters, right ventricular function catheters, continuous cardiac output catheters, and oximetric catheters for continuous mixed venous oxygen saturation monitoring. Prior to ﬂoating the catheter, the following must be done:

insertion, patients, and pathology, one should keep these approximate lengths in mind. If the catheter is being advanced past 60 cm without a right ventricle, PA, or wedge tracing, it is necessary to reevaluate and consider obtaining a chest x-ray or readvancing the catheter because the risk of coiling or improper placement increases.

1. All ports are ﬂushed. 2. Catheter is placed through a sterile sheath to allow future adjustments. 3. Balloon is checked by inﬂating air to 1.5 cc. 4. PA port is connected to a pressure transducer. 5. Frequency response of the transducer is checked by moving the tip to see an appropriately changing waveform on the monitor. 6. All catheters are manufactured with a natural curve. Curve should be adjusted to allow for easier ﬂow through the right ventricular outﬂow tract. 7. If patient was placed in Trendelenburg position for venous access, he or she should be leveled or placed slightly head up.

COMPLICATIONS OF PULMONARY ARTERY CATHETER FLOTATION

Next, the PA catheter is ready for insertion. One must be aware of the characteristic waveforms as the catheter advances to the PA. 1. Place catheter to 20 cm, then inﬂate balloon (never advance catheter with balloon down). 2. With balloon inﬂated, advance as the waveform changes from a CVP pattern to a right ventricular pattern. This is characterized by systolic pressure 15 to 30 mm Hg and diastolic pressure approximating right atrial (CVP) pressure 0 to 5 mm Hg. 3. Continue advancement to the PA as evidenced by the identiﬁcation of a dicrotic notch and a higher diastolic pressure: normally 15 to 30 mm Hg systolic, 8 to 12 mm Hg diastolic. 4. Careful, slow advancement will lead to PA occlusion pressure which approximates PA end-diastolic pressure (8–12 mm Hg). 5. At this point, the balloon should be deﬂated and the PA tracing should once again be identiﬁed; if not, the balloon should be withdrawn slightly and readvanced to PA occlusion. 6. Obtain chest x-ray to look for placement. If the appropriate tracings are unable to be identiﬁed, the catheter should be withdrawn, with the balloon down, to 20 cm and readvanced. A study by Tempe and associates13 showed approximate insertion lengths in patients undergoing cardiac surgery. They found, from a right internal jugular approach, that the right ventricle is reached at 24.6 cm (95% conﬁdence interval [CI] 24.2–24.9), the pulmonary artery at 36 cm (95% CI 35.6–36.5), and pulmonary artery occlusion at 42.8 cm (95% CI 42.2– 43.5 cm). Although PAC varies with different routes of

Arrhythmia Arrhythmias are the most common complication during PAC, occurring in up to 87% of patients. However, they are often short-lived and benign. Certain patient populations have a higher incidence of arrhythmias such as myocardial infarction, myocarditis, hypokalemia, hypoxia, and acidosis.14 ● Consequence Atrial ectopic beats, ventricular tachycardia, ventricular ﬁbrillation, right bundle branch block, or complete heart block may occur; most are short-lived and recover spontaneously. Ventricular tachycardia requiring treatment occurs in approximately 1% of catheterizations. Right bundle branch block occurs in 0.5% to 5%, and in the presence of a left bundle branch block, a complete heart block may occasionally occur.8 Grade 1/2 complication ● Repair Upon recognition of an arrhythmia, back up the catheter and reﬂoat. If the arrhythmia continues, administration of lidocaine or other antiarrythmic agent may be necessary. Occasionally, transvenous or transdermal pacing is required. ● Prevention If the patient has risk factors for arrhythmia, appropriate medications should be nearby. If a preexisting left bundle branch block is present, consider a transvenous pacing PA catheter versus being prepared for transcutaneous pacing. However, because the risk of complete heart block in the presence of left bundle branch block is less than 1%, prophylactic pacing is not warranted.15 Prophylactic lidocaine may decrease the incidence of mechanically induced arrhythmias.16 Decreased catheterization times also may lead to fewer arrhythmias.17

Coiling of Pulmonary Artery Catheter PA catheters are responsible for two thirds of coiled intravascular devices. This complication results most often from looping of the catheter in the right ventricle, but it can become knotted in the vena cava or PA. Occasionally, it can result in looping around intracardiac structures (papillary muscles or tricuspid valve).18

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SECTION II: BEDSIDE PROCEDURES procedure with interventional radiology, in which the catheter knot is guided to a more accessible location such as the internal jugular vein and removed through a venotomy.20 If the catheter becomes ﬁxed to an intracardiac ﬁxture, open heart surgery may be required for removal. ● Prevention The most important concept in preventing this complication is to avoid excessive catheter length prior to encountering PA pressures or a wedge tracing. In addition, looping may be suspected if multiple ventricle ectopia are seen. In both cases, the catheter should be withdrawn to the 20-cm mark and reﬂoated.

Figure 9–2 Chest radiographic ﬁlm shows the knotted (encircled) pulmonary artery catheter ﬁxed in the superior vena cava. (Reprinted with permission from Georghiou GP, Vidne BA, Raanani E, et al. Knotting of a pulmonary artery catheter in the superior vena cava: surgical removal and a word of caution. Heart 2004;90: e28; BMJ Publishing Group Ltd.)

Figure 9–3 Knot in the removed pulmonary artery catheter. (Reprinted with permission from Georghiou GP, Vidne BA, Raanani E, et al. Knotting of a pulmonary artery catheter in the superior vena cava: surgical removal and a word of caution. Heart 2004;90: e28; BMJ Publishing Group Ltd.)

● Consequence If the catheter becomes knotted, it will not be able to be removed and will not function properly. The mortality rate in one study was 8%18 (Figs. 9–2 and 9–3). Grade 2/3/5 complication ● Repair Initially, interventional radiologic approaches are used to aid in removal. Various techniques have been described, including untying the knot under ﬂuoroscopy with the use of guidewires or balloon catheters. Other techniques involve tightening the knot under ﬂuoroscopic control in order to remove it with the introducer sheath.19 If the coil is large and contains many loops, surgical removal is required. Most commonly, this is a combined

Pulmonary Artery Rupture ● Consequence PA rupture is a relatively rare event; however, it is the most serious complication arising from ﬂotation of a PA catheter. The incidence ranges from 0.03% to 0.2% with a mortality rate of 50% to 70%.21 Risk factors for rupture include female gender, advanced age over 60 years, anticoagulation, pulmonary hypertension, balloon hyperinﬂation, steroid use, multiple and frequent catheter manipulation, peripheral placement of the catheter, and inﬂating the balloon with ﬂuids other than air. In addition, surgically induced hypothermia and cardiac decompression and manipulation during cardiac surgery may increase the risk for rupture.10 PA rupture leads to hemorrhage, pseudoaneurysm formation, hemoptysis, hypoxia, and hemodynamic instability. Pseudoaneurysm may be discovered in a delayed fashion days to months or years after removal of a PA catheter and can be identiﬁed as an incidental ﬁnding of imaging studies (Figs. 9–4 to 9–6). Grade 2–5 complication ● Repair The management of PA rupture depends largely upon two factors: location of the patient (i.e., operating room, ICU, or outpatient setting) and the presence of hemodynamic instability. If the patient is in the operating room undergoing cardiac surgery, the rupture is often repaired directly and may include direct repair of the PA, ligation, or lobectomy or pneumonectomy, depending on the degree of hemorrhage and hemodynamic stability. If the patient is not undergoing cardiac surgery and PA rupture is entertained, transcatheter embolization should be performed, if possible. If the patient is in the ICU or an outpatient setting, a pulmonary angiogram should be performed to diagnose the site of bleeding and deﬁnitively treat the lesion. A high index of suspicion must be maintained, and any new hemoptysis during placement should be followed by pulmonary angiogram. Keeping the catheter in place is debatable but may lead to faster identiﬁcation of the injury, and maintaining the balloon inﬂated may decrease ﬂow to the ruptured segment thereby limiting hemorrhage.

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125

A

Figure 9–5 Extravasation of contrast medium is visible on peripheral placement of the catheter during angiography. (Reprinted with permission from Kierse R, Jensen U, Helmberger H, et al. Value of multislice CT in the diagnosis of pulmonary artery pseudoaneurysm from Swan-Ganz catheter placement. J Vasc Interv Radiol 2004;15:1133–1137.)

B Figure 9–4 A, Multislice computed tomography (CT) shows exact visualization of the aneurysm revealing perfused and thrombosed areas. B, The organ-optimized reconstruction with nearly isometric resolution permits direct identiﬁcation of the feeder vessel and its connection to the aneurysm. (A and B, Reprinted with permission from Kierse R, Jensen U, Helmberger H, et al. Value of multislice CT in the diagnosis of pulmonary artery pseudoaneurysm from Swan-Ganz catheter placement. J Vasc Interv Radiol 2004;15:1133–1137.)

Other important principles to remember when dealing with this devastating complication include reversal of anticoagulation, protecting the nonaffected lung from aspirated blood by decubitus positioning (nonaffected side up), placement of a double-lumen endotracheal tube, and application of positive end-expiratory pressure. Figure 9–7 shows a treatment algorithm.

Figure 9–6 The aneurysm is sealed after placement of coils in the feeder vessel. Note the stretched vessels associated with the lesion. (Reprinted with permission from Kierse R, Jensen U, Helmberger H, et al. Value of multislice CT in the diagnosis of pulmonary artery pseudoaneurysm from Swan-Ganz catheter placement. J Vasc Interv Radiol 2004;15:1133–1137.)

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Suspected pulmonary artery perforation

Remove PA catheter

Hemodynamic instability (without airway hemorrhage)

Major airway hemorrhage

Minor hemoptysis (or herald hemorrhage)

Defer elective surgery Expectant treatment A. Establish adequate gas exchange (ET and MV) B. Isolation of lung---(DLET or BB) C. Control of hemorrhage

Pre/post-op Hemodynamically stable

Intra-operative (hemorrhage on weaning CPB)

Pre/post-op Hemodynamically unstable

(Open bil.pleura/reinstitute CPB)

(Appraisal of injury)

Contained parenchymal hemorrhage

Emergent thoracotomy clamp hilum

Extensive parenchymal hemorrhage or pleural rupture

Injured central and branch PA

Pulmonary reserve

Arterial repair

Poor

Good

Persistent hypoxemia?

Temporary ECLS

Conservative therapy Mechanical ventilation and PEEP

PA loop

Chest X ray and CT scan Pulmonary angiogram

Bleeding PA perforation PA pseudo aneurysm

Arterial embolization

Recurrent hemorrhage?

Pulmonary resection

Figure 9–7 Treatment algorithm. (Adapted from Sirivella S, Gielchinsky I, Parsonnet V, et al. Management of catheter-induced pulmonary artery perforation: a rare complication. Ann Thorac Surg 2001;72:2056–2059.)

9 PULMONARY ARTERY CATHETERIZATION ● Prevention Although Mullerworth and coworkers22 concluded that “catheter-induced pulmonary rupture is unavoidable,” education and training of those involved with insertion is of utmost importance. Most ruptures occur with the balloon inﬂated and trying to obtain a PAOP, or wedge, pressure. The inﬂation time should be kept to a minimum, and the person advancing the catheter should watch the tracing. Upon insertion, once a PAOP pattern is identiﬁed, the catheter must not be advanced further. If a PAOP pattern is identiﬁed with partial inﬂation of the balloon or with the balloon deﬂated, the catheter should be moved back. The balloon inﬂation syringe should be kept on the balloon port at all times to avoid inadvertent ﬂuid injection into the balloon. In addition, consider using the pulmonary end-diastolic pressure to approximate PAOP, especially in patients with pulmonary hypertension or other risk factors for rupture.

Other Complications Many rare complications have been reported. Most can be avoided by remembering and practicing the principles for safe insertion. Catheter emboli, usually caused by shearing of the catheter just proximal to a knot, have been reported. This can occur with any central vein catheter, and conservative management carries a morbidity risk of 45% to 73%, with mortality rates as high as 60%. Catheter emboli can result in arrhythmias, thrombus, pulmonary emboli, sepsis, and myocardial inﬂammation or endocarditis.23–27 Interventional radiologic techniques should be used to remove these fragments, which often requires placing the fragment in an accessible vein such as internal jugular or femoral. Conservative management should be discouraged, unless comorbid conditions create an absolute contraindication to any invasive procedure (grade 3/4/5). Damage of the tricuspid and pulmonary valves has been reported, usually occurring by removing the catheter with the balloon inﬂated or coiling of the catheter around these structures (grade 3/4/5).28 Most PA catheters are heparin-coated and may lead to thrombocytopenia or even heparin-induced thrombocytopenia. As always with this condition, a high index of suspicion is required for timely diagnosis and intervention. Non–heparin-coated PA catheters are available (grade 1/2). Pulmonary infarction can occur and usually results from placing the catheter too distal in the pulmonary arterial system. It can also be a consequence of one of the aforementioned complications, for example, catheter emboli or postangiographic embolization. Catheters have been reported to be placed in the coronary sinus or persistent left-sided superior vena cava (grade 1).29,30 Migration through a patent ductus arteriosus and into the aorta has been described in pediatric patients (grade 1).31 Perforation of the right ventricle by a PA

127

catheter has been described, and in one such case, cardiac output and mixed venous saturation measurements continued (grade 3/4).32

SUMMARY PAC is associated with numerous complications. Maintaining proper technique, careful examination of waveforms, and postprocedure x-rays should help minimize complications and their morbidity.

REFERENCES 1. Swan HJC, Ganz W, Marcus H, et al. Catheterization of the heart in men with use of a ﬂow-directed balloontipped catheter. N Engl J Med 1970;183:447–451. 2. Connors AF Jr, Speroff T, Dawson NV, et al. The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA 1996;276:889–897. 3. Gattinoni L, Pelosi P, Crotti S, Valenza F. Effects of positive end-expiratory pressure on regional distribution of tidal volume and recruitment in adult respiratory distress syndrome. Am J Respir Crit Care Med 1995;151:1807– 1814. 4. Bender JS, Smith-Meek MA, Jones CE. Routine pulmonary artery catheterization does not reduce morbidity and mortality of elective vascular surgery: results of a prospective randomized clinical trial. Ann Surg 1997;226:229– 237. 5. Harvey S, Harrison D, Singer M, et al. An assessment of the clinical effectiveness of pulmonary artery catheters in patient management in intensive care (PAC-Man): a randomized controlled trial. Lancet 2005;366:472– 477. 6. Ivanov R, Allen J, Calvin J. The incidence of major morbidity in critically ill patients managed with pulmonary artery catheters: a meta-analysis. Crit Care Med 2000;28: 615–619. 7. Wilson J, Woods I, Fawcett J, et al. Reducing the risk of major elective surgery: randomized controlled trial of preoperative optimisation of oxygen delivery. BMJ 1999; 318:1099–1103. 8. Truwit J. The pulmonary artery catheter in the ICU, part 1: technique and measurements. J Crit Illness 2003;18:9– 19. 9. Mueller HS, Chatterjee K, Davis KB, et al. ACC Expert Consensus Document. Present use of bedside right heart catheterization in patients with cardiac disease. J Am Coll Cardiol 1998;32:840–864. 10. Pybus A. The “St. George” Guide to Pulmonary Artery Catheterisation. Available at HONcode accreditation seal. www.manbit.com/PAC/chapters/PAC.cfm (accessed May 7, 2008). 11. De Lange S, Boscoe MJ, Stanley TH. Percutaneous pulmonary artery catheterization via the arm before anaesthesia: success rate, frequency of complications and arterial pressure and heart rate responses. Br J Anaesth 1981;53:1167–1172.

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12. Sparks CJ, McSkimming I, George L. Shoulder manipulation to facilitate central vein catheterization from the external jugular vein. Anaesth Intensive Care 1991;19: 567–568. 13. Tempe DK, Gandhi A, Datt V, et al. Length of insertion for pulmonary artery catheters to locate different cardiac chambers in patients undergoing cardiac surgery. Br J Anaesth 2006;97:147–149. 14. Ermakov S, Hoyt JW. Pulmonary artery catheterization. Crit Care Clin 1992;8:773–806. 15. Shah KB, Rao TL, Laughlin S, El-Etr AA. A review of pulmonary artery catheterization in 6,245 patients. Anesthesiology 1984;61:271–275. 16. Sprung CL, Marcial EH, Garcia AA, et al. Prophylactic use of lidocaine to prevent advanced ventricular arrhythmias during pulmonary artery catheterization. Prospective double-blind study. Am J Med 1983;75:906–910. 17. Iberti TJ, Benjamín E, Gruppi L, Raskin JM. Ventricular arrhythmias during pulmonary artery catheterization in the intensive care unit. Am J Med 1985;78:451–454. 18. Karanikas ID, Polychronidis A, Vrachatis A, et al. Removal of knotted intravascular devices. Case report and review of the literature. Eur J Endovasc Surg 2002;23:189– 194. 19. Tan C, Bristol PJ, Segal P, Bell RJ. A technique to remove knotted pulmonary artery catheters. Anaesth Intensive Care 1997;25:160–162. 20. Baqul NB, Menon NJ, Pathak R, et al. Knot in the cava— an unusual complication of Swan-Ganz catheters. Eur J Vasc Endovasc Surg 2005;29:651–653. 21. Abreau AR, Campos MA, Krieger BP. Pulmonary artery rupture induced by a pulmonary artery catheter: a case report and review of the literature. J Intensive Care Med 2004;19:291–296. 22. Mullerworth MH, Angelopoulos P, Couyant MA, et al. Recognition and management of catheter-induced

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

pulmonary artery rupture. Ann Thorac Surg 1998;66: 1242–1245. Nellore A, Trerotola SO. Delayed migration of a catheter fragment from the left to the right pulmonary artery. J Vasc Interv Radiol 2004;15:497–499. Fisher RG, Ferreyro R. Evaluation of current techniques for nonsurgical removal of intravascular iatrogenic foreign bodies. AJR Am J Roentgenol 1978;130:541–548. Bernhardt LC, Mendenhall JT, Wegner GP. Intravenous catheter embolization to the pulmonary artery. Chest 1970;57:329–332. Richardson JD, Grover FL, Trinkle JK. Intravenous catheter emboli. Experience with twenty cases and collective review. Am J Surg 1974;128:722–727. Wellmann KF, Reinhard A, Salazar EP. Polyethylene catheter embolism. Review of the literature and report of a case with associated fatal tricuspid and systemic candidiasis. Circulation 1968;37:380–392. O’Toole JD, Wurtzbacher JJ, Weaner NE, Jain AC. Pulmonary-valve injury and insufﬁciency during pulmonary-artery catheterization. N Engl J Med 1979;22:301: 1167–1168. Baciewicz FA, Nirdlinger MA, Davis JT. An unusual position of a Swan Ganz catheter. Intensive Care Med 1987;13:211–212. Lai YC, Goh JCY, Lim SH, Seah TG. Difﬁcult pulmonary artery catheterization in a patient with persistent left superior vena cava. Anaesth Intensive Care 1998;26: 671–673. Moore RA, McNicholas K, Gallagher JD, Niguidula F. Migration of pediatric pulmonary artery catheters. Anesthesiology 1983;58:102–104. Chuang KC, Lan AKM, Luk HN, et al. Perforation of the right ventricle by a pulmonary artery catheter that continues to measure cardiac output and mixed venous saturation. J Clin Anesth 2005;17:124–127.

10

Arterial Catheterization Elizabeth A. David, MD and Stephen R. T. Evans, MD INTRODUCTION Continuous arterial pressure monitoring and direct arterial blood samplings are the two most common indications for arterial catheterization, which is typically used for perioperative monitoring during major surgical procedures and in critically ill patients. Common sites of cannulation include radial, femoral, and axillary arteries, and the most frequently reported complications include vascular insufﬁciency, bleeding, and infection. Despite reported complications, numerous studies have demonstrated the safety of arterial cannulas for monitoring in both the surgical and the medical intensive care settings.1 In an extensive review of the literature from 1978 to 2001, Scheer and coworkers1 reported a major complication rate of less than 1% in over 25,505 attempts at cannulation of the radial, femoral, and axillary arteries.

INDICATIONS ● Continuous arterial pressure monitoring ● Direct arterial blood sampling

OPERATIVE PROCEDURE Radial Artery Cannulation Scheer and coworkers1 found temporary occlusion of the radial artery to be the most common complication, with an incidence rate from 1.5% to 35%. Complications after radial cannulation have also been reported: hematoma formation (14% incidence rate), local infection (0.7%), bleeding (0.5%), pseudoaneurysm (0.09%), and permanent ischemic damage (0.09%).1

whereas vascular insufﬁciency and bleeding were more common after line changes over a guidewire.2 Grade 1/2 complication ● Repair Catheter removal is typically sufﬁcient therapy except in extreme circumstances, as noted under “Pseudoaneursym,” later in this chapter. ● Prevention Thrombotic complications can be avoided and minimized through the use of smaller-gauge catheters (20gauge) and Teﬂon catheters.3 Minimizing the number of punctures has also been shown to be an effective means of minimizing the chance of thrombotic complications.4 Slogoff and associates4 also demonstrated an increased risk of occlusive complications in patients who also have hematoma, which is also related to multiple puncture attempts. Beards and colleagues5 in a randomized, controlled trial demonstrated that arterial cannula insertion using a Seldinger technique resulted in fewer puncture attempts and fewer occlusive problems than a direct puncture method of cannula insertion. Similarly, Mangar and coworkers6 demonstrated an 82% success rate when cannulating the radial artery using a guidewire versus only 65% success when a direct puncture method was used. The use of heparinized ﬂush solution made no difference in the maintenance of cannula patency versus ﬂushing with normal saline; however, more accurate blood pressure monitoring was recorded in patients receiving heparinized ﬂush solutions than in those with cannulas ﬂushed with normal saline only.7 Low-dose aspirin or low-dose heparin therapy pretreatment has been demonstrated to minimize the risk of occlusive complications after arterial cannulation.8

Infection Thrombosis ● Consequence Occlusive complications plague all of the common sites for arterial cannulation. Arterial spasm and pulseness are more commonly seen after new-site insertion,

● Consequence Whether or not cannula site inﬂuences infection rate after arterial cannulation is controversial. Frezza and associates2 found that the infection rate of 0.4% to 0.7% does not vary regardless of line site and that serial

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changing of the arterial cannulation site made no difference in terms of the complications reported. However, in a large prospective observational study, Lorente and coworkers9 demonstrated a higher risk of catheter-related line infections and catheter-related bloodstream infections with femoral arterial cannulas than with radial cannulas.9 Grade 1 complication ● Repair Appropriate antibiotic therapy and catheter removal will typically provide sufﬁcient therapy. ● Prevention Sterile insertion technique, adequate disinfection of cannulation site, and length of cannulation have been demonstrated to be crucial factors for decreasing the incidence of cannula-related infections.10 Mimoz and colleagues10 compared the use of chlorhexidine with iodine preparation solutions for both sterilization of the insertion site and maintenance of indwelling cannula sites in a prospective, randomized trial and found that the chlorhexidine solution was more effacious at prevention of infection at cannula sites. This effect was attributed to chlorhexidine’s effect on gram-positive organisms.10

Pseudoaneurysm (Fig. 10–1) Pseudoaneurysm after radial cannulation has a mean incidence of 0.09% in the literature and is typically managed

with ligation of the radial artery after an Allen test demonstrates collateral ﬂow.11 ● Consequence Perez and associates12 reported a case of pseudoaneurysm requiring ligation of the radial artery and eventually resulting in septic shock. Grade 1–3 complication ● Repair Ligation of the radial artery may be required if an Allen test demonstrates sufﬁcient ulnar arterial collateral ﬂow.12 ● Prevention Pseudoaneurysm is typically seen later after catheterization (7–40 days). Factors that were associated with pseudoaneurysm included repeated puncture attempts, alterations of vessel walls, and catheter infections.12 Ganchi and coworkers13 demonstrated that the presence of Staphylococcus aureus infection and signs of infection lasting longer than 48 hours after cannula removal or initiation of antibiotics are directly correlated with the development of pseudoaneurysm.13 Therefore, early recognition of signs of infection and minimizing the time of catheterization may help reduce the incidence of pseudoaneurysm after radial cannulation.

Proper palmar digital arteries

Proper digital arteries of thumb

Common palmar digital arteries Palmar metacarpal arteries

Radial indicis artery Princeps pollicis artery

Deep palmar arterial arch

Ulnar artery

Superfical palmar branch of radial artery

Radial artery

Figure 10–1 The radial and ulnar arteries provide collateral ﬂow to the hand, which allows for ligation in the presence of a pseudoaneurysm.

10 ARTERIAL CATHETERIZATION

131

Hand Ischemia Hand ischemia is a rare, but reported complication of radial arterial cannulation.

further exacerbated by the systemic heparinization required for bypass.15 Grade 1–5 complication

● Consequence Valentine and associates14 reported a series of eight patients (incidence estimated to be 1 in 1000) who experienced hand ischemia after radial arterial thrombosis following arterial cannulation. Patient outcomes included hospital death, ﬁnger gangrene requiring amputation, chronic pain, and cold intolerance; one patient was asymptomatic.14 Grade 1–5 complication

● Repair Primary repair and mechanical tamponade via pressure or packing are the most readily available options for repair.

● Repair Patients were treated with a combination of thrombectomy, patch angioplasty, vein graft interposition, and medical therapies.14 ● Prevention Risk factors for hand ischemia included coronary artery disease, diabetes mellitus, end-stage renal disease, heparin-induced thrombocytopenia, and peripheral arterial occlusive disease. Duration of cannulation varied from 1 to 14 days prior to presentation with ischemic symptoms. All patients were noted to have compromised ulnar arterial ﬂow at the time of vascular surgery evaluation. Embolization from radial arterial thrombus leading to occlusion of distal arteries supplied by the palmar arch may be responsible for hand ischemia and provide explanation for the persistence of digital ischemia despite thrombectomy and reperfusion therapies.14 Recognizing risk factors, minimizing duration of cannulation, and maintaining ulnar arterial ﬂow are keys to preventing hand ischemia.

Femoral Artery Cannulation The femoral artery is the second most common site cannulated for invasive blood pressure monitoring and frequent blood sampling. Unlike complications with the radial artery, hematoma and bleeding were the most frequently reported complications (mean incidence of 6.1% and 1.58%, respectively) followed by temporary occlusion (mean incidence of 1.45%).1 The literature contains reports of pseudoaneursym, local infection, and even death after retroperitoneal bleeding.

Retroperitoneal Bleeding (Fig. 10–2) ● Consequence Death after retroperitoneal bleeding after placement of a right femoral arterial catheter was reported by Muralidhar15 in a 22-year-old patient who had undergone correction of tetralogy of Fallot requiring cardiopulmonary bypass. The patient’s death was attributed to multiple attempts at cannulation that led to bleeding

● Prevention Muralidhar15 suggested puncture of the femoral artery below the inguinal ligament, adequate compression of the puncture site after failed attempts, using a smallgauge catheter, and avoiding cannulation by inexperienced personnel as means of avoiding this morbidity associated with femoral cannulation.15

Axillary Artery Cannulation The axillary artery is the third most common site for arterial cannulation, and although it requires cutdown for access to be safely attained, some studies suggest a lower complication rate than with alternate sites of cannulation. The most common complications reported by Scheer and coworkers1 were hematoma and local infection (mean incidence of 2.28% and 2.24%, respectively).

Local Infection ● Consequence The rates of local infection are the highest for axillary cannulation of the three common sites. Some studies have attributed an increased incidence of sepsis in the presence of local infection to care and monitoring of the actual system.16 Grade 1 complication ● Repair Antibiotics are typically necessary only in cases of sepsis. Local infection will clear when the catheter is removed. ● Prevention Maki and Hassemar16 suggested that the pressure monitoring apparatus should be changed every 48 hours to minimize the risk of infection and sepsis in patients with in-dwelling cannulas.

Hand Paresthesia (Fig. 10–3) ● Consequence A unique complication for axillary cannulation is paresthesia of the hand secondary to pressure on the brachial plexus, which has been described by Brown and colleagues,17 who concluded that despite this complication and others described earlier, the axillary artery is wa safe alternative site when the radial artery is unavailable. Grade 1/2 complication

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B

C

A

Figure 10–2 A, The femoral artery above and below the inguinal canal. C, Below the inguinal canal, the femoral artery can be compressed using direct pressure against the femoral head. B, Above the inguinal ligament, pressure cannot be applied which can increase the risk of retroperitoneal bleeding.

10 ARTERIAL CATHETERIZATION

133

Lateral cord Medial cord Axillary artery

Musculocutaneous nerve Median nerve Ulnar nerve Brachial artery

Medial cutaneous nerve of forearm

C5 C6 C7 C8 T1 Inferior trunk Middle trunk Superior trunk

Radial artery

B

Lateral cord Posterior cord Medial cord

Median nerve Ulnar nerve Ulnar artery

A

Musculocutaneous nerve

Median nerve Axillary artery

Ulnar nerve Brachial artery Biceps muscle

Median nerve Ulnar nerve

Figure 10–3 A and B, The axilla demonstrates the relationship between the axillary artery and the brachial plexus. C, When the brachial plexus is compressed during arterial cannulation, hand ischemia can result.

C

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● Repair Catheter removal will generally restore normal sensation to the hand. ● Prevention Positioning of the catheter and short duration of catheterization may minimize this complication.

SUMMARY In summary, arterial cannulation is a safe and effective means of perioperative monitoring and frequent blood sampling in critically ill patients. The radial artery is the preferred site of cannulation, but when it is unavailable, the femoral and axillary arteries have been demonstrated to be safe. The common complications of thrombosis and infection can be minimized by using small-gauge catheters, chlorhexidine preparation solutions, Seldinger technique for insertion, and early removal of cannulas to minimize the duration of catheterization.

REFERENCES 1. Scheer BV, Perel A, Pfeiffer UJ. Clinical Review: Complications and risk factors of peripheral arterial catheters used for hemodynamic monitoring in anesthesia and intensive care medicine. Crit Care 2002;6:198–204. 2. Frezza EE, Mezghebe H. Indications and complications of arterial catheter use in surgical or medical intensive care units: analysis of 4932 patients. Am Surg 1998;64:127– 131. 3. Davis FM. Radial artery cannulation: inﬂuence of catheter size and material on arterial occlusion. Anesth Intensive Care 1978;6:49–53. 4. Slogoff S, Keats AS, Arlund C. On the safety of radial artery cannulation. Anesthesiology 1983;59:42–47. 5. Beards SC, Doedens L, Jackson A, Lipman J. A comparison of arterial lines and insertion techniques in critically ill patients. Anaesthesia 1995;50:576.

6. Mangar D, Thrush DN, Connell GR, Downs JB. Direct or modiﬁed Seldinger guide wire–directed technique for arterial catheter insertion. Anesth Analg 1993;76(4):714– 717. 7. Kulkarni M, Elsner C, Ouellet D, Zeldin R. Heparinized saline versus normal saline in maintaining patency of the radial artery catheter. Can J Surg 1994;37:37–42. 8. Bedford RF, Ashford TP: Aspirin pretreatment prevents post-cannulation radial-artery thrombosis. Anesthesiology 1979;51:176–178. 9. Lorente L, Santacreu R, Martin MM, et al. Arterial catheter–related infection of 2,949 catheters. Crit Care 2006;10:R83 10. Mimoz O, Pierone L, Lawrence C, et al. Prospective, randomized trial of two antiseptic solutions for prevention of central venous or arterial catheter colonization and infection in intensive care unit patients. Crit Care Med 1996;24:1818–1823. 11. Stansby G, Smout J, Chalmers R, Lintott R. MRSAinfected pseudoaneurysms of the radial artery. Surgeon 2003;1:108–110. 12. Perez L, Jiminez G, Ruiz J. Pseudoaneurysm in the radial artery after catheterization. Rev Esp Anestesiol Reanim 2006;53:119–121. 13. Ganchi PA, Wilhelmi BJ, Fujita K, Lee WP. Ruptured pseudoaneurysm complicating an infected radial artery catheter: case report and review of the literature. Ann Plast Surg 2001;46:647–650. 14. Valentine RJ, Modrall JG, Clagett GP. Hand ischemia after radial artery cannulation. J Am Coll Surg 2005;201: 18–22. 15. Muralidhar K. Complication of femoral artery pressure monitoring. J Cardiothorac Vasc Anesth 1998;12:128– 129. 16. Maki DG, Hassemar C. Endemic rate of ﬂuid contamination and related septicemia in arterial pressure monitoring. Am J Med 1981;70:733–738. 17. Brown M, Gordon LH, Brown OW, Brown EM. Intravascular monitoring via the axillary artery. Anaesth Intensive Care 1985;13:38–40.

11

Chest Tube Insertion Aarti Mathur, MD and Stephen R. T. Evans, MD INTRODUCTION Drainage of the pleural space by means of tube thoracostomy is a common procedure performed for a variety of well-established indications. Although chest tube insertion is considered a simple procedure by experienced physicians, morbidity rates as high as 36% have been reported.1,2 Factors associated with a higher complication rate include technique of insertion, emergent placement of chest tube, operator performing the procedure, and the length of time that the tube is in place.2,3 In addition, increased severity of injury correlates with a higher complication rate, although the mechanism of chest injury, blunt versus penetrating, does not.2

INDICATIONS 1,4 A chest tube essentially functions to remove air, ﬂuid, or pus from the intrathoracic space.

Place a gloved ﬁnger into the incision and sweep 360° Step 8 Advance a proximally clamped thoracostomy tube and direct it in the desired direction Step 9 Connect the end of the thoracostomy tube to an underwater-seal apparatus Step 10 Suture the tube in place and apply a dressing Step 11 Obtain a chest x-ray Step 7

OPERATIVE PROCEDURE Patient Positioning The ideal position for chest tube insertion is supine on a bed, slightly rotated, with the arm on the side of the lesion behind the patient’s head to expose the axillary area. This positioning exposes the “safe triangle” and reduces the risk of injuring underlying muscle and breast tissue.5

Choose Drain Insertion Site ● ● ● ● ● ●

Pneumothorax Tension pneumothorax Hemothorax Penetrating chest injury Drainage of malignant pleural effusion Parapneumonic effusions: simple or complicated with empyema ● Pleurodesis for intractable symptomatic effusions ● Chylothorax ● Bronchopleural ﬁstula

OPERATIVE STEPS Step 1 Step 2

Step 3 Step 4 Step 5 Step 6

Position the patient Choose the drain insertion site—nipple level (ﬁfth intercostal space) just anterior to the midaxillary line Prepare and drape the chest using sterile technique at the chosen site of insertions Anesthetize the skin and periosteum Skin incision and blunt dissection through subcutaneous tissue down to the rib Puncture the parietal pleura just above the rib

Diaphragmatic Perforation ● Consequence Placement of a chest tube outside of the thoracic cavity or a diaphragmatic injury will result in an iatrogenic pneumothorax, an unresolved pneumothorax, or a tension pneumothorax.6,7 Placement of the chest tube through or below the diaphragm will cause the tube to become lodged in the abdominal cavity, and the pulmonary pathology initially requiring the tube will persist. The consequences, repair, and prevention of intra-abdominal placement of a tube are discussed later. Grade 1/2 complication ● Repair A second chest tube must be placed into the pleural space and the initial tube removed. The diaphragm does not need to be repaired as long as a functional chest tube is present on that side. ● Prevention Insertion should be in the safe triangle bordered by the anterior border of the latissimus dorsi, the lateral

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Cupula (dome) of pleura

Apex of lung

Spleen Diaphragm

Liver Stomach Pancreas

Figure 11–1 During full expiration, the diaphragm rises to the ﬁfth rib/fourth intercostal space. Therefore, identifying a site in the fourth intercostal space helps to avoid diaphragmatic and abdominal cavity penetration.

border of the pectoralis major muscle, a line superior to the horizontal level of the nipple, and an apex below the axilla.5 During full expiration, the diaphragm rises to the ﬁfth rib/fourth intercostal space (Fig. 11–1). Identifying a site in the fourth intercostal space midaxillary line helps to avoid diaphragmatic and abdominal cavity penetration. The highest rib space in the axilla adjacent to the nipple is usually the fourth or ﬁfth, or alternatively, the rib spaces may be counted down from the second rib at the sternomanubrial joint (Fig. 11–2; see also Fig. 11–1).8

Aseptic Technique/Surgical Preparation and Draping Wound Site Infection ● Consequence Infection of the wound site results in cellulitis, leukocytosis, and an increased risk of developing an empyema or necrotizing soft tissue infection. Necrotizing soft tissue infection typically presents with wound pain; crepitus; foul, watery wound discharge; skin blistering; and rapid progression to septic shock 3 to 5 days after insertion of a chest tube.9 A chest tube placed for an empyema is associated with an increased risk of developing a necrotizing chest wall infection. Grade 2/3 complication ● Repair A simple wound site infection typically consists of Staphylococcus aureus and responds to antibiotics. Necrotizing soft tissue infections are highly lethal and require aggressive surgical débridement and high-

dose antibiotics. Reconstructive surgery may eventually be required. ● Prevention A large area of skin cleansing using iodine or chlorhexidine should be undertaken.5 Prophylactic antibiotics do not reduce the incidence of wound infections in routine chest tube placement and are, therefore, not indicated.10,11 However, they may be considered in the setting of penetrating trauma. The wound site should be examined daily.

Thoracic Empyema ● Consequence An empyema may cause respiratory compromise/ failure. The incidence of this complication reported in the literature varies widely from 1% to 25%.12 The true source and route of infection may be difﬁcult to determine; however, the rate of empyema is higher when a pleural effusion is present prior to tube insertion.12 Grade 2/3 complication ● Repair An empyema can be drained via closed tube thoracostomy and treated with intravenous antibiotics. However, if it continues to persist, a thoracotomy and decortication will be required. ● Prevention Although tube thoracostomy may lead to infectious complications by providing an entrance for contamina-

11 CHEST TUBE INSERTION

137

B

C

Figure 11–2 During inspiration, the diaphragm lies several rib spaces lower.

A

tion, the true route and source of infection for development of an empyema are difﬁcult to determine.12 The best way to prevent empyema is by use of the aseptic technique. Prophylactic antibiotics have not been shown to reduce the incidence and, therefore, are not recommended for routine use of chest tube placement.10,11,13

Anesthesia/Analgesia14 Lack of Appropriate Analgesia ● Consequence Lack of appropriate analgesia creates a mobile patient, which increases the difﬁculty of the procedure. This

increases the likelihood of most of the complications discussed in this chapter. Grade 1 complication ● Repair If the patient is experiencing pain causing her or him to move, the procedure should be placed on hold until adequate analgesia or sedation is administered. ● Prevention Providing the patient with adequate analgesia aids in ease of performing the procedure. It has been recommended to use about 10 to 20 ml of lidocaine to ﬁrst create a dermal bleb and then to direct the needle perpendicular to the skin to inﬁltrate the muscles of the

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chest wall. This includes the intercostal muscles, down to the rib, injecting around the periosteum of the rib. The needle is then angled above the rib until air is aspirated. The remaining 5 ml can be injected into the pleural space.

Incision and Blunt Dissection Damage to Intercostal Artery or Vein ● Consequence Damage to an intercostal vessel may cause an iatrogenic hemothorax. In rare instances, it may result in an arteriovenous ﬁstula either between an intercostal artery and a subcutaneous vein or from an internal thoracic artery draining into a lobar pulmonary artery.15 The clinical manifestations of a ﬁstula may be immediate or delayed. Grade 2/3 complication

Intercostal v. Intercostal a. Intercostal n.

Kelly clamp parallel to body

● Repair The hemothorax is best treated by adequate pleural drainage with the chest tube; however, if it is massive, a thoracotomy may be required. Treatment of arteriovenous ﬁstulas is based on clinical symptoms, and options range from surgical removal of the ﬁstula to transcatheter embolization.15 ● Prevention A transverse incision is made parallel to and along the upper border of the rib below the intercostal space to be used. The size of the incision should be slightly larger than the operator’s ﬁnger and the tube. Blunt dissection using a Kelly clamp is carried out until the surface of the rib is encountered. A drain track is then created cranially using a Kelly clamp and blunt ﬁnger dissection so that it is directed over the top of the rib. This avoids the intercostal vessels lying below each rib.1 Excessive bleeding during insertion of a chest tube should raise the possibility of development of a ﬁstula.15

Figure 11–3 The Kelly clamp should be directed immediately above the rib to avoid injury to the intercostal neurovascular bundle.

Damage to the Intercostal Nerve16

Lung Laceration

● Consequence Neuritis/neuralgia from intercostal nerve damage can present with pain, numbness, tingling, and muscle atrophy. Grade 1 complication

● Consequence A lung laceration may manifest in several different ways including bleeding; development of a new, iatrogenic, or unresolving persistent pneumothorax; and in severe cases, a bronchopleural ﬁstula (BPF) or bronchocutaneous ﬁstula.17,18 A BPF typically presents with suddenonset dyspnea, hypotension, subcutaneous emphysema, and cough with expectoration of purulent ﬂuid. Although rare, BPF presents a challenging management problem and is associated with high morbidity and mortality.17 A bronchocutaneous ﬁstula slowly develops after a chest tube has been in place for a longer period of time and is diagnosed with radiography after that tube is removed. Grade 3/4 complication

● Repair The mainstay in treatment is analgesia, physiotherapy, and occasionally, topical capsaicin. ● Prevention The intercostal nerve runs with the artery and vein below each rib. Thus, in attempting to prevent injury to the vessels, the nerve will be preserved as well (Fig. 11–3).

Fingersweep

11 CHEST TUBE INSERTION

139

Lung

Adhesions from lung to chest wall

Gloved hand is left of nipple

Diaphragm

Figure 11–4 A ﬁngersweep is performed by rotating a ﬁnger 360 degrees inside the pleural cavity to break down any pleural adhesions to avoid lung laceration, pneumothorax, bronchocutaneous ﬁstula, and bleeding.

● Repair Pneumothorax, bronchocutaneous ﬁstula, and bleeding will require tube thoracostomy drainage. A thoracotomy is indicated for massive hemothorax. Initial management of a patient with a BPF includes continued chest drainage and positioning of the patient on his or her side, with the side of the BPF being down. Long-term management involves various procedures including bronchoscopy with different glues, coils, and sealants.17 ● Prevention The thoracic cavity is entered using the clamp immediately above the rib. Excessive force is not necessary and may cause a lung laceration. Once the cavity is punctured, the clamps should be spread open widely to allow insertion of a ﬁnger and the tube. A ﬁnger is then inserted and rotated around 360°. This allows breakdown of any pleural adhesions that may position the lung against the chest wall and make it prone to injury (Fig. 11–4).8

Intra-Abdominal Placement ● Consequence Intra-abdominal placement of a chest tube has a wide variety of sequelae ranging from laceration of the spleen or liver, resulting in bleeding, to avulsion injury or perforation of stomach or colon, resulting in

peritonitis.7 In addition, the primary pulmonary pathology requiring the tube remains untreated.8 Grade 3/4 complication ● Repair Intra-abdominal placement can be conﬁrmed by a plain ﬁlm. Another chest tube must be placed in the chest, the intra-abdominal tube should be removed, and the patient should be closely monitored. In the case of a liver or splenic laceration, serial hematocrits and followup imaging should be obtained to ensure cessation of bleeding. Peritonitis may result from perforated viscus. Hemodynamic instability and peritonitis necessitate operative intervention. ● Prevention Initial choice of an appropriate drain site is critical to prevent intra-abdominal placement, as described earlier. The ﬁngersweep conﬁrms placement into the thoracic cavity. The ﬁrst solid organ felt after a gloved ﬁnger is inserted should be the lung. The surface of the diaphragm may also be felt when the ﬁnger is rotated inferiorly to ensure placement into the thoracic cavity and evaluate for a diaphragmatic laceration.1,6 Although placement into the chest may be conﬁrmed, injury to intra-abdominal organs may also result from emergent chest tube placement in a patient with an unrecognized diaphragmatic hernia (Fig. 11–5).6

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Finger sweep below diaphragm

track into the pleural cavity until the last hole of the drain is inside of the cavity. The tube should slide in easily; if excessive force is required, the tube should be taken out and another attempt made to slide it in the pleural cavity opening.

Placement Too Far into Apex or Mediastinum

Figure 11–5 A ﬁngersweep will aid in detection of intraabdominal penetration and avoid incorrect placement of a chest tube.

Placement of Tube and Position of Tube Tip Placement into Subcutaneous Tissue8 ● Consequence Placement of a chest tube outside the thoracic cavity in the subcutaneous tissues will result in an unresolved pnemothorax or effusion. In addition, it may cause a tension pneumothorax because air has been allowed to enter the thoracic cavity from the initial puncture site. These complications may also be noted in a chest tube that has been placed inside the correct cavity when all of the holes of the tube are not inside the cavity. ● Repair Subcutaneous chest tube placement can be conﬁrmed by chest x-ray and/or worsening clinical symptoms. An intra-thoracic chest tube must be immediately placed. After conﬁrmation of correct placement of the second chest tube, the ﬁrst tube may be removed. ● Prevention The actual placement of the tube into the puncture site created by the Kelly clamp can often be difﬁcult and challenging. However, an appropriate-sized track and a large enough opening into the thoracic cavity will make this step of the procedure easier and reduce the risk of subcutaneous tissue placement. The blunt dissection should be minimal, creating a single track until the pleural cavity is punctured. A track that is too wide or has gone more superior than the puncture site may make it easier to miss the opening into the thoracic cavity. This can also occur if the entrance to the cavity is not wide enough. Once the thoracic cavity is punctured, the Kelly clamp should be widely opened to provide a large enough space to accommodate the chest tube and a clamp. Before the tube is inserted, it should be mounted on a clamp and passed along the

● Consequence A variety of complications have been reported from chest tubes that have been placed too far into the lung apex or that abut the mediastinum. The tube may abut major vascular structures such as the subclavian artery and cause an obstruction or even disruption.19,20 Direct injury to the artery is unlikely at the time of insertion; however, it may occur secondary to vessel erosion from direct contact with the tube over a period of time. Rarer complications include brachial plexus compression causing pain, sudden death from vagus nerve irritation, extubation failure secondary to phrenic nerve injury, partial aortic obstruction, contralateral pneumothorax, and esophageal perforation.19,21 Grade 3/4 complication ● Repair A chest radiograph should be obtained immediately after insertion, and any tube that is found to be in a dangerous position, too far into the apex, or abutting the mediastinum should be repositioned immediately. If profuse bleeding is noted from a chest tube, thoracotomy is indicated to determine the source and control the bleeding. Cessation of bleeding may be managed with careful repositioning of the chest tube and subsequent radiographic conﬁrmation. ● Prevention The tip of any intrathoracic tube should not rest in either the apex of the thorax or the mediastinum. The ﬁnal resting place of the tube is determined in part by the direction of the track it follows through the chest wall. If a drain is to lie anteriorly in the chest, the track should be developed in a slightly anterior direction. Typically, a chest tube is placed apically for a pneumothorax and basally for drainage of an effusion.5 Placement should not require excessive force. Because most chest tubes placed too far into the apex cause symptoms related to the duration of placement of the tube, the best way to prevent these complications is to check a chest ﬁlm immediately after the tube has been placed and to reposition any suspicious tube.

Placement Abutting Mediastinum ● Consequence If a chest tube is placed with excessive force, perforation of the left ventricle or right atrium may occur, resulting in cardiac tamponade.22,23 Cardiogenic shock

11 CHEST TUBE INSERTION and various arrhythmias, especially rapid atrial ﬁbrillation, may result if a tube abuts and irritates the mediastinum.24 Rarely, in patients who have had a previous coronary bypass, vein compression can produce myocardial ischemia.19 Rarely, the phrenic nerve may be injured where it runs over the mediastinum.19,25 Patients with cardiomegaly are at increased risk for these complications. Grade 3/4/5 complication ● Repair If the chest radiograph obtained after insertion of the chest tube shows the tube to abut the cardiac silhouette, the tube should be repositioned and placement conﬁrmed with x-ray. If cardiac tamponade or perforation is suspected, an echocardiogram may conﬁrm the diagnosis. However, operative intervention is necessary. ● Prevention Simple pneumothorax causes mediastinal shift toward the affected side, making the pericardium prone to laceration. Therefore, no excessive force should be used to place a chest tube. Placement of a chest tube ideally should be performed under electrocardiographic monitoring to assess for mediastinal irritation. If electrocardiographic changes are present during the procedure or if resistance is met while inserting the tube, it should be repositioned. In addition, a chest radiograph should be checked immediately after placement; if the tube appears to be abutting the mediastinum, it should be repositioned.

Drain Becomes Nonfunctional (Kink/Clot)7,19 ● Consequence A nonfunctional drain will result in an undrained effusion, hemothorax, unresolved pneumothorax, or in extreme instances, a tension pneumothorax. A tube typically becomes nonfunctional once it is ﬁlled with clot, debris, or lung tissue, which can result in infarction of lung tissue. Grade 3/4 complication ● Repair Once a nonfunctional drain is identiﬁed, a second drain needs to be placed and, after radiographic conﬁrmation of successful placement, the ﬁrst drain should be removed. ● Prevention Key to preventing clotting of a chest tube is to choose the appropriate drain size. Smaller drains tend to kink/ clot easier than larger drains, especially when used in the setting of trauma because of the high incidence of hemothorax.26 The major determinant to size selection is the ﬂow rate of either the air or the liquid that can

141

accommodated by the tube. The internal diameter (bore) of the tube and, less so, the tube length are the critical ﬂow determinants. Twenty percent of patients with chest trauma have accompanying hemothorax and pneumothorax. Therefore, given the potential need for evacuation of both air and blood, a large-bore (28– 36 Fr) chest tube is recommended. In hemodynamically stable, nonmechanically vented patients with primary or secondary spontaneous pneumothorax, a small-bore chest tube (16 or 22 Fr) may be placed. A mechanically vented patient with an iatrogenic pneumothorax or a patient who needs ﬂuid drained should have a tube greater than 28 Fr placed.13,27–29 The inadvertent occlusion of drains by normal patient positioning can be potentially life-threatening. Because the tubing is soft and elastic, it is predisposed to frequent bending and kinking, which if done at right angles, has the effect of clamping outﬂow. This can be minimized by frequent monitoring of the tube and appropriate taping. It has been suggested that ﬁtting a standard corrugated ventilator circuit over the drain can provide an outer support layer to stiffen the tubing.30 The drain may also be blocked with lung tissue. If a track is directed posteriorly, the drain can fall back to lie in the oblique ﬁssure where it may become blocked. Chest radiographs must be checked, and this blockage can be suspected in a patient who is clinically deteriorating with no chest tube output.

Secure Drain Pneumothorax or Effusion ● Consequence A pneumothorax or effusion may persist if the tube starts to come out of or fall out of the thoracic cavity, and in severe cases, a tension pneumothorax may result.19 Subcutaneous emphysema may be noted around the skin site. Grade 1/2 complication ● Repair A second chest tube needs to be placed for a nonfunctional chest drain in the setting of a persistent effusion, pneumothorax, or tension pneumothorax. ● Prevention Once a chest tube is placed, ensuring that the last hole of the drain is inside of the thoracic cavity, it should be appropriately sutured and a sterile dressing placed.

Complications of Chest Tube Insertion Reexpansion Pulmonary Edema31–33 This refers to a unilateral pulmonary edema that can rarely occur on either the ipsilateral or the contralateral side after evacuation of a pleural effusion or pneumothorax. This is

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a rare but serious complication that carries a mortality rate as high as 20%. Although the pathophysiology remains obscure, both mechanical and inﬂammatory processes are believed to contribute to its development. The risk of developing reexpansion pulmonary edema is associated with duration and severity of lung collapse and the rate of reexpansion.

REFERENCES 1. Millikan JS, Moore EE, Steiner E. Complications of tube thoracostomy for acute trauma. Am J Surg 1980;140:738–741. 2. Etoch SW, Bar-Natan MF, Miller FB, Richardson JD. Tube thoracostomy. Factors relating to complications. Arch Surg 1995;130:521–525. 3. Resnick DK. Delayed pulmonary perforation: a rare complication of tube thoracostomy. Chest 1993;103:311– 313. 4. Miller KS, Sahn SA. Chest tubes: indications, technique, management and complications. Chest 1987;91:258–264. 5. Laws D, Neville E, Duffy J. BTS guidelines for the insertion of a chest drain. Thorax 2003;58(suppl II):ii53– ii59. 6. Hyde J. Reducing morbidity from chest drains. BMJ 1997;314:914–915. 7. Bailey RC. Complications of tube thoracostomy in trauma. Emerg Med J 2000;17:111–114. 8. Advanced Trauma Life Support Team Manual. Chest trauma management. In American College of Surgeons Advanced Trauma Life Support for Doctors, 7th ed. Chicago: First Impression, 2004; p 125. 9. Urschel JD, Takita H, Antkowiak JG. Necrotizing soft tissue infections of the chest wall. Ann Thorac Surg 1997; 64:276–279. 10. Luchette FA, Barrie PS, Oswanksi MF, et al. Practice management guidelines for prophylactic antibiotic use in tube thoracostomy for traumatic hemothorax: the EAST Practice Management Guidelines Work Group. J Trauma 2000;48:753–757. 11. Wilson RF, Nichols RL. The EAST practice management guidelines for prophylactic antibiotic use in tube thoracostomy for traumatic hemothorax: a commentary. J Trauma 2000;48:758–759. 12. Chan L, Reilly KM, Henderson C. Complication rates of tube thoracostomy. Am J Emerg Med 1997;15:368–370. 13. Baumann MH. What size chest tube? What drainage system is ideal? And other chest tube management questions. Curr Opin Pulm Med 2003;9:276–281. 14. Luketich JD, Kiss MD, Hershey J, et al. Chest tube insertion: a prospective evaluation of pain management. Clin J Pain 1998;14:152–154. 15. Coulter TD, Maurer JR, Miller MT, Mehta AC. Chest wall arteriovenous ﬁstula: an unusual complication after chest tube placement. Ann Thorac Surg 1999;67:849– 850.

16. Verdigo RJ, Cea JG, Campero M, Castillo JL. Pain and temperature. In Goetz CG, Pappert EJ (eds): Textbook of Clinical Neurology, 2nd ed. Philadelphia: Saunders, 2003; p 351. 17. Lois M, Noppen M. Bronchopleural ﬁstulas: an overview of the problem with special focus on endoscopic management. Chest 2005;128:3955–3965. 18. John S, Jacob S, Piskonowski T. Bronchocutaneous ﬁstula after chest-tube placement: a rare complication of tube thoracostomy. Heart Lung 2005;34:279–281. 19. Taub PJ, Lajam F, Kim U. Erosion into the subclavian artery by a chest tube. J Trauma 1999;47:972–979. 20. Moskal TL, Liscum KR, Mattox KL. Subclavian artery obstruction by tube thoracostomy. J Trauma 1997;43: 368–369. 21. Shapira OM, Aldea GS, Kupferschmid J, Shemin RJ. Delayed perforation of the esophagus by a closed thoracostomy tube. Chest 1993;104:1897–1898. 22. Abad C, Padron A. Accidental perforation of the left ventricle with a chest drainage tube. Tex Heart Inst J 2002;29:143. 23. Hesselink DA, Van Der Klooster JM, Bac EH, et al. Cardiac tamponade secondary to chest tube placement. Eur J Emerg Med 2001;8:237–239. 24. Barak M, Iaroshevski D, Ziser A. Rapid atrial ﬁbrillation following tube thoracostomy insertion. Eur J Cardiothorac Surg 2003;24:461–462. 25. Williams O, Greenough A, Mustafa N, et al. Extubation failure due to phrenic nerve injury. Arch Dis Child Fetal Neonatal Ed 2003;88:72–73. 26. Collop NA, Kim S, Sahn S. Analysis of tube thoracostomy performed by pulmonologists at a teaching hospital. Chest 1997;112:709–713. 27. Baumann MH, Strange C, Heffner JE, et al. Management of spontaneous pneumothorax. An American College of Chest Physicians Delphi consensus statement. Chest 2001; 119:590–602. 28. Antony VB, Loddenkemper R, Astoul P, et al. Management of malignant pleural effusions. Am J Respir Crit Care Med 2000;162:1987–2001. 29. Colice GL, Curtis A, Deslaurier B, et al. Medical and surgical treatment of parapneumonic effusions. An evidence-based guideline. Chest 2000;118:1158– 1171. 30. Konstantakos AK. A simple and effective method of preventing inadvertent occlusion of chest tube drains: the corrugated tubing splint. Ann Thorac Surg 2005;79:107– 111. 31. Gordon AH, Grant GP, Kaul SK. Reexpansion pulmonary edema after resolution of tension pneumothorax in the contralateral lung of a previously lung injured patient. J Clin Anesth 2004;16:289–292. 32. Sherman SC. Reexpansion pulmonary edema: a case report and review of the current literature. J Emerg Med 2003; 24:23–27. 33. Mahfood S, Hix WR, Aaron BL, et al. Reexpansion pulmonary edema. Ann Thorac Surg 1988;45:340– 345.

12

Paracentesis Stacy Loeb, MD and Stephen R. T. Evans, MD INTRODUCTION

OPERATIVE PROCEDURE

A myriad of clinical conditions can lead to the development of ascites. Abdominal paracentesis is both diagnostic and therapeutic and can aid in the differential diagnosis. Although in the United States, the majority of cases are now caused by alcoholic liver disease, other common causes include infection, malignancy, congestive heart failure, and nephrotic syndrome. Paracentesis allows the peritoneal ﬂuid to be sent for analysis. The ﬂuid is considered sterile if there are fewer than 250 polymorphonuclear leukocytes/mm3.1 For patients with new-onset ascites, a useful calculation is the serum–ascites albumin gradient (SAAG), which can help distinguish between some of the more common etiogies.2 Paracentesis can also be useful to evaluate a patient with known ascites for the development of spontaneous bacterial peritonitis. Not only is paracentesis a critical diagnostic tool, but it also provides therapeutic beneﬁt. Ascites can cause sequelae ranging from early satiety, abdominal pain, fullness, and umbilical hernias to shortness of breath and adverse effects on cardiovascular function.3,4 Paracentesis has been shown to remove ascitic ﬂuid more rapidly than diuretics,5 thus providing symptomatic relief for the patient.

The patient should be encouraged to empty the bladder before paracentesis. It is also useful to document baseline vital signs, serum chemistries, and complete blood count prior to the procedure. Paracentesis is most commonly performed with the patient in a supine position. Strict adherence to sterile technique should be exercised when draping and preparing the abdominal area. The abdomen should be inspected and percussed for an appropriate entry site. In addition, many institutions, including our own, use ultrasound routinely for localization. Local anesthesia (such as lidocaine) is then administered to the skin and subcutaneous tissues. Depending upon physician preference, patient characteristics such as abdominal girth and the volume of ascites present, a variety of different needles, catheters, or kits may be used to withdraw the ﬂuid. Drainage can take up to several hours. Once the drainage begins to taper off, the abdominal position may be slightly shifted to facilitate the drainage of any residual areas. When the aspiration is complete, the needle or catheter can be removed, and sterile 4 × 4 dressings taped securely over the area. Blood pressure, heart rate, serum chemistries (with particular attention to sodium and creatinine), and complete blood count (to monitor the hematocrit) should be obtained after the procedure.

INDICATIONS Abdominal ascites ● Diagnostic ● Therapeutic

OPERATIVE STEPS Step Step Step Step Step Step

1 2 3 4 5 6

Prep and drape in supine position Inspect for entry site Inject local anesthetic agent Use appropriate needle/kit to withdraw ﬂuid Remove needle and apply sterile dressing Monitor vital signs and labs following the procedure

Failed Attempt to Localize Ascitic Fluid ● Consequence If a needle is placed into the abdomen and no ascitic ﬂuid can be withdrawn, the patient is subject to the morbidity of a needle stick without any of the diagnostic or therapeutic beneﬁt. Furthermore, the patient may then need a second procedure. Grade 1 complication ● Prevention Some authors recommend using a needle insertion site in the midline,1 whereas others advocate a left lower quadrant insertion site.4,6 Paracentesis has also been successfully performed via a right lower quadrant or infraumbilical insertion site. Regardless, percussion should be utilized to help select the most appropriate

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Bowel with adhesions Umbilical hernia

Surgical scar Neurogenic full bladder

Figure 12–1 Anatomical obstacles/areas to avoid during paracentesis.

site. If it is difﬁcult to localize the area of dullness with percussion, ultrasound should be employed to help guide the site selection. In modern intensive care units and surgical ﬂoors, the liberal use and wide availability of ultrasound should facilitate its routine use in this setting as well. Another suggestion for difﬁcult cases is to reposition the patient. Although paracentesis is traditionally performed with the patient lying semirecumbent, a handknee position may be used instead.7 If the patient is unable to maintain this position, he or she can be positioned prone between two beds with the physician performing the tap from the ﬂoor beneath.

Failure due to Inappropriate Needle Selection ● Consequence Attempts to perform paracentesis may not be successful owing to improper needle selection. Based upon the body habitus or the quantity of ﬂuid to be removed, the likelihood of success may depend upon the equipment used. With a small-gauge needle, the potential for complications is minimized. Conversely, larger needles permit faster drainage but increase the risk of complications. Thus, these risks and beneﬁts should be carefully weighed. Grade 1 complication ● Prevention A variety of metal needles have been used to perform routine paracentesis, typically ranging in size from 16 to 22 gauge.1,4 Although in an average-sized patient, a 1.5-inch (3.8-cm) needle is generally sufﬁcient, for obese patients, a 3.5-inch (8.9-cm) needle may be necessary to successfully penetrate the pannus. For largevolume paracentesis, other options include multiple-hole

blunt cannulas with sharp removable inner trocars8 or a 10-Fr Teﬂon peritoneal dialysis catheter, which can be connected to a Foley bag and drained to gravity.6

Distorted Anatomy Leading to Perforation of Adjacent Organ ● Consequence The bowel, bladder, and pregnant uterus are the anatomic obstacles most commonly encountered when performing paracentesis (Fig. 12–1). Whereas under normal circumstances, the intestine tends to ﬂoat away from the advancing paracentesis needle, the presence of adhesions or other anatomic impediments can prevent this from occurring. The bladder is more likely to be breached in cases of neurogenic bladder or other causes of distention. An abnormal position of abdominal structures could lead to a failed attempt to localize ﬂuid or a more difﬁcult needle placement. It could also lead the operator to inadvertently traverse adjacent organs or structures, potentially leading to further complications. In one large series of diagnostic paracenteses, two bowel perforations were reported.9 Grade 1–5 complication ● Repair Possible need for laparotomy/surgical repair. ● Prevention Before paracentesis is performed, the abdomen should be inspected for any surgical scars, and if possible, the needle should be introduced away from such areas.10 In cases in which complicated anatomy is suspected or in pregnant patients, ultrasound should be used to guide the paracentesis. For neurogenic bladder, catheterization can be performed to empty the bladder prior to the paracentesis.

12 PARACENTESIS

Infection The association between paracentesis and an increased risk of infection is controversial. In a randomized, controlled trial, Runyon and coworkers11 compared the levels of complement and opsonic activity between patients undergoing medical diuretic therapy and those receiving daily therapeutic paracentesis. Serum levels of complement C3 and C4 were stable in the paracentesis group, whereas both serum and ascitic ﬂuid levels of C3 signiﬁcantly increased after diuretic management. Overall, opsonic activity was unchanged by paracentesis, but it increased with diuretics (presumably through the effects of ﬂuid concentration). Although the lack of increase in opsonic activity theoretically could increase the risk of infection after paracentesis compared with diuretics alone, there was no difference in the incidence of spontaneous bacterial peritonitis between the two groups in this or other studies. In a separate study, Runyon1 compared the frequency of infected ﬂuid aspirate between initial and repeat paracenteses during a patient’s hospital stay and found no difference in the presence of infected ascites in repeat paracenteses. Thus, the author concluded that paracentesis does not lead to an increased risk of peritonitis. ● Consequence/Prevention No evidence exists that paracentesis considerably increases the risk of peritonitis in patients with ascites. Moreover, the presence of suspected spontaneous bacterial peritonitis should not be considered a contraindication to paracentesis. In fact, paracentesis is highly useful in the setting of infection to enable both susceptibility testing and the use of culture-speciﬁc antibiotics. Grade 1 complication

Bleeding Because alcoholic liver disease is the most common etiology of ascites, many of the patients undergoing paracentesis are coagulopathic. Several studies have evaluated the safety and risk of bleeding complications in this population. Among 242 diagnostic paracenteses performed in patients with liver disease, Mallory and associates9 reported 4 hemorrhagic complications. Overall, most paracentesis series report the incidence to be less than 1% to 2%. The risk of bleeding does not completely subside after the immediate postparacentesis period. There are also case reports of delayed hemoperitoneum after large-volume paracentesis in patients with liver disease.12 ● Consequence Although in the majority of cases, bleeding from paracentesis does not lead to any major long-term sequelae, nevertheless, severe hemorrhage leading to death has been reported.13 Grade 1–5 complication

145

● Repair Attempts should be made to stabilize the patient with ﬂuid resuscitation and blood products. However, if these measures fail, laparotomy may be necessary, with control of the bleeding vessels. Nonetheless, the source of bleeding may not be found intraoperatively, and the surgery itself could lead to further decompensation in these patients. Therefore, the selection of therapy should be guided by the speciﬁc clinical situation. ● Prevention Some authors have recommended the use of prophylactic blood products for patients with coagulopathies prior to undergoing paracentesis. However, McVay and colleagues14 found that even in patients with mild to moderate coagulopathies, the frequency of serious bleeding complications was extremely low, and they concluded that the use of prophylactic transfusions is not warranted. In their study, the only subgroup with a signiﬁcantly greater risk of bleeding were patients with a markedly elevated serum creatinine. In addition, if abdominal veins are engorged secondary to the alcoholic liver disease, such areas should be avoided, and ultrasound guidance is advisable. We conclude that prophylactic transfusions are unwarranted, because bleeding complications are so infrequent even in the presence of coagulopathy.

Fluid and Electrolyte Imbalance In patients undergoing large-volume paracentesis (>5 L), some reports have suggested a risk of triggering an acute reduction in intravascular volume or electrolyte abnormalities. ● Consequence In 18 patients undergoing large-volume paracentesis, Kao and coworkers15 found no signiﬁcant difference in pre- and postprocedure sodium, blood urea nitrogen, hematocrit, or postural systolic blood pressure.15 Pinto and associates4 measured plasma volume using a dilution method involving 125I-labeled human serum albumin in 12 patients undergoing large-volume paracentesis. They did not ﬁnd any difference in the mean plasma volume, serum sodium, creatinine, or blood urea nitrogen at 24 and 48 hours after the procedure as compared with preparacentesis levels. Nevertheless, in large hepatology services, overaggressive paracentesis has led to severe hypotension and death (personal communication, 2007). Grade 1–5 complication ● Repair Aggressive ﬂuid resuscitation; monitor and replete electrolytes.

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● Prevention Simple steps for prevention are to establish a good ﬂuid and electrolyte balance prior to performing the paracentesis. Furthermore, the paracentesis should be limited to removing enough ﬂuid for symptomatic relief and diagnostic purposes, without being overzealous. Albumin may also be useful with paracentesis in some cases, taking into account factors such as the presence or absence of peripheral edema and the volume of ﬂuid removed.6

Ascitic Fluid Leak In a series of 52 patients undergoing 73 large-volume paracenteses, Wilcox and colleagues6 reported that the most common complication was ascitic ﬂuid leak in 5 procedures (7%). In all cases, the leak was self-limited. Nevertheless, in 2 patients the drainage persisted for a few days. ● Consequence All cases of ascitic ﬂuid leak in the literature have been self-limited. Grade 1 complication ● Repair Although in most paracenteses, a sterile 4 × 4 dressing is sufﬁcient to cover the puncture site, in the presence of a leak, additional dressings may be needed. Wilcox and colleagues6 recommended placing an ostomy bag over the site until the drainage ceases. ● Prevention It is possible that the use of peritoneal dialysis catheters led to the increased rate of ascitic ﬂuid leakage in the series of Wilcox and colleagues6 and that there is less risk with smaller-bore needles. However, it is also possible that other authors simply did not report this as a complication. Another suggestion for prevention is to position the patient opposite to the paracentesis site for a period of time after the procedure.6

Other Complications In a prospective series of 229 abdominal paracenteses performed on 125 patients, Runyon1 reported 1 abdominal wall hematoma requiring transfusion and 2 that did not require transfusion. Additional morbidities that have been reported in association with paracentesis include scrotal edema (grade 1) and retained catheter fragments left in abdomen9 (grade 2).

CONCLUSIONS/CLINICAL PEARLS ● Use sterile technique. ● Include routine use of ultrasound for localization.

● Make careful needle selection. ● Avoid anatomic obstacles (e.g., surgical scars, varices). ● Monitor ﬂuid and electrolyte status both before and

after the procedure.

REFERENCES 1. Runyon BA. Paracentesis of ascitic ﬂuid. A safe procedure. Arch Intern Med 1986;146:2259–2261. 2. Pare P, Talbot J, Hoefs JC. Serum-ascites albumin concentration gradient: a physiologic approach to the differential diagnosis of ascites. Gastroenterology 1983;85: 240–244. 3. Angueira CE, Kadakia SC. Effects of large-volume paracentesis on pulmonary function in patients with tense cirrhotic ascites. Hepatology 1994;20(4 pt 1):825–828. 4. Pinto PC, Amerian J, Reynolds TB. Large-volume paracentesis in nonedematous patients with tense ascites: its effect on intravascular volume. Hepatology 1988;8: 207–210. 5. Gines P, Arroyo V, Quintero E, et al. Comparison of paracentesis and diuretics in the treatment of cirrhotics with tense ascites. Results of a randomized study. Gastroenterology 1987;93:234–241. 6. Wilcox CM, Woods BL, Mixon HT. Prospective evaluation of a peritoneal dialysis catheter system for large volume paracentesis. Am J Gastroenterol 1992;87:1443– 1446. 7. Lawson JD, Weissbein AS. [The puddle sign; an aid in the diagnosis of minimal ascites.] N Engl J Med 1959;260: 652–654. 8. Shaheen NJ, Grimm IS. Comparison of the Caldwell needle/cannula with Angiocath needle in large volume paracentesis. Am J Gastroenterol 1996;91:1731–1733. 9. Mallory A, Schaefer JW. Complications of diagnostic paracentesis in patients with liver disease. JAMA 1978; 239:628–630. 10. Runyon BA. Patient selection is important in studying the impact of large-volume paracentesis on intravascular volume. Am J Gastroenterol 1997;92:371–373. 11. Runyon BA, Antillon MR, Montano AA. Effect of diuresis versus therapeutic paracentesis on ascitic ﬂuid opsonic activity and serum complement. Gastroenterology 1989; 97:158–162. 12. Martinet O, Reis ED, Mosimann F. Delayed hemoperitoneum following large-volume paracentesis in a patient with cirrhosis and ascites. Dig Dis Sci 2000;45:357– 358. 13. Pache I, Bilodeau M. Severe haemorrhage following abdominal paracentesis for ascites in patients with liver disease. Aliment Pharmacol Ther 2005;21:525–529. 14. McVay PA, Toy PT. Lack of increased bleeding after paracentesis and thoracentesis in patients with mild coagulation abnormalities. Transfusion 1991;31:164– 171. 15. Kao HW, Rakov NE, Savage E, Reynolds TB. The effect of large volume paracentesis on plasma volume—a cause of hypovolemia? Hepatology 1985;5:403–407.

Section III

GASTROINTESTINAL SURGERY Stephen R. T. Evans, MD Reason and free inquiry are the only effectual agents against error. —Thomas Jefferson

STOMACH, DUODENUM AND SMALL BOWEL 13

Open Gastrostomy Feeding Tube Placement and Percutaneous Endoscopic Gastrostomy Tube Placement Rebecca Evangelista, MD and Eleanor Faherty, MD INTRODUCTION Gastric tube placement is a common procedure for the delivery of supplemental or total enteral nutrition and for drainage in cases of distal obstructing masses. A number of approaches are available depending on the patient’s previous surgical history, comorbidities, and reason for requiring tube placement. Open gastrostomy placement by Stamm and Janeway techniques as well as percutaneous endoscopic gastrostomy (PEG) tube placement are

addressed in this chapter. Most retrospective studies have shown little or no statistical difference in the complication rates between these procedures. The most serious complication reported is tube dislodgement, with all other complications falling into the minor category.1 Reported overall complication rates range from 9% to 46%, in which a vast majority are minor complications.1–5 Most steps discussed in this chapter are related to reducing risk of tube dislodgement in the early and late postoperative periods and reduction in risk of visceral injury during each

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procedure. Choosing to perform a Janeway gastrostomy with gastric stoma maturation can be the best choice in those cases in which early tube dislodgement is more likely, in cases of signiﬁcant mental status changes, essentially avoiding all related and subsequent complications.

INDICATIONS ● ● ● ● ●

Functional dysphagia or other risks for aspiration Gastric outlet obstruction Distal obstructing masses Proximal obstructing masses Other poor nutritional states

Open Gastrostomy Tube Placement OPERATIVE STEPS OPEN STAMM GASTROSTOMY TUBE Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7 Step 8

Upper midline incision Mobilization of the stomach Placement of the pursestring suture in the anterior stomach Gastrostomy Placement of the gastrostomy tube into the stomach through the abdominal wall Suturing the anterior stomach to the peritoneum around the tube tract and insertion site Closure of the midline incision External suturing of the tube to the anterior abdominal wall

OPEN JANEWAY GASTROSTOMY TUBE Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7

Upper midline incision Mobilization of the stomach Creation of the gastric tube along the anterior stomach Creation of the tract through the anterior abdominal wall for the gastric tube Maturation of the gastric stoma Insertion of the gastrostomy tube through the stoma Closure of the midline incision

OPERATIVE PROCEDURE OPEN STAMM GASTROSTOMY Upper Laparotomy Intra-Abdominal Injuries with Midline Incision To obtain access to and adequate exposure of the stomach, an upper midline is the standard incision of choice for

an open gastrostomy tube placement. Occasionally, a left subcostal incision can be used. Complications related to laparotomy incisions are discussed in Section I, Chapter 7, Laparoscopic Surgery.

Mobilization of the Stomach and Lysis of Adhesions Bowel Perforation ● Consequence Leak from the injured stomach, small bowel, or transverse colon, leading to postoperative peritonitis. A minority of patients will have dense adhesions from previous surgery or a partially or completely intrathoracic stomach owing to paraesophageal hernia. The stomach will require adequate mobilization to allow the anterior portion along the greater curvature to approximate the anterior abdominal wall two ﬁngerbreadths below the left costal margin without undue tension. Grade 3/4 complication ● Repair Two-layer suture repair of all full-thickness injuries. Single-layer suture repair of all serosal tears. ● Prevention The position of the stomach must be fully visualized through an adequate fascial incision and any degree of herniation directly visualized. Sharp dissection should be used for lysis of adhesions and cautery avoided to reduce the risk of delayed thermal perforation.

Placement of the Pursestring Suture in the Anterior Stomach Inadequate Suture Thickness ● Consequence Tear of the gastric wall with pull-through of the suture. This can result in an immediate or delayed perforation in the stomach, allowing for potential leak if not repaired adequately. Suture that is visible through the serosal surface layer is too shallow, has a higher risk of tear, and should be replaced. Grade 3 complication ● Repair Two-layer repair and repositioning of the pursestring suture for a separate site of intended tube insertion. ● Prevention Sutures should be placed to a seromuscular thickness by fully pronating the wrist and driving the needle perpendicular with an almost immediate supination of the wrist. If a seromuscular placement cannot be ensured, a full-thickness bite is adequate.

13 GASTROSTOMY TUBE PLACEMENT

Gastrostomy in the Center of the Pursestring Injury to the Posterior Wall of the Stomach ● Consequence Immediate or delayed intra-abdominal leak through the posterior wall. Grade 3/4 complication ● Repair Two-layer suture repair from the posterior surface of the stomach requires exposure of the posterior stomach through a window into the lesser sac through the gastrocolic ligament. ● Prevention Retract the anterior stomach wall with atraumatic forceps or Babcocks while creating the gastrostomy. The gastrostomy can also be made by opening the individual layers of the gastric wall, sequentially retracting each subsequent deeper layer. Avoid prolonged application of the cautery and using pressure on the tip of the cautery to create tension while making the gastrostomy.

Placement of the Gastrostomy Tube into the Stomach through the Anterior Abdominal Wall Tube Damage/Inadequate Closure of Pursestring Sutures ● Consequence Immediate or delayed failure of the balloon to retain inﬂation. Immediate or delayed leak from or around the tube. An early consequence of deﬂation of a balloon, if used, is bleeding from the gastrotomy owing to lack of tamponade. Leak from the tube early through a hole in the tube can result in extravasation of tube contents into the abdomen or along the abdominal wall tract leading to peritonitis or localized fasciitis, respectively. Grade 1/2 complication ● Repair After passing the tube through the tract in the abdominal wall, test a balloon, if used, or ﬂush the tube with saline and look for a leak. A dilute solution of methylene blue can also be used if damage to the tube is suspected but unclear with saline ﬂush. ● Prevention After the tract in the anterior abdominal wall is made with a tonsil clamp use a broader Kelly clamp to pull the tube through the tract. Also clamp the entire tube rather than feeding the lumen of the tube onto one tine of the clamp to avoid damage to the tube as it is being pulled through the layers of the abdominal wall.

149

Suturing the Anterior Stomach to the Peritoneum around the Tube Tract and Insertion Site Tension and Tearing of Stomach around Gastrostomy Site/Loss of Tube Tract ● Consequence Leak around the tube insertion site. Slippage of stomach away from the anterior abdominal wall or tube from within the stomach. Early, this can lead to free intraabdominal leak of gastric contents and inability to replace the tube by ﬂuoroscopic guidance. Grade 3 complication ● Repair Fluoroscopic guidance to replace a slipped tube may be possible 3 to 5 days after placement. Seldinger technique can be used to identify the tract and determine whether access to the stomach is present. If access to the stomach cannot be veriﬁed, open exploration and replacement of the tube or repair of the original gastrotomy will be necessary. ● Prevention Place multiple interrupted sutures of nonabsorbable material around the tube site. Be sure that the sutures are placed seromuscular or full thickness in the stomach and obtain adequate purchase of each suture on the peritoneum. Ensure that the balloon is deﬂated during this step and inﬂated before closing the abdomen.

Closure of the Midline Incision Injury to Intra-Abdominal Structures/Dehiscence See Section I, Chapter 7, Laparoscopic Surgery.

External Suturing of the Tube to the Anterior Abdominal Wall Tube Dislodgement ● Consequence Slippage of stomach from the anterior abdominal wall with subsequent leak and loss of percutaneous access to the stomach. Grade 3 complication ● Repair See “Suturing the Anterior Stomach to the Peritoneum around the Tube Tract and Insertion Site,” earlier. Replace any sutures that have pulled through the skin or been inadvertently cut. ● Prevention Place several permanent interrupted sutures around the tube and/or external bumper to the skin. Air knots

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may keep the skin from necrosis, but skin sutures should be full thickness to avoid tearing through. Abdominal binders can also be placed for the ﬁrst week to minimize access to the tube before the tract becomes epithelialized.

OPEN JANEWAY GASTROSTOMY For upper midline incision and mobilization of the stomach, see “Open Stamm Gastrostomy,” earlier.

● Repair Lengthen the gastric tube to allow for tension-free passage and reduce torque through the abdominal wall. Enlarge the diameter of the fascial opening. ● Prevention Complete the creation of the gastric tube prior to making the tract through the abdominal wall to allow for more accurate placement of the tract. The tract should be straight through the abdominal wall up from the base of the gastric tube and should be at least 2 to 3 cm below the left costal margin.

Creation of the Gastric Tube along the Anterior Stomach Wall

Maturation of the Gastric Stoma

Inadequate Length or Width of Gastric Tube/Inadequate Blood Supply to Gastric Tube

● Consequence Leak of gastric or tube contents into abdominal wall owing to slippage of the gastric tube end below the skin surface. Inability to pass tube into the stomach. Grade 3 complication

● Consequence Inability to evert a stoma at the skin surface or undue tension on the gastric tube to evert the stoma. If the tube is not developed from the midanterior stomach toward the greater curvature, there may be too much tension on the gastric tube through the abdominal wall or poor blood supply along the staple line. Grade 1 complication ● Repair If the tube appears dusky or cannot deliver completely with 1 cm above the skin, a new tube needs to be created or extended toward the greater curvature. ● Prevention Start the creation of the gastric tube in the midportion of the anterior gastric wall and remain parallel to the greater curvature. Based on the thickness of the abdominal wall, estimate the length needed to ensure a 1-cm extension above the skin. Maintain a tube diameter of approximately 1.5 cm for the full length.

Creation of the Tract through the Anterior Abdominal Wall for the Gastric Tube Inadequate Position/Inadequate Diameter of Tract ● Consequence Inability to place a tube of adequate diameter through the gastric tube into the stomach, undue tension on the base of the gastric tube, or impingement of tube through too narrow a tract. Grade 3 complication

Inadequate Eversion of Gastric Tube

● Repair Increase the length of the gastric tube and resuture the circumference of the gastric tube. ● Prevention Place interrupted sutures from the gastric tube end, seromuscular through the gastric tube 1 cm deep to the end and ﬁnally through deep dermis. This will ensure complete eversion of the end of the gastric tube.

Insertion of the Gastrostomy Tube through the Stoma Inadequate Positioning below the Level of the Abdominal Wall ● Consequence Leak and inadequate nutrition delivery. Grade 2 complication ● Repair Release any balloon at the end of the tube, remove, and replace after lubricating the tip. A contrast study can be done if there is any question about complete tube advancement into the stomach below the level of the posterior fascia. ● Prevention A contrast study can be done if there is any question about complete tube advancement into the stomach below the level of the posterior fascia.

Closure of the Midline Incision See “Open Stamm Gastrostomy,” earlier.

13 GASTROSTOMY TUBE PLACEMENT

Percutaneous Gastrostomy Tube Placement OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7 Step 8

Insertion of endoscope through the esophagus into the stomach Insufﬂation of the stomach Identiﬁcation of the “one-to-one” position on the abdominal wall Percutaneous insertion of the angiocatheter into the stomach Endoscopic capture of the guidewire and removal Pull-through of PEG tube from the oral cavity into the stomach via guidewire Placement of external bumper and external anchoring suture Repeat endoscopy

OPERATIVE PROCEDURE Insertion of the Endoscope into the Stomach Perforation ● Consequence Anywhere along the path of the endoscope, a visceral tear and perforation can occur. Leak from an esophageal tear can be into the thorax or the abdomen depending on the location of the perforation. Perforation of the stomach is rare but possible. Although rare, it can be fatal.6 Grade 3/4 complication ● Repair If found early after endoscopy, exploration and repair of the perforation may be necessary by either open surgical repair or esophageal stent placement.7 If diagnosed late, many esophageal perforations can be treated with a course of total parenteral nutrition and nothing by mouth. ● Prevention Maintain the view of the lumen in the center of the scope at all times. Recognize the appearance of bright white, signifying the end of the scope up against the visceral wall. Use of small amounts of insufﬂation will also help open the lumen ahead of the scope, allowing for maintaining the proper view during scope advancement.

151

Insufﬂation of the Stomach Inadequate Distention of the Stomach ● Consequence Inability to ﬁnd the best one-to-one position and/ or pass the angiocatheter percutaneously into the stomach. Grade 1 complication ● Repair Close all nonworking ports and cover the insufﬂation button on the scope. Watch as the rugae of the stomach ﬂatten as an indicator of the proper amount of insufﬂation. Insufﬂate until the stomach grossly distends the anterior abdominal wall. If one-to-one position cannot be well deﬁned, convert to an open gastrostomy. ● Prevention Prior to the start of the endoscopy, ensure that all systems for the scope are in proper working order including the insufﬂation. Look over the head of the scope and ensure that all instrument ports are capped or closed while not in use.

Identiﬁcation of One-to-One Position on the Abdominal Wall Colonic or Small Bowel Injury/Placement of PEG Tube through Bowel ● Consequence Peritonitis from leak, sepsis, bowel obstruction. Grade 3 complication ● Repair Exploratory laparotomy and resection of involved bowel with possible temporary colostomy. ● Prevention Look for the one-to-one position where minimal compression on the anterior abdominal wall shows obvious depression of the stomach on endoscopy. In addition, transilluminating can show the end of the scope clearly through the anterior abdominal wall indicating minimal tissue between the scope and the skin and proper location for tube placement (Fig. 13–1).

Percutaneous Insertion of the Angiocatheter into the Stomach Laceration of Short Gastric Vessels/Injury to Bowel ● Consequence Ongoing intra-abdominal bleeding. Grade 2/3/4 complication

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Colon

Rib

Liver

Small intestine

A

Stomach

Endoscope Gastrostomy tube secured

Colon

Rib

Liver

Small intestine

C

Stomach

B

Figure 13–1 A, Poor “one-to-one” with a wide gastric indentation may indicate the presence of transverse colon, omentum, or small bowel between the abdominal wall and the anterior gastric wall. B, Example of poor one-to-one palpation with a wide gastric indentation (arrow). C, Example of percutaneous endoscopic gastrostomy (PEG) placement through intervening tissue if good oneto-one palpation is not identiﬁed.

● Repair Exploratory laparotomy and suture ligation of bleeding vessels.

guidewire. Laceration of the tongue will result in local pain and bleeding. Grade 1 complication

● Prevention Establish proper one-to-one position and do not go below two ﬁngerbreadths under the costal margin, increasing the risk of needle insertion at the greater curvature rather than on the anterior surface of the stomach. Do not attempt multiple passes of the angiocatheter. If good one-to-one position cannot be established or two passes of the angiocatheter are unsuccessful, convert the procedure to an open gastrostomy placement.

● Repair Repeat placement of the endoscope to locate the end of the guidewire to recapture. If the end is not seen or it is not possible to safely grasp the end within the esophagus, pull the wire back into the stomach under direct visualization, reinsufﬂate, and regrasp the guidewire. A tongue laceration from this step will very rarely require any speciﬁc treatment other than direct pressure and suctioning of the mouth until the bleeding ceases.

Endoscopic Capture of the Guidewire and Removal through the Mouth Loss of Guidewire/Laceration of Tongue ● Consequence Inability to attach and pull the PEG tube into place, requiring repeat endoscopy to locate the end of the

● Prevention When grasping the wire, be sure to allow sufﬁcient guidewire through the loop of the grasper. Assign a single person to maintain a tight grasp on the guidewire until it is retrieved from the grasper after pulling the entire scope and grasper from the mouth. To avoid tongue laceration, minimize the amount of movement of the guidewire after pulling through the mouth (Fig. 13–2).

13 GASTROSTOMY TUBE PLACEMENT

Figure 13–2 Grasp the guidewire well beyond the end to avoid loss of the wire during delivery through the esophagus and oropharynx.

Pull-through of the PEG Tube into the Stomach and through the Abdominal Wall via the Guidewire Laceration of Tongue/Loss of PEG from Guidewire For laceration of the tongue, see “Endoscopic Capture of the Guidewire and Removal through the Mouth,” earlier. ● Consequence Loss of the tract as the guidewire is pulled through the abdominal wall without the PEG tube. Grade 1 complication ● Repair Restart the procedure from Step 1, “Insertion of the Endoscope through the Esophagus into the Stomach.” ● Prevention Prior to pulling the PEG through the esophagus and stomach, ensure that the guidewire is securely attached to the PEG tube and manually guide them as a unit into the posterior oropharynx before pulling into the stomach and through the abdominal wall. Also ensure that the stab incision in the abdominal skin is long enough to accommodate the diameter of the PEG tube to avoid undue resistance while pulling through the abdominal wall.

153

Figure 13–3 Repeat endoscopy is done to ensure adequate approximation of the PEG button to the gastric wall and good hemostasis.

Placement of the External Bumper and the External Anchoring Suture Abdominal Wall Necrosis/Bleeding/Accidental Loss of PEG Tube ● Consequence Tight placement of the bumper can lead to abdominal wall abscess and/or necrotizing fasciitis around the tube site. Loose placement can allow for bleeding around the tube insertion site from the gastric mucosa. Grade 2/3 complication ● Repair Loosen the bumper at the bedside as soon as tight placement is recognized. Local wound care may be all that is necessary. However, with worsening necrosis, operative wide débridement may be necessary. If ongoing blood loss is suspected and a loose position is recognized, the bumper can be tightened at the bedside. Endoscopy can conﬁrm this problem and guide tightening to a point of tamponade. ● Prevention In most patients, the bumper position should be around 3 cm on the tube at the exit point from the abdominal wall. Repeating the endoscopy after tube securing can conﬁrm adequate tamponade.

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Repeat Endoscopy This is done primarily to ensure proper tension of the PEG tube on the gastric wall to promote hemostasis and evaluate for any injury (Fig. 13–3). See “Insertion of the Endoscope into the Stomach,” earlier.

4.

5.

REFERENCES 1. MacLean AA, Alverez NR, Davies JD, et al. Complications of percutaneous endoscopic and ﬂuoroscopic gastrostomy tube insertion procedures in 378 patients. Gastroenterol Nurs 2007;30:337–341. 2. Möller P, Lindberg CG, Zilling T. Gastrostomy by various techniques: evaluation of indications, outcome, and complications. Scand J Gastroenterol 1999;34:1050–1054. 3. Bankhead RR, Fisher CA, Rolandelli RH. Gastrostomy tube placement outcomes: comparison of surgical, endo-

6.

7.

scopic, and laparoscopic methods. Nutr Clin Pract 2005; 20:607–612. Hoffman MS, Cardosi RJ, Lemert R, Drake JG. Stamm gastrostomy for postoperative gastric decompression in gynecologic oncology patients. Gynecol Oncol 2001;82: 360–363. Rustom IK, Jebreel A, Tayyab M, et al. Percutaneous endoscopic, radiological and surgical gastrostomy tubes: a comparison study in head and neck cancer patients. J Laryngol Otol 2006;120:463–466. Freeman RK, Van Woerkom JM, Ascioti AJ. Esophageal stent placement for the treatment of iatrogenic intrathoracic esophageal perforation. Ann Thorac Surg 2007;83:2003–2007; discussion 2007–2008. Panos MZ, Reilly H, Moran A, et al. Percutaneous endoscopic gastrostomy in a general hospital: prospective evaluation of indications, outcome, and randomised comparison of two tube designs. Gut 1994;35:1551– 1556.

14

Open Jejunostomy Tube Placement Eleanor Faherty, MD and Rebecca Evangelista, MD INTRODUCTION

Step 5

Enteral nutrition is the preferred method of feeding patients who are unable to meet their caloric needs through the conventional oral route. Feeds are most commonly initiated via the stomach, but the jejunum is an acceptable alternative. Jejunal feeding tubes are often placed in patients who are at increased risk of aspiration of gastric contents. It is also an option when the stomach is not suitable for a gastrostomy tube because of previous surgery, distal obstruction, or disease. Jejunostomy tubes are also often placed during extensive enteric reconstructions in which delayed oral intake is anticipated. Such tubes provide distal access for enteral nutrition and help to avoid the need for parenteral nutrition and prolonged vascular access.1

Step 6 Step 7 Step 8

Placement of jejunostomy tube into jejunum through abdominal wall* Suturing of jejunal wall to anterior abdominal wall around tube insertion site Close midline incision External suturing of tube to anterior abdominal wall

OPERATIVE PROCEDURE Upper Midline Incision Intra-Abdominal Injuries with Midline Incision To obtain access and adequate exposure of the jejunum for an open jejunostomy tube placement, an upper midline incision is the standard choice. Care should be taken if the patient has had prior laparotomies and, thus, has resultant scar tissue. Complications related to laparotomy incisions are discussed in Section I, Chapter 7, Laparoscopic Surgery.

INDICATIONS ● ● ● ● ● ●

High risk for aspiration Gastric outlet obstruction Gastric dysmotility (i.e., gastroparesis) Previous gastric resection or gastric bypass Status after esophagogastrectomy Inability to place percutaneous endoscopic gastrostomy (PEG) tube ● Enteral access needed after extensive surgical procedure ● Long-term enteral access for chemotherapy patients2,3

OPERATIVE STEPS 2 Step 1 Step 2 Step 3 Step 4

Upper midline incision Identiﬁcation of the jejunum approximately 20 cm distal to ligament of Treitz Placement of pursestring suture in antimesenteric side of jejunum Jejunostomy

Identiﬁcation of the Jejunum Incorrect Identiﬁcation of the Ligament of Treitz If the ligament of Treitz is not identiﬁed or is incorrectly identiﬁed, the placement of the jejunostomy tube may not be in the correct location in the jejunum. Ideal placement is considered to be approximately 20 to 30 cm distal to the ligament of Treitz. ● Consequence Malabsorption may result if the tube is placed too distally. If the tube is too proximal, it is possible that enteral feeds could reﬂux via the duodenum into the stomach and possibly cause aspiration. Grade 2/3 complication

*Some surgeons add a step here to additionally secure tube via the Witzel technique. To do this, place seromuscular sutures on either side of feeding tube to wrap about 5 cm of tube proximally with jejunal wall. Potential pitfalls with this technique are intestinal obstruction owing to excessive imbrication of the bowel wall circumference.

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● Repair If incorrect placement of the tube is noticed intraoperatively, the tube may be removed and the jejunostomy closed primarily. If proximal or distal placement is suspected from clinical factors, a contrast study may be performed to conﬁrm tube location. If the study conﬁrms either proximal or distal placement and the patient is not tolerating enteral feeding, a new tube should be placed. ● Prevention Correct identiﬁcation of the ligament of Treitz will aid in proper tube placement. Locating the ligament is most easily accomplished by reﬂecting the transverse colon and omentum superiorly and following the transverse colon mesentery to its posterior origin. The ligament of Trietz should be visualized and palpated just to the left of midline in its posterior location.

Placement of the Pursestring Suture in the Antimesentric Jejunum Inadequate Suture Thickness ● Consequence Tear of the jejunal wall with pull through of the suture. This can result in an immediate or delayed fullthickness tear in the jejunal wall, allowing for potential leak. Grade 2/3 complication ● Repair Primary repair of any jejunal injury and repositioning of the pursestring suture for tube placement. ● Prevention Pursestring sutures should be anchored in the seromuscular layer of the jejunum for adequate strength. Sutures can be placed by fully pronating the wrist and driving the needle perpendicular to the tissue with an almost immediate supination of the wrist. Suture that is visible through the serosal surface is likely too shallow and has a higher risk of pulling through the tissue and, thus, should be replaced.

Jejunostomy in the Center of the Pursestring Suture

injury. Avoid prolonged application of the cautery or using signiﬁcant pressure on the tip of the cautery or knife when making the jejunostomy.

Mesenteric Hematoma if the Jejunostomy Is Made Too Close to the Mesentery ● Consequence Bowel ischemia at the associated small bowel, resulting in bowel necrosis and/or intra-abdominal leak. Grade 3 complication ● Repair If the hematoma is small and detected intraoperatively, direct pressure may be sufﬁcient or a small suture ligature to the mesentery may be needed. If the hematoma is large, or if there are signs of ischemia or stricture of the jejunum, a resection with primary anastomosis may be necessary. ● Prevention Careful placement of jejunostomy on the antimesenteric side of the jejunum.

Placement of the Jejunostomy Tube into the Jejunum through the Anterior Abdominal Wall Failure of the Pursestring to Secure the Jejunostomy Tube ● Consequence Tube dislodgement and possible intra-abdominal leak. Grade 2/3 complication ● Repair If recognized intraoperatively, a new pursestring suture may be placed to secure the tube. If recognition is delayed, a repeat laparotomy would be needed for jejunal repair and new tube placement. ● Prevention Ensure that the pursestring suture is placed in the seromuscular layer (see earlier). When tying the suture around the tube, maintain tension to avoid placement of an air knot.

Injury to the Posterior Wall of the Jejunum

Injury to the Epigastric Vessels

● Consequence Immediate or delayed leak through the posterior wall. Grade 3 complication

● Consequence Abdominal wall hematoma and, rarely, pseudoaneurysm of the epigastric artery. Grade 1/2/3 complication

● Repair Primary repair of the posterior wall injury. ● Prevention Retraction of the antimesenteric side of the jejunum with atraumatic forceps will help avoid a posterior wall

● Repair Evacuation of hematoma and oversewing of vessels if active bleeding is still apparent. Surgical excision of the pseudoaneurysm may be necessary to relieve pain at the site.

14 OPEN JEJUNOSTOMY TUBE PLACEMENT ● Prevention Knowledge of the normal and variant anatomy of the superior and inferior epigastric vessels is essential to avoiding injury. Placement of the jejunostomy tube at least 8 cm lateral to the midline should avoid vessel injury. Also direct visualization of the tube and instrument entry into the abdomen from the peritoneal side of the abdominal wall will allow identiﬁcation of the epigastric vessel course and avoidance of injury.

157

Closure of the Midline Incision See Section I, Chapter 7, Laparoscopic Surgery.

External Suturing of the Tube to the Anterior Abdominal Wall Tube not Adequately Secured to the External Abdominal Wall

Suturing of the Jejunal Wall to the Anterior Abdominal Wall around the Tube Insertion Site

● Consequence Tube dislodgement. Grade 2/3 complication

Inadequate Anchoring of the Jejunum to the Anterior Abdominal Wall Owing to a high risk of obstruction, most surgeons do not use tubes with distal balloons in the jejunum. The tubes are not routinely ﬁxed to the small bowel other than to secure the pursestring sutures. This differs from the procedure for gastrostomy tubes in that the anchoring sutures to the anterior abdominal wall are signiﬁcant in jejunostomy tube placement.

● Repair If this occurs early (<1 wk), an attempt may be made to replace the tube at same site with wire-guided ﬂuoroscopy. If the tube is dislodged after a week, it may be possible to replace the tube into epithelialized tract and to conﬁrm placement in the jejunum with a contrast study. If neither is possible, a repeat laparotomy will be needed for tube replacement.

● Consequence High tension from the jejunum pulling away from the anterior abdominal wall can result in tube dislodgement, loss of percutaneous access to the jejunostomy, and likely intra-abdominal leak. Grade 3 complication

● Prevention Use of a ﬁxation device is included with some commercially available feeding tubes, or adequate sutures to the skin covered by a dressing should assist in avoiding tube dislodgement.

● Repair Repeat laparotomy for primary repair of the jejunostomy site and new tube placement.

REFERENCES

● Prevention Seromuscular sutures in the jejunum should be placed on four sides of the jejunostomy tube insertion site to distribute any tension away from the tube. These sutures should then be securely tied (avoid air knots) to the internal side of the anterior abdominal wall to minimize jejunal mobility at the tube insertion site.

1. Kudsk KA. Clinical applications of enteral nutrition. Nutr Clin Prac 1994;9:165. 2. Kudsk KA. Enteral nutrition. In Baker RJ, Fisher JE (eds): Mastery of Surgery, 4th ed. Philadelphia: Lippincott Williams & Wilkins 2001; pp 80–92. 3. Chand B, Ponsky JL. Flexible endoscopy and enteral access. In Mastery of Endoscopic and Laparoscopic Surgery, 2nd ed. Philadelphia: Lippincott Williams & Wilkins 2005; pp 185–192.

15

Graham Patch Repair Babak Sarani, MD and Andrea Badillo, MD INTRODUCTION The surgical management of peptic ulcer disease (PUD) has changed dramatically since the 1970s primarily owing to the advancement of medical therapy. With the introduction and widespread use of histamine-2 (H2)–receptor blockers, proton pump inhibitors, and effective treatment of Helicobacter pylori (H. pylori), classic acid-reducing procedures are rarely performed.1 Despite these pharmacologic advances, however, the incidence of perforated duodenal ulcer has changed little. Therefore, a much larger proportion of surgery for PUD is emergent.2,3 In addition to presenting emergently, the typical patient with perforated PUD (PPUD) is 50 to 60 years of age4,5 with comorbid disease and limited physiologic reserve. Therefore, the general surgeon must be adept at identifying which of these patients require surgery and how to perform the necessary procedure(s) and must be familiar with the pitfalls associated with taking care of such patients. This chapter discusses repair of duodenal and juxtapyloric ulcers and excludes other more proximal or distal ulcers. Perforated duodenal ulcer disease (DUD) is associated with a 2% to 10% mortality rate, with septicemia being the most common cause of death.6–8 Preoperative shock, perforation for greater than 24 hours prior to surgical intervention, and concurrent signiﬁcant illness have consistently been shown to be predictive of mortality, and the presence of all three risk factors carries a near 100% mortality.7,9–11 Furthermore, some investigators have found that the amount and type of ﬂuid in the abdomen and the patient’s preoperative nutritional status may also be predictive of mortality.8 Given that up to 50% of perforated ulcers seal by the time of operation,12 the challenge is to identify which patients require emergent operation to control the source of sepsis versus those patients that can be treated nonoperatively, thereby avoiding the additional morbidity of a laparotomy. Omental patch or Graham patch closure of perforated duodenal ulcers was ﬁrst described in 1929 by Cellen-Jones13 and by Graham in 1937.14 In its original description, a tongue of omentum is held in place over the perforation with suture. More recently, this technique has been performed using a laparoscopic approach.

Although multiple reports have documented the safety of laparoscopic repair, no good studies demonstrate the superiority of this approach.10,15–20 Overall, these reports suggest that there is very little difference in outcome between patients undergoing laparoscopic or those having an open approach if the surgeon has advanced laparoscopic training and experience. The postoperative ileus, pain, wound infection rate, and hospital stay are very similar, and any differences noted may be due to bias in the trial design. As such, the decision to proceed laparoscopically should be made based on the surgeon’s experience and comfort with one modality versus the other. Nonoperative treatment for PPUD can be instituted in very speciﬁc circumstances (Box 15–1) and includes antibiotics, treatment for H. pylori, and nasogastric decompression.12,16,21,22 A contrast study is essential to conﬁrm that the perforation has sealed because the physical examination is unreliable for this determination. Assuming that the perforation has, in fact, sealed, this group of patients has an expected mortality rate of 35% to 50% owing to the delay in presentation or severity of comorbid illness(es).23 Of note, patients whose symptoms and physiologic status do not improve within 12 hours of the institution of nonoperative therapy require surgery.12

INDICATIONS Perforated duodenal ulcer

KEY STEPS 14,17,23 Step 1

Step Step Step Step

2 3 4 5

Step 6

Midline incision. Can also use transverse incision, if desired. Trocar placement if procedure is to be done laparoscopically Expose area of perforation Irrigate surrounding tissues and spaces Place sutures across the perforation Mobilize tongue of greater omentum on a wide vascular pedicle Place omentum over the perforation

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SECTION III: GASTROINTESTINAL SURGERY

Box 15–1 ● ● ● ● ●

Indications for Nonoperative Treatment

Symptoms >48 hr old No indices of systemic sepsis present No diffuse peritonitis Documentation with contrast radiography that the perforation has sealed Signiﬁcant comorbid conditions rendering the patient American Society of Anesthesiologists’ Class 4–5, if all of the above conditions are also present

From Donovan AJ, Berne TV, Donovan JA. Perforated duodenal ulcer: an alternative therapeutic plan. Arch Surg 1998;133:1166–1171; Jamieson GG. Current status of indications for surgery in peptic ulcer disease. World J Surg 2000;24:256–258; Berne T, Donovan A. Nonoperative treatment of perforated duodenal ulcer. Arch Surg 1989;124:830–832; and Taylor H. Peptic ulcer perforation treated without operation. Lancet 1946;2:441–444.

ulation of inﬂamed tissues to re-create a seal over the defect and may increase the postoperative leak rate. Grade 2 complication ● Repair See later steps for how to proceed with a Graham patch repair. ● Prevention Tissues that appear to be adherent to the duodenum in cases in which no perforation is seen should not be manipulated. Rather, air or liquid can be gently injected into the duodenum by nasogastric tube to test the integrity of the existing seal.

Placement of Sutures across the Perforation Enlargement of the Perforation

Step 7 Step 8

Secure sutures over the omentum Close fascia and skin. Remove trocars.

OPERATIVE PROCEDURE Midline Incision Injury to Visceral Organs A standard laparotomy incision beginning just caudad to the xyphoid and ending several centimeters above the umbilicus is most often used. A transverse incision can also be used based on the patient’s previous surgical history or surgeon preference. Many, though not all, studies suggest that transverse incisions may be associated with a lower postoperative hernia rate.24–26 Complications related to midline incision and fascial closure are discussed separately in Section I, Chapter 5, Anesthesia for the Surgeon.

● Consequence An increase in the size of the perforation can amplify the difﬁculty of repair, with a possible increase in the postoperative leak rate. Grade 1 complication ● Repair A slight increase in the size of the perforation does not require a change in operative technique. A giant duodenal defect (>3 cm) may not be amenable to Graham patch repair.27 In this circumstance, other procedures such as vagotomy/pyloroplasty, pyloric exclusion with proximal gastric diversion, or side-to-side duodenojejunostomy may be necessary. However, the latter procedure is very rarely needed in the majority of patients undergoing surgery for PPUD, even with iatrogenic enlargement of the perforation. Pitfalls related to anastomoses involving the duodenum are discussed elsewhere.

Exposure of the Area of Perforation and Irrigation of Surrounding Spaces

● Prevention Three to four interrupted 3-0 silk sutures are placed across the perforation. The sutures are inserted approximately 1 cm away from the edge of the perforation to accommodate the tendency of the suture to pull through the friable, inﬂamed duodenum. Ideally, all sutures should be placed through normal intestine, away from the area of inﬂammation. The needle should be retrieved and reintroduced from within the perforation during suture placement so as to place the suture using two passes of the needle (Figs. 15–1 and 15–2). This minimizes torque or undue force on the duodenum itself and helps prevent inadvertent worsening of the perforation.

Opening of a Sealed Perforation

Stenosis of the Duodenal Lumen

● Consequence At the time of surgery, tissues in the area have sealed the duodenal perforation in 50% of cases.12 Disruption of this closure results in the need for additional manip-

● Consequence Stenosis of the duodenum may result in small bowel obstruction postoperatively. Grade 2/3 complication

Trocar Insertion Injuries (Laparoscopic Approach) Trocar placement varies based on surgeon preference and experience. One approach utilizes a Hassan trocar in the infraumbilical position, an 11-mm trocar in the left midclavicular line approximately just above the level of the umbilicus, and a 5-mm trocar in the right midclavicular line just above the umbilicus. Complications of trocar insertion are discussed separately in Section I, Chapter 7.

161

O

m

en

tum

15 GRAHAM PATCH REPAIR

er ss Le

Perforated duodenal ulcer

MC

er

Om e

ntu m

Figure 15–1 Incorrect placement of sutures across the perforation. Passage of the needle across the perforation in one pass can result in undue force and tension, resulting in tearing of the indurated tissue. The suture should be placed across the perforation using two passes of the needle.

ss Le

Perforated duodenal ulcer

A

B

C Figure 15–2 Correct placement of sutures across the perforation. Placement of the suture and needle across the perforation using two passes of the needle (A and B) minimizes undue tension across the site and decreases trauma to the indurated tissue. C shows the correct placement of sutures across the defect.

● Repair Sutures that are noted to narrow the lumen of the bowel or that may have apposed the posterior and anterior walls of the duodenum should be removed and replaced. ● Prevention Utilizing two passes of the needle as described previously decreases the possibility of suturing the posterior and anterior walls of the duodenum.

Mobilization of the Tongue of the Greater Omentum Necrosis of the Omental Tongue ● Consequence Necrosis of the tongue of the omentum used to fashion a repair can manifest as a postoperative leak with subsequent peritonitis and sepsis. This signiﬁcantly

162

SECTION III: GASTROINTESTINAL SURGERY

Mobilized pedicle of greater omentum Securing greater omentum over ulcer

Figure 15–3 Mobilization of the omentum to the perforation. A wide pedicle must be mobilized to prevent ischemia of the omentum.

Figure 15–4 Securing the omentum across the perforation. The sutures should be tied to keep the omentum in place. Excessively tight knots will result in ischemia and necrosis of the omentum and disruption of the repair.

increases the morbidity and mortality associated with PPUD.28 Grade 3 complication ● Repair Necrosis of the omental tongue is rarely noted intraoperatively because of the operative time associated with repair of DUD. However, if noted intraoperatively, a separate, better-vascularized portion of the omentum should be used and the ischemic ﬂap should be resected. ● Prevention Creating a wide, well-vascularized pedicle on the greater omentum and placing the omentum over the perforation in a tension-free manner best prevents this complication (Fig. 15–3). Similarly, there is no need to push the omentum into the perforation because this can strangulate the omentum in a mechanism similar to that of an incarcerated, strangulated hernia.

Placement of the Omentum over the Perforation and Securing of Sutures Strangulation of the Omentum The original Graham patch describes using the previously placed sutures to hold the omental tongue in place, as opposed to using them to formally close the perforation itself (Figs. 15–4 to 15–6). However, care must be taken not to strangulate the omentum when securing it in place. ● Consequence As noted previously, strangulation of the omentum can lead to an increase in the postoperative leak rate and a signiﬁcant increase in the morbidity and mortality associated with PPUD.28 Grade 3 complication

Figure 15–5 Securing the omentum across the perforation. The sutures should be tied to keep the omentum in place. Excessively tight knots will result in ischemia and necrosis of the omentum and disruption of the repair.

● Repair Sutures tied too tightly may cause omental necrosis and should be removed and replaced. ● Prevention Sutures should be tied to prevent displacement of the omentum without compromising vascular ﬂow.

Lack of Omentum ● Consequence Some patients may not have sufﬁcient omentum to allow for a Graham patch repair. However, other tissues can be used in place of an omental patch, and the same

15 GRAHAM PATCH REPAIR

163

Greater omental pedicle Duodenum

Omental plug inside of perforated ulcer

Figure 15–6 Cross-sectional view of the omentum secured across the perforation. The intent of the omentum is to plug the defect, as opposed to closing the defect primarily and buttressing the repair with the omentum.

principles as that of the Graham patch can be employed for fashioning a tissue repair Grade 1 complication ● Repair The perforation can be suture-repaired primarily without further reinforcement,29 though there are no studies comparing differences in outcome in those patients undergoing suture repair alone with those undergoing Graham patch repair. There are also case reports on the use of ﬁbrin glue both to reinforce suture closure of the duodenum and also as a sole modality to seal a perforation.30,31 However, there are no controlled studies evaluating the safety and efﬁcacy of ﬁbrin glue as the only modality to seal a perforation, and its use as the sole method of ulcer repair is not advised. Finally, another option involves creating a “serosal” patch by suturing the serosal surface of a loop of jejunum over the perforation. ● Prevention This situation is not preventable because it is often due to previous surgery or omentectomy. Previous abdominal surgery should raise a surgeon’s index of suspicion, and arrangements should be made for other types of repairs should the patient be found to have insufﬁcient omentum.

Fascial and Skin Closure Postoperative Drainage of the Dissection Bed Routine drainage of the dissection bed postoperatively has no role.32 Although there are no studies evaluating the role of nasogastric decompression after duodenal ulcer repair, most surgeons leave a nasogastric tube to continuous suction for 24 to 48 hours after repair.

Stomach

● Consequence Postoperative drainage of the area of repair is rarely required and has been reported to increase the risk for infection.23,32 Grade 1 complication ● Prevention Drains should not be placed in the operative site.

Skin Closure ● Consequence Closure of skin after a delayed perforation can lead to an increase in the wound infection rate. Wound infection has been shown to increase hospital stay, cost, and the incidence of incisional hernia.33 Grade 1 complication ● Repair Wounds that become infected after closure should be opened at the bedside and allowed to heal by secondary intent. ● Prevention Although there are no studies evaluating the time at which skin closure becomes prohibitive, skin should not be closed if the perforation is greater than 12 hours old. In such instances, delayed primary closure can be performed in 2 to 3 days if the wound remains clean.

Other Complications Treatment for Helicobacter pylori Deﬁnitive acid-reducing operation may not be necessary until H. pylori infection is addressed. It is well established that the overwhelming majority of duodenal ulcers are

164

SECTION III: GASTROINTESTINAL SURGERY

Box 15–2 Risk Factors for Reperforation in the Early Postoperative Period ● ● ● ● ● ●

Admission heart rate >110 beats per minute Systolic blood pressure <90 mm Hg Hemoglobin <10 g/dl on admission Albumin <2.5 g/dl Lymphocyte count <1800 cells/mm3 Perforation size >5 mm

From Kumar K, Pai D, Srinivasan K, et al. Factors contributing to releak after surgical closure of perforated duodenal ulcer by Graham’s patch. Trop Gastroenterol 2002;23:190–192.

associated with H. pylori infection and that persistent infection is predictive of ulcer recurrence or perforation.12,34–41 Thus, patients should not be considered to have failed medical therapy until an attempt is made to eradicate this infection.12 ● Consequence Failure to test and treat patients who are noted either to have antibody to H. pylori or to carry the organism itself increases the risk for ulcer recurrence. Grade 1 complication ● Repair There are many treatment options for H. pylori. The most recent recommendations include either an H2receptor antagonist or proton pump inhibitor for 2 to 4 weeks and clarithromycin with or without amoxicillin for 2 weeks.42 ● Prevention All patients should be tested and treated for H. pylori. Given the near-ubiquitous presence of this infection in patients with DUD, treatment should be started empirically pending the results of testing.

Postoperative Reperforation and Leak Box 15–2 lists the risk factors that predict reperforation and leak in the immediate postoperative period. ● Consequence As noted previously, leakage from the area of repair in the immediate postoperative period increases the perioperative mortality from 2% to 55%.28 Grade 2–5 complication depending on severity of leak and septic response ● Repair There are no studies evaluating the best procedure in such patients, but attempt at revision of Graham patch alone is not recommended. Patients with reperforation in the immediate postoperative period require more deﬁnitive repair. Pitfalls related to complex duodenal repairs are discussed elsewhere, but in addition to control of the perforation, such patients should also either undergo vagotomy or be placed on long-term proton pump inhibitors.

● Prevention Patients with several of the previously noted risk factors should not undergo Graham patch repair alone.23,28 Other options in such patients include vagotomy and pyloroplasty or antrectomy, in acceptable operative candidates.

REFERENCES 1. Hermansson M, Stael von Holstein C, Zilling T. Peptic ulcer perforation before and after the introduction of H2receptor blockers and proton pump inhibitors. Scand J Gastroenterol 1997;32:523–529. 2. Tonus C, Weisenfeld E, Appel P, Nier H. Introduction of proton pump inhibitors—consequences for surgical treatment of peptic ulcer. Hepatogastroenterology 2000; 47:285–290. 3. Gustavsson S, Kelly KA, Melton LJ 3rd, Zinsmeister AR. Trends in peptic ulcer surgery. A population-based study in Rochester, Minnesota, 1956–1985. Gastroenterology 1988;94:688–694. 4. Svanes C. Trends in perforated peptic ulcer: incidence, etiology, treatment, and prognosis. World J Surg 2000;24: 277–283. 5. Svanes C, Salvesen H, Stangeland L, et al. Perforated peptic ulcer over 56 years. Time trends in patients and disease characteristics. Gut 1993;34:1666–1671. 6. Boey J, Wong J, Ong GB. Bacteria and septic complications in patients with perforated duodenal ulcers. Am J Surg 1982;143:635–639. 7. Boey J, Wong J, Ong GB. A prospective study of operative risk factors in perforated duodenal ulcers. Ann Surg 1982;195:265–269. 8. Makela JT, Kiviniemi H, Ohtonen P, Laitinen SO. Factors that predict morbidity and mortality in patients with perforated peptic ulcers. Eur J Surg 2002;168:446–451. 9. Lee FY, Leung KL, Lai BS, et al. Predicting mortality and morbidity of patients operated on for perforated peptic ulcers. Arch Surg 2001;136:90–94. 10. Lunevicius R, Morkevicius M. Management strategies, early results, beneﬁts, and risk factors of laparoscopic repair of perforated peptic ulcer. World J Surg 2005;8:8. 11. Svanes C, Lie RT, Svanes K, et al. Adverse effects of delayed treatment for perforated peptic ulcer. Ann Surg 1994;220:168–175. 12. Donovan AJ, Berne TV, Donovan JA. Perforated duodenal ulcer: an alternative therapeutic plan. Arch Surg 1998; 133:1166–1171. 13. Cellen-Jones C. A rapid method of treatment in perforated duodenal ulcer. Br Med J 1929;1:1076. 14. Graham R. The treatment of perforated duodenal ulcers. Surg Gynecol Obstet 1937;64:235–238. 15. Druart ML, Van Hee R, Etienne J, et al. Laparoscopic repair of perforated duodenal ulcer. A prospective multicenter clinical trial. Surg Endosc 1997;11:1017– 1020. 16. Jamieson GG. Current status of indications for surgery in peptic ulcer disease. World J Surg 2000;24:256–258. 17. Khoursheed M, Fuad M, Safar H, et al. Laparoscopic closure of perforated duodenal ulcer. Surg Endosc 2000; 14:56–58.

15 GRAHAM PATCH REPAIR 18. Lau H. Laparoscopic repair of perforated peptic ulcer: a meta-analysis. Surg Endosc 2004;18:1013–1021. Epub 2004;May 12. 19. Lunevicius R, Morkevicius M. Comparison of laparoscopic versus open repair for perforated duodenal ulcers. Surg Endosc 2005;5:5. 20. Robertson GS, Wemyss-Holden SA, Maddern GJ. Laparoscopic repair of perforated peptic ulcers. The role of laparoscopy in generalised peritonitis. Ann R Coll Surg Engl 2000;82:6–10. 21. Berne T, Donovan A. Nonoperative treatment of perforated duodenal ulcer. Arch Surg 1989;124:830–832. 22. Taylor H. Peptic ulcer perforation treated without operation. Lancet 1946;2:441–444. 23. Baker R. Operation for acute perforated duodenal ulcer. In Nyhus L, Baker R, Fischer J (eds): Mastery of Surgery, 3rd ed. Boston: Little, Brown, 1997; pp 916–920. 24. Fassiadis N, Roidl M, Hennig M, et al. Randomized clinical trial of vertical or transverse laparotomy for abdominal aortic aneurysm repair. Br J Surg 2005;92: 1208–1211. 25. Burger JW, van’t Riet M, Jeekel J. Abdominal incisions: techniques and postoperative complications. Scand J Surg 2002;91:315–321. 26. Grantcharov TP, Rosenberg J. Vertical compared with transverse incisions in abdominal surgery. Eur J Surg 2001;167:260–267. 27. Gupta S, Kaushik R, Sharma R, Attri A. The management of large perforations of duodenal ulcers. BMC Surg 2005; 5:15. 28. Kumar K, Pai D, Srinivasan K, et al. Factors contributing to releak after surgical closure of perforated duodenal ulcer by Graham’s patch. Trop Gastroenterol 2002;23: 190–192. 29. Koninger J, Bottinger P, Redecke J, Butters M. Laparoscopic repair of perforated gastroduodenal ulcer by running suture. Langenbecks Arch Surg 2004;389:11–16. Epub 2003;Nov 15. 30. Mutter D, Evrard S, Keller P, et al. [Treatment of perforated duodenal ulcer: the celioscopic approach]. Ann Chir 1994;48:339–344.

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31. Benoit J, Champault GG, Lebhar E, Sezeur A. Sutureless laparoscopic treatment of perforated duodenal ulcer. Br J Surg 1993;80:1212. 32. Pai D, Sharma A, Kanungo R, et al. Role of abdominal drains in perforated duodenal ulcer patients: a prospective controlled study. Aust N Z J Surg 1999;69:210–213. 33. Yahchouchy-Chouillard E, Aura T, Picone O, et al. Incisional hernias. I. Related risk factors. Dig Surg 2003; 20:3–9. 34. Ng EK, Chung SC, Sung JJ, et al. High prevalence of Helicobacter pylori infection in duodenal ulcer perforations not caused by non-steroidal anti-inﬂammatory drugs. Br J Surg 1996;83:1779–1781. 35. Tokunaga Y, Hata K, Ryo J, et al. Density of Helicobacter pylori infection in patients with peptic ulcer perforation. J Am Coll Surg 1998;186:659–663. 36. Kate V, Ananthakrishnan N, Badrinath S. Effect of Helicobacter pylori eradication on the ulcer recurrence rate after simple closure of perforated duodenal ulcer: retrospective and prospective randomized controlled studies. Br J Surg 2001;88:1054–1058. 37. Kauffman GL Jr. Duodenal ulcer disease: treatment by surgery, antibiotics, or both. Adv Surg 2000;34:121– 135. 38. Kumar D, Sinha AN. Helicobacter pylori infection delays ulcer healing in patients operated on for perforated duodenal ulcer. Indian J Gastroenterol 2002;21:19–22. 39. McFarlane G. Effect of Helicobacter pylori eradication on the ulcer recurrence rate after simple closure of perforated duodenal ulcer: retrospective and prospective randomized controlled studies. Br J Surg 2002;89:493; author reply 494. 40. Mihmanli M, Isgor A, Kabukcuoglu F, et al. The effect of H. pylori in perforation of duodenal ulcer. Hepatogastroenterology 1998;45:1610–1612. 41. Sebastian M, Chandran VP, Elashaal YI, Sim AJ. Helicobacter pylori infection in perforated peptic ulcer disease. Br J Surg 1995;82:360–362. 42. Helicobacter pylori and peptic ulcer disease. 2001. Available at http://www.cdc.gov/ulcer/keytocure.htm# treatment (accessed May 11, 2008).

16

Vagotomy and Pyloroplasty Tamica White, MD and Patrick G. Jackson, MD INTRODUCTION Pyloroplasty was ﬁrst performed by Heineke in 1886 for a patient with an obstructing pyloric mass.1 Less than 1 year later, Mikulicz2 described a similar operation for the treatment of a bleeding duodenal ulcer. Because of the temporal relationship of these two reports, the technique of opening the pylorus longitudinally and closing it transversely is known as the Heineke-Mikulicz pyloroplasty.3 Over the next several decades, other methods of gastric drainage were developed. In 1892, the Jaboulay pylorplasty, a misnomer because it is actually a gastroduodenostmy, was described for the treatment of an obstructing pyloric mass.4,5 In 1902, Finney6 reported a method of pyloroplasty that also incorporated a gastroduodenostomy.3 It was not until 1943 that Dragstedt sectioned the vagus nerves just above the diaphragm to control hyperacidity and popularized truncal vagotomy in conjunction with pyloroplasty.7 Although described several decades ago, the Heineke-Mikulicz pyloroplasty and Finney pyloroplasty continue to be two of the most common techniques performed by surgeons today for the treatment of peptic ulcer disease. Recurrence rates after truncal vagotomy are unaffected by the type of pylorplasty performed.8,9 The HeinekeMikulicz pyloroplasty is recommended for routine cases because of its ease and simplicity.10 However, in patients with a very tight pyloric obstruction, this approach can be difﬁcult to perform.11 In cases in which the stomach lays primarily in the longitudinal axis (i.e., is J-shaped), the Finney pyloroplasty is the preferred technique.3,5 The Finney pyloroplasty is also recommended in patients with ulcers in the second portion of the duodenum or when chronic inﬂammation has displaced the pylorus and duodenum under the liver.10 In cases of severe scarring and ﬁbrosis of the pylorus, the Jaboulay gastroduodenostomy is an alternative for gastric drainage.5 Vagotomy and pyloroplasty is considered a relatively quick and simple operation with good postoperative results.12 Long-term ulcer recurrence rates range from 5% to 15%.3,7,8,10,13,14 Complications, although rare, do occur.13 Chan and coworkers15 reported a less than 1% mortality rate. Skellenger and colleagues3 reported a major operative complication rate of 5%, which included serious complica-

tions such as esophageal perforation, splenic rupture, and anastomotic leak. Although vagotomy and pyloroplasty has the potential to be mastered in a relatively short period of time, its success is directly related to the training, experience, and attention to detail of the operating surgeon.12,13 Vagotomy and pyloroplasty can be approached laparoscopically as well.16,17 The laparoscopic technique closely duplicates the open approach and, therefore, is not discussed here. Complications of general laparoscopy are discussed in Section I, Chapter 8, Laparoscopic Surgery.

INDICATIONS ● ● ● ● ●

Obstructing gastric and/or duodenal ulcer Bleeding gastric and/or duodenal ulcer Perforated gastric and/or duodenal ulcer Gastric replacement after esophagectomy Pyloric stenosis (pyloroplasty only)

OPERATIVE STEPS Vagotomy18–20 Step 1 Step 2 Step 3 Step 4 Step 5 Step 6

Mobilization of the left lobe of the liver (if necessary) Incision of the peritoneal reﬂection over the distal esophagus Encirclement and placement of a Penrose drain around the esophagus Exposure and resection of a segment of the anterior vagus nerve Anterolateral traction on the esophagus to expose the posterior vagus nerve Division and resection of a segment of the posterior vagus nerve

Heineke-Mikulicz Pyloroplasty5,18,21 Step 1 Step 2

Kocher maneuver Placement of stay sutures superiorly and inferiorly to the planned incision site

168 Step 3

Step 4 Step 5

SECTION III: GASTROINTESTINAL SURGERY Longitudinal incision anteriorly through all layers of the pylorus extending onto the stomach and duodenum Transverse closure of the incision Placement of an omental patch over the pyloroplasty (optional)

Finney Pyloroplasty5,18,21 Step 1 Step 2

Step 3

Step 4

Step 5

Step 6 Step 7

Kocher maneuver Placement of stay sutures (at the superior margin of the pyloric ring and 10 cm proximal and distal to the pylorus on the stomach and duodenum) Interrupted row of posterior seromuscular sutures through the apposing walls of the stomach and duodenum U-shaped incision into the lumen of the stomach extending to the duodenum transecting the pylorus Running closure of the posterior and anterior inner layers between the stomach and the duodenum Interrupted row of anterior seromuscular sutures Placement of an omental patch over the pyloroplasty (optional)

Jaboulay Pyloroplasty5,21 Step 1 Step 2 Step 3

Step 4 Step 5

Step 6 Step 7

Kocher maneuver Placement of traction sutures to approximate the duodenal and gastric walls Interrupted row of seromuscular sutures through the apposing walls of the stomach and duodenum Incisions into the lumen of the stomach and duodenum leaving the pylorus intact Running closure of posterior and anterior inner layers between the stomach and the duodenum Interrupted row of anterior seromuscular sutures Placement of an omental patch over the pyloroplasty (optional)

OPERATIVE PROCEDURE

● Consequence Bleeding. Grade 2/3 complication ● Repair The vein can be ligated with impunity once identiﬁed. ● Prevention The phrenic vein should be anticipated during the dissection to avoid transecting it unexpectedly. In those patients with a particularly turgid or ﬁbrotic left lobe, mobilization is futile because the lobe will be extremely difﬁcult to fold.22

Encircling the Esophagus and Identiﬁcation of the Vagus Nerves Esophageal Perforation ● Consequence Intra-abdominal leak with peritonitis. Esophageal perforation during vagotomy is a rare complication with an incidence of less than 1%22–24 (Fig. 16–1). However, the morbidity of this complication is high, particularly if it goes unrecognized during the original procedure.25 Skellenger and colleagues3 reported that esophageal perforation during vagotomy is usually the result of blind ﬁnger dissection of the esophagus. Factors contributing to esophageal perforation include the obese, patients with friable inﬂamed tissue, portal hypertension, or previous surgery in that region.22 Grade 3/4/5 complication ● Repair Esophageal perforation identiﬁed intraoperatively should be repaired primarily in layers. Postoperative esophageal leak can be managed with nasogastric tube decompression and antibiotics when appropriate. Larger postoperative leaks with evidence of peritonitis and hemodynamic instability require reoperation.

Diaphragm Finger passed behind esophagus Hiatus

Mobilization of the Left Lobe of the Liver Injury to the Phrenic Vein In some cases, the left lobe of the liver must be taken down in order to provide exposure to the gastroesophageal junction. Care must be taken not to enter the rather large phrenic vein located within the diaphragm in this region.21

Figure 16–1 Encircling esophagus at hiatus.

16 VAGOTOMY AND PYLOROPLASTY

169

● Prevention When encircling the esophagus, the surgeon should stay wide on the esophagus in order to prevent inadvertent entry into the lumen.10 In addition, care should be taken to encircle the esophagus above the diaphragm to be certain that the posterior vagus is included in the maneuver.19 The posterior vagus nerve can be found by palpation superiorly on the esophagus to localize the vagus nerve before it is separated from the esophageal tissue. If the nerve is still not found, inspection in the tissue on the right crus as well as the para-aortic region can often expose the posterior vagus nerve.19 Unwarranted dissection within the posterior muscular wall of the esophagus in search of vagal strands increases the chance of perforation.

● Prevention The cisterna chyli, when present, lies to the right side of the abdominal aorta, in front of the ﬁrst two lumbar vertebrae, and is usually well covered by the right crus. Frequently, a true cisterna is not present and the thoracic duct is formed directly by the collecting lymphatic vessels.26 The lymphatics can be as small as 2 to 3 mm in diameter, making them difﬁcult to identify. Therefore, during dissection, any neighboring structures suspicious of being lymphatics must be properly isolated and ligated.

Splenic Injury

● Repair Esophageal dilation is usually successful in treating most patients.3 If unsuccessful, reoperation with esophageal myotomy may be required.

● Consequence Bleeding. Grade 2/3/4 complication ● Repair Wirthlin and associates22 reported a 2.7% incidence of splenic injury with vagotomy. A tear in the splenic capsule can usually be controlled with electrocautery or Gelfoam. If the tear is more extensive and bleeding cannot be controlled, splenectomy may be required. In cases in which an uncontrolled short gastric artery is the cause of hemorrhage, care must be taken to gently reﬂect the stomach toward the left lobe of the liver in order to allow for optimal visualization during ligation of the vessels. ● Prevention Meticulous attention to the splenic tip is required when dissecting in the region of the gastroesophageal junction. Minimizing blind or unwarranted dissection will aid in avoiding inadvertent injury to the spleen.

Injury to the Thoracic Duct ● Consequence Chylous ascites following vagotomy is very rare. Only a handful of case reports are found in the literature.26 This complication is believed to result from injury to an aberrant lymphatic trunk at the lower portion of the esophagus. Grade 2/3 complication ● Repair Cox and colleagues27 reported a case of spontaneous resolution of chylous ascties after treatment with only simple drainage. Nonoperative treatment with drainage and total parenteral nutrition followed by a low-fat diet can be attempted ﬁrst. Patients who do not improve within 6 weeks may require reoperation with ligation of the injured lymphatic channel.28,29

Dysphagia ● Consequence Prolonged inability and/or difﬁculty with solid foods. Grade 2/3 complication

● Prevention The overall incidence of postvagotomy dysphagia ranges from 1% to 3%.22,24,30 The onset may be early or months after the operation. Periesophageal ﬁbrosis and denervation of the lower esophagus have been suggested as factors contributing to dysphagia.30 Complete knowledge of the anatomy in the region of the gastroesophageal junction is required in order to avoid unnecessary dissection of the lower esophagus. In addition, complete stripping of the lower esophagus during isolation of the vagus nerves should be avoided to prevent denervation and devascularization.

Division and Resection of the Vagus Nerves Incomplete Vagotomy ● Consequence Recurrent ulceration. Not all patients with incomplete vagotomy develop recurrent ulcers. However, it is generally accepted that ulcer recurrence after vagotomy is due to incomplete nerve section (Fig. 16–2).31 Soybel and coworkers18 reported that approximately two thirds of patients with duodenal or pyloric channel ulcer recurrence after initial vagotomy have evidence of intact vagal innervation. The majority of patients with recurrent ulcers present with intractable pain or bleeding. Grade 2/3 complication ● Repair Some recurrences will be amenable to medical treatment. However, patients who are refractory to medical management will require reoperation. Skellenger and colleagues3 reported that revagotomy alone for the treatment of recurrent ulcers is indicated only for those patients with elevated basal acid secretion or a clear-cut

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SECTION III: GASTROINTESTINAL SURGERY Longitudinal line of incision through anterior wall of pylorus

Figure 16–2 Division of posterior vagus. Figure 16–4 Location of Heineke-Mikulicz pyloroplasty.

separated and ligated. However, failure to identify each cord will result in incomplete vagotomy. When identifying the posterior vagus nerve, care must be taken to make sure that the “criminal nerve” of Grassi is distal to the area of proposed resection. Although this nerve is usually found wrapping around the cardiac notch from its origin at the posterior vagal trunk, it can occasionally ramify more proximally above the gastroesophageal junction.18 After each nerve resection, a specimen of the vagus should always be sent to the pathologist for histologic conﬁrmation.

Incision through the Pylorus and/or Stomach/Duodenum Figure 16–3 Division of anterior vagus.

Failure of Adequate Drainage 32

vagal response to insulin. Kennedy and associates reported a 16% re-recurrence rate after revagotomy alone compared with a 1.4% rate after revagotomy and antrectomy. The majority of patients with ulcer recurrence after truncal vagotomy and pyloroplasty are best treated with revagotomy and antrectomy. ● Prevention Although incomplete vagotomy is more common with other types of vagotomies (highly selective, parietal cell), careful attention is imperative when dividing the vagus nerves during truncal vagotomy to avoid leaving small ﬁbers behind. During dissection of the anterior vagus nerve (approximately 2–4 cm above the gastroesophageal junction), the surgeon must be aware that it is not uncommon for vagal ﬁbers to be distributed among two or three smaller cords at this level (Fig. 16–3). These cords are usually quite visible and easily

● Consequence Level 1 evidence shows that persistent vomiting, epigastric fullness, dyspepsia, or heartburn occurs in approximately 10% of patents after vagotomy and pyloroplasty.33–35 Many of these symptoms resolve after the immediate postoperative period. Prolonged symptoms are usually due to an inadequate pyloroplasty that does not allow sufﬁcient drainage of gastric contents through the pyloroplasty and into the duodenum3 (Fig. 16–4). Grade 1/2/3 complication ● Repair Patients with mild symptoms can be treated medically. Gastric outlet obstruction with severe, intractable symptoms will require reoperation with construction of a new drainage procedure. Patients with both reﬂux esophagitis and painful alkaline reﬂux gastritis may require a Roux-en-Y diversion procedure.3

16 VAGOTOMY AND PYLOROPLASTY First (back) row of serosal sutures in place Line of incision through wall of duodenum

171

Traction suture Line if incision through wall of stomach

Posterior through and through suture

Figure 16–7 Inner layer of Finney pyloroplasty. Figure 16–5 Creation of back row of Finney pyloroplasty.

Figure 16–8 Weinberg modiﬁcation of closure for HeinekeMikulicz pyloroplasty.

Closure of the Pyloroplasty Anastomotic Leak Figure 16–6 Closure of anterior wall of Finney pyloroplasty.

● Prevention Except for cases of pyloric stenosis, pyloroplasty is performed to overcome the gastric stasis caused by vagotomy. During pyloroplasty, if the incision through the pylorus is not long enough, drainage of the stomach into the duodenum will be insufﬁcient (see Fig. 16–4). A minimal 5-cm incision is recommended for a Finney or Jaboulay pyloroplasty (Figs. 16–5 to 16–7). During the Heineke-Mikulicz pyloroplasty, the pylorus should be palpated to ensure complete transaction of the muscle with clear extension onto the stomach and duodenum. In addition, any dog-ears at the ends of the incision after closure should not be infolded because this can narrow the lumen.

● Consequence Peritonitis, abscess. Grade 3/4/5 complication ● Repair Drainage and/or reoperation with repair or revision of the anastomosis. Any patient having unexplained fever or inappropriate abdominal pain postoperatively should be evaluated for possible anastomotic leak (Fig. 16–8). Depending on the severity of the leak, surrounding inﬂammation, and stability of the patient, either primary repair or diversion can be performed. ● Prevention With respect to the Heineke-Mikulicz pyloroplasty, there is no evidence in the literature to suggest that a two-layer closure is superior to a single-layer closure

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(Weinberg modiﬁcation) in preventing an anastomotic leak. In fact, many advocate this modiﬁcation because it is believed to result in a larger opening with improved gastric emptying.5 Two-layer closures are indicated for the Finney and Jaboulay pyloroplasties. When closing the defect, full-thickness sutures must be placed through all layers of the bowel to ensure a proper anastomosis. Although level 1 evidence is lacking from the literature, placing a tongue of vascularized omentum over the anastomosis to buttress the pyloroplasty is advocated.

Other Complications Inadequate/Incomplete Kocher Maneuver Grade 2/3 complication It is essential to fully mobilize the duodenum by performing a complete Kocher maneuver. Little is reported in the literature about this complication. However, failure of adequate mobilization of the duodenum results in undue tension on the anastomosis of the pyloroplasty. Moreover, proper apposition of the stomach and duodenum when performing a Finney or Jaboulay pyloroplasty is nearly impossible without full mobilization of the duodenum. Pneumothorax Grade 2 complication Wirthlin and associates22 reported 1 case of pneumothorax from their series over 1000 vagotomies. The patient was treated conservatively without a chest tube and had no long-term sequelae. Although rare, this complication must be considered particularly when a patient presents with respiratory difﬁculties postoperatively. Prevention of a pneumothorax is best accomplished by avoiding unnecessary proximal esophageal dissection into the chest. If the pleura is visualized, care should be taken to reﬂect it laterally without entering the pleural space. Aortic Injury Grade 5 complication Aortic injury during the esophageal dissection portion of the vagotomy is extremely rare. Inexperience with dissecting around the gastroesophageal junction is usually the cause of injury. It is imperative that the surgeon understands the anatomic relationship between the esophagus, the crura, and the aorta. The aorta lies just behind the esophagus and can be hidden by the left crus. When dissecting around the esophagus, care must be taken not to injure the aorta inadvertently. Immediate primary repair is required.

REFERENCES 1. Fronmuller F. Operation der Pylorusstenose [Erlangen dissertation]. Furth, Schroder, 1886; pp 1–19. 2. Mikulicz J. Zur operativen behandlung des stenosirenden magengeschwures. Arch Klin Chir 1888;37:79–90.

3. Skellenger ME, Jordan PH. Complications of vagotomy and pyloroplasty. Surg Clin North Am 1983;63:1167– 1180. 4. Jaboulay M. La gastro-enterostomie, la jejunoduodenostomie, la resection du pylore. Arch Prov Chir 1892;1:11–12. 5. Sawyers JL, Richards WO. Selective vagotomy and pyloroplasty. In Baker RJ, Fisher JE (eds): Mastery of Surgery, 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2001; pp 933–941. 6. Finney JMT. A new method of pyloroplasty. Johns Hopkins Bull 1902;13:155–161. 7. Woodward ER. The history of vagotomy. Am J Surg 1987;153:9–17. 8. Pemberton JH, VanHeerden JA. Vagotomy and pyloroplasty in the treatment of duodenal ulcer: long-term results. Mayo Clin Proc 1980;55:10–18. 9. Stempien SJ, Dagradi AE, Lee ER. Status of duodenal ulcer patients ten years or more after vagotomypyloroplasty. Am J Gastroenterol 1971;56:99–108. 10. Thompson BW, Read RC. Long-term randomized prospective comparison of Finney and Heineke-Mikulicz pyloroplasty in patients having vagotomy for peptic ulceration. Am J Surg 1975;129:78–81. 11. Samsi AB, Pandya AP, Kulkarni VR, et al. Finney’s pyloroplasty in chronic pyloric obstruction. J Postgrad Med 1980;26:112–115. 12. Robles R, Parrilla P, Lujan JA, et al. Long-term follow-up of bilateral truncal vagotomy and pyloroplasty for perforated duodenal ulcer. Br J Surg 1995;82:665. 13. Stabile BE. Current surgical management of duodenal ulcers. Surg Clin North Am 1992;72:335–355. 14. Welch CE, Rodkey GV, vonRyll Gryska P. A thousand operations for ulcer disease. Ann Surg 1986;204:454– 467. 15. Chan VM, Reznick RK, O’Rourke K, et al. Meta-analysis of highly selective vagotomy versus truncal vagotomy and pyloroplasty in the treatment of uncomplicated duodenal ulcer. Can J Surg 1994;37:457–464. 16. Prietraﬁtta JJ, Schultz LS, Graber JN. Experimental transperitoneal laparoscopic pyloroplasty. Surg Laparosc Endos 1992;2:104. 17. Snyders D. Laparoscopic pyloroplasty for duodenal ulcer. Br J Surg 1993;80:127. 18. Soybel DI, Zinner MJ. Stomach and duodenum: operative procedures. In Zimmer MJ, Schwartz SI, Ellis H (eds): Mangoit’s Abdominal Operations. New York: Appleton and Lange, 1997; pp 1079–1097. 19. Pappas TN. Truncal vagotomy. In Sabiston DC (ed): Atlas of General Surgery. Philadelphia: WB Saunders, 1994; pp 328–332. 20. Roberts JP, Debas HT. A simpliﬁed technique for rapid truncal vagotomy. Surg Gynecol Obstet 1989;168:539– 541. 21. Meyers WC: Heineke-Mukulicz pyloroplasty. In Sabiston DC (ed): Atlas of General Surgery. Philadelphia: WB Saunders, 1994; pp 251–253. 22. Wirthlin LS, Malt RA. Accidents of vagotomy. Surg Gynecol Obstet 1972;135:913–916. 23. Simmons RL, Back VR, Harvey HD, Herter FP. Technical complications of trans-abdominal vagotomy. Arch Surg 1966;92:922.

16 VAGOTOMY AND PYLOROPLASTY 24. Postlethwait RN, Kim SK, Dillon ML. Esophageal complications of vagotomy. Surg Gynecol Obstet 1969;128:481–488. 25. Hauser JB, Lucas RJ. Esophageal perforation during vagotomy. Arch Surg 1970;101:466. 26. Al-Mousawi M, Abu-Nema T. Chylous ascites: a rare complication of vagotomy. Eur J Surg 1991;157:149– 150. 27. Cox WD, Schmitz RT, Gillesby WJ. Unusual complications of vagotomy and pyloroplasty. Am J Surg 1966;32:259. 28. Clain A. Chylous ascites following vagotomy. Br J Surg 1991;58:312. 29. Hocking MA, Barth CE. Chylous ascites, a complication of vagotomy. J R Coll Surg Edinb 1978;23:232. 30. Anderson HA, Schlegel JF, Olsen AM. Post vagotomy dysphagia. Gastrointest Endosc 1966;12:13.

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31. Johnson AG, Baxter HK. Where is your vagotomy incomplete? Observations on operative technique. Br J Surg 1977;64:583–586. 32. Kennedy T, Roger-Green WE. Stomal and recurrent ulceration: medical or surgical management. Am J Surg 1980;139:18–21. 33. Kennedy T, Connell AM, Love AGH. Selective or truncal vagotomy? Five year results of a double blind randomized controlled trial. Br J Surg 1973;60:944–948. 34. Robb JV, Banks S. Marks IN, et al. A comparison between selective vagotomy and truncal vagotomy with drainage in duodenal ulceration. South Afr Med J 1973;47:1391– 1396. 35. Hojlund B, Madsen P. The clinical results of selective vagotomy and pyloroplasty 6–9 years later. Dan Med Bull 1980;27:164–167.

17

Laparoscopic Nissen Fundoplication Stephen R. T. Evans, MD and Elizabeth A. David, MD INTRODUCTION Since the early 1990s, laparoscopic Nissen fundoplication (LNF) has come to replace open fundoplication as the surgical “gold standard” and procedure of choice for gastroesophageal reﬂux disease (GERD). Some data suggest that LNF is associated with more life-threatening complications than open fundoplication, but when the learning curve is taken into account, in experienced hands, the laparoscopic approach has proved to have signiﬁcant advantages over the open procedure.1 The less life-threatening complications of splenectomy and pneumonia seen in open Nissen fundoplication are rare in LNF, but these are replaced with more potentially serious injuries. Despite articles speciﬁcally focused on error prevention in LNF, life-threatening and lethal complications still occur.2 First reported in the literature in 1991, LNF is a complex advanced laparoscopic procedure that has excellent outcomes when performed by experienced surgeons. However, even in the best of hands, serious complications can result.3 Rantanen and coworkers1 reported a prevalence of 1.3% for life-threatening complications and 1.2% for non– life-threatening complications. Predictors of success for this operation have been published elsewhere, but overall patient satisfaction has been extremely high.4 Certain patient populations, speciﬁcally morbidly obese patients with body mass indexes (BMIs) greater than 30, may be at increased risk for complications with LNF.5 Presumably, in the morbidly obese patient, visibility can be limited in the upper abdomen, creating a more difﬁcult gastroesophageal (GE) junction dissection and more difﬁculty with takedown of the short gastric and other vessels, leading to a higher complication rate both intraoperatively and postoperatively. However, good data indicate no increased risk of complications in the elderly or the pediatric population.6–8 The only other population at increased risk for complications are those patients with prior extensive upper abdominal surgery.

INDICATIONS ● Young patient population well controlled on proton

pump inhibitors

● Progressive regurgitant symptoms ● Extraesophageal manifestations ● Proton pump inhibitor failures

OPERATIVE STEPS 2 Step Step Step Step

1 2 3 4

Step 5 Step 6 Step Step Step Step Step Step Step

7 8 9 10 11 12 13

Positioning and trocar placement Liver retraction Division of the hepatogastric ligament Dissection of the crura and phrenoesophageal ligament Lengthening of the abdominal esophagus (if necessary) Stomach mobilization and ligation of short gastric vessels Retroesophageal dissection at the GE junction Bougie and nasogastric tube placement Closure of the esophageal hiatus Retroesophageal wrap Suture placement for the wrap Fixation of the wrap to the right crus Trocar removal

OPERATIVE PROCEDURE Trocar Insertion Trocar Insertion Injuries Life-threatening and less serious complications can occur with trocar insertion. A standard ﬁve-trocar technique is used: a 5-mm port in the right midabdomen, a 10-mm port subxiphoid, a 5-mm port to the left of the xiphoid, a 10-mm port in the left midabdomen, and a Hasson port supraumbilically. Complications of trocar insertion are discussed in Section I, Chapter 7, Laparoscopic Surgery.

Division of the Hepatogastric Ligament Injury to an Aberrant Left Hepatic Artery As the hepatogastric ligament is dissected to visualize the right crus and right phrenoesophageal ligament, approximately 10% of patients will have an aberrant left hepatic

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artery branching off the left gastric artery, making this vessel prone to injury if it is not visualized.9 ● Consequence Excessive bleeding with uncontrolled transection of the aberrant left hepatic artery and/or potential left hepatic lobe compromise with ischemia. If the patient has cirrhosis and/or signiﬁcant hepatic compromise, ligation of this aberrant left hepatic artery (36% are accessory, 64% are replaced) may lead to clinically signiﬁcant hepatic ischemia. Grade 2–4 complication ● Repair Ligation may be carried out if there is no obvious hepatic compromise. However, end-to-end anastomosis may be necessary in patients with limited hepatic reserve. ● Prevention Visualization of the aberrant vessel through what is usually a transparent hepatogastric ligament is critical, especially in light of the frequency of this anatomic vascular anomaly (Fig. 17–1A). Frequently, the vessel can be reﬂected out of the operating ﬁeld while still maintaining full visualization and allowing takedown of the right phrenoesophageal ligament and dissection of the GE junction. A small-caliber aberrant left hepatic artery would strongly suggest this to be an accessory vessel; it could be ligated if necessary to obtain adequate access to the GE junction and phrenoesophageal ligament. However, a larger-caliber vessel (e.g., >3– 4 mm in diameter) should be reﬂected out of the operating ﬁeld and spared for the reasons mentioned previously (see Fig. 17–1B).

Dissection of the Crura and Phrenoesophageal Ligament with Lengthening of the Abdominal Esophagus (GE Junction Dissection)

A

B Figure 17–1 A, The hepatogastric ligament is shown above the caudate lobe (small arrow) with evidence of an aberrant left hepatic artery (large arrow) and the left lateral segment reﬂected anteriorly (curved arrow). B, Dissection of the aberrant left hepatic artery out of the operating ﬁeld with retraction. The size of this vessel strongly suggests this is a replacement vessel, which would be spared and not ligated merely for convenience of the dissection.

Vagus Nerve Injury ● Consequence Postvagotomy diarrhea (10%–15%) and delayed gastric emptying. Grade 1 complication

Esophageal Injury

● Prevention The operating surgeon must visualize both anterior and posterior vagal trunks during the dissection of the GE junction and takedown of the right, left, and anterior phrenoesophageal ligaments (Fig. 17–2A). Some surgeons actually insert the wrap inside of the vagal nerve trunks, making sure that both trunks have been clearly delineated. The anterior nerve can be tethered up close to the phrenoesophageal ligament and must be reﬂected back onto the esophagus anteriorly. The posterior trunk is most commonly injured when the retroesophageal window is created. Care must be taken to again

● Consequence Intra-abdominal leak with peritonitis. The reported incidence for this complication is roughly 1%; however, it carries a mortality rate of greater than 20%, making it one of the most important and lethal complications of LNF.10 This complication has been well described in the literature. When looking at speciﬁc mechanisms of esophageal perforations, Schauer and associates10 identiﬁed the majority of injuries occurring from improper retroesophageal dissection. Obesity and large hiatal hernias were found to contribute to esophageal injury secondary to excessive fatty tissue in the periesophageal

reﬂect the nerve anteriorly onto the esophagus to prevent injury (see Fig. 17–2).

17 LAPAROSCOPIC NISSEN FUNDOPLICATION

177

appropriate positioning of a nasogastric tube, antibiotics, and a swallow study that conﬁrms no on-going leak (prior to removal of the nasogastric tube). ● Prevention Retraction of the esophagus should be carried out only with Penrose drains around the GE junction (Fig. 17– 3A) or with retraction bluntly such as with the endoscopic Babcock retractor (see Fig. 17–3B). Grasping of the esophagus or junction with the retractors as previously discussed will lead to a high incidence of linear tears within the esophagus and catastrophic outcomes (see Fig. 17–3C). Dissection should be performed away from the esophagus to minimize the risk of injury and devascularization. Retroesophageal dissection should proceed from right to left, anterior to the left crus of the diaphragm—dissection too superior can lead to pneumothorax secondary to pleural penetration, too anterior can lead to esophageal perforation, and too inferior may lead to gastric perforation. If a tear is suspected (and commonly, these may be linear through the longitudinal muscle and difﬁcult to visualize), insufﬂation with the nasogastric tube proximal to this area, with distal occlusion using a noncrushing bowel clamp and saline over the esophagus and stomach inspecting for leak, has been shown in animal studies to be a useful modality. This may hasten diagnosis of occult injuries, which may decrease the morbidity of perforation injuries in the future.11

A

B Figure 17–2 A, The right and left crura are outlined (small arrows) and the anterior vagus is easily visualized in its midposition on the esophagus (large arrow). At this point in the dissection, with mobilization of the right and left phrenoesophageal ligaments completed, the dissection anteriorly should extend well above the anterior vagal trunk, pushing the vagus down onto the esophagus to minimize risk of injury. B, The posterior vagal trunk is shown by the arrow. The esophagus is being reﬂected anteriorly. The retroesophageal window is created, and at this point in the dissection, the posterior vagal trunk should be reﬂected anteriorly with the esophagus to minimize the risk of injury.

region that obscures tissue planes and complicates dissection. As with other complications of LNF, experience of the surgeon is a risk factor for this complication. Schauer and associates10 reported that 10 of 17 esophageal perforations identiﬁed collectively from several institutions occurred during the ﬁrst 10 LNFs performed by each surgeon. Grade 2–5 complication ● Repair The esophageal perforations can be closed laparoscopically if the surgeon has an extensive experience and comfort level with this. Otherwise, conversion to an open procedure should be performed with a layered closure. Proper postoperative management includes

Pneumothorax, Pneumomediastinum, and Pneumopericardium ● Consequence Hypercarbia and increased airway pressures. Murdock and colleagues12 studied over 900 laparoscopic cases to identify which patients were at risk for developing hypercarbia, subcutaneous emphysema, pneumothorax, and pneumomediastinum. They concluded that longer operative times (>200 min), higher maximum measured end-tidal CO2, a greater number of surgical ports, older patient age, and Nissen fundoplications all predisposed to hypercarbia-related complications during laparoscopy. Of note, the relation between LNF and hypercarbia was attributed to the length of the procedure (mean 227 min), which would increase the risk of pneumothorax/pneumomediastinum by 20 times based on procedure length alone.12 Grade 1/2 complication ● Repair The vast majority of patients with CO2 pneumothoraces will resolve spontaneously on their own and do not require chest tubes. Extensive dissections into the chest for mobilization of the esophagus commonly leads to subcutaneous emphysema and hypercarbia. Communication between the surgeon and the anesthesiologist will allow for the ventilators to be set at higher rates

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A

C

B

Figure 17–3 A, The Penrose drain is placed around the gastroesophageal (GE) junction for retraction in an atraumatic fashion. Both right and left crura are shown by arrows. This atraumatic retraction minimizes the risk of gastric or esophageal tears or perforations. B, Other options for retraction include simple reﬂection of the GE junction and esophagus in the appropriate vector necessary. Here, the blunt side of the endoscopic Babcock reﬂects the esophagus anteriorly, exposing the hiatus and the right and left crura (arrows). C, Grasping the esophagus or the GE junction in this fashion will clearly lead to a high incidence of linear tears in the esophagus and should be avoided at all cost. Of note is the aorta behind the left crus in this view (arrow).

with higher minute ventilations to reduce end-tidal CO2 such that it can be maintained at a safe rate. Positive end-expiratory pressure (PEEP) has been used to correct the respiratory changes related to the effects of CO2 retention during extensive laparoscopic surgeries with a high rate of success. By decreasing the pressure gradient between the abdominal and the pleural cavities during both inspiration and expiration, PEEP therapy provides a means of reinﬂating a collapsed lung without invasive intervention.13 ● Prevention The close proximity of the right and left pleura (especially the left pleura) in the mediastinal dissection must be understood during mobilization of the esophagus to achieve abdominal esophageal lengthening. The dissection should push the pleura away from the operative ﬁeld (i.e., in the lateral plane of the thoracic dissection). Commonly, in an attempt for the surgeon to stay off the esophagus, the dissection extends out too far laterally into the chest and the pleural space (Fig. 17–4).

Figure 17–4 The edge of the right pleura (arrow) is visualized in the intrathoracic dissection. Care should be taken to reﬂect the pleura out laterally on the right and left sides and not to dissect straight through it; otherwise, the CO2 pneumothorax will occur.

17 LAPAROSCOPIC NISSEN FUNDOPLICATION

especially if there is a tear on the splenic capsule. This requires meticulous visualization with suctioning, and frequently, an additional trocar must be placed to allow an additional set of hands to expose the vessels or the site of the splenic tip.

Ligation of the Short Gastric Vessels Splenic Injury and/or Bleeding ● Consequence Bleeding. Grade 2/3 complication ● Repair Ligation of the short gastric vessels requires excellent visualization when moving superiorly and posteriorly into the upper abdomen. This requires reﬂection of the stomach toward the left lateral segment of the liver. The harmonic scalpel is most commonly used at this step. Sponges and Gelfoam may be used to control bleeding and aid in visualization. In situations in which hemostatic control is not excellent, conversion to an open procedure may be required to achieve hemostasis,

179

● Prevention An extensive gastric mobilization of the entire fundus and cardia allows the stomach to be reﬂected so that visualization of the posterior wall is facilitated. This allows an easier dissection down to the short gastric vessels with the spleen reﬂected off to the side. When a harmonic scalpel is used to ligate the short gastric vessels, the common mistakes are that the scalpel is not held in the neutral position and that the vessels separate prematurely without complete closure (Fig. 17–5).

A

B

C

D

Figure 17–5 A, The harmonic scalpel used to mobilize the greater curve of the stomach and the short gastrics is shown here in the correct neutral position allowing tissue with retraction medially and laterally to release upon completion of sealing of the tissue. B, The harmonic scalpel is being retracted anteriorly, which can lead to premature release of the tissues and bleeding, especially in difﬁcult areas, as the short gastrics are taken in closer proximity to the spleen. C, The second error in technique that can lead to bleeding from the harmonic scalpel is incomplete control of the vessel as shown here in which only partial approximation of the vessels is obtained, again leading to potential uncontrolled bleeding. D, The stomach is reﬂected anteriorly to allow exposure posteriorly, which minimizes the risk of injury along the greater curve of the stomach and also allows better visualization of the short gastric and the relationship between the spleen and the stomach as the dissection moves proximally.

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Figure 17–6 The harmonic scalpel is in too close proximity to the stomach. This can lead to thermal injury and delayed gastric perforation with subsequent peritonitis and sepsis. The harmonic scalpel in this setting should be moved to the right, allowing an adequate distance of at least 2 to 3 mm to minimize thermal injury to the stomach. Even as one moves in closer proximity to the stomach and the spleen, the harmonic scalpel should err on the side of the spleen, not on the side of the stomach.

Gastric Injury, Acute or Delayed (Thermal) ● Consequence Perforation with peritonitis. Extensive retraction of the stomach for better visualization can lead to serosal and full-thickness tears of the stomach. In addition, use of the harmonic scalpel in close proximity to the stomach can contribute to thermal injuries, leading to delayed perforations and, subsequently, to delayed peritonitis with potentially serious or life-threatening consequences (Fig. 17–6). Grade 2–5 complication ● Repair Primary closure of these esophageal injuries can be carried out without difﬁculty both laparoscopically (depending on the surgeon’s comfort level) and by conversion to an open procedure. The more challenging and difﬁcult issue is the problem of thermal injury with delayed perforation. In the setting of what appears to be a thermal injury, which may or may not be full thickness, excising or oversewing this area may be useful. The use of prolonged nasogastric suctioning, administering perioperative antibiotics, and using omentum to buttress this area have also proved useful. Testing the stomach for occult perforations has proved to be useful, as previously outlined, with insufﬂation and saline wash.11 ● Prevention When the short gastric vessels are being ligated, the harmonic scalpel needs to be held in the neutral position. Especially when the vessels are extremely short,

Figure 17–7 The most ﬂoppy portion of the cardia utilizing the short gastrics as the landmark has been brought through the retroesophageal window, as shown by the arrow. There is no retraction on this. The left portion of the cardia now can easily be brought up in proximity for a tension-free “ﬂoppy” approximation.

the harmonic scalpel must be moved on the side of the spleen, not on the side of the stomach, to minimize the risk of full-thickness thermal injuries to the stomach. Gastric tears can be minimized by appropriate retraction of the stomach with blunted instruments. Penrose drain retraction of the GE junction is used so that tears with retraction are minimized.

Gas Bloat Syndrome ● Consequence The reported incidence of poor quality of life with inability to burp or belch is approximately 1% to 7% postoperatively.14 Grade 1/2 complication ● Prevention The inability to burp or belch after LNF is believed by many surgeons to be due to a wrap under tension because all the short gastric vessels were not ligated. Level-one evidence suggests that there is no relationship between the takedown of the short gastric vessels and the incidence of gas bloat syndrome.15 However, this author and several other surgeons believe that extensive mobilization does lead to a more ﬂoppy wrap and, considering the very low incidence, may in fact require an extremely large randomized study to prove otherwise16 (Fig. 17–7).

Bougie and Nasogastric Tube Insertion Esophageal and Gastric Perforation ● Consequence Viscus leak with peritonitis (Fig. 17–8). Grade 2–5 complication

17 LAPAROSCOPIC NISSEN FUNDOPLICATION

Figure 17–8 Intraoperative photograph depicts a nasogastric tube perforating the retroesophageal portion of the Nissen wrap. The placement of this tube was done without communication between the anesthesiologist and the surgeon, so that direct visualization of the placement of the tube was not done. Direct visualization would allow proper placement of the tube along the greater curve of the stomach. The nasogastric tube in this case was subsequently pulled back, the gastric perforation repaired primarily under laparoscopic visualization, and the patient had an uneventful postoperative course.

● Repair Two-layer repair of the stomach or esophagus. Any LNF patient who, in the ﬁrst 24 to 48 hours postoperatively, develops an unexplained fever should be ruled out for an occult GE perforation. In addition, if the patient develops increasing abdominal pain in the setting of tachycardia, she or he should be ruled out for a GE perforation. Having a high suspicion and a low threshold for assessment of this potentially lifethreatening injury is critical in the post-LNF patient. A two-layer repair of the stomach or esophagus can be carried out (see “Gastric Injury, Acute or Delayed [Thermal],” earlier). ● Prevention Excellent communication between the anesthesiologist and the surgeon is required at the time of the bougie insertion. It is critical that the anesthesiologist and the surgeon understand this potential complication. The dilator should be passed slowly and under direct visualization by an individual experienced in this technique. Placement of the bougie dilator or insertion of the nasogastric tube was the second most common cause of gastric and esophageal perforations during LNF reported by Schauer and associates.10 The risk of esophageal and gastric perforation has been shown to be increased during LNF secondary to many factors including inexperience of both the surgeon and the anesthesia personnel, absence of manual palpation,

181

Figure 17–9 Hidden anatomy. The retroesophageal window is depicted with the potential for injury to the esophagus or stomach if the dissection occurs too far anteriorly or too far distally. Also depicted are potential injuries of placement of the nasogastric tube or the bougie if the GE junction is not properly oriented during placement and positioning.

improper retraction on the esophagus or stomach, the presence of an esophageal myotomy, and pathologic changes of the esophagus. Lowham and coworkers17 clearly showed that lack of communication during insertion was a primary risk factor for this mechanism of injury. These authors also suggested that distal esophageal angulation after crural closure was a primary risk factor for perforation and needed to be corrected by anterior and caudal traction on the gastric fundus17 (Fig. 17–9). Making the diagnosis of postoperative gastric perforation can be difﬁcult in patients status post LNF. Hughes and coworkers18 reported one case in which the diagnosis was eventually made using a retrograde sinogram through a right upper quadrant drain placed for an abscess found on computed tomography (CT) scan on postoperative day 8, despite negative Gastrograﬁn and barium swallow studies and a negative CT scan of the abdomen on postoperative day 3.18 Again, the surgeon must be acutely aware of the associated risk of occult injury to the esophagus or stomach that requires diligent assessment to identify the injury and aggressive management postoperatively. All patients who develop upper abdominal abscesses or infectious processes documented by CT scans or other imaging studies should be suspected of having a gastric or esophageal perforation until proved otherwise. The frequency of GE perforation (1%–2%) and its severity (fatal in 20%–50%) mandate that it be considered in all patients with postoperative leukocytosis and fever.18

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SECTION III: GASTROINTESTINAL SURGERY cially with the most posterior sutures, are critical (Fig. 17–10).

Closure of the Esophageal Hiatus Aortic Injury ● Consequence Life-threatening bleeding. Grade 5 complication ● Repair Energent open primary vascular repair. ● Prevention It is critically important that the laparoscopic surgeon understand the relationship between the crura and the aorta, especially the left crus and its close relationship to the aorta. Needle injuries into the aorta resulting in death have been reported in addition to other similar vascular injuries at the level of the aortic hiatus.19,20 Baigrie and associates20 reported three cases of signiﬁcant hemorrhage that required conversion to open procedures for control of hemostasis involving injuries to the left inferior phrenic vein, an aberrant left hepatic vein, and the aorta. These authors suggested that minimal use of hook diathermy for dissection, early conversion to laparotomy, and early recognition of aberrant anatomy are critical to prevent vascular injury that may be life-threatening.20 Visualization and protection of the aorta during the crus closure, espe-

Dysphagia ● Consequence Long-term potential difﬁculties with solid foods. Grade 1/2 complication ● Repair Esophageal dilation or possible reoperation. ● Prevention Dysphagia is a commonly accepted complication of the Nissen procedure. The classic procedure has been modiﬁed in several ways—including decreasing the length of the fundoplication from 4 to 1 cm, dividing the short gastric vessels, and increasing the size of the esophageal bougie—to minimize the incidence of postoperative dysphagia. Attempts to “eyeball” the hiatus closure have been fraught with difﬁculty because this commonly leads to dysphagia. To reemphasize the importance of an esophageal dilator to determine the size of the hiatus, Patterson and colleagues19 carried out a prospective, blinded, randomized trial showing the efﬁcacy of esophageal bougie placement during LNF. This level-one evidence demonstrated that the

A

B Figure 17–10 A, The suture has been placed in the most posterior aspect approximating the left and right crura. The aorta sits in close proximity behind the left crus, and care should be taken with these most posterior sutures to protect against aortic injury at this time. The aorta (arrow) is seen behind the crus. B, Hidden anatomy. The positioning of the aorta and its relationship to the left and right crus are shown along with the risk for injury to the aorta with approximation of the left and right crura, especially with posterior sutures. In addition, the anterior phrenic vessels commonly come in close proximity to the anterior aspect of the hiatus, and care must be taken with dissection of the anterior phrenoesophageal ligament to minimize injury to these vessels. Lastly, the inferior vena cava is seen posterior to the caudate lobe, and an aberrant left hepatic artery may be seen in this region, again reemphasizing the potential risk of vascular injury with dissection of the GE junction.

17 LAPAROSCOPIC NISSEN FUNDOPLICATION incidence of long-term dysphagia is reduced in patients in whom a 56-Fr bougie is used during LNF (17%) versus patients who underwent LNF without the use of an esophageal bougie (31% with long-term dysphagia).21 Other causes of dysphagia that can occur postoperatively include esophageal motility disorders not detected through preoperative manometric studies, a tight wrap with poor or inadequate mobilization of the greater curve of the stomach, and short gastric vessels.

Breakdown of the Crus Closure ● Consequence Herniation of the wrap into the chest or mediastinum with pain, possible dysphagia, and recurrent GERD. Grade 2/3 complication ● Repair Reoperation with reinforcement of the hiatus with mobilization of the thoracic esophagus to achieve 6 to 8 cm of abdominal esophagus and reinforcement of the hiatus with biomaterial. ● Prevention Intrathoracic herniation of the Nissen wrap or “slipped Nissen” is a commonly described complication after LNF, typically attributed to inadequate closure of the crura, excessive tension on the crural closure, or failure to recognize a shortened esophagus.20 Currently, several reports discuss the use of synthetic materials to reinforce the hiatus in LNF, but now, level-one evidence exists to support its application in hiatal hernias larger than 8 cm in greatest diameter.22–25 In a prospective, randomized trial, Frantzides and coworkers25 showed that using polytetraﬂuoroethylene (PTFE) to repair hiatal hernia defects larger than 8 cm lowered the incidence of breakdown of the hiatus from 22% with primary crura closure to zero. They also failed to see evidence of erosions or strictures of the esophagus, which have been cited as potential pitfalls of mesh repair of large diaphragmatic hiatal hernias.25 However, mesh repair is not benign. Granderath and associates23 reported an increased incidence of postoperative dysphagia within the ﬁrst 3 months in patients who received mesh hiatoplasty compared with those who received standard nonabsorbable polypropylene suture hiatal closure. The signiﬁcant difference of the incidence of postoperative dysphagia between the groups did resolve at the 1-year follow-up evaluation. Although only case reports currently exist, biomaterials such as AlloDerm may prove to be better synthetic agents because of their capacity to revascularize. Vecchia and colleagues26 demonstrated in the pediatric population that AlloDerm may be useful for diaphragmatic repair because of the potential for ﬁbroblastic incorporation and small capillary ingrowth.

183

Suture Placement for the Wrap Intraluminal Sutures in the Esophagus ● Consequence Ulceration and odynophagia. Grade 2/3 complication ● Repair Endoscopic removal of the sutures. ● Prevention When sutures are placed to prevent a slipped Nissen, sutures from the wrap are commonly taken from the left portion of the cardia through the anterior wall of the esophagus and then to the retroesophageal portion of the cardia to complete the 360° wrap. Care must be taken when placing the esophageal sutures to get muscularis only and not full-thickness intraluminal bites.

Other Complications Gastric Ulceration Gastric ulceration has been reported as a cause for postoperative hemorrhage. Etiologies of these ulcerations are theorized to include trauma to the external wall of the stomach and/or full-thickness sutures with subsequent suture erosion and ulceration or from nasogastric or bougie trauma intraoperatively.27,28 Pianka and coworkers27 reported a case of acute upper gastrointestinal hemorrhage from a Nissen wrap ulcer, which they suggested could result from devascularized segments of the fundus secondary to division of the short gastric vessels, the surgical dissection, and gastric distention. Cueto-Garcia and associates28 also reported a case of postoperative gastric Nissen wrap ulcer in which two surgical clips were found at the inferior aspect of the ulceration. They concluded that devascularization from division of the short gastric vessels and dissection technique in the retroesophageal space may contribute to postoperative ulceration. Concurrent peptic ulcer disease, even when an adequate vagotomy has been performed, should be managed medically postoperatively with proton pump inhibitors to prevent hyperacidity and hypersecretion, which may also contribute to postoperative Nissen wrap ulceration.28 At least 15 cases have been reported in the open Nissen literature of aortoenteric ﬁstulas occurring at the point of the Nissen wrap eroding into the aorta. The cases reported suggest primary erosion from a gastric ulcer, but the question must be raised as to whether any degree of aortic injury or partial aortic wall tear at the time of the original surgery predisposed to this disastrous complication. The damage to the gastric blood supply and the mucosal barrier that occurs as a result of the trauma of surgery, as well as the new anatomic proximity created between the stomach wall and the aorta after LNF, may contribute to ﬁstula formation.29 Gastric ulcers are not the only reported

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entity to erode into the aorta and result in life-threatening hemorrhage. McKenzie and colleagues30 reported a single case of an adventitial aortic granuloma closely associated with a polypropylene suture placed at the fundoplication. The authors suggested the use of braided suture for both fundoplication and crural sutures to prevent the formation of granulomas and erosion into the aorta.30

Pancreatitis Pancreatitis from both gallstones and iatrogenic injury has been reported in patients postoperatively after LNF. Hughes and coworkers18 suggested that postoperative pancreatitis typically occurs as a result of blunt pancreatic trauma and that thin patients may be more susceptible owing to the limited amount of working space within the abdomen. The close proximity of the pancreas to the posterior wall of the stomach is important during stomach retraction and manipulation of instruments with retraction. Liver Hematoma Because of retraction of the left lateral segment of the liver to expose the GE junction and hepatogastric ligament, liver hematomas and retraction injuries are not uncommon but rarely lead to serious complications other than pain and discomfort. Pasenau and colleagues31 reviewed retraction injuries associated with LNF and reasserted the requirement for gentle retraction and use of atraumatic and blunt instruments to reﬂect the left lateral segment to allow full exposure. Speciﬁcally, they asserted that the type of retractor, the size of the patient’s left lobe of the liver, and the force applied on the retractor all contribute to safe retraction. They suggested monitoring the color of the retracted liver during difﬁcult cases to indicate when a pause in the procedure may be appropriate to prevent ischemia or venous engorgement injuries.31 Cardiac Injury Beyond the danger of hematoma and infarction during liver retraction for the LNF, Firoozmand and coworkers32 reported a case of cardiac tamponade resulting from right ventricular injury secondary to the use and positioning of the fan liver retractor. They suggested that the acute edge of the fan liver retractor may have led to the development of right ventricular laceration because continuous beating of the heart against the retractor edge contributed to the formation of a hematoma in the ventricular wall. The diaphragm is believed to have protected the pericardial sac from injury, but tamponade resulted when the ventricular wall hematoma ruptured as the mechnical strain on the ventricle wall intensiﬁed. Firoozmand and coworkers32 suggested careful evaluation of retractor positioning, frequent repositioning of the liver retractor, and early recognition of this fatal complication. An additional report of cardiac tamponade during LNF indicated that the etiology of the tamponade was believed to be secondary to right ventricular injury attributed to damage from a perforating

needle during ventricular contraction.33 Swide and associates34 reported a second case of ventricular injury secondary to direct myocardial trauma from a laparoscopic instrument. However, their patient did not suffer lifethreatening hemorrhage or tamponade, but experienced only intraoperative and postoperative electrocardiogram changes. These two cases demonstrate the need for constant vigilance with laparoscopic instruments, especially during the critical moments of crus dissection during the LNF.

Celiac and Superior Mesenteric Artery Thrombosis Mitchell and colleagues35 reported a case of celiac axis and mesenteric arterial thrombosis as the cause of the only mortality from their series of 156 LNF procedures. They described a patient with severe postoperative abdominal pain, leukocytosis, and elevated bilirubin status after LNF whose clinical picture deteriorated and who required an exploratory laparotomy. At the time of exploration, the proximal stomach and lower sixth of the esophagus were noted to be infarcted and gastric contents were leaking from all suture sites. The patient recovered from her initial exploration only to require a second reexploration that revealed further infarction of the remaining proximal stomach, gallbladder, spleen, and small and large intestine, sparing the duodenum and proximal jejunum. The patient eventually expired from hepatic infarction and overwhelming sepsis. The postmortem examination revealed a congenitally narrowed ostium of the celiac arterial trunk. Although rare, the danger of mesenteric ischemia must be considered during laparoscopic procedures because CO2 pneumoperitoneum has been shown to contribute to decreased splanchnic blood ﬂow as a result of vasoconstriction of the vascular bed and increased resistance to blood ﬂow across the liver. Prevention of mesenteric ischemia is best accomplished by avoiding hypercapnia through increasing minute ventilation and minimizing insufﬂation pressures (10–11 mm Hg).

REFERENCES 1. Rantanen T, Salo J, Sipponen J. Fatal and life-threatening complications in anti-reﬂux surgery: analyses of 5502 operations. Br J Surg 2000;87:967–968. 2. Evans SRT, Jackson PG, Czerniach DR, et al. A stepwise approach to laparoscopic Nissen fundoplication. Arch Surg 2003;135:723–728. 3. Dallemagne B, Weerts JM, Jahaes C, et al. Laparoscopic Nissen fundoplication: preliminary report. Surg Laparosc Endosc 1991;1:138–143. 4. Jackson PG, Gleiber MA, Askari R, Evans SRT. Predictors of outcome of 100 consecutive laparoscopic antireﬂux procedures. Am J Surg 2001;181:231–235. 5. Hahnloser D, Schumacher M, Cavin R, et al. Risk factors for complications of laporoscopic Nissen fundoplication. Surg Endosc 2002;16:43–47.

17 LAPAROSCOPIC NISSEN FUNDOPLICATION 6. Coelho JCU, Campos ACL, Costa MAR, et al. Complications of laparoscopic fundoplication in the elderly. Surg Laparosc Endosc Percutan Tech 2003;13:6–10. 7. Sydorak RM, Albanese CT. Laparoscopic anti-reﬂux procedures in children: evaluating the evidence. Semin Laparosc Surg 2002;9:133–138. 8. Powers CJ, Levitt MA, Tantoco J, et al. The respiratory advantages of laparoscopic Nissen fundoplication. J Pediatr Surg 2003;38:886–891. 9. Skandalakis JE, Gray SW, Rowe JS (eds). Liver. In Anatomical Complications in General Surgery. New York: McGraw Hill, 1983; p 110. 10. Schauer PR, Meyers WC, Eubanks S, et al. Mechanisms of gastric and esophageal perforations during laparoscopic Nissen fundoplication. Ann Surg 1996;223:43–52. 11. Flum DR, Bass RC. The accuracy of gastric insufﬂation in testing for gastroesophageal perforations during laparoscopic Nissen fundoplication. J Soc Laparoendosc Surg 1999;3:267–271. 12. Murdock CM, Wolff AJ, Van Geem T. Risk factors for hypercarbia, subcutaneous emphysema, pneumothorax and pneumomediastinum during laparoscopy. Obstet Gynecol 2000;95:704–709. 13. Joris JL, Chiche JD, Lamy ML. Pneumothorax during laparoscopic fundoplication: diagonsis and treatment with positive and expiratory pressure. Anesth Analg 1995;81: 993–1000. 14. Khajanchee YS, Hong D, Hansen PD, Swanstrom LL. Outcomes of antireﬂux surgery in patients with normal preoperative 24-hour pH test results. Am J Surg 2004; 187:599–603. 15. Watson DI, Pike GK, Baigrie RJ, et al. Prospective double-blind randomized trial of laparoscopic Nissen fundoplication with division and without division of short gastric vessels. Ann Surg 1997;226:642–652. 16. Dallemagne B, Weerts JM, Jehaes C, Markiewicz S. Causes of failures of laparoscopic antireﬂux operations. Surg Endosc 1996;10:305–310. 17. Lowham AS, Filipi CJ, Hinder RA, et al. Mechanisms and avoidance of esophageal perforation by anesthesia personnel during laparoscopic foregut surgery. Surg Endosc 1996;10:979–982. 18. Hughes SG, Chekan EG, Ali A, Reintgen KL. Unusual complications following laparoscopic Nissen fundoplication. Surg Laparosc Endosc Percutan Tech 1999;9:143– 147. 19. Leggett PL, Bissell CD, Churchman-Winn R. Aortic injury during laparoscopic fundoplication: an underreported complication. Surg Endosc 2002;16:362. 20. Baigrie RJ, Watson DI, Game PA, Jamieson GG. Vascular perils during laparoscopic dissection of the esophageal hiatus. Br J Surg 1997;84:556–557. 21. Patterson EJ, Herron DM, Hansen PD, et al. Effect of an esophageal bougie on the incidence of dysphagia follow-

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ing Nissen fundoplication: a prospective, blinded, randomized trial. Arch Surg 2000;135:1055–1061. Dahlberg PS, Deschamps C, Miller DL, et al. Laparoscopic repair of large paraesophageal hiatal hernia. Ann Thorac Surg 2001;72:1125–1129. Granderath FA, Schweiger UM, Kamolz T, et al. Laparoscopic anti-reﬂux surgery with routine mesh-hiatoplasty in the treatment of gastroesophageal reﬂux disease. J Gastrointest Surg 2002;6:347–353. Granderath FA, Schweiger UM, Kamolz T, et al. Laparoscopic Nissen fundoplication with prosthetic hiatal closure reduces postoperative intrathoracic wrap herniation: preliminary results of a prospective randomized functional and clinical study. Arch Surg 2005;140:40–48. Frantzides CT, Madan AK, Carlson MA, Stavropoulos GP. A prospective randomized trial of laparoscopic polytetraﬂuoreoroethylene (PTFE) patch repair vs simple cruroplasty for large hiatal hernia. Arch Surg 2002;137: 649–652. Vecchia LD, Engum S, Kogon B, et al. Evaluation of small intestine submucosa and acellular dermis as diaphragmatic prostheses. J Pediatr Surg 1999;34:167– 171. Pianka JD, Smith CD, Waring JP. Acute upper gastrointestinal hemorrhage from an ulcer on a Nissen fundoplication. Am J Surg 1999;177:359–363. Cueto-Garcia J, Rodrigues-Diaz M, Salas J, et al. Postoperative ulcer and hemorrhage: an uncommon complication of laparoscopic Nissen fundoplication. Surg Laparosc Endosc 1998;8:219–222. Wasvary H, Wease G, Bierema T, Glover J. Gastro-aortic ﬁstula: an uncommon complication of Nissen fundoplication. Am Surg 1997;63:455. McKenzie T, Esmore D, Tulloh B. Haemorrhage from aortic wall granuloma following laparoscopic Nissen fundoplication. Aust N Z J Surg 1997;67:816–818. Pasenau J, Mamazza J, Schlachta CM, et al. Liver hematoma after laparoscopic Nissen fundoplication: a case report and review of retraction injuries. Surg Laparosc Endosc Percutan Tech 2000;10:178–181. Firoozmand E, Ritter M, Cohen R, Peters J. Ventricular laceration and cardiac tamponade during laparoscopic Nissen fundoplication. Surg Laparosc Endosc 1996;6:394– 397. Farlo J, Thawgathurai D, Mikhail M, et al. Cardiac tamponade during laparoscopic Nissen fundoplication. Eur J Anaesthesiol 1998;15:246–247. Swide CE, Nyberg PF. Cardia trauma: an unusual cause of dysrhythmias and electrocardiographic changes during laparoscopic Nissen fundoplication. Anesthesiology 1996; 85:209–211. Mitchell PC, Jamieson GG. Coeliac axis and mesenteric arterial thrombosis following laparoscopic Nissen fundoplication. Aust N Z J Surg 1994;64:728–730.

18

Laparoscopic Esophagomyotomy with Dor Fundoplication Alexander Wohler, MD and Stephen R. T. Evans, MD INTRODUCTION Achalasia is a rare, acquired disorder characterized by the triad of aperistalsis of the esophagus, a hypertonic lower esophageal sphincter (LES), and a failure of LES relaxation in response to swallowing.1 The primary pathophysiology in LES hypertension is related to the destruction of myenteric ganglion cells via an inﬂammatory, possibly infectious, mechanism.2 This process leads to hypertonicity of the LES and its failure to relax normally in response to swallowing. The resulting functional obstruction, which causes dysphagia, leads with time to abnormal dilation of the more proximal esophagus. In fact, the abnormalities seen in the peristalsis of the esophagus may be solely a secondary phenomenon related to its prolonged abnormal distention.2 The “gold standard” for diagnosing achalasia, after an appropriate history and physical examination has suggested the disease process, is esophageal manometry, revealing the triad described previously. Some physicians choose to start with a barium swallow,2 which can suggest achalasia as well as evaluate for other disease processes and anatomic variations that may make endoscopy/ manometry more difﬁcult. An esophagogastroduodenoscopy (EGD), however, is essential in the preoperative work-up to evaluate not only for other disease processes such as malignancy or a stricture (both potential causes of pseudoachalasia) but also anatomy. Any suspicion of pseudoachalasia related to a malignant process warrants a computed tomography (CT) scan and other work-up as appropriate. Although multiple nonsurgical treatment modalities for achalasia exist, none is as effective as deﬁnitive surgical esophagomyotomy, usually performed via a minimally invasive technique. The response to pharmacologic agents such as calcium channel blockers and nitrates is usually poor and short-lived.2 Furthermore, nonsurgical interventions, such as forceful endoscopic dilation of the LES and LES botulinum toxin injection, are not without risk. Okike and coworkers3 found that the risk

of esophageal leak and mediastinal sepsis was four times higher in those patients undergoing endoscopic forceful dilation than in those treated with surgical esophagomyotomy. In addition, these interventions often increase the difﬁculty and morbidity of subsequent surgical myotomy1,4,5 and can also decrease the effectiveness of the procedure.2 The signiﬁcant reduction in operative morbidity afforded by minimally invasive surgery has increased the attractiveness of surgical esophagomyotomy over nonsurgical procedures. Both video-assisted thoracic surgery (VATS) and laparoscopic approaches are options, but studies have suggested that the latter is associated with a shorter hospital stay, decreased conversion rate, and better relief of dysphagia.6,7 Most series report a success rate of approximately 90% or higher in relieving symptoms with laparoscopic esophagomyotomy.1,4,8 This compares quite favorably with the long-term success seen with botulinum toxin injection or pneumatic dilation. Most patients who receive botulinum toxin injections do not achieve longterm relief, and the long-term success rate of pneumatic dilation is only about 65% to 70%.2,9 Although the majority of patients who undergo laparoscopic esophagogastric myotomy obtain excellent symptom relief, the procedure is not without complications. The operative mortality is low (e.g., <0.5%), if not zero, in most series. The most common serious complication, especially if not identiﬁed and repaired, is esophageal or gastric injury with immediate or delayed perforation. Other complications to be discussed include persistent or recurrent dysphagia, gastroesophageal reﬂux disease (GERD), bleeding, and paraesophageal hernia.

INDICATIONS ● Symptoms of dysphagia and/or regurgitation ● Manometric ﬁndings of: hypoperistalsis of the esopha-

gus, hypertonicity of the LES, and failure of relaxation of the LES

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● Failure of nonoperative techniques (although initial

operative correction is preferable in the absence of contraindications) ● No evidence of pseudoachalasia or advanced megaesophagus, neoplasia, and the like in preoperative work-up that would alter the operative plan

OPERATIVE STEPS

endoscopic identiﬁcation of the GEJ (squamocolumnar junction) but also is helpful in assessing the mucosa and myotomy after the dissection. The lighted endoscope, with the aid of insufﬂation, allows for inspecting the mucosa for small injuries or for residual uncut muscle ﬁbers overlying the mucosa (Figs. 18–1 and 18–2). Endoscopy is also useful in assessing the adequacy of the myotomy. To that end, some have even advocated intraoperative manometry to ensure the absence of residual high-pressure zones of the GEJ.9

Endoscope placement (left at the gastroesophageal junction [GEJ]) (optional) 2 Positioning and trocar placement 3 Takedown of the hepatogastric ligament/ removal of gastroesophageal fat pad 4 Takedown of the anterior phrenoesophageal ligament 5 Dissection anterior to the esophagus into the mediastinum 6 Takedown of the short gastric vessels 7 Esophageal and gastric myotomy 8 Inspection of the mucosa/myotomy 9 Dor fundoplication 10 Trocar removal and closure

Step 1 Step Step Step Step Step Step Step Step Step

OPERATIVE PROCEDURE Endoscope Placement Many surgeons place an endoscope at the GEJ prior to beginning the procedure. This not only allows for

Figure 18–1 Note the presence of residual muscle ﬁbers overlying the mucosa (black arrow), preventing complete separation of the myotomy edges (white arrows) in this segment.

Residual muscle fiber

Figure 18–2 Residual muscle ﬁbers constrict the otherwise bulging mucosa. Failure to divide these ﬁbers (often visually less obvious than illustrated here) will lead to persistent postoperative dysphagia.

18 LAPAROSCOPIC ESOPHAGOMYOTOMY WITH DOR FUNDOPLICATION

189

Positioning/Trocar Insertion Positioning and trocar placement and insertion are the same as those used for laparoscopic Nissen fundoplication (see Section III, Chapter 17).

Trocar Insertion Injuries Injuries related to trocar insertion are discussed in Section I, Chapter 8, Laparoscopic Surgery.

Takedown of the Hepatogastric Ligament/ Removal of the Gastroesophageal Fat Pad Injury to an Aberrant Left Hepatic Artery See Section III, Chapter 17, Laparoscopic Nissen Fundoplication.

Takedown of the Anterior Phrenoesophageal Ligament and Anterior Dissection into the Mediastinum Paraesophageal Hernia In contrast to the dissection performed in an antireﬂux procedure or takedown of a hiatal/paraesophageal hernia, the hiatal dissection should ideally remain limited in laparoscopic Heller myotomy.9,10 ● Consequence In gaining exposure to the anterior aspect of the GEJ, not only is extensive (i.e., circumferential) dissection usually unnecessary, but it also alters the GEJ physiologically and thereby may predispose to reﬂux. Furthermore, Chapman and associates9 described a postoperative paraesophageal hernia as a complication they encountered with laparoscopic myotomy, which necessitated repeat operation for repair. Grade 2/3 complication ● Repair One should inspect the hiatus after completion of the procedure to ensure that it is not excessively loose. The presence of a hiatal hernia or a shortened “sigmoid” esophagus, for example, may necessitate more thorough dissection around the GEJ than would normally be required. If the hiatal opening appears loose, it should be corrected with posterior crural sutures, keeping in mind that dysphagia may result from a tootight closure. ● Prevention Whereas some dissection is needed to expose the esophagus for an effective myotomy, this should mainly be performed anteriorly,11 with a minimum of lateral and posterior dissection. However, some make a small opening posterior to the esophagus in order to place a Penrose drain for traction.9 Regardless, the size of the hiatus and the potential for herniation must be assessed prior to closure (Fig. 18–3). This is particularly true if

Figure 18–3 The rather large hiatal opening in this patient predisposes to postoperative gastroesophageal reﬂux (GER) and paraesophageal hernia. Sutures are placed in the posterior aspects of the crura to minimize these risks (the ﬁrst suture is shown).

a signiﬁcant amount of dissection has been necessary, for example, in those patients with advanced disease and resulting “sigmoid” or shortened esophagus.12

Vagal Nerve Injury See later and Section III, Chapter 17, Laparoscopic Nissen Fundoplication. Esophageal Injury See later and Section III, Chapter 17, Laparoscopic Nissen Fundoplication. Pneumothorax, Pneumomediastinum, and Pneumopericardium See Section III, Chapter 17, Laparoscopic Nissen Fundoplication.

Ligation of the Short Gastric Vessels Ligation of the short gastric vessels allows for gastric mobilization such that the fundoplication can be performed.1 We perform complete ligation of the short gastric vessels with the harmonic scalpel. Others advocate limiting this dissection to the more cephalad short gastric vessels,1,9 presumably in the interest of minimizing disruption of the LES/GEJ physiology. Regardless, usually at least some of the short gastric vessels must be ligated in order to provide enough mobility of the proximal fundus to complete a fundoplication.

Bleeding See Section III, Chapter 17, Laparoscopic Nissen Fundoplication. Gastric Injury See Section III, Chapter 17, Laparoscopic Nissen Fundoplication.

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Gas Bloat Syndrome See Section III, Chapter 17, Laparoscopic Nissen Fundoplication.

Esophageal and Gastric Myotomy Esophageal or Gastric Perforation Certainly the most common serious complication of this procedure, especially if not recognized and repaired intraoperatively, is that of esophageal or gastric injury/ perforation, which occurs in approximately 5% of cases.2 The incidence of this complication can be signiﬁcantly higher, however (≥10%), in those who have undergone previous pneumatic dilation or botulinum toxin injection.1,9 ● Consequence The most feared complication of the procedure is mediastinal sepsis from esophageal leak or perforation (immediate or delayed). Mediastinal sepsis is particularly dangerous, with a high risk of mortality. Therefore, protecting against mucosal injury (or identifying it and repairing it should injury occur) is of utmost importance. That being said, the key to successful relief of dysphagia is effective myotomy, which leaves mucosa as the only barrier between the esophageal lumen and the mediastinum. This underscores the need for great caution with respect to avoiding mucosal damage. Furthermore, in addition to frank esophageal perforation, partial-thickness damage to the mucosa, especially from electrocautery (Fig. 18–4), can lead to delayed perforation, manifesting as mediastinal sepsis postoperatively. Grade 3–5 complication ● Repair Detection of mucosal injury is of utmost importance. Mucosal tears identiﬁed intraoperatively should be

Figure 18–4 The mucosal damage (arrow) occurred during the myotomy. Although this is not a frank perforation, subsequent necrosis of this portion of the mucosa may occur, causing a delayed perforation.

immediately repaired with a sutured closure, which can be performed laparoscopically, if the surgeon has sufﬁcient expertise, but may warrant conversion to an open procedure in some circumstances. An endoscope can be very helpful in identifying perforation by using insufﬂation and transillumination to identify problem areas of the mucosa. Repaired mucosal injuries or concern for mucosal damage in the absence of frank perforation can be effectively buttressed by the anterior Dor fundoplication,8 which is one of the reasons we prefer to perform this particular antireﬂux procedure in conjunction with myotomy. Postoperative care of patients in whom mucosal injury occurs includes keeping a nasogastric tube in place past the GEJ (intraoperatively positioned), nothing-by-mouth (NPO) status, and antibiotics. These measures are continued until a postoperative swallow study conﬁrms the absence of a leak. ● Prevention Although avoiding mucosal injury is of concern in every patient, the surgeon should be particularly cautious in those who have had previous esophageal procedures. Several series have reported a higher incidence of esophageal injury (some >10%) in patients who have undergone previous pneumatic dilations.1,4,5 One key to preventing mucosal injury is to minimize the use of electrocautery during the myotomy. In addition to causing full-thickness injury, electrocautery can damage the mucosa (see Fig. 18–4) such that a delayed perforation develops. Avoiding the excessive use of cautery will lessen the chance of mucosal injury, and to this end, a harmonic scalpel (our preference) or laparoscopic scissors can be used to complete the myotomy in the cephalad direction. Ultrasonic dissectors such as the harmonic scalpel are known to cause less collateral injury to surrounding tissue than electrocautery. Whereas the use of laparoscopic scissors eliminates the concern for collateral injury, the hemostasis afforded by ultrasonic dissectors is a distinct advantage. Great care must be taken to ensure that the appropriate plane is developed between the mucosa and the muscle ﬁbers and that the ultrasonic dissector (e.g., hook electrocautery) is pulled away from the mucosa prior to dissecting the muscle (Figs. 18–5 and 18–6). Failure to maintain sufﬁcient traction away from the mucosa (Fig. 18–7) greatly increases the chances of mucosal injury. When performing the gastric portion of the myotomy, it is important to realize that the plane just superﬁcial to the mucosa can be more difﬁcult to identify and develop in this region. Avoidance of mucosal injury, therefore, requires meticulous identiﬁcation of muscle ﬁbers and traction away from mucosa as they are divided.

Incomplete or “Healed” Myotomy The most important factor involved in ensuring the effective relief of dysphagia is the myotomy itself. Incomplete

18 LAPAROSCOPIC ESOPHAGOMYOTOMY WITH DOR FUNDOPLICATION myotomy is a major reason for operative failure, as is the failure to prevent “healing” of the myotomy by appropriately separating the muscle ﬁbers.9,11,13 ● Consequence Ineffective relief of dysphagia. Failure to perform a myotomy that extends appropriately in both cephalad and caudad directions from the GEJ will lead to early postoperative failure. Healing of insufﬁciently separated muscle ﬁbers of the myotomy will lead to delayed failure with recurrence of dysphagia. Grade 2/3 complication ● Repair An endoscope placed at the GEJ prior to the dissection allows for the assessment of myotomy completeness.

Figure 18–5 Proper technique. Note the traction that is placed on the muscle ﬁbers (away from the mucosa) prior to dividing them.

If, after the myotomy, the endoscope reveals any areas of remaining constriction, these areas are addressed with further identiﬁcation and division of muscle ﬁbers (see Fig. 18–1). Some have also used intraoperative manometry to ensure elimination of high-pressure zones, either at the distal or proximal aspects of the myotomy or related to initially unidentiﬁed residual muscle ﬁbers.9 Postoperative dysphagia can be effectively treated with pneumatic dilation.11 In order to reduce the risk of perforation, Zaninotto and colleagues11 recommended waiting at least 4 months postoperatively before performing forceful dilation. ● Prevention Accurate predissection identiﬁcation of the GEJ (i.e., by identifying the squamocolumnar junction endoscopically) can assist with ﬁnding the appropriate “starting point” for the myotomy. The myotomy should extend 8 cm proximally and also 2 cm distally onto the gastric cardia. One should see the mucosa bulging out from the myotomy site, and any residual muscle ﬁbers seen on the mucosa should be identiﬁed and divided. After the dissection is completed, the edges of the myotomy should be bluntly dissected away from each other to lessen the likelihood that they will reapproximate and heal (Fig. 18–8). As mentioned previously, the plane between the mucosa and the muscle ﬁbers can be more difﬁcult to develop distally at the gastric portion of the myotomy. Also, the mucosal bulge that results from effective myotomy is usually less prominent in this region. Both of these factors increase the risk of incomplete or healed myotomy and mucosal injury at the distal aspect of the myotomy. One

Circular m. layer

Mucosal layer

Longitudinal m. layer Anterior vagus n.

Figure 18–6 The appropriate technique of retracting away from the mucosa while dividing the muscle ﬁbers. Also shown is the expected bulging of the mucosa between the myotomized edges.

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A Figure 18–8 The rather large hiatal opening in this patient may warrant posterior crural sutures. Also demonstrated are the properly separated edges (arrows) of the myotomy as well as the resultant bulging of the mucosa from underneath.

B Figure 18–7 A, Improper technique. Note the relative lack of traction placed on the muscle ﬁbers (compare with Fig. 18–5). The proximity of the lower blade of the instrument to the esophageal mucosa will increase the risk of direct or collateral damage from the harmonic scalpel if it is activated in this location. B, Mucosal perforation due to harmonic scalpel injury identiﬁed during the procedure prior to laparoscopic repair.

should be especially careful, therefore, in dividing the muscle ﬁbers in this region, proceeding in a “ﬁber-byﬁber” fashion. Finally, the speciﬁc location of the myotomy with respect to the horizontal plane may be as important to its effectiveness as is its completeness vertically. Korn and coworkers14 described the importance of both the semicircular “clasp” muscle ﬁbers and the oblique “sling” ﬁbers in contributing to the tone of the LES. A myotomy that does not divide both of these ﬁbers may be less effective. To that end, as a general rule the myotomy should be made slightly to the left of the anterior vagal trunk (Fig. 18–9).

Gastroesophageal Reﬂux/Dysphagia Although minimally invasive esophagomyotomy, usually laparoscopic, is generally considered the preferred treatment for achalasia, considerable controversy exists regard-

ing whether a concomitant antireﬂux procedure is necessary as well as which type of antireﬂux procedure should be used.8,15,16 On one end of the spectrum, Ellis and associates17 and Okike and coworkers3 have advocated a limited myotomy (extension of the myotomy to only 0.5–1 cm onto the gastric cardia) without a concomitant antireﬂux procedure. In contrast, others advocate a full 360° fundoplication.16 Such a fundoplication, in the setting of an aperistaltic esophagus, can be easily complicated by postoperative dysphagia.13 A common, perhaps moderate, practice (and our preferred technique) is to perform a full myotomy, 8 cm above the GEJ and extended onto the cardia of the stomach for 2 cm, and then a subsequent Dor fundoplication. This, we believe, minimizes the risks of both dysphagia (related to incomplete myotomy or excessive tension from the fundoplication) and gastroesophageal reﬂux (GER) postoperatively. ● Consequence Failure to provide some barrier to reﬂux often leads to pathologic GER, whether or not it is symptomatic. Given the changes that occur in the distal esophagus from the underlying achalasia, it is possible that only a fraction of those patients with pathologic reﬂux complain of symptoms, which may be even more concerning, considering the long-term risks of reﬂux with respect to Barrett’s esophagitis and carcinoma. Grade 1/3 complication ● Repair If conservative measures are not effective, postoperative GER may necessitate reoperation for creating/revising a fundoplication. ● Prevention We recommend a partial “Dor” fundoplication, which has been demonstrated to provide excellent protection

18 LAPAROSCOPIC ESOPHAGOMYOTOMY WITH DOR FUNDOPLICATION

193

Incision

Anterior vagus n.

Figure 18–9 The prominence of the oblique “sling” ﬁbers on the left side of the gastroesophageal junction (GEJ). Performing the myotomy to the left of midline is generally recommended to ensure that both the clasp and the sling ﬁbers are divided.

against GERD18 while avoiding the potential complications of a more circumferential fundoplication. Others have utilized a 180° posterior “Toupet,” with good results. Whereas the Toupet does have the advantage of being able to prevent a healed myotomy (the fundoplication is secured to the edges of the myotomy, thus theoretically holding the edges apart),1 the anteriorly placed Dor protects against esophageal leak by buttressing the mucosa of the myotomized segment (Fig. 18–10).

Dor (or Toupet) Fundoplication Dysphagia Although some controversy exists in the literature regarding the necessity of an antireﬂux procedure after esophageal myotomy,16 it is generally recommended. The incidence of GER in those who undergo myotomy without fundoplication has been reported to be as high as 60%.7 However, whereas the myotomy may predispose a patient to GER, a major concern with including an antireﬂux procedure is that the very dysphagia that led to the procedure may persist as a result of an excessively tight fundoplication. Some authors recommend a “ﬂoppy” Nissen,16 but we and many others1,4,5,11,12,19 advocate partial fundoplication. Speciﬁcally, we perform an anterior Dor fundoplication.

Figure 18–10 Anterior Dor fundoplication buttresses the mucosa exposed by the myotomy, which protects against the development of delayed leak.

● Consequence Excessive LES tension created by fundoplication can lead to treatment failure. The debate over whether to perform a fundoplication and which type to employ is as yet unresolved. Given that the underlying symptomatology of achalasia is dyphagia and that esophageal hypomotility is one third of the diagnostic triad, it is not surprising that most authors advocate a partial

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fundoplication only. A complete myotomy followed by an inappropriately tight fundoplication serves only to re-create dysphagia. Furthermore, Dor fundoplication has been shown to be very effective in the prevention of postoperative GER. In their series, Richards and colleagues18 reported GER in 47.6% of those patients who underwent myotomy only, compared with only 9.1% in those who underwent a combined Heller-Dor procedure. Grade 2/3 complication ● Repair Intraoperative endoscopy can be used not only to guide and inspect the dissection but also to evaluate the GEJ after fundoplication. If the fundoplication leads to excess resistance to endoscope advancement, it should be revised. ● Prevention The use of a partial fundoplication, especially the Dor fundoplication, should not, if done correctly, provide undue resistance in the LES. Furthermore, in contrast to the Toupet fundoplication, the anteriorly placed Dor fundoplication buttresses any potential mucosal injury and also any mucosal repair that may have been necessary. Another theoretical advantage of Dor fundoplication over the posterior Toupet is that the former is less disruptive to the physiology of the LES. Bringing the stomach posterior to the GEJ may angulate the stomach anteriorly, increasing the likelihood of dysphagia. A fundoplication more circumferential than the Dor, if performed, should be decidedly loose to lessen the risk of postoperative dysphagia.

Other Complications Bleeding Bonavina and coworkers12 had one patient in their series who required reoperation secondary to bleeding from the myotomy site. Although this series dates from before the laparoscopic era, it seems relevant as a study of the potential complications of minimally invasive techniques. Especially when sharp dissection is used to perform the myotomy, bleeding from the cut surfaces may occur. Electrocautery or suture may be used to obtain hemostasis, provided that the muscle edges have been sufﬁciently dissected away from the mucosa. Alternatively, an ultrasonic dissector can be used to complete the myotomy, which is our preference. Although less collateral damage is generated with the ultrasonic instruments than with electrocautery, one must still be mindful of the potential for damaging the mucosa and maintain traction away from the mucosa while performing the dissection. Anterior Vagal Nerve Injury The anterior vagal trunk is at risk for injury during the dissection, myotomy, and fundoplication. Posterior vagal

trunk injuries are much less likely because dissection posterior to the esophagus should be limited, if not avoided altogether. Although postvagotomy diarrhea and delayed gastric emptying are more commonly complications of simultaneous anterior and posterior trunk injury, care should be taken to identify the anterior vagal trunk. Not only is it an important structure to preserve, it is also a landmark for where to perform the myotomy (slightly to the left of the anterior trunk) (see Fig. 18–9).

Splenic Injury Several series have reported splenic injuries,4,12,20 some of which have required open splenectomy. Whereas splenic injury is a risk during any laparoscopic procedure (see Section I, Chapter 8, Laparoscopic Surgery), it is of particular concern when working near the GEJ and proximal stomach. Excess traction on the stomach can lead to avulsion of short gastric vessels. Retractors and other instruments can also obviously lead to splenic injury. Poor exposure/visualization of gastrosplenic attachments, especially when dividing the more cephalad short gastric vessels, signiﬁcantly increases the risk of splenic injury. Patience (and sometimes an additional port site) is the best insurance against this problem.

REFERENCES 1. Luketich JD, Fernando HC, Christie NA, et al. Outcomes after minimally invasive esophagomyotomy. Ann Thorac Surg 2001;72:1909–1913. 2. Arain MA, DeMeester TR. Achalasia of the esophagus. In Cameron JC (ed): Current Surgical Therapy, 8th ed. Philadelphia: Mosby, 2004; pp 14–18. 3. Okike N, Payne WS, Neufeld DM, et al. Esophagomyotomy versus forceful dilation for achalasia of the esophagus: results in 899 patients. Ann Thorac Surg 1979;28: 119–125. 4. Peracchia A, Rosati R, Bona S, et al. Laparoscopic treatment of functional diseases of the esophagus. Int Surg 1995;80:336–340. 5. Marino M, Rebecchi F, Festa V, Garrone C. Surgical laparoscopy with intraoperative manometry in the treatment of esophageal achalasia. Surg Laparosc Endosc 1997;7:232–235. 6. Stewart KC, Finley RJ, Clifton JC, et al. Thoracoscopic versus laparoscopic modiﬁed Heller myotomy for achalasia: efﬁcacy and safety in 87 patients. J Am Coll Surg 1999;189:164–169. 7. Patti MG, Pelligrini CA, Horgan S, et al. Minimally invasive surgery for achalasia: an 8-year experience with 168 patients. Ann Surg 1999;230:587–593. 8. Wang PC, Sharp KW, Holzman MD, et al. The outcome of laparoscopic Heller myotomy without antireﬂux procedure in patients with achalasia. Am Surg 1998;64: 515–520. 9. Chapman JR, Joehl RJ, Murayama KM, et al. Achalasia treatment: improved outcome of laparoscopic myotomy with operative manometry. Arch Surg 2004;139:508–513.

18 LAPAROSCOPIC ESOPHAGOMYOTOMY WITH DOR FUNDOPLICATION 10. Sharp KW, Khaitan L, Scholz S, et al. 100 consecutive minimally invasive Heller myotomies: lessons learned. Ann Surg 2002;235:631–639. 11. Zaninotto F, Costantini M, Portale G, et al. Etiology, diagnosis, and treatment of failures after laparoscopic Heller myotomy for achalasia. Ann Surg 2002:235:186– 192. 12. Bonavina L, Nosadini A, Bardini R, et al. Primary treatment of esophageal achalasia: long-term results of myotomy and Dor fundoplication. Arch Surg 1992;127:222–227. 13. Ellis FH. Failure after esophagomyotomy for esophageal motor disorders. Causes, prevention, and management. Chest Surg Clin North Am 1997;7:477–487. 14. Korn O, Braghetto I, Burdiles P, Csendes A. Cardiomyotomy in achalasia: which ﬁbers do we cut? Dis Esophagus 2000;13:104–107. 15. Streitz JM, Ellis FH, Williamson WA, et al. Objective assessment of gastroesophageal reﬂux after short esoph-

16.

17.

18.

19. 20.

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agomyotomy for achalasia with the use of manometry and pH monitoring. J Thor Cardiovasc Surg 1996;111:107– 113. Frantzides CT, Moore RE, Carlson MA, et al. Minimally invasive surgery for achalasia: a 10-year experience. J Gastrointest Surg 2004;8:18–23. Ellis FH, Crozier RE, Watkins E Jr. Operation for esophageal achalasia. J Thorac Cardiovasc Surg 1984;88:344– 351. Richards WO, Torquati A, Holzman MD, et al. Heller myotomy versus Heller myotomy with Dor fundoplication for achalasia: a prospective randomized double-blind clinical trial. Ann Surg 2004;240:405–412. Swanstrom LL, Pennings J. Laparoscopic esophagomyotomy for achalasia. Surg Endosc 1995;9:286–290. Cacchione RN, Tran DN, Rhoden DH. Laparoscopic Heller myotomy for achalasia. Am J Surg 2005;190:191– 195.

19

Laparoscopic Gastric Bypass Bruce Schirmer, MD INTRODUCTION During the 5 years from 1998 to 2003, the ﬁeld of bariatric surgery in the United States underwent a veritable revolution. The number of Roux-en-Y gastric bypass (RYGB) procedures performed annually in the country increased from approximately 20,000 to 140,000.1 The major reason for this may be debatable, but this author’s hypothesis is that the explosion in popularity of the operation was driven largely by the availability of the performance of the operation using a laparoscopic approach. The temporal relationship of the advent of the laparoscopic approach and the rise in popularity of the operation are strongly correlated. Laparoscopic surgery was popular among young surgeons, and the popularity spread to bariatric surgery. The public and referring physicians had already demonstrated the inclination to view a laparoscopic approach to surgery as much more acceptable as a treatment option for operations such as cholecystectomy and antireﬂux surgery. This pattern continued with bariatric surgery. Multimedia and the Internet made the spread of information about laparoscopic gastric bypass much more rapid and prevalent. Laparoscopic Roux-en-Y gastric bypass (LRYGB) surgery became one of the most commonly performed abdominal operations in this country by the year 2003. During that year, approximately 130,000 gastric bypass operations were performed in the United States; in 1998, the number was approximately 20,000. The rapid proliferation of the operation resulted in the need for training opportunities for surgeons interested in beginning their experience with the operation. The complications that could occur with an inexperienced surgeon performing the operation became problematic in some situations. The large number of procedures performed led to a variety of complications being reported in the surgical literature. Although these were often not well quantitated in terms of frequency, the author’s own signiﬁcant institutional experience along with the literature will serve as the primary basis for judging such frequencies, in instances in which the literature is lacking. The relative brief duration of performance of LRYGB in large volume may preclude a true estimation of the incidence of certain long-term complications, yet the operation itself, done as an open procedure, has a track

record of over 40 years of careful scrutiny by the bariatric and surgical community.2 Unless directly related to the method of access, such long-term complications are as likely to occur after open as after laparoscopic RYGB. Therefore, an underestimation of their frequency is less likely. The literature already supports the fact that two considerable advantages to the laparoscopic over the open approach for RYGB are the signiﬁcantly lower incidence of wound complications and the remarkably lower incidence of incisional hernias.3 This chapter is dedicated to assisting the novice bariatric surgeon, as he or she initiates an experience with the performance of LRYGB, with the hope its contents may decrease the incidence of complications during that process. The trainee considering its performance in training or fellowship will hopefully similarly beneﬁt from this text. The experienced bariatric surgeon may ﬁnd these remarks interesting in a self-comparison assessment of his or her own experience with the pitfalls of performing LRYGB.

INDICATIONS ● LRYGB is performed to achieve surgically induced

weight loss for patients who are morbidly obese, as deﬁned next: ● Individuals who have a body mass index (BMI = weight in kg/height in m2) of 40 or greater with no comorbid medical conditions associated with or caused by obesity or those with a BMI of 35 or greater with at least one such comorbidity.4 ● Individuals should have demonstrated a failure to lose weight through nonsurgical dietary measures. Although data to support this indication are lacking, it is generally accepted.

OPERATIVE STEPS Step 1 Step 2 Step 3

Creation of a pneumoperitoneum Placement of trocars (ports) Laparoscopic survey and assessment of abdominal organs

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Enterolysis if necessary to free omentum and clear left upper quadrant Step 5 Division of small bowel and creation of Rouxen-Y limb Step 6 Enteroenterostomy Step 7 Closure of mesenteric defect Step 8 Creation of gastric pouch Step 9 Passage of Roux-en-Y limb Step 10 Gastrojejunostomy Step 11 Closure of remaining mesenteric defects Step 12 Closure of port sites Step 4

OPERATIVE PROCEDURE Creation of a Pneumoperitoneum Viscus Injury ● Consequence If the injury was created with a Veress needle, it is often of a relatively minor nature. Tangential laceration may cause hemorrhage or perforation, leading to leakage, infection, and peritonitis. If the injury to the hollow viscus was created by a cutdown to insert a Hassan trocar, the degree of injury may often be more severe and the perforation or injury of greater size. Creation of the pneumoperitoneum with a directly inserted trocar using visualization through the trocar without pneumoperitoneum is advocated by some. This approach, should visceral injury occur, would almost certainly lead to a more severe degree of injury than that with the Veress needle, similar to the severity rarely seen with the Hassan approach. Failure to detect and repair any signiﬁcant size injury often results in severe peritonitis and sepsis, frequently presenting after discharge. Delay in having the patient return for treatment often results in the patient representing in extremis, and mortality is not uncommon. Grade 1–5 complication

geons (SAGES).5 FLS instructs all trainees in the appropriate steps to minimize visceral injury during creation of the pneumoperitoneum. These steps include the elevation of the abdominal wall during Veres needle insertion. In the morbidly obese patient, this becomes problematic at the umbilical area. We recommend the use of a tracheostomy hook to elevate the fascia in the left subcostal midclavicular region, where underlying viscera are less common and less prone to injury. Use of this location for creation of the pneumoperitoneum in the morbidly obese patient is documented to be safe and effective.6 The Veress needle is then inserted through the elevated fascia. Use of a Hassan trocar is discouraged in the morbidly obese patient because of the large incision needed to reach the peritoneum with adequate visualization and, hence, the inability of that site to hold the pneumoperitoneum. Previous surgery in the left upper quadrant is an indication to insert the Veress needle in the right subcostal region, with care being taken to avoid liver injury. We do not favor the direct visualization technique because, in this author’s opinion, its best aspect is that it allows excellent visualization of the mucosa of the hollow organ being entered. It is contraindicated to use this approach in any area in which previous surgical scarring is likely.

Vascular Injury Whereas vascular injury may occur during creation of the pneumoperitoneum, it is usually more common with insertion of the trocars, unless the direct visualization technique is improperly used for creation of the pneumoperitoneum. Therefore, this complication is discussed later. Gas Embolism

● Repair Suture repair is indicated if hemorrhage or any appreciable perforation of a hollow viscus is evident. Solid organ injury with hemorrhage can usually be controlled with hemostatic energy sources. Extensive injury is reason for conversion to an open procedure to ensure adequate repair. Extensive injury may even require segmental intestinal resection.

● Consequence Gas embolism, although rare, is a life-threatening complication of creation of a pneumoperitoneum. CO2 gas is uniformly used to create the pneumoperitoneum during LRYGB. The solubility of the gas at least allows the potential for patient recovery if the complication is immediately recognized and treated. Failure to do so results in anoxic brain injury, pulmonary or visceral ischemia, and potentially, death from cardiovascular collapse. Grade 1–5 complication

● Prevention Surgeons who routinely perform laparoscopic surgery should be well versed in the potential complications of the creation of a pneumoperitoneum. It is recommended that all surgeons have documented training and accreditation in the performance of basic laparoscopy through the completion of the Fundamentals of Laparoscopic Surgery (FLS) program currently offered by the Society of Gastrointestinal and Endoscopic Sur-

● Repair The problem arises from insertion of the Veress needle into an intravascular space. The hemodynamic effects are similar to that seen with a massive pulmonary embolism. Sudden decrease in end-tidal CO2 with accompanying hypoxia and hypotension should alert the anesthesiologist and surgeon to this problem. Immediate action is needed. The Veress needle must be removed, the pneumoperitoneum decompressed,

19 LAPAROSCOPIC GASTRIC BYPASS the patient turned to a right-side-up position, and a central venous catheter passed to aspirate as much of the CO2 that still occupies the superior aspect of the right atrium as possible. ● Prevention Gas embolism occurs essentially exclusively with the Veress needle approach to pneumoperitoneum. Its incidence is very low, but attention to proper technique in terms of needle insertion, conﬁrmation of the “hanging drop” saline test to ensure the needle is in a free space of low resistance, and not persisting with insufﬂation at elevated intra-abdominal pressures on the insufﬂation monitor will prevent this complication.7

Cardiac Arrhythmia ● Consequence During insufﬂation of the pneumoperitoneum, a notuncommon problem is sudden development of cardiac arrhythmias, usually of the supraventricular type. Bradycardia is the most frequent arrhythmia seen. These are believed to arise because of the sudden change in venous return coupled with the change in intra-abdominal pressure. If appropriately managed, these are usually of little consequence and resolve quickly. However, persistence can mean conversion to an open operation for the procedure, cancellation of the operation altogether if too persistent and hemodynamically consequential, and further treatment, including pharmacologic therapy, as appropriate for bradyarrhythmias.8 Grade 1–3 complication ● Repair The immediate measure that must be taken is cessation of insufﬂation of CO2 and full decompression of the pneumoperitoneum, which normally resolves the arrhythmia. Occasionally, a pharmacologic agent is additionally needed. If the patient is suspected to be hypovolemic, this should be corrected. Once cardiac rhythm and hemodynamic stability have been achieved, it is appropriate to cautiously and slowly reinsufﬂate the abdomen to establish the pneumoperitoneum. In most instances, this will not result in a return of the arrhythmia. Should the arrhythmia return, the laparoscopic approach must be abandoned and a decision made by the surgeon as to whether to proceed with conversion to an open operation. The latter is appropriate only if hemodynamic stability occurs with decompression once again of the pneumoperitoneum. ● Prevention There is no guaranteed method of prevention of this complication. However, appropriate pharmacologic treatment of known existing cardiac arrhythmias preoperatively, adequate hydration and intravascular volume, excellent oxygenation, and inquiring about any previous arrhythmia history are all appropriate measures that will lessen the incidence of this complication.

199

Subcutaneous Emphysema ● Consequence Subcutaneous emphysema, including preperitoneal emphysema, and organ emphysema such as insertion of gas into the tissue planes of the omentum, are all considered under this heading. The occurrence of subcutaneous emphysema may not manifest itself until later during a long laparoscopic operation. Insufﬂation of the preperitoneal space or of the omentum will be immediately apparent on initial laparoscopic exploration. These latter two problems become issues only if they prevent the ability of the surgical team to safely visualize the organs in the operative ﬁeld. In this case, the operation may need to be converted to an open incision, delayed while the CO2 gas is absorbed, or cancelled. Rarely do further complications occur. In the case of subcutaneous emphysema, the increased CO2 load to the patient’s system can result in systemic acidosis. This may not be apparent simply from the measurement of end-tidal CO2 on the ventilator, which will be elevated as a result of the emphysema but may remain static although elevated. In patients with preexisting cardiopulmonary disease, inability to process the excess CO2 that is absorbed may lead to a systemic acidosis with resultant hemodynamic and metabolic complications.9 Grade 1–5 complication ● Repair Insufﬂation of CO2 into the preperitoneal space or the omentum will resolve with time. Placement of the trocar with the CO2 gas input securely within the peritoneal cavity will expedite the resolution of preperitoneal emphysema by exerting the pneumoperitoneum pressure on the peritoneal surface, which hastens gas absorption and decompression. Placement of an arterial line should be done if one is not in place and the procedure may be lengthy or if the patient has a history of preexisting cardiopulmonary disease. Serial arterial blood gases during the remainder of the operation are indicated to monitor systemic pH. Subcutaneous emphysema may occur because the port is only partially into the peritoneal cavity, causing direct insufﬂation of CO2 into the abdominal wall. Correction of the port position is indicated. If systemic pH drops, the operation may need to be completed using an open approach. ● Prevention Organ and preperitoneal insufﬂation can best be prevented by attention to technique with Veress needle insertion and stopping insufﬂation if the pressure rises to high levels after an amount of insufﬂated gas is less than expected. Reinserting the needle from the ﬁrst step is indicated in this situation. Subcutaneous emphysema is best prevented by visually conﬁrming that the port in which CO2 is being insufﬂated has its end

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securely within the peritoneal cavity. Avoiding repositioning, removing, and reinserting trocars during the operation will lessen the incidence of this problem. The thin elderly patient, with loose subcutaneous tissue, is at particular risk for the development of subcutaneous emphysema. Correct port placement technique is particularly important in these patients, and they should be carefully monitored for signs of this problem. Arterial blood gas measurement is indicated if the condition develops and persists. Lengthy laparoscopic procedures on such patients should be undertaken only when absolutely necessary and with the understanding that subcutaneous emphysema may result in conversion to an open incision to complete the operation.

Organ Injury ● Consequence Injury to an organ from trocar insertion after or before the creation of a pneumoperitoneum carries a signiﬁcantly higher likelihood of severe injury to the organ than does penetration with a Veress needle. Repair is almost always indicated, and the need for conversion to an open procedure is more likely. Unrecognized injury to a hollow viscus with a trocar carries an almost certain likelihood of delayed leak and peritonitis. Grade 1–5 complication ● Repair Repair of the injury is as described previously for such injuries in the section “Creation of a Pneumoperitoneum.” The principles are to arrest any hemorrhage and to repair any hollow visceral wall injury. ● Prevention Placement of trocars using a controlled twisting pressure, with care to avoid sudden rapid advancement of the trocar through the abdominal wall, is the best means of preventing this complication. Making an adequate skin incision such that the skin is not a source of resistance to the trocar insertion is important. Using a blunt-tip noncutting trocar will decrease but not prevent such injuries. Placing trocars only once an adequate pneumoperitoneum exists to serve as a counterresistance to the insertion pressure is also an important preventive and safety step. The initial trocar placement must by necessity be a blind maneuver, and this trocar has the overwhelming likelihood of creating such an injury. Inspection of the organs in the area of initial trocar insertion is always mandatory to conﬁrm that its insertion caused no injury. Subsequent trocars must always be placed under direct laparoscopic vision.

Vascular Injury ● Consequence The mechanism of vascular injuries is the same as that for hollow viscus injury: from the uncontrolled

initial trocar insertion into the peritoneal cavity. Whenever such a situation occurs, the patient is in a life-threatening situation. This is further compounded if the surgeon fails to realize the presence of the vascular injury, allowing untreated hemorrhage to occur. This complication is fortunately rare.10 However, many of the deaths from simple diagnostic and therapeutic laparoscopic procedures have been a direct result of vascular injuries from trocar insertion with resultant hemorrhage, hypovolemic shock, and death. Grade 1–5 complication ● Repair Vascular injury is treated with emergent control of the vascular injury. Direct pressure, followed by obtaining both proximal and distal control of the injured vessel, is indicated. This most often requires an emergent conversion to an open incision if a major vascular injury has occurred. Direct suture repair of the vascular injury is imperative as soon as such control is established. Ligation is an option if a smaller vessel is injured and ligation does not lead to untoward consequence. Visceral ischemia secondary to any vascular injury may necessitate partial or complete organ removal, as indicated. Major vascular injury is such a severe complication that accomplishing its repair is usually all the surgery that should be done at that setting, and of necessity, the original operation proposed should be postponed. ● Prevention Prevention of vascular injury is via the same measures as those used for prevention of organ injury, discussed previously.

Abdominal Wall Vascular Injury/Hematoma ● Consequence Insertion of a trocar through the epigastric vessels of the abdominal wall will result in potential uncontrolled arterial bleeding, at worst, or subsequent abdominal wall hematoma, at best. This complication may result in some morbidity to the patient if it is unrecognized or delayed, usually in the form of a painful and large hematoma. Intraoperative arterial bleeding is generally recognized and treated with the usual minor consequence. Failure to immediately recognize it does put the patient at risk for signiﬁcant hemorrhage and hypovolemic shock. Grade 1–4 complication ● Repair When the epigastric vessels have been lacerated and arterial bleeding is evident from around a trocar, control of the hemorrhage can usually be easily accomplished by passing two ligatures, at right angles to each other

19 LAPAROSCOPIC GASTRIC BYPASS and through the trocar site, using a suture passer. Each ligature should pass through surrounding tissue of the trocar opening, encompassing a bite of subcutaneous tissue, muscle, and fascia. The suture passer is used to retrieve the end of the suture to form a U-shaped suture. Two such sutures of permanent material, passed at right angles to each other and tied over external bolsters, will normally control hemorrhage from the vascular injury of the abdominal wall. The more transverse of the two sutures must be placed to occlude the arterial inﬂow side of the injured vessel. Ligatures should be pulled up taught before tying to conﬁrm that they will arrest the hemorrhage. The ligatures can be removed in 1 to 2 days, as can the bolsters. ● Prevention Maintaining an awareness of the location of the epigastric vessels during trocar insertion, and avoiding their location and potential injury, is the best prevention.

Inappropriate Port Placement ● Consequence This complication is mentioned only to conﬁrm its minimal consequences. Placement of a trocar that subsequently proves to be in a poor location, or in a direction that is almost useless for performing the operation, should NOT be viewed as a major problem. A different, appropriately placed trocar should be inserted as a substitute. Far more danger arises from trying to persist in the performance of an operation in which the trocars limit surgical maneuvering, suturing, or visualization than does the minimal danger or morbidity of placing an additional trocar. The inexperienced surgeon is much more prone to persist in using a suboptimally placed trocar, to the potential detriment of the operation. Grade 1 complication ● Repair Simple insertion of a better, more appropriately placed trocar is in the patient’s best interest if it allows safer and more rapid completion of the operation. ● Prevention Experience with the performance of an operation and the insertion of trocars will prevent location misplacement and inappropriate direction misplacement of a trocar, respectively. Trocar placement by experienced surgeons, or having the senior surgeon present to indicate trocar location, is the best prevention. Understanding that an inappropriately placed trocar is NOT a major problem and that it should NOT necessitate struggling throughout the remainder of the operation just to complete it must be a principle taught to all ﬂedgling laparoscopic surgeons.

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Laparoscopic Survey and Assessment of the Abdominal Organs Missed Abdominal Lesion ● Consequence The initial survey of the abdominal organs done during LRYGB should constitute a careful assessment of the liver, intestine, and pelvic organs as appropriate. The most likely unexpected pathology will be ovarian tumors in women. These can present as large cysts, dermoid tumors, or even unexpected ovarian carcinoma. Uterine pathology, intestinal diverticula, gastrointestinal stromal tumors (GIST), and other lesions are also possible unexpected ﬁndings. The consequence of missing these lesions is the delay in appropriate treatment, including excision, which may be indicated, with the potential for allowing the existence of lifethreatening pathology in the worst-case scenario. Grade 1–3 complication ● Repair Repair is not appropriate because this is an error of omission. ● Prevention The discipline to routinely look at the abdominal viscera, using a laparoscopic-guided approach, is the best prevention for missing such lesions. The liver is generally very obvious, and fatty inﬁltration or injury as severe as cirrhosis is usually unmistakable. However, the surgeon must take the time to look in the pelvis and, especially with women, conﬁrm that there are no tumors of signiﬁcant size that pose a potential threat to the patient’s life more severe than the obesity being addressed at surgery.

Fatty Liver with Cirrhosis ● Consequence Morbidly obese patients are predisposed to development of fatty liver and, if long-standing, to nonalcoholic steatotic hepatitis (NASH). NASH is present when scarring has occurred as a result of the fatty liver inﬁltration. NASH may progress, in a small number of patients, to cirrhosis and liver failure. Patients with diabetes are at the highest risk.11 Determination of disease presence and severity can help with the prognosis. Severe fatty liver and hepatomegaly can prevent a laparoscopic approach to the operation and make an open approach exceedingly difﬁcult. Cirrhosis is not in and of itself a contraindication to surgery, although this is controversial. Cirrhosis with accompanying portal hypertension is a contraindication to proceeding with LRYGB. Grade 1/2 complication ● Repair No surgical treatment exists for this lesion. Liver biopsy is always indicated to stage the disease whenever gross

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fatty inﬁltration of the liver is present. Some authorities recommend routine liver biopsy. Treatment is medical, primarily centered upon weight loss. ● Prevention Prevention of fatty liver that can make the exposure of the stomach for RYGB difﬁcult is done by two measures. First, patients should have a preoperative abdominal ultrasound to determine liver size and consistency and whether gallstones are present. Second, if the liver is fatty, the patient should be placed on a lowcarbohydrate diet for at least 6 weeks. Because liver fat is derived from the storage of glycogen and triglyceride from carbohydrate metabolism, a low-carbohydrate diet will shrink the liver and remove much of its fat content. Although level-one evidence to this effect is lacking, numerous personal experiences by bariatric surgeons with individual cases using this strategy for successful performance of LRYGB after an initial aborted attempt have led the bariatric surgical community to generally accept this practice. However, it has been shown that visceral obesity was most strongly correlated with hepatomegaly and steatosis in women undergoing gastric banding.12 Hepatologists recommend that, for the patient diagnosed with NASH, ingestion of any substance that is potentially hepatotoxic should be avoided and weight loss should be undertaken.

Excessive Adhesions ● Consequence Previous abdominal surgery may result in a large number of intra-abdominal adhesions, which are obvious after the initial trocar placement and peritoneoscopy. The surgeon must decide whether the adhesions preclude a safe and relatively feasible performance of laparoscopic RYGB or whether conversion to an open approach is indicated. This decision is one of individual judgment, based on the surgeon’s comfort with laparoscopic adhesiolysis. Severe adhesions may result in undetected organ injury during the adhesiolysis portion of the operation. Grade 1–3 complication

avoid injury to organs during adhesiolysis is the overriding concern.

Hernia of the Abdominal Wall ● Consequence Most hernias of the abdominal wall are readily apparent preoperatively by physical examination. Occasionally, owing to body wall thickness, unexpected small hernias may be encountered. They may require repair, which will lengthen the operative procedure. Failure to repair them could lead to incarceration of the small intestine in them postoperatively, Richter’s hernia. This causes a mechanical small bowel obstruction that, if untreated, can result in retrograde distention of the lower stomach and rupture of the staple lines with consequent peritonitis, sepsis, and potentially, death. Level 1–5 complication ● Repair Repair is recommended for all hernias large enough (roughly ≥1.5 cm) to potentially incarcerate bowel. Repair is best done using a piece of biologic mesh or small intestine submucosa for the repair. This material resists infection and functions well to patch the hernia. Principles of laparoscopic abdominal wall hernia repair are followed. For very large hernias, in which incarceration is most unlikely, repair is not indicated at the time of the initial LRYGB. ● Prevention Preexisting abdominal wall hernias cannot be prevented. The consequences of not repairing them can be prevented by repairing at the time of LRYGB, if indicated by the hernia size and location.13

Enterolysis If Necessary to Free the Omentum and Clear the Left Upper Quadrant Injury to the Abdominal Organs

● Repair Excessive adhesions may be dealt with using either a laparoscopic approach or converting to an open approach. The latter is faster for the adhesiolyis and must be entertained if the process will be excessively long laparoscopically. Otherwise, using progressively placed trocars in locations appropriate for LRYGB, the surgeon performs the necessary adhesiolysis to free up the upper abdominal organs and the omentum.

● Consequence Consequences of such an event are proportional to its recognition and correct repair. Should both occur, consequences, other than a prolongation of the operation, are minimal. Should the injury be severe, resection of a portion of the organ may be required. This leads to complications associated with such a procedure. The most severe consequence is an unrecognized injury of a hollow viscus. As discussed earlier in the section “Creation of a Pneumoperitoneum,” this situation usually results in a delay in diagnosis of a severe and life-threatening peritonitis. Grade 1–5 complication

● Prevention Adhesions from a previous operation cannot be prevented. They simply must be overcome. Taking care to

● Repair If the injury results in a perforation of a hollow viscus, repair must be complete, such that postoperative leak

19 LAPAROSCOPIC GASTRIC BYPASS and infection do not occur. Severe injury to a section of intestine or its blood supply may warrant resection and reanastomosis. ● Prevention Careful performance of the enterolysis, with good visualization of the tissue to be divided, avoidance of excessive retraction on the scarred tissue, and avoidance of the use of energy sources near any hollow viscus are the principles that minimize organ injury during enterolysis.

Hemorrhage ● Consequence Injury to a vascular solid organ, or to the mesentery or larger vessels in the abdomen during enterolysis may produce signiﬁcant hemorrhage. This can be life-threatening. Grade 1–5 complication ● Repair Standard measures to control hemorrhage are employed, including direct pressure, application of energy sources, and suture ligature. Outcomes are optimal if the injury is promptly recognized and appropriately treated using one of these methods. Conversion to an open incision may be necessary if laparoscopic means are not working. The need to always have a set of open abdominal instruments available for all LRYGB cases is emphasized by this potential complication. ● Prevention As with prevention of injury to a hollow viscus, the same principles of excellent visualization, careful tissue division, avoidance of excessive traction, and avoidance of any maneuvers outside of the direct visualization of the camera are the most important measures to prevent this complication.

Division of the Small Bowel and Creation of the Roux-en-Y Limb The ligament of Treitz is ﬁrst identiﬁed and then the proximal jejunum is measured for division to create the Roux-en-Y limb.

Misidentiﬁcation of the Proximal Jejunum for Division ● Consequence Failure to recognize the proximal jejunum and to then begin the operation by dividing more distal bowel will result in an unnecessary bowel division subsequently requiring reanastomosis to repair the problem. The danger of an extraintestinal anastomosis that could leak, the increased operative time, and the location of a potential postoperative internal hernia are all

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consequences of this complication. Should the surgical team continue with the operation after division of the bowel considerably beyond the ligament of Treitz, a signiﬁcant malabsorptive component to the operation will have been created that was not planned for or wished by the patient. Postoperative deﬁciency in iron and calcium will almost certainly occur and may be more refractory to correction with oral supplements. Steatorrhea, proliﬁc diarrhea as is seen after duodenal switch operations, fat-soluble vitamin deﬁciency, and protein calorie malnutrition can all result if the length of the biliopancreatic limb is excessive and the length of small intestine beyond the enteroenterostomy is too short. Grade 1–4 complication ● Repair Recognition of the error is the ﬁrst and most important step. Then the surgeon must determine whether the excess length of the biliopancreatic limb will likely produce any of the untoward effects noted above. If so, reanastomosis of the divided bowel is needed and then repeat creation of the Roux-en-Y limb—this time at the appropriate distance from the ligament of Treitz. ● Prevention Absolute conﬁrmation of the ligament of Treitz is imperative to prevent this complication. Factors that predispose to it and must be avoided include a poor camera operator who fails to keep the operative ﬁeld in constant vision, excessive scarring making identiﬁcation more difﬁcult, and massive obesity similarly making identiﬁcation difﬁcult. An inappropriately placed camera port can also predispose to this. Any time the surgeon is not clearly seeing the operation, the situation must be reassessed to correct the reasons. These may include placement of a more optimal trocar for the camera, ﬁnding a more expert camera operator, and better coordinating the team’s efforts to visualize the ligament of Treitz.

Tear/Injury in Handling the Small Bowel ● Consequence The potential to tear the small bowel exists in many stages of the operation, but it is discussed here. If tear or injury is recognized, appropriate repair minimizes this complication to simply a few minutes of additional operating time. If unrecognized, it has the same potential as any visceral perforation to cause peritonitis, sepsis, and death. Grade 1–5 complication ● Repair Repair must be preceded by recognition. Once the tear or injury is recognized, the injury is sutured laparoscopically to effect a good repair. If conversion to an open incision is necessary, it should be done. Rarely

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is such an injury severe enough to require bowel resection. Repair of a late, unrecognized injury involves bowel resection, reanastomosis, placement of drains, thorough peritoneal lavage, and consideration of creation of an ostomy proximal to or at the injury site if the tissue quality is not appropriate for secure anastomosis. Such patients are usually extremely ill and require the highest level of intensive care expertise postoperatively. ● Prevention The most important factor in preventing this injury is the use of good technique by the surgical team when handling the bowel. Bowel must be grasped with a large surface area of the grasper, handled gently, and not pulled excessively. Preoperative bowel preparation to decompress the bowel improves the lightness of the bowel and may help decrease this complication, although no data exist to prove that.

Ischemia of the Tip of the Small Bowel after Division ● Consequence A mild degree of ischemia can occur after small bowel division. Resection of the ischemic end of the bowel is needed. This complication, prevalent enough to not actually be considered a major adverse event, occurs because often the bowel mesenteric vessels are not easily seen through the overlying adipose tissue. They are divided unevenly, dividing too close to one side of the divided bowel. That side will suffer ischemia of the tip of the bowel. If ischemia is recognized and resected, minimal consequence results. If ischemia is allowed to persist, it could lead to postoperative breakdown of the stapled end of the bowel with leakage of bowel contents, peritonitis, sepsis, and death. Grade 1–5 complication ● Repair The problem is easily repaired by resecting back to viable and well-perfused intestine. This may at times mean several inches of bowel. The resected piece should be placed in a bag and removed immediately, unless it is so large as to require trocar site enlargement. Then, a notation of the presence of the bag must be made so it is not forgotten at the end of the operation. Reresection of the bowel is easily accomplished with the use of the linear stapler for both bowel and mesentery or with an energy source such as the harmonic scalpel for the mesentery division.

Hemorrhage of the Small Bowel Mesentery ● Consequence Figure 19–1 shows division of the small bowel mesentery, maintaining hemostasis. If some bleeding occurred during mesenteric division, a not-uncommon event, the surgeon must remain calm and methodically address

Figure 19–1 Dividing the small bowel mesentery.

the bleeding point or points. Small bleeding areas of the divided mesentery will often be evident after stapled division of the mesentery. Treatment is usually accomplished with no morbidity. If the bleeding arises from vessels at the base of the mesentery, in which case the division of the mesentery was carried down further than needed, then major bleeding may result that can require more severe measures for control, transfusion, and may even rarely be life-threatening if the patient has poor hemodynamic reserves. Conversion to an open incision is usually needed in cases of severe hemorrhage. Grade 1–5 complication ● Repair Small areas of mesenteric bleeding along the divided mesentery are easily treated with limited and local application of the harmonic scalpel for vessel coaptation and achievement of hemostasis. If the harmonic scalpel is used for mesenteric division, small vessels will not usually bleed. If the division of the mesentery is carried down inappropriately deep into the base of the mesentery, some mesenteric vessels in that area will not be adequately controlled with a single application of the harmonic scalpel or a stapler. In these cases, direct grasping of the mesenteric base to limit blood ﬂow followed by application of the harmonic scalpel in several adjoining locations on the vessel or careful placement of clips or sutures will achieve hemostasis. It is rare for hemorrhage along the more superﬁcial mesenteric edges to be severe enough to require conversion to an open incision. Major hemorrhage from deeper vessels will often require this measure. ● Prevention Once the bowel is divided, we usually use the harmonic scalpel to divide the mesentery. However, the linear stapler with a white load or gray load will also sufﬁce to achieve good hemostasis. Careful division of the

19 LAPAROSCOPIC GASTRIC BYPASS mesentery to provide adequate Roux-en-Y limb mobilization but avoid dissection to the very base of the mesentery, where larger and more difﬁcult to control vessels exist, is the key to preventing this complication (see Fig. 19–1).

Inadequate Length of Roux-en-Y Limb Mobilization ● Consequence The Roux-en-Y limb will not reach the proximal gastric pouch, necessitating efforts to later further mobilize it, which are much more difﬁcult after creation of the enteroenterostomy and closure of the mesenteric defect. This risks injuring the distal anastomosis. The Rouxen-Y limb may just barely reach the pouch, in which case tension on the anastomosis puts it at high risk for postoperative leak, resulting in peritonitis, sepsis, and death. Grade 1–5 complication ● Repair The steps to correct this include further division of the mesentery at the base of the Roux-en-Y limb, with care being taken to maintain hemostasis but avoid ischemia to the Roux-en-Y limb. Alternatively, passage of the Roux-en-Y limb retrocolic (retrogastric if the original plan was for an antecolic passage) lessens the distance needed to reach the gastric pouch. If tension is suspected after anastomosis, suturing the Roux-en-Y limb just distal to the anastomosis to the undersurface of distal stomach can help alleviate some of the tension on the anastomosis, especially with patient positional changes postoperatively. ● Prevention By experience, the surgeon can usually determine whether mobilization is adequate. We recommend approximately a 5-inch or longer division of the mesentery. Once division is accomplished, but before creating the enteroenterostomy, a quick check of the likelihood of the end of the Roux-en-Y limb to reach above the incisura of the stomach can be performed. If not, further division and mobilization is needed. For larger patients (BMI > 60), division of the jejunum at a point over 50 cm distal to the ligament of Treitz will provide greater mobility of the Roux-en-Y limb and should be strongly considered. It is always wise to prevent this complication rather than to have to deal with it later in the operation.

Misidentiﬁcation of the Roux-en-Y Limb Versus the Biliopancreatic Limb ● Consequence This occurs when the gastric pouch is made ﬁrst, then the jejunum is divided and brought up to do the gas-

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trojejunostomy ﬁrst, prior to the enteroenterostomy.14 If the biliopancreatic limb is mistakenly identiﬁed as the Roux-en-Y limb and anastomosed to the proximal gastric pouch, the surgeon then realizes when going to create the enteroenterostomy, that this has occurred. Great unhappiness results in the operating room when it is realized the infamous Roux-en-O has been created. If the anastomosis is left this way, food would go from the proximal gastric pouch to the distal gastric pouch. The proximal anastomosis must be taken down and redone, and the biliopancreatic limb must have the anastomosis point resected. Not only is excessive time spent doing this, but the proximal anastomosis, being revised, is now much more prone to leak. Grade 1–5 complication ● Repair If this complication does occur, the gastrojejunostomy should be taken down by dividing the biliopancreatic limb just distal to the anastomosis and resecting as little as possible of the proximal gastric pouch to remove the old anastomosis. It is preferable to resect the anastomosis, if the gastric pouch is large enough to allow a stapler to be placed above the anastomosis. Then that staple line must be tested for integrity. A new, stapled anastomosis is made between the correct end of the Rouxen-Y limb and the more proximal part of the gastric pouch. This new anastomosis should be treated as a redo anastomosis; a drain is placed adjacent to it, as well as a gastrostomy in the lower stomach. The biliopancreatic limb is correctly repositioned for appropriate placement and creation of the enteroenterostomy. ● Prevention Creation of the enteroenterostomy usually precludes this potential complication. To be absolutely certain it does not occur, once the proximal jejunum is divided to create the Roux-en-Y limb, a Penrose drain is sutured to the proximal end of the Roux-en-Y limb, for ease in later passage as well as for positive identiﬁcation. The Roux-en-Y limb must be constantly viewed with the camera from time of division to attachment of the drain to prevent misidentiﬁcation.

Enteroenterostomy Misalignment of the Bowel to Create the Twisted Mesentery of the Roux-en-Y Limb ● Consequence Creation of the enteroenterostomy is performed by aligning a portion of the Roux-en-Y limb, usually from 75 to 150 cm distal to the end of the Roux-en-Y limb, with the distal end of the biliopancreatic limb. The alignment must position the Roux-en-Y limb such that the proximal end is pointed upward toward the head, so that when it is passed to the proximal stomach the bowel is straight. Observing from the patient’s feet, the

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left side of the Roux-en-Y limb is the side to which the anastomosis must be made to conform to keep it straightly aligned. If during the alignment of the bowel segments, the end of the Roux-en-Y limb is allowed to slide down toward the feet and the portion of the Roux-en-Y limb is twisted such that the right side of the limb is now aligned next to the biliopancreatic limb, creating the enteroenterostomy with the bowel in this position will cause a twist in the Roux-en-Y limb mesentery as it passes back up toward the stomach. This is not acceptable, and the anastomosis must be totally revised. Once again, excessive operating room time is used, a segment of the biliopancreatic limb and the Roux-en-Y limb are lost, and there are two stapled anastomoses instead of one, multiplying the danger of leakage. Although harder to imagine, if the anastomosis were so incorrectly created and the twist in the Rouxen-Y limb not recognized, ischemia of the Roux-en-Y limb postoperatively could result, along with subsequent bowel infarction, peritonitis, sepsis, and death. Grade 1–5 complication ● Repair Once recognized, the anastomosis must be resected and revised. The biliopancreatic limb is divided just proximal to the anastomosis. There is enough length of it to create a new anastomosis, given that the usual length of division of the jejunum is at 30 cm or greater beyond the ligament of Treitz. It is best to resect the length of the Roux-en-Y limb involved in the anastomosis, and then perform an enteroenterostomy of the Roux-en-Y limb to reconstitute it. The new enteroenterostomy to the biliopancreatic limb is made a safe distance beyond this anastomosis. Mesenteric defects of both anastomoses must be closed at the time of their creation. ● Prevention When measuring the Roux-en-Y limb for length, and to determine the place for creation of the enteroenterostomy, the Roux-en-Y limb must always be passed upward and toward the left upper quadrant while being measured. This prevents the end from falling toward the feet. It is mandatory that this stage of the operation be carefully and constantly viewed by the camera operator and that the surgeon and ﬁrst assistant work together to effect a safe measurement of the Roux-enY limb while uniformly passing it in this direction. Once the locations of the two segments of bowel (Roux-en-Y limb and biliopancreatic limb) are determined, they are sutured together with a stay suture on the antimesenteric side. Before the anastomosis is created, a ﬁnal check to prevent this complication is mandatory to be certain that the Roux-en-Y limb is not twisted underneath this suture and coming back through the opening of the area below the bowel segments.

Misﬁring of the Stapler ● Consequence Misﬁring of the stapler may occur at any time during the operation. However, in creation of the enteroenterostomy, it carries particular potential morbidity. Injury to the bowel tissue, an incorrectly formed anastomosis, hemorrhage from the bowel edge if cut but not stapled, stenosis of the anastomosis from reﬁring over the area again, and leakage of the anastomosis owing to tissue weakening from two overlapping staple lines are all potential complications of this problem. Postoperative hemorrhage, bowel obstruction, and anastomotic leakage are potential resulting complications, all of which can be life-threatening. Grade 1–5 complication ● Repair The repair needed is based on what results after the misﬁring. If few staples were ﬁred and no tissue divided (when the cartridge essentially falls off because it was misloaded), little damage is done and a new ﬁring of the stapler is performed. It is essential to remove all unﬁred staples that may be in the way of the new staple line. Retrieval of the cartridge is, of course, necessary. If the stapler has divided tissue but the staples are incompletely ﬁred, the damaged bowel must be suturerepaired to prevent leakage and hemorrhage. If the staples have ﬁred only partially, the loose staples are removed, a new load is ﬁred to create the anastomosis, and the new anastomosis is both carefully inspected for integrity of staple line and, if possible, checked for leakage afterward by milking the bowel contents through the anastomosis and observing for signs of any leakage. Reinforcing sutures are always helpful to prevent leakage after a staple misﬁre at an anastomosis. Conﬁrmation that the newly created anastomosis is adequate is also necessary before closing the stapler defect. ● Prevention Fully trained scrub nurses and surgeons who handle the staplers are the ﬁrst and most important prevention. Loading the stapler correctly and positioning and ﬁring it correctly are usually the steps violated when stapler misﬁre occurs. However, there is no question that a stapler may be defective and misﬁre. All experienced surgeons have had this occur. The incidence of it is kept to a minimum by avoiding the human operator errors noted.

Perforation of the Bowel with the Stapler ● Consequence The surgeon may insert one jaw of the stapler too forcefully into the lumen, causing a perforation of the bowel. This most commonly occurs when the bowel segments are not appropriately aligned and one segment

19 LAPAROSCOPIC GASTRIC BYPASS of bowel is kinked at an angle, allowing the side of the bowel to be encountered by the advancing jaw of the stapler. Zeal of the surgeon to make sure the stapler is inserted to its full length while not observing the bowel near the tip of the stapler can lead to this complication. If recognized, it must be repaired; the patient is at risk for leak from the perforation site. If unrecognized, it will result in postoperative leak, peritonitis, sepsis, and potentially, death. Grade 1–5 complication ● Repair The perforation is repaired using sutures in most cases. If a major tear has occurred in the biliopancreatic limb and sufﬁcient length is available to resect this area and still have adequate biliopancreatic limb for an anastomosis, resection of the injured section of the biliopancreatic limb is best. The repair must be carefully performed and the damaged area securely closed. ● Prevention This complication is easily prevented by having the surgeon constantly being able to visualize the stapler jaws in their entirety. The enterotomies made for the stapler jaws should be of adequate size to prevent difﬁculty in inserting the jaws. The bowel segments must be aligned side by side without kinking so that the stapler jaws can be advanced smoothly into the two lumens of the bowel (Fig. 19–2). The process requires good cooperation on the part of the ﬁrst assistant and camera person to optimally assist the surgeon during insertion.

Inadequate Closure of the Stapler Defect ● Consequence The defect left by the linear stapler after creating the enteroenterostomy must be closed securely to prevent

Figure 19–2 Inserting the stapler the second time, from right to left, to perform the double-stapling technique.

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postoperative leakage of intestinal contents. If not closed securely, such leakage may result in localized abscess, potential scarring and obstruction, free leakage with peritonitis, sepsis, and death. Grade 3–5 complication ● Repair Suture closure of the enteroenterostomy stapler defect has been performed at our center with excellent results. Some surgeons advocate the “double-stapling technique” in which the linear stapler is ﬁred both proximally and distally at the enteroenterostomy site (see Fig. 19–2), the stapler defect can then be closed with another ﬁring of the stapler.15 This will work if the stapled edges are both held together and totally placed within the jaws of the closing stapler. We prefer to sew this defect closed, because the accuracy of suturing seems more appropriate to this step of the procedure. No data exist to show whether stapling or suturing is best. Should any leakage in the stapled or sutured closure be detected, suture repair is indicated. ● Prevention Careful suturing or stapling techniques to conﬁrm that a secure and complete closure of the defect made by the stapler is the only prevention. It is difﬁcult to do a leak test of this anastomosis, as is commonly performed for the gastrojejunostomy.

Stenosis of the Enteroenterostomy at Creation ● Consequence Stenosis of the enteroenterostomy, if severe, can lead to distention of the biliopancreatic limb and the distal stomach. Because this portion of the stomach has no “pop-off” valve, it cannot be decompressed without intervention. Failure to intervene quickly enough can result in rupture of the distal gastric staple line with peritonitis, sepsis, and death.16 Stenosis of the enteroenterostomy can also cause postoperative vomiting, which can lead to dehydration, ﬂuid and electrolyte imbalances and acute thiamine deﬁciency if prolonged, and places stress on the proximal anastomosis. Emergent operative treatment is usually indicated. Grade 3–5 complication ● Repair It is most important for the surgeon to recognize the problem early in its symptomatic development. We have found the major value of the postoperative day 1 Gastrograﬁn swallow is to alert us to the potential for this complication. Whereas percutaneous distal gastrostomy placement has been advocated by some as a means of acutely treating the distal gastric distention,17 we recommend emergent reoperation. This is usually accomplished in as rapid a time frame and allows for distal gastric decompression with an operatively placed gastrostomy as well as revision of the enteroenteros-

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tomy. We have found, through experience, that revision of the anastomosis is advisable unless a clear alternative mechanical reason, such as a kink in the distal jejunum just beyond the enteroenterostomy or another cause of obstruction, is found. Creating a new enteroenterostomy between the segment of Roux-en-Y limb just proximal to the existing anastomosis and the segment of distal jejunum just distal to the anastomosis, in a side-to-side fashion, is recommended. After the anastomosis is stapled, but before closure of the stapler defect, an instrument is inserted into the lumen of the jejunum to be certain there is still an adequate opening into the biliopancreatic limb for drainage. The operation can be accomplished laparoscopically, provided the distal stomach is not so distended as to preclude this approach. Also, placing the gastrostomy tube laparoscopically is quite feasible, but controlling any spillage of gastric contents as the tube is inserted can be a technical challenge without losing the pneumoperitoneum and visualization of the operation. ● Prevention We advocate using a double-staple technique for creation of the enteroenterostomy and closing the stapler defect with sutures. Beginning the suture closure at the alimentary tract side of the defect will minimize the risk of a suture catching the back wall of the intestine and causing narrowing (Fig. 19–3). We believe this approach minimizes the risk for postoperative distal anastomotic obstruction. Mesenteric closure prevents kinking of the jejunum just distal to the anastomosis (the “Brolin stitch” of open gastric bypass).18

Obstruction of the Anastomosis from Edema, Hemorrhage, or Technical Error ● Consequence This complication is identical to the one just described, except the lumen is totally obstructed and the etiolo-

gies may be from technical error, edema, or hemorrhage with intraluminal hematoma causing obstruction. The potential complications are identical. Grade 3–5 complication ● Repair The principles of repair are identical to those listed previously (see “Stenosis of the Enteroenterostomy at Creation”). However, in some cases in which edema is suspected to be the cause (swallow study shows minimal passage initially past the anastomosis), careful monitoring of the patient and conservative treatment can be justiﬁed only if the patient is clinically doing well and radiographic studies are done that deﬁnitively rule out a dilated distal stomach. Intraluminal hemorrhage will require the additional operative steps of evacuating the hematoma from the anastomosis, being sure the distal jejunum is not similarly obstructed with hematoma, and directly visualizing the anastomosis staple line to conﬁrm whether the hemorrhage has stopped. If hemorrhage is still ongoing, suture ligature to control it is indicated. An enterotomy adjacent to the area of the anastomosis is often the best way to do this. If a new enteroenterostomy is planned, this may be done with the stapler insertion site serving as the enterotomy. ● Prevention Prevention is similar to the prevention of stenosis of the anastomosis listed previously. Hemorrhage at the time of initial operation that is seen from the lumen of the bowel must of course be sutured to arrest the hemorrhage from the anastomotic staple line. Vomiting blood postoperatively must alert the surgeon to the potential for this complication, which needs attention, as does the hemorrhage itself, which could arise from either the enteroenterostomy staple line or the gastrojejunostomy staple line.

Closure of the Mesenteric Defect Hemorrhage from the Mesentery ● Consequence Suturing the mesenteric defect closed is mandatory to prevent postoperative internal hernia. Sutures placed too deeply into the mesentery may cause hemorrhage or hematoma. Hemorrhage is rarely of signiﬁcant volume but can require energy or sutures to repair if it is signiﬁcant. These sutures or the compression of a hematoma may impair blood supply to the jejunum of the enteroenterostomy, causing it to become ischemic. The entire anastomosis must then be redone, with resection of the ischemic area and two new enteroenterostomies performed. Grade 1–3 complication

Figure 19–3 Closing the stapler defect with sutures.

● Repair Repair of the bleeding is done initially with direct pressure. If this is insufﬁcient, use of a suture is more likely

19 LAPAROSCOPIC GASTRIC BYPASS to achieve hemostasis. If the bleeding point is very superﬁcial and easily identiﬁed, the harmonic scalpel may be applied with good effect. If ischemia of the jejunum occurs, the ischemic portion must be resected. Treatment is identical to that described in the section on “Misalignment of the Bowel to Create the Twisted Mesentery of the Roux-en-Y Limb” in that a portion of the Roux-en-Y limb must be resected, the biliopancreatic limb cut back, and two new anastomoses created. ● Prevention Careful suturing technique to take a very superﬁcial, although lengthy, bite of peritoneum when closing the mesenteric defect is essential to preventing this complication. Observation to avoid visible vessels in the mesentery with the superﬁcial sutures is also essential.

Ischemia of the Anastomosis ● Consequence The ischemia that may result from a hematoma from bleeding can also result from sutures placed too deeply into the mesentery during closure of the mesenteric defect. The resulting ischemia has the same consequence. Grade 1–3 complication ● Repair Repair is as described in the section on “Misalignment of the Bowel to Create the Twisted Mesentery of the Roux-en-Y Limb.” ● Prevention As with prevention of hemorrhage, prevention of ischemia also requires that the bite of tissue taken is a superﬁcial one, including just the peritoneum. The needle must be placed just under the peritoneum and passed parallel to it to include a sufﬁciently long length of peritoneum to have strength to hold the suture line together.

Failure to Close the Mesentery ● Consequence Failure to close the mesenteric defect after a bowel anastomosis leaves the patient at risk for an internal hernia. This can cause a closed-loop bowel obstruction with ischemia and gangrene of a signiﬁcant portion of the small bowel. This is life-threatening. The frequency of this complication has increased since a laparoscopic approach to RYGB was instituted.19 This is because few intra-abdominal adhesions form postoperatively, and the bowel is more mobile to slide into tissue crevices like the mesenteric defect. In addition, that defect is less likely to scar down on its own after a laparoscopic than after an open operation. Grade 1–5 complication

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● Repair Closure of the mesenteric defect is performed with permanent suture placed carefully, to prevent bleeding or ischemia but to close the peritoneal edges of the cut mesentery together. Either a running or an interrupted technique may be used. Exposure of the edges is often difﬁcult, and this can be a technically challenging portion of the operation. ● Prevention Prevention is by performing closure with adequate technique.

Creation of the Gastric Pouch Hemorrhage along the Lesser Curvature ● Consequence Dissection along the lesser curvature to create an opening for the stapler jaws to divide the stomach can be met with hemorrhage. This is usually easily controlled but can, if dissection is misplaced or technically incorrectly performed, result in signiﬁcant hemorrhage from the left gastric artery or its main branches along the lesser curvature. If hemorrhage is not easily controlled, this may lead to conversion to an open incision, signiﬁcant blood loss requiring transfusion, and hypotensive shock. Grade 1–4 complication ● Repair An experienced laparoscopic surgeon will usually control this hemorrhage with a combination of compression, application of the harmonic scalpel, and a suture ligature or an Endo loop. ● Prevention Careful dissection in an area just adjacent to the lesser curvature surface of the stomach is required to create an opening for the stapler. The harmonic scalpel is used for division of smaller vessels along or just superﬁcial to the gastric surface. Careful spreading dissection from the right upper quadrant trocar (at the surgeon’s left hand) creates the opening in the appropriate orientation such that the instrument breaks through the peritoneum into the lesser sac. Avoiding dissection too far off the stomach surface and too high up on the lesser curvature minimizes the risk for severe hemorrhage. Careful retraction of the mesentery is also necessary to avoid tearing the vessels.

Division of the Stomach Too Proximal ● Consequence Division of the stomach too close to the gastroesophageal junction leaves inadequate room for a technically easy gastrojejunostomy. The subsequent difﬁculty in

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creating an anastomosis close to the esophagus increases the risk for postoperative leak. Grade 1–5 complication ● Repair No repair for this problem once it is created. However, the anastomosis must be done to the very proximal stomach or, perhaps, almost directly to the esophagus. Only a highly proﬁcient laparoscopic surgeon should perform this anastomosis, because it is difﬁcult. Hand suturing is probably the best option for the anastomosis, but an end-to-end anastomosis stapler could conceivably be used, with the anvil passed through the esophagus. A linear stapler will not work owing to inadequate length of the gastric pouch. ● Prevention Careful assessment of the stapler placement before ﬁring the initial load of staples to start gastric division is important. The stapler jaws should be approximately 3 cm or more, preferably 4 cm, from the gastroesophageal junction along the lesser curvature. They can be placed even further distally, especially if there is concern that the Roux-en-Y limb may have difﬁculty reaching the proximal gastric pouch. By having the pouch longer yet still very small in terms of its diameter, we have not seen any difference in weight loss between those individuals who had slightly longer-length gastric pouches versus those with standard shorter ones. However, these data are observational impressions only.

Creation of Too Large a Pouch ● Consequence Creation of too large a proximal gastric pouch is not a major complication in and of itself. However, it will decrease the effectiveness of the operation, allowing the patient to eat more and potentially lose less weight. It also will allow for an increased incidence of both marginal ulcer and recurrent gastroesophageal reﬂux disease long-term. Grade 1–4 complication ● Repair The pouch can be cut down in size if this complication is recognized intraoperatively. This is much more easily done before the creation of the gastrojejunostomy. The surgeon should assess the pouch, and if she or he believes it is clearly too large, it should be resected further to a more appropriate size. If this results in intersecting staple lines, suture reinforcement at that point and testing for pouch integrity (leak test) are advised intraoperatively prior to performing the gastrojejunostomy. ● Prevention Careful assessment of pouch size as the staple loads are being ﬁred to divide the stomach is crucial. Some surgeons use a bougie, a lavage tube, or a Baker tube to

Figure 19–4 Creating the gastric pouch but taking care to exclude the fundus. It is best if the Ewald tube can be seen as it makes a distortion of the proximal gastric pouch.

help size the pouch. Others pass a ﬂexible endoscope. We use a Ewald or gastric lavage tube, placed by the anesthesiologist under laparoscopic vision and adjusted to lie along the upper lesser curvature of the stomach. The tube serves as a guide for pouch size. When stapling near the gastroesophageal junction to divide the stomach, the surgeon must be careful to exclude as much of the fundus as possible, because this part of the stomach is much more distensible and should not compose a signiﬁcant percentage of the pouch (Fig. 19–4).

Stapling across the Tube in the Stomach ● Consequence This unfortunate complication results in a tube that is stapled and usually divided. The portions of the tube must be removed from each staple line by resecting back those sections of the staple line. This allows the proximal tube to be withdrawn and the distal tube segment to be removed. Both staple lines, even if repaired, are now at increased risk for leakage, with the already deﬁned risks of staple line leakage. Grade 1–5 complication ● Repair One hopes this complication is always realized intraoperatively, and not postoperatively when the nasogastric tube is attempted to be removed. Reoperation is required in the latter case. Repair of this problem intraoperatively involves resecting enough of each staple line, usually with a laparoscopic scissors, to allow the tube segments to be freed up. This is usually less than a 1-cm length of staples. The defect is then sutured closed, preferably with a two-layer closure to encompass some of each side of the staple line. A leak test of the proximal pouch must then be performed. Strong consideration should be given to placing a laparoscopic gastrostomy in the distal stomach.

19 LAPAROSCOPIC GASTRIC BYPASS ● Prevention This complication is preventable if the surgeon ascertains from the anesthesiologist that the tubes are withdrawn from the stomach (including nasogastric tubes as well as temperature probes) before the ﬁrst stapler load is ﬁred. If a tube is used to help size and create the gastric pouch, the surgeon must be certain the tube position remains where intended and it is not allowed to shift or be withdrawn slightly and then pushed back in. This can result in the tube being caught in the stapler. Direct verbal communication every time with the anesthesiologist must be done at this step of the operation. We use a plastic and, hence, see-through upper drape during our LRYGB procedures, which visually conﬁrms the act of removing the tubes.

Stapler Misﬁre ● Consequence Stapler misﬁring during creation of the proximal gastric pouch carries the potential that the area of divided stomach during the misﬁre is incompletely and insecurely stapled. This can lead to postoperative staple line leak and its already stated sequelae. If the stapler knife cuts and staples are not ﬁred, the gastrotomy created is a risk for bleeding and leakage and must be repaired. Grade 1–5 complication ● Repair Repair is based on the injury. If a staple line is unstable or insecure, it must be sutured to prevent leakage. If there is hemorrhage, it must also be sutured to arrest it. Any defects in either the gastric pouch or the distal stomach staple lines must be repaired, reinforced, and tested (proximal is possible, distal is not). Distal gastrostomy may also be needed if there is concern about the staple line. ● Prevention As mentioned previously for the jejunojejunostomy, most stapler misﬁres involve operator error. Either the stapler is misloaded or the amount of tissue attempted to be divided may be too thick or have preexisting staples in it that prevent clean ﬁring. These operator errors are best prevented by training in loading the stapler as well as in ﬁring and using it. Because staple misﬁres do occur, there is no absolute way to prevent this complication.

Hemorrhage from the Staple Line ● Consequence Minor immediate and recognized hemorrhage is easily treated intraoperatively, with no consequence. Major intraoperative hemorrhage is rare but is usually also controlled without the need for transfusion or conversion to an open procedure. Postoperative hemorrhage

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can be signiﬁcant in volume and can, if sufﬁcient, subject the patient to hypovolemic shock and its sequelae. Transfusions may be needed. Reoperation, endoscopy, and angiography may all potentially be needed to arrest the hemorrhage, depending on its site and severity. Intraluminal hematoma from the stomach that passes to the area of the enteroenterostomy can cause alimentary tract obstruction and vomiting. If the distal stomach is the site, it may distend to the point at which staple lines rupture; massive contamination, peritonitis, and a high likelihood of death may follow. Grade 1–5 complication ● Repair Bleeding that occurs during operation and is identiﬁed can be treated with suture ligature or, for smaller amounts of hemorrhage, a brief application of the harmonic scalpel to the vessel lumen site. The most common site for this occurrence is at the edge of the lesser curvature during the ﬁrst stapler ﬁring. Inspection of the staple line after creation may demonstrate small bleeding sites as well. These are similarly treated. If a patient presents with postoperative tachycardia, decrease in hematocrit, and a radiographic picture of distal gastric distention (on computed tomography scan) or obstruction at the enteroenterostomy (swallow study), the site of bleeding must be presumed to be the distal stomach staple line. Treatment is emergent operative decompression of the distal stomach with a gastrostomy tube. We recommend this be done operatively, although success has been reported with percutaneous techniques (but for air not hematoma distention). Oversewing the distal gastric staple line, evacuating the distal stomach hematoma, and placement of a distal stomach gastrostomy are indicated. Hemorrhage from the proximal gastric pouch staple line will usually manifest itself with hematemesis as the primary symptom, even before hemodynamic changes occur. Upper endoscopy and direct endoscopic injection of the bleeding site is the treatment of choice.20 At the sign of hemorrhage of any type postoperatively, the patient’s deep vein thrombosis prophylaxis must be stopped and a coagulation panel checked to be certain that no element of coagulopathy is contributing to the problem. ● Prevention The incidence of postoperative signiﬁcant hemorrhage after LRYGB is under 3% and includes all types and sources of hemorrhage.21 Measures to prevent gastric staple line hemorrhage include a careful intraoperative inspection of these staple lines and avoiding overdosing any postoperative anticoagulation medication (including using any combinations that may be synergistic such as coumadin and low-molecular-weight heparin, given in therapeutic doses simultaneously). Aggressive management of hemorrhage can minimize the complications.

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Leak from the Staple Line ● Consequence Gastric staple line leakage postoperatively can result in massive peritonitis, sepsis, and death. Smaller, more contained leakages may result in intra-abdominal abscesses, often in the left subphrenic region. Grade 3–5 complication ● Repair Distal gastric staple line leaks. Recognition of the problem is the major obstacle to appropriate and timely care. The diagnosis of a distal gastric staple line leak is made more difﬁcult by the fact that an oral gastrograﬁn swallow study, considered the standard test for leaks from the gastrojejunostomy or proximal gastric pouch, will be normal in this setting. A high index of suspicion and any untoward signs such as unexplained tachycardia, tachypnea, excessive abdominal pain, fever, and persistent oliguria are all tips to the potential presence of this problem.22 Distal gastric distention from biliopancreatic intestinal limb obstruction and distention must raise the immediate suspicion of this problem existing or potentially occurring. Repair of distal gastric distention is via immediate operation, usually open but laparoscopic can be appropriate in some settings, with closure of the staple line, thorough lavage and elimination of contaminating ﬂuids in the abdomen, and placement of a gastrostomy tube in the distal stomach. Leakage from the proximal gastric staple line is treated identically as leakage from the gastrojejunostomy, described later. ● Prevention There is, unfortunately, no guaranteed method of preventing this complication entirely. Major series of LRYGB report leaks, which would include this site, at from 1% to 5%.23 Careful intraoperative attention to successful and complete division and closure of the stomach is the most important step. If staple misﬁre, staple line bleeding, or other problems arise to suggest that the staple line could be compromised, our approach is to be as certain as possible that excellent closure of the staple line has occurred intraoperatively (including testing the proximal pouch if indicated) and consideration of placement of a drain in the area as well as a distal gastrostomy, depending on the concern for the staple line integrity. Although the drain and gastrostomy may not prevent the leak, they can be useful in its management.24

Inadequate Division of the Stomach ● Consequence Inadequate division of the stomach leaves an isthmus of intact stomach, always at the area of the greater curvature near the angle of His. This passageway allows

for decompression and, hence, defeat of the process of proximal gastric restriction of intake of food. It also is a pathway for distal gastric juice, causing a high incidence of marginal ulcer when present. Grade 1–4 complication ● Repair The situation in which this usually occurs is in the very superobese patient undergoing LRYGB, in whom visualization of the area of the angle of His is difﬁcult. BMI alone may not be an accurate reﬂection of this difﬁculty: men with central obesity and a BMI of 50 may be more difﬁcult than a woman with a hips-and-buttocks fat distribution pattern and a BMI in excess of 70. Once recognized, treatment depends on the resultant symptoms from the remaining gastric communication. If weight loss is suboptimal or if a marginal ulcer develops, reoperation to complete division of the stomach is indicated. ● Prevention The best means of preventing this complication is to ensure the surgeon and the whole operating team see the two sides of the completely divided stomach at the area of the angle of His. If liver retraction prevents this, a second liver retractor should be placed. If telescope position is not optimal, an additional port should be placed to allow good visualization of the area. If these measures fail, conversion to an open incision may be necessary to accomplish this task, although the exposure and visualization using that approach are often less optimal than the laparoscopic approach, in this author’s experience.

Ischemia of the Proximal Gastric Pouch ● Consequence Fortunately, the stomach is very vascular, and this complication is rarely seen or reported. If it occurs, the surgeon must have ligated the left gastric artery near its takeoff. If recognized, resection of the remaining stomach and esophagojejunostomy is indicated. This is an operation with at least a ﬁve times higher leak rate for the anastomosis.25 If unrecognized, the ischemic gastric pouch will break down and a postoperative anastomotic leak, with its potentially lethal result, will occur. Grade 2–5 complication ● Repair The repair is hopefully done during the original operation when the condition is recognized. Reports of this are so scarce as to make it an extremely unlikely complication. If it occurs, the gastric pouch must be resected back to viable tissue, likely the distal esophagus, and an esophagojejunostomy performed. This anastomosis, because of its high potential for leak, should be treated

19 LAPAROSCOPIC GASTRIC BYPASS by placement of a perianastomotic drain and a distal gastrostomy tube. Conversion to an open operation may be needed to accomplish all these tasks. ● Prevention Avoiding hemorrhage from the upper lesser curvature of the stomach during dissection for initiating the creation of the proximal gastric pouch is the key preventive step. Only if the left gastric artery and its main feeding vessels to the proximal stomach are totally ligated would this result occur. This is unlikely, but avoidance during mesenteric dissection is key.

Passage of the Roux-en-Y Limb Injury to Colon ● Consequence If recognized and repaired successfully, there is minimal consequence. If unrecognized or inadequately repaired, colonic contents leaking postoperatively will cause fecal peritonitis, sepsis, and potentially, death. Grade 1–5 complication ● Repair Recognizing that this has occurred is key. In the retrogastric passage of the Roux-en-Y limb, this is unlikely unless there is difﬁculty, the gastrocolic ligament is opened to visualize the lesser sac, and the opening is made too close to the colon and causes injury. In the antegastric approach, usually the omentum is divided. At the base of that division, extending it too far can cause colon injury. Once recognized, the injury is usually small enough that two-layer suture repair is appropriate and satisfactory. ● Prevention Using the retrocolic approach, keeping the mesenteric opening at the base of the mesentery, and being careful to avoid opening the gastrocolic ligament very far from the greater curvature of the stomach (the ideal location is just beyond the gastroepiploic vascular arcade) will prevent this injury. Using the antecolic approach, halting omental division before the surface of the colon is encountered is imperative.

Injury to the Stomach ● Consequence Injury to the stomach, from the harmonic scalpel or traction injury, can potentially result in postoperative gastric necrosis and leak. The same consequences as for anastomotic leak would follow. Grade 1–5 complication ● Repair Repair of any gastric injury should be by immediate suturing, usually with an imbricating suture, to buttress

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the injury site and avoid postoperative perforation and leakage. The incidence of this injury is extremely low. ● Prevention Prevention of injury to the stomach is by clearly visualizing any use of an energy source in the creation of a mesenteric opening to the lesser sac. Avoiding touching the stomach with the energy source will prevent this complication. Similarly, avoiding excessive traction on the stomach that could result in an injury to its wall is also imperative.

Hemorrhage ● Consequence During retrocolic advancement of the Roux-en-Y limb, an opening is made in the mesentery of the transverse colon. If that opening is made through a major vessel of the colon mesentery, signiﬁcant hemorrhage may occur. This can lead to the need for further surgical maneuvers to stop it, at best, or conversion to an open operation and signiﬁcant blood loss with consequent hemodynamic shock, at worst. Grade 1–5 complication ● Repair If hemorrhage from the colonic mesentery is encountered, it must be controlled with direct pressure and grasping. Then either use of the harmonic scalpel (for a vein or smaller artery) or clips or sutures (for larger arteries) will affect an adequate control of the bleeding. If the bleeding has caused hemodynamic changes, appropriate ﬂuid resuscitation and transfusion should be performed as indicated. ● Prevention Creating a defect in the transverse colon mesentery that will minimize the risk of bleeding can be done if the defect is made just to the patient’s left of the ligament of Treitz and relatively low on the surface of the underside of the transverse colon mesentery. Staying to the patient’s left of the ligament of Treitz usually prevents injury to the middle colic vessels. Keeping the mesenteric defect relatively low on the transverse colon mesentery avoids the often-present large crossing vessel in the upper portions of the colon mesentery (marginal artery of Drummond or other crossing vessels that may exist and be unnamed).

Inadequate Length of the Roux-en-Y Limb ● Consequence If the Roux-en-Y limb will not stretch up to meet the proximal gastric pouch, the operation is already in trouble. Because the proximal gastric pouch is likely already created, it cannot be revised to make it longer. The mesentery of the jejunum must be

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further undercut to mobilize the Roux-en-Y limb further, and this presents the potential for bleeding and ischemia. Finally, once the anastomosis is created, it may be under tension, increasing the risk for leakage postoperatively. Grade 1–5 complication ● Repair If the Roux-en-Y limb is not long enough to reach the proximal gastric pouch, it must be further mobilized. If the distal anastomosis has already been performed, this task becomes very difﬁcult. The mesenteric closure must be taken down. The mesentery then must be further divided to allow enough mobilization of the Roux-en-Y limb to reach the proximal gastric pouch. This can be a difﬁcult technical maneuver, fraught with the potential for hemorrhage or ischemia to the existing Roux-en-Y limb or biliopancreatic limb. ● Prevention Adequate mobilization and length of the Roux-en-Y limb must be ascertained early in the operation when this maneuver is performed. Experience will usually allow the surgeon to visually assess whether the bowel will reach the proximal stomach. If any doubt exists, simply attempting to bring the bowel up to the proximal stomach immediately after creating the Roux-en-Y limb will conﬁrm adequate length. We have found that in patients with high BMI, the bowel mesentery can be short and the distance to the stomach longer. In these patients, we construct the gastric pouch longer, starting just above the incisura, to decrease the distance the Roux-en-Y limb must reach. The pouch can be cut back if the limb is long enough to reach higher.

Twist of the Roux-en-Y Limb Mesentery ● Consequence The Roux-en-Y limb must be passed upward to the proximal gastric pouch with no twists in it or its mesentery. Such undetected twists may result in postoperative ischemia, gangrene, necrosis, leakage of intestinal contents, peritonitis, sepsis, and death.26 Twists may also cause partial to complete bowel obstruction. Ischemic stenosis may occur over a longer time frame if none of the these manifest themselves ﬁrst. Grade 1–5 complication ● Repair If the twist is discovered prior to creation of the gastrojejunostomy, the Roux-en-Y limb is simply untwisted. If it is discovered at surgery after creating the anastomosis, the anastomosis must be taken down and revised after untwisting the Roux-en-Y limb. In our experience, this usually requires conversion to an open incision and puts the revised gastrojejunostomy at higher risk for leakage.

Figure 19–5 Passing the Roux-en-Y limb with emphasis on being sure the mesentery is downward.

● Prevention During passage of the Roux-en-Y limb, the entire surgical team must focus on the fact that the mesentery of the limb is straight and not twisted. Imaging the mesentery during passage is important to conﬁrm this. Using a retrocolic approach, which we do for LRYGB, the passage of the end of the Roux-en-Y limb into the lesser sac is carefully done to maintain the mesentery location straight downward (Fig. 19–5). Once the Roux-en-Y limb is passed up after dividing the stomach, the orientation of the limb must be identical to that which it had previously: the mesentery down, the staple line pointing toward the patient’s right side as it is brought up to just clear the distal stomach. If this is not true, the gastrocolic ligament must be opened to clearly visualize the entire Roux-enY limb and its mesentery, and the area at which the Roux-en-Y limb passes through the transverse colon mesentery must also be visualized to conﬁrm appropriate orientation.

Roux-en-Y Limb Obstruction at the Colonic Mesentery ● Consequence This complication occurs only with the retrocolic route of the Roux-en-Y limb. The mesenteric opening may be too tight or, more likely, later postoperatively develop scarring at the opening that kinks or narrows the Roux-en-Y limb. Partial to complete bowel obstruction can occur, with the need for reoperation to revise this area. Grade 2–4 complication ● Repair The opening in the transverse colon mesentery must be adequately large to allow the Roux-en-Y limb to pass

19 LAPAROSCOPIC GASTRIC BYPASS through it without constriction. If scar tissue has developed to form a constricting ring about the opening, it must be divided to alleviate the obstruction. If the surgeon used a running permanent suture to close the mesenteric opening, it can result in stenosis at the mesenteric opening. This suture must be divided and the resultant scar released. If the Roux-en-Y limb was not appropriately sutured to the mesentery at surgery, partial herniation of the limb into the retrogastric space can mimic the same types of obstructive symptoms as can scarring at the mesenteric opening. Reduction and resuturing of the bowel is indicated. ● Prevention Creating an adequate mesenteric opening, then suturing the bowel to it appropriately with interrupted permanent sutures will prevent this complication.

Gastrojejunostomy Stapler Misﬁre ● Consequence Staple misﬁring to create the gastrojejunostomy carries the same potential problems as it does for the jejunojejunostomy. In addition, it is particularly hard to correct this problem at the gastrojejunostomy site because only a small amount of gastric tissue is available for a new staple ﬁring. A new stapled or a revised handsewn anastomosis must be created after the misﬁring. This may involve conversion to an open procedure. Increased chance for postoperative leakage exists, the consequences of which were well deﬁned previously (see “Creation of the Gastric Pouch, Stapler Misﬁre”). Grade 1–5 complication ● Repair The repair required is based on the tissue injury caused by the misﬁre. If it is minimal, a new staple load may be ﬁred carefully, ensuring good tissue apposition and visually inspecting the anastomosis for competence and security. A postoperative leak test is indicated after closing the stapler defect. More severe injury to the tissues could require resecting back a portion of the gastric pouch or Roux-en-Y limb or both and creating a new anastomosis. If not enough gastric tissue is available and an opening exists in the gastric pouch, a handsutured gastrojejunostomy is the best option for constructing the anastomosis. Placement of a perianastomotic drain and a distal gastrostomy should be considered if the revised anastomosis is considered high risk for leakage. ● Prevention Prevention is similar to that for stapler misﬁrings, described previously for the jejunojejunostomy. There is no absolute prevention.

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Leak from the Anastomosis ● Consequence Postoperative leaks from the gastrojejunostomy represent the most frequent site for leaks after LRYGB.27,28 Leaks here pose the same risks to the patient’s health as in the other areas described previously (jejunojejunostomy and gastric staple line). Leaks may persist for months despite reoperation and closure. Grade 1–5 complication ● Repair The signs and symptoms of a leak are the same as that of leakage from the gastric staple line described previously. A high index of suspicion must be maintained by the surgeon for any patient with any such symptoms. Aggressive evaluation includes an emergent swallow test, which even if negative does not rule out the chance for a leak because these are known to be inaccurate in a signiﬁcant percentage of cases. Persistence of any untoward signs suggesting a leak is indication for emergent reoperation. If a leak is found, oversewing, buttressing the repair with tissue such as omentum, thorough drainage of the area, and placement of a distal gastrostomy are indicated. The surgeon must be prepared to care for a potentially very sick patient postoperatively, and all available intensive care facilities and consultants should be appropriately used as indicated. Persistent ﬁstulas may require many weeks to close, and drains should be monitored until no further output is seen. Then a swallow test should be conducted to conﬁrm no further leak before oral intake is restarted. Enteral feeding via gastrostomy during the recovery is indicated. Recent evidence suggests leaks from the gastrojejunostomy may be treated with a high rate of success using an endoscopically placed stent. Stent migration is the major complication when such an approach is used.29,30 ● Prevention Use of good technique to create the anastomosis is the best prevention (Fig. 19–6). Having no tension on the

Figure 19–6 Creating the proximal stapled anastomosis with the linear stapler. The stapler is in place, ready to ﬁre.

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anastomosis, having a cleanly ﬁred stapler to create it, and careful oversewing of the staple defect are all necessary. Good blood supply to both the stomach and the Roux-en-Y limb is important. An intraoperative leak test is highly recommended. Despite these measures used by surgeons, the leak rate after LRYGB is at or over 1% in most series, indicating that even these measures do not guarantee that this complication cannot occur. However, because it is the leading cause for postoperative legal action against bariatric surgeons, the surgeon is wise to follow all precautions. In addition, maintaining a high index of suspicion for a leak postoperatively will improve the likelihood it is promptly diagnosed and treated, and thus minimize complications from it.

Tension on the Anastomosis ● Consequence Finding that the anastomosis is under some tension at the time of its creation poses the risk for a higher incidence of postoperative leakage. This leakage can result in peritonitis, sepsis, and death, as described in the section “Leak from the Anastomosis.” Tension on the anastomosis may also result in postoperative stenosis of the anastomosis from chronic ischemic stricture. This typically presents 6 to 12 weeks postoperatively with symptoms of vomiting and food intolerance.31 Grade 1–5 complication ● Repair The repair is based on the degree of tension. If only a very small amount exists, we suture the Roux-en-Y limb to the side of the proximal gastric pouch (done in all cases), and that process provides us with further feedback on the tension, if any, present. If after creating this suture line, the tension issue seems resolved, we proceed with anastomosis. If the tension seems too severe before creating the anastomosis, we proceed to lengthen the Roux-en-Y limb as described previously under “Inadequate Length of the Roux-en-Y Limb.” A leak test is always done. ● Prevention Prevention involves recognition of tension and alleviating the situation. The same measures indicated for preventing an inadequate length of the Roux-en-Y limb, described previously, should be followed here as well.

Hemorrhage from the Anastomosis ● Consequence Hemorrhage from the gastrojejunostomy during surgery requires suture ligature repair or harmonic scalpel energy to stop the hemorrhage. Care must be

taken to avoid tissue necrosis or stenosis of the anastomosis during this process. Hemorrhage postoperatively can result in hematemesis, aspiration, need for hospitalization and transfusion, hypovolemic shock, and need for endoscopic or even operative measures to arrest the hemorrhage. Hemorrhage can be life-threatening. Grade 1–5 complication ● Repair Repair involves stabilization of the patient, assessment for amount of blood loss, resuscitation with intravenous ﬂuids and blood products as indicated, ruling out any coagulopathy, and aggressive use of upper endoscopy to assess the bleeding site and perform epinephrine injection to arrest the bleeding.20 Other endoscopic measures such as heater probe or bicap cautery may be used but are less advisable because of a higher likelihood of tissue injury leading to perforation. Operative suturing of the anastomosis is indicated if endoscopic measures fail. ● Prevention There is no absolute prevention for this problem, as noted previously for hemorrhage from the gastric staple line. Oversewing or use of suture line buttress materials to perform the anastomosis has not been shown to totally eliminate this complication. The incidence of this complication is fortunately low, probably in the 1% range.23 Noting and treating intraoperative suture line bleeding is important to prevent postoperative problems from large amounts of blood loss.

Stenosis of the Anastomosis ● Consequence Stenosis of the gastrojejunostomy may present very early after surgery (postoperative days 1–2) from edema or technical error in creating too small an anastomosis. Subsequent stenosis usually presents at 6 to 12 weeks postoperatively, but later presentation is possible associated more with concurrent marginal ulcer and the edema and scarring from it.31 Stenosis causes nausea, vomiting, food intolerance, dehydration, electrolyte disturbances, acute thiamine deﬁciency, and even renal injury if dehydration persists too long. Thiamine deﬁciency can produce permanent neurologic deﬁcits such as Wernicke’s encephalopathy picture if not appropriately treated.32 Endoscopic, ﬂuoroscopic, and operative procedures may be needed to treat this problem. Protein calorie malnutrition may also evolve if stenosis is chronic and untreated. Grade 1–5 complication ● Repair Usually, the problem is suggested by the patient’s symptoms. If highly suspected, we recommend an upper endoscopy to both diagnose and treat the problem. Endoscopic balloon dilation is indicated for

19 LAPAROSCOPIC GASTRIC BYPASS any anastomosis with a diameter less than 10 mm, essentially one that does not allow the scope to pass through. Usually one or two dilations will sufﬁce to treat the stenosis, but further dilations may sometimes be needed. A ﬂuoroscopic dilation may be indicated if more than one endoscopic dilation has failed, because the radiologist can use a larger-diameter balloon than can the endoscopist. Reoperation is rare; in our experience, it is limited to those few patients with associated marginal ulcers that failed to heal without severe stenosis.31 Any patient who presents postoperatively after a bariatic operation, including LRYGB, should be given intravenous thiamine and B vitamins (similar to treatment for alcoholism) before the administration of intravenous glucose. Fluid resuscitation, electrolyte replacement, and even short-term parenteral nutrition may be indicated depending on the severity of dehydration and malnutrition seen. ● Prevention The incidence of gastrojejunostomy stenosis after LRYGB can be minimized by several measures. The type of stapler used to create the anastomosis has been related to the incidence of stenosis.33 The linear stapler is associated with an exceedingly low incidence of this problem (<1% in our recent experience34) The use of a circular stapler is associated with an incidence of between 9% and 14% stenosis.35 Smaller-circumference circular staplers are associated with the higher end of this spectrum. Hand-sewn anastomoses are associated with a lower stenosis rate, usually in the 3% to 5% range.36 Use of totally absorbable suture is reported to be associated with a lower incidence than use of permanent suture.37 Tension and ischemia will also increase the incidence of this problem. The development of a marginal ulcer should be promptly treated in its early stages to allow resolution with the minimum amount of residual scarring.

Marginal Ulcer at the Anastomosis ● Consequence Marginal ulcers develop at or just distal to the gastrojejunostomy. They cause epigastric pain, and may also cause dyspepsia, nausea, food intolerance; in cases in which the ulcer becomes severe and deep, bleeding and gastrogastric ﬁstula may occur. Although medical treatment may cure most ulcers, those associated with the latter complications can cause life-threatening bleeding and will need operative treatment. The incidence of marginal ulcers after LRYGB is reported as between 2% and 12%.38 Grade 2–5 complication ● Repair Marginal ulcers are diagnosed by using ﬂexible endoscopy to visualize the gastrojejunostomy anastomotic

217

area. Upper gastrointestinal series have a sensitivity that is too low to be reliable. Persistent epigastric pain after LRYGB is an indication for upper endoscopy. If marginal ulcer is conﬁrmed, the treatment is medical. Triple antibiotic therapy effective against Helicobacter pylori as well as a proton pump inhibitor (PPI) at standard twice-daily dosing for 3 to 6 months then once daily for an additional 6 months are indicated. Repeat upper endoscopy is needed only if symptoms persist or stenosis symptoms occur. Patients must avoid smoking and intake of nonsteroidal anti-inﬂammatory drugs (NSAIDs), because these will prevent ulcer healing or cause them, respectively. If a marginal ulcer is large or deep on endoscopy, if symptoms have been present for weeks, or if the ulcer fails to heal with standard therapy, an upper gastrointestinal contrast series is indicated to rule out ﬁstulization of the ulcer from the proximal gastric pouch to the lower stomach.38 In addition, if there has been incomplete division of the stomach such that a gastrogastric ﬁstula at any location exists, the patient will need operative therapy to divide the ﬁstula, resect the area of involved stomach, and dilate the gastrojejunostomy. If the patient is severely stenotic, the gastojejunostomy may need to be revised. ● Prevention The prevention of marginal ulcer is improved by making the proximal gastric pouch small to decrease potential acid production, minimizing foreign material in performing the anastomosis (such as reinforcing with permanent suture), treating patients with documented H. pylori infection preoperatively to eradicate the organism,30 and ensuring complete division and separation of the proximal gastric pouch from the lower stomach. In addition, patients complaining of persistent epigastric pain should be aggressively endoscoped to rule out this problem, and treated early if the condition is present. It must be stressed to patients that they must stop smoking and they must refrain from ingesting NSAIDs. Nonessential steroid usage should be eliminated.

Closure of the Remaining Mesenteric Defects Internal Hernia via the Colonic Mesentery Opening ● Consequence If a retrocolic passage of the Roux-en-Y limb has been used for LRYGB, the mesenteric defect in the transverse colon mesentery must be closed to prevent postoperative herniation. If it is not, herniation of another loop of bowel adjacent to the Roux-en-Y limb into the retrogastric space or herniation of the Roux-en-Y limb itself to form an accordion-like mass of bowel behind the stomach will result in postoperative bowel obstruc-

218

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tion with potential for bowel ischemia and necrosis. Vomiting, dehydration, electrolyte imbalances, tissue necrosis with perforation and peritonitis, and death may potentially occur. Grade 1–5 complication ● Repair Bowel obstruction after LRYGB is a surgical problem. Conservative therapy is inappropriate and dangerous because of the high incidence of closed-loop obstruction and internal hernia.39 Because adhesion formation is low after LRYGB, bowel obstruction is most likely to be from an internal hernia of some type. Diagnosis is by symptoms and computed tomography scan. Plain ﬁlms may be suggestive if air-ﬂuid levels are seen in the left upper quadrant behind the stomach. Computed tomography scan may be diagnostic if it demonstrates loops of small bowel behind the stomach. Operative therapy is indicated. We have usually been able to use a laparoscopic approach. If the Roux-en-Y limb itself has been herniated behind the stomach, careful reduction, with or without enlargement of the mesenteric opening as needed, is performed. When completely reduced, the Roux-en-Y limb is resutured to both the mesentery and the adjacent ligament of Treitz with permanent suture. The bowel must obviously appear healthy and without any areas of suspected necrosis after reduction. If another loop of bowel has passed into the lesser sac adjacent to the Roux-en-Y limb, it is reduced and inspected. If viable, resuturing the Rouxen-Y limb to the mesentery is all that is needed. If the bowel is not viable, resection and reanastomosis are indicated. ● Prevention The incidence of this problem is zero when the antecolic passage of the Roux-en-Y limb is performed. When the retrocolic passage of the Roux-en-Y limb is performed, we have found a dramatic reduction in the incidence of this complication with the use of permanent suture to stitch the side of the Roux-en-Y limb to the patient’s right as it passes through the colon mesentery to the biliopancreatic limb just distal to the ligament of Treitz. Two sutures placed approximately 1.5 cm apart create a ﬁxed segment of the two loops of bowel. The uppermost suture used for this joining of the two bowel segments also includes two bites of the colon mesentery, one at 1 o’clock and another at 10 o’clock on the mesenteric opening (Fig. 19–7). This effectively closes the excess mesenteric space around the Roux-en-Y limb, with the exception of the side of the limb on the patient’s left. That side is then sutured to the transverse colon mesentery using at least one additional permanent suture in the 3 o’clock position. Using this “triple stitch” technique, we have observed a herniation rate of all types involving the colon mesentery defect of approximately 1%.

Figure 19–7 Creating the “triple-stitch.” The suture is being placed in the mesentery after it was ﬁrst placed in the bowel, just before tying.

Petersen’s Space Hernia ● Consequence Herniation of the small bowel underneath the mesentery of the Roux-en-Y limb after gastric bypass has been termed Petersen’s hernia. This complication may occur after any Roux-en-Y limb operation. If it occurs, the symptoms may be minimal if the space is large and the bowel can freely pass back and forth beneath the mesentery. However, if the space is small, herniation of a signiﬁcant portion of the bowel will result in its entrapment under the mesentery, with potential ischemia to the entrapped bowel as well as, potentially, the Rouxen-Y limb. Bowel obstruction symptoms, followed by sequelae of bowel ischemia and necrosis, will follow if operative treatment is delayed and the problem not promptly treated. Recently, centers that perform small bowel transplantation have seen a number of referrals for patients who had loss most of the small intestine after gastric bypass owing to this complication. Death has also been reported.40 Grade 1–5 complication ● Repair Recognition of the problem is the ﬁrst and foremost issue. Most bariatric surgeons will quickly appreciate this possible problem in a patient after LRYGB who presents with a clinical and radiographic picture of small bowel obstruction. The problem is that a bariatric surgeon is often not the person who initially treats and evaluates such patients. Well-intentioned but ignorant general surgeons may often hospitalize the patient, place a nasogastric tube, and give intravenous ﬂuids— the accepted initial treatment for adhesive postoperative small bowel obstruction. However, after LRYGB, adhesive obstruction is much less likely than internal herniation and closed-loop obstruction. Therefore, the treatment for any patient after LRYGB who presents with a clinical and radiographic picture consistent with small bowel obstruction is operative. Emergent lapa-

19 LAPAROSCOPIC GASTRIC BYPASS rotomy or laparoscopy is indicated, based on the surgeon’s talents and the patient’s bowel distention. Reduction of any internal hernias is necessary. Often, the identiﬁcation of which piece of bowel is which becomes very confusing. It is recommended that the terminal ileum at the ileocecal valve be positively identiﬁed, then the ileum be traced retrograde to the jejunum and then to the area of the enteroenterostomy. Petersen’s hernia will be evident because some of this distal bowel will be herniated under the mesentery of the Roux-en-Y limb. Decompressing and reversing any such volvulus and herniation are indicated, after which the bowel must be assessed for viability. If no ischemia is present, the Petersen defect is closed. If a retrocolic Roux-en-Y limb is present, the limb can be sutured to the ligament of Treitz (see previous section). If an antecolic Roux-en-Y limb is present, the defect between the base of the Roux-en-Y limb mesentery and the transverse colon mesentery must be closed. This is a very difﬁcult technical procedure, and one of the contributing reasons we prefer the retrocolic approach to Roux-en-Y limb passage. Use of an omental patch into the space can be considered if the defect is large. If the reduced bowel is necrotic in any area, resection and reanastomosis are indicated. Patients who have had bowel necrosis from such an obstruction may be extremely ill owing to the consequences of the bowel ischemia; multiorgan system failure must be anticipated and all measures taken to combat it. ● Prevention The closure of Petersen’s space is always indicated after retrocolic LRYGB. Some surgeons who perform antecolic LRYGB do not advocate closure of this space, but accumulating case reports of bowel loss from herniation through this space strongly suggest this defect should always be closed.41 Important to the prevention of bowel ischemia is the prompt diagnosis and operative treatment of any patient who presents with a picture of bowel obstruction after LRYGB.

Stenosis of the Roux-en-Y Limb at the Mesentery ● Consequence This complication is rare and is a result of either chronic obstruction at the Roux-en-Y limb mesentery (described previously under “Roux-en-Y Limb Obstruction at the Colonic Mesentery”) or chronic ischemia of the bowel from tight scarring in this area or excess tension and ischemia on the Roux-en-Y limb mesentery. The consequence is a stenotic area of bowel that, if symptomatic, is usually not amenable to endoscopic dilation but requires operative resection and reanastomosis. Grade 1–4 complication ● Repair This complication is rare. However, if it occurs, it will present with obstructive symptoms similar to those of

219

gastrojejunostomy stenosis. The same sequelae as that complication (described in the section on “Stenosis of the Anastomosis,” under “Gastrojejunostomy,” previously) may occur. Treatment is similar in terms of initial resuscitation with attention to thiamine replacement followed by intravascular rehydration. Nutritional status must be addressed. Upper gastrointestinal series will conﬁrm the diagnosis, and reoperation to resect the stenotic section of bowel is usually indicated. Dilation may on occasion be successful. ● Prevention This problem is rare and can be prevented by avoiding excess tension on the Roux-en-Y limb, as well as avoiding excess tightness and scarring of the mesenteric closure around the Roux-en-Y limb by using an interrupted and not a continuous running permanent suture for mesenteric closure.

Hemorrhage from the Mesentery ● Consequence Rarely, suturing the Roux-en-Y limb to the transverse colon mesentery can be met with bleeding from the transverse colon mesentery. This is usually easily arrested. The colon is rarely in danger of ischemia because of the collateral circulation that exists within the upper portions of the mesentery. Grade 1/2 complication ● Repair The hemorrhage is controlled with placement of additional interrupted sutures in the area of the bleeding of the mesentery, with care being taken not to suture too high on the mesentery and injure the collateral crossing vessels of the colon. ● Prevention This complication is prevented by taking care to avoid visible vessels in the transverse colon mesentery when sutures are placed to close the mesenteric defect.

Hematoma of the Roux-en-Y Limb ● Consequence Suturing the mesenteric defect closed as described previously (under “Closure of the Mesenteric Defect”) can involve a hematoma of the Roux-en-Y limb or the biliopancreatic limb. Because the biliopancreatic limb must allow the passage of only bile and pancreatic juice, this hematoma is inconsequential. However, if a larger hematoma were to result in the wall of the Roux-en-Y limb, a partial bowel obstruction could potentially occur. However, this complication is exceedingly rare. Grade 1/2 complication

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● Repair Compression to limit the size of the hematoma is all that can be done intraoperatively. Conservative therapy postoperatively until the hematoma resolves, with the retention of a liquid diet only for a longer than usual period of time, is usually all that is needed. ● Prevention This complication is prevented by avoiding an excessively large bite of the Roux-en-Y limb when closing the mesenteric defect.

Closure of the Port Sites Richter’s Hernia ● Consequence Failure to close the port sites, especially those 10 mm and larger, is associated with a very low but deﬁnite possibility of Richter’s hernia, in which a loop of small intestine becomes partially incarcerated into the port site opening. Intestinal obstruction may occur. The incarcerated portion of the bowel may become ischemic. Perforation and peritonitis with its sequelae could develop. This process can be seen with complete herniation of the bowel into an abdominal wall hernia defect as well.42 Grade 3–5 complication ● Repair The problem must ﬁrst be recognized. Unexplained bowel obstruction symptoms, especially within the ﬁrst few days after surgery and with a more distal bowel location as the obstruction site, should make one think of this potential complication. Diagnosis is by computed tomography scan and index of suspicion. If the scan is not conﬁrmatory and symptoms persist, diagnostic laparoscopy is deﬁnitive. Treatment is then based on bowel condition. Resection of any ischemic bowel is indicated. Repair of the port site hernia defect is also indicated. ● Prevention Closure of all port sites of 10 mm or larger should be performed at the conclusion of all LRYGB procedures in order to best prevent this complication. Data from bladeless trocars suggest that perhaps these trocars do not leave a large enough hernia defect to need closure.43 However, closure is still the best prevention.

Wound Infection ● Consequence The incidence of wound infection after LRYGB is considerably less than that after open surgery. Comparisons between the two approaches have shown a decrease of from approximately 7% to a 1 to 2% incidence of wound

infections in open versus laparoscopic approaches.23 The severity of the laparoscopic wound infections is usually minor as well owing to their size. Our experience with over 1000 LRYGBs is that we have seen only 1 port site wound infection that went on to develop an abdominal wall fascial infection and loss of some tissue of the abdominal wall. Most infections are superﬁcial and treated as outpatient problems. Grade 1–3 complication ● Repair Treatment of port site wound infections is a combination of local treatment involving opening the wound and draining and débriding any nonviable tissue at the site. Packing and wound care are then indicated. Oral antibiotics are sufﬁcient in most instances, and culture is appropriate if purulence is present to conﬁrm antibiotic sensitivity. Rarely does inpatient admission and intravenous antibiotics or operative therapy for tissue débridement because of deep-seated abdominal wall infection occur. However, these measures may be needed if standard outpatient wound care and oral antibiotics do not reverse the infectious process. ● Prevention Use of appropriate sterile technique, avoiding wound contamination by not removing any contaminated tissue through the port site without placing it in a bag, gentle technique of wound closure to avoid tissue injury, hemostasis at the wound site to prevent hematoma, and appropriate use of immediately preoperative parenteral broad-spectrum antibiotics with appropriate intraoperative redosing as indicated are the measures that will, if used routinely, limit the incidence of wound infections. Appropriate early wound drainage, local care, and antibiotics with careful follow-up for treatment effectiveness will minimize the likelihood of a more serious wound infection developing.

Hemorrhage from/Hematoma of the Abdominal Wall ● Consequence Closure of the port sites may be complicated by injury to abdominal wall vessels that produce a hematoma or hemorrhage from the port site. The consequences are identical to those of hematoma and hemorrhage that may occur at the start of operation with trocar insertion. Intraoperative measures can usually limit the problem to a small hematoma or amount of blood loss. Unrecognized bleeding that occurs slowly postoperatively may accumulate to form a large and painful postoperative hematoma of the abdominal wall, usually within the rectus sheath. Treatment is usually nonoperative, and the hematoma absorbs over 6 to 8 weeks. Rarely, hemorrhage or hematoma immediately after surgery can require reoperation. Grade 1–3 complication

19 LAPAROSCOPIC GASTRIC BYPASS ● Repair Intraoperative treatment is the use of sutures passed with a suture passer through the abdominal wall, as described previously for hemorrhage following trocar placement (under “Creation of a Pneumoperitoneum”). Two well-placed sutures at right angles to each other will usually arrest the hemorrhage or hematoma formation. ● Prevention Prevention of this problem is highly likely if the suture used to close the trocar sites is passed through the abdominal wall at the 12 and 6 o’clock locations of the wound. This minimizes the likelihood of injuring the epigastric vessels, if the port is near them.

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31. Schirmer B, Erenoglu C, Miller A. Flexible endoscopy in the management of patients undergoing Roux-en-Y gastric bypass. Obes Surg 2002;12:634–648. 32. Salas-Salvado J, Garcia-Lorda P, Cuatrecasas G, et al. Wernicke’s syndrome after bariatric surgery. Clin Nutr 2000;19:371–373. 33. Gonzalez R, Lin E, Venkatesh KR, et al. Gastrojejunostomy during laparoscopic gastric bypass: analysis of 3 techniques. Arch Surg 2003;138:181–184. 34. Lee SK, Dix J, Miller MS, et al. The inﬂuence of a laparoscopic approach for the performance of Roux-en-Y gastric bypass on surgical outcomes at a university teaching hospital during the past decade. Surg Obes Relat Dis 2006;2:289–290. 35. Nguyen NT, Stevens CM, Wolfe BM. Incidence and outcome of anastomotic stricture after laparoscopic gastric bypass. J Gastrointest Surg 2003;7:997–1003. 36. Higa KD, Boone KB. Laparoscopic Roux-en-Y gastric bypass for morbid obesity: technique and preliminary results of our ﬁrst 400 patients. Arch Surg 2000;135: 1029–1034. 37. Capella JF, Capella RF. Gastro-gastric ﬁstulas and marginal ulcers in gastric bypass procedures for weight reduction. Obes Surg 1999;9:22–28.

38. Schirmer BD. Strictures and marginal ulcers in bariatric surgery. In Buchwald H, Cowan GSM, Pories WJ (eds): Surgical Management of Obesity. Philadelphia, Saunders Elsevier, 2007; pp 297–303. 39. Higa KD, Ho T, Boone KB. Internal hernias after laparoscopic Roux-en-Y gastric bypass: incidence, treatment and prevention. Obes Surg 2003;13:350– 354. 40. Mason EE, Renquist KE, Huang YH, et al. Causes of 30day bariatric surgery mortality: with emphasis on bypass obstruction. Obes Surg 2007;17:9–14. 41. Paroz A, Calmes JM, Giusti V, Suter M. Internal hernia after laparoscopic Roux-en-Y gastric bypass for morbid obesity: a continuous challenge in bariatric surgery. Obes Surg 2006;16:1482–1487. 42. Sukeik M, Alkari B, Ammori BJ. Abdominal wall hernia during laparoscopic gastric bypass: q serious consideration. Obes Surg 2007;17:839–842. 43. Rosenthal RJ, Szomstein S, Kennedy CI, Zundel N. Direct visual insertion of primary trocar and avoidance of fascial closure with laparoscopic Roux-en-Y gastric bypass. Surg Endosc 2007;21:124–128.

20

Gastrectomy with Reconstruction Aimee M. Crago, MD, PhD, Gitonga Munene, MD, and Stephen R. T. Evans, MD INTRODUCTION As the incidence of gastric ulcer disease has decreased and medical management of the disorder has improved, partial and complete resection of the stomach is most commonly performed for neoplastic processes and is described in this chapter predominantly as it pertains to this pathology. Although wedge resection may be adequate for gastrointestinal stromal tumors and small polyps, anatomic resection is essential for malignant growths. Preoperative preparation and staging should be carefully performed because morbidity related to gastrectomy remains as high as 21% to 33% and mortality is about 6% to 9%.1–4 Meticulous surgical technique, thorough knowledge of anatomy, and experience are all essential components in minimizing operative morbidity and mortality. Choice of procedure depends on the underlying disease process, with antrectomy indicated as a portion of therapy in gastric ulcer disease and in distal tumors. Proximal gastrectomy is appropriate for gastroesophageal junction cancers (discussed in Section XI, Chapter 70, Esophageal Surgery), and total gastrectomy is essential for diffuse bleeding from stress gastritis, in many lesser curve tumors, and in large masses inadequately treated by a lesser procedure. Standard therapy for gastric cancer mandates that a 6-cm margin be achieved and lymph node resection be performed for adequate cancer staging.5

INDICATIONS ● Gastric cancer ● Complicated gastric ulcer disease ● Gastric ulcer disease refractory

to

management

OPERATIVE STEPS Step Step Step Step

1 2 3 4

Duodenal or gastric transection and division of right vessels Kocher maneuver 6 Ligation of left gastroepiploic and short gastric vessels 7 Division of the proximal specimen In total gastrectomy In distal or subtotal gastrectomy 8 Ligation of left gastric vessels in total gastrectomy 9 Lymphadenectomy 10 Reconstruction Billroth I reconstruction Billroth II reconstruction Roux-en-Y gastrojejunostomy Roux-en-Y esophagojejunostomy

Step 5

Patient, provider, and facility selection Anesthetic management Incision and exploration Entrance to the lesser sac

medical

●

Step Step ● ●

Step Step Step ● ● ● ●

PREOPERATIVE CONSIDERATIONS Patient, Provider, and Facility Selection As previously noted, the rate of morbidity associated with gastrectomy makes it essential that meticulous preoperative preparation be made. Guidelines such as those described in Section I, Chapter 4, Preoperative Pitfalls, should be followed to ensure that patients with locoregional disease, who are considered candidates for resection, are medically optimized prior to surgery. An aspect of preoperative preparation unique to the gastrectomy and other complex procedures is selection of hospital facilities. Hospital volume is an important factor in patient outcome after gastrectomy, with mortality being 8.7% in very high volume centers and 13% in centers in which the procedure is rarely performed. Very high volume centers were deﬁned in these series as those performing 21 or more cases each year. This concept is also reﬂected in studies comparing outcomes in patients treated at National Cancer Institute–designated cancer centers versus other institutions, with patients faring better at the specialty facilities.1,6 Preoperative evaluation should also address the extent of disease in patients with gastric cancer. This prevents unnecessary procedures and maximizes the surgeon’s

224

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preparedness to perform the procedure. Initial staging typically begins with a computed tomography (CT) scan of the abdomen, pelvis, and often, chest. CT can identify metastatic disease in 66% to 77% of patients when used in conjunction with endoscopic ultrasound (EUS).7,8 Preoperative laparoscopy may identify an additional 23% to 37% of patients with M1 disease because CT fails to identify peritoneal implants and liver metastases less than 5 mm in diameter. Its use has been integrated in the National Cancer Center Network’s staging guidelines for gastric cancer, although its beneﬁt may be limited to those patients with gastroesophageal junction tumors and tumors involving the whole stomach.9,10

Anesthetic Management Section I, Chapter 4, Preoperative Pitfalls, addressing preoperative work-up of patients, also described the contribution of regional anesthetic techniques in minimizing morbidity and mortality after major abdominal procedures such as the gastrectomy. Epidural placement may result in decreased narcotic requirements and improved pulmonary toilet.

OPERATIVE PROCEDURE: TOTAL/ PROXIMAL GASTRECTOMY Positioning, Incision, and Exploration with Entrance into the Lesser Sac The patient is positioned in a supine fashion on the operating table. A midline incision is made from the xiphoid process to the umbilicus or lower abdomen, depending on necessity. Superiorly, the xiphoid process can be grasped and removed with electrocautery in order to reach the region of the esophageal hiatus. A thorough exploration of the abdominal cavity is made to conﬁrm the absence of peritoneal implants and liver metastases. After exploration, the lesser sac is entered to begin mobilization of the stomach.

Injury to the Middle Colic Vessels ● Consequence Injury to the middle colic artery in the setting of insufﬁcient collaterals can result in segmental ischemia between the hepatic and the splenic ﬂexures. The transverse colon should be repeatedly evaluated throughout the remainder of the procedure. If collateralization to this area of bowel is poor and signs of ischemia develop, resection of the involved colon is essential to prevent septic complications. Grade 4 complication ● Prevention While the lesser sac is entered, the omentum can be detached from the transverse colon in cancer proce-

Posterior layer of greater omentum

Middle colic vessels

Posterior layer of transverse Mesocolon

Figure 20–1 The stomach is retracted superiorly, demonstrating the avascular plane between its posterior wall and the transverse mesocolon. Dissection outside of this plane and into the mesocolon can result in injury to the middle colic artery and vein. (Redrawn from Fischer JE, Bland KI, Callery MP, et al. [eds]: Mastery of Surgery, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.)

dures because it will always be resected with the specimen. An avascular plane provides the line of dissection between the omentum and the transverse colon. This plane continues superiorly along the transverse mesocolon, and separation of the transverse mesocolon and posterior stomach along this plane allows for superior retraction of the stomach. Dissection outside of this plane can result in the injury to the middle colic vessels and subsequent ischemia of the transverse colon (Fig. 20–1).

Transection of the Distal Margin and Division of the Right Gastric and Gastroepiploic Vessels The distal margin of resection in total gastrectomy is just past the pylorus. Transection of the duodenum is generally performed by staple technique (Fig. 20–2). The staple line can be oversewn with a two-layer suture closure if the duodenum is scarred or if there is evidence that the staple line is poorly approximated. During this portion of a total gastrectomy, the right gastric and gastroepiploic arteries will be ligated where they give off branches to the distal stomach, unlike in the proximal gastrectomy for gastroesophageal junction tumor, as described in Section XI, Chapter 70, Esophageal Surgery, which requires preservation of these vessels. Mobilization of the duodenum to allow transection may also involve complete Kocherization of the duodenum to examine paraortic lymph nodes for metastatic disease or clearing the ﬁrst portion of the duodenum by incision of the hepatoduodenal ligament. Section IV, Chapter 35, Pancreaticoduodenectomy, describes duodenal dissection and the Kocher procedure in the context of pancreaticoduodenectomy because these

20 GASTRECTOMY WITH RECONSTRUCTION

A Tract of hepatic artery ( hidden by stomach) Site of ligated right gastric artery Stapler Surgeon hand retracting stomach caudally

B Site of ligated right gastroepiploic artery

Entrance to lesser sac Tract of pancreaticodualend artery

Figure 20–2 A, Transection of the duodenum occurs just past the pylorus in distal or total gastrectomy. To isolate this portion of the duodenum, the right gastric and gastroepiploic arteries are ﬁrst ligated and the liver is retracted superiorly. Care must be taken to avoid the nearby portal structures. B, Major structures are outlined.

maneuvers must be performed carefully to prevent injury to the portal structures.

Duodenal Stump Blow-out Duodenal stump blow-out occurs most often in the context of severe scarring of the duodenum related to chronic ulcer disease. Obstruction of the afferent limb has also been associated with the complication. ● Complication Peritonitis and widespread sepsis can result from duodenal stump blow-out. Grade 3–5 complication ● Repair Repair of ruptured duodenal stump cannot be treated with conservative measures. Reexploration is required. Attempts at primary repair with an omental patch can be attempted, but wide drainage of the right upper quadrant and tube duodenostomy are also commonly employed to create a controlled duodenocutaneous ﬁstula that can subsequently be treated with bowel rest, enteric drainage, and parenteral nutrition.

225

● Prevention Modiﬁcation of the standard duodenal stump closure should be made in the context of a scarred duodenal stump. Numerous methods to prevent leakage have been described. Tube duodenostomy involves insertion of a small feeding tube through the duodenal stump to encourage formation of a controlled duodenocutaneous ﬁstula. Similarly, a feeding tube can be threaded through the wall of the second portion of the duodenum or through the wall of the jejunum downstream and into the lumen of the duodenal stump to provide decompression of this portion of the afferent limb. Use of tube jejunostomy results in signiﬁcantly lower rates of persistant enterocutaneous ﬁstula after removal of the drainage tube than does use of the previously mentioned tube duodenostomy. The Bancroft closure is a procedure in which the stomach is transected proximal to the pylorus. The mucosal layer of the antral stump and the pylorus are dissected away from the submucosa and removed. The submucosa and the muscularis layers of the prepyloric stomach are then used to reinforce the closure of the duodenal stump (Fig. 20–3B). Alternatively, the Nissen closure can be used to reinforce a difﬁcult stump. After the duodenum is transected, the open lumen is anastomosed to the capsule of the pancreas (see Fig. 20–3A). No level-one evidence directly compares these methods of duodenal stump repair, but familiarity with all methods may provide the surgeon with the ability to adapt to a given set of obstacles.

Retained Gastric Antrum ● Complication Recurrent peptic ulcer disease or gastritis can occur after distal gastrectomy and Billroth II reconstruction when retained antrum tissue is continuously exposed to the unopposed bicarbonate secretion of the pancreas. Grade 2–4 complication ● Repair Medical management via histamine receptor type-2 or proton pump inhibitors can help over 50% of patients. Following the diagnosis of retained antrum, generally performed by technetium scan, deﬁnitive repair may require resection of the duodenal stump or conversion to a Billroth I reconstruction, in which gastric acid would ﬂow across the anastomosis to neutralize pancreatic secretions. ● Prevention Antral tissue may extend 0.5 cm past the pylorus, and therefore, transection of the duodenum past this point can prevent this type of complication. Historically, complete antral resection has been conﬁrmed by visualizing the presence of Brunner’s glands, deﬁning duodenal tissue, at the distal margin of the specimen.

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Figure 20–3 A, Nissen closure. This method, often employed when the duodenum is scarred to the pancreatic capsule, is performed by ﬁrst transecting the duodenum. The duodenal stump is then anastomosed to the pancreatic capsule or duodenal wall left in place on the pancreatic capsule. B, Bancroft closure. In this method of duodenal stump closure, the stomach is transected proximal to the pylorus, where tissue is less ﬁbrotic. The gastric mucosa in the duodenal stump is then dissected away from the submucosa into the duodenum. This is secured with a pursestring suture, and the seromuscular layer is closed over the stump. (A and B, Reproduced with permission from Burch JM, Cox CL, Feliciano DV, et al. Management of the difﬁcult duodenal stump. Am J Surg 1991;162:523–524.)

A

B

Division of Proximal Specimen in Distal Gastrectomy In distal gastrectomy, mobilization of the stomach proceeds only to the level of the incisura and the third branch of the right gastroepiploic artery. Dissection should be performed between the stomach and the vascular supply to preserve the right gastroepiploic artery. Transection is generally performed using a surgical stapler ﬁred from the incisura to the greater curvature. More proximal transection may be necessary to obtain adequate margins with adequate blood supply if the short gastric vessels are left in place. Following proximal transection, the surgeon proceeds to lymphadenectomy in total gastrectomy.

Ligation of the Left Gastroepiploic and Short Gastric Vessels Dissection of the upper aspect of the greater curvature requires transection of the short gastric arteries. Complications associated with ligation of the short gastric arteries and the left gastroepiploic artery are covered in Section III, Chapter 17, Laparoscopic Nissen Fundoplication. Of note, surgeons should ensure that no undue traction is placed on the spleen. This can result in splenic laceration and hemorrhage, requiring repair of the splenic capsule or a splenectomy.

Exposure and Isolation of the Gastroesophageal Junction and the Left Gastric Vessels with Transection of the Esophagus During proximal or total gastrectomy, dissection of the gastrohepatic ligament (lesser omentum) allows mobilization of the lesser curve of the stomach. The left triangular ligament can also be incised to provide better exposure to the esophageal hiatus. As the stomach is retracted superiorly and to the patient’s right, the surgeon is able to visualize the left gastric artery entering the stomach just distal to the gastroesophageal junction (Fig. 20–4). Complications encountered during this portion of the procedure include damage to the hepatic veins (during incision of the left triangular ligament), injury to a replaced left hepatic artery (during transection of the hepatogastric ligament), pneumothorax, and esophageal perforation. These complications have been previously addressed in Section III, Chapter 17, Laparoscopic Nissen Fundoplication. In a total gastrectomy, dissection of the gastroesophageal junction is followed by esophageal stapling. To prevent retraction of the mobilized esophagus into the chest, suture tags should be placed on the distal end of the esophagus prior to transection.

Lymphadenectomy The extent of lymphadenectomy required for gastric adenocarcinoma remains controversial. Whereas Japanese

20 GASTRECTOMY WITH RECONSTRUCTION

227

Table 20–1 Comparison of Billroth I and II Reconstructions

Figure 20–4 The left gastric artery branches from the celiac trunk to enter the posterior aspect of the stomach. (Redrawn from Fischer JE, Bland KI, Callery MP, et al. [eds.] Mastery of Surgery, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.)

surgeons have shown signiﬁcant beneﬁt from extended lymph node dissection in retrospective studies,11–13 initial reports from Western countries14,15 demonstrated no survival beneﬁt in patients with D2 (extended) versus D1 (limited) resection and found increased morbidity associated with more extensive procedures. Because of this, recent meta-analyses have argued against routine performance of the D2 lymphadenectomy during resection for gastric cancer.16 High-volume centers can, however, perform the procedure with low morbidity and mortality, and because of faults associated with the trials addressing this topic, many surgeons believe that recurrence rates and survival in at least a subset of gastric cancer patients may be positively affected by performing D2 resections. Complications related to performing D2 resection have often centered around splenectomy and distal pancreatectomy, and one should refer to chapters on these topics when planning to perform this procedure.

Reconstruction Reconstruction after total or subtotal gastrectomy (greater than two thirds of the stomach) is performed by completing an antecolic or retrocolic Roux-en-Y esophagogastrectomy to prevent reﬂux of bile into the esophagus. Partial gastrectomies are most often reconstructed with a Billroth II gastrojejunostomy or, less frequently, with a Billroth I gastrojejunostomy, which has theoretical beneﬁt in certain circumstances (Table 20–1). In the context of malignant disease, Billroth I reconstruction is contraindicated, because it will make subsequent procedures—necessary in the context of cancer recurrence—signiﬁcantly more complicated.

Billroth I

Billroth II

• Potentially lower rates of remnant carcinoma

• Risk of marginal ulcer related to retained antrum

• Decreased rates of postprandial dumping

• Recurrent cancer unlikely to occur adjacent to the pancreatic head

• Potential improvement in gastroesophageal junction function

• Facilitates lymphatic dissection • Risk of afferent loop syndrome

• Histologic changes related to gastritis in 80%–90% of patients

• Decreased rates of bile reﬂux and gastritis

• Retains normal physiologic passage of food into duodenum, maintaining innate regulatory pathways of bicarbonate and pancreatic enzymes

• Potentially lower rates of anastomotic stricture owing to anastomotic caliber • Anastomosis can be performed in context of extensive duodenal scarring

Multiple methods of Billroth II reconstruction have been reported with variation in the position of gastric transection, variation in the placement of the gastrojejunostomy along the line of gastric transection, and antecolic versus retrocolic positioning of the gastrojejunostomy deﬁning the types of reconstruction (Fig. 20–5). The Billroth I reconstruction has less variation, although opinion has differed on the line of gastric transection and placement of the gastrojejunostomy along this anastomosis (Fig. 20–6). No clear data exist to support a preference of Billroth I or Billroth II methods.

Anastomotic Leak Rates of anastomotic leak are approximately 1% to 4% after gastrectomy with gastroduodenostomy or gastrojejunostomy and 5% to 15% in esophagogastrostomy with Rouxen-Y reconstruction.17,18 ● Consequence Intra-abdominal leak, peritonitis, sepsis, multiorgan failure, and death. Early signs of leak include fever, tachycardia, and worsening abdominal pain. Grade 2–5 complication ● Repair Patients with anastomotic leak normally present with evidence of systemic inﬂammatory response and infection. Unexplained fevers and tachycardia can herald the presence of this complication and should be investigated by upper gastrointestinal series or CT scan. Initiation of antibiotic therapy and nasogastric decompression or percutaneous drainage can control many leaks, as demonstrated in the literature describing anastomotic leakage after gastric bypass surgery and in retrospective analyses of gastrectomy patients.17,19,20 More recently, the use of expandable, covered stents, placed

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Billroth 1851

Wolfler 1881

Curvoisier 1883

Billroth 1885

Heineke and Mikulicz 1886

Hofmeister 1888

Brown and Jaboulay 1892

Schoemaker 1898

Roux 1898

Polya 1911

Balfour 1917

Von Haberer-1922 Finney-1924

Figure 20–5 Methods of Billroth II reconstructions. (Redrawn from Shackleford’s Surgery of the Alimentary Tract, Vol 2. Philadelphia, WB Saunders, 1981.)

endoscopically, has been shown to result in sealing of leaks at the site of both esophagojejunostomy and gastrojejunostomy sites.21,22 Persistent evidence of inﬂammation, peritonitis, or worsening symptoms may require reoperation with abdominal washout and repair of the anastomosis. ● Prevention A list of risk factors related to leakage after gastrointestinal anastomosis is presented in Box 20–1. In our practice, three of these risk factors led us to perform a proximal diverting ostomy when a colocolostomy is performed. Such measures cannot be used to protect a more proximal anastomosis such as that used for reconstruction after a partial or total gastrectomy. Meticulous technique remains the primary means of preventing anastomotic leak. A gastrojejunostomy can be performed in one or two layers, but it is essential to take strong seromuscular bites to ensure integrity of the suture line. Rates of anastomotic leakage in a stapled anastomosis are not shown to be consistently different to those seen after a hand-sewn reconstruction.

Box 20–1 Risk Factors for Gastrointestinal Anastomotic Leak Malnutrition (albumin < 3.25) Weight loss Alcohol abuse Smoking Intraoperative contamination Long operative time (>4–6 hr) Multiple blood transfusions Chronic obstructive pulmonary disease Peritonitis Bowel obstruction Use of corticosteroids Radiation Based on references 18 and 57–61.

Special care should be taken when constructing an anastomosis between the esophagus and the jejunum after total gastrectomy. The anastomosis is particularly difﬁcult because a layer of fatty tissue between the mucosa and the submucosa causes frequent retraction of the mucosa on the cut end of the esophagus. It is essential that this layer

20 GASTRECTOMY WITH RECONSTRUCTION

Billroth 1881

A

Billroth 1881

B

C

v. Haberer, 1922 Finney, 1923

F

Kocher 1890

D

Winkelbauer 1927

G

Kutscha-Lissberg 1925

v. Haberer 1920

E

Schoemaker 1911

H

229

Harkins, Nyhus 1960

I

Figure 20–6 Billroth I reconstructions. (Reproduced with permission from Sieivert JR, Bumm R. Distal gastrectomy with Billroth I, Billroth II or Roux-en-Y reconstruction. In Fischer JE, Bland KI, Callery MP, et al. [eds]: Mastery of Surgery, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.)

be incorporated in a full-thickness stitch used to create the hand-sewn esophagojejunostomy in a Roux-en-Y reconstruction after total gastrectomy. No beneﬁt of stapled versus hand-sewn anastomosis has been consistently demonstrated,23,24 and when choosing to create this anastomosis with a circular stapler, a tight pursestring suture through the esophageal wall and around the anvil helps to ensure a sturdy anastomosis. After the stapler is ﬁred, two complete rings of tissue, one obtained from each limb, should be visualized. Incomplete tissue rings serve to identify potential defects in construction. A second technical point, uniquely applicable to the Billroth I reconstruction, is the importance of addressing the “angle of sorrow” or Jammerecke. This area deﬁnes the junction of the gastroduodenostomy and the stapled end of the stomach. A triple seromuscular suture placed outside to in on the anterior wall of the stomach, inside to out on the duodenum, and inside to out on the posterior stomach can be used to secure this region.

● Repair Anastomotic bleeding normally resolves spontaneously postoperatively and can be treated with correction of coagulopathy and limited transfusion. Upper endoscopy can identify the site of bleeding and allow for placement of clips or electrocautery. Rarely does anastomotic bleeding require operative intervention that involves gastrostomy and direct control of hemorrhage. ● Prevention Although some surgeons consider rates of anastomotic bleeding to be higher in stapled versus sutured anastomoses, large series in postgastrectomy patients do not consistently show this to be the case.25 Regardless, a two-layered hand-sewn anastomosis with one layer being full-thickness with absorbable sutures results in good hemostasis. Careful inspection and oversewing of exposed staple lines can prevent some episodes of staple line bleeding.

Anastomotic Bleeding ● Consequence Hemorrhage and increased transfusion requirement. Grade 2/3 complication

Postgastrectomy Syndromes Numerous chronic complications related to gastrectomy with reconstruction are discussed in references 26 to 28.

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SECTION III: GASTROINTESTINAL SURGERY

Afferent Loop Syndrome Afferent loop syndrome is an uncommon complication most often associated with Billroth II reconstruction in which the afferent loop becomes obstructed owing to stasis, adhesions, volvulus, or herniation. ● Consequence This complication can occur in the immediate postoperative period and present as unrelenting epigastric pain, which reﬂects a closed-loop obstruction. This may result in duodenal stump dehiscence. Late presentation of afferent loop syndrome is characterized by postprandial fullness, nausea, and eventually, projectile, bilious vomiting followed by relief of symptoms. Patients may have jaundice owing to biliary outﬂow obstruction, pancreatitis, and postprandial epigastric mass. Deﬁnitive diagnosis can be made by CT scan, upper gastrointestinal series, or endoscopy. Grade 3 complication ● Repair Lysis or adhesions, reduction of internal hernia, shortening of the afferent loop, or bowel resection treating the underlying cause of obstruction may correct the problem. In emergent procedures, in which markedly dilated loops of bowel are present, enteroenterostomy between the afferent and the efferent loops of the gastrojejunostomy is an option. In the chronic syndrome, shortening of the afferent loop (to 10–15 cm) or conversion to either Billroth I or Roux-en-Y gastrojejunostomy will treat the condition. ● Prevention Afferent loop syndrome is associated with long afferent loops (generally >30 cm in length), which can also present with diarrhea, marginal ulcer, or malabsorption. Antecolic reconstruction, antiperistaltic gastrojejunostomy, and poor positioning of the gastrojejunostomy along the greater curve of the stomach are also risk factors in development of the syndrome and should be considered when deciding the appropriate reconstruction for a given patient. Closure of the retroanastomotic opening by tacking the anastomosis to the transverse mesocolon can reduce the risk of retroanastomotic hernia.

Efferent Loop Syndrome Efferent loop syndrome is associated primarily with internal hernia but may also reﬂect adhesive disease or jejunogastric or jejunojejunal intussusceptions. ● Consequence Efferent loop syndrome presents in a manner similar to small bowel obstruction with colicky abdominal pain, nausea, and vomiting. Grade 3 complication

● Repair Repair centers on correction of the underlying problem, that is, hernia reduction and repair or lysis of adhesions. ● Prevention Proper closure of mesocolic defects and anchoring the jejunum to the mesocolon are the most effective ways of preventing internal herniation.

Anastomotic Stricture Anastomotic stricture is seen in 1.5% to 13% of patients after gastric resections.24,29 It can occur in the acute postoperative period or many years after the initial operation. The etiology of anastomotic stricture or stenosis can be anastomotic edema, extraluminal adhesion or compression,30 cancer recurrence, or long-term ﬁbrosis and scarring. Chronic changes that result in strictures may occur owing to ulceration, inadequate perfusion at the anastomosis, or poor technique. The diagnostic work-up of stricture should begin with a contrast study to evaluate the etiology of the obstruction. Recurrent tumor at the gastrojejunal anastomosis may be seen as plaquelike, ulcerative, or polypoid lesions at or near the anastomosis on upper gastrointestinal series. In esophagogastric anastomosis, strictures resulting from anastomotic technique typically appear as short, ringlike areas of narrowing, whereas strictures from alkaline reﬂux esophagitis appear as long segments of smooth, tapered narrowing in the distal esophagus. Eccentric anastomotic narrowing would suggest recurrent tumor.31 ● Consequence Patients present with dysphagia when related to esophagogastrostomy stricture or with gastric outlet obstruction after gastric to small bowel anastomosis. Grade 2/3 complication ● Repair After a contrast study is performed, an esophagogastroduodenoscopy should be performed as a diagnostic and potentially therapeutic intervention. Benign anastomotic strictures can be treated successfully with either endoscopic balloon dilation or ﬂuoroscopy-guided balloon dilation.32 For complete resolution of the stricture, multiple dilations may have to be performed, risking perforation.33 There have been several reports of benign strictures being treated successfully with selfexpandable stents, but long-term data are still forthcoming.34 The operation of choice for recalcitrant stricture is anastomotic revision. If structuring is due to recurrent tumors, the patient should be restaged, and if resection is possible, surgical intervention should include lymphadenectomy and completion gastrectomy with reconstruction. In those patients with unresectable disease, palliation with metallic stents should be considered.35

20 GASTRECTOMY WITH RECONSTRUCTION ● Prevention Risk factors for anastomotic stricture include inadequate blood supply at the anastomosis, alkaline reﬂux, ulcer formation, anastomotic dehiscence, and smallerdiameter stapled anastomosis. The surgeon should be conscious of the blood supply preserved during resection, and the largest possible end-to-end anastomosis stapler should be used to create the esophagogastrectomy.36 These principles are particularly important in laparoscopic resection because there have been reports of increased anastomotic stricture (≤40%) after these procedures compared with open gastrectomy.37

Roux Stasis Syndrome Roux stasis syndrome presents in 30% of patients with Roux-en-Y gastrojejunostomy. ● Consequence Early satiety, postprandial vomiting, and epigastric pain.38 The etiology of this dysmotility is believed to be related to disconnection of the transected Roux limb from the duodenal pacemaker,39 but it may also be related to gastric dysmotility or to anastomotic stricture. Grade 2/3 complication ● Repair Patients are initially treated with promotility agents such as metoclopramide or erythromycin.40 Endoscopy may be useful for dilating anastomotic strictures. Failure to improve with medical and endoscopic management indicates the need for surgical intervention. Standard therapy consists of subtotal gastrectomy with reconstruction. This is essential if evidence of severe gastric dysmotility is observed. More recently, conversion to an “uncut” Roux-en-Y gastrojejunostomy, as described later, has been shown to improve symptoms associated with Roux stasis syndrome.41 ● Prevention The Roux stasis syndrome can be prevented by performing the uncut Roux-en-Y as initial reconstruction (Fig. 20–7).38,41 Studies have also noted that longer length of the Roux limb was associated with higher rates of Roux syndrome, but as noted previously, this must be balanced against the risk of afferent loop syndrome.

Bile Reﬂux Gastritis Bile reﬂux gastritis is most commonly seen after Billroth II reconstruction as a consequence of a defective pyloric channel and results from exposure of the gastric mucosa to bile, pancreatic secretions, and duodenal contents. ● Consequence Symptoms result in only 3% to 30% of patients with endoscopic evidence of bile reﬂux,42 and include burning epigastric pain, bilious emesis, oral aversion,

231

Gastric enteric stream Bilious enteric stream Propagation of enteric pacesollar potantlias Staple line

Figure 20–7 Conversion to an “uncut” Roux-en-Y gastrojejunostomy is believed to restore the physiologic ﬂow of enteric contents, improving dysmotility of the small bowel and relieving symptoms related to Roux stasis syndrome. (From Collen JJ, Kelly KA: Gastric motor physiology and pathophysiology. Surg Clin North Am 1993;71:1145–1160.)

and weight loss. Pain is unrelieved by acid suppression and is aggravated by both oral intake and the recumbent position. Bile reﬂux gastritis is a diagnosis of exclusion owing to the low speciﬁcity of endoscopic ﬁndings and histologic ﬁndings (intestinalization of gastric glands with inﬂammation). Zollinger-Ellison syndrome and other postgastrectomy syndromes should be ruled out prior to operative repair aimed at correction of this condition. Grade 2–4 complication ● Repair Medical management of bile reﬂux gastritis includes prokinetic agents, antispasmodic therapy, cholestyramine, and dietary modiﬁcation. The aim of reoperative surgery in this setting is to divert duodenal contents away from the gastric remnant and may be accomplished by any of several procedures: ● Conversion to Roux-en-Y gastrojejunostomy with a

Roux limb of at least 40 cm is associated with symptomatic relief in up to 85% of patients.42 ● Distal Braun enterostomy (see Fig. 20–5) has been shown to improve symptoms of bile reﬂux gastritis in 53% of patients.43 ● The Henley procedure is a gastrojejunoduodenostomy constructed with an interposition of a jejunal segment approximately 40 cm in length between the gastric remnant and the duodenum (Fig. 20–8).44 Symptomatic relief is seen in 70% of patients undergoing this procedure.

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SECTION III: GASTROINTESTINAL SURGERY ● Repair Most patients will respond to medical management of dumping syndrome. Low-carbohydrate, high-protein meals and ﬁber supplementation have been shown to reduce dumping symptoms. If symptoms persist despite dietary modiﬁcation, the long-acting somatostatin analogue, octreotide, can be administered with good effect or the alpha-glucosidase inhibitor acarbose may prevent absorption of the carbohydrate load, treating late dumping symptoms.47–49 Surgical therapy is rarely necessary and historically centered on reconstruction of the pylorus whether by direct repair after pyloromyotomy or by creation of an antiperistaltic jejunal interposition limb anastomosed between the stomach and the duodenum. Use of jejunal interposition has been largely abandoned owing to high rates of postoperative obstruction and gastric stasis. The most commonly employed revision procedure to treat dumping syndrome is currently the Roux-en-Y gastrojejunostomy, which results in near-complete symptom resolution in 86% of patients.50

Figure 20–8 The Henley procedure creates a gastrojejunoduodenostomy with interposition of a 40-cm jejunal segment between the gastric remnant and the duodenum. (From Aranow JS, Matthews JB, Garcia-Aguilar J, et al. Isoperistaltic jejunal interposition for intractable postgastrectomy alkaline reﬂux gastritis. J Am Coll Surg 1995;180:648–653.) ● Biliary diversion using Roux-en-Y hepaticojejunos-

tomy can be performed by converting the gastric anastomosis to a gastroduodenostomy and performing choledochojejunostomy. ● Prevention Rates of bile reﬂux are lowest in the Roux-en-Y gastrojejunostomy, although the possibility of Roux stasis syndrome should be weighed against this beneﬁt when choosing reconstruction.

Dumping Syndrome Dumping is a well-recognized complication of distal gastrectomy, occurring in as many as 25% of patients owing to alteration in the pyloric outﬂow mechanism.45,46 ● Consequence Early dumping results from a hyperosomotic load delivered to the small bowel and causes abdominal cramping and diarrhea. Late dumping is less common, is related to hyperinsulinemia, and presents with hypoglycemic symptoms that are relieved with carbohydrate administration. Grade 2/3 complication

● Prevention No clear measures are known to prevent dumping when Billroth I or Billroth II reconstruction is planned, and complications speciﬁc for Roux-en-Y gastrojejunostomy should be weighed when choosing this as a means to prevent dumping.

Delayed Gastric Emptying Delayed gastric emptying occurs owing to either mechanical outﬂow obstruction or dysmotility related to alteration in vagal innervation of the stomach or the gastric pacemaker owing to surgery. ● Consequence Delayed gastric emptying can occur in the immediate postoperative period, presenting as inability to tolerate an oral diet. In the chronic setting, it is associated with abdominal pain and bloating, nausea, vomiting, weight loss, and malnutrition. Diagnosis is made by gastric emptying studies that demonstrate delayed emptying of solids. Endoscopy will show evidence of retained food and, potentially, bezoar formation. Grade 2–4 complication ● Repair Anastomotic strictures should be treated with endoscopic dilation, if possible, and adhesive disease should be treated with reoperation. As in Roux stasis syndrome, promotility agents are the ﬁrst-line therapy when no evidence of mechanical obstruction is found. Metoclopramide, doperamide, and cisapride may provide some symptomatic relief.40,51,52 In refractory cases, patients may require a subtotal or complete gastrectomy with Roux-en-Y reconstruction.53,54 Place-

20 GASTRECTOMY WITH RECONSTRUCTION ment of implantable pacemakers have been of some use in severe gastroparesis after bariatric surgery and may provide relief for some patients after gastrectomy.55 ● Prevention Careful dissection around the esophageal hiatus to preserve vagal innervation should minimize damage to the autonomic innervation of the gastric remnant. Maintenance of as much residual stomach as possible will prevent inadvertent resection of the gastric pacer. In patients undergoing Roux-en-Y reconstruction after distal gastrectomy, higher rates of gastric stasis were seen in patients who underwent more extensive lymph node dissection.56 Risk factors associated with postoperative delayed gastric emptying include diabetes and gastric outlet obstruction. In patients with these conditions, consideration should be given to placement of gastrostomy and feeding jejunostomy tube placements at the time of operation. Preoperative nasogastric decompression may provide some improvement in outcomes.27

4.

5.

6.

7. 8.

9.

10.

Other Complications Nutritional deﬁcits after gastrectomy can result in anemia, neuropathy, and osteoporosis. Attention to adequate vitamin replacement therapy must continue throughout the patient’s lifespan and address malabsorption of iron, vitamin B12, folate, vitamin D, and calcium. Stump carcinoma is most common with Billroth II reconstruction, occurring several decades after operation, and should be considered in the differential diagnosis of patients presenting with vague abdominal complaints or weight loss. No deﬁnitive recommendations for screening have been published, but low threshold for endoscopy is appropriate. Gastroesophageal reﬂux disease is a common complication of gastric surgery and may result from damage to the lower esophageal sphincter, gastric dysmotility, or bile reﬂux. Medical management with metoclopramide or domperidone and histamine receptor or proton pump inhibitors should be attempted. Fundoplication (if possible) or revision surgery, as discussed previously and aimed at addressing gastric dysmotility or bile reﬂux, may be required.

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22. Lee BI, Choi KY, Kang HJ, et al. Sealing an extensive anastomotic leak after esophagojejunostomy with an antimigration-modiﬁed covered self-expanding metal stent. Gastrointest Endosc 2006;64:1024–1026. 23. Seufert RM, Schmidt-Matthiesen A, Beyer A. Total gastrectomy and oesophagojejunostomy—a prospective randomized trial of hand-sutured versus mechanically stapled anastomoses. Br J Surg 1990;77:50–52. 24. Takeyoshi I, Ohwada S, Ogawa T, et al. Esophageal anastamosis following gastrectomy for gastric cancer: a comparison of hand-sewn and stapling technique. Hepatogastroenterology 2000;47:1026–1029. 25. Hori S, Ochiai T, Gunji Y, et al. A prospective, randomized trial of hand-sutured versus mechanically stapled anastomosis for gastroduodenostomy after distal gastrectomy. Gastric Cancer 2004;7:24–30. 26. Dempsey DT. Reoperative gastric surgery and postgastrectomy syndromes. In Yeo C, Zuidema GD (eds): Shackleford’s Surgery of the Alimentary Tract, Vol 2. Philadelphia: WB Saunders, 2001; pp 161–177. 27. Jaffe BM, Florman SS. Postgastrectomy and postvagotomy syndromes. In Fischer JE (ed): Mastery of Surgery, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2007; pp 938–954. 28. Sawyers JL. Management of postgastrectomy syndromes. Am J Surg 1990;159:8–14. 29. Date RS, Panesar KJ. D2 gastrectomy—a safe operation in experienced hands. Int J Clin Pract 2005;59:672– 674. 30. Takahashi T, Yamashiro M, Hashimoto H, et al. Stomal stenosis following gastrectomy in the elderly. Nippon Ronen Igakkai Zasshi 1992;29:758–764. 31. Woodﬁeld CA, Levine MS. The postoperative stomach. Eur J Radiol 2005;53:341–352. 32. Inagake M, Yamane T, Kitao Y, et al. Balloon dilatation for anastomotic stricture after upper gastrointestinal surgery. World J Surg 1992;16:541–544. 33. Carrodeguas L, Szomstein S, Zundel N, et al. Gastrojejejunal anastomotic stricture following laparoscopic Rouxen-Y gastric bypass: analysis of 1291 patients. Surg Obes Relat Dis 2006;2:92–97. 34. Ustündag Y, Köseglu T, Cetin F, et al. Self-expandable metallic stent therapy of esophagojejunal stricture in a stapled anastomosis: a case report and review of the literature. Dig Surg 2001;18:211–213. 35. Sugimoto K, Hiroto S, Imanaka K, et al. Application of self expanding metallic stents to malignant stricture following mechanically stapled esophagojejunostomy: report of two cases. Radiat Med 2000;18:133–137. 36. Wong J, Cheung H, Lui R, et al. Esophagogastric anastomosis performed with a stapler: the occurrence of leakage and stricture. Surgery 1987;101:408–415. 37. Varela JE, Hiyasha M, Nguyen T, et al. Comparison of laparoscopic and open gastrectomy for gastric cancer. Am J Surg 2006;192:837–842. 38. Gustavsson S, Ilstrup DM, Morrison P, Kelly KA. Rouxen-Y stasis syndrome after gastrectomy. Am J Surg 1988; 155:490–494. 39. Tu BN, Kelly KA. Elimination of the roux stasis syndrome using a new type of “uncut Roux” limb. Am J Surg 1995; 170:381–386.

40. Petrakis J, Vassilakis JS, Karkavitasas N, et al. Enhancement of gastric emptying of solids by erythromycin in patients with Roux-en-Y gastrojejunostomy. Arch Surg 1998;133:709–714. 41. Noh SM. Improvement of the Roux limb function using a new type of “uncut Roux” limb. Am J Surg 2000;180: 37–40. 42. Zobolas B, Sakorafas GH, Kouroukli I, et al. Alkaline reﬂux gastritis: early and late results of surgery. World J Surg 2006;30:1043–1049. 43. Vogel SB, Drane WE, Woodward ER. Clinical and radionucleotide evaluation of bile diversion by Braun enteroenterostomy: prevention and treatment of alkaline reﬂux gastritis. An alternative to Roux-en-Y diversion. Ann Surg 1994;219:458–465. 44. Aranow JS, Matthews JB, Garcia-Aguilar J, et al. Isoperistaltic jejunal interposition for intractable postgastrectomy alkaline reﬂux gastritis. J Am Coll Surg 1995;180:648– 653. 45. Carvajal SH, Mulvihill SJ. Postgastrectomy syndromes: dumping and diarrhea. Gastrointest Clin North Am 1994; 23:261–279. 46. Mix CL. “Dumping stomach” following gastrojejunostomy. Surg Clin North Am 1922;2:617–622. 47. Gerard J, Luyckx AS, Lefebvre PJ. Acarbose in reactive hypoglycemia: a double-blind study. Int J Clin Pharmacol Toxicol 1984;22:25–31. 48. Gray JL, Debas HT, Mulvihill SJ. Control of dumping symptoms by somatostatin analogue in patients after gastric surgery. Arch Surg 1991;126:1231–1235. 49. Hasegawa T, Yoneda M, Nakamura K, et al. Long-term effect of alpha-glucoside inhibitor on later dumping syndrome. J Gastroenterol Hepatol 1998;13:1201– 1206. 50. Vogel SB, Hocking MP, Woodward ER. Clinical and radionucleotide evaluation of Roux-Y diversion for postgastrectomy dumping. Am J Surg 1988;155:57–62. 51. Ramirez B, Eaker EY, Drane WE, et al. Erythromycin enhances gastric emptying in patients with gastroparesis after vagotomy and antrectomy. Dig Dis Sci 1994;39: 2295–2300. 52. Tomita R, Ikeda T, Fujisaki S, et al. Effects of mosapride, citrate on patients after vagal nerve preserving distal gastrectomy reconstructed by interposition of a jejunal J pouch with a jejunal conduit for early gastric cancer. World J Surg 2006;30:205–212. 53. Eckhause FE, Conrad M, Knol JA, et al. Safety and longterm durability of completion gastrectomy in 81 patients with postsurgical gastroparesis syndrome. Am Surg 1998; 64:711–716. 54. McCallum RW, Polepalle SC, Schirmen B. Completion gastrectomy for refractory gastroparesis following surgery for peptic ulcer disease. Long-term follow-up with subjective paramenters. Dig Dis Sci 1991;36:1156–1161. 55. Salameh JR, Schmeig RE, Runnels JM, Abell TL. Refractory gastroparesis after roux-en-Y gastric bypass: surgical treatment with implantable pacemaker. J Gastrointest Surg. 2007;11:1669–1672. 56. Hirao M, Fujitani K, Tsujinaka T. Delayed gastric emptying after distal gastrectomy for gastric cancer. Hepatogastreoenterology 2005;52:305–309.

20 GASTRECTOMY WITH RECONSTRUCTION 57. Makela JT, Kiviniemi H, Laitinen S. Risk factors for anastomotic leakage after left-sided colorectal resection with rectal anastamosis. Dis Colon Rect 2003;46:653– 660. 58. Sorenson LT, Jørgensen T, Kirkeby LT, et al. Smoking and alcohol abuse are major risk factors for anastomotic leakage in colorectal surgery. Br J Surg 1999;86:927– 931. 59. Golub R, Golub RW, Cantu R Jr, Stein HD. A multivaried analysis of factors contributing to leakage of

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21

Enterectomy Reid B. Adams, MD INTRODUCTION Enterectomy is a common procedure used primarily for resection of small bowel or in combination with other gastrointestinal procedures. Enterectomy also is used in conjunction with reconstructive procedures for replacement of the gastrointestinal or urologic tract. This discussion focuses on primary enterectomy for treatment of small bowel conditions. The complications discussed here are common to those procedures requiring small bowel resection for other reasons. Enterectomy has been part of the abdominal surgeons’ repertoire for much of the history of surgery, yet the risks and complications associated with this procedure have remained constant over its recent history. Whereas we may understand the pathophysiology and predisposing factors for their development, complications persist and all abdominal surgeons should be familiar with their development, consequences, repair, and prevention. This chapter focuses on these issues related to enterectomy. The reported leak rates for intestinal anastomosis range from 1% to 8%.1–6 Speciﬁc leak rates for enterectomy are more difﬁcult to ﬁnd in the literature. One review reported a 1.1% leak rate in 798 patients undergoing enterectomy.7 The primary aspects necessary for construction of a successful anastomosis include careful approximation of well-vascularized bowel wall in a tension-free manner. Clearly, a technically inadequate anastomosis will lead to anastomotic failure.8 However, despite a technically suitable anastomosis, complications such as anastomotic failure can occur. Signiﬁcant efforts have focused on understanding the nontechnical factors that contribute to anastomotic failure. Poor nutrition, hypoalbuminemia, infection, smoking, diabetes, obesity, and many others have been implicated in various studies.1–4,7,9–11 Despite extensive investigation, study results are conﬂicting and no consensus on predisposing factors has been reached. In Pickleman and coworkers’ review,7 the only factor predicting anastomotic leak after enterectomy was hypertension. How this contributed to anastomotic failure was unclear from this study. No differences were seen in stapled versus sewn anastomoses or between different types of anastomoses. Overall, their ﬁndings reinforced

the concept that a clear set of factors predisposing to anastomotic leak have not been delineated.

INDICATIONS ● ● ● ● ● ● ●

Small bowel obstruction Small bowel neoplasm Small bowel inﬂammatory disease (e.g., Crohn’s disease) Small bowel herniation with vascular compromise Enterocutaneous ﬁstula Small bowel intussusception Mesenteric tumors when resection leads to small bowel ischemia ● Traumatic injury to the small bowel

OPERATIVE STEPS Incision Evaluation of small bowel from ligament of Treitz to ileocecal valve 3 Identiﬁcation of transection sites proximal and distal to diseased segment 4 Creation of anastomosis Creating a mesenteric defect Transection of bowel Ligation and division of small bowel mesentery Small bowel anastomosis Inspection of anastomosis for bleeding Closure of enterotomy resulting from small bowel anastomosis 5 Assessment of anastomosis patency by palpation 6 Suture closure of mesenteric defect 7 Closure of incision

Step 1 Step 2 Step Step ● ● ● ● ● ●

Step Step Step

OPERATIVE PROCEDURE Incision Injuries upon Entry into the Peritoneal Cavity All grades of injuries can occur during this step. This is primarily the case during reoperative surgery or during a

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primary procedure when the bowel is grossly dilated. Careful dissection and controlled entry into the peritoneal cavity under these conditions are required to avoid entry complications, as discussed in Section I, Chapters 6 and 7.

Evaluation of the Small Bowel Missed Lesions Many small bowel conditions (neoplasia, ischemia, strictures, or obstruction) requiring enterectomy can be multifocal. Identiﬁcation of all diseased segments is important to facilitate complete treatment. ● Consequence Persistent neoplasm with development of obstruction or metastasis. Residual ischemia leading to stricture, obstruction, or perforation with peritonitis. Grade 3/4/5 complication ● Repair Repeat operation for resection of residual tumor, ischemia, stricture, or obstruction. ● Prevention A thorough evaluation of the entire small bowel and its mesentery is important to rule out additional lesions, particularly if the procedure is being done for small bowel neoplasm or ischemia. Identiﬁcation of mass lesions, strictures, or injuries is accomplished by “milking” the bowel between the index and the middle ﬁngers (Fig. 21–1) and visually examining both sides of the bowel during this process. This allows identiﬁcation of small lesions. Similarly, the mesentery in the area of a small bowel neoplasm is palpated for lymphadenopathy and tumor involvement. When assessing for ischemia, ﬂuorescein staining or Doppler studies may aid in distinguishing viable from ischemic segments when determining the extent of enterectomy. One ampule of ﬂuorescein is given, and the small bowel is examined under a Wood lamp. Nonviable segments of bowel will be demarcated by this method. When areas are indeterminate for ischemia at the initial laparotomy, a planned repeat laparotomy 24 hours later will allow assessment of the questionable areas of ischemia. Additional enterectomy may be required at the second operation.

Identiﬁcation of Transection Sites Proximal and Distal to the Diseased Segment Missed or Recurrent Disease The site chosen for transection of the small bowel is dependent upon the disease process being treated. Historically, a distance of 5 to 10 cm away from the lesion being resected has been advocated to ensure an adequate resection margin when treating a neoplasm. However, there does not appear to be literature providing solid evidence to support a speciﬁc transection distance. The

Figure 21–1 Lesions within the bowel can be identiﬁed by “milking” the bowel between the index and the middle ﬁngers. This allows small lesions to be palpated, preventing missed pathologic ﬁndings. In addition, enteric contents can be milked away from the site of an enterotomy, minimizing the risk of operative site contamination by enteric contents.

transection site of the bowel is partly dictated by the amount of mesenteric resection necessary to encompass the lymphatic drainage in the area of the neoplasm. Transection for ischemic disease should be at sites that are well vascularized. Transection for inﬂammatory disease, such as Crohn’s disease, is done just outside the area of grossly involved bowel. The consequences, repair, and prevention of this complication are similar to those in the prior section.

Creation of the Anastomosis Several techniques are described for enterectomy with anastomosis. Currently, the most commonly practiced is a stapled side-to-side, functional end-to-end anastomosis. In some circumstances, this anastomosis is not technically feasible and a sewn anastomosis is required. The stapled anastomosis is used for illustrative purposes for this discussion, because the general complications for enterectomy with anastomosis are similar in both the stapled and the sewn techniques.

21 ENTERECTOMY

Figure 21–2 Backlighting the mesentery (transillumination) allows identiﬁcation of the vascular arcade (arrows). This permits precise identiﬁcation of the bowel’s edge (arrowhead) and the vessels (arrows). As a result, careful ligation can be done, preventing injury to the bowel or the vascular arcade.

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Figure 21–3 Wound contamination is minimized by covering the wound edges with a saline-moistened towel. This and the strategies shown in Figures 21–1 and 21–4 limit enteric spillage and contamination.

Injuries during Creation of a Mesenteric Defect Injury to the small bowel or the adjacent mesentery can occur during this step. ● Consequence Leakage of enteric contents, wound contamination, and increased postoperative infection risk. Mesenteric injury with bleeding, hematoma, or compromise of the blood supply to the remaining small bowel. Any of these injuries may lead to the unintended resection of additional normal small bowel. Grade 1/2 complication ● Repair The injured small bowel can be incorporated into the stapled transection line or the resection specimen. The mesenteric injury can be oversewn and/or incorporated into the resection specimen. ● Prevention Transillumination of the mesentery (Fig. 21–2) will allow identiﬁcation of the small mesenteric vessels and the edge of the bowel, thereby avoiding these injuries. Removing the lights from the operative ﬁeld followed by direct light on the back side of the mesentery will allow the surgeon to identify these structures. The avascular window is then marked with cautery or punctured with a tonsil clamp to mark its position. Prevention of infection is facilitated by covering the wound with a moist towel to keep the enteric contents from contaminating the edges (Fig. 21–3). The bowel involved in the anastomosis also can be surrounded by moist towels to contain any spillage of enteric contents. Milking enteric contents away from the transection sites (see Fig. 21–1) and occluding the bowel proximally and distally with a noncrushing bowel clamp (Fig. 21–4) will minimize enteric contents in the enterectomy site. Placement of the occluding clamp should be done in a fashion that does not include the mesentery. Finally, administra-

Figure 21–4 After the enteric contents are milked away from the enterectomy site, noncrushing bowel clamps can be used to occlude the lumen proximally and distally from the resection site, preventing reﬂux into the operative ﬁeld. The clamps are placed to the edges of the bowel, but not onto the adjacent mesentery (arrows).

tion of perioperative antibiotics, covering gram-negative bacilli and anaerobes, will minimize the risk of perioperative infections.

Difﬁculties during Bowel Transection Complications at this step usually are the result of device malfunction. ● Consequence Spillage of enteric contents, intra-abdominal abscess formation, or wound infection. Additional loss of healthy bowel can result if further intestinal resection is required to repair the misﬁre site. An inadequate staple line can lead to anastomotic leak, as discussed later. Grade 1/2/3 complication

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● Repair The site of malfunction typically results in an open or injured piece of small intestine. Reapplication of the stapler at an adjacent site of healthy bowel will treat this complication. ● Prevention Stapler malfunctions are uncommon.8 Experienced surgeons frequently know whether the stapler has not operated correctly. Occluding the bowel adjacent to the stapler to prevent spillage of enteric contents can be done while the stapler is removed and the staple line inspected. If the bowel is not intact or is injured, the stapler can be reapplied adjacent to the occluding bowel clamp. Anticipating/recognizing a misﬁring will minimize opportunities for enteric spillage. Stapler malfunctions can result from educational deﬁciencies or the introduction of new equipment or models. Adequate staff and surgeon training regarding the use and reloading of the devices will minimize these errors. Finally, multiuse staplers should be ﬁred according to the manufacturer’s speciﬁcations. Firing the stapler more times than recommended may lead to malfunction.

Inadequate Ligation and Division of the Small Bowel Mesentery ● Consequence Bleeding or hematoma formation. Imprecise ligation can cause small bowel ischemia, leading to unnecessary resection of healthy intestine. Unrecognized, inadequate ligation can result in immediate or delayed major intra-abdominal hemorrhage. Grade 1/3/4 complication ● Repair Bleeding sites can be transﬁxed with a suture ligature or reclamped and ligated to achieve hemostasis. Care should be taken to prevent occlusion of adjacent major vessels and subsequent ischemic injury. Expanding hematomas can be treated with a suture ligature to achieve hemostasis of a retracted mesenteric vessel. Although rarely required, opening of the hematoma may be necessary to ensure accurate and complete ligation of the bleeding site. Ligation resulting in ischemic intestine requires additional resection of intestine back to adequately perfused bowel. Delayed hemorrhage typically requires reoperation and ligation of the bleeding site. This may result in intestinal ischemia, requiring re-resection of the small intestine including the site of the anastomosis. Alternatively, interventional angiography may allow identiﬁcation and embolization of the bleeding site if it can be selectively cannulated. ● Prevention Transillumination of the mesentery (see Fig. 21–2) will allow determination of the exact location of the mesenteric vessels. This ensures accurate and adequate liga-

tion. Occasionally, a fatty mesentery prevents accurate location of the vessels or an adequate purchase for a tie. A suture ligature used in this instance will prevent dislodgement of the tie. Good communication between the surgeon and the assistant will prevent premature removal of the clamp before the suture is secured.

Difﬁculties during the Anastomosis A number of complications can occur during this step as a result of equipment malfunction or operator error. Attention to the technical details of this and the following steps will minimize complications during this part of the procedure. ● Consequences Failure to accurately line up the proximal and distal ends of the bowel can result in a distorted, torqued, and dysfunctional anastomosis with a stricture or obstruction. Stapler malfunction can occur, as described previously. However, loss of this staple line results in a much greater loss of healthy intestine because both the proximal and the distal bowel ends will require resection back to healthy bowel. Alternatively, suture repair of the injury may sufﬁce. Perforation of the bowel with the end of the stapler can occur if both limbs are not adequately seen during stapler insertion. Again, this will require repair or resection of healthy bowel. Enteric spillage during this step can lead to infection, as discussed previously. Bleeding from the staple line can result in immediate or delayed hemorrhage. Delayed hemorrhage can result in obstruction at the anastomosis or disruption of the anastomosis owing to distention, which can result in an anastomotic leak. An inadequate or disrupted staple line can lead to anastomotic leak, as discussed later. Grade 1/2/3/4/5 complication ● Repair Mechanical problems resulting in a strictured or obstructed anastomosis may require resection of the anastomosis and construction of a new one. Similar treatment is used for stapler malfunctions that result in an inadequate staple line or anastomosis. Bleeding at the anastomosis can be treated with a transﬁxing suture. ● Prevention Careful approximation of the proximal and distal limbs of the bowel involved in the anastomosis will prevent misalignment complications (Fig. 21–5). A traction suture placed at the cut ends of the bowel will help ensure that the two pieces are pulled equally onto the stapler jaws (Fig. 21–6). Rotation of the bowel so the antimesenteric edges are in approximation will ensure a technically precise anastomosis (Fig. 21–7). Adequate inspection and palpation during stapler placement will prevent perforation injuries (Fig. 21–8).

21 ENTERECTOMY

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Enteric spillage can be prevented, as described previously. Opening of the stapler jaws completely, prior to removing the stapler, will prevent traction injuries, including bleeding, once the stapler is ﬁred. Retraction of the edges of the enterotomy and direct inspection of the staple line will allow identiﬁcation and oversewing of any bleeding sites and will prevent delayed hemorrhage complications (Fig. 21–9).

A

Failure at the Enterotomy Closure Site ● Consequence Strictured anastomosis. An inadequate staple line can lead to anastomotic leak, as discussed later. Grade 1/2/3/4 complication

B

● Repair Reapplication of the stapler or oversewing of the inadequately closed enterotomy. Narrowing/stricture requires construction of a new anastomosis.

Figure 21–5 A, The proximal and distal ends of the bowel are aligned by traction sutures (arrowheads). Careful approximation prevents misalignment complications, such as kinking or twisting of the bowel limbs. B, To anastomose the proximal and distal bowel limbs, an enterotomy is made in the antimesenteric border of each limb. The proximal traction suture (not seen, behind the stapler) is then used to pull the bowel ends up onto the stapler arms, bringing them into appropriate alignment (arrows).

● Prevention Care to include the entire length of the enterotomy is required to prevent this problem. At each corner of the enterotomy, an Allis clamp is placed with one jaw into the lumen of the anastomosis (Fig. 21–10). The Allis is partially closed while withdrawing the clamp, thereby grabbing the mucosa to ensure that full-thickness bowel is included in the enterotomy closure. This prevents inadequate closure at the corners of the enterotomy. Alternatively, a suture through each corner of the anastomosis and a suture in the middle of the anastomosis, all of which include the full thickness of the bowel, can be used to hold the bowel edges in apposition to allow precise closure. The staple lines are offset slightly from

A B Figure 21–6 A, The proximal traction sutures (arrows) help pull the bowel ends onto the stapler arms. This suture ensures that the bowel ends are aligned (arrowheads). B, Inspection of the posterior part of the staple line ensures that the entire anastomosis is appropriately aligned.

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B

Figure 21–7 Once the stapler jaws are closed, proper alignment of the bowel limbs includes the ends at the enterotomy sites (arrowheads) and the small bowel mesentery (arrow), which is held out directly opposite (180°) from the anastomosis. The surgeon’s ﬁngers are placed behind the bowel as shown to insure no other structures are caught in the staple line.

Figure 21–8 A, The distal end of the staple line requires inspection as the stapler arms are inserted into the bowel lumen. This prevents a through-and-through bowel injury from the tip of the stapler (arrows) coming out the bowel wall. B, This is particularly true when an anastomosis is done deep in the abdominal cavity and the distal end of the anastomosis is difﬁcult to see.

each other (see Fig. 21–10) and the two edges of bowel between the corner clamps are held in approximation with additional Allis clamps (Fig. 21–11). Application of the linear non-cutting stapler just below the Allis clamps will prevent narrowing of the anastomosis and subsequent stricture formation (Fig. 21–12). A buttressing suture placed at the end of the staple line will prevent tension at this portion of the anastomosis (Fig. 21–13). Assessment of the patency of the anastomosis is done by palpation of the lumen (Fig. 21–14). In addition, intraluminal air can be milked into the anastomosis to distend it and ensure an airtight seal. Likewise, passage of succus through the anastomosis ensures an adequate size of the opening.

Anastomotic Failure Anastomotic disruption and leakage are dreaded and potentially fatal complications of enterectomy. Although

Figure 21–9 The staple line (arrow) can be inspected directly to ensure hemostasis. Bleeding along the staple line can be suture-ligated to prevent delayed anastomotic bleeding resulting in obstruction or disruption.

21 ENTERECTOMY

243

these fears are warranted, the incidence of anastomotic failure for enterectomy is low, 1.1% in one series, resulting in a mortality of 0.4%.7 ● Consequence Anastomotic leak, intra-abdominal abscess, enterocutaneous ﬁstula, peritonitis, and death. Grade 2/3/4/5 complication

Figure 21–10 An Allis clamp is placed at each corner of the enterotomy. One side of the clamp is placed into the lumen, partially closing it and pulling outward to include the mucosa (arrows) within the closed clamp. This insures that full-thickness bowel and the entire corners are included in the enterotomy closure. The initial (gastrointestinal anastomosis) staple lines are offset (arrowheads) during closure of the enterotomy to avoid multiple overlapping staple lines.

● Repair Contained leaks without generalized peritonitis can be treated with supportive care, antibiotics, and percutaneous drainage. Failure of this treatment, a free leak or generalized peritonitis requires laparotomy for repair. In these circumstances, drainage alone is associated with increased mortality. Repair of the anastomosis can be done, but most authors favor construction of a new anastomosis. Either way, a proximal diverting ostomy is recommended by some authors as part of the procedure.7 ● Prevention All authors believe that attention to the technical details during construction is critical. In addition, all adhere to the primary tenets of this and any other anastomosis that the minimum requirements for a successful anastomosis are adequate approximation of wellvascularized tissue in a tension-free manner. Despite a technically excellent anastomosis, leaks still occur. As noted earlier, although signiﬁcant efforts have been devoted to detecting risk factors for anastomotic failure, the results from these studies have been mixed and variable. Consequently, no consistent risks have been identiﬁed that might be optimized preoperatively to minimize the nontechnical risks of anastomotic failure.

Inadequate Closure or Injury during Closure of the Mesenteric Defect

Figure 21–11 Allis or Babcock clamps are used to approximate the bowel edges to insure complete closure of the enterotomy site.

● Consequence Internal herniation, bleeding, hematoma, and anastomotic failure. Grade 1/2/3/4/5 complication ● Repair Internal herniation requires laparotomy to reduce the hernia. Ischemic injury may require resection and reconstruction of the ischemic bowel. Injury typically results in bleeding or hematoma, requiring suture ligation of the bleeding site.

Figure 21–12 The linear non-cutting stapler is placed just beneath the clamps, allowing complete closure of the enterotomy without narrowing the anastomosis.

● Prevention When closing the mesenteric defect include small bites of the peritoneum only (Fig. 21–15). Deeper bites into the mesenteric adipose tissue result in vascular injury. Avoid placing sutures at sites where the sutures used to ligate the mesentery during mesenteric division are present. Vessels extend to the edge of the mesentery at these sites and are more easily injured with the superﬁcial bites of the closing sutures. Inspection after

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A

B

Figure 21–13 A, The “corner” of the staple line (arrow). B, A suture is placed adjacent to the linear staple line (arrow) to prevent tension at this site. This is the “buttressing” suture.

Figure 21–14 The lumen of the anastomosis (indicated by the bracket) can be palpated between the thumb and the index ﬁnger to ensure that it is patent.

closure insures adequate approximation to prevent subsequent herniation.

Closure Injury during Closure of the Incision All grades of injury can occur at this step. Careful fascial approximation will avoid these complications, as discussed in Section I, Chapters 6 and 7.

Figure 21–15 During closure of the mesenteric defect (edge indicated by small arrowheads), small superﬁcial bites of the peritoneum (see the needle) are obtained to avoid injury to the mesenteric vessels. Care is used to avoid the mesentery ligation sites (arrows), where vessels come to the cut edge of the mesentery and, therefore, are easily injured.

Other Complications Short Bowel Syndrome Grade 4 complication Although not a technical complication of enterectomy, short bowel syndrome is a consequence of massive intestinal resection. Symptoms can be avoided if more than 150 cm of small bowel remain intact. A minimum of

21 ENTERECTOMY 50 cm of small bowel in the absence of any colon is required to allow adaptation.12,13 Jejunal resection is tolerated better than ileal resection, because the ileum adapts better than the jejunum.13 Maintaining the ileocecal valve and as much colon as possible also diminishes the onset and severity of symptoms from massive enterectomy. Finally, stricturoplasty and other techniques to maintain length in patients with small bowel disease, such as Crohn’s disease, will prevent short bowel syndrome in those patients in whom even minimal resections may lead to symptoms owing to their diseased bowel.

Nutritional Deﬁciencies Grade 1 complication Resection of signiﬁcant ileum can lead to nutritional deﬁciencies, most notably vitamin B12. Patients with extensive ileal resection should have B12 supplementation. Malabsorption of fat, fat-soluble vitamins, and bile salts also occurs with extensive ileal resection. Fat malabsorption may require supplementation for fat-soluble vitamins A, D, and E.14 It also can lead to nephrolithiasis.15 Bile salt malabsorption can lead to diarrhea and cholelithiasis. Ileus Grade 1 complication A common feature of abdominal surgery, ileus prolongs hospital stay and increases patient discomfort. Although not unique to enterectomy, ileus may be decreased by a number of interventions including the use of thoracic epidural catheters, avoidance of systemic opioid analgesics, administration of new pharmacologic agents, and the use of laparoscopic techniques, all feasible in enterectomy.16,17 In addition, the effects of postoperative ileus may be minimized by a number of strategies. Numerous studies demonstrate no beneﬁt in the routine use of nasogastric tubes postoperatively.18 Likewise, early postoperative feeding has become standard, because only 10% to 20% of patients fail the early initiation of a diet.19 Together, these strategies minimize the effects of an ileus, lessening patient discomfort and shortening the length of stay. Postoperative Bowel Obstruction Grade 1/3/4 complication Early or late bowel obstruction can occur after enterectomy. Like an ileus, this is not a technical error in the conduct of the operation, but a consequence of laparotomy. Early obstruction can mimic ileus, and distinguishing the two may be difﬁcult.20 Ileus usually resolves after 3 to 5 days. Lack of bowel activity or progressive distention after this time typically represents an early small bowel obstruction. The risk of occurrence is reported to be 0.7% at 4 weeks after operation,21 although Fazio and associates22 reported that 30% of all bowel obstructions in their series occurred within 30 days of the operation. Resolution with conservative therapy occurs in approxi-

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mately 90% of patients by 10 to 14 days. The risk of strangulation obstruction is reported to be extremely small, allowing prolonged conservative therapy in this group of patients. Late postoperative bowel obstruction most commonly occurs as a result of adhesions. Up to 90% of patients will develop adhesions postoperatively.23 However, a smaller percentage, approximately 3% to 30%, will develop a small bowel obstruction as a result of adhesions.22,24–28 Whereas signiﬁcant research has been devoted to minimizing postoperative adhesions and subsequent bowel obstruction, reliable means for doing so have been elusive. Recently, adhesion-prevention products have proved successful in decreasing the risk of adhesive small bowel obstruction based on randomized, controlled trials.22

REFERENCES 1. Jex RK, van Heerden JA, Wolff BG, et al. Gastrointestinal anastomoses. Factors affecting early complications. Ann Surg 1987;206:138–141. 2. Carty NJ, Keating J, Campbell J, et al. Prospective audit of an extramucosal technique for intestinal anastomosis [see comment]. Br J Surg 1991;78:1439–1441. 3. Golub R, Golub RW, Cantu R Jr, Stein HD. A multivariate analysis of factors contributing to leakage of intestinal anastomoses. J Am Coll Surg 1997;184:364–372. 4. Max E, Sweeney WB, Bailey HR, et al. Results of 1,000 single-layer continuous polypropylene intestinal anastomoses. Am J Surg 1991;162:461–467. 5. Kaidar-Person O, Person B, Wexner SD. Complications of construction and closure of temporary loop ileostomy. J Am Coll Surg 2005;201:759–773. 6. Hautmann RE, de Petriconi R, Gottfried HW, et al. The ileal neobladder: complications and functional results in 363 patients after 11 years of followup. J Urol 1999;161: 422–427; discussion 427–428. 7. Pickleman J, Watson W, Cunningham J, et al. The failed gastrointestinal anastomosis: an inevitable catastrophe? J Am Coll Surg 1999;188:473–482. 8. Baker RS, Foote J, Kemmeter P, et al. The science of stapling and leaks. Obes Surg 2004;14:1290–1298. 9. Irvin TT, Goligher JC. Aetiology of disruption of intestinal anastomoses. Br J Surg 1973;60:461–464. 10. Pruett TL, Simmons RL. Failure of Gastrointestinal Anastomosis. Chicago: Year Book Medical, 1984. 11. Resegotti A, Astegiano M, Farina EC, et al. Side-to-side stapled anastomosis strongly reduces anastomotic leak rates in Crohn’s disease surgery. Dis Colon Rectum 2005;48:464–468. 12. Sax HC. Speciﬁc nutrients in intestinal failure: one size ﬁts no one. Gastroenterology 2006;130(2 suppl 1): S91–S92. 13. Tappenden KA. Mechanisms of enteral nutrient–enhanced intestinal adaptation. Gastroenterology 2006;130(2 suppl 1):S93–S99. 14. Jeejeebhoy KN. Management of short bowel syndrome: avoidance of total parenteral nutrition. Gastroenterology 2006;130(2 suppl 1):S60–S66.

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15. Buchman AL. Etiology and initial management of short bowel syndrome. Gastroenterology 2006;130(2 Suppl 1): S5-S15. 16. Saclarides TJ. Current choices—good or bad—for the proactive management of postoperative ileus: a surgeon’s view. J Perianesth Nurs 2006;21(2A suppl):S7–S15. 17. Wolff BG, Michelassi F, Gerkin TM, et al. Alvimopan, a novel, peripherally acting mu opioid antagonist: results of a multicenter, randomized, double-blind, placebocontrolled, phase III trial of major abdominal surgery and postoperative ileus. Ann Surg 2004;240:728–734; discussion 734–735. 18. Vermeulen H, Storm-Versloot MN, Busch OR, Ubbink DT. Nasogastric intubation after abdominal surgery: a meta-analysis of recent literature. Arch Surg 2006;141: 307–314. 19. Behrns KE, Kircher AP, Galanko JA, et al. Prospective randomized trial of early initiation and hospital discharge on a liquid diet following elective intestinal surgery. J Gastrointest Surg 2000;4:217–221. 20. Sajja SB, Schein M. Early postoperative small bowel obstruction. Br J Surg 2004;91:683–691. 21. Stewart RM, Page CP, Brender J, et al. The incidence and risk of early postoperative small bowel obstruction. A cohort study. Am J Surg 1987;154:643–647. 22. Fazio VW, Cohen Z, Fleshman JW, et al. Reduction in adhesive small-bowel obstruction by Sepraﬁlm adhesion

23.

24.

25.

26.

27.

28.

barrier after intestinal resection. Dis Colon Rectum 2006; 49:1–11. Menzies D, Ellis H. Intestinal obstruction from adhesions—how big is the problem? Ann R Coll Surg Engl 1990;72:60–63. Parker MC, Ellis H, Moran BJ, et al. Postoperative adhesions: ten-year follow-up of 12,584 patients undergoing lower abdominal surgery. Dis Colon Rectum 2001;44: 822–829; discussion 829–830. Nieuwenhuijzen M, Reijnen MM, Kuijpers JH, van Goor H. Small bowel obstruction after total or subtotal colectomy: a 10-year retrospective review. Br J Surg 1998; 85:1242–1245. Ellis H, Moran BJ, Thompson JN, et al. Adhesion-related hospital readmissions after abdominal and pelvic surgery: a retrospective cohort study.[see comment]. Lancet 1999; 353:1476–1480. Beck DE, Opelka FG, Bailey HR, et al. Incidence of small-bowel obstruction and adhesiolysis after open colorectal and general surgery [erratum appears in Dis Colon Rectum 1999;42:578]. Dis Colon Rectum 1999; 42:241–248. Matter I, Khalemsky L, Abrahamson J, et al. Does the index operation inﬂuence the course and outcome of adhesive intestinal obstruction? Eur J Surg 1997;163: 767–772.

22

Ileostomy James FitzGerald, MD INTRODUCTION Proper construction of an ileostomy is a fundamental and essential skill for all surgeons operating in the abdomen. It can be performed either as a separate operation or as a part of a larger procedure and can be created using a traditional open incision or laparoscopic techniques.1 Depending upon the indication, an ileostomy may be constructed in a variety of ways. Because both ends of the small bowel are accessible on the surface of the skin, loop ileostomies are generally easier to close and intended to be temporary stomas. However, a recent study of patients undergoing surgery for rectal cancer showed that approximately 19% of these “temporary” stomas will never be reversed.2 End ileostomies may be either permanent or temporary depending upon the remaining bowel anatomy, but generally require a laparotomy to restore bowel continuity. An “end-loop” ileostomy is generally used when there is difﬁculty reaching through the abdominal wall (Fig. 22–1). Ileostomies have a signiﬁcant impact on the quality of life of patients, with up to 80% experiencing some change in their lifestyle after the creation of a stoma.3 The degree of social impact appears to be related to the number of stoma care problems.4 Regardless of the indication for the procedure or the technique used, surgeons must adhere to several basic principles in order to minimize postoperative stoma-related complications.

INDICATIONS ● After surgical resection of the colon and rectum ● Protection of a high-risk anastomosis ● Temporary fecal diversion for perineal infections

OPERATIVE STEPS Step Step Step Step Step

1 2 3 4 5

Site selection Selection and preparation of bowel segment Alignment of layers of abdominal wall Skin and subcutaneous tissue incision Anterior rectus sheath fascial incision

Step Step Step Step

6 7 8 9

Separation of rectus muscle ﬁbers Posterior rectus sheath fascial incision Passing bowel through abdominal wall Placing the bridge and maturing the stoma

OPERATIVE PROCEDURE Site Selection Poorly Fitting or Leaking Stoma Appliance ● Consequence Breakdown of the skin surrounding the ileostomy. Approximately 28% of patients with an ileostomy would prefer the stoma to be relocated, and the percentage is higher in patients undergoing an emergency procedure (37%) than in those undergoing elective surgery (23%).3 Thirty percent to 61% of patients experience excoriation of the skin around the stoma, and 22% to 57% of patients experience leakage4–6 (Fig. 22–2). Grade 1 complication ● Repair Patient education and changing the type of appliance may be effective. In extreme cases, laparotomy with stoma relocation may be necessary. ● Prevention Ideally, the stoma should be placed through the rectus muscle centered on a ﬂat area or on the crest of a fat roll away from scars, creases, or bony prominences. The site should be chosen prior to the operation after examining the patient in the supine and sitting positions. Marking the patient preoperatively in the proper site can signiﬁcantly reduce skin problems in the immediate postoperative period.7

Selection of the Bowel Segment and Preparation of the Bowel High-Output Stoma ● Consequence Electrolyte imbalances or dehydration potentially leading to acute renal failure. A prospective analysis of

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A

Figure 22–1 An end-loop ileostomy. The mesentery to the bowel is not divided, enabling the bowel to be brought through a thick abdominal wall without the risk of ischemia. (Adapted from Wu JS. Ileostomy. Oper Tech Gen Surg 2003;5:257–263.)

60 patients undergoing restorative colectomy with a defunctioning ileostomy showed that ileostomy output peaked at postoperative day 4 and that the critical period for acute dehydration was from 3 to 8 days after the operation. During this time, ileostomy output is increasing, but oral intake is still limited.8 Overall, dehydration occurs in 5% to 20% of patients with ileostomies.6,9 Grade 1 complication ● Repair Replacement ﬂuids should be given while monitoring standard parameters of resuscitation. Serum electrolytes should be checked and replaced as needed. Loperamide has been shown to decrease ileostomy output by 22%.10 Bismuth subgallate, lomotil, tincture of opium, and codeine sulfate have also been shown to reduce ileostomy output.11 ● Prevention During surgery, every effort should be made to preserve the distal small bowel and use the most distal portion of the small bowel for the ileostomy. Postoperatively, ileostomy output should be carefully measured and recorded. On discharge, patients should be instructed and taught to continue to track the stoma output.

B Figure 22–2 The site for this ileostomy was not marked prior to the operation. In the operating room, it looks to be in good position. However, postoperatively, when the patient is seated the ileostomy is low, making care difﬁcult.

Stoma Retraction ● Consequence Leakage around the stoma, leading to peristomal skin irritation. Retraction of a loop ileostomy can result in incomplete defunctionalization of the distal bowel.6,12 Stoma retraction occurs in up to 17% of ileostomy patients followed for 20 years.13 Grade 3 complication

22 ILEOSTOMY

249

Figure 22–3 To determine the depth of ischemia or necrosis of a stoma, a test tube is gently inserted into the stoma opening. A penlight is used to help visualize the mucosa. If the ischemia extends below the fascial level, an urgent laparotomy is required.

● Repair Stoma revision may be accomplished by a local procedure at the ileostomy site, but the majority of cases will require a laparotomy. ● Prevention Stoma retraction is caused by tension on the bowel or loss of the distal stoma from necrosis. Retraction often is associated with a high body mass index.14 In obese patients, an end-loop ileostomy should be considered. Some data indicate a higher rate of retraction in contaminated stoma cases, although this is not speciﬁc for ileostomies.15

Necrotic/Ischemic Stoma ● Consequence Superﬁcial necrosis of the stoma, resulting in stenosis or retraction of the stoma. If the ischemic segment extends below the fascia, peritonitis can result. A simple bedside test can be performed to assess the depth of necrosis (Fig. 22–3). Grade 2/3 complication ● Repair Superﬁcial necrosis can be observed. If it results in stenosis or difﬁculty ﬁtting the appliance, the stoma will need to be revised. If the ischemic segment extends below the fascia, an emergent laparotomy is required. ● Prevention Mesenteric tension or excessive trimming of the mesentery may result in an ischemic stoma. The last vascular arcade of the small bowel mesentery should be preserved. Again, consideration should be given to constructing an end-loop ileostomy, especially in obese patients.

Figure 22–4 Ischemia at the distal end of the ileostomy or tension on the mesentery of the bowel can lead to stenosis. This will make it difﬁcult for the patient to properly ﬁt the appliance.

Stoma Stenosis ● Consequence Difﬁculty ﬁtting the appliance, stoma leakage, and noise while passing ﬂatus (Fig. 22–4). Grade 2/3 complication ● Repair If the stenosis is at the skin level, local repair is possible. In cases resulting from ischemia or Crohn’s disease, a formal laparotomy is usually required. ● Prevention Stenosis is believed to be secondary to ischemia of the distal bowel or to result from tension at the mesentery. See comments for “Prevention” in the section on “Necrotic/Ischemic Stoma,” earlier.

Skin and Subcutaneous Tissue Incision Mucocutaneous Separation ● Consequence Difﬁculty ﬁtting the appliance, leading to breakdown of the skin around the stoma. Grade 2/3 complication ● Repair Local revision is possible in simple cases. V-Y ﬂaps have been used to decrease the size of the incision.16 In extreme cases, laparotomy and resitting of the stoma may be necessary. ● Prevention Proper assessment of the diameter of the bowel to be used for the stoma. It is generally advisable to start small and increase the size as needed.

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Alignment of the Layers of the Abdominal Wall and Incision of the Anterior Rectus Fascia Peristomal Hernia ● Consequence Difﬁculty ﬁtting the appliance, bowel obstruction, and strangulation leading to bowel ischemia. Loop ileostomies are associated with a 1% to 3% incidence of peristomal hernia. For end ileostomies, the rate is between 6% and 7%. The cumulative probability after 20 years of developing a peristomal hernia is 16% (Figs. 22–5 and 22–6). Grade 3 complication ● Repair Local tissue repairs overall have poor results, with recurrence rates ranging from 40% to 100%. Stoma relocation fares slightly better, with recurrence rates ranging from 0% to 76%. Mesh repairs have the lowest reported recurrence rate (0%–33%), but carry the risk of infection in a contaminated ﬁeld.17 ● Prevention The fascial incision should be just large enough to allow passage of the limb of bowel, generally 2.5 cm. Whereas it is generally believed that placing the stoma through the rectus muscle reduces the incidence of a peristomal hernia, the data are mixed18,19 (Fig. 22–7).

Stoma Prolapse ● Consequence Difﬁculty ﬁtting the appliance and irritation of the bowel. In extreme cases, incarceration of the prolapsed

bowel may occur, leading to strangulation. The cumulative risk of prolapse over a 20-year period is approximately 11%.13 Grade 2/3 complication ● Repair Local revision of the stoma with excision of the prolapsed bowel is generally required. In cases of incarceration, application of sugar on the edematous bowel will act as an osmotic agent and may reduce the bowel. Strangulated bowel requires an emergent laparotomy and stoma revision. ● Prevention See comments for “Prevention,” in the section on “Parastomal Hernia,” previously.

Separation of the Rectus Fibers Injury to the Inferior Epigastric Vessels ● Consequence Excessive bleeding. Grade 1 complication ● Repair Ligation of the vessel. ● Prevention Careful separation of the rectus ﬁbers by spreading in a longitudinal direction may reduce the risk of injury to this vessel (Figs. 22–8 and 22–9).

Incision of the Posterior Rectus Fascia and Peritoneum Parastomal Hernia and Prolapse See the section on “Alignment of the Layers of the Abdominal Wall and Incision of the Anterior Rectus Fascia,” earlier.

Injury to the Underlying Bowel ● Consequence Enterotomy, possible peritonitis postoperatively if not identiﬁed at the time of injury. Grade 2/3 complication ● Repair Primary repair or resection as required. Figure 22–5 Although there are no speciﬁc data regarding the exact size of the stoma opening, either too large or too small an opening can lead to complications. In general, the stoma incision should be two ﬁngerbreadths for a loop ileostomy and slightly smaller for an end ileostomy.

● Prevention The assistant should place a laparotomy pad under the peritoneum and lift up the undersurface of the abdominal wall (Fig. 22–10).

22 ILEOSTOMY Lateral edge of rectus muscle

251

Medial edge of rectus muscle Fascial edge

Skin

A Stoma opening

Skin Fat

Clamps

Ructus muscle

B

Fascia

Figure 22–6 Hidden anatomy. A, In patients with thick abdominal walls, the fascia tends to retract laterally relative to the midline skin incision. If proper alignment is not restored, the stoma opening will be made tangential to the muscular wall of the abdomen. The opening in the fascia for the stoma will be too close to the midline incision. This can lead to difﬁculty closing the midline incision and could result in kinking of the bowel as it traverses the abdominal wall. B, By placing a clamp on the fascia and on the dermal layer of the midline incision, proper alignment can be restored.

Passing the Bowel through the Stoma Opening

pressure should be exerted from the abdominal side to deliver the bowel segment onto the skin surface.

Tearing the Bowel ● Consequence Enterotomy, contamination of ﬁeld, and possibly peritonitis if not identiﬁed at the time of injury. Grade 2/3 complication ● Repair Use the enterotomy site as the stoma opening if possible; otherwise, primary repair or resection is required. ● Prevention The bowel should be guided through the abdominal wall from the skin side, but not pulled. Rather, gentle

Twisting of the Bowel ● Consequence Bowel obstruction, ischemia, and maturing wrong end of a loop ileostomy. Grade 2/3 complication ● Repair Rotate bowel for proper alignment if noted intraoperatively; otherwise reoperation is required. ● Prevention For an end ileostomy, following the divided mesentery of the right colon up to the underside of the

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Figure 22–9 A clamp is passed through the stoma opening. When the surgeon grasps the tip of the clamp, the abdominal wall can be closely inspected for signs of bleeding. The inferior epigastric artery lies just below the rectus muscle.

Figure 22–7 At the base of this stoma incision, the ﬁbers of the external oblique muscles can be visualized. Most surgeons believe that placing a stoma in this location increases the possibility of hernia formation.

Figure 22–8 To reduce the chance of injury to the inferior epigastric vessel, the rectus muscle should be separated in the direction of its ﬁbers. (Adapted from Wu JS. Ileostomy. Oper Tech Gen Surg 2003;5:257–263.)

Figure 22–10 Proper alignment of the skin and fascial layers is crucial to ensure that the bowel passes perpendicular to the abdominal wall. A Kocher clamp is placed on the rectus fascia and a second on the dermal layer. A folded lap pad is placed under the stoma site. The assistant holds the two clamps and presses up on the underside of the abdominal wall.

22 ILEOSTOMY

Figure 22–11 Once the bowel has been passed through the abdominal wall, it is essential to be certain that it is not rotated. Placing a seromuscular suture through one side of a loop ileostomy can help maintain proper orientation.

abdominal wall will ensure proper alignment. For a loop ileostomy, marking one side with a seromuscular suture is helpful, but careful attention to detail is essential (Fig. 22–11).

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Figure 22–12 Skin implants at the mucocutaneous junction are the result of passing a suture through the epidermal skin layer. Ideally, the suture should be placed at the dermal level. (Reprinted with permission from Wu JS. Ileostomy. Oper Tech Gen Surg 2003;5:257–263.)

Placing the Bridge and Maturing the Stoma Enterocutaneous Fistula ● Consequence Poor-ﬁtting appliance and peristomal irritation. Fistulas develop in 7% to 11% of ileostomy patients with Crohn’s disease.20 Grade 2/3 complication ● Repair Simple ﬁstulas may be amenable to local revision of the stoma. In patients with Crohn’s disease, laparotomy with resection of the distal bowel and peristomal skin and revision of the stoma are frequently required.21 ● Prevention Fistulas arise either from a technical error maturing the ileostomy, Crohn’s disease, or pressure necrosis from the appliance on the side of the ileostomy (Fig. 22–12). When the end of the ileostomy is being everted, the ﬁrst bite should be full thickness through the distal cut edge of the bowel. The second should be a seromuscular bite approximately 5 cm proximal to the cut edge. A full-thickness bite at this level has the potential to develop into a ﬁstula. Finally, the last bite should be of the dermis at the edge of the ileostomy incision. Placing the suture full thickness through the skin can lead to mucosal implants around the stoma (Fig. 22–13). Care should be taken to avoid pressure from the stoma wafer on the ileostomy.

Figure 22–13 The appliance has irritated the side of the ileostomy. If this is not corrected, it can result in ﬁstula formation.

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Other Complications Diversion Colitis Grade 1 complication Segments of the colon excluded from the fecal stream can develop inﬂammatory changes. Up to 50% of patients experience symptoms, commonly mucous discharge, abdominal pain, or low-grade fevers. The endoscopic appearance of the diverted segment can be normal or inﬂamed. Diversion colitis is believed to be caused by the absence of luminal short chain fatty acids, which are used as an energy source for colonic mucosal cells. Symptoms generally resolve with closure of the ileostomy.22 In cases in which this is not possible, short chain fatty acid enemas may be useful.23,24 Pyoderma Gangrenosum Grade 1 complication Pyoderma gangrenosum is a chronic, painful ulceration of the skin associated with inﬂammatory bowel disease. Although it usually affects the lower extremity, several cases of peristomal pyoderma gangrenosum have been described. The painful ulcerations around the stoma create difﬁculty ﬁtting the appliance. Meticulous care of the stoma is essential. Injection of corticosteroids, inﬂiximab, antibiotics, and systemic steroids have all been tried with limited success.25 Carcinoma Grade 3/4/5 complication Forty-four cases of primary adenocarcinoma of an ileostomy have been reported in the literature. The average time from creation of the ileostomy to appearance of the adenocarcinoma is 24 years. The pathologic features suggest a transition from ileal mucosa to colonic mucosa to colonic dysplasia to adenocarcinoma. Chronic irritation of the stoma may predispose the ileal mucosa to these changes. Patients with ileostomies older than 15 years should be followed closely for this complication.26 Stomal excision is advised for any dysplastic changes, and segmental excision is recommended for adenocarcinoma.27 Stomal Varices Grade 3/4/5 complication Patients with portal hypertension may develop varices at the mucocutaneous junction. Local control measures and revision of the mucocutaneous junction may provide local control. Portal decompression or liver transplantation offers a more permanent solution.28

3. 4.

5.

6. 7.

8. 9.

10.

11. 12.

13.

14.

15.

16.

17. 18.

19.

20. 21.

REFERENCES 1. Khoo RE, Montrey J, Cohen MM. Laparoscopic loop ileostomy for temporary fecal diversion. Dis Colon Rectum 1993;36:966–968. 2. Den Dulk M, Smit M, Peeters KMJ, et al. A multivariate analysis of limiting factors or stoma reversal in patients

22. 23.

with rectal cancer entered into the total mesorectal excision (TME) trial: a retrospective study. Lancet Oncol 2007;8:278–279. Nugent KP, Daniels P, Stewart B, et al. Quality of life in stoma patients. Dis Colon Rectum 1999;42:1569–1574. Gooszen AW, Gelkerken RH, Hermans J, et al. Quality of life with a temporary stoma: ileostomy vs. colostomy. Dis Colon Rectum 2000;43:650–655. Robertson I, Leung E, Hughes D, et al. Prospective analysis of stoma-related complications. Colorectal Dis 2005;7:279–285. Feinberg SM, McLeod RS, Cohen Z. Complications of loop ileostomy. Am J Surg 1987;153:102–107. Bass EM, Del Pino A, Tan A, et al. Does preoperative stoma marking and education by the enterostomal therapist affect outcome? Dis Colon Rectum 1997;40: 440–442. Tang CL, Yunos A, Leong APK, et al. Ileostomy output in the early postoperative period. Br J Surg 1995;82:607. Wexner SD, Taranow DA, Johansen OB, et al. Loop ileostomy is a safe option for fecal diversion. Dis Colon Rectum 1993;36:349–354. Tytgat GN, Huibregtse K, Meuwissen SG. Loperamide in chronic diarrhea and after ileostomy: a placebo-controlled double-blind cross-over study. Arch Chir Neerl 1976;28: 13–20. Kramer P. Effect of antidiarrheal and antimotility drugs on ileal excreta. Am J Dig Dis 1977;22:327–332. Winslet MC, Drolc Z, Allan A, Keighley MRB. Assessment of the defunctioning efﬁciency of the loop ileostomy. Dis Colon Rectum 1991;34:699–703. Leong APK, Londono-Schimmer EE, Phillips RKS. Lifetable analysis of stomal complications following ileostomy. Br J Surg 1994;81:727–729. Arumugam PJ, Bevan L, Macdonald L, et al. A prospective audit of stomas—analysis of risk factors and complications and their management. Colorectal Dis 2003;5:49– 52. Leenen LPH, Kuypers JHC. Some factors inﬂuencing the outcome of stoma surgery. Dis Colon Rectum 1989;32: 500–504. Edington HD, Lorze MT. V-Y closure for abdominal wall stomal reduction. Surg Gynecol Obstet 1987;164:381– 382. Carne PWG, Robertson GM, Frizelle FA. Parastomal hernia. Br J Surg 2003;90:784–793. Sjodahl R, Anderberg B, Bolin T. Parastomal hernia in relation to site of the abdominal stoma. Br J Surg 1988; 75:339–340. Williams JG, Etherington R, Hayward MWJ, Hughes LE. Paraileostomy hernia: a clinical and radiological study. Br J Surg 1990;77:135–137. Shellito PC. Complications of abdominal stoma surgery. Dis Colon Rectum 1998;41:1562–1572. Greenstein AJ, Dicker A, Meyers S, Aufses AH. Periileostomy ﬁstulae in Crohn’s disease. Ann Surg 1983;197:179– 182. Giardiello FM, Lazenby AJ. The atypical colitides. Gastroenterol Clin North Am 1999;28:479–490. Harig JM, Soergel KH, Komorowski RA, et al. Treatment of diversion colitis with short chain fatty acids irrigation. N Engl J Med 1989;320:23–28.

22 ILEOSTOMY 24. Kiely EM, Ajayi NA, Wheeler RA, Malone M. Diversion procto-colitis: response to treatment with short-chain fatty acids. J Pediatr Surg 2001;36:1514–1517. 25. Kiran RP, O’Brien-Ermlich B, Achkar JP, et al. Management of peristomal pyoderma gangrenosum. Dis Colon Rectum 2005;48:1397–1403. 26. Quah HM, Samad A, Maw A. Ileostoma carcinomas a review: the latent risk after colectomy for ulcerative colitis and familial adenomatous polyposis. Colorectal Dis 2005; 7:538–544.

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27. Gadacz TR, McFadden DW, Gabrielson EW, et al. Adenocarcinoma of the ileostomy: the latent risk of cancer after colectomy for ulcerative colitis and familial polyposis. Surgery 1990;107:698–703. 28. Roberts PL, Martin FM, Schoetz DJ, et al. Bleeding stomal varices: the role of local treatment. Dis Colon Rectum 1990;33:547–549.

COLON, RECTUM AND ANUS Eugene F. Foley, MD 23

Right Colectomy: Open and Laparoscopic David W. Larson, MD INTRODUCTION The operative choices available for right colectomy expanded in May of 2004. With the publication of Clinical Outcomes Surgical Therapy (COST),1 laparoscopic or minimally invasive surgery (MIS) for the treatment of malignant disease had the evidence needed to ethically offer it to patients with cancer. Since the early 1990s, laparoscopic colectomy for benign and, more importantly, malignant disease suffered from poor adoption. The reasons for this are many, including technical difﬁculty, poor instrumentation, and concerns over the oncologic impact of laparoscopic surgery. These important factors and concerns crystallized the importance of open right colectomy as the standard by which MIS is judged. Despite the slow growth of MIS, the evidence supplied by trials like COST, Conventional vs. Laparoscopic Assisted Surgery in Colorectal Cancer (CLASICC), and Colon Cancer Laparoscopic or Open Resection (COLOR)1–3 have allowed for the dramatic increase in the use of this technique. Right colectomy remains a classic and standard operation that results in outstanding outcomes with relatively few lasting complications. However, even well-known and successful operations have pitfalls. These potential problems can be avoided by careful planning and meticulous technique. The best data to date would suggest that morbidity associated with this procedure is around 20% with 2% to 4% of these occurring intraoperatively.1,3 Most complications from this operation involve two areas: those common to all operations of the right colon and those important to cancer speciﬁcally. The complications common to all operations of the right colon include trocar complications (<1%), bleeding (1%–4%), bowel injury

(1%–2%), ureteral injury (1%), wound infection and dehiscence (2%–5%), anastomotic failure (2%–3%), deep vein thrombosis (DVT; 1%–2%), and death (0.5%–5%).1–3 Complications related to oncologic concern arise mainly from the risk of trocar site implants and the inability to adequately assess the abdomen for metastatic disease. Trocar site recurrences have been reported as high as 24%,4 although with the publication of recent randomized trials, the percentage, in the setting of well-trained surgeons, should approach only 1%.1 This rate of recurrence is similar to that seen in open surgery. Although failure to detect metastatic disease is a risk, with proper preoperative work-up, this risk remains small and can be attested to by the results of the COST, CLASICC, and COLOR trials.1–3

INDICATIONS Pathology of the right colon includes a number of benign and malignant conditions. ● Endoscopically unresectable polyps ● Malignancy (adenocarcinoma, carcinoid) ● Inﬂammatory bowel disease (IBD)—Crohn’s disease

OPERATIVE STEPS Step 1 Step 2 Step 3

Positioning and/or trocar placement Thorough exploration of the abdomen with both malignant disease and IBD Mobilization of the distal small bowel and cecum

258

SECTION III: GASTROINTESTINAL SURGERY rence with malignancy secondary to poor technique remains an important aspect of trocar use. The consequences and repair of such injury are self-evident. Grade 2–5/5 complication

Figure 23–1 Trocar site placement. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

Step Step Step Step

4 5 6 7

Mobilization of the hepatic ﬂexure Vascular control Anastomotic techniques Closure

OPERATIVE PROCEDURE Positioning and Trocar Placement All operations begin with positioning. It is our practice to position patients on the table in a supine position. Ankle straps are utilized in both open and laparoscopic techniques to allow for Trendelenburg position. The surgeon stands on the patient’s left and across from the ﬁrst assistant. Trocar placement can be seen in Figure 23–1.

Trocar Injuries and Future Wound Site Recurrence ● Consequence Injuries associated with trocar placement can be lifethreatening. Although relatively uncommon, bowel injury and intra-abdominal or abdominal wall bleeding can occur. Likewise, the association of port site recur-

● Prevention We suggest that the placement of the ﬁrst trocar be performed in either an open or a modiﬁed open technique. The modiﬁed open technique of placing the camera through a transparent trocar and passing it under direct vision through the abdominal wall provides a signiﬁcant advantage in many obese patients or those with a “hostile abdomen.” Once the ﬁrst trocar is placed and secured, all other trocars are placed under direct vision after appropriate insufﬂations. Care must be taken when placing any lateral port to avoid the inferior epigastric vessel. If bleeding from the abdominal wall occurs, cautery, suture ligation, or tamponade can be used. Speciﬁcally, the use of a small Foley catheter placed through the trocar with subsequent inﬂation of the balloon and back-pressure on the abdominal wall will stop most bleeding. Prevention of port site recurrence includes making sure all trocars are securely in place and allowing gas to escape only through the trocars. By preventing gas or irrigation from exiting the abdomen around or through an unprotected trocar site, you will prevent the so-called chimney effect, which has been theorized as the cause for the high rates of recurrence.

Exploration Exploration is a critical step in the surgical management of both benign and malignant disease. It remains most critical for malignant disease because rates of unsuspected M1 disease range from 1% to 4%.1 Once the abdomen is entered, a thorough exploration of the abdomen is the ﬁrst order of business. The liver must be palpated or visualized in the case of laparoscopic surgery, the gallbladder must be assessed for stones, and the surrounding organs of the upper and midabdomen must be examined. The small bowel is run from the ligament of Treitz to the ileocecal valve. In women, the uterus and ovaries must be inspected for any pathology because metastatic disease may occur in up to 3% of patients. One must remember that intraoperative ultrasound can also be used to enhance the hepatic evaluation for metastasis. During exploration, we determine whether adhesions, altered anatomy, or tumor characteristics will require conversion to open surgery. If so, conversion is performed promptly. ● Consequence Improper exploration will lead to incomplete operation in both malignancy and IBD. Grade 2–5/5 complication

23 RIGHT COLECTOMY: OPEN AND LAPAROSCOPIC

259

● Repair If metastatic disease is identiﬁed, surgical resection of isolated metastatic disease or biopsy of unresectable metastatic disease may take place. In the setting of multisite IBD, further surgical intervention such as strictureoplasty, resection, or bypass may be used. ● Prevention In the setting of malignant disease, preoperative staging with computed tomography (CT), laboratory evaluation, and physical examination will have lower than 1% risk of identifying unsuspected M1 disease, as attested to by COST.1 Special consideration should be given to locally aggressive tumors. If adjacent organs are involved such as duodenum, small bowel, omentum, or retroperitoneal structures such as the ureter or gonadal vessels, every attempt must be made to complete an en-bloc resection. The surgeon must not violate oncologic principles by attempting to separate intra-abdominal structures from the tumor because this would adversely affect patient outcome. A R0 resection must be the goal of every operation regardless of technique.

Mobilization of the Cecum and Small Bowel Although technical details differ between open and laparoscopic surgery, the actual dissection remains exactly the same. For a right colon cancer, the line of dissection depends on the location of the tumor. For tumors located in the cecum, a 10-cm margin of terminal ileum is generally taken. If the tumor is located in the ascending colon, only a few centimeters of ileum is required as a margin. This line of resection should extend to the transverse colon at the level of the right branch of the middle colic vessels (Fig. 23–2). Ureteral injury and adjacent bowel injury are most likely during this portion of the dissection.

Injury to the Ureter (1%) or the Surrounding Small Bowel (1%–3%) (Thermal Injury) ● Consequence The degree of complication depends on the extent of the injury and the timing of the repair. Grade 2–4/5 complication (ureteral injury); grade 2–5/5 complication (small bowel injury) ● Repair Primary repair of the ureter over a stent or repair of the small bowel injury can be performed either laparoscopically or in an open fashion depending on the surgeon’s comfort level. In the setting of thermal injury that is not full thickness, the use of an oversew stitch or buttressing the area with an omental patch may prove useful.

Figure 23–2 Line of resection for a right hemicolectomy done for cancer. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

● Prevention Prevention starts with meticulous technique and proper equipment and retraction. The patient is placed in the Trendelenburg position with the right side tilted up. The ﬁrst step of dissection is ureter identiﬁcation, which can usually be done at the level of the pelvic brim. In obese patients, one must ﬁrst score the peritoneum to identify the ureter. With appropriate retraction and positioning, one can separate the bowel of interest from loops of adjacent bowel. It is important to understand the intrinsic limitations of the different dissection tools we have at our disposal from sharp dissection to electrocautery to ultrasonic dissectors to various radiofrequency devices. Each has its own intrinsic risk of injuring adjacent structures, and one must be constantly aware of one’s surrounding, especially with a laparoscopic approach. Mobilization of the right colon begins by separating the retroperitoneal structures (gonadal vessels and ureter) from the terminal ileum and cecum. This is performed by incising the virtually transparent peritoneal attachments to these structures laterally and rotating the cecum anteriorly and medially (Fig. 23–3). Once this mobilization is completed, the medial and posterior attachments to the right

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SECTION III: GASTROINTESTINAL SURGERY

Figure 23–4 Inferior and medial dissection of the cecum and ascending colon. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

colon and terminal small bowel are incised up toward the junction of the third and fourth portions of the duodenum (Fig. 23–4). Mobilization of the colon and the ileocolic vessel is complete once the surgeon has identiﬁed the middle colic vessel as it crosses the inferior border of the duodenum.

Hepatic Flexure Mobilization

Figure 23–3 A, Lateral line of dissection for open right colectomy. B, Lateral to medial dissection of the cecum and ascending colon. (A and B, By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

Continuing the lateral dissection up and around the hepatic ﬂexure during open resection, the surgeon’s index ﬁnger provides the plane of dissection for the ﬁrst assistant to cauterize upon (Fig. 23–5). Retracting the midtransverse colon inferiorly, one can complete the exposure of the hepatic ﬂexure. The thin plane between the mesocolon and the gastrocolic ligament can be developed bluntly and dissected to complete the ﬂexure mobilization. Once this has been completed, the right colon is retracted superiorly and medially, exposing the anterior edge of the duodenum and head of the pancreas. Release of these ﬁlmy attachments is the last step in the dissection. Similarly, the laparoscopic approach begins medially at the transverse colon and proceeds toward the previous

23 RIGHT COLECTOMY: OPEN AND LAPAROSCOPIC

Figure 23–5 Line of resection for the lateral peritoneal attachments of the right colon and hepatic ﬂexure. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

261

Figure 23–6 Hepatic ﬂexure mobilization, laparoscopic technique. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

lateral dissection of the cecum and ascending colon. The patient is placed in reverse Trendelenburg with the right side up. Mobilization of the colon at the hepatic ﬂexure begins with the gastrocolic ligament, which is grasped near but not on the bowel and elevated toward the anterior abdominal wall and the feet. This thin ligament can often be separated from the deeper tissues of the colonic mesentery. By identifying and then entering the correct plane between the gastrocolic ligament and the transverse colon mesentery, one can easily mobilize the hepatic ﬂexure. Proper mobilization allows for visualization of the duodenum, which is protected (Fig. 23–6). Once these planes of dissection are connected, the remaining ﬁlmy attachments anterior to the duodenum are divided, in a manner similar to that performed in the open approach.

● Prevention Meticulous dissection at the level of the duodenum and around the head of the pancreas is the standard that must be upheld. During laparoscopic dissection, this area is at particular risk, given the more limited nature of retraction. It is, therefore, crucial to elevate the gastrohepatic ligament off the retroperitoneal structure prior to dissecting them (see Fig. 23–6). Without this critical step, one is apt to place the duodenum at risk for thermal or ultrasonic injury. It is important that the dissection of the cecum and the posterior and medial attachments up to the duodenum be completely freed (see Fig. 23–4). This mobilization will allow for greater separation of tissues that now hold the hepatic ﬂexure close to the duodenal edge.

Duodenal Injury

Vascular Control

● Consequence Perforation or delayed perforation with peritonitis. Grade 2–5/5 complication

The avascular window between the right branch of the middle colic artery and the right or ileocolic artery is an important anatomic landmark. The right colic artery rarely branches directly off the superior mesenteric artery (SMA). The right colic most often (90% of the time) is a branch of the ileocolic artery and rarely requires separate ligation. The vessels of interest in an operation for cancer are, of course, the ileocolic, the right colic, and the right branch of the middle colic.

● Repair As stated in the previous section, if injury is noted, one must repair the defect. If noted during a laparoscopic resection, one can either convert and repair or repair with laparoscopic techniques.

262

SECTION III: GASTROINTESTINAL SURGERY ● Consequences Anastomotic leak occurs in 2% to 3% of patients. Grade 3–5/5 complication ● Repair and Prevention Standard surgical dictum of proper blood supply, limited tension, and meticulous technique is the hallmark of every successful anastomosis. Our techniques include two broad categories of anastomosis: handsewn and stapled anastomoses. Three standard anastomotic techniques can be performed: end-to-end, side-to-side, or end-to-side.5

Hand-Sewn Anastomosis (Fig. 23–8)

Figure 23–7 Intracorporeal vascular ligation. Pedicle ligation of the ileocolic and right colic artery is accomplished with the use of a laparoscopic device. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

● Consequence Bleeding (1%–2%). Grade 1–2/5 complication (if at the time of operation); grade 3–5/5 complication (if delayed) ● Repair and Prevention Again, one must know the limitations of each particular method of ligation. The ﬁrst step in proper ligation either laparoscopically or in the open approach begins with the avascular area between the ileocolic and the right branch of the middle colic vessel. This space is incised down to the base of the ileocolic vessels at the level where it crosses the lateral or inferior edge of the duodenum (Fig. 23–7). The peritoneum overlying the ileocolic and right colic vessels is incised, and the vessels are doubly ligated and/or divided with a laparoscopic device. Next, the marginal branches to the ileum are divided, thus preparing the proximal line of resection. The ﬁnal step divides the marginal and the right branch of the middle colic artery.

Anastomosis For the purpose of this chapter, the techniques of anastomosis are the same for both the laparoscopy-assisted and the open approach. Although exposure is certainly different between the two approaches, both are performed extracorporeally.

With this anastomosis, our preference is to ﬁrst make certain that the two ends of bowel are approximated. We use 3-0 stay sutures in the corners of the bowel to aid with approximation. A posterior row of Lembert sutures is placed ﬁrst. These sutures should be placed deep enough to incorporate most of the muscle layer. Next, an inner layer of running 3-0 suture is used to approximate the mucosal and submucosal layers. The corner of the bowel is secured ﬁrst, and the running suture is then advanced along the posterior aspect of the anastomosis. This suture is continued around the opposite corner to complete the anterior mucosal approximation. The suture is then tied to itself at the corner. The occluding bowel clamps are removed from the bowel to allow blood ﬂow to return to the ends of the bowel. The ﬁnal step includes the anterior second layer of 3-0 Lembert sutures approximating the serosal layer, thus, bolstering the anastomotic line.

Stapled Anastomosis (Fig. 23–9) Our standard stapled functional end-to-end anastomosis6 employs two ﬁrings of a disposable linear cutting stapler. On the specimen side of the resection line, a 1-cm transverse incision is made on the antimesenteric borders of the ileum and colon. Placing one of the two sides of the linear cutting stapler into each of the holes in the small bowel ﬁrst and then the colon, the stapler is gently closed, approximating the small bowel and the colon along the antimesenteric border. Ensuring that the mesentery is clear and the stapler is in good position, it is ﬁred and then removed. Upon doing this, the previously separate ileal and colonic enterotomies become joined into a single enterotomy, and a pair of Babcock clamps are used to grasp opposite borders of this enterotomy at the anterior and posterior staple lines. A reloaded, long (75–100-mm) linear cutting stapler is then placed across the ileum and transverse colon, at a right angle to the previous staple line. By retracting the previous enterotomy, the stapler is ﬁred, completing the surgical resection and anastomosis.

23 RIGHT COLECTOMY: OPEN AND LAPAROSCOPIC

263

Figure 23–8 A, Hand-sewn anastomosis. Posterior row of interrupted suture. B, Posterior running layer of suture. C, Anterior running layer of suture. D, Anterior row of interrupted suture. (A–D, By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

Other Complications Wound Infection or Dehiscence Grade 1–2/5 complication Postoperative wound infections have been a chronic problem for all bowel surgery, affecting 2% to 5% of patients undergoing this operation.1–3 The data from the three randomized trials have not found any improvement for those patients who undergo a laparoscopic approach.1–3 Recently, new wound-protecting devices along with continued proper tissue handling and perioperative antibiotic may reduce this risk, but the data on this subject are limited. It is our standard practice to utilize a woundprotecting device on all our laparoscopic cases. Deep Vein Thrombosis Grade 1–2/5 complication Standard treatment with subcutaneous heparin or low-molecular-weight heparin 1 to 2 hours prior to oper-

ation and postoperatively as well as concomitant use of pneumatic compression and compression stockings have proved efﬁcacy in abdominal operations. These treatments are most important for those patients with increased risk factors for venous thrombotic events such as cancer and IBD. Early ambulation will also decrease the risk of this particular morbidity.

CONCLUSION Surgical resection of the right colon is a classic standard operation in the training of all surgeons. Surgical technique and anatomic dissection are the keys to oncologic outcome and postoperative success, regardless of the technique employed. Following these principles will allow continued excellent outcomes.

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Figure 23–9 A, Stapled anastomosis. One-centimeter transverse incisions are made on the antimesenteric borders of the ileum and colon to begin a stapled anastomosis. B, First staple line in the stapled anastomosis. C, Second staple line, which completes the stapled anastomosis. D, Oversewing the staple line with interrupted suture. (A–D, By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

REFERENCES 1. A comparison of laparoscopically assisted and open colectomy for colon cancer. N Engl J Med 2004;350: 2050–2059. 2. Guillou PJ, Quirke P, Thorpe H, et al. Short-term endpoints of conventional versus laparoscopic-assisted surgery in patients with colorectal cancer (MRC CLASICC trial): multicentre, randomised controlled trial. Lancet 2005;365:1718–1726. 3. Veldkamp R, Kuhry E, Hop WCJ, et al. Laparoscopic surgery versus open surgery for colon cancer: short-term

outcomes of a randomised trial. Lancet Oncol 2005;6:477– 484. 4. Berends FJ, Kazemier G, Bonjer HJ, Lange JF. Subcutaneous metastases after laparoscopic colectomy. Lancet 1994; 344:58. 5. Devine R, Pemberton JH. Right and left hemicolectomy. In Donohue J, Van Heerden J, Monson J (eds): Atlas of Surgical Oncology. Cambridge, MA: Blackwell Science, 1995; pp 215–221. 6. Meagher AP, Wolff BG. Right hemicolectomy with a linear cutting stapler. Dis Colon Rectum 1994;37:1043– 1045.

24

Left Colectomy: Open and Laparoscopic Edward C. Lee, MD and Kelly Garrett, MD INTRODUCTION A left colectomy is indicated for pathologic processes involving the distal third of the transverse colon, the descending colon, and the sigmoid colon. In general, this encompasses diseases such as diverticulitis, ischemic colitis, segmental Crohn’s colitis, and neoplasms, both benign and malignant. In resection of malignant diseases, lymphatic drainage and blood supply generally control the extent of dissection. A minimum of 5 cm on either side of the lesion is considered an adequate margin. Bowel margins are also important when resection is undertaken for benign diseases.1 For instance, in the treatment of diverticular disease, the entire distal sigmoid colon should be removed and anastomosed to the rectum. It has been shown that retaining a distal sigmoid cuff may contribute to recurrent diverticulitis.2,3 In comparison, conservative resection margins are recommended in the treatment of inﬂammatory bowel disease. The presence of residual microscopic disease at resection margins has not been shown to reduce recurrence rates. Therefore, resection margins should be determined by gross inspection only.4 As a ﬁnal point, in benign diseases, dissection of the mesentery can be carried out at any level; however, it is most often carried out at the same level as it is for malignant disease for the sake of convenience in ligation of vessels and lymphatics.1 Open left colectomy has traditionally been the operation of choice. Some literature has demonstrated laparoscopic colon resection to be a safe and practical approach for resecting both benign and malignant diseases.5–8 Both surgical procedures generally involve the same concept. In the open procedure, however, dissection starts at the white line of Toldt, whereas laparoscopically, it is often done using a medial to lateral approach. Overall, a steep learning curve, approaching between 30 to 70 cases, is associated with the laparoscopic technique.9 However, laparoscopic colectomies are gradually becoming the standard of care at major institutions. Patients undergoing laparoscopic colectomy have been shown to resume a diet quicker, to need less narcotic analgesia, to have a quicker return of bowel function and a shorter hospital stay.6

This chapter reviews both the open and the laparoscopic procedures, along with their respective complications and outcomes. Although each technique may differ with regard to operative steps, the risks and pitfalls are similar.

INDICATIONS ● Neoplasms involving the distal transverse colon, splenic

ﬂexure, descending colon, and sigmoid colon ● Segmental Crohn’s colitis ● Diverticulitis ● Ischemic colitis

OPERATIVE STEPS Open Procedure Incision of lateral peritoneal reﬂection and mobilization of sigmoid colon Step 2 Identiﬁcation of left iliac artery and ureter Step 3 Mobilization along left pericolic gutter Step 4 Takedown of gastrocolic ligament and enter lesser sac Step 5 Mobilization of splenic ﬂexure Step 6 Division of proximal colon with gastrointestinal anastomosis (GIA) stapler Step 7 Ligation of mesenteric vessels Step 8 Ligation of superior rectal artery Step 9 Division of mesorectum Step 10 Division of rectosigmoid colon with TA stapler Step 11 Anastomosis with end-to-end anastomosis (EEA) stapler or hand-sewing Step 12 Test anastomosis with rigid sigmoidoscope by ﬁlling with air while occluding lumen proximally Step 1

Laparoscopic Procedure Step 1 Step 2

Trocar placement Retract sigmoid colon laterally and score medial peritoneal attachment

266 Step 3 Step 4 Step 5 Step 6 Step 7 Step 8

Step 9 Step 10 Step 11 Step 12 Step 13 Step 14 Step 15

Step 16 Step 17 Step 18

SECTION III: GASTROINTESTINAL SURGERY Identify superior rectal artery and left ureter from medial to lateral Ligate superior rectal artery with GIA stapler (vascular load) Develop plane between rectosigmoid and mesorectum Division of rectosigmoid colon with GIA stapler Division of mesorectum with harmonic scalpel or GIA stapler (vascular load) Takedown of lateral peritoneal attachment proceeding cephalad toward splenic ﬂexure with harmonic scalpel Takedown gastrocolic ligament and enter lesser sac Mobilization of splenic ﬂexure Extraction of left colon through umbilical port after extension of port site incision Division of mesocolon Division of proximal colon extracorporally Pursestring suture and insertion of EEA anvil into proximal colon Partial closure of umbilical incision, reinsertion of trocar, and reestablishment of pneumoperitoneum Insertion of EEA through anus and intracorporeal anastomosis Test anastomosis with rigid sigmoidoscope Removal of trocars

OPERATIVE PROCEDURE Incision of the Lateral Peritoneal Reﬂection and Mobilization of the Sigmoid Colon with Ligation of the Superior Rectal Artery Ureter Injury The left ureter is in close proximity to the rectosigmoid colon in the region where it crosses over the left common iliac artery. Injuries to the ureter most commonly occur while taking down the lateral peritoneal reﬂection at the white line of Toldt and during identiﬁcation and ligation of the superior rectal artery. When the colon is retracted medially, the left ureter may be elevated with the sigmoid mesocolon and mistaken for the superior rectal artery or another mesenteric vessel10 (Fig. 24–1). ● Consequence Iatrogenic injury is most often to the left ureter. Injury can occur in several ways during this step of the procedure. Most common injuries consist of complete transection, excision of an entire segment or portion of the ureteral wall, suture ligation, heat damage from electrocautery, devascularization, or accidental crush with a surgical clamp.10,11 Awareness of these injuries allows for immediate repair. However, 50% to 70% of

Figure 24–1 In medial to lateral dissection, the left ureter is swept lateral to medial to expose the superior rectal artery, as seen here.

the time iatrogenic ureteral injuries go unnoticed until symptoms become apparent postoperatively.10 Grade 2/3 complication ● Repair When injury to the ureter is recognized intraoperatively, urologic consultation should be obtained. The plan for repair is based on the length and location of the injury as well as the patient’s overall condition. One third of iatrogenic injuries will involve the distal ureter. These are primarily repaired with ureteroneocystostomy and stent placement. Vesicopsoas hitch can be done with greater loss of distal ureter length. Although rare during left colectomy, upper and midureteral injuries are generally repaired by ureteroureterostomy over an internal stent. Transureteroureterostomy or a Boari tabularized bladder ﬂap is indicated with more signiﬁcant loss of length. Other options include autotransplantation and ileal transposition; however, these are rarely indicated.10 Injuries identiﬁed during the postoperative course present more of a challenge. Flank pain and fevers are the most common presenting signs and symptoms. Other manifestations include ureterovaginal and ureterocutaneous ﬁstulas. Diagnosis is generally made by cystoscopy, and the level of injury can be conﬁrmed by retrograde pyelogram.12,13 If these injuries present within the immediate postoperative period, operative intervention and repair are warranted. When injury recognition is delayed further, endourologic management with percutaneous nephro-stomy can be carried out prior to deﬁnitive surgical repair. ● Prevention When the sigmoid colon is mobilized, the left ureter should be identiﬁed as it crosses anterior to the common iliac artery (Fig. 24–2). Before ligation of the superior rectal artery and stapling through the rectosigmoid junction, care should be taken to keep the location of

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Figure 24–2 In lateral to medial dissection, the left ureter is swept medial to lateral to make the sigmoid colon into a midline structure. In this dissection, stay as close to the sigmoid colon as possible because all the critical structures—left ureter, left iliac vessels, and left gonadal vessels—need to be exposed laterally.

the ureter in mind (Fig. 24–3A). Sometimes, it is useful to identify the pulsation of the iliac artery and then look for the ureter crossing over5 (see Fig. 24–3B). In the open procedure, the ureter is generally mobilized laterally, whereas it is mobilized medially in the laparoscopic procedure away from the superior rectal artery. Gentle palpation is useful for identiﬁcation; however, the ureter should not be snapped or pulled. More so, extensive skeletonization should not be performed because of the risk of compromising the local blood supply. This can result in ischemic necrosis.11 If there is suspicion of a ureteral injury intraoperatively, 12.5 g of mannitol can be injected intravenously followed by 5 ml of indigo carmine dye or methylene blue. The diagnosis is made if blue dye inﬁltrates the operative ﬁeld.14 Some patients are considered at risk preoperatively secondary to a history of previous pelvic surgery, radiation therapy, or large pelvic masses. In these cases, the anatomy can be deﬁned with a preoperative excretory urogram and placement of ureteral stents prior to incision.11 Stents do not absolutely protect against injury but may help to clearly identify damage if and when it occurs.

Vascular Injury ● Consequence During mobilization of the rectum and sigmoid, injury to the gonadal and iliac vessels can occur. This results in active hemorrhage with or without hypotension. Early recognition of these injuries is important to avoid subsequent morbidity. Grade 1/2 complication ● Repair Ligation of the gonadal vessels in either sex does not usually produce any harmful effects. This is due to the ample collateral circulation to the gonads provided by

Figure 24–3 A, Prior to ligating or stapling the superior rectal artery, once again the left ureter needs to be visualized crossing under the artery and the stapler. B, Another situation in which the left ureter may be injured is when ligating or stapling the mesorectum. The left ureter needs to be identiﬁed coursing laterally medial to the iliac vessels.

the artery to the vas deferens and external spermatic artery in the male and the uterine artery in the female.15 Injuries involving the iliac artery require repair. First and foremost, it is important to gain proximal and distal control. Placing sponge sticks on either side of the lesion can provide hemostasis quickly. Repair of the artery can be done by means of a lateral arteriorrhaphy with 4-0 or 5-0 polypropylene sutures. Injury to the iliac veins should be exposed and controlled in a similar fashion. Repair can be performed by a lateral venorrhaphy, being careful not to cause narrowing of the vein, which can lead to subsequent thrombosis.16 In cases involving injuries to major arteries and veins, consultation with a vascular surgeon is beneﬁcial.17 Comparable injuries sustained during the laparoscopic approach should initiate conversion to a laparotomy.18 Indications for conversion should include blood via Veres needle aspiration, hemodynamic instability, active

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Figure 24–4 Laparoscopically, the right ureter and the right iliac vessels may be at risk because the dissection of the superior rectal artery start from right to left or medial to lateral under the artery. Care needs to be taken to stay close to the superior rectal artery when making the peritoneal incision by the sacral promontory.

Figure 24–5 When mobilizing the splenic ﬂexure, stay close to the colon and away from the spleen. With a gentle downward retraction, the splenocolic ligament, which is relatively avascular, can be released.

intra-abdominal hemorrhage, or an expanding retroperitoneal hematoma.19

Colon resection with concurrent splenectomy is associated with a ﬁvefold increased morbidity rate. The risk of postoperative infectious complications in patients undergoing colorectal cancer surgery is approximately 50% when splenectomy is also performed.23 Therefore, every effort should be made to preserve the spleen. Grade 3/4 complication

● Prevention Similar to prevention of ureteral injuries, adequate visualization and identiﬁcation of anatomic structures and their relationships can preclude vascular injury. This is true for both the open and the laparoscopic approach. In addition, laparoscopic injuries can also be avoided by obtaining pneumoperitoneum using the open (Hasson) technique as opposed to the percutaneous insufﬂation needle (Veres), inserting other trocars under direct vision, elevating the abdominal wall prior to trocar insertion, and training surgeons in laparoscopic techniques adequately.18–20 Moreover, in the medial to lateral approach, the right iliac vessels may be at risk. These injuries can be avoided by dissecting close to the superior rectal vessels while incising the peritoneum along the right sacral promontory (Fig. 24–4).

Mobilization along the Left Pericolic Gutter, Takedown of the Gastrocolic Ligament, and Division of the Proximal Colon Splenic Injury ● Consequence Iatrogenic splenic injury is uncommon, with percentages ranging between 0.8% to 2.4%.21,22 This most commonly occurs owing to inadequate exposure and forceful traction on the colon during mobilization of the splenic ﬂexure. Most injuries result from a capsular tear with avulsion of a small segment of the splenic pulp.14 Splenic salvage is preferred, however; occasionally, splenectomy will need to be performed secondary to uncontrollable bleeding.

● Repair Attempt to control bleeding should begin with packing. Efforts can be made to stop bleeding with several maneuvers, including topical hemostatic agents such as Gelfoam, thrombin, Fibrillar, or Surgicel. Use of an argon beam coagulator has also been employed. If blood loss continues, splenorrhaphy can be performed. This can be accomplished by suture repair with Teﬂon pledgets and buttressing the repair with omentum if necessary. More recently, a technique has been described using topical hemostatic agents combined with a Vicryl mesh wrap.24 ● Prevention Splenic injury is best prevented by avoiding excess traction on the spleen, creating adequate visualization during mobilization, and dissecting close to the colon (Fig. 24–5). In the open technique, pushing in an upward direction with the ﬁngertips instead of pulling caudad can avoid unnecessary pulling on the splenic attachments.22 Another technique that has been suggested entails “early release of the spleen.” This involves mobilizing the spleen in the beginning of the operation and has been shown to reduce the incidence of splenectomy.25 In the laparoscopic approach, the patient is generally in a reverse Trendelenburg position. Rotation of the patient to the right side can help better visualize the splenic

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ﬂexure. Splenic injury seems to be less common in laparoscopic surgery because the visualization is better and forceful retraction is less.

Anastomosis Anastomotic Leak ● Consequence Published leakage rates have been anywhere from 1.7% to 5.1% in some studies.26,27 Anastomotic leaks generally become apparent between postoperative days 4 and 12.28 Leaks may manifest with symptoms of generalized peritonitis, as a localized collection found on fever workup, or as a subclinical leak detected on a contrast study.27 Predictive signs and symptoms include fevers and leukocytosis, slow return of bowel function, diarrhea, increasing drain output, oliguria, and renal failure.28 A leak after colon anastomosis contributes a large amount of morbidity to the postoperative course. It most often requires a drainage procedure or a second operation necessitating creation of a temporary colostomy.27–29 Grade 3–5 complication

Figure 24–6 Hidden anatomy. When the proximal colon needs more mobilization to decrease tension, the left colic artery needs to be ligated close to its takeoff to preserve the collateral vessels. Care needs to be taken not to injure the ligament of Treitz and the tail of the pancreas.

● Repair Clinical suspicion of a leak justiﬁes reexploration in the operating room. If inspection of the anastomosis reveals a defect in the suture or staple line, reinforcing sutures can be placed. Most of the time, however, a proximal diverting ostomy will need to be created.14,28,29 Occasionally, patients can develop a subclinical leak detected on routine contrast enema or on work-up for fevers or leukocytosis. If there are no associated peritoneal signs, these leaks can be treated expectantly or with a percutaneous drainage procedure.14,27 ● Prevention Many local and systemic factors are believed to contribute to an increased rate of anastomotic leak. Maintaining blood supply to the site of anastomosis is important. This ensures the viability of adjacent bowel. If an extended left colectomy needs to be completed, the left colic artery may need to be ligated. This should be done as close as possible to the takeoff from the inferior mesenteric artery (Fig. 24–6). This retains the marginal blood supply and helps to keep the area at risk well vascularized. To conﬁrm intact blood supply, I often use intraoperative Doppler to assess adequate signals by the proximal margin. Most literature supports the fact that an anastomosis performed with either single-layer interrupted sutures or staples will preserve blood supply.1 Another factor shown to contribute to leak is tension on the anastomosis. Normally, the transverse colon should be adequately mobilized in order to be anastomosed to the sigmoid without tension. If the colon does not appear to reach, further mobilization should be performed. After the colon has been divided, the ends must be prepared for anastomosis. One centimeter to 2 cm of each

Figure 24–7 Make sure that not too much of the mesentery is cleared prior to the anastomosis. Vigorous stripping of the mesentery will result in ischemia that can lead to an anastomotic leak. The mesentery should be cleaned sufﬁciently so that the anastomotic site is free of thick, mesenteric fat.

end should be débrided to provide a space sufﬁcient for anastomosis without incorporating any fat1,30 (Fig. 24–7). Too much “clean out” will cause devascularization, which needs to be avoided. A hand-sewn anastomosis is generally performed using 3-0 or 4-0 long-term absorbable sutures. A generous amount of the seromuscular layer is incorporated with a minimal amount of mucosa. This functions to invert the suture line. A single layer is adequate; however, some surgeons may choose to add a second layer of Lembert sutures for reinforcement.14 Typically, interrupted sutures are used; however, use of a running stitch has been shown to be just as effective.31 For stapled anastomosis, an appropriate-sized EEA stapler should be chosen. The largest size should be used whenever possible so as not to create a functional stenosis.14 Once the

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anastomosis is complete, two complete doughnuts should be veriﬁed. Although circular staples are used frequently in colorectal surgery, this method has not been proved to be better than sutured anastamoses.32 Some preventive measures are employed by many surgeons to protect the suture or staple line. Removal of blood and cellular debris from the pelvis to avoid hematoma formation has been recommended.33 However, other methods including prophylactic drainage and omentoplasty have not been shown to reduce the rate of anastomotic dehiscence.34,35 In patients with systemic factors affecting the healing process or in a technically difﬁcult anastomosis, some may choose to perform a temporary diverting ostomy to protect the suture line. This does not reduce the rate of anastomotic leak but can reduce mortality rate.34

Other Complications Bowel Injury Accidental bowel injury is a recognized complication with any intra-abdominal procedure. Most laparoscopyinduced bowel injuries are recognized intraoperatively and can be repaired immediately. However, 10% of injuries are missed and are recognized during the postoperative course. Most missed injuries are secondary to electrocautery and blind trocar insertion. Less frequently, grasping forceps and scissors are the cause. Injuries that are overlooked are associated with a mortality rate of approximately 3.6%.5,36 If injuries are identiﬁed intraoperatively, conversion to lapartotomy is often necessary. Most injuries including serosal damage from electrocautery can be repaired with simple suturing. Less often, bowel resection with reanastomosis and proximal diverting ostomy is required.36 Inadvertent bowel injuries can be prevented in several ways. Similar to the prevention of other injuries, using the Hasson technique to gain access to the abdomen is judicious. Furthermore, it is important to diligently follow movements of the electrocautery and sharp dissecting instruments with the camera in order to avoid damage occurring out of view.36 Conversion to Open Procedure During any laparoscopic procedure, conversion to the open approach is an accepted risk. A reasonable conversion rate is approximately 10% to 20%.5,7,9 However, this varies with experience of the operating surgeon. Conversion to an open procedure should be performed if there is difﬁculty with technical aspects of the procedure including adequate exposure, mobilization of the bowel, and identiﬁcation of the ureters.6 In addition, if there are anatomic issues that preclude safe dissection such as metastatic tumor or excessive adhesions, laparotomy should be considered. Finally, as discussed previously, inadvertent injury to the ureter, bowel, or vessels supports modifying the procedure to the open approach.5,37

REFERENCES 1. Condon RE. Resection of the colon. In Zuidema GD (ed): Shackelford’s Surgery of the Alimentary Tract. Philadelphia: WB Saunders, 1996; pp 207–224. 2. Benn PL, Wolff BG, Ilstrup DM. Level of anastomosis and recurrent colonic diverticulitis. Am J Surg 1986;151: 269–271. 3. Thaler K, Baig MK, Berho M, et al. Determinants of recurrence after sigmoid resection for uncomplicated diverticulitis. Dis Colon Rectum 2003;46: 385–388. 4. Fazio VW, Marchetti F, Church M, et al. Effect of resection margins on the recurrence of Crohn’s disease in the small bowel. A randomized controlled trial. Ann Surg 1996;224:563–571; discussion 571–573. 5. Regadas FS, Rodrigues LV, Nicodemo AM, et al. Complications in laparoscopic colorectal resection: main types and prevention. Surg Laparosc Endosc 1998;8:189– 192. 6. Hong D, Lewis M, Tabet J, Anvari M. Prospective comparison of laparoscopic versus open resection for benign colorectal disease. Surg Laparosc Endosc Percutan Tech 2002;12:238–342. 7. Clinical Outcomes of Surgical Study Group. A comparison of laparoscopically assisted and open colectomy for colon cancer. N Engl J Med 2004;350:2050–2059. 8. Patankar SK, Larach SW, Ferrara A, et al. Prospective comparison of laparoscopic vs. open resections for colorectal adenocarcinoma over a ten-year period. Dis Colon Rectum 2003;46:601–611. 9. Tekkis PP, Senagore AJ, Delaney CP, Fazio VW. Evaluation of the learning curve in laparoscopic colorectal surgery: comparison of right-sided and left-sided resections. Ann Surg 2005;242:83–91. 10. Elliott SP, McAninch JW. Ureteral injuries: external and iatrogenic. Urol Clin North Am 2006;33:55–66, vi. 11. Fry DE, Milholen L, Harbrecht PJ. Iatrogenic ureteral injury. Options in management. Arch Surg 1983;118: 454–457. 12. Dowling RA, Corriere JN Jr, Sandler CM. Iatrogenic ureteral injury. J Urol 1986;135:912–915. 13. Lask D, Abarbanel J, Luttwak Z, et al. Changing trends in the management of iatrogenic ureteral injuries. J Urol 1995;154:1693–1695. 14. Corman ML (ed). Carcinoma of the colon. In Colon and Rectal Surgery. Philadelphia: Lippincott Williams & Wilkins, 2005; pp 804–856. 15. Walsh PC, Wein AJ, Kavoussi LR, et al. Surgical anatomy of the retroperitoneum, kidneys, and ureters. In Kabalin J (ed): Campbell’s Urology, 8th ed. Philadelphia: Saunders, 2002; p 7. 16. Bongard F. Thoracic and abdominal vascular trauma. In Vascular Surgery. Philadelphia: WB Saunders, 2005; pp 886–887. 17. Barbosa Barros M, Lozano FS, Queral L. Vascular injuries during gynecological laparoscopy—the vascular surgeon’s advice. Sao Paulo Med J 2005;123:38–41. 18. Guloglu R, Dilege S, Aksoy M, et al. Major retroperitoneal vascular injuries during laparoscopic cholecystectomy and appendectomy. J Laparoendosc Adv Surg Tech A 2004;14:73–76.

24 LEFT COLECTOMY: OPEN AND LAPAROSCOPIC 19. Usal H, Sayad P, Hayek N, et al. Major vascular injuries during laparoscopic cholecystectomy. An institutional review of experience with 2589 procedures and literature review. Surg Endosc 1998;12:960–962. 20. Dixon M, Carrillo EH. Iliac vascular injuries during elective laparoscopic surgery. Surg Endosc 1999;13:1230– 1233. 21. Ignjatovic D, Djuric B, Zivanovic V. Is splenic lobe/ segment dearterialization feasible for inferior pole trauma during left hemicolectomy? Tech Coloproctol 2001;5:23– 25. 22. Langevin JM, Rothenberger DA, Goldberg SM. Accidental splenic injury during surgical treatment of the colon and rectum. Surg Gynecol Obstet 1984;159: 139–144. 23. Varty PP, Linehan IP, Boulos PB. Does concurrent splenectomy at colorectal cancer resection inﬂuence survival? Dis Colon Rectum 1993;36:602–606. 24. Bochicchio GV, Arciero C, Scalea TM. “The hemostat wrap”: a new technique in splenorraphy. J Trauma 2005; 59:1003–1006. 25. Killingback M, Barron P, Dent O. Elective resection and anastomosis for colorectal cancer: a prospective audit of mortality and morbidity 1976–1998. Aust N Z J Surg 2002;72:689–698. 26. Pickleman J, Watson W, Cunningham J, et al. The failed gastrointestinal anastomosis: an inevitable catastrophe? J Am Coll Surg 1999;188:473–482. 27. Walker KG, Bell SW, Rickard MJ, et al. Anastomotic leakage is predictive of diminished survival after potentially curative resection for colorectal cancer. Ann Surg 2004; 240:255–259. 28. Alves A, Panis Y, Pocard M, et al. Management of anastomotic leakage after nondiverted large bowel resection. J Am Coll Surg 1999;189:554–559.

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29. Makela JT, Kiviniemi H, Laitinen S. Risk factors for anastomotic leakage after left-sided colorectal resection with rectal anastomosis. Dis Colon Rectum 2003;46:653– 660. 30. Scott-Conner CE. Right and left colon resections. In Scott-Connor CE, Dawson DL (eds): Operative Anatomy. Philadelphia: Lippincott Williams & Wilkins, 2003; pp 478–482. 31. Burch JM, Franciose RJ, Moore EE, et al. Single-layer continuous versus two-layer interrupted intestinal anastomosis: a prospective randomized trial. Ann Surg 2000; 231:832–837. 32. Fingerhut A, Hay JM, Elhadad A, et al. Supraperitoneal colorectal anastomosis: hand-sewn versus circular staples— a controlled clinical trial. French Associations for Surgical Research. Surgery 1995;118:479–485. 33. Hirsch CJ, Gingold BS, Wallack MK. Avoidance of anastomotic complications in low anterior resection of the rectum. Dis Colon Rectum 1997;40:42–46. 34. Merad F, Hay JM, Fingerhut A, et al. Omentoplasty in the prevention of anastomotic leakage after colonic or rectal resection: a prospective randomized study in 712 patients. French Associations for Surgical Research. Ann Surg 1998;227:179–186. 35. Merad F, Yahchouchi E, Hay JM, et al. Prophylactic abdominal drainage after elective colonic resection and suprapromontory anastomosis: a multicenter study controlled by randomization. French Associations for Surgical Research. Arch Surg 1998;133:309–314. 36. van der Voort M, Heijnsdijk EA, Gouma DJ. Bowel injury as a complication of laparoscopy. Br J Surg 2004;91: 1253–1258. 37. Chen C-C YH, Sato M, Nakajima K, et al. Long-term outcome of laparoscopic surgery for colorectal cancers. Dig Endosc 2005;17:191–197.

25

Low Anterior Resection Charles M. Friel, MD INTRODUCTION Surgical resection of all or part of the rectum with a primary anastomosis is referred to as a low anterior resection. This procedure is most commonly performed for rectal cancer. However, on occasion, the rectum is removed for a variety of other benign and malignant conditions. When done for mid and low rectal cancers, the operation includes a total mesorectal excision1,2 with an anastomosis at the level of the pelvic ﬂoor. For upper rectal cancers, a partial mesorectal excision with a 5-cm distal and mesorectal margin is probably adequate.3 In this circumstance, the anastomosis is usually done in the midrectum. When done for cancer, obtaining a negative circumferential margin is critical to decrease the likelihood of local recurrence.4,5 Therefore, the dissection must stay outside the fascia propria and closer to the pelvic sidewall. This may increase the likelihood of complications, including bleeding and autonomic nerve injury. For benign disease, there is no circumferential margin, so violation of the fascia propria has no signiﬁcant implications. Therefore, in benign disease, it is probably better to veer the dissection closer to the rectum to decrease the probability of these other complications. For the purpose of this discussion, it is assumed that the indication for surgery is cancer and the technical points will stress adequate oncologic technique. These principles are generally applicable to benign conditions as well. However, on occasion, there are differences in patients with benign disease, and this is noted in the text.

● Severe pelvic infection/inﬂammation causing stricture

(e.g., radiation injury, pelvic inﬂammatory disease, rectal perforation, previous anastomotic leak) ● Severe endometriosis ● Upper rectal vaginal ﬁstulas ● Other malignancies (e.g., ovarian cancer, retrorectal tumors, rectal sarcomas)

OPERATIVE STEPS Step Step Step Step Step Step

1 2 3 4 5 6

Positioning and incision Mobilization of sigmoid and left colon Takedown of splenic ﬂexure Ligation of vasculature Rectal mobilization Anastomosis

OPERATIVE PROCEDURE Patient Positioning Patients are placed in a modiﬁed lithotomy position to perform a low anterior resection. This allows access to the perineum for a stapled anastomosis. The patient’s arms are usually extended to allow access for the anesthesiologist. In addition, a self-retaining retractor is quite helpful for exposure. Proper positioning of the patient and the retractor is critical to prevent iatrogenic nerve injuries.

Peripheral Nerve Injuries

INDICATIONS This is a partial list of surgical indications for a low anterior resection. These procedures involve rectal resection and a primary colorectal anastomosis. The most common indication is ● Upper, mid, and low rectal cancer

Other indications include ● Large polyp not amenable to other techniques (e.g.,

endoscopy, transanal, transmission electron microscopy [TEM])

● Consequence Clearly, the consequences of this complication depend on the severity of the injury. Most peripheral nerve injuries occur from prolonged compression or stretch. Often, this is just neuropraxis and will resolve completely with time. Less commonly, permanent injury can result that will leave a permanent disability. Grade 1 complication (if resolves); grade 4 (if permanent) ● Repair Generally, there is no operative repair for patients with peripheral nerve injury from compression or stretch.

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Figure 25–1 Self-retaining retractor. To prevent femoral nerve injury, great care must be used when placing retractor blades (marked with an X) in the inguinal region.

Treatment is just supportive, which would include physical and occupational therapy. ● Prevention Careful patient positioning is key to prevent injuries.6 Well-padded stirrups are necessary. The patient’s heel should be placed ﬁrmly in the foot of the stirrup so that the weight of the leg is supported by the patient’s heel. It is also helpful to tilt the stirrup posteriorly to prevent pressure from being applied to the posterior and lateral aspects of the lower extremity, which will aid in preventing common peroneal nerve injury. This area can be further padded if necessary. To prevent brachial plexus injuries, the patient’s arms should rest easily and should not be extended more than 90°.6 Furthermore, nothing should be placed between the shoulder blades that can stretch the brachial plexus by elevating the chest. The anesthesiologist and operating staff should also monitor the position of the arms because they may shift during the procedure, particularly if the patient is placed in Trendelenburg position to gain additional exposure. Finally, to prevent femoral injuries, great care must be taken when utilizing a self-retaining retractor.7 Retractors over the inguinal region should be used with caution, especially in thin patients (Fig. 25–1). However, if necessary, use the most superﬁcial retractor available (e.g., the bladder blade) (Fig. 25–2) because deeper retractors are more likely to compress the femoral nerve, which runs just beneath the psoas muscle. If the operation is prolonged, periodically release and replace the retractors to limit the potential for prolonged compression to an isolated spot. If a perineal approach is necessary at any time, take care to remove the abdominal wall retractors as well. This injury is more common with a transverse incision, which is being utilized more frequently as surgeons adopt a laparoscopy-assisted approach to rectal surgery.

Figure 25–2 Examples of self-retaining retractors. Arrow identiﬁes the retractor with the least depth and, therefore, the least likely to damage the femoral nerve.

Incision Most low anterior resections can be accomplished through a midline incision. Exposure is critical to safely complete all portions of the procedure. To properly expose the pelvis, the incision frequently needs to go all the way to the pubis. This will allow the best visualization of the deep pelvic structures. For most low anterior resections, complete mobilization of the splenic ﬂexure is also necessary. Therefore, the upper extent of the incision is often well above the umbilicus. In patients who are thin or have a low splenic ﬂexure, the incision may need to extend only to the umbilical region. It is best to start with a lower midline incision and then extend as necessary to gain the required exposure.

Bladder Injury Although rare, iatrogenic injuries to intra-abdominal structures can occur while the abdomen is being opened. Clearly, these injuries are more likely to occur in patients who have had previous abdominal surgery. However, when doing a low anterior resection, special consideration should be given to the lower portion of the incision. While extending to the pubis, an injury to the dome of the bladder is possible and care must be taken to avoid this problem. ● Consequence Fortunately, an injury to the bladder while making an incision is usually in the bladder dome. This is generally readily apparent and can be promptly ﬁxed. When this is done, there are few long-term consequences, except for prolonged catheterization. An unrecognized injury will lead to an intra-abdominal urine leak and can result in sepsis. Repair is also greatly complicated and will require long-term bladder drainage.

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275

Bleeding

Figure 25–3 Opening incision. To avoid bladder injury, incise the anterior fascia all the way to the pubis, staying anterior to the underlying muscle.

Grade 2 complication (if recognized); grade 3 complication (if not recognized) ● Repair The bladder dome is easily repaired and generally forgiving. Closure of the defect is generally done in two layers with an absorbable suture. Permanent suture is avoided to prevent future calculi and granulomas. To keep the bladder decompressed, a Foley catheter is generally kept for approximately 7 to 10 days.8 ● Prevention When opening the abdomen, it is important to get all the way to the pubis for proper pelvic exposure. However, most of the beneﬁt is from incising the anterior fascia. The bladder will lie beneath the pyramidalis and rectus muscles. Therefore, if the dissection is always above these muscles, the bladder cannot be injured (Fig. 25–3). Division of the posterior peritoneum is not always necessary in this region because it is easily retracted with a self-retaining retractor. If division of this peritoneum is necessary, it can be done carefully layer by layer to identify the bladder dome. Furthermore, the dissection of the peritoneum can veer a bit off midline, which will help avoid the bladder dome.

Colon Mobilization and Ligation of the Mesenteric Vessels In order to perform a low anterior resection of the rectum, the sigmoid colon must be fully mobilized. Furthermore, in most instances, complete mobilization of the descending colon and splenic ﬂexure is also required to perform a tension-free anastomosis (see later). Most mishaps that can occur during this portion of the procedure are similar for any left-sided colonic operation and are well described in Chapter 24 (Left Colectomy: Open and Laparoscopic). These complications are brieﬂy reviewed here.

● Consequence If the proper planes are found and dissected properly, bleeding from colonic mobilization should not be signiﬁcant. When bleeding is encountered, the surgeon should question whether he or she is in the proper plane and adjust accordingly. Most bleeding is easily controlled without any signiﬁcant sequelae. Some evidence suggests that patients who get a blood transfusion are more likely to have a cancer recurrence and/or an infectious complication of surgery.9–11 Whether this is due to the immunosuppression of the transfusion or is just a marker for a difﬁcult case has not been determined.12,13 Nevertheless, to prevent the unnecessary risk of a blood transfusion, bleeding should be kept to a minimum whenever possible. Grade 1 complication ● Repair Identiﬁcation and ligation are all that is necessary for proper control of bleeding. If necessary, the gonadal vessels can be ligated once the ureter is clearly identiﬁed. Bleeding from the major vascular structures, such as the aorta or iliac vessels, is unusual but can be directly repaired after proper proximal and distal control. ● Prevention Proper identiﬁcation of the avascular planes is necessary to prevent unnecessary bleeding. The descending colon and its mesentery lie just anterior to the retroperitoneum and its associated structures. An areolar plane exists between the mesocolon and the retroperitoneum and, when dissected, allows the colon and the mesocolon to be fully mobilized to the midline position. The dissection is begun by dividing the lateral peritoneum of the sigmoid and descending colon. Rapid identiﬁcation of the gonadal vessels can be quite helpful because these vessels are the most anterior of the retroperitoneal structures and should be swept posteriorly off the colonic mesentery (Fig. 25–4). Care must be taken to stay above the gonadal vessels because they are quite fragile and will bleed with too much manipulation. However, when this plane is properly identiﬁed, there should be little bleeding; if this plane is followed, the colon and the mesocolon should be lifted off the left kidney to prevent inadvertent kidney mobilization. As the gonadal vessels are swept posteriorly, the mesocolon and, speciﬁcally, the inferior mesenteric vessels are elevated to a midline position. The ureter, which passes beneath the gonadal vessels, can be identiﬁed as it crosses the iliac vessels. Once the gonadal vessels and kidney have been swept posteriorly, the peritoneum on the right-hand side should be divided just at the sacral promontory and underneath the superior rectal artery. This will allow entrance into the retrorectal space, which is also avascular. This dissection should meet the

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Figure 25–4 Dissection of the gonadal vessels off the mesentery of the colon. This plane is avascular and will guide the surgeon to the plane separating the colon and its mesentery from the retroperitoneum.

previous dissection on the left-hand side and create a window under the superior rectal artery (Fig. 25–5). The superior rectal artery can then be further dissected on the right-hand side all the way to the aorta, where it is now the inferior mesenteric artery (IMA). If the dissection on the left-hand side was done properly, the gonadal vessels and ureter should be easily visualized from the right-hand side underneath the IMA. An avascular window can now be identiﬁed through the mesocolon on the left-hand side of the IMA. The inferior mesenteric vein (IMV) is just to the left of the IMA and can be dissected out separately. Care should be taken to identify the duodenum, which should be located just superior to the IMA (Fig. 25–6). Once these vessels are properly identiﬁed, they can be divided and doubly ligated (Fig. 25–7). It is advisable to leave a stump for the IMA in case vascular control is lost. Reclamping and ligating the base of the IMA is considerably easier than repairing a defect in the aorta.

A

B

Figure 25–5 Mesentery of rectosigmoid colon from the right-hand side. A, Line shows the approximate course of the superior rectal artery. Shaded area represents avascular window posterior to the superior rectal artery at the level of sacral promontory. B, Avascular window is opened, posterior to the superior rectal pedicle.

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Figure 25–6 Position of the duodenum in relation to the pedicle of the inferior mesenteric vessels. Yellow shows the approximate location of the inferior mesenteric artery (IMA). Note that the peritoneum to the left of the IMA has been incised and the IMA is being lifted off the aorta by the left dissecting hand.

Great care with the IMV is also critical because this vessel is prone to retract underneath the pancreas, which will make vascular control quite difﬁcult once it is lost. This describes a high ligation of the IMA and IMV. From an oncologic perspective, this may not be necessary,14 and division of the IMA and IMV can be done together with a single clamp just distal to the takeoff of the left colic artery. However, for a very low anastomosis, division of these vessels is often required to provide the necessary colonic length to do a safe, tension-free anastomosis (see the section on “Anastomosis”). A

B Figure 25–7 Inferior mesenteric vessels are identiﬁed and clamped (A) and then ligated (B). Forceps point to the ureter and the retroperitoneum, which have been swept posteriorly (A). Note the proximity of the ureter to the inferior mesenteric vessels at the point of ligation (B).

Ureteral Injury An intra-abdominal injury to the ureter is possible when the sigmoid and descending colon is mobilized. This is fully described elsewhere in the text so it is only reviewed here. Clearly, proper identiﬁcation of the ureter is essential to preventing injuries. The ureter is usually identiﬁed as it crosses the iliac vessels but must be followed superiorly and swept posteriorly to prevent injury when ligating the IMA and IMV. It is important to remember that the ureter lies beneath the gonadal vessels, so if the dissection is above the gonadal vessels, the ureter should also be posterior and out of harm’s way. Sometimes, the ureter is difﬁcult to clearly identify and is most often confused with the gonadal vessels. Under these circumstances, it is important to remember several principles. The ureter runs longitudinally through the retroperitoneum. It never branches, as do blood vessels, and when manipulated, it should show evidence of peristalsis (Fig. 25–8). If the ureter cannot be identiﬁed secondary to inﬂammation or tumor, the ureter should be identiﬁed higher in the abdomen, where the anatomy may be more normal, and followed distally. If it is anticipated that ureteral identiﬁca-

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Figure 25–8 Retroperitoneum after dissection and removal of the rectum and associated lymphatics. Note the direction of the ureter, which is parallel to the aorta, compared with the gonadal vessels, which veer laterally. Also note that the ureter passes beneath the gonadal vessels.

tion will be difﬁcult, placing ureteral stents preoperatively can be quite helpful. Grade 2 complication

Splenic Injury When the splenic ﬂexure is mobilized, the spleen can be injured and cause troublesome bleeding.15 This complication is possible with any intra-abdominal colon operation and is reviewed in detail elsewhere. Most splenic injuries originate from omental attachments to the splenic capsule. With downward retraction on the colon, these attachments are torn off the splenic capsule, causing bleeding from the injured spleen. Fortunately, these attachments are unusual, but when identiﬁed, they need to be carefully divided (Fig. 25–9). If the splenic ﬂexure is torn, troublesome bleeding will ensue. Most of the time, this bleeding is well controlled with simple packing, but on occasion, bleeding will persist. Although other maneuvers to control bleeding are available, the surgeon should not hesitate to perform a splenectomy if the bleeding is not well controlled. Grade 1/2 complication

A

Rectal Mobilization An understanding of rectal anatomy is critical to proper rectal mobilization. The rectum is surrounded by a large amount of fat containing the mesentery and lymphatics to the rectum itself. This tissue is enveloped by a thin layer of fascia, known as the fascia propria. An avascular plane exists between the fascia propria and the presacral fascia, which is adherent to the periosteum of the sacrum. The retrorectal fascia, or Waldeyer’s fascia, is a thick layer of fascia connecting the presacral fascia to the fascia propria of the rectum. Division of this fascia is necessary to mobilize the distal rectum, and when divided, the rectum will lift from the sacral hollow and begin a more anterior

B Figure 25–9 Omental attachments to the spleen (A), which needs to be divided (B) to prevent injury to the spleen with downward retraction of the colon.

25 LOW ANTERIOR RESECTION approach. This greatly lengthens the rectum, especially posteriorly. For this reason, a low-lying posterior tumor may elevate signiﬁcantly after division of the retrorectal fascia, allowing for a low anterior resection. Anteriorly, the rectum is more ﬁxed and will not lengthen as much with mobilization. Therefore, a low-lying anterior tumor will more likely require an abdominal perineal resection than would a posterior-based tumor at the same preoperative level. Rectal mobilization begins by entering the retrorectal space at the level of the sacral promontory (see Fig. 25–5). Division of the peritoneum at this level will identify the avascular plane between the mesorectum and the presacral fascia. The peritoneum lateral to the rectum is then incised toward the anterior cul-de-sac bilaterally. Finally, the anterior peritoneum also needs to be divided, which will allow entrance into the proper plane to mobilize the vagina in a woman, or the seminal vesicles and prostate in a man. Once the peritoneum is completely incised, the rectum is further mobilized by dividing the areolar tissue that exists between the fascia propria of the rectum and the fascia of the pelvic sidewall, collectively referred to as the endopelvic fascia. This dissection is greatly facilitated by proper deep pelvic retractors and anterior retraction of the rectum (Fig. 25–10). This dissection should be continued posteriorly and in the midline as deep as possible (Fig. 25–11). This will help identify the proper lateral plane, which should continue just adjacent to the mesorectum. Finally, the anterior plane needs to be developed, separating either the vagina or the prostate from the rectum (Figs. 25–12 and 25–13). This is greatly facilitated by using a lipped pelvic retractor and anterior traction on the vagina or prostate while using the hand for posterior traction of the rectum. Whereas this description implies that the posterior, lateral, and anterior dissections are done sequentially, in reality the surgeon needs to constantly adjust her or his retractors to dissect the area that is currently best exposed and continue this dissection circumferentially all the way to the pelvic ﬂoor. When this is done properly, there should be no mesorectum at the pelvic ﬂoor, thus com-

Figure 25–10 Deep pelvic retractors.

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pleting a total mesorectal excision. Therefore, all that should be left is the rectum itself as it enters the rectal ampulla between the muscles of the pelvic ﬂoor. Division of the rectum at this level can almost always be done with one ﬁre of a 30-mm transverse stapling device. Figure 25–14 shows the ﬁnal appearance of the sacral hollow after complete removal of the rectum and the associated mesorectum.

Hemorrhage Although uncommon, massive and life-threatening bleeding can be encountered with rectal mobilization. This is most commonly from the presacral plexus and can occur when the presacral fascia is injured. Bleeding is venous in nature and can be quite profuse. The bleeding source is from either the veins just below the presacral fascia or the basivertebral veins, which are within the sacrum itself. The basivertebral veins, when injured, will retract within the sacral foramen and can be extremely difﬁcult to control. Other sources of major pelvic bleeding include the vessels of the pelvic sidewall, the most signiﬁcant being the internal iliac artery and vein. ● Consequence Signiﬁcant and even life-threatening bleeding can occur from either the presacral plexus or the internal iliac vessels. In general, signiﬁcant venous bleeding is more difﬁcult to control, due partly to the poor exposure of these venous structures and to the nature of their thin walls, which can tear easily and cause more excessive bleeding. Clearly, massive blood loss can be immediately life-threatening. But even if controlled, this complication can lead to continued postoperative problems, including multisystem organ failure and delayed death. Grade 2 complication (if quickly controlled); grade 4 complication (if not controlled quickly) ● Repair When profuse bleeding is initially encountered, direct pressure is most appropriate. Because venous bleeding is low, this pressure will quickly control the signiﬁcant blood loss. Prolonged pressure may in fact stop the bleeding but will at least allow the anesthesiologist time to get proper access and blood products available. To the surgeon, the bleeding may only seem “brisk,” but it is important to remember that blood loss of 100 ml/ min will result in a 1-L blood loss in only 10 minutes and can quickly lead to patient instability. If the bleeding appears to be coming from the presacral veins, no attempt should be made to dissect this further, because this generally results in more signiﬁcant bleeding. Suture ligation can be quite tempting but often further disrupts the presacral fascia, potentially exposing the sacral foramina and the basivertebral veins, resulting in worsening bleeding.16 Direct pressure and utilization of any variety of hemostatic products can be used

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Ureter

A

B

Figure 25–11 Posterior dissection. A, Pelvic retractor provides anterior retraction on the rectum. Yellow line shows the approximate plane of dissection, dissecting the mesorectum from the sacral hollow using either sharp dissection or electrocautery. B, Retrorectal (Waldeyer’s) fascia in the deep posterior midline. Rectum is anteriorly retracted and not visible. Yellow line shows the approximate plan of dissection, which is done sharply or with electrocautery to minimize bleeding.

Figure 25–12 Anterior dissection in a male. Pelvic retractor provides anterior retraction on the seminal vesicles and prostate while the hand is pushing the rectum posteriorly, exposing the anterior cul-de-sac. Straight arrow shows the point of dissection. Denonvilliers’ fascia is the white tissue just posterior to the line of dissection, denoted by curved arrow.

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A Figure 25–14 Sacral hollow after completion of low anterior resection and simultaneous hysterectomy and oopherectomy, shows complete removal of the sigmoid and rectal mesentery, the position of the left ureter and preservation of the hypogastric nerves.

B Figure 25–13 Anterior dissection in a woman with a previous hysterectomy. A, Lateral peritoneum has already been incised. Entrance to the rectovaginal septum is obtained by dividing the peritoneum anteriorly, along the dotted line. B, Demonstration of the rectal stump, after the rectum has been removed, shows the posterior vaginal wall. The rest of the vagina is being retracted anteriorly.

effectively.16,17 If this is not successful, sterile titanium thumbtacks can be used to directly compress the bleeding vein16,18 (Fig. 25–15). As a last resort, the pelvis can be packed and the patient taken to the intensive care unit for 24 to 48 hours. The patient is then taken back to the operating room and the packs removed. By that time, the bleeding has usually stopped and the operation can be completed. Bleeding from the internal iliac vessels is also uncommon. It is most likely encountered with a large tumor adherent to the vessels or with signiﬁcant pelvic scarring from previous infection or radiation. For venous bleeding, proximal and distal control is best accomplished with sponge sticks and direct pressure.19 The vein lies behind the artery, so exposure can be difﬁcult. The vein can be repaired directly if the injury is small and easily visualized. If necessary, both the internal iliac artery and vein can be ligated without signiﬁcant sequelae. In these difﬁcult situations, an experienced vascular surgeon can be quite helpful.19 ● Prevention Presacral bleeding usually occurs if the presacral fascia is disrupted. This is best avoided by using sharp dissection in the retrorectal space. Blunt dissection should be discouraged. This is particularly true when dividing the retrorectal fascia (Waldeyer’s fascia), which is often very

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tough tissue and is adherent to the presacral fascia (see Fig. 25–11B). Attempts to bluntly dissect through this tissue are more likely to disrupt the presacral fascia and lead to bleeding. To prevent bleeding from the pelvic sidewall, including the internal iliac vessels, careful dissection should be done just adjacent to the fascia propria of the rectum. Whereas for oncologic reasons, it is important to keep the fascia propria intact, if the dissection is done too laterally, troublesome bleeding can be encountered. Occasionally, the dissection must be done more laterally to get circumferential tumor clearance. Under these circumstances, the surgeon should clearly identify the iliac vessels, including the bifurcation of the internal and external iliac vessels, well above the tumor and be prepared to intervene if bleeding from these vessels ensues. A

B

Sexual and Bladder Dysfunction Both sympathetic and parasympathetic nerves can be damaged with rectal surgery. The sympathetic ﬁbers begin in the aortic plexus near the IMA. These ﬁbers coalesce to form two main hypogastric nerves, which are readily identiﬁable at the level of the sacral promontory (Fig. 25–16; see also Fig. 25–14). These nerves carry sympathetic innervation to the pelvic plexus. Parasympathetic innervation is supplied by the nervi ergentes, which pass through the sacral foramen and run laterally and then forward to also join the pelvic plexus. The pelvic nerves tend to be lateral, near the pelvic sidewall, but will course anteriorly as they approach the prostate and seminal vesicles, forming the periprostatic plexus. Although the two main hypogastric nerves can be readily seen during surgery, most nerve ﬁbers are not identiﬁable and knowledge of their location is necessary to minimize nerve injury.

Figure 25–15 A, Sterile thumbtacks and applicator. B, Close up of sterile thumbtacks.

Figure 25–16 Position of hypogastric nerves. Forceps point to the trunks of the hypogastric nerves.

25 LOW ANTERIOR RESECTION ● Consequence Injury to the sympathetic and parasympathetic nerves can cause both bladder and sexual dysfunction. Whereas the incidences of bladder and sexual dysfunction are reportedly similar, to most clinicians, sexual dysfunction seems more common and problematic. This is probably related to the observation that minor changes in bladder dysfunction may not be as readily apparent as sexual dysfunction to the clinician. Sexual dysfunction in men can be either the inability to have an erection or the failure to ejaculate ﬂuid despite achieving orgasm and are related to different types of neural injuries.20 Woman may experience dyspareunia after rectal surgery. Bladder dysfunction can present as urgency, dribbling, leaking, or the inability to completely void.20 All of these problems are considerably more common as patients get older and are probably related to both aging and the use of concomitant radiation commonly employed for the treatment of rectal cancer.20,21 It is important to discuss these issues with patients prior to surgery and to get a good understanding of their preoperative sexual and urologic function, because sexual and urologic dysfunction is quite common, especially as people get older.21 Grade 2/4 complication ● Repair No surgical repair exists for nerve injuries during rectal surgery. Some problems with bladder and sexual dysfunction will improve with time.22 The treatment is symptomatic. Continued bladder dysfunction will require either prolonged catheterization or a selfcatheterization program. For patients with persistent sexual dysfunction, both medical and surgical options exist to improve potency, and a urologic consultation is warranted. ● Prevention Precise dissection is the best way to prevent nerve injuries.20,22 When the IMA is ligated, care should be taken to stay right underneath the vessel because the nerves tend to course over the aorta. The hypogastric nerves can usually be seen right at the sacral promontory and begin to sweep laterally. Gaining access to the retrorectal space right in the midline is less likely to damage these nerves. Dissection should be right on the fascia propria, which will ensure that the dissection is anterior to these nerves. Frequently, the hypogastric trunks will be adherent to the fascia propria, and they need to be carefully dissected off and swept laterally. To further minimize injury to the pelvic nerves, care should be taken to stay just adjacent to the fascia propria of the rectum because the nerves tend to be closer to the pelvic sidewall. This is true for the entire rectal dissection, but it is most important during the anterior lateral dissection near the seminal vesicles. Precise dissection is critical to best preserve nerve function while doing an oncologically appropriate operation. Clearly, for

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benign disease, it is best to veer closer to the rectum to help further decrease the likelihood of permanent nerve injury.

Anastomosis Anastomotic Leak Anastomotic leak is the dreaded complication associated with colon and rectal surgery and is the most common cause of death after an elective colon or rectal resection. For rectal surgery, the incidence can vary from approximately 3% to 10%, depending on the level of the anastomosis. Very low pelvic anastomoses will leak more frequently than those performed to the midrectum.3,23 Other factors contributing to a higher leak rate include pelvic radiation, male gender, and prolonged surgery,23 which is most likely a surrogate for a difﬁcult operation. The clinical presentation of an anastomotic leak can be quite varied. Whereas some leaks will present as frank peritonitis, others can be more subtle, such as a pelvic abscess. The diagnosis must be suspected in any patient who has a new rectal anastomosis and has a cardiopulmonary collapse of an unclear etiology. Failure to promptly make this diagnosis will contribute to ongoing sepsis and will likely lead to a poor outcome. ● Consequence The clinical consequences of an anastomotic leak depend on the severity of the leak itself. For small leaks resulting in a pelvic abscess, a percutaneous drain may be all that is necessary, with little long-term signiﬁcance. However, a leak associated with fecal peritonitis is clearly life-threatening. It generally will require a reoperation and the creation of a diverting stoma. Intensive care monitoring is often required to deal with the septic sequelae of the leak. Once a patient does recover, restoration of intestinal continuity may be compromised. Some patients will have a permanent stoma, whereas others will be reversed but ﬁbrosis will result in an anastomotic stricture or poor function. In addition to these complications, data also suggest that local/regional cancer recurrence rates are higher in patients who have had an anastomotic leak.24,25 Grade 2/4/5 complication ● Repair If a patient has a well-contained leak without evidence of systemic illness, percutaneous drainage is appropriate and often successful. For patients who do not improve with catheter drainage or those who are systemically ill at presentation, operative management is warranted. Reexploration after an anastomotic leak can be very challenging, because the adhesions can be quite difﬁcult, especially near the leaking anastomosis. If the anastomosis can be readily identiﬁed and there is a large dehiscence, resecting the anastomosis and creating an end colostomy are appropriate. However, the anastomosis frequently cannot be easily seen. Under these

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Figure 25–17 Fully mobilized descending colon, which will easily reach low in the pelvis. Yellow line shows the approximate location of the marginal artery, which must be carefully preserved to provide adequate blood supply to the mobilized colon.

circumstances, extensive dissection can be troublesome and should be avoided. Pelvic drainage and proximal diversion, with either a loop colostomy or an ileostomy, can be done.26 Whereas some authors have expressed concern about ongoing sepsis from a stool-ﬁlled colon, recent evidence suggests that sepsis can be well controlled with proper drainage and proximal diversion.26 Furthermore, with this approach, many low-lying anastomoses that have leaked can be salvaged, thus increasing the likelihood of restoring intestinal continuity. Occasionally, a small leak is easily visualized. Under these circumstances, simple repair of the anastomosis is quite tempting. However, this approach is frequently unsuccessful, and the consequences of a second leak are usually devastating. Therefore, simple closure without proximal diversion should be discouraged. ● Prevention Proper construction of a low-lying anastomosis is critical to minimize the likelihood of an anastomotic leak. For an anastomosis to properly heal, healthy bowel must be available on either end of the anastomosis in addition to a good blood supply and no signiﬁcant tension. For a low pelvic anastomosis, complete mobilization of the splenic ﬂexure is almost always required. However, even after all the avascular retroperitoneal attachments are divided, it still can be difﬁcult to get the descending colon to reach the pelvic ﬂoor. Under these circumstances, the colon is still tethered by the colonic mesentery. Therefore, in order to get the necessary length, either the IMA needs to divided at the aorta or the left colic vessel is divided just as it branches off the IMA (see Fig. 25–7). Great care must be taken not to damage the marginal artery, which runs parallel to the colon and only a few centimeters from the mes-

enteric border of the colon (Fig. 25–17). Once the IMA or left colic artery is ligated, the entire blood supply to the left colon is from the middle colic artery via the marginal artery. If, after dividing the arterial blood supply, there is still tension, the IMV should also be divided near the duodenum and pancreas. Once this is done, the avascular portion of the colonic mesentery can be divided all the way to the middle colic vessels, and the colon will have plenty of length to reach the pelvic ﬂoor (see Fig. 25–17). Furthermore, as long as the marginal artery is not damaged, blood supply to the distal descending colon will be adequate. An understanding of this anatomy and faith in the marginal artery are paramount to constructing a proper low anastomosis without tension and with good blood supply. The last factor, ensuring healthy ends of bowel, is usually not problematic with good tissue handling. However, because more patients receive preoperative radiation for rectal cancer, the distal bowel is not normal, which may impair proper healing. All distal anastomoses should be thoroughly evaluated by ﬁrst examining the integrity of the anastomotic doughnuts and then by air insufﬂation. If a leak is identiﬁed, attempts at suture repair are warranted. If, as is frequently the case, the anastomosis cannot be visualized, large leaks may, under some circumstances, be repaired via a transanal approach. Small leaks that cannot be repaired are best treated with proximal diversion and drainage. Under most circumstances, these small leaks will seal on their own and the ostomy can be reversed at a later date. Debate continues about whether a low-lying anastomosis should be routinely protected by proximal diversion. Critics of proximal diversion correctly assert that diversion itself does not prevent an anastomotic leak.27 Furthermore, there is associated morbidity from the reversal of

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the proximal stoma. However, proponents of proximal diversion will note that in most series a low rectal anastomosis will leak approximately 10% of the time3,28 and that, although diversion does not prevent an anastomotic leak, the clinical consequences of the leak are greatly diminished in patients who are proximally diverted.23,28,29 Therefore, proximal diversion should be strongly considered for any patients who have had previous radiation, who have a low anastomosis, if there is any concern about the integrity of the anastomosis, or who cannot medically tolerate the signiﬁcant morbidity of fecal peritonitis.23,28,29

Anastomotic Bleeding ● Consequence Clinically signiﬁcant bleeding from a colorectal anastomosis occurs approximately 2% of the time. Fortunately, most bleeding is self-limited and will stop on it own accord.30 Very rarely, an intervention will be necessary. Grade 1/2 complication ● Repair If a low-lying anastomosis does bleed, it is usually readily apparent because blood will pass through the rectum. Most bleeding is self-limited and will stop.30 Therefore, as long as the patient is hemodynamically stable, support is all that is necessary. Occasionally, the bleeding will be persistent and perfuse (Fig. 25–18A). Under these circumstances, it is best to attempt endoscopic management.31 A low-lying anastomosis is easily seen with the colonoscope and the bleeding identiﬁed. Bleeding can be frequently controlled with epinephrine injection or with an endoscopically applied clip (see Fig. 25–18B). If this is unsuccessful or not available, surgery will be necessary. For an anastomosis in the upper rectum, simply overseeing the anastomosis may be all that is necessary. For a very low-lying anastomosis, stitches can be applied via a transanal approach. Redoing the anastomosis can be very difﬁcult and should be done only as a last resort. ● Prevention No good way exists to prevent anastomotic bleeding for a low pelvic anastomosis.

Anastomotic Stricture ● Consequence A stricture can have an impact on bowel function. The clinical impact depends on the severity of the stricture. Obviously, for very tight strictures, evacuation will be difﬁcult and, on rare occasions, impossible. Many strictures are mild and can be managed with a combination of gentle dilation and bowel management, such as a high-ﬁber diet and stool softeners. More signiﬁcant strictures will require either an endoscopic or a surgical treatment. Grade 1/2 complication

A

B Figure 25–18 A, Anastomotic bleeding. B, Treatment with endoscopically applied endoclips.

● Repair Only symptomatic strictures should be treated. Generally, these are in patients in whom, on endoscopic examination, a standard colonoscope cannot be passed. Once symptoms do occur, endoscopic management should be attempted. This is usually accomplished with balloon dilation and is frequently successful. For very tight stenosis, the stricture can be partially pretreated with electrocoagulation or an argon beam coagulator prior to balloon dilation.32 Other options include selfexpanding colonic stents and endoscopic transanal resections of strictures. However, the long-term results of these latter approaches are still unclear.33 For very tight or long strictures, operative management may be necessary. This usually involves resection and the

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creation of a new colorectal or coloanal anastomosis. These operations are generally reserved for patients with mid or upper rectal strictures and can be very challenging.34 Temporary diversion after anastomotic revision is almost always done. Patients with low-lying strictures that cannot be managed with endoscopic means may require a permanent colostomy for symptomatic control. ● Prevention Many anastomotic strictures are associated with a clinical anastomotic leak. Presumably, many of the other strictures may be secondary to subclinical leaks, although this is difﬁcult to demonstrate. Prevention of anastomotic strictures is, therefore, similar to that for preventing anastomotic leaks. Proper anastomotic technique, with particular attention to lack of tension and blood supply, is critical. Reportedly anastomotic strictures are more common in stapled than in hand-sewn anastomoses.35 An association also seems to exist between fecal diversion and an increased stricture rate.36 However, the beneﬁts of diversion may outweigh the risk of subsequent stricture.

Vaginal Injury and Rectal Vaginal Fistulas ● Consequence Injury to the vagina and subsequent rectovaginal ﬁstula are uncommon but have been reported in the literature.37,38 Whereas some ﬁstulas result from direct injury to the vagina, others develop from an anastomotic leak and subsequent pelvic abscess.39 Symptoms will vary depending on the size of the resulting ﬁstula. For patients with minimal symptoms, observation and a bowel-conﬁning program may result in spontaneous healing. If unsuccessful, operative management will be necessary. Grade 2–4 complication ● Repair If the vagina is injured during the operative procedure, it can be repaired with nonabsorbable sutures. This may require careful and additional development of the rectovaginal septum to identify the injury. After the repair is complete, it is advisable to place well-vascularized omentum between the anastomosis and the vagina to help prevent ﬁstula formation. Under these circumstances, proximal diversion may also be advised. Once a rectovaginal ﬁstula is identiﬁed, it is critical to identify the exact location of the ﬁstula. A high ﬁstula may require further resection and the creation of a coloanal anastomosis.39 A low-lying ﬁstula may be amenable to an endorectal mucosal advancement ﬂap39 or a ﬂap using either bulbocavernosus tissue or the gracilis muscle. Results from these procedures may be impaired by previous pelvic radiation. Proximal diversion may be necessary for symptomatic relief and may, in some situations, lead to spontaneous healing.

● Prevention In order to perform a very low anastomosis, complete mobilization of the rectovaginal septum is necessary. This is facilitated by using a lipped pelvic retractor and anterior retraction on the posterior wall of the vagina. If the surgeon encounters “troublesome bleeding,” he or she is usually too anterior and may risk injuring the posterior vaginal wall, which will readily bleed. It is very important to mobilize the vagina all the way to the pelvic ﬂoor. This will completely separate the rectum and vagina so that a stapler can be safely placed around the rectum. When performing the end-to-end stapled anastomosis, the pelvic retractor should elevate the vaginal wall and the stapler should be lowered under direct visualization, taking care that the posterior wall of the vagina is not inadvertently incorporated into the stapling device (see Fig. 25–7B). Palpation of the vagina is recommended prior to ﬁring the stapler to reassure the surgeon that the vagina is not involved in the anastomosis.

Lower Ureteral Injury ● Consequence Unrecognized injury can result in urinary leak and urinoma. Although uncommon, injury to the lower ureter usually will occur as the ureter courses more medially to the trigone and is most vulnerable during the anterior lateral dissection, especially if there is a bulky tumor or signiﬁcant radiation ﬁbrosis. Grade 2–4 complication ● Repair Injury to the ureter at this level is problematic and usually warrants a urologic consultation. When the injury is recognized intraoperatively, the proximal ureter can be fully mobilized and often reimplanted into the bladder in a tunneled fashion.40 Primary repair over a urologic stent is also possible, but stricture may result, especially in a radiated ﬁeld. If the injury is identiﬁed postoperatively, drainage is initially required41 and may necessitate temporary urinary diversion with a percutaneous nephrostomy tube.42 Occasionally, the ureteral injury will resolve with proximal urinary diversion.42 However, if the injury persists, subsequent operative repairs will include reimplantation using either a psoas hitch40 or a Boari ﬂap. Another option involves a ureteroureterostomy43 and, as a last resort, nephrectomy. ● Prevention As the rectal dissection continues more distally, the pelvis becomes more narrow. The ureters, which course into the pelvis quite laterally, begin to veer more medially to join the trigone. If the dissection of the rectum is done just along the fascia propria, ureteral injury should be avoided because the ureter should stay both lateral and anterior. If the injury is due to tumor size

25 LOW ANTERIOR RESECTION or pelvic ﬁbrosis, the dissection is more lateral and the surgeon should clearly identify the ureter at the pelvic brim and dissect out the ureter distally for its entire length. If necessary, the dissection can be done all the way to the bladder itself. If, after this dissection, it is determined the distal ureter needs resection to obtain proper tumor clearance, a controlled resection and reimplantation can be done. The preoperative placement of ureteral stents can facilitate identiﬁcation of the ureter and any intraoperative injuries and should be considered in difﬁcult cases. The use of intraoperative indigo carmine can also be employed to identify a suspected intraoperative injury to the distal ureter.

Anterior Resection Syndrome ● Consequences Many patients after a low anterior resection have imperfect bowel function. Common complaints include increased frequency, urgency, fragmentation, incontinence, and constipation.44 Collectively, these symptoms have been referred to as the anterior resection syndrome. Unfortunately, these symptoms can be quite debilitating and can render a technical success a functional failure. Functional results seem to deteriorate as the anastomosis is lower in the pelvis.45–47 Whereas there is some improvement with time,48,49 many patients will have permanent and signiﬁcant alterations of their bowel function.50 Not surprisingly, bowel function seems worse in patients who have had pelvic radiation.45,51,52 Grade 1 complication ● Repair No surgical solution exists for the anterior resection syndrome. Symptoms are probably worse in patients who have had anastomotic complications, but even those patients with technically perfect operations can experience poor bowel function. Because improvement can occur with time, frustrated patients should be encouraged to persevere for at least 12 months.48 Symptomatic treatment includes the use of antidiarrhea agents, a high-ﬁber diet, and the use of barrier creams to protect the perineal skin. Patients will frequently need some psychological support and encouragement.53 Whereas many patients have a poor functional outcome, patient satisfaction is often higher than expected.48,51 This suggests that some patients, despite less than ideal function, still prefer their situation to the alternative: a permanent colostomy. Nevertheless, if patients have continued and life-limiting symptoms, conversion to a colostomy may be reasonable. ● Prevention There is no way to completely prevent the anterior resection syndrome. However, because of these signiﬁcant symptoms, alternative techniques have been developed. These include the use of the colonic J pouch

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and coloplasty. Most studies suggest improved function within the ﬁrst year, but over time, the functional outcomes between these alternative techniques and a straight colorectal anastomosis seem similar. Nevertheless, because of the improved immediate result, a colonic J pouch may be preferred if technically feasible. A preoperative assessment of anorectal function does seem warranted prior to performing a very low anastomosis. In patients who have poor anorectal function prior to surgery, a low anastomosis is likely to provide poor function and a colostomy may be considered. This may also be true for patients who have limited access to bathroom facilities for either personal or professional reasons. Caution should also be exercised in patients who are elderly and frail because poor anorectal function can be extremely debilitating under these circumstances. Frank discussions about postoperative function are essential to help patients make informed decisions.

REFERENCES 1. Heald RJ, Husband EM, Ryall RD. The mesorectum in rectal cancer surgery—the clue to pelvic recurrence? Br J Surg 1982;69:613–616. 2. Heald RJ, Ryall RD. Recurrence and survival after total mesorectal excision for rectal cancer. Lancet 1986;1:1479– 1482. 3. Law WL, Chu KW. Anterior resection for rectal cancer with mesorectal excision: a prospective evaluation of 622 patients. Ann Surg 2004;240:260–268. 4. Quirke P, Durdey P, Dixon MF, et al. Local recurrence of rectal adenocarcinoma due to inadequate surgical resection. Histopathological study of lateral tumour spread and surgical excision. Lancet 1986;2:996–999. 5. Adam IJ, Mohamdee MO, Martin IG, et al. Role of circumferential margin involvement in the local recurrence of rectal cancer. Lancet 1994;344:707–711. 6. Sawyer R, Richmond MN, Hickey JD, et al. Peripheral nerve injuries associated with anaesthesia. Anaesthesia 2000;55:980–991. 7. Brasch RC, Bufo AJ, Kreienberg PF, et al. Femoral neuropathy secondary to the use of a self-retaining retractor. Report of three cases and review of the literature. Dis Colon Rectum 1995;38:1115–1118. 8. Armenakas NA, Pareek G, Fracchia JA. Iatrogenic bladder perforations: long-term follow-up of 65 patients. J Am Coll Surg 2004;198:78–82. 9. Mynster T, Christensen IJ, Moesgaard F, et al. Effects of the combination of blood transfusion and postoperative infectious complications on prognosis after surgery for colorectal cancer. Danish RANX05 Colorectal Cancer Study Group. Br J Surg 2000;87:1553–1562. 10. Beynon J, Davies PW, Biol M, et al. Perioperative blood transfusion increases the risk of recurrence in colorectal cancer. Dis Colon Rectum 1989;32:975–979. 11. Edna TH, Bjerkeset T. Perioperative blood transfusions reduce long-term survival following surgery for colorectal cancer. Dis Colon Rectum 1998;41:451–459.

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12. Busch OR, Hop W, van Papendrecht MH, et al. Blood transfusions and prognosis in colorectal cancer. N Engl J Med 1993;328:1372–1376. 13. Donohue JH, Williams S, Cha S, et al. Perioperative blood transfusions do not affect disease recurrence of patients undergoing curative resection of colorectal carcinoma: a Mayo/North Central Cancer Treatment Group study. J Clin Oncol 1995;13:1671–1678. 14. Kawamura YJ, Umetani N, Sunami E, et al. Effect of high ligation on the long-term result of patients with operable colon cancer, particularly those with limited nodal involvement. Eur J Surg 2000;166:803–807. 15. Cassar K, Munro A. Iatrogenic splenic injury. J R Coll Surg Edinb 2002;47:731–741. 16. Khan FA, Fang DT, Nivatvongs S. Management of presacral bleeding during rectal resection. Surg Gynecol Obstet 1987;165:274–276. 17. Losanoff JE, Richman BW, Jones JW. Cyanoacrylate adhesive in management of severe presacral bleeding. Dis Colon Rectum 2002;45:1118–1119. 18. Nivatvongs S, Fang DT. The use of thumbtacks to stop massive presacral hemorrhage. Dis Colon Rectum 1986; 29:589–590. 19. Oderich GS, Panneton JM, Hofer J, et al. Iatrogenic operative injuries of abdominal and pelvic veins: a potentially lethal complication. J Vasc Surg 2004;39:931– 936. 20. Havenga K, Enker WE, McDermott K, et al. Male and female sexual and urinary function after total mesorectal excision with autonomic nerve preservation for carcinoma of the rectum. J Am Coll Surg 1996;182:495–502. 21. Heriot AG, Tekkis PP, Fazio VW, et al. Adjuvant radiotherapy is associated with increased sexual dysfunction in male patients undergoing resection for rectal cancer: a predictive model. Ann Surg 2005;242:502–510; discussion 510–511. 22. Pocard M, Zinzindohoue F, Haab F, et al. A prospective study of sexual and urinary function before and after total mesorectal excision with autonomic nerve preservation for rectal cancer. Surgery 2002;131:368–372. 23. Marusch F, Koch A, Schmidt V, et al. Value of a protective stoma in low anterior resections for rectal cancer. Dis Colon Rectum 2002;45:1164–1171. 24. Bell SW, Walker KG, Rickard M, et al. Anastomotic leakage after curative anterior resection results in a higher prevalence of local recurrence. Br J Surg 2003;90:1261– 1266. 25. Chang SC, Lin JK, Yang SH, et al. Long-term outcome of anastomosis leakage after curative resection for mid and low rectal cancer. Hepatogastroenterology 2003;50:1898– 1902. 26. Hedrick TL, Sawyer RG, Foley EF, et al. Anastomotic leak and the loop ileostomy: friend or foe? Dis Colon Rectum 2006;49:1167–1176. 27. Wong NY, Eu KW. A defunctioning ileostomy does not prevent clinical anastomotic leak after a low anterior resection: a prospective, comparative study. Dis Colon Rectum 2005;48:2076–2079. 28. Gastinger I, Marusch F, Steinert R, et al. Protective defunctioning stoma in low anterior resection for rectal carcinoma. Br J Surg 2005;92:1137–1142.

29. Leester B, Asztalos I, Polnyib C. Septic complications after low anterior rectal resection—is diverting stoma still justiﬁed? Acta Chir Iugosl 2002;49:67–71. 30. Cirocco WC, Golub RW. Endoscopic treatment of postoperative hemorrhage from a stapled colorectal anastomosis. Am Surg 1995;61:460–463. 31. Mayer G, Lingenfelser T, Ell C. The role of endoscopy in early postoperative haemorrhage. Best Pract Res Clin Gastroenterol 2004;18:799–807. 32. Suchan KL, Muldner A, Manegold BC. Endoscopic treatment of postoperative colorectal anastomotic strictures. Surg Endosc 2003;17:1110–1113. 33. Forshaw MJ, Maphosa G, Sankararajah D, et al. Endoscopic alternatives in managing anastomotic strictures of the colon and rectum. Tech Coloproctol 2006;10: 21–27. 34. Schlegel RD, Dehni N, Parc R, et al. Results of reoperations in colorectal anastomotic strictures. Dis Colon Rectum 2001;44:1464–1468. 35. MacRae HM, McLeod RS. Handsewn vs. stapled anastomoses in colon and rectal surgery: a meta-analysis. Dis Colon Rectum 1998;41:180–189. 36. Lucha PA Jr, Fticsar JE, Francis MJ. The strictured anastomosis: successful treatment by corticosteroid injections—report of three cases and review of the literature. Dis Colon Rectum 2005;48:862–865. 37. Sugarbaker PH. Rectovaginal ﬁstula following low circular stapled anastomosis in women with rectal cancer. J Surg Oncol 1996;61:155–158. 38. Rex JC Jr, Khubchandani IT. Rectovaginal ﬁstula: complication of low anterior resection. Dis Colon Rectum 1992;35:354–356. 39. Fleshner PR, Schoetz DR Jr, Roberts PL, et al. Anastomotic-vaginal ﬁstula after colorectal surgery. Dis Colon Rectum 1992;35:938–943. 40. Ahn M, Loughlin KR. Psoas hitch ureteral reimplantation in adults–analysis of a modiﬁed technique and timing of repair. Urology 2001;58:184–187. 41. Katz R, Meretyk S, Gimmon Z. Abdominal compartment syndrome due to delayed identiﬁcation of a ureteral perforation following abdomino-perineal resection for rectal carcinoma. Int J Urol 1997;4:615–617. 42. Lask D, Abarbanel J, Luttwak Z, et al. Changing trends in the management of iatrogenic ureteral injuries. J Urol 1995;154:1693–1695. 43. Paick JS, Hong SK, Park MS, et al. Management of postoperatively detected iatrogenic lower ureteral injury: should ureteroureterostomy really be abandoned? Urology 2006;67:237–241. 44. Rasmussen OO, Petersen IK, Christiansen J. Anorectal function following low anterior resection. Colorectal Dis 2003;5:258–261. 45. Bretagnol F, Troubat H, Laurent C, et al. Long-term functional results after sphincter-saving resection for rectal cancer. Gastroenterol Clin Biol 2004;28:155–159. 46. Nesbakken A, Nygaard K, Lunde OC. Mesorectal excision for rectal cancer: functional outcome after low anterior resection and colorectal anastomosis without a reservoir. Colorectal Dis 2002;4:172–176. 47. Lewis WG, Martin IG, Williamson MER, et al. Why do some patients experience poor functional results after

25 LOW ANTERIOR RESECTION anterior resection of the rectum for carcinoma? Dis Colon Rectum 1995;38:259–263. 48. Efthimiadis C, Basdanis G, Zatagias A, et al. Manometric and clinical evaluation of patients after low anterior resection for rectal cancer. Tech Coloproctol 2004;8(suppl 1):s205–s207. 49. Ho YH, Seow-Choen F, Tan M. Colonic J-pouch function at six months versus straight coloanal anastomosis at two years: randomized controlled trial. World J Surg 2001;25:876–881. 50. Williamson ME, Lewis WG, Finan PJ, et al. Recovery of physiologic and clinical function after low anterior

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resection of the rectum for carcinoma: myth or reality? Dis Colon Rectum 1995;38:411–418. 51. Matzel KE, Bittorf B, Gunther K, et al. Rectal resection with low anastomosis: functional outcome. Colorectal Dis 2003;5:458–464. 52. Pollack J, Pahlman L, Gunnarsson U, et al. Late adverse effects of short-course preoperative radiotherapy in rectal cancer. Br J Surg 2006;93:1519–1525. 53. Desnoo L, Faithfull S. A qualitative study of anterior resection syndrome: the experiences of cancer survivors who have undergone resection surgery. Eur J Cancer Care (Engl) 2006;15:244–251.

26

Abdominal Perineal Resection with Colostomy Charles M. Friel, MD INTRODUCTION An abdominal perineal resection (APR) is the complete removal of the rectum and anus. The most common indication for surgery is adenocarcinoma of the lower rectum, when performing a primary anastomosis is not feasible. When APR is done for cancer, obtaining a negative circumferential margin is critical, so the dissection is wide to provide adequate oncologic clearance. Sometimes, the rectum and anus need to be removed for benign conditions. Under these circumstances, the dissection can be closer to the rectal wall, which may help prevent complications. For the purpose of this discussion, it is assumed that the indication for surgery is cancer and the technical points will stress appropriate oncologic technique. These principles are generally applicable to benign conditions as well. However, on occasion, there are differences in patients with benign disease, and this is noted in the text.

● Fecal diversion due to perineal sepsis (e.g., Fournier’s

gangrene, Crohn’s disease, severe perianal hidradenitis, radiation injury) ● Disabling incontinence ● Distal benign or malignant stricture ● Emergency surgery, when an anastomosis is deemed not safe

OPERATIVE STEPS Step 1 Abdominal dissection Step 2 Perineal dissection ● Incision ● Posterior and lateral dissection ● Division of anococcygeal ligament ● Division of levator ani ● Anterior dissection ● Closure of perineal wound Step 3 Creation of end colostomy

INDICATIONS This is a partial list of surgical indications for an APR and colostomy. These procedures involve the complete removal of the rectum and anus and the creation of an end colostomy. The most common indication is ● Very low rectal cancer.

Other indications include ● Large polyp not amenable to other techniques (e.g.,

endoscopy, transanal, transmission electrom microscopy [TEM]) ● Severe pelvic or perineal infection/inﬂammation (e.g., radiation injury, pelvic inﬂammatory disease, rectal perforation, previous anastomotic leak, Crohn’s disease) ● Other malignancies (e.g., ovarian cancer, retrorectal tumors, rectal sarcomas, urologic cancer) Additional indications for a colostomy include

OPERATIVE PROCEDURE Abdominal Perineal Resection An APR consists of two separate dissections. When performed by one operating surgeon, the abdominal dissection is completed ﬁrst and then the surgeon will reposition himself or herself and perform the perineal dissection. Because there are two distinct areas of dissection, some surgeons advocate a synchronous approach, utilizing two surgeons and a simultaneous abdominal and perineal dissection.1 Such an approach decreases operative time and can help both surgeons during a difﬁcult case.

Abdominal Dissection The abdominal portion of the procedure is similar to a very low anterior resection. It is helpful to continue the abdominal dissection as low as possible, preferably all the way to the pelvic ﬂoor and below the coccyx. As one gets

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lower in the pelvis, the surgeon needs to be cognizant of the tumor location and make sure she or he does not cone in on the rectum, leaving a positive circumferential radial margin. Otherwise, the abdominal dissection is the same as for a low anterior resection. Therefore, the complications and anatomy are also similar. The reader is referred to Section III, Chapter 25, Low Anterior Resection, for complications associated with the abdominal portion of this procedure.

Perineal Dissection Upon completion of the abdominal dissection, the surgeon must reposition himself or herself for the perineal dissection. An elliptical incision is made around the anus, approximately 2 to 3 cm from the anal verge (Fig. 26–1). Once the skin is incised, the dissection is greatly facilitated by the use of a self-retaining retractor (Fig. 26–2). The incision is then carried deeper into the ischiorectal fossa bilaterally (Fig. 26–3). No vital structures are located in the posterior or lateral positions, so dissection in this area is safe and should be continued more deeply using elec-

trocautery. The inferior rectal artery does pass through the ischiorectal fossa and may result in some minor bleeding. This artery can usually be controlled with electrocautery but does occasionally require ligation. As the dissection is carried posteriorly, there is a tendency for the operating surgeon to travel too far and get behind the coccyx (Fig. 26–4). Therefore, careful palpation of the coccyx is critical to guide the surgeon’s dissection above the coccyx. Once the coccyx is clearly identiﬁed (Fig. 26–5), a ﬁbrous band extends from the coccyx in the midline position. This is the anococcygeal ligament and needs to be divided. The surgeon is now ready to enter the peritoneal cavity just above the coccyx. This is best done with an assistant placing a hand behind the rectum all the way to the coccyx from the abdominal cavity. Then the operating surgeon should be able to palpate the assistant’s ﬁnger. Mayo scissors are then used to poke through the pelvic ﬂoor, just above the coccyx (Fig. 26–6). This hole is widened, which allows the operating surgeon to insert a ﬁnger into the peritoneal cavity and hook the levator ani muscles. Using electrocautery, these muscles can be divided in both directions (Fig. 26–7). Once 75% of this dissection is complete,

Figure 26–1 Perineum in a patient with rectal cancer. Purple line demonstrates the location of the incision for malignant disease, which is outside the external sphincter.

Figure 26–3 Perineum in a patient with Crohn’s disease. A selfretaining retractor is in place. Yellow dotted line demonstrates the location of the incision for an intersphincteric dissection. This dissection is appropriate for benign disease.

Figure 26–2 Final appearance after removal of the rectum and anus. Forceps point to the posterior wall of the prostate.

Figure 26–4 Abdominal perineal resection (APR), lateral dissection.

26 ABDOMINAL PERINEAL RESECTION WITH COLOSTOMY

Figure 26–5 APR, posterior dissection.

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Figure 26–7 APR, posterior dissection. The surgeon is about to use Mayo scissors to poke into the peritoneal cavity just above the coccyx.

Figure 26–6 APR, posterior dissection. Forceps point to the coccyx, which should be palpated.

the top of the rectum can be grasped and pulled through the perineal defect (Fig. 26–8). This helps deﬁne the anterior plane of dissection, which can be the most challenging. With a hand behind the rectum, the anterior plane between the rectum and the prostate or the vagina is developed (Fig. 26–9). In a man, palpation of the Foley catheter can help deﬁne this plane (Fig. 26–10). In a woman, a ﬁnger in the vagina can be advantageous. The specimen is ﬁnally freed and removed. The perineal wound is then closed, using several layers of an absorbable suture, and the skin closed with a subcuticular stitch.

Urethral Injury ● Consequence The anterior portion of the perineal dissection can be the most problematic. If the dissection is carried too far anteriorly in a man, a urethral injury is possible. Usually, this is immediately evident as the Foley catheter is visualized. Attempts at repair can be made. However, after a repair, a urethral stricture is possible. If a leak persists, a urethral perineal ﬁstula can develop. If tumor is at the anterior margin, a pelvic exenteration with a cystectomy and ileal conduit should be performed.

Figure 26–8 Division of the levator ani muscles.

Grade 2/3 complication; grade 4 (if need for pelvic exenteration) ● Repair Small defects can be oversewn, using an absorbable stitch. A frank transaction can be more difﬁcult to treat and would require an end-to-end anastomosis. If repair

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SECTION III: GASTROINTESTINAL SURGERY risk of injury.2 In these cases, palpation is even more critical. If the proctectomy is being done for benign disease, an intersphincteric dissection may be more appropriate.3 In this dissection, the intersphincteric groove is identiﬁed and the circular dissection is done between the internal and the external sphincters (see Fig. 26–2). The dissection follows this plane into the peritoneal cavity. With this dissection, the levators are not divided. The dissection stays very close to the rectal wall, decreasing the chances of a urethral injury.

Vaginal Injury Figure 26–9 Anterior dissection. The rectum pulled through the perineum.

Figure 26–10 Anterior dissection.

dissection

line

of

the

anterior

is attempted, prolonged catheterization is warranted. The catheter should not be removed until radiographic evidence indicates that a leak has sealed. Unfortunately, healing can be greatly impaired in an irradiated ﬁeld, which is common if the patient has received neoadjuvant treatment for a locally advanced rectal cancer. An intraoperative urologic consultation may be warranted. ● Prevention Careful palpation of the Foley catheter is important while performing the anterior dissection. This palpation will help guide the surgeon to the proper plane between the prostate and the rectum. Persistent bleeding should alert the surgeon that she or he has ventured too anteriorly and is getting into the prostate, increasing the likelihood of urethral injury. Between the rectum and the urethra, there is generally enough prostate to avoid a urethral injury. However, on occasion, the tumor will extend just adjacent to the capsule of the prostate or superﬁcially invade the prostate. Under these circumstances, the dissection can deliberately extend into the prostate, putting the urethra at greater

● Consequences In women, the vagina is just anterior to the rectum. Therefore, the vagina is susceptible to injury during the perineal dissection. Because the rectum is being removed, this rarely results in any long-term sequelae. In fact, in women with anterior tumors of the rectum, strong consideration should be given to a posterior vaginectomy to facilitate adequate tumor clearance, which can help to decrease the rate of local recurrence. Grade 1 complication ● Repair If an inadvertent injury to the vagina does occur, primary closure with an absorbable stitch should be done. However, because the rectum is being removed, even if this repair were to fail, the posterior wall of the vagina will often heal by secondary intention without development of a ﬁstula. ● Prevention As in men, careful identiﬁcation of the anterior plane is important to prevent inadvertent injury to the vagina. Persistent bleeding should alert the surgeon that the well-vascularized vagina is being traumatized and the plane of dissection should be adjusted more posteriorly. If the proctectomy is being done for benign disease, an intersphincteric dissection is appropriate and may prevent this complication (see the section on “Urethral Injury,” earlier).3

Perineal Wound Breakdown ● Consequences Perineal wound breakdown can range from a minor separation of the skin to a complete disruption of the wound. This problem is more common in patients who have had preoperative radiation.4,5 This is particularly true for patients with a remote history of pelvic radiation who now require surgery.6 For minor disruptions, healing can be rapid,4 but major wound breakdown can take months to fully heal.4,5 Grade 1/2 complication (if treated conservatively); grade 3 complication (if myocutaneous ﬂap required)

26 ABDOMINAL PERINEAL RESECTION WITH COLOSTOMY

295

● Repair Proper drainage and wound débridement are necessary if there is an associated wound infection. Once the sepsis is controlled, the wound can be packed and allowed to heal by secondary intention. A vacuumassisted closure (VAC) device can also be used, which may speed up wound healing.7 For a very large defect that is failing to close, a myocutaneous ﬂap, using either the gracilis6 or the rectus muscle,8 can be done.9 ● Prevention Wound breakdown is often associated with a wound infection. Therefore, it is important to limit fecal contamination during the perineal dissection. Proper hemostasis is important to prevent a hematoma that may get superinfected. Pelvic drains may also help prevent accumulation of peritoneal ﬂuid in the pelvis, which can leak and cause perineal wound maceration and subsequent breakdown. Whether to perform a primary rectus or gracilis muscle ﬂap on patients who have been previously radiated continues to be debated. Proponents of a primary ﬂap note the relatively high rate of perineal wound complications.8 They believe wound problems will be lessened if nonirradiated tissue is used to reconstruct the perineum. Unfortunately, even with primary ﬂap closures, wound complications can be encountered.10,11 Therefore, it seems reasonable to save valuable muscle for reconstruction in those patients who develop a long-term perineal wound complication. An exception to this approach may be in patients who have had a remote history of pelvic radiation. In these patients, the abnormal perineal tissue is less likely to heal and a primary ﬂap can be considered.6,8 This scenario is commonly found in patients with recurrent anal cancer who have been treated previously with chemoradiation,10 who have a very high rate of wound failure after primary closure.

Colostomy Creation

Figure 26–11 Circular incision for colostomy at the previously marked location.

Figure 26–12 Cruciate incision in the anterior rectus sheath has been done, exposing the rectus abdominus muscle.

Once the perineal dissection is completed, an end colostomy is created. A circular incision is made at a previously marked location (Fig. 26–11). The dissection is carried through the subcutaneous adipose tissue to the anterior sheath of the rectus muscle. A cruciate incision is made in the fascia, and the rectus is identiﬁed (Fig. 26–12). The ﬁbers of the rectus muscle are then separated and the posterior sheath exposed. The posterior sheath is also divided using a cruciate incision (Fig. 26–13), and the defect is dilated to about two ﬁngerbreadths (Fig. 26–14). The colon is then delivered through the abdominal wall (Fig. 26–15) and matured using an absorbable stitch (Fig. 26–16).

Stomal Necrosis ● Consequences If superﬁcial, stomal necrosis may result only in some mucosal sloughing without long-term sequelae. If more

Figure 26–13 Cruciate incision in the posterior rectus sheath.

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Figure 26–14 Colostomy site is dilated to two ﬁngerbreadths.

Figure 26–16 Final mature colostomy.

Figure 26–15 Distal colon is delivered through the colostomy site without tension.

extensive, the distal portion of the stoma will slough and lead to a stenotic and recessed stoma. In the worstcase scenario, the colon will necrose below the level of the fascia, which can lead to a free intraperitoneal perforation and leakage of stool. Grade 1/2 complication (if superﬁcial); grade 3 complication (if deep) ● Repair Stoma necrosis is a postoperative diagnosis. If the stoma is just “dusky,” there may be some minor sloughing but no further intervention is necessary. When the mucosa is clearly not viable, the extent of necrosis should be assessed. This is easily done using a narrow proctoscope or anoscope. It is necessary to examine only the distal few centimeters. Usually, there will be pink mucosa just below the skin. Under these circumstances, conservative management is reasonable, recognizing that stenosis may develop in the future. If the mucosa is not viable below the level of the fascia, an immediate revision of the colostomy may be necessary. In patients who will require a permanent stoma, early revision may be appropriate if revision seems inevitable.

In patients with temporary stomas, a conservative approach is reasonable because the subsequent stenosis can be addressed at the time of colostomy closure. ● Prevention Stomal necrosis results from poor blood supply to the distal colon. Proper mobilization of the descending colon will help decrease the tension on the colon and prevent this complication. Furthermore, it may be necessary to divide additional mesenteric vessels to also prevent unnecessary tension. As with an anastomosis, when colonic mesentery is divided, care must be taken to protect the marginal artery, which will provide blood to the distal colon. Finally, the blood supply of the distal colon can be easily damaged as the surgeon pulls the colon through the fascial defect, particularly in obese patients. Therefore, the fascial defect must be large enough to permit passage of the colon without undo force. A larger defect will also prevent venous outﬂow obstruction, which is another cause for ischemia and stomal necrosis. While the surgeon is maturing the stoma, she or he should pay particular attention to its viability. If, while closing, the mucosa is clearly ischemic, it may be wise to revise the stoma prior to leaving the operating room. This is particularly true in an elective case and if the stoma is intended to be permanent.

26 ABDOMINAL PERINEAL RESECTION WITH COLOSTOMY

Figure 26–17

Colostomy stenosis.

Other Complications Stomal Stenosis Stomal stenosis (Fig. 26–17) usually occurs as a result of stomal necrosis. Once the distal colon sloughs completely, the stoma will recess and the surrounding skin will begin to close. Surprisingly, even with a tight stenosis, stool often passes and some patients can successfully keep a bag on the opening. As long as the patient is asymptomatic and a colonoscope can be passed, allowing for surveillance of the colon, revision may not be necessary. However, if the patient is symptomatic or if surveillance of the colon is not possible, a revision of the colostomy should be done. An attempt can be made via a peristomal incision. Through this incision, it may be possible to free up some underlying healthy colon and advance the colon a few centimeters to redo the colostomy. However, if this is not possible, a complete revision can be done via an open or laparoscopic approach. If the stoma is not permanent, a reversal can be performed when the patient is medically ﬁt. Parastomal Hernia By deﬁnition, a colostomy creates a defect in the fascia. This defect must be large enough to pass the colon without undo force or tension. Furthermore, if the defect is too small, venous outﬂow may be obstructed and cause stomal necrosis and subsequent stenosis. However, when the defect is too large, a parastomal hernia may result. Unfortunately, these hernias are quite common.12 Because of high failure rates, asymptomatic hernias are often handled conservatively. If surgical treatment is necessary, two general approaches are available. Either the surgeon attempts to tighten or close the fascial defect, leaving the colostomy in the same location, or the colostomy is completely resituated.13 The former can be done either via a peristomal incision or via a transabdominal approach. Shaping a piece of mesh into a “key” hole is also commonly used, but this is associated with a high recurrence rate. In general, resituating the stoma is associated with the lowest recurrence rate.13,14 However, no matter

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Figure 26–18 Colostomy marks in an obese patient. Note the very high marks (purple circles) necessary under these circumstances.

the approach, recurrence is common, which may make the conservative management of an asymptomatic hernia reasonable.13,14

Leakage A poorly constructed or poorly placed colostomy can be extremely morbid. Patients will have a difﬁcult time keeping a stomal appliance attached, and stool leakage results. This can lead to signiﬁcant skin irritation and is socially unacceptable. This problem is considerably exacerbated if a stoma is placed in a skin crease. For these reasons, patients should be clearly marked by an experienced enterostomal therapist whenever possible prior to surgery. This is particularly true in patients who are obese (Fig. 26–18) or in those who have multiple abdominal scars, when stomal placement can be particularly challenging. It is also best to have a colostomy protrude approximately 1 cm above the skin. Flush stomas should be avoided, because these will often leak and make applying a stomal appliance difﬁcult. An experienced enterostomal therapist is critical in marking patients preoperatively and in assisting with postoperative stomal problems.15

REFERENCES 1. de Canniere L, Rosiere A, Michel LA. Synchronous abdominoperineal resection without transfusion. Br J Surg 1993;80:1194–1195. 2. Ike H, Shimada H, Kamimukai N, et al. Extended abdominoperineal resection with partial prostatectomy for T3 rectal cancer. Hepatogastroenterology 2003;50:377– 379. 3. Lubbers EJ. Healing of the perineal wound after proctectomy for nonmalignant conditions. Dis Colon Rectum 1982;25:351–357. 4. Bullard KM, Trudel JL, Baxter NN, et al. Primary perineal wound closure after preoperative radiotherapy and

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5.

6.

7.

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abdominoperineal resection has a high incidence of wound failure. Dis Colon Rectum 2005;48:438–443. Chadwick MA, Vieten D, Pettitt E, et al. Short course preoperative radiotherapy is the single most important risk factor for perineal wound complications after abdominoperineal excision of the rectum. Colorectal Dis 2006;8:756–761. Shibata D, Hyland W, Busse P, et al. Immediate reconstruction of the perineal wound with gracilis muscle ﬂaps following abdominoperineal resection and intraoperative radiation therapy for recurrent carcinoma of the rectum. Ann Surg Oncol 1999;6:33–37. Greer SE, Duthie E, Cartolano B, et al. Techniques for applying subatmospheric pressure dressing to wounds in difﬁcult regions of anatomy. J Wound Ostomy Continence Nurs 1999;26:250–253. Chessin DB, Hartley J, Cohen AM, et al. Rectus ﬂap reconstruction decreases perineal wound complications after pelvic chemoradiation and surgery: a cohort study. Ann Surg Oncol 2005;12:104–110.

9. Anthony JP, Mathes SJ. The recalcitrant perineal wound after rectal extirpation. Applications of muscle ﬂap closure. Arch Surg 1990;125:1371–1376; discussion 1376–1377. 10. Christian CK, Kwaan MR, Betensky RA, et al. Risk factors for perineal wound complications following abdominoperineal resection. Dis Colon Rectum 2005;48:43–48. 11. Kapoor V, Cole J, Frank I, et al. Does the use of a ﬂap during abdominoperineal resection decrease pelvic wound morbidity? Am Surg 2005;71:117–122. 12. Arumugam PJ, Bevan L, Macdonald L, et al. A prospective audit of stomas—analysis of risk factors and complications and their management. Colorectal Dis 2003;5:49–52. 13. Rieger N, Moore J, Hewett P, et al. Parastomal hernia repair. Colorectal Dis 2004;6:203–205. 14. Rubin MS, Schoetz DJ Jr, Matthews JB. Parastomal hernia. Is stoma relocation superior to fascial repair? Arch Surg 1994;129:413–418; discussion 418–419. 15. Park JJ, Del Pino A, Orsay CP, et al. Stoma complications: the Cook County Hospital experience. Dis Colon Rectum 1999;42:1575–1580.

27

Laparoscopic Appendectomy C. Joe Northup, MD INTRODUCTION Laparoscopic appendectomy (LA) is rapidly becoming the standard of care for surgical removal of the appendix. Acute appendicitis is a diagnostic possibility in nearly every patient who presents emergently with abdominal pain. Despite the recent improvements in diagnostic imaging, appendicitis is often confused with other inﬂammatory processes, and it presents a challenging clinical diagnosis. Ovarian torsion/abscess, diverticulitis, inﬂammatory bowel disease, and other conditions can all present with symptoms similar to those of acute appendicitis.1 A thorough history and physical examination continue to be the most efﬁcient methods of clinical diagnosis. Generalized abdominal pain migrating to the right lower quadrant (RLQ) with associated leukocytosis is the classic presentation for acute appendicitis. Frequently, however, the source of abdominal pain is less certain, especially in the female patient. Diagnostic studies such as computed tomography (CT) scan and ultrasound have been shown to be beneﬁcial when the diagnosis is not clear.2,3 Yet no imaging study has been able to replace careful evaluation of the patient’s symptoms and physical examination ﬁndings.4 Indications for LA remain the same as those for open appendectomy (OA), with acute appendicitis being the most common reason for appendectomy. Chronic appendicitis is a more controversial diagnosis, most commonly associated with patients in the pediatric population. Recurrent RLQ pain, which does not go on to develop into severe pain or localized peritonitis, is the most frequent complaint associated with chronic appendicitis. Some surgeons advocate elective appendectomy in this group and have demonstrated relief of symptoms in many patients.5 Perforated appendicitis with subsequent abscess formation can be safely managed with percutaneous drainage and interval appendectomy once the acute inﬂammation has resolved. Tumors of the appendix can demonstrate a wide variety of pathology. The presence of a lesion in the appendix is an indication for appendectomy, and the differential diagnosis includes appendiceal cysts, adenocarcinoma, and carcinoid tumors.

The addition of the laparoscopic approach over traditional appendectomy has yielded many beneﬁts. Improved visualization of the abdominal cavity obtained with laparoscopy is particularly beneﬁcial when the diagnosis of acute appendicitis is uncertain. LA has been found to have a decreased length of stay, a lower readmission rate, and a decrease in overall complications.6 In recent articles, there has not been a signiﬁcant increase in cost between LA and OA. As with many laparoscopic procedures, LA has been demonstrated to have a decrease in narcotic use and an earlier return to work than OA.7 Complications from LA may be increased in patients who are elderly or morbidly obese or in those with perforated appendicitis.8 Also, the previously operated abdomen can add further challenge to any laparoscopic procedure. Consideration must be given to peritoneal access and port placement depending on previous surgical history. The overall complication rates of LA range from 6% to 13% with a very low risk of mortality.9,10 Careful identiﬁcation of structures and careful dissection will help avoid many intraoperative and postoperative complications.

INDICATIONS ● ● ● ●

Acute appendicitis Chronic appendicitis Interval appendectomy Neoplasm

OPERATIVE STEPS Step Step Step Step Step Step Step

1 2 3 4 5 6 7

Patient positioning and trocar insertion Mobilization of appendix/cecum Dissection of appendix and mesoappendix Division of mesentery Resection of appendix Specimen removal Trocar removal

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OPERATIVE PROCEDURE Trocar Insertion Trocar Insertion Injuries For general injuries related to trocar placement, refer to Section I, Chapter 7, Laparoscopic Surgery. Bladder Injury ● Consequence Intra-abdominal contamination. Early diagnosis of this injury is critical. Patients with missed injuries will often present to the emergency department with complaints of atypical abdominal pain, frequently associated with large amounts of drainage from the wound. Associated hematuria is also common. Imaging studies are very helpful in diagnosing this complication because a CT scan will typically demonstrate a large amount of nonloculated peritoneal ﬂuid. Contrast extravasation may be present in the pelvis on a standard CT scan, and a CT cystogram is the most accurate method for conﬁrmatory diagnosis of this injury. Delayed presentation of this complication can present with oliguria and acute renal failure. Patients can also go on to develop peritonitis and, eventually, sepsis. Grade 2/3 complication ● Repair Bladder injuries are repaired with a two-layer, primary closure and can be completed laparoscopically. If there is a question of injury during the procedure, retrograde ﬁlling of the bladder may be helpful in demonstrating the injury. The distended bladder will also allow for an easier repair of the injury. A urinary catheter should be left in place for 10 to 14 days after the repair to allow for adequate healing.11 Prior to removal of the urinary catheter, a formal cystogram should be performed to conﬁrm that the repair has healed satisfactorily. ● Prevention Trocar insertion in the pelvis, and in all areas of the abdomen, should be done under direct vision (Fig. 27–1). A distended bladder can often reach as high as the umbilicus in some patients, and a urinary catheter should be placed prior to the start of any laparoscopic pelvic surgery. Injury to the bladder with instrumentation is uncommon during LA; however, care should always be taken when dissecting an inﬂamed appendix from the peritoneum.

Figure 27–1 Trocar insertion. The operating port in the left lower quadrant is placed under direct vision to avoid injury to the sigmoid colon (C) or other structures.The trocar should be inserted just lateral to the epigastric vessels (E).

occur until the trocar is removed and the pneumoperitoneum is released. Considerable bleeding can result from this injury, requiring transfusion, reoperation, or the development of a large rectus sheath hematoma. Grade 2 complication ● Repair Once the vessel has been injured, it typically requires ligation to control bleeding. Using a port closure device and absorbable suture is typically the most efﬁcient method to manage this complication. Two to three sutures placed perpendicular to the path of the vessel are usually required to adequately ligate the vessel. If unsuccessful, increasing the incision of the port site is required to directly suture the vessels. Once the bleeding is under control, the abdominal pressure should be decreased to allow for identiﬁcation of further hemorrhage that may be controlled by the presence of the distended abdomen. ● Prevention Visualization of the epigastric vessels should be attempted before placing the trocar in the vicinity of the vessels. Also, an estimation of the border of the rectus muscle should be made. Trocars for this procedure should be placed just lateral to the rectus edge in the left lower quadrant.

Wound Infection Epigastric Vessel Injury ● Consequence Severe bleeding. Before trocars are placed along the midclavicular line, thought must be given to the location of the epigastric vessels. Injuries to these vessels are often missed at the time of surgery owing to compression by the trocar and the presence of a pneumoperitoneum. Frequently, signiﬁcant hemorrhage does not

● Consequence Severe complications. The overall wound infection for LA remains quite low. However, superﬁcial skin infections can increase the rate of incisional hernia and result in increased pain and delayed recovery. Rarely, a superﬁcial skin infection can progress to more aggressive infection or necrotizing fasciitis. Grade 1/2 complication

27 LAPAROSCOPIC APPENDECTOMY

Figure 27–2 Removal of the specimen. The appendix has been placed into a specimen pouch and is being removed from the abdomen. This prevents the contaminated appendix from coming into direct contact with the subcutaneous tissue.

301

Figure 27–3 Identiﬁcation of the appendix. The appendix can often be difﬁcult to identify when inﬂamed. Identiﬁcation of the superior taenia coli (T) and following it toward the cecum (C) will lead to the base of the appendix (A).

● Repair The vast majority of superﬁcial infections can be managed with simple wound management. Allowing the wound to heal by secondary intention with daily dressing changes is often the only intervention necessary. Cultures should be taken when the wound is opened and antibiotics reserved for patients with associated cellulitis. ● Prevention Most studies demonstrate that preoperative antibiotics are indicated prior to an appendectomy to decrease the rate of wound infection.12 In the presence of a perforated appendix or severe contamination, primary wound closure may not be indicated. Perforated appendicitis increases the wound infection rate to 15%.13 If the intra-abdominal ﬁndings increase the concern of a wound infection, the skin incision can be left open to allow drainage of any subcutaneous wound infections. Wound contamination may also occur during removal of the specimen. Placing the resected appendix into a specimen pouch is advocated to decrease wound exposure to the contaminated tissue (Fig. 27–2).

Figure 27–4 Attachments to the appendix. The appendix is often located in a retrocolic position, or it will have ﬁbrous attachments to the retroperitoneum.

Dissection of the Appendix and the Mesoappendix Injury to the Colon ● Consequence Intra-abdominal contamination with development of peritonitis or abscess. Careful dissection must be performed when mobilizing the appendix, especially in the presence of periappendiceal inﬂammation (Figs. 27–3 to 27–5). During laparoscopic procedures, the expected incidence of intestinal injury is less than 1%.14 Delayed presentation of a colonic injury can have severe consequences. A patient with an unrecognized colonic injury typically presents with abdominal pain and fever. If the

Figure 27–5 Mobilization of the appendix (A) and cecum (C). The attachments to the appendix are being taken down sharply. Thermal energy is avoided to decrease the risk of injury to the colon.

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Figure 27–6 Dissection of appendix. In this ﬁgure, a space is being developed between the appendix and its mesentery. The relationship of the appendix to the cecum must be maintained to avoid cecal injury.

injury was small, the patient may have a simple abscess that can be treated with intravenous antibiotics and percutaneous drainage. The patient can also arrive with peritonitis and develop sepsis or further complications. Grade 3/4 complication ● Repair Nearly all enterotomies can be closed primarily, even without mechanical bowel preparation. An identiﬁed injury should be carefully inspected for evidence of devitalized tissue or potential narrowing after repair. Also, routine inspection of the cecum and the appendiceal stump should be done upon removal of the appendix to search for possible bowel injury, because this is a much more devastating problem if missed. If the surgeon has a high degree of suspicion of an injury that cannot be clearly identiﬁed laparoscopically, she or he should not hesitate to convert to an open procedure. An enterotomy can easily be repaired laparscopically if the surgeon is familiar with intracorporeal suturing techniques. Otherwise, an RLQ or lower midline incision will be required to repair the colon injury. Primary repair with a two-layer closure is typically adequate. Drain placement can be avoided unless peritoneal contamination is signiﬁcant. ● Prevention The operating surgeon should always maintain careful dissection when mobilizing the cecum and appendix. The relationship of the appendix and cecum should be determined to help identify the angle to approach the space posterior to the appendix. This is especially important when creating a space between the appendix and its mesentery (Fig. 27–6). The tip of the instrument should be clearly visualized while developing this plane (Fig. 27–7). Also, minimal use of cautery is advocated during dissection to avoid indirect thermal injury to the intestine.

Figure 27–7 Completion of the dissection. An instrument has been passed between the appendix and the mesoappendix. Adequate space has been developed to allow passage of a stapling device.

Ureteral Injury ● Consequence Contamination of the abdominal cavity. Iatrogenic ureteral injury is an uncommon yet signiﬁcant injury during LA. These injuries are often not identiﬁed at the time of surgery and are diagnosed postoperatively. Delayed presentation of this injury will often bring the patient into the emergency department with abdominal pain, leukocytosis, and fever. A CT scan will demonstrate free ﬂuid in the abdomen with or without hydronephrosis. If the injury results in occlusion of the ureter, a delay in diagnosis may result in renal parenchymal damage. Grade 2/3 complication ● Repair The type of injury dictates the method of repair. Immediate identiﬁcation of the injury with prompt primary repair results in the best long-term outcome. A monoﬁlament suture should be used to close the defect or perform an ureteroureterostomy in the case of complete transection. With late presentation, the injured ureter may not be viable and requires resection to healthy tissue. Primary repair is used for an injury in the proximal two thirds and bladder reimplantation for injuries in the distal one third. In the case of signiﬁcant loss of length, anastomosis to the contralateral ureter may be necessary. Stenting of the injured area will assist in decreasing the rate of postoperative stricture. ● Prevention The ureter is most at risk during the dissection of the appendix and cecum. This risk is increased with a retrocecal appendix or in the presence of severe inﬂammation. The operating surgeon should be aware of the possible location of the ureter during the mobilization of the cecum (see Fig. 27–5). Maintaining careful dis-

27 LAPAROSCOPIC APPENDECTOMY

303

section within the avascular plane will allow for careful identiﬁcation of structures and avoidance of this injury.

Division of the Mesentery Mesenteric Bleeding ● Consequence Postoperative bleeding requiring reoperation or development of infected hematoma. Tearing of the mesoappendix can result in bleeding from the appendiceal artery or its branches. Whereas this can appear to be a signiﬁcant problem initially, clinically signiﬁcant postoperative hematomas occur in less than 1% of patients after LA.15 Despite these data, careful hemostasis should always be maintained. Grade 1–3 complication ● Repair The majority of intraoperative bleeding from the mesentery will be controlled with direct pressure using a blunt grasper. When approaching hemorrhage in this area, ﬁrst start with a clear operative ﬁeld. Irrigate the area to help precisely identify the area of the mesoappendix that is bleeding. If the mesentery remains of adequate length, an endoloop may be placed around the entire mesoappendix. Otherwise, cautery can be used to coagulate small bleeders from the staple line. The surgeon must be careful to identify the proximity of the terminal ileum and the cecum before trying to control bleeding using thermal energy. Suture ligation may be performed to control hemorrhage if the previous steps fail. ● Prevention No study has demonstrated a comparative advantage regarding division of the mesoappendix. The primary step to prevent bleeding from the mesentery is to conﬁrm that the stapler, endoloop, and other instruments are completely around the mesoappendix (Figs. 27–8 and 27–9). When using a stapling device, the surgeon should make sure to use a staple load appropriate for the thickness of the tissue. The staple lines of both the mesentery and the appendix should be evaluated for bleeding or intestinal injury (Fig. 27–10).

Figure 27–8 Division of the mesoappendix. A stapler has been placed completely around the mesoappendix. The tip of the stapler should be visualized beyond the mesentery to ensure complete division.

Figure 27–9 Division of the appendix. When placing the stapler on the appendix, the tips must be visualized as well as conﬁrming the cecum is not entrapped by the device.

Resection of the Appendix Appendiceal Stump Leak ● Consequence Tearing of the appendix at its base or avulsion of the appendix from the cecum. In the presence of a perforated appendix or severe inﬂammation, the appendix can become extremely friable. Upon delayed presentation, the appendix may perforate near its base and not allow adequate space to safely secure the base. This complication can lead to intra-abdominal contamination, increasing the risk of a postoperative abscess or wound complication. Grade 2 complication

Figure 27–10 Evaluation of the staple lines. The staple lines should always be inspected to conﬁrm that there is no bleeding and no injury to the surrounding tissue.

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SECTION III: GASTROINTESTINAL SURGERY easily tear, leaving inadequate tissue for ligation of the stump.

Stump Appendicitis

Figure 27–11 Difﬁcult appendiceal stump. Here the appendiceal stump is completely involved with carcinoid tumor.

● Consequence Abscess or abdominal contamination. Stump appendicitis is an uncommon complication after appendectomy.17 The greatest obstacle in dealing with this problem is the diagnostic challenge it creates. RLQ pain in a patient with a previous appendectomy can create confusion for the evaluating physician and commonly results in a delay in treatment. Owing to the previous resection, diagnostic imaging is not beneﬁcial. The most common presentation will appear very late in the course of appendicitis, with the diagnosis delayed until the patient develops an abscess or peritonitis.18 Grade 2 complication ● Repair Management of stump appendicitis can be performed by partial cecectomy. However, if the patient has a delayed presentation, the resultant inﬂammation and contamination may require an ileocecectomy. ● Prevention The resection of the appendix should leave a stump approximately 1 cm in length. A stump longer than this will be at risk for recurrent appendicitis.

Postoperative Abscess

Figure 27–12 Partial cecectomy. The laparoscopic stapler has been placed below the lesion (T) and across the end of the cecum. The insertion of the terminal ileum (TI) into the right colon (RC) must be carefully identiﬁed.

● Repair Management of the complicated appendiceal stump varies depending on the severity of the injury. Several techniques can be used to control the appendix base.16 If the base is easily visualized, a laparoscopic stapler can be used to perform a partial cecectomy with resection of the appendiceal stump. A similar technique can be used in the presence of a tumor in the appendix (Fig. 27–11). Again, the relationship to the terminal ileum must be identiﬁed so as not to inadvertently injure or narrow the intestinal lumen (Fig. 27–12). ● Prevention Often, the difﬁcult appendiceal stump is due to perforation or severe inﬂammation of the appendix and unavoidable. During the mobilization of the appendix, the surgeon must be careful not to place too much tension on the appendix. The tissue can be extremely friable in advanced or perforated appendicitis and can

● Consequence Abdominal pain, fever, and possibly, sepsis. This complication occurs in approximately 8% to 25% of patients after appendectomy and is increased in the presence of perforation.19 These patients will most often present to the emergency department with pain, fever, and leukocytosis between 3 and 7 days after an appendectomy. If not treated promptly, the abscess can develop into a ﬁstula or generalized sepsis. Grade 2 complication ● Repair CT- or ultrasound-guided drainage and antibiotics will resolve the abscess in the majority of patients with this complication. If percutaneous drainage fails, the patient can be explored laparoscopically for drainage of the abscess. In this situation, the surgeon should carefully evaluate the cecum and terminal ileum for a possible missed bowel injury or stump leak. A high index of suspicion and early CT scan in patients who have an atypical postoperative course will allow for prompt identiﬁcation and treatment of an intraperitoneal abscess. ● Prevention Avoidance of intra-abdominal contamination is the primary method of postoperative abscess prevention.

27 LAPAROSCOPIC APPENDECTOMY Controversy exists whether preoperative antibiotics, or prolonged intravenous antibiotics in the case of perforation, will decrease the incidence of abscess formation.

REFERENCES 1. Lally KP, Cox CS Jr, Andrassy RJ. The appendix. In Townsend CM Jr, Beauchamp RD, Evers BM, Mattu KL (eds): Sabiston Textbook of Surgery, 16th ed. Philadelphia: WB Saunders, 2001; p 920. 2. Zielke A, Hasse C, Sitter H, Rothmund M. Inﬂuence of ultrasound on clinical decision making in acute appendicitis: a prospective study. Eur J Surg 1998;164:201–209. 3. Raman SS, Lu DS, Kadell BM, et al. Accuracy of nonfocused helical CT for the diagnosis of acute appendicitis: a 5-year review. AJR Am J Roentgenol 2002;178:1319– 1325. 4. Lee SL, Walsh AJ, Ho HS. Computed tomography and ultrasonography do not improve and may delay the diagnosis and treatment of acute appendicitis. Arch Surg 2001;136:556–562. 5. Onders RP, Mittendorf EA. Utility of laparoscopy in chronic abdominal pain. Surgery 2003;134:549–552. 6. Nguyen NT, Zainabadi KM, Mavandadi SA, et al. Trends in utilization and outcomes of laparoscopic versus open appendectomy. Am J Surg 2004;188:813–820. 7. Ortega AE, Hunter JG, Peters JH, et al. A prospective, randomized comparison of laparoscopic appendectomy with open appendectomy. Am J Surg 1995;189:208–212. 8. Carbonell AM, Burns JM, Lincourt AE, Harold KL. Outcomes of laparoscopic versus open appendectomy. Am Surg 2004;70:759–765.

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9. Ball CG, Kortbeek JB, Kirkpatrick AW, Mitchell P. Laparoscopic appendectomy for complicated appendicitis: an evaluation of postoperative factors. Surg Endosc 2004; 18:969–973. 10. Schirmer BD, Schmieg RE Jr, Dix J, et al. Laparoscopic versus traditional appendectomy for suspected appendicitis. Am J Surg 1993;165:670–675. 11. Armenakas NA, Pareek G, Fracchia JA. Iatrogenic bladder perforations: long-term follow-up. J Am Coll Surg 2004; 198:78–82. 12. Busuttil RW, Davidson RK, Fine M, Topkins RK. Effect of prophylactic antibiotics in acute nonperforated appendicitis: a prospective, randomized, double-blind clinical study. Ann Surg 1981;194:502–509. 13. Lin HF, Wu JM, Tseng LM, et al. Laparoscopic versus open appendectomy for perforated appendicitis. J Gastrointest Surg 2006;10:906–910. 14. Thomson SR, Fraser M, Stupp C, Baker LW. Iatrogenic and accidental colon injuries—what to do? Dis Colon Rectum 1994;37:496–502. 15. Vo N, Hall FM. Severe post appendectomy bleeding. Am Surg 1983;49:560–562. 16. Poole GV. Management of the difﬁcult appendiceal stump: how I do it. Am Surg 1993;59:624–625. 17. Liang MK, Lo HG, Marks JL. Stump appendicitis: a comprehensive review of the literature. Am Surg 2006;72: 162–166. 18. van den Broek WT, Bijnen AB, de Ruiter P, Gouma DJ. A normal appendix found during diagnostic laparoscopy should not be removed. Br J Surg 2001;88:251– 254. 19. Piskun G, Kozik D, Rajpal S, et al. Comparison of laparoscopic, open, and converted appendectomy for perforated appendicitis. Surg Endosc 2001;15:660–662.

28

Hemorrhoidectomy Eugene F. Foley, MD INTRODUCTION

OPERATIVE STEPS

Although many nonresective procedures have been described for the treatment of hemorrhoidal disease over the years, surgical hemorrhoidectomy continues to maintain an important role in the therapy of hemorrhoids and may be one of the most common anorectal operations performed by the general surgeon. Because surgical hemorrhoidectomy has been done for many decades, ample evidence indicates that this procedure can be done safely, with a low complication rate and with a high degree of effectiveness in the reduction of hemorrhoidal symptoms.1 Despite this efﬁcacy, surgical hemorrhoidectomy has well-described, speciﬁc complications, and their existence and the steps in their prevention should be well understood by the surgeon embarking upon these cases. In addition, the substantial postoperative pain associated with surgical hemorrhoidectomy is well recognized.2 In an attempt to reduce this morbidity, a new technique, stapled hemorrhoidectomy (also referred to as procedure for prolapse and hemorrhoids [PPH]), has been introduced. This chapter describes both the traditional closed Ferguson excisional hemorrhoidectomy3 and the stapled hemorrhoidectomy, with emphasis on the operative steps and the avoidance of the speciﬁc technical complications associated with each.

Step Step Step Step Step Step Step

Traditional Hemorrhoidectomy

● Repair Urinary retention after hemorrhoidectomy is treated by temporary urinary drainage with a Foley catheter, typically over a 48-hour period. The need for formal urologic evaluation is rare, except in patients with substantial urologic difﬁculties that were present preoperatively. Conservative measures, including voiding while submerged in a tub of warm water, may avoid the need for catheterization.

INDICATIONS ● Hemorrhoidal symptoms not amenable to conservative

bowel manipulation ● Internal hemorrhoids larger than grade 2, not amen-

able to ofﬁce procedures such as banding hemorrhoids with a large external component

● Symptomatic

1 2 3 4 5 6 7

Prone positioning/anesthetic considerations Anoscopy and operative planning Ligation of the pedicle Excision of the hemorrhoidal complex Religation of the pedicle and incision closure Attention to other quadrants Application of local anesthesia

OPERATIVE PROCEDURE Anesthetic Considerations Urinary Retention Urinary retention, due to overdistention of the bladder during surgery or postoperative levator spasm from incisional pain, is one of the most common complications of anorectal surgery, including hemorrhoidectomy. Large series have reported this complication as frequently as 25% to 35%.4 ● Consequence Urinary retention after anorectal surgery can substantially increase the morbidity of hemorrhoidectomy by delaying the discharge of patients after this day-surgery procedure or by requiring emergent reevaluation of the patient later in the day. The need for urinary drainage may also increase the potential for urinary tract infection. Grade 1/2 complication

● Prevention Steps taken to avoid acute overdistention of the bladder, including the use of a heparin lock rather than con-

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tinuous intravenous ﬂuid administration and preoperative voiding, have been shown to decrease the incidence of urinary retention after hemorrhoidectomy.5–7 Adequate administration of local anesthetics (bupivacaine [Marcaine]) may also reduce early postoperative levator spasm, leading to less urinary retention after surgery.

Anoscopy and Operative Planning Inappropriate Hemorrhoidal Excision Prior to excision, a full operative plan needs to be established by careful anoscopy. Typically, either two or three hemorrhoidal complexes are excised. Even most “circumferential” hemorrhoids can be grouped for excision into the common hemorrhoidal quadrants: left lateral, right posterior, and right anterior. ● Consequences Failure to fully plan the excisions at the start of the operation will lead either to inadequate excision and persistent symptoms or to overaggressive resection and subsequent anal stenosis. Grade 1/2/3 complication

Figure 28–1 Ligation of the hemorrhoidal pedicle, including the mucosa, submucosa, and hemorrhoidal plexus.

● Repair If an inadequate resection is initially made, additional resection can be done at the end of the case. Anal stenosis and its treatment are discussed later. ● Prevention Careful preexcision planning is mandatory to obtain an adequate and appropriate hemorrhoid resection.

Ligation of the Pedicle Hemorrhage ● Consequences Failure to adequately ligate the plexus can result in signiﬁcant postoperative bleeding from the pedicle, which can require reoperation to control. The rate of this complication should be less than 1%,8 but it represents one of the most serious complications of hemorrhoidectomy. Grade 2/3 complication ● Repair Pedicle bleeding recognized at the time of initial surgery can be simply religated. Identiﬁcation and resuturing of the pedicle may be facilitated by leaving the pedicle suture long and in place while the excision and incisional closure are completed. Once the excisions are all completed and the incisions closed, the pedicles can all be examined carefully for persistent bleeding. Signiﬁcant hemorrhage in the early postoperative period requires reexploration and ligation. ● Prevention Deeply ligating the pedicle well within the rectal vault, including the mucosa and submucosa and encircling

Figure 28–2 The pedicle suture secured well within the rectal vault, high above the dentate line.

the entire hemorrhoidal plexus, will minimize the incidence of postoperative bleeding (Fig. 28–1).

Anal Stenosis Placing the pedicle sutures too low, within the narrow anal canal rather than the capacious distal rectum, may lead to an increase in the likelihood of postoperative anal stenosis (Fig. 28–2). The consequences and repair of this complication are discussed later.

Excision of the Hemorrhoidal Pedicle Sphincter Injury Once ligated in the distal rectum, the hemorrhoidal plexus and its overlying epithelium are sharply excised starting peripherally on the perianal skin. A plane is developed between the hemorrhoid and the underlying sphincter complex, which should be easily identiﬁed (Fig. 28–3).

28 HEMORRHOIDECTOMY

309

Figure 28–3 The sphincter complex underlying the hemorrhoidal plexus.

Figure 28–4 A narrow epithelial excision, reducing the likelihood of postoperative anal stenosis.

● Consequence Inadequate visualization of the underlying sphincter complex can lead to sphincter injury and weakening. The incidence of this complication should be extremely low, less than 0.5%.9 Grade 2/3 complication

● Repair Persistent symptomatic anal stenosis after hemorrhoidectomy is an indication for anoplasty, often requiring the use of local skin ﬂaps to reconstruct and reepithelialize the resected anal canal mucosa. This procedure is typically done at a second stage.11,12 Primary repair when this complication is recognized at the initial operation could be accomplished by conversion to a Whitehead hemorrhoidectomy. When done correctly, this involves primary mobilization of the perianal skin circumferentially, reepithelializing the distal anal canal with perianal skin advanced to the native dentate line.

● Repair Although quite unusual, future sphincteroplasty to repair sphincter injury after surgical hemorrhoidectomy may be indicated.9 ● Prevention Careful identiﬁcation and preservation of the sphincter beneath the hemorrhoid should essentially eliminate the chance of signiﬁcant sphincter injury during hemorrhoidectomy.

Anal Stenosis Anal stenosis remains one of the most serious complications of hemorrhoidectomy. Poor planning or execution of a number of steps during the hemorrhoidectomy— including poor exposure, inadequate anesthesia, low ligation of the pedicles, and excessive excision—may contribute to this complication. ● Consequence The excision of excessive anal canal mucosa during the hemorrhoid excision is the most common factor leading to anal stenosis. This serious complication of hemorrhoidectomy occurs with a frequency of 2% to 4%.10 It is potentially a source of symptomatic distal gastrointestinal obstruction, which may carry substantial morbidity and, in its more severe forms, may require surgical correction. Grade 2/3 complication

● Prevention Prevention of anal stenosis requires substantial vigilance in maintaining adequate anal canal epithelium during excision. General or spinal anesthesia is critical to allow adequate visualization during the dissection, and prone positioning also facilitates the exposure. The extent of epithelial resection should be small, leaving narrow incisions that can be closed without stricture (Fig. 28–4). This is especially true with larger hemorrhoids or during emergency surgery for incarcerated hemorrhoids. Larger hemorrhoids can be excised by raising anal mucosal ﬂaps bilaterally and removing additional hemorrhoidal tissue while preserving overlying mucosa. Care should also be made to preserve some anal canal mucosa between resection lines. The placement of a large Hill-Ferguson anal retractor during the resection, and the ability to place this retractor at the end of the procedure, usually indicates that the anal canal will not be stenotic (Fig. 28–5).

Inadequate Hemorrhoidal Excision ● Consequences Inadequate excision of the hemorrhoidal plexus will lead to persistent symptoms of hemorrhoidal disease,

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Religation of the Pedicle and Incisional Closure Postoperative Hemorrhage Religation of the pedicle is another important step in reducing the incidence of postoperative bleeding, as discussed earlier. Whitehead Deformity

Figure 28–5 A large Hill-Ferguson anal retractor in the anal canal at completion of the surgery, indicating adequate preservation of the anoderm.

● Consequence During the incisional closure, care is taken to align the incision edges, re-creating the dentate line, and realigning rectal mucosa, anal mucosa, and perianal skin. Failure to do so may result in a Whitehead deformity, which is created by malalignment of these layers, suturing rectal mucosa to the perianal skin, resulting in chronic anal drainage from externalized mucosa.14 Grade 1/2 complication ● Repair The formation of a symptomatic Whitehead deformity requires a second operation for repair in the form of an anoplasty to re-create the dentate line and internalize all mucosa.14 ● Prevention Care taken in full religation of the pedicle and judicious realignment of the mucosal levels will reduce the likelihood of these complications.

Figure 28–6 A completed hemorrhoidectomy, with incisions extending well out onto the perianal skin, fully resecting all external tags and preventing a dog ear at the external end of the incision.

including prolapsing tissue, bleeding, and excessive perianal skin tags. A properly done hemorrhoidectomy should lead to an acceptable resolution of hemorrhoidal symptoms in 90% of patients.13 Grade 1/2 complication ● Repair Persistent symptoms after hemorrhoidectomy may require additional hemorrhoid surgery, an incidence that should be less than 5% to 10%.13 ● Prevention Adequate excision of the hemorrhoids needs to be evaluated at the time of the initial surgery. Persistent perianal skin tags may be prevented by starting the excision out at the periphery on the perianal skin, fully excising the entire external component, and reducing the possibility of a persistent perianal skin dog ear (Fig. 28–6).

Stapled Hemorrhoidectomy (Procedure for Prolapse and Hemorrhoids) INDICATIONS ● Symptomatic hemorrhoids refractory to conservative therapy, with a predominance of internal component

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5 Step 6

Anesthetic considerations and positioning Placement of operating anoscope and obturator Pursestring placement Introduction of stapling device and securing of pursestring Closure and ﬁring of stapling device Removal and inspection of staple line and excised tissue

28 HEMORRHOIDECTOMY

Figure 28–7 The pursestring suture being placed during a procedure for prolapse and hemorrhoids (PPH).

OPERATIVE PROCEDURE Anesthetic and Positioning Considerations Prone positioning, general or spinal anesthesia, and judicious ﬂuid management are highly recommended for stapled hemorrhoidectomy, for the same reasons outlined for excisional hemorrhoidectomy.

Placement of the Anoscope, Obturator, and Pursestring Suture The operating anoscope and obturator are placed well into the distal rectum to allow an adequately high placement of the pursestring suture. A 2-0 Prolene pursestring suture is then placed at a level well within the rectal vault and deep enough to include the mucosal and submucosal layers. Care is taken to leave only small gaps between the bites and to try to keep the pursestring at a uniform distance from the dentate line circumferentially (Figs. 28–7 and 28–8).

Inadequate Excision ● Consequence Large gaps between the pursestring bites or uneven levels of the pursestring in relation to the dentate line will increase the chances of an incomplete circumferential resection. This difﬁculty will lead to a greater chance of persistent hemorrhoidal symptoms or bleeding.15 Grade 2/3 complication ● Repair Incomplete hemorrhoidal resection can be corrected after stapling by excising remaining hemorrhoid in a fashion analogous to the open technique. ● Prevention Placement of the pursestring with small travel between the bites (total of six to eight bites), with care taken to

311

Figure 28–8 The completed pursestring suture placed during a PPH procedure, well above the dentate line.

keep the bites at the same level in the rectum, will minimize the incidence of an incomplete doughnut and the resulting incomplete resection of a quadrant.

Rectovaginal Fistula An inappropriately deep pursestring suture may also increase the possibility of a surgically created rectovaginal or rectourethral ﬁstula when the stapler is ﬁred. This complication is discussed later. Postoperative Pain and Stricture If the pursestring suture is placed too low in the distal rectum or anal canal, the excision may take place in the sensate portion of the anal canal, leading to unexpected postoperative pain. Furthermore, low excision within the anal canal may lead to postoperative stricture. Both of these potential complications are discussed later.

Introduction of the Stapler and Securing the Pursestring Inadequate Excision ● Consequences Securing the pursestring suture through the stapler once it is introduced is also critical to ensure adequate hemorrhoidal excision. The stapler is introduced into the rectum and the pursestring suture is secured around the stem of the stapler. Once tied around the shaft, the ends of the pursestring are then brought out through the pursestring guides on the side of the stapler and tied loosely together. Inadequate tightening of the pursestring around the shaft of the stapler may lead to an incomplete circumferential resection, causing persistent symptoms from remaining hemorrhoids. Grade 2 complication

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● Repair Repair of an incomplete resection is treated by an open excision of the remaining hemorrhoid, as noted previously. ● Prevention Care when securing the pursestring around the shaft, and upward traction on the loop of the pursestring when the stapler is closed, will help prevent this complication.

Closing and Firing the Stapler Rectovaginal Fistula ● Consequences A surgically created rectovaginal ﬁstula (or, analogously, a rectourethral ﬁstula in men) can occur if the pursestring bites are too deep anteriorly, causing full-thickness rectal wall excision when the stapler is ﬁred. This is a disastrous complication of stapled hemorrhoidectomy, which should be entirely avoidable by adequate technique. It has, however, been reported.16 Grade 3/4 complication ● Repair Primary surgical repair of the rectovaginal ﬁstula should be performed if this complication is noted at the time of surgery. This could be accomplished by a direct, layered repair of the vagina, rectovaginal septum, and rectal wall. Recognition of this complication postoperatively would require a delayed repair. ● Prevention Care needs to be taken to place the pursestring sutures, especially anteriorly in women, only deep enough to include the mucosa, submucosa, and hemorrhoidal plexus. Prior to ﬁring the stapler, the posterior vaginal wall should always be palpated to ensure it is not included in the staple line.

Figure 28–9 The PPH stapler in fully closed position, sitting well within the rectum and anus, with only the 3- and 4-cm marks visible, indicating an acceptably proximal position.

● Repair There is no speciﬁc initial repair of this problem once the excision has occurred, and therapy is directed to analgesic care. Symptomatic anal stenosis diagnosed in the postoperative period would be treated by elective anoplasty. ● Prevention Careful placement of the pursestring suture well into the rectal vault, above the dentate line, will minimize the likelihood of this complication. This adequate positioning is conﬁrmed after the stapler is inserted and closed. Prior to closure, only the 3- or 4-cm mark should be visible at the anal verge. If the 1- or 2-cm marks are visible, the stapler is too low in the anal canal and should be repositioned (Fig. 28–9).

Removal of the Stapler and Inspection of the Excision

Excessive Postoperative Pain and Stricture

Incomplete Excision

● Consequence If the pursestring suture is placed too low in the rectum or anal canal or the stapler is positioned within the anal canal, the excision will occur in an area of sensation for the patient, near or below the dentate line. This will result in unexpectedly high amounts of postoperative pain, negating the reported advantages of decreased postoperative pain associated with the stapling technique over the traditional surgical hemorrhoidectomy. Furthermore, this may also lead to anal stenosis, owing to the presence of the staple line in the narrowest part of the anorectum, the anal canal. Grade 2/3 complication

● Consequences Once ﬁred, the stapler should be loosened and removed. The stapler should have two complete tissue doughnuts, analogous to the appropriately completed low anterior stapled anastomosis. Incomplete doughnuts may suggest an incomplete excision, leading to persistent symptoms from the unexcised quadrant17 (Fig. 28–10). Grade 1/2 complication ● Repair If the incomplete excision is identiﬁed, that quadrant may be simply excised by the open technique.

28 HEMORRHOIDECTOMY

313

REFERENCES

Figure 28–10 Complete tissue doughnuts after PPH.

● Prevention As noted above, multiple (six to eight) bites placed close together in the pursestring will help reduce this problem. Careful inspection of the tissue excised and the staple line will allow easy repair if it has occurred.

Postoperative Hemorrhage ● Consequence Staple line bleeding can occur, and failure to recognize it at this point of the operation may result in the need for reexploration in the early postoperative period. Staple line bleeding will be more likely in patients with incomplete tissue doughnuts. Grade 2/3 complication ● Repair Identiﬁcation of suture line bleeding at the time of operation can be easily controlled by resuture ligation. Substantial bleeding in the early postoperative period requires reexploration. ● Prevention Careful staple line and tissue doughnut inspection will prevent the morbidity of reoperation for early postoperative bleeding.

1. Shanmugam V, Campbell K, Louden M, et al. Rubber band ligation versus excisional haemorrhoidectomy for haemorrhoids. Cochrane Database of Systemic Review 2005;3:CD005034. 2. Shanmugan V, Thaha MA, Rabindranath KS, et al. Systemic review of randomized trials comparing rubber band ligation with excisional haemorrhoidectomy. Br J Surg 2005;92:1481–1487. 3. Senagore AJ. Surgical management of hemorrhoids. J Gastrointest Surg 2002;6:295–298. 4. Zaheer S, Reilly WT, Pemberton JH, Ilstrup D. Urinary retention after operations for benign anorectal diseases. Dis Colon Rectum 1998;41:696–704. 5. Bailey HR, Ferguson JA. Prevention of urinary retention by ﬂuid restriction following anorectal operations. Dis Colon Rectum 1976;19:250–252. 6. Hoff SD, Bailey HR, Butts DR, et al. Ambulatory surgical hemorrhiodectomy—a solution to postoperative urinary retention? Dis Colon Rectum 1994;37:1242–1244. 7. Lau H, Lam B. Management of postoperative urinary retention: a randomized trial of in-out vs. overnight catheterization. Aust N Z J Surg 2004;74:658–661. 8. Goldberg SM. Hemorrhoids. In Goldberg SM, Gordon PH, Nivatvong S (eds): Essentials of Anorectal Surgery. Philadelphia: Lippincott, 1980; pp 42–72. 9. Johannsen HO, Graf W, Pahlman L. Long-term results of haemorrhoidectomy. Eur J Surg 2002;168:485–489. 10. Gearhart SL. Symptomatic hemorrhoids. Adv Surg 2004; 38:167–182. 11. Eu KW, Teoh TA, Seow-Choen F, Goh HS. Anal stricture following haemorrhoidectomy: early diagnosis and treatment. Aust N Z J Surg 1995;65:101–103. 12. Neeklakandan B. Double Y-V plasty for post surgical anal stricture. Br J Surg 1996;83:1599. 13. Mazier WP. Hemorrhoids, ﬁssures, and pruritis ani. Surg Clin North Am 1994;74:1277–1292. 14. Ferguson JA. Whitehead deformity of the anus, S-plasty repair. Dis Colon Rectum 1979;22:286–287. 15. Nisar PJ, Acheson AG, Neal KR, Scholeﬁeld JH. Stapled hemorrhoidopexy compared with conventional hemorrhoidectomy: a systematic review of randomized, controlled trials. Dis Colon Rectum 2004;47:1837–1845. 16. McDonald PJ, Bona R, Cohen CR. Rectovaginal ﬁstula after stapled hemorrhoidopexy. Colorectal Dis 2004;6:64– 65. 17. Brusciano L, Ayabaca SM, Pescatori M, et al. Reinterventions after complicated or failed stapled hemorrhoidopexy. Dis Colon Rectum 2004;47:1846–1851.

29

Anal Fistulotomy Eugene F. Foley, MD INTRODUCTION The surgical treatment of perianal ﬁstulous disease is one of the most common, minor, benign anorectal procedures performed by the general surgeon. Despite its frequency and “size,” the appropriate balance between resolution of the troubling symptoms of persistent ﬁstulas and the potential for devastating functional consequences with overly aggressive surgical treatment of ﬁstulas can be very challenging. The major elements of successful anal ﬁstulotomy surgery are described later, with emphasis on the reduction of speciﬁc complications.

INDICATIONS Although not all surgically drained perianal or perirectal abscesses will result in a chronic ﬁstula-in-ano, it is estimated that as many as 50% will.1 The symptoms of a persistent ﬁstula include recurrent abscess formation, chronic perianal drainage, and pain. The diagnosis of a persistent ﬁstula-in-ano in most patients is an indication for consideration of ﬁstulotomy to reduce or eliminate these chronic symptoms and the frequency of recurrent abscess formation. Notable exceptions would include patients with complex ﬁstulas due to Crohn’s disease, perineal radiation, or uncontrolled distal gastrointestinal tract or gynecologic malignancy.

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4

Anesthetic considerations Examination and identiﬁcation of internal opening Assessment of sphincter complex in relation to ﬁstula track Incision of ﬁstula

OPERATIVE PROCEDURE Anesthetic Considerations Urinary Retention Urinary retention is one of the most common complications of all anorectal surgery. The extent and complexity

of surgery correlates with the incidence of this complication. A large institutional study has reported the incidence of urinary retention after ﬁstula surgery as 5%.2 ● Consequences Postoperative urinary retention may lead to the need for urinary catheterization, delaying the discharge of patients after this day-surgery procedure. It may also require emergent reevaluation of the patient later in the day after surgery. Grade 1/2 complication ● Repair Urinary retention after anorectal surgery is treated by temporary urinary catheterization, usually over a 24to 48-hour period. Conservative measures, including voiding while submerged in a tub of warm water, may avoid the need for catheterization. Formal urologic evaluation is reserved for the minority of patients who fail these measures, usually those with preoperative urologic difﬁculties. ● Prevention Judicious use of perioperative intravenous ﬂuid has been shown to decrease this complication after hemorrhoidectomy.3,4 Although not conclusively shown in the literature to reduce this rate after ﬁstula surgery, analogous recommendations of limiting overdistention of the bladder with excessive intravenous ﬂuid and the liberal use of local anesthetic (bupivacaine [Marcaine]) to decrease postoperative levator spasm seem reasonable.

Examination under Anesthesia and Identiﬁcation of the Internal Opening Failure to Identify the Internal Opening Finding the internal opening of the ﬁstula-in-ano is the ﬁrst of two critical steps in the successful surgical treatment of a ﬁstula. Benign ﬁstulas are the result of cryptglandular infection at the dentate line and are perpetuated by a persistent internal opening at the inciting gland at the dentate line.

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● Consequence Failure to identify the internal opening of the ﬁstulain-ano will result in failure of the surgery to correct the problem, resulting in persistent symptoms of recurrent abscess formation or perianal drainage. Fistula surgery should be successful in 85% to 90% of cases.5 Grade 2/3 complication ● Repair If the internal opening is not found, the external opening and track should be opened and débrided, to improve drainage. Attempts at blindly cutting or forcing the ﬁstula probe through the dentate line without seeing an internal opening are unlikely to resolve the ﬁstula and more likely to damage the underlying sphincter complex. If the internal opening is not identiﬁed or opened, recurrent symptoms will likely mandate another operative exploration at a later date. ● Prevention Several things may be done to facilitate identifying the internal opening. It is important to be familiar with Goodsall’s rule, which describes the usual locations of the internal opening of the ﬁstula based on the location of the external opening. Goodsall’s rule suggests that if the external opening is within 3 cm of the anal verge, an external opening posterior to the midsagittal line will generally course to a posterior midline internal opening, whereas an anteriorly based external opening will course radially on a straight line to its internal opening (Fig. 29–1). Knowledge of this rule will help immensely in concentrating one’s search for the internal opening in the most likely location. With Goodsall’s rule in mind, most internal openings can be found by simply passing a ﬁstula probe through the external opening along the track and out the internal opening (Fig. 29–2). If this proves difﬁcult, many surgeons also inject the external opening with a liquid substance such as methylene blue or milk to help identify the internal opening. Dilute hydrogen peroxide serves well in this role, because it is easily seen on anoscopy and can be repeated several times without staining the tissues the way methylene blue does6 (Fig. 29–3).

Assessment of the Sphincter Complex in Relationship to the Fistula Track

Figure 29–1 Goodsall’s rule predicting the location of the internal opening of a ﬁstula-in-ano based on the location of the external opening.

Figure 29–2 A ﬁstula probe passed through the external opening, coursing the ﬁstula, and entering the anal canal through the internal opening at the dentate line.

Weakening of the Anal Sphincter and Incontinence Once the internal opening is identiﬁed and the ﬁstula probe is passed through the track, a careful assessment of the amount of sphincter that will be cut with a ﬁstulotomy is made. This is the second key step in successful ﬁstulotomy.

these complications of ﬁstula surgery varies depending on the study and degree of disability reported. Some reports suggest the frequency of “minor” continence alterations to be as high as 30% to 50%.5,7,8 Major incontinence after ﬁstula surgery should be lower than 10%.5,7,8 Grade 3 complication

● Consequence Proceeding with a ﬁstulotomy in the presence of a high or deep ﬁstula may result in temporary or permanent sphincter weakness and incontinence. The frequency of

● Repair Permanent, disabling incontinence after ﬁstula surgery may be repaired by anal sphincteroplasty at an elective, secondary surgery.9

29 ANAL FISTULOTOMY

Figure 29–3 Hydrogen peroxide bubbling through the internal opening of a ﬁstula-in-ano after injection at the external opening.

● Prevention Prevention of inadvertent sphincter injury causing incontinence is an essential element of ﬁstula surgery, and perhaps the most difﬁcult to assess without signiﬁcant experience. It should be noted that many ﬁstulas require some sphincter division and that many transsphincteric ﬁstulas can be safely treated by ﬁstulotomy. Furthermore, many factors contribute to “how much muscle can be safely cut,” including preoperative sphincter function, patient age, sex, and ﬁstula location. Much less muscle can be safely cut in patients with some preoperative weakness, older patients, and women, particularly in anteriorly based ﬁstulas where there is typically a very thin amount of sphincter complex.10 In young, healthy men with a posteriorly based ﬁstula, a ﬁstulotomy can safely be performed as long as the puborectalis at the top of the sphincter complex is preserved. Recognition of the factors that make incontinence more likely and a conservative approach to patients with these factors will reduce the likelihood of this serious complication of ﬁstula surgery. Generally, with the ﬁstula probe through the track, the amount of muscle encompassed by the probe (which will be cut) and the amount of muscle deep to the probe (which will be left) are palpated (Fig. 29–4). A determination regarding the safety of the ﬁstulotomy is then made based on these ﬁndings, the location of the ﬁstula, and the preoperative factors listed previously. If a surgeon is concerned about the depth of the ﬁstula or the presence of risk factors for incontinence, a number of techniques have been described to surgically treat the high ﬁstula that do not involve cutting muscle.11 They include the use of a cutting seton, a Park ﬁstulectomy, the use of ﬁbrin glue, or a transanal sliding advancement ﬂap. Each of these techniques has proponents, although, in general, each is not typically as effective at resolving the

317

Figure 29–4 Identiﬁcation of the sphincter complex cut at the time of a transsphincteric ﬁstulotomy.

Figure 29–5 The remaining, intact puborectalis at the top of the sphincter left after a transsphincteric ﬁstulotomy.

ﬁstula as ﬁstulotomy and will be needed in only a minority of ﬁstula cases.

Cutting the Fistulotomy Once the internal opening is identiﬁed and the amount of muscle to be cut is deemed safe, the ﬁstulotomy is created, typically by electrocautery. Chronic granulation tissue is curetted from the track, and scar around the internal and external openings is débrided. The remaining intact sphincter is evaluated for adequacy (Fig. 29–5).

Persistent Fistula ● Consequences Inadequately opening and débriding the track may lead to an increased rate of a persistent ﬁstula. Overag-

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gressive muscle cutting leading to incontinence is discussed previously. Grade 2/3 complication ● Repair/Prevention The repair and prevention of persistent ﬁstulas or anal incontinence after ﬁstula surgery are discussed earlier.

REFERENCES 1. Vasilevsky CA, Gordon PH. The incidence of recurrent abscesses or ﬁstula-in-ano following anorectal suppuration. Dis Colon Rectum 1984;27:126–130. 2. Zaheer S, Reilly WT, Pemberton JH, Istrup D. Urinary retention after operations for benign anorectal diseases. Dis Colon Rectum 1998;41:696–704. 3. Bailey HR, Ferguson JA. Prevention of urinary retention after operations for benign anorectal diseases. Dis Colon Rectum 1976;19:250–252. 4. Hoff SD, Bailey HR, Butts DR, et al. Ambulatory surgical hemorrhoidectomy—a solution to postoperative urinary retention?. Dis Colon Rectum 1994;37:1242–1244.

5. Garcia-Aguilar J, Belmonte C, Wong WD, et al. Anal ﬁstula surgery—factors associated with recurrence and incontinence. Dis Colon Rectum 1996;39:723– 729. 6. The American Society of Colon and Rectal Surgeons. Practice parameters for treatment of ﬁstula-in-ano— supporting documentation. The Standards Practice Task Force. Dis Colon Rectum 1996;39:1363–1372. 7. Gustafsson UM, Graf W. Excision of anal ﬁstula with closure of the internal opening: functional and manometric results. Dis Colon Rectum 2002;45:1672–1678. 8. Cavanaugh M, Hyman N, Osler T. Fecal incontinence severity index after ﬁstulotomy. Dis Colon Rectum 2002;45:349–353. 9. Engel AF, Lunniss PJ, Kamm MA, Phillips RK. Sphincteroplasty for incontinence after surgery for idiopathic ﬁstula-in-ano. Int J Colorectal Dis 1997;12:323– 325. 10. Billingham RP, Isler JT, Kimmins MH, et al. The diagnosis and management of common anorectal disorders. Curr Probl Surg 2004;41:586–645. 11. Rickard MJ. Anal abscesses and ﬁstulas. Aust N Z J Surg 2005;75:64–72.

Section IV

HEPATOBILIARY SURGERY Lynt B. Johnson, MD Mistakes are a fact of life. It is the response to error that counts.—Nikki Giovanni

30

Gallbladder: Cholecystectomy (Laparoscopic vs. Open) Amy D. Lu, MD INTRODUCTION Although Langenbuch reported the ﬁrst cholecystectomy in 1882,1 it was not until 1905 that the ﬁrst complication of bile duct strictures was reported by Mayo. Since then, the numbers have continued to increase.2 Complications in the open technique have been as low as 0.2% with training and the standardization of surgical technique.3 Two techniques are used to perform a cholecystectomy. In the retrograde method, the hilar structure dissection occurs ﬁrst, followed by removal of the gallbladder. The antegrade or “fundus-down” approach separates the gallbladder from the liver before the duct and artery are ligated. The antegrade technique is generally considered safer because it allows for the progressive demonstration of the anatomy down to the infundibulocystic junction. With the improvement in the quality of ultrasound and the innovation of laparoscopic technique, more patients are being operated on, and laparoscopic cholecystectomy has become the standard of care for cholelithiasis. Open cholecystectomy is rarely performed anymore, usually when laparoscopy fails. In this case, the conversion is because of adhesions, bleeding, or anatomy. However, with the increasing number of laparoscopic cholecystectomies done, a parallel increase in complica-

tions has occurred.4,5 The most common complication and also potentially the most devastating for the patient are bile duct injuries. It has been reported that up to 40% of the surgeons performing laparoscopic cholecystectomies have caused a major bile duct injury and that the early recognition of the injury affects outcome.6,7 Evidence also suggests that outcome is improved if the injuries are managed by an experienced hepatobiliary surgeon.8 Patients treated by the injuring surgeon have an increased risk of death,9 yet between 50% and 75% of the complications are still repaired by the injuring surgeon.10–12 With the introduction of any innovative technique, there is a period of evaluation and learning for surgeons to develop the skill set required to perform the procedure. As the technique becomes broadly accepted and utilization increases, experience also increases and the learning process is foreshortened. This is the case for laparoscopic cholecystectomy. When the laparoscopic technique was ﬁrst introduced, only a few people were performing the procedure. As this innovation was found to be scientiﬁcally sound and beneﬁcial to the patient, more surgeons learned the technique and it became widely adopted in the surgical community. Now, laparoscopic cholecystectomy is routine in general surgical training; it is now being supervised and taught by experienced surgeons. The learning

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curve variable has greatly diminished from the equation. Because most bile duct injuries are perceived to be preventable, they are one of the most commonly litigated surgical procedures in the United States.13 The most common cause of bile duct injury is the misidentiﬁcation of the major duct for the cystic duct. Way and coworkers14 found the primary reason for the error to be a visual perceptual illusion and not related to technical skill. The argument follows then that most laparoscopic cholecystectomy injuries do not meet the criteria for medical negligence. Monetary remuneration occurs when a physician falls below the practice standard. Human error in laparoscopic cholecystectomies is not the result of purposeful substandard performance, but rather, a consequence of response to certain uncommon anatomic illusions.14 These mistakes may be inevitable in high-risk technologic settings.15 However, the further issue of diagnosis and management may ultimately affect litigation. Other complications may occur and may be related to the surgeon’s operative experience.16 These complications include injuries to the liver; less common are bowel and other vascular trauma.

Laparoscopic Cholecystectomy INDICATIONS ● ● ● ●

Biliary dyskinesia Cholelithiasis Cholecystitis with or without cholelithiasis Gallbladder polyps

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5 Step 6

Positioning and trocar placement Retraction of gallbladder Exposure, cholangiography, and ligation of cystic artery and duct Dissection of gallbladder Removal of gallbladder Trocar removal

OPERATIVE PROCEDURE Trocar Insertion Trocar Insertion Injuries Complications can be minimized by utilizing an open technique with a Hassan port to ﬁrst enter the abdomen for insufﬂation at the umbilicus. The standard umbilicus and epigastric ports are 10 to 12 mm in size, whereas two other ports are 5 mm each. Before starting a laparoscopic cholecystectomy, I usually mark the location for a subcos-

Traction applied to gallbladder in a superior direction only

Liver

Ill-defined biliary anatomy

CHD

Duodenum

Lateral view: CHD behind cystic duct

Figure 30–1 The gallbladder being retracted.

tal incision. After entering the abdomen, try to place the epigastric port along the subcostal line and enter the abdomen to the right lateral aspect of the falciform ligament. Next, the two remaining 5-mm ports should be placed laterally to retract the gallbladder superiorly (Fig. 30–1). The patient should be positioned in reverse Trendelenburg. Complications for trocar insertion are discussed in Section I, Chapter 7, Laparoscopic Surgery.

Exposure, Cholangiography, and Ligation of the Cystic Artery and Duct Injury to the Common Bile Duct ● Consequence Serious morbidity and mortality can result. Studies have shown the incidence of injury to be 0.1% to 0.5% after the use of the laparoscopic approach.4,5 Jaundice, biloma, biliary peritonitis, and sepsis can result earlier, with later presentations of recurrent cholangitis and secondary biliary cirrhosis. The level of the injury would determine its grade of complication. Many classiﬁcations have been used to attempt to delineate these injuries. Bismuth ﬁrst classiﬁed bile duct strictures based on the level of the stricture in relation to the hepatic ducts. In an analysis of 252 cases, Way and coworkers14 identiﬁed and classiﬁed four types of injuries (Fig. 30–2 and Table 30–1) based on the mechanism of the injury. Grade 2/3/4/5 complication ● Repair Unfortunately, most injuries are not recognized at the time of surgery. Therefore, biliary reconstruction in the form of a hepaticojejunostomy is usually required. If the injury is recognized at the time of surgery, conversion to an open approach should be done to address the injury. In some cases, a repair may be able to be performed over a T-tube stent when there is no loss or

30 GALLBLADDER: CHOLECYSTECTOMY (LAPAROSCOPIC VS. OPEN)

321

STEWART-WAY CLASSIFICATION LAPAROSCOPIC BILE DUCT INJURIES

Cystic duct

Class I

Class II

Right hepatic duct Rouviere’s sulcus

Class III

Class IV

Figure 30–2 Classiﬁcation of laparoscopic bile duct injuries. (From Way LW, Stewart L, Gantert W, et al. Causes and prevention of laparoscopic bile duct injuries. Ann Surg 2003;237:460–469, by permission of the Annals of Surgery.) Table 30–1 Mechanism of Injury Class I

CBD mistaken for cystic duct, but recognized Cholangiogram incision in cystic duct extended into CBD

Class II

Lateral damage to the CHD from cautery or clips placed on duct Associated bleeding, poor visibility

Class III

CBD mistaken for cystic duct, not recognized CBD, CHD, R, L hepatic ducts transected and/or resected

Class IV

RHD mistaken for cystic duct, RHA mistaken for cystic artery, RHD and RHA transected Lateral damage to the RHD from cautery or clips placed on duct

From Carroll BJ, Birth M, Phillips EH. Common bile duct injuries during laparoscopic cholecystectomy that result in litigation. Surg Endosc 1998;12:310–313, by permission of the Annals of Surgery.

damage of tissue and the repair will be tension free. If the viability of the tissue is in any doubt, the best approach would be to perform a Roux limb reconstruction. It is advisable in these repairs to temporarily stent the bile duct. ● Prevention Identiﬁcation of Rouviere’s sulcus and dissection ventral to this point ensures no unexpected anatomy and identiﬁcation of signiﬁcant structures before ligation (Fig. 30–3). Also, utilization of a 30° telescope, avoidance of diathermy near the common hepatic duct, dissection close to the gallbladder–cystic duct junction, and conversion to the open approach when uncertain all decrease the chance of injury. No dissection should occur in the hepatoduodenal ligament at the base of

Figure 30–3 Rouviere’s sulcus and the relationship of the right hepatic duct.

segment IV because the left hepatic duct lies extrahepatically within this tissue. It may be helpful to divide the cystic artery ﬁrst. This allows retraction of the infundibulum laterally to better expose the cystic duct junction with the bile duct. Early recognition of possible injury is also very important. When clipping the presumed cystic duct, if a large clip does not fully encompass the duct, one should reassess whether it is in fact the cystic duct. During dissection, if one encounters the presence of another ductal structure or extravascular structures, the common bile duct may have been inadvertently perceived as the cystic duct. Controversy exists as to whether intraoperative cholangiograms prevent bile duct injury.17,18 However, intraoperative cholangiogram will likely identify the injury at the time of surgery. Cholangiograms should be used whenever the anatomy is confusing or biliary anomaly is suspected (Box 30–1).

Injury to the Hepatic Artery ● Consequence Excessive bleeding may occur with uncontrolled transection of an aberrant right hepatic artery or hepatic ischemia with complete ligation and transection. Right hepatic artery injury is most commonly associated with injury to the right hepatic duct or with dissection under the mistakenly identiﬁed common bile duct for the cystic duct. If the patient has hepatic compromise (i.e., cirrhosis) or it is the main right hepatic artery, ligation may lead to ischemia, liver failure, biloma, and/or other biliary problems. Grade 2/3/4 complication

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Box 30–1 Rules of Thumb to Help Prevent Bile Duct Injuries Optimize Imaging ●

Use high-quality imaging equipment.

Initial Steps and Objectives ●

● ● ● ●

Before starting the dissection, use the triangle of Calot for orientation; ﬁnd the cystic duct starting at the triangle. Pull the gallbladder infundibulum laterally to open the triangle of Calot. Clear the medial wall of the gallbladder infundibulum. Make sure the cystic duct can be traced uninterrupted into the base of the gallbladder. Open any subtle tissue plane between the gallbladder and the presumed cystic duct; the real cystic duct may be hidden in there.

Figure 30–4 The cystic artery (arrow) above the cystic duct.

Factors that Suggest One May Be Dissecting the Common Duct Instead of the Cystic Duct ● ●

● ● ● ●

The duct when clipped is not fully encompassed by a standard M/L clip (9 mm). Any duct that can be traced without interruption to course behind the duodenum is probably the common bile duct. Another unexpected ductal structure is present. A large artery is behind the duct—the right hepatic artery runs posterior to the common bile duct. Extralymphatic and vascular structures are encountered in the dissection. The proximal hepatic ducts fail to opacify on operative cholangiograms.

Cystic artery

Obtain Operative Cholangiograms Liberally ● ● ●

Whenever the anatomy is confusing. When inﬂammation and adhesions result in a difﬁcult dissection. Whenever a biliary anomaly is suspected; assume that what appears to be anomalous anatomy is really normal and confusing until proved otherwise by cholangiograms.

Avoid Unintended Injury to Ductal Structures ● ●

●

●

Place clips only on structures that are fully mobilized; the tip of a closed clip should not contain tissue. The need for more than eight clips suggests the operation may be bloody enough to warrant conversion to an open procedure. Consideration of a need for blood transfusion suggests the operation should be converted to an open procedure. Open when inﬂammation or bleeding obscures the anatomy.

Illusions ●

Compelling anatomic illusions to which everyone is susceptible are the primary cause of bile duct injuries. Experience, knowledge, and technical skill by themselves are insufﬁcient protection against this complication.

From Way LW, Stewart L, Gantert W, et al. Causes and prevention of laparoscopic bile duct injuries. Ann Surg 2003;237:460–469, by permission of the Annals of Surgery.

R. hepatic a.

Cystic duct

Figure 30–5 The relationship of the right hepatic artery and cystic duct.

● Repair Conversion to an open approach is necessary for repair. An attempt may be made at end-to-end anastomosis unless an accessory artery is involved and collateral ﬂow is adequate. ● Prevention The cystic artery normally lies above the cystic duct (Figs. 30–4 and 30–5). It is important to identify the ﬁnal distribution of the artery into the gallbladder wall. A looped right hepatic artery may give rise to a short cystic artery, which, if not identiﬁed, will lead to transection of the right hepatic artery.

30 GALLBLADDER: CHOLECYSTECTOMY (LAPAROSCOPIC VS. OPEN)

Dissection of the Gallbladder Injury to the Liver ● Consequence Excessive bleeding. Anomalies in the position of the gallbladder, such as an intrahepatic position, may make the dissection of the gallbladder from its fossa difﬁcult. When the liver is enlarged or ﬁbrotic, it may not be pliable and will have a tendency to bleed when lifted or manipulated. This is the case in cirrhotic and fatty livers, in which it is difﬁcult to retract the fundus over the liver. Portal hypertension results in increased venous collateralization and may make dissection dangerous. Grade 1/2 complication ● Repair Cauterization of the liver bed for hemostasis. ● Prevention Identiﬁcation of the plane of dissection. In patients with portal hypertension, conversion to open is prudent.

Perforation of the Gallbladder ● Consequence Spillage of bile or stones. Five percent to 40% incidence in laparoscopic procedures, but complications occur rarely. Complications can occur months to years after the laparoscopic cholecystectomy. Isolated reports of stone spillage resulting in abscess formation, sinus formation, port site infections, and intestinal obstruction have been described. Migration to other systems has been documented,19–21 resulting in hernia sacs and ﬁstula. Recently, Zehetner and colleagues22 published a review of the literature and case reports for lost gallstones and found the most frequent consequence was an abscess in the abdominal wall. Grade 1/2 complication ● Repair If possible, the hole in the gallbladder should be closed by the grasp forceps or an endoclip. In case of spillage, efforts should be made at stone retrieval and irrigation of the peritoneal cavity to dilute any infected bile. Use of a retrieval bag is recommended to prevent further spillage. There is no indication for conversion to open surgery. ● Prevention The incidence of perforation is higher in patients with acute cholecystitis, especially when hydrops is present. Aspiration of a tense gallbladder can facilitate dissection, and all attempts should be made to identify the correct planes. If spillage occurs, patients should be informed to minimize the legal implications and aid in the diagnosis of later complications, should they occur.

323

Bile Leaks ● Consequence Rarely, there may be leaks from the ducts of Lushka (ducts draining directly from the liver into the gallbladder, not via the cystic duct). Bile leaks may also occur from incomplete ligation of the cystic duct. Grade 1/2 complication ● Repair None. May need persistent Jackson-Pratt drainage until the ducts seal and may consider postoperative sphincterotomy with endoscopic retrograde cholangiopancreatography (ERCP) to expedite the process. An ERCP would be the procedure of choice for bile leaks. It can be both diagnostic and therapeutic. If there is a cystic duct leak, a stent can be placed across the leak to facilitate closure. The ERCP would also identify more serious pathology such as a common bile duct injury. ● Prevention None. Examine the bed of the gallbladder carefully prior to closing to determine the need for Jackson-Pratt drain placement.

Trocar Removal Trocar Site Hernias These are described in Section I, Chapter 7, Laparoscopic Surgery.

Other Complications Hemobilia has been reported as a complication after laparoscopic cholecystectomy.23,24 This complication has been seen to occur usually within 4 weeks of the surgery, but rare case reports of late onset have also been documented.25 The mechanism of injury is unclear, but thermal or mechanical injury to the cystic or hepatic arteries and common bile duct is the presumed pathogenesis. Patients may require a combination of endoscopy and angiography for diagnosis and management. In some case reports, infection may have facilitated the ﬁstulization.26 Viscus injuries, especially duodenum or colon, are very uncommon in laparoscopic cholecystectomy and are discussed in greater detail in Section I, Chapter 7, Laparoscopic Surgery. Although rare, they can be one of the most lethal complications of laparoscopic surgery. Unfortunately, these injuries are not usually recognized at the time of surgery and are diagnosed later when patients experience sepsis, peritonitis, or intra-abdominal abscess. The late recognition of these injuries contributes to the associated high mortality rates. The incidence of occurrence has been rare: around 0.1% to 0.4% of laparoscopic cholecystectomy cases.27,28 Duodenal injuries have been reported in laparoscopic cholecystectomies as a result of thermal injury or laceration.29,30 Small bowel ischemia has

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also been reported as an adverse affect of pneumoperitoneum-associated intra-abdominal hypertension.31 This results in the compromise of the mesenteric circulation. Transient right shoulder pain is a common symptom after laparoscopic cholecystectomy and is believed to be the result of a combination of the smoke, CO2, and ﬂuid. However, persistent pain may be the ﬁrst sign of a missed injury to the bowel. A high index of suspicion is necessary when the postoperative course is anything but routine.

Open Cholecystectomy Since the advent of laparoscopic surgery, open cholecystectomy procedures have been on the decline. However, when such procedures are performed, it is usually the result of conversion from the laparoscopic approach because of anatomic difﬁculties, excessive bleeding, or complications. Acute and chronic inﬂammation may obscure anatomy. In these patients, the inﬂammation may result in increased vascularity. In many cases of open cholecystectomy, the gallbladder is severely inﬂamed, and an attempt to dissect the gallbladder from the liver may not be easy. Utilization of the antegrade technique is important in these surgically difﬁcult situations. Opening the fundus and introducing a ﬁnger into the gallbladder are helpful to guide dissection. A portion of the wall may need to be left behind, and it is better to ligate the cystic duct as close to the neck of the gallbladder as possible to avoid injury to the common bile duct. Sometimes, ligation of the neck is impossible to do and leaks occur. A Jackson-Pratt drain should be left in the pouch for drainage. These leaks will eventually seal. To avoid more serious complications, it is important in these cases to have the pouch adequately drained to avoid formation of a biloma. Sealing of the leaks may be expedited with endoscopic stent placement in the common bile duct and occlusion of the cystic duct. ERCP can be performed with sphincterotomy and provides both diagnostic and therapeutic intervention. Small leaks of the ducts of Luschka will seal off rather quickly within a few days. Cystic duct leaks may take several weeks. In those cases, a JacksonPratt drain should be left in place for 6 weeks and then may be safely removed.

INDICATIONS ● Failed laparoscopic approach ● Previous right upper quadrant surgery with hostile ● ● ● ● ● ●

environment Gangrenous cholecystitis Suspected gallbladder cancer Other pathologic ﬁndings (e.g., ﬁstula, hydrops) Unclear anatomy Failed ERCP with retained common bile duct stones Suspected injury to bile duct, viscus, or major blood vessel

● Porcelain gallbladder ● Mirizzi’s syndrome

OPERATIVE STEPS Step Step Step Step Step Step

1 2 3 4 5 6

Incision Exposure of gallbladder Dissection of gallbladder Possible cholangiogram Ligation of cystic duct and artery Wound closure

OPERATIVE PROCEDURE Incision A right subcostal approach is taken. A midline incision is also acceptable.

Bleeding from the Epigastric Vessels ● Consequence Bleeding may occur from the epigastric vessels during the incision. Grade 1 complication ● Repair There is a rich collateralization in the abdominal wall, so ligation of the epigastric vessels can be done with impunity. ● Prevention Increased vascularity occurs in the setting of portal hypertension, and therefore, these vessels may be quite large and require suture ligation.

Exposure A surgical pad placed behind the right lobe of the liver can facilitate exposure.

Dissection of the Gallbladder and Possible Cholangiogram Injury to the Liver See the section on “Injury to the Liver,” under “Laparoscopic Cholecystectomy,” earlier. Perforation of the Gallbladder See the section on “Perforation of the Gallbladder,” under “Laparoscopic Cholecystectomy,” earlier.

Ligation of the Cystic Duct and Artery In the open approach, antegrade dissection of the gallbladder allows for safe identiﬁcation of the artery and duct. By coming from lateral to medial as one approaches the neck of the gallbladder and staying close to the gall-

30 GALLBLADDER: CHOLECYSTECTOMY (LAPAROSCOPIC VS. OPEN) bladder, identiﬁcation and safe ligation of the appropriate structures are facilitated.

325

Extent of node clearance

Injury to the Hepatic Artery See the section on “Injury to the Hepatic Artery,” under “Laparoscopic Cholecystectomy,” earlier. Injury to the Common Bile Duct See the section on “Injury to the Common Bile Duct,” under “Laparoscopic Cholecystectomy,” earlier. a

Wound Closure

b

Wound Infection A postoperative wound infection from this approach is rare. ● Consequence Opening of the wound may be required and antibiotics in the setting of cellulitis. Grade 1 complication ● Repair Opening of the wound and packing.

Incisional Hernias ● Consequence Hernias may arise from poor closure technique. Grade 3 complication ● Repair If there is no incarceration, the hernia can be repaired electively or when symptomatic. Hernia repair in this area will require mesh. ● Prevention Closure may be achieved as a two-layer closure; however, previous right upper quadrant surgery may necessitate a one-layer closure.

Combined Cholecystectomy with Liver Resection Combined cholecystectomy with liver resection is performed in many cases. Cholecystectomy is required for any formal right or left hepatectomy, trisegmentectomy, or bile duct tumor resections. These procedures are discussed in Section IV, Chapter 32, Left Hepatectomy; Chapter 33, Trisectionectomy; and Chapter 39, Resection and Reconstruction of the Biliary Tract. This section of this chapter focuses on partial hepatectomy with cholecystectomy. The most common indication for this procedure is gallbladder cancer. Sometimes, it has been termed an extended cholecystectomy. The extended cholecystectomy

c

d e

Figure 30–6 The nodal dissection around the porta hepatis.

involves en-bloc removal of adventitia and contained lymphatics surrounding the bile duct, portal vein, and hepatic artery as well as excision of the liver substance adjacent to the gallbladder bed (Fig. 30–6). Unfortunately, gallbladder cancer often presents too late for a curative resection to be a viable option. However, about one third of the cases of gallbladder cancer are found at the time of cholecystectomy. When cancer is found, controversy still exists about the optimum surgical procedure for treatment. The spectrum of resections has included simple cholecystectomy, nonanatomic wedge resection of the gallbladder bed, formal removal of segments IV and V, and combined liver resection with pancreaticoduodenectomy.32 Wedge resection may seem to be the least radical of the procedures, but it can be difﬁcult and associated with signiﬁcant blood loss because it is a nonanatomic resection. Extended resections were once believed unnecessary for T2 tumors. These tumors by deﬁnition remain subserosal but have invaded through the muscular layer. However, the plane of dissection in a simple cholecystectomy is in the subserosal plane between the liver and the gallbladder, where tumor may be violated.33 Data have shown that T2 tumors are also reported to have a high incidence of regional nodal metastases from 33% to 43%.34,35 Improved 5-year survival of upward of 80% with radical resection36,37 are seen compared with simple cholecystectomy survival rates of 20% to 40%.38,39 When the cancer has grossly penetrated the wall or locally advanced disease is present, further controversy exists concerning treatment. For tumors located in the fundus of the gallbladder, a radical cholecystectomy allows for an adequate margin. However, when the tumors arise near the neck of the gallbladder, in Hartmann’s pouch or extend into the hilum, there may be a role for an extended hepatectomy.40

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Until recently, the operations for complete resection were associated with a high incidence of morbidity, ranging from 5% to 54%,41 and mortality rates up to 21%.27,42 However, several studies have shown surgical resection for T3 or T4 tumors can result in long-term survival.40,43,44 During the late 1980s and 1990s, studies reported increasing safety24 and an operative mortality of less than 5%,45 providing additional support for an aggressive approach to gallbladder cancer utilizing an extended cholecystectomy. A signiﬁcant number of gallbladder cancers will present for deﬁnitive therapy after prior cholecystectomy. There have been suggestions that patients subjected to two operations have a less favorable prognosis than patients with a single procedure. With experienced surgeons, the outcome is sufﬁciently favorable, and the outcome of incomplete resection dismal, to warrant additional radical resection. The resection must provide at least a 2-cm margin of noninvolved liver tissue.

INDICATIONS ● Early gallbladder cancer Figure 30–7 The placement of chromic sutures for hemostasis prior to transection of the liver parenchyma.

OPERATIVE STEPS Step Step Step Step Step

1 2 3 4 5

Incision Exposure Transection of liver Ligation of cystic duct and artery Closure of wound

OPERATIVE PROCEDURE Incision A right subcostal approach is taken.

Bleeding from the Epigastric Vessels See the section on “Bleeding from the Epigastric Vessels,” under “Open Cholecystectomy,” earlier.

Exposure

Bleeding ● Consequence As mentioned previously, because this is not an anatomic resection, bleeding can be more difﬁcult to control. Grade 1 complication ● Repair Parenchymal bleeding of the liver can usually be controlled with direct cauterization; suture ligatures may be needed with larger vessels. ● Prevention Careful dissection or use of large chromic sutures may decrease the risk of serious hemorrhage (Fig. 30–7).

A surgical pad placed behind the right lobe of the liver can facilitate exposure.

Injury to the Hepatic Artery See the section on “Injury to the Hepatic Artery,” under “Laparoscopic Cholecystectomy,” earlier.

Transection of the Liver

Bile Leak

A minimum of a 2-cm margin of healthy liver tissue should be excised with the gallbladder. The plane of dissection can be initially demarcated with electrocautery or argon beam. With current improvements in instrumentation, one can utilize various methods for parenchymal dissection including harmonic scalpel, Cavitron ultrasonic aspirator (CUSA), tissue link, or electrocautery.

● Consequence While transecting liver, small bile ducts may be transected. Grade 1 complication ● Repair Suture ligation.

30 GALLBLADDER: CHOLECYSTECTOMY (LAPAROSCOPIC VS. OPEN) ● Prevention Ligation of any vascular or duct structures while transecting the parenchyma. A Jackson-Pratt drain should be placed in order to drain the space if a bile leak occurs. Usually, they will seal without further intervention.

Ligation of the Cystic Duct and Artery See the section on “Ligation of the Cystic Duct and Artery,” under “Open Cholecystectomy,” earlier.

Nodal Dissection The nodes around the porta hepatis should be removed by skeletonizing the adventitia around the major structures. In this way, there is little risk of injury to any of the structures in the porta hepatis.

Injury to the Common Bile Duct See the section on “Injury to the Common Bile Duct,” under “Laparoscopic Cholecystectomy,” earlier. Injury to the Hepatic Artery See the section on “Injury to the Hepatic Artery,” under “Laparoscopic Cholecystectomy,” earlier. Injury to the Portal Vein ● Consequence Immediate bleeding and possible ischemia to the liver. Grade 4/5 complication ● Repair Suture repair needs to be performed. A Pringle procedure may need to be done in order to facilitate safe repair of the vein. If there is tissue loss, one may need to utilize a patch of vein as a graft. ● Prevention Careful identiﬁcation of the anatomy. The portal vein lies posterior to the hepatic artery and medial to the common bile duct.

Closure of the Wound Incisional Hernias See the section on “Incisional Hernias,” under “Open Cholecystectomy,” earlier.

Wound Infection See the section on “Wound Infection,” under “Open Cholecystectomy,” earlier.

327

REFERENCES 1. Braasch JW. Historical perspectives of biliary tract injuries. Surg Clin North Am 1994;74:731–740. 2. Chapman WC, Halevy A, Blumgart LH, Benjamin IS. Postcholecystectomy bile duct strictures: management and outcome in 130 patients. Arch Surg 1995;130:597– 604. 3. Roslyn JJ, Binns GS, Hughes EFX, et al. Open cholecystectomy. A contemporary analysis of 42,474 patients. Ann Surg 1993;218:129–137. 4. Fletcher DR, Hobbs MS, Tan P, et al. Complications of cholecystectomy: risks of the laparoscopic approach and protective effects of operative cholangiography: a population-based study. Ann Surg 1999;229:449–457. 5. Russell JC, Walsh SJ, Mattie AS, Lynch JT. Bile duct injuries, 1989–1993. A statewide experience. Connecticut Laparoscopic Cholecystectomy Registry. Arch Surg 1996; 131:382–388. 6. Archer SB, Brown DW, Smith CD, et al. Bile duct injury during laparoscopic cholecystectomy: results of a national survey. Ann Surg 2001;234:549–559. 7. Savader SJ, Lillemoe KD, Prescott CA, et al. Laparoscopic cholecystectomy–related bile duct injuries: a health and ﬁnancial disaster. Ann Surg 1997;225:268–273. 8. Stewart L, Way LW. Bile duct injuries during laparoscopic cholecystectomy. Factors that inﬂuence the results of treatment. Arch Surg 1995;130:1123–1129. 9. Hugh TB. New strategies to prevent laparoscopic bile duct injury—surgeons can learn from pilots. Surgery 2002;132:826–835. 10. Flum DR, Cheadle A, Prela C, et al. Bile duct injury during cholecystectomy and survival in Medicare beneﬁciaries. JAMA 2003;290:2168–2173. 11. Francoeur JR, Wiseman K, Buczkowski AK, et al. Surgeons’ anonymous response after bile duct injury during cholecystectomy. Am J Surg 2003;185:468– 475. 12. Shah SR, Mirza DF, Afonso R, et al. Changing referral pattern of biliary injuries sustained during laparoscoic cholecystectomy. Br J Surg 2000;87:890–891. 13. Carroll BJ, Birth M, Phillips EH. Common bile duct injuries during laparoscopic cholecystectomy that result in litigation. Surg Endosc 1998;12:310–313. 14. Way LW, Stewart L, Gantert W, et al. Causes and prevention of laparoscopic bile duct injuries. Ann Surg 2003;237:460–469. 15. Perrow C. Normal accidents. In Living with High-Risk Technologies. Princeton, NJ: Princeton University Press, 1999. 16. Hobbs MS, Mai Q, Knuiman MW, et al. Surgeon experience and trends in intraoperative complications in laparoscopic cholecystectomy. Br J Surg 2006;93:844– 853. 17. Flum DR, Koepsell T, Heagerty P, et al. Common bile duct injury during laparoscopic cholecystectomy and the use of intraoperative cholangiography: adverse outcome or preventable error? Arch Surg 2001;136:1287–1292. 18. Wright KD, Wellwood JM. Bile duct injury during laparoscopic cholecystectomy without operative cholangiography. Br J Surg 1998;85:191–194.

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19. Sathesh-Kumar T, Saklani AP, Vinayagam R, Blackett RL. Spilled gallstones during laparoscopic cholecystectomy: a review of the literature. Postgrad Med J 2004;80:77–79. 20. Schafer M, Suter C, Klaider C, et al. Spilled gallstones after laparoscopic cholecystectomy. A relevant problem? A retrospective analysis of 10,174 laparoscopic cholecystectomies. Surg Endosc 1998;12:291–293. 21. Woodﬁeld JC, Rodgers M, Windsor JA. Peritoneal gallstones following laparoscopic cholecystectomy: incidence, complications, and management. Surg Endosc 2004;18:1200–1207. 22. Zehetner J, Shamiyeh A, Wayand W. Lost gallstones in laparoscopic cholecystectomy: all possible complications. Am J Surg 2007;193:673–678. 23. Zilberstein B, Cecconello I, Ramos AC, et al. Hemobilia as a complication of laparoscopic cholecystectomy. Surg Laparos Endosc 1994;4:301–303. 24. Genyk YS, Keller FS, Halpern NB. Hepatic artery pseudoaneurysm and hemobilia following laser laparoscopic cholecystectomy. Surg Endosc 1994;8:201–204. 25. Rebeiro A, Williams H, May G, et al. Hemobilia due to hepatic artery pseudoaneurysm thirteen months after laparoscopic cholecystectomy. J Clin Gastroenterol 1998; 26:50–53. 26. Porte RJ, Coerkamp EG, Koumans RKJ. False aneurysm of a hepatic artery branch and a recurrent subphrenic abscess. Surg Endosc 1996;10:161–163. 27. Deziel DJ, Millikan KW, Economou SG, et al. Complications of laparoscopic cholecystectomy: a national survey of 4,292 hospitals and analysis of 77,604 cases. Am J Surg 1993;165:9–14. 28. Southern Surgeons Club. A prospective analysis of 1,518 laparoscopic cholecystectomies. N Engl J Med 1991;324: 1073–1078. 29. Avrutis O, Meshoulam J, Yutkin O, et al. Brief clinical report: duodenal laceration presenting as massive hematemesis and multiple intra-abdominal abscesses after laparoscopic cholecystectomy. Surg Laparosc Endosc Percutan Tech 2001;11:330–333. 30. Eden CG, Williams TG. Duodenal perforation after laparoscopic cholecystectomy. Endoscopy 1992;24:790– 792. 31. Andrei VE, Schein M, Wise L. Small bowel ischemia following laparoscopic cholecystectomy. Dig Surg 1999; 16:522–524.

32. Nimura Y, Hayakawa N, Kamiya J, et al. Hepaticopancreatoduodenectomy for advanced carcinoma of the biliary tract. Hepatogastroenterology 1991;38:170– 175. 33. Yamaguchi K, Tsuneyoshi M. Subclinical gallbladder carcinoma. Am J Surg 1992;163:382–386. 34. Fong Y, Jarnagin W, Blumgart L. Gallbladder cancer: comparison of patients presenting initially for deﬁnitive operation with those presenting after prior noncurative intervention. Ann Surg 2000;232:557–569. 35. Matsumoto Y, Fujii H, Aoyama H, et al. Surgical treatment of primary carcinoma of the gallbladder based on the histologic analysis of 48 surgical specimens. Am J Surg 1992;163:239–245. 36. Shirai Y, Yoshida K, Tsukada K, et al. Radical surgery for gallbladder carcinoma. Ann Surg 1992;216:565– 568. 37. Bartlett DL, Fong Y, Fortner JG, et al. Long-term results after resection of gallbladder cancer: implications for staging and management. Ann Surg 1996;224:639– 646. 38. Oertli D, Herzog U, Tondelli P. Primary carcinoma of the gallbladder: operative experience during a 16-year period. Eur J Surg 1993;159:415–420. 39. de Aretxabala X, Roa IS, Burgos LA, et al. Curative resection in potentially resectable tumours of the gallbladder. Eur J Surg 1997;163:419–426. 40. Reddy SK, Marroquin CE, Kuo PC, et al. Extended hepatic resection for gallbladder cancer. Am J Surg 2007; 194:355–361. 41. Ogura Y, Mizumoto R, Isaji S, et al. Radical operations for carcinoma of the gallbladder: present status in Japan. World J Surg 1991;15:337–343. 42. Donohue JH, Nagorney DM, Grant CS, et al. Carcinoma of the gallbladder: does radical resection improve outcome? Arch Surg 1990;125:237–241. 43. Gall FP, Kockerling F, Scheele J, et al. Radical operations for carcinoma of the gallbladder: present status in Germany. World J Surg 1991;15:328–336. 44. Onoyama H, Yamamoto M, Tseng A, et al. Extended cholecystectomy for carcinoma of the gallbladder. World J Surg 1995;19:758–763. 45. Nakamura S, Sakaguchi S, Suzuki S, Muro H. Aggressive surgery for carcinoma of the gallbladder. Surgery 1989; 106:467–473.

31

Right Hepatectomy Jay A. Graham, MD and Lynt B. Johnson, MD INTRODUCTION In Le Foie: Études Anatomiques et Chirurgicales, Claude Couinaud ﬁrst described the anatomic liver segments and nomenclature widely used by surgeons today. His indepth understanding of the hepatobiliary anatomy helped create the framework for much of liver surgery because it provided a systematic approach for safe resection. The ﬁrst published hepatectomy was performed by Jean Louis Lortat Jacob in 1952.1 Since then, the associated morbidity and mortality have decreased tremendously. Improved surgical technique using the “roadmap” laid out by Couinaud has undoubtedly been responsible for most of the decline in operative complications. In the last few years, surgeons have sought to bridge the gap between excellent operative technique and better outcomes through the use of newer technology. One of the main hurdles of liver surgery and predictors of poor outcomes is operative blood loss. Given the vascular nature of the liver parenchyma, surgeons have employed many devices intraoperatively to help identify and control large vascular structures. Notably, ultrasound has emerged as an essential tool to assess the intraparenchymal liver anatomy intraoperatively. This provides the surgeon with a powerful tool to evaluate the relationship between the large vessels and the planned resection plane. Harnessing ultrasonic energy, the ultrasonic dissector has also revolutionized parenchymal dissection. Using ultrasonic energy to fragment liver tissue, this technique spares blood vessels, which are made of ﬁrmer ﬁbrous tissue. Other devices implement a pressurized jet of water to accomplish this same task. The harmonic scalpel, which can be used to precisely cut and cauterize these vessels, also utilizes ultrasonic energy. Most recently, radiofrequency ablation has emerged and been used in conjunction with surgery to provide salvage therapy for large tumors. While the gamut of surgical instruments continues to grow, certain core surgical principles remain relevant in the discussion of operative morbidity. The use of the Pringle maneuver and measures taken to lower central venous pressure (CVP) are two precepts that are proven to minimize bleeding during resection. In this vain, this chapter proposes other techniques that can be used by the hepatobiliary surgeon to reduce complication rates during

right and left hepatectomies and provides a guide to common pitfalls encountered during surgery. However, much of the prevention strategies outlined in our chapter are secondary to an inherent and thorough understanding of the segmental liver anatomy.

OPERATIVE STEPS Operative incision Division of falciform ligament Division of right triangular ligament and coronary ligament with mobilization of right lobe of the liver. 4 Division of short hepatic veins between right hepatic lobe, caudate lobe (segments 1, 6, and 7), and inferior vena cava (IVC) 5 Cholecystectomy 6 Extrahepatic dissection of porta hepatis Isolation and division of right hepatic artery Isolation and division of right portal vein 7 Isolation and division of right hepatic vein 8 Hepatic parenchymal transection 9 Intraparenchymal division of right hepatic duct

Step 1 Step 2 Step 3

Step

Step Step ● ●

Step Step Step

OPERATIVE PROCEDURE A right hepatectomy involves resection of segments 5, 6, 7, and 8.

Operative Incision Hernia ● Consequence The use of the Mercedes versus an extended right subcostal incision is a matter of surgical preference. Both give adequate visualization for a right hepatectomy (Figs. 31–1 and 31–2). The midline incision extension to the xyphoid is often the site of hernia formation. Grade 3 complication ● Repair If the ventral hernia does not pose an incarceration risk, it can be repaired electively or when symptomatic.

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SECTION IV: HEPATOBILIARY SURGERY ● Prevention A recent study comparing 856 patients with Mercedes incisions with 570 patients with right subcostal incisions demonstrated discrepancies with wound healing. Patients with Mercedes incisions had a higher incidence of hernias, 9.8% versus 4.8%.2 However, any incision is prone to herniation without proper surgical technique with regard to reapproximation of the fascia.

Persistent Bleeding from the Superior Epigastric Arteries

Figure 31–1 A right subcostal incision with a midline incision gives adequate exposure to perform this operation.

● Consequence The superior epigastric arteries are invested in the rectus muscle near the xiphoid and can be lacerated during upper transverse incisions. These vessels can bleed signiﬁcantly if they are not controlled. Grade 1 complication ● Repair There is a rich collateral bed of vessels in this area. Therefore, ligation of the superior epigastric arteries is permissible. ● Prevention Surgical exposure is paramount during this operation. Therefore, these vessels can be sacriﬁced for optimization of the surgical view.

Division of the Falciform and Left Triangular Ligaments Torsion of the Left Lobe D B

C

A

Figure 31–2 Incisions for a right hepatectomy are depicted: A→ B is a right subcostal incision, A→B→D is an extended right subcostal incision and A→B→C with B→D is a chevron (Mercedes) incision.

● Consequence Extended division of the falciform and left triangular ligaments can lead to torsion, which can disrupt venous outﬂow that leads to venous congestion and severe liver dysfunction. The left triangular ligament helps to suspend the liver in anatomic position. After a right hepatectomy, the left lobe tends to rotate into the right subphrenic space. Excessive left triangular ligament division can exacerbate this occurrence and lead to torsion. Therefore, it is prudent to maintain the left triangular ligamentous attachments. Grade 4/5 complication ● Repair A study that analyzed 44 right hepatic resections concluded that venous outﬂow was improved when the left lobe was placed in its original anatomic position.3 Thus, it is recommended that after a right hepatectomy, the left lobe of the liver should be ﬁxed into anatomic position. ● Prevention When possible, an excessive division of the falciform ligament, and especially the left triangular ligament, should be avoided to prevent exacerbation of venous outﬂow obstruction. If the left lobe shifts from ana-

31 RIGHT HEPATECTOMY

Figure 31–3 The divided falciform ligament is reapproximated to secure the left lobe of the liver using 4-0 Prolene.

tomic position after a right lobe hepatectomy, it is advisable to secure the remnant (Fig. 31–3). Other options are to mobilize the hepatic ﬂexure and allow the right colon to partially ﬁll in the space.

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Figure 31–4 The dome of the right liver has been exposed by careful dissection of the right triangular and coronary ligaments. The blue rubber tie is placed around the right hepatic vein. The inferior vena cava (IVC) is located posterolateral to this blue rubber tie. The surgeon must be mindful of this structure when dissecting the ligamentous attachments.

movolemic hemodilution have been shown to minimize the use of banked blood.4

Injury to the Suprahepatic IVC ● Consequence Great care should be taken when cutting the falciform ligament as one approaches the bare area of the liver. The vena cava lies just posterior to the inferior edge of the falciform ligament and may be readily injured with aggressive dissection. Grade 5 complication ● Repair The vena cava should be immediately repaired to prevent further blood loss and possible air embolus. ● “The ﬁrst rule is do not panic.” ● The surgeon should tamponade the injury by placing

the index ﬁnger of the nondominant hand over the hole. ● Using 4-0 Prolene, place whip stitches until the hole is closed. ● Avoid using clamps to control the bleeding because this will often tear the vessel wall, causing bigger problems. Make an effort to get good visualization of the injury. Placing errant sutures can often lead to narrowing or obstructing the lumen of the vessel ● Prevention The surgeon should be aware of the anatomy in this area to prevent inadvertent injury to the vena cava. It is imperative that patients undergoing a right hepatectomy have adequate central venous access to monitor CVP and for resuscitation as necessary. In the event of moderate blood loss, preoperative autologous blood donation, intraoperative cell savage, and nor-

Division of the Right Triangular Ligament and the Right Side of the Coronary Ligament with Mobilization of the Right Lobe of the Liver Injury to the Right Hepatic Vein or Suprahepatic IVC Mobilization of the right lobe of liver begins with dissection through the lateral peritoneal reﬂection of the right triangular ligament. This dissection is carried medially through this relatively avascular areolar tissue plane. Superior mobilization of the right lobe involves taking down the right coronary ligament. As the dissection proceeds medially, care should be taken to avoid injury to the right hepatic vein or the IVC in the bare area of the liver. ● Consequence Dissection through the superior and medial aspects of this avascular tissue can lead to inadvertent injury to the right hepatic vein or IVC. Transection of the right hepatic vein without ligation poses a serious problem because the surgeon is confronted with controlling a large hole in the IVC without adequate exposure. Grade 5 complication ● Repair Any bleeding that is encountered should be controlled and the defect closed with suture. ● Prevention Again, meticulous dissection in the medial aspects of the coronary ligament can prevent inadvertent venotomies (Fig. 31–4). One of the rare complications with

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injury to these large veins can be air embolism. During this stage of the operation, it has been proposed that the patient have a positive CVP and be placed in Trendelenberg position to prevent air embolus. However, with increased CVP, bleeding will increase.

Injury to the Diaphragm Diaphragm puncture can occur with dissection of the infradiaphragmatic plane of the right triangular ligament. Also, sometimes intentional diaphragmatic resection is necessitated by liver tumors that are adherent to the diaphragm. ● Consequence Diaphragmatic injury can occur during dissection of the bare area of the liver. When this occurs, negative pleural pressure is lost and must be restored. Grade 1/2 complication ● Repair Negative pleural pressure needs to be reestablished during the operative case after violation of the thoracic cavity. All diaphragmatic holes can be repaired primarily using a nonabsorbable suture. One technique that is readily used in our hospital to restore a normal pulmonary environment is the use of a small catheter with suction. A red rubber catheter with suction is placed in the defect, and a pursestring suture is cinched down as the catheter is quickly removed. ● Prevention Careful dissection of the peritoneal reﬂections of the posterior liver while an assistant rotates the liver medially and inferiorly may decrease the incidence of diaphragmatic injury. The central portion of the diaphragm is often stretched thin owing to large right lobe tumors. When this occurs, the triangular ligament is draped over the right lobe and is much higher than anticipated. A right-angle clamp inserted under the edge will allow the surgeon to safely identify the insertion of the ligament and the capsule of the liver (Fig. 31–5).

Duodenal Injury ● Consequence Duodenal injuries can occur while dissecting in the inferior planes of the right triangular ligament. The duodenum usually sits away from the right triangular ligament so that gentle retraction with a ﬁnger can protect its integrity. However, a duodenum that sits in a more cephalad position may be more prone to injury. Dissection of the triangular ligament around the right renal peritoneal reﬂection can place the duodenum at risk (Fig. 31–6). Grade 1/2 complication ● Repair Simple duodenal lacerations may be repaired primarily with a monoﬁlament suture.

Figure 31–5 A right-angle clamp is inserted under the edge of triangular ligament to safely facilitate the dissection of the right lobe of the liver from the diaphragm.

Figure 31–6 The location of the duodenum can obscured by omental fat (▼). Electrocautery should be used sparingly when dissecting in this plane. The arrow demonstrates the portal vein.

● Prevention Electrocautery should be used sparingly in the inferior aspects of the triangular ligament because the duodenum may be injured.

Injury to the Adrenal Gland ● Consequence The adrenal gland may also be injured with dissection in the right coronary avascular planes. An adrenal hematoma due to injury of the parenchyma is a known consequence of right hepatectomy.5 Grade 1 complication ● Repair The adrenals are rarely the site of major blood loss, and these hematomas can be followed up with serial imaging.6

31 RIGHT HEPATECTOMY There is tremendous collateral circulation to the adrenal gland. Therefore, any problematic vessels can be oversewn without severe consequence. ● Prevention The medial reﬂections of the right coronary ligament should be divided close to the liver to avoid injury to the adrenal glands. Once renal fascia is encountered, the surgeon should direct his or her dissection in an anterior fashion. Of note, once the adrenal gland is visualized, the IVC is very nearby.

Recognition of the Phrenic Vessels ● Consequence In dividing the right triangular ligament, it is not uncommon to come across suprarenal and phrenic vessels as they drain their respective structures. There is adequate collateralization of the inﬂow and outﬂow to the diaphragm and adrenal gland. Therefore, these vessels can be ligated and divided as the surgeon continues in superomedial dissection. Grade 0 complication ● Repair No repair is needed because these vessels may be divided. ● Prevention The bare area of the liver must be followed closely when dissecting the coronary ligaments to prevent phrenic vessel injury.

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IVC (Fig. 31–7). Their division allows greater mobility of the right liver lobe. IVC injury can occur during this portion of the operation, and management of this injury is detailed previously.

Injury to the IVC with Division of the Ligamentous Band of the Caudate Lobe ● Consequence In many patients, a ligamentous band attaches the Spieghel portion of the caudate lobe to segment 7 of the liver (Fig. 31–8). This attachment passes posterolateral to the IVC and can contain liver parenchyma. This band must be divided in order to mobilize the right liver. Grade 5 complication ● Repair This ligamentous band often contains liver parenchyma and separate venous drainage. This band must be divided, ligated, and oversewn. ● Prevention Special care must be taken when dividing this structure, given the immediate proximity of the IVC (Fig. 31–9).

Cholecystectomy The gallbladder is taken down in standard dome-down fashion. Complications are detailed in Section IV, Chapter 30, Gallbladder: Cholecystectomy (Laparoscopic vs. Open).

Extrahepatic Dissection of the Porta Hepatis Division of the Short Hepatic Veins Between Segments 1, 6, 7, and the IVC Mobilization of the right lobe reveals short hepatic veins that may be ligated and divided as they come off of the

Extrahepatic dissection of the porta hepatis is a popular method for inﬂow control. However, hilar dissection can put contralateral structures at risk through devascularization or injury.

Figure 31–7 Rolling the liver medially, one can appreciate the ligation of the short hepatic veins between segments 1, 6, 7, and the IVC (▼).

Figure 31–8 The Kelly clamp illustrates the parenchymal connection between the Spiegel portion of caudate lobe and segment 7.

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Ligamentous band Inferior vena cava Caudate lobe

Bare area

Renal impression

Left gastric a.

Portal vein Proper hepatic artery

Proper hepatic a. Right replaced hepatic a

Left hepatic a.

Colic impression Segment IV

Figure 31–9 The ligamentous band between the caudate lobe and segment 7 of the liver is clearly seen. When dividing this band, the surgeon must be mindful of the proximity of the IVC.

For this reason, we do not advocate extrahepatic bile duct division. Moreover, with extrahepatic biliary dissection, the surgeon may place the common hepatic duct in jeopardy.

Common Hepatic Duct Vascular Compromise ● Consequence Attempts to ﬁnd the conﬂuence of the right and the left hepatic ducts in the hilum often necessitate dissection around the common bile duct. The vascular supply of the common hepatic duct runs along this structure at the 3 and 9 o’clock positions. Therefore, minimal dissection of this crucial structure should ensue when attempting to isolate the right hepatic duct. Grade 1/2/3 complication ● Repair Common hepatic duct vascular compromise leading to stenosis is often manifested with pain, increasing bilirubin, and possible cholangiitis.7 Radiographic studies usually will demonstrate intrahepatic bile duct dilatation. The stenosis can usually be endoscopically stented with good results. However, when endoscopic stenting fails, the injury must be addressed with a Roux-en-Y hepaticojejunostomy.8,9 ● Prevention Some surgeons advocate performing a cholecystectomy and extrahepatic dissection of the common hepatic duct to trace its bifurcation. However, we prefer intraparenchymal right hepatic duct division to prevent common hepatic duct vascular disruption. Typically, the bifurcation of the hepatic ducts is situated under segment 4. It is safer to divide the bile duct in the parenchymal division phase of the operation rather than to try and isolate this structure outside the liver.

Figure 31–10 The lateral position of a replaced right hepatic artery with regard to the portal triad.

Division of the Right Hepatic Artery Recognition of the Replaced Right Hepatic Artery ● Consequence The right hepatic artery usually courses posterior to the common hepatic duct. A multitude of anatomic variants are present in the right hepatic arterial vasculature, the most common being the replaced right hepatic artery (Fig. 31–10). Grade 0 complication ● Repair No repairs are needed because all right-sided hepatic anomalous arteries should be divided to ensure safe transection of the liver parenchyma. ● Prevention The prevalence of a replaced right hepatic artery is approximately 17%.10 Intraoperative assessment by palpation of the portal triad helps to identify a replaced right hepatic artery (Fig. 31–11). A pulse posterolateral to the common hepatic duct should raise suspicions for this anomalous artery.

Division of the Right Portal Vein Injury to the Left Portal Vein ● Consequence All attempts to maintain the luminal diameter of the left portal vein branch should be taken to ensure adequate venous ﬂow. The right branch of the portal vein is very short, and careless ligation can encroach upon the left portal vein, causing stenosis.11 Grade 1/2 complication

31 RIGHT HEPATECTOMY

Figure 31–11 The right-angle clamp clearly demonstrates a replaced right hepatic artery lateral to the portal vein, which is being lifted by a vein retractor. Also, ﬁnger palpation of the proximal replaced right hepatic artery is being demonstrated with the right index ﬁnger.

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Figure 31–13 Hilar shelf elevation with a vein retractor demonstrates the caudate venous supply from the right portal vein (suture encircling).

Use a vein retractor to lift the common duct so that the bifurcation can be adequately visualized. The ligation of the right portal vein should not cause stenosis of the segment between the main and the left portal veins.

Injury to the Posterior Portal Vein Feeding the Caudate Lobe ● Consequence Given the short segment of extrahepatic right portal vein, meticulous dissection is needed to preserve portal vein ﬂow to the caudate lobe. Grade 1 complication

Figure 31–12 A malleable retractor has been positioned under segment 4 to allow the hilar shelf to move caudally. Next, a vein retractor is used to lift the common hepatic duct and expose the right portal vein (arrow). The right hepatic artery (▼) has been divided prior to this portion of the operation.

● Repair Usually, short segments of stenosis will not impede the venous ﬂow sufﬁciently to cause lasting morbidity. However, if the portal vein to the left portal vein conduit is deemed to be inadequate (signiﬁcantly small diameter), it should be revised. ● Prevention Segment 4 should be elevated, and the hilar shelf will move caudally, giving the surgeon a better operative view (Fig. 31–12). Care must be taken to clearly identify the bifurcation before extrahepatic division.

● Repair Usually, there is adequate arterial collateralization to the caudate lobe to ensure viability. Therefore, no repair is needed if the posterior portal venous ﬂow to caudate lobe is interrupted. However, most liver surgeons believe that it is better to preserve this caudate lobe blood supply. ● Prevention The right portal vein usually gives off a branch that feeds the caudate lobe (Fig. 31–13). This branch lies posterior to the bifurcation of the right and left portal veins. Injury to this structure may occur with dissection of a short right portal vein in the posterior planes. When attempting to circumscribe the right portal vein, the surgeon must be aware of the portal vein supply of the caudate lobe (Fig. 31–14).

Left-sided Gallbladder Left-sided gallbladder describes the two anatomic variants in which the gallbladder lies against the left segments or is characterized by a right-sided round ligament. In the

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Ligamentous band Caudate lobe Caudate branches of portal v. Portal vein

surgeon must carry out dissection on the right side of the gallbladder to prevent unwarranted portal vein or hepatic duct injury.

Isolation and Division of the Right Hepatic Vein The right hepatic vein is the largest of the three veins and drains most of the right lobe of the liver. Identiﬁcation and ligation can be done either during or before parenchymal division. We prefer to identify and divide the right hepatic vein before parenchymal transection to minimize backbleeding through the venous tributaries. Our approach is to divide the right hepatic vein with an endovascular gastrointestinal anastomosis (GIA) stapler.

Hepatic Vein Bleeding Figure 31–14 Right and left portal veins are shown to give off branches to the caudate lobe. The surgeon should be familiar with this anatomy so as to preserve blood ﬂow to the caudate lobe and to minimize bleeding.

latter variant, the gallbladder lies in a normal position but the round ligament is on the right, giving the appearance of a left-sided gallbladder.12 Left-sided gallbladders are worrisome because of the anatomic challenges they provide. ● Consequence The presence of a left-sided gallbladder heralds the potential of biliary and portal venous variation.13 The left and right hepatic ducts usually converge at the hepatoduodenal ligament. This also holds true for the left and right portal veins. However, in patients with left-sided gallbladders, care must be taken when dividing the liver parenchyma. In this situation, the left portal vein takeoff is more distal in position, and injury can occur if it is not recognized. Also, the left hepatic duct may traverse through a portion of the right lobe. Grade 1/2/3 complication ● Repair An injury to the left-sided portal venous vasculature may signiﬁcantly compromise the vascular supply of the remaining left lobe. If a major portal venous injury is encountered, immediate vascular repair must ensue with either primary anastomosis or venous patch angioplasty. If the left hepatic duct is injured and cannot be repaired primarily, a Roux-en-Y hepaticojejunostomy will need to be done. ● Prevention Dissection of liver parenchyma should be done carefully to identify all structures. In this situation, the

● Consequence Brisk bleeding can arise from the right hepatic vein if it is not clamped and ligated properly. Grade 1 complication ● Repair Stump bleeding from the right hepatic vein can occur after its division. Usually, this is secondary to a ligation tie that is improperly placed. Using 4-0 Prolene, the defect can be whip stitched until the hole is closed. ● Prevention Adequate right hepatic vein length should be obtained via hepatic parenchyma resection prior to ligation and division.

Hepatic Parenchymal Transection Blood Loss ● Consequence Through the years, blood loss has been responsible for the signiﬁcant morbidity associated with this operation. Given the vascular nature of the liver and that this organ receives 25% of the cardiac output; hepatic resection often leads to a signiﬁcant blood loss. In an attempt to lessen blood loss intraoperatively, many surgical instruments have been employed in the operative theater. Today, parenchymal division is usually accomplished by using a Cavitron ultrasonic surgical aspirator (CUSA), harmonic scalpel, or saline-enhanced cautery (Figs. 31–15 to 31–17). These instruments have been shown to decrease blood loss.14 However, even with these instruments, the surgeon can encounter signiﬁcant blood loss. Increased blood loss mandates transfusion and places the patient at risk for blood-borne infections, shock, and in some series, increased risk of recurrence in malignancies. Grade 1/3/4/5 complication

31 RIGHT HEPATECTOMY

337

● Repair In patients with catastrophic uncontrolled hemorrhage or with tumors that require reconstruction of the IVC, total vascular occlusion can be employed.15 This technique involves placing clamps across the infradiaphragmatic IVC, infrahepatic IVC, and portal triad. In addition, the right adrenal vein must be ligated in order to achieve total vascular isolation.

Figure 31–15 Parenchymal division proceeds in anterior to posterior plane using a Cavitron ultrasonic aspirator (CUSA). The small intraparenchymal vessels are cauterized with the Bovie.

● Prevention In the early 1900s, Hogarth Pringle described an inﬂow occlusion technique to limit blood loss during liver surgery.16 The Pringle maneuver requires that the vascular structures in the hepatoduodenal ligament be temporarily occluded. This technique has been used by surgeons for close to 100 years, and one study veriﬁed that it reduced blood loss.17 In patients with chronic liver disease, intermittent occlusion is often used to prevent signiﬁcant ischemia times. Decreasing the CVP during a hepatectomy can lower blood loss.18 In a prospective, randomized, controlled trial, 25 patients underwent hepatectomies with a CVP of 2 to 4 mm Hg, while the control group underwent the same operation but with higher CVPs. On average, the control group lost approximately 600 ml more blood than the group with low CVPs.19 Isovolemic hemodilution (IH) can be used to reduce the transfusion requirement during hepatic resection. IH is safe, and its use is reported to result in a 60% reduction in mean packed red blood cell transfusion.20 Adverse effects of homologous blood transfusions are well documented, and IH may be implemented to lessen the associate risks.

Intraparenchymal Division of the Right Hepatic Duct Figure 31–16 Larger vessels are clipped or tied.

Bifurcation of the common hepatic duct lies in the posterior aspect of segment 4. We believe that it is much safer to identify this structure during intrahepatic parenchymal dissection between segments 4 and 5.

Bile Leak ● Consequence Biliary leakage is a serious consequence after right or left hepatic division during major hepatic resections. Leaks more often occur at the cut surface of the liver parenchyma but can also present secondary to inadequate ligation of the hepatic ducts.21 Grade 1/2 complication

Figure 31–17 The cauterized left lobe of the liver can be seen after completion of the right hepatectomy.

● Repair Several approaches have been used to manage a bile leak after major hepatic resection. Endoscopic retrograde cholangiopancreatography with stenting has been shown to be very effective for biliary control, but it is only necessary if the leak is greater than 100 ml for longer than 7 days. More minor leaks will often seal.

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● Prevention Meticulous attention to bile staining of the cut edge of the liver will direct the surgeon to areas that may leak bile. If a leak is seen, it should be oversewn.

REFERENCES 1. Lortat-Jacob JL, Robert HG, Henry C. Hepatectomie lobaire droite reglee pour tumour maligne secondaire. Arch Mal Appareil Digestif 1952;41:662–667. 2. D’Angelica M, Maddineni S, Fong Y, et al. Optimal abdominal incision for partial hepatectomy: increased late complications with Mercedes-type incisions compared to extended right subcostal incisions. World J Surg 2006;30: 410–418. 3. Ogata S, Kianmanesh R, Belghiti J. Doppler assessment after right hepatectomy conﬁrms the need to ﬁx the remnant left liver in the anatomical position. Br J Surg 2005;92:592–595. 4. Lutz JT, Valentin-Gamazo C, Gorlinger K, et al. Blood-transfusion requirements and blood salvage in donors undergoing right hepatectomy for living related liver transplantation. Anesth Analg 2003;96:351– 355. 5. Gouliamos AD, Metafa A, Ispanopoulou SG, et al. Right adrenal hematoma following hepatectomy. Eur Radiol 2000;10:583–585. 6. Bowen AD, Keslar PJ, Newman B, Hashida Y. Adrenal hemorrhage after liver transplantation. Radiology 1990; 176:85–88. 7. Bagia JS, North L, Hunt DR. Mirizzi syndrome: an extra hazard for laparoscopic surgery. Aust N Z J Surg 2001;71: 394–397. 8. Rothlin MA, Lopfe M, Schlumpf R, Largiader F. Longterm results of hepaticojejunostomy for benign lesions of the bile ducts. Am J Surg 1998;175:22–26.

9. Williams GR. Experiences with surgical reconstruction of hepatic duct. Ann Surg 1974;179:540–548. 10. Calne RY. Partial resection of the liver for primary cancer. In Najarian JS, Delaney JP (eds). Hepatic, Biliary and Pancreatic Surgery. Miami, Symposia Specialists, 1980; pp 605–619. 11. Ong GB. Right hemihepatectomy. In Calne RY, Querci Della Rovere G (eds). Liver Surgery. Padua, Piccin Medical Books, 1982; pp 23–32. 12. Nagai M, Kubota K, Kawasaki S, et al. Are left-sided gallbladders really located on the left side? Ann Surg 1997;225:274–280. 13. Regimbeau JM, Panis Y, Couinaud C, et al. Sinistroposition of the gallbladder and the common bile duct. Hepatogastroenterology 2003;50:60–61. 14. Wu W, Lin XB, Qian JM, et al. Ultrasonic aspiration hepatectomy for 136 patients with hepatocellular carcinoma. World J Gastroenterol 2002;4:763–765. 15. Huguet C, Nordlinger B, Galopin JJ, et al. Normothermic hepatic vascular exclusion for extensive hepatectomy. Surg Gynecol Obstet 1978;147:689–693. 16. Troitskii RA. Current aspects of liver surgery. Review of the literature. Eksp Khir Anesteziol 1965;4:48–50. 17. Man K, Fan ST, Ng IO, et al. Prospective evaluation of Pringle maneuver in hepatectomy for liver tumors by a randomized study. Ann Surg 1997;226:704–713. 18. Jones RM, Moulton CE, Hardy KJ. Central venous pressure and its effect on blood loss during liver resection. Br J Surg 1998;85:1058–1060. 19. Wang WD, Liang LJ, Huang XQ, Yin XY. Low central venous pressure reduces blood loss in hepatectomy. World J Gastroenterol 2006;14:935–939. 20. Johnson LB, Plotkin JS, Kuo PC. Reduced transfusion requirements during major hepatic resection with use of intraoperative isovolemic hemodilution. Am J Surg 1998; 176:608–611. 21. Reed DN, Vitale GC, Wrightson WR, et al. Decreasing mortality of bile leaks after elective hepatic surgery. Am J Surg 2003;185:316–318.

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Left Hepatectomy Jay A. Graham, MD and Lynt B. Johnson, MD INTRODUCTION In regard to the performance of a left hepatectomy, the operative concepts remain unchanged from that of a rightsided resection. While technically easier than a right hepatectomy, the detailed understanding of liver anatomy is paramount to reproducibly performing safe left-sided hepatectomies. Moreover, the surgical pitfalls we discuss should prompt a thorough examination of hepatic anatomy as it relates to form and function to prevent the forthcoming outcomes.

INDICATIONS ● Benign tumors (e.g., hepatic adenoma or symptomatic hemangioma) ● Malignancies ● Primary liver cancer (hepatoma or cholangiosarcoma) ● Metastases

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7 Step 8

Operative incision Division of falciform ligament Division of left triangular and coronary ligaments Division of hepatogastric ligament Ligation and division of left hepatic artery and left portal vein branch Liver parenchymal division Left hepatic duct division Middle and left hepatic vein division

OPERATIVE PROCEDURE Operative Incision Typically, a right subcostal or chevron incision with midline extension is used to provide excellent exposure during a left hepatectomy.

Division of the Falciform Ligament The falciform ligament and ligamentum teres should be divided so that the left lobe can be fully mobilized.

Division of the Left Triangular and Coronary Ligaments Injury to the Phrenic Vessels As the phrenic vessels course along the diaphragm in an oblique fashion, they can be inadvertently transected during dissection of the left coronary ligaments (Fig. 32– 1). During this phase of left lobe mobilization, it is best to hug the surface of the liver. See Section IV, Chapter 31, Right Hepatectomy. Injury to the Inferior Vena Cava ● Consequence During division of the coronary and left triangular ligaments, the inferior vena cava (IVC) may be injured with medial dissection. Grade 5 complication ● Repair Management is discussed in Section IV, Chapter 31, Right Hepatectomy. ● Prevention Dissection of the coronary ligaments should be done with great care to minimize the chance of an inadvertent IVC puncture.

Esophageal Injury ● Consequence The esophagus lies at the inferior edge of the triangular ligament (Fig. 32–2). Esophageal injury may occur during stray dissection in this area. Grade 2/3 complication ● Repair Unrecognized esophageal injuries can be catastrophic. Therefore, the esophagus should be inspected carefully

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SECTION IV: HEPATOBILIARY SURGERY and primarily repaired immediately if an injury is found. Drains should be left in the vicinity and the patient kept on postoperative antibiotics that target enteric organisms. ● Prevention The left triangular ligament should be taken down at the peritoneal reﬂection of the left lobe. Dissecting along the inferior edge of the liver should keep the surgeon superior to the esophagus. A right angle can be used to pull the triangular ligament and peritoneal attachments away from crucial structures during this mobilization.

Division of the Hepatogastric Ligament Figure 32–1 The left coronary and triangular ligaments have been divided to reveal the bare area of the liver (↓). The left phrenic vein (▼) is prominent and observed to be coursing through this area. After dividing the left coronary and triangular ligaments, the surgeon rotates the left lobe medially to reveal the remnant of the ligamentum venosum as it enters the left hepatic vein just cephalad to the caudate lobe (䉮).

Injury to an Accessory or Replaced Left Hepatic Artery An accessory or replaced left hepatic artery branches off the left gastric artery. The aberrant artery lies in the hepatogastric ligament and can be injured during dissection (Fig. 32–3). The incidence of this anomaly is approximately 12.5%.1 ● Consequence Uncontrolled bleeding may result from inadvertent transection of an aberrant left hepatic artery traveling in the hepatogastric ligament. Grade 1 complication

Left triangular lig.

Right triangular lig.

Esophagus

Abdominal aorta IVC

Figure 32–2 The proximity of the left triangular ligament with the esophagus. The surgeon must be aware of this spatial anatomy to avoid inadvertent esophageal injury during left triangular ligament division.

32 LEFT HEPATECTOMY

341

Left gastric a. Left replaced hepatic a.

Right hepatic a. Proper hepatic a.

Figure 32–3 A replaced left hepatic artery should be recognized and controlled before division of the hepatogastric ligament to avoid potential bleeding.

● Repair The aberrant left hepatic artery must be ligated to stop any potential hemorrhage. If necessary, the left gastric artery can be sacriﬁced to control bleeding. ● Prevention Inoperative assessment with palpation can delineate any structures that lie within the hepatogastric ligament. The hepatogastric ligament should be palpated for an aberrant left hepatic artery prior to division.

MC

controlled. Once the hilar plate is retracted superiorly, ﬁrst palpate to conﬁrm normal hepatic artery anatomy or replaced variants. The adventitial tissue above the hepatic artery can be divided to expose the vessel. It is imperative that the surgeon trace back the surmised left hepatic artery to the common hepatic artery to avoid inadvertent injury to the right arterial supply. To gain access to the portal vein, lift the bile duct with a vein retractor to expose the left portal vein.

Gastric Perforation

Caudate Portal Vein Injury

● Consequence The stomach is tented against the liver by the hepatogastric ligament. Division of the tissue is often carried parallel to the lesser curve of the stomach, and injury may result. Grade 1 complication

● Consequence The left portal vein may give off a branch that feeds the caudate lobe. Ligation of the left portal vein proximal to this vein will cut off the portal venous supply to the caudate lobe. Grade 1 complication

● Repair If a gastric injury is noted, the opening should be primarily repaired immediately. An omental patch can be placed to bolster the repair. ● Prevention Angle the plane of dissection to hug the left lobe of the liver. Injury to the left lobe of liver is of no consequence since it will be resected.

Ligation and Division of the Left Hepatic Artery and the Left Portal Vein Branch The portal triad is easily viewed lying under the hilar plate of the quadrate segment, and the inﬂow vessels can be

● Repair Whereas the ligation of the left portal vein in this area is not ideal, there should be sufﬁcient inﬂow to the caudate lobe from arterial vessels. ● Prevention The caudate lobe portal venous supply can be preserved if the ligation of the left portal vein is distal to this branch. Every attempt should be made to adequately dissect the left portal vein before division to ensure salvation of the caudate portal inﬂow. If dissection is difﬁcult, dividing the left portal vein at the umbilical ﬁssure can be done, because the caudate portal vein is usually proximal to this point (Figs. 32–4 and 32–5).

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Liver Parenchymal Division Delayed Gastric Emptying ● Consequence Delayed gastric emptying is a known complication of left hepatectomy as the stomach contacts the surface of the cut liver. Delayed gastric emptying usually presents with early satiety, decreased appetite, weight loss, and nausea and vomiting. Grade 1 complication ● Repair In our clinical practice, gastric emptying is a rare entity seen after left hepatectomy. Although the clear cause is not understood, it is assumed that the postoperative inﬂammatory mediators from the cut surface of the liver decrease gastric motility. As the inﬂammatory

Figure 32–4 The caudate vein (blue tie) coming from the left portal vein. The surgeon’s index ﬁnger is placed on the caudate lobe for anatomic reference.

response subsides in the postoperative period, gastric motility usually returns to normal. If delayed gastric emptying persists, a specialist in gastroenterology should be involved to rule out mechanical obstruction and to help with possible prokinetic medical therapy. ● Prevention A recent study purports that tacking the omentum to the peritoneum prevents delayed gastric emptying by reducing stomach and liver contact.2 However, there is no clear consensus on the best preventive therapy.

Gastric Volvulus ● Consequence Mesenteroaxial gastric volvulus has been described after left-sided hepatic resections. The clinical presentation is variable, but often, the patient presents with symptoms related to a chronic intermittent gastric outlet obstruction. In the living related donor, the occurrence is reported as 11%.3 Grade 3 complication ● Repair Mesenteroaxial volvulus has been described in partial lobectomy or complete transplantation of the liver.4 Typically, gastric volvulus can be managed with nonoperative therapy, including proton pump inhibitors, nasogatric tube suction, and attempted reduction via endoscopy.5 If the patient’s symptoms persist or the clinical presentation deteriorates, exploratory laparotomy with gastropexy should be done. Vascular compromise is uncommon in mesenteroaxial gastric volvulus, so the need for resection of nonviable stomach is rare. ● Prevention Mesenteroaxial gastric volvulus associated with left hepatectomy is almost certainly associated with division

Caudate lobe outline Branches to caudate lobe

Portal vein

Figure 32–5 The caudate lobe venous supply is shown.

32 LEFT HEPATECTOMY

343

Aberrant dorsal caudal branch of the right hepatic duct

Right hepatic duct Left hepatic duct

Common hepatic duct

Common hepatic duct

A

B

Figure 32–6 A, Hilar hepatic duct division is fraught with potential risks owing to the prevalence of biliary anatomic aberration. Intraparenchymal division of the left hepatic duct improves the chance that injury will be avoided. B, An aberrant dorsal caudal branch of the right hepatic duct is shown.

of the hepatogastric ligament. However, division of this structure is inevitable with left-sided liver resection. Therefore, patients should be counseled with regard to the risk of this potentially chronic problem and corrective surgery. There is no precedent in the literature to perform gastropexy at the time of liver resection, and we do not employ this technique in our practice because we believe the risks outweigh the beneﬁts.

Left Hepatic Duct Division (Fig. 32–6) Injury to the Aberrant Dorsal Caudal Branch of the Right Hepatic Duct Whereas some groups advocate division of the left hepatic duct during hilar dissection, we do not use this technique. Biliary anatomic aberration poses potentially disastrous complications to the liver surgeon. We believe these risks are signiﬁcantly minimized by opting to divide the left hepatic duct during liver parenchymal division, rather than at the hilum. ● Consequence The biliary system is prone to anatomic variation. These variations can be problematic in patients undergoing a left hepatectomy. Aberrant posterior right hepatic ducts that drain into the left hepatic duct in the intrahepatic

umbilical ﬁssure are estimated at 11%.6 A closed biliary system can arise if this type of anatomy is encountered. Division of the left hepatic duct proximal to the aberrant posterior right hepatic insertion will result in an open posterior right biliary system. Grade 3 complication ● Repair In general, if the injury is signiﬁcant, a Roux-en-Y right hepaticojejunostomy must be created in order to drain the right posterior segmental of the biliary tree. Other options include attempted primary anastomosis with a T tube, but these surgical reconstructions often have a high rate of failure. If the duct is less than 2 mm, often simple ligation can be employed. Closure may lead to atrophy of the corresponding posterior right segments. ● Prevention We believe that the left hepatic duct should be divided during parenchymal division to avoid unintentional biliary tract injury. We believe this approach gives the surgeon the best opportunity to correctly identify the left hepatic duct. Moreover, biliary branches traveling in the left lobe encountered during parenchymal division are likely to solely feed the left lobe. The same cannot be said for biliary branches traversing the hilum.

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Middle and Left Hepatic Vein Division Many liver surgeons prefer extrahepatic control of the hepatic veins prior to parenchymal division. Whereas surgical preference dictates the techniques used for control of the hepatic veins, we believe that employment of intraoperative ultrasound and intraparechymal division confers many advantages. Namely, the liver surgeon can avoid difﬁcult dissection and isolation of the hepatic veins, especially the left hepatic vein that typically joins the middle hepatic vein within 2 cm of the IVC.

Injury to the IVC See Section IV, Chapter 31, Right Hepatectomy. Injury to the Spleen Overaggressive mobilization and rotation of the left lobe anterior and to the right prior to complete division of the left triangular ligament can lead to inadvertent splenic tears. ● Consequence During mobilization of the left hepatic lobe in a medial and anterior fashion, ligamentous attachments may avulse the spleen. Grade 4 complication ● Repair Splenic injury necessitates either splenorrhaphy or splenectomy to control bleeding. Capsular tears can sometimes be repaired by placing surgical ties over the

injury and welding them in place with the argon beam coagulator. ● Prevention Splenic avulsion can be prevented by ensuring that all posterolateral peritoneal reﬂections to the spleen are divided prior to mobilizing the liver.

REFERENCES 1. Varotti G, Gondolesi GE, Goldman J, et al. Anatomic variations in right liver living donors. J Am Coll Surg 2004; 198:577–582. 2. Yoshida H, Mamada Y, Taniai N, et al. Fixation of the greater omentum for prevention of delayed gastric emptying after left-sided hepatectomy: a randomized controlled trial. Hepatogastroenterology 2005;65:1334–1337. 3. Akamatsu T, Nakamura N, Kiyosawa K, et al. Gastric volvulus in living, related liver transplantation donors and usefulness of endoscopic correction. Gastrointest Endosc 2002;55:55–57. 4. Franco A, Vaughan KG, Vukcevic Z, et al. Gastric voluvlus as complication of liver transplant. Pediatr Radiol 2005;35: 327–329. 5. Wasselle JA, Norman J. Acute gastric volvulus: pathogenesis, diagnosis, and treatment. Am J Gastroenterol 1993;8: 1780–1784. 6. Cheng YF, Huang TL, Chen CL, et al. Anatomic dissociation between the intrahepatic bile duct and portal vein: risk factors for left hepatectomy. World J Surg 1997;21:297– 300.

33

Trisectionectomy John E. Scarborough, MD, Carlos E. Marroquin, MD, Bryan M. Clary, MD, and Paul C. Kuo, MD, MBA INTRODUCTION Trisectionectomy is the most extensive hepatic resection procedure possible, short of total hepatectomy in preparation for orthotopic liver transplantation. Left trisectionectomy, also called extended left hepatectomy, involves the resection of the left hepatic segments (2, 3, and 4) as well as the right anterior sector (segments 5 and 8). Resection of the caudate lobe (segment 1) is also occasionally included in this procedure. Right trisectionectomy, also referred to as extended right hepatectomy, involves resection of the right lobe of the liver (segments 5, 6, 7, and 8) as well as segment 4 of the left lobe. These extensive procedures are primarily indicated in patients with extremely large hepatocellular carcinomas involving both hepatic lobes, large hepatoblastomas in pediatric patients, and centrally located (hilar) cholangiocarcinomas. Trisectionectomy has also been described in case reports for the management of a variety of metastatic lesions and for a host of benign hepatic diseases. As experience with hepatic resection has evolved since the late 1980s, signiﬁcant improvements in perioperative morbidity and mortality have been realized. Nonetheless, because it involves the resection of up to 70% to 80% of functional hepatic mass, trisectionectomy places patients at considerable risk for postoperative morbidity. In a study of over 1800 liver resections performed at Memorial Sloan-Kettering from 1991 to 2001, investigators found that the incidence of postoperative morbidity and mortality increased signiﬁcantly as the number of segments involved in the resection increased. For patients undergoing trisectionectomy at that institution, the complication rate of 75% and operative mortality rate of 7.8% were signiﬁcantly higher than for patients undergoing less extensive resections.1 When the same authors analyzed a subgroup of 226 patients undergoing only extended hepatic resections, they were able to identify a total of ﬁve factors that were most predictive of in-hospital mortality: cholangitis, creatinine greater than 1.3 mg/dl, total bilirubin greater than 6 mg/dl, intraoperative blood loss greater than 3 L, and vena caval resection.2 The presence of any two of these factors was associated with 100%

mortality, whereas the absence of any of these factors was associated with only 3% mortality. In the largest series of left hepatic trisectionectomies published to date, from Nishio and colleagues,3 revealed an overall morbidity rate of 46% and a 30-day mortality rate of 7%. Preoperative jaundice and intraoperative blood transfusion were identiﬁed by multivariate analysis to be the major risk factors for postoperative morbidity in this group of 70 patients. Knowledge of the variables most predictive of postoperative morbidity has stimulated a number of modiﬁcations in the preoperative and intraoperative management of patients undergoing extended hepatic resection. Preoperative management options such as portal venous embolization and biliary drainage, as well as intraoperative techniques aimed at limiting blood loss, have enabled trisectionectomy to be performed with minimal perioperative mortality and major postoperative morbidity. One analysis of 58 major hepatic resections, including 49 trisectionectomies, reported 0% perioperative mortality and a 43% morbidity rate, with no cases of postoperative liver failure.4 Other groups are reporting similar outcomes, indicating that trisectionectomy for oncologic diagnoses can be performed with minimal short-term mortality.5,6

INDICATIONS ● Large hepatocellular carcinoma involving bilateral hepatic lobes ● Large hepatoblastomas (pediatric patients) ● Hilar cholangiocarcinomas involving bilateral hepatic ducts ● Metastatic tumors to liver involving bilateral hepatic lobes (e.g., colorectal metastases)

OPERATIVE STEPS COMMON TO BOTH RIGHT AND LEFT TRISECTIONECTOMY 7 Step 1 Step 2

Diagnostic laparoscopy to detect unresectable disease Incision: bilateral subcostal incision with midline extension to xyphoid process

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Abdominal exploration and intraoperative ultrasonography of hepatic lesions and major vascular structures 4 Mobilization of liver 5 Conﬁrmation of arterial anatomy via palpation of gastrohepatic ligament and gastroduodenal ligament to rule out accessory/replaced hepatic arteries 6 Ligation of cystic duct and artery, cholecystectomy 7 Control of inﬂow vessels via extrahepatic dissection and ligation 8 Control of outﬂow vessels 9 Parenchymal transection 10 Closure of abdominal wall in one or two layers and skin closure

Step 3

Step Step

Step Step Step Step Step

OPERATIVE STEPS SPECIFIC TO RIGHT TRISECTIONECTOMY Control of inﬂow vessels via extrahepatic dissection and ligation Open sheath of porta hepatis, dissection of plane between common bile duct and portal vein, ligation and division of right portal vein, ligation and division of right hepatic artery Dissection of umbilical ﬁssure to identify vascular pedicles to segments 2, 3, and 4. Identiﬁcation, ligation, and division of hepatic arterial and portal venous branches to segment 4 8R Control of right hepatic vein Division of right triangular ligament to completely mobilize right lobe off retroperitoneum Ligation/division of small hepatic venous tributaries from caudate process and posterior aspect of right lobe to inferior vena cava (IVC) Isolation, ligation, and division of right hepatic vein Isolation, ligation, and division of middle hepatic vein 9R Parenchymal transection Plane of transection is to immediate right of falciform ligament, starting from anterior surface and proceeding back toward divided right hepatic vein

Step 7R ●

●

Step ● ●

● ●

Step ●

OPERATIVE STEPS SPECIFIC TO LEFT TRISECTIONECTOMY Control of inﬂow vessels via extrahepatic dissection and ligation (see Fig. 33–1) ● Dissection of umbilical ﬁssure to identify, ligate, and divide left hepatic artery ● Identiﬁcation, ligation, and division of left portal vein at base of umbilical ﬁssure (proximal or distal

Step 7L

Step ● ● ●

Step ●

to caudate branch, depending on whether caudate lobe to be included in resection) 8L Control of outﬂow vessels (middle and left hepatic veins) Retract left liver to patient’s right after division of lesser omentum Identify and divide ligamentum venosum between caudate lobe and back of segment 2 Individual division of left and middle hepatic veins using vascular stapler 9L Parenchymal transection Plane of transection is lateral to gallbladder fossa and anterior to main right hepatic venous trunk halfway between right anterior and posterior pedicles

OPERATIVE PROCEDURE Skin Incision Inadequate Exposure The standard skin incision used for trisectionectomy is the bilateral subcostal incision with extension of the midline cephalad toward the xyphoid process. In special cases, however, this incision may not provide optimal exposure. This is especially true for redo hepatic resections involving the right hepatic lobe, for large tumors in the superior portions of the right or left hepatic lobes, or when the IVC requires dissection above the level of the diaphragm. ● Consequence Difﬁculty in hepatic venous identiﬁcation and control owing to inadequate liver mobilization increases the potential for hepatic venous injury and subsequent massive hemorrhage. Grade 5 complication ● Repair Maximizing the position of a self-retaining retractor may permit better visualization of the suprahepatic and retrohepatic IVC.8 In cases in which manipulation of the retractor still does not provide adequate exposure, extension of the subcostal incision further to the right or left may help to improve exposure. Rarely, creating a modiﬁed thoracoabdominal incision permits exposure to the chest and supradiaphragmatic vena cava and may be especially useful in patients with bulky tumors of the superoposterior portions of the right hepatic lobe, especially in large patients.9 ● Prevention An alternative to the bilateral subcostal incision is an upper midline incision from the xyphoid process to 2 cm superior to the umbilicus connecting to a right transverse abdominal incision extending to the midaxillary line halfway between the lowest rib and the right iliac crest.7 This incision usually provides sufﬁcient

33 TRISECTIONECTOMY exposure for all types of hepatic resection, including resections involving the right lobe of the liver. A right anterolateral thoracoabdominal incision will permit access to both the chest and the abdominal cavity and should be considered preoperatively either in patients with a large tumor of the right lobe or in those who require repeat resection after a previous right hepatic lobectomy. In the Memorial Sloan-Kettering series of over 1800 hepatic resections, a thoracoabdominal incision was required in only 3% of patients.1

Mobilization of the Liver Postoperative Pleural Effusion Pleural effusion is one of the most common complications after major hepatectomy and likely has a multifactorial etiology. A retrospective review of 254 patients undergoing liver resection for hepatocellular carcinoma at one institution found the incidence of patients developing postoperative intractable pleural effusion to be 5.9%.10 The pressure differential between the abdominal and the thoracic spaces, combined with compromise of the diaphragmatic barrier owing liver mobilization, can cause ascitic ﬂuid to traverse the diaphragm and accumulate in the right pleural space. Patients with some degree of underlying cirrhosis are also commonly hypoalbuminemic and may also have high portal venous pressures that are transmitted to the azygous vein, thus promoting transudation into the pleural space.11 ● Consequence Although often asymptomatic, postoperative pleural effusions may compromise the respiratory function of posthepatectomy patients. The effusion can cause pulmonary atelectasis and poses a risk factor for nosocomial pneumonia. In patients on the ventilator, signiﬁcant pleural effusion can increase the number of days that mechanical ventilation is necessary, whereas in patients who have already been extubated, pleural effusion may increase the incidence of reintubation. Grade 2 complication ● Repair Intraoperatively, pleural drainage using an indwelling central venous catheter in the pleural cavity has been shown to be efﬁcacious in preventing the accumulation of pleural ﬂuid after hepatectomy.12 Postoperative drainage for pleural effusion is indicated either in patients who are experiencing difﬁculty weaning from mechanical ventilation or in those who have marginal respiratory function postextubation. Management options include diuretic administration, pleural drainage via either thoracentesis or a pleural drainage catheter, and pleurodesis. In a study of 10 patients with postoperative pleural effusion, 4 responded to conservative management with diuretics, 4 required pleural drainage, and 2 required pleurodesis.11

347

● Prevention Multivariate analysis of patients with intractable posthepatectomy pleural effusion revealed increased serum levels of type IV collagen, preoperative transcatheter arterial embolization, and resections including segments 7 and/or 8 to be independent risk factors for the development of this complication.10 A separate investigation conﬁrmed that resections involving segments 7 and 8, via either right hepatectomy or posterior segmentectomy, led to increased risk of postoperative pleural effusion.13 The difference between the positive pressure of the abdominal cavity and the negative pressure of the intrathoracic space may contribute to the unidirectional diffusion of ascitic ﬂuid into the pleural space, especially as the dissociation of the liver from its diaphragmatic attachments can lead to an increase in the development of small holes in the diaphragm. Simply extending the duration of postoperative mechanical ventilation by 1 day postoperatively has been shown to reduce the development of pleural effusion after hepatectomy, presumably by providing persistent positive intrathoracic pressure to allow ﬁbrin deposits to seal the small diaphragmatic communications between the abdomen and the thoracic cavity and thus preventing the migration of ascitic ﬂuid.14 Alternatively, argon beam coagulation of the dissected diaphragmatic surfaces may help to seal these tiny routes for ﬂuid migration intraoperatively. Yan and colleagues12 compared two groups of hepatectomy patients, one who underwent separation of the liver from the diaphragm using argon beam coagulation and the other undergoing suture ligation of bleeding points from the diaphragmatic attachments. Patients in the argon beam coagulation group had a 3.8% incidence of postoperative pleural effusion, whereas patients in the suture ligation group had a 10.5% incidence (P < .01). In a separate prospective, randomized trial of 60 patients undergoing hepatectomy, 28 underwent argon beam coagulation of the cut surface of the hepatic ligaments and bare area of the retroperitoneum whereas 32 did not. The two groups of patients were similar with respect to demographic characteristics as well as preoperative and postoperative liver function. One of the 28 patients receiving argon beam coagulation developed postoperative pleural effusion at 3 days postoperatively compared with 9 of the 32 patients who did not receive argon beam coagulation.11 An alternative to the use of argon beam coagulation is to apply ﬁbrin sealant to the cut surface of the diaphragmatic attachments after liver mobilization. This technique resulted in a signiﬁcant reduction in the development of postoperative pleural effusion among 25 patients undergoing hepatectomy compared with a control group of 39 patients in whom ﬁbrin sealant was not used.15 Avoidance of routine use of the thoracoabdominal approach to liver resection has also been suggested as a means to reduce the incidence of postoperative pleural effusion and the

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necessity for subsequent thoracentesis because up to 73% of patients in whom this incision is used will develop pleural effusion postoperatively.16

Control of Inﬂow Vessels Hepatic Necrosis due to Hepatic Arterial or Portal Venous Injury or Thrombosis Because trisectionectomy involves the removal of a large majority of functional hepatic mass, injury to any of the major structures that provide vascular inﬂow to the remnant liver can have severe consequences. ● Consequence The hepatic artery is responsible for up to 50% of the oxygen supply to the liver. Because the oxygen consumption is expected to be elevated after hepatectomy as the remnant liver undergoes regeneration, compromise of oxygen delivery to the remnant liver owing to hepatic arterial injury can result in acute necrosis of the remaining hepatic tissue. In addition, compromise of the portal venous ﬂow postoperatively can also result in hepatic necrosis because the portal vein normally provides 75% of blood ﬂow to the liver. Acute hepatic necrosis is typically characterized by acute abdominal pain and abrupt, marked increases in transaminase levels. Other sequelae of fulminant hepatic failure may soon follow. The diagnosis can be conﬁrmed by duplex ultrasonography, which will document reduced or absent hepatic arterial or portal venous ﬂow and hypoechogeneic areas within the remnant liver. Computed tomography can verify the absence of portal ﬂow and arteriography can verify the absence of hepatic arterial ﬂow, if ultrasound is equivocal.17 Grade 4 complication ● Repair Injuries to the hepatic artery or portal vein that are recognized intraoperatively can usually be repaired. Hepatic arterial injuries that do not involve excessive segment lengths can be repaired using a direct end-toend anastomosis or a saphenous vein interposition graft. Portal venous injuries, meanwhile, can usually be repaired by venoplasty using the greater saphenous vein. Vascular reconstruction of either the hepatic artery or the portal vein in patients undergoing hepatic resection for cholangiocarcinoma has been shown to result in survival rates comparable with those in patients who do not require such reconstruction.6 Unrecognized hepatic arterial injuries that lead to hepatic arterial thrombosis postoperatively are usually not necessary to repair because the resulting hepatic necrosis is irreversible. However, in order to maximize the function of the remaining liver tissue, some groups have reported performing portal arterialization in these situations. This procedure involves the construction of a shunt

between the portal vein and a mesenteric artery, thereby increasing the delivery of oxygen to regenerating hepatic tissue that is spared of necrosis.17,18 ● Prevention The best way to prevent hepatic arterial injury is to have a thorough knowledge of variants to normal hepatic arterial anatomy and to carefully assess the anatomy of individual patients through preoperative multisection computed tomographic arteriography. “Normal” hepatic arterial anatomy, which is present in only 55% of patients, consists of a common hepatic artery coming off of the celiac axis, giving off a gastroduodenal branch to then become the proper hepatic artery.19 The proper hepatic artery travels toward the liver within the hepatoduodenal ligament, lying anterior to the portal vein and to the left of the common bile duct. In up to 20% to 30% of patients, a left hepatic artery arises from the left gastric artery. This can be either an accessory left hepatic artery (which occurs in addition to a left branch of the proper hepatic artery) or a replaced left hepatic artery (which represents the sole arterial supply to the left segments of the liver). In approximately 17% of patients, a right hepatic artery arises from the superior mesenteric artery. This artery, which can also serve as either an accessory or a replaced right hepatic artery, travels within the hepatoduodenal ligament posterior to the common bile duct, then to the right of the common hepatic duct as it approaches the hilum of the liver.20 Portal venous anatomy tends to be more consistent from patient to patient, although variants do exist. The portal vein lies posterior to both the common bile duct and the hepatic artery within the hepatoduodenal ligament. The most common anomaly requiring attention during left trisectionectomy is trifurcation of the portal vein, in which the portal vein branches to the right paramedian and lateral sectors originate from the main portal vein in addition to the left portal vein.21 In patients with a normal portal vein bifurcation undergoing left trisectionectomy, care must be taken in dissecting the right portal vein because this branch is much shorter than the left portal vein (Fig. 33–1). In addition to thorough knowledge of these types of variants, avoiding injury or excessive manipulation of the hepatic artery and portal vein that is to supply the remnant liver is also essential for preventing postoperative hepatic necrosis owing to hepatic arterial injury. For example, when performing a Pringle maneuver, a tourniquet made from a Penrose drain to obtain vascular inﬂow occlusion should be used in order to avoid intimal disruption within the proper hepatic artery that can be caused by direct application of vascular clamps.17 In addition, veriﬁcation of pulsatile blood ﬂow to the planned hepatic remnant during occlusion of arterial inﬂow into liver to be resected will assist in prevention of this complication.

33 TRISECTIONECTOMY

349

Left hepatic duct Left superior, inferior hepatic ducts

Right hepatic duct

Gall bladder

Hepatic portal vein

Figure 33–1 Isolation of hepatic arterial and portal venous inﬂow of the planned resection. Careful dissection of the left hepatic artery, and left portal vein is critical in order to prevent damage to the vascular inﬂow of the remnant liver. The point of ligation of the left portal vein will depend on whether the caudate lobe is to be resected with the specimen or left with the remnant liver.

Cystic duct Common hepatic duct Common bile duct Inferior vena cava

Injury to the Arterial Supply of the Biliary System ● Consequence Injury to the right hepatic artery, or its branches that supply the major bile ducts, can result in ischemic injury to the duct and subsequently long-term bile duct stenosis. Such stenosis can subsequently lead to recurrent episodes of cholangiitis or even the development of cirrhosis of the remnant liver. Grade 3 complication ● Repair Accidental division of the major bile duct that is to drain the remnant liver after trisectionectomy requires intraoperative reestablishment of biliary continuity. This can be accomplished either through a direct endto-end anastomosis of the proximal duct and distal common bile duct or by Roux-en-Y hepaticojejunostomy. Although primary anastomosis can be considered for dilated ducts, a bilioenteric anastomosis is usually preferred for ducts that are of normal caliber because the risk of postoperative biliary stenosis is minimized. In cases of unrecognized biliary injury due to ischemic damage to the major bile duct draining remnant liver, repair involves reoperation and Roux-en-Y hepaticojejunostomy. If the patient presents with postoperative cholangiitis due to biliary obstruction, the percutaneous transhepatic drainage of the remnant biliary system should be performed prior to deﬁnitive repair. ● Prevention Knowledge of the arterial blood supply to the extrahepatic biliary system is important in order to avoid isch-

Abdominal aorta Common hepatic artery

emic insult to the biliary drainage of the remnant liver after trisectionectomy. The epicholedochal plexus at the biliary bifurcation derives its blood supply primarily from the right hepatic artery, which sends a branch to the plexus when it passes posterior to the common bile duct. Therefore, dissection and division of the right hepatic artery during right trisectionectomy should be performed to the right of the common bile duct in order to avoid damaging this branch.21 Furthermore, division of biliary structures during major hepatectomy should be delayed until after parenchymal resection in order to avoid biliary injury. Minimization of hilar dissection is also preferable in order to avoid injury to the vascular supply of the remnant biliary duct. Recently described techniques in which the glissonian sheaths of the segments to be resected are isolated and divided individually can help limit the degree of hilar dissection necessary to achieve resection.22 In cases in which extrahepatic bile duct excision is necessary, especially when the indication for resection is a perihilar cholangiocarcinoma, the common bile duct should be excised extrahepatically as close to the pancreas as possible in order to ensure negative resection margins. After the bile duct has been resected, the sectional bile duct draining the remnant liver can then usually be reconstructed using a Roux-en-Y hepaticojejunostomy.

Control of Outﬂow Vessels Massive Hemorrhage due to Injury to the Hepatic Vein or the IVC The best way to prevent massive, life-threatening hemorrhage during major hepatic resection is to establish ade-

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quate control of vascular inﬂow and outﬂow prior to dissection of juxtacaval adhesions or tumor. ● Consequence Massive hemorrhage due to vena caval or hepatic venous injury is the primary cause of intraoperative mortality during hepatectomy. Grade 5 complication ● Repair If bleeding results from a tear of a hepatic vein at its junction with the liver, then the vessel loops or umbilical tape previously placed around the hepatic veins and the hepatoduodenal ligament should be tightened so as to prevent blood ﬂow into and out of the liver. The venous injury can then be repaired primarily. If bleeding arises from the IVC, then rapid control proximal and distal to the site of injury may be required. Control of the infrahepatic cava can be achieved rather quickly using direct pressure. Control of the suprahepatic cava may be more difﬁcult. If access to this area is obscured by the liver or by tumor, the patient’s incision can be extended at the midline into a median sternotomy in order to obtain rapid control of the supradiaphragmatic vena cava. The vena caval injury can then be repaired using either primary repair or venoplasty with the greater saphenous vein. ● Prevention Adequate control of the vascular inﬂow and outﬂow of the liver to permit total hepatic vascular isolation is essential for prevention of massive hemorrhage during major hepatectomy. This is especially true for trisectionectomy, when complete mobilization of the liver is required, and for tumors abutting the IVC or hepatic veins. Control of hepatic inﬂow is described later. The technique needed to obtain proper control of the hepatic veins requires division of the falciform ligament in a cephalad direction to the upper peritoneal folds of the right and left triangular ligaments.23 The gutter between the liver, the right hepatic vein, and the middle hepatic vein is then developed by blunt dissection from an anterior approach. The right lobe is then fully mobilized and retracted upward and medially. The numerous short posterior tributaries between the vena cava and the posterior right lobe or caudate lobe that are invariably present must then be ligated and divided. If a right inferior hepatic vein is also present, as is the case for 20% of patients, it should also be ligated and divided, unless it is large or a left trisectionectomy with preservation of the right posterior segments is being performed. After ligation and division of the hepatocaval ligament, the right hepatic vein can then be safely encircled with a tape. For extrahepatic control of the middle and left hepatic veins, the peritoneal reﬂection above the caudate lobe is divided, followed by ligation and division of the ligamentum venosum.24 The junc-

tion of the left hepatic vein and vena cava are thereby exposed. A blunt dissector can then be passed into the gutter between the right and the middle hepatic veins, and the common trunk to the middle and left hepatic veins thereby encircled with a tape.

Parenchymal Transection Intraoperative Bleeding Intraoperative blood loss is an inevitable part of major hepatectomy. Massive hemorrhage owing to major hepatic venous or caval injury is immediately life-threatening. Steps to avoid this type of hemorrhage have been outlined previously. Bleeding that occurs during hepatic parenchymal transection may be more insidious, but the total amount of blood lost during this part of the procedure can be signiﬁcant. This is especially true during left trisectionectomy, when the plane of transection is relatively large compared with that in right trisectionectomy. ● Consequence Intraoperative bleeding requiring blood transfusion has been frequently cited as a signiﬁcant predictor of posthepatectomy morbidity.2,24–27 Analysis of trisectionectomy patients reinforces this relationship. In a review of 70 patients undergoing left hepatic trisectionectomy, Nishio and colleagues3 identiﬁed intraoperative blood transfusion as an independent risk factor for postoperative morbidity. The mechanism underlying this relationship between intraoperative blood loss and increased postoperative morbidity is likely multifactorial. For example, the immunosuppressive effects of transfused blood products have been shown to increase the incidence of postoperative infectious complications after hepatectomy.27,28 In addition, the ﬁnding that perioperative blood transfusion is an independent risk factor for recurrence of hepatocellular carcinoma status after hepatectomy suggests that the immunosuppressive effects of blood products may have adverse oncologic consequences as well.29 Grade 5 complication ● Repair Unlike hepatic venous or caval injuries, for which repair of the injury will stop the bleeding, no speciﬁc repair exists for hemorrhage that occurs during parenchymal transection. Instead, efforts should be focused on preventing such bleeding through meticulous transection technique combined with judicious use of vascular inﬂow and potentially outﬂow occlusion. When bleeding does occur and is not associated with hemodynamic instability, avoidance of routine blood product transfusion is probably desirable. Ancillary management options to help limit the need for blood transfusion include preoperative autologous blood donation, the use of erythropoietic stimulants, selective transfusion criteria, and isovolumic hemodilution. The best way to

33 TRISECTIONECTOMY avoid the need for blood transfusion, however, is to prevent excessive blood loss intraoperatively. ● Prevention Techniques for prevention of blood loss during parenchymal transection, and thus the need for perioperative blood transfusions, have focused on the use of vascular inﬂow and outﬂow occlusion and on techniques for parenchymal transection. The simplest method for limiting blood loss by vascular inﬂow occlusion is to clamp the main hepatic pedicle, a technique popularly known as the Pringle maneuver.30 To perform this maneuver, the hepatoduodenal ligament is dissected free of surrounding adhesions and encircled with tape. The ligament is then compressed using either a Rommel tourniquet or a vascular clamp while the parenchymal transection is being performed, with complete occlusion of the pedicle being conﬁrmed by absence of the hepatic arterial pulse. The hemodynamic changes associated with hepatic pedicle clamping are mild and usually very well tolerated.31 The duration of inﬂow occlusion that the remnant hepatic parenchyma will tolerate depends on whether the clamp is applied continuously or intermittently. Continuous clamping will be tolerated for up to 60 minutes by a normal liver but for less than 30 minutes in a steatotic or cirrhotic liver.31,32 Continuous clamp times beyond these will considerably increase the risk for postoperative hepatic insufﬁciency. If intermittent clamping is used, in which clamped periods of 15 to 20 minutes are alternated with unclamped periods of 5 minutes, the duration of ischemia tolerated by a normal liver can be increased to up to 120 minutes.33 The reason for the increased tolerance of hepatic parenchyma to intermittent rather than continuous hepatic pedicle clamping likely involves a favorable preconditioning of hepatic parenchyma to ischemia reperfusion provided by the intermittent clamping method.34 Because of this hepatoprotective effect, the greater extent of splanchnic congestion that occurs with continuous clamping, and the prospective observation that continuous clamping does not result in less total operative blood loss compared with intermittent clamping, intermittent hepatic pedicle clamping appears to be the preferred mode of hepatic vascular inﬂow interruption.35 Alternatives to occlusion of the entire hepatic vascular inﬂow include hemihepatic clamping or segmental vascular clamping.24 These techniques involve the selective interruption of hepatic arterial and portal venous inﬂow of the hepatic segments to be resected, without interruption of inﬂow to the remnant liver. The theoretical advantages of these selective inﬂow occlusion techniques are that they avoid ischemic insult to the remnant liver, demarcate the area of liver that is to be resected, and limit the negative effects of hepatic pedicle clamping on splanchnic circulation and overall hemodynamics.36 Disadvantages to selective vascular inﬂow occlusion include the signiﬁ-

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cant hilar dissection required for selective clamping and the potential for bleeding from the transected edge of the nonoccluded liver. Because of these disadvantages, the selective technique appears to be most useful in cases in which a clear demarcation of the segment to be resected is desirable, such as in patients with cirrhosis in whom it is important to limit the degree of resection.31 There are several reasons why hepatic pedicle clamping may fail to adequately suppress blood loss during parenchymal transection: (1) incomplete clamping of the hepatic pedicle, (2) unrecognized replaced or accessory left hepatic artery, (3) the existence of hypervascular adhesions, which can occur in patients who have undergone prior hepatic resection or preoperative arterial chemoembolization, and (4) signiﬁcant backﬂow bleeding from the hepatic venous system. If the ﬁrst three possibilities have been ruled out and bleeding remains signiﬁcant, consideration can be given to minimizing hepatic venous ﬂow. The simplest and easiest way to minimize hepatic venous ﬂow is to reduce the central venous pressure, which constitutes the driving force for hepatic venous backbleeding, to less than 5 cm H2O.37 This can usually be achieved by careful volume restriction, but it requires an anesthesiology team speciﬁcally trained in this technique. The combination of intermittent hepatic pedicle occlusion and low central venous pressure anesthesia appears to result in a signiﬁcant reduction in intraoperative blood loss and may, therefore, contribute to a reduction in postoperative morbidity and mortality.38 Patients with heart failure or pulmonary arterial hypertension may be refractory to attempts to lower central venous pressure. In these situations, caval or hepatic venous occlusion may be necessary in addition to inﬂow occlusion. Total hepatic venous exclusion (THVE) involves placing clamps on the infrahepatic and suprahepatic IVC. This technique requires complete mobilization of the liver from its ligamentous attachments and adhesions. The right adrenal vein may require division in order to completely mobilize the infrahepatic cava. Once exposure to the cava is completed, clamps are applied to the hepatoduodenal ligament, the infrahepatic cava, and the suprahepatic cava, in that order. Maximal tolerable clamping durations, either for continuous clamping or for intermittent clamping, are similar to those tolerated during hepatic pedicle clamping alone. Once the parenchymal transection is complete, the clamp on the infrarenal vena cava is partially released in order to release any trapped air, and the clamps are removed in the reverse of the order in which they were originally placed.31 The major disadvantage to THVE is the effects that complete interruption of inferior vena caval ﬂow have on the cardiovascular system and splanchnic circulation. Owing to loss of preload by up to 60%, cardiac output will decrease signiﬁcantly. Reﬂexive increases in the heart rate and systemic vascular resistance by up to 80% will usually limit the resulting decrease in mean arterial pressure to only 10% to 12%, with the cardiac index being

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reduced by up to 50%.24 In approximately 10% to 15% of patients, however, the necessary sympathetic reﬂex does not occur, and as a result, the cardiac output will drop by more than 50% and the mean arterial pressure by more than 30%.35 It is difﬁcult to determine preoperatively which patients will not tolerate THVE, but an initial 2- to 5-minute trial of total vascular exclusion is generally predictive of a patient’s hemodynamic tolerance of this technique. Other potential deleterious effects of THVE include renal compromise, splanchnic congestions, and hyperamylasemia.24 In addition, patients who have undergone preoperative arterial chemoembolization may have dense adhesions between the vena cava and the caudate lobe and may risk signiﬁcant injury to the caudate or cava during placement of the infrahepatic clamp. Therefore, it is generally recommended that THVE be avoided in cirrhotic patients, patients with preexisting renal dysfunction, or patients who have undergone preoperative arterial chemoembolization.35 In these patients, and in those who do tolerate THVE hemodynamically, selective hepatic venous exclusion can be attempted in order to limit venous backbleeding during parenchymal transection. Selective hepatic venous exclusion (SHVE) involves the isolation and extrahepatic control of the right hepatic vein and the common trunk of the middle and left hepatic veins. The techniques required to isolate the hepatic veins have already been described. Because vena caval ﬂow is not interrupted, the hemodynamic effects of SHVE are similar to those seen with hepatic pedicle clamping and, thus, are generally well tolerated.31 Persistent venous backbleeding despite SHVE generally implies that a major venous tributary, from either an inferior right hepatic vein into the posterior right lobe, a short tributary from the cava to the posterior right lobe or the caudate lobe, or a left phrenic vein into the left hepatic vein, has not been properly identiﬁed. Whereas SHVE may be more technically challenging than THVE, it offers clear advantages in terms of hemodynamic stability and sparing of deleterious renal or splanchnic effects. Therefore, it should be considered the preferred technique for achieving hepatic vascular outﬂow occlusion when needed to limit venous backbleeding during parenchymal transection.35 The presence of tumor at the cavohepatic junction may make the dissection required for SHVE too dangerous, however, in which cases, THVE or potentially even venovenous bypass will be required. Other approaches toward minimizing blood loss and the need for transfusion during major hepatic resections such as trisectionectomies have focused on the technique used for parenchymal transection. The traditional method for dividing hepatic parenchyma involved crushing the parenchyma with either a pair of clamps or the thumb and foreﬁnger and then ligating and dividing the bile ducts and vessels isolated in this manner. More recently, several devices have been developed in an attempt to limit the blood loss associated with parenchymal transection and potentially to limit the duration of hepatic vascular inﬂow

occlusion that is needed during transection.39 One such device is the ultrasonic dissector (Cavitron ultrasonic surgical aspirator, Tyco Healthcare, Mansﬁeld, MA), which uses ultrasonic energy to locate ducts and vessels, thereby facilitating their identiﬁcation prior to ligation and division. Another device is the Hydrojet (Erbe, Tübingen, Germany), which uses a pressurized water jet to dissect the hepatic parenchyma, thus exposing vessels for ligation and division. The dissecting sealer (TissueLink, Dover, NH) device, meanwhile, combines radiofrequency and saline in order to precoagulate hepatic parenchyma prior to ligation and division of vessels. Only a few randomized, prospective trials have been performed to compare these various techniques of parenchymal transection. The traditional clamp-crushing technique was compared with an ultrasonic dissector in one study of 132 patients undergoing partial hepatectomies.40 The ultrasonic dissector did not result in any signiﬁcant improvement in blood loss, transection time, or transection speed, but it did cause more frequent tumor exposure at the surgical margin. Another prospective, randomized trial compared the ultrasonic dissector with a water-jet dissector and found that the water-jet dissector resulted in signiﬁcant reductions in transection time, transfusion requirements, and duration of hepatic pedicle occlusion required.41 In a more recent trial, 100 consecutive patients undergoing liver resection were randomized to one of four different transection strategies: (1) the traditional clampcrushing technique with routine inﬂow occlusion, (2) ultrasonic dissection without inﬂow occlusion, (3) waterjet dissection without inﬂow occlusion, and (4) salinelinked dissecting sealer without inﬂow occlusion.39 The authors found that patients who underwent transection using the clamp-crush technique had the quickest transection times and lowest blood loss of the four different techniques. Furthermore, the clamp-crush technique was shown to be the least costly, and the number of surgical clips or sutures required during parenchymal transection was no greater with the clamp-crush technique than with the other three techniques. These results suggest that parenchymal transection using the traditional clamp-crush technique may be more cost effective than using the newer devices. Ultimately, the choice of which transection technique to use seems to depend mostly on surgeon preference.

Postoperative Biliary Leak Postoperative bile leakage occurs in approximately 3% to 12% of patients undergoing hepatectomy, with the incidence being highest in those patients undergoing the most extensive resections.42,43 There are several potential mechanisms for this complication. Biliary leakage from smaller, peripheral biliary ductules can occur postoperatively from the cut surface of the hepatic parenchyma, either because such leaking ductules are not ligated sufﬁciently intraoperatively or because the cut surface of the

33 TRISECTIONECTOMY liver necroses and sloughs off, thus exposing these ductules. Leaks from major bile ducts can occur owing to intraoperative injury, inadequate ligation, or ischemia of the ligated stump with resulting necrosis and bile leakage. Other potential mechanisms for postoperative biliary leakage include leakage from bilioenteric anastomoses (when bile duct excision is required for complete resection of hilar cholangiocarcinoma), or leakage from immature T-tube sites. Of these potential mechanisms, leakage from peripheral ductules on the cut surface of the liver appears to be the most common culprit. ● Consequence The consequences of posthepatectomy biliary leakage stem from the presence of bile in the peritoneal cavity. Postoperative biliary leaks can cause exacerbation of abdominal pain, as well as other nonspeciﬁc gastrointestinal symptoms such as ileus. Postoperative bile collections can lead to intra-abdominal sepsis as well. Because patients undergoing trisectionectomy have little hepatic reserve immediately postoperatively, the development of such infection can lead to excessive metabolic demands on the hepatic remnant and, thus, the development of postoperative hepatic failure.44 For this reason, postoperative biliary leakage has been associated with an increased risk of postoperative liver failure and death, as well as prolonged hospitalization.43 Grade 3 complication ● Repair The traditional management of postoperative biliary leakage often involved reoperation in order to identify and repair the site of leakage and to ensure adequate external drainage of the leaking bile. However, reoperation for bile leakage is associated with a signiﬁcant increase in mortality rates, especially in patients with marginal posthepatectomy hepatic reserve owing to extensive resection. One retrospective review of patients with biliary leakage after hepatectomy found that the mortality rate of patients requiring reoperation owing to major bile leakage was almost 80%.43 Other studies support the extremely challenging nature of reoperations for biliary leakage.45 With the increasing availability of nonoperative management options for this complication, reoperation should therefore be reserved for patients with leaks from major bile ducts, those with life-threatening sepsis, and those in whom nonoperative management has failed to control or resolve the biliary leak. There are two primary considerations in managing patients with posthepatectomy leaks. First, appropriate control of leaking bile is necessary in order to prevent the development of intra-abdominal sepsis and, potentially, liver failure and death. Therefore, a patient with signs of infection that may be due to bile leakage should undergo ultrasound or computed tomography in order to assess for ﬂuid collections. Percutaneous drainage of such col-

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lections can then be performed as needed, with the ﬂuid returned being sent for bilirubin levels and bacterial culture. Broad-spectrum antibiotics should be started until culture and antibiotic sensitivity data from the drainage ﬂuid are available. If such measures result in adequate drainage of the bile leak and control of intra-abdominal infection, the patient can be managed expectantly. Drains can eventually be removed if the volume of output reduces to zero and the patient remains clinically well. In patients with persistent or high volumes of bilious drainage, efforts to determine the site of biliary leakage are warranted. Endoscopic retrograde cholangiopancreatography (ERCP) is probably the preferred diagnostic test in this case because it is minimally invasive and offers the potential for simultaneous therapeutic intervention. Patients with a major duct injury can then undergo temporary covered stent placement over the injury site, with a follow-up ERCP 4 to 6 weeks later to remove the stent and assess duct integrity. Patients without extravasation of contrast on initial ERCP can be assumed to be leaking bile from the cut surface of the liver. In such cases, several groups have shown that endoscopic sphincterotomy with or without placement of a temporary stent across the sphincter of Oddi may be helpful. These measures help to reduce the intraluminal pressure within the biliary system and, therefore, may facilitate healing of the leakage site. Alternatively, a nasobiliary drain can be placed, although this approach is less desirable from the standpoint of patient comfort. Several groups have reported successful management of persistent posthepatectomy biliary leaks using ERCP and stent or nasobiliary drainage placement, making this the preferred approach for patients with this complication.42,46,47 Finally, some groups have advocated injecting ablative substances such as ethanol or ﬁbrin glue into the percutaneous drains of patients who develop persistent postoperative biliary leaks that show no communication of the leakage point with the main biliary system on postoperative cholangiography.45,47,48 Whereas this technique offers the theoretical possibility of ﬁstula closure, and has met with some anecdotal success, there are no published studies comparing this technique to other methods of biliary ﬁstula management. ● Prevention In patients in whom a left trisectionectomy is planned, preoperative cholangiography is suggested in order to delineate potential biliary anatomic variations. In some patients, biliary ducts from the caudate lobe or right posterior segment will drain into the left hepatic duct close to the hilum. These patients are, therefore, at higher risk for postoperative biliary leakage during left trisectionectomy because the left hepatic duct will require division close to the hilum. Knowledge of any existing anatomic variants in these patients will therefore help to minimize the risk of postoperative biliary leakage.43

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Regarding biliary leakage from the cut surface of the liver, three major intraoperative techniques to detect potential leakage points have been developed: intraoperative cholangiography, bile leakage testing using methylene blue or normal saline, and application of ﬁbrin glue to the cut surface of the liver. Injection of diluted methylene blue or isotonic normal saline into the cystic duct after parenchymal transection can reveal leaking peripheral biliary ductules at the cut surface. These ductules can then be individually ligated. Alternatively, an intraoperative cholangiogram can be performed if the integrity of major bile ducts is in question. In a retrospective review of the usefulness of these detection techniques in 616 patients undergoing hepatic resection, Lam and coworkers49 found that the postresection methylene blue test resulted in a signiﬁcant reduction in postoperative biliary leak rates, whereas intraoperative cholangiography did not signiﬁcantly lower leak rates. In this same study, however, 10% of patients in whom the methylene blue test failed to demonstrate leak still developed biliary leaks postoperatively, indicating that this leak detection method is not always successful. Furthermore, a prospective study by Ijichi and associates50 randomized patients undergoing hepatic resection to receiving or not receiving a biliary leakage test intraoperatively. This study failed to show any signiﬁcant beneﬁcial effect of intraoperative leakage testing on the development of postoperative biliary leaks. Other authors have echoed the belief that intraoperative leakage tests are not signiﬁcantly effective in preventing postoperative biliary leaks, potentially because the segment of liver at which the leak originates may no longer be in continuity with the main biliary system.43 Based on the available literature, therefore, routine intraoperative bile leak testing cannot be recommended. Substances such as ﬁbrin glue have also been applied to the cut surface of the liver intraoperatively to prevent the development of postoperative biliary leakage.51 A recent prospective, randomized trial showed that patients who had ﬁbrin glue applied to the cut surface of their liver postresection had signiﬁcant reductions in postoperative drainage volumes compared with patients who did not receive ﬁbrin glue application.52 There was no analysis of drain content in these patients, however, and thus the incidence of postoperative biliary leakage in the two groups of patients was not known. Only one other prospective, randomized trial of topical sealants has been performed.53 In this trial, patients undergoing hepatic resection were randomized to either microcrystalline collagen powder or ﬁbrin glue applied topically to the cut surface of the liver. Despite the absence of a control population of patients in this study, patients in both the collagen powder and the ﬁbrin glue groups had a 6% rate of postoperative biliary leakage. Other groups have retrospectively analyzed the use of ﬁbrin glue application and have found that it does not reduce the incidence of postoperative biliary leakage.49 Therefore, routine use of ﬁbrin glue to the cut surface of the liver cannot be recom-

mended as a reliable method for preventing postoperative biliary leakage. In summary, the development of postoperative biliary leakage is a common complication among patients undergoing major hepatectomy. No intraoperative technique has yet been developed that fully prevents this complication. Intraoperative cholangiograpy may help to detect injury to major bile ducts if there is some reason to suspect such injury, and injection of saline or methylene blue into the cystic duct after cholecystectomy may help to identify potential sites of leakage from the postresection cut surface, but neither of these detection methods nor the topical application of ﬁbrin glue has been found to reliably prevent postoperative bile leaks from occurring. Necrosis of the cut surface, possibly in combination with intraabdominal infection, may help to explain why such maneuvers do not prevent postoperative biliary leakage. Meticulous surgical technique, therefore, remains the primary method for minimizing the development of this complication.

Other Complications Postoperative Hepatic Insufﬁciency Postoperative hepatic insufﬁciency is a dreaded complication of hepatic resection. The incidence of postoperative hepatic failure varies from institution to institution and depends in part on the deﬁning parameters. In a retrospective analysis of over 1000 patients undergoing hepatectomy at one center, Imamura and colleagues54 reported only 1 patient who developed hepatic failure postoperatively. This group deﬁned hepatic failure as a bilirubin level greater than 5.0 mg/dl and/or a prothrombin rate of less than 50% for 3 or more consecutive days. Because trisectionectomy involves resection of up to 80% of functioning liver parenchyma, it is expected that this procedure would be associated with higher rates of postoperative hepatic failure than those of lesser resections. Indeed, Nagino and coworkers55 reviewed the postoperative complications in 105 patients who underwent hepatectomy for hilar cholangiocarcinoma. This group found that postoperative hepatic failure developed in 16.7% of patients who had less than 50% of their liver resected versus 36.8% of patients who had resection of greater than 50%. In an analysis of 70 patients undergoing left trisectionectomy, 17% of patients developed transient hepatic insufﬁciency postoperatively.3 Other reports cite a 3% incidence of this complication after 51 extended left hepatectomies and a 6.7% incidence in 33 patients undergoing right trisectionectomy.5,56 ● Consequence The sequelae of this complication depend on the extent of organ insufﬁciency that develops. In general, the metabolic and reticuloendothelial functions of the liver will be impaired, resulting in decreased protein synthesis and compromised host-defense functions. As a

33 TRISECTIONECTOMY consequence, patients with postoperative hepatic insufﬁciency become more prone to malnutrition, infectious complications, and impaired healing of incisions and anastomoses. These patients are also more prone to respiratory and/or renal failure, with the stress of systemic infection or other organ failure further compromising the already failing liver. The mortality rate associated with isolated postoperative liver failure is 6.1%, although this increases to up to 33% when patients with concomitant failure of other organs are included.1,55 Grade 4 complication ● Repair Management of mild or moderate postoperative hepatic insufﬁciency is generally supportive, with the duration of insufﬁciency usually correlating with the amount of time required for adequate functional hepatic regeneration to occur (typically about 3 wk).57 In cases of severe, life-threatening postoperative liver failure, hepatic transplantation may be a viable therapeutic option, depending on the indication for resection. ● Prevention Two general measures can be taken to prevent the development of hepatic insufﬁciency after major hepatic resection. Postoperatively, it is important to avoid conditions that place excessive stress on the metabolic functions of the liver. Thus, the avoidance of gastrointestinal hemorrhage, systemic infection, or renal failure will help to prevent pushing a patient with borderline hepatic function into catastrophic liver failure. Because the risk of developing postoperative hepatic dysfunction is directly related to the amount of functional hepatic tissue that is resected, a considerable amount of research has been directed toward determining preoperatively the amount of liver tissue that can be safely resected in a given patient. This ability of individual patients to tolerate major hepatic resections such as trisectionectomy depends both on the extent of resection needed to achieve oncologic beneﬁt (assuming the resection is for malignancy) and on the quality of the remnant hepatic tissue. Generally, a patient with normal hepatic function preoperatively and no evidence of cirrhosis or chronic hepatitis can tolerate removal of as much as 75% to 80% of their total hepatic volume. Patients with compromised hepatic function due to steatosis, cirrhosis, or hepatitis, however, may not be able to tolerate this much resection. Several techniques have been developed that attempt to predict postoperative residual liver function in these patients with preoperative cirrhosis.58 Indocyanine green (ICG), for example, is taken up by the hepatocytes after intravenous injection and excreted into the bile unchanged. Serial measurement of ICG levels at 5-minute intervals after its injection can help to detect the clearance rate of this substance by the liver, which is generally greater than 90% after 15 minutes.59 Patients with cirrhosis and ICG

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retention greater than 14% after 15 minutes have been found by some groups to have increased risk of postoperative mortality after liver resection.59,60 Several groups have successfully incorporated ICG clearance rates into their preoperative assessment of patients with cirrhosis in order to plan the extent of hepatic resection in these patients, a strategy that has resulted in favorable mortality rates.54,61 ICG clearance rates should generally not be used as the sole determinant of the extent of resection to undertake, or of whether or not to perform resection in the ﬁrst case, because the test is not completely accurate as a predictor of postoperative hepatic dysfunction.58 Another test of preoperative hepatocyte function is the monoethylglycinexylidide (MEGX) test, which assesses the ability of the hepatic cytochrome P-450 pathways to convert lidocaine to monoethylglycinexylidide. Low venous concentrations of MEGX 15 minutes after injection of lidocaine have been shown to correlate both with the degree of cirrhosis and with the risk of hepatic dysfunction after hepatectomy.62 This test has been shown to compare favorably with ICG clearance testing as a measure of liver function, although both tests are somewhat limited by their dependence on hepatic blood ﬂow.63 Several other methods for determining the extent of hepatocyte dysfunction have also been developed, including the hippurate ratio, the aminopyrine breath test, the amino acid clearance test, the caffeine clearance test, galactose elimination capacity, and the arterial ketone body ratio. These methods have variable prognostic efﬁcacy compared with that of ICG and MEGX in predicting which cirrhotic patients who undergo liver resection will develop postoperative hepatic failure and death.58 Another potentially useful method for determining a patient’s risk for developing hepatic dysfunction after liver resection is to estimate the anticipated volume of hepatic tissue that will remain with the patient after resection (i.e., the remnant liver volume). Such estimations are achieved by volumetric analysis using computed tomography and have been shown to correlate well with the amount of hepatic tissue actually resected.58 Furthermore, the ratio of the anticipated remnant liver volume to total liver volume has been shown to correlate well with a patient’s risk of postoperative hepatic dysfunction. In an analysis of 126 patients undergoing liver resection for colorectal metastases, the group at Memorial Sloan-Kettering found that 90% of patients with a remnant liver volume of less than 25% based on preoperative volumetric analysis developed postoperative hepatic dysfunction, compared with none of the patients undergoing trisectionectomy who had a remnant liver volume greater than 25%.64 The clinical utility of preoperative hepatic function testing and volumetric analysis will depend on how this information is used. Not only will the data obtained from these studies help in estimating the maximum extent of resection that can be tolerated by the patient, the information derived from these tests may also assist in determining

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whether the patient might beneﬁt from preoperative portal vein embolization. The use of preoperative portal vein embolization was ﬁrst reported in 1990 as a potential method for promoting compensatory hypertrophy in the future remnant liver of cirrhotic patients who require major hepatic resection for malignancy.65 The ideal candidates for portal vein embolization are those patients requiring extensive resection but who have only borderline hepatic function (corresponding to an ICG clearance value of 10%–20% at 15 min).66 This technique does not appear to be as useful for patients with hepatic tumors and more severe liver dysfunction (ICG retention > 20%) because the amount of time required for adequate compensatory hypertrophy of the anticipated remnant liver would be excessive in light of the relative urgency of proceeding from an oncologic perspective. The use of portal venous embolization combined with preoperative biliary drainage in patients with obstructive jaundice has been shown to expand the surgical options for patients needing extensive hepatic resection. In a retrospective study of 79 patients undergoing major hepatic resection for hilar cholangiocarcinoma, preoperative biliary drainage was performed in 65 patients who had obstructive jaundice and in 41 of 51 patients undergoing extended right hepatectomy. The in-hospital mortality rate for the patients in this series was only 1.3%, and the incidence of postoperative hepatic failure was zero.67 The combination of portal venous embolization and preoperative biliary drainage for patients with obstructive jaundice has enabled the safe performance of trisectionectomy with minimal postoperative mortality and hepatic failure in other recent series as well and should, therefore, be considered in any patient needing major hepatic resection who has preoperative evidence of obstructive jaundice and borderline hepatic function.6

REFERENCES 1. Jarnagin WR, Gonen M, Fong Y, et al. Improvement in perioperative outcomes after hepatic resection: analysis of 1,803 consecutive cases over the past decade. Ann Surg 2002;236:397–407. 2. Melendez J, Ferri E, Zwillman M, et al. Extended hepatic resection: a 6-year retrospective study of risk factors for perioperative mortality. J Am Coll Surg 2001;192:47– 53. 3. Nishio H, Hidalgo E, Hamady Z, et al. Left hepatic trisectionectomy for hepatobiliary malignancy: results and an appraisal of its current role. Ann Surg 2005;242:267– 275. 4. Seyama Y, Kubota K, Sano K, et al. Long-term outcome of extended hemihepatectomy for hilar bile duct cancer with no mortality and high survival rate. Ann Surg 2003; 238:73–83. 5. Rui JA, Wang SB, Chen SG, Zhou L. Right trisectionectomy for primary liver cancer. World J Gastroenterol 2003;9:706–709.

6. Fong Y, Blumgart LH. Hepatic resection. In ACS Surgery: Principles and Practice. Available at http://www. acssurgery.com (accessed May 10, 2006). 7. Pinson CW, Drougas JG, Lalikos JL. Optimal exposure for hepatobiliary operations using the Bookwalter self-retaining retractor. Ann Surg 1995;61:178– 181. 8. Nagano Y, Togo S, Tanaka K, et al. The role of median sternotomy in resection for large hepatocellular carcinomas. Surgery 2005;137:104–108. 9. Tanaka S, Kubo S, Tsukamoto T, et al. Risk factors for intractable pleural effusion after liver resection. Osaka City Med J 2004;50:9–18. 10. Kwon AH, Matsui Y, Satoi S, et al. Prevention of pleural effusion following hepatectomy using argon beam coagulation. Br J Surg 2003;90:302–305. 11. Yan JJ, Zhang XH, Chu KJ, et al. Preservation and management of pleural effusions following hepatectomy in primary liver cancer. Hepatobiliary Pancreat Dis Int 2005; 4:375–378. 12. Nanashima A, Yamaguchi H, Shibasaki S, et al. Comparative analysis of postoperative morbidity according to type and extent of hepatectomy. Hepatogastroenterology 2005; 52:844–848. 13. Matsumata T, Kanematsu T, Okudaira Y, et al. Postoperative mechanical ventilation preventing the occurrence of pleural effusion after hepatectomy. Surgery 1987;102:493–497. 14. Uetsuji S, Komada Y, Kwon AH, et al. Prevention of pleural effusion after hepatectomy using ﬁbrin sealant. Int Surg 1994;79:135–137. 15. Kise Y, Takayama T, Yamamoto J, et al. Comparison between thoracoabdominal and abdominal approaches in occurrence of pleural effusion after liver cancer surgery. Hepatogastroenterol 1997;44:1397–1400. 16. Tanabe G, Kawaida K, Hamanoue M, et al. Treatment for accidental occlusion of the hepatic artery after hepatic resection: report of two cases. Surg Today 1999;29:268– 272. 17. Shimada H, Endo I, Sugita M, et al. Hepatic resection combined with portal vein or hepatic artery reconstruction for advanced carcinoma of the hilar bile duct and gallbladder. World J Surg 2003;27:1137–1142. 18. Iseki J, Tamaki N, Touyama K, et al. Mesenteric arterioportal shunt after interruption. Surg Today 1998;123:58– 66. 19. Sahani D, Mehta A, Blake M, et al. Preoperative hepatic vascular evaluation with CT and MR angiography: implications for surgery. RadioGraphics 2004;24:1367– 1380. 20. Skandalakis JE, Skandalakis LJ, Skandalakis PN, Mirilas P. Hepatic surgical anatomy. Surg Clin North Am 2004;84: 413–435. 21. Imamura H, Makuuchi M, Sakamoto Y, et al. Anatomical keys and pitfalls in living donor liver transplantation. J Hepatobiliary Pancreat Surg 2000;7:380–394. 22. Machado MA, Herman P, Makdissi FF, et al. Anatomic left hepatic trisegmentectomy. Am J Surg 2005;190:114– 117. 23. Makuuchi M, Yamamoto J, Takayama T, et al. Extrahepatic division of the right hepatic vein in hepatectomy. Hepatogastroenterology 1991;38:176–179.

33 TRISECTIONECTOMY 24. Smyrniotis V, Farantos C, Kostopanagiotu G, Arkadopoulos N. Vascular control during hepatectomy: review of methods and results. World J Surg 2005;29:1384–1396. 25. Gozzetti G, Mazziotti A, Grazi GL, et al. Liver resection without blood transfusion. Br J Surg 1995;82:1105–1110. 26. Belghiti J, Hiramatsu K, Benoist S, et al. Seven hundred forty-seven hepatectomies in the 1990s: an update to evaluate the actual risk of liver resection. J Am Coll Surg 2000;191:38–46. 27. Kooby DA, Stockman J, Ben-Porat L, et al. Inﬂuence of transfusions on perioperative and long-term outcome in patients following hepatic resection for colorectal metastases. Ann Surg 2003;237:860–870. 28. Matsumata T, Yanaga K, Shimada M, et al. Occurrence of intraperitoneal septic complications after hepatic resection between 1985 and 1990. Surg Today 1995;25:49–54. 29. Poon RT, Fan ST, Irene OL, Wong J. Signiﬁcance of resection margin in hepatectomy for hepatocellular carcinomas: a critical reappraisal. Ann Surg 2000;231:544– 551. 30. Pringle JH. Notes on the arrest of hepatic haemorrhage due to trauma. Ann Surg 1909;48:541–549. 31. Abdalla EK, Noun R, Belghiti J. Hepatic vascular occlusion: which technique? Surg Clin North Am 2004;84: 563–585. 32. Huguet C, Gavelli A, Chieco PA, et al. Liver ischemia for hepatic resection: where is the limit? Surgery 1992;111: 251–259. 33. Elias D, Desruennes E, Lasser P. Prolonged intermittent clamping of the portal triad during hepatectomy. Br J Surg 1991;78:42–44. 34. Clavien PA, Yadav S, Sindram D, Bentley RC. Protective effects of ischemic preconditioning for liver resection performed under inﬂow occlusion in humans. Ann Surg 2000;232:155–162. 35. Belghiti J, Noun R, Zante E, et al. Portal triad clamping or hepatic vascular exclusion for major liver resection: a controlled study. Ann Surg 1996;224:155–161. 36. Makuuchi M, Mori T, Gunven P, et al. Safety of hemihepatic vascular occlusion during resection of the liver. Surg Gynecol Obstet 1987;164:155–158. 37. Jones RM, Moulton CE, Hardy KJ. Central venous pressure and its effect on blood loss during liver resection. Br J Surg 1998;85:1058–1060. 38. Chen H, Merchant NB, Didolkar MS. Hepatic resection using intermittent vascular inﬂow occlusion and low central venous pressure anesthesia improves morbidity and mortality. J Gastrointest Surg 2000;4:162–167. 39. Lesurtel M, Selzner M, Petrowsky H, et al. How should transection be performed?: a prospective randomized study in 100 consecutive patients comparing four different transection strategies. Ann Surg 2005;242:814–823. 40. Takayama T, Makuuchi M, Kubota K, et al. Randomized comparison of ultrasonic versus clamp transection of the liver. Arch Surg 2001;136:922–928. 41. Ray HG, Wichmann MW, Schinkel S, et al. Surgical techniques in hepatic resections: ultrasonic aspirator versus Jet-Cutter. A prospective randomized clinical trial. Zentralbl Chir 2001;126:586–590. 42. Reed DN, Vitale GC, Wrightson WR, et al. Decreasing mortality of bile leaks after elective hepatic surgery. Am J Surg 2003;185:316–318.

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43. Lo CM, Fan ST, Liu CL, et al. Biliary complications after hepatic resection: risk factors, management, and outcome. Arch Surg 1998;133:156–161. 44. Yanaga K, Kanematsu T, Takenaka K, Sugimachi K. Intraperitoneal septic complications after hepatectomy. Ann Surg 1986;203:148–152. 45. Yamashita Y, Hamatsu T, Rikimaru T, et al. Bile leakage after hepatic resection. Ann Surg 2001;233:45–50. 46. Bhattacharyja S, Puleston J, Davidson B. Hepatic resection: early endoscopic drainage in bile leak management. Gastrointest Endosc 2003;57:526–530. 47. Tanaka S, Hirohashi K, Tanaka H, et al. Incidence and management of bile leakage after hepatic resection for malignant hepatic tumors. J Am Coll Surg 2002;195:484– 489. 48. Kyokane T, Nagino M, Sano T, Nimura Y. Ethanol ablation for segmental bile duct leakage after hepatobiliary resection. Surgery 2002;131:111–113. 49. Lam CM, Lo CM, Liu CL, Fan ST. Biliary complications during liver resection. World J Surg 2001;25:1273–1276. 50. Ijichi M, Takayama T, Toyoda H, et al. Randomized trial of usefulness of bile leakage test during hepatic resection. Arch Surg 2000;135:1395–1400. 51. Kraus TW, Mehrabi A, Schemmer P, et al. Scientiﬁc evidence for application of topical hemostats, tissue glues, and sealants in hepatobiliary surgery. J Am Coll Surg 2005;200:418–427. 52. Eder F, Meyer F, Nestler G, et al. Sealing of the hepatic resection area using ﬁbrin glue reduces signiﬁcant amount of postoperative drain ﬂuid. World J Gastroenterol 2005; 11:5984–5987. 53. Kohno H, Nagasue N, Chang Y, et al. Comparison of topical hemostatic agent in elective hepatic resection: a clinical prospective randomized trial. World J Surg 1992; 16:966–970. 54. Imamura H, Seyama Y, Kokudo N, et al. One thousand ﬁfty-six hepatectomies without mortality in 8 years. Arch Surg 2003;138:1198–1206. 55. Nagino M, Kamiya J, Uesaka K, et al. Complications of hepatectomy for hilar cholangiocarcinoma. World J Surg 2001;25:1277–1283. 56. Povoski SP, Fong Y, Blumgart LH. Extended left hepatectomy. World J Surg 1999;23:1289–1293. 57. Stone MD, Benotti PN. Liver resection: preoperative and postoperative care. Surg Clin North Am 1989;69:383– 391. 58. Mullin EJ, Metcalfe MS, Maddern GJ. How much liver resection is too much? Am J Surg 2005;120:87–97. 59. Lau H, Man K, Fan ST, et al. Evaluation of preoperative hepatic function in patients with hepatocellular carcinoma undergoing hepatectomy. Br J Surg 1997;84:1255– 1259. 60. Fan ST, Lai EC, Lo CM, et al. Hospital mortality of major hepatectomy for hepatocellular carcinoma associated with cirrhosis. Arch Surg 1995;130:198–203. 61. Kubota K, Makuuchi M, Kusaka K, et al. Measurement of liver volume and hepatic functional reserve as a guide to decision-making in resectional surgery for hepatic tumors. Hepatology 1997;26:1176–1181. 62. Ercolani G, Grazi GL, Calliva R, et al. The lidocaine (MEGX) test as an index of hepatic function: its clinical usefulness in liver surgery. Surgery 2000;127:464–471.

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63. Huang YS, Chiang JH, Wu JC, et al. Risk of hepatic failure after transcatheter arterial chemoembolization for hepatocellular carcinoma: predictive value of monoethylglycineexylidide test. Am J Gastroenterol 2002;97:1223– 1227. 64. Shoup M, Gonen M, D’Angelica M, et al. Volumetric analysis predicts hepatic dysfunction in patients undergoing major liver resection. J Gastrointest Surg 2003;7:325– 330. 65. Makucchi M, Thai BL, Takayasu K, et al. Preop portal embolization to increase safety of major hepatectomy for

hilar bile duct carcinoma: a preliminary report. Surgery 1990;107:521–527. 66. Takayama T, Makuuchi M. Preoperative portal vein embolization: is it useful? J Hepatobiliary Surg 2004;11: 17–20. 67. Kawasaki S, Imamura H, Kobayashi A, et al. Results of surgical resection for patients with hilar bile duct cancer: application of extended hepatectomy after biliary drainage and hemihepatic portal vein embolization. Ann Surg 2003;238:84–92.

34

Laparoscopic Liver Resection Amit D. Tevar, MD, Mark J. Thomas, MD, and Joseph F. Buell, MD INTRODUCTION The rapid evolution of technology and experience with laparoscopic surgery has led to the feasibility of safe minimally invasive hepatic resection. The ﬁrst laparoscopic liver resection was reported by Gagner and coworkers in 1992.1 Ferzli and colleagues2 subsequently reported an additional hepatic resection in 1995. Azagra and associates3 were the ﬁrst to perform a segmental resection, describing a left lateral segmentectomy in 1996. Since these initial reports, multiple institutional series and a few multicenter groups have reported segmental and nonsegmental resection for benign and malignant disease.4–24 The application of laparoscopic techniques for liver resection has demonstrated equivalent morbidity and mortality rates to those of open techniques. In addition, the laparoscopic approach has resulted in decreased blood loss, shorter postoperative stay, and reduced postoperative analgesic requirement for pain.18,25,26 Although technologic advancement and surgeon experience have rapidly advanced the extent and safety of laparoscopic liver resection, concern remains regarding the oncologic integrity of laparoscopic resection for malignant disease and of multiple potential complications. These complications include those that are possible with any liver resection—including functional synthetic reserve in a cirrhotic liver, tumor recurrence, bleeding, biliary leak—and those that are unique to laparoscopic liver resection, such as CO2 embolism and port site metastasis.

INDICATIONS The indications for laparoscopic liver resection are similar to those for open procedure in regard to patient and lesion characteristics. No liver resection should be performed using a laparoscopic technique that would not be indicated using an open technique. Special consideration should be given to preoperative imaging and the proximity of the lesions with the hepatic vein conﬂuence and the portal bifurcation. The most common benign lesions and

indications that would be considered for liver resection include ● Hemangioma ● Severe symptoms ● Hemorrhage ● Focal nodular hyperplasia ● Severe symptoms ● Growth on serial imaging ● Uncertain diagnosis ● Liver cell adenoma ● Simple liver cysts ● Severe symptoms The most common malignant lesions that would be considered for liver section include ● Hepatocellular carcinoma ● Noncirrhotic patients ● Child’s A cirrhotic patients with lesion smaller than

5 cm ● Metastatic colon adenocarcinoma ● Metastatic lesions noncolonic ● Include gastrointestinal stromal tumor (GIST),

melanoma, renal cell carcinoma, and others, only if no extrahepatic metastatic lesions and primary has been controlled

OPERATIVE STEPS Step Step Step Step Step Step

1 2 3 4 5 6

Patient positioning Port placement Liver mobilization Laparoscopic intraoperative hepatic ultrasound Parenchymal division Closure

OPERATIVE PROCEDURE Patient Positioning Patient positioning is paramount to a successful laparoscopic liver resection. Left lateral, left median segment,

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12 mm 5 mm lap disk

Surgeon

12 mm

First assistant

Figure 34–1 Surgeon, laparoscopic and hand port placement for left hepatic laparoscopic resection.

Figure 34–2 Operative table in full ﬂexion for decubitus positioning of patients for right sided laparoscopic liver resection.

and caudate lesions are best performed with the patient in a supine position with the arms out6,7 (Fig. 34–1). This allows for uncomplicated and safe division of the left triangular and coronary, falciform, and gastrohepatic ligaments. Lesions involving the right lobe (segments 5, 6, 7, and 8) are best laparoscopically approached with the patient in a left decubitus position with the operative bed in full ﬂexion (Fig. 34–2).

Port Placement All laparoscopic liver resections at the University of Cincinnati are performed with a hand-assist device (Lap-Disc; Ethicon, Cincinnati, OH) in combination with low-proﬁle balloon ports. The hand-assist technique allows for tactile feedback, which is an important tool in the armamentarium for obtaining adequate margins in the malignant hepatic resection (Fig. 34–3). The hand-assist also allows for

Figure 34–3 Laparoscopic hand port placement.

digital compression of parenchymal or vascular bleeding, preventing unnecessary blood loss or CO2 air embolism. As with any laparoscopic surgery, appropriate port and surgeon placement greatly facilitates the operative technique, allowing for a safer and shorter case. The primary surgeon leads the case by placement of his or her hand in the hand port. In the case of left-sided lesions, the primary surgeon resides on the patient’s right side in order to place his or her right hand intracorporeally through a hand port placed on the right to guide mobilization and parenchymal division. Resection of the right lobe of the liver involves the primary surgeon on the patient’s left side with his or her assistant directly opposite. The primary surgeon’s left hand is placed through a right-sided hand port to facilitate dissection, mobilization, and resection. Some groups have placed the hand port in the midline with success. The low-proﬁle balloon port is used, and the initial port is placed using an open Hasson technique. In the cirrhotic patient, the initial 12-mm balloon port is placed infraumbilically in order to avoid the large recannulized umbilical vein circuit. If a varix is encountered, hemostasis should be obtained with direct suture ligation. In the noncirrhotic patient, the initial port is placed supraumbilically, again using an open technique. The remaining ports are placed under direct visualization after pneumoperitoneum is obtained. Right-sided lesions require placement of two additional subcostal 12-mm ports. These should be placed under direct visualization, and great care should be taken to avoid cephalad or caudal placement of these ports. Working ports placed too high will result in difﬁculty opening the jaws of a laparoscopic vascular staple owing to the proximity to the liver. Working ports placed too low will lead to inability of instrument to reach the right and middle hepatic veins. The hand port is placed in the right upper quadrant, just above and lateral to the supraumbilical port. It is recommended that the hand port be placed more cephalad for right-sided lesions to allow for hand retraction of the liver for dissection of the hepatic veins and the bare area. Left-sided lesions require two

34 LAPAROSCOPIC LIVER RESECTION

12 mm lap disk

First assistant

361

● Prevention All patients with end-stage liver disease should be identiﬁed preoperatively by laboratory values. Even with normal liver function tests and coagulation studies and no evidence of ascites or encephalopathy, all patients should be carefully examined after general anesthesia is obtained for evidence of a caput medusae. The presence of other physical examination ﬁndings classically seen in portal hypertension suggest that periumbilical varices may have developed, even if they are not readily visible on visual examination. Port placement for patients with end-stage liver disease should begin with an infraumbilical 12-mm port using an open Hasson technique. This generally will avoid disruption of any periumbilical varices.

12 mm

12 mm

Surgeon

Figure 34–4 Surgeon, laparoscopic and hand port placement for right hepatic laparoscopic resection.

additional left subcostal ports, placed in a similar fashion. Our group routinely places the hand port in the right side for left-sided resections, and it may be placed more caudally than for right-sided lesions (Fig. 34–4).

Trocar Insertion Hollow Viscus Injury This is an unnecessary complication that deserves special consideration because the patient population undergoing laparoscopic liver resection has often undergone previous surgery or may have end-stage liver disease. The standard trocar insertion is described previously, and the initial port should be placed using an open technique. See Section I, Chapter 7, Laparoscopic Surgery. Trocar Insertion Bleeding The patient population undergoing laparoscopic liver surgery often has end-stage liver failure with impressive superﬁcial periumbilical vein circuits originating from a recannulized umbilical vein. ● Consequence Variceal bleeding can be somewhat problematic because of the large-volume, low-pressure, and thin-walled veins. In addition, the variceal veins will often retract into the subcutaneous fat and, when working through a small 12-mm port skin incision, a signiﬁcant volume of blood may be lost before the vein is visualized. ● Repair Direct digital pressure should be applied to the area in order to minimize a potentially large volume of blood loss. Blind electrocautery into the area of the bleeding is usually ineffective. Visualization is key in controlling this bleeding. Retraction with Army-Navy retractors or extension of the skin incision may facilitate this. Identiﬁcation and direct ligation of both ends of the varix with suture is the appropriate way to treat this bleeding.

Liver Mobilization Mobilization is performed in a manner similar to that of the traditional open technique. The left lobe is mobilized by having the primary surgeon retract the left lateral segment in an inferior and posterior position. The laparoscopic ultrasonic cutting and coagulation device (Harmonic Scalpel; Ethicon Endo-Surgery, Inc.) is then used to divide the coronary and triangular ligament. The dissection is taken to circumferentially clear the left and middle hepatic veins. Great care should be taken at this time to avoid injury to the phrenic vein. Injury to this should be managed with digital compression and clip or ultrasonic ligation. The left lateral segment is now retracted in an anterior fashion, and the gastrohepatic ligament is divided with the ultrasonic shears. In case an accessory left hepatic artery is encountered, it should be divided using the ultrasonic shears or ligated with clips and divided. After complete mobilization of the left lateral segment, the caudate lobe can also be mobilized for resection. The peritoneum overlying the inferior vena cava is ﬁrst divided with the ultrasonic shears. The posterior aspect of the left hepatic vein is then fully mobilized, followed by the superior aspect of the caudate lobe. Once the small caudate veins are ligated and divided, the main caudate vein is circumferentially dissected and can be taken with a reloadable laparoscopic articulating vascular stapler (Endo GIA Roticulator; Autosuture, Tyco, Norwalk, CT). Caudate portal vein branches may also be taken if needed. The right lobe is mobilized by retracting the lobe medially and caudally with the primary surgeon’s hand through the hand port. Ligament attachments are then divided with the ultrasonic shears (Fig. 34–5). A combination of blunt and sharp dissection is used to fully mobilize the right lobe to the right hepatic vein. The inferior vena cava ligament may be divided to facilitate visualization of the right hepatic vein. The right hepatic and middle hepatic veins are circumferentially dissected. The lateral attachments of the inferior vena cava are divided using the ultrasonic shears. Small branches from the vena cava to the liver may be taken with the laparoscopic vessel sealant device (LigaSure Lap; Valleylab, Boulder, CO) or with clip ligation and laparoscopic shear division.

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Figure 34–6 Laparoscopic liver ultrasound. Figure 34–5 Mobilization of lateral attachments of the right lobe using a laparoscopic ultrasonic cutting device.

Pneumothorax Mobilization of the right lobe often requires ultrasonic dissection. This thermal heat can lead to a diaphragm injury and a spontaneous pneumothorax. This is extremely vexing when the working space becomes compromised with the mobile diaphragm. ● Consequence Airway pressures suddenly rise while the working space becomes inhibited. Each pulmonary excursion results in a billowing of the diaphragm, making continued operating difﬁcult. ● Repair Repair can be performed through open operative conversion or a laparoscopic approach. In our practice, we have elected to utilize continuous suction during suture repair of the diaphragm. First, the diaphragm injury is identiﬁed. Either a ﬁgure-of-eight or an interrupted suture repair is performed around the injury. This can be done with a suture passer device or free-hand suturing with intracorporeal knot tying. Once this is repaired, an endoscopic suction device is placed in the thoracic cavity. Aspiration of the free air is accomplished, and a forced inspiration is performed to minimize the free space. At that juncture, the suture is secured and the suction device removed. ● Prevention This is achieved though meticulous placement of the ultrasonic device. Pass pointing and adjacent thermal injuries can be avoided by either conservative or meticulous placement of these devices.

Laparoscopic Intraoperative Hepatic Ultrasound The ultrasound examination remains a crucial aspect of any liver operation, and surgeons performing laparoscopic

hepatectomy should be familiar with the equipment and well versed in assessment of the obtained images. The laparoscopic ultrasound probe (8666 probe; B-K Medical, Denmark) is used to methodically evaluate all segments of the liver, looking for additional lesions, boundaries of known lesions, and the relationship with the vascular anatomy (Fig. 34–6). If the patient is still a candidate for resection, a 2-cm margin around the lesion is marked with the argon beam coagulator.

Inadequate Intrusion Laparoscopic hepatic resection is dependent on adequate working space. When there is insufﬁcient space to deploy or articulate instrumentation, this operative procedure becomes impossible. ● Consequence Inadequate working space incapacitates most forms of technology that are critical to the performance of these operations. ● Repair Unfortunately, there are few remedies for the lack of intrusion. The most widespread or universally accepted procedure is the technique of laprolift. In this scenario, the abdominal wall is elevated by the technique of laprolift.

Parenchymal Division Our group has avoided routine employment of the Pringle maneuver. If brisk bleeding is encountered, direct compression of the porta with the primary surgeon’s hand can be performed while a laparoscopic vascular clamp is put into position. Parenchymal transection begins with division of the Glisson capsule using the ultrasound shears at a line marked with the laparoscopic ultrasound (Figs. 34–7 and 34–8). The technique used by our group involves liberal use of 60-mm-long, 2.5-mm staple loads. The staple load

34 LAPAROSCOPIC LIVER RESECTION

Figure 34–7 Division of Glisson’s capsule along an argon beam marking line using a laparoscopic ultrasonic cutting device.

363

Figure 34–8 Division of Glisson’s capsule using a laparoscopic ultrasonic cutting device.

Figure 34–9 Hepatic parenchymal resection using a reticulating laparoscopic vascular staple.

is guided into position using the intracorporeal hand. The thin blade is guided into the liver parenchyma and then ﬁred. The staples ligate any hepatic vessels or bile ducts. As the cutting blade distance is shorter that the staple length, partial division of large vessels remains hemostatic

(Fig. 34–9). Alternative methods to parenchymal division include a saline infusion, radiofrequency ablation device (TissueLink ﬂoating ball; TissueLink, Dover, NH) (Fig. 34–10), with selective stapling or clip placement of large vascular or biliary structures.

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SECTION IV: HEPATOBILIARY SURGERY ● Consequence The resulting blood loss can be quite signiﬁcant and result in hemodynamic compromise if not recognized and treated effectively in a timely manner. If not controlled quickly, this blood loss will invariably result in conversion to an open procedure or reexploration for continued bleeding.

Figure 34–10 Hepatic parenchymal resection using a saline infusion, radiofrequency ablation device.

Figure 34–11 ulation device.

Cut surface hemostasis with an argon beam coag-

Upon completion of the resection, cut surface liver parenchymal bleeding can be controlled by argon beam coagulation of the cut surface (Fig. 34–11). Bile leakage or focused arterial bleeding is controlled with free-hand suturing or clip application. A hemostatic matrix of collagen and topical thrombin (Floseal; Baxter, Deerﬁeld, IL) is then applied to the cut surface. After hemostasis and absence of bile leak is appropriately assessed, the specimen is removed through the hand port. The port itself acts as a wound protector and prevents tumor seeding of the wound.

Venous and Arterial Bleeding Hepatic arterial or venous bleeding can become a signiﬁcant problem in the conﬁned space of a laparoscopic procedure. This results from disruption of the small or large portal or hepatic veins resting in the liver parenchyma. Intraparenchymal hepatic arterial bleeding is another potential source of bleeding when the liver parenchyma is divided. This may be further complicated by a baseline coagulopathy of the cirrhotic patient.

● Repair Intraoperatively, all patients should have their coagulopathies corrected with fresh frozen plasma, cryoprecipitate, and/or platelets before proceeding with hepatic resection. Central venous pressure should be continuously measured through a central venous line and be kept below 6 mm Hg. Again, recognition is paramount in successfully controlling the bleeding. Our group does not perform a Pringle maneuver before beginning parenchymal division, which allows for early identiﬁcation of bleeding. The ﬁrst maneuver in controlling bleeding is direct compression with the primary surgeon’s intra-abdominal hand. This keeps blood loss to a minimum and prevents the possibility of CO2 embolism if large hepatic veins are divided. In addition, it safely allows for the remainder of the hepatic resection to be completed so that the entire cut surface can be visualized, greatly simplifying direct permanent control of bleeding vessels. Laparoscopic suturing or clip application in the crevice of a partially completed resection is extremely difﬁcult and does not allow for direct visualization. In almost all cases, direct pressure with the intraabdominal hand and a laparotomy sponge will maintain hemostasis until the surgeons are ready to perform more permanent hemostatic maneuvers. In the case of a cirrhotic liver in which direct compression of the liver does not always adequately stop bleedings, the surgeon’s hand can be used to compress the portal structures. Visible venous or arterial vessels on the cut surface should be permanently ligated with clip application, direct laparoscopic suture ligation, or a laparoscopic vascular stapler. Avoid argon beam coagulation of large vessels because this does not provide permanent hemostasis and can lead to gas embolization. After major vessels have been ligated, the cut surface parenchyma may be cauterized with the argon beam coagulator. We often spread a collagen and thrombin hemostatic matrix over the cut surface before closing. ● Prevention Among the different techniques available for parenchymal division, our group employs liberal use of 60-mm length, 2.5-mm staple loads. The staple load is guided into position using the intracorporeal hand. The thin blade is guided into the liver parenchyma and then ﬁred. The staples ligate any hepatic vessels or bile ducts. This results in a very hemostatic cut surface. When using the Tissuelink device, it is important to identify vessels and staple or clip them directly to avoid bleed-

34 LAPAROSCOPIC LIVER RESECTION ing. Vigilant attention should also be given toward correction of the patient’s coagulopathy and maintenance of adequate body temperature and central venous pressure throughout the procedure.

Bile Leak Biliary leakage remains a signiﬁcant problem in major open hepatic resection. Reports from recent series have shown the rate of biliary complications to range from 3% to 10%, with mortality from major leaks to be as high as 40% to 50%.27,28 ● Consequence The cut surface of the liver with associated cut bile duct is a signiﬁcant source of bile leak. Many leaks are small and will resolve without intervention. Larger leaks can result in abdominal pain, bile peritonitis, abscess, or abdominal sepsis. The large symptomatic leaks can be high as 40% to 50%. ● Repair Intraoperative recognition and repair of bile leaks is paramount to avoiding postoperative complications. This involves thorough investigation for bile leak on the cut surface prior to closure. This can be done through direct visualization with the laparoscope or by placing a clean laparotomy sponge on the cut surface and looking for bile staining. We do not perform routine cholangiogram on open or laparoscopic liver resections to search for bile leaks. Once a bile leak is discovered, it is repaired in the same fashion as that for open hepatic resection, with free-hand suture ligation or clip application. Again, intraoperative recognition and repair of bile leaks are important. If leaks are discovered postoperatively, they should be treated aggressively with early endoscopic retrograde cholangiography and stent placement. If ﬂuid collections are not adequately resolved by operatively placed drains, computed tomography scan should be obtained and interventional radiology percutaneous drains should be placed. ● Prevention Meticulous attention and focused search and repair of bile leaks intraoperatively will invariably result in fewer biliary complications.

Closure Particular attention should be given to closure of all port incisions because early herniation is an unnecessary complication in laparoscopy. Also, because patients with endstage liver disease may have large-volume ascites with diminished healing capacity, attention should be given to meticulous technique to avoid closure breakdown in this subgroup of patients. Our technique involves a 1-0 permanent suture twolayer closure for the hand port incision. The 12-mm port sites should be closed using the laparoscopic fascial closure device or an open technique.

365

Other Complications Intraoperative Hypotension Pneumoperitoneum often leads to unexpected hypotension, as a result of patient intravascular volume depletion and subsequent susceptibility to pneumoperitoneal pressures. In laparoscopic liver resection, the patient is often placed in a reverse Trendelenburg position, which worsens central venous return. Subsequently, the blood pressure is extremely sensitive to patient positioning. ● Consequence Often transient but signiﬁcant and dramatic hypotension can occur. Associated with this hypotension is bradycardia rather than the expected tachycardia resulting from hypotension. ● Repair Hypotension and bradycardia are responsive to atropine and/or ﬂuid resuscitation utilizing normal saline or 5% albumin. In more extreme cases, immediate release of the pneumoperitoneum or repositioning of the patient until adequate central volume resuscitation is achieved is required. ● Prevention Adequate resuscitation of the patient is critical. The goal of central venous pressure is 6 to 8 mm Hg. However, excessive volume depletion is inappropriate and dangerous. Management of these patients with a central venous line to monitor pressures is very helpful in monitoring volume status.

Major Air Embolism A potentially fatal complication of minimally invasive hepatic resection is major air embolism. Signiﬁcant disruption of the hepatic venous system in the face of CO2 pneumoperitoneum may result in air embolism to the central venous system. Subsequent air lock hypotension and fatal arrhythmia may follow. This is the most feared complication of hepatic transection performed under positive pressure. ● Consequence Air embolism is a known complication of hepatic resection. This rare complication is the result of air entering a vessel and becoming trapped within the atrium. The most susceptible patients to fatal complications are those with patent foramen ovale. This allows for trapp-ing of air in the right ventricle outﬂow tract, resulting in air lock with resultant hypotension or even cardiac arrest. ● Repair Procedure-related hypotension should be monitored closely. In the event of a signiﬁcant drop in end-tidal CO2 along with decreases in oxygen saturation and/or hypotension, the pneumoperitoneum should be

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released and the patient hand-ventilated. The most sensitive test for air embolism remains transesophageal echocardiography, which can detect less than 0.02 ml/ kg of air. Treatment should be instituted immediately on suspicion of air embolism. The patient should immediately be placed in a Trendelenburg and left lateral decubitus position. Administration of 100% oxygen should begin immediately because it may decrease bubble size. Pulmonary artery or central venous catheters should be advanced into the heart and aspirated, in hopes of aspirating trapped air. In the case of circulatory collapse, advanced cardiac life support protocol should be instituted with cardiopulmonary resuscitation because this may break bubbles and advance air into pulmonary vessels and out of the heart.

11. 12.

13.

14.

15.

● Prevention Several authors have advocated the elimination of pneumoperitoneum and the use of a laprolift.29,30 Others advocate use of low pneumoperitoneum. Several air embolisms have been documented in the performance of laparoscopic hepatic resection. One reported fatality resulted from air embolism after an argon beam use in the liver.31 Avoidance of direct gas instillation in an open hepatic vein is critical to preventing this complication. In our practice, the use of high pneumoperitoneal (15–18 mm Hg) pressures is common. Another consideration is avoidance of nitrous oxide anesthetic because it will cause expansion of any air embolus. Despite these elevated pressures, we have not experienced an increased incidence of air embolism.

16.

REFERENCES

23.

1. Gagner MRM, Dubuc JE. Laparoscopic partial hepatectomy for liver tumor. Surg Endosc 1992;6:99. 2. Ferzli G, David A, Kiel T. Laparoscopic resection of a large hepatic tumor. Surg Endosc 1995;9:733–735. 3. Azagra JS, Georgen M, Gilbart E, Jacobs D. Laparoscopic anatomical (hepatic) left lateral segmentectomy—technical aspects. Surg Endosc 1996;10:758–761. 4. Antonetti MC, Killelea B, Orlando R 3rd. Hand-assisted laparoscopic liver surgery. Arch Surg 2002;137:407–411; discussion 412. 5. Are C, Fong Y, Geller DA. Laparoscopic liver resections. Review. Adv Surg 2005;39:57–75. 6. Buell JF, Koffron AJ, Thomas MJ, et al. Laparoscopic liver resection. J Am Coll Surg 2005;200:472–480. 7. Buell JF, Thomas MJ, Doty TC, et al. An initial experience and evolution of laparoscopic hepatic resectional surgery. Surgery 2004;136:804–811. 8. Descottes B, Glineur D, Lachachi F, et al. Laparoscopic liver resection of benign liver tumors. Surg Endosc 2003; 17:23–30 [erratum appears in Surg Endosc 2003;17:668]. 9. Gigot JF, Glineur D, Azagra JS, et al. Laparoscopic liver resection for malignant liver tumors: preliminary results of a multicenter European study. Ann Surg 2002;236:90–97. 10. Huang M, Lee W, Wag W, et al. Hand-assisted laparoscopic hepatectomy for solid tumor in the posterior

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portion of the right lobe. Ann Surg 2003;238:674– 679. Kaneko H, Otsuka Y, Takagi S, et al. Hepatic resection using stapling devices. Am J Surg 2004;187:280–284. Kaneko H, Takagi S, Otsuka Y, et al. Laparoscopic liver resection of hepatocellular carcinoma. Am J Surg 2005;189:190–194. Kurokawa T, Inagaki H, Sakamoto J, et al. Hand-assisted laparoscopic anatomical left lobectomy using hemihepatic vascular control technique. Surg Endosc 2002;16:1637– 1638. Linden BC, Humar A, Sielaff TD. Laparoscopic stapled left lateral segment liver resection–technique and results. J Gastrointest Surg 2003;7:777–782. Laurent A, Cherqui D, Lesurtel M, et al. Laparoscopic liver resection for subcapsular hepatocellular carcinoma complicating chronic liver disease. Arch Surg 2003;138:763–769. Lesurtel M, Cherqui D, Laurent A, et al. Laparoscopic versus open left lateral hepatic lobectomy: a case-control study. J Am Coll Surg 2003;196:236–242. Mala T, Rosseland AR, Gladhaug I, et al. Laparoscopic liver resection: experience of 53 procedures at a single center. J Hepatobiliary Pancreat Surg 2005;12:298–303. Morino M, Morra I, Rosso E, et al. Laparoscopic vs open hepatic resection: a comparative study. Review. Surg Endosc 2003;17:1914–1918. O’Rourke N, Fielding G. Laparoscopic right hepatectomy: surgical technique. J Gastrointest Surg 2004;8:213–216. Takagi S, Kaneko H, Ishii A. Laparoscopic hepatectomy for extrahepatic growing tumor. Surg Endosc 2002;16: 1573–1578. Tang CN, Li MK. Laparoscopic-assisted liver resection. J Hepatobiliary Pancreat Surg 2002;9:105–110. Teramoto K, Kawamura T, Sanada T, et al. Hand-assisted laparoscopic hepatic resection. Surg Endosc 2002;16:1363. Teramoto K, Kawamura T, Takamatsu S, et al. Laparoscopic and thoracoscopic approaches for the treatment of hepatocellular carcinoma. Am J Surg 2005;189:474–478. Vibert E, Perniceni T, Levard H, et al. Laparoscopic liver resection. Br J Surg 2006;93:67–72. Rau H, Buttler E, Meyer G, et al. Laparoscopic liver resection compared with conventional partial hepatectomy—a prospective analysis. Hepatogastroenterology 1998;45:2333–2338. Cherqui D, Husson E, Hammond R, et al. Laparoscopic liver resections: a feasibility study in 30 patients. Ann Surg 2000;232:753–762. Nakai T, Kawabe T, Shiraishi O, Shiozaki H. Prevention of bile leak after major hepatectomy. Hepatogastroenterology 2004;51:1286–1288. Pol B, Campan P, Hardwigsen J, et al. Morbidity of major hepatic resections: a 100-case prospective study. Eur J Surg 1999;165:446–453. Intra M, Viani MP, Ballarini C, et al. Gasless laparoscopic resection of hepatocellular carcinoma (HCC) in cirrhosis. J Laparoendosc Surg 1996;6:263–270. Gutt CN, Kim ZG, Schmandra T, et al. Carbon dioxide pneumoperitoneum is associated with increased liver metastases in a rat model. Surgery 2000;127:566–570. Fatal gas embolism caused by overpressurization during laparoscopic use of argon enhanced coagulation. Health Devices 1994;23:257–259.

35

Pancreaticoduodenectomy Lynt B. Johnson, MD and Rupen Amin, MD INTRODUCTION A pancreaticoduodenectomy (PD) or Whipple procedure is one of the most complex general surgical operations. Owing to the complexity of this procedure, pitfalls that lead to major complications can occur. In this operation, experience of the surgeon is paramount to successful outcomes. This operation is most commonly performed to remove benign and malignant tumors that involve the head of the pancreas, duodenum, periampullary region, or distal common bile duct (CBD). The classic technique of PD consists of the en-bloc removal of the distal segment of the stomach (antrum), the ﬁrst and second portions of the duodenum, the head of the pancreas, the distal CBD, and the gallbladder. Another approach to this procedure is known as a pylorus-sparing PD. In this approach, a small segment of duodenum is left in situ with the entire stomach to preserve the pylorus and prevent post–gastrectomyrelated symptoms and complications. The classic Whipple and pylorus-preserving operations are associated with comparable operation times, blood loss, hospital stays, mortality, morbidity, and incidence of delayed gastric emptying. The overall long-term and disease-free survival is comparable in both groups. Both surgical procedures are equally effective for the treatment of pancreatic and periampullary carcinoma.1 Although the mortality associated with this procedure has remained low, around 2% at major surgical centers,1 signiﬁcant morbidity of 20% to 50% still occurs after this operation.1,2 Several series have demonstrated that results are improved when the procedure is performed by highvolume surgeons, deﬁned as those surgeons that perform more than 24 procedures per year.3 Common complications after PD are postoperative pancreatic ﬁstula (POPF), gastroparesis, wound infection, hemorrhage, and pancreatitis.1,4 Complications of the procedure generally result in prolonged hospital stay, delayed adjuvant therapy, diminished quality of life, or death. The most common complication after PD is POPF. The occurrence of POPF with release of autolytic digestion enzymes in the peritoneal cavity is an underlying source of other complications such as peripancreatic collections, abscess, and hemorrhage.5 Many series have demonstrated ﬁstula rates ranging from 1% to 20%.6,7 The wide range of this reported com-

plication is likely a result of varying deﬁnitions of POPF as well as some patient and surgeon factors. Currently, the International Study Group Pancreatic Fistula (ISGPF) deﬁnition of POPF remains the most useful for diagnosis.8 This deﬁnition includes any amount of drainage ﬂuid that has an amylase level greater than three times the normal limit of serum amylase. The deﬁnition further classiﬁes POPF into subcategories based on the clinical consequences of the ﬁstula.6 Risk factors for the development of POPF after PD include patients with soft texture of the gland, small pancreatic ducts, and low preoperative albumin and prealbumin.5 In pancreatic adenocarcinoma and chronic pancreatitis, the pancreas has a more ﬁbrotic consistency and is more likely to maintain anastomotic integrity. In patients with duodenal, neuroendocrine, or small bile duct tumors, the duct remains small and the gland maintains a soft normal gland consistency.5 Small duct size has also been shown to result in a higher incidence of POPF. However, duct size may be a surrogate for gland consistency because small ducts are more often seen in patients with soft glands.

INDICATIONS ● ● ● ● ● ●

Carcinoma of head of the pancreas Carcinoma of ampulla of Vater Chronic pancreatitis Duodenal cancer Distal bile duct cancer (cholangiocarcinoma) Cystic tumors of pancreas

OPERATIVE STEPS Step Step Step Step Step Step

1 2 3 4 5 6

Step 7

Laparotomy and exploration Kocher’s maneuver Cholecystectomy and transection of CBD Division of gastroduodenal artery Ligation of gastrocolic ligament Identiﬁcation and dissection of superior mesenteric vein (SMV) Division of duodenum or stomach

368 Step 8 Step 9 Step 10 Step 11 Step 12 Step 13 Step 14

SECTION IV: HEPATOBILIARY SURGERY Division of ligament or Treitz and division of jejunum Division of neck of pancreas Dissection of portal vein branches from uncinate process Division and ligation of branches from superior mesenteric artery (SMA) to uncinate process Pancreaticojejunostomy Hepaticojejunostomy Duodenojejunostomy or gastrojejunostomy

OPERATIVE PROCEDURE Kocher’s Maneuver Damage to the Inferior Vena Cava or the Left Renal Vein The peritoneum overlying the second and third portions of the duodenum is divided to mobilize the duodenum. The inferior vena cava (IVC) lies directly posterior to the pancreatic head and thus can be inadvertently injured if the dissection does not occur in the correct plane. ● Consequence Excessive bleeding with injury to the anterior wall of the IVC. Venous bleeding is often more difﬁcult to control because the venous walls will collapse when incised. Grade 3 complication ● Repair The ﬁrst thing to do when faced with IVC bleeding is to remain calm. The second objective is to accurately visualize the injury before attempting repair. A good technique is to apply digital pressure for control initially and then compress the IVC with two sponge sticks above and below the injury. The IVC wall is often fragile so one should refrain from attempts to clamp the injured walls because this can result in an extension of the injury. Once the injury is visualized, closure with simple oversewing with monoﬁlament suture will repair the injury. ● Prevention Knowledge of the anatomic position of the IVC with respect to the duodenum and pancreas is critical. The relationship is constant. Once the peritoneum is divided, the index ﬁnger of the right hand can be used to guide the dissection through the loose areolar tissue behind the duodenum and anterior to the IVC.

Cholecystectomy and Transection of the CBD Injury to the Right Hepatic Artery (Normal or Replaced) In the normal course, the proper hepatic artery bifurcates to the left of the CBD and the right hepatic artery courses behind the common hepatic duct to reach the right hepatic lobe. In almost 20% of patients, the right hepatic artery

will be replaced from the SMA. The replaced right branch reaches the right hepatic lobe by running parallel and adjacent to the right side of the CBD in the hilum. The aberrant replaced right hepatic artery is particularly prone to injury if not expected. ● Consequence Either excessive bleeding or arterial compromise to the right hepatic lobe and right intrahepatic biliary tree. On most occasions, the hepatic ischemia will be limited and not catastrophic. However, long-term strictures or necrosis of the right-sided intrahepatic biliary radicles may occur, resulting in inadequate intrahepatic biliary drainage or intrahepatic abscesses (Fig. 35–1). Grade 3 complication ● Repair End-to-end anastomosis with interrupted ﬁne monoﬁlament suture (7-0 or 8-0) should be carried out under loupe or microscope magniﬁcation. ● Prevention Aberrant anatomy to the liver occurs in upward of 30% of patients. Surgeons should always open the gastrohepatic ligament and manually palpate the hilar vessels to gain an understanding of the arterial supply to the liver. Knowledge of the course of a replaced hepatic artery is essential and should guide palpation to the lateral posterior area of the bile duct to ascertain whether there is a replaced right hepatic artery. Extreme care is taken to gently dissect the right hepatic artery away from the wall of the bile duct prior to transection of the CBD. The replaced right hepatic artery is then dissected proximally to separate it from the areolar tissue holding it close to the pancreatic head or the injury may recur when dividing the uncinate process.

Identiﬁcation and Dissection of the SMV Injury to the SMV The SMV is identiﬁed at the inferior border of the pancreas. Injury to the SMV at this location can be catastrophic if it occurs behind the neck of the pancreas. ● Consequence Excessive bleeding. Grade 3 complication ● Repair Gently lifting the inferior border of the neck of the pancreas with a vein retractor may expose the injury so that repair with oversewing of the injury with ﬁne monoﬁlament suture can occur (Fig. 35–2). If the injury occurs at the middle of the neck of the pancreas, packing the injury with hemostatic sponge or gauze and proceeding with division of the neck of the pancreas may then allow for better exposure to repair the injury.

35 PANCREATICODUODENECTOMY

369

Pancreas

Superior mesenteric vein

Figure 35–2 The inferior border of the neck of the pancreas is lifted to visualize the superior mesenteric vein and portal vein. This maneuver is more easily accomplished with benign tumors.

● Prevention Typically, no branches from the SMV are exactly anterior to the vein. During the dissection, it is paramount to stay in this orientation and not deviate to either side. Lifting on the inferior border of the neck of the pancreas with a vein retractor will provide some additional visualization, but inevitably, a portion of the dissection will be performed without direct visualization to completely mobilize the neck of the pancreas from the portal vein and SMV.

Dissection of the Portal Vein Branches from the Uncinate Process Portal Vein Injury Injury to the portal vein most often occurs when the tumor is closely abutting or adherent to the portal vein. ● Consequence Excessive bleeding or narrowing of the portal vein leading to portal vein thrombosis. Grade 3 complication

Figure 35–1 Hepatic infarcts after Whipple resection. Contrastenhanced axial computed tomography (CT) images demonstrate peripheral geographic areas of diminished attenuation in the liver, most prominent in segment 1. The main portal vein and hepatic artery are patent.

● Repair The initial goal when bleeding from the portal vein occurs is to control the bleeding site to visualize the injury and prepare for repair. Lifting of the head of the pancreas and vein by placing a hand in the retroperitoneal space behind the duodenum will often control the bleeding. If the injury can be easily visualized, repair with simple oversewing can be performed. However, often the specimen prevents adequate visualization. Thus, if the specimen can be removed while controlling the bleeding site with digital pressure, this may allow for better visualization of the injury and a more satisfactory repair (Fig. 35–3). The goal of repair of the portal vein is to prevent narrowing at the closure site. If the vein cannot be repaired with primary closure, mobiliza-

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SECTION IV: HEPATOBILIARY SURGERY tumors, this dissection can be quite perilous because the tumor may be quite adherent in this area.

Transected pancreas

Uncinate process

Portal vein

Figure 35–3 Short branches from the portal vein to the uncinate process must be carefully dissected and secured. Malignant neoplasms, especially in the uncinate process, can make this dissection difﬁcult. In this situation, obtaining control of the portal vein, superior mesenteric vein, and splenic vein will allow control of hemorrhage in the event of branch avulsion.

tion of the portal vein by dividing the peritoneal attachments of the hepatic ﬂexure as well as dissecting distally to free the vein of perihepatic lymphatic and areolar tissue may allow for repair by complete transection followed by an end-to-end anastomosis of the portal vein. The authors, however, prefer to perform a vein patch angioplasty at the injury site. Typically, the saphenous vein is harvested from the groin to create a repair with a vein patch angioplasty. ● Prevention Branches from the portal vein and SMV are fragile in nature and are easily torn. Gentle retraction and dissection of the areolar tissue between the portal vein and the uncinate process is necessary to prevent injury. If the tumor is adherent, an early decision to excise part of the lateral wall of the portal vein and repair with saphenous vein patch angioplasty will prevent foolhardy attempts to dissect the tumor away from the portal vein. If the surgeon anticipates a difﬁcult dissection, control of the portal vein, SMV, and splenic vein with vessel loops prior to dissecting the uncinate process away from the portal vein may allow for rapid control and minimize blood loss owing to an inadvertent injury of the portal vein.

Division and Ligation of Branches from the SMA to the Uncinate Process SMA Injury During the ﬁnal portion of dissection, the specimen is freed in the region of the uncinate process. Small branches for the SMA course through the soft tissue in this area. Knowledge of these branches and the course of the SMA is paramount to prevent injury. With large and bulky

● Consequence Excessive blood loss may occur from avulsion of a side branch of the SMA or direct injury to the SMA itself. Ligation or clamping of the main SMA will result in intestinal ischemia with a disastrous outcome if not easily recognized and repaired. Grade 3 complication ● Repair The critical maneuver is to lift the SMA with the specimen attached so manual control of the bleeding can occur. If the injury site is visualized, simple oversewing of the vessel with monoﬁlament suture can be used for repair. Often, the specimen itself prevents adequate visualization for repair. In this instance, the remainder of the specimen dissection will be unnecessary while maintaining digital or clamp control of the bleeding site. Often, proximal and distal control with clamps applied to the SMA is necessary to prevent catastrophic hemorrhage. Once the specimen is removed, repair of the vessel can be performed under better visualization.

Pancreaticojejunostomy Pancreatic Leak or Postoperative Pancreatic Fistula POPF is the most feared complication after a PD procedure. In this situation, amylase-rich ﬂuid escapes from the pancreatic duct owing to a loss of the integrity of the pancreatic to jejunal or gastric anastomosis. The release of autodigestive enzymes in the peritoneal cavity can lead to other secondary complications. Some series have reported that intra-abdominal abscess has been related to POPF in 50% to 60% of cases.5,9–12 ● Consequence POPF can result in abscess, sepsis, and mortality in its severest form. However, if handled properly, POPF does not necessarily present serious clinical consequences. Recently, the ISGPF devised a classiﬁcation system for POPF. The complication is graded as A, B, or C, depending on the consequences of the POPF— grade A: biochemical ﬁstula without clinical sequelae; grade B: ﬁstula requiring any therapeutic intervention; and grade C: ﬁstula with severe clinical sequelae.13 Grade A ﬁstulas occurred 15% of the time; grade B, 12%; and grade C, 3%.14 Grade 3 complication ● Repair Reoperation for POPF is generally unnecessary unless an undrained ﬂuid collection is unattainable by percutaneous drainage. If reoperation is necessary, controlling the ﬁstula with a closed-suction drain is typically

35 PANCREATICODUODENECTOMY

371

all that is necessary. A few buttress repair sutures can be placed if the site of the leak is obvious, but dedicated attempts to locate the ﬁstula site with aggressive dissection is unnecessary and often will result in further damage or disruption. Patients with the clinical diagnosis of pancreatic ﬁstula usually undergo a computed tomography (CT) scan to assess for associated abscess formation, but approximately 80% of ﬁstulas heal with conservative management.4 Ten percent to 15% of patients with pancreatic ﬁstulas require percutaneous drainage, whereas only 5% require repeat surgery.4 ● Prevention Numerous strategies have been employed to prevent POPF. Accurate suture placement by an experienced pancreatic surgeon is warranted. Whether one chooses a duct-to-mucosa two-layered anastomosis or a singlelayered dunking technique does not seem to differ in the occurrence of POPF. Other strategies have included the use of octreotide, although the effect has been variable in different reported series. In addition, it appears that a standardized approach to the pancreatic anastomosis and a consistent practice of a single technique can help to reduce the incidence of complications after PD.15

Figure 35–4 Pseudoaneurysm of hepatic artery jump graft after Whipple resection. Immediate postoperative contrast-enhanced axial CT image shows peripancreatic inﬂammation.

Other Complications Foregut Ischemia due to Ligation of the Gastroduodenal Artery in Patients with Celiac Artery Stenosis or Occlusion An unusual but potentially devastating complication can occur in patients who undergo a Whipple procedure who have celiac artery stenosis or occlusion. This can occur in patients with atherosclerotic disease or arcuate ligament syndrome. In this situation, the blood supply to the liver and pancreas will be supplied by retrograde ﬂow through the gastroduodenal artery via collaterals from the SMA. If unrecognized, division of the gastroduodenal artery will result in foregut ischemia. ● Consequence Liver, pancreatic, and stomach ischemia. Grade 4/5 complication

Figure 35–5 Pseudoaneurysm of hepatic artery jump graft after Whipple resection. Follow-up CT 3 weeks later shows complex ﬂuid in the lesser sac, consistent with blood products.

● Repair Aorta to hepatic artery bypass graft with saphenous vein is necessary in most cases. If the stenosis is recognized preoperatively, endovascular dilation and stenting may prevent the need for bypass and ischemic insult to the aforementioned organs. If a bypass graft is necessary, strong consideration should be given to performing a completion pancreatectomy to prevent the need for a tenuous pancreaticojejunostomy. In this situation, the risk of leak from the pancreatic anastomosis can lead to devastating complications of abscess, sepsis, or pseudoaneurysm owing to disruption of the pancreatic enteric anastomosis (Figs. 35–4 to 35–7).

● Prevention A thorough review of the visceral vessel anatomy with preoperative imaging can demonstrate signiﬁcant narrowing of the celiac axis.

Delayed Gastric Emptying Delayed gastric emptying is deﬁned as the persistent need for a nasogastric tube for longer than 10 days and is seen in 11% to 29% of patients.16–18 This is one of the most common complications after PD. Most cases occur owing to edema at the anastomosis or dysmotility after partial gastrectomy and loss of the duodenal pacemaker. The classic Whipple and pylorus-sparing operations are

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SECTION IV: HEPATOBILIARY SURGERY embolization if the site can be identiﬁed. Post-PD pancreatitis is rarer, occurring in fewer than 5% of patients.17,18

OVERALL MORBIDITY AND MORTALITY

Figure 35–6 Pseudoaneurysm of hepatic artery jump graft after Whipple resection. On a more inferior image, a pseudoaneurysm of the hepatic artery is seen as a new ﬁnding.

Many questions remain regarding the morbidity and mortality associated with the two different approaches to this complicated procedure. Several studies clearly demonstrated no statistical difference in morbidity between the two types of procedures. Further, the overall mortality of this procedure remains steady at approximately 3%, but no difference in mortality has been described between the two different approaches to this procedure. Therefore, pylorus-preserving PD is an acceptable alternative to the classic Whipple procedure in the treatment of periampullary cancer. Long-term survival and type of recurrence are not inﬂuenced by selection of surgical procedures.22–25

REFERENCES

Figure 35–7 Pseudoaneurysm of hepatic artery jump graft after Whipple resection. A multiplanar reformatted image demonstrates the pseudoaneurysm of the hepatic artery and associated hematoma.

associated with comparable operation times, blood loss, hospital stays, mortality, morbidity, and more importantly, incidence of delayed gastric emptying.1,19 The incidence of delayed gastric emptying can possibly be reduced by shortening the operative time and using antecolic duodenojejunostomy.20

Hemorrhage Hemorrhage in the postoperative period occurs in approximately 7% of patients. Endoluminal hemorrhage generally requires endoscopic evaluation or arteriography with embolization.21 Early intraperitoneal hemorrhage generally requires urgent surgical exploration. Delayed hemorrhage is often best managed with arteriography and

1. Tran KT, Smeenk HG, van Eijck CH, et al. Pylorus preserving pancreaticoduodenectomy versus standard Whipple procedure: a prospective, randomized, multicenter analysis of 170 patients with pancreatic and periampullary tumors. Ann Surg 2004;240:738–745. 2. Crist DW, Sitzmann JV, Cameron JL. Improved hospital morbidity, mortality, and survival after the Whipple procedure. Ann Surg 1987;206:358–365. 3. Urbach DR, Bell CM, Austin PC. Differences in operative mortality between high- and low-volume hospitals in Ontario for 5 major surgical procedures: estimating the number of lives potentially saved through regionalization. CMAJ 2003;168:1409–1414. 4. Gervais DA, Fernandez-del Castillo C, O’Neill MJ, et al. Complications after pancreatoduodenectomy: imaging and imaging-guided interventional procedures. Radiographics 2001;21:673–690. 5. Crippa S, Bassi C, Salvia R, et al. Enucleation of pancreatic neoplasms. Br J Surg 2007;94:1254–1259. 6. Bassi C, Dervenis C, Butturini G, et al. Postoperative pancreatic ﬁstula: an International Study Group Pancreatic Fistula (ISGPF) deﬁnition. Surgery 2005;138:8–13. 7. Kazanjian KK, Hines OJ, Eibl G, et al. Management of pancreatic ﬁstulas after pancreaticoduodenectomy: results in 437 consecutive patients. Arch Surg 2005;140:849– 854; discussion 54–56. 8. Liang TB, Bai XL, Zheng SS. Pancreatic ﬁstula after pancreaticoduodenectomy: diagnosed according to International Study Group Pancreatic Fistula (ISGPF) deﬁnition. Pancreatology 2007;7:325–331. 9. Li-Ling J, Irving M. Somatostatin and octreotide in the prevention of postoperative pancreatic complications and the treatment of enterocutaneous pancreatic ﬁstulas: a systematic review of randomized controlled trials. Br J Surg 2001;88:190–199. 10. Popiela T, Kedra B, Sierzega M, et al. Risk factors of pancreatic ﬁstula following pancreaticoduodenectomy for

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periampullary cancer. Hepatogastroenterology 2004;51:1484–1488. Buchler MW, Friess H, Wagner M, et al. Pancreatic ﬁstula after pancreatic head resection. Br J Surg 2000;87:883– 889. Balsam JH, Ratter DW, Warsaw AL, et al. Ten-year experience with 733 pancreatic resections: changing indications, older patients, and decreasing length of hospitalization. Arch Surg 2001;136:391–398. Pratt W, Maithili SK, Vanounou T, et al. Postoperative pancreatic ﬁstulas are not equivalent after proximal, distal, and central pancreatectomy. J Gastrointest Surg 2006;10:1264–1278; discussion 1278–1279. Pratt WB, Maithel SK, Vanounou T, et al. Clinical and economic validation of the International Study Group of Pancreatic Fistula (ISGPF) classiﬁcation scheme. Ann Surg 2007;245:443–451. Shrikhande SV, Barreto G, Shukla PJ. Pancreatic ﬁstula after pancreaticoduodenectomy: the impact of a standardized technique of pancreaticojejunostomy. Langenbecks Arch Surg 2008;393:87–91. Fernandez-del Castillo C, Rattner DW, Warshaw AL. Standards for pancreatic resection in the 1990s. Arch Surg 1995;130:295–299; discussion 299–300. Yeo CJ, Cameron JL, Sohn TA, et al. Six hundred ﬁfty consecutive pancreaticoduodenectomies in the 1990s: pathology, complications, and outcomes. Ann Surg 1997; 226:248–257; discussion 257–260.

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18. Barens SA, Lillemoe KD, Kaufman HS, et al. Pancreaticoduodenectomy for benign disease. Am J Surg 1996;171: 131–134; discussion 134–135. 19. van Berge Henegouwen MI, van Gulik TM, DeWit LT, et al. Delayed gastric emptying after standard pancreaticoduodenectomy versus pylorus-preserving pancreaticoduodenectomy: an analysis of 200 consecutive patients. J Am Coll Surg 1997;185:373–379. 20. Gao HQ, Yang YM, Zhuang Y, et al. [Inﬂuencing factor analysis of delayed gastric emptying after pylorus-preserving pancreaticoduodenectomy]. Zhonghua Wai Ke Za Zhi 2007;45:1048–1051. 21. Rumstadt B, Schwab M, Korth P, et al. Hemorrhage after pancreatoduodenectomy. Ann Surg 1998;227:236– 241. 22. Pellegrini CA, Heck CF, Raper S, et al. An analysis of the reduced morbidity and mortality rates after pancreaticoduodenectomy. Arch Surg 1989;124:778–781. 23. Itani KM, Coleman RE, Meyers WC, et al. Pyloruspreserving pancreatoduodenectomy. A clinical and physiologic appraisal. Ann Surg 1986;204:655–664. 24. Takao S, Aikou T, Shinchi H, et al. Comparison of relapse and long-term survival between pylorus-preserving and Whipple pancreaticoduodenectomy in periampullary cancer. Am J Surg 1998;176:467–470. 25. Grace PA, Pitt HA, Tompkins RK, et al. Decreased morbidity and mortality after pancreatoduodenectomy. Am J Surg 1986;151:141–149.

36

Distal Pancreatectomy Kiran K. Dhanireddy, MD and Thomas M. Fishbein, MD INTRODUCTION Distal pancreatectomy is performed for a variety of benign and malignant indications. The tail of the pancreas can be resected for lesions that are to the left of the superior mesenteric vessels. The procedure can be performed with or without splenic preservation, depending on the initial indication and intraoperative ﬁndings. Pancreatic malignancy generally requires splenectomy, whereas benign indications for distal pancreatectomy allow for splenic preservation. Although the ultimate outcome of the procedure depends on the underlying disease process, the complications associated with distal pancreatectomy are readily avoided through an intimate knowledge of pancreatic anatomy and meticulous surgical technique. The most discussed complication of pancreatic surgery is pancreatic leak and ﬁstula1–3; however, several additional pitfalls to be avoided in the course of executing distal pancreatectomy will also limit postoperative morbidity and mortality. Whereas laparoscopic distal pancreatectomy with or without splenic preservation is currently possible, speciﬁc discussion of the laparoscopic aspects of this operation are beyond the scope of this chapter.4–7

INDICATIONS ● ● ● ● ● ● ● ●

Pancreatic adenocarcinoma Benign cystadenoma Cystadenocarcinoma Neuroendocrine tumor Traumatic pancreatic duct disruption Pancreatic pseudocyst Chronic pancreatitis Acute pancreatic necrosis

OPERATIVE STEPS Step 1 Step 2 Step 3

Incision Entry into lesser sac and exposure of pancreas Dissection of inferior border of pancreatic tail

Distal Pancreatectomy with Splenectomy Step 4a Splenic mobilization Step 5a Medial rotation of spleen pancreas Step 6a Ligation of splenic vessels

and

tail

of

Splenic Preservation Vascular control of splenic vessels medial to lesion Step 5b Ligation of perforating branches of splenic vein and artery Step 7a/6b Pancreatic division Step 8a/7b Drain placement and closure of abdomen Step 4b

OPERATIVE PROCEDURE Incision The patient should be in the supine position on the operative table in slight reverse Trendelenburg. Either an upper midline or a left subcostal incision may be used because both provide excellent exposure of the pancreas. The midline incision may be preferable when the patient has a narrow costal arch, whereas the subcostal incision is superior in patients in whom the costal arch is wide.

Entry into the Lesser Sac and Exposure of the Pancreas To enter the lesser sac, the gastrocolic ligament is divided in a relatively avascular area. The anterior surface of the pancreas is then fully exposed. Occasionally, the inferior short gastric vessels must be ligated to facilitate full exposure of the tip of the pancreatic tail. This has no implication for splenic function if the spleen is preserved.

Hemorrhage from the Veins Communicating between the Right Gastroepiploic Vessels and the Middle Colic Vein Occasionally, a branch of the right gastroepiploic vessels will communicate with the middle colic vessels inferior to the pylorus. In the process of elevating the stomach, this vein may be torn.

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● Consequence Unnecessary blood loss can obscure the operative ﬁeld and prolong the course of the operation. Grade 1 complication

splenorenal, and splenogastric ligaments, must be fully mobilized.

● Repair Ligation of the torn ends of the vessel.

● Consequence The spleen has a rich blood supply from both the splenic artery and the short gastric vessels. Injury to the splenic capsule or failure to recognize all the short gastric vessels can result in bothersome bleeding. Grade 1 complication

● Prevention Prior to elevating the antrum and pylorus of the stomach, all vascular attachments should be identiﬁed and ligated using silk or Vicryl ties of the appropriate caliber. Entering through the gastrocolic omentum in the correct avascular plane and continuing toward the short gastric vessels to the spleen will help avoid this complication.

Dissection of the Inferior Border of the Pancreatic Tail After the pancreas has been fully exposed, the peritoneum overlying the inferior margin of the pancreatic tail is incised. This maneuver allows for superior reﬂection of the pancreas and exposure of the splenic vessels.

Injury to the Middle Colic Vein or the Inferior Mesenteric Vein The middle colic vein runs in the transverse mesocolon in close proximity to the inferior border of the pancreas. This vein may be encountered during the medial portion of the dissection. Similarly, the inferior mesenteric vein may be encountered more laterally as it drains into the splenic vein. ● Consequence Unnecessary blood loss and increased operative time are the consequences of unrecognized middle colic and inferior mesenteric vein injury. Grade 1 complication

Bleeding from the Spleen

● Repair Meticulous ligation of the short gastric vessels will control bleeding from these vessels. ● Prevention Ligation of the splenic artery at the hilum of the spleen early in the course of mobilization will limit blood loss if splenic injury occurs. Argon beam coagulation or other local measures can temporarily halt splenic capsular or ligamentous bleeding.

Medial Reﬂection of the Spleen and the Tail of the Pancreas After the splenic attachments have been released, the spleen and tail of the pancreas may be rotated medially. The attachments of the pancreatic tail to the retroperitoneum are avascular and can therefore be freed using a combination of gentle blunt and sharp dissection. The splenic vessels are included in the mobilization.

Injury to the Left Renal Vein or the Adrenal Vein The left renal vein lays posterior to the inferior margin of the tail of the pancreas (Fig. 36–1). The left adrenal vein enters the superior surface of the renal vein, and the adrenal gland can sometimes be adherent to the posterior

● Repair The middle colic and inferior mesenteric veins may be ligated if they are injured because there is a rich network of collateral venous drainage for the large intestine.

Adrenal

● Prevention During the course of dissection, these vessels should be identiﬁed and spared injury. Dissection of the pancreatic tail should proceed from distally (near the spleen) toward the body. Identiﬁcation of the splenic vein along the inferior margin of the pancreas allows one to directly identify where these veins will potentially enter, avoiding injury.

Splenic Mobilization If the spleen is not to be preserved during the conduct of the operation, the attachments, including the leinocolic,

Spleen

IVC

Renal vein

Kidney

Pancreas

Figure 36–1 Hidden anatomy – relationship of left renal vein/left adrenal vein to tail of pancreas.

36 DISTAL PANCREATECTOMY capsule of the pancreas, making this mobilization of the pancreas more difﬁcult. During the course of medial reﬂection, the left renal vein, adrenal gland, or adrenal vein may be inadvertently injured. ● Consequence Renal vein injury can result in brisk bleeding and signiﬁcant blood loss. Based on the severity of the laceration, a signiﬁcant prolongation of the operative procedure may result. If a branch of the renal vein is inadvertently ligated and unrecognized, venous congestion and subsequent loss of renal function may result. The left adrenal gland may be controlled with electrocautery, and the vein may be ligated without consequence. Grade 1/2 complication ● Repair The left renal vein should be repaired primarily using a nonabsorbable monoﬁlament suture such as Prolene. This requires vascular control of the vein proximally and distally. This may be facilitated by ligation of the left gonadal vein and retroperitoneal collateral vein from the left renal vein in order to gain mobility for repair with good visualization. ● Prevention Knowledge of the relationship between the left renal vein and the tail of the pancreas along with careful dissection during the course of medial reﬂection will prevent this complication.

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supply to the tail of the pancreas consists of multiple perforating vessels directly from the splenic vessels.

Bleeding from the Pancreatic Branches of the Splenic Vessels These vessels must be carefully dissected and ligated with small clips, suture ligature, or harmonic scalpel. If an unsecured vessel is transected, the vessel may retract out of the operative ﬁeld and cause bleeding that is difﬁcult to control. ● Consequence Unnecessary blood loss and prolonged operative time will result from bleeding branches of the splenic vessels. Grade 1 complication ● Repair Identiﬁcation and ligation of the bleeding vessels halts blood loss. The pancreatic side is best controlled with ﬁne monoﬁlament suture, whereas the splenic vein side may be tied or sutured if it tears. ● Prevention Early vascular control of the splenic vessels proximal to the site of proposed pancreatic transection allows for minimization of any bleeding from the perforating vessels. The use of suture ligation of these very short branches with ﬁne Prolene may speed the conduct of the operation.

Pancreatic Division Ligation of the Perforating Branches of the Splenic Vein and Artery If the spleen is to be preserved during the conduct of the operation, the splenic artery and vein must be separated from the tail of the pancreas (Fig. 36–2). The blood

Spleen

Pancreas

The pancreatic parenchyma can be divided using a gastrointestinal anastomosis (GIA) stapler with a vascular load or using nonabsorbable horizontal mattress sutures. Data suggest that the incidence of complications is lower in stapled transections.8

Pancreatic Leak/Fistula Pancreatic ﬁstula after distal pancreatectomy is reported to occur in approximately 25% of patients.9,10 This complication adds signiﬁcant morbidity and mortality to the operation. ● Consequences Pancreatic ﬁstula infrequently necessitates reoperation but does add signiﬁcantly to length of hospital stay, the need for parenteral nutrition, and overall costs.7 Grade 4 complication

Figure 36–2 Small vessels directly from splenic vessels to tail of pancreas. Note added branches from splenic vein.

● Repair Few would advocate direct repair of the pancreatic stump for management of a pancreatic ﬁstula. Current strategies include drainage and the use of parenteral nutrition to prevent pancreatic stimulation by enteral diet. The use of a somatostatin analogue has been examined as a means to decrease the production of

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pancreatic enzymes.11 Low-volume leaks usually seal with drainage alone, whereas those ﬁstulas with highvolume output are likely to seal with a period of prolonged parenteral nutrition in the absence of oral intake. ● Prevention There have been numerous reports of strategies to reduce the risk of pancreatic leak after distal pancreatectomy. Most of these techniques have been unsuccessful. For example, the use of ﬁbrin glue had been advocated but has recently been shown to not signiﬁcantly change the rate of ﬁstula development.12 Another technique that might alter the rate of ﬁstula development is direct ligation of the pancreatic duct, even if a stapler is used for transecting the pancreatic tissue.13 The mainstay of treatment is closed-suction drainage of the pancreatic bed after surgery, the institution of a low-fat diet, and the judicious use of antibiotics to treat superinfection when it occurs.

REFERENCES 1. Rodriguez JR, Germes SS, Pandharipande PV, et al. Implications and cost of pancreatic leak following distal pancreatic resection. Arch Surg 2006;141:361–365. 2. Kuroki T, Tajima Y, Kanematsu T. Surgical management for the prevention of pancreatic ﬁstula following distal pancreatectomy. J Hepatobiliary Pancreat Surg 2005;12: 283–285. 3. Knaebel HP, Diener MK, Wente MN, et al. Systematic review and meta-analysis of technique for closure of the pancreatic remnant after distal pancreatectomy. Br J Surg 2005;92:539–546. 4. Toniato A, Meduri F, Foletto M, et al. Laparoscopic treatment of benign insulinomas localized in the body and tail

5.

6.

7.

8.

9.

10.

11.

12.

13.

of the pancreas: a single-center experience. World J Surg 2006;30:1916–1919. Palanivelu C, Shetty R, Jani K, et al. Laparoscopic distal pancreatectomy: results of a prospective non-randomized study from a tertiary center. Surg Endosc 2007;4:250– 254. Aluka KJ, Long C, Rickford MS, et al. Laparoscopic distal pancreatectomy with splenic preservation for serous cystadenoma: a case report and literature review. Surg Innov 2006;13:94–101. Pierce RA, Spitler JA, Hawkins WG, et al. Outcomes analysis of laparoscopic resection of pancreatic neoplasms. Surg Endosc 2007;4:579–586. Takeuchi K, Tsuzuki Y, Ando T, et al. Distal pancreatectomy: is staple closure beneﬁcial? Aust N Z J Surg 2003; 73:922–925. Fahy BN, Frey CF, Ho HS, et al. Morbidity, mortality, and technical factors of distal pancreatectomy. Am J Surg 2002;183:237–241. Pannegeon V, Pessaux P, Sauvanet A, et al. Pancreatic ﬁstula after distal pancreatectomy: predictive risk factors and value of conservative treatment. Arch Surg 2006;141: 1071–1076. Suc B, Msika S, Piccinini M, et al, and the French Associations for Surgical Research. Octreotide in the prevention of intra-abdominal complications following elective pancreatic resection: a prospective, multicenter randomized controlled trial. Arch Surg 2004;139:288– 294. Suc B, Msika S, Fingerhut A, et al, and the French Associations for Surgical Research. Temporary ﬁbrin glue occlusion of the main pancreatic duct in the prevention of intra-abdominal complications after pancreatic resection: prospective randomized trial. Ann Surg 2003;237:57– 65. Bilimoria MM, Cormier JN, Mun Y, et al. Pancreatic leak after left pancreatectomy is reduced following main pancreatic duct ligation. Br J Surg 2003;90:190–196.

37

Lateral Pancreaticojejunostomy (Puestow) Procedure Eleanor Faherty, MD and Patrick G. Jackson, MD INTRODUCTION

OPERATIVE STEPS

Surgical approaches to chronic pancreatitis are indicated in the setting of intractable pain or anatomic complications of the disease process, such as symptomatic obstruction of the common bile duct, pancreatic duct, or duodenum. From a conceptual standpoint, the surgical procedures offered for chronic pancreatitis can be segregated into resection procedures, drainage procedures, or combinations of the two. The speciﬁc approach to surgical management must be individualized because there is a wide variability in symptomatology, gland pathology, and anatomic manifestation.1 Ductal drainage procedures are used for patients with dilated pancreatic ductal systems, under the theory that the pancreatic duct has a symptomatic and functional obstruction. With a limitation to enzyme secretion into the duodenum, there is a lack of inhibitory feedback, thus allowing an increase in cholecystokinin, which induces further enzyme secretion into a functionally obstructed duct. The increased ductal distention then causes pain.2 No clear consensus exists regarding the deﬁnition of a dilated ductal system. Whereas most would agree that pancreatic ducts greater than 1 cm (Fig. 37–1) constitute sufﬁcient dilation, greater controversy exists regarding ducts between 5 mm and 1 cm.1,3 Although no prospective study exists correlating greater ductal size with superior long-term outcome, increased ductal dilation does facilitate a number of the steps in the procedure. Surgical management of chronic pancreatitis and ductal drainage is technically challenging, requiring a comprehensive and coherent surgical approach to avoid common pitfalls.

Step 1 Step 2

INDICATIONS ● Intractable abdominal pain and/or back pain ● Symptomatic duodenal obstruction ● Symptomatic common bile duct obstruction

Skin incision Exploration of peritoneal contents for additional pathology Step 3 Enter lesser sac to expose anterior pancreas Step 4 Wide Kocher maneuver Step 5 Location of pancreatic duct with palpation and needle aspiration Step 6 Unrooﬁng of pancreatic duct from duodenum to splenic hilum Step 7 Ensure adequate pancreatic drainage Step 8 Construction of Roux-en-Y jejunal loop of approximately 60 cm Step 9 Anastomosis of Roux-en-Y loop in retrocolic, two-layer, side-to-side pancreaticojejunostomy Step 10 Fixation of Roux-en-Y jejunal loop to transverse mesocolon Step 11 Closure4,5

OPERATIVE PROCEDURE Exploration of Peritoneal Contents for Additional Pathology Unexpected Intraoperative Findings ● Consequence Change in operative strategy. Grade 1/2 complication ● Repair Appropriate surgical management of another disease process such as pancreatic cancer. ● Prevention Preoperative planning in the management of chronic pancreatitis is critical to success. Noninvasive imaging with high-quality dynamic bolus-enhanced computed tomography (CT) with thin cuts to evaluate the pancreas helps avoid errors in the management algorithm. Pancreatic cancers will generally appear as

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Figure 37–1 calciﬁcations.

Dilated

pancreatic

duct

with

parenchymal

hypodense lesions. Preoperative CT scans can also delineate biliary ductal dilation, pseudocysts, and pancreatic duct size.1 Endoscopic retrograde cholangiopancreatography (ERCP) can provide valuable information about intraductal pathology and should be used when the diagnosis of chronic pancreatitis is in doubt, to evaluate possible ampullary lesions, or to assess duct size if CT cannot provide adequate information. Endoscopic ultrasound (EUS), a newer diagnostic technique, is the most sensitive modality for the diagnosis of pancreatic carcinoma, and although it is invasive, it poses fewer risks than ERCP.4 With its ability to assess the pancreatic parenchyma and determine duct size and an increased sensitivity for mass lesions, EUS is becoming a valuable tool in the preoperative planning of chronic pancreatitis management.

Figure 37–2

Needle aspiration of dilated duct system.

The posterior wall of the stomach may be densely adhered to the pancreas and will require meticulous dissection in the avascular place for separation. Critical in this step is exposure of the entire anterior surface of the pancreas, with careful preservation of the gastroepiploic vessels.6

Location of the Pancreatic Duct with Palpation and Needle Aspiration and Unrooﬁng of the Pancreatic Duct from the Duodenum to the Splenic Hilum Inability to Identify the Pancreatic Duct

Enter the Lesser Sac to Expose the Anterior Pancreas and Perform a Wide Kocher Maneuver Inadequate Exposure ● Consequence Technical inability to complete the procedure. Grade 2/3 complication ● Repair Appropriate exposure of the abdomen and the anterior surface of the entire pancreas. ● Prevention A generous midline incision is employed for the procedure, and the entire abdomen is explored. A wide Kocher maneuver helps in the exposure of the head of the pancreas. The gastrocolic ligament is divided to enter the lesser sac with subsequent mobilization of the stomach superiorly and the transverse colon inferiorly.

● Consequence Bleeding or inadvertent injury to the pancreatic parenchyma. Grade 2/3/4 complication ● Repair Hemostasis and wide postoperative drainage. ● Prevention The pancreatic duct can usually be palpated as a soft compressible area in the body of the gland. Intraoperative ultrasound should be used liberally to conﬁrm the identiﬁcation of the duct and thus avoid unwarranted pancreatotomy. Accessory or side branch ducts may also be dilated, so aspiration of clear secretions does not conﬁrm location of the main duct (Fig. 37–2). With intraoperative ultrasound, a needle can be easily placed into the pancreatic duct by aspiration, with the syringe then removed, leaving the needle in the duct to serve as a guide.

37 LATERAL PANCREATICOJEJUNOSTOMY (PUESTOW) PROCEDURE

Aggressive Attempts to Identify and Open the Duct ● Consequence Injury to the superior mesenteric vein/portal vein. Grade 2/3/4 complication ● Repair Meticulous hemostasis using ﬁne sutures. ● Prevention Clear and careful identiﬁcation of the superior mesenteric vein during exposure of the pancreas will help avoid this potentially disastrous event. In addition, the duct should be entered using electrocautery through its anterior surface at the midbody, thus avoiding the splenoportal conﬂuence.6

Ensure Adequate Pancreatic Drainage Insufﬁcient Decompression ● Consequence Anastomotic stricture, reduced likelihood of symptomatic relief. Grade 2/3/4 complication

381

intraductal concretions must be removed.4 The entire duct from tail to head should be opened to allow sufﬁcient drainage of the entire pancreatic parenchyma (Fig. 37–4). Studies suggest that a pancreaticojejunostomy less than 6 cm in length has a higher risk of stricture and therefore inadequate drainage.7 Although this is factually correct, focusing too heavily on the minimum requirement fails to emphasize the goal of adequate decompression of the entire pancreas because the minimum requirement becomes the deﬁnition of adequacy. Therefore, unrooﬁng of the entire duct from tail to head with subsequent longitudinal pancreaticojejunostomy will provide sufﬁcient drainage.

Anastomosis of the Roux-en-Y Loop in a Retrocolic, Two-Layer, Side-to-Side Pancreaticojejunostomy Inadequate Orientation of the Roux-en-Y Limb ● Consequence Difﬁculty in subsequent biliary decompression. Grade 2/3 complication ● Repair Additional biliary enteric bypass limb.

● Prevention Using the needle as a guide, the pancreatic duct is opened. Once the pancreatotomy is sufﬁcient to allow passage of a ﬁne right-angle clamp or probe, the course of the duct can be determined (Fig. 37–3). This allows incision of the overlying pancreatic parenchyma. All

● Prevention The blind end of the Roux-en-Y limb used for pancreaticojejunostomy should be oriented toward the splenic hilum (Fig. 37–5). Orientation in the opposite direction will not allow for decompression of the biliary tree, should this prove necessary later. With orientation of the blind end toward the spleen, additional length of this limb can be drawn through the rent in the transverse mesocolon for creation of a tension-free biliary enteric anastomosis if necessary.1

Figure 37–3 incision.

Figure 37–4 Exposure of entire length of pancreatic duct.

● Repair Further endoscopic or surgical procedures to decompress the ductal system.

Right angle clamp used to extend pancreatic duct

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REFERENCES Figure 37–5 Construction of pancreaticojejunostomy.

Leak from the Pancreaticojejunostomy ● Consequence Intra-abdominal autodestruction from activated pancreatic enzymes. Grade 2/3 complication ● Repair Wide drainage with prolonged bowel rest. ● Prevention Given the ﬁbrotic parenchymal changes from chronic pancreatitis, leak from this anastomosis should be

1. Prinz R. Pancreatic duct drainage. In Pancreas. p 829. 2. Owyang C. Control of exocrine pancreatic secretion. Regul Pept 1989;1:107. 3. Prinz RA. Surgical options in chronic pancreatitis. Int J Pancreatol 1993;14:97–105. 4. Nakeeb A, Lillemoe K, Cameron JL. Procedures for benign and malignant pancreatic disease. In Souba WS (ed): ACS Surgery: Principles and Practice. Hamilton, Ontario: BC Decker, 2008. 5. Sakorafas GH, Sarr MG. Tricks in the technique of lateral pancreaticojejunostomy. Eur J Surg 2000;166:498–500. 6. Nealon WH, Thompson JC. Progressive loss of pancreatic function in chronic pancreatitis is delayed by main pancreatic duct decompression. A longitudinal analysis of the modiﬁed Puestow. Ann Surg 1993;217:458–468.

38

Pancreatic Cyst/Debridement Lynt B. Johnson, MD, Patrick G. Jackson, MD, and Trevor Upham, MD Inﬂammatory Pancreatic Cyst Drainage Lynt B. Johnson INTRODUCTION Cysts of the pancreas are typically inﬂammatory in nature or neoplastic. Pancreatic pseudocysts generally occur as a consequence of acute or chronic pancreatitis. Unlike pseudocysts of the pancreas due to chronic pancreatitis, pseudocysts that occur as a result of acute pancreatitis more often can spontaneously resolve over time; however, some of these cysts persist and require intervention. Distinction should be made between a pancreatic pseudocyst with a low viscous liquid ﬂuid and other peripancreatic collections that include phlegmons and tissue necrosis, which are more semisolid or solid in consistency. The consistency of the material encountered greatly inﬂuences the appropriate treatment options. Typically for noninfected collections, it is prudent to wait 6 weeks from the inﬂammatory incident to allow time for the cyst to resolve or for the cyst wall to mature. During this 6-week period, the consistency of the ﬂuid can change dramatically from a toothpaste consistency to pure liquid. The diagnosis of the pseudocyst is typically identiﬁed through abdominal imaging. Computed tomography, magnetic resonance imaging, or ultrasound can be used to conﬁrm the diagnosis. One must be cautious to not misdiagnose a cystic neoplasm as a pseudocyst. Suspicion of the diagnosis should occur if there has not been a precedent history of pancreatitis. Clinical signs of infection such as fevers and gas within the collection often warrant early intervention. Although studies utilizing percutaneous drainage as well as endoscopic drainage have reported some success, the selection of the appropriate patient for these treatments is paramount. In general, patients with semisolid or solid components in the collection should be managed with

operative drainage. The choices for operative drainage include internal drainage by cystenterostomy or external drainage. Internal drainage is preferred when the cyst is not infected and has low-viscosity ﬂuid. For giant pseudocysts, the author prefers a Roux-en-Y cystgastrostomy performed through the transverse mesocolon. This allows for complete resolution of the cyst through dependent drainage. Although cystgastrostomy is regarded as a mainstay for internal drainage cases, stasis and retroperitoneal sepsis have occurred, especially in large pseudocysts, owing to lack of adequate dependent drainage. External drainage can also be accomplished through a transverse mesocolon approach for patients with phlegmons or infected pseudocysts to allow for manual débridement of the necrotic tissue and placement of large-caliber drains.

Cystgastrostomy or Endoscopic Drainage INDICATIONS ● Small, less than 5 cm persistent pseudocyst located pos-

terior to stomach ● Low viscosity of cyst ﬂuid

OPERATIVE STEPS Step Step Step Step

1 2 3 4

Anterior gastrotomy Creation of posterior gastrotomy Cyst wall and posterior stomach anastomosis Closure of anterior gastrotomy

OPERATIVE PROCEDURE Anterior Gastrotomy Anterior Gastrotomy Bleeding Typically, a transverse incision using electrocautery directly overlying the cyst should be made. The gastric wall is very vascular, and thus, bleeding can occur if other nonhemostatic incisions are made in the stomach wall.

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● Consequence Bleeding can occur and obscure adequate vision. Grade 1 complication

verse mesocolon, one can identify the pseudocyst bulging through the mesocolon. If not, apply the same maneuvers as listed previously.

● Repair Oversewing of the gastrotomy edges typically will control the bleeding.

Injury to the Mesocolon Vessels

● Prevention Alternatively, the gastrotomy can be performed with a dividing stapling device.

Creation of the Posterior Cystgastrostomy Inability to Locate the Cyst The cyst can typically be felt by palpation or visualized owing to an impression on the posterior gastric wall. ● Consequence Creation of a gastrotomy not in continuity with the pseudocyst. Grade 1 complication ● Repair Closure of the aberrant opening and reassessment. ● Prevention The cyst cavity can be detected by aspiration with a 22-gauge needle through the posterior gastric wall. Alternatively, intraoperative ultrasound can be used to localize the cyst.

Roux-en-Y Cystjejunostomy INDICATIONS ● Large, greater than 5 cm persistent pseudocyst.

OPERATIVE STEPS Step 1 Step 2

Identiﬁcation and opening of pseudocyst wall through transverse mesocolon Creation of Roux-en-Y cystjejunostomy

● Consequence Hemorrhage. Grade 1 complication ● Repair Oversewing of the bleeding vessel should control the bleeding. If it occurs from the pancreatic bed, oversewing of the vessel or topical coagulation should be attempted. If these maneuvers are not effective, packing of the cavity and immediate angiographic embolization of the bleeding vessel may be warranted. ● Prevention Great caution should be used when creating the opening to perform this through an avascular plane in the mesocolon. Aspirating with a small-gauge needle may provide some safety before making the opening. One should avoid carrying the opening too medial to avoid injury to the middle colic vessels. Typically, the opening should be to the left of the ligament of Treitz to avoid this complication.

Creation of the Roux-en-Y Cystjejunostomy Anastomotic Leak ● Consequence Undrained ﬂuid collection or abscess, sepsis. Grade 1 complication ● Repair Percutaneous drainage of the ﬂuid collection to try to create a controlled ﬁstula is paramount. If the ﬂuid is amylase rich, the patient should be started on octreotide. Once the drain has been left for 6 weeks, a drain study can be performed. If there is no collection, the drain can be removed and the epithelialized tract will generally seal. ● Prevention Closed-suction drains should be left above and below the anastomosis. These drains should be left in place until there is certainty that no leak has occurred.

OPERATIVE PROCEDURE Identiﬁcation and Opening of the Pseudocyst Wall through the Transverse Mesocolon

External Drainage

Inability to Locate the Cyst See the section on “Inability to Locate the Cyst,” under “Cystgastrostomy,” earlier. Typically by lifting the trans-

INDICATIONS ● Infected pseudocyst or phlegmon.

38 PANCREATIC CYST/DEBRIDEMENT

OPERATIVE STEPS Step 1 Step 2 Step 3

Identiﬁcation and opening of pseudocyst wall through transverse mesocolon Débridement of necrotic or infected tissue Placement of large-bore sump drains

OPERATIVE PROCEDURE Identiﬁcation and Opening of the Pseudocyst Wall through the Transverse Mesocolon Same pitfalls as in the sections on “Inability to Locate the Cyst,” and “Injury to the Mesocolon Vessels,” under “Roux-en-Y Cystjejunostomy,” earlier.

Débridement of Necrotic or Infected Tissue The ﬂuid and tissue within the phlegmon is typically of a semisolid consistency much like that of toothpaste. As the ﬁrst step, the author prefers to manually dislodge and remove this tissue through the opening created. The tissue separates fairly easily from the underlying viable pancreatic tissue. Russian forceps can then be used to extricate the hard-to-reach areas. Irrigation with a red rubber catheter can also be employed to remove dislodged particles.

Pancreatic Bed Hemorrhage Overaggressive débridement can result in hemorrhage from the pancreatic bed. Minor bleeding can occur from surface branches. More substantial bleeding can occur from the pancreatoduodenal vessels or dorsal pancreatic vessels. ● Consequence Major hemorrhage during or after the procedure can lead to disastrous consequences. Grade 3 complication ● Repair When hemorrhage is recognized during the procedure, suture ligation should be attempted. If this fails, packing the opening and quickly transporting the patient for angiographic embolization is the indicated treatment. ● Prevention The necrotic tissue is generally of a different consistency than the underlying parenchyma and should elevate quite easily. Densely adherent tissue that does not easily elevate with manual débridement or irrigation should be left behind.

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Placement of Large-Bore Sump Drains Large-bore sump drains should be placed in the pancreatic bed and brought external. These drains should have an opening of sufﬁcient size such that particulate material can be drained adequately. A drain in the style of a Waterman sump is one variation. Alternatively, some surgeons use stuffed Penrose drains as packing, with sequential removal once they stop draining.

Surgical Management of Pancreatic Necrosis Patrick G. Jackson and Trevor Upham INTRODUCTION Pancreatic necrosis occurs as a sequela of approximately 15% to 30% of the 185,000 cases of acute pancreatitis in the United States every year.1 Pancreatic necrosis exists as a continuum from sterile pancreatic necrosis to infected pancreatic necrosis (Fig. 38–1). Bacteria infect the sterile necrotic pancreas, probably via translocation from the colon, in a time-dependent manner from the onset of pancreatitis. The infection rate of the sterile pancreatic bed ranges from approximately 24% within 1 week to 71% within 3 weeks in the absence of treatment.2 If untreated, infected pancreatic necrosis can progress to a dense walled-off collection of pus and liqueﬁed necrosis. To prevent the associated systemic complications, early recognition of infection and proper treatment, medically or surgically, are critical. In the setting of known infected pancreatic necrosis or worsening clinical presentation indicative of infection, pancreatic débridement is necessary to prevent the lethal systemic inﬂammatory response syndrome (SIRS) and possible multiple organ system failure. Surgical treatment of a necrotic pancreas requires careful approach, débridement, and postoperative management to resuscitate the critical organ. Surgeons select the appropriate surgical protocol from the three primary methods that exist for surgical débridement and packing: (1) open débridement with closed packing, (2) open débridement with closed lavage, and (3) open débridement with open packing. Open débridement consists of gentle blunt ﬁnger dissection to carefully identify all necrotic tissue and ﬁnger abrasion with sponges covering the ﬁngertips to remove the necrotic tissue. Because the necrotic tissue may be very poorly demarcated, a preoperative computed tomography (CT) scan can be used as a guide to identify and débride all necrotic areas of the pancreas and any necrotic attachment to local structures. Generous interoperative lavage is encouraged.

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Closed packing involves placement of ¾-inch Penrose drains or an Abramson drain in conjunction with several Jackson-Pratt (JP) drains. Closed lavage consists of placement of single- and double-lumen catheters in the cavity. The drains on the left traverse from the cavity posterior to the large bowel, inferior to the spleen, and anterior to the kidney through separate skin stab wounds. On the right, the drains traverse from the cavity through the foramen of Winslow to separate skin stab wounds. The gastrocolic ligament and transverse mesocolon are closed with sutures to create a conﬁned space for concentrated lavage. Hyperosmolar potassium-free dialysis ﬂuid is used postoperatively to lavage the cavity at a rate of 2 L/hr until the efﬂuent lacks necrotic tissue and does not contain amylase. Open packing involves an approach through a horizontal incision. The cavity is packed with moist gauze. Redébridement with lavage is performed ﬁrst after 48 to 72 hours and then every 48 hours until the cavity is clean with healthy granulation tissue at the base. The cavity is then managed with surgical drains. Choosing between these strategies must be done in the scope of the clinical details of the necrotizing process as well as the available surgical expertise and ancillary support staff. In that all strategies have equivalent outcomes, the choice of approach is largely surgeon dependent. Regardless of the chosen surgical protocol, minimizing surgical complications while optimally preserving the remaining pancreatic function proves a delicate task that favors foresight to prevent surgical management pitfalls. Although all operative strategies have equivalent outcomes, open débridement with close packing is preferred. To avoid the following pitfalls, carefully planned surgical management of pancreatic necrosis is mandated in the setting of known infected pancreatic necrosis or worsening clinical presentation indicative of infection. Surgical outcomes can be maximized with complete débridement

Figure 38–1 Retroperitoneal air with infected necrosis.

of the necrotic tissue and management of the residual cavity with carefully chosen closed packing, closed lavage, or open packing.

INDICATIONS ● Infected pancreatic necrosis ● Worsening clinical symptomatology of infection in

setting of pancreatic necrosis

OPERATIVE STEPS Step Step Step Step Step Step

1 2 3 4 5 6

Skin incision Entrance into lesser sac to expose pancreas Débridement of necrotic pancreas Surgical drainage Closed packing Abdominal closure

Skin Incision Delayed Pancreatic Débridement ● Consequence SIRS and possible multiple organ system failure. Grade 3/4 complication ● Repair Surgical débridement. ● Prevention Surgical débridement is indicated in the setting of (1) infection, (2) increasing toxicity in the absence of infection, (3) failure to improve clinically despite continued support over 3 to 4 weeks, or (4) an acute abdominal catastrophe.3 A commonly used and helpful means of identifying infection in pancreatic necrosis is the liberal use of cross-sectional imaging, with the identiﬁcation of retroperitoneal gas from gas-forming bacteria. Extensive studies have failed to deﬁne a universally concrete time point to operate in the setting of sterile pancreatic necrosis. Sterile pancreatic necrosis requires careful consideration for surgical débridement on a case-by-case basis. In the setting of true sterile pancreatic necrosis, conservative management without surgery is warranted. Patients must be closely monitored for signs of organ failure or SIRS including tachycardia, tachypnea, leukocytosis, fever, or hypoxia. Concurrently, imipenem/cilastin may be used to reduce the progression to pancreatic necrosis.4 Fluoroquinolones also provide broad coverage and good pancreatic penetration. Cautionary use of antibiotics in this setting is advised because progression to pancreatic infection by typical enteric pathogens may be supplanted by fungal or gram-positive nosocomial infections.5 In addition to antibiotics, ﬁne-needle aspiration may be used, and repeated, whenever sterile necrosis is

38 PANCREATIC CYST/DEBRIDEMENT

Transverse mesocolon

Middle colic artery

387

ligament or through the transverse mesocolon (Fig. 38–2). A local inﬂammatory response often makes the gastrocolic ligament access difﬁcult enough to warrant access via the mesocolon. The middle colic vessels must be carefully identiﬁed to avoid ligation. If the middle colic vessels are the sole blood supply to areas of the colon, ligation of this sole blood supply will lead to an ischemic bowel, requiring resection. Thus, access to the lesser sac via the mesocolon should be carefully made on either side, or on both sides, of the middle colic vessels.1 Ligation of the middle colic vessels is reserved only for necessary surgical access to the pancreas when other approaches are not possible.

Débridement of the Necrotic Pancreas Damage to Peripancreatic Critical Vascular Structures Figure 38–2 Infra-mesocolic exposure of pancreatic bed.

clinically ambiguous. In the absence of retroperitoneal gas, repeat CT imaging is an unreliable marker of progression to infection. In addition, repeat images are advised when surgical débridement would be seriously considered—following the second week after initial pancreatitis presentation, unless the clinical picture mandates otherwise. Again, the assumption of sterile pancreatic necrosis must always be questioned. Surgical débridement must be considered in the setting of unresolving or signiﬁcant new signs of SIRS that warrant surgical intervention.6,7 If pancreatic necrosis is known to be infected, surgical intervention is required. If pancreatic necrosis has progressed to a welldeveloped, uncomplicated true pancreatic abscess, primary treatment with concurrent culture-sensitive antibiotics and percutaneous drainage or endoscopic drainage of the abscess cavity through the posterior wall of the stomach may prevent surgical necessity. Before this treatment is begun, the diagnosis of a true pancreatic abscess must be questioned and obscured necrotizing processes ruled out.

Entrance into the Lesser Sac to Expose the Pancreas Ligation of the Middle Colic Vessels ● Consequence Possible large bowel ischemia. Grade 2/3/4 complication ● Repair Bowel resection. ● Prevention Surgical access to the lesser sac for surgical débridement of the pancreas can be approached via the gastrocolic

● Consequence Operative blood loss secondary to inferior vena cava, splenic, or portal vein damage. Grade 3/4 complication ● Repair Surgical repair of the vasculature. ● Prevention Extensive necrotic involvement may attach to local structures. Excessive débridement may leave the portal vein near the head of the pancreas and the splenic vein near the tail of the pancreas vulnerable to avoidable damage. Extensive retroperitoneal involvement may compromise the structure of the vena cava. Although demarcation of necrotic borders may not be present, only semisolid necrotic tissue must be gently débrided without unnecessarily disrupting the vasculature.

Endocrine or Exocrine Insufﬁciency ● Consequence Diabetes mellitus results from lack of endocrine function of the pancreas. Malabsorption, steatorrhea, and associated abdominal symptomatology result from insufﬁcient exocrine secretions. Grade 2 complication ● Repair Medical management of glucose control and supplementation of pancreatic enzymes. ● Prevention Maximal preservation of healthy pancreatic endocrine tissue is ideal. Exocrine and endocrine deﬁciencies do not result from débridement because the majority of débrided tissue is peripancreatic inﬂammatory soft tissue, and débridement removes only the alreadydemarcated necrotic tissue, rather than viable pancreas.

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Rather, exocrine and endocrine deﬁciencies result from the inﬂammatory insult of necrotizing pancreatitis to the islets of Langerhans and exocrine glands. In order to maximize pancreatic function in the setting of necrotizing pancreatitis, physicians must be diligent with the treatment of sterile pancreatic necrosis and carefully monitor for surgical indication.

Surgical Drainage

Limited Surgical Drainage

Pancreaticocutaneous Fistula ● Consequence Leakage of pancreatic amylase and proteins onto the skin may induce inﬂammatory mediators and potential hypercholeraemic or normal anion gap metabolic acidosis. Grade 2/3 complication ● Repair Suppression of pancreatic enzymes with octreotide, catheter manipulation or replacement, and possible surgical correction. ● Prevention Recognition of patients with a high risk of pancreaticocutaneous ﬁstula formation and carefully coordinated surgical drainage of the surgical cavity are the best methods to avoid the occurrence and complications of a pancreaticocutaneous ﬁstula. The more severely the pancreatic parenchyma is disrupted by disease, the more likely a pancreaticocutaneous ﬁstula will occur. Consequently, severe pancreatitis and, possibly, pancreatitis of biliary cause are most likely to result in a pancreaticocutaneous ﬁstula.8 Percutaneous drainage, either used alone or postoperatively, must be monitored daily in critically ill patients

Jp

in order to determine necessary (1) changes in nutrition or antibiotic treatment, (2) catheter ﬂushing, manipulation, or replacement, and (3) indication for surgical intervention. Prophylactic octreotide9,10 may also be used when a high likelihood of pancreaticocutaneous ﬁstula exists, such as in severe pancreatitis.

Jp Jp

Jp

Figure 38–3 Extensive drainage of pancreatic infection.

● Consequence Persistent infection. Grade 2/3/4 complication ● Repair Redébridement. ● Prevention The large residual cavity following pancreatic débridement must be carefully managed to prevent further infection, visceral communication, and erosion of blood vessels. The Penrose or Abramson drain must be removed before JP drains to prevent pancreatic ascites or a pancreatocutaneous ﬁstula (Fig. 38–3). If Penrose drains are used, sequential removal, one drain per day, 7 to 10 days postoperatively, carefully allows the cavity to collapse in a stepwise fashion.

Pancreatic Ascites and Pancreatic Pleural Effusion ● Consequence Fistula formation and erosion of peripancreatic structures by exocrine secretions. Grade 2/3/4 complication ● Repair Conservative treatment consists of gastrointestinal rest, nasogastric suction, octreotide, and total parenteral nutrition. Treatment of the ﬁstula is fostered by repeat paracentesis and thoracocentesis as well as chest tube drainage. Surgical intervention is indicated when there is no clinical improvement from conservative measures. Endoscopic placement of a pancreatic duct stent may also be useful. ● Prevention Although clinical symptoms of pancreatic ascites and effusions are very similar to those of other pancreatic disease, any patient clinically suspected to have pancreatic ascites or pleural effusion should have the appropriate bodily ﬂuids sampled for amylase and albumin via paracentesis or thoracocentesis. If pancreatic ascites has occurred, the amylase level will always be markedly elevated (>1000 Somogyi units/100 ml), and in the absence of hypoalbuminemia, the albumin level will be greater than 3 g/100 ml. If conservative management

38 PANCREATIC CYST/DEBRIDEMENT of the pancreatic ascites or pleural effusion fails to reverse the course of disease, surgical correction is warranted based upon the pancreatic duct anatomy and the extent of damage from the ascites.11

Abdominal Closure Intra-Abdominal Swelling with Challenging Abdominal Wall Closure ● Consequence Dehiscence, wound infection, or abdominal hernia. Grade 2/3 complication ● Repair Antibiotics. Possible surgical correction of the incision or hernia. ● Prevention Two types of incisions—horizontal and vertical—may be made to gain access to the pancreas. Horizontal transverse or subcostal “chevron” incisions leave the incision more difﬁcult to approximate and often require mesh fortiﬁcation. The preferable vertical midline incision allows better approximation and rarely involves mesh placement. Properly placed retention sutures are used to best close the abdominal wall.

REFERENCES 1. Jackson PG, Rattner DW. Pancreatic abscess. In Cameron JL (ed): Current Surgical Therapy, 7th ed. St. Louis: Mosby, 2001; pp 539–543.

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2. Rau B, Pralle V, Uhl W, et al. Management of sterile necrosis in instances of severe acute pancreatitis. J Am Coll Surg 1995;181:279–288. 3. Bouvet M, Moossa AR. Pancreatic abscess. In Cameron JL (ed): Current Surgical Therapy, 8th ed. Philadelphia: Mosby, 2004; pp 476–479. 4. Bassi C, Falconi M, Talamini G, et al. Controlled clinical trial of perﬂoxacin versus imipenem in severe acute pancreatitis. Gastroenterology 1998;115:1513– 1517. 5. Buchler M, Malfertheiner P, Friess H, et al. Human pancreatic tissue concentration of bactericidal antibiotics. Gastroenterology 1992;103:1902–1908. 6. Buchler MW, Gloor B, Muller CA, et al. Acute necrotizing pancreatitis: treatment strategy according to the status of infection. Ann Surg 2000;232:619–626. 7. Warshaw AL. Pancreatic necrosis: to débride or not to débride?—That is the question. Ann Surg 2000;232:627– 629. 8. Fotoohi M, D’Agostino HB, Wollman B, et al. Persistent pancreatocutaneous ﬁstula after percutaneous drainage of pancreatic ﬂuid collections: role of cause and severity of pancreatitis. Radiology 1999;213:573–578. 9. Rosenberg L, MacNeil P, Turcotte L. Economic evaluation of the use of octreotide for prevention of complications following pancreatic resection. J Gastrointest Surg 1999;3:225–232. 10. Yeo CJ. Does prophylactic octreotide beneﬁt patients undergoing elective pancreatic resection? J Gastrointest Surg 1999;3:223–224. 11. Kaman L, Behera A, Singh R, Katira RN. Internal pancreatic ﬁstulas with pancreatic ascites and pancreatic pleural effusions: recognition and management. Aust N Z J Surg 2001;71:221–225.

39

Resection and Reconstruction of the Biliary Tract David A. Bruno, MD and Thomas M. Fishbein, MD INTRODUCTION

OPERATIVE STEPS

In 1891, in Dresden, Germany, Oskar Sprengel published the ﬁrst report of a choledochoenterostomy. In this patient, after a successful cholecystectomy, Dr. Sprengel was unable to clear the distal common bile duct of stones. A choledochotomy was made, and the common bile duct was anastomosed to the duodenum. Although the ﬁrst patient survived, subsequent attempts resulted in several deaths, presumably from bile peritonitis followed by sepsis.1,2 Not until a successful series of cases in the early 20th century was the operation accepted as standard of care.3 Many years later, it was recognized that hepatic ducts could also be resected and reconstructed with attention to two simple principles: The anastomosis must be performed free of tension and with direct mucosal apposition to facilitate proper healing. These principles still maintain today. Safe and effective biliary reconstruction requires intimate knowledge of normal anatomy as well as commonly recognized variations in biliary and vascular anatomy of the liver and porta hepatis. Proper exposure allowing careful dissection in this region is of paramount importance. Resection and reconstruction, performed to establish biliary continuity with the small bowel, is the usual goal, regardless of the speciﬁc pathology. When malignancy is the indication for surgery, anatomic planes are frequently altered owing to inﬂammation, desmoplastic reaction, and sometimes, tumor mass, increasing the complexity of the procedure. All procedures involving the biliary tract involve several operative steps: exposure, dissection, and establishment of biliary continuity.

Step Step Step Step Step Step

1 2 3 4 5 6

Incision Exposure of hepatoduodenal ligament Dissection of common bile duct Duct division Duct resection or closure Reestablishment of biliary continuity

OPERATIVE PROCEDURE Resection and restoration of biliary continuity above or below the hepatic bifurcation.

Operative Incision This is reviewed in Section IV, Chapter 32, Right Hepatectomy. Brieﬂy, this can be optimally accomplished through a right subcostal incision, a midline incision, or a bilateral subcostal incision. Prior operations may dictate which of these is chosen, whereas in patients with no prior operations, a right or bilateral subcostal incision is preferred.

Bile Duct Isolation Extrahepatic Bile Duct—Blood Supply The blood supply to the extrahepatic bile duct is derived from vessels on the medial and lateral walls of the duct, sometimes referred to as “9 o’clock and 3 o’clock position”4 (Fig. 39–1). Blood ﬂow derives both from intrahepatic arteriobiliary collateral circulation downward and upward from the gastroduodenal artery.

Bleeding from Peribiliary Vessels

INDICATIONS ● Bile duct obstruction ● Biliary injury—trauma ● Biliary ﬁstula

● Consequence Failure to avoid or ligate these vessels and adequately control hemorrhage can lead to three possible complications. First, poor visualization may increase the likelihood of injury to other vital structures, most

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Right hepatic artery Common hepatic artery

3 o’clock vessels

9 o’clock vessels Common bile duct

Figure 39–1 Bile duct lateral vessels. Note the right hepatic artery courses posterior to the common bile duct.

commonly, the right hepatic artery. Second, postoperative bleeding from the anastomosis may occur. Third, injury and extensive coagulation may lead to ischemia of the duct, leading to late stricture formation at the anastomosis. Grade 3 complication ● Repair Careful ligation of larger peribiliary vessels at the point of transaction of the duct should be undertaken, usually with ﬁne monoﬁlament suture. Smaller vessels may be controlled with electrocautery. Care must be taken when using electrocautery because thermal damage to the biliary tree may result in late stricture.5 ● Prevention Preoperative understanding of the normal and variant anatomy of the biliary tree and its surrounding vessels is essential. In normal anatomy, the common bile duct is derived from one left and one right hepatic duct joining at the hepatic hilum. The right hepatic artery branches from the proper hepatic artery medial to the duct, giving off small branches to the bile duct. Additional branches may be derived from the right hepatic artery lateral in the porta hepatis once it has passed posterior to the duct. The right hepatic artery bifurcates into anterior and posterior sectoral branches lateral to the duct. A replaced right hepatic artery sometimes courses lateral to the portal vein and gives off branches to the bile duct.

Common Hepatic Artery Injury ● Consequence Hepatic artery anatomy can sometimes be obscured by pathology and variations in anatomy.6–12 As the duct is

dissected and prepared for division or resection, identiﬁcation of the common hepatic artery origin should be noted. Inadvertent injury to the hepatic artery will result in brisk hemorrhage. Complete ligation and division may result in ischemia of the right hepatic lobe of the liver. This can result in hepatic parenchymal damage postoperatively, sometimes leading to intrahepatic biliary necrosis, biloma formation, or abscess. Grade 3 complication ● Repair Incomplete transection of the proper hepatic artery should immediately be recognized. Control of the proximal and distal segments with vascular clamps should immediately be obtained. The artery itself should be repaired with an appropriately sized monoﬁlament suture. Repair should be made in a transverse fashion in order to avoid narrowing of the artery. If the artery has suffered injury that makes a clean complete primary repair impossible, the authors recommend completing transection of the artery at the site of the injury and direct end-to-end anastomosis.13,14 ● Prevention Never transect the common bile duct until the hepatic artery has been positively identiﬁed at the level of planned transection. Encircle only the bile duct if possible.

Proper Hepatic Artery Injury ● Consequence Variations in both the right and the left hepatic arteries are common.15 Division of the proximal common bile duct without identiﬁcation of arterial supply in the porta should be avoided (Fig. 39–2). Early proper hepatic arterial injury can lead to hemorrhage and hepatic parenchymal ischemia. Unrecognized division of these arteries has been associated with strictures and the formation of bilomas late after surgery.16–18 Grade 4 complication ● Repair Inadvertent transection of the right or left hepatic artery should be repaired with an end-to-end anastomosis after proximal and distal control is established.19–22 Nonabsorbable monoﬁlament sutures are appropriate for repair. In the patient in whom an accessory hepatic artery branch exists and either it or the proper branch is injured, an injury of one may not require repair. The proximal stump of the injured vessel may be examined for backbleeding, which if it is judged to be pulsatile and sufﬁcient, implies adequate intraparenchymal collateral circulation. Such an accessory branch may be ligated. High injuries of right hepatic artery branches may not allow distal control, thus requiring direct suture repair or closure.

39 RESECTION AND RECONSTRUCTION OF THE BILIARY TRACT

393

Figure 39–3 Right hepatic artery (RHA) is shown coursing anterior to a fusiform choledochal cyst (CDC) and entering the hilum anteriorly. Blue loop identiﬁes the common bile duct, which usually is anterior to the RHA. CBD, common bile duct; CHA, common hepatic artery; LHA, left hepatic artery. Atrophic left lobe with no portal vein seen

Figure 39–2 Replaced right hepatic artery. This usually runs posterior to the portal vein, but may then course anteriorly to lie just behind the bile duct above the cystic duct.

● Prevention Proper hepatic artery injury prevention begins with an intimate knowledge of variations before entering the operating room. Potentially hazardous variations of hepatic artery anatomy include an early trifurcation branching into (1) right and (2) left hepatic artery branches and the (3) gastroduodenal artery low in the porta hepatis, the right hepatic artery deriving from the superior mesenteric artery posterior to the portal vein, the right hepatic artery passing anterior to the common bile duct, and the entire proper hepatic artery arising from the gastroduodenal artery (Fig. 39–3).4 Early identiﬁcation of the proper hepatic artery by palpation medial to the bile duct low in the porta hepatis is advantageous.

Portal Vein Injury ● Consequence Inﬂammatory reactions, secondary to benign or malignant disease, may result in a proximal common bile duct or hepatic ducts that are adherent to the portal vein. These may occur in the setting of pancreatitis, chronic biliary infections, biliary ﬁstula, and cholangiocarcinoma. Excessive dissection can cause disruption of the sometimes-attenuated anterior wall of the portal vein. Hilar cholangiocarcinoma frequently directly invades the vein or small portal branches, such as branches draining the left caudate (Fig. 39–4). This vascular invasion must be recognized to avoid injury. Grade 3 complication

Figure 39–4 Computed tomography (CT) scan shows hilar cholangiocarcinoma invading the left portal vein.

● Repair The portal vein can be manually compressed and then occluded with a Pringle maneuver proximal to the disruption in order to allow sufﬁcient exposure during bleeding. A vascular clamp is then placed on the vein, and primary repair with nonabsorbable monoﬁlament suture can be undertaken.23–25 The vein wall should be directly visualized and transverse repair performed to avoid narrowing the vein, which can lead to late portal thrombosis. Freeing a length of the vein, when possible, allows tension-free repair. This sometimes requires the ligation of a small pancreatic branch on the right anterior portal vein wall. Division of the gastroduodenal artery allows easy visualization of the proximal portal vein. ● Prevention Recognition of a portal vein that is densely adherent to the common bile duct is the ﬁrst step in prevention of

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this injury. In such cases, circumferential control of the bile duct may not be required. Instead, in the case of benign disease or unresectable malignancy, the duct may be incised anteriorly, leaving the adherent posterior wall intact. Anastomosis to the intestine may be accomplished safely by placing sutures into the intact posterior wall after suturing the distal portion of the duct closed. Alternatively, if the bile duct can be transected, minimal dissection proximally up to the liver may be performed to allow suture placement without injuring the anterior portal vein wall. Placing the posterior wall sutures on the inside of the anastomosis decreases the potential for injury in patients in whom the duct is adherent to the portal vein.

Excision Distal Stump Leak ● Consequence Failure to ligate the distal remnant of the common bile duct in procedures that call for complete common bile duct resection can result in a retrograde reﬂux from the duodenum. This may result in peritonitis and abscess formation from reﬂuxed enteric contents. Grade 2 complication ● Repair This complication sometimes presents in the late postoperative period. Endoscopic stent placement via endoscopic retrograde cholangiopancreatography (ERCP) to decrease intrabiliary pressure and allow duodenal drainage can result in closure of the leak.18,26–30 ● Prevention Closure of the distal ductal remnant with suture or tying is critical to prevent this injury. One must ensure that all lumens seen at the point of division of the duct are closed adequately. Recognition of aberrant biliary anatomy, including a low insertion of the right posterior sectoral bile duct or an accessory right bile duct running parallel to the common bile duct prior to entry, may leave a lateral opening in the common bile duct wall that may leak. A low insertion of the cystic duct below the level of transection likewise may lead to the same complication (Fig. 39–5).

Biliary Stricture ● Consequence Hepatic duct and common bile duct blood supplies run axially along the length of the ducts (see Fig. 39–1). Excessive dissection of the duct beyond the area of excision may lead to ischemia, which in turn may lead to either early bile leak or late stricture formation.31 Grade 2/3 complication ● Repair When anastomotic disruption due to ischemia, tension, or late stricture occurs, two repair options exist. Early

LHA

RHA

Figure 39–5 Normal level of insertion of cystic duct (CD) and cystic artery (CA) in Calot’s triangle. LHA, left hepatic artery; RHA, right hepatic artery.

leak may be managed by early reoperation in the absence of systemic sepsis and if diagnosed promptly. Late diagnosis of leak may be best managed with conservative measures of drainage and delayed repair if stricture ensues. Stricture late after anastomosis may be managed utilizing decompression (transhepatic access is usually preferable) and either balloon dilation or deﬁnitive surgical repair.28,32–35 In patients in whom access cannot be obtained via the transhepatic approach, a transjejunal approach can occasionally be used for dilation of the stricture.36–39 ● Prevention Adequate blood supply at the point of transection of the bile duct is critical to ensure prevention of complications. This is generally ensured by observation of good bleeding from the cut edge of the transected duct. This usually requires direct suture ligation of the bleeding vessels. Dissection of the duct near the area to be transected should be lateral to the ductal tissue, leaving periadventitial tissue undisturbed. The area should not be skeletonized in the manner of vascular dissection. If there is any indication that the duct has been devascularized, further resection to bleeding tissue is required prior to anastomosis. Vessels running along the duct should be directly ligated with ﬁne monoﬁlament suture.

Reconstruction and Reestablishment of Biliary Continuity Anastomotic Leak ● Consequence Irrespective of the method for reestablishing biliary continuity, tension on the biliary-enteric anastomosis may result in a bile leak. This may result in sterile

39 RESECTION AND RECONSTRUCTION OF THE BILIARY TRACT

395

biloma, which can be drained, or uncontrolled peritonitis. Grade 2/3 complication ● Repair Anastomotic tension should be recognized immediately. A primary choledochocholedochostomy should be performed only if the duct is freshly cut, with no loss of bile duct length, as with a direct division during another procedure. If duct edges are not cleanly divided or there is any tension, a Roux-en-Y choledochojejunostomy should be performed. A drain is generally placed in the pouch of Morrison, the most dependent portion of the abdomen, near the anastomosis. This will usually control bile leakage if it occurs. ● Prevention Any sign of anastomotic tension will result in an anastomosis that is prone to leakage. Such an anastomosis should not be completed, with or without an internal stent such as a T-tube. We recommend a Roux-en-Y anastomosis that is retrocolic and approximately 40 cm long. Mobilization of an adequate length of intestinal mesentery will alleviate tension on the intestinal loop utilized for anastomosis.

Hepatic Duct Leak ● Consequence Resections above the biliary bifurcation may result in three or more hepatic ducts requiring reconstruction. When a smaller stump is not recognized, it may not be included in the hepaticojejunostomy. In this case, bile will freely drain into the peritoneum and a biliary leak will occur. As previously discussed, uncontrolled biliary ﬁstula will result in bile peritonitis. Grade 3 complication ● Repair Early recognition of all proximal extrahepatic ducts and subsequent inclusion into the anastomosis will prevent this complication. Smaller ducts such as those draining the caudate lobe can be oversewn without loss of signiﬁcant hepatic parenchymal function. Those draining larger areas of functional liver, such as anterior and posterior sectoral ducts, may be joined together using an intact back wall to provide a single larger anastomosis. Repair of a missed duct postoperatively usually requires reoperation and revision with construction of an additional anastomosis. ● Prevention Preoperative imaging of the biliary tree above the site of resection helps to prevent this by identifying the intrahepatic anatomy. This is best accomplished with percutaneous transhepatic cholangiography for totally obstructing lesions but may sometimes be accomplished

Figure 39–6 Completed hepaticojejunostomy with an aberrant right hepatic artery anterior to a Roux-en-Y loop of jejunum performed tension free with mucosal apposition.

with imaging from below in cases in which dye will pass through the area requiring repair. Magnetic resonance cholangiography is increasingly used for this purpose. Cholangiitis should be prevented by treating with systemic antibiotics during these imaging studies, and imaging from below should be accompanied by a drainage procedure (stent placement). Intraoperative recognition of each duct transected as identiﬁed by imaging will help prevent this complication. One must also recognize that little bile may be produced by liver segments that have been chronically obstructed at the time of transaction, later to be followed by improved bile ﬂow after surgery. Thus, oriﬁces encountered that appear consistent with biliary radicals should be tagged and reconstructed despite the lack of good bile ﬂow intraoperatively. Probing what appear to be very small ducts with a lacrimal probe will often demonstrate direct access into a major lobe of the liver, making clear the requirement for drainage (Fig. 39–6).

REFERENCES 1. Sprengel O. Uber eienen fall von exstirpation der gallenblase mit anlegung einer kommunikation zwischen dudenum und ductus choledochus. Zentralbl Chir 1891; 18:121–122. 2. Horgan E. Reconstruction of the biliary tract: a review of all the methods that have been employed. New York: Macmillan, 1932. 3. Sasse F. Uber choledochoduodenostomie. Zentralbl Chir 1913;40:942–943. 4. Northover JM, Terblanche J. A new look at the arterial supply of the bile duct in man and its surgical implications. Br J Surg 1979;66:379–384.

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5. Hochstadetr H, Bekavac-Beslin M, Doko M, et al. Functional liver damage during laparoscopic cholecystectomy as the sign of the late common bile duct stricture development. Hepatogastroenterology 2003;50:676– 679. 6. Abdullah SS, Mabrut JY, Garbit V, et al. Anatomical variations of the hepatic artery: study of 932 cases in liver transplantation. Surg Radiol Anat 2006;28:468–473. 7. Chaib E, Ribeiro MA Jr, Saad WA, Gama-Rodrigues J. The main hepatic anatomic variations for the purpose of split-liver transplantation. Transplant Proc 2005;37:1063– 1066. 8. Chen CY, Lee RC, Tseng HS, et al. Normal and variant anatomy of hepatic arteries: angiographic experience. Chin Med J (Free China ed) 1998;61:17–23. 9. Koops A, Wojciechowski B, Broering DC, et al. Anatomic variations of the hepatic arteries in 604 selective celiac and superior mesenteric angiographies. Surg Radiol Anat 2004;26:239–244. 10. Mlakar B, Gadzijev E, Ravnik D, et al. Anatomical variations of the arterial pattern in the left hemiliver. Eur J Morphol 2002;40:115–120. 11. Mlakar B, Gadzijev EM, Ravnik D, Hribernik M. Anatomical variations of the arterial pattern in the right hemiliver. Eur J Morphol 2002;40:267–273. 12. Mlakar B, Gadzijev EM, Ravnik D, Hribernik M. Congruence between the courses of the biliary ductal and the hepatic arterial systems. Eur J Morphol 2005;42:135– 141. 13. Mathisen O, Soreide O, Bergan A. Laparoscopic cholecystectomy: bile duct and vascular injuries: management and outcome. Scand J Gastroenterol 2002;37:476–481. 14. Doctor N, Dooley JS, Dick R, et al. Multidisciplinary approach to biliary complications of laparoscopic cholecystectomy. Br J Surg 1998;85:627–632. 15. Hiatt JR, Gabbay J, Busuttil RW. Surgical anatomy of the hepatic arteries in 1000 cases. Ann Surg 1994;220:50–52. 16. Krotovskii GS, Shcherbiuk AN, Gerasimov VB. [Intraoperative injury to the hepatic artery proper]. Khirurgiia (Soﬁia) 1983;5:105–106. 17. Sankot J. [Injury of the hepatic artery]. Rozhl Chir 1998; 77:121–122. 18. Gupta N, Solomon H, Fairchild R, Kaminski DL. Management and outcome of patients with combined bile duct and hepatic artery injuries. Arch Surg 1998;133:176– 181. 19. Schmidt SC, Langrehr JM, Raakow R, et al. Right hepatic lobectomy for recurrent cholangitis after combined bile duct and right hepatic artery injury during laparoscopic cholecystectomy: a report of two cases. Langenbecks Arch Surg 2002;387:183–187. 20. Schmidt SC, Langrehr JM, Settmacher U, Neuhaus P. [Surgical treatment of bile duct injuries following laparoscopic cholecystectomy. Does the concomitant hepatic arterial injury inﬂuence the long-term outcome?]. Zentralbl Chir 2004;129:487–492. 21. Schmidt SC, Settmacher U, Langrehr JM, Neuhaus P. Management and outcome of patients with combined bile

22.

23. 24. 25. 26.

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38.

39.

duct and hepatic arterial injuries after laparoscopic cholecystectomy. Surgery 2004;135:613–618. Shiraishi M, Hiroyasu S, Kusano T, Muto Y. Vascular reconstruction for intraoperative major vascular injuries. Int Surg 1997;82:141–145. Snyder CJ. Injuries to the portal triad. Am J Surg 1993; 166:318. Jurkovich GJ, Hoyt DB, Moore FA, et al. Portal triad injuries. J Trauma 1995;39:426–434. Dawson DL, Johansen KH, Jurkovich GJ. Injuries to the portal triad. Am J Surg 1991;161:545–551. Binmoeller KF, Katon RM, Shneidman R. Endoscopic management of postoperative biliary leaks: review of 77 cases and report of two cases with biloma formation. Am J Gastroenterol 1991;86:227–231. Familiari L, Scafﬁdi M, Familiari P, et al. An endoscopic approach to the management of surgical bile duct injuries: nine years’ experience. Dig Liver Dis 2003;35:493–497. Katsinelos P, Kountouras J, Paroutoglou G, et al. The role of endoscopic treatment in postoperative bile leaks. Hepatogastroenterology 2006;53:166–170. Katsinelos P, Paroutoglou G, Beltsis A, et al. Endobiliary endoprosthesis without sphincterotomy for the treatment of biliary leakage. Surg Endosc 2004;18:165–166. Sandha GS, Bourke MJ, Haber GB, Kortan PP. Endoscopic therapy for bile leak based on a new classiﬁcation: results in 207 patients. Gastrointest Endosc 2004;60:567– 574. Sawaya DE Jr, Johnson LW, Sittig K, et al. Iatrogenic and noniatrogenic extrahepatic biliary tract injuries: a multiinstitutional review. Am Surg 2001;67:473–477. Hillis TM, Westbrook KC, Caldwell FT, Read RC. Surgical injury of the common bile duct. Am J Surg 1977; 134:712–716. Sava P, Camelot G, Kahn J, Gillet M. [Operative trauma of the common bile duct. Report of eight cases (author’s transl)]. J Chir 1978;115:663–671. Michelassi F, Ranson JH. Bile duct disruption by blunt trauma. J Trauma 1985;25:454–457. Mergener K, Strobel JC, Suhocki P, et al. The role of ERCP in diagnosis and management of accessory bile duct leaks after cholecystectomy. Gastroint Endosc 1999;50: 527–531. Sugiyama M, Izumisato Y, Ubukata N, et al. Peroral jejunoscopy for treating stenosis of hepaticojejunostomy after pancreatoduodenectomy. Hepatogastroenterology 2001;48:681–683. Severini A, Cozzi G, Salvetti M, et al. Management of complications from hepatobiliary surgery using the percutaneous transjejunal approach. Tumori 1997;83:912– 917. Ruiz J, Torres R. Translaparoscopic jejunal approach for benign stricture of Roux-en-Y hepaticojejunostomy. Surg Endosc 2001;15:518. McPherson SJ, Gibson RN, Collier NA, et al. Percutaneous transjejunal biliary intervention: 10-year experience with access via Roux-en-Y loops. Radiology 1998;206: 665–672.

Section V

ENDOCRINE SURGERY Gerard M. Doherty, MD A life spent making mistakes is not only more honorable but more useful than a life spent doing nothing.—George Bernard Shaw

40

Thyroid Surgery Michael McLeod, MD and Gerard M. Doherty, MD

INTRODUCTION

● Local symptoms due to mass effects of enlarged

gland Thyroid operations are usually safe procedures with rare life-threatening complications. Complications common to any operation, such as bleeding, infection, and anesthetic reactions, are all quite unusual. Almost never is sufﬁcient blood lost during the operation to require transfusion. After the procedure, bleeding can cause dangerous local effects but only rarely requires blood replacement. The neck is a privileged site for wound healing that can withstand substantial contamination without clinical infection. These procedures are typically performed as ambulatory or overnight hospitalizations, with short (1–3 hr) general or regional anesthetic techniques, which limit the risk of anesthetic or pulmonary complications and deep venous thrombotic events. However, thyroid surgery is considered a delicate area of clinical practice. Signiﬁcant technical complications can occur that can create permanent changes for the patient. The most common of these are hypoparathyroidism and nerve injury. Other less-frequent complications include cervical hematoma and aerodigestive tract damage.

OPERATIVE STEPS (UNILATERAL LOBECTOMY) Step 1 Step 2

Step 3 Step 4

Step 5 Step 6 Step 7

INDICATIONS Step 8 ● Hyperthyroidism ● Malignancy or suspicion of malignancy

Induce general anesthesia and secure airway Transverse incision along skin lines inferior to thyroid isthmus through platymus, raising subplatysmal ﬂaps Separate strap muscles in midline, exposing thyroid gland Expose upper pole vessels by dissecting between cricothyroid muscle and thyroid gland and lateral to thyroid gland Divide upper pole vessels Reﬂect thyroid medially and dissect lateral aspect of gland Identify inferior thyroid artery, recurrent laryngeal nerves (RLNs), and parathyroid glands in tracheoesophageal groove Divide inferior thyroid artery branches, thyroid attachment to trachea anterior to RLN insertion, and inferior pole vessels

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Divide thyroid isthmus. For bilateral procedures, isthmus is usually left intact, and same steps are followed for contralateral lobe Step 10 Obtain hemostasis and close wound in layers Step 9

OPERATIVE PROCEDURE The potential complications of thyroid operations include the immediate complication of cervical hematoma, as well as the more chronic complications of hypoparathyroidism, nerve injury, and injuries to the aerodigestive tract. Finally, chronic problems can arise from iatrogenic hyper- or hypothyroidism.

Securing the Airway At the outset of the operation, for most patients, general anesthesia is induced and an endotracheal tube is placed. For most patients, this is a routine and uneventful portion of the procedure; however, this can be the most dangerous portion of the procedure for a patient with a large goiter or tumor (Fig. 40–1).

Airway Management ● Consequence Because the thyroid lies directly anterior to the trachea, enlargement of the thyroid or direct invasion of the trachea by tumor can cause airway compromise that can become critical during the induction of anesthesia.1–4

Compression of the trachea can cause loss of airway patency in the supine patient under anesthesia. Once the negative intrathoracic pressure needed to lift the thyroid and keep the trachea patent is lost, it may be difﬁcult or impossible to ventilate the patient with positive pressure. This can be avoided by using awake intubation to maintain airway patency. Grade 2/3 complication ● Prevention Compression of the trachea in the neck can narrow the lumen substantially and require placement of a smaller endotracheal tube at intubation. However, the more difﬁcult management issue can be signiﬁcant lateral deviation of the trachea. Although these patients can usually be ventilated by positive-pressure mask ventilation, the shift of the larynx can make it difﬁcult or impossible to access the vocal cords for placement of an endotracheal tube. Intubation over a ﬁberoptic laryngobronchoscope can be helpful in most patients. However, some patients cannot be intubated in spite of all attempts, who require tracheostomy at the outset of the thyroidectomy in order to safely perform the operation. Anticipation of the difﬁculties that may be faced, the assembly of a team expert in airway management, and the readiness of an experienced surgeon prepared to access the airway operatively are critical to the safe outcome of these occasionally extremely challenging and dangerous situations.

Dissection and Identiﬁcation of Cervical Structures After exposure of the thyroid gland (Fig. 40–2), the upper pole vessels are divided (Fig. 40–3). The thyroid lobe is

78 mm

45 mm

Thyroid

Trachea

Upper pole

Left thyroid lobe

Figure 40–1 Tomographic reconstruction of a substernal goiter with airway compromise. The compression and shift of the trachea in patients such as this can be particularly dangerous during the induction of anesthesia. Intubation can be difﬁcult, and the airway can be lost with induction.

Figure 40–2 Exposure of the left lobe of the thyroid gland. The sternohyoid and sternothyroid muscles are held by the retractor.

40 THYROID SURGERY

399

Upper parathyroid gland

Upper pole vessels Ligament of Berry

Left thyroid lobe

Figure 40–3 Division of the left upper pole vessels. These vessels can be divided using a number of techniques, including division between ligatures or clips or using powered hemostasis equipment, as illustrated here.

Left upper parathyroid Thyroid lobe

Recurrent laryngeal nerve Nerve stimulator probe

Figure 40–4 Demonstration of the tracheoesophageal groove dissection. The nerve is carefully exposed and may be conﬁrmed using intraoperative nerve monitoring, as demonstrated here. The upper parathyroid is typically posterior to the recurrent nerve position and superior to the inferior artery, as in this patient.

reﬂected anteriorly in order to expose the tracheoesophageal groove (Fig. 40–4). The dissection is carried down along the medial surface of the carotid artery to the prevertebral fascia. The inferior thyroid artery can be identiﬁed passing deep to the carotid in its course toward the

Recurrent laryngeal nerve

Figure 40–5 The posterior attachment of the thyroid to the trachea anterior to the recurrent laryngeal nerve (ligament of Berry) is divided with careful avoidance of the recurrent nerve.

lower pole of the thyroid. Careful dissection is performed around the inferior thyroid artery to identify the RLN as it passes underneath or, less commonly, anterior to the artery. If the RLN is not visible, it can usually be identiﬁed caudally (in previously undissected areas) as it ascends in the tracheoesophageal groove. The cephalad course of the nerve is deﬁned, taking care to preserve branches that arise proximal to its disappearance under the caudal border of the cricothyroid muscle. The right RLN arises more laterally in the chest than the left, leading to a more oblique course. The superior and inferior parathyroid glands may be preserved by dissecting them away from the posterior capsule of the thyroid gland with their vascular pedicles. The superior glands are most commonly located on the dorsal surface of the thyroid lobe at the level of the upper two thirds of the gland (see Fig. 40–4). Although their location is more variable, the lower glands usually lie caudal to the inferior thyroid artery. With the course of the RLN directly visualized, the branches of the inferior thyroid artery are divided adjacent to their entrance into the thyroid gland to preserve the parathyroid blood supply. The inferior pole is then dissected. A variable number of inferior thyroid veins and, in some cases, a thyroid ima artery are divided. The RLN is also vulnerable to injury in this area. With its upper and lower poles free, the thyroid lobe remains ﬁxed to the trachea by the ligament of Berry. The thyroid gland is rolled medially, and with the RLN separated from the thyroid gland and in clear view, the ligament is encircled, ligated, and divided (Figs. 40–5 and 40–6). During this active dissection, most complications of thyroidectomy can occur.

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SECTION V: ENDOCRINE SURGERY

Thyroid isthmus

Cricothyroid muscle Ligament of Left upper Berry ligature parathyroid gland

Left thyroid lobe

Trachea

Recurrent laryngeal nerve

Figure 40–6 Completed dissection of the left lobe of the thyroid gland. With the ligament of Berry divided, the thyroid lobe is attached only by the isthmus, and the trachea returns to its natural position. Careful hemostasis must be ensured.

Hypoparathyroidism ● Consequence The parathyroid glands are delicate structures that share a blood supply with the thyroid gland. Their diminutive size (normally 30–60 mg) and fragile nature make them particularly prone to damage during thyroidectomy. Patients who have markedly diminished or absent parathyroid function after thyroidectomy have severe hypocalcemia that requires replacement. If permanent, this complication can be palliated by calcium and vitamin D supplements, but this requires multiple doses each day, and uncomfortable symptoms occur if doses are late or missed. In addition, there is cumulative bone damage over time. The symptoms of hypoparathyroidism are those of severe hypocalcemia. Patients have numbness and tingling in the distal extremities and around the mouth or tongue in the earliest phases. With more severe hypocalcemia, patients develop muscle cramping at rest or, especially, with use. The anxiety that often accompanies these symptoms exacerbates them because the patient hyperventilates. The consequent respiratory alkalosis shifts more calcium intracellularly, lowering the serum level of calcium and worsening the symptoms. Severe tetany can result. Patients can then be limited in their ability to help themselves resolve the episode with calcium supplements because their hands and forearms are often severely affected by the muscle spasms. The classic signs of hypocalcemia are Chvostek’s sign and Trousseau’s sign. Chvostek’s sign is generated by tapping gently over the facial nerve in the lateral cheek to demonstrate facial muscle contraction due to increased nerve irritability. This sign is present in a minority of people with a normal serum level of calcium and so is not entirely reliable in the diagnosis of hypocalcemia.

Trousseau’s sign is elicited by placing a sphygmomanometer cuff on the upper arm and inﬂating to systolic pressure. Within a few minutes, the patient develops severe carpal spasm, with ﬂexion of the wrist and ﬁngers, and abduction of the thumb. This sign is very uncomfortable for the patient and should not be used clinically. In general, the symptoms of hypocalcemia are much more reliable and useful than the signs for patient assessment. Grade 1/2 complication ● Repair The acute management of hypocalcemia in the postoperative patient depends upon the severity of the hypocalcemia and symptoms. Total serum calcium levels correlate roughly with symptoms but are quite variable between individuals. Some patients can have extremely low total serum levels of calcium with no symptoms, whereas others can have severe symptoms and signs, with nearly normal calcium levels. Ionized calcium measurements correlate better than total serum calcium levels, but there is still variability. Replacement is generally guided by symptoms. For mild hypocalcemia with tingling, oral calcium supplements (calcium carbonate, 500–1500 mg by mouth, two to four times a day) are often sufﬁcient to resolve the hypocalcemia. Daily doses of calcium above 3000 mg provide little incremental beneﬁt, however, because of the limits of gastrointestinal absorption of calcium. If supplementation beyond this level is necessary, the addition of supplemental vitamin D (calcitriol 0.25–1.0 mcg daily) will increase the gastrointestinal absorption of calcium. Vitamin D requires 48 to 72 hours to have its effect, however, so intravenous calcium supplementation may be needed until then. Anticipation of the need for vitamin D can smooth patient management considerably by starting it early. Hypocalcemia not controlled by oral supplements, or accompanied by severe symptoms such as muscle cramping, is best managed by intravenous calcium administration. Intravenous calcium gluconate is the only option for calcium supplementation. Calcium chloride can cause severe tissue damage if accidental tissue inﬁltration occurs and should be used only for the acute, life-threatening cardiac emergency. Bolus administration of calcium gluconate (supplied in 1000-mg ampules containing 90 mEq calcium) corrects serum levels of calcium rapidly and safely, although the effect is short lived. A preferable alternative is to use a calcium gluconate solution (6 ampules calcium gluconate = 6 g calcium gluconate = 540 mEq calcium in 500 ml D5W) infused at 1 ml/kg/hr. This provides a steady calcium supplement and can be adjusted to maintain the calcium in the normal range while oral supplements are absorbed. Temporary hypocalcemia occurs in about 10% of patients after total thyroidectomy, and permanent hypocalcemia occurs in about 1% (Table 40–1).5–11 The temporary hypocalcemia can be severe and requires intravenous and oral

40 THYROID SURGERY

401

Table 40–1 Incidence of Complications after Total Thyroidectomy Authors, Yr Thompson, 19786

Farrar, 19805

Schroder, 19867

Clark, 19888

Ley, 19939

Tartaglia, 200310

Rosato, 200411

No. of Patients

165

29

56

160

124

1636

9599

Transient nerve paresis, N (%)

NR

NR

1 (2%)

4 (2.5%)

1 (0.8%)

31 (1.9%)

195 (2%)

Permanent nerve paresis, N (%)

0

1 (3%)

0

3 (2%)*

1 (0.8%)

15 (0.9%)

94 (1%)

Transient hypoparathyroidism, N (%)

NR

2 (7%)

9 (17%)

NR

13 (10%)

NR

797 (8.3%)

Permanent hypoparathyroidism, N (%)

<2%

4 (14%)

3 (6%)

1 (0.6%)

2 (1.6%)

14 (0.9%)

163 (1.7%)

*Each from deliberate sacriﬁce of the recurrent laryngeal nerve due to tumor involvement. NR, not reported.

supplementation for the duration of the effect. Permanent hypoparathyroidism requires life-long support with calcium supplements and vitamin D analogues. Missing doses of the supplements will usually produce symptoms of varying severity, and which, although manageable, are often quite bothersome for patients. In addition to the discomfort and inconvenience of the supplements, patients develop lowturnover bone disease, which resembles osteomalacia. Although dysmorphic, bone mass is generally preserved or increased in hypoparathyroidism, and fracture risk is not apparently increased. Finally, the calcium and vitamin D supplements with low parathyroid hormone (PTH) lead to an increased daily urinary excretion of calcium and signiﬁcant risk of nephrolithiasis. The recent availability of pharmacologic PTH for exogenous administration has opened the opportunity to replace PTH in patients with postoperative hypoparathyroidism. The experience with this to date is limited, but early results demonstrate that PTH delivered subcutaneously twice daily can maintain serum calcium levels in the same range as oral calcium and vitamin D supplements and decreases the amount of hypercalciuria.12 Further experience with this strategy will be necessary before the full long-term effects are clear. ● Prevention Avoidance of permanent hypoparathyroidism is far more desirable than its treatment. This can be accomplished by preservation of the parathyroid glands on their native blood supply or autografting of parathyroid tissue to a muscular bed.13 During thyroidectomy, the blood supply to each parathyroid gland should be identiﬁed and speciﬁcally considered during dissection. Every parathyroid gland should be treated as though it were the only remaining gland. The parathyroid glands receive their blood supply via the inferior thyroid artery. During dissection of the thyroid, the inferior thyroid artery branches should be divided distal to the branching of the parathyroid end-arteries. The parathyroid glands can then be moved posteriorly in the neck away from the thyroid to allow safe dissection of the RLN and thyroid attachments to the trachea.

If the parathyroid glands cannot be preserved on their native blood supply, transfer of the gland to a convenient grafting site can maintain function.13,14 For normal parathyroid glands, transfer to the sternocleidomastoid muscle provides a convenient vascular bed for transplant. The parathyroid gland must be reduced to pieces that can survive on the diffusion of nutrients temporarily while neovascular in-growth occurs over several weeks. This strategy is effective, as is clear from operative series in which all parathyroid glands were autografted in order to try to optimize the long-term outcome of normal parathyroid function. All patients became temporarily hypoparathyroid, but all recovered to become dependent fully on their autografts. Although this strategy is effective, it leads to signiﬁcant short-term morbidity owing to the uniform, severe hypocalcemia that occurs before graft function begins. A selective strategy of autografting only the parathyroid glands that are devascularized during dissection is equally effective and more comfortable for the majority of the patients.

Nerve Injuries Several nerves adjacent to the thyroid gland can be deliberately or inadvertently affected during thyroidectomy. These include the RLN immediately adjacent to the thyroid and the vagus nerve, which is slightly more removed but causes the same symptoms when damaged. The external branch of the superior laryngeal nerve can be injured during dissection of the upper pole of the thyroid gland, and the sympathetic chain and stellate ganglion can be injured near the posterior aspect of the upper pole of the gland as well. Recurrent Laryngeal Nerve ● Consequence The RLN ﬁbers are a part of the vagus nerve on each side, until they branch off in the upper chest, course around the ligamentum arteriosum (left RLN) or the subclavian artery (right RLN), and back along the tracheoesophageal groove on each side. They pass between the thyroid and the larynx and insert in the larynx at

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the inferior border of the cricopharyngeal muscle. The nerve often branches at about the level of the lower pole of the thyroid and inserts to the larynx as two or more adjacent ﬁbers. There is also an esophageal branch that extends posteriorly from about the level of the thyroid lower pole. Damage to the RLN causes unilateral paralysis of the muscles that control ipsilateral vocal cord tension. Unilateral RLN injury changes the voice substantially in most patients and also signiﬁcantly affects the swallowing mechanism. The voice can range from a soft, whispery voice, with the inability to increase the volume at all, to a nearly normal-sounding voice, which cannot be raised to a yell. The difference between these is based on the ability of the contralateral vocal cord to cross the midline and appose the affected cord. If the cords cannot meet, the voice will be soft and breathy. If the cords can meet, the speaking voice will be more normal in timbre, but the affected cord prolapses with increased airway pressure and the ability to yell is lost. Swallowing is affected also, and the aspiration of liquids is a mark of severe RLN paresis. This improves with time and can be helped by swallowing training. Bilateral RLN injury causes paralysis of both cords and usually results in a very limited airway lumen at the cords. These patients usually have a normal-sounding speaking voice but severe limitations on inhalation velocity because of upper airway obstruction. They often require reintubation to maintain ventilation. Grade 2/3 complication ● Repair RLN paresis is usually temporary and resolves over days to months (see Table 40–1).5–11 There is no known method of aiding or speeding recovery. If a unilateral paresis proves to be permanent, palliation of the cord immobility and voice changes can be achieved with vocal cord injection or laryngoplasty. These procedures stiffen and medialize the paralyzed cord in order to allow the contralateral cord to appose the paralyzed cord during speech. If both cords are affected, the palliative procedures are more limited and involve creating an adequate airway for ventilation. Improvements in voice quality are not likely because there is no muscular control of the cord function. ● Prevention Avoidance of RLN injury is far superior to palliation. Great care must be taken during the dissection of the nerve in order to protect it. In some clinical situations, the RLN is sacriﬁced in order to allow an adequate tumor resection. Absent this unusual circumstance, though, careful dissection can generally preserve cord function. The principles of the dissection are 1. Avoid dividing any structures in the tracheoesophageal groove until the nerve is deﬁnitively identiﬁed.

Small branches of the inferior thyroid artery may seem like they can clearly be safely transected; however, the distortion of tumor, retraction, or previous scar may lead the surgeon to mistakenly divide a branch of the RLN. The identifying feature of the RLN is that the more it is dissected, the more it looks like the correct structure. This is based upon the morphologic appearance and the anatomic course. The nerve can tolerate manipulation but not cutting. Once cut, repair of the nerve is of unproven beneﬁt. 2. Identify the nerve low in the neck, well below the inferior thyroid artery, at the level of, or below, the lower pole of the thyroid gland. This allows dissection of the nerve at a site where it is not tethered by its attachments to the larynx or its relation to the inferior thyroid artery. Traction injuries to the nerve can occur when the nerve is manipulated near a site of ﬁxation. 3. Keep the nerve in view during the subsequent dissection of the thyroid from the larynx. Once the nerve is identiﬁed, the dissection can generally proceed from inferior to superior along the nerve, dividing the inferior thyroid artery branches and preserving the parathyroid glands. This allows careful dissection of the tissues with minimal manipulation of the RLN. 4. Minimize the use of powered dissection posterior to the thyroid. Although the electrocautery and highfrequency ultrasonic scalpel are useful tools in dissection, they have some risk of lateral thermal spread, which can damage adjacent tissues. Careful cold dissection and hemostasis with ligatures or clips will avoid this risk. This is particularly important at the entry of the RLN to the larynx, immediately adjacent to the ligament of Berry and its vessels. The use of nerve stimulators and laryngeal muscle potential monitors has been investigated as a tool to try to limit or avoid nerve injuries.15,16 The data do not currently support the routine use of these devices as reducing the rate of RLN injury. This may be because they help to identify the nerve, whereas the portion of the operation most likely to produce damage in experienced hands is the dissection of the RLN at the ﬁxed point of the cricopharyngeus. Further investigation may identify speciﬁc circumstances in which this technology is helpful. About 10% of patients have some evidence of RLN paresis after thyroidectomy; however, this resolves in most patients. About 1% or fewer patients have permanent nerve injury when total thyroidectomy is performed by experienced surgeons (see Table 40–1).

External Branch of the Superior Laryngeal Nerve ● Consequence This nerve courses adjacent to the superior pole vessels of the thyroid gland, before separating to penetrate the

40 THYROID SURGERY cricopharyngeus muscle fascia at its superoposterior aspect. The nerve supplies motor innervation of the inferior constrictor muscles of the larynx. Damage to this nerve changes the ability of the larynx to control high-pressure phonation, such as high-pitched singing (soprano/falsetto) or yelling.11,17 Grade 1/2 complication ● Prevention To avoid damaging this nerve, the dissection of the upper pole vessels should proceed from a space at which the nerve is safely sequestered under the cricopharyngeal fascia to the superior vessels themselves, thus safely separating the nerve from the tissue to be divided.

Sympathetic Chain ● Consequence Although it is separated from the posterior aspect of the thyroid, the sympathetic chain and stellate ganglion can be damaged during thyroidectomy, producing Horner’s syndrome (ipsilateral ptosis, miosis, and anhidrosis). This is probably due to retractor-induced injury because the sympathetic chain and ganglion itself are out of the operative ﬁeld. These injuries are nearly always temporary. Grade 1/2 complication ● Prevention Avoid traction on the nerve.

Injury to Other Cervical Structures Thoracic Duct ● Consequences The thoracic duct empties into the left internal jugular vein, posterior to the clavicular insertion of the sternocleidomastoid muscle. Damage to the thoracic duct can cause a large collection of lymph or chyle in the operative bed. Grade 1–3 complication ● Repair This can heal spontaneously after drainage if the leak is small. However, frequently the leak continues in spite of attempts to allow healing by decreasing output (a fat-free diet or total dietary abstention, total parenteral nutrition, and octreotide injections). If the leak persists for more than 3 weeks, the thoracic duct can be divided in the left hemithorax using thoracoscopic techniques. This will nearly always allow the leak to heal. ● Prevention Identiﬁcation of the duct can avoid injury. Identiﬁcation of a leak intraoperatively allows obliteration of the leak at that time to avoid postoperative leak.

403

Trachea ● Consequences Tracheal injuries can occur, particularly during removal of large invasive tumors. Untreated injuries can result in wound infection and tracheocutaneous ﬁstula. Grade 1–3 complication ● Repair Most tracheal injuries can be repaired primarily with resorbable suture. For defects larger than 10 mm, it may be preferable to patch the trachea with a pedicle of the sternocleidomastoid muscle or to perform a sleeve resection of the affected area. If resected, the cut ends of the trachea are reapproximated with absorbable suture. A drain should be placed to evacuate any air that escapes through the repair. This is less of an issue if the patient is extubated at the completion of the operation, avoiding the effects of positive-pressure ventilation on the repair. A tracheostomy is rarely necessary, although if there are other issues concerning airway safety, placement of a temporary tracheostomy may be preferable to prolonged intubation. ● Prevention Avoid injury to the trachea by careful dissection or planned resection.

Esophagus ● Consequence Esophageal injuries rarely occur during thyroidectomy. Untreated injury can result in deep space wound infection and esophageal-cutaneous ﬁstula. Grade 2–4 complication ● Repair If the esophageal lumen is entered, the operative options include primary repair or closure of the distal lumen and construction of a cervical esophagostomy. Primary repair is generally preferable, unless there is extensive tissue loss or damage. ● Prevention Avoid injury to the esophagus via careful dissection or planned resection.

Obtain Hemostasis and Close in Layers After the completion of the central neck procedure, the operative bed must be carefully inspected for hemostasis. In particular, the area immediately anterior to the RLN insertion under the inferior border of the cricothyroid muscle is a site of frequent residual bleeding. This is the site of the ligament of Berry division (see Figs. 40–5 and 40–6). Careful management of these bleeding sites is necessary to ensure hemostasis without damaging structures preserved during the dissection.

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Neck Hematoma ● Consequences A neck hematoma requiring reoperation develops after operation in about 1 of every 150 thyroidectomies.18,19 The hematoma nearly always appears within the initial 6 hours after the completion of the procedure, although with therapeutic anticoagulation, the hematoma can appear up to several days later. This complication is manifest by increasing pain, neck swelling, and often marked anxiety. The hematoma can collect either between the platysma muscle and the sternohyoid muscles (superﬁcial) or deep to the strap muscles along the larynx (deep). The deep hematomas are the more dangerous because they can be sequestered on one side of the larynx, causing a shift and compression of the airway. Grade 1–5 complication ● Repair Although a minority of patients with postoperative hematomas develop airway compromise requiring emergent evacuation at the bedside, this possibility exists with every neck hematoma. Patients with a hematoma of the neck should not be left alone until the hematoma has been evacuated. Medical personnel with the capability of opening the wound to decompress the airway must stay with the patient until the situation is resolved. For most patients, the hematoma is less immediately threatening, and the patient can be urgently returned to the operating room, placed under anesthesia, and the hematoma evacuated and bleeding controlled. Often, no speciﬁc bleeding site can be identiﬁed at reoperation, although when one is found, the most likely areas are the anterior jugular veins under the platysma ﬂaps, the superior pole vascular pedicle, and the vessels of the ligament of Berry, adjacent to the RLN insertion. The risk of cervical hematoma has led some to question the safety of outpatient thyroidectomy because there would be some possibility of the hematoma developing after discharge.18,19 The current experience with outpatient thyroid surgery by experts in the ﬁeld has demonstrated that this can be done safely, although postoperative observation for 6 hours is routine in order to detect this complication prior to facility discharge. ● Prevention Careful hemostasis during the initial operation is required, with particular attention to these areas, to try to prevent this complication.

Postoperative Thyroid Hormone Management Iatrogenic Hyperthyroidism or Hypothyroidism ● Consequences After total thyroidectomy, and as a part of the therapy for most thyroid carcinomas, patients receive thyroid

hormone replacement therapy.20 As a chronic medication, thyroid hormone is among the most well tolerated. It has a long half-life, which makes daily dosing adequate and means that patients do not develop symptoms if they miss or change the timing of doses. The problems with thyroid hormone administration, however, are (1) its long half-life allows adjustment of dosage only once per month or so, making the titration of the proper dose a slow process; (2) its narrow therapeutic window means that small changes in dosing or medication preparation can change the physiologic effect; and (3) it is largely protein-bound so other protein-bound drugs or changes in the proteins themselves can change the effects of a given dose of the drug. Grade 1/2 complication ● Prevention Patients must understand that the process of titration can take time. Trying to speed the process by making more frequent changes often delays the identiﬁcation of the appropriate dose by overcorrection. The narrow therapeutic window of thyroid hormone efﬁcacy is another aspect that patients should understand. In particular, the effect of changing thyroid hormone preparations, from one brand to another, or to generic preparations, may change the patient’s response to the drug. Patients should be encouraged to be consistent about the preparation that they use, or, if a change is unavoidable, to recheck their thyroid-stimulating hormone levels a month after a change to document the effect. This has been well documented in the medical and lay literature, and most pharmacists are also sensitive to this issue.21–30 A more frequent problem is the addition or subtraction of some other chronic medication, such as oral contraceptive pills or estrogen replacement therapy, that changes the serum protein binding of the thyroid hormone dose. Patients should be informed of this potential effect and the need to redocument and adjust thyroid hormone dosing after these changes in other medications.

REFERENCES 1. Kitamura Y, Shimizu K, Nagahama M, et al. Immediate causes of death in thyroid carcinoma: clinicopathological analysis of 161 fatal cases. J Clin Endocrinol Metab 1999; 84:4043–4049. 2. Rudow M, Hill AB, Thompson NW, Finch JS. Heliumoxygen mixtures in airway obstruction due to thyroid carcinoma. Can Anaesth Soc J 1986;33:498–501. 3. Allo MD, Thompson NW. Rationale for the operative management of substernal goiters. Surgery 1983;94:969– 977. 4. Sippel RS, Gauger PG, Angelos P, et al. Palliative thyroidectomy for malignant lymphoma of the thyroid. Ann Surg Oncol 2002;9:907–911.

40 THYROID SURGERY 5. Farrar WB, Cooperman M, James AG. Surgical management of papillary and follicular carcinoma of the thyroid. Ann Surg 1980;192:701–704. 6. Thompson NW, Nishiyama RH, Harness JK. Thyroid carcinoma: current controversies. Curr Probl Surg 1978; 15:1–67. 7. Schroder DM, Chambous A, France CJ. Operative strategy for thyroid cancer, is total thyroidectomy worth the price? Cancer 1986;58:2320. 8. Clark OH, Levin K, Zeng QH, et al. Thyroid cancer: the case for total thyroidectomy. Eur J Cancer Clin Oncol 1988;24:305–313. 9. Ley PB, Roberts JW, Symmonds RE Jr, et al. Safety and efﬁcacy of total thyroidectomy for differentiated thyroid carcinoma: a 20-year review. Am Surg 1993;59:110–114. 10. Tartaglia F, Sgueglia M, Muhaya A, et al. Complications in total thyroidectomy: our experience and a number of considerations. Chir Ital 2003;55:499–510. 11. Rosato L, Avenia N, Bernante P, et al. Complications of thyroid surgery: analysis of a multicentric study on 14,934 patients operated on in Italy over 5 years. World J Surg 2004;28:271–276. 12. Winer KK, Ko CW, Reynolds JC, et al. Long-term treatment of hypoparathyroidism: a randomized controlled study comparing parathyroid hormone-(1-34) versus calcitriol and calcium. J Clin Endocrinol Metab 2003;88: 4214–4220. 13. Olson JA Jr, DeBenedetti MK, Baumann DS, Wells SA Jr. Parathyroid autotransplantation during thyroidectomy. Results of long-term follow-up [see comment]. Ann Surg 1996;223:472–478; discussion 478–480. 14. Thomusch O, Machens A, Sekulla C, et al. The impact of surgical technique on postoperative hypoparathyroidism in bilateral thyroid surgery: a multivariate analysis of 5846 consecutive patients. Surgery 2003;133:180–185. 15. Rea JL, Khan A. Clinical evoked electromyography for recurrent laryngeal nerve preservation: use of an endotracheal tube electrode and a postcricoid surface electrode. Laryngoscope 1998;108:1418–1420. 16. Otto RA, Cochran CS. Sensitivity and speciﬁcity of intraoperative recurrent laryngeal nerve stimulation in predicting postoperative nerve paralysis. Ann Otol Rhinol Laryngol 2002;111:1005–1007. 17. Stojadinovic A, Shaha AR, Orlikoff RF, et al. Prospective functional voice assessment in patients undergoing thyroid surgery [see comment]. Ann Surg 2002;236:823–832.

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18. Burkey SH, van Heerden JA, Thompson GB, et al. Reexploration for symptomatic hematomas after cervical exploration. Surgery 2001;130:914–920. 19. Abbas G, Dubner S, Heller KS. Re-operation for bleeding after thyroidectomy and parathyroidectomy. Head Neck 2001;23:544–546. 20. Mazzaferri EL. An overview of the management of papillary and follicular thyroid carcinoma. Thyroid 1999; 9:421–427. 21. Mikosch P, Obermayer-Pietsch B, Jost R, et al. Bone metabolism in patients with differentiated thyroid carcinoma receiving suppressive levothyroxine treatment. Thyroid 2003;13:347–356. 22. Sawka AM, Gerstein HC, Marriott MJ, et al. Does a combination regimen of thyroxine (T4) and 3,5,3′triiodothyronine improve depressive symptoms better than T4 alone in patients with hypothyroidism? Results of a double-blind, randomized, controlled trial. J Clin Endocrinol Metab 2003;88:4551–4555. 23. Walsh JP, Shiels L, Lim EM, et al. Combined thyroxine/ liothyronine treatment does not improve well-being, quality of life, or cognitive function compared to thyroxine alone: a randomized controlled trial in patients with primary hypothyroidism [see comment]. J Clin Endocrinol Metab 2003;88:4543–4550. 24. Walsh JP. Dissatisfaction with thyroxine therapy—could the patients be right? Curr Opin Pharmacol 2002;2:717– 722. 25. Saravanan P, Chau WF, Roberts N, et al. Psychological well-being in patients on ‘adequate’ doses of L-thyroxine: results of a large, controlled community-based questionnaire study [see comment]. Clin Endocrinol 2002;57: 577–585. 26. Woeber KA. Levothyroxine therapy and serum free thyroxine and free triiodothyronine concentrations. J Endocrinol Invest 2002;25:106–109. 27. Wiersinga WM. Thyroid hormone replacement therapy. Horm Res 2001;56(suppl 1):74–81. 28. Fischman J. Reports of thyroid drug’s demise were exaggerated. US News World Rep 2001;131:57. 29. What is going on with levothyroxine? Med Lett Drugs Ther 2001;43(1108):57–58. 30. Bell DS, Ovalle F. Use of soy protein supplement and resultant need for increased dose of levothyroxine. Endocr Pract 2001;7:193–194.

41

Parathyroid Surgery Lawrence T. Kim, MD INTRODUCTION Surgical treatment of parathyroid disease is highly successful, with a very low complication rate. In expert hands, the cure rate of hyperparathyroidism approaches 99% in large series, whereas signiﬁcant morbidity may be very rare.1 As with all operations, however, the results achieved by experts depends on long-term experience with the potential difﬁculties of the procedure. The purpose of this chapter is to expand on these potential problems so that the reader may either avoid them or deal with them appropriately.

DIAGNOSIS Hyperparathyroidism is usually a straightforward diagnosis. However, misdiagnosis is a common cause of operative failure. The combination of hypercalcemia, elevated parathyroid hormone (PTH), and elevated urinary calcium is diagnostic. However, many patients do not ﬁt this simple paradigm. The surgeon is often faced with patients who have marginal laboratory abnormalities or diseases that may masquerade as hyperparathyroidism. Surgery performed in cases in which parathyroid adenoma or hyperplasia is absent is frustrating for the surgeon and dangerous for the patient. This section brieﬂy focuses on disorders that commonly present a diagnostic challenge. The collaboration of an endocrinologist who is expert in parathyroid disease and mineral metabolism cannot be overemphasized. Not infrequently, patients referred to the author for hyperparathyroidism do not in fact have the disease. The surgeon always has the ﬁnal responsibility for establishing the correct diagnosis. Normocalcemic hyperparathyroidism, as its name suggests, is characterized by normal serum calcium, at least on most occasions. Normocalcemic hyperparathyroidism has been clearly deﬁned as an entity and may represent a very early stage of the disease.2 In these cases, PTH may be only slightly elevated and is usually lower than in patients with hypercalcemia. Urinary calcium excretion may occasionally be markedly elevated which helps to conﬁrm the diagnosis of hyperparathyroidism.

Coexisting vitamin D deﬁciency, a common occurrence, may mask the hypercalcemia that would normally occur. Hyperparathyroidism may occur as part of a genetic syndrome. These syndromes include familial isolated hyperparathyroidism, multiple endocrine neoplasia (MEN) 1, MEN 2a, and hyperparathyroidism–jaw tumor syndrome. It is vital to obtain family history for all patients with hyperparathyroidism. Questions should be relevant not only to hyperparathyroidism but also to other manifestations of these syndromes. Speciﬁc questions about peptic ulcer disease, Zollinger-Ellison syndrome, thyroid tumors, adrenal tumors, and pituitary tumors should be included. Failure to diagnose a genetic syndrome may lead to inappropriate surgery for the patient. Familial hypocalciuric hypercalcemia (FHH) is an uncommon disease characterized by mild elevations of serum calcium, normal to modestly elevated PTH, and a low urinary calcium. It is an autosomal dominant genetic disease. Approximately two thirds of patients have a mutation in the calcium-sensing receptor. A 24-hour urinary calcium usually shows very low calcium excretion. The best test to differentiate FHH from hyperparathyroidism is the ratio of urinary calcium to creatinine clearance (UCa × SCr/UCr × SCa, where U is the 24-hr urinary excretion and S is the serum concentration).3 Most patients with FHH will have a ratio less than 0.01. It is important to rule out FHH prior to surgical exploration, particularly if the serum calcium and PTH are nearly normal. This disease will usually not require surgical treatment.

CHOICE OF OPERATION The “gold standard” surgical approach for primary hyperparathyroidism is full neck exploration with visualization of all parathyroid glands. This has the advantage of an extremely high cure rate in expert hands. But dissection is fairly extensive, even in simple cases, which results in a longer operative time, longer hospital stay, and more patient discomfort. A newer technique for parathyroidectomy is the directed parathyroidectomy. With the directed parathyroidectomy, preoperative imaging is used to locate an abnormal gland, and only that gland is visualized and

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removed. A variation of this technique is to use intraoperative radioactivity detection to locate the abnormal gland to facilitate localization and dissection. The intraoperative parathyroid hormone (IOPTH) assay is used to conﬁrm that no other abnormal tissue remains. Advantages of the minimally invasive technique include a shorter operative time, a much smaller incision with less dissection, a shorter hospital stay (usually done as an outpatient), and a quicker recovery. Directed parathyroidectomy particularly lends itself to performance under local anesthesia.4,5 A disadvantage is that the cure rate may be lower with this procedure, especially if the IOPTH assay is omitted. However, the risks of reoperation are believed to be lower, given the fact that most of the neck will not have been dissected. The approach should be chosen based on the available technology and the clinical details of the patient (Fig. 41–1).

Full Neck Exploration, Including Subtotal and Total Parathyroidectomy INDICATIONS ● Primary

hyperparathyroidism (especially in cases without availability of IOPTH monitoring or with no visible lesion after preoperative imaging) ● Familial hyperparathyroidism ● Secondary hyperparathyroidism ● Calciphylaxis

Diagnosis of hyperparathyroidism

Intraop PTH assay available?

Yes No Good ultrasound and sestamibi available?

Yes No Full neck exploration

Plan directed parathyroidectomy

No Gland seen on imaging?

Yes

Gland seen on ultrasound and sestamibi.

Directed parathyroidectomy

Gland seen on ultrasound only.

Gland seen on sestamibi only.

Directed parathyroidectomy with intraoperative gamma probe

Figure 41–1 Management algorithm for primary hyperparathyroidism.

41 PARATHYROID SURGERY

409

T

I Figure 41–2 View of the left parathyroids. The view is of the left side of the neck. The head is to the right. The thyroid is retracted superiorly and to the patient’s right (away from the viewer). The superior (S) and inferior (I) parathyroids are seen, as is the recurrent laryngeal nerve (N). Of note is the typical relationship of the superior and inferior parathyroid glands to the recurrent nerve, with the superior gland posterior and the inferior gland anterior.

OPERATIVE STEPS Transverse collar incision Vertical incision through strap muscles Exposure of thyroid Dissection and identiﬁcation of parathyroids Biopsy of parathyroids (optional) Removal of abnormal parathyroid(s) Thymectomy (included with total parathyroidectomy) Step 8 Approximation of strap muscles Step 9 Closure of platysma Step 10 Skin closure Step Step Step Step Step Step Step

1 2 3 4 5 6 7

Transverse Collar Incision The incision is ideally placed within a transverse skin crease. A more inferior incision usually provides a more pleasing cosmetic result, although access to the superior pole of the thyroid gland may be difﬁcult.

Dissection and Identiﬁcation of Normal and Abnormal Parathyroids Failure to Locate an Abnormal Parathyroid ● Consequence Noncurative operation. Grade 2–4 complication ● Repair Reoperation. ● Prevention Intraoperative localization of the parathyroids requires an intimate familiarity with their anatomy and embryol-

N S

ogy (Fig. 41–2). The parathyroid glands arise from the third and fourth pharyngeal pouches. The superior glands arise from the fourth pouch along with the Ccells of the thyroid. They migrate inferiorly and typically come to rest on the posterior aspect of the thyroid in the midbody of the gland, near the intersection of the inferior thyroid artery and the recurrent laryngeal nerve. Because of its embryologic relationship with the C cells, superior glands may occur within the substance of the thyroid. The inferior glands arise from the third pouch, which also gives rise to the thymus. These glands migrate farther inferiorly than the superior glands and are usually located near the tip of the inferior pole of the thyroid. Because of their embryologic origin, they are frequently within the thymus or the fat pad containing the thymic remnant. This fat pad lies inferior to the thyroid and is bounded roughly by the thyroid superiorly, the sternocleidomastoid muscles and recurrent laryngeal nerves laterally, the trachea posteriorly, the aortic arch inferiorly, and the strap muscles and sternum anteriorly. Inferior parathyroid glands are somewhat more prone than superior glands to be found in unusual locations. All parathyroid glands can migrate into unusual or “ectopic” locations. Superior glands may be found near the superior pole of the thyroid along the course of the superior thyroid artery. Parathyroids may occur anywhere along the posterior or lateral surface of the thyroid gland. They are frequently just under the thyroid capsule and may be thinned considerably from pressure applied by the surgeon during dissection or retraction. Frequent inspection of the thyroid during the dissection (and during thyroidectomy) may reveal these subcapsular glands. Either superior or inferior parathyroids may be within the

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substance of the thyroid parenchyma and undetectable grossly. Ultrasound either preoperatively or intraoperatively may help locate these glands. Parathyroids may lie posteriorly near the esophagus and even in the retropharyngeal or retroesophageal space. Glands may also be found in the carotid sheath. As mentioned previously, inferior glands may be found within the thymus or its associated fat pad. Thymic tissue can easily be mistaken for a parathyroid adenoma. Thymic tissue is more gray in color, slightly more dense, and less vascular than the typical adenoma. Inferior parathyroids may migrate as inferiorly as the heart. Therefore, they can be out of reach from a cervical incision, although this is distinctly unusual. The surgeon should make every attempt to carry the search down to and along the innominate artery and aortic arch as long as the patient’s body habitus allows a safe dissection. In addition to unusual locations, there may be more than four parathyroid glands. In his classic anatomic study, Gilmour6 found that 6.5% of cadavers had more than four parathyroids. Other studies have found a lower incidence.7 Although some studies including these have shown fewer than four glands in some subjects, one can never be certain if other glands have simply been overlooked. During dissection of parathyroids, meticulous technique is required. Lighting and magniﬁcation are critical to successful parathyroid surgery. A headlight is useful, particularly when working through small incisions, and loupes provide a signiﬁcant advantage. A bloodless ﬁeld must be maintained at all times. Staining with blood impairs detection of subtle colorations. thereby making identiﬁcation of parathyroids more difﬁcult. A useful technique to expose the gland is to grasp the overlying tissue with ﬁne forceps, nicking the tissue with ﬁne scissors or occasionally cautery, and gently pulling the tissue apart between forceps. Gentle spreading with a ﬁne instrument is also useful. Care must be taken, however, not to disrupt ﬁne blood vessels, which may cause pesky bleeding. Indiscriminate use of electrocautery may damage a parathyroid or recurrent laryngeal nerve. If a full exploration is completed and only three normal glands are found, what should be done? In almost all cases, there is an adenoma somewhere. Assuming that all of the areas for ectopic location have been explored, a thymectomy should be performed ﬁrst. That tissue should be carefully inspected for the presence of a parathyroid. A thyroid lobectomy would then be indicated if no adenoma is found. If the surgeon or pathologist still cannot ﬁnd the gland after sectioning the thyroid lobe or thymus, the search must be continued until the entire neck from the larynx to the aortic arch and posteriorly to the vertebrae have been explored. Avoidance of this difﬁcult situation is one of the strongest arguments for preoperative parathyroid imaging. In these difﬁcult cases, the IOPTH assay is also very useful if available.

Failure to Recognize Multigland Disease ● Consequence Noncurative operation or early recurrence. Grade 2–4 complication ● Prevention The gold standard for differentiation between normal and abnormal glands is their gross appearance to an experienced surgeon. As mentioned previously, current parathyroid imaging studies are poor at detecting multigland parathyroid disease such as multiple adenomas or hyperplasia. Therefore, imaging of a gland does not mean that it is the only abnormal gland. Normal parathyroid glands usually weigh 30 to 70 mg and have a yellowish-brown color variously described as “salmon” or “peanut butter.” Visually, the typical size is about that of a lentil, but they may range in size from that of a plump grain of rice to a ﬂattened, elongated pea. Parathyroids are, like all other endocrine glands, highly vascular and bleed briskly if biopsied. Adenomas are often more of a deep red color than normal parathyroids (Fig. 41–3). A typical appearance is that of a “chicken heart.” In some cases, especially smaller adenomas, a rim of normal parathyroid tissue can be seen adjacent to the adenoma. In very small adenomas, color alone may distinguish them from normal parathyroids. Adenomas can vary in size from 1 to 2 mm and encompassed completely within a normal parathyroid to walnutsized or even larger. A typical adenoma is the size and shape of a kidney bean. Adenomas are universally soft. A hard adenoma must lead one to consider parathyroid cancer. Lymph nodes and thyroid tissue also are typically ﬁrmer than a parathyroid adenoma. Hyperplastic glands are also highly variable in size. Some hyperplastic glands are only slightly larger than normal and have a normal color and appearance. Other hyperplastic glands may grow to considerable size. Small hyperplastic glands may look exactly the same as an adenoma. Large ones tend to be ﬁrmer than adenomas and often lack the ruddy appearance of an adenoma. Hyperplastic glands usually do not grow uniformly, and there can be an order of magnitude variation in size within one patient. Adenomas may be multiple.8 Therefore, removal of even a large, typical adenoma may not result in a cure. Currently, the best modalities to ensure a curative operation are a full neck exploration to grossly evaluate all parathyroids or use of the IOPTH assay.

Failure to Locate Four (All) Parathyroids after Discovery of an Adenoma ● Consequence Probably none; possibly failure to diagnose multigland disease. Grade 1–3 complication

41 PARATHYROID SURGERY

411

T

S I

Figure 41–3 Left superior parathyroid adenoma. The view is from roughly the same perspective as in Figure 41–2. The superior gland (S) is enlarged and ruddy with the typical appearance of an adenoma. Note its lack of surface vasculature, which helps distinguish it from thyroid tissue (T). Also seen are the inferior parathyroid (I), the recurrent laryngeal nerve (N), and the inferior thyroid artery (I).

● Prevention If the initial dissection shows a parathyroid adenoma, the surgeon is often faced with the dilemma of determining when enough dissection is enough. Clearly, the standard is to complete the dissection until four glands are identiﬁed. Unless the IOPTH assay is used (see later), less than a full dissection will probably result in more treatment failures. Parathyroid disease may be manifested by two or even three distinct adenomas. Therefore, ﬁnding one abnormal gland and one normal gland on one side is not deﬁnitive. Knowing, however, that 85% or so of hyperparathyroidism is caused by a single adenoma, the odds are with the surgeon if she or he stops dissection. However, expert parathyroid surgeons should expect a 98% to 99% cure rate. Therefore, most experts would recommend that dissection be continued until four glands are found. However, there are patients in whom an adenoma has been found, two other normal glands have been found, both sides of the neck have been explored, and a fourth gland cannot be found. In the case of adenoma, normal glands may be suppressed and may even be smaller than normal. This may make ﬁnding that last normal gland very difﬁcult. If a diligent exploration has been carried out and the surgeon feels that the existence of another sizeable adenoma within the dissected area is unlikely, it is reasonable to stop. Certainly, if the surgeon feels that further dissection would increase the possibility of surgical morbidity, the risks of further dissection outweigh any potential beneﬁt. When making the decision to stop any further search, however, the surgeon should always consider that a repeat dissection in the future will be far more difﬁcult and hazardous

A N

for the patient. As always, intraoperative consultation from another experienced surgeon is appropriate in difﬁcult cases.

Injury to the Remaining Glands ● Consequence Hypoparathyroidism. Grade 4 complication ● Repair Reimplantation of normal parathyroid if suspected. ● Prevention Extreme care must be taken to avoid damage to the blood supply of normal glands. Devascularized glands rapidly become dusky and eventually turn very dark. If this occurs to a normal gland, it should immediately be excised and placed on ice until it can be reimplanted (see under “Parathyroid Autotransplantation,” later).

Injury to the Recurrent Laryngeal Nerve ● Consequence Vocal cord paralysis; hoarseness. Grade 4 complication ● Repair Primary repair of nerve (immediately). Vocal cord medialization (later). ● Prevention All parathyroid surgeons should be very familiar with the course and potential aberrant locations of the recurrent laryngeal nerve so as not to injure it. Even if the

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nerve is not cut, it may be injured by dissection in close vicinity. Cautery should be used only when one is certain that electric current will not injure a nearby nerve. Bipolar cautery is safer when working near the nerve. Clips and sutures may impinge on the nerve or may kink it, thereby impairing its blood supply.

Biopsy of the Parathyroids Frozen section may be used to identify parathyroid glands. This is most useful for simple conﬁrmation that the tissue in question actually is parathyroid. Differentiation between adenoma and hyperplasia on histology is unreliable. Frozen section can be useful if appearances are unusual or confusing. It is usually optional and becomes less necessary as surgeon experience increases. It is mandatory, however, in cases in which a gland will be cryopreserved or reimplanted (see later), because misidentiﬁcation may lead to disaster. Frozen section is not generally useful in distinguishing an adenoma from hyperplasia. For that, the surgeon will need to rely on inspection of all glands or the IOPTH assay. If a parathyroid needs to be biopsied for identiﬁcation, care must be taken to avoid damage to the blood supply to the gland. A tip of the gland is exposed away from the vascular pedicle. Fine scissors are placed across this tip with the gland well proximal to the tip of the scissors. If only the scissor tip is used, the gland has a tendency to slide out before it is transected completely. As with all endocrine organs, the transected parathyroid should bleed briskly (for its size). Bipolar electrocautery is used sparingly for hemostasis. Monopolar cautery should not be used or should be used only at very low settings to avoid injury to the remaining gland and blood supply.

Removal of Abnormal Parathyroids Disruption of the Capsule ● Consequence Possible parathyromatosis. Grade 3 complication ● Repair Reoperation at a future date. ● Prevention When dissecting a parathyroid, care should be taken to avoid damage to the capsule. Spilling cells from an adenoma may lead to parathyromatosis (i.e., multiple foci of enlarging parathyroid tissue). This may cause recurrent disease at a later date and can be a difﬁcult problem to correct. While dissecting a normal-sized parathyroid, the surgeon should avoid grasping or retracting the gland directly. Pressure or retraction on adjacent tissue should expose the gland. However, adenomas sometimes require direct traction, especially when working through a small incision. If the adenoma

must be grasped, the whole gland may be gently grasped with a larger forceps such as a DeBakey. Small, ﬁne forceps are too prone to puncture the capsule. Gentle pressure only can be used, because too ﬁrm a grip will crush the gland. When ﬁrmer traction is required, the gland may be pushed or pulled with open DeBakey forceps. The capsule alone should not be grasped because it is likely to tear. Once the vascular pedicle is ligated, the suture may be cut relatively long to provide a “handle” to pull the gland from surrounding tissue. After ligation of this pedicle, the whole gland can usually be pulled free of surrounding areolar tissue with gentle traction and blunt dissection.

Subtotal Parathyroidectomy Subtotal parathyroidectomy is chosen in cases of sporadic four-gland hyperplasia. It may also be chosen by some surgeons for secondary hyperparathyroidism. Hyperplasia is diagnosed by ﬁnding diffuse enlargement of all glands. With hyperplasia, the size of the abnormal parathyroids is highly variable, both within a single patient and between different patients. In some patients, the glands may be virtually normal in size. In these cases, a careful search for an ectopic supernumerary gland and a thymectomy should be undertaken, although these normal or near-normal size glands may in fact be the cause of the disease. If a subtotal parathyroidectomy is chosen, the most normalappearing gland is chosen to remain in situ. If there is more than one good candidate, the gland that would be most accessible at reoperation is chosen to remain in situ. If the gland chosen to remain is signiﬁcantly enlarged, the remnant is trimmed to allow approximately 50 to 70 mg of normal parathyroid tissue to remain. Technically, this is performed as described earlier under “Biopsy of the Parathyroids.” The remnant is marked with a nonabsorbable suture (polypropylene) and clips for identiﬁcation at a later date should reoperation be required. The suture is usually easier to ﬁnd during operation, and clips will facilitate sonographic or radiographic localization. Care must be used to ensure that the blood supply to the gland is not damaged during dissection. If there is a question about the viability of the remnant, complete excision should be performed followed by autotransplantation of tissue whose viability is certain.

Supernumerary Glands ● Consequence Persistent hyperparathyroidism. Grade 2–4 complication ● Repair Reoperation. ● Prevention The possibility of supernumerary glands is a much more signiﬁcant problem when operating for hyperplasia.

41 PARATHYROID SURGERY Anatomic studies have shown a prevalence of supernumerary parathyroid glands from 2.5% to 11%.6,7,9 Retained, unidentiﬁed glands left in situ may be the source of recurrent or persistent disease. A careful search should be made at the time of operation for supernumerary glands. Presumably, the IOPTH assay could be used to prove that no source of PTH has been left. It has been shown that the IOPTH assay should be performed after resection of multigland disease.10,11 Proof that this assay can rule out supernumerary glands is lacking, but practically, if the IOPTH level falls to very low levels, the likelihood of a signiﬁcant gland remaining is low.

Total Parathyroidectomy Total parathyroidectomy with autotransplantation can be performed for genetic disease including familial hyperparathyroidism and MEN. It may also be chosen for secondary hyperparathyroidism due to renal failure. Total parathyroidectomy without autotransplantation is indicated for calciphylaxis. Some authors have also recommended total parathyroidectomy without autotransplantation in renal failure, although this is currently a minority opinion.12 An advantage of total parathyroidectomy with autotransplantation is a potential decrease in recurrence of hyperparathyroidism. In one small, randomized, prospective trial, patients with secondary hyperparathyroidism treated this way had a lower recurrence over those treated with subtotal parathyroidectomy.13 However, long-term follow-up suggests that many patients with secondary hyperparathyroidism due to renal failure may recur regardless of technique, although the data again favor total parathyroidecomy.14 In any case, reoperation on autotransplanted glands in the forearm is less risky to the patient than reoperating in the neck. Locating hyperfunctioning glands within a muscle belly is often difﬁcult. Ultrasound preoperatively may occasionally show the location of an enlarged autotransplant. If a total parathyroidectomy is chosen (with or without autotransplantation), a cervical thymectomy should be included as part of the procedure for removal of potential supernumerary glands. A thymectomy is performed by removing all tissue between the thyroid superiorly, the aortic arch inferiorly, the trachea posteriorly, the recurrent laryngeal nerves laterally and posteriorly, and the strap muscles anteriorly. Dissection is begun at the inferior border of the thyroid. The recurrent nerves are traced inferiorly bilaterally, and these serve to mark the posterior and lateral extent of the dissection. All tissue is elevated off the trachea. Thymic and fatty tissue is elevated out of the mediastinum by gentle traction with Allis clamps. Dissection is completed by transecting the tissue at or just above the aortic arch. A harmonic scalpel is useful to cut through this amorphous tissue.

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Temporary Postoperative Hypocalcemia ● Consequence Symptoms of hypocalcemia (e.g., muscle spasm, paresthesias). Grade 1 complication ● Repair Calcium should be checked every 6 to 8 hours after total parathyroidectomy. Patients will usually require intravenous calcium infusion beginning 24 to 72 hours after surgery. They may then be started on oral supplementation and calcitriol until stable levels can be maintained. Over several weeks, the supplementation can be gradually decreased as the residual or autotransplanted parathyroid becomes functional. ● Prevention Hypocalcemia is the routine after total parathyroidectomy with autotransplantation. Its absence should cause worry that a supernumerary gland has been overlooked.

Wound Closure Inaccurate Closure of the Platysma ● Consequence Poor cosmetic result. Grade 1 complication ● Repair Possibly, wound revision in extreme cases. ● Prevention Closure of the platysma is important for a good cosmetic result. In placing sutures into the platysma, it is easy to hook the dermis with the needle. This results in a dimpling of the skin that may remain long term. Accurate closure of this muscle also helps to prevent “step-offs” that produce an unsightly result.

Directed Parathyroidectomy INDICATIONS ● Sporadic primary hyperparathyroidism WITH ● Available IOPTH monitoring ● Positive preoperative imaging ● Sporadic primary hyperparathyroidism with positive

preoperative imaging but WITHOUT available IOPTH monitoring (controversial).

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OPERATIVE STEPS Preoperative imaging Preoperative injection with 99Tc sestamibi (optional) Step 3 Insertion of peripheral intravenous shunt for blood draws Step 4 Blood sample for baseline IOPTH assay Step 5 Small transverse neck incision Step 6 Identiﬁcation of parathyroid adenoma Step 7 Blood sample for preexcision IOPTH assay Step 8 Excision of parathyroid Step 9 Blood samples 5 and 10 minutes postexcision for IOPTH assay Step 10 Extension of operation to full exploration if indicated by assay Step 11 Closure Step 1 Step 2

A

Preoperative Imaging Prior to widespread acceptance of the directed parathyroidectomy, parathyroid imaging was widely considered unnecessary because a full neck exploration would be performed anyway. The radiologist John Doppman was widely quoted that, “The only localization technique needed is to localize an experienced parathyroid surgeon.” Increased attention to and acceptance of directed parathyroidectomy have led to wider use of preoperative parathyroid imaging. Parathyroid imaging can be extremely helpful, but it has major pitfalls. The two most commonly used techniques are ultrasound examination and nuclear scintigraphy with 99Tc-labeled sestamibi. Ultrasound is convenient, inexpensive, and potentially very accurate. It may be performed in the surgeon’s ofﬁce at the time of the initial visit.15,16 The exact sensitivity and speciﬁcity of ultrasound have varied widely in the literature, no doubt because of these technical issues. Sensitivity in good hands is probably around 70% to 80%, with speciﬁcity over 90%. Because the results of ultrasound vary so widely, it is important that a parathyroid surgeon understand the accuracy in his or her institution. If detection rates are consistently under 50%, the technique is clearly not being used to its potential. Accuracy may be improved by working with radiology to encourage a radiologist and a sonographer to become expert in this area. Another alternative is for the surgeon to perform the ultrasound (Fig. 41–4). It is well documented that ultrasound can be expertly performed by surgeons in these focused areas.15,17,18 Training in ultrasound is available from the American College of Surgeons and a variety of other sources. There are major advantages to the surgeon performing his or her own ultrasound in appreciating the anatomic location of the lesion. Ultrasound can reveal fairly small adenomas (3–4 mm on occasion), but it is not particularly good at detecting ectopic parathyroids, especially low in the mediastinum. Ultrasound is also poor at detecting multigland disease, especially hyperplasia. Even

B

Figure 41–4 A, Transverse ultrasound view of a left superior parathyroid adenoma. Note the homogeneous, hypoechoic lesion. B, Longitudinal ultrasound view of the same left superior parathyroid adenoma.

large hyperplastic glands can be missed, probably because their echotexture and density may be the same as the thyroid or surrounding tissue. The sestamibi scan is also widely available. Sestamibi (Cardiolite) was initially developed for cardiac imaging. It was subsequently found to concentrate in parathyroid adenomas and has since been widely used for parathyroid imaging. Sestamibi accumulates in mitochondria, which are abundant in parathyroid cells. This scan is somewhat time-consuming for the patient but is very low risk. The patient receives an injection of the labeled compound. After a short period of time (15 min), scintigraphy is performed of the neck and upper chest. This will show uptake in the thyroid, parathyroid, and salivary glands. Occasionally, a parathyroid will be visible because it is either ectopic or sufﬁciently large to cause asymmetry of the thyroid image, but usually the parathyroid adenoma is not visible in this early image. Over a period of time, the sestamibi will wash out of the thyroid but remain in the parathyroid. An image is taken 2 to 3 hours after the initial injection to look for retention in a parathyroid

41 PARATHYROID SURGERY

10 MINUTE POST INJECTION

415

3 HOUR POST INJECTION

3 HOUR POST INJECTION

Figure 41–5 Typical sestamibi scan indicates the presence of a right inferior parathyroid adenoma. Note the early uptake in the thyroid gland that dissipates in the 3-hour view. The parathyroid is indicated by the arrows. The salivary glands are shown by the intense uptake in the upper part of the images.

(Fig. 41–5). This imaging technique is particularly useful in locating ectopic parathyroid glands, including the mediastinum. The main problems with sestamibi scanning are sensitivity and its poor efﬁcacy in detecting multigland disease. Although, as with ultrasound, a wide range of accuracy with sestamibi scanning has been reported, on average, a sestamibi scan should show a lesion in about 60% to 80% of cases.19–21 If a gland is seen, the likelihood that it is indeed a parathyroid is very high. Multiplane scans should be obtained for the best possible localization. Sensitivity and speciﬁcity can also be improved with single photon emission computed tomography (SPECT) imaging. A potential cause of a false-positive scan can be uptake in a thyroid nodule. Abnormal thyroid tissue may trap sestamibi, yielding a false-positive result. Correlation with ultrasound in these cases can be very helpful. The combination of high-quality ultrasound and sestamibi is complementary, and many parathyroid experts use both techniques preoperatively.

Other imaging tests are occasionally useful preoperatively. Computed tomography (CT) scanning is not an imaging method of choice because of poor sensitivity, but it can show adenomas on occasion. Magnetic resonance imaging (MRI) can be helpful, particularly for locating an ectopic gland in the mediastinum. Positronemission tomography (PET) has been performed using 11 C-methionine with results similar to those of sestamibi.22,23 Another alternative, used primarily after a failed exploration, is venous sampling from neck veins by an experienced interventional radiologist to detect an area of high PTH secretion. Usually, this technique should be reserved for referral centers. Further developments in imaging are necessary for improved resolution, sensitivity, and speciﬁcity. If a preoperative imaging study shows a parathyroid lesion, the surgeon is faced with the choice of a directed parathyroidectomy or the standard complete neck exploration. With the development of the IOPTH assay in the

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1990s (see later), more and more surgeons are choosing a directed parathyroidectomy. If the ultrasound shows a typical parathyroid adenoma, there should be enough anatomic information to readily guide the surgeon to the abnormal gland. If the gland shows only on sestamibi scan, anatomic information is limited. In this case, intraoperative detection using a hand-held gamma detector (see later) may speed dissection. Intraoperative localization with ultrasound may be done but is not as good as preoperative ultrasound. In this technique, the incision is ﬁlled with saline, and imaging is performed through the saline. Sterile ultrasound gel may also be used on the skin or on solid organs. Intraoperative ultrasound may be performed to inspect the thyroid when an intrathyroidal parathyroid is suspected. Its use to localize an adenoma in other locations during surgery is more problematic. The numerous electrical devices present in an operating room often degrade the image on the ultrasound screen. Air introduced into the tissues during dissection is particularly troublesome because tiny air bubbles scatter the ultrasound beam and degrade the image considerably. This author typically uses ultrasound preoperatively in the clinic or just before incision to plan the incision, particularly in reoperative cases.

Intraoperative Radio-guided Localization If this procedure is chosen, the patient is taken to nuclear medicine for injection with 99Tc Sestamibi the morning of surgery. A hand-held gamma probe with collimator is then used to localize the area of highest emission, similar to the technique used with sentinel lymph node biopsy. These hand-held probes are now found in most operating rooms, often for use with sentinel lymph node biopsy. Dissection is carried toward the area of highest activity in a fashion similar to that used for a sentinel node biopsy. Some authors have advocated routine use of intraoperative gamma detection.24 Advantages include better incision planning and a focused, directed dissection. In this author’s opinion, good sestamibi scanning along with preoperative ultrasound provides adequate anatomic information in most cases without the need for the intraoperative gamma probe. However, for cases in which a lesion is seen on sestamibi scan but not ultrasound, especially in reoperative cases or when an ectopic gland is suspected, intraoperative gamma probe localization is very useful. Intraoperative gamma detection is not useful if the sestamibi scan performed in nuclear medicine does not detect a parathyroid.

Intraoperative PTH Monitoring The IOPTH assay has been used since the mid-1990s to monitor PTH during surgery. PTH has a short halflife, approximately 4 minutes. If an adenoma is removed, the PTH level should fall rapidly. If other abnormal glands remain, the level should fall to less of a degree. Therefore, if the level falls appropriately, the gland in

question was a single adenoma. If it does not fall appropriately, other abnormal glands probably remain. This allows the operation to be terminated without direct visualization of the other glands. This concept was conﬁrmed by Irvin and coworkers25–27 and has been validated by several other groups. IOPTH is measured at baseline prior to or just after incision. Ideally, this should be done from a peripheral venous line. The best placement is usually in the saphenous vein at the ankle. However, in practical terms, samples obtained from neck veins (away from the parathyroid, such as an anterior jugular vein) or arterial lines tend to have quite similar values. It is important that a new sample be drawn as baseline at the time of surgery rather than relying on previous clinic levels. As the putative adenoma is dissected, just prior to its removal, a second level is drawn, which is termed the preexcision level. This level is important because, on occasion, the PTH level may rise substantially from manipulation during dissection. After the gland is excised, levels are drawn at 5 minutes and 10 minutes after excision. Criteria for successful removal of abnormal tissue is a drop of 50% at 10 minutes compared with either the baseline or the preexcision level, whichever is higher. The IOPTH assay may be performed in the operating room using a portable instrument. However, a dedicated technician must be present to prepare and operate the machine. This is often not cost effective for clinical laboratory personnel. Direct transport to the laboratory by a tube system or a courier is usually adequate. However, direct communication between laboratory staff and operating room staff is crucial both prior to and during the procedure. The instrument may require several hours of setup and calibration time, making a last-minute request for the testing impossible to fulﬁll. The IOPTH assay, although fast, is usually not back by the time the wound is closed. It is important to remain in the operating room with the sterile ﬁeld maintained until a deﬁnitive laboratory value returns. This author has, on several occasions, had to reopen the neck based on the IOPTH results, even though a typical adenoma was found. Other disadvantages of the IOPTH assay are its cost and lack of widespread availability. A separate setup to perform IOPTH assays alone is often impractical for hospitals with a small volume of parathyroidectomies. However, newer instruments can be incorporated into the general clinical laboratory to run these and other assays. Such multifunction can greatly reduce the ﬁxed costs associated with the assay, making its purchase more attractive to hospitals. It is essential that the surgeon work closely with a clinical laboratory specialist when determining how best to make this test available.

False-Positive Drop in PTH Levels ● Complication Persistence of hyperparathyroidism. Grade 2 complication

41 PARATHYROID SURGERY ● Repair Reoperation. ● Prevention If the Irvin criteria are met, the false-positive rate (falsely indicating complete resection) has been reported from 6% (based on evaluation of all other glands)28 down to 0% (based on clinical cure rate).29 These data raise the question as to whether some glands may be enlarged but not hyperfunctional. Current data suggest that this is indeed the case.18 Therefore, when interpreting studies that clearly show grossly abnormal glands missed by the IOPTH assay, one must not assume for certain that these glands would produce clinical disease. More precise answers about the relationship between gross morphology and abnormal function will await further developments in imaging. If a failure does occur after directed parathyroidectomy and reexploration is required, it may not be as hazardous because most of the neck has not been dissected. Whereas the Irvin guidelines have proved very reliable, certain patterns in the parathyroid level should raise concern for the surgeon. If the level drops by about 50% after 5 minutes, but does not drop by another 50% at 10 minutes, the surgeon should be concerned. For example, if the baseline level was 150, the preexcision level was 140, the 5-minute level was 60, and the 10minute level was 50, the criteria for a complete excision have been met. However, one would expect the 10minute level to be around 30, given the half-life of PTH, especially because the normal glands should be suppressed. In these cases, another level can be drawn that will usually resolve the question. If a 15- or 20-minute level is the same or rising, further exploration is probably warranted.30 However, if it has fallen further, the operation can probably be terminated. If signiﬁcant concern remains, conversion to a full exploration is warranted. However, some judgment and interpretation are vital. Factors such as patient age, health, operative risk, desire to avoid repeat surgery, and desire to avoid the cosmetic and recovery disadvantages associated with complete exploration should be considered. Strict adherence to the Irvin guidelines is a safe, effective approach. But attention to the patterns of PTH decline will occasionally avoid an operative failure even when the criteria are met.

Incision For a directed parathyroidectomy, the location and length of the incision may vary. With good localization using either ultrasound or the hand-held gamma probe, the location of the putative adenoma may be very accurately identiﬁed prior to incision. Some surgeons prefer to make the incision directly over the lesion and dissect through the strap muscles at that location. The main advantage of this approach is a direct, minimal dissection. This can be

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a signiﬁcant advantage for glands that are particularly superior or inferior. This approach can also be especially helpful in reoperative cases because the surgeon may be able to operate in previously unviolated planes, allowing a safer dissection. A disadvantage of this approach is that conversion to a full neck exploration may require a new incision. For directed parathyroidectomy, this author prefers a transverse incision approximately 1.5 to 3 cm long (longer for larger necks, occasionally smaller for thin necks) centered in the midline. This is made within a skin crease nearest the parathyroid. Small subplatysmal ﬂaps are created, and the strap muscles are opened vertically in the midline. The skin is retracted with a Weitlaner retractor. The strap muscles and thyroid gland may be retracted with an Army-Navy or similar retractor. This approach allows exposure of a parathyroid adenoma in any typical location and can, therefore, be used in cases in which preoperative localization is uncertain. The main disadvantage is the long distance between the incision and the adenoma in certain cases making visualization and dissection difﬁcult. Although technically possible in some cases, use of this small incision to identify all normal glands or subtle hyperplasia is usually not advisable. If it is suspected that a full neck exploration will be required, a larger, standard incision is preferable. In addition, if a search of ectopic locations is necessary, conversion to the larger incision is needed.

Identiﬁcation of Parathyroid Adenoma As described previously, under “Full Neck Exploration.”

Blood Sample for Preexcision IOPTH Assay Usually, this is obtained after manipulation of the adenoma but prior to ligation of the vascular pedicle.

Extension of the Operation to Full Exploration if Indicated by the Assay If the assay shows that the ﬁrst excision is not complete, it is usually best to extend the incision for a full neck exploration. Whereas it should be possible to access the most common locations of a parathyroid adenoma from a well-placed central incision, a larger incision allows for easier detection of small adenomas or mildly hyperplastic parathyroids.

Parathyroid Autotransplantation Parathyroid autotransplantation may be performed as an adjunct to total parathyroidectomy or when a parathyroid gland is devascularized unintentionally during thyroid surgery. If this procedure is anticipated during total para-

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thyroidectomy, several specimen cups should be available as well as an ice bath (this may be prepared either on the sterile ﬁeld or outside the sterile ﬁeld). As each gland is removed, it is placed in a sterile container along with a few drops of saline. The container is tightly sealed and then immediately immersed in ice. This slows the metabolism of the ex vivo gland. After all glands are removed, the most normal-appearing gland is selected for autotransplantation. A portion of the chosen gland is sent for frozen section to conﬁrm its identity. At this time, if the autotransplant will be placed in the forearm, the neck is closed and the nondominant arm is extended, prepared, and draped. A small incision is made over the ﬂexor muscles, and dissection is carried down through the muscle fascia. If the gland will be placed in the sternocleidomastoid or strap muscle, a suitable muscle belly is exposed. About a 50- to 70-mg (about the size of a normal parathyroid) piece of parathyroid tissue is selected and dissected free of any attached fat or connective tissue. The portion chosen for reimplantation is then minced into small pieces. The author usually divides it into 8 to 12 pieces. Muscle ﬁbers are spread, and a piece is placed into the pocket. The pocket is then closed with a polypropylene suture. Each piece is then placed in turn until all tissue has been reimplanted. The author usually places 2 pieces in each muscle pocket. Other surgeons use separate pockets for each piece or place all pieces into a large pocket. A few surgeons place the parathyroids in other locations such as in subcutaneous fat.31,32 If a normal parathyroid is to be reimplanted during thyroid surgery, an alternative technique has been suggested. In this technique, the parathyroid is placed in a small volume (1.5–2 ml) of saline and minced into very ﬁne pieces. These are then drawn into a syringe and injected into the muscle belly. This has the advantages of being fast and easy. A small randomized study of this technique showed no disadvantages when compared with the reimplantation technique.33 It should be cautioned, however, that this should be limited to reimplantation of normal glands only until its safety has been demonstrated with abnormal glands. The concern would be that diffusion of cells throughout a muscle might cause a signiﬁcant problem if genetically abnormal or hyperplastic cells continued their unregulated growth. Intuitively at least, removal of this diffuse process in the case of recurrent disease might be more difﬁcult than using individual pieces of tissue.

Permanent Hypoparathyroidism ● Consequence Severe hypocalcemia. Grade 4 complication ● Repair Treated with high-dose calcium and calcitriol.

● Prevention Cryopreservation of excised parathyroid tissue. Permanent hypoparathyroidism and chronic hypocalcemia can be a debilitating complication of a total parathyroidectomy. If a total parathyroidectomy is performed, cryopreservation provides a safety net should the autograft fail or prove hypofunctional. Cryopreserved tissue will remain viable for a long time, probably years. This can be reimplanted if the need arises, although the need for reimplantation is an admittedly rare event. If cryopreservation is to be performed, all parathyroid tissue should be placed on ice immediately after excision. Any tissue chosen for reimplantation or cryopreservation should be examined by frozen section to ensure correct identiﬁcation. Tissue chosen for cryopreservation must then be placed into medium supplied by the cryopreservation unit and transported to the facility on ice. Most standard pathology laboratories will not be able to perform cryopreservation. Facilities must follow stringent guidelines and comply with federal and state regulations. Many tertiary facilities will have this service on site, but other facilities will likely need to send tissue off-site for cryopreservation. Obviously, procedures must be established well prior to the need for this service. In the author’s experience, the surgeon will have to take the lead in ensuring that cryopreservation is available.

Parathyroidectomy for Genetic Disease Hyperparathyroidism may be part of a genetic syndrome such as familial isolated hyperparathyroidism, MEN 1, MEN 2a, or the hyperparathyroidism–jaw tumor syndrome. Failure of recognition that the syndrome is genetic is the greatest pitfall for the surgeon in dealing with these diseases. A detailed and focused family history including parathyroid, thyroid, adrenal, pituitary, and pancreatic endocrine tumors should be elicited in all patients with hyperparathyroidism. A history of severe peptic ulcer disease should also be investigated. A review of surgery for these familial syndromes has recently been presented.34 For MEN 1, a subtotal parathyroidectomy or total parathyroidectomy with autotransplantation is the procedure of choice because all glands are usually affected. This author prefers a total parathyroidectomy with autotransplantation because persistent or recurrent disease should be more easily treated. Permanent hypoparathyroidism is a concern with this approach, although it has not been a problem in the author’s experience. MEN 2a with known hyperparathyroidism is treated similarly to MEN 1. The hallmark disease for MEN 2a, however, is medullary thyroid cancer, and the surgeon may be faced with a decision about how to handle the parathyroid glands when treating the medullary cancer in a patient who has not manifested any signs of hyperparathyroidism. Genetic testing for the RET gene should be

41 PARATHYROID SURGERY done and a detailed family history obtained. Certain mutations in RET that cause MEN 2a, such as C634, have a higher risk than others to cause hyperparathyroidism. If the family history is strong and gene sequencing reveals a mutation known to cause hyperparathyroidism, more aggressive treatment of the parathyroids is indicated. This may include removal of normal-appearing glands and autotransplantation in some cases. If the family history is not deﬁnitive, however, the surgeon may proceed with thyroidectomy to treat the medullary cancer and inspect the parathyroids. Abnormal parathyroids should certainly be removed, and a rational argument could be made to proceed with total parathyroidectomy and autotransplantation. If all parathyroids appear normal at thyroidectomy, most surgeons would leave them in situ, although some may opt, at least in certain circumstances, to proceed with parathyroidectomy on at least one side of the neck. If the parathyroids are left in situ, they should be marked with polypropylene suture and clips for future identiﬁcation. Familial isolated hyperparathyroidism may cause solitary adenomas or multigland disease, and treatment should probably be the same as for isolated hyperparathyroidism. The hyperparathyroid–jaw tumor syndrome is a rare cause of hyperparathyroidism. This syndrome has a high risk of parathyroid cancer, which the surgeon must take into account when planning the operation.

Parathyroid Cancer Parathyroid cancer is rare and probably accounts for less than 0.5% of cases of hyperparathyroidism. Failure to recognize parathyroid cancer in a patient with hyperparathyroidism is a signiﬁcant pitfall for the surgeon. Patients who present with sudden onset, more severe disease, and aggressive renal symptoms should be suspected of parathyroid cancer. Calcium and PTH levels tend to be much higher than those in most patients with hyperparathyroidism. A palpable mass at the suspected location of a parathyroid should be considered parathyroid cancer until proved otherwise. An absolute preoperative diagnosis of cancer usually cannot be made by current biopsy techniques. When operating on any patient for hyperparathyroidism, the surgeon should be attuned to signs that the putative adenoma is in fact a cancer. The lesion is usually much ﬁrmer than usual and is frequently adherent to surrounding thyroid or other tissue. It typically has a pale gray to white color rather than the usual reddish-brown appearance of an adenoma. Frozen section may show signs suggestive of cancer, such as ﬁbrous septations or capsular invasion, but is usually not deﬁnitive at conﬁrming a diagnosis of cancer. This tumor is sufﬁciently rare that there are no evidence-based guidelines to guide the extent of resection. If parathyroid cancer is suspected, however,

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most surgeons would recommend a wide excision including the thyroid lobe and any adjacent lymph nodes.

REFERENCES 1. van Heerden JA, Grant CS. Surgical treatment of primary hyperparathyroidism: an institutional perspective. World J Surg 1991;15:688–692. 2. Silverberg SJ, Bilezikian JP. “Incipient” primary hyperparathyroidism: a “forme fruste” of an old disease. J Clin Endocrinol Metab 2003;88:5348–5352. 3. Brown EM. Familial hypocalciuric hypercalcemia and other disorders with resistance to extracellular calcium. Endocrinol Metab Clin North Am 2000;29:503–522. 4. Inabnet WB, Fulla WB, Richard B, et al. Unilateral neck exploration under local anesthesia: the approach of choice for asymptomatic primary hyperparathyroidism. Surgery 1999;126:1004–1009. 5. Lo Gerfo P. Bilateral neck exploration for parathyroidectomy under local anesthesia: a viable technique for patients with coexisting thyroid disease with or without sestamibi scanning. Surgery 1999;126:1011–1014. 6. Gilmour JR. The gross anatomy of the parathyroid glands. J Pathol 1938;46:133–149. 7. Wang C. The anatomic basis of parathyroid surgery. Ann Surg 1976;83:271–275. 8. Tezelman S, Shen W, Shaver JK, et al. Double parathyroid adenomas. Clinical and biochemical characteristics before and after parathyroidectomy. Ann Surg 1993;218:300– 307. 9. Thompson NW, Eckhauser FE, Harness JK. The anatomy of primary hyperparathyroidism. Surgery 1982;92:814– 821. 10. Stratmann SL, Kuhn JA, Bell MS, et al. Comparison of quick parathyroid assay for uniglandular and multiglandular parathyroid disease. Am J Surg 2002;184: 578–581. 11. Arciero CA, Peoples GE, Stojadinovic A, et al. The utility of a rapid parathyroid assay for uniglandular, multiglandular, and recurrent parathyroid disease. Am Surg 2004;70: 588–592. 12. Conzo G, Celsi S, Buffardi R, et al. Total parathyroidectomy with or without autoimplantion in the therapy of secondary hyperparathyroidism. Minerva Chir 2002;57: 309–315. 13. Rothmund M, Wagner PK, Schark C. Subtotal parathyroidectomy versus total parathyroidectomy and autotransplantation in secondary hyperparathyroidism: a randomized trial. World J Surg 1991;15:745–750. 14. Hargrove GM, Pasieka JL, Hanley DA, et al. Short- and long-term outcome of total parathyroidectomy with immediate autografting versus subtotal parathyroidectomy in patients with end-stage renal disease. Am J Nephrol 1999;19:559–564. 15. Van Husen R, Kim LT. Accuracy of surgeon-performed ultrasound in parathyroid localization. World J Surg 2004;28:1122–1126. 16. Milas M, Stephen A, Berber E, et al. Ultrasonography for the endocrine surgeon: a valuable clinical tool that

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enhances diagnostic and therapeutic outcomes. Surgery 2005;138:1193–1200. Solorzano CC, Carneiro-Pla DM, Irvin GL III. Surgeonperformed ultrasonography as the initial and only localizing study in sporadic primary hyperparathyroidism. J Am Coll Surg 2006;202:18–24. Carneiro DM, Irvin GL III. Late parathyroid function after successful parathyroidectomy guided by intraoperative hormone assay (QPTH) compared with the standard bilateral neck exploration. Surgery 2000;128: 925–929. Arici C, Cheah WK, Ituarte PH, et al. Can localization studies be used to direct focused parathyroid operations? Surgery 2001;129:720–729. Clark PB, Case D, Watson NE, et al. Experienced scintigraphers contribute to success of minimally invasive parathyroidectomy by skilled endocrine surgeons. Am Surg 2003;69:478–483. Pappu S, Donovan P, Cheng D, et al. Sestamibi scans are not all created equally. Arch Surg 2005;140:383–386. Athanasoulis T. 11C-methionine PET versus 99mTcsestamibi in the pre-operative localisation of hyperfunctional parathyroid tissue. Eur J Nucl Med Mol Imaging 2005;32:514. Otto D, Boerner AR, Hofmann M, et al. Pre-operative localisation of hyperfunctional parathyroid tissue with 11Cmethionine PET. Eur J Nucl Med Mol Imaging 2004;31:1405–1412. Norman J, Chheda H. Minimally invasive parathyroidectomy facilitated by intraoperative nuclear mapping. Surgery 1997;122:998–1003. Irvin GL III, Solorzano CC, Carneiro DM. Quick intraoperative parathyroid hormone assay: surgical adjunct to allow limited parathyroidectomy, improve success rate,

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Adrenal Surgery Arsalla Islam, MD, William H. Snyder, MD, and Fiemu Nwariaku, MD INTRODUCTION Adrenalectomy is performed primarily for functioning and nonfunctioning tumors of the adrenal glands. Many technical variations have evolved since the ﬁrst description by Thornton in 1899. Laparoscopic adrenalectomy is now the most common type reported in the United States. Originally described by Gagner in 1992,1 laparoscopic adrenalectomy has dramatically reduced the lengths of the hospital stay and of the postoperative recovery. This chapter discusses potential pitfalls associated with adrenalectomy. These misadventures can result from inappropriate or inadequate preoperative evaluation or a lack of technical expertise.

Evaluation of Adrenal Masses Given the large number of available diagnostic tests, a focused and streamlined approach to preoperative testing is necessary to control cost and limit patient anxiety. Two questions are important from a surgical perspective: (1) Is the mass biochemically functional and (2) is it malignant? The detailed biochemical evaluation is beyond the scope of this chapter but has been reviewed previously.1a The clinician must exclude common functioning adrenal tumors such as pheochromocytomas, aldosterone-producing adenomas, and cortisol-producing adenomas. A history of hypertension, unprovoked kaliuresis, palpitations or episodic “spells” associated with resistant hypertension, or unexplained weight gain or bruising is important to determine if the adrenal mass is associated with hormone hypersecretion. However, biochemical testing is the standard method of excluding hypersecretion. This should include 24-hour urinary estimation of catecholamines and their degradation products (metanephrines), cortisol, potassium, and aldosterone. The plasma aldosterone–to–renin ratio is a useful screening tool for primary hyperaldosteronism, whereas the combination of 24-hour urinary free cortisol levels and a dexamethasone suppression test can identify cortisol hypersecretion. The diagnosis of malignancy in an adrenal mass is much more challenging because of the rarity of primary adrenal

cancer,2 the poor speciﬁcity of noninvasive imaging for cancer, and the lack of reliable biomarkers to diagnose adrenal cancer. Radiologic methods such as delayed contrast-enhanced computed tomography (CT) show the most promise in estimating malignancy risk.3,4 Malignant tumors retain intravenous contrast dye for longer periods (e.g., there is less washout) than benign tumors. This approach has a reported sensitivity of 88% and speciﬁcity of 96% for the diagnosis of adenoma.5 Size is also an important factor, and many endocrine surgeons recommend adrenalectomy based on the size of adrenal tumors.6–8 Investigators at a recent NIH consensus conference statement9 determined the risk of malignancy in adrenal masses to be 2% in tumors less than 2 cm, 6% in tumors 2 to 4 cm, and 25% in tumors greater than 4 cm. Based on these factors, we offer the algorithm in Figure 42–1 for the preoperative evaluation of adrenal tumors.

INDICATIONS FOR ADRENALECTOMY As shown in Figure 42–1, we recommend adrenalectomy for biochemically functioning lesions regardless of size and for nonfunctioning tumors larger than 4 cm or those that increase in size during observation. The choice of surgical approach depends on patient-related factors such as prior abdominal surgery, comorbid conditions, and body habitus and on tumor characteristics such as size and invasiveness.

SPECIFIC PITFALLS IN ADRENAL SURGERY Radiologic Pitfalls High-resolution CT and magnetic resonance imaging (MRI) studies can now identify subtle radiologic abnormalities that may mimic adrenal masses. Such ﬁndings occasionally lead to inappropriate abdominal exploration. Common mimics of adrenal tumors include renal tumors, tortuous splenic vessels and pseudoaneurysms, accessory spleens, pancreatic cysts, and gastric tumors. Figures 42–2 to 42–4 show examples of such lesions.

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Asymptomatic Patient with Incidental Adrenal Mass

Biochemical testing Elevated 24 hr UFC, ± Positive low dose dex suppression, size > 4cm Elevated aldo-renin ratio Elevated plasma and/or urinary metanephrines.

+

Adrenalectomy

Interval growth or hyperfunction

− Non-enhanced CT

<10

Surveillance

A

>10H

Delayed enhanced CT or chemical shift MRI

>50% contrast washout (15min) OR signal drop on out-of-phase MRI

<50% contrast washout OR NO signal drop on out-of-

Adrenalectomy

B

Figure 42–1 Algorithm for the preoperative evaluation of adrenal tumors.

Figure 42–3 Varix mimicking adrenal tumor on CT scan.

Figure 42–2 Gastric fundus mass can mimic adrenal tumor on computed tomography (CT) scan.

Figure 42–4 Accessory spleen.

● Consequence Eagerness to perform surgery on such patients without appropriate evaluation can result in unnecessary procedures. ● Prevention Multiphase, thin-section (3–5 mm) CT scan is most useful. Density measurements and examination of the

images by an experienced radiologist can reduce errors in diagnosis. Figures 42–5 and 42–6 show CT images of adrenal long limb variant and metastasis of the adrenal gland, respectively.

Biochemical Pitfalls The full scope of biochemical evaluation of patients with adrenal masses is beyond the scope of this chapter.

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morbidity and death during the surgical treatment of pheochromocytoma. Conversely, inadequate α-adrenergic blockade can result in perioperative cardiovascular morbidity and death. We use selective α1-adrenergic receptor antagonists such as phenoxybenzamine and doxazosin 1 to 3 weeks prior to surgery. This may be supplemented with β-adrenergic blockade for patients who develop tachycardia or cardiac arrhythmia during α-adrenergic blockade. Intravascular volume depletion in patients with pheochromocytoma is the result of persistent vasoconstriction. Therefore, preoperative volume expansion is necessary to avoid profound perioperative hypotension. Cortisol-Secreting Adrenal Tumors

Figure 42–5 Adrenal long limb variant.

Patients with cortisol hypersecretion have a fourfold increased risk of thromboembolic complications compared with the general population.10 Therefore, thrombosis prophylaxis with low-dose heparin and pneumatic leg compression devices is particularly important in these patients. Perioperative steroids may be required to prevent hypotension after unilateral adrenalectomy and deﬁnitely after bilateral resection. Nelson’s syndrome is a complication of bilateral total adrenalectomy for Cushing’s disease. It may occur in up to 30% of such patients and manifests as progressive pituitary enlargement and cutaneous pigmentation from increased adrenocorticotropic hormone (ACTH) hypersecretion. Pituitary irradiation may limit the progression of Nelson’s syndrome in selected patients. Aldosterone-Producing Adenomas

Correction of hypokalemia with oral potassium chloride in patients with Conn’s syndrome is necessary to prevent cardiac arrhythmias during general anesthesia.

Figure 42–6 Adrenal metastasis shown on CT scan.

However, the minimal evaluation should include measurement of plasma aldosterone concentration and renin activity, plasma or 24-hour urinary metanephrines, and 24-hour urinary free cortisol. ● Consequence Unnecessary surgical procedures. Intraoperative hemodynamic instability can be fatal for patients undergoing adrenalectomy for pheochromocytoma who have not undergone appropriate preoperative adrenergic blockade. ● Prevention The use of rigorous criteria to conﬁrm biochemical hyperfunction can reduce errors in diagnosis. Pheochromocytoma

Adequate preoperative adrenergic blockade may be the single most important factor in reducing perioperative

OPERATIVE APPROACHES Operative approaches for open adrenalectomy include the anterior (transperitoneal), ﬂank (extraperitoneal),11–13 posterior (retroperitoneal),14 thoracoabdominal, and transdiaphragmatic approaches. We restrict this discussion to the common approaches including anterior transperitoneal and posterior retroperitoneal operations.

Anterior Transperitoneal Approach Advantages ● Surgeon familiarity with anatomic landmarks. ● Evaluation and surgical therapy of coexisting intraperitoneal diseases. Contraindications and Disadvantages15,16 ● Extensive intra-abdominal adhesions due to prior intraabdominal surgery or infection. ● High potential for bowel injury and postoperative ileus.

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Posterior Retroperitoneal Approach Advantages ● Avoids peritoneal adhesions due to prior intraabdominal surgery or infection. ● Less postoperative ileus and lower risk for bowel injury.

Contraindications and Disadvantages ● Smaller operating space limits manipulation and excision of large tumors. ● Few landmarks for the surgeon. ● Previous renal/perirenal surgery. ● Retroperitoneal ﬁbrosis. ● Severe scoliosis.11,14

Laparoscopic Transperitoneal Adrenalectomy Indications ● Benign tumors, whether or not functional. ● Bilateral adrenal hyperplasia. ● Selected solitary adrenal metastases. Contraindications ● Adrenal tumors more than 10 cm in size.17 ● Adrenal cancers and other malignant adrenal tumors. Advantages ● Fewer wound complications.18,19 ● Decreased hospital stay and postoperative analgesia requirement.19 ● Faster return of normal bowel function.20 ● Decreased transfusion requirements. ● Improved patient comfort and satisfaction and early return to normal daily activities.

Open Transperitoneal Adrenalectomy Indications ● Large tumors (>6–8 cm). ● Malignant tumors, particularly with evidence of invasion. ● Conversion to open procedure during a laparoscopic approach.21 ● Primary or metastatic invasive adrenal malignancies because extensive en-bloc excision and node dissection may be necessary. ● Previous extensive upper abdominal surgery in the area of adrenal dissection (e.g., nephrectomy, partial hepatectomy, or splenectomy). ● Intracranial hypertension (may be exacerbated by CO2 insufﬂation). ● Diaphragmatic hernias. ● Cardiovascular and respiratory diseases that preclude laparoscopic surgery.

Advantages ● Better en-bloc resection and lymphatic clearance for malignant tumors. Disadvantages ● More postoperative ileus compared with laparoscopic approach.

Retroperitoneal Adrenalectomy—Posterior Approach Advantages ● Reduced operative time for bilateral adrenalectomy. ● Fewer wound complications than with the open retroperitoneal approach. Disadvantages ● Limited operative space. ● Poor organ and tissue landmarks. ● Requires speciﬁc experience.

Open Posterior Adrenalectomy Advantages ● Bilateral adrenalectomy without the need to reposition the patient. ● Less postoperative ileus. ● Fewer wound complications. Disadvantages ● Less visualization and control of potential hemorrhage. ● Difﬁcult dissection with larger tumors (>7 cm). ● The adrenal vein is identiﬁed at a later phase in dissection. Therefore, pheochromocytomas are a relative contraindication because early ligation of the adrenal vein may prevent excessive intra-operative hemodynamic instability. ● Subcostal nerve injury.

Thoracoabdominal Adrenalectomy Indications ● Tumors greater than 12 cm. ● Tumors adherent to the diaphragm, liver, and extraadrenal structures. Advantages ● Excellent exposure for large tumors. Disadvantages ● Postoperative pulmonary dysfunction. Division of the diaphragm peripherally, 2 cm from its insertion into the chest wall, may reduce postoperative pulmonary dysfunction. ● Postoperative pain.

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Dissection of inferior pole of adrenal gland and superior pole of kidney Removal of adrenal gland and desufﬂation Closure of trocar sites

Laparoscopic Anterior Transperitoneal Adrenalectomy

Step 7

OPERATIVE STEPS (Table 42–1)

Figure 42–8 shows the positioning for the laparoscopic anterior transperitoneal approach during right adrenalectomy.

Step 1 Step 2 Step 3 Step 4 Step 5 Step 6

Positioning Trocar insertion and CO2 insufﬂation Liver mobilization (spleen and pancreas for left adrenal gland) Dissection of inferior vena cava (IVC) Identiﬁcation and ligation of adrenal vein Dissection of arterial supply (medial) of adrenal gland

Table 42–1 Steps for Laparoscopic Anterior Transperitoneal Adrenalectomy Step

Description

Position of the patient

Full left lateral decubitus position, lower leg ﬂexed, cushion under left ﬂank, table ﬂexed to open the space between the inferior costal margin and the anterior superior iliac spine.

Trocar placement

Usually three or four trocars (one 12 mm and three 5 mm) and a 30° laparoscope are required.

Liver retraction

An atraumatic liver retractor is used to gently retract the liver superiorly and medially.

Mobilization of the liver (spleen and pancreas for left adrenal)

Using electrocautery hook, scissors, or ultrasonic shears, the subhepatic peritoneum is incised lateral to the inferior vena cava. Complete mobilization of the liver to include dissection of the right triangular ligament.

Identiﬁcation of the inferior vena cava and the renal vein

Lateral border of the inferior vena cava is dissected superiorly to the level of the right crus of the diaphragm and can be dissected inferiorly to visualize the renal vein.

Identiﬁcation of the main and accessory adrenal veins

Main adrenal vein is divided between surgical clips. An accessory adrenal vein may be present inferiorly.

Dissection of the arteries

Multiple adrenal arteries supply the adrenal gland from the aorta and the phrenic and renal arteries. These can usually be controlled by electrocautery or with ultrasonic shears.

Extraction of the gland

Attachments between the inferior aspect of the gland and the upper pole of the kidney are dissected. The gland is grasped with an atraumatic grasper and introduced into an extraction bag. The port site may be slightly enlarged depending on the size of the gland. Figure 42–7 shows placement of adrenal gland in an endobag.

Postoperative care

Liquid diet and ambulation on the day of surgery. Discharge home in 1 or 2 days.

Step 8 Step 9

Positioning

Nerve Injuries; Brachial Plexus, Peroneal Nerve Injury ● Consequence Transient or permanent neuropathy with disability. Grade 1/3 complication ● Repair No speciﬁc repair. Physical therapy and rehabilitation may improve function. ● Prevention Padding of all bony prominences, especially the dependent lower extremity. Correct placement of axillary roll

Figure 42–7 Placement of the adrenal gland in an Endobag.

Figure 42–8 Position for the laparoscopic right adrenalectomy— transperitoneal approach.

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prior to laparoscopic adrenalectomy. Avoidance of excessive shoulder stretching. The lower leg is slightly ﬂexed to provide stability and the upper leg extended. A pillow placed between the legs should support the upper leg and prevent stress on the knee joint.

Skeletal Fractures May Occur with Patients with Severe Osteoporosis from Cushing’s Syndrome ● Consequence Inability to ambulate. Grade 4 complication

● Repair Intraoperative repair when possible. Control of bleeding with energy sources (electrocautery, argon beam coagulator) or hemostatic agents. May require open conversion. ● Prevention Careful dissection, leaving a peritoneal ﬂap during splenic or liver dissection.

Dissection of the IVC and Adrenal Vein Vascular Injury (IVC, Renal or Adrenal Vein)

● Repair Open reduction and internal ﬁxation. ● Prevention Padding of all bony prominences and preventing excessive torsion on joints.

Trocar Insertion and CO2 Insufﬂation Figure 42–9 shows port placement from above.

Bowel and Vascular Injuries Grade 3 complication Bowel and vascular injuries during entry into the abdomen may occur during laparoscopic procedures. Their consequences and steps for prevention are detailed in Section I, Chapter 7, Laparoscopic Surgery.

Liver Mobilization (Spleen and Pancreas for Left Adrenal Gland) Solid Organ Injury ● Consequence Bleeding (intraoperative and postoperative). May require open conversion and splenorrhaphy or splenectomy. Pancreatic ﬁstula and intra-abdominal abscess formation. Grade 3 complication

● Consequence Intraoperative bleeding and hypotension. ischemia or infarction with possible renal loss. Grade 3 complication

Renal

● Repair Small tears may be controlled with surgical clips. Larger tears will require open conversion and suture repair. Direct gentle caval compression may be attempted with an endoscopic Kittner dissector during a laparoscopic procedure to control blood loss. Conversion to open adrenalectomy should be performed early if there is difﬁculty maintaining hemostasis. ● Prevention Careful dissection with minimal tension on the adrenal gland or adrenal vein. Clear visualization of the space between the IVC and the right adrenal gland. The right adrenal vein drains directly into the right hepatic vein in 4% of patients.22 An accessory right adrenal vein can also drain into the inferior phrenic vein, and rarely, the main adrenal vein can divide into two branches, each entering the IVC separately.

Identiﬁcation and Ligation of the Adrenal Vein Adrenal Vein Injury ● Consequence Same as for “Vascular Injury (IVC, Renal or Adrenal Vein),” earlier. An example of adrenal hemorrhage from possible adrenal vein injury during adrenal vein sampling is shown in Figure 42–10. Grade 3 complication Figures 42–11 and 42–12 show adrenal vein and its relation to inferior vena cava.

Dissection of the Arterial Supply (Medial) to the Adrenal Gland Bleeding from Adrenal Arteries Figure 42–9 Trochar placement for adrenalectomy–transperitoneal approach.

laparoscopic

right

● Consequence Intraoperative or postoperative hemorrhage. Grade 3 complication

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Figure 42–13 Partial diaphragmatic injury. Figure 42–10 Adrenal hemorrhage.

IVC

● Repair Control of small adrenal arteries can usually be accomplished with surgical clips. The use of a suction irrigator device as a retractor is helpful to keep the operative ﬁeld dry. ● Prevention Careful use of ultrasonic shears or electrocautery to coagulate small arteries prior to dividing them.

Adrenal vein

Injury to the Diaphragm or Stomach (Left Adrenalectomy) Figure 42–11 Adrenal vein going into the inferior vena cava (IVC).

● Consequence Postoperative bleeding. Postoperative abdominal abscess. Gastrocutaneous ﬁstula. Diaphragmatic hernia. Figure 42–13 shows diaphragmatic injury during laparoscopic right adrenalectomy. Grade 3 complication ● Repair Laparoscopic or open suture repair of the stomach or diaphragm. ● Prevention Sharp dissection under direct vision.

Clips on adrenal vein

IVC

Dissection of the Inferior Pole of the Adrenal Gland and the Superior Pole of the Kidney Renal Vascular Injury

Figure 42–12 Clipped adrenal vein—right adrenalectomy.

● Consequence, Repair, and Prevention Similar to those of “Vascular Injury (IVC, Renal or Adrenal Vein),” earlier. Grade 3 complication

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Removal of the Adrenal Gland Hollow Viscus or Solid Organ Injury ● Consequence and Repair Same as for “Bowel and Vascular Injuries,” and “Solid Organ Injury,” under “Liver Mobilization (Spleen and Pancreas for Left Adrenal Gland),” earlier. Grade 3 complication ● Prevention Direct visualization of the bag during extraction from the abdominal cavity will prevent the bowel being pulled up and injured during removal of the adrenal gland.

Closure of Trocar Sites Similar to that for other laparoscopic procedures. Entrapped bowel and postoperative hernias may occur; therefore, closure of trocar sites should be performed under direct vision (laparoscopically or anteriorly).

Open (Right) Anterior Adrenalectomy OPERATIVE STEPS Step Step Step Step Step

1 2 3 4 5

Step 6 Step 7

Entering abdomen Mobilizing liver Dissection of IVC Identiﬁcation and ligation of adrenal vein Dissection of arterial supply (medial) of adrenal gland Dissection of inferior pole of adrenal gland and superior pole of kidney Removal of adrenal gland

Duodenal Injury ● Consequence Duodenal ﬁstula. Abscess formation. Grade 3 complication ● Repair Two-layer suture repair and drainage. ● Prevention Dissecting the IVC cephalad to the duodenum.

Colonic Injury (Hepatic Flexure) ● Consequence, Repair, and Prevention This is rare during right adrenalectomy; however, the consequences and repair are similar to those of “Bowel and Vascular Injuries” under “Laparoscopic Anterior Transperitoneal Adrenalectomy,” earlier. Figures 42–14 and 42–15 show the laparoscopic dissection for a right adrenalectomy. Figure 42–16 shows the mobilization of the liver in an open approach. Grade 3 complication

Open (Left) Anterior Adrenalectomy OPERATIVE STEPS Step Step Step Step

1 2 3 4

Step 5 Step 6

Entering abdomen Entering lesser sac and mobilizing pancreas Identiﬁcation and ligation of adrenal vein Dissection of arterial supply (medial) of adrenal gland Dissection of inferior pole of adrenal gland Removal of adrenal gland

Abdominal Entry Small Bowel Injury

Abdominal Entry

● Consequence, Repair, and Prevention Similar to consequences during “Laparoscopic Anterior Transperitoneal Adrenalectomy,” earlier. In the presence of adhesions, sharp dissection under direct vision may reduce the risk of bowel injury. Grade 3 complication

Bowel Injury

Hepatic Flexure Injury

Entering the Lesser Sac and Mobilizing the Pancreas

● Consequence, Repair, and Prevention Similar to those of “Bowel and Vascular Injuries” under “Laparoscopic Anterior Transperitoneal Adrenalectomy,” earlier. Grade 3 complication

● Consequence, Repair, and Prevention Same as those of “Bowel and Vascular Injuries” under “Laparoscopic Anterior Transperitoneal Adrenalectomy,” earlier. Grade 3 complication

Stomach Injury Same as those of “Bowel and Vascular Injuries” under “Laparoscopic Anterior Transperitoneal Adrenalectomy,” earlier.

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Liver

A

Figure 42–15

Dissection—right adrenalectomy.

Adrenal

Kidney

B

Figure 42–16 adrenalectomy.

Mobilization

of

the

liver

for

a

right

● Prevention Gentle upward retraction of the pancreas with blunt retractors.

Colonic Injury (Splenic Flexure)

C Figure 42–14

Dissection—right adrenalectomy.

● Consequence, Repair, and Prevention Similar to those of “Bowel and Vascular Injuries” under “Laparoscopic Anterior Transperitoneal Adrenalectomy,” earlier. Grade 3 complication

Splenic Injury Pancreatic Injury ● Consequence Pancreatic ﬁstula or abscess. Pancreatitis. Grade 3 complication ● Repair No repair for small injuries. However, larger injuries may require distal pancreatectomy. All injuries should be drained to create a controlled pancreatic ﬁstula.

● Consequence Intraoperative or postoperative hemorrhage requiring splenorrhaphy or splenectomy. Postsplenectomy infection. Grade 4 complication ● Repair Electrocautery, argon beam coagulator, hemostatic agents, splenorrhaphy. or splenectomy.

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● Prevention Sharp dissection of splenocolic and splenophrenic ligaments under direct vision and leaving a ﬂap of peritoneum attached to the spleen during dissection. This ﬂap can be used to retract the spleen without avulsing the splenic capsule.

Step 3 Step 4 Step 5 Step 6 Step 7 Step 8

Retroperitoneal entry Dissection of upper pole of kidney Dissection of arterial supply (medial) of adrenal gland Ligation of adrenal vein Removal of adrenal gland Wound closure

Identiﬁcation and Ligation of the Adrenal Vein Discussed under “Laparoscopic Anterior Transperitoneal Adrenalectomy” under “Dissection of the IVC & Adrenal Vein.”

Patient Positioning Patient is placed prone with arms extended. There is a risk of brachial plexus injury from stretching, especially in prolonged cases.

Dissection of the Arterial Supply (Medial) of the Adrenal Gland

Incision Placement and Muscle Dissection

Injury to thoracic duct or intestinal lymphatics around the left crus may occur.

The classic Young curvilinear (hockey-stick) incision or a 12th rib incision (parallel to the 12th rib) may be used.

Injury to the Lymphatics

Rib Resection and Pleural Reﬂection

● Consequence Chylous ﬁstulas. Grade 3 complication ● Repair Initial therapy is pharmacologic. Etilefrine chlorhydrate is an α-adrenergic agonist that acts on the muscular ﬁbers of the thoracic duct. Patients can also be placed on a medium chain triglyceride diet. Persistent chylous ﬁstulas may require reoperation. ● Prevention Dilated lymphatic connections should be individually ligated.

Dissection of the Inferior Pole of the Adrenal Gland Complications and pitfalls are similar to those of laparoscopic anterior transperitoneal adrenalectomy under “Dissection of the Inferior Pole of the Adrenal Gland and Superior Pole of the Kidney.”

Injury to the Intercostal Blood Vessels and the Subcostal Nerve ● Consequence Intraoperative or postoperative hemorrhage. Retroperitoneal hemorrhage. Postoperative abdominal wall hypesthesia and muscle laxity. Grade 2 complication ● Repair Suture ligation of intercostal blood vessels. No repair for nerve injury. ● Prevention Subperiosteal dissection prior to rib resection ensures that only the rib is resected.

Injury to the Pleura ● Consequence Pneumothorax. Lung injury. Grade 3 complication

Removal of the Adrenal Gland

● Repair Suture repair and thoracostomy tube drainage.

Complications and pitfalls are as discussed under “Removal of the Adrenal Gland” under “Laparoscopic Anterior Transperitoneal Adrenalectomy.”

● Prevention Subperiosteal dissection.

Open Posterior Adrenalectomy OPERATIVE STEPS Step 1 Step 2

Patient positioning Incision placement and muscle dissection

Dissection of the Upper Pole of the Kidney Injury to the Kidney, Hemorrhage ● Consequence Intraoperative or postoperative hemorrhage. Grade 3 complication ● Repair Hemostasis with ligatures and electrocautery.

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Fascial edge

Phrenic vein

Lumbar hernia

Lumbar hernia

Adrenal vein

Figure 42–18 adrenalectomy.

Bilateral lumbar hernias after an open posterior

● Prevention Use of the kidney for retraction and avoidance of excessive traction on the adrenal vein.

Wound Closure Figure 42–17 Left adrenal—dissection showing the conﬂuence of adrenal and phrenic veins.

Lumbar Hernias (Fig. 42–18)

● Prevention Sharp dissection under direct vision.

● Consequence Pain and discomfort. Grade 3 complication

Dissection of the Arterial Supply (Medial) to the Adrenal Gland Complications are similar to those of “Dissection of the Arterial Supply (Medial) to the Adrenal Gland” under “Laparoscopic Anterior Transperitoneal Adrenalectomy,” earlier.

Ligation of the Adrenal Vein

● Repair Operative hernia repair. ● Prevention Multilayer closure with nonabsorbable or delayed absorbable sutures.

Complications are similar to those of “Dissection of the Arterial Supply (Medial) to the Adrenal Gland” under “Laparoscopic Anterior Transperitoneal Adrenalectomy,” earlier.

Retroperitoneoscopic (Posterior) Adrenalectomy

Injury to the Vena Cava or the Renal Vein Figure 42–17 shows the left adrenal vein and the phrenic vein.

OPERATIVE STEPS

● Consequence Intraoperative or postoperative hemorrhage. Renal injury. Grade 3 complication

Step Step Step Step Step

● Repair Suture repair suture.

Step 6 Step 7 Step 8

with

monoﬁlament

nonabsorbable

1 2 3 4 5

Patient positioning Incision placement and muscle dissection Retroperitoneal entry Dissection of upper pole of kidney Dissection of arterial supply (medial) of adrenal gland Ligation of adrenal vein Removal of adrenal gland Wound closure

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Figure 42–19 Stapler for partial adrenalectomy.

The complications of this approach are similar to those that occur after “Open Posterior Adrenalectomy.” However, the incidence of wound complications is lower.23,24 Partial adrenalectomy may be necessary in situations in which preservation of adrenal function is desirable in a patient with no contralateral adrenal gland. The challenge of partial adrenalectomy is parenchymal bleeding and remnant devascularization. However, these can be minimized using careful dissection, bipolar electrocautery, and topical hemostatic agents. Stapling devices can also be used for partial resections (Fig. 42–19).

REFERENCES 1. Gagner M, Lacroix A, Bolte E. Laparoscopic adrenalectomy in Cushing’s syndrome and pheochromocytoma. N Engl J Med 1992;327:1033. 1a. Brunt LM. Current approach to the adrenal incidentaloma. In Problems in General Surgery. Philadelphia: Lippincott, 1984; pp 81–91. 2. Suzuki H. Laparoscopic adrenalectomy for adrenal carcinoma and metastases. Curr Opin Urol 2006;16:47– 53. 3. Caoili EM, Korobkin M, Francis IR, et al. Delayed enhanced CT of lipid-poor adrenal adenomas. AJR Am J Roentgenol 2000;175:1411–1415.

4. Boland GW, Hahn PF, Pena C, et al. Adrenal masses: characterization with delayed contrast-enhanced CT. Radiology 1997;202:693–696. 5. Anca M, Avram LMF, Gross MD. Adrenal gland scintigraphy. Semin Nucl Med 2006;36:212–227. 6. Favia G, Lumachi F, Basso S, et al. Management of incidentally discovered adrenal masses and risk of malignancy. Surgery 2000;128:918–924. 7. Korobkin M, Dunnick NR. Characterization of adrenal masses. AJR Am J Roentgenol 1995;164:643–644. 8. Outwater EK, Siegelman ES, Radecki PD, et al. Distinction between benign and malignant adrenal masses: value of T1-weighted chemical-shift MR imaging. AJR Am J Roentgenol 1995;165:579–583. 9. NIH state-of-the-science statement on management of the clinically inapparent adrenal mass (“incidentaloma”). NIH Consens State Sci Statements 2002;19:1–25. 10. Small M, Lowe GDO, Forbes CD, et al. Thromboembolic complications in Cushing’s syndrome. Clin Endocrinol 1983;19:503–511. 11. Bonjer HJ, Bruning HA. Endoscopic retroperitoneal— ﬂank approach. Oper Tech Gen Surg 2002;4:322–330. 12. Hanssen WE, Kuhry E, Casseres YA, et al. Safety and efﬁcacy of endoscopic retroperitoneal adrenalectomy. Br J Surg 2006;93:715–719. 13. Berends FJ, Harst EVD, Giraudo G, et al. Safe retroperitoneal endoscopic resection of pheochromocytomas. World J Surg 2002;26:527–531. 14. Berber E, Siperstein AE. Laparoscopic retroperitoneal adrenalectomy—posterior approach. Oper Tech Gen Surg 2002;4:331–337. 15. Brunt LM, Doherty GM, Norton JA, et al. Laparoscopic adrenalectomy compared to open adrenalectomy for benign adrenal neoplasms. J Am Coll Surg 1996;183:1–10. 16. Saunders BD, Doherty GM. Laparoscopic adrenalectomy for malignant disease. Lancet Oncol 2004;5:718–726. 17. Shen W, Sturgeon C, Clark OH, et al. Should pheochromocytoma size inﬂuence surgical approach? A comparison of 90 malignant and 60 benign pheochromocytomas. Surgery 2004;136:1129–1136. 18. Gagner M. Laparoscopic adrenalectomy. Surg Clin North Am 1996;76:523–537. 19. Gagner M, Pomp A, Heniford BT, et al. Laparoscopic adrenalectomy: lessons learned from 100 consecutive procedures. Ann Surg 1997;226:238–246; discussion 246–247. 20. Fazeli-Matin S, Gill IS, Hsu THS, et al. Laparoscopic renal and adrenal surgery in obese patients: comparison to open surgery. J Urol 1999;162:665–669. 21. Shen W, Kebebew E, Clark O. Reasons for conversion from laparoscopic to open or hand-assisted adrenalectomy: review of 261 laparoscopic adrenalectomies from 1993 to 2003. World J Surg 2004;28:1176–1179. 22. Proye CAG, Lokey JS. Thoracoabdominal adrenalectomy for malignancy. Oper Tech Gen Surg 2002;4:338–345. 23. Walz MK, Alesina PF, Wenger FA, et al. Laparoscopic and retroperitoneoscopic treatment of pheochromocytomas and retroperitoneal paragangliomas: results of 161 tumors in 126 patients. World J Surg 2006;30:899–908. 24. Walz MK, Petersenn S, Koch JA, et al. Endoscopic treatment of large primary adrenal tumours. Br J Surg 2005;92:719–723.

Section VI

BREAST SURGERY Shawna C. Willey, MD It is on our own failures that we base a new and different and better success. —Havelock Ellis

43

Image-Guided Breast Biopsy Richard E. Fine, MD and Kenneth J. Bloom, MD

INTRODUCTION Increased utilization of mammography screening is believed to have resulted in a relative increase in breast abnormalities of sufﬁcient risk to warrant a biopsy. It is estimated that approximately 1.5 million breast biopsies are performed each year in the United States. Many of these biopsies are for nonpalpable lesions and, therefore, require some type of image guidance. A signiﬁcant number of these biopsies will be performed for benign disease because the average positive predictive value for mammography is only 20% (range 15%–35%).1–4 If traditional methods for histologic conﬁrmation were utilized, all women with nonpalpable breast lesions would proceed to the operating room after a wire localization procedure was performed in the radiology suite. Percutaneous imageguided breast biopsy has become an effective minimally invasive alternative to open surgical breast biopsy for the diagnosis of both palpable and nonpalpable imagedetected abnormalities.5–7 Although the risk of bleeding and infection may be comparable with those of open surgical breast biopsy, some potential difﬁculties are unique to image-guided breast biopsy.8 With the early introduction by the Karalinski Institute in 1989 of stereotactic-guided ﬁne-needle aspiration cytology of nonpalpable breast abnormalities,9 imageguided percutaneous breast biopsy has been shown to provide a secondary level of screening in a less-invasive,

cost-effective manner to obtain a histologic diagnosis without sacriﬁcing accuracy.5–7,10 The evolution of the biopsy tools used with image guidance (stereotaxic, ultrasound, and recently, magnetic resonance imaging [MRI]) has added to the accuracy of minimally invasive imageguided breast biopsy,11,12 keeping a greater portion of women with probably benign disease out of the operating room for a diagnostic procedure. However, advancement in technology has also added to the potential procedural risks.13

INDICATIONS Almost any palpable or nonpalpable, indeterminate breast abnormality, which is visualized with imaging modalities (ultrasound, mammography, MRI), can be evaluated with image-guided breast biopsy. The lesions will fall into the following categories established by the American College of Radiology (ACR) lexicon14: ● BI-RADS 3 (probably benign, short-interval follow-up

[6 mo], <2% risk of malignancy) abnormalities identiﬁed in a patient with a strong family history, difﬁcult clinical and imaging examination, or a high level of anxiety. ● BI-RADS 4 (suspicious abnormality, biopsy should be considered) abnormalities, which require biopsy, may

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avoid a trip to the operating room for an abnormality with perhaps only a 20% risk of malignancy. ● BI-RADS 5 (highly suggestive of malignancy, appropriate action should be taken) abnormalities can provide a histologic diagnosis for preoperative patient consultation.

Stereotactic Breast Biopsy Stereotaxis mammography determines the position of a nonpalpable breast abnormality by utilizing computerized triangulation of the targeted lesion visualized with two stereo images, separated by a 30° arc.5,15 The equipment for performing a stereotactic breast biopsy is either a dedicated prone table or an add-on unit, which utilizes a targeting and biopsy platform attached to a standard upright mammogram system.15,16 Add-on stereotactic breast biopsy units have been traditionally less popular because the upright patient position and patient visualization of the procedure have the potential for producing increased syncopal episodes.5,17 The advantages of the prone position include gravity to assist the technologist with posterior lesions and a greatly enhanced workspace beneath the table.18 Both are important for positioning and access, which limit many of the potential difﬁculties in achieving a successful biopsy.

OPERATIVE STEPS Evaluate mammogram and lesion as well as patient and choose image approach to breast (craniocaudal [CC], mediolateral [ML], lateromedial [LM]) Step 2 Position patient on stereotactic biopsy table for visualization of image-detected abnormality Step 3 Obtain scout and stereotactic digital images Step 4 Target lesion on stereo images Step 5 Anesthetize skin and breast parenchyma and make skin incision after appropriate antiseptic skin preparation Step 6 Insert biopsy device based on calculated coordinates Step 7 Assess appropriate alignment between lesion and biopsy device on prebiopsy and/or postbiopsy alignment stereo digital images Step 8 Adequately sample lesion for diagnosis and/or potential therapeutic removal Step 9 Place postprocedure marker and obtain postprocedure/clip placement stereo images Step 10 Obtain specimen radiograph Step 11 Obtain adequate hemostasis and apply appropriate dressing and/or wrap Step 1

Step 12 Check pathology for concordance with radiologic impression Step 13 Obtain follow-up imaging

OPERATIVE PROCEDURE Evaluating the Mammogram and the Patient and Choosing the Approach to the Breast Choosing an Inappropriate Mammogram Lesion Type for Biopsy ● Consequence It is important to anticipate that some patients and some lesions will be difﬁcult to biopsy. The characteristics of certain lesions (low-density nodules, faint microcalciﬁcations, and vague asymmetrical densities) make them more difﬁcult to visualize with digital imaging despite postprocessing features. Also, when the ﬁeld of view of the breast is limited to a 5 × 5-cm area (the size of the biopsy window in the front compression paddle), the abnormality is not visualized in relation to the remainder of the breast as it is on the mammogram. An asymmetrical density may represent only a summation shadow of overlapping ﬁbroglandular tissue. Loosely clustered calciﬁcations may become more diffuse on stereo images and be impossible to target with any certainty because of varying depth. Grade 2 complication ● Prevention Recognizing these demanding lesions may avoid unnecessary scheduling and the possibility of procedures being canceled. Complete diagnostic workup, including spot compression views and possibly ultrasound for asymmetrical densities and microfocus magniﬁcation for microcalciﬁcation, is essential. A true lateral (90°) view may successfully demonstrate “tea cup” calciﬁcations associated with “milk of calcium,” in which benign calcium deposits layer out within microcysts. It is sometimes prudent to send patients with a complete diagnostic evaluation and a persistent but questionable imaging abnormality to the stereotactic suite ahead of time to see whether the lesion can be successfully visualized.

Failure to Recognize Patient Characteristics that Will Result in an Unsuccessful Stereotactic Breast Biopsy ● Consequence There are also patient characteristics that will interfere with the success of a stereotactic breast biopsy. Patients with neurologic or musculoskeletal conditions may not tolerate positioning on the already-uncomfortable stereotactic biopsy table. Any condition that increases the

43 IMAGE-GUIDED BREAST BIOPSY likelihood of patient movement will cause a greater risk of missing the target lesion. This includes patients with acute or chronic respiratory conditions with associated coughing and patients with a high level of anxiety, especially those suffering from claustrophobia or agoraphobia. A history of bleeding abnormalities or use of anticoagulants, as with any biopsy, creates the potential for bleeding and complications such as hematoma. Grade 2 complication ● Prevention When recognizing the kyphotic patient or those who may not tolerate the table positioning, it is helpful to ask the patient to try lying on the ﬂoor at home, with her head turned to one side for approximately 20 to 30 minutes. Having cough suppressants available will deal with most respiratory conditions. Although most stereotactic breast biopsies are performed with only local anesthesia, it may be helpful to use a diazepam for sedation in those anxious patients. If time allows, schedule the biopsy after 10 days of restriction from anticoagulants working on platelet function and allow for the reversal of warfarin. However, because the patient facing a possible diagnosis of breast cancer may not want to wait 10 days or if reversal of warfarin is medically inadvisable, most procedures can still be accomplished with only marginal risk. Using a smallergauge biopsy device and wrapping the patient with a pressure-style dressing may be helpful.

Not Choosing the Ideal Approach to the Breast ● Consequence The shortest skin-to-lesion distance and the ability to clearly visualize the imaged abnormality are both factors the technologist and physician consider when working together to choose the correct approach (CC, LM, ML, and with the Hologic Multi-Care Platinum table, caudocranial) to the breast. Once the shortest skin-tolesion distance is chosen, the lesion must be well visualized. The visibility of the breast abnormality may occasionally take priority over the shortest distance from the skin to the lesion. Although a lesion in the breast at 12 o’clock may suggest a CC approach, if the lesion is seen better on the patient’s mediolateral oblique (MLO) mammogram view, then an ML approach may be preferable. A situation may arise (on the Fischer Mammotest table) in which the abnormality is best seen in the CC view but the lesion appears to be in the inferior aspect of the breast on the MLO mammogram view. Therefore, it may not be possible to insert the biopsy instrument without traversing most of the breast tissue and striking the back of the patient’s breast (negative stroke margin), because in contrast to the Hologic Multicare Platinum table, the Fischer Mammotest table does not provide a caudocranial approach. Grade 1 complication

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● Repair/Prevention Determining the true position of the lesion within the breast starts with an understanding of the virtual position of the lesion created by the usual 60° MLO mammogram. A lesion that is in the lateral breast appears to be higher on the MLO view than its true position and a medial lesion appears lower on the MLO view than its true position. Therefore, if the patient’s abnormality is visualized best in the CC view, but the lesion is in the medial aspect of the breast, the biopsy using this approach will be successful and may not impale the underside of the breast because the medial lesion is actually more superior in the breast than it is perceived on the MLO mammogram view.

Failure to Recognize the Position of the Lesion in the Breast ● Consequence The technologist may have difﬁculty in locating a lesion for biopsy when positioning the patient on the stereotactic table if the correct position of the lesion in the breast is not appreciated. Grade 1 complication ● Repair Remember that when positioning a patient on a prone stereotactic table for an LM or ML approach that this is a 90° angle to the breast compared with the 60° angle associated with the traditional MLO mammogram view. Therefore, the lesion in the lateral aspect of the breast will “move” to a more inferior position with the LM stereotactic approach compared with its apparent position on the MLO mammogram. A lesion in the medial aspect of the breast will “move” to a more superior position with an ML (90°) stereotactic approach compared with its apparent position on the MLO mammogram.

Failure to Visualize the Lesion on Both Stereo Images ● Consequence When a lesion well visualized on the scout image lacks visibility on both stereo images, another difﬁculty arises, especially when the physician has already considered the shortest skin-to-lesion distance and the clarity of the image on each mammogram view. This is most often due to ﬁbroglandular tissue that superimposes itself over the target lesion in one of the stereo images because of the angle of exposure. Grade 1 complication ● Repair A technique known as target on scout can be utilized to resolve the issue of limited clarity of the lesion on one of two stereotactic images. The stereo image, with poor lesion visibility, is replaced by the original scout image in which the lesion is clearly identiﬁed. The

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targeting is then performed on the one remaining stereo image and the scout image. The software is able to recognize the 15° separation between the two targeted images and then calculate the appropriate coordinates. It is important to maintain all follow-up preﬁre and postﬁre images consistent with the targeting images. On the replaced scout image on the Hologic Multi-Care Platinum table, with the biopsy device in position, it is more difﬁcult to visualize the targeted lesion because of the cartesian targeting platform.

Patient Positioning Failure to Image a Lesion that is Deep against the Pectoral Muscle

Obtain Scout and Stereo Digital Images Acquisition of the ﬁrst digital image is the 0°, scout image. Regardless of the approach to the breast (CC, ML, LM, or caudocranial), this image is taken perpendicular to the compressed breast. Next, the technologist obtains a set of stereo images by rotating the tube head to the +15° and the –15° positions to yield an arc of separation between the two stereo images of 30°.

Not Correctly Positioning the Breast Lesion within the Compression Window

● Consequence The position of certain lesions, including those against the chest wall or in the tail of the breast or axilla, may require innovative positioning by the experienced technologist. Grade 1 complication

● Consequence Failure to position the breast so that the lesion to be biopsied falls within the 5 × 5 cm opening of the compression paddle such that it appears in the middle third of the scout image will result in the lesion being “thrown” outside the visualization/targeting window on one of the two stereo images (Fig. 43–2). Grade 1 complication

● Repair One commonly used positioning technique involves placing the patient’s arm and part of the shoulder through the table aperture with the breast. This allows compression with the paddles of the most posterior aspect of the breast (Fig. 43–1).

● Repair Repositioning the patient and the breast so that the breast abnormality falls within the middle third of the compression paddle–biopsy window should correct the problem. The technologist will frequently recognize and correct this problem.

Failure to Recognize the Depth of a Lesion in the Breast

Figure 43–1 The patient is positioned with her arm through the table aperture so the surgeon can gain access to a posterior lesion.

● Consequence A lesion that is too superﬁcial may interfere with the successful function of certain biopsy devices that may require the sampling portion of the device to be within the skin. A vacuum-assisted biopsy (VAB) device requires maintaining a suction vacuum to pull tissue toward the sampling portion of the device. If the entire sampling portion is not beneath the skin because the lesion is too superﬁcial, the vacuum is unable to maintain enough suction to pull the tissue in for biopsy (Fig. 43–3). The newer large, intact sampling devices utilize radiofrequency-activated tissue cutting and must, therefore, be a certain distance beneath the skin to avoid any inadvertent burns. If a lesion is too deep, insertion of the biopsy device without encroaching on the backside of the breast will be difﬁcult, and a stroke margin problem will be encountered. This is especially true for devices that have a springloaded mechanism to advance the biopsy portion of the device forward into the breast. A stroke margin is the distance from the device tip after advancing forward to the back of the breast. There is a problem when this distance is less than the stroke (forward motion) of the particular device (negative stroke margin) (Fig. 43–4). Grade 1 complication

43 IMAGE-GUIDED BREAST BIOPSY

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Correct positioning Image receptor Scout

Stereo

⫹15

⫺15

Incorrect positioning Image receptor Scout

Stereo

⫹15

⫺15

Figure 43–2 Correct positioning with the lesion in the middle third of the biopsy window. Incorrect positioning will cause the lesion to be taken out of view on one of the stereo images.

Negative Stroke Margin Stroke (mm) Stroke (⬍0) margin

Post-fire

Lesion

Figure 43–3 The back end of the sampling portion of a vacuumassisted biopsy device is shown outside the skin during an attempt to biopsy a superﬁcial lesion.

● Repair The use of skin hooks can retract the skin so the back of the VAB device is covered; thus, there will be adequate suction for biopsy and the skin can be protected from the heat of the radiofrequency-activated large intact sample device (Fig. 43–5). Repositioning the patient for a different approach to the breast may be all that is required (e.g., changing from a CC to an ML or LM approach) to deal with lesions that are determined to be too deep.

Compression thickness

Figure 43–4 A negative stroke margin occurs when the stroke margin is less that the forward motion (stroke) of the biopsy device.

● Prevention The ability to recognize the signiﬁcance of lesion movement from one stereo image to the next can alert the astute physician to the depth (superﬁcial or deep) of the lesion and further predict a problem of a lesion too close to the skin or too deep against the back of the breast or rear image receptor.

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SECTION VI: BREAST SURGERY sary amount of tissue behind the lesion. Using a biopsy device that has a shorter-throw (forward movement of an automated device) or a biopsy tool that has a shorter sample notch can reduce the required breast thickness. Manual insertion of the biopsy instrument (avoiding the automated ﬁring) allows a controlled forward motion of the sampling notch into appropriate position. Use of the lateral arm allows insertion of the biopsy device through the side of the compressed breast, parallel to the compression paddles. Also, use of the double-paddle technique adds an additional buffer between the back of the breast and the back compression paddle.

Figure 43–5 Skin hooks are one method to adjust for potential complications related to the biopsy device and a superﬁcial lesion.

Targeting the Lesion A target is chosen on the abnormality in each of the stereotactic images. The computer software determines the horizontal, parallax shift of the lesion from stereo image number one to stereo image number two. The software then calculates the horizontal, vertical, and depth coordinates. The software can either use the 30° separation of stereo images or substitute the 15° between the stereo and the scout images when using the “target on scout” technique. It may be important to consider the biopsy device type when placing the target on the lesion in each of the stereo images. If the abnormality in the breast is small, the size of certain devices when inserted into the breast may hinder visualization of the lesion. Therefore, placing the targets inferior to the lesion will allow the lesion to appear superior to the biopsy device once it is in position and easily visualized.

A Negative Stroke Margin ● Consequence Once the target information is acquired, whether there will be an adequate stroke margin becomes evident. The stroke margin again is the distance from the postﬁred position of the biopsy probe to the back of the breast or rear-image receptor. A negative stroke margin is encountered when the breast is very thin or the lesion is in a posterior position in the breast. This situation may result in the biopsy needle striking the rear-image receptor and piercing the back of the patient’s breast skin (see Fig. 43–4). Grade 1 complication ● Repair Several methods are available for eliminating the negative stroke margin. Taking a different approach to the breast lesions (e.g., changing from a lateral approach to a medial approach) may actually provide the neces-

● Prevention Small or ptotic breasts create one of the most common difﬁculties in stereotactic breast biopsy. A minimal compression thickness is required to avoid stroke margin problems. This minimal compression thickness varies between biopsy devices. It is important to recognize the patient with these characteristics. Once again, the ability to accurately access the position of the lesion and appropriately position the patient for the correct approach will limit these difﬁculties.

Prepare the Breast: Skin Preparation, Local Anesthesia, and Skin Incision The appropriate level of local anesthesia is crucial to limit patient discomfort and resultant movement. The position of the biopsy device to the calculated horizontal and vertical coordinates determines the entry site into the breast. The physician makes a small skin incision with usually a No. 11 blade scalpel. The incision size may vary from just a few millimeters to slightly greater than 1 cm, depending on the biopsy device and whether the incision is oriented vertically.

Using Local Anesthetic with Epinephrine in the Skin ● Consequence The skin wheal is raised, usually with 1% lidocaine. For stereotactic biopsy, it is important to avoid the use of local anesthesia combined with epinephrine. The constant pressure of the 5 × 5 cm biopsy window (in the compression paddle) on the breast for the entire length of the procedure (sometimes >30–45 min) will cause a decrease in blood ﬂow and result in skin necrosis at the entrance site. Local anesthesia with epinephrine (1 : 100,000) is commonly used with the deeper injection into the breast parenchyma. Grade 1 complication ● Repair The area of necrosis is usually limited to the size of the skin wheal. Local wound care is sufﬁcient and rarely requires surgical excision of the necrotic skin.

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Injecting Too Much Local Anesthetic ● Consequence Too much local anesthetic injected into the biopsy site can also pose potential problems. The injection is not performed in real time as is done with ultrasoundguided procedures and, therefore, can cause inadvertent lesion movement, and faint, noncalciﬁed lesions can become difﬁcult if not impossible to see on additional imaging. Grade 2 complication ● Repair If the injection is too large, a quantity of local anesthetic results in the movement of the lesion such that adequate sampling may be altered; in this situation, it will be necessary to remove the biopsy device from the breast and retarget the lesion. If the lesion is faint and/or noncalciﬁed, correction is more difﬁcult. Occasionally, waiting a few minutes for reabsorption or dilution of the local anesthetic is sufﬁcient. Sometimes, a review of the stereo digital images taken for initial targeting can help judge the correct position of the lesion by comparing the surrounding breast architecture. A last resort would be postponing the procedure and rescheduling. ● Prevention Physicians have employed different techniques for providing the patient with adequate anesthesia and avoiding the difﬁculties outlined. One technique utilizes a skin wheal followed by injection of deep local anesthetic at the four quarters of the clock (12, 3, 6, 9 o’clock positions) positioned at the lateral aspect of the skin wheal. The 1½ inch needle is inserted to the hub and the local anesthetic is injected gently as the needle is withdrawn. This technique disperses the local anesthetic evenly and provides a region of anesthesia where tissue sampling will occur. Another technique involves placing local anesthetic directly at the biopsy site only after a skin wheal has been raised. A spinal needle can be directed with stereotactic guidance to the correct x-, y-, and z-axis (depth) coordinates, and 1 or 2 ml of local anesthetic is directed in a limited fashion to the biopsy site. However, the most accurate prevention starts with recognition of which lesions will be difﬁcult to visualize when larger amounts of local anesthetic are injected (faint asymmetrical densities and microcalciﬁcations). Prior to injecting larger quantities of local anesthetic, deploying a metallic clip in the lesion will eliminate nonvisualization. In addition, allowing injection of deep local anesthesia only after the biopsy device is in position and visually aligned with the target lesion will usually accomplish the goal.

Insertion of the Biopsy Device The physician inserts the biopsy device into the breast to the depth determined by the system software.

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Failure to Recognize Speciﬁc Insertion Depths for Different Devices ● Consequence Certain devices require placement at a depth less than that calculated by the system software. The “pullback” is calculated by the individual manufacturers because of the device mechanics such as the forward motion or throw with the amount of “dead space” at the front of the needle along with the length of the sampling portion of the needle. If the required pullback in depth is ignored for a particular device, the device may be too deep or not aligned correctly with the lesion and adequate tissue sampling will not occur. Grade 1 complication ● Prevention It is crucial not only to be familiar with the biopsy mechanism of the device but also to know the speciﬁcations from the manufacturers for stereotactic targeting, including the pullback depth. The Fischer MammoTest table allows the speciﬁcations for all the biopsy devices physicians will use to be programmed into the system. The Lorad Multi-Care table requires calibration of each device to the system on each patient (z-axis = zero), and the physician manually sets the depth.

Inability to Avoid a Negative Stroke Margin ● Consequence If a negative stroke margin cannot be prevented by changing the positioning or approach to the breast or utilizing any of the other previously discussed options, the negative stroke margin must be recognized and manipulated to prevent injury to the patient or the equipment. Grade 1 complication ● Repair The most commonly employed correction method is pulling back the preﬁre position of the biopsy needle a determined number of millimeters until the calculated stroke margin is adequate. Care must be taken not to pull back the biopsy device to a distance that places the sampling notch or biopsy mechanism too far in front of the lesion such that the lesion will be missed.

Assess Appropriate Alignment between the Lesion and the Biopsy Device on Prebiopsy and/or Postbiopsy Alignment Stereo Digital Images Failure to Recognize Targeting Errors ● Consequence Interpretation of the stereotactic digital images allows the physician to determine whether the breast-imaged abnormality is within the range required by the device for adequate sampling. Correct targeting demonstrates

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Vertical error 12

9

3

6

Probe is above

12

9

3

6

Probe is below

Figure 43–6 Y or vertical axis targeting error: The device is visualized above or below the lesion. The directed sampling is illustrated by the shaded areas on the clock.

symmetrical alignment of the lesion and the biopsy portion of the device in each stereo image. There are three types of targeting errors that can occur: x-, y-, and z-axis targeting errors. X-axis deviation occurs when the lesion is pushed to the right or the left of the biopsy needle. Y-axis errors represent movement of the lesion above or below the needle/probe. Z-axis error occurs when the sampling notch or biopsy mechanism is too proximal or too distal to the depth of the breast abnormality. Grade 1 complication ● Repair Fortunately, most x- and y-axis targeting errors that present a problem with stereotactic needle-core biopsy have a limited effect on the success of a stereotactic biopsy performed with either a VAB or a large-intake sample device because these devices can be directed for speciﬁc sampling (Fig. 43–6). However, if the deviation from the target is signiﬁcant enough to risk a poor biopsy, the lesion must be retargeted. After the device is removed from the breast, it is redirected and inserted with new coordinates. ● Prevention To avoid missing a lesion because of an incorrect depth (z-axis) coordinate caused by forward motion of the lesion because of the “plowing” effect as the biopsy device is inserted; targets can be placed on the lesion in each of the new stereo images and the resultant zaxis depth compared with the original z-axis depth. The

position of the target in each stereo image can also be helpful in preventing lesion movement and improve the probability of being able to easily visualize a very small lesion once the biopsy needle/probe is fully inserted into the breast. By targeting beneath the lesion, some of the plowing effect is dispersed, and because the lesion will be elevated above the device, even a very small lesion will not be hidden and its position will be easily assessed.

Adequately Sample the Lesion for Diagnosis and/or Potential Therapeutic Removal Failure to Choose the Correct Biopsy Device ● Consequence The tools for specimen acquisition have evolved from ﬁne-needle aspiration, automated Tru-Cut core needle, VAB devices to large-intact sampling instruments, and the technologic advancements have closely paralleled the acceptance of image-guided breast biopsy.19 Fineneedle aspiration has long been recognized to have several potential pitfalls. This includes insufﬁcient sampling, as high as 38% in some series, with sensitivity ranges between 68% and 93% and speciﬁcity between 88% and 100%.18,19 Cytology rarely provides a speciﬁc benign diagnosis and cannot distinguish between invasive and in situ carcinoma. The automated Tru-Cut core needle has a lower false-negative rate compared with that of ﬁne-needle aspiration.5–7 Standard use of the 14-gauge needle essentially eliminated the issue of insufﬁcient sampling.

43 IMAGE-GUIDED BREAST BIOPSY Several different gauge needles have been evaluated for Tru-Cut biopsy. The lower rate of insufﬁcient sampling and increased sensitivity, without increased complications, has led to a minimum size of 14-gauge as a standard.5,19 The issue of how many cores are needed was addressed by Dr. Laura Lieberman from Sloan-Kettering in New York.20 In this study, 145 lesions were biopsied: 92 were nodular densities, and 53 were microcalciﬁcations. Five cores with a 14-gauge automated Tru-Cut needle yielded a diagnosis in 99% of biopsies for breast masses. Five cores yielded a diagnosis in only 87% of the microcalciﬁcation cases, and more than six cores yielded a diagnosis in 92% of the cases. The accuracy of needle-core biopsy of microcalciﬁcations came into question. Studies demonstrated upgrading to carcinoma from 48% to 52% of atypical hyperplasia identiﬁed on stereotactic core biopsy.21–23 Not surprisingly, atypical hyperplasia diagnosed at stereotactic core biopsy has become an indication for open biopsy. Grade 2 complication ● Repair The VAB device was developed to satisfy the requirement of increasing the size of the core sample and the contiguous nature of the sampling as a proposed solution to the upgrading issue.24,25 The VAB system was ideal for performing an image-guided biopsy of calciﬁcations under stereotactic guidance. The spring-loaded mechanism to advance the biopsy probe could eliminate the potential z-axis targeting error by rapidly penetrating the tissue and avoiding the plowing effect of pushing the lesion forward. But the ability to manually insert the device without having to utilize the ﬁring mechanism could help deal with the small breast and potential stroke margin issues. The vacuum applied to the sampling portion of the device eliminates the pinpoint accuracy required with automated Tru-Cut biopsy needles by pulling the lesion toward the sampling chamber, and the ability of the VAB sampling to be directional is helpful in dealing successfully with mild x-axis and y-axis targeting errors.18,24 The improved accuracy with the directional VAB device lowered the upgrading of diagnosis compared with that of needlecore biopsy technology.11,12

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large intact sample devices. Fortunately, the vacuum associated with these devices will continue to pull blood from the biopsy site and allow the inherent biopsy mechanism the opportunity to continue to obtain tissue samples. Therefore, from personal experience, the most important step in dealing with bleeding during a stereotactic breast biopsy is to continue to take core samples with appropriate rapidity. The injection of additional local anesthesia with 1 : 100,000 epinephrine can be helpful. ● Prevention During the imaging phase of the procedure, it should be determined whether there are vessels near the lesion that may be in the pathway of the biopsy device. This is accomplished by placing a target on the vessel in each stereo image to check whether the depth is the same as the lesion. If the lesion and the vessel are at the same depth, the patient should be repositioned to try to manipulate the breast so the approach to the lesion avoids the vessel.

Place a Postprocedure Marker and Obtain Postprocedure/Clip Placement Stereo Images Postprocedure digital images are required to document removal of the microcalciﬁcations and, at the same time, to verify the presence of residual calciﬁcations. If the postprocedure images are taken after clip placement, it is important to verify accurate and successful clip deployment. In addition, accuracy is improved when calciﬁcations are documented within the core samples on a digital specimen radiograph.26,27 Even in open biopsy surgical literature, pathologic assessment has identiﬁed atypical hyperplasia and ductal carcinoma in situ (DCIS) at a “distance” from the targeted calciﬁcations.28

Clip Placement and Migration

● Consequence During the course of any image-guided breast biopsy procedure, bleeding can occur. An excessive amount of intraprocedural bleeding can potentially interfere with sampling and, as a result, an accurate biopsy. Grade 2 complication

● Consequence At the conclusion of a stereotactic breast biopsy, the placement of a marker has become standard. The marker has two purposes. The ﬁrst and foremost is to be able to localize a stereotactic biopsy site when all image evidence of the target lesion has been removed, and second, to track the site on future mammograms. The initial clip (Micromark; Ethicon Endosurgery) was developed as an adjunct to the Mammotome VAB device to mark the complete removal of calciﬁcations where pathology resulted in the need for follow-up surgery.29 Clip migration was a reported event.30 The result would be a failure to accurately localize a biopsy site. Grade 1 complication

● Repair When performing a stereotactic breast biopsy, the most common biopsy devices used include VAB devices and

● Prevention The prevention of clip migration involved careful technique, including pulling the device back to position the

Failure to Appropriately Manage Intraprocedural Bleeding

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ramping up of the clip into the center of the biopsy cavity, applying active suction to pull the tissue in the breast toward the clip applier, and rotating and closing the device away from the clip position (to avoid accidental removal). Postprocedure mammograms could accurately ensure good clip placement. The issue of clip migration has also been avoided by the use of clips or markers that do not require attachment to the breast tissue. The newer markers include a metallic component along with an absorbable component such as Vicryl or collagen that can be visualized by ultrasound. These newer markers are simply deposited into the biopsy cavity. As the biopsy site heals, the cavity contracts and the clip is trapped at the biopsy site.

Obtain a Specimen Radiograph Postprocedure digital images and specimen radiographs of calciﬁcations and the relationship to diagnostic upgrading have been addressed earlier. Additional sampling to remove a greater portion of the targeted lesion can easily be accomplished if inadequate calciﬁcations are visualized on postprocedure images.

Obtain Adequate Hemostasis and Apply Appropriate Dressing and/or Wrap Techniques to avoid hematomas are discussed in the section on “Image-Guided Breast Biopsy with Ultrasound Guidance,” later.

Check Pathology for Concordance with Radiologic Impression This topic is addressed in the section on “Pathologic Pitfalls in Image-Guided Breast Biopsy,” later.

Image-Guided Breast Biopsy with Ultrasound Guidance

Adequately sample lesion for diagnosis and/or potential therapeutic removal Step 8 Place postprocedure marker and obtain postprocedure/clip placement mammogram Step 9 Obtain adequate hemostasis and apply appropriate dressing and/or wrap Step 10 Check pathology for concordance with radiologic impression Step 11 Obtain follow-up imaging Step 7

Evaluate the Ultrasound Failure to Recognize a Possible Cystic Lesion ● Consequence The ultrasound characteristics of a complex cyst frequently mimic those of a solid lesion. If the complex cystic lesion is not recognized and the physician moves forward with an image-guided biopsy of a presumed solid lesion, the physician may waste a more costly disposable biopsy device instead of a simple syringe or a needle that would be adequate for a cyst aspiration. By evaluating the ultrasound images and appreciating the depth (superﬁcial or deep) of the lesion or its relationship to an implant, the patient can be better positioned (see the section on “Position the Patient and Equipment [Ultrasound and Biopsy System], later) and the optimal biopsy device chosen. To be discussed further in the section on “Sample the Lesion for Diagnosis and/or Potential Therapeutic Removal,” later, certain biopsy instruments are more ideally suited for a very deep or very superﬁcial lesion. Grade 1 complication ● Prevention Careful evaluation of the diagnostic ultrasound performed at an outside institution can sometimes eliminate the unnecessary wasting of an expensive disposable biopsy tool for a lesion that may actually turn out not to be solid and can be aspirated. Any suggestion of posterior enhancement or other characteristics of a possible complex cyst should ﬁrst lead to an attempt at aspiration, even with a larger-gauge needle. Occasionally, duct ectasia may be associated with cystic ﬂuid that requires a needle as large as 14-gauge to aspirate the contents.

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5 Step 6

Evaluate ultrasound Position patient and equipment (ultrasound and biopsy system) Identify lesion with ultrasound and optimize image Anesthetize skin and make skin incision after appropriate antiseptic skin preparation Insert biopsy device Conﬁrmation scan for alignment of lesion with biopsy device

Position the Patient and Equipment (Ultrasound and Biopsy System) Poor Positioning of the Patient and Equipment ● Consequence/Prevention Regardless of the imaging modality, the most signiﬁcant error in image-guided breast biopsy is of course missing the lesion or a failure to accurately sample the breast abnormality and providing the patient a false sense of security. With ultrasound intervention, the ability to perform a successful procedure starts with

43 IMAGE-GUIDED BREAST BIOPSY comfort for the patient and the physician. Positioning of the physician, the patient, and the ultrasound equipment will greatly facilitate the required alignment of the biopsy device with the lesion. Standing opposite to the ultrasound unit will eliminate the physician from turning his or her head away from the biopsy ﬁeld to see the ultrasound monitor. The optimal setup to provide the best visualization of the advancing biopsy device is a straight line between the physician’s vision and the physician’s arm down the length of the biopsy device, along the long axis of the ultrasound transducer, and up to the ultrasound monitor. Grade 1 complication

Identify the Lesion with Ultrasound and Optimize the Image Inappropriate Gain and Focal Zone Setting ● Consequence/Repair Optimal scanning is achieved by adjusting the time gain compensation slope to provide a uniform gray scale. An altered overall gain setting may change the appearance of the internal echo pattern and limit the ability to distinguish solid from cystic lesions. To achieve the optimal lateral resolution, the sonographer must align the focal zone with the target lesion as illustrated in Figure 43–7. This will better demonstrate the retrotumoral characteristics such as posterior enhancement. Grade 1 complication

Poor Optimization of the Lesion Position for Biopsy ● Consequence If the ultrasound transducer is not positioned so that the greatest diameter of the lesion is within the ultrasound plane, the needle-core biopsy device may miss the lesion by veering off the edge of a solid mass. If the lesion is not positioned correctly on the ultrasound

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monitor, the shortest skin-to-lesion distance will not be achieved. Grade 2 complication ● Prevention Two scanning techniques are crucial for identifying the area of greatest lesion diameter and positioning the lesion on the ultrasound monitor to limit the skin-tolesion distance. Movement of the transducer perpendicular to the long axis of the transducer allows the scanner to visualize the lesion from end to end and ﬁnd the widest portion of the lesion. Sliding the transducer in the direction parallel with the long axis will change the position of the lesion on the ultrasound monitor.

Prepare the Breast: Skin Preparation, Local Anesthesia, and Skin Incision Failure to Judiciously Administer Local Anesthetic ● Consequence Too much local anesthetic injected into the breast parenchyma carries the risk of the inability to visualize a smaller target lesion. In addition, the injection of too much local anesthetic in one area can create a false lesion that mimics a cyst. This can be especially frustrating when the target lesion is cystic. Grade 2 complication ● Repair If the visibility of the target lesion has been hindered by the local anesthetic administration, few alternatives are available to continue the biopsy. A very skilled sonographer could use an aspiration needle to aspirate any collections of local anesthetic that are interfering with the biopsy. However, the usual course of action would be to wait until the local anesthetic has been reabsorbed. Attempting to perform the biopsy without optimal visualization of the lesion could result only in

Figure 43–7 Alternating the focal zone, as seen with this breast phantom, will alter the lateral resolution. The ideal lateral resolution occurs when the focal zone is aligned with the target.

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an inadequate sampling of the lesion and a diagnosis that may falsely reassure the patient. ● Prevention After a sterile or “clean” preparation of the skin and the ultrasound transducer, local anesthetic (usually 1% lidocaine) is injected at the proximal end of the ultrasound transducer. Once a skin wheal is made, intraparenchymal injection of local anesthetic is performed under direct ultrasound visualization. By monitoring the injection with ultrasound, adequate anesthesia is obtained without compromising visibility. The technique of injection under direct visualization is discussed further with prevention of inadvertent biopsy of the skin and prevention of pneumothorax below.

Insert the Biopsy Device Failure to Visualize the Advancing Biopsy Device Tip ● Consequence Pneumothorax, hemothorax, and biopsy of pectoral muscle (with associated increased bleeding and pain) are among the potential problems associated with the inability to conﬁrm the position of the advancing biopsy device. Grade 2 complication ● Repair The details of treatment of a rare pneumothorax or hemothorax, and the placement and management of chest tubes are not discussed in this section. Management of “Bleeding and Hematoma” are discussed later. ● Prevention To avoid potential advancement of the device into the pectoral muscle or lung, multiple issues are addressed. The key to visualizing the advancing tip of any device resides in both maintaining alignment of the device with the ultrasound scan plane and keeping the advancing device as parallel with the face of the ultrasound transducer as possible. To achieve parallel positioning with the transducer, regardless of the lesion depth, will require that the patient be positioned in lateral decubitus with a pillow behind the shoulder. In addition, the ultrasound transducer can be gently tilted into the breast away from the advancing device. Local anesthesia can also be injected under direct ultrasound visualization; by directing the needle beneath the lesion, it can be raised off or away from the pectoral muscle. Another way to avoid inadvertent pneumothorax is to use a nonﬁring device. The VAB as well as the large intact sample devices are positioned below a lesion without a spring-loaded ﬁring mechanism and the acquisition of tissue is directed superiorly.

Conﬁrmation Scans for Alignment of the Lesion with the Biopsy Device Failure to Align the Lesion with the Biopsy Device ● Consequence Failure to conﬁrm with ultrasound imaging that the biopsy device tip or its sampling area is aligned correctly with the lesion will of course lead to inadequate biopsy of the lesion and potentially falsely reassuring a patient of a benign diagnosis. Grade 2 complication ● Prevention To avoid missing signiﬁcant portions of the lesion with ultrasound-guided needle core biopsy, by the forward movement of the inner and outer cannula, the needle tip is brought just to the front edge of the lesion and does not penetrate into the lesion prior to ﬁring. When performing a needle-core biopsy, in which it is crucial to know whether the needle has penetrated the lesion, a conﬁrmation scan is needed to avoid a false image created by the overlap of the narrow ultrasound scan plane with the needle just at the edge of the lesion (image averaging). The physician may view the ultrasound image and interpret it as a successful biopsy although the needle has not actually penetrated the lesion (Fig. 43–8). By moving the ultrasound transducer perpendicular to its long axis, the lesion can be visualized from one end through its middle to the other end of the lesion. It is necessary to see a portion of the lesion without the needle, followed by the needle with the lesion, and then continuing the scan in the same direction to again visualize the lesion without the needle. This will conﬁrm that the needle is in the lesion. The success of ultrasound-guided VAB or large intact biopsy is enhanced by careful attention to the technical aspect of the procedure. Patient positioning (lateral decubitus), injection of local anesthetic posterior to the lesion for a lifting effect, and torquing down of the biopsy device handle as the probe approaches the underside of the lesion all serve to provide a shallow angle of insertion and easier access underneath the lesion, especially when the lesion is deep within the breast parenchyma. When the biopsy device is in position for a biopsy, ensuring an adequate sampling requires a conﬁrmation scan to assess the relationship of the device and the lesion. VAB devices and one of the large intact sample devices (Rubicor Medical, Halo, Redwood City, CA) are positioned below the lesion. If these are not positioned beneath the breast target lesion, the artifact created by the device would eliminate visualization of any portion of the lesion below the biopsy probe. To conﬁrm that the device is centered beneath the lesion, the ultrasound transducer is rotated 90°. The device is then visualized in crosssection, and it becomes obvious whether it is centered underneath the lesion, also seen in cross-section.

43 IMAGE-GUIDED BREAST BIOPSY

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Figure 43–8 When the biopsy needle and the edge of a lesion are both within the ultrasound scan plane, image averaging occurs and creates the perception that the needle is in the lesion.

Sample the Lesion for Diagnosis and/or Potential Therapeutic Removal Failure to Choose the Appropriate Biopsy Device for Ideal Sampling ● Consequence Cytologic or histologic conﬁrmation of malignancy is the minimum requirement for ultrasound-guided biopsy of “indeterminate” or suspicious solid lesions. Fine-needle aspiration biopsy is a quick, inexpensive technique to delineate benign from malignant solid breast masses. However, the same issues surrounding the use of ﬁne-needle aspiration in stereotactic imageguided breast biopsy apply to ultrasound-guided procedures. Grade 2 complication ● Prevention Ultrasound ﬁne-needle aspiration is ideally suited to evaluate lesions in areas such as the axilla where more invasive biopsy devices may be difﬁcult or dangerous. The diagnosis of lymph node metastasis by ﬁne-needle aspiration can assist with preoperative staging in consideration of neoadjuvant chemotherapy or eliminating sentinel lymph node biopsy by conﬁrming positive cytology in clinically suspicious lymph nodes. The use of automated Tru-Cut needle-core biopsy eliminates the same problems with ﬁne-needle aspiration that are seen with stereotactic breast biopsy such as insufﬁcient sampling and the inability to provide the histologic type and grade of a diagnosed cancer. VAB and large intact sample technology are also available with ultrasound guidance. The indications for an ultrasound-guided VAB are similar to those for needlecore biopsy, including any indeterminate, ultrasoundvisible, palpable or nonpalpable solid masses. If the physician is interested in the potential therapy of probably benign breast abnormalities, VAB devices or large intact sampling devices would be required. Both of these device categories have successfully demonstrated their ability to

Figure 43–9 A postprocedure hematoma after a vacuum-assisted biopsy. No surgical intervention was required.

remove image evidence and especially palpability of probably benign solid masses.31

Place a Postprocedure Marker and Obtain Postprocedure/Clip Placement Mammogram Clip placement and potential pitfalls have been addressed previously.

Obtain Adequate Hemostasis and Apply Appropriate Dressing and/or Wrap Bleeding and Hematoma ● Consequence The incidence of hematoma with image-guided breast biopsy is reported to be 2% to 8% (Fig. 43–9). It is extremely rare for bleeding or hematoma to result in any post–image-guided surgical procedures. This author’s experience is that no patient has required operative intervention. Bruising and small hematoma

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formation are common, especially near the biopsy insertion site. The size of the hematoma will, of course, contribute to the level of pain and discomfort. Grade 1 complication ● Prevention/Repair Manual compression is the mainstay for achieving hemostasis in image-guided breast biopsy and preventing hematomas. It is important for the pressure to be applied across the biopsy track created by the device. When a VAB or large intact sample device has been used to remove the image evidence of the lesion, a larger biopsy cavity is created and there is a greater risk of bleeding/hematoma. It is important that the manual pressure and the pressure dressing, in particular, be applied to the site of the lesion and not only at the incision. Prevention of a hematoma can also be inﬂuenced by placing the patient in a chest wrap. Conservative management with ice and pressure wraps is sufﬁcient.

Check Pathology for Concordance with Radiologic Impression This topic is addressed in the section on “Pathologic Pitfalls in Image-Guided Breast Biopsy.”

PATHOLOGIC PITFALLS IN IMAGE-GUIDED BREAST BIOPSY Not Performing a Further Procedure with a Diagnosis of Benign Papillary Lesion on Core Biopsy ● Consequence The pathologist is confronted with the following decision points when presented with a papillary lesion: 1. Distinguishing benign, atypical, and malignant papillary lesions with limited material. 2. Establishing a diagnosis with the realization that the sample may not contain the most worrisome histology present in the lesion. 3. Distinguishing invasive carcinoma from a fragmented and distorted sclerosing papillary lesion. Papillary lesions of the breast can be divided into benign and malignant categories. Benign lesions include solitary intraductal papilloma, multiple papillomas, and atypical hyperplasia within a papilloma. If a diagnosis of atypia is mentioned, further surgical excision needs to be performed. What is less clear is whether or not complete surgical excision is required for a diagnosis of benign intraductal papilloma. Solitary intraductal papilloma usually presents as a well-deﬁned mass, whereas multiple intraductal papillomas typically present as a nodular mass or with microcalciﬁcations.32 In both instances, a cystic component may be identiﬁed on ultrasound examination.

The signiﬁcance of either diagnosis is an increased risk of developing breast cancer. Based on a review of 372 solitary papillomas and 41 multiple papillomas published from the Mayo clinic, there is an approximately twofold increased risk in the case of solitary papilloma and a threefold increase in the case of multiple papillomas.33 Atypia, when present, is more often associated with multiple papillomas than with solitary central papillomas.34 The atypia in papillary lesions is frequently unevenly distributed and is usually present in less than 50% of the papilloma.35 The relative risk of developing carcinoma when atypia is present versus when atypia is not identiﬁed is a 7.5-fold increase.36 In addition, that risk is in the ipsilateral breast as opposed to a more generalized risk associated with atypical intraductal hyperplasia (AIDH). Studies have demonstrated the presence of atypia and/ or malignancy in 0% to 44% of excision specimens when a diagnosis of benign papillary lesion is rendered on a core biopsy.37–46 In general, a relationship exists between the presence of atypia and/or malignancy in excisional specimens and the amount of residual lesion remaining after core biopsy. This is not surprising given the focal nature of atypia, when present. Because of the possibility of missing the most worrisome histology and the fact that papilloma with atypia is a precursor lesion, most experts recommend complete radiographic excision of the imaging abnormality if a diagnosis of benign papillary lesion is rendered by the pathologist. When sclerosing papillary lesions are removed in small fragments, they can be difﬁcult to distinguish from radial sclerosing lesions and invasive carcinomas. The sclerosis can entrap benign epithelial elements, simulating an invasive carcinoma. The use of immunostains can effectively demonstrate the presence or absence of a myoepithelial cell layer to aid in the differential diagnosis of an invasive cancer but cannot help to distinguish a radial sclerosing lesion. It should be noted, however, that most malignant papillary lesions behave in a relatively indolent manner.47 Whereas they occasionally metastasize to lymph nodes, distant metastasis is rare. ● Prevention Complete removal of the imaging abnormality should be performed.41,42,45,46,48 The biopsy device chosen by the surgeon may dictate further procedures. For example, if a lesion, highly suspicious for a papilloma, is sampled with a 14-gauge spring-loaded biopsy device, a second procedure will need to be performed even if a diagnosis of a benign papillary lesion is rendered. Limited sampling of a papillary lesion may miss atypia, which is usually present only focally, and atypia is believed to be a precursor lesion. Therefore, when the probability of a papillary lesion, such as a welldeﬁned subareolar mass, is high, a large-core biopsy device or whole intact excisional biopsy device should be used.

43 IMAGE-GUIDED BREAST BIOPSY

Figure 43–10 Low-power hematoxylin and eosin (H&E) microscopic image of a completely resected intraductal papilloma. The biopsy was obtained using a whole intact biopsy device, preserving the architecture and eliminating the need for further surgery.

A second factor in selecting a biopsy device is preservation of tissue architecture. Biopsy devices can be thought of as providing puzzle pieces to the pathologist. The larger the pieces, the less the architecture is distorted and the easier it is for a pathologist to establish a diagnosis. In addition to deciding how much tissue should be sampled, the radiologist or surgeon must also decide whether to remove the lesion in one piece (whole intact), to optimally preserve the architecture, or in pieces. If the lesion is to be sampled in pieces, the size of the pieces must be determined. Because architecture is critical in differentiating a sclerosing papillary lesion from other lesions, larger pieces allow the pathologist to obtain a better overall assessment of the architecture. Removing all imaging evidence of a potential papillary lesion will greatly reduce the need for further surgery if a diagnosis of benign papillary lesion is rendered (Fig. 43–10).

Obtaining a HER-2 Result on a Core Biopsy Specimen ● Consequence HER-2 is an oncogenic protein that may be overexpressed in up to 20% of high- and intermediate-grade invasive breast carcinomas. It is rarely overexpressed in low-grade ductal or classic invasive lobular carcinomas.49 Patients with HER-2 overexpression beneﬁt from targeted anti–HER-2 therapies, such as trastuzumab, in both the adjuvant and the metastatic settings.50–52 The assessment of HER-2 overexpression is most commonly performed by immunohistochemistry, and patients whose tumor cells show 3+ overexpression have the greatest likelihood of response to anti–HER-2 therapy.

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The ability of a pathologist to accurately assess a HER2 immunostain can be compromised by four major artifacts: tissue crush, tissue retraction, thermal injury, and edge artifact. These artifacts can cause the HER-2 antibody to diffuse unevenly, causing the tumor cells in the area of artifact to see a higher concentration of antibody than expected. Tissue crush is caused when a thin needle is forced into tissue and the cells along the edge are crushed. The cytoplasm becomes streamed and distorted. Tissue retraction is deﬁned as the separation of breast epithelial cells, benign or malignant, from stromal elements, creating a cleftlike space. The use of VAB devices can accentuate this artifact, but it may also occur as part of routine tissue processing. Thermal injury is caused by the use of cautery. It causes the cells to take on a windswept appearance and increases nuclear chromasia. Edge artifact is seen in all tissues and is caused by antibody pooling along the edge of a specimen, affecting tissue located within 1 mm of the edge. Thus, a core biopsy measuring 2 mm in diameter is mostly edge artifact, with the exception of the exact middle of the core. Core biopsies with a small diameter, such as a 14-gauge springloaded core, are virtually all edge artifact. Fluorescence in situ hybridization (FISH) is a method that allows detection of the HER-2 gene.53 The technique involves exposing the tumor nuclei via digestion of the cell membrane and cytoplasm, heating the DNA until it uncoils, ﬂooding the sample with a ﬂuorescently tagged complementary sequence to the HER-2 gene, and then cooling the DNA allowing it to recoil with the HER-2 gene now ﬂuorescently tagged. The number of HER-2 genes in each tumor nucleus can then be enumerated. Because two HER-2 genes are present in all normal cells, one from mom and one from dad, it is essential that only tumor nuclei be assessed. The key to counting only the tumor nuclei is preservation of tissue architecture. It has been noted that approximately 18% of breast tumors scored as 3+ by HER-2 immunohistochemistry and 12% of breast tumors assessed as having gene ampliﬁcation do not show overexpression or gene ampliﬁcation when repeated in a central reference laboratory.54,55 This high rate of error has resulted in the American Society of Clinical Oncology (ASCO) and the College of American Pathologists (CAP) issuing joint guidelines in an effort to improve HER-2 assessment in breast cancer.56 ● Prevention The artifacts caused by core biopsy all lead to potential overstaining by immunohistochemistry. Thus, tumors assessed as 3+ may be truly 3+ or may be falsely positive as a result of an artifact. If the diameter of the biopsy core is less than 2 mm, cores assessed as 3+ should be conﬁrmed with FISH testing or be repeated on the lumpectomy specimen, because the majority of the core is edge artifact. Even if large-core biopsy devices are used, care must be taken to avoid scoring artifacts because these will still be present in the biopsy.

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Figure 43–11 Low-power HER-2 immunostained slide shows apparent strong expression of the protein. However, the staining cannot be clearly visualized on the membrane and is the result of both edge and crush artifact typical of a core biopsy specimen.

Before relying on the results of a FISH test, you must be assured that the correct cells were examined. Because only tumors can show ampliﬁcation of the HER-2 gene, if gene ampliﬁcation is detected, tumor cells must have been examined. The only possibility for error is if in situ and invasive carcinoma are both present and only the in situ carcinoma shows ampliﬁcation of the HER-2 gene. Although this does occur, it is unusual. More problematic is when FISH testing does not show ampliﬁcation of the HER-2 gene. In this circumstance, one must always question whether tumor cells were observed. It can be difﬁcult to distinguish tumor cells from normal cells on ﬂuorescence microscopy, especially when the tumor is limited and intermixed with benign pathology such as adenosis. The pathologist relies on architecture and comparison with an adjacent hematoxylin and eosin (H&E)–stained section to select the tumor cells. As a general rule, if the pathologist is struggling to establish the diagnosis on the H&E slide, it will be difﬁcult to identify the tumor cells by ﬂuorescence. The larger the core biopsy, the better the preservation of tissue architecture, and the more reliable the FISH result (Fig. 43–11).

Not Obtaining an Estrogen Receptor Immunostain on a Core Biopsy Specimen ● Consequence The determination of estrogen receptor (ER) should be performed on all breast carcinomas. The accurate determination of ER status is largely dependent on the amount of tumor assessed, tissue ﬁxation, and the assay used. Currently, ER status is usually assessed by immunohistochemistry. Unlike HER-2, which is a membrane protein, ER is a nuclear stain and is not affected by the artifacts such as edge artifact, tissue crush, tissue retraction, or cautery artifact.

Studies have shown that ER status is an excellent predictor of response to antiestrogen therapy.57,58 The initial studies were performed by ligand-binding assay. This assay requires a large amount of fresh tissue, which is ground up and assessed quantitatively. Assessment of ER on formalin-ﬁxed parafﬁn-embedded tissue was found to be even more predictive of response to antiestrogen therapy when using a speciﬁc immunohistochemical assay with a speciﬁc scoring system.58 This is not surprising because the tissue included in the ligand-binding assay usually included a mixture of tumor cells, stroma, and often, benign breast epithelial cells. Unfortunately, in current practice, many different immunohistochemical assays and scoring systems are used to assess ER status, leading to signiﬁcant errors in ER testing results. These errors can be broken down into several problems including tissue ﬁxation, tissue processing, antigen retrieval methods, antibody clones, amount of tissue assessed, scoring system, and cutoff levels. With respect to core biopsies, tissue ﬁxation and the amount of tissue examined are of most concern. ER determination is greatly affected by tissue ﬁxation. Underﬁxation of breast tissue can cause a marked decrease in the ability of immunohistochemistry to detect ER.59 Because core biopsies tend to be signiﬁcantly smaller than excisional specimens, they ﬁx more rapidly, which is optimal for ER assessment. It is not unusual to see weak expression of ER on a core biopsy while no expression is noted on the excision specimen. ● Prevention ER determination should be performed on all core biopsies because of more optimal tissue ﬁxation.60 If no expression of ER is noted, ER status should be reassessed on the excisional specimen. Expression in as little as 1% of the invasive tumor cells is associated with signiﬁcantly greater responsiveness to antiestrogen therapy than those tumors showing no expression. Because the amount of tissue examined in a core biopsy is typically less than the amount examined in an excisional specimen, lack of expression in a core biopsy may be the result of incomplete sampling.

Not Performing a Further Procedure with a Diagnosis of AIDH on Core Biopsy ● Consequence The diagnosis and signiﬁcance of AIDH are deﬁned based on the follow-up of patients who underwent excisional biopsy. When AIDH is found on a core biopsy, the question is whether it is representative of the entire lesion or whether it is indicative of a more worrisome pathology. On a molecular level, AIDH and low-grade intraductal carcinoma are undistinguishable.61–63 The two lesions are sometimes difﬁcult for the pathologist to separate, even on excisional specimens, let alone on core biopsy samples in which more limited tissue is available. Even when a deﬁnitive diagnosis of

43 IMAGE-GUIDED BREAST BIOPSY AIDH can be rendered on core biopsy, it is frequently associated with low-grade DCIS. When diagnosed on core biopsy, AIDH is frequently upgraded to DCIS or invasive carcinoma once the lesion is excised.21,64–68 In general, the more tissue removed at core biopsy, the smaller the percentage of cases that will be diagnosed as carcinoma on excision. Approximately 40% of core biopsies diagnosed as AIDH using a 14-gauge biopsy device will show carcinoma on excision whereas only about 20% will show carcinoma when AIDH is diagnosed with an 11-gauge VAB device.69 Recently, it has been suggested that it may be important to note the number of foci of AIDH on core biopsy and that the number of foci may be predictive of the presence of carcinoma on the excisional biopsy.70 When AIDH was limited to only one or two foci, carcinoma was not seen on the subsequent excisional biopsy specimen; the incidence of carcinoma was 50% when three foci of AIDH were identiﬁed and 87% when four or more foci were identiﬁed. I believe this approach is too simplistic and that attention should be paid to the type and extent of the mammographic lesion. If the lesion presents as microcalciﬁcations, carcinoma is more often detected if the mammographic lesion is not completely removed. However, even if the mammographic microcalciﬁcations are completely removed, carcinoma may still be found at excision. If the mammographic lesion presents as a mass, there is only a 5% incidence of carcinoma at excision.71 It has been noted that when a micropapillary pattern is identiﬁed, most excisional specimens will contain a micropaillary DCIS.70 ● Prevention Whereas there continues to be much interest in deﬁning a subset of AIDH patients who do not require subsequent excision, no such category can be deﬁned reliably. AIDH has similar molecular alterations to those seen in low-grade DCIS and should be treated. It is frequently found at the periphery of DCIS, and thus, a concurrent carcinoma can be truly excluded only if the surrounding tissue is examined and no carcinoma is seen.66 AIDH is a signiﬁcant risk factor for the development of invasive breast cancer, conferring a relative risk of four to ﬁve times and is about equal in both breasts.72,73

Not Performing a Further Procedure with a Diagnosis of Angiolymphoid Hyperplasia/Lobular Carcinoma In Situ on Core Biopsy ● Consequence When angiolymphoid hyperplasia (ALH) or lobular carcinoma in situ (LCIS) is found on excisional biopsy, no further surgery is performed because the lesions are believed to be markers of a generalized increased risk of developing invasive breast carcinoma that occurs

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with equal frequency in both breasts.74–80 LCIS/ALH is not typically associated with a mammographic or ultrasound abnormality and, thus, is usually an incidental ﬁnding rather than the pathology that led to the core biopsy. It has an incidence of less than 2% in most core biopsy studies.42,79,81–84 Because of its low incidence, our knowledge of ALH/LCIS on core biopsy is mostly derived from retrospective trials. Pooling these studies, approximately 19% of excisional biopsies after a diagnosis of ALH/LCIS show carcinoma.85 Approximately 55% of these show invasive carcinoma (30% invasive lobular), and 45% show intraductal carcinoma. Liberman and coworkers84 put forth criteria strongly recommending surgical excision if there is radiologicpathologic discordance, if another lesion requiring excisional biopsy (such as atypical ductal hyperplasia [ADH]) is also present, or if the histologic features of the ALH/ LCIS cannot be easily distinguished from DCIS.84 ● Prevention Because ALH/LCIS is not associated with a radiographic abnormality, there is likely to be radiologicpathologic discordance. Although concern has been raised that these studies might be biased because not all patients who were diagnosed with ALH/LCIS on core biopsy underwent excisional biopsy, until further studies are available, excisional biopsy seems prudent.

Not Performing a Further Procedure with a Diagnosis of Flat Epithelial Atypia (Atypical Columnar Cell Alteration) on Core Biopsy ● Consequence Columnar cell lesions are the most common cause of pleomorphic microcalciﬁcations seen on core biopsy. These lesions have been described under a number of different names ranging from “blunt duct adenosis” on the benign side to “clinging carcinoma” on the malignant side. The signiﬁcance of columnar cell lesions is the company they keep. Atypical columnar cell lesions (ﬂat epithelial atypia) have been associated with lowgrade in situ and invasive ductal and/or lobular carcinomas.86 In one review, 95% of cases of pure tubular carcinoma were associated with atypical columnar cell lesions.87 On a molecular level, columnar cell lesions frequently show loss on chromosome 16 similar to those seen in low-grade carcinomas.88 For years, these lesions were largely ignored when identiﬁed in excisional biopsy specimens and the association with lowgrade carcinomas was not appreciated. Retrospective studies looking at benign breast biopsies containing overlooked atypical columnar cell lesions did not show a subsequent invasive carcinoma. When columnar cell alterations were present without an associated carcinoma, the lesions did not appear to confer an increased risk of malignancy.

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Figure 43–12 H&E-stained microscopic slide shows ﬂat epithelial atypia. The nuclei in the lining cells are more vesicular with visible nucleoli. They have lost their polarity and have a much more uniform and focally rounded appearance.

● Prevention Columnar cell alterations are commonly seen because of their frequent association with pleomorphic microcalciﬁcations. If a dedicated breast pathologist is not available at your institution, it is worth asking your pathologists if they are aware of this entity and the current histologic criteria. It is essential that the pathologist be familiar with the terminology and criteria. If atypia is present, complete surgical excision of the lesion is advised because of the possible association with an in situ or invasive carcinoma. If no associations are found, the probability of developing into an invasive carcinoma is exceedingly low (Fig. 43–12).

Pathology Does not Correlate with Imaging Findings?/No Calciﬁcations Found on Pathology When Calciﬁcations Were Identiﬁed on Your Imaging Study (Tissue Processing in General) ● Consequence Although they are not encountered very often, the inability to demonstrate microcalciﬁcations on histologic examination can be problematic. If calciﬁcations cannot be demonstrated, and the lack of microcalciﬁcations cannot be explained, complete excision of the lesion should be performed, assuming microcalciﬁcations are still remaining in the breast. When performing an image-guided biopsy for microcalciﬁcations, large-core or whole intact biopsy devices should be utilized. Studies have shown that larger biopsy samples and more cores will remove more of the calciﬁcations and require few excisional biopsies owing to radiographic-pathologic discrepancies.89–91 ● Prevention This is deﬁnitely the case in which an ounce of prevention is worth a pound of cure. The radiologist/surgeon

should radiograph all of the removed cores as well as obtain a postbiopsy ﬁlm to ensure that the calciﬁcations have been removed and a specimen radiogram to ensure that they are present in the core biopsy specimens. Once documented, the cores containing the microcalciﬁcations should be submitted separately from the cores that do not show radiographic evidence of calciﬁcations. This will allow the pathologist to concentrate on the more suspicious cores and potentially examine more levels on sections thought to contain calciﬁcations. If microcalciﬁcations are not identiﬁed by the pathologist, several steps should be taken. The ﬁrst step is for the pathologist to polarize the H&E slides. Calciﬁcations composed of calcium oxylate are not easily demonstrated on the H&E stain but are easily demonstrated on polarization.92,93 This type of calciﬁcation is most commonly seen associated with apocrine metaplasia. Assuming that calciﬁcations are still not identiﬁed, the next step should be to x-ray the tissue block. If no calciﬁcations are identiﬁed within the block, but preprocessing radiographs demonstrated the microcalciﬁcations, it can be assumed that the calciﬁcations dissolved in processing. This happens very rarely. If calciﬁcations are still demonstrated in the parafﬁn-embedded block, deeper sections should be obtained. The sections should be cut on a fresh microtome blade, if possible. Occasionally, microcalciﬁcations cannot be cut by a microtome blade and the calciﬁcations are launched as small projectiles rather than being cut. These can be detected as holes in the tissue that represent remnants of where the microcalciﬁcations used to reside.

Lack of Radiographic and Pathologic Correlation, Whatever the Cause, Requires Complete Surgical Excision Not Performing a Further Procedure with a Diagnosis of Radial Scar on Core Biopsy ● Consequence Most radial scars are incidental ﬁndings measuring approximately 4 mm in size. Based on data from the Nurses’ Health Study, women with radial scars demonstrate a twofold increase in risk of invasive breast cancer; this risk increases with the size of the radial scar.94 The risk is believed to be bilateral, but larger radial scars may be associated with DCIS and invasive carcinomas. Carcinomas arising in association with radial scars are frequently located at the periphery of the lesion, causing them to be missed if the center of the lesion is targeted. It is important to note whether a radial scar is an incidental ﬁnding or whether it is the targeted lesion. There is a signiﬁcantly higher association of carcinoma and AIDH in lesions identiﬁed mammographically than those lesions found incidentally. There does not appear to be any distinguishing mammographic feature that allows

43 IMAGE-GUIDED BREAST BIOPSY

7.

8.

9.

10.

11.

Figure 43–13 Triple immunostaining for P63, cytokeratin 5/6, and cytokeratin 18 in the same radial sclerosing lesion as seen on the H&E stain. P63 and cytokeratin 5/6 highlight cells with myoepithelial/basal differentiation. Both antibodies are visualized with diaminobenzidine (DAB) (brown). P63 is a nuclear, and cytokeratin 5/6 is a cytoplasmic. Cytokeratin 18, a cytoplasmic stain, is visualized with fast red. The presence of two cell types conﬁrms the proliferation as benign.

radiographic separation of radial scars harboring carcinomas from those that do not harbor such foci.95 ● Prevention All mammographically detected radial scars and all radial scars measuring 6 mm or larger should undergo excision. Sloane and Meyers96 reported a 30% incidence of carcinoma when the radial scar measures 6 mm or larger and an incidence of only 2.6% with smaller radial scars. Given the small number of radial scar studies and the low incidence of radial scars in general, it seems prudent to recommend excision for all mammographically detected radial scars and certainly all radial scars measuring larger than 6 mm (Fig. 43–13).

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44

Breast Biopsy and Breast-Conserving Surgical Techniques Lorraine Tafra, MD and Zandra Cheng, MD INTRODUCTION Surgical procedures of the breast have changed signiﬁcantly since the late 1990s. With improved imaging techniques, the detection of radiologic abnormalities is increasing and the size of detected malignancies is decreasing. These factors have led to a shift in management strategies toward more precise and aesthetic surgical approaches. Just as the surgical management has changed, so have other subspecialty management strategies such that the multidisciplinary aspect of breast cancer has become more complex. Comprehensive care, therefore, involves surgical strategies and decisions with input from a team of multidisciplinary specialists. The operating surgeon’s ﬁrst and crucial step to avoid surgical pitfalls with the breast patient is to ensure easy and frequent communication with the other specialists. A strategy used by many centers to ensure this communication is the multidisciplinary tumor board. A signiﬁcant change in breast surgery was the shift from open surgical biopsy to image-guided needle-core biopsy (for the diagnosis of breast abnormalities). The current literature supports the superiority of an image-guided needle biopsy over an open surgical biopsy for the vast majority of patients with a breast abnormality.1–7 This technology has decreased the frequency of operative procedures, allowed for tailored care of proven malignancies, and improved the accuracy of deﬁnitive surgical management of breast cancer. It is also convenient for the patient and expedites the diagnosis. A very small group of patients remain who present with a palpable abnormality, with no imaging correlate, who will still require an open surgical biopsy for a deﬁnitive diagnosis. The vast majority of patients who do need to go to the operating room for a diagnosis (1) are being evaluated for a nonpalpable, image-detected lesion for which the core biopsy pathology result is equivocal or (2) were constrained by the limitations of the image-guided techniques (e.g., thin breast, very faint microcalciﬁcations).

Partial mastectomy, which is also commonly referred to as lumpectomy, is the breast-conserving surgical procedure performed for a breast cancer. Although many of the steps of a lumpectomy are similar to those of a biopsy, the goals of each are very different and are considered separately.

Breast Biopsy INDICATIONS ● Patient with a deﬁned mass on palpation but no

evidence of abnormality on mammography or ultrasound ● Patient with an image-detected abnormality who, on core biopsy, has insufﬁcient tissue for a deﬁnitive diagnosis, or the benign pathology results are not concordant with imaging ﬁndings ● Patient with a benign diagnosis on core biopsy but who exhibits growth or other concerning symptomatic or physiologic behavior over time ● Patient with an image-detected abnormality who is not a candidate for image-guided biopsy (presence of implants, thin breasts, needle phobias, obese [stereotactic tables have a weight limit of about 350 lbs], or bleeding disorders)

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5

Mark palpable lesion in preoperative area Ensure adequate localization if lesion is nonpalpable Mark incision on breast Resect Palpate lesion resection, perform a specimen radiograph as indicated, and close

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OPERATIVE PROCEDURE Marking the Lesion Failure to Remove the Correct Area of Concern ● Consequence Occasionally, the patient will have a subtle abnormality; something the patient can feel well, but for the surgeon, the abnormality is not well deﬁned. Removing the wrong area may warrant a return to the operating room. Besides avoiding the dreaded scenario of doing a breast biopsy on the wrong breast, marking the site of the lesion and obtaining consensus on its location ensure the precise removal of the area of concern. Grade 3 complication ● Prevention Preoperative discussion of the area, marking and ﬁnding the lesion, and reaching consensus between the surgeon and the patient on the site of the abnormality.

Adequate Localization Failure to Remove the Correct Area of Concern ● Consequence Lesions that are not palpable require some form of localization. This is an active area of investigation because this scenario continues to increase in frequency.8 Wire localization has been the standard procedure for localizing a lesion for the surgeon since its introduction in the 1980s,9–11 but there is much room for improvement. Standard wire localization is frequently imprecise. In addition, when addressing a malignancy, it does not assist with obtaining negative margins and is not very convenient for the patient who must endure an additional procedure prior to the initial surgery. It has typically been performed outside of the operating room by the radiologist, but fortunately with increasing use of ultrasound by surgeons, a shift is occurring, allowing the patient to be localized in the operating room. Intraoperative localization has many advantages: it avoids the time delays that come with coordination of a second department; scheduling is simpliﬁed; patient satisfaction is maximized; staff inconvenience is minimized; and ﬁnally, the accuracy is probably better when the physician localizing the lesion is also removing it. The precision and accuracy of the localization of the lesion are far more important than who performs it. The worst consequence of inadequate localization is missing the lesion and having to return the patient to the operating room for a second attempt at excision. This is obviously disconcerting to the patient, but it also delays the diagnosis and potential treatment. In addition, because cosmesis is related to the amount of tissue removed, a second trip to the operating room to remove more tissue

could negatively affect cosmesis, patient satisfaction, and future imaging. Grade 3 complication ● Prevention The localization procedure needs to adhere to the following basic principles, whether performed by the radiologist or the surgeon: 1. Ensure that the correct area has been targeted, and if a clip is the target, that the clip has, in fact, remained at the area of interest since the time of needle biopsy. 2. Ensure that the site of the wire entering the skin has been marked with a marker visible in the postlocalization ﬁlms (if the localization is done by someone other than the surgeon) and that another point of reference on the breast (most commonly, the nipple) is also marked so that the surgeon can determine how far the lesion is from the entry of the wire through the skin and within the breast tissue. 3. Ensure that the location of the wire is within 2 to 3 mm of the clip (if a clip is targeted). 4. Ensure that two views (both the craniocaudal [CC] and the mediolateral [ML]) have been obtained and sent with the patient to conﬁrm that the locations of the lesion, the clip, and the wire can be determined by the surgeon. Once this has been established, it is the surgeon’s goal to remove the area of concern. If the target is a clip or calciﬁcations or if the lesion remains nonpalpable even with dissection down to the area, a specimen radiograph is needed. If there has been clip migration or if the localization is not where the surgeon believes the original lesion is, it is imperative that good communication occurs between the radiologist and the surgeon prior to the procedure. In these cases, retrieval of the clip on specimen radiograph may not be necessary. If the lesion becomes palpable with dissection, a specimen radiograph need not be performed if the operating surgeon is conﬁdent the lesion has been obtained. Caution should be exercised with this approach, however, because a palpable hematoma from the prior core biopsy may masquerade as the lesion. Once the best determination of the site of the lesion is made based upon direct review intraoperatively of the mammographic or ultrasound images, the lesion is marked and the incision is placed directly over the abnormality. Occasionally, the more cosmetic periareolar incision is used, especially if the lesion is in close proximity to the nipple-areolar complex. Dissection then proceeds toward the wire. The wire is then delivered into the wound. Palpation of the tissue surrounding the wire will ensure an adequate removal of the tissue that needs further assessment. It is worth emphasizing that the incision usually is not placed at the site of the entrance of the wire to the skin. If the lesion is localized by the surgeon in the operating room, the surgeon must have prior, precise knowledge of the lesion’s location. It is best if the surgeon retains

44 BREAST BIOPSY AND BREAST-CONSERVING SURGICAL TECHNIQUES a copy of the ultrasound or mammogram for reference in the operating room. The use of intraoperative ultrasound is justiﬁably increasing. If a lesion is visible on ultrasound and the surgeon has ultrasound skills, localization in the operating room is easier and safer, requires less time, and is more convenient for the patient and surgeon. With experience, localizing a lesion in the operating room is usually straightforward, but it can be challenging with small lesions. If the lesion is small (<5 mm), consideration should be given to having the patient’s breast marked preoperatively by another physician (surgeon or radiologist) to get consensus by two physicians of the lesion’s location. Sometimes, after a core biopsy, a hematoma is well visualized, but with time, it resolves, leaving little at the site of the biopsy. If the surgical procedure is to be scheduled more than a few weeks after the core biopsy, consideration should be given to performing a repeat ultrasound to ensure the surgeon can still visualize the lesion in the absence of the hematoma. Clips placed at the time of core biopsy have, in the past, not been echogenic enough to visualize with ultrasound. However, the newer clips retain materials around the clip itself that can be seen by a surgeon experienced with ultrasound. Use of these types of clips can also increase the number of patients who are candidates for localization in the operating room. A number of standard localization devices are on the market (Kopans [Cook, Bloomington, IN]), Hawkins (Boston Scientiﬁc, Watertown, MA [Fig. 44–1]), and Bard (CR Bard, Inc., Covington, GA), but new devices are being introduced in an attempt to solve the inherent

Hawkins

Hawkins II

457

problems of the traditional needles. The Anchor Guide (SenoRx, Aliso Viejo, CA [Fig. 44–2]) is a device that uses an umbrella basket–type deployment that creates a palpable lesion from a nonpalpable lesion, assisting in localization and resection.12 No device to date has been remarkable enough to gain wide acceptance in the surgical market. For now, the particular device used is probably less important than ensuring that the wire or localization device is placed accurately.

Incision Placement Poor Cosmesis and Inadequate Planning for Mastectomy, if Needed ● Consequence Imprecise placement of the incision will result in more breast dissection than is necessary. The cosmetic incisions on the breast are generally circumlinear; however, in the inner and 6 o’clock positions, the incision that results in the best cosmesis remains controversial. Large incisions placed in other than these orientations can deform the breast and result in poor cosmesis. Large incisions in the upper outer quadrant near the axilla may also negatively affect lymphatic drainage of the breast, potentially leading to breast lymphedema. Although the entire lesion needs to be removed, removing large amounts of breast tissue is rarely indicated and will lead to a poor cosmetic result. Grade 1 complication

Hawkins III

Figure 44–1 Hawkins needle localization devices. (Courtesy of Boston Scientiﬁc, Watertown, MA.)

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Resection Hematoma and Poor Cosmesis ● Consequence and Prevention Few complications occur during resection or after a breast biopsy. The most common are hematoma, infection, and poor cosmesis. The breast is not tolerant of bleeding, and meticulous hemostasis should be the rule. The biopsy cavity should be carefully inspected and be perfectly hemostatic prior to closure of the wound. Poor cosmesis should not occur after a breast biopsy. The amount of tissue needed for a diagnosis is rarely a large amount and, therefore, should not result in a deformity of the breast. Little data are available on the cosmetic outcome of a breast biopsy and the factors that may affect the appearance of the breast. The prevailing philosophy is that the cosmesis varies inversely with the amount of tissue resected and will be worse if deep sutures are placed into the biopsy cavity, leading to breast contour deformity. Grade 2 complication

Palpate Lesion Resected, Perform Specimen Radiograph, and Close A

Missing the Lesion ● Consequence Every effort should be made to ensure the lesion has been adequately sampled for histologic examination, to avoid having to return to the operating room. Grade 3 complication

B Figure 44–2 A, SenoRx localization device with adjustable bracketing wires. B, Diagram of the device in the breast. (A and B, Courtesy of SenoRx, Aliso Viejo, CA.)

● Prevention The surgeon should take time to draw the incision, as well as the site of the lesion, directly onto the patient. The size of the incision should be kept to the minimum size that still allows adequate retrieval of the targeted lesion as well as palpation and visualization of the cavity for hemostasis. Usually, this is not more than 3 to 4 cm in length. The nipple and entry of the wire can serve as useful points of reference if the lesion is fairly deep and it is difﬁcult to feel the needle tip. To ensure the location of the lesion or the direction of the wire, gently tug on the wire and palpate the breast simultaneously. Usually, the incision is not placed where the wire enters the skin and, if placed by the radiologist, can enter the skin quite a distance from the lesion.

● Prevention Small lesions can often be palpated, obviating the need for a specimen radiograph. Patients with calciﬁcations or a clip almost always require a specimen radiograph. Occasionally, the minute clip can be visualized or the hematoma from the biopsy can easily be palpated. Even in these circumstances, it is reassuring to see the calciﬁcations in the specimen. Clinical judgment is needed if the surgeon does not see the clip on the specimen radiograph. The questions that should be considered include (1) Was the correct site targeted? or (2) Did the clip fall out during surgical excision? Blind re-resection if the area is believed to be close to the surgical site of dissection is warranted; however, extensive dissection, which could deform the breast, should be avoided. Meticulous cosmetic closure of the breast should be the rule.

Partial Mastectomy INDICATIONS ● Patient with a diagnosed breast cancer who does not

have

44 BREAST BIOPSY AND BREAST-CONSERVING SURGICAL TECHNIQUES ● ● ● ●

A contraindication for radiation therapy Previous radiation therapy The presence of widespread local breast disease Large tumor–to–breast size ratio (i.e., locally advanced disease) without prior neoadjuvant therapy or with contraindications or a poor response to neoadjuvant therapy ● Patient with a phyllodes tumor

LUMPECTOMY STEPS Step Step Step Step Step

1 2 3 4 5

Mark palpable lesion in preoperative area Localization Incision Resection and specimen orientation Palpate lesion resection, perform specimen radiograph as indicated, and close

459

Accurate localization of the malignancy and determining the extent of the malignancy for palpable lesions can assist in obtaining negative margins, but it does not guarantee this outcome. The same principles outlined for biopsy are used for localization of malignancies, with a few additions. If the patient is found to have a large area of ductal carcinoma in situ (DCIS) based on imaging, it is helpful to use bracketing wires to outline the area of disease for the surgeon.15 Other creative approaches to localizing a malignancy have included leaving a hematoma behind at the time of biopsy to mark the site for ultrasound localization in the operating room16 and using radioactive seed localization. This latter technique requires 99Tc injection or radioactive seed placement at the time of the biopsy. The gamma probe (commonly being used for sentinel node biopsy) can then be used to track the site of the malignancy.17

Incision OPERATIVE PROCEDURE Marking the Lesion See the section on “Marking the Lesion,” under “Breast Biopsy,” earlier.

Adequate Localization Failure to Remove the Entire Lesion with a Negative Margin ● Consequence A consequence of inadequate localization and precise resection is positive or close margins, which usually requires returning to the operating room. This is usually well tolerated and can be performed without general anesthesia, but it is obviously disconcerting to the patient. Although the same principles for localization for breast biopsies apply to localization for malignancies, the goals are very different. With localization for malignancy, the entire extent of the lesion must be mapped to allow the surgeon to perform an accurate lumpectomy. Grade 2 complication ● Prevention The goals of partial mastectomy are to obtain negative margins and a good cosmetic result. This can be difﬁcult because both goals are poorly deﬁned and there is no universally acceptable standard. It has been well established, however, that the status of the margin affects the local recurrence rate.13 The deﬁnition of a negative or adequate margin may range from no tumor at the margin to 3 to 5 mm of normal tissue intervening between the tumor and the edge of the specimen.14 Even with no acceptable standard, attention to the issue is crucial for good long-term results.

The principles for incision placement remain the same for lumpectomy as they do for a biopsy (see earlier). Although the incision may need to be larger than a biopsy incision, the procedure can usually be carried out through an incision half the size of the specimen (Fig. 44–3). The largest dimension of the specimen can usually be predicted to be 2 cm plus the size of the tumor in centimeters. Therefore, a 2-cm malignancy can be removed through a 2-cm incision. Closure of dead space can deform the breast. However, if a large amount of dead space is present, the area may also retract down or deform secondary to radiation and still cause a signiﬁcant defect in the contour of the breast. Recently, oncoplastic strategies have been introduced to rotate breast tissue into the area of the defect to minimize the defect.18–20 However, this can affect the area of the radiation boost. Therefore, marking the boundaries of the original lumpectomy with clips or radiopaque markers is important for patients eligible for radiation therapy after breast conservation. It is hopeful that in the future, techniques will be developed to maintain the exact contour of the breast, even after a large lumpectomy.

Resection and Orientation of the Specimen Failure to Obtain Negative Margins; Failure to Orient the Specimen ● Consequence Similar to the localization step, the steps followed for the surgical resection of a malignancy should decrease the chance of a positive margin, but with our current technology, this unfortunate result cannot be eliminated altogether. A second important pitfall after resection of the tumor is failing to orient the specimen. Without adequate orientation of the partial mastectomy specimen, a targeted re-resection, if needed, cannot be done. If the patient is found to have positive

460

SECTION VI: BREAST SURGERY

A

B Figure 44–3 A and B, Partial mastectomy performed through a small incision.

margins and it is not clear which speciﬁc margin is involved, the patient is subjected to excision of all margins, leading to a potentially poor cosmetic outcome. In this situation, it is possible that the only cosmetically acceptable choice is a mastectomy. Grade 2/3 complication ● Prevention In addition to the techniques described for localization, other methods can be applied during the resection that can potentially decrease the reexcision rate of positive margins. In a few series with small numbers, the use of intraoperative ultrasound has been shown to decrease the rate of positive margins.21,22 Intraoperative ultrasound can assist in mapping the extension of the tumor on the breast and in imaging the specimen to guide further resection of margins deemed to be close.

Frozen section analysis of margin sampling and cytology imprinting of the margin have also been used successfully, although these are criticized for being time consuming for the pathologist and requiring a long wait in the operating room for the surgeon.23,24 A recent prospective, randomized trial looked at using a cryoprobe for localizing ultrasound visible tumors.25 The localization was accompanied by growing an ice ball template around the tumor with the hope of obtaining a more accurate lumpectomy.25 The amount of tissue resected was decreased compared with that in the group that underwent standard needle localization. However, the positive margin rate remained high (30%) in both groups. This relatively high rate occurred despite well-selected patients (inﬁltrating ductal tumors [no inﬁltrating lobular], all tumors <1.7 cm). This study, perhaps better than any other, has elucidated the fact that our current imaging technology fails to accurately visualize the extent of breast malignancies in a signiﬁcant number of patients. Precautions need to be taken with the handling of the specimen itself. Specimen handling can result in falsepositive margins for a number of reasons.26 Specimen compression for needle wire–localized specimens can lead to false-positive margins and should be avoided.27 Other reasons for false-positive margins include seepage of ink into crevices of the specimen, fatty tissue surrounding the tumor that tends to separate from the tumor, and retraction artifact. If the chance of a positive margin is to be minimized, the operating surgeon should develop some strategy that works for him or her to use on all patients undergoing a lumpectomy. The surgeon should consider: (1) frequent use of ultrasound, particularly for ultrasound-visible tumors, to locate the tumor in the operating room; (2) liberal use of bracketing wires for large areas of calciﬁcations believed to represent extension of DCIS; (3) frequent use of ultrasound to evaluate the partial mastectomy specimen; (4) orienting the surgical specimen; (5) obtaining and reviewing the oriented specimen radiograph28; and (6) avoiding compression. Although the goal in breast conservation is also to maintain cosmesis, little data are available that guide the surgeon as to what actually is an acceptable cosmetic result (Fig. 44–4). To compound this, it has now been appreciated that the concordance between the surgeon and the patient with respect to the postoperative appearance of the breast is poor.29 Thus, what we, as surgeons, may view as terrible results may be viewed by the patient as acceptable and vice versa. Studies are needed to better deﬁne cosmesis after lumpectomy from both the surgeon’s and the patient’s point of view, immediately postoperative and long term. To not orient the lumpectomy specimen is to possibly commit the patient to more extensive breast surgery than might be required. There are many methods of specimen orientation including suture marking, using preﬁxed tags to identify the various margins of the tissue, and painting

44 BREAST BIOPSY AND BREAST-CONSERVING SURGICAL TECHNIQUES

461

A

A

B

C Figure 44–4 A–C, Examples of a poor cosmetic result after a lumpectomy.

B Figure 44–5 A and B, Faxitron device for intraoperative specimen evaluation. (A and B, Courtesy of Faxitron, X-Ray Corp., Wheeling, IL.)

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intraoperatively with pathology dyes by the surgeon. The exact method chosen is probably less important than the practice of using the same method on all patients and frequently communicating with the pathologist on deviations from that method.

Cavity and Specimen Palpation, Specimen Radiograph if Needed, and Skin Closure

5.

6.

Leaving Tumor in the Breast and a Poor Cosmetic Outcome ● Consequence Failure to palpate the resected specimen or the cavity or to view the specimen radiograph could result in leaving tumor behind. Closing the skin with staples or placing large sutures for closure can result in visible hash marks that do not always fade with time. Grade 2/3 complication ● Prevention After the breast specimen is removed, both the specimen and the cavity should be meticulously examined for residual tumor. However, this must be balanced with the temptation to perform extensive reexcisions, leading to poorer cosmetic results. For breast patients, in whom the issue of cosmesis is a relatively high priority, it is recommended to perform a cosmetic subcuticular closure, which can leave the breast with an excellent cosmetic outcome. Performing a specimen radiograph can also help determine how close the margins may be and is especially important for DCIS and the presence of calciﬁcations. This can be very inconvenient if the radiology department or the mammography suite is not located adjacent to the operating room (which it rarely is). An exciting new device to enter the market is a digital specimen radiograph device (Faxitron, X-Ray Corp., Wheeling, IL [Fig. 44–5]) that is portable and can be rolled from one operating room to another. More data are becoming available on the use of this device, but it is anticipated that this should make intraoperative conﬁrmation less time consuming.30

REFERENCES 1. Hatmaker AR, Donahue RM, Tarpley JL, Pearson AS. Cost-effective use of breast biopsy techniques in a Veterans health care system. Am J Surg 2006;192:e37– e41. 2. Silverstein MJ, Lagios MD, Recht A, et al. Image-detected breast cancer: state of the art diagnosis and treatment. J Am Coll Surg 2005;201:586–597. 3. Sauer G, Deissler H, Strunz K, et al. Ultrasound-guided large-core needle biopsies of breast lesions: analysis of 962 cases to determine the number of samples for reliable tumour classiﬁcation. Br J Cancer 2005;92:231–235. 4. Groenewoud JH, Pijnappel RM, van den Akker-Van Marle ME, et al. Cost-effectiveness of stereotactic large-

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core needle biopsy for nonpalpable breast lesions compared to open-breast biopsy. Br J Cancer 2004;90: 383–392. Verkooijen HM, and the Core Biopsy after Radiological Localization (COBRA) Study Group. Diagnostic accuracy of stereotactic large-core needle biopsy for nonpalpable breast disease: results of a multicenter prospective study with 95% surgical conﬁrmation. Int J Cancer 2002;99: 853–859. Smyczek-Gargya B, Krainick U, Müller-Schimpﬂe M, et al. Large-core needle biopsy for diagnosis and treatment of breast lesions. Arch Gynecol Obstet 2002;266: 198–200. Pijnappel RM, van den Donk M, Holland R, et al. Diagnostic accuracy for different strategies of imageguided breast intervention in cases of nonpalpable breast lesions. Br J Cancer 2004;90:595–600. Coburn NG, Chung MA, Fulton J, et al. Decreased breast cancer tumor size, stage, and mortality in Rhode Island: an example of a well-screened population. Cancer Control 2004;11:222–230. Rissanen TJ, Makarainen HP, Mattila SI, et al. Wire localized biopsy of breast lesions: a review of 425 cases found in screening or clinical mammography. Clin Radiol 1993;47:14–22. Vuorela AL, Ahonen A. Preoperative stereotactic hookwire localization of nonpalpable breast lesions with and without the use of a further stereotactic check ﬁlm. Anticancer Res 2000;20:1277–1279. Homer MJ. Nonpalpable breast lesion localization using a curved-end retractable wire. Radiology 1985;157:259– 260. Israel P, Gittleman M, Fenoglio M, et al. A prospective, randomized, multicenter clinical trial to evaluate the safety and effectiveness of a new lesion localization device. Am J Surg 2002;184:318–321. Aziz D, Rawlinson E, Narod SA, et al. The role of reexcision for positive margins in optimizing local disease control after breast-conserving surgery for cancer. Breast J 2006;12:331. Taghian A, Mohiuddin M, Jagsi R, et al. Current perceptions regarding surgical margin status after breastconserving therapy: results of a survey. Ann Surg 2005; 241:629–639. Liberman L, Kaplan J, Van Zee KJ. Bracketing wires for preoperative breast needle localization. AJR Am J Roentgenol 2001;177:565–572. Smith LF, Rubio IT, Henry-Tillman R, et al. Hematomadirected ultrasound-guided breast biopsy. Ann Surg 2001; 233:669–675. Gray RJ, Salud C, Nguyen K, et al. Randomized prospective evaluation of a novel technique for biopsy or lumpectomy of nonpalpable breast lesions: radioactive seed versus wire localization. Ann Surg Oncol 2001;8:711–715. Anderson BO, Masetti R, Silverstein MJ. Oncoplastic approaches to partial mastectomy: an overview of volumedisplacement techniques. Lancet Oncol 2005;6:145–157. Choi JY, Alderman AK, Newman LA. Aesthetic and reconstruction considerations in oncologic breast surgery. J Am Coll Surg 2006;202:943–952. Masetti R, Di Leone A, Franceschini G, et al. Oncoplastic techniques in the conservative surgical treatment of breast

44 BREAST BIOPSY AND BREAST-CONSERVING SURGICAL TECHNIQUES

21.

22.

23.

24.

25.

cancer: an overview. Breast J 2006;12(5 suppl 2):S174– S180. Moore MM, Whitney LA, Cerilli L, et al. Intraoperative ultrasound is associated with clear lumpectomy margins for palpable inﬁltrating ductal breast cancer. Ann Surg 2001;233:761–768. Rahusen FD, Bremers AJ, Fabry HF, et al. Ultrasoundguided lumpectomy of nonpalpable breast cancer versus wire-guided resection: a randomized clinical trial. Ann Surg Oncol 2002;9:994–998. Cendán JC, Coco D, Copeland EM. Accuracy of intraoperative frozen-section analysis of breast cancer lumpectomy-bed margins. J Am Coll Surg 2005;201:194–198. Hakam A, Khin N. Intraoperative imprint cytology in assessment of sentinel lymph nodes and lumpectomy surgical margins. Clin Lab Med 2005;25:795–807, viii. Tafra L, Fine R, Whitworth P, et al. Prospective randomized study comparing cryo-assisted and needle-wire

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localization of ultrasound-visible breast tumors. Am J Surg 2006;192:462–470. Dooley WC, Parker J. Understanding the mechanisms creating false positive lumpectomy margins. Am J Surg 2005;190:606–608. Méndez JE, Meulen D, Padussis J, et al. Tissue compression is not necessary for needle-localized lesion identiﬁcation. Am J Surg 2005;190:580–582. McCormick JT, Keleher AJ, Tikhomirov VB, et al. Analysis of the use of specimen mammography in breast conservation therapy. Am J Surg 2004;188:433– 436. Arenas M, Sabater S, Hernández V, et al. Cosmetic outcome of breast conservative treatment for early stage breast cancer. Clin Transl Oncol 2006;8:334–338. Kaufman CS, Bachman BA, Jacobson L, et al. Intraoperative digital specimen mammography: prompt image review speeds surgery. Am J Surg 2006;192:513–515.

45

Axillary Surgery Sara A. Bloom, MD and Donna-Marie Manasseh, MD INTRODUCTION Although breast cancer surgery can be traced back to AD 200, it was not until the early 18th century that French surgeon Jean Louis Petit ﬁrst noted the signiﬁcance of enlarged axillary nodes and that they should be removed along with the diseased breast tissue.1 Axillary metastasis has since been shown to be the most important prognostic indicator of both patient survival2 and breast cancer recurrence.3 Therefore, axillary surgery is a crucial step in the proper management of patients with carcinoma of the breast. William Halsted’s4 revolutionary radical mastectomy excised all three levels of axillary nodes as well as the breast and pectoralis major. This effectively eliminated all regional diseased tissue, but at the cost of great deformity to the patient. Subsequent management of both the breast and the axilla has trended toward conservation of as much nondiseased tissue as possible. Today, an axillary dissection removes most of the level I and II nodes. The extent of this dissection has been shown to be sufﬁcient enough to reduce local recurrence, stage the patient’s level of disease, and determine the most effective treatment.5 Level III nodes are removed only if palpable or otherwise suspected of containing malignancy. Seventy percent of patients with a clinically negative axilla will also prove to be microscopically free of axillary metastases.6 Axillary dissection carries signiﬁcant longterm morbidity for these patients. The advent of the sentinel lymph node biopsy (SLNB), ﬁrst successfully applied by Morton and colleagues7 for use in melanoma surgery, has allowed node-negative patients to be spared complete axillary dissection. When compared with axillary dissection, SLNB results in less postoperative morbidity (arm numbness and swelling) and allows for faster recovery.8 The sentinel lymph node is deﬁned as the ﬁrst lymph node to which a primary tumor will drain. In breast cancer, this is typically a level I node. SLNB can reliably predict the status of a regional lymph node basin. Giuliano and coworkers9 and Krag and associates10 applied this technique to breast cancer. Giuliano and coworkers used isosulfan blue dye to localize the sentinel node in 65.5% of patients. The rate improved to 78% with

accumulated experience, accurately predicting axillary status in 95.6% of patients. Krag and associates used unﬁltered technetium sulfur colloid to identify the sentinel node in 82% of patients, accurately predicting each case. Albertini and colleagues11 utilized both isosulfan blue dye and technetium sulfur colloid, identifying a sentinel node in 92% of patients.

Axillary Dissection INDICATIONS ● Invasive carcinoma with positive sentinel node ● Inability to identify a sentinel node in an invasive carcinoma patient ● Breast cancer with a clinically positive axilla (palpable nodes)

Operative Steps Step 1 Step 2

Step 3 Step 4 Step 5 Step 6 Step 7

Incision Axillary dissection and identiﬁcation of structures: axillary vein, long thoracic nerve, thoracodorsal nerve, intercostobrachial nerves En-bloc removal of level I and II nodes Palpation and possible excision of level III and Rotter’s nodes Acquisition of hemostasis Drain placement Two-layer closure

OPERATIVE PROCEDURE Incision Inappropriate Placement of Incision ● Consequence Wound contraction and breast deformity. Grade 1 complication ● Prevention If the patient will be undergoing a tissue-sparing procedure of the breast, a separate U-shaped or oblique

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SECTION VI: BREAST SURGERY

Axillary vein

Pectoralis major Intercostal-brachial nerve Thoracodorsal nerve

Intercostal-brachial nerve

Long thoracic nerve Latissimus dorsi

Thoracodorsal nerve Serratus anterior

Long thoracic nerve

Figure 45–1 Axillary anatomy.

incision from the lateral border of the pectoralis major to the anterior border of the latissimus dorsi, just inferior to the hairline, gives the best exposure and cosmetic result. The incision should not be visible from the frontal view of the patient. Radial or angled incisions and those that are continuous with the breast excision site result in more deformity of the breast owing to wound contraction during the healing process.

Axillary Dissection and Identiﬁcation of Pertinent Nerves and Blood Vessels (Fig. 45–1) Nerve Damage ● Consequence Multiple nerves course through the axilla (Fig. 45–2), damage to which causes the following patient morbidities: ● Damage to the long thoracic nerve, which inner-

vates the serratus anterior, causes winging of the scapula, shoulder pain, and inability to raise the arm above shoulder level. ● Damage to the thoracodorsal nerve, which innervates the latissimus dorsi, causes weakened arm pullups and adduction. ● Damage to the intercostobrachial nerves causes numbness and pain of the upper inner arm. These are the most commonly damaged nerves of an axillary dissection because they course through the axillary space and must sometimes be sacriﬁced with the specimen.

Medial

Lateral

Figure 45–2 Nerves of the axilla. ● Damage to the lateral pectoral nerve, which inner-

vates the pectoralis major, causes muscle atrophy and limitation of shoulder motion. Grade 1–3 complication ● Repair Typically, there is no repair for injury to these nerves. Some improvement does occur with time, especially with regard to sensory dysfunction. Although 76.5% of axillary dissection patients studied by Roses and coworkers12 initially complained of medial arm/axillary numbness or paresthesias, 82% of these had resolution of symptoms on follow-up assessment. Recovery is less likely with damage to the motor nerves. On long-term follow-up of patients with injury to the long thoracic nerve, 81% cannot lift or pull heavy objects, 58% cannot play sports (such as tennis or golf), and 54% are unable to work with their hands above shoulder level.13 Attempts have been made to surgically restore normal scapulohumeral dynamics in cases of serratus anterior paralysis by transferring the pectoralis major tendon14 or ﬁxing the inferior angle of the scapula.15 These therapies are still experimental and, if they prove successful, may be applied more readily in the future. The overall incidence of motor nerve damage secondary to axillary dissection is not well reported. It appears to be so low that the most common presentation in the literature is in case report format.

45 AXILLARY SURGERY

467

increased with longer patient follow-up. Petrek and associates17 studied a cohort of breast cancer survivors at 20 years after surgery and found that 49% reported the sensation of lymphedema. Although most of these patients (77%) developed this complication within the ﬁrst 3 years, additional patients developed lymphedema at a rate of approximately 1% per year. Grade 3 complication Axillary vein

● Repair No surgical repair is possible. Patients can undergo physical therapy and may wrap the affected arm with compressive dressings to decrease swelling.

Thoracodorsal nerve Intercostal-brachial nerve Medial

Lateral

Figure 45–3 Operative anatomy of the axilla.

● Prevention All major nerves should be identiﬁed and preserved. As the dissection proceeds inferiorly from the axillary vein (Fig. 45–3), the long thoracic nerve of Bell should be identiﬁed coursing longitudinally along the investing fascia of the chest wall anterior to the subscapularis muscle and inserting into the serratus anterior. It passes approximately 2 cm deep to where the intercostobrachial nerve exits the chest wall. It should be separated from the specimen and allowed to remain against the chest wall. The thoracodorsal nerve should be identiﬁed deep in the axilla, alongside the subscapular vessels, traversing laterally and inferiorly toward the latissimus dorsi. The intercostobrachial nerves course transversely through the axilla, and although not always possible, an attempt should be made to spare these nerves. An attempt should also be made to preserve the pectoral neurovascular bundle as it passes laterally around the pectoralis major, inferior to the axillary vein. Use of cautery should be limited in the axilla, because it can transmit and cause damage to these nerves. Use clips and ties as necessary.

Lymphedema ● Consequence Breast cancer patients frequently develop upper extremity lymphedema, distal to the site of axillary dissection. It is due to an overload of the lymphatic system, which can no longer adequately remove the amount of lymph made by the tissue. This problem is then compounded by an accumulation of macromolecules, causing increased oncotic pressure and, subsequently, more tissue edema. This stagnant, protein-rich ﬂuid can invite further complications of cellulitis and lymphangitis. It is difﬁcult to precisely deﬁne the incidence of lymphedema. In a review of the literature, lymphedema occurred in 6% to 30% of patients.16 It should be noted that these studies varied in length of follow-up from 14 months to 11 years and that the incidence of lymphedema clearly

● Prevention Risk factors for the development of lymphedema include the extent of the dissection (particularly near the axillary vein), number of nodes removed, postoperative radiotherapy, obesity, and arm infection or trauma.17–19 In Petrek and associates’ study,17 the lateonset lymphedema was associated with a postsurgery history of arm infection/injury or weight gain. The surgeon has little control over many of these factors but can be careful not to strip the axillary vein of its overlying tissue. The patient can reduce risk factors by controlling postoperative weight gain and arm injury/ infection.

Dissection above the Axillary Vein ● Consequence Extension of the dissection above the level of the axillary vein increases the likelihood of damage to the axillary vein, axillary artery, or brachial plexus. Grade 2 complication ● Repair The repair should be tailored to the speciﬁc structure injured. ● Prevention The dissection should proceed from the lateral border of the pectoralis major and minor to the anterior border of the latissimus dorsi, maintaining a superior border 1 cm below the axillary vein.

Acquisition of Hemostasis Lack of Hemostasis ● Consequence Hematoma will form in the cavity created by the excised tissue. Grade 1 or 2b complication ● Repair The hematoma may be treated by percutaneous drainage in the ofﬁce or, if there is persistent bleeding, may need a return to the operating room to ligate the bleeding vessel.

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● Prevention Ensure excellent hemostasis prior to closure.

Drain Placement

● Cases of ductal carcinoma in situ (DCIS) that are

aggressive, widespread, and palpable, requiring mastectomy or when immediate reconstruction is to be performed

Inadequate or Failure of Drain Placement ● Consequence Seromas are the most common complication of axillary surgery, resulting from disruption of both capillary and lymphatic vessels. The exact incidence varies wildly from study to study (range 4%–92%), based on the authors’ classiﬁcation criteria.5,20–22 Serous ﬂuid naturally collects in the excision cavity and can be identiﬁed sonographically in 92% of patients.21 It is when these seromas become large enough to require aspiration (42%) that they can lead to further infection, ﬂap necrosis, wound dehiscence, nerve injury, and an increased incidence of arm lymphedema.23–26 Grade 1 complication ● Repair Seromas are typically treated in the ofﬁce by percutaneous aspiration. ● Prevention The use of a closed suction drain does not necessarily prevent seromas, but it is believed to decrease the degree and subsequent complications of seroma formation.27 Divino and colleagues28 found that the use of drains decreased the rate of axillary seroma formation from 40% to 6%. Kopelman and coworkers29 noted a decrease in seroma formation if the drain was left until there was less than 35 ml of drainage over 24 hours. Generally, a closed suction drain should be placed inferior to the incision through a separate stab incision and should be removed when the output has decreased to 30 to 40 ml per 24-hour period. Attempts have been made to use ﬁbrin glue to decrease seroma formation.30,31 The results have been mixed, and more investigation into this potential therapy is still needed. Risk factors for seroma formation include increased age, patient weight, amount of drainage in the ﬁrst 72 hours, a large number of positive nodes, and no previous surgical biopsy.32,33 Although there have been reports to the contrary, Petrek and associates33 found no increase in seroma formation with early arm mobilization.

Sentinel Lymph Node Biopsy INDICATIONS 34 ● T1 or T2 invasive carcinoma of the breast, with clini-

cally negative lymph nodes

CONTRAINDICATIONS 34 Large and locally advanced (>5 cm) invasive breast carcinoma.

RELATIVE CONTRAINDICATIONS Previous Axillary Surgery Although a history of axillary surgery has previously been viewed as a contraindication to SLNB, some studies support the use of SLNB even if the patient has previously undergone an axillary dissection. Port and colleagues35 reported a 75% success rate in identifying sentinel nodes in patients with previous axillary surgery. The success rate was higher if fewer than 10 lymph nodes were removed previously (87%) versus removal of 10 or more nodes (44%). In these cases, the sentinel node may map to the internal mammary or contralateral axillary lymph node basins.36 In patients with a history of axillary surgery, SLNB may be attempted, and it may be advantageous to perform preoperative lymphoscintigraphy.

Clinically Positive Axillary Nodes Any clinically positive lymph node, identiﬁed either preoperatively or during surgery, is also considered a sentinel lymph node and should therefore be excised. Although some surgeons may advocate proceeding with an axillary dissection, 25% of clinically positive nodes yield falsepositive ﬁndings.34 The use of blue or radiolabeled dye may help identify additional sentinel nodes. If all of these nodes return negative for cancer, these patients can be spared the morbidity of an axillary dissection.

Inﬂammatory Breast Cancer34 SLNB false-negative rate may be elevated owing to subdermal lymphatics that are partially obstructed or contain tumor emboli.

Multicentric Tumors34 Many surgeons exclude patients with multicentric disease; however, several nonrandomized studies have shown that intradermal or subareolar injection yields comparable results to SLNB in women with unifocal disease.

Allergy to the Dye34 Avoid blue dye, and use radiolabeled colloid.

45 AXILLARY SURGERY

Pregnancy Vital dyes should not be used. However, when using radiolabeled colloids, the dose of radiation received by the fetus is minimal and most likely safe for use.

Preoperative Radiation or Chemotherapy At this time, data are insufﬁcient to recommend use of SLNB in this setting.

Recent Reduction Mammoplasty Data are insufﬁcient, but it is believed that the more extensive the prior surgery, the higher the likelihood of false-negatives or SLNB failure.

OPERATIVE STEPS Step Step Step Step Step Step Step

1 2 3 4 5 6 7

Injection of dye and/or radioisotope Incision Dissection and identiﬁcation of sentinel node Excision of sentinel node Inspect for palpable nodes Acquisition of hemostasis Closure

469

can then be given β-blockers and glucagon. These patients may experience recurrent episodes of hypotension and should, therefore, be admitted for 24-hour observation. Blue urticaria is treated like other type I hypersensitivity reactions, with intravenous hydrocortisone and diphenhydromine. The urticaria regresses within 24 hours and is typically gone within a week. ● Prevention Isosulfan is identical in chemical structure to substances used in cosmetics and hand lotions as well as other household products. Exposure to these products has led to sensitization of approximately 3% of the population, as determined by skin-prick testing.40 Although skin-prick testing could determine who is at risk for anaphylaxis from isosulphan, it is not routinely practiced. Ultimately, SLNB should be performed only in a setting in which the personnel is able to recognize and treat anaphylaxis.

Artiﬁcial Decrease in Pulse Oximeter Reading Of note: The blue dye causes a pseudodesaturation, frequently decreasing the reading of the pulse oximeter by 1% to 2%.37 The saturation may appear to be low, but the arterial PO2 remains within normal limits.

Dissection (Figs. 45–4 and 45–5) OPERATIVE PROCEDURE Injection of Dye and/or Radioisotope Allergic Reaction ● Consequence Approximately 1% of patients have allergic reactions to the isosulfan blue dye that is used in sentinel lymph node biopsies. The dye has been associated with severe anaphylactic reactions, requiring vigorous resuscitation.37,38 The reaction typically occurs 15 to 30 minutes after injection. It is diagnosed by a combination of cardiovascular collaspse, erythema, angioedema, bronchospasm, urticaria, and/or pulmonary edema, secondary to massive histamine release. Less severe allergic reactions have also been reported, consisting of “blue hives” (diffuse, blue, maculopapular rashes) without anaphylaxis.39 Grade 2 complication ● Repair Anaphylaxis should be aggressively treated with ﬂuid resuscitation and medications as necessary.38 As a ﬁrst line of therapy, the anesthetic agents are stopped, and the patient is treated with 100% oxygen, large volumes of intravenous ﬂuid, and epinephrine. The second line of therapy consists of H1-blockers and corticosteroids. If the hypotension is refractory, patients

Nerve Damage Patients report sensory deﬁcits after SLNB that are approximately half of those reported by axillary dissection patients.41 This is secondary to damage to branches of the intercostobrachial nerves (as explained previously in this chapter). Most cases improve within 3 months. Grade 1 complication Seroma/Lymphedema The dissection required to identify and excise the sentinel node can lead to complications such as seroma formation

Site of dye injection (peritumoral) Previous incision

Sentinel lymph node

Clavipectoral fascia

Figure 45–4 Sentinel lymph node biopsy: the injection site of the blue dye and its migration to the sentinel lymph node.

470

SECTION VI: BREAST SURGERY

Blue node Blue lymphatic

Figure 45–5 Sentinel lymph node biopsy: a blue lymphatic leading to the sentinel lymph node.

and lymphedema, as discussed previously. The minimal amount of dissection (as compared with axillary dissection), makes lymphedema an uncommon complication of SLNB. Sener and colleagues42 noted only a 3% incidence of lymphedema in patients who underwent SLNB compared with a 17% incidence in patients who had SLNB followed by axillary dissection. They also noted for most of these patients that the mass was located in the upper outer quadrant. The incidence and severity of seroma formation after SLNB are not typically great enough to warrant drain placement. Grade 1–3 complication

Excision of Sentinel Node Failed Sentinel Node ● Consequence If the surgeon is unable to ﬁnd a sentinel node, she or he must proceed to an axillary dissection. This inﬂicts upon the patient the morbidity associated with axillary dissection, even if no positive nodes are ultimately identiﬁed. Grade 2 complication ● Repair A failed SLNB dissection.

necessitates

an

axillary

node

● Prevention The choice of lymphatic tracer inﬂuences the falsenegative rate. A review of the literature found sentinel node identiﬁcation rates to be 81% for blue dye, 92% for radioisotope, and 93% for a combined method.43 SLNB has been less successful in older patients and obese patients.44 As patients age, nodal tissue is replaced by increasing amounts of adipose tissue. For older patients, success of the SLNB is somewhat improved by the combined technique.45

When using blue dye, 2 to 5 ml is injected 5 minutes prior to incision. The injection can be peritumoral, intradermal, retroareolar, or some combination of these. The breast is massaged from the site of injection toward the axilla to enhance the lymphatic migration of the dye. When using radiocolloid, injection is made anywhere from 2 to 24 hours prior to the incision. Lymphoscintigraphy can be performed, but it has not been shown to improve results.46 The background gamma probe count, taken after nodal excision, should be less than 10% of the highest node count.10 Although there is high concordance between intradermal and peritumoral injection,47 an analysis of 966 patients performed at Memorial Sloan-Kettering showed that intradermal injection is associated with a higher success rate.48 McMasters and coworkers49 also showed better results with the dermal technique, identifying sentinel nodes in 98% of dermal injections compared with 89.9% of peritumoral injections. This is likely due to the high density of lymphatic vessels in the skin. Peritumoral injection has been found to be more accurate for localizing nonaxillary sentinel nodes; however, the likelihood of having nonaxillary metastases without having a positive axillary node is very low.43

False-Negative Node ● Consequence A false-negative node is either (1) a negative sentinel node with subsequent discovery (by backup axillary dissection) of positive nodes elsewhere in the axilla or (2) a node found negative by frozen section but subsequently positive by further microscopic studies. The false-negative node can lead to the downstaging of the patient’s disease and failure to implement the appropriate adjuvant therapy. Residual tumor is left in the patient’s axilla, increasing the likelihood of local recurrence. Grade 1–3 complication ● Repair Studies are unclear about returning to the operating room for axillary dissection if a node found negative by frozen section ultimately reveals micrometastases. Radiation has been suggested as an alternative therapy, but at this time, data are insufﬁcient on the subject. Therefore, the current recommendation is to proceed with axillary dissection.6,43 ● Prevention The choice of lymphatic tracer inﬂuences the falsenegative rate. In a review of the literature, falsenegative rates were 9% for blue dye, 7% for radioisotope, and 5% for a combination method.43 The combined method may decrease false-negative rates owing to the increased removal of multiple sentinel nodes.49 The false-negative rate decreases from 14.3% to 4.3% when

45 AXILLARY SURGERY multiple sentinel nodes are removed instead of one, and the only factor independently associated with identiﬁcation of a single sentinel node is the use of blue dye alone.50 More importantly, the experience of the surgeon is directly related to the false-negative rate. Most falsenegative results occur in a surgeon’s ﬁrst 15 cases and are, therefore, best prevented by increased experience of the surgeon.51 Location of the tumor in the lateral half of the breast may increase the false-negative rate when radiocolloid is used, secondary to masking of true sentinel nodes situated close to the site of injection.52 Contrary to initial thoughts, a previous excisional biopsy does not increase the likelihood of a false-negative node.53 It is also important to palpate the axilla for abnormal nodes throughout surgery. A node with a high amount of tissue replacement by tumor cells may not have good uptake of the dye. For both failed and false-negative SLNB: McMasters and associates54 showed that sentinel lymph node identiﬁcation and false-negative rates are greatly improved after a surgeon’s ﬁrst 20 cases. Surgeons new to SLNB should perform backup axillary dissections to validate their results. This means a training period of 20 to 30 SLNBs with subsequent axillary dissection, conﬁrming an identiﬁcation rate greater than 90% and a false-negative rate less than 5%.6 With more experience, the surgeon should be able to improve to an identiﬁcation rate of 95%.55 The axillary dissection should not be abandoned until the surgeon can achieve this level of performance. All palpable lymph nodes are also considered sentinel nodes and should be excised in addition to the node(s) identiﬁed by blue dye or radioactive colloid.

Other Complications Wound Infection ● Consequence Surgical wounds are naturally at risk for infection. The Axillary Lymphatic Mapping Against Nodal Axillary Clearance (ALMANAC) trial56 identiﬁed a 15% infection rate for axillary dissection and an 11% rate for SLNB. The most common organisms identiﬁed are Staphylococcus aureus and Staphylcococcus epidermidis.57 Grade 2a complication ● Repair Treat with the appropriate antibiotic. Open and pack the wound when indicated. ● Prevention Preoperative antibiotics can decrease the rate of infection after breast and axillary surgery by 50%.58 However, most of these cases are associated with a recent previous biopsy.57,59 Thus, preoperative antibiotics are generally not required, except in those patients at increased risk for infection (recent previous open biopsy, alteration of host defense).

471

REFERENCES 1. Degenshein GA, Ceccarelli F. The history of breast cancer surgery. Part I. Early beginning to Halsted. Breast 1977; 3:28–35. 2. Carter CL, Allen C, Nenson DE. Relation of tumor size, lymph node status, and survival in 24,740 breast cancer cases. Cancer 1989;63:181–187. 3. Fisher ER, Sass R, Fisher B. Pathologic ﬁndings from the National Surgical Adjuvant Project for Breast Cancers (protocol no. 4). Cancer 1984;53:712–723. 4. Halsted WS. The results of operations for the cure of cancer of the breast performed at The Johns Hopkins Hospital from June 1889 to January 1894. Johns Hopkins Hosp Bull 1894–1895;4:297. 5. Siegal B, Mayzel K, Love S. Level I and II axillary dissection in the treatment of early stage breast cancer. Arch Surg 1990;125:1144. 6. Schwartz GF. Clinical practice guidelines for the use of axillary sentinel lymph node biopsy in carcinoma of the breast: current update. Breast J 2004;10:85–88. 7. Morton DL, Wen DR, Wong JH, et al. Technical details of intraoperative mapping for early stage melanoma. Arch Surg 1992;127:392–399. 8. Burak WE, Hollenbeck ST, Zervos EE, et al. Sentinel lymph node biopsy results in less postoperative morbidity compared with axillary lymph node dissection for breast cancer. Am J Surg 2002;183:23–27. 9. Giuliano AE, Kirgan DM, Guenther JM, et al. Lymphatic mapping and sentinel lymphadenectomy for breast cancer. Ann Surg 1994;220:391–401. 10. Krag DN, Weaver DL, Alex JC, et al. Surgical resection and radiolocalisation of the sentinel lymph node in breast cancer using a gamma probe. Surg Oncol 1993;2:335– 340. 11. Albertini JJ, Lyman GH, Cox C, et al. Lymphatic mapping and sentinel node biopsy in the patient with breast cancer. JAMA 1996;276:1818–1822. 12. Roses DF, Brooks AD, Harris MN, et al. Complications of level I and II axillary dissection in the treatment of carcinoma of the breast. Ann Surg 1999;230:194–201. 13. Kauppila L, Vastamaki M. Iatrogenic serratus anterior paralysis: long-term outcome in 26 patients. Chest 1996; 109:31–34. 14. Perlmutter GS, Leffert RD. Results of transfer of the pectoralis major tendon to treat paralysis of the serratus anterior muscle. J Bone Joint Surg 1999;81:377–384. 15. Vukov V, Bumbasirevic M, Pecotic G, et al. Isolated serratus anterior paralysis: a simple surgical procedure to reestablish scapulo-humeral dynamics. J Orthop Trauma 1996;10:341–347. 16. Petrek JA, Heelan MC. Incidence of breast carcinoma– related lymphedema. Cancer 1998;83:2776. 17. Petrek JA, Senie RT, Peters M, Rosen PP. Lymphedema in a cohort of breast carcinoma survivors 20 years after diagnosis. Cancer 2001;92:1368. 18. Herd-Smith A, Russo A, Muraca MG, et al. Prognostic factors for lymphedema after primary treatment of breast carcinoma. Cancer 2001;92:1783. 19. Kissen MW, Querci della Rovere G, Easton D, Westburg G. Risk of lymphoedema following treatment of breast cancer. Br J Surg 1986;73:580–584.

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20. Somers RG, Jablon LK, Kaplan MJ, et al. The use of closed suction drain after lumpectomy and axillary node dissection for breast cancer: a prospective randomized trial. Ann Surg 1992;215:146. 21. Jeffrey SS, et al. Axillary lymphadenectomy for breast cancer without axillary drainage. Arch Surg 1995;130:909. 22. Zavotsky J, et al. Evaluation of axillary lymphadenectomy without axillary drainage for patients undergoing breast conserving therapy. Ann Surg Oncol 1998;5:227. 23. Bridges M, Morris D, Hall JR, Deitch EA. Effect of wound exudates on in vitro immune parameters. J Surg Res 1987;43:133–138. 24. Tejler G, Aspergren K. Complications and hospital stay after surgery for breast cancer: a prospective study of 385 patients. Br J Surg 1985;72:542–544. 25. Budd DC, Cochran RC, Sturtz DL, Fouty WJ. Surgical morbidity after mastectomy operations. Am J Surg 1978; 135:218–220. 26. Say CS, Donegan WA. A biostatistical evaluation of complications from mastectomy. Surg Gynecol Obstet 1974;138:370–376. 27. Soon PSH, Clark J, Magarey CJ. Seroma formation after axillary lymphadenectomy with and without the use of drains. Breast 2005;14:103–107. 28. Divino CM, Kuerer HM, Tartter PI. Drains prevent seromas following lumpectomy with axillary dissection. Breast J 2000;6:31–33. 29. Kopelman D, Klemm O, Bahous H, et al. Postoperative suction drainage of the axilla: for how long? Prospective randomized trial. Eur J Surg 1999;165:117–120. 30. Ulusoy AN, Polat C, Alvar M, et al. Effect of ﬁbrin glue on lymphatic drainage and on drain removal time after modiﬁed radical mastectomy: a prospective randomized study. Breast J 2003;9:393–396. 31. Moore M, Burak WE, et al. Fibrin sealant reduces the duration and amount of ﬂuid drainage after axillary dissection: a randomized prospective clinical trial. J Am Coll Surg 2001;192:591–599. 32. Burak WE Jr, Goodman PS, Young DC, Farrar WB. Seroma formation following axillary dissection for breast cancer: risk factors and lack of inﬂuence of bovine thrombin. J Surg Oncol 1997;64:27. 33. Petrek JA, Peters MM, Nori S, et al. Axillary lymphadenectomy: a prospective, randomized trial of thirteen factors inﬂuencing drainage, including early or delayed arm mobilization. Arch Surg 1990;125:378–382. 34. Lyman GH, Giuliano AE, Somerﬁeld MR, et al. American Society of Clinical Oncology guideline recommendations for sentinel lymph node biopsy in early-stage breast cancer. J Clin Oncol 2005;23:7703–7720. 35. Port ER, Fey J, Gemignani ML, et al. Reoperative sentinel lymph node biopsy: a new option for patients with primary or locally recurrent breast carcinoma. J Am Coll Surg 2002;195:167–172. 36. Roumen RMH, Kuijt GP, Liem IH. Lymphatic mapping and sentinel node harvesting in patients with recurrent breast cancer. J Cancer Surg 2006;32:1076–1081. 37. Leong SP, Donegan E, Hefferrnon W, et al. Adverse reactions to isosulfan blue during selective sentinel lymph node dissection in meloanoma. Ann Surg Oncol 2000;7: 361–366.

38. Albo D, Wayne JD, Hunt KK, et al. Anaphylactic reactions to isosulfan blue dye during sentinel lymph node biopsy for breast cancer. Am J Surg 2001;182:393. 39. Komenaka IK, Bauer VP, Schnabel FR, et al. Allergic reactions to isosulfan blue in sentinel lymph node mapping. Breast J 2005;11:70–72. 40. Kalimo K, Jansen CT, Kormano M. Sensitivity to patent blue dye during skin-prick testing and lymphography. Radiology 1981;141:365–367. 41. Temple LKF, Baron R, Cody HS, et al. Sensory morbidity after sentinel lymph node biopsy and axillary dissection: a prospective study of 233 women. Ann Surg Oncol 2002; 9:654–652. 42. Sener SF, Winchester DJ, Martz CH, et al. Lymphedema after sentinel lymphadenectomy for breast carcinoma. Cancer 2001;92:748–752. 43. Bonnema J, van de Veld CJH. Sentinel lymph node biopsy in breast cancer. Ann Oncol 2002;13:1531– 1537. 44. Morrow M, Rademaker AW, Bethke KP, et al. Learning sentinel node biopsy: results of a prospective randomized trial of two techniques. Surgery 1999;126:714. 45. Motomura K, Inaji H, Komoike Y, et al. Combination technique is superior to dye alone in identiﬁcation of the sentinel node in breast cancer patients. J Surg Oncol 2001;76:95. 46. McMasters KM, Wong SL, Tuttle TM, et al. Preoperative lymphoscintigraphy for breast cancer does not improve the ability to identify axillary sentinel lymph nodes. Ann Surg 2000;231:724–731. 47. Borgstein PJ, Meijer S, Pijpers RJ, van Diest PJ. Functional lymphatic anatomy for sentinel node biopsy in breast cancer: echoes from the past and the periareolar blue method. Ann Surg 2000;232:81–89. 48. Cody HS III, Fey J, Akhurst T, et al. Complementarity of blue dye and isotope in sentinel node localization for breast cancer: univariate and multivariate analysis of 966 procedures. Ann Surg Oncol 2001;8:13–19. 49. McMasters KM, Wong SL, Martin RC, et al. Dermal injection of radioactive colloid is superior to peritumoral injection for breast cancer sentinel lymph node biopsy: results of a multiinstitutional study. Ann Surg 2001;233: 676–687. 50. Wong SL, Edwards MJ, Chao C, et al. Sentinel lymph node biopsy for breast cancer: impact of the number of sentinel nodes removed on the false-negative rate. J Am Coll Surg 2001;192:684–689. 51. Cody HS III, Hill ADK, Tran KN, et al. Credentialing for breast lymphatic mapping: How many cases are enough? Ann Surg 1999;229:723–728. 52. Krag D, Weaver D, Ashikaga T, et al. The sentinel node in breast cancer. N Engl J Med 1998;339:941– 946. 53. Haigh PI, Hansen NM, Qi K, et al. Method of biopsy and excision volume do not affect success rate of subsequent sentinel lymph node dissection in breast cancer. Ann Surg Oncol 2000;7:21–27. 54. McMasters KM, Wong SL, Chao C, et al. Deﬁning the optimal surgeon experience for breast cancer sentinel lymph node biopsy: a model for implementation of new surgical techniques. Ann Surg 2001;234:292–299.

45 AXILLARY SURGERY 55. Schwartz GF, Giuliano A, Veronesi U, and the Consensus Conference Committee. Proceedings of the consensus conference on the role of sentinel lymph node biopsy in carcinoma of the breast, April 19–22, 2001, Philadelphia. Cancer 2002;94:2542–2551. 56. Mansel RE, Fallowﬁeld L, Kissin M, et al. Randomized multicenter trial of sentinel node biopsy versus standard axillary treatment in operable breast cancer: the ALMANAC trial. J Natl Cancer Inst 2006;98:599– 609.

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57. Beatty J, Robinson GV, Zaia JA, et al. A prospective analysis of nosocomial wound infection after mastectomy. Arch Surg 1983;118:1421. 58. Platt R, Zaleznik DF, Hopkins CC, et al. Perioperative antibiotic prophylaxis for herniorrhaphy and breast surgery. N Engl J Med 1990;322:153. 59. Wagman LD, Tegtmeier B, Beatty JD, et al. A prospective, randomized double blind study of the use of antibiotics at the time of mastectomy. Surg Gynecol Obstet 1990;170:12.

46

Mastectomy Shawna C. Willey, MD and Elizabeth D. Feldman, MD INTRODUCTION

● Persistent positive margins after multiple attempts at

Although the trend in surgical management of breast cancer is toward less extensive surgery, a signiﬁcant number of patients are still not candidates for minimally invasive procedures who go on to have a mastectomy. Up to 50% of women who are diagnosed with breast cancer undergo mastectomy as their primary surgical therapy.1 Almost all women with breast cancer are candidates for mastectomy. The approach to mastectomy has evolved since William Halsted2 ﬁrst described what is referred to today as the “Halstedian” radical mastectomy in 1894. The Auchincloss modiﬁcation of the radical mastectomy is most consistent with the modiﬁed radical mastectomy (MRM) of today, which includes removal of the entire breast, nipple-areolar complex (NAC), and axillary lymph nodes (levels I, II, and occasionally, III if involved) with preservation of both pectoralis muscles.3 Further modiﬁcation of the MRM occurred with the development of the total mastectomy, which preserves the axillary lymph nodes as well as both pectoralis muscles. Based on the premise that breast cancer is a systemic disease,4 axillary node dissection is not performed if sentinel lymph node biopsy (SLNB) is negative, because it is unlikely to affect survival and has associated morbidity.5 In addition, skin-sparing mastectomy (SSM) has emerged as another approach to surgical therapy for breast cancer since its ﬁrst description by Toth and Lappert in 1991.6 SSM involves the removal of breast parenchyma, the NAC, previous biopsy sites, and skin in close proximity to the lesion and preserves the breast envelope, which facilitates the cosmetic result of the breast reconstruction.

● Recurrence in a breast previously treated with partial

breast-conserving surgical procedures mastectomy and radiation ● Tumor size relative to breast size that does not

allow for an acceptable cosmetic outcome for breast conservation ● Contraindication to radiation ● Patient preference The indications for MRM are similar to those for total mastectomy as they relate to treatment of the breast. However, an axillary dissection is performed in conjunction with the mastectomy if a patient has clinically suspicious axillary disease, circumstances that exclude her from undergoing an SLNB, or a positive sentinel lymph node.5 A mastectomy is an operation with low morbidity and mortality and is well tolerated by patients. However, it is not without complications including seroma, hemorrhage and hematoma, wound infection, skin ﬂap necrosis, recurrence, and pain syndromes, and rarer complications such as pneumothorax, chylous ﬁstula, and air embolism.

OPERATIVE STEPS Step 1

Step Step Step Step Step

2 3 4 5 6

Diagnosis with core needle biopsy (when possible) at two different sites to conﬁrm multicentricity Incision Flap elevation Extent of dissection Wound closure Postoperative concerns

Preoperative Core Needle Biopsy INDICATIONS FOR TOTAL MASTECTOMY ● Multicentricity of disease (two or more primary

tumors in separate quadrants) or diffuse malignant calciﬁcations

Wound Infection ● Consequence Increase in cost, psychological trauma, and cosmetic consequences. Wound infections result in additional medical care including prolonged hospitalization,

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outpatient physician visits, antibiotics, hospital readmissions, or possible surgical drainage. The rates of wound infection are reported to range from 2.8% to 15%.7–9 Grade 1/2 complication ● Repair Antibiotics or, if severe, surgical drainage. ● Prevention Witt and colleagues10 demonstrated that patients who underwent core needle biopsy within 1 to 3 days of a deﬁnitive surgical procedure were at signiﬁcantly higher risk for developing a wound infection (P = .001).10 This effect remained constant even with control for potential confounders such as age, diabetes, benign versus malignant disease, and preoperative marking. The authors suggested increasing the interval between core needle biopsy and deﬁnitive surgery but could not recommend an appropriate interval because most of their patients underwent surgery within 24 hours of biopsy. The use of prophylactic antibiotics has not generally been recommended for clean procedures such as mastectomy. However, in a randomized, double-blind trial of 606 patients undergoing breast surgery (lumpectomy and MRM) with and without perioperative antibiotic prophylaxis, Platt and coworkers11 demonstrated a decrease in infectious complications from 12.2% to 6.6% in those treated with cefonicid no more than 90 minutes prior to incision.11 There were 51% fewer deﬁnite wound infections (deﬁned as a wound with erythema and drainage, one with purulent drainage, and/or one opened and reclosed) and the incidence of purulent drainage decreased by 57%. Staphylococcus aureus was the principal pathogen, accounting for 78% of all isolates.

Incision Skin Flap Necrosis (Fig. 46–1) ● Consequence Local wound care and possible débridement. The incidence of skin ﬂap necrosis has been estimated to be 11% and is similar in SSM and non–skin-sparing mastectomy.12 Grade 1–3 complication ● Repair Hultman and Daiza13 recommend conservative management if possible, including the application of topical antimicrobial creams, minimal débridement, and the use of a supportive brassiere.13 For patients with moderate ﬂap loss as evidenced by full-thickness skin necrosis, stable eschars develop and separate in weeks to months, permitting salvage of the ﬂaps. Severe ﬂap loss involving extensive infarction of the skin envelope often requires operative intervention after demarcation of ﬂap viability.

A

B Figure 46–1 A patient with skin ﬂap necrosis after a mastectomy. A, Far-ﬁeld view of a patient with skin ﬂap necrosis after a mastectomy. B, Close-up view.

● Prevention Factors believed to contribute to necrosis include inadequate blood supply to the ﬂap, wound closure under tension, external pressure from compression dressings, obesity, and type of incision (vertical vs. transverse). Hultman and Daiza13 also found that diabetes and a history of radiation as well as increased body mass index (BMI) were associated with native skin ﬂap complications. Interestingly, unlike previous reports, recent or active tobacco use did not seem to contribute to ﬂap necrosis. Vlajcic and colleagues14 described the use of an omega or inverted omega incision around the NAC in order to preserve the “mesentery-like” horizontal septum of the breast that carries the main vascular and nerve channeling structure of the NAC ﬁrst noted by Wuringer and associates in 199815 (Fig. 46–2). They proposed that periareolar or circumareolar incisions were inappropriate for peripheral lesions because they mandated tunneling, which can compromise the ﬂaps. The horizontal lateral extension of the omega can be used for tumors in the lateral hemisphere of the breast, axillary dissection, and exposure of the thoracodorsal vessels.

46 MASTECTOMY

12

12

9

3 6

6

A

B Figure 46–2 The omega incision constructed both superior and inferior to the nipple-areolar complex. A, Frontal view. B, Oblique view.

The dissection of skin ﬂaps with a constant thickness is important in maintaining the viability of the ﬂap. The application of clamps (Lahey or Adairs) or skin hooks on the underside of the ﬂap with constant, even tension by the assistant at right angles to the chest wall allows visualization of the dissection plane and ﬂap development. Similarly, long, even strokes with a cautery or knife in parallel with the ﬂap contribute to the “evenness” of the ﬂap and minimize accidental “burns” and “buttonholes.”

Inability to Reconstruct ● Consequence Diminished cosmetic outcome and psychological trauma. Grade 1 complication ● Prevention The choice of incision is dependent both on the location of the primary tumor and on the reconstructive options considered (Fig. 46–3). Generally, a skinsparing incision with adequate margins is used if immediate reconstruction is planned. Conventional SSM

477

entails the excision of the NAC and previous biopsy scars with the preservation of the skin envelope. The same amount of breast parenchyma is removed. SSM beneﬁts the aesthetic outcomes for all types of reconstruction in that it preserves or accurately restores the inframammary fold (IMF), improves shaping of the breast mound, retains sensibility of the skin envelope, and uses the breast skin in the ﬁnal reconstruction.16 SSM is not indicated in patients with inﬂammatory carcinoma, large tumors, and locally advanced disease in which the risk of recurrence is high.17 An SSM generally includes removal of the NAC as well as all previous biopsy scars, especially if associated with a previous excision with positive margins. Laronga and coworkers18 showed that nodal positivity, subareolar tumor location, and multicentricity were signiﬁcant risk factors for NAC involvement. Although these authors quoted a NAC positivity for occult carcinoma of 5.6%, a literature review by Cense and colleagues19 found that the NAC was involved in as many as 58% of mastectomy specimens. They concluded that the best candidates for NAC conservation, a new trend in mastectomy, were T1 tumors more than 4 cm from the nipple. If no reconstruction is planned, a transverse or slightly oblique elliptical incision is used (see Fig. 46–3). Vertical incisions are avoided because they can limit upper extremity range of motion.

Flap Elevation Seroma Formation ● Consequence Discomfort, repeated aspiration, and wound infection. Seroma formation arises from the inﬂammatory exudates and the transection of blood vessels and lymphatics. Some studies have demonstrated an increase in seroma formation with the use of electrocautery compared with scalpel (38% vs. 13%, P = .01),20 whereas others have not found a statistically signiﬁcant difference.21,22 Seromas not only can cause discomfort but also may delay the start of adjuvant therapy. Grade 1/2 complication ● Repair Treatment may include aspiration or placement of a drain if repeated aspiration is unsuccessful. ● Prevention The use of a closed suction drain beneath the skin ﬂaps may decrease dead-space and subsequent seromas, as ﬁrst proposed by Murphy in 1947.23 However, Puttawibul and associates24 demonstrated no statistically signiﬁcant difference in complications in patients with and without drains in the pectoral area. More recently, Jain and coworkers25 demonstrated that the use of suction catheter drainage did not prevent seroma formation and was associated with prolonged postoperative stay and higher postoperative pain scores. In

478

SECTION VI: BREAST SURGERY

A Central

B Upper outer

C Upper inner

D Lower outer

E Lower inner

addition, the incidence and rate of seroma formation in patients having mastectomy without drainage but with ﬁbrin sealant installation were both signiﬁcantly reduced compared with closed drainage as in the standard technique. The type of drain placed has also been reviewed. Porter and colleagues20 noted in their comparison of JacksonPratt to Blake drains that Blake drains were more effective in reducing seroma formation (P = .006). In addition, Coveney and associates26 suggested that suturing the skin ﬂaps to the underlying muscle can minimize seroma formation. They found that the incidence of seroma in patients who underwent closed suction drainage was signiﬁcantly less (P < .05) and there was a decreased number of seromas in the group that had their ﬂaps sutured compared with those that did not.

Figure 46–3 Creation of an elliptical incision with respect to the location of the tumor and margins. The vector of the ellipse is modiﬁed to include the tumor with appropriate margins. A, Central. B, Upper outer. C, Upper inner. D, Lower outer. E, Lower inner.

Smaller studies have examined the use of the harmonic scalpel in performing the dissection without direct comparison with either electrocautery or scalpel.27,28 It was postulated that the harmonic scalpel has decreased thermal injury compared with electrocautery and results in sealing of vascular and lymphatic channels. Deo and Shukla28 noted a diminished postoperative drain volume in patients with mastectomies performed with harmonic scalpel compared with conventional mastectomy (430 ml/patient vs. 1100 ml/patient). In contrast to the studies by Jain and coworkers25 noted earlier, there have also been studies using intraoperative ﬁbrin sealant29 as well as sclerosing agents such as tetracycline to reduce dead space30 that have not demonstrated statistically signiﬁcant decreases in seroma formation compared with control.

46 MASTECTOMY The removal of the pectoralis major fascia may also contribute to seroma formation. Dalberg and coworkers31 randomized 247 patients to removal or preservation of the pectoralis major fascia and did not detect a statistically signiﬁcant difference in seroma formation between groups.

Hemorrhage and Hematoma Formation ● Consequence Anemia, blood transfusion, and wound infection. Blood transfusion has long been associated with morbidity and mortality with multiple potential and actual adverse effects including allergic reactions and transmission of communicable diseases. The detrimental effect of perioperative blood transfusion on survival after operations for cancer surgery has been reported.32–34 The percent of patients who undergo mastectomy and require blood transfusion is not consistently reported. Patients may also suffer from postmastectomy pain syndrome secondary to axillary hematoma formation.35 This chronic neuropathic pain syndrome is a long-lasting continuous pain in the axilla, medial upper arm, and lateral chest wall beginning shortly after surgery. The pain is characterized as paroxysms of lancinating pain against a background of burning, aching, and tightening sensations.36–38 Grade 1 complication ● Prevention Several studies have demonstrated statistically signiﬁcant increases in intraoperative blood loss as well as postoperative packed cell volume transfusion in mastectomy performed with scalpel compared with electrocautery.21,22 Electrocautery has the principal advantage of being able to coagulate as it cuts or dissects. An alternative may be the harmonic scalpel, which uses high-frequency ultrasonic waves for dissection and hemostasis and has had encouraging results in the laparoscopic and cardiovascular surgical ﬁelds.39,40 It causes breakdown of hydrogen bonds and forms a protein coagulum to occlude the vascular and lymphatic channels.28 Again, multiple small studies have suggested the feasibility of using the harmonic scalpel for ﬂap dissection, removal of the breast parenchyma from the pectoralis muscle, and axillary dissection.27,28 However, direct comparison with conventional instruments is not yet available, and the expense related to the instrument may be prohibitive.

Extent of Dissection Recurrence ● Consequence Chest wall (68%) and supraclavicular nodes (41%) were the most common sites of locoregional recurrence in a review of 1031 patients who were treated with mastectomy and doxorubicin-based chemotherapy without irradiation in ﬁve prospective trials.41 Skin ﬂap recurrence is a frequent type of local recurrence after mas-

479

tectomy42 and depends on ﬂap thickness. In addition, a proportion of breast tissue may be left behind in attempts to preserve the IMF during mastectomy to facilitate breast reconstruction. The IMF is a zone of adherence of the superﬁcial fascial system to the underlying chest wall43 and is anatomically deﬁned as the area where the skin of the lower pole of the glandular breast tissue meets the chest wall. At this junction, the breast parenchyma is bound down tightly to the deep fascia of the thoracic wall. A proportion of breast tissue may be left behind in attempts to preserve the IMF during mastectomy to facilitate breast reconstruction. Grade 2/3 complication ● Repair Postoperative radiation therapy or reexcision depending on anatomy. ● Prevention Skin ﬂap recurrence might result from tumor emboli implantation in the wound or small, unrecognized foci in thick skin ﬂaps. Tumor emboli can escape from blood vessels or lymphatics cut during the operation. The thickness of the skin ﬂap that is elevated is often debated among surgeons. Tewari and associates42 took biopsies of four quadrants under the skin ﬂaps of 37 patients with stages ranging from T1N1 to T4bN1. They found residual breast tissue in 8 (21.6%), with carcinoma cells in 3 of 8 patients (37.5%). Skin involvement is also signiﬁcantly related to the site of the tumor, clinical T staging, skin tethering, pathologic tumor size, and perineural inﬂammation as demonstrated by Ho and coworkers44 in a detailed serial-section examination of 30 total mastectomy specimens. Traditionally, the technique is to dissect the ﬂaps just above the superﬁcial layer of the superﬁcial fascia of the breast. In a study of ﬂap thickness, Krohn and colleagues45 compared the survival and recurrence rates of women who had “ultrathin” ﬂaps with patients with thicker ﬂaps during mastectomy. The authors found similar 5- and 10-year survival rates as well as recurrence rates. However, patients with the ultrathin ﬂaps had increased incidences of wound complications, length of hospital stay, and lymphedema. More recently, Beer and associates46 found that the superﬁcial layer of the superﬁcial fascia of the breast was absent in 44% of the resected specimens. They noted that when the superﬁcial layer was present, there were islands of breast tissue within the superﬁcial layer in 42% of the specimens. When present, the superﬁcial layer had an undulating appearance rather than a straight horizontal interface. Furthermore, the distance between the superﬁcial layer and the dermis varied within a single specimen and across all specimens (from <5 mm in 82% to >10 mm in 5.1%), as did the thickness of the superﬁcial layer itself. Thus, Beer and associates46 recommended looking for the presence of the superﬁcial layer, and if visible, it should be used as a plane of dissection, provided that the skin ﬂaps left behind appear viable.

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A Figure 46–5 The “crinkly layer.” The caudal extension of the breast is approximately 2 to 3 cm below the IMF layer, as identiﬁed by loose areolar tissue resembling tissue paper.

B Figure 46–4 The dotted line represents the boundaries of dissection during a mastectomy. A, The boundaries are the anterior border of the latissimus dorsi laterally, the sternal border medially, the inferior border of the clavicle superiorly, and the inframammary fold (IMF) inferiorly. B, Also depicted is the technique of ﬂap elevation.

At our institution, we aim to identify a plane of dissection that separates visible breast tissue from the region just above the superﬁcial layer. We have observed that this plane of dissection varies between patients, depending on body habitus, and leaves a ﬂap thickness on average of 7 to 8 mm. The IMF is another anatomic point of contention. Although the lateral (anterior border of the latissimus dorsi), medial (sternal border), and superior (inferior border of the clavicle) borders of the breast are well deﬁned, the inferior border of the breast is less concrete (Fig. 46–4). Carlson and colleagues47 examined 24 mastectomy specimens obtained from 22 female breast cancer patients. They removed the IMF specimens separately by elevating the inferior skin ﬂaps over the anterior rectus sheath and removing the underlying ﬁbrofatty tissue off the rectus sheath. After the tissue was ﬁxed, parafﬁn-embedded, and sectioned, the slides were screened for breast parenchyma composed of either ductal or lobular elements. The authors demonstrated a mean value of 0.02% breast tissue in the

IMF after the total volume of the specimens was calculated from the dimensions of the fresh tissue. All cases were negative for carcinoma of the residual breast tissue. In a study of 580 consecutive patients, Behranwala and Gui48 identiﬁed only four tumors affecting the IMF (0.7%), all of which were clinically palpable and proven malignant on ﬁne-needle aspiration cytology. They did not note any incidental ﬁnding of breast cancer from additional specimens during their series. Because the IMF may not be fully included on conventional mammographic views, the importance of good palpation of the IMF should be routine during preoperative examination as well as intraoperative assessment. At our institution, we deﬁne the caudal extension of the breast as approximately 2 to 3 cm below the IMF identiﬁed by a layer of loose areolar tissue resembling tissue paper that is referred to as the “crinkly layer” (Fig. 46–5). The preservation of the pectoral fascia is an additional point for discussion. Dalberg and coworkers31 noted a trend toward increased chest wall recurrences in patients with preserved fascia, although the overall and eventfree survival did not differ. The total 5-year-cumulative chest wall recurrence rate in patients with preserved fascia was 12% compared with 7% in patients with removed fascia, and the 5-year-local control rates were 86 and 91%, respectively.

Wound Closure Redundant Skin at the Lateral Edge of the Mastectomy Scar ● Consequence Discomfort and poor cosmetic result. This skin can lie at or above the bra line and can be distracting to patients. It can interfere with wearing of an external breast prosthesis and/or require surgical correction.49 Grade 1/3 complication

46 MASTECTOMY

481

A

B

C

D

E Figure 46–6 The technique for the creation of a ﬁsh-tail plasty as described by Hussein and coworkers. A, The elliptical incision of the mastectomy scar. B, The wound after a mastectomy is completed. C, The upper and lower skin ﬂaps stitched at the anterior axillary line. D, The redundant skin is advanced medially and stitched to the skin ﬂaps such that the “dog ears” can be excised. E, Fish-tail plasty after wound closure. (A–E, From Hussein M, Daltrey I, Dutta S, et al. Fish-tail plasty: a safe technique to improve cosmesis at the lateral end of mastectomy scars. Breast 2004;13:206–209.)

● Repair Operative correction. ● Prevention Farrar and Fanning50 ﬁrst described the idea of Yshaped closure of the mastectomy wound in 1988, and the term ﬁsh-shaped incision was introduced by Nowacki and associates in 1991.51 Hussein and coworkers49 performed 30 ﬁsh-tail plasties in 28 patients (27 primarily,

3 delayed) to prevent “dog-ear deformity” (Fig. 46–6). They achieved good cosmetic results in all 28 patients, and none required surgical revision. Patients who were older (>70 yr) and obese (BMI > 30) with large breasts (mean weight of resected tissue 1015 g) needed to undergo a ﬁsh-tail plasty in their study. This technique did not prolong hospitalization. Similarly, Gibbs and Kent52 described their technique for creating a lateral V-Y advancement ﬂap by retracting

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B

A

C

D

E Figure 46–7 Modiﬁed V-Y advancement technique for mastectomy closure. A, Standard incision for mastectomy. B, The lateral apex is retracted for marking the superior and inferior ﬂaps. C, The superior and inferior ﬂaps are excised along the dotted line. D, The lateral apex is retracted medially and secured to the superior and inferior skin edges. E, The closure as it appears after completion. (From Gibbs ER, Kent RB 3rd. Modiﬁed V-Y advancement technique for mastectomy closure. J Am Coll Surg 1998;187:632–633.)

the lateral apex medially and securing it to the approximated transverse incision about one third of the way medial in the incision (Fig. 46–7). The incision is closed with a newly created Y conﬁguration. Other techniques include extending the ellipse (by further lengthening of the wound) and excising excess tissue. The scar may eventually extend around the back and further diminish the cosmetic result. Flap length discrepancy is a key factor in the creation of dog ears. Gold53 described a technique similar to the one we use at our institution whereby skin length of both the superior and the inferior ﬂaps is measured with a silk suture to avoid length asymmetry between both limbs of the ellipse (Fig. 46–8). The technique was applied to over 250 patients and was especially effective in patients with small breasts and relatively large tumors situated large distances from the NAC.

Suture-Associated Issues ● Consequence Suture removal may provoke patient anxiety and result in suture tracks. It also requires an additional follow-up visit. Grade 1 complication ● Repair Use of tissue adhesive as an alternative to sutures. ● Prevention Gennari and colleagues54 conducted a prospective, randomized trial comparing skin closure with the tissue adhesive 2-octylcyanoacrylate (OCA) with subcuticular monoﬁlament suture and then blindly assessed cosmetic and economic outcome at various time points. They found that tissue adhesive skin closure was faster

46 MASTECTOMY

B A

A B

A

B

C

D

E

Figure 46–8 Measurement with silk sutures for ﬂap length. A, Marking the long and short axes of the intended skin incision. B, A snugly clamped suture to mark the superior skin incision. C, A second suture placed to mark the inferior skin incision, leaving the superior suture undisturbed. D, The intended ellipse is traced with a skin marker. E, The wound after a cosmetic closure along the long axis. F, Photographic depiction of the technique.

F

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Lateral pectoral n. Pectoralis major m.

Pectoralis minor m. Medial pectoral n.

Figure 46–9 An artistic rendition of the anatomy of the lateral and medial pectoral nerves as they relate to the pectoralis minor muscle. The lateral pectoral nerve courses along the undersurface of the pectoralis minor muscle, and the medial pectoral nerve courses through the pectoralis minor muscle in 62% and exits around the lateral aspect of the muscle in the remaining 38%.

than the suture closure, the OCA patients developed less tissue reaction, and the total cost in the OCA group was signiﬁcantly lower (P < .001). The cost saving was mostly due to reduced physician and ancillary services and reduced equipment needs. However, there is a learning curve in applying the OCA in that hemostasis must be meticulous because the adhesive polymerizes upon contact with blood and ﬂuid. If polymerization occurs too rapidly, the adhesive can form an unsightly plastic mass on top of the wound. In addition, subcutaneous sutures must be placed to minimize dead space, maximize skin eversion, avoid depressed scarring, and improve cosmetic outcome. Lastly, the preference of staples over sutures for wound closure in mastectomy is not directly addressed in the literature in terms of cosmetic outcome or infectious complications. At our institution, we use subcuticular sutures to approximate the skin edges in mastectomy patients because the psychological impact of staple removal and the skin imprinting from the staples can be devastating to the patient.

Postoperative Concerns Postoperative Muscle Atrophy/Limitation of Shoulder Movement ● Consequence Injury to the lateral pectoral nerve by accidental division, cautery injury, or avulsion produces variable postoperative atrophy, ﬁbrosis, and shortening of the lower third of the pectoralis major muscle (PMM). This limits

shoulder motion and changes the cosmetic contour of the pectoral region of the chest. Grade 3 complication ● Repair Reconstruction with skin-muscle ﬂaps, as opposed to breast implants or tissue expansion, to correct the infraclavicular depression followed with breast implants. ● Prevention Awareness of the anatomic distribution and course of the medial and lateral pectoral nerves is essential to the preservation of the PMM and its function. The upper part of the PMM is innervated by the medial pectoral nerve, whereas the lateral pectoral nerve supplies the lower third of the muscle.55 The lateral pectoral nerve courses along the undersurface of the PMM and may be compromised during division and retraction of removal of the pectoralis minor muscle (Fig. 46–9). In 100 cadaver dissections, Moosman55 demonstrated that the medial pectoral nerve coursed through the pectoralis minor muscle in 62% of the specimens, whereas it exited around the lateral aspect of the muscle in the remaining 38% (see Fig. 46–9). Hoffman and Elliot56 had similar ﬁndings and suggested that dissection between the PMM and the pectoralis minor muscle is more likely to result in disruption of a signiﬁcant portion of the innervation to the PMM. In addition, capsule formation around breast implants has been implicated as causing compression of the medial and lateral pectoral nerves under the PMM.

46 MASTECTOMY

Phantom Breast Phenomena ● Consequence Psychological consequences as well as need for pain management. Phantom breast syndrome (PBS) refers to both painful and painless sensations of persistence of the entire breast or parts of it despite its absence. Onset may be immediately after mastectomy or more than 1 year after mastectomy58 and may persist for years. The incidence of PBS is reported to vary from 17% to 64%.59,60 Grade 1 complication ● Prevention PBS sensation may be the nonpainful variety: numbness, tension, twinging, pressuring, pounding, itching, pricking, and bothering as described by Rothemund and associates.61 The authors also addressed the painful variant, which included sensations such as twinging, tearing, tense, cutting, sharp, convulsive, pressing, and cramplike. Whereas Rothemund and associates61 found no relation of PBS to age, Staps and coworkers62 reported that in their study of 89 women surveyed, those with PBS tended to be younger (<55 yr) and premenopausal, they more often had children and a preoperative history of breast sensation.62 Kroner and colleagues63 performed a prospective study of 120 women who underwent mastectomy in order to investigate the clinical picture of PBS, its temporal course, and the possible relationship between premastectomy breast pain and PBS. They found that the incidence of PBS was 25% initially and decreased to about 12% at 1 year and that the location of the sensations changed from periareolar to the remainder of the breast over time. Like Rothemund and associates,61 Kroner and colleagues63 did not note a relationship with PBS and age, but they did ﬁnd a signiﬁcant relationship between preoperative breast pain and PBS. The majority of patients described their pain as knifelike, sticking, shooting, or exteroceptive-like pain that could be provoked or relieved by various environmental stimuli such as emotional distress, exercise, or touch. The attacks tended to be of high intensity but of very short duration.

Other Complications Pneumothorax Pneumothorax is reported to have an incidence of approximately 1% after MRM.64 This may be secondary to technique or preexisting medical conditions like asthma. Treatment may include observation, chest tube insertion, or even video-assisted thoracoscopic surgery with pleurodesis in the event of failure of resolution of the pneumothorax with simple chest tube insertion. Grade 1/2 complication

485

Chylous Fistula A chylous ﬁstula after an MRM is a rare occurrence. However, major anatomic variations in the termination of the thoracic duct may occur, rendering it susceptible to injury.65 Nakajima and associates66 described four cases of chylous ﬁstula after breast operations. In this paper, the authors were able to treat all patients with conservative management including cessation of oral intake and institution of intravenous nutrition for several weeks. However, in the face of failure of nonoperative management, surgical ligation of the leaking thoracic duct or branch thereof may be necessary. This complication is technically a function of the axillary dissection component of the MRM. Grade 2/3 complication Rare Complications We surveyed multiple, highly regarded breast surgeons in order to ascertain the incidence of more unusual complications associated with mastectomies, given the paucity of literature on this subject. Their experiences totaled more than 3500 mastectomies over 20 years and included 1 deep venous thrombosis, 8 examples of ﬂap necrosis requiring operative intervention, 1 pneumothorax secondary to injection of local anesthetic, 5 instances of hemorrhage mandating blood transfusion, 6 postoperative hematomas requiring reoperation, 4 wound infections needing exploration in the operating room, 13 persistent seromas necessitating operative intervention, 1 air embolism, and 1 death secondary to sepsis originating from an infected hematoma. None of the surgeons reported any experiences with chylothorax, which has been suggested in the literature but not documented.

Acknowledgments We would like to thank Alison Estabrook, MD, Lorraine Tafra, MD, Victor Zannis, MD, and Mel Silverstein, MD, for contributing data from their vast experience.

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24. Puttawibul P, Sangthong B, Maipang T, et al. Mastectomy without drain at pectoral area: a randomized controlled trial. J Med Assoc Thai 2003;86:325–331. 25. Jain PK, Sowdi R, Anderson AD, et al. Randomized clinical trial investigating the use of drains and ﬁbrin sealant following surgery for breast cancer. Br J Surg 2004;91:54–60. 26. Coveney EC, O’Dwyer PJ, Geraghty JG, et al. Effect of closing dead space on seroma formation after mastectomy—a prospective randomized clinical trial. Eur J Surg Oncol 1993;19:143–146. 27. Galatius H, Okholm M, Hoffmann J. Mastectomy using ultrasonic dissection: effect on seroma formation. Breast 2003;12:338–341. 28. Deo SV, Shukla NK. Modiﬁed radical mastectomy using harmonic scalpel. J Surg Oncol 2000;74:204–207. 29. Johnson L, Cusick TE, Helmer SD, et al. Inﬂuence of ﬁbrin glue on seroma formation after breast surgery. Am J Surg 2005;189:319–323. 30. Rice DC, Morris SM, Sarr MG, et al. Intraoperative topical tetracycline sclerotherapy following mastectomy: a prospective, randomized trial. J Surg Oncol 2000;73:224– 227. 31. Dalberg K, Johansson H, Signomklao T, et al. A randomised study of axillary drainage and pectoral fascia preservation after mastectomy for breast cancer. Eur J Surg Oncol 2004;30:602–609. 32. Blumberg N, Agarwal MM, Chuang C. Relation between recurrence of cancer of the colon and blood transfusion. Br Med J (Clin Res Ed) 1985;290:1037–1039. 33. Blumberg N, Heal JM, Murphy P, et al. Association between transfusion of whole blood and recurrence of cancer. Br Med J (Clin Res Ed) 1986;293:530–533. 34. Eickhoff JH, Andersen PM, Norgard H. Effect of perioperative blood transfusion on recurrence and death after mastectomy for breast cancer. Acta Chir Scand 1988; 154:425–428. 35. Blunt C, Schmiedel A. Some cases of severe postmastectomy pain syndrome may be caused by an axillary haematoma. Pain 2004;108:294–296. 36. Carpenter JS, Andrykowski MA, Sloan P, et al. Postmastectomy/postlumpectomy pain in breast cancer survivors. J Clin Epidemiol 1998;51:1285–1292. 37. Kwekkeboom K. Postmastectomy pain syndromes. Cancer Nurs 1996;19:37–43. 38. Stevens PE, Dibble SL, Miaskowski C. Prevalence, characteristics, and impact of postmastectomy pain syndrome: an investigation of women’s experiences. Pain 1995;61:61–68. 39. Amaral JF. Laparoscopic cholecystectomy in 200 consecutive patients using an ultrasonically activated scalpel. Surg Laparosc Endosc 1995;5:255–262. 40. Ohtsuka T, Wolf RK, Hiratzka LF, et al. Thoracoscopic internal mammary artery harvest for MICABG using the harmonic scalpel. Ann Thorac Surg 1997;63(6 suppl): S107–S109. 41. Katz A, Strom EA, Buchholz TA, et al. Locoregional recurrence patterns after mastectomy and doxorubicinbased chemotherapy: implications for postoperative irradiation. J Clin Oncol 2000;18:2817–2827. 42. Tewari M, Kumar K, Kumar M, et al. Residual breast tissue in the skin ﬂaps after Patey mastectomy. Indian J Med Res 2004;119:195–197.

46 MASTECTOMY 43. Lockwood TE. Superﬁcial fascial system (SFS) of the trunk and extremities: a new concept. Plast Reconstr Surg 1991;87:1009–1018. 44. Ho CM, Mak CK, Lau Y, et al. Skin involvement in invasive breast carcinoma: safety of skin-sparing mastectomy. Ann Surg Oncol 2003;10:102–107. 45. Krohn IT, Cooper DR, Bassett JG. Radical mastectomy: thick vs thin skin ﬂaps. Arch Surg 1982;117:760– 763. 46. Beer GM, Varga Z, Budi S, et al. Incidence of the superﬁcial fascia and its relevance in skin-sparing mastectomy. Cancer 2002;94:1619–1625. 47. Carlson GW, Grossl N, Lewis MM, et al. Preservation of the inframammary fold: what are we leaving behind? Plast Reconstr Surg 1996;98:447–450. 48. Behranwala KA, Gui GP. Breast cancer in the inframammary fold: is preserving the inframammary fold during mastectomy justiﬁed? Breast 2002;11:340–342. 49. Hussien M, Daltrey IR, Dutta S, et al. Fish-tail plasty: a safe technique to improve cosmesis at the lateral end of mastectomy scars. Breast 2004;13:206–209. 50. Farrar WB, Fanning WJ. Eliminating the dog-ear in modiﬁed radical mastectomy. Am J Surg 1988;156:401– 402. 51. Nowacki MP, Towpik E, Tchorzewska H. Early experience with “ﬁsh-shaped” incision for mastectomy. Eur J Surg Oncol 1991;17:615–617. 52. Gibbs ER, Kent RB 3rd. Modiﬁed V-Y advancement technique for mastectomy closure. J Am Coll Surg 1998; 187:632–633. 53. Gold JP. Assurance of ﬂap symmetry following mastectomy using intraoperative measurement. Surg Gynecol Obstet 1984;158:169–172. 54. Gennari R, Rotmensz N, Ballardini B, et al. A prospective, randomized, controlled clinical trial of tissue adhesive (2octylcyanoacrylate) versus standard wound closure in breast surgery. Surgery 2004;136:593–599.

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55. Moosman DA. Anatomy of the pectoral nerves and their preservation in modiﬁed mastectomy. Am J Surg 1980; 139:883–886. 56. Hoffman GW, Elliott LF. The anatomy of the pectoral nerves and its signiﬁcance to the general and plastic surgeon. Ann Surg 1987;205:504–507. 57. Wallace MS, Wallace AM, Lee J, et al. Pain after breast surgery: a survey of 282 women. Pain 1996;66:195–205. 58. Ackerly W, Lhamon W, Fitts WT Jr. Phantom breast. J Nerv Ment Dis 1955;121:177–178. 59. Bressler B, Cohen SI, Magnussen F. The problem of phantom breast and phantom pain. J Nerv Ment Dis 1956;123:180–187. 60. Lorenzoni E, Heidenreich W. [Phantom sensations following mastectomy (author’s transl)]. Geburtshilfe Frauenheilkd 1982;42:63–65. 61. Rothemund Y, Grusser SM, Liebeskind U, et al. Phantom phenomena in mastectomized patients and their relation to chronic and acute pre-mastectomy pain. Pain 2004;107:140–146. 62. Staps T, Hoogenhout J, Wobbes T. Phantom breast sensations following mastectomy. Cancer 1985;56:2898– 2901. 63. Kroner K, Krebs B, Skov J, et al. Immediate and long-term phantom breast syndrome after mastectomy: incidence, clinical characteristics and relationship to pre-mastectomy breast pain. Pain 1989;36:327–334. 64. Hoefer RA Jr, DuBois JJ, Ostrow LB, et al. Wound complications following modiﬁed radical mastectomy: an analysis of perioperative factors. J Am Osteopath Assoc 1990;90:47–53. 65. Purkayastha J, Hazarika S, Deo SV, et al. Post-mastectomy chylous ﬁstula: anatomical and clinical implications. Clin Anat 2004;17:413–415. 66. Nakajima E, Iwata H, Iwase T, et al. Four cases of chylous ﬁstula after breast cancer resection. Breast Cancer Res Treat 2004;83:11–14.

Section VII

SOFT TISSUE AND SKIN Steven K. Libutti, MD Experience is simply the name we give our mistakes.—Oscar Wilde

47

Management of Soft Tissue Sarcoma James C. Yang, MD INTRODUCTION The surgical approach to soft tissue sarcomas (STS) has evolved extensively and, in some cases, paradoxically since the mid 1980s. During the 1950s and 1960s, insufﬁciently aggressive surgery was considered the shortfall in the treatment of primary sarcomas, but with improvements in diagnosis, imaging, and adjunctive therapies, this is no longer the case. Although changes in technique and procedures have occurred, these have not been nearly as dramatic as those for sarcomas of bony origin. Therefore, the pitfalls for the surgeon treating STS tend to be errors in judgment rather than in technique. This chapter reviews the potential causes of suboptimal therapy at each stage of dealing with STS, including imaging, biopsy, pathology, surgical plann-ing, resection, and adjuvant therapies.

planned with the elements of a future deﬁnitive cancer operation in mind. Such an operation must be able to encompass any sites that were violated during a biopsy or other manipulation of the mass. If the planning of a deﬁnitive cancer operation is not clear from clinical examination, imaging of the mass and surrounding tissues should precede a biopsy and help determine its placement. If the approach to a resection is apparent, the biopsy and all violated tissues should lie well within the margins of that potential resection. The best chance of an adequate resection is at the ﬁrst operation, and therefore, attention to detail with respect to adequacy of resection and incorporation of any biopsy sites is critical to a successful outcome. Both imaging and biopsy will be required for all but small, simple, or superﬁcial masses. These evaluation modalities are examined individually.

POTENTIAL PITFALLS IN MAKING THE DIAGNOSIS

POTENTIAL PITFALLS INVOLVING PROPER STAGING

When a patient presents with a newly discovered soft tissue mass, most often of the extremities, the ﬁrst decision is what amount of investigation is warranted. Nearly all soft tissue masses over 3 cm or with symptoms will require a deﬁnitive investigation to determine their identity and risk to the patient. Many smaller masses may also need vigorous investigation unless a benign clinical diagnosis can be made with assurance. If suspicion of malignancy cannot be allayed, any invasive intervention must be

A potential pitfall in the work-up of a soft tissue mass is in the misclassiﬁcation of the lesion or in an inadequate staging of the extent of the disease. Prior to discussing management, a brief description of STS is in order. Sarcomas in general are divided into pediatric versus adult tumors and soft tissue versus bony tumors. This is because there are signiﬁcant differences in clinical behavior, prognosis, and treatment between these entities. Pediatric “small, round, blue cell tumors”

SECTION VII: SOFT TISSUE AND SKIN

(including alveolar and embryonal rhabdomyosarcomas, Ewing’s sarcoma, and primitive neuroectodermal tumors) often disseminate widely and require chemotherapy as the mainstay of treatment. These can also occur in young adults in whom they lead to diagnostic dilemmas and mistreatment. Many of the pediatric tumors have been found to have molecular markers that facilitate deﬁnitive diagnosis,1 and these should be investigated if any doubts are raised that a tumor in a young adult is an atypical presentation of a pediatric sarcoma, because treatment may be radically altered. Conversely, for true adult sarcomas, surgery is the primary treatment for localized as well as limited metastatic disease, and dissemination is often conﬁned to the lungs, where chemotherapy is of minimal beneﬁt. Osteosarcomas and other bony tumors of young adults differ from adult STS in diagnostic and surgical approaches, as well as in the use of adjuvant chemotherapy, which is effective in the former but not the latter.

An Approach to Proper Staging to Avoid Misdiagnosis For true adult STS, there are hundreds of potential individual tumor types, but the majority share similar therapeutic approaches as well as similar staging and prognosis. Localized tumors are staged partially by histologic grade, size (≤5 cm or >5 cm in diameter), and depth of involvement (superﬁcial or deep to fascia). Nodal involvement is rarely a consideration in the presentation of STS (but is a poor prognostic factor when present). The dominant prognostic parameter is the histologic grade, based on its microscopic appearance. An experienced pathologist will use characteristics such as pleomorphism, cellularity, mitotic rate, and necrosis to assign a grade to a tumor; this drives the clinical staging system. The ability of different pathologists to do this accurately varies widely,2 and here, the surgeon is at the mercy of the anatomic pathologist. The latest American Joint Committee on Cancer (AJCC) staging system is presented in Table 47–1, and the prognosis of these stages is shown in Figure 47–1.3 Thus, it is evident that misidentiﬁcation and mistakes in staging of STS can be some of the earliest and most detrimental pitfalls for those treating this disease, because these errors will lead to mistreatment. Therefore, the biopsy is critical to sarcoma management.

PROPER APPROACH TO PREOPERATIVE BIOPSY TO AVOID LOCAL RECURRENCE For uncomplicated, superﬁcial masses less than 3 cm, simple excision is the indicated biopsy. This has the advantages of complete histologic sampling and deﬁnitive treatment if malignancy is not found. Major errors in this area can occur if the lesion proves to be a sarcoma. The exci-

Table 47–1 Staging of Adult Soft Tissue Sarcomas Stage

Primary Tumor

Metastases*

Grade

Size

Depth

I

Low

Any

Any

No

II

High

≤5 cm

Any

No

High

>5 cm

Superﬁcial

No

III

High

>5 cm

Deep

No

IV

Any

Any

Any

Yes

*Nodal or distant. From Fleming ID, Cooper JS, Henson DE, et al (eds): AJCC Cancer Staging Manual, 5th ed. Philadelphia: Lippincott-Raven, 1997.

Probability of metastasis-free survival

490

1.0

Stage I

.9 .8

Stage II

.7 .6 .5

Stage III

.4 .3 .2 .1 0

0 12 24 36 48 60 72 84 96 108120132144156168180 Months from diagnosis

Figure 47–1 Metastasis-free survival by the American Joint Committee on Cancer (AJCC) stage (minimal differences from current staging) for localized adult soft tissue sarcomas. Low-grade lesions (stage I) have a very low risk of metastasis, even with prolonged follow-up. (From Wunder JS, Healey JH, Davis AM, Brennan MF. A comparison of staging systems for localized extremity soft tissue sarcoma. Cancer 2000;88:2721–2730.)

sion scar should be longitudinal on the limb to facilitate wide reexcision, and drains should be avoided if at all possible or, when necessary, placed immediately adjacent to the wound. Hemostasis is of the highest priority because many sarcomas can be quite vascular, and hematoma can carry malignant cells throughout tissue planes within a limb, leading to an otherwise avoidable amputation. For larger or more complex lesions, a diagnostic biopsy is indicated. This can often be accomplished adequately by core needle biopsy, depending on the experience of the facility and pathologist. Some institutions advocate ﬁneneedle assessment, but in our hands, this is often inadequate for complete staging and occasionally incorrect (owing to sampling error) when compared with the ultimate resection specimen.4 A bruit, thrill, or pulsation should alert one to the possibility of a vascular sarcoma and the potential for major bleeding from a biopsy. Hematuria, abdominal mass, or associated bony destruction should raise the possibility of a bony metastasis from renal

47 MANAGEMENT OF SOFT TISSUE SARCOMA cancer with a soft tissue component masquerading as a sarcoma because these are particularly prone to hemorrhage after biopsy. Very large or ﬁxed lesions should have imaging performed prior to biopsy to identify areas of solid tumor versus liquefaction and to evaluate the structures that may need to be sacriﬁced in future operations. For instance, when an amputation is a possibility for a large, deep, proximal thigh lesion, consideration should be given to preserving the appropriate anterior or posterior hemipelvectomy ﬂap and not compromise it with a biopsy site. Prebiopsy imaging suggesting bone or major neurovascular involvement would particularly raise such a concern. Conversely, if an unequivocal diagnosis of lowgrade (grade I) sarcoma is made from a biopsy, a lesser, nonablative surgical option may be entertained. In such a situation, the surgeon relies heavily on the pathologist to accurately “predict” the biologic behavior of the tumor based on histology. A relatively small number of experienced sarcoma pathologists have seen sufﬁcient cases and have an adequate clinical database to assess and reﬁne their own reliability. For most experts, designating a sarcoma as “grade I” indicates that there is less than a 10% chance (and in most cases, 5% or less) that this lesion will ever show metastatic behavior. Even large grade I lesions, when correctly identiﬁed, are typically limb-threatening rather than life-threatening malignancies, and the options for local therapy are perhaps more ﬂexible. Although the causal link between local recurrence and metastatic disease has come under major scrutiny based on animal data as well as prospective, randomized clinical studies, the surgeon undoubtedly feels more comfortable considering a function-sparing procedure with a higher risk of local recurrence if he or she knows he or she is dealing with a lesion with minimal metastatic potential. In a published

491

experience from our institution, none of 67 patients with a diagnosis of low-grade (grade I) sarcoma of the extremities required an amputation at their initial presentation.5 The metastasis-related mortality in this group was only 4%, with a maximum follow-up extending beyond 10 years. Therefore, limb-sparing and function-sparing operations within this group of patients with low-grade sarcomas are the rule, and the major pitfall in their care is not adequately considering these options. If the biopsy reveals an unequivocal high-grade lesion, the appropriate deﬁnitive procedure can be planned without further disturbing tissue planes.

PROPER APPROACH TO PREOPERATIVE IMAGING Imaging of extremity sarcomas is also a point of some controversy. Plain radiographs have little utility, and the main competing modalities are computed tomography (CT) scanning and magnetic resonance imaging (MRI). Because the radiodensity and vascularity of some sarcomas differ minimally from surrounding tissues, they can be difﬁcult to delineate on CT (Fig. 47–2). Conversely, the effects that very large compressive masses can have on surrounding tissue vis-à-vis inﬂammation, edema, and ischemia can exaggerate the apparent size of the malignancy on MRI. This can lead to procuring excess margins at a high functional cost. As an example, a patient with a large high-grade sarcoma was evaluated by MRI (Fig. 47–3), and there appeared to be intimate contact between the tumor and the femur over a signiﬁcant portion of its circumference. Rather than plan an amputation, exploration to evaluate local resection showed the periosteum to

Figure 47–2 Computed tomography (CT) scan (left) and magnetic resonance imaging (MRI) (right) of a patient with low-grade liposarcoma of the thigh. Lesion is indistinct on CT, but precisely delineated by MRI.

492

SECTION VII: SOFT TISSUE AND SKIN

Figure 47–3 MRI of high-grade sarcoma of the thigh shows what appears to be intimate contact with the femur over a large portion of the femoral circumference. The signal of MRI may overestimate the extent of malignancy owing to edema or inﬂammation in compressed adjacent tissue. This patient had limb-sparing resection with a histologically negative periosteal margin.

be uninvolved, and a small periosteal stripping and local resection achieved a satisfactory margin, which was then followed by postoperative radiotherapy. Although she subsequently developed aggressive metastatic disease and expired, there was never any evidence of local recurrence. This patient would have been disserved by an amputation performed in anticipation of a positive margin based on the MRI and demonstrates the potential for MRI to overestimate tumor extent. In difﬁcult cases, both CT and MRI may be needed to preoperatively assess and anticipate the need for resection of important structures. In rare cases in which bona ﬁde bony involvement is the critical point, a nuclear medicine bone scan can also be quite revealing. In general, the burden of proof in this preoperative assessment and planning is on those who advocate resecting vital functional structures; that approach is usually reserved for high-grade or recurrent lesions in which imaging indicates substantial direct involvement of the structure by surrounding, unequivocally malignant tissue.

AVOIDING RECURRENCE AFTER DEFINITIVE SURGICAL RESECTION The major pitfall for the surgeon in the planning of the deﬁnitive resection of an STS is to underestimate the size of the lesion and the involved compartments. Local recurrence can be a signiﬁcant problem, and therefore, adequate planning and execution are critical. The approach to surgical procedures for sarcoma has swung back and

forth over the last 50 years, and apparent contradictions have been generated that are not completely resolved. Prior to the work of Pack, Stout, and others, minimal excisional procedures were often utilized and typically failed to control local disease. Advocating more radical resections, sarcoma surgeons of the 1950s and 1960s pointed to improved local control and a consistent cure rate in uncontrolled trials as evidence of the efﬁcacy of this approach. Then, the major success story from the 1970s was the addition of radiation to lesser, limb-sparing surgeries to achieve comparable local control and survival rates (again, with only one small randomized trial on the subject).6,7 Finally, randomized, prospective trials of limb-sparing surgery with and without adjuvant radiation therapy supported the concepts that many lesions could be treated with limb-sparing procedures without radiation and that salvage of patients with local recurrence was often possible without clearly impairing overall survival.8,9 At ﬁrst glance, this seems to effect the complete undoing of 50 years of “progress” in the surgical management of sarcomas. Yet other factors, also evolving over this time interval, may offer a better interpretation. Earlier diagnosis and improved recognition of sarcomatous lesions with lower lethality have improved the overall prognosis of sarcomas as a group. Improvements in surgical imaging, planning, and technique have also allowed the more satisfactory extirpation of these tumors without violating tumors, encountering hemorrhage, or destroying function. In addition, when needed, radiation remains a proven adjunct to surgery to improve local control for difﬁcult lesions, and improvements in technique have

47 MANAGEMENT OF SOFT TISSUE SARCOMA dramatically reduced the complications and morbidity of this modality.

AVOIDING THE PITFALL OF OVERAGGRESSIVE THERAPY AND POOR FUNCTIONAL OUTCOME In view of the developments previously discussed, current pitfalls in surgical management of sarcomas are as likely to be from overtreatment as from undertreatment or technical misadventure. The surgeon should have a clear grasp of the minimum of structures needed to retain a productive extremity. Although largely outmoded by new developments in prostheses, the original Tikoff-Lindberg procedure as a substitution for forequarter amputation was an early example of this concept. Neurovascular service to the hand and forearm still maintained a productive extremity even without shoulder joint integrity. Often, the argument is made that major resections of muscle groups will result in a poorly functioning limb with more protracted rehabilitation than even an amputation. Yet, it is often underappreciated that several major lower extremity muscle groups can be largely removed with only speciﬁc and minor deﬁcits. Loss of the lower extremity biceps group has minimal impact in daily function and normal ambulation. Loss of the quadriceps group causes most difﬁculty in ascending and descending stairs, but if even a trace of knee extensor activity is preserved, this allows knee hyperextension that supports weight-bearing in normal ambulation with only a minor alteration in gait. Knee bracing can often compensate for even total loss of quadriceps function when walking on level ground. The concept that sarcomas do not have true capsules and that the “pseudocapsule” often surrounding them does not represent a safe excision plane, has been well established. This envelope encompassing the obvious sarcomatous mass does not represent a true ﬁbrous capsule, but is rather compressed reactive normal tissue, frequently inﬁltrated by malignant cells. Therefore, a truly negativemargin surgical procedure remains outside of this transition zone. Conversely, surgeons often fail to realize that a true ﬁbrous or fascial structure adjacent to a sarcomatous mass is often an adequate boundary if not invaded by malignant cells. Thus, the fascia of a major muscle group or the periosteal membrane, even when in direct apposition to the tumor, can represent an adequate margin if not directly invaded. In those cases, there is no arbitrary radial distance that deﬁnes the term wide (as in “wide local excision”). This is important because most large extremity sarcomas, high and low grade, will abut the fascia of a muscle compartment, and performing multiple compartment excisions or amputations is typically not necessary to procure a sufﬁcient margin at that interface. The determination of actual bony invasion on preoperative studies can be problematic. Often, the limits of an STS are vague on CT scanning because tumor and normal soft tissue

493

densities are similar. MRI can be more sensitive but will detect inﬂammation and edema as well as malignancy and not discriminate well between these entities. As mentioned, we often use both modalities to estimate likely surgical margins, realizing that the former can suffer from false negatives whereas the latter can have false positives. Without clear evidence of bony destruction, we will typically assume that the periosteal margin will be adequate and conﬁrm this at surgery by frozen sections. When determining adequate margins intraoperatively, one must proceed with a clear contingency plan in mind in the event that bony involvement is encountered. This can be orthopedic and prosthetic backup or amputation, and the initial approach to the tumor must not compromise the backup plan. The initial incision should respect the layout for optimal closure of a possible amputation or allow a satisfactory approach to a segmental or total bone resection en bloc with the primary tumor mass. Often, one encounters the “minimal” positive margin, in which, for example, tumor closely approaches a major nerve or vessel over a very limited segment without frank involvement. If this is the only point of compromise for an otherwise satisfactory resection, a segmental resection of the neurovascular structure versus a potential compromise of the resection must be weighed. Segmental vascular resection results in a more consistently satisfactory functional outcome than that of nerve resection and grafting or repair. Ultimately, the preservation of a poorly functional limb is not a desired outcome, so careful marking of the point of compromise (as well as the wider limits of the entire surgical ﬁeld) by surgical clips and the administration of postoperative adjuvant radiotherapy can be a realistic choice. A randomized study showed that local recurrences of low-grade tumors were reduced to very low frequency with adjuvant, postoperative external beam radiotherapy (Fig. 47–4A).8 In the case of low-grade tumors, one should select this option without much reservation if the alternative is signiﬁcantly morbid. Randomized studies also indicate that even highgrade lesions can be well managed by this approach in many circumstances. The signiﬁcant retrospective association in many studies between local recurrence and metastatic recurrence and death led many to conclude that improved survival would result if one achieved better local control. Yet, when this was subjected to randomized, prospective studies testing local control measures, this hypothesis was not substantiated. Two studies of postoperative radiotherapy for high-grade tumors after limb-sparing surgery (one by external beam and the other using brachytherapy) demonstrated signiﬁcantly improved local control with radiation, but neither documented an improvement in overall survival8,9 (see Fig. 47–4B). In one study, the local recurrences without radiotherapy were either accompanied by prompt and aggressive metastatic relapse (in which local recurrence was not a major component of the clinical picture) or durably salvaged by reresection of the local recurrence, implying that the local relapse was not seeding new metastatic sites after failure

494

SECTION VII: SOFT TISSUE AND SKIN Radiation

Percent without local recurrence

100 90 80 70

No radiation

60 50 40 30 20

P2⫽.016

10 0

2

4

A

6 8 Follow-up (years)

10

12

90

No radiation

80 70 60 50 40 30 20

80

Radiation

70

No radiation

60 50 40 30 20

P2⫽.003

10 0

B

100

Percent survival

Percent without local recurrence

Radiation 100 90

P2⫽.71

10 0 2

4

6

8

10

12

Follow-up (years)

2

4

6

8

10

12

Follow-up (years)

Figure 47–4 A, Randomized trial of adjuvant postoperative external beam radiotherapy versus no radiotherapy after limb-sparing resection of low-grade extremity sarcomas. Radiation signiﬁcantly reduced local recurrences in this malignancy. B, Randomized trial of adjuvant postoperative external beam radiotherapy versus no radiotherapy after limb-sparing resection of high-grade extremity sarcomas. Local recurrences were signiﬁcantly reduced with radiotherapy (left), but this had no demonstrable effect on overall survival (right). (A and B, From Yang JC, Chang AE, Baker AR, et al. Randomized prospective study of the beneﬁt of adjuvant radiation therapy in the treatment of soft tissue sarcomas of the extremity. J Clin Oncol 1998;16:197–203.)

of the primary resection.8 Therefore, it is misguided to apply a radical approach to resection when there are other lesser options because of the concept that it is somehow more “curative.” The strong retrospective association between local recurrence and death10 is more plausibly due to the aggressive intrinsic biology of some tumors, and successfully reducing local recurrences does not affect their tendency for distant metastases. This ﬁnding should not be misconstrued as an excuse for poor or inadequate surgery or neglect of the primary. Local recurrences can severely affect quality of life, and the limited size of the studies cited cannot exclude all possibility of an impact of poorer local control on metastatic disease. Rather, these studies indicate that after optimal limb-sparing surgery by experienced sarcoma surgeons, the application of postoperative adjuvant radiotherapy can further reduce the already low incidence of local recurrence. Yet those patients who do not receive this adjuvant do not suffer a demonstrably reduced overall survival. Both ﬁndings (adjuvant

radiotherapy is locally effective, and local recurrences do not clearly degrade overall survival) support the alternative of relying on postoperative adjuvant radiotherapy in the case of “minimally compromised” surgical margins in which the surgical procedure necessary to rectify this compromise is morbid or defunctionalizing. A relatively dramatic example of this is illustrated in Figure 47–5 in which a patient with a very large low-grade sarcoma of the quadriceps was explored and transfascial inﬁltration into the lateral portion of the biceps compartment was found. Because hemipelvectomy was the only procedure that could achieve widely negative margins and because the lesion was of low grade, it was elected to resect the majority of the quadriceps compartment and all gross disease in the biceps compartment and apply postoperative radiation. Care was taken to preserve the posterior thigh skin in the event that hemipelvectomy was ultimately necessary. With 6 years of follow-up, this patient has a functional gait without prosthesis and is free of evident disease.

47 MANAGEMENT OF SOFT TISSUE SARCOMA

495

EARLY DETECTION, DIAGNOSIS, AND TREATMENT OF RECURRENCES

Figure 47–5 A patient with very large low-grade liposarcoma of the quadriceps compartment with transfacial extension to the posterior compartment found at surgery. Rather than proceed to amputation, a local resection of all gross disease was performed followed by postoperative adjuvant radiotherapy. The patient has useful function of the extremity, requires no assistance with ambulation, and has shown no sign of recurrence for over 6 years. The low metastatic risk of low-grade lesions supports the safety of such a conservative surgical approach.

At this point, even if he suffers a local recurrence and requires an amputation, he will have beneﬁted from the use of the functional limb for a substantial time and have a survival expectation not signiﬁcantly affected by the attempt at lesser surgery. Although such an approach is not recommended for extensively inﬁltrating high-grade tumors, in this case, the main pitfalls in trying this strategy for a low-grade tumor are poor follow-up that does not detect the local recurrence until it is not amenable to amputation or not technically preserving the amputation as a salvage option during the ﬁrst procedure. The merit of this approach seems evident when dealing with lowgrade lesions, and the two randomized trials cited earlier indicate that it can also be entertained safely for many high-grade tumors that are marginally resected. Gross high-grade residual disease is not likely to be controlled with this approach (and such patients were not included in the randomized studies), but adjuvant radiotherapy, careful follow-up, and a fall-back plan can be a safe option for avoiding amputation after a marginal resection for many of these tumors.

If a recurrence occurs despite the best efforts of the surgical team to properly plan and execute a deﬁnitive surgical resection, a salvage operation may be required. Adult STS recur either locally or systemically. Although retrospective studies indicate that local recurrences can be harbingers of poor outcome, as noted previously, that appears to be a reﬂection of underlying aggressive biology rather than a result of a cause and effect relationship. Therefore, when a local recurrence appears in the absence of disseminated disease, it should be treated vigorously, and there would be some expectation that some of these patients can yet be cured. If the patient has already been treated with limb-sparing surgery and adjuvant radiotherapy for a high-grade lesion, most surgeons will have to proceed to an amputation as their salvage procedure. If no adjuvant radiation therapy was given originally and the recurrence is small or localized, a second limb-sparing operation is possible in many patients. In almost all such cases, this second procedure should be accompanied by adjuvant radiotherapy because the primary has already demonstrated its propensity for local recurrence. For lowgrade tumors, the option of amputation is reserved for those patients with very large and inﬁltrating recurrent lesions that cannot be cleanly re-resected. Otherwise, adjuvant external beam radiotherapy is also a useful component of treatment after re-resection of these recurrences if not already used. The more difﬁcult situation is when dissemination is systemic and hematogenous. Fortunately, there is a marked predilection for metastases to go exclusively to the lungs. Here, a common pitfall is to not pursue pulmonary metastasectomy adequately. In our experience, even the third metastatic recurrence from sarcoma can be exclusively pulmonary and still technically resectable.11 Because systemic therapies such as chemotherapy are, at best, of brief beneﬁt to a small minority of patients, surgery is the mainstay of treatment for limited metastases conﬁned to the lungs. Although the success of pulmonary metastasectomy is reduced with a higher number of lesions and a shorter disease-free interval, there can still be extended periods of tumor-free survival for some of these patients,12–14 and the real limitations are technical, related to pulmonary reserve and resectability.

SUMMARY OF POTENTIAL PITFALLS AND HOW TO AVOID THEM Most often, mistakes in the management of primary adult STS result from inadequate or inaccurate pathologic grading and selection of suboptimal function-destroying choices in surgery. Randomized studies have shown that intrinsic biologic determinants are probably driving prognosis more than are therapeutic options, implying that

496

SECTION VII: SOFT TISSUE AND SKIN

draconian therapeutic options are less likely to improve outcome than to impair quality of life. Yet, knowing when a lesser, conservative resection is appropriate and safe is still one of the most difﬁcult clinical decisions. Isolated local recurrences after limited surgery are often amenable to curative surgical salvage procedures if one carefully allows for such an “exit strategy” during planning for the ﬁrst procedure. Lastly, aggressive pulmonary metastasectomy represents the best and only route to cure or prolonged disease-free survival once metastatic disease occurs. The potential beneﬁts of such a resection should be considered for each patient with metastatic disease and should be rejected only when the clinical course or technical considerations clearly predict rapid failure of this strategy.

REFERENCES 1. Helman LJ, Meltzer P. Mechanisms of sarcoma development. Nat Rev Cancer 2003;3:685–694. 2. Alvegard TA, Berg NO. Histopathology peer review of high-grade soft tissue sarcoma: the Scandinavian Sarcoma Group experience. J Clin Oncol 1989;7:1845–1851. 3. Wunder JS, Healey JH, Davis AM, Brennan MF. A comparison of staging systems for localized extremity soft tissue sarcoma. Cancer 2000;88:2721–2730. 4. Barth RJ Jr, Merino MJ, Solomon D, et al. A prospective study of the value of core needle biopsy and ﬁne needle aspiration in the diagnosis of soft tissue masses. Surgery 1992;112:536–543.

5. Marcus SG, Merino MJ, Glatstein E, et al. Long-term outcome in 87 patients with low-grade soft-tissue sarcoma. Arch Surg 1993;128:1336–1343. 6. Rosenberg SA, Tepper J, Glatstein E, et al. The treatment of soft-tissue sarcomas of the extremities: prospective randomized evaluations of (1) limb-sparing surgery plus radiation therapy compared with postoperative radiotherapy in the treatment of soft tissue sarcomas in adults. Am J Roentgenol 1975;123:123–129. 8. Yang JC, Chang AE, Baker AR, et al. Randomized prospective study of the beneﬁt of adjuvant radiation therapy in the treatment of soft tissue sarcomas of the extremity. J Clin Oncol 1998;16:197–203. 9. Pisters PW, Harrison LB, Leung DH, et al. Long-term results of a prospective randomized trial of adjuvant brachytherapy in soft tissue sarcoma. J Clin Oncol 1996; 14:859–868. 10. Pisters PW, Leung DH, Woodruff J, et al. Analysis of prognostic factors in 1,041 patients with localized soft tissue sarcomas of the extremities. J Clin Oncol 1996;14: 1679–1689. 11. Potter DA, Glenn J, Kinsella T, et al. Patterns of recurrence in patients with high-grade soft-tissue sarcomas. J Clin Oncol 1985;3:353–366. 12. Pogrebniak HW, Roth JA, Steinberg SM, et al. Reoperative pulmonary resection in patients with metastatic soft tissue sarcoma. Ann Thorac Surg 1991;52:197–203. 13. Rizzoni WE, Pass HI, Wesley MN, et al. Resection of recurrent pulmonary metastases in patients with soft-tissue sarcomas. Arch Surg 1986;121:1248–1252. 14. Weiser MR, Downey RJ, Leung DH, Brennan MF. Repeat resection of pulmonary metastases in patients with soft tissue sarcoma. J Am Coll Surg 2000;191:184–190.

48

Isolated Limb Perfusions and Extremity Amputations Joseph A. Blansﬁeld, MD and James F. Pingpank, Jr., MD INTRODUCTION In-transit metastatic disease in melanoma is deﬁned as recurrent melanoma within the intradermal or subcutaneous lymphatics that does not enter the nodal basins. In the current American Joint Committee on Cancer (AJCC) staging system, in-transit disease without metastatic lymph nodes is considered stage IIIb and carries with it a 5year survival of 30% to 50%.1 For recurrent melanoma conﬁned to an extremity, simple excision can usually eradicate the disease. Simple excision is sufﬁcient and a wide local excision is not necessary because it does not improve recurrence rates. For larger numbers of lesions, simple excision becomes technically prohibitive. For these patients, isolated limb perfusion (ILP) is the treatment of choice. ILP involves surgical isolation of an extremity’s circulation and placing that circulation into an extracorporeal circulation, which is separated from the systemic circulation. After creating the new circuit, the isolated limb is perfused with high doses of heated chemotherapy. ILP should be contemplated in patients with intradermal or subcutaneous in-transit melanoma metastases conﬁned to an extremity when there is no evidence of systemic metastatic disease. ILP was ﬁrst used to treat melanoma in the late 1950s by Creech and coworkers.2 His group introduced the practice of using an extracorporeal oxygenator to treat melanoma conﬁned to an extremity. Stehlin and associates3 modiﬁed the technique 20 years later to include hyperthermia to enhance the cytotoxic effects of the chemotherapy. Hyperthermia can enhance the cytotoxicity of some chemotherapeutic agents and can cause selective killing of neoplastic cells.3 Hyperthermic ILP with melphalan leads to an objective response rate in 79% of patients, with a complete response in 54%.4 Patients with a complete response have the best prognosis. In patients with a complete response after perfusion, the 3-year survival is 60%, versus 35% in patients not obtaining a complete response.4 Unfortunately, despite the high objective response rates including a majority of

patients with complete remissions after ILP, there is a 22% to 100% recurrence rate.5 Patients can be eligible for repeat ILPs for recurrence. Melphalan is the chemotherapeutic agent of choice for ILP.6 Melphalan is an alkylating agent that is a derivative of phenylalanine. Phenylalanine is a precursor in melanin synthesis and is taken up preferentially by melanocytes, making it an optimal choice for the treatment of melanoma.7 Other agents, including cisplatin, interferon, and tumor necrosis factor–alpha (TNF-α), have been used in combination with or separately from melphalan, but response rates and durations of response are not signiﬁcantly higher than with melphalan alone. The high tissue levels of chemotherapy obtained in the bypass circuit can lead to some tissue toxicity. Also, if the chemotherapy leaks into the systemic circulation, there can be some systemic toxicity. Regional side effects include skin, nerve, and muscle toxicity from the melphalan. Systemic side effects include nausea and vomiting as well as bone marrow suppression.

Isolated Limb Perfusion in Melanoma INDICATION ● Patients with in-transit metastatic melanoma conﬁned

entirely to an extremity whose melanoma is not amenable to surgical excision

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4

Blood vessel dissection and collateral ligation Cannulation and attachment to pump oxygenator Tourniquet application Reestablishment of circulation with ﬂush

498

SECTION VII: SOFT TISSUE AND SKIN

OPERATIVE PROCEDURE

Box 48–1 Wieberdink Grading System for Regional Tissue Toxicity after ILP11

Blood Vessel Dissection and Collateral Ligation

Grade I Grade II Grade III

The ﬁrst step in ILP is to isolate inﬂow and outﬂow vessels to the perfused extremity. ILP of the lower extremity is most commonly performed through the external iliacs but can also be performed via the femoral or popliteal vessels. The location of vessel dissection depends on the distribution of the in-transit metastases as well as technical considerations. These technical points include the patient’s body habitus as well as history of previous lymph node dissections or previous surgeries in the area. ILP in the upper extremity is most commonly performed via the axillary vessels; however, brachial vessels can also be used, depending on the circumstances. In the lower extremity, a more proximal perfusion does not improve the rate of inguinal nodal recurrence. Thus, inguinal nodal recurrences are comparable for iliac and femoral vessels.8 The external iliac vessels are found via a retroperitoneal approach. This approach is made in the lower abdominal wall via a hockey-puck “transplant”–type incision. Both the artery and the vein are circumferentially dissected distally, and all collaterals arising proximally or at the inguinal ligament are ligated and divided.

Vascular Injuries as a Result of Dissection See Section X, Chapter 60, Infrainguinal Revascularization.

Cannulation and Attachment to the Pump Oxygenator The external iliac vessels are cannulated and connected to the inﬂow and outﬂow lines of an extracorporeal bypass circuit. The perfusion circuit contains a heat exchanger, an oxygenator, and a roller pump. The circuit is primed using 700 ml of balanced salt solution, 1 unit of packed red blood cells, and 1500 units of heparin. The typical hematocrit in the circuit is 25%. One unit of blood is used because regional toxicity cannot be further prevented by providing a higher hematocrit.9 Flow rates of 300 to 500 ml/min for the lower extremity and 150 to 300 ml/ min in the upper extremity are optimal for the perfusion. Flows are adjusted depending on line pressure and volume of the reservoir or because of systemic leak.10 The circuit is warmed using a heat exchanger, and the extremity is covered in external warming blankets to maintain tissue temperatures of 38.5°C to 40°C. Temperatures are monitored by thermistor probes placed in the lower extremity. Dosing for melphalan is based either on body weight or on actual limb volume. Older series used dosing regimens based on body weight and ranged from 0.8 to 2.0 mg/kg for the lower extremity and 0.45 to 0.75 mg/ kg for the upper extremity. Wieberdink and coworkers11 modiﬁed the dosing regimen so that it was based on measuring the actual volume of the limb. They then developed

No subjective or objective evidence of reaction Slight erythema and/or edema Considerable erythema and/or edema with some blistering; slight disturbed mobility permissible Grade IV Extensive epidermolysis and/or obvious damage to the deep tissues, causing deﬁnite functional disturbances; threatening or manifest compartmental syndromes Grade V Reaction that may necessitate amputation

a system to grade regional toxicity related to the perfusion11 (Box 48–1). The volume of the extremity is determined by the volume of water it disperses when submerged in a container of water, with an additional 10% added for the lower extremity to estimate the volume of the lateral thigh that is not submerged. Based on this regimen, an optimal dose of melphalan was found that resulted in reversible grade II or III toxicity in the majority of perfusions. In the lower extremity, this dose is 10 mg/L. The upper extremity can tolerate a slightly higher dose of 13 mg/L. These doses are currently used by most centers.

Toxicities of Melphalan Toxicities of melphalan are due to the direct effect of melphalan in the perfusion circuit or to melphalan that leaks into the systemic circulation. Regional side effects in the ﬁeld of perfusion include effects on the skin, nerve, and muscle.12 In one group of 425 patients after ILP, 85% of patients had Wieberdink grade I or II toxicity, 15% had grade II/IV toxicity, and 0.5% (2 patients out of 425) had grade V toxicities.13 ● Consequence Virtually all patients undergoing ILP have some evidence of skin toxicity and dependent edema. Most of these reactions are transient, and most patients recover completely. Skin erythema typically starts 2 to 5 days after the perfusion and reaches its maximal intensity at about day 35. Over the subsequent 2 to 3 months, the erythema fades to a bronze. Skin reaction can be more severe including blistering or peeling of the skin, especially of the soles of the feet and the palms of the hands. Dependent edema can also occur and may be a result of the lymph node dissection that accompanies the vessel isolation. Peripheral neuropathy occurs in about half of the patients undergoing ILP. Shooting pains down the treated extremity typically occurs 2 to 3 weeks after a perfusion and can last up to 3 months.14 A subset of patients has longer-lasting neuropathy. Twenty percent of patients after axillary perfusion and 2% of patients after iliac perfusion have neuropathy that is considered long term (deﬁned as lasting >3 mo).15

48 ISOLATED LIMB PERFUSIONS AND EXTREMITY AMPUTATIONS Muscle effects tend to be the most troublesome longterm effects after ILP.2,14 The clinical presentation of the muscle injury can be extremely variable. Patients may have little to no muscle effects with transient myalgias or may have direct myotoxicity that leads to chronic pain and atrophy. Grade 1/2/3/4 complication, but typically grade 1/2 complication ● Repair Skin effects including erythema, blistering, and edema can be managed by supportive care and applying silver sulfadiazine (Silvadene) to blisters once they have unroofed. Edema can be controlled with Jobst stockings and is typically self-resolving. Neuropathy is also self-resolving about 3 months after treatment but can be treated with gabapentin for pain relief. Myotoxicity occurs in a signiﬁcant form in up to 10% of patients and is so far idiopathic. Fasciotomy does not improve the direct effects of melphalan on muscle and should be performed only with high compartmental pressures. Regional toxicities must be carefully documented in patients, especially myotoxic effects of the melphalan. Patients who are reperfused tend to have enhanced muscle toxicity with each subsequent perfusion.16 ● Prevention Unfortunately, these complications of perfusion cannot be prevented except by strictly compliance with dosing regimens, as outlined previously.

Tourniquet Application An Esmarch tourniquet is placed around the root of the extremity to occlude any superﬁcial veins that may allow leakage of the chemotherapy into the systemic circulation. Meticulous surgical ligation of all collaterals and tourniquet application to control superﬁcial vessels avoids perfusate ﬂow into the systemic circulation and also prevents systemic blood from entering the perfusion circuit.

Systemic Leakage of Melphalan Melphalan leak into the systemic circulation can cause a variety of side effects including gastrointestinal upset and bone marrow suppression. Nausea and vomiting occurs within 24 hours of a perfusion if there is systemic absorption, and the bone marrow can be suppressed beginning about 7 to 10 days after the perfusion. Blood leakage into or out of the perfusion circuit must be monitored during the course of the perfusion. Reservoir volume is a key indicator for blood leakage into or out of the circuit. An increase in the amount of blood in the reservoir is indicative of a leak of blood into the perfusion circuit from either the arterial or the venous side. Increasing ﬂow rates will increase the line pressure, which can overcome arterial ﬂow into the circuit. By partially occluding the venous outﬂow and thus

499

increasing the venous perfusion pressure, venous side leakage into the circuit will stop. A decrease in the amount of blood in the reservoir is indicative of a leak into the systemic circulation. Flow rates can be decreased and/or the tourniquet can be tightened to stop leakage into the circulation. Continuous intraoperative assessment of perfusate leakage into the systemic circulation is an important technique to discriminate small amounts of leakage. 131Iradiolabeled albumin or 99Tc-labeled red blood cells is allowed to circulate in the isolated circulation during the procedure. A gamma counter is placed precordially to provide continuous intraoperative monitoring of leak during a perfusion.17 This system can discriminate a leak of less than 1%.18 Systemic leak rates of less than 1% can be achieved in the vast majority of patients (90%) using the leak-monitoring systems.19 ● Consequence The nausea and vomiting associated with melphalan is self-limiting. Bone marrow suppression can lead to possible neutropenic fevers, thrombocytopenia and anemia, and infectious complications. With intraoperative continuous assessment of leak detection, and consequently low levels of systemic melphalan, most patients experience only transient nausea and vomiting for a day after surgery and low levels of bone marrow suppression approximately 7 to 10 days after treatment. Grade 1 complication ● Repair Nausea and vomiting can be treated supportively with antiemetics postoperatively. Bone marrow suppression should be treated with neupogen if neutropenia is present and with transfusions for anemia or thrombocytopenia.

Reestablishment of Circulation The perfusion circuit is disconnected after a 60-minute perfusion, and residual drug is washed out of the tissues with a 3-L ﬂush of the extremity. This ﬂushes any residual drug from the vascular system to further lessen systemic exposure to melphalan.

Extremity Amputations In the era of ILP and immunotherapy to treat melanoma, amputation is performed rarely to treat locoregionally intractable extremity melanoma. Kapma and colleagues20 presented a series of 451 patients who underwent 501 ILPs over a 23-year period with only 11 patients (2.4%) who needed to undergo an amputation for locoregionally intractable melanoma. Amputation for melanoma confers no increase in survival6,21 and should be performed only for palliation.

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SECTION VII: SOFT TISSUE AND SKIN

REFERENCES 1. Balch CM, Buzaid AC, Soong SJ, et al. Final version of the American Joint Committee on Cancer staging system for cutaneous melanoma. J Clin Oncol 2001;19:3635– 3648. 2. Creech O, Krementz ET, Ryan RF, Winblad JN. Chemotherapy of cancer: regional perfusion utilizing an extracorporeal circuit. Ann Surg 1958;148:616–632. 3. Stehlin JS, Giovanella BC, de Ipolyi PD, et al. Results of hyperthermic perfusion for melanoma of the extremities. Surg Gynecol Obstet 1975;140:339–348. 4. Klaase JM, Kroon BB, van Geel AN, et al. Prognostic factors for tumor response and limb recurrence-free interval in patients with advanced melanoma of the limbs treated with regional isolated perfusion with melphalan. Surgery 1994;115:39–45. 5. Thompson JF, Hunt JA, Shannon KF, Kam PC. Frequency and duration of remission after isolated limb perfusion for melanoma. Arch Surg 1997;132:903–907. 6. Fraker DL. Hyperthermic regional perfusion for melanoma and sarcoma of the limbs. Curr Probl Surg 1999;36:841–907. 7. Luck JM. Action of p-dichloroethyl amino-L-phenylalanine on Harding-Passey mouse melanoma. Science 1956;123: 984–985. 8. Klaase JM, Kroon BB, van Geel AN, et al. The role of regional isolated perfusion in the eradication of melanoma micrometastases in the inguinal nodes: a comparison between an iliac and femoral perfusion procedure. Melanoma Res 1992;2:407–410. 9. Klaase JM, Kroon BB, van Slooten GW, et al. Comparison between the use of whole blood versus a diluted perfusate in regional isolated perfusion by continuous monitoring of transcutaneous oxygen study: a pilot study. J Invest Surg 1994;7:249–258. 10. Alexander HR, Fraker DL, Bartlett DL. Isolated limb perfusion for malignant melanoma. Semin Surg Oncol 1996;12:416–428. 11. Wieberdink J, Benckhuysen C, Braat RP, et al. Dosimetry in isolation perfusion of the limbs by assessment of

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

perfused tissue volume and grading of toxic tissue reactions. Eur J Cancer Clin Oncol 1982;18:905–910. Olieman AF, Koops HS, Geertzen JH, et al. Functional morbidity of hyperthermic isolated regional perfusion of the extremities. Ann Surg Oncol 1994;3:382–388. Klaase JM, Kroon BB, van Geel BN, et al. Patient and treatment related factors associated with acute regional toxicity after isolated perfusion for melanoma of the extremities. Am J Surg 1994;167:618–620. Bonifati DM, Ori C, Rossi CR, et al. Neuromuscular damage after hyperthermic isolated limb perfusion in patients with melanoma or sarcoma treated with chemotherapeutic agents. Cancer Chemother Pharmacol 2000; 46:517–522. Vrouenraets BC, Eggermont AM, Klaase JM, et al. Longterm neuropathy after regional isolated perfusion with melphalan for melanoma of the limbs. Eur J Surg Oncol 1994;20:681–685. Vrouentaets BC, Hart GA, Eggermont AM, et al. Relation between limb toxicity and treatment outcomes after isolated limb perfusion for recurrent melanoma. JAMA 1999;188:522–530. Barker WC, Andrich MP, Alexandre HR, et al. Continuous intraoperative external monitoring of perfusate leak using I-131 human serum albumin during isolated perfusion of the liver and limbs. Eur J Nucl Med 1995; 22:1242–1248. Hoekstra HJ, Naujocks T, Schraffordt-Koops H, et al. Continuous leaking monitoring during hyperthermic isolated regional perfusion of the lower limb: techniques and results. Reg Cancer Treat 1992;4:301–304. Klaase JM, Kroon BB, van Geel AN, et al. Systemic leakage during isolated limb perfusion for melanoma. Br J Surg 1993;80:1124–1126. Kapma MR, Vrouenraets BC, Nieweg OE, et al. Major amputation for intractable extremity melanoma after failure of isolated limb perfusion. Eur J Surg Oncol 2005;31:95–99. Lienard D, Eggermont AM, Kroon BB. Thirty-ﬁve years of isolated limb perfusion for melanoma: indications and results. Br J Surg 1996;83:1319–1328.

Section VIII

HERNIA Stephen R. T. Evans, MD and Leigh A. Neumayer, MD Every great mistake has a halfway moment, a split second when it can be recalled and perhaps remedied.—Pearl S. Buck

49

Open Inguinal Hernia Repair with Plug and Patch Technique Derrick D. Cox, MD and Parag Bhanot, MD INTRODUCTION Groin hernias, which can be further classiﬁed as inguinal and femoral hernias, are among the most common conditions for which patients undergo surgical intervention, with approximately 800,000 cases performed annually.1 The lifetime risk of having a groin hernia repair is estimated to be 14% for men and 2% for women.2 Elective surgical repair is usually advised because of concerns regarding incarceration and/or strangulation, particularly with femoral hernias. A number of clinical studies have proved elective surgical repair to be safe and effective with a very low morbidity rate. This is in contrast to emergency operations, which are associated with a substantial morbidity and mortality; especially when concomitant bowel resections are performed.3 A number of open repairs have been described and classiﬁed depending on the type of dissection (anterior, posterior) and the use of different mesh (Lichtenstein, plug and patch, Prolene hernia system). The type of repair performed is primarily based on the type of hernia as well as the surgeon’s expertise. This chapter is dedicated to the plug and patch technique; although much of the discussion also applies to groin hernia repairs in general.

INDICATIONS AND CONTRAINDICATIONS The most common indications for groin hernia repair are listed in Box 49–1. Repair of groin hernias in minimally symptomatic individuals is still an area of debate. A randomized clinical trial conducted by Fitzgibbons and associates4 of 720 men concluded that this cohort can be followed by delaying surgical intervention with minimal morbidity. Femoral hernias represent a different clinical entity with an increased incidence of complications and emergent operations.5 Although there are few contraindications to groin hernia repair, a number of considerations may delay repair (Box 49–2).

OPERATIVE STEPS Although there is some variance in the technical aspects of the plug and patch repair, the operation has welldeﬁned steps. Step 1 Step 2

Patient preparation Skin incision

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Box 49–1 ● ● ● ●

Symptomatic hernias Prevention of progression of symptoms Prevention of complications (incarceration, strangulation) Treatment of complications (incarceration, strangulation)

Box 49–2 Repair ● ● ● ●

Indications for Groin Hernia Repair

Contraindications to Groin Hernia

Uncontrollable ascites Soft tissue infection Pregnancy Reversible causes of increased intra-abdominal pressure (benign prostates hyperplasia [BPH], acute respiratory issues)

Step 3 Step 4 Step 5 Step 6 Step 7 Step 8

Dissection of subcutaneous layer and Scarpa’s fascia Incision of external oblique fascia Mobilization of spermatic cord Identiﬁcation and reduction of hernia (direct and/or indirect) Mesh ﬁxation Anatomic closure of abdominal wall layers

OPERATIVE PROCEDURE Dissection of the Subcutaneous Layer and Scarpa’s Fascia Hemorrhage ● Consequence Signiﬁcant postoperative bleeding would be very unusual from this dissection. However, ecchymosis or superﬁcial hematoma may result from improper ligation of smaller venous branches. Grade 1 complication ● Repair Hematomas of signiﬁcant size may need to be evacuated to prevent subsequent soft tissue infection. Otherwise, conservative measures may be employed. ● Prevention Preoperatively, patients should be instructed to avoid antiplatelet and other anticoagulation medications. A number of small veins encountered in the subcutaneous layer can simply be cauterized. One or two prominent superﬁcial epigastric veins are also located in the incision near the pubic tubercle, and these must be sutureligated to prevent bleeding.

Incision of the External Oblique Fascia Ilioinguinal Nerve Injury The ilioinguinal nerve is solely a sensory nerve with a distribution of the upper and medial aspects of the thigh

and scrotum. It is located overlying the spermatic cord directly underneath the external oblique fascia and is at risk for transection at this stage. ● Consequence Inadvertent transaction of the ilioinguinal nerve will result in sensory deprivation in the associated dermatomes described. Inability to recognize that the nerve has been transected may also lead to a neuroma and chronic inguinal pain.

Grade 1/2 complication ● Prevention An understanding of the anatomy of the nerve is crucial to recognizing its usual course through the ﬁeld of dissection. Care should be taken when incising the external oblique fascia to ensure that the nerve has been separated from its underside. This can be accomplished by ﬁrst partially transecting the fascia in the direction of the superﬁcial ring and then lifting up on the medial and lateral leaﬂets to further expose the inguinal canal (Fig. 49–1).

Mobilization of the Spermatic Cord Ischemic Orchitis/Testicular Injury ● Consequence Ischemic orchitis is the result of venous congestion within the testicle secondary to venous thrombosis within the spermatic cord. This process may lead to testicular atrophy. The reported incidence is less than 1%.6 Grade 3/4 complication ● Repair The management of orchitis includes observation and use of nonsteroidal anti-inﬂammatory medications for several weeks. A duplex ultrasound should be performed to assess perfusion of the testicle. Ischemia and/or infarction may warrant orchiectomy. ● Prevention This injury can be prevented by limiting dissection within the spermatic cord. This requires precise identiﬁcation of the indirect hernia sac to safely mobilize it from the medial aspect of the cord (Fig. 49–2). In patients in whom the hernia sac is large and adherent, the distal portion of the sac can be left in situ with a high ligation proximally.

Hemorrhage ● Consequence Mobilization of the spermatic cord usually requires division of the cremasteric muscle ﬁbers overlying the hernia sac. Improper recognition of bleeding from the transected muscle ﬁbers may result in hematomas. Grade 1/2 complication

49 OPEN INGUINAL HERNIA REPAIR WITH PLUG

503

A Figure 49–2 The Penrose drain encircles both the indirect hernia sac and the spermatic cord. The testicular vessels (tip of the hemostat) are directly adjacent to the hernia sac and can be easily injured.

istration.7 An increased risk is associated with incarcerated and femoral hernias. The sequela of an infection is dependent upon the source of infection, the degree of infection, and the type of mesh placed for the repair. Exposed mesh is considered to be contaminated and is included in the same algorithm. Grade 3/4/5 complication

B Figure 49–1 A, The external oblique fascia has been transected into medial and lateral leaﬂets. The ilioinguinal nerve is just visible overlying the spermatic cord (tip of the forceps). B, The ilioinguinal nerve has been carefully dissected along its course from the internal ring to the pubic tubercle without the use of cautery or excessive retraction.

● Repair Hematomas of signiﬁcant size may need to be evacuated to prevent subsequent soft tissue infection. Otherwise, conservative measures may be employed. ● Prevention Division of the cremasteric muscle is necessary to fully mobilize the hernia sac from the spermatic cord. Cautery is usually sufﬁcient to prevent bleeding from the muscle ﬁbers, but it must be done before retraction occurs.

Mesh Fixation Mesh Infection and/or Exposure ● Consequence Mesh infection accounts for over 40% of all adverse events, as reported by the U.S. Food and Drug Admin-

● Repair The majority of plug and patch meshes are constructed from polypropylene. This type of mesh can resist bacterial colonization and has the ability to incorporate into native tissue. This accounts for a higher likelihood of being able to salvage the mesh with long-term antibiotic administration and/or drainage of any associated abscess. However, if the source of infection is an enteric ﬁstula, mesh removal is required. In the presence of sepsis, aggressive measures are instituted with immediate operative exploration and systemic antibiotics. ● Prevention The most important preventive measure is to maintain strict sterile technique throughout the operation. The surgical team has to be vigilant in not compromising the surgical ﬁeld or contaminating the mesh before its placement. Preoperatively, any remote sources of infection, such as pneumonia, urinary tract infection, or soft tissue infections, should be addressed before the operation. Although there has been some debate in the literature on the use of intravenous antibiotics for hernia cases, the authors believe that this is an important measure coinciding with the conclusions from several randomized studies.8–11 Lastly, despite the lack of level-one evidence, the authors believe that the use of adhesive surgical barriers that serve as physical barriers against bacterial migration between the skin and the mesh is important.

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Enterocutaneous Fistula ● Consequence The reported incidence of enterocutaneous ﬁstulas is less than 1% in large series and is described as isolated case reports.12 Consequences include mesh infection, intra-abdominal abscess, sepsis, and mortality. Grade 3/4/5 complication ● Repair The management of intestinal ﬁstulas should follow surgical principles in terms of patient resuscitation and sepsis control. Eventually, the treatment also needs to take into account the associated mesh infection. The operation will include exploratory laparotomy, excision of mesh, repair of ﬁstula, and closure of the abdominal wall without mesh. ● Prevention Prolene mesh is known to be associated with signiﬁcant adhesion formation that may lead to mesh erosion into the bowel and resultant ﬁstula.13,14 The principal concept in prevention is to avoid direct opposition of the mesh with bowel. This is particularly relevant with the plug placement because a signiﬁcant portion is placed into the preperitoneal space for direct hernias and adjacent to the hernia sac in indirect hernias. If the hernia sac has been opened, a secure high ligation must be performed.

Hernia Recurrence ● Consequence The lifetime recurrence rate is less than 5% in most large series.15,16 Multiple risk factors include morbid obesity, diabetes, connective tissue disorders, smoking, ascites, and previous hernia repair. Patients will present with symptoms similar to their initial complaints of the presence of a bulge, new onset of inguinal pain, and incarceration with possible strangulation. It is important to note that most failures are secondary to technical causes and can be prevented. The major complication of a recurrent hernia repair is the increased recurrence rate of approximately 20%.17 Hematomas, seromas, testicular atrophy, and chronic pain all have an increased incidence as well. Grade 3/4 complication ● Repair With symptomatic recurrences in surgical candidates, a repeat attempt at a hernia repair is warranted. Many large series, including the randomized clinical trial by Neumayer and associates,18 have demonstrated superior results with a laparoscopic approach to the repair of a recurrent hernia. This approach has the advantage of avoiding scar tissue and altered anatomy caused by the previous repair. However, depending on the surgeon’s expertise, an open approach may be used with placement of an additional plug and patch.

Figure 49–3 Although the onlay portion of the mesh has been secured to the edges of the inguinal canal, the repair is compromised secondary to improper reconstruction of the internal ring.

● Prevention There are several important technical considerations to ensure the lowest rate of failure. As previously listed, there are individual considerations of each patient that may warrant delaying the operation. The identiﬁcation of all concomitant hernias (direct and indirect components) is critical. A recurrence through the internal ring can occur if the indirect hernia sac is not properly dissected and reduced prior to placement of the plug component or if the onlay mesh is excessively loose around the proximal spermatic cord (Fig. 49–3). A direct hernia recurs if the onlay portion does not adequately reinforce the inferomedial portion of the inguinal ﬂoor.

Vas Deferens Obstruction ● Consequence Vasal obstruction related to inguinal herniorrhaphy is an uncommon complication, but it is recognized as a cause of azoospermia in the male infertility patient with an incidence of 0.3%.19 The obstruction is due to a foreign body reaction to the mesh with resultant decreased vasal luminal diameter. Grade 2/3 complication ● Repair Vasogram is the “gold standard” to diagnose the injury. In addition to the presence of mesh, vasal obstruction can also result from direct iatrogenic injury caused by ligation or cauterization, vascular compromise, or extrinsic compression. Most of these injuries may be identiﬁed intraoperatively and a primary repair may be attempted, maintaining fertility. Microsurgical repair of an injury to the vas deferens has excellent outcomes with a patency rate of 65% at follow-up.20 Vasal obstruction secondary to a desmoplastic reaction to the mesh will ultimately require reexploration of the groin.

49 OPEN INGUINAL HERNIA REPAIR WITH PLUG

505

● Prevention The use of mesh results in a desmoplastic reaction, and thus, it is important to avoid placement of the plug component in direct contact with the vas deferens. The spermatic cord should be handled carefully during dissection of the hernia sac to reduce the risk of exposing a bare vas deferens to the mesh. Also, the patch placed for reinforcement of the transversalis fascia should have a slit large enough to allow safe passage of the spermatic cord through the deep ring.

Nerve Entrapment/Chronic Inguinal Pain ● Consequence The literature is equivocal with regard to elective division of the ilioinguinal nerve to reduce the risk of an inadvertent injury and consequent chronic pain. A randomized, controlled trial by Picchio and coworkers21 concluded that the occurrence of postoperative pain is unaffected by elective division of the ilioinguinal nerve. Moreover, the purposeful transection of the ilioinguinal nerve was related to sensory disturbances in the corresponding dermatome. Grade 2/3 complication ● Repair Chronic pain secondary to nerve entrapment can be frustrating to manage. Outpatient management includes injection of local anesthetic combined with steroids in the location of the nerve and/or point of tenderness. If this is not effective, exploration of the groin is warranted. However, identiﬁcation of the affected nerve may be difﬁcult secondary to scar tissue. If the nerve can be located, it should be freed from the scar tissue with possible reimplantation. Neurectomy of either the ilioinguinal, the iliohypogastric, and/or the genitofemoral nerves may ameliorate the neuralgia.22 ● Prevention Meticulous attention must be paid to identifying all nerves and branches in the surgical ﬁeld, especially the ilioinguinal nerve. When obtaining exposure and repairing the hernia, care should be taken not to damage the nerves by entrapment with staples, sutures, or prosthetic materials (Fig. 49–4). One should avoid excessive retraction on the nerve. Cautery should be kept away from the nerve to prevent electrical injury.

Femoral Vessel Injury ● Consequence Injury of the femoral vein as a result of unobserved constriction by suture placement can manifest with subsequent thromboembolic complications. Femoral artery injury may cause vascular compromise depending on the presence of collateral arterial ﬂow. In addition, delayed complications include aneurysms and arteriovenous ﬁstulas. Grade 3/4 complication

A

B Figure 49–4 A, The plug component has been properly secured at the level of the internal ring oriﬁce. However, the ilioinguinal nerve is clearly in contact with the mesh, predisposing to nerve entrapment and chronic pain. B, The onlay component used to reinforce the transversalis fascia has entrapped the ilioinguinal nerve with one of the permanent sutures.

● Repair Management of the vascular injury depends on the severity of the complication and the vessel involved. Patients with acute venous injury presenting with deep venous thrombosis should be appropriately anticoagulated. If there is severe compromise of venous outﬂow from the lower extremity, an angiogram may be needed to determine the extent of the thrombosis and possible intervention. Reoperation may be needed to remove the offending suture(s). Intraoperative arterial injury can be repaired primarily with adequate exposure. Most suture needle injuries can be controlled with direct pressure without placement of additional sutures. Long-term sequela such as aneurysms and arteriovenous ﬁstulas has to be evaluated with additional studies before repair is attempted.

SECTION VIII: HERNIA

506

Cord

Ext. oblique

Poupart’s lig. Femoral v.

Cooper’s lig.

Ant. femoral fascia

Figure 49–5 The external iliac vessels become the femoral vessels as they transverse underneath the inguinal ligament. These vessels can be injured during dissection of the inguinal ﬂoor or during placement of sutures into the shelving edge of the ligament.

● Prevention The surgeon has to be aware of the anatomy of the underlying femoral vessels when placing sutures for ﬁxation of the mesh (Fig. 49–5). This is important speciﬁcally during repair of femoral hernias in which the femoral vein is situated lateral to the hernia sac. Compression of the femoral vein is a well-reported complication of the McVay repair.23 For inguinal hernias, the lateral border of the mesh should be secured to the shelving edge of the inguinal ligament, which will avoid the anterior wall of the vein. Injury to the femoral artery can occur during reconstruction of the inguinal ﬂoor near the deep inguinal ring, at which point the artery is situated just posterior to the transversalis fascia. Lastly, any signiﬁcant bleeding must be controlled with appropriate exposure and direct visualization.

Anatomic Closure of Incision Seroma ● Consequence A postoperative seroma will develop in 1.2% of patients.6 Most seromas are usually asymptomatic and resolve without any intervention (Fig. 49–6). Grade 1/2 complication ● Repair The management of a symptomatic or infected seroma follows a different algorithm. Seromas that are persistent can be aspirated if large and symptomatic. This must be done under sterile conditions, and the risk of contamination of the wound and underlying mesh has

Figure 49–6 Computed tomography (CT) scan obtained in the early postoperative period to evaluate for a recurrence demonstrates a moderate-size seroma in an asymptomatic patient. This seroma resolved after 2 months without any intervention.

to be considered. Infected seromas may be a sequela of a deeper infection. As with any abscess and soft tissue infection, the wound may have to be opened and explored formally to ensure a potential bowel injury does not exist. ● Prevention Careful dissection of the appropriate tissue planes will help to prevent seromas. Excessive subcutaneous tissue should be suture-ligated to control lympathics.

Other Complications Bowel Obstruction Small or large bowel obstruction may occur during reduction of the indirect hernia sac.24,25 If a high ligation is performed before placement of the plug component, it is important to assess whether there is bowel within the sac and to completely reduce it before ligation is completed to avoid trapping the bowel. Conservative measures may be employed, but there should be a low threshold for exploration. Grade 2/3 complication Mesh Migration The plug component may migrate from its desired location at the oriﬁce of the internal ring and be found entirely in the preperitoneal space, intraperitoneal, or the scrotum (Fig. 49–7). Depending on the location of the migrated mesh and resulting sequela, it may have to be removed. This complication can be avoided by proper anchoring of the plug of the mesh to the inguinal ﬂoor. Grade 3/4 complication

49 OPEN INGUINAL HERNIA REPAIR WITH PLUG

Figure 49–7 Laparoscopic view of the intraperitoneal migration of the plug component. The external iliac vessels are adhered to the mesh, which precluded its safe removal. In addition, the potential for a bowel injury exists because the sigmoid colon is in close proximity.

Ileovaginal Fistula This complication has been cited as case reports in the literature after repair of a strangulated femoral hernia.26 Care should be taken to ensure adequate reduction of all herniated contents to avoid the risk of perforation secondary to suture placement. The presence of a ﬁstula should raise the concern for infected mesh, and the algorithm previously described should be followed. Grade 3/4 complication Paravesical Abscess This rare complication has been reported in a case series of six patients by Imamoglu and colleagues.27 These individuals underwent operations for treatment of paravesical abscess related to previous inguinal hernia repairs. The injury was determined to be caused by sutures that had been placed into or adjacent to the urinary bladder. Fixation sutures for the mesh must be appropriately placed. Grade 3/4 complication

REFERENCES 1. Rutkow IM. Demographics and socioeconomic aspects of hernia repair in the United States in 2003. Surg Clin North Am 2003;83:1045–1051. 2. Ruhl CE, Everhart JE. Risk factors for inguinal hernia among adults in the United States population. Am J Epidemiol 2007;167:1154–1161. 3. Nilsson H, Stylianidis G, Haapamaki M, et al. Mortality after groin hernia surgery. Ann Surg 2007;245:656–660. 4. Fitzgibbons RJ Jr, Giobbie-Hurder A, Gibbs JO, et al. Watchful waiting versus repair of inguinal hernia in minimally symptomatic men: a randomized clinical trial. JAMA 2006;295:285–292.

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5. Alimoglu O, Kaya B, Okan I, et al. Femoral hernia: a review of 83 cases. Hernia 2006;10:70–73. 6. Bittner R, Auerland S, Schmedt CG. Comparison of endoscopic techniques versus Shouldice and other open nonmesh techniques for inguinal hernia repair: a metaanalysis of randomized controlled trials. Surg Endosc 2005;19:605–615. 7. Robinson TN, Clarke JH, Schoen J, et al. Major meshrelated complications following hernia repair: events reported to the Food and Drug Administration. Surg Endosc 2005;19:1556–1560. 8. Rios A, Rodriguez JM, Munitiz V, et al. Antibiotic prophylaxis in incisional hernia repair using prosthesis. Hernia 2001;5:148–152. 9. Yerdel MA, Akin EB, Dolalan S, et al. Effect of singledose prophylactic ampicillin and sulbactam on wound infection after tension-free inguinal hernia repair with polypropylene mesh: the randomized, double-blind, prospective trial. Ann Surg 2001;233:26–33. 10. Aufenacker TJ, van Geldere D, van Mesdag T, et al. The role of antibiotic prophylaxis in prevention of wound infection after Lichenstein open mesh repair of primary inguinal hernia: a multicenter double-blind randomized controlled trial. Ann Surg 2004;240:955–960. 11. Perez AR, Roxas MF, Hilvano SS. A randomized, doubleblind, placebo-controlled trial to determine effectiveness of antibiotic prophylaxis for tension-free mesh herniorrhaphy. J Am Coll Surg 2005;200:393–397. 12. Losanoff JE, Rochman BW, Jones JW. Enterocutaneous ﬁstula: a late consequence of polypropylene mesh abdominal wall repair: a case report and review of literature. Hernia 2002;6:144–147. 13. Harrell AG, Novitsky YW, Peindle RD, et al. Prospective evaluation of adhesion formation and shrinkage of intraabdominal prosthetics in a rabbit model. Am Surg 2006; 72:808–813. 14. Mahmouduslu HY, Erkek AB, Cakmak A, et al. Incisional hernia treatment with polypropylene graft: results of 10 years. Hernia 2006;10:380–384. 15. Bringman S, Ramel S, Heikknen TJ, et al. Tension-free inguinal hernia repair: TEP versus mesh-plug versus Lichtenstein: a prospective randomized controlled trial. Ann Surg 2003;237:142–147. 16. Frey DM, Wildisen A, Hamel CT, et al. Randomized controlled trial of Lichtenstein’s operation versus meshplug for inguinal hernia repair. Br J Surg 2007;94:36–41. 17. Eklund A, Rudberg C, Leijonmarck CE, et al. Recurrent inguinal hernia: randomized multicenter trial comparing laparoscopic and Lichenstein repair. Surg Endosc 2007; 21:634–640. 18. Neumayer L, Giobbie-Hurder A, Jonasson G, et al. Open mesh versus laparoscopic repair of inguinal hernia. N Engl J Med 2004;350:1819–1827. 19. Shin D, Lipshultz LI, Golstein M, et al. Herniorrhaphy with polypropylene mesh causing inguinal vasal obstruction: a preventable cause of obstructive azoospermia. Ann Surg 2005;241:553–558. 20. Sheynkin YR, Hendin BN, Schlegel PN, et al. Microsurgical repair of iatrogenic injury to the vas deferens. J Urol 1998;159:139–141. 21. Picchio M, Palimento D, Attanasio U, et al. Randomized controlled trial of preservation or elective division of

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ilioinguinal nerve on open inguinal hernia repair with polypropylene mesh. Arch Surg 2004;139:755–758. 22. Alﬁeri S, Rotondi F, DiGiorgio A, et al. Inﬂuence of preservation versus division of ilioinguinal, iliohypogastric, and genital nerves during open mesh herniorrhaphy: prospective multicenter study of chronic pain. Ann Surg 2006;243:553–558. 23. Normington EY, Franklin DP, Brotman SI. Constriction of the femoral vein after McVay inguinal hernia repair. Surgery 1992;111:343–347. 24. Ferrone R, Scarone PC, Natalini G. Late complication of open inguinal hernia repair: small bowel obstruction

caused by intraperitoneal mesh migration. Hernia 2003;7:161–162. 25. Chuback JA, Singh RS, Sills C, et al. Small bowel obstruction resulting from mesh plug migration after open inguinal hernia repair. Surgery 2000;127:475–476. 26. Deshpande PV. Ileovaginal ﬁstula: A complication following repair of a strangulated femoral hernia. Br J Clin Pract 1964;18:744–745. 27. Imamoglu M, Cay A, Sarihan H, et al. Paravesical abscess as an unusual late complication of inguinal hernia repair in children. J Urol 2004;171:1268–1270.

50

Prolene Hernia System— Hernia Repair Edward W. Nelson, MD INTRODUCTION The ideal method to accomplish the successful and durable repair of groin hernias remains a topic of ongoing debate; centuries after these defects were ﬁrst described by early anatomists and more than 100 years after the ﬁrst reported “surgical cures” by Marcy (1881), Bassini (1887), and Halsted (1889). Today, entire surgical texts and journals are devoted to the history, evolution, and ongoing progress in surgery for hernia repair.1,2 The most current literature describing the relative merits of the open versus the laparoscopic approach is a prime example of both the science and the emotion still generated by this common yet difﬁcult problem.3 Ideally, repair of groin hernias should be safe, reliable, and easy to learn and, above all, have a low recurrence rate. Champions exist for a variety of currently popular repairs, but today, most surgeons performing open repairs have adopted the concept, ﬁrst introduced by Usher and colleagues in 1960,4 of using mesh as part of the repair. Current literature comparing these various mesh repairs is limited by nonrandomization, short follow-up, and operative variability.5–7 Today, the Lichtenstein “tension-free” mesh repair, the plug and patch repair reported by Robbins and Rutkow, the preperitoneal Kugel repair, and the Prolene hernia system (PHS) are the most common anterior tension-free mesh repairs performed, all with excellent overall results and minimal recurrence rates when performed by experienced surgeons.8–12 Groin hernia repair using the PHS was ﬁrst reported by Gilbert and associates in 1999,11 and numerous follow-up reports continue to document the ease of use and low recurrence rate of this system when compared with other methods.13–15 Unique to this system is the intent to have a mesh repair designed to cover the entire myopectineal oriﬁce.16 With this intent, potential defects at the internal ring, inguinal ﬂoor, and femoral canal are covered with both onlay and underlay patches held together by a connector inserted into the hernia defect16 (Fig. 50–1). When the PHS repair is completed, the onlay patch covers the entire ﬂoor of the inguinal canal as in the Lichtenstein repair, the underlay patch covers and supports the preperi-

toneal space as in a Kugel or laparoscopic approach, and the connector “plugs” the defect without the risk of migration seen with the two-piece plug patch repair17 (Fig. 50–2). Using this repair in over 11,000 procedures, recurrence rates of 0.014% have been reported.13 A systematic series of steps have been well described in the correct use of the PHS to minimize the risk of pitfalls in its use in the repair of groin hernias.

INDICATIONS ● Inguinal hernia repair ● Direct hernia repair ● Indirect hernia repair

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5 Step 6

Exposure of inguinal ﬂoor Conﬁrm type of hernia present Development of external pocket for onlay patch Prepare posterior space for underlay patch Deployment of underlay patch Secure onlay component

OPERATIVE PROCEDURE Exposure of the Inguinal Floor Like all open inguinal hernia repairs, the PHS repair requires a standard inguinal incision, opening in the subcutaneous fat, Scarpa’s fascia, and the external oblique fascia in the direction of its ﬁbers to the external ring. Assuming a correctly placed incision, the complications that can occur during exposure of the inguinal ﬂoor and mobilization of the spermatic cord include excessive bleeding and hematoma formation in the subcutaneous space, incorrect placement of the external oblique fascial opening, and injury to the ilioinguinal nerve or spermatic cord.

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Figure 50–1 A stem connector inserted through the hernia defect holds together the onlay and the underlay mesh patches.

● Prevention Subcutaneous vessels, when encountered, require careful attention to hemostasis with either electrocautery or absorbable ties, if necessary. The external oblique fascial opening should be oriented on clear identiﬁcation of the external ring. A carefully placed incision in the direction of the fascial ﬁbers with clear identiﬁcation of the nerve and cord prior to completion of the opening is mandatory. For the PHS repair, the ilioinguinal nerve need not be elevated off the cord, thereby minimizing traction and potential injury.

Conﬁrm the Type of Hernia Present Once the cord is mobilized, the ﬂoor of the inguinal canal can be inspected for the presence of a direct hernia. If a direct hernia is found, the possibility of an indirect hernia must also be perused by opening the external spermatic fascia at the anterior medial aspect of the cord near the internal ring. If the preoperative examination suggested a femoral hernia, Cooper’s ligament must be exposed to allow inspection for a femoral defect.

(B) (A)

● Consequence Unless the cord is inspected for an indirect sac, the potential for recurrence at the internal ring will be greatly increased. ● Prevention Methodical and consistent inspection for both direct and indirect defects is mandatory in all hernia repairs.

Development of the External Pocket for the Onlay Patch Figure 50–2 The underlay patch (A) supports the preperitoneal space and is connected to the onlay patch (B) covering the ﬂoor of the inguinal canal.

● Consequence Excessive bleeding in the subcutaneous space can result in hematoma formation and increased risk of secondary infection. Making the opening in the external oblique fascia either too high or too low can compromise exposure of the cord, risk injury to the iliohypogastric nerve as it penetrates the abdominal musculature, and make closure of the fascia over the onlay patch more difﬁcult. Careless technique in opening the external oblique fascia and mobilization of the cord can result in injury to the ilioinguinal nerve with resultant postoperative numbness in its area of sensation, or injury to the spermatic cord or its contents resulting in cord hematoma, vas deferens injury, or compromise of testicular circulation with secondary pain, swelling, and possible atrophy.

The space between the external oblique fascia and the internal oblique muscle must be opened to allow placement of the onlay patch. This dissection includes clearing the attachments from the shelving edge of the inguinal ligament and opening the space lateral to the internal ring to the upper third of the ligament (Fig. 50–3). ● Consequence Injury to the iliohypogastric nerve during the superior part of the dissection can occur, and several perforating vessels may also be disrupted. Most importantly, if the lateral and superior spaces are not opened completely enough, the onlay mesh will not lie ﬂat in order to conform to the abdominal wall. Especially in thin patients, onlay mesh that is not ﬂat may be palpable or cause discomfort. ● Prevention The space for the onlay mesh must be developed with attention to creating a space large enough to cover not only the ﬂoor of the inguinal canal but also the superior and lateral areas beyond the area normally covered by other open mesh repairs. When done under direct

50 PROLENE HERNIA SYSTEM—HERNIA REPAIR

511

Figure 50–3 The fascial plane beneath the external oblique fascia is dissected to create a space for the onlay patch.

Figure 50–4 The preperitoneal space is dissected through the hernia oriﬁce to allow space for the underlay patch.

vision and with adequate care, the space can be opened without nerve or vessel injury. If necessary, the onlay mesh can be trimmed slightly in smaller patients to appropriately cover the area needed.

neum will result in the underlay mesh laying directly on the abdominal viscera.

Prepare the Posterior Space for the Underlay Patch The preperitoneal space, between the abdominal wall and the preperitoneal fat, is developed to allow space for the underlay patch. For indirect inguinal hernias, this is done through the internal ring; for direct hernias, it is created through the posterior ﬂoor defect. At the internal ring, this requires taking down all ﬁbers remaining between the cord and the hernia sac; for direct hernias, any remaining attenuated ﬁbers of the inguinal ﬂoor must be opened to fully expose the direct sac. For both indirect and direct defects, the sac is not opened or ligated but rather inverted back into the abdominal cavity. In either case, the space is carefully created using ﬁnger dissection to sweep circumferentially to actualize the preperitoneal space (Fig. 50–4). A moist 4 × 4 gauze sponge can be used to facilitate this dissection and hold the space open. To be complete, the preperitoneal space should extend to Cooper’s ligament inferiorly and well back, beyond the defect in all other directions. ● Consequence Failure to completely actualize the preperitoneal space will not permit the underlay patch to ﬂatten out against the underside of the abdominal wall to cover the entire myopectineal oriﬁce. Opening or tearing the perito-

● Prevention The space for the underlay mesh must be carefully and completely developed. Although mesh trimming may be needed, it should be minimized. Any inadvertent holes in the peritoneum should be closed with running absorbable suture to prevent direct contact between the mesh and the abdominal viscera.

Deployment of the Underlay Patch The onlay patch is folded and grasped with a clamp or sponge forceps with the long axis parallel to the inguinal ligament. The entire underlay patch is inserted into the previously developed preperitoneal space, and with the onlay patch held above the defect, the underlay patch is spread out away from the connector using a ﬁnger or forceps (Fig. 50–5). Increased intra-abdominal pressure, when the patient later stands or strains, will enhance deployment by ﬂattening the underlay mesh against the inside of the abdominal wall. If the defect is considerably larger than the connector, interrupted sutures should be placed to snug up the tissue around the connector. ● Consequence Failure to ﬂatten the underlay mesh as much as possible will result in failure to adequately cover all areas where recurrent hernias may occur: the femoral canal, inguinal ﬂoor, and internal ring. Unless the underlay patch is

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Figure 50–5 The underlay patch is inserted and spread out in the preperitoneal space whereas the onlay patch is held above with the long axis parallel to the inguinal ligament.

deployed as completely as possible, the repair will be compromised and the risk of recurrence increased. If the defect is considerably larger than the connector, added risk of recurrence next to the connector or extrusion of the underlay mesh is possible. ● Prevention Correct deployment of the underlay patch begins with the careful creation of the preperitoneal space as described earlier in the section on “Development of the External Pocket for the Onlay Patch.” Once in place, the underlay mesh must be carefully and patiently spread out, to be as ﬂat as possible. If the defect is much larger than the connector, the tissues around the connector should be approximated to ensure a snug ﬁt.

Secure the Onlay Component Once the underlay patch is completely deployed, the onlay component is ﬂattened and positioned in the previously created space between the external oblique fascia and the ﬂoor of the inguinal canal. The lateral ﬂap is positioned ﬁrst and the mesh trimmed to allow a ﬂat ﬁt, held in place with sutures at the pubic tubercle, transverse arc, and inguinal ligament. A slit is made to accommodate the cord and sutures placed between the mesh and the shelving edge of the inguinal ligament on either side of the cord. Fixation sutures should be placed at least ¼ inch from the edge of the mesh and the mesh fashioned to lie as ﬂat as possible (Fig. 50–6).

Figure 50–6 The onlay patch should lie ﬂat against the inguinal ﬂoor and under the external oblique fascia with anchoring sutures on either side of the cord and at the pubic tubercle.

● Consequence Failure to adequately open the pocket between the external oblique fascia and the abdominal wall as described earlier in the section on “Conﬁrm the Type of Hernia Present,” can cause folding or wrinkling of the onlay mesh. Placing more sutures than needed will increase the risk of postoperative pain, especially when placed too deeply at the pubic tubercle. Sutures placed too tightly around the spermatic cord can result in compromise of cord circulation, with testicular swelling, pain, and atrophy. Sutures placed too close to the mesh edge can pull through. ● Prevention The PHS is a groin hernia repair requiring few sutures to secure the mesh, and the temptation to place more sutures than necessary must be resisted. A minimal number of stitches to attach the mesh to the tubercle, around the cord, and if needed, to the anterior abdominal wall should be used.

SUMMARY When appropriately applied, groin hernia repair using the PHS has a competitively low recurrence rate with minimal and largely preventable complications. To maximize the advantages of both an onlay and an underlay mesh system, special attention in creation of the space below the external oblique fascia and in the preperitoneum is required.

50 PROLENE HERNIA SYSTEM—HERNIA REPAIR

REFERENCES 1. Condon RE, Nyhus LM. Hernia, 4th ed. Philadelphia: JB Lippincott, 1995. 2. Lichtenstein IL. Hernia Repair Without Disability, 2nd ed. St. Louis: Ishiyaku Euroamerica, 1987. 3. Neumayer L, Giobbie-Hurder A, Jonasson O, et al, and the Veterans Affairs Cooperative Studies Program 456 Investigators. Open mesh verses laparoscopic mesh repair of inguinal hernia. N Engl J Med 2004;350:1819–1827. 4. Usher FC, Cogan JE, Lowery TI. A new technique for the repair of inguinal and incisional hernias. Arch Surg 1960;81:847–854. 5. Nienhuijs SW, van Oort I, Keemers-Gels ME, et al. Randomized trial comparing the Prolene Hernia System, mesh plug repair and Lichtenstein method for open inguinal hernia repair. Br J Surg 2005;92:33–38. 6. Mayagoitia JC. Inguinal hernioplasty with the Prolene hernia system. Hernia 2004;8:64–66. 7. Huang CS, Huang CC, Lien HH. Prolene hernia system compared with mesh plug technique: a prospective study of short- to mid-term outcomes in primary groin hernia repair. Hernia 2005;9:167–171. 8. Lichtenstein IL, Shulman AG. Ambulatory outpatient hernia surgery. Including a new concept, introducing the tension-free repair. Int Surg 1986;71:1–7. 9. Robbins AW, Rutkow IM. The mesh-plug hernioplasty. Surg Clin North Am 1993;73:501–512.

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10. Kugel RD. The Kugel repair for inguinal hernias. In Bendavid R, Abrahamson J, Arregui ME, et al (eds): Abdominal Wall Hernias: Principles and Management. New York, Berlin: Springer-Verlag, 2001; pp 504–507. 11. Gilbert AI, Graham MF, Voigt WJ. A bilayer patch device for inguinal hernia repair. Hernia 1999;3:161–166. 12. Amid PK, Lichtenstein IL. Long-term result and current status of the Lichtenstein open tension-free hernioplasty. Hernia 1998;2:89–94. 13. Gilbert AI, Young J, Graham MF, et al. Combined anterior and posterior inguinal hernia repair: intermediate recurrence rates with three groups of surgeons. Hernia 2004;8:203–207. 14. Kingsnorth A, Wright D, Porter C, Robertson G. Prolene hernia system compared with Lichtenstein patch: a randomised double-blind study of short-term and medium-term outcomes in primary inguinal hernia repair. Hernia 2002;6:113–119. 15. Murphy JW. Use of the Prolene hernia system for inguinal hernia repair: retrospective, comparative time analysis versus other inguinal repair systems. Am Surg 2001;67: 919–923. 16. Fagan SP, Awad SS. Abdominal wall anatomy: the key to a successful inguinal hernia repair. Am J Surg 2004;188(6A suppl):3S–8S. 17. LeBlanc KA. Complications associated with the plug-andpatch method of inguinal herniorrhaphy. Hernia 2001;5: 135–138.

51

Laparoscopic Inguinal Hernia Repair Benjamin Kim, MD and Quan-Yang Duh, MD INTRODUCTION Laparoscopic inguinal hernia repair has evolved to become a safe and effective alternative for inguinal herniorrhaphy. The ﬁrst report of a laparoscopic approach was in 1990 by Ger and associates1 in which indirect inguinal hernias were repaired by a transabdominal laparoscopic staple closure of a patent processus vaginalis. Following this study, other reports were published including a transabdominal rolled mesh plug technique2 and an intraperitoneal onlay mesh technique.3 These methods were eventually abandoned owing to high recurrence rates. Over time, the laparoscopic approach built upon the idea of applying a prosthetic to the posterior wall of the groin developed by Nyhus, Stoppa, and Wantz.4 The hallmarks of this approach included complete dissection of the groin in the preperitoneal space, identiﬁcation of all myopectineal oriﬁces, and placement of mesh over the entire inguinal-femoral region (Fig. 51–1). This has now become the laparoscopic procedure of choice. Several reports have demonstrated the efﬁcacy of the laparoscopic approach to inguinal hernia repairs. Liem and coworkers5 compared laparoscopic versus conventional anterior hernia repair and found that the laparoscopic group had faster postoperative recovery and a recurrence rate similar to that of the open group. A study by Andersson and colleagues6 found that laparoscopic totally extraperitoneal hernia repair resulted in less postoperative pain, shorter time to recovery, earlier return to work, and no difference in overall complications when compared with open tension-free repair. The results from the Veterans Administration (VA) Cooperative Study showed that, although laparoscopic repair of inguinal hernias resulted in less pain and earlier return to normal activity, recurrence was signiﬁcantly more common after laparoscopic repair.7 However, this study also reported similar recurrence rates between laparoscopic and open inguinal hernia repairs when surgeons with a large volume of experience performed the laparoscopic procedures. This ﬁnding underscores the challenge in learning this approach and the need for technical mastery in order to achieve consistently satisfactory results.8

The laparoscopic approach to inguinal hernia repair can be divided into two types: the transabdominal preperitoneal approach (TAPP) and the totally extraperitoneal approach (TEP). Initially, most procedures were performed with the TAPP approach for exposure of the posterior ﬂoor of the groin because the groin anatomy was easier to delineate. However, the TEP approach avoids violation of the peritoneal cavity, potentially reducing some of the complications associated with the TAPP technique. Although understanding the inguinal anatomy from an extraperitoneal posterior view can be difﬁcult, hernia surgeons have become more comfortable with this exposure and can achieve similarly low recurrence rates using this technique.4 By and large, the TEP approach can be applied to most clinical circumstances in which laparoscopic inguinal hernia repair is performed, and it is described here.

INDICATIONS ● ● ● ●

Recurrent inguinal hernias Bilateral inguinal hernias Patients who are able to tolerate general anesthesia Patients who are eager to return to normal activity earlier

RELATIVE CONTRAINDICATIONS ● Prior or planned extraperitoneal operations (e.g., radical

prostatectomy) ● Previous pelvic irradiation ● Extremes of age ● Contraindications to laparoscopy (e.g., severe chronic

obstructive pulmonary disease)

OPERATIVE STEPS Step 1 Step 2

Positioning and trocar insertion Dissection of preperitoneal space

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Inf

D I

F

Vas Sper

X x

Figure 51–2

x

Port placement.

Figure 51–1 Posterior view of potential right groin myopectineal defects. D, direct hernia defect; F, femoral hernia defect; I, indirect hernia defect; Inf, inferior epigastric vessels; Sper, spermatic vessels; Vas, vas deferens.

Step 3 Step Step Step Step

4 5 6 7

Exposure of pubic bone ligament Dissection of direct hernia Dissection of indirect hernia Placement of mesh Trocar removal

and

Cooper’s

OPERATIVE PROCEDURE Positioning The monitor is placed at the foot of the operating bed with the surgeon standing by the patient’s shoulder on the opposite side of the hernia. If bilateral inguinal hernias are present, the surgeon starts opposite the side of the larger, more symptomatic hernia. Both of the patient’s arms are tucked to the side, and the patient is placed in the Trendelenburg position once the dissecting ports are inserted. The patient needs to be paralyzed to allow for insufﬂation of the preperitoneal space.

Trocar Insertion Trocar insertion should be controlled and under direct vision to avoid serious complications. A standard threetrocar technique is used: a 10-mm port subumbilically, a

5-mm port in the right lower quadrant, and a 5-mm port in the left lower quadrant (Fig. 51–2). All ports are placed within the preperitoneal space. Complications of trocar insertion are discussed in Section I, Chapter 7, Laparoscopic Surgery. The ﬁrst trocar placed is the 10-mm subumbilical port, using an open technique. This port is placed slightly off of the midline to stay in the space behind the rectus muscle and in front of the posterior rectus sheath. If it is placed in the midline, where the anterior and posterior rectus sheaths merge, it will enter the peritoneal cavity. Following this port placement, a 10-mm, 30° angled laparoscope is inserted and used to bluntly dissect the areolar tissue in the preperitoneal space, using a gentle sweeping motion. The preperitoneal space is cleared out laterally toward the anterior superior iliac spine to provide enough space for placement of the other ports. Alternatively, a balloon dissector can be used instead of manual dissection, although it is more expensive. The temptation here is to take down the areolar tissue and move toward the symphysis pubis rather than toward the anterior superior iliac spine. However, by making a conscious effort to move the dissection laterally, enough space can be created to place the other ports, after which the remaining areolar tissue can be dissected in a more precise fashion, using laparoscopic graspers.

51 LAPAROSCOPIC INGUINAL HERNIA REPAIR

517

Right

Left

Coop Pubic Bladder

Dir

Figure 51–3 Midline view of preperitoneal space. Left, left Cooper’s ligament; Right, right Cooper’s ligament.

A

Exposure of the Pubic Bone and Cooper’s Ligament Coop

This step is done at the outset of the procedure in order to clearly deﬁne the midline. Cooper’s ligaments are found just lateral and slightly cephalad to the pubic bone (Fig. 51–3). Cooper’s ligament is where the mesh will be anchored medially. Small veins overlie the pubic bone, and they can be injured during exposure.

Injury during Exposure ● Consequence Bleeding can occur if these small veins are injured by excessive manipulation of the pubic bone, thereby obscuring the view of Cooper’s ligaments. Grade 1 complication ● Repair The bleeding will typically stop on its own. ● Prevention Identify the symphysis pubis and then, by gently probing, conﬁrm the position of the pubic bone. There is no need for excessive rubbing.

Injury to the Bladder ● Consequence Injury to the bladder can occur during exposure of the pubic bone, given that this structure lies in close proximity to it and Cooper’s ligaments. Grade 2 complication ● Repair Bladder injuries can be repaired laparoscopically by suture closure. This is followed by suprapubic or Foley catheter drainage of the bladder. Urology consultation is often necessary. ● Prevention Emptying the bladder immediately preoperatively can reduce its size. Once the size of the bladder is reduced,

Dir

B Figure 51–4 A, Right direct hernia defect with contents reduced. Coop, Cooper’s ligament; Dir, direct hernia defect. B, Corresponding pictorial view.

avoid it and dissect the pubic bone under direct vision.

Dissection of Direct Hernia Identiﬁcation of a Direct Hernia As Cooper’s ligament is exposed, a direct hernia, if present, will generally be reduced (Fig. 51–4). If it is not, gentle traction on the peritoneal attachments should provide enough force to reduce the sac. Occasionally, in chronic direct hernias, a “pseudosac” may be present. The pseudosac is a posterior invagination of the transversalis fascia and should be distinguished from the direct hernia sac, which is continuous with the peritoneum (Fig. 51–5). ● Consequence If not recognized, the pseudosac can be vigorously dissected, leading to confusion in identifying the groin anatomy and potential injury to the peritoneum or the iliac vein. The peritoneal tear can then result in entry

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Injury to the Inferior Epigastric Vessels

Coop Inf

● Consequence Bleeding from this injury can obscure the view of the groin anatomy. Unrecognized and untreated blood loss can potentially result in transfusions and lead to postoperative hematomas. Grade 2 complication ● Repair If the inferior epigastric artery or vein is injured, it is best controlled with endoclips.

Psd

● Prevention It is critical to identify the inferior epigastric vessels to prevent injury. It is a key landmark of the groin, and it separates the direct and indirect inguinal hernia defects. These vessels are identiﬁed behind the rectus muscles and are best left adhered to them during dissection of the preperitoneal space. Dissecting the inferior epigastric vessels off the rectus muscles will cause more bleeding during the procedure and makes placement of the mesh difﬁcult.

A

Coop Inf

Dissection of Indirect Hernia Injury to the External Iliac Vessels

Psd

● Consequence Injury to the external iliac artery or vein causes severe bleeding and, potentially, a CO2 embolus. Grade 3/4 complication ● Repair Laparoscopic repair is very difﬁcult, and open exploration and repair are usually required.

B Figure 51–5 A, Right-sided pseudosac is being dissected free from the direct hernia defect. Coop, Cooper’s ligament; Inf, inferior epigastric vessels; Psd, pseudosac. B, Corresponding pictorial view.

of air into the peritoneal space, obscuring the view of the anatomy. Grade 1 complication ● Repair Tears of the peritoneum can be repaired using an endoloop, clips, or suture. In general, peritoneal tears can be closed after the hernia is repaired. ● Prevention Recognizing the pseudosac can prevent confusion regarding the anatomy and avoid unnecessary dissection of this structure. The pseudosac needs to be dissected away from the true sac and left along the anterior abdominal wall, allowing the true sac and peritoneum to fall back toward the abdominal cavity. Gently pulling the peritoneum posteriorly while providing countertraction on the pseudosac anteriorly will peel the true hernia sac off.

● Prevention The external iliac vessels are located just below the area ﬂanked medially by the vas deferens and laterally by the spermatic vessels. Dissecting within this area risks injury to the external iliac vessels. They can usually be identiﬁed by their pulsation and are best avoided by identifying the peritoneal edge of the hernia sac and gently pulling it away from the preperitoneal tissue under direct vision.

Identiﬁcation of an Indirect Hernia The indirect hernia sac is found along the spermatic cord and just cephalad to it. Within the spermatic cord, the vas deferens and the spermatic vessels are located medial and lateral, respectively, merging through the internal ring. Together with the inferior epigastric vessels, the vas deferens and the spermatic vessels form the so-called Mercedes-Benz sign (Fig. 51–6). Cord lipomas, if identiﬁed, are usually found laterally along the spermatic vessels. Usually, the indirect hernia sac is reduced from the internal ring by gentle traction and dissection (Fig. 51–7). If the sac is too long or too large, it can be dissected

51 LAPAROSCOPIC INGUINAL HERNIA REPAIR

519

Inf Inf

Coop

Ind

Vas

A Sper Inf

Coop

Figure 51–6 “Mercedes-Benz” sign. The inferior epigastric vessels (Inf), the vas deferens (Vas), and the spermatic vessels (Sper) represent the three spokes seen in the Mercedes-Benz symbol. Ind

at the internal ring and divided. The proximal part of the sac, which is continuous with the peritoneum, is dissected off of the cord structures and ligated with an endoloop. The distal end of the transected sac should be left open and not ligated. Ligating the distal sac will cause a hydrocele.

B

● Consequence During dissection of the cord structures, the indirect hernia sac can be torn, creating a pneumoperitoneum. Sometimes, the sac is intentionally transected, also creating a pneumoperitoneum. This can hinder the view of the anatomy in the preperitoneal space. Grade 1 complication

Figure 51–7 A, Left indirect hernia defect (Ind) with contents nearly completely reduced. Cooper’s ligament (Coop) has been exposed, and the inferior epigastric vessels (Inf) have been seen. B, Corresponding pictorial view.

● Repair Tears in the peritoneum are best repaired with endoloops. Clips or sutures can also be used for closure. If not repaired, loops of bowel can herniate through the defect, creating a “preperitoneal hernia.” Grade 3 complication

Avoiding Recurrence The mesh should be large enough to cover all potential hernia defects in the groin. It is also important to ﬁx the mesh to minimize shrinkage and to prevent migration. Inappropriate mesh placement can lead to hernia recurrence because the mesh shrinks over time and can move within the preperitoneal space. The mesh also needs to lie ﬂat against the anterior abdominal wall in order to prevent hernia recurrence around the edges of the mesh.

● Prevention Complete dissection of the indirect sac off of the spermatic cord is not necessary if the sac is long. The sac can be divided and the proximal end closed with an endoloop. Dividing the sac at the internal ring frequently helps in the dissection of the remaining spermatic cord structures.

Placement of Mesh

● Consequence Laparoscopic hernia repair should have similar or lower recurrence rates than those of open operation. Grade 3 complication

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Figure 51–9 Mesh placement in right indirect hernia repair. Figure 51–8 Mesh placement in right direct hernia repair.

● Repair If a hernia recurs, it can be re-repaired with either an open or a laparoscopic technique. ● Prevention Using a large piece of mesh and ﬁxing the mesh decrease the chance of recurrence. Enough space should be dissected out laterally in order for the mesh to lie ﬂat against the abdominal wall. The edge of dissected peritoneum should be beyond the edge of the mesh to prevent recurrence. When repairing direct hernias, preformed, contoured mesh (Bard, 3D Max Mesh, Davol Inc., Cranston, RI) can be used (Fig. 51–8). The contoured surface and stiffness of the mesh make it easy to manipulate, and it tends not to move much within the preperitoneal space. For an indirect hernia, however, we use a large (16 × 12 cm) piece of ﬂat mesh that is slit medially, passing the lower tail around the spermatic cord structures (Fig. 51–9). The two tails are then overlapped and ﬁxed to Cooper’s ligament medially. Slitting the mesh medially and placing the lower tail below the cord structures ensures complete coverage of the indirect inguinal hernia site without having to add additional points of ﬁxation of the mesh.

Fixating the Mesh ● Consequence Unﬁxed mesh can move and compromise the repair. The mesh is usually ﬁxed with an endotacker in two or three points. Inappropriate placement of the tacks, however, can cause painful neuralgias. Grade 2/3 complication

● Repair When a speciﬁc nerve is entrapped or injured, it can be diagnosed by pain in its distribution immediately after the operation. In such cases, the tacks should be removed. ● Prevention The mesh is ﬁxated medially at Cooper’s ligament and laterally onto the anterior abdominal wall above the iliopubic tract (Fig. 51–10). Deep tacking into the pubic bone, instead of Cooper’s ligament, can cause chronic pain. There are several nerves at risk for injury by the tacks as well (Fig. 51–11). These nerves run at or below the iliopubic tract to innervate the upper thigh. When placing the tacks laterally onto the abdominal wall, the surgeon needs to be able to palpate the end of the tacking device with the opposite hand. If the tip is not palpable, the tacks can be placed below the iliopubic tract and cause nerve injury. The tacks are designed to simply hold the mesh in place. Do not use excessive force on the tacking device because the tacks can cause skin dimpling or even puncture the skin in very thin persons. After palpating the endotacker tip, gently push and simply allow the tack to hold the mesh in place against the anterior abdominal wall.

SUCCESSFUL LAPAROSCOPIC INGUINAL HERNIA REPAIR ● ● ● ● ●

Select appropriate patients Understand preperitoneal anatomy Use proven techniques Avoid common pitfalls Learn from experience

51 LAPAROSCOPIC INGUINAL HERNIA REPAIR

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Genital branch

Femoral branch

Lateral femoral cutaneous nerve

A Genital femoral nerve

Figure 51–11 Nerves at risk for injury during laparoscopic inguinal hernia repair.

REFERENCES

B

C Figure 51–10 A, Medial mesh ﬁxation over a left-sided inguinal hernia defect. Two endotacks are placed in Cooper’s ligament. B, Lateral mesh ﬁxation over a left-sided inguinal hernia defect, taking care to place the endotack above the iliopubic tract. The tip of the tacking device should be palpable with the opposite hand along the abdominal wall. C, Final orientation of the mesh covering all left-sided myopectineal oriﬁces.

1. Ger R, Monroe K, Duvivier R, Mishrick A. Management of indirect inguinal hernias by laparoscopic closure of the neck of the sac. Am J Surg 1990;159:370–373. 2. Schultz L, Cartuill J, Graber JN, Hickok DF. Transabdominal preperitoneal procedure. Semin Laparosc Surg 1994;1: 98–105. 3. Kingsley D, Vogt DM, Nelson MT, et al. Laparoscopic intraperitoneal onlay inguinal herniorrhaphy. Am J Surg 1998;176:548–553. 4. Conlon KC, Johnston SM. Surgical endoscopy for staging palliation of upper gastrointestinal malignancy. In Soper NJ, Swanstrom LL, Eubanks WS (eds). Mastery of Endoscopic and Laparoscopic Surgery. Philadelphia: Lippincott Williams & Wilkins, 2005; p 50. 5. Liem MS, van der Graaf Y, van Steensel CJ, et al. Comparison of conventional anterior surgery and laparoscopic surgery for inguinal-hernia repair. N Engl J Med 1997;336: 1541–1547. 6. Andersson B, Hallen M, Leveau P, et al. Laparoscopic extraperitoneal inguinal hernia repair versus open mesh repair: a prospective randomized controlled trial. Surgery 2003;133:464–472. 7. Neumayer L, Giobbie-Hurder A, Jonasson O, et al, and the Veterans Affairs Cooperative Studies Program 456 Investigators. Open mesh versus laparoscopic mesh repair of inguinal hernia. N Engl J Med 2004;350:1819–1827. Epub 2004; April 25. 8. Grunwaldt L, Schwaitzberg SD, Rattner DW, Jones DB. Is laparoscopic inguinal hernia repair an operation of the past? J Am Coll Surg 2005;200:616–620.

52

Umbilical and Epigastric Hernias Kamal M. F. Itani, MD INTRODUCTION

OPERATIVE PROCEDURE

About 10% of all primary hernias consist of umbilical and epigastric hernias.1 Umbilical hernias are classiﬁed into congenital, infantile, and adult types, based on their actual time of development in life. This section covers only the adult umbilical hernia, which in 90% of the cases, is an acquired hernia and represents an indirect herniation through the umbilical canal.2 Epigastric hernias are protrusions of the intra-abdominal contents through the linea alba between the umbilicus and the xyphoid. The origin and development of the epigastric hernia is still an enigma. Although originally considered a congenital defect,3 it is now assumed to be an acquired lesion.4 It is important to note that as many as 20% of these hernias are multiple, although it may not be apparent clinically that more than one hernia exists.5

Repair of umbilical and epigastric hernias can be performed through the open approach or laparoscopically. As with incisional hernias, smaller umbilical and epigastric hernias (<3 cm) can be repaired with primary tissue approximation with sutures.6 Repair of larger defects generally requires the use of prosthetic materials, which allow for a tension-free repair. Laparoscopic techniques may be used for repair of hernias greater than 3 cm in diameter, recurrent hernias of any size, hernias in obese patients and in those who had to return to strenuous activity shortly after surgery.7

INDICATIONS Complications of umbilical hernias are few, with strangulation, incarceration, or evisceration being reported in 5% of patients in large series.5 Hernias smaller than 1.5 cm in diameter become incarcerated twice as often as do larger hernias. The skin over larger hernias is stretched and often very thin and may even become ulcerated by pressure necrosis. In cirrhotic patients with ascites, skin ulceration and necrosis may lead to rupture with chronic ascitic ﬂuid leak or peritonitis. In obese patients, contact dermatitis with resulting ulceration can occur between the inferior fold of the hernia and the abdominal wall. Many patients seek surgery for esthetic reasons and for relief of discomfort. However, the real danger is the risk of the previously discussed complications, and repair is therefore advocated as soon as feasible. For epigastric hernias, the smaller hernias may become painful because of strangulation of the preperitoneal fat incarcerating in the defect. Omentum in the sac may also strangulate, in which case, the hernia may become swollen, painful, and tender, and the overlying skin reddens. Larger hernias containing bowel may also strangulate, but this is rare. Epigastric hernias are managed in the same way as umbilical hernias.

Open Repair The classic repair for umbilical hernias is the Mayo hernioplasty.8 In this operation, a vest-over-pants imbrication of the superior and inferior aponeurotic segments is performed. Smaller umbilical and epigastric hernias are closed with a to-and-fro continuous or interrupted nonabsorbable suture (Fig. 52–1).

Prosthetic Mesh Repair Mesh repair for umbilical and epigastric hernias can be used as sublay or onlay. Mesh plugs have also been used to repair these hernias. In the sublay technique, the RivesStoppa repair described for ventral incisional hernias is used in which the mesh is placed between the rectus abdominis muscle and the posterior rectus sheath (Fig. 52–2). With the onlay technique, the defect is primarily closed as described previously for primary repair and an onlay mesh is sutured circumferentially on top of the primary repair to reinforce the defect (Fig. 52–3). A mesh plug has also been used with care to avoid placing the plug in direct contact with bowel. The sac is carefully dissected and reduced. The preperitoneal space is dissected to allow placement of the mesh in that space. The mesh plug is subsequently sutured to the fascial edges (Fig. 52–4). The Prolene hernia system has been successfully used recently to repair umbilical and epigastric hernias. The Prolene hernia system combines a sublay, a plug, and an

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A

C

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MC

B

D

Figure 52–1 Primary repair of a small umbilical hernia with interrupted monoﬁlament suture. A, Infraumbilical curvilinear incision and (B) primary repair with either (C) a running monoﬁlament suture or (D) interrupted monoﬁlament sutures.

A

B

Figure 52–2 Rives-Stoppa repair with a sublay mesh placed between the rectus abdominis muscle and the posterior rectus sheath. A, Anterior and (B) sagittal view of the sublay mesh with anchoring transmuscular sutures.

52 UMBILICAL AND EPIGASTRIC HERNIAS

A

525

B Figure 52–3 Continuous or interrupted mass closure of hernia opening (A) with onlay reinforcement of the repair with mesh sutured circumferentially (B).

A

B

Figure 52–4 Mesh plug repair. A, The mesh is placed in the preperitoneal space after dissection and reduction of the hernia sac. B, The mesh is sutured to the fascial edges.

onlay repair. The posterior leaﬂet of the Prolene hernia system is placed in the preperitoneal space after carefully reducing the sac and dissecting the preperitoneal space underneath the fascial edges. The connector between the posterior and the anterior leaﬂet of the mesh acts as a plug. The anterior leaﬂet of the Prolene hernia system is tacked to the anterior rectus fascia with running or interrupted nonabsorbable monoﬁlament sutures (Fig. 52–5). The laparoscopic repair uses the concept of a sublay technique with a smooth mesh used intraperitoneally with a 3- to 4-cm overlap over the edges of the defect. Transabdominal ﬁxation of the mesh with nonabsorbable sutures every 6 cm in addition to the tacks has been shown to reduce recurrence. Although various prosthetic materials have been used in contaminated ﬁelds, it is advisable to avoid their use under this condition and perform a primary suture repair or use allografts (Fig. 52–6).

Complications Recurrence of Hernia One of the most signiﬁcant problems in hernia surgery is recurrence. Recurrence rates as high as 13% have been reported for umbilical hernias repaired primarily without mesh.9 ● Consequence Recurrence will defeat the purpose of the original primary repair. Subsequent repairs are generally more difﬁcult and place the patient at higher risk for higher recurrence rates in the future.10 Grade 3 complication ● Repair Placement of a mesh should be considered in the repair of a recurrent hernia in which the original defect was

SECTION VIII: HERNIA

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Skin Subcuaneous fat

Subcutis

Onlay patch of PHs Umbilicus

Connector of PHS

Peritoneum

Figure 52–6 Intraperitoneal placement of a polytetraﬂuoroethylene (PTFE) mesh during laparoscopic repair of an epigastric hernia. The mesh is ﬁxed to the abdominal wall with a nonabsorbable suture every 6 cm in addition to tacks circumferentially.

closed primarily. Laparoscopic repair might allow for an alternative approach and avoid dissection of scarred tissues if the open approach was originally used. Alternatively, an open approach in a recurrent laparoscopic hernia might avoid intra-abdominal adhesions and should be used by surgeons with little laparoscopic experience. ● Prevention Among open repairs, the Mayo technique is no longer favored11 owing to high recurrence rates ranging between 20% and 28%.12 The use of mesh in umbilical or epigastric hernias should reduce the recurrence rate from 13%9 to less than 1%.13 In a prospective, randomized trial comparing primary suture repair with polypropylene mesh or plug in 200 patients with a primary umbilical hernia and a mean follow-up of 69 months, recurrence was 11% in the primary repair group and 1%

Anterior rectus sheath

Musculus rectus abdominis Underlay of patch of PHS

Figure 52–5 Prolene hernia system. The posterior leaﬂet of the mesh is placed in the preperitoneal space. The anterior leaﬂet of the mesh is anchored to the anterior rectus fascia.

in the mesh repair group. Overall recurrence rates were similar for defects greater and smaller than 3 cm diameter (8% vs. 5%, respectively).14 There are no studies that evaluate the recurrence rate of sublay repair and few reported with onlay mesh in the repair of primary umbilical or epigastric hernias. The sublay technique requires extensive preparation of the preperitoneal space. Recurrence rates of 0%15 to 10.4%16 have been reported with this technique in ventral incisional hernias. With the onlay mesh, recurrence varies from 2.5%17 to 14.8%18 in ventral incisional hernias and 0% in a small series of primary umbilical hernias.19 With the plug repair, no recurrence has been reported for primary umbilical and epigastric hernias; a recurrence rate of 2.3% was reported for the repair of recurrent umbilical hernias, and 0% was reported for the repair of recurrent epigastric hernias.20 With the Prolene hernia system, recurrence has been reported to be 0%.19,21 The laparoscopic repair is gaining popularity with larger (>3 cm) umbilical and epigastric hernias. Recurrence rate was nonexistent in two small series with less than 2 years follow-up.22,23 No relationship has been observed between obesity and recurrence.9

Seroma Seroma occurs in 2.9% of open umbilical hernia repairs and 3.5% of open epigastric hernia repairs.20 The incidence of seroma in the laparoscopic group is higher, at 10%.22 ● Consequence Seromas can be tender or uncomfortable to the patient. They can also become secondarily infected in both the open and the laparoscopic procedures, ultimately requiring removal of the mesh and recurrence of the ventral hernia. Treatment by aspiration or repeated aspiration of the seroma can be uncomfortable and annoying to the patient and has the risk of introducing bacteria. Grade 2 complication

52 UMBILICAL AND EPIGASTRIC HERNIAS ● Repair Most seromas will resolve with expectant therapy. Symptomatic seromas, large seromas, and persistent seromas can be aspirated; repeated aspirations might be required. A chronic seroma might need operative intervention using the open or laparoscopic approach with drainage of the ﬂuid and removal of the pseudocapsule. ● Prevention Placement of subcutaneous drains has been advocated in the open repair that requires extensive dissection and development of ﬂaps in order to prevent ﬂuid accumulation and seroma. The use of a pressure dressing with a binder for 7 to 10 days after laparoscopic repair has also been advocated.24 Premature removal of a drain can result in ﬂuid accumulation; however, this should be weighed against leaving a drain for a prolonged period of time with the potential for an infection to occur. It is believed that repeated aspiration of the ﬂuid in a third of the patients is less morbid than placement of a drain in all patients undergoing the laparoscopic procedure. A small study suggested that cauterization of the hernia sac during the laparoscopic repair prevents seroma formation.25

Infection Despite the use of prophylactic antibiotics and advances in anesthesia techniques, infection rates of 3.3% with laparoscopic and 10% with open repair are still reported for umbilical and epigastric hernia repairs.22 Body habitus, diabetes, immunosuppression, and cigarette smoking are all risk factors for a surgical site infection in these patients. ● Consequence Postoperative cellulitis occurring around the incision is self-limited and usually resolves with oral or intravenous antibiotics. When unrecognized, it can progress to a deep surgical site infection. Grade 1/2 complication ● Repair In cases of cellulitis, antibiotic therapy is recommended until resolution of the redness and return of the temperature and white blood cell to normal. In cases of abscesses with no mesh placement, percutaneous or open drainage with local wound care and antibiotics should be performed. In the presence of a mesh, open drainage and removal of the mesh should be considered; in the cases of polypropylene mesh, consideration can be given to leaving the mesh in place and applying local wound care with wet to dry dressings and antibiotic therapy. All necrotic tissue should be débrided. ● Prevention Intravenous antibiotic prophylaxis within 60 minutes of incision time is recommended in patients at higher

527

risk for infection undergoing mesh placement.26 Optimization of patient risk factors and adequate preparation of the surgical site should be observed.26 No relationship was found between wound infection and obesity.

Hematoma Hematomas are most commonly the result of trocar injury to abdominal wall vessels in the laparoscopic repair. In the open repair, hematomas are due to poor hemostasis at the time of dissection of the subcutaneous ﬂaps. Hematomas in both procedures can also be the result of intraabdominal organ or mesenteric injury. ● Consequence Hematomas have been associated with pain at the surgical site, wound infections, intra-abdominal abscess formation, need for reexploration, and blood transfusion. Grade 1/2 complication ● Repair Most hematomas can be treated expectantly. Progression of a hematoma with a continuous drop in hematocrit will require reexploration of the surgical site, ligation of the bleeder, and proper hemostasis. Hematomas that are symptomatic or infected will need to be drained. A liqueﬁed hematoma can be aspirated if symptomatic or persistent. ● Prevention Proper surgical technique and cauterization or ligation of all bleeders should be performed. Blunt dissection in the preperitoneal space can result in unrecognized bleeding. Inspection of all entered spaces for adequate hemostasis should be performed prior to ﬁnal closure.

Bowel Injury, Intra-abdominal Abscess, Enterocutaneous Fistula Unrecognized serosal tear during laparoscopic dissection, placement of a polyester or polypropylene mesh within the peritoneal cavity, or migration of a plug into the peritoneal cavity can all result in bowel perforation, postoperative intraperitoneal abscess, and/or delayed enterocutaneous ﬁstulas. ● Consequence When this complication occurs, removal of the mesh with recurrence of the hernia is inevitable. Resection of the involved bowel is necessary. Grade 3 complication ● Repair Percutaneous drainage of an intra-abdominal abscess, antibiotic therapy, and stabilization of the septic patient should be performed. Spontaneous closure of an enterocutaneous ﬁstula secondary to bowel injury during the hernia repair or mesh erosion will not occur.

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In these cases, removal of the mesh and resection of the involved loop of bowel is the next step. The use of a bioprosthesis to bridge the fascial defect and prevent the recurrence of a hernia should be considered but is not proved to prevent hernia recurrence in the long term. ● Prevention The use of polypropylene and polyester meshes within the peritoneal cavity should be avoided and restricted to the preperitoneal space. In the laparoscopic repair, polytetraﬂuoroethylene should be used. Newer material such as allografts and combined material (Proceed) are under consideration. Inspection of the bowel for any sign of injury should be performed during laparoscopic cases and in open procedures in which the peritoneal cavity is entered.

Skin Necrosis Skin necrosis is rare and is the result of devascularization of the skin ﬂaps at the time of dissection. ● Consequence Although small areas of skin necrosis can be self-limited, larger areas might get secondarily infected or result in skin dehiscence. Grade 1/2 complication ● Repair Areas of skin necrosis will usually require skin débridement and local care of the wound. In cases of infection, it should be treated as described previously. With mesh exposure, consideration should be given to ﬂap advancement or skin grafting if the involved area is large and after proper granulation. ● Prevention Dissection of the skin and subcutaneous tissue ﬂap should be carefully undertaken in order to avoid devascularization of the ﬂaps and subsequent skin necrosis.

Umbilical Hernia Repair in Patients with End-Stage Liver Disease and Refractory Ascites Umbilical hernia is seen in up to 20% of patients with longstanding cirrhosis and ascites27 (Fig. 52–7). The strategy for treating umbilical hernia in patients with ascites has evolved considerably. Initial management consisted of nonoperative therapy secondary to fear of precipitating bleeding from esophageal varices. ● Consequence Occasionally, a patient will present with spontaneous rupture of an umbilical hernia and leaking ascites. Patients with ascites who present acutely with ruptured umbilical hernias have two distinct problems that need to be treated, namely, the ruptured umbilical hernia and the underlying ascites. Grade 3 complication

Figure 52–7 Patient with intractable ascites and protruding umbilical hernia at risk for rupture (Reproduced with permission from www.mef.hr/patologija/ch_3/c3_ascites_umb_hernia.jpg).

● Repair Prevention of infection and adequate ﬂuid and electrolyte management in ruptured umbilical hernias in cirrhotic patients with ascites are crucial. Management of ascites with transjugular intrahepatic portosystemic shunting (TIPS) is currently favored, followed by repair of the umbilical hernia. ● Prevention Elective repair of an umbilical hernia in patients with ascites should be performed after proper optimization of the patient. Aggressive medical management of ascites with diuretics is advocated prior to elective hernia repair. In cases of refractory ascites, the treatment of choice becomes primary repair of the hernia with either concomitant or staged peritoneovenous shunting (PVS).27 Recently, transjugular intrahepatic portosystemic shunting (TIPS) has supplanted PVS as the treatment of choice in patients with intractable ascites prior to umbilical hernia repair.28

REFERENCES 1. Muschaweck U. Umbilical and epigastric hernia repair. Surg Clin North Am 2003;83:1207–1221. 2. Jackson OJ, Moglen LH. Umbilical hernia: a retrospective study. Calif Med 1970;113:8. 3. Larson GM, Vandertoll MD. Approaches to repair of ventral hernia and full thickness losses of the abdominal wall. Surg Clin North Am 1978;60:40–42. 4. Lang B, Lau H, Lee F. Epigastric hernia and its etiology. Hernia 2002;6:148–150. 5. Nyhus LM, Pollack R. Epigastric, umbilical, and ventral hernias. In Decker BC (ed): Current Surgical Therapy. St. Louis: Mosby, 1992; pp 536–539. 6. SSAT Patient Care Guidelines. Surgical repair of incisional hernias. J Gastrointest Surg 2004;8:369–370. 7. Evidence mounts for lap umbilical hernia repair. Two hernia giants report their ﬁndings. Gen Surg News

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8. 9.

10.

11.

12.

13.

14.

15.

16.

2002;29:14–15. Available at www.generalsurgerynews.com (accessed October 2002). Mayo WJ. An operation for the radical cure of umbilical hernia. Ann Surg 1901;34:276–278. Holm JA, Heisterkamp J, Veen HF, et al. Long term follow-up after umbilical hernia repair: are there risk factors for recurrence after simple and much repair? Hernia 2005;26:1–4. Flum DR, Horvath K, Koepsell T. Have outcomes of incisional hernia repair improved with time? A population based analysis. Am Surg 2003;237:129–135. Bennett D. Incidence and management of primary abdominal wall hernias: umbilical epigastric and spigelian. In Fitzgibbons RJ Jr, Greenburg AG (eds): Nyhus and Condon’s Hernia, 5th ed. Philadelphia: JB Lippincott, 2002; pp 389–398. Celdran A, Bazire P, Garcia-Urena MA, et al. Hernioplasty: a tension free repair for umbilical hernia. Br J Surg 1995;82:371–372. Arroyo SA, Perez F, Serrano P, et al. Is prosthetic umbilical hernia repair bound to replace primary herniorrhaphy in the adult patient? Hernia 2002;6:175– 177. Arroyo A, Garcia P, Perez F, et al. Randomized clinical trial comparing suture and mesh repair of umbilical hernia in adults. Br J Surg 2001;88:1321–1323. Bauer JJ, Harris MT, Gorﬁne SR, et al. Rives-Stoppa procedure for repair of large incisional hernias. Experience with 57 patients. Hernia 2002;6:120–123. Petersen S, Henke G, Freitag M, et al. Experiences with reconstruction of large abdominal wall cicatricial hernias using Stoppa-Rives pre peritoneal meshplasty. Zentralbl Chir 2000;125:152–156.

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17. Kennedy GM, Matyas JA. Use of expanded polytetroﬂuoroethylene in the repair of the difﬁcult hernia. Am J Surg 1994;168:304–306. 18. Leber GE, Garb J, Albert A, Reed WP. Long-term complications associated with prosthetic repair of incisional hernias. Arch Surg 1998;133:378–382. 19. Cafer P, Dervisoglu A, Senyurek G, et al. Umbilical hernia repair with the Prolene hernia system. Am J Surg 2005; 190:61–64. 20. Muscharveck U. Umbilical and epigastric hernia repair. Surg Clin North Am 2003;83:1207–1221. 21. Perrakis E, Velimezis G, Vezakis A, et al. A new tensionfree technique for the repair of umbilical hernia, using the Prolene hernia system—early results from 48 cases. Hernia 2003;7:178–180. 22. Wright BE, Beckerman J, Cohen M, et al. Is laparoscopic umbilical hernia repair with mesh a reasonable alternative to conventional repair? Am J Surg 2002;184:505–508. 23. Lou H, Patil NG. Umbilical hernia in adults. Surg Endosc 2003;17:2016–2020. 24. Chowbey PK, Sharma A, Khullar R, et al. Laparoscopic ventral hernia repair. J Laparoendosc Adv Surgl Tech 2000;10:79–84. 25. Tsimoyiannis EC, Siakas P, Glantzounis G, et al. Seroma in laparoscopic ventral hernioplasty. Surg Laparosc Endosc Percutan Tech 2001;11:317–321. 26. Barie PS, Eachempati SR. Surgical site infections. Surg Clin North Am 2005;85:1115–1135. 27. Belghetti J, Durand F. Abdominal wall hernias in the setting of cirrhosis. Semin Liver Dis 1997;17:219–226. 28. Fagan SP, Awad SS, Berger DH. Management of complicated umbilical hernias in patients with end stage liver disease and refractory ascites. Surgery 2004;135:679–682.

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Open Primary and Mesh Repairs Mary Hawn, MD INTRODUCTION Incisional hernias complicate approximately 10% of all laparotomies. Repair of an incisional hernia is a challenging case and recurrence rates remain high. The ﬁrst repair of an incisional hernia has the highest likelihood of success; therefore, considerable attention should be given to the surgical strategies that achieve optimal outcomes.1 The key factor associated with decreased likelihood of recurrence is the use of mesh for the repair.2 Long-term results of a randomized trial comparing suture with mesh repair demonstrated a 62% recurrence for suture repair and 32% for mesh repair.3 For small defects (<10 cm2), the efﬁcacy of mesh was even greater, with a 67% recurrence in the suture arm and 17% in the mesh arm. This highlights the fact that even small hernias should have a mesh repair. However, mesh is associated with a twofold increase in the complication rate, some of which, such as mesh infection and ﬁstula formation, can be devastating.3 Therefore, it is important to understand factors associated with increased risk of mesh complications. Primary reapproximation of the fascial edges without a mesh overlay or component separation technique should be reserved for patients with a contraindication to mesh placement and, given the current literature, should not be considered a deﬁnitive hernia repair. Many different technical approaches to mesh placement are available, and they can essentially be divided into three categories: (1) intraabdominal (underlay), (2) interfascial (interlay), and (3) suprafascial (overlay). We have an ongoing study of incisional hernia repairs performed in the Veterans healthcare system, and all three types of open repair are used equivalently. Without adequate outcomes data, we currently cannot advocate one approach over the other.

INDICATION ● Presence of an incisional hernia

PREOPERATIVE CONSIDERATIONS 1. Misdiagnosis. Eventration can be difﬁcult to distinguish from herniation, especially in obese patients.

a. Diastasis recti. Upper midline attenuation of linea alba. b. Lateral eventration. Most often seen after ﬂank incisions for nephrectomy and results from denervation of the oblique musculature. A computed tomography (CT) scan can be useful in conﬁrming the diagnosis of eventration. 2. Prior surgical history a. History of cancer i. Does the patient need to be restaged? Will you need to biopsy tissue during your laparotomy? b. Presence of an ostomy i. Can it be reversed? If so, these patients should be evaluated for concomitant ostomy reversal. ii. Consider a bowel preparation preoperatively. c. Prior mesh placement i. Important to review prior operative notes to understand where the mesh was placed and what type of mesh was used. 3. Contraindications to mesh placement a. Preexisting infection. Whenever possible, the preexisting infection should be deﬁnitely treated prior to hernia repair. Preexisting infection increases the risk for wound infection and subsequent failure of the repair (Fig. 53–1). b. Concomitant bowel surgery. This is a relative contraindication. If the bowel surgery is elective and the bowel is prepared, mesh can be placed with relative safety.4 4. Modiﬁable factors that may improve outcome a. Prostatism. A history of prostatism in men increases the risk for recurrence.2 Although there are no studies to evaluate the efﬁcacy of treating the symptoms, it seems logical to have men with symptoms of prostatism evaluated prior to elective surgery. b. Smoking cessation. Smoking doubles the risk of surgical site infection.5 Surgical site infection is associated with a greater than 50% recurrence rate for incisional hernia repair.3 If the patient is at high risk, consideration should be given to smoking cessation prior to undertaking elective repair. c. Obesity. Obesity is a risk factor for both surgical site infection and recurrence. If a patient has failed a prior repair without other explanation, consideration

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Figure 53–2 Infection of mesh prosthesis. Air bubbles (arrow) are present in the perimesh ﬂuid collection.

Figure 53–1 Incisional hernia with concomitant infection. An infected peripancreatic ﬂuid collection (arrow) is shown.

should be given to a weight loss intervention prior to undertaking repair of a recurrent hernia. 5. Nonmodiﬁable risk factors for recurrence a. History of an abdominal aortic aneurysm (AAA). Patients with a history of an AAA are at fourfold risk for recurrence.2 b. Chronic steroid use is associated with a fourfold increase in postoperative wound infections.5

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7 Step 8

Preparation of patient Excise old scar Excise peritoneal hernia sac from subcutaneous tissue Identify fascial edges and raise subcutaneous ﬂaps Reduce hernia contents to abdominal cavity, sharp adhesiolysis if necessary Placement of mesh prosthesis or component separation repair Drain subcutaneous space Skin closure

OPERATIVE PROCEDURE Preparation of the Patient Wound Infection ● Consequence Wound infections are a signiﬁcant morbidity for incisional hernia repair. The occurrence of a postoperative

wound infection can lead to a hernia recurrence rate of 80%.3 Furthermore, if the mesh prosthesis becomes infected, it usually needs to be explanted (Fig. 53–2). Grade 2/3 complication ● Repair The surgical site needs to be opened and the purulent material evacuated. If the infection involved a mesh prosthesis, especially polytetraﬂuoroethylene (PTFE), it will likely need to be explanted and either a primary fascial closure or an absorbable mesh placement performed. ● Prevention Preoperative antibiotics. A randomized trial has shown that a single dose of preoperative antibiotics decreases the incidence of postoperative surgical site infections for incisional hernia repair.6 Gram-positive coverage is sufﬁcient unless concomitant bowel resection is planned. Antimicrobial skin barrier (Ioban) or other skin barrier to limit the direct contact of the prosthesis with the patient’s skin.7

Deﬁnition of the Facial Edges Missed concomitant defect or inadequate overlap between mesh and fascia. ● Consequence The rate of hernia recurrence after incisional hernia repair remains high. Common causes for hernia recurrence are the failure to recognize or repair all defects at the time of the initial surgery and inadequate overlay of mesh with the repair2 (Fig. 53–3). Grade 3 complication ● Repair Operative repair of the recurrent hernia may be undertaken. Repair of recurrent hernias is less likely to be successful and is associated with more complications.1

53 OPEN PRIMARY AND MESH REPAIRS

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otomy increases the complexity of the operation and potentially increases the risk of mesh infection. Grade 3/4 complication ● Repair Prior to closure of the abdomen, all of the intestine should be inspected for evidence of inadvertent injury or deserosilization. ● Prevention Careful, sharp dissection for the adhesiolysis of intestine is recommended. Avoid using cautery to take down dense intestinal adhesions to prevent thermal injury to the intestine. Prompt repair of any recognized enterotomies or deserosilation should be undertaken. If multiple enterotomies are made in a short segment of bowel, or if the enterotomy comprises more than 50% of the bowel circumference, consideration should be given to resecting that portion of the intestine.

Enterocutaneous Fistula ● Consequence Intestinal ﬁstulas occur more frequently with mesh repair, and the incidence appears to be approximately 2% to 4%.3 Intestinal ﬁstulas in combination with a ventral hernia are very difﬁcult to manage and are discussed in more detail later in this chapter. Grade 3/4 complication

Figure 53–3 A, Recurrent incisional hernia after prior mesh repair. Intact mesh overlay (arrow) is shown. B, Incarcerated bowel (arrow) is shown between the fascia and the mesh.

● Prevention Raise subcutaneous ﬂaps circumferentially for at least 3 to 5 cm from the hernia defect to expose healthy fascia. If an underlay technique is employed, lyse adhesions from the undersurface of the peritoneum for at least 5 cm from the hernia defect. Palpate cephalad and caudad to the hernia defect to ensure that there are not any concomitant defects.

Adhesiolysis and Reduction of Hernia Contents Enterotomy or Deserosalization ● Consequence Intestinal contents may be in the subcutaneous tissue, and thermal injury to the bowel from cautery can increase the risk of postoperative intestinal leak and ﬁstula. An unrecognized or missed enterotomy may result in sepsis and death. Repair of a recognized enter-

● Repair All enterocutaneous ﬁstulas involving a foreign body will require removal of the foreign body and operative repair. If the ﬁstula is distal in the small intestine or involves the colon and can be adequately managed with an ostomy appliance, conservative therapy can be considered. ● Prevention Enterocutaneous ﬁstulas are believed to result from erosion of the mesh prosthesis into the adjacent intestine. Therefore, omentum, peritoneum, or fascia should be placed between the intestine and the mesh. If this is not possible, then an expanded PTFE (ePTFE) mesh appears to have the lowest rate of ﬁstula formation.8

Placement of the Mesh Prosthesis Mesh to Skin Fistula ● Consequence A chronic sinus tract between the mesh and the skin is inconvenient for the patient but does not mandate mesh removal (Fig. 53–4). Grade 1/2 complication ● Repair A course of antibiotics can be attempted and is usually successful in decreasing the amount of drainage from

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Figure 53–4 Mesh sinus tract. Localized mesh infection (solid arrow) results in a persistent sinus tract. The fascial edges (broken arrows) illustrate that the majority of the mesh is incorporated and not infected.

Figure 53–5 Subcutaneous seroma after primary incisional hernia repair (arrow). This collection was aspirated and was sterile. A percutaneous drain was placed and resulted in resolution of the collection.

the wound. The sinus tract can be explored and any unincorporated mesh removed. ● Prevention Excise the old scar and any attenuated or nonviable skin prior to closure of the incision. Local skin necrosis can lead to mesh exposure and chronic sinus tract formation.

Wound Closure Seroma Formation ● Consequence A seroma causes pain and discomfort for the patient. It also leads to a cosmetically undesirable outcome. Occasionally, seromas can become infected and need more aggressive treatment (Fig. 53–5). Grade 1/2 complication

Figure 53–6 Off-midline incisional hernia with concomitant loss of abdominal domain (arrow).

● Repair Aspiration of the seroma can usually be performed in the clinic setting. An abdominal binder can be placed to help decrease the likelihood of the seroma reforming. Care should be taken to perform the aspiration in an aseptic manner so that the seroma does not become secondarily infected.

Emergency Repair with Concomitant Bowel Obstruction Patients who present with obstructed or strangulated intestine present several challenges for incisional hernia repair. Any nonviable bowel should be resected. If the small bowel is involved and the patient is stable, primary anastomosis is preferable. If the large intestine is involved or the patient is unstable, creation of an ostomy and mucous ﬁstula or Hartman’s pouch is the safest approach. If the ﬁeld is contaminated, a primary closure with or without reinforcement of an absorbable mesh should be performed. If there is too much tension on the repair owing to either the size of the defect or the dilated intestine, a mesh repair can be performed to prevent facial dehiscence postoperatively. If any intraoperative enteroto-

● Prevention Excise the peritoneal sac from the subcutaneous tissue and ensure meticulous hemostasis prior to closure. Place drains at the time of surgery if subcutaneous ﬂaps were raised. Use a closed drainage system to decrease risk of infection. Consider placing an abdominal binder to decrease the likelihood of seroma formation.

Special Considerations at the Time of Incisional Hernia Repair

53 OPEN PRIMARY AND MESH REPAIRS mies or bowel resections occurred, that bowel should be protected from the fascial closure when possible. Enterocutaneous ﬁstulas are much more likely to develop if a repaired enterotomy is present immediately below a fascial or mesh repair.

Off-Midline Hernias The challenges for off-midline hernias include (1) exposure of the defect, (2) ability to deal with intraoperative

535

complications, and (3) ﬁnding adequate tissue to secure the repair (Fig. 53–6). Off-midline hernias in the ﬂank position are best repaired with the patient in the decubitus position, whereas an off-midline hernia in a prior cholecystectomy or ostomy site incision is best approached with the patient supine. Flank hernias often require securing the mesh to the rib cage or the iliac crest. MiTek screws can be used to secure the mesh repair to these bony structures.

Figure 53–7 A, Extra-abdominal repair of enterocutaneous ﬁstula with an incisional hernia. Computed tomography (CT) scan demonstrates ﬁstula arising in the hernia defect (arrow). B, Rectus femoris ﬂap raised in preparation for ﬁstula (arrow) closure. C, Completion of the closure with 14-Fr red rubber catheter through the rectus femoris ﬂap and ﬁstula.

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Loss of Domain and/or Loss of Abdominal Wall Loss of domain occurs when a signiﬁcant amount of the intra-abdominal contents are chronically incarcerated in the hernia sac (see Fig. 53–6). Returning these contents to the abdominal cavity at the time of repair will increase the intra-abdominal pressure. This can both cause undue tension on the repair and increase the risk for dehiscence and also pulmonary compromise from the increased pressure on the diaphragm. Peak airway pressures should be monitored before and after the fascial repair to help determine whether pulmonary compromise is a risk postoperatively. Likewise, loss of abdominal wall, from either prior fasciitis or retraction of the muscles laterally, will require signiﬁcant ﬂaps to be raised to identify adequate fascial edges to secure the repair. Fistula An enterocutaneous ﬁstula signiﬁcantly increases the complexity of ventral hernia repair. All considerations of factors that impede ﬁstula closure must be addressed. Particular scenarios often seen in this setting are the presence of either a foreign body, especially prior mesh placement, or a short ﬁstula track owing to lack of fascia at the hernia site. A ﬁstula in the presence of a prosthetic material will not close until the foreign body is removed and the ﬁstula repaired. Every attempt must be made to get muscle or fascia directly over the ﬁstula repair, or the likelihood of success is low. This is a scenario in which component separation is very useful to provide autogenous muscle and/or fascia for the closure. If a ﬁstula is present in the middle of a granulating wound without mesh or distal obstruction, consideration can be given to a ﬂap repair to close the ﬁstula.9 This extra-abdominal repair has a high rate of success for ﬁstula closure, but it does not address repair of the underlying hernia. We have used this technique successfully to close ﬁstulas when the patient has a signiﬁcant loss of abdominal wall and no evidence of distal obstruction (Fig. 53–7). The basis of this technique is to take a short, likely epithelialized tract and convert it into a long tract. We have used both rectus abdominus and rectus femorus muscle rotational ﬂaps. We raise subcutaneous ﬂaps around the ﬁstula and abdominal wall defect. We then freshen up the edges of the ﬁstula and place a pursestring suture around the edges. We then place a 14-Fr red rubber Robinson

catheter through the skin and muscle ﬂap into the intestine, much like a feeding jejunostomy tube. The ﬂap is then inset, and the tube is left to dependent drainage for 2 weeks. The tube is then removed, and if successful, the tract closes.

SUMMARY In summary, incisional hernia repair is a commonly performed operation. There are no “gold standards” for technique of repair. Complications presenting at the time of incisional hernia repair or as a consequence of the repair pose major challenges for treatment.

REFERENCES 1. Flum DR, Horvath K, Koepsell T. Have outcomes of incisional hernia repair improved with time? A populationbased analysis. Ann Surg 2003;237:129–135. 2. Luijendijk RW, Hop WC, van den Tol MP, et al. A comparison of suture repair with mesh repair for incisional hernia. N Engl J Med 2000;343:392–398. 3. Burger JW, Luijendijk RW, Hop WC, et al. Long-term follow-up of a randomized controlled trial of suture versus mesh repair of incisional hernia. Ann Surg 2004;240:578– 583; discussion 583–585. 4. Geisler DJ, Reilly JC, Vaughan SG, et al. Safety and outcome of use of nonabsorbable mesh for repair of fascial defects in the presence of open bowel. Dis Colon Rectum 2003;46:1118–1123. 5. Finan KR, Vick CC, Kiefe CI, et al. Predictors of wound infection in ventral hernia repair. Am J Surg 2005;190: 676–681. 6. Abramov D, Jeroukhimov I, Yinnon AM, et al. Antibiotic prophylaxis in umbilical and incisional hernia repair: a prospective randomised study. Eur J Surg 1996;162:945– 948; discussion 949. 7. French ML, Eitzen HE, Ritter MA. The plastic surgical adhesive drape: an evaluation of its efﬁcacy as a microbial barrier. Ann Surg 1976;184:46–50. 8. Diaz JJ Jr, Gray BW, Dobson JM, et al. Repair of giant abdominal hernias: does the type of prosthesis matter? Am Surg 2004;70:396–401; discussion 402. 9. Kearney R, Payne W, Rosemurgy A. Extra-abdominal closure of enterocutaneous ﬁstula. Am Surg 1997;63:406– 409.

54

Laparoscopic Incisional Hernia Repair Parag Bhanot, MD INTRODUCTION Incisional hernia formation after laparotomy is a complication that occurs in approximately 20% of patients.1 Several open hernia repair methods have been developed, but they are associated with signiﬁcant recurrence rates and woundrelated complications secondary to extensive tissue dissection.2,3 The application of minimally invasive surgery techniques has led to the development of laparoscopic methods for repairing incisional hernias. Several comparative studies now demonstrate the high rate of success and low associated morbidity compared with those of the open approach.4–7 Since they were ﬁrst reported in the literature in 1992, the number of laparoscopic ventral hernia repairs (LVHR) performed has signiﬁcantly grown as excellent outcomes have been published. Although complications have been reported to occur less frequently when compared with those of the open approach, they continue to remain an issue, especially in less experienced hands. Heniford and coworkers8 reported an overall complication rate of 13.2% in a series of 850 patients.

Relative ● Active wound infection ● Loss of abdominal domain ● Severe abdominal adhesions

OPERATIVE STEPS Although the technical aspects of LVHR vary, the operation involves a series of well-deﬁned steps. Step Step Step Step Step Step Step Step Step

1 2 3 4 5 6 7 8 9

Patient preparation and positioning Abdominal access Trocar placement Lysis of adhesions Reduction of hernia contents Evaluation of fascial defect Mesh selection and preparation Mesh ﬁxation Trocar removal and fascial closure

INDICATIONS ● ● ● ●

Hernia defect 4 cm or greater Recurrent hernia Multiple hernias Morbidly obese individuals

CONTRAINDICATIONS Absolute ● ● ● ● ● ●

Surgeon inexperience Inability to tolerate general anesthesia Inability to tolerate laparotomy Advanced cardiopulmonary disease Uncorrectable coagulopathy Portal hypertension with abdominal wall varices

OPERATIVE PROCEDURE Abdominal Access and Trocar Placement Trocar Insertion Injuries An open or closed technique may be used for access to the peritoneal cavity. A number of complications can occur while gaining access to the peritoneal cavity because a signiﬁcant number of these patients may have had multiple abdominal procedures. The total number of trocars placed is dependent on several factors, including the extent of adhesions and the size and location of the hernias. Trocars should be placed at least 5 cm away from the fascial defect to allow mesh placement with appropriate fascial overlap (Fig. 54–1). Complications of trocar insertion are discussed in Section I, Chapter 7, Laparoscopic Surgery.

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SECTION VIII: HERNIA ● Repair The decision on the approach used to repair the bowel injury is based on surgeon experience and degree of contamination. Conversion to an entirely open procedure should not be considered a failure. Alternatively, a smaller incision can be used to allow repair of the enterotomy followed by continuation of the laparoscopic approach. With increasing surgeon experience, a laparoscopic repair of the enterotomy may be performed.

A

B Figure 54–1 A, Although the mesh has been sized to provide appropriate overlap to cover the fascial defect, its ﬁxation is compromised as the edge of the mesh overlaps with one of the 5-mm trocars. B, The trocars are placed at an appropriate distance from the fascial defect to allow circumferential ﬁxation of the mesh.

Lysis of Adhesions Intestinal Injury Adhesiolysis can be the most difﬁcult and technically challenging portion of the operation. This is especially evident in patients with multiple previous surgeries and/or previously placed mesh. Soper and associates9 reported their results of 121 consecutive patients that showed an enterotomy rate of 11.4% in patients with prior hernia repairs compared with 0% in patients undergoing a ﬁrst-time repair.9 ● Consequence An enterotomy can jeopardize the remainder of the operation by affecting the ability to proceed with mesh placement. This is dependent on the degree of contamination and the portion of the bowel injured. An unrecognized bowel injury can have catastrophic consequences with resultant intra-abdominal sepsis. Grade 3/4/5 complication

● Prevention A complete visualization of all of the adhesions is critical to ascertain whether or not bowel is adherent to the abdominal wall (Fig. 54–2A). This usually requires changing the camera port to the contralateral side. A plane allowing for a safe dissection should be developed between the abdominal wall and the adhesions. A majority of the dissection should be performed without the use of energy sources such as ultrasonic shears, especially adjacent to the bowel wall, to prevent thermal injury (see Fig. 54–2B and C). If dense adhesions are present, dividing the hernia sac or adjacent fascia may aid the adhesiolysis (see Fig. 54–2D). The surgeon should avoid grasping the bowel directly and instead use the surrounding adhesions to provide countertraction.

Hemorrhage Minimal bleeding can result from a number of sources. However, signiﬁcant bleeding is rare and usually recognized intraoperatively. Major sources are raw surfaces of the abdominal wall after extensive adhesiolysis, injury to abdominal wall vessels such as the inferior epigastric vessels, or from large-caliber vessels found within the adhesions. ● Consequence Signiﬁcant postoperative bleeding is very rare, with a reported incidence of less than 2% of patients requiring a blood transfusion. Grade 1 complication ● Repair Abdominal wall bleeding can be controlled with direct pressure and/or placement of sutures to ligate the vessel. Larger-caliber vessels present in mature adhesions or omentum are controlled with ultrasonic shears or clips. ● Prevention The development of an avascular plane between the adhesions and the peritoneum will prevent violation of the dissection into the abdominal wall muscles. Transillumination of the abdominal wall to visualize the vessels before trocar placement and placement of ﬁxation sutures should be employed when possible. This may not be possible when operating on an obese individual. All adhesions should be examined for the presence of large-caliber vessels before lysing (Fig. 54–3).

54 LAPAROSCOPIC INCISIONAL HERNIA REPAIR

A

B

C

D

539

Figure 54–2 A, In addition to the omental adhesions to the anterior abdominal wall, which can be taken down with blunt dissection, a loop of small bowel is also clearly seen inside the fascial defect. This should be carefully cleared off of the peritoneum with sharp dissection to prevent serosal injury. B, The majority of the adhesiolysis can be performed with sharp dissection without use of energy sources. An avascular plane is developed between the peritoneum and the adhesions. C, As the adhesions are taken down close to the proximity of small bowel, it is critical to visualize the tips of the scissors, as depicted in this photograph, in which a potential for injury is evident. The use of ultrasonic shears would most deﬁnitely cause a thermal injury to the bowel wall. D, When there are a number of adhesions or dense adhesions, it is safer to divide the hernia sac from the edge and reduce the contents with the peritoneum attached to the adhesions. Normally, this is unnecessary and the hernia sac is left in situ.

Reduction of Hernia Contents Intestinal Injury In most cases, the hernia contents can be reduced without much difﬁculty. Excessive manipulation of incarcerated bowel can result in a bowel injury. ● Consequence See the section on “Lysis of Adhesions,” earlier. Grade 3/4 complication

serosal injuries. If the hernia contents cannot be reduced, external manual compression should be used. In those patients in whom the previous two maneuvers are not successful, sharp dissection is employed along the fascial edges away from bowel wall to facilitate reduction. A small incision can be made directly over the hernia on the abdominal wall as well. This is particularly useful if a bowel injury is possible and the bowel can be explored extracorporeally.

● Repair See the section on “Lysis of Adhesions,” earlier.

Mesh Selection and Preparation

● Prevention When bowel is incarcerated within a hernia defect, it is important to avoid excessive tension to reduce the contents. The use of atraumatic graspers will help avoid

● Consequence Mesh infection accounts for over 40% of all adverse events, as reported by the U.S. Food and Drug Administration.10 The resulting consequences of an infection

Mesh Infection and/or Exposure

540

SECTION VIII: HERNIA infection, such as pneumonia, urinary tract infection, or open skin lesions, should be addressed and resolved before the operation. Although there has been some debate in the literature on the use of intravenous antibiotics for hernia cases, the authors believe that this is an important measure coinciding with the conclusions from several randomized studies.19–22 Lastly, despite the lack of level-one evidence, the authors believe that the use of adhesive surgical barriers to serve as physical barriers against bacterial migration between the skin and the mesh is important.

Enterocutaneous Fistula

Figure 54–3 Adjacent to the portion of bowel involved within the adhesion, there is also a large-caliber vessel separate from the mesentery. This vessel needs to be ligated before it is separated for the abdominal wall to prevent hemorrhage that would obscure dissection planes.

depend upon the source of infection, the degree of infection, and the type of mesh placed for the repair. Exposed mesh is considered to be contaminated and is included in the same algorithm. Grade 3/4/5 complication ● Repair If the source of the infection is a missed intestinal injury, the patient will require a second operation.11,12 The injury needs to be explored and repaired, followed by complete excision of the contaminated mesh. Reconstruction of the abdominal wall can be performed with a rectus abdominis myofascial advancement ﬂap and/or placement of bioabsorbable mesh.13 Mesh infection not secondary to intestinal injury can be treated depending on the type of mesh placed. Two broad categories of mesh are those constructed with polypropylene or expanded polytetraﬂuoroethylene (ePTFE). Several medium-sized studies described the advantages of the former.14–17 Polypropylene meshes can resist bacterial colonization and have the ability to incorporate into native tissue. This accounts for a higher likelihood of salvaging the mesh with long-term antibiotics and/or drainage of any associated abscess. However, if mesh migration or ﬁstulas are present, mesh removal is required. ePTFE meshes are not amenable to nonoperative modalities and require excision. Only one case study, by Kercher, reported infected ePTFE mesh that was able to be treated without excision.18 ● Prevention The most important preventive measure is to maintain strict sterile technique throughout the operation. The surgical team has to be vigilant in not compromising the surgical ﬁeld or contaminating the mesh before its placement. Preoperatively, any remote sources of

● Consequence The reported incidence of enterocutaneous ﬁstulas is less than 1% in large series and is described as isolated case reports.23,24 Consequences include mesh infection, intra-abdominal abscess, sepsis, and mortality. Grade 3/4/5 complication ● Repair The management of intestinal ﬁstulas should follow surgical principles in terms of patient resuscitation and sepsis control. Eventually, the treatment also needs to take into account the associated mesh infection. The operation will include exploratory laparotomy, excision of mesh, repair of ﬁstula, and closure of the abdominal wall by options previously described (Fig. 54–4). ● Prevention In addition to the preventive measures previously described for avoidance of intestinal injury, additional surgical principles need to be adhered to. Any mesh that does not have a speciﬁc composite layer on the visceral surface to prevent adhesions should not be placed in direct opposition to bowel. Certain mesh types such as Marlex or exposed polypropylene are known to be associated with a higher rate of adhesion formation, which potentially may lead to mesh erosion into the bowel and resultant ﬁstula.25,26

Mesh Fixation Hernia Recurrence ● Consequence Hernia recurrence after laparoscopic repair is associated with several factors: mean defect size, longer operating times, previous hernia repairs, morbid obesity, and higher complication rate.8 Patients will present with symptoms similar to their initial complaints of abdominal pain, presence of bulge, and/or incarceration. Unlike the open procedure, the published recurrence rate of approximately 5% in the laparoscopic cohort is much lower in long-term outcomes.27,28 Most failures are secondary to technical causes and can be prevented. Grade 3/4 complication

54 LAPAROSCOPIC INCISIONAL HERNIA REPAIR

Figure 54–4 At time of exploration, the point of erosion between the mesh and the underlying small bowel is evident with visible mucosa and leakage of bile-tinged contents into the surrounding tissues. The mesh is excised followed by a short-segment, small bowel resection and alternative closure of the abdominal wall. The use of permanent mesh in this setting is absolutely contraindicated.

● Repair With symptomatic recurrences in surgical candidates, a second laparoscopic attempt at hernia repair is warranted. Additional placement of mesh with appropriate ﬁxation sutures and surgical tacks will be required. ● Prevention Several important technical considerations can ensure the lowest rate of failure. It is critical to be able to visualize the entire abdominal wall and clearly identify all of the fascial defects (Fig. 54–5). This ability to detect multiple hernias is a signiﬁcant advantage over the open approach and likely accounts for a lower recurrence rate. After the fascial defects have been assessed, the mesh must be sized appropriately to allow for at least 3 cm of overlap. Although there are conﬂicting data regarding the use of ﬁxation sutures, the authors as well as data from the largest series conﬁrm that this step should not be omitted.29–31 Depending on the quality of the fascia, these sutures should be placed at least every 5 cm and serve as the primary source of ﬁxation. Hernia tacks are used as secondary ﬁxation points between these sutures. The type of mesh placed may also have some impact on recurrence rates as it relates to mesh shrinkage. An evaluation of speciﬁc mesh types with regards to prosthetic shrinkage revealed that ePTFE had statistically signiﬁcant more shrinkage than other standard meshes.25

541

Figure 54–5 The typical Swiss-cheese–type appearance of fascial defects along the entire length of a midline incision. Each fascial defect if left unrecognized would ultimately lead to a “recurrence” of the hernia repair. The mesh will be sized to account for all the defects in greatest dimension.

Other Complications Ileus In patients who required extensive lysis of adhesions or had large fascial defects, a postoperative ileus may result. It is important not to advance the diet in these cases to minimize abdominal distention and emesis. A nasogastric tube may be required for decompression, even in the absence of bowel resection. Unnecessary manipulation of bowel is the only preventive measure. Grade 1 complication Seroma A postoperative seroma will develop in approximately 10% of patients11 and account for approximately 40% of all complications.9 Most seromas are associated with large hernia defects, with a resultant dead space between the mesh and the overlying skin. They are usually asymptomatic and resolve without any intervention.32 A symptomatic or persistent seroma may need to be aspirated under sterile technique. Appropriate mesh size and ﬁxation will prevent excessive dead space and ﬂuid accumulation. The use of abdominal binders has not been shown to reduce the incidence or size of seroma formation. Grade 1/2 complication Suture Site Pain In addition to incisional pain associated with trocar sites, patients may also complain of pain at the transabdominal suture ﬁxation sites, related to tissue or nerve entrapment. In most patients, the pain will resolve with time and can be treated with narcotics and/or nonsteroidal antiinﬂammatory drugs. For severe or persistent pain, injection of local anesthetic may be necessary and is effective.33 Depending on the number of ﬁxation sutures utilized, a

542

SECTION VIII: HERNIA

single suture may be removed if it corresponds directly to the site of tenderness and the surgeon is conﬁdent about the time interval for the mesh to fully incorporate within the native abdominal wall. Grade 1/2 complication

Mesh Migration into the Urinary Bladder Several publications have described the migration of mesh into the urinary bladder after laparoscopic inguinal hernia repairs. One case report, in addition to the case Heniford described in his large series, has been published about the same complication after LVHR.8,34 The urinary bladder ﬁstula was treated with reoperation without a deﬁnitive cause of the ﬁstula. In repairing lower abdominal incisional hernias, the surgeon has to be familiar with the pelvic anatomy to avoid placing sutures or tacks in vital structures. When the fascial defect extends to the suprapubic area, the peritoneum is divided and dissected to the pubis where it, along with the bladder, can be displaced posteriorly. This maneuver exposes Cooper’s ligament bilaterally and allows for ﬁxation of the mesh inferiorly without injury to the urinary bladder. The use of a threeway Foley catheter is also recommended. Grade 3/4 complication Small Bowel Perforation Secondary to Spiral Tacks Spiral titanium tacks are routinely used in the repair of abdominal wall hernias. Small bowel perforation due to a protruding spiral tack is a very rare complication and is described in a case report occurring 2 weeks postoperatively.35 Management of this complication is previously described in the section on “Intestinal Injury.” The surgeon should be certain that the tacker is perpendicular to the abdominal wall so that the tack becomes properly

Figure 54–6 After the four-quadrant sutures have been secured, spiral tacks are placed circumferentially. These 4-mm tacks should be ﬂush with the mesh and not protruding excessively where they can “hook” the underlying bowel.

situated into the wall (Fig. 54–6). Any loose or fallen tacks should be promptly removed. Grade 3/4/5 complication

REFERENCES 1. Winslow ER, Fleshman JW, Birnbaum EH, et al. Wound complications of laparoscopic versus open colectomy. Surg Endosc 2002;16:1420–1425. 2. Luijendijk RW, Hop WC, van den Tol P, et al. A comparison of suture repair with mesh repair for incisional hernia. N Engl J Med 2000;343:392–398. 3. Burger JW, Luijendijk RW, Hop WC, et al. Long-term follow-up of a randomized controlled trial of suture versus mesh repair of incisional hernia. Ann Surg 2004;240:578– 585. 4. LeBlanc KA, Booth WV, Whitaker JM, et al. Laparoscopic incisional and ventral herniorrhaphy in 100 patients. Am J Surg 2000;180:193–197. 5. Carbajo MA, Martin del Olmo JC, Blanco JI, et al. Laparoscopic approach to incisional hernia. Surg Endosc 2003;17:118–122. 6. Rosen M, Brody F, Ponsky J, et al. Recurrence after laparoscopic ventral hernia repair: a ﬁve-year experience. Surg Endosc 2003;17:123–128. 7. Ujiki MB, Weinberger J, Varghese TK, et al. One hundred consecutive ventral hernia repairs. Am J Surg 2004;188:593–597. 8. Heniford BT, Park A, Ramshaw BJ, et al. Laparoscopic repair of ventral hernia: nine year’s experience with 850 consecutive hernias. Ann Surg 2003;238:391–400. 9. Perrone JH, Soper NJ, Eagon JC, et al. Perioperative outcomes and complications of laparoscopic ventral hernia repair. Surgery 2005;138:708–715. 10. Robinson TN, Clarke JH, Schoen J, et al. Major meshrelated complications following hernia repair: events reported to the Food and Drug Administration. Surg Endosc 2005;19:1556–1560. 11. Berger D, Bientzle M, Muller A. Postoperative complications after laparoscopic incisional hernia repair. Incidence and treatment. Surg Endosc 2002;16:1720–1723. 12. Wright BE, Niskanen BD, Peterson DJ, et al. Laparoscopic ventral hernia repair: are there comparative advantages over traditional methods of repair? Am Surg 2002;68:291–295. 13. Szczerba SR, Dumanian GA. Deﬁnitive surgical treatment of infected or exposed ventral hernia mesh. Ann Surg 2003;237:437–441. 14. Birolini C, Utiyama EM, Rodrigues AJ, et al. Elective colonic operation and prosthetic repair of incisional hernia: does contamination contraindicate abdominal wall prosthetic use? J Am Coll Surg 2000;191:366–372. 15. Bleichrodt RP, Malyar AW, de Vries Reilingh TS, et al. The omentum-polypropylene sandwich technique: an attractive method to repair large abdominal-wall defects in the presence of contamination or infection. Hernia 2007;11:71–74. 16. Alaedeen DI, Lipman J, Medalie D, et al. The singlestaged approach to the surgical management of abdominal wall hernias in contaminated ﬁelds. Hernia 2007;11:41– 45.

54 LAPAROSCOPIC INCISIONAL HERNIA REPAIR 17. Kelly ME, Behrman SW. The safety and efﬁcacy of prosthetic hernia repair in clean-contaminated and contaminated wounds. Am Surg 2002;68:524– 528. 18. Kercher KW, Sing RF, Matthews BD, et al. Successful salvage of infected PTFE mesh after ventral hernia repair. Ostomy Wound Manage 2002;48:40–42. 19. Rios A, Rodriguez JM, Munitiz V, et al. Antibiotic prophylaxis in incisional hernia repair using prosthesis. Hernia 2001;5:148–152. 20. Yerdel MA, Akin EB, Dolalan S, et al. Effect of singledose prophylactic ampicillin and sulbactam on wound infection after tension-free inguinal hernia repair with polypropylene mesh: the randomized, double-blind, prospective trial. Ann Surg 2001;233:26–33. 21. Aufenacker TJ, van Geldere D, van Mesdag T, et al. The role of antibiotic prophylaxis in prevention of wound infection after Lichenstein open mesh repair of primary inguinal hernia: a multicenter double-blind randomized controlled trial. Ann Surg 2004;240:955–960. 22. Perez AR, Roxas MF, Hilvano SS. A randomized, doubleblind, placebo-controlled trial to determine effectiveness of antibiotic prophylaxis for tension-free mesh herniorrhaphy. J Am Coll Surg 2005;200:393–397. 23. Losanoff JE, Rochman BW, Jones JW. Enterocutaneous ﬁstula: a late consequence of polypropylene mesh abdominal wall repair: case report and review of literature. Hernia 2002;6:144–147. 24. Ott V, Groebli Y, Schneider R. Late intestinal ﬁstula formation after incisional hernia using intraperitoneal mesh. Hernia 2005;9:103–104. 25. Harrell AG, Novitsky YW, Peindl RD, et al. Prospective evaluation of adhesion formation and shrinkage of intraabdominal prosthetics in a rabbit model. Am Surg 2006;72:808–813.

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26. Mahmoud uslu HY, Erkek AB, Cakmak A, et al. Incisional hernia treatment with polypropylene graft: results of 10 years. Hernia 2006;10:380–384. 27. Pierce RA, Spitler JA, Frisella MM, et al. Pooled data analysis of laparoscopic versus open ventral hernia repair: 14 years of patient data accrual. Surg Endosc 2007;21: 378–386. 28. Lomanto D, Iyer SG, Shabir A, et al. Laparoscopic versus open ventral hernia mesh repair: a prospective study. Surg Endosc 2006;20:1030–1035. 29. van’t Riet M, de Vos van Steenwijk PJ, Kleinrensink GJ, et al. Tensile strength of mesh ﬁxation methods in laparoscopic incisional hernia repair. Surg Endosc 2002; 16:1713–1716. 30. Heniford BT, Park A, Ramshaw BJ, et al. Laparoscopic ventral and incisional hernia repair in 407 patients. J Am Coll Surg 2000;190:645–650. 31. LeBlanc KA, Booth WV, Whitaker JM, et al. Laparoscopic incisional and ventral herniorraphy: our initial 100 patients. Hernia 2001;5:41–45. 32. Susmallian S, Gewurtz G, Ezri T, et al. Seroma after laparoscopic repair of hernia with PTFE patch: is it really a complication? Hernia 2001;5:139–141. 33. Carbonell AM, Harold KL, Mahmutovic A, et al. Local injection for the treatment of suture site pain after laparoscopic ventral hernia repair. Am Surg 2003;69:688– 691. 34. Riaz AA, Ismail M, Barsam A, et al. Mesh erosion into the bladder: a late complication of incisional hernia repair. A case report and review of the literature. Hernia 2004;8: 158–159. 35. Ladurner R, Mussack T. Small bowel perforation due to protruding spiral tackers: a rare complication in laparoscopic incisional hernia repair. Surg Endosc 2004;18: 1001.

55

Component Separation for Complex Abdominal Wall Reconstruction and Recurrent Ventral Hernia Repair Brian Reuben, MD, Daniel Vargo, MD, and Marga F. Massey, MD INTRODUCTION Since the 1980s, signiﬁcant changes have occurred in the operative management of the abdomen in patients requiring large-volume resuscitation secondary to hemorrhagic or septic shock. “Damage control” laparotomies with rapid management of life-threatening conditions and temporary wound closure are increasingly more common and designed to avoid the dreaded triad of death—hypothermia, coagulopathy, and hemorrhage. In addition, intra-abdominal hypertension or “abdominal compartment syndrome” has become a well-recognized entity that often mandates management of a complex abdominal wall hernia with signiﬁcant “loss of domain.” With damage control laparotomies and abdominal compartment syndrome, large abdominal wall defects are the resultant surgical challenge. A mesh-independent technique of abdominal wall reconstruction was ﬁrst introduced in 1990 to address large, complex abdominal wall hernias with either a prior history of infection or a signiﬁcant loss of domain.1 This autologous reconstruction method, commonly known as component separation, has achieved widespread acceptance for these types of problems before the introduction of the acellular dermal regenerative tissue matrix AlloDerm (LifeCell, Branchburg, NJ).2,3 Component separation, as it was initially introduced, utilizes bilateral, innervated, bipedicle, rectus abdominis muscle and fascial composite ﬂaps transposed medially to reconstruct the central abdominal wall. Several procedural variations have appeared in the literature, all based on central mobilization of the rectus abdominis muscle and associated overlying fascia and a distinct independence from synthetic mesh materials.3–8 All effective methods of abdominal wall reconstruction address ﬁve basic goals: (1) restoration of function and integrity of the musculofascial abdominal wall; (2) prevention of visceral eventration; (3) provision of dynamic muscle support; (4) provision of a tension-free repair; and

(5) optimizing an aesthetically acceptable appearance.3,4,9 Immediate reconstruction of a large abdominal wall defect is optimal. However, it may be suitable only in a medically stable patient with a clean wound bed and reliable reconstructive options that provide a tension-free closure. A delayed approach potentially involving multiple, staged surgical procedures is more common for the high-risk patient with an unstable or contaminated wound and multiple medical problems. Staged reconstructions commonly require the temporary use of absorbable mesh materials and delayed split-thickness skin grafting followed by a component separation procedure 6 to 12 months later. These extreme cases may require combined tissue expansion techniques to provide stable skin coverage over the fascial repair. They may require mesh in addition to a component separation procedure with the distinct goal of re-creating the majority of the abdominal wall with a tension-free predominance of innervated muscle ﬂaps, which promote function (Fig. 55–1). Component separation is ideal for midline defects with fascial defects greater than 3 cm in transverse diameter.9 Bilateral component separation provides 8 to 10 cm of mobilization in the epigastric area, 10 to 15 cm in the midabdomen, and 6 to 8 cm in the suprapubic region.10 It is ideal for the high-risk, loss-of-domain patient who has failed a synthetic mesh repair secondary to infection. It is a signiﬁcant reconstructive option for patients with stomas within the operative ﬁeld. It should be considered superior and a ﬁrst line of reconstruction for patients who have had prior irradiation, who have a bowel injury in the setting of a laparoscopic hernia repair attempt, who have suffered prior enterocutaneous ﬁstula, or who have risk factors for wound healing problems that preclude the use of synthetic mesh materials. Coordinated preoperative evaluation by general and plastic surgeons with a focus on abdominal wall reconstruction is effective in the completion of these difﬁcult surgical procedures with acceptable levels of morbidity and mortality.

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SECTION VIII: HERNIA

A1

A2

B1

A3 Figure 55–1 Staged abdominal wall reconstruction for abdominal compartment syndrome. A, A 56-year-old man with a history of necrotizing pancreatitis and abdominal compartment syndrome presented for a near-total abdominal wall reconstruction. His reconstruction was delayed secondary to a multiple laparotomy requirement for pancreatic débridement. Once he was medically stable, his open abdominal wound was managed by Vicryl mesh placement followed by dressing changes and progression to a Wound V.A.C. A staged split-thickness skin graft (STSG) was then placed at a second operative procedure. The patient had tissue expanders placed under his abdominal skin ﬂaps to recruit skin for ﬁnal skin ﬂap closure as well as expanders beneath bilateral tensor fascia lata (TFL) ﬂaps 12 months after his initial presentation. These expanders were ﬁlled weekly in preparation for his ﬁnal reconstructive procedure.

55 COMPONENT SEPARATION FOR COMPLEX ABDOMINAL WALL

547

B2 C1

C2

C3

Figure 55–1, cont’d B, STSG and abdominal wall tissue expanders are removed at a delayed component separation procedure 15 months after his initial absorbable mesh placement. Bilateral “backup” expanded TFL ﬂaps were not required to achieve a ﬁnal closure. C, The patient is shown at 27 months after his initial presentation, 12 months after his deﬁnitive repair with midline approximation of his skin ﬂaps as facilitated by abdominal wall tissue expansion. His fascia was reconstructed by a component separation procedure in addition to Prolene mesh, given the size of is fascial defect. Bilateral expanded TFL ﬂaps, designed to supplement his component separation, were preserved, given an intraoperative ﬁnding of a 20-cm pancreatic pseudocyst requiring enteric diversion. It was believed that the patient was at risk for revisional intra-abdominal surgery, given his pancreatic pathology. At 1 year, he has no evidence of hernia recurrence, with a majority of his abdominal wound having been reconstructed by autologous, innervated rectus abdominis myocutaneous ﬂaps.

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SECTION VIII: HERNIA

INDICATIONS ● Large

● ● ● ● ● ● ●

abdominal wall defect (>40 cm2)—loss-ofdomain ventral hernia ● Epigastic (≤8–10 cm horizontal advancement requirement) ● Midabdominal (≤10–15 cm horizontal advancement requirement) ● Suprapubic (≤6–8 cm horizontal advancement requirement) Recurrence of hernia defect after prior primary closure attempt and contraindication for synthetic mesh Failed primary mesh hernia repair secondary to infection Bowel injury in setting of laparoscopic hernia repair Exposed mesh with unstable surrounding skin Presence of enterocutaneous ﬁstula or ostomy in operative ﬁeld Prior abdominal wall irradiation Systemically compromised patient ● Concurrent malignancy ● Systemic immunosuppression secondary to organ transplantation ● Active human immunodeﬁciency virus (HIV) infection ● Corticosteroid dependence ● Malnutrition ● Large body surface area burn

OPERATIVE STEPS Skin incision Enter peritoneal cavity with excision of splitthickness skin graft (STSG) 3 Develop adipocutaneous advancement ﬂaps 4 Excise poorly incorporated mesh 5 Excise hernia sac 6 Lyse adhesions to an intraperitoneal level 4 cm lateral to fascial defect 7 Vertical incision of external oblique fascia 1 cm lateral to linea semilunaris 8 Muscle ﬂap advancement and approximation 9 Adipocutaneous ﬂap advancement and approximation 10 Assimilation of postoperative secrets for success

Step 1 Step 2 Step Step Step Step Step Step Step Step

OPERATIVE PROCEDURE Skin Incision Skin Necrosis and Dermal Dehiscence ● Consequence The surgical incision must be carefully planned to prevent unnecessary skin necrosis, skin ﬂap dermal

dehiscence, and the need for prolonged dressing changes. Previous incisions should be used or extended when possible.9 Otherwise, the midline incision is recommended because it is the least damaging to neurovascular and functional structures.11 Grade 1/2/3 complication ● Repair Operative débridement of necrotic skin should be followed by the initiation of wet to dry dressing changes three times daily. The wound should be inspected routinely and repeat débridements completed at the bedside when indicated. If the wound appears well at 5 days, one may either return to the operating room for adipocutaneous ﬂap readvancement and closure or initiate the placement of a wound V.A.C. (KCI, San Antonio, TX) negative-pressure dressing with changes every 3 days. Traditional dressing changes should continue if there is any question of ongoing infection. Speciﬁcally, V.A.C. therapy should not be used to control infected wounds. ● Prevention Careful attention should be addressed toward previous scars, surgical incisions, ostomy sites, and drain sites because these may have disrupted the blood supply from the intercostal arteries and may result in skin ﬂap ischemia and necrosis. Midline incisions are most appropriate for thin patients. It is best to avoid transverse and subcostal incisions, which can interrupt the superﬁcial epigastric arcades and the segmental vessels of the intercostal system.12 Morbidly obese patients with signiﬁcant hernias may require a more sophisticated reconstructive plan. When massive hernias are repaired for these patients, the dependent pannus may be resected to promote wound healing. It is best to approach these patients with a limited midline skin incision that is excised in its entirety with an inferior adipocutaneous ﬂap advancement and transverse closure. It is imperative not to place this ﬁnal transverse incision at the juncture of the mons as in a traditional abdominoplasty because it is associated with a high risk of infection in obese patients. In addition, it limits revisional surgery in the context of wound dehiscence (Fig. 55–2). Extreme care must be extended to patients with prior ostomies. Skin bridges between midline incisions and the ostomy site are at high risk for ischemia. If the ostomy is to remain, one should consider a unilateral component separation procedure (Fig. 55–3). If intestinal reconstruction is a part of the operative intervention, one should consider complete excision of the ostomy site including the intervening skin bridge (Fig. 55–4). If not feasible, typically in the thin patient, we recommend primary closure of the ostomy site with expectant management. Wound dehiscence at the previous ostomy site can be treated with dressing changes and staged closure at 5 days or wound V.A.C. management.

55 COMPONENT SEPARATION FOR COMPLEX ABDOMINAL WALL

A1

A3

549

A2

B

Figure 55–2 Surgical incision placement in the morbidly obese patient with a plan for panniculectomy to reduce postoperative wound complications. A, Preoperative appearance of a 64-year-old man with a recurrent giant abdominal wall hernia with retained mesh, loss of domain and prior midline incision. B, Intraoperative wound closure with an inferior adipocutaneous ﬂap advancement. The initial exploration was via a limited midline incision centered at the umbilicus. The access incision was completely excised with the advancement of an inferior adipocutaneous ﬂap and a transverse closure remote from the mons and the native inferior skin fold to avoid potential wound infection.

C1

C2

Figure 55–2, cont’d C, Postoperative appearance of skin ﬂap closure at 4 months with no evidence of adipocutaneous skin ﬂap necrosis or dermal dehiscence.

C3

A1

A2

Figure 55–3 Unilateral component separation for maintained ostomy in the operative ﬁeld. A, Intraoperative appearance of a 43-yearold woman treated for ovarian cancer to include a total colectomy and end ileostomy complicated by multiple small bowel ﬁstulas–to– composite mesh placed to treat a prior midline evisceration event.

55 COMPONENT SEPARATION FOR COMPLEX ABDOMINAL WALL

A3

551

A4

B

C Figure 55–3, cont’d B, No component separation is performed on the ipsilateral side of the end ileostomy in order to preserve ostomy function and to avoid possible parastomal hernia. C, Postoperative appearance at 6 months with no evidence of midline hernia and persistent good stoma function.

Enter Peritoneal Cavity with Excision of STSG Iatrogenic Enterotomy ● Consequence Reentry into the peritoneal cavity of patients with complex hernias with or without STSG can potentially result in iatrogenic enterotomies with contamination of the surgical ﬁeld. Such a complication can be limited to wound cellulitis. In its most extreme form, the patient may develop an enterocutaneous or enteroenteric ﬁstula heralded by possible intra-abdominal abscess and sepsis. Grade 1/2/3/4 complication

● Repair Simple oversewing of the enterotomy with running 30 polydioxanone (PDS) suture is appropriate for minor serosal injuries. More extensive devascularization injuries should be approached with possible bowel resection using accepted stapling techniques. ● Prevention Timing of exploration and STSG excision can be assessed on physical examination preoperatively. Typically, most patients are not ready for reoperation until the STSG can be lifted from the underlying bowel. Surgery should be delayed until this simple maneuver

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SECTION VIII: HERNIA

A1

A2

A3 B1 Figure 55–4 Adipocutanteous ﬂap advancement and excision of prior colostomy site to promote wound healing. A, A 46-year-old woman with a history of rectal injury in the setting of open hysterectomy requiring diverting colostomy and open wound care, resulting in a midline hernia for repair. The patient has a prior Phanansteil incision concealed beneath her dependent pannus in addition to a right subcostal incision secondary to an open cholecystectomy.

55 COMPONENT SEPARATION FOR COMPLEX ABDOMINAL WALL

B2

553

B3

Figure 55–4, cont’d B, A midline incision was used for her exploration, given the patient’s prior right subcostal incision as a contraindication for an immediate transverse skin ﬂap closure. Her transverse colostomy site was completely excised with medial advancement of her right-sided adipocutaneous ﬂap to promote wound healing and improved abdominal wall contour.

injuries. Not all such injuries are preventable, particularly in patients with prior synthetic mesh placement. Judicious repair must be completed when injuries occur. We suggest aggressive staged irrigation of the abdomen and skin ﬂaps during closure overtop of closed suction drains in the setting of iatrogenic bowel injuries.

Postoperative Ileus

Figure 55–5 Assessing time of elective hernia repair. Lifting the STSG from the underlying bowel should be a pain-free assessment in the clinic prior to elective hernia repair.

● Consequence A prolonged ileus is a common complication with a reported incidence of 27%.13 Uncomplicated ileus is the direct result of extensive enterolysis during the takedown of the hernia. It can be secondary to electrolyte abnormalities in patients having received a preoperative bowel preparation. Of more clinical concern, it can be an early sign of an intra-abdominal infectious process or intestinal anastomotic leak. Grade 1/2/3/4 complication

can be preformed in the clinic with minimal pain (Fig. 55–5). Patients without STSG should be delayed for a minimum of 6 months after they have achieved a closed wound. Meticulous sharp dissection during adhesiolysis using the surgical principles of traction and countertraction to develop dissection planes between loops of bowel and the abdominal fascia are necessary to prevent iatrogenic bowel

● Repair Potentially correctable sources for prolonged ileus should be examined to include serum electrolytes, leukocyte count, and urinary analysis. Fever, abdominal pain, leukocytosis, and abdominal distention associated with profound emesis should prompt consideration of abdominal computed tomography (CT) scanning to deﬁne possible intra-abdominal ﬂuid collections and/ or abscess.

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SECTION VIII: HERNIA

● Prevention Patients are on nothing by mouth (NPO) with or without a nasogastric tube until they demonstrate evidence of bowel function. Ileus in an afebrile patient with a normal leukocyte count, normal serum electrolytes, and uncontaminated urine can be managed expectantly. Radiographic investigation should be concordant with the clinical setting.

Develop Adipocutaneous Advancement Flaps Ischemia and/or Venous Congestion ● Consequence Adipocutaneous ﬂap ischemia and/or venous congestion can lead to partial or full-thickness necrosis and an open wound with its associated problems of caloric consumption, risk for infection and potential for fascial dehiscence/evisceration, and extended ﬁnancial requirements of dressing supplies and continued surveillance. Grade 1/2/3 complication ● Repair Threatened adipocutaneous ﬂaps require expectant management. Serial physical examinations with an experienced eye will facilitate the timing of surgical débridement. Initial steps to prevent progression of ischemia and venous congestion include bedside release of the skin closure sutures and edema control. Persistent tension on ﬂap closure can result in progression of necrosis. Early release of tension is a preventive measure. Timely débridement and ﬂap readvancement after the diuresis of third-space ﬂuids may alleviate this problem. Incomplete wound closure can be addressed with dressing changes or wound V.A.C. placement. ● Prevention Adipocutaneous ﬂaps should be elevated at the juncture of the anterior fascia, with minimal fat being left behind on the fascia. The technical focus is ﬂap development using low-setting cautery and precise control of the perforators extending through the fascia. Distinct coagulation or clip and/or suture ligature of these perforators is necessary in order to prevent thermal injury down into the pedicle vessels supplying the underlying muscles or up into the adipocutaneous ﬂap. Precise use of the cautery is imperative to prevent areas of fat necrosis within the ﬂap. In addition, it is important to protect adipocutaneous ﬂaps from traction, avulsion, and compression injury by surgical assistants. Some patients may require a signiﬁcant ﬂuid resuscitation secondary to a prolonged operative course in the setting of concomitant secondary procedures. Tissue edema may become problematic, particularly in patients with multiple prior skin incisions. Intraoperative use of colloid over crystalloid has been advantageous.14,15 Delaying the skin

ﬂap closure or purposefully leaving marginal skin in place for 5 days is advised. Return to the operating room after a physiologic postoperative diuresis and skin ﬂap margination is the sign of a thoughtful surgeon. All patients should be counseled preoperatively of this possible “staging” of their abdominal wall closure (Fig. 55–6).

Excise Poorly Incorporated, Previously Placed Mesh Infection and Recurrent Hernia ● Consequence Lack of mesh incorporation into surrounding tissues is consistent with a clinical diagnosis of chronic infection. Retained, poorly incorporated mesh may lead to persistent wound infection. Retained mesh with areas of suture line dehiscence from the fascia can lead to hernia recurrence and need for unplanned reoperation. Grade 2/3 complication ● Repair Retained infected mesh and missed suture line dehiscence from prior hernia repairs will necessitate redo exploration and secondary hernia repair. ● Prevention Intraoperative examination of previously placed mesh as a distinct step in the operative procedure is imperative. Aggressive débridement with care to preserve the vascular supply to the remaining abdominal wall is preferable over leaving chronically infected mesh or small suture-line hernias clinically not apparent preoperatively on physical examination.

Excise Hernia Sac Seroma and Possible Infection ● Consequence Retained hernia sac may lead to postoperative seroma. Devascularized retained hernia sac will result in wound infection and possible dehiscence and evisceration. Complete excision of the hernia sac will eliminate these complications and facilitate ease to a technically competent fascial closure. Grade 2/3 complication ● Repair Suprafascial seromas secondary to retained viable hernia sac can be treated expectantly with aggressive use of closed bulb suction drains that remain in situ until drain output is less than 30 ml/day per drain. Ultrasound-guided percutaneous drain placement is an acceptable approach to early postoperative seroma formation. Persistent drain output from a percutaneous drain or recurrence after 3 weeks is suggestive of the formation of a seroma capsule, which requires a surgical excision and reclosure.

55 COMPONENT SEPARATION FOR COMPLEX ABDOMINAL WALL

A1

555

A2

B1

A3 Figure 55–6 Staging of adipocutaneous ﬂap closure. A, A 64-year-old man with history of bladder extrophy presents with a recurrent hernia secondary to infected synthetic mesh in the setting of bilateral paramedian abdominal incisions and a right-sided sigmoidureterostomy. B, The patient was explored through a left paramedian incision with removal of a staged superior tissue expander. His fascial reconstruction was completed by the use of acelluar dermal matrix. Adipocutaneous ﬂaps were allowed to marginate for 4 days prior to return to the operating room for ischemic ﬂap excision and staged closure.

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SECTION VIII: HERNIA

B2

B3

C1

C2

Figure 55–6, cont’d C, The patient’s postoperative appearance at the time of Jackson-Pratt drain removal.

Infection secondary to retained nonviable hernia sac requires débridement and open management of the wound with a staged, secondary abdominal wall reconstruction. ● Prevention Precise excision of the hernia sac is the best prevention. Occasionally, we have used well-vascularized hernia sac

atop of synthetic mesh in the setting of threatened skin ﬂaps (Fig. 55–7). If synthetic mesh or acellular dermis is used in combination with a component separation beneath thin adipocutaneous ﬂaps with overlying hernia sac, one must use multiple closed suction drains, which receive aggressive stripping and perioperative surveillance. If the adipocutaneous ﬂaps are lost, a portion of the hernia sac may protect the underlying mesh or

55 COMPONENT SEPARATION FOR COMPLEX ABDOMINAL WALL

557

AlloDerm against infection until an STSG can be applied in a staged fashion.

Complete Lysis of Adhesions to an Intraperitoneal Level 4 cm Lateral to the Fascial Defect Bowel Injury ● Consequence Small or large bowel adherent to the undersurface of the abdominal wall in near proximity to the hernia sac may inadvertently be injured or included in the suture used to reapproximate the fascia. Grade 3/4 complication ● Repair Unrecognized iatrogenic injury to or inclusion of the bowel within the fascial closure will require reoperation for an intra-abdominal catastrophe heralded by abdominal sepsis and possible dehiscence or evisceration. This too leads to open wound management followed by a staged, secondary reconstruction. C3 Figure 55–6, cont’d.

A1

● Prevention Surgeons of all ages and degrees of experience should maintain a level of attentiveness to prevent the inadvertent inclusion of a loop of bowel within the suture line of a fascial closure. Lysis of adhesions to a 4-cm margin will facilitate the ease of fascia reapproximation.

A2

Figure 55–7 Use of preserved, well-vascularized hernia sac beneath thin adipocutaneous ﬂaps. A, A 64-year-old man presents for abdominal wall reconstruction for recurrent failed infected mesh. Comorbidities included obesity, diabetes mellitus, and congestive heart failure.

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SECTION VIII: HERNIA

A3

B1

B2 B3 Figure 55–7, cont’d B, Hernia sac was preserved for use overtop of an acellular dermal matrix repair, given the anticipated thin nature of his skin ﬂaps.

55 COMPONENT SEPARATION FOR COMPLEX ABDOMINAL WALL

inadvertent transection of both the external and the internal oblique muscle layers has been reported in the literature with repair using onlay polypropylene mesh.16 AlloDerm should be considered in patients with a risk of infection. Intra-abdominal acellular dermal matrix or mesh placement can be completed using modiﬁed techniques of laparoscopic hernia repair, namely, transfascial lateral permanent suture placement and the use of efﬁcient hernia tackers (Salute Fixation System, Davol, Inc., Cranston, RI) (Fig. 55–8).

Vertical Incision of External Oblique Fascia 1 cm Lateral to the Semilunaris Spigelian Hernia ● Consequence Dissection deep to the external oblique muscle can injure the internal oblique fascia or muscle, resulting in a defect similar to a spigelian hernia. This injury results in loss of fascial continuity and dynamic support with loss of intra-abdominal domain relative to the chronicity of a failure to diagnose or treat this unusual defect. Grade 3/4 complication

● Prevention Meticulous dissection and observation of proper anatomic landmarks are imperative. The linea semilunaris is noted by the insertion of the external oblique fascia at the lateral rectus abdominis border. The initial longitudinal incision should be placed 1 cm lateral to the linea semilunaris. Generally, the fascial planes are quite distinct and allow for easy dissection. The plane between the external and the internal oblique may be opened out to the posterior axillary line. However, the mobility of the innervated rectus abdominis–internal oblique– transversus abdominis muscle complex should routinely

● Repair If unintended injury to the underlying internal oblique fascia occurs, interrupted reinforcing stitches may be placed. Typically, the internal oblique fascia is friable and a braided Vicryl suture is best, although leaving one with a high risk of remote hernia formation. If the resulting defect or weakness is large, a piece of synthetic mesh may be placed to reinforce the area using an onlay technique, again noting a risk for hernia recurrence. Frank rupture of the transverse abdominal muscle after

A

C

559

B

Figure 55–8 Intra-abdominal acellular dermal matrix placement for lateral fascial weakness secondary to internal oblique injury. A, A 54-year-old woman presented with a lateral abdominal wall hernia secondary to an avulsion injury in the setting of a motor vehicle accident. Her oblique muscles were avulsed from the right rectus abdominis muscle, and a delayed reconstruction included Vicryl mesh placement followed by AlloDerm, utilizing an open inlay technique. B, Percutaneous transfascial ﬁxation sutures were used for lateral AlloDerm advancement in the manner they would be applied in the setting of a laparoscopic hernia repair. C, Salute laparoscopic hernia clips were then applied to reduce postoperative pain and surgical time.

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be evaluated to prevent excessive dissection laterally, therefore decreasing the chances for an accidental deep fascial injury. The typical component separation release separates the external oblique muscle and aponeurosis from its connection to the anterior rectus fascia from the costal margin to the iliac crest at a level just lateral to the linea semilunaris. The external oblique can then be separated off the internal oblique with blunt dissection, avoiding injury to the internal oblique fascia and allowing the muscles to slide relative to one other (Fig. 55–9).

● Prevention Finding the proper plane of dissection is crucial to avoid this potential complication. The surgical dissection plane is between the external and the internal obliques and is avascular. Excessive bleeding should prompt a higher level of attention to this potential complication. The intercostal nerves supplying the rectus abdominis run deep to the fascia of the internal oblique muscle lateral to the linea semilunaris.

Muscle Flap Advancement and Approximation

Denervation of Rectus Abdominis Muscle

Failure to Obtain Closure

● Consequence Dissection deep to the internal oblique muscle may cause denervation of the rectus abdominis muscle and resulting atrophy and “pseudohernia” or the appearance of an eventration. Nerve injury such as this theoretically can also result in neuromas and chronic pain syndromes. Grade 2/3/4 complication

● Consequence Not all hernias can be repaired by a component separation procedure. Fascial defects may be underestimated on physical examination by the operative surgeon. Flap advancements may fail to approach reported ranges. Lack of a concerted surgical plan can result in an acute failure to close the fascial defect. Skin ﬂap closure over this type of a remaining fascial defect results in an immediate hernia and risk for skin ﬂap necrosis and dehiscence and/or evisceration. Unstable or insufﬁcient skin for closure results in a full-thickness open wound requiring staged reconstructive operative interventions. This last situation would likely result in a Vicryl mesh–based reconstruction in most centers (see Fig. 55–1). As is shown, expanded bilateral tensor fascia lata (TFL) ﬂaps were designed as a backup plan

● Repair Intercostal nerve transection can be repaired with interrupted 9-0 nylon suture using microscopic magniﬁcation. Often, these injuries are of a traction/avulsion-type injury and respond poorly to repair. One should seek assistance from a consulting surgeon experienced in nerve repairs.

A1

A2

Figure 55–9 Component separation surgical procedure. A, A 23-year-old woman with ovarian cancer presented with midline incision hernia for autologous repair. Risk factors for hernia recurrence included body mass index (BMI) greater than 30, active malignancy, and dependent pannus.

55 COMPONENT SEPARATION FOR COMPLEX ABDOMINAL WALL

A3

B2

561

B1

C

Figure 55–9, cont’d B, The hernia sac has been completely excised, leaving a 6-cm midline fascial defect for repair. Methylene blue has been applied, outlining the linea semilunaris bilaterally. The umbilical stalk has been preserved with circumferential incision. C, The external oblique fascia is incised 1 cm lateral to the linea semilunaris (inked in blue) from the costal margin inferiorly to the iliac crest. The internal oblique is viewed dorsally within the component separation.

for reconstruction, should component separation have failed to provide a tension-free fascial closure. Grade 3/4 complication ● Repair Backup, or salvage, reconstructive options should be outlined preoperatively for the surgical team and for informed consent of the patient. Synthetic mesh hernia reconstruction can be used in combination with a component separation procedure. For patients at risk for or with active infection, we have used rotational

TFL ﬂap reconstructions (Figs. 55–10 and 55–11). More recently, we have converted to AlloDerm cadaveric acellular regenerative tissue matrix, given its ease of acquisition and elimination of the donor site (Fig. 55–12). Long-term recurrent hernia rates utilizing acellular dermis are currently unavailable. Giant hernias repaired with acellular dermal matrices may display increased abdominal girth over time without a discrete hernia, necessitating excision of a midportion of the matrix to restore a functionally acceptable result. AlloDerm can have retained antibiotics, which may

562

SECTION VIII: HERNIA

D1

D2

E

F1 Figure 55–9, cont’d D, The right-sided component separation is advanced to the midline and closed with running Prolene suture. The umbilicus is preserved at the midline. E, A superior-based adipocutaneous ﬂap is advanced to the level of the mons for total excision of the dependent pannus to promote wound healing and function. This technique does require the creation of a full-thickness defect for umbilical reconstruction. Drains exit the lateral aspect of the incision to prevent additional drain site exit wounds. F, Postoperative appearance of right-sided component separation independent of synthetic mesh, with superior adipocutaneous ﬂap advancement and closure resulting in a functional and esthetically pleasing result.

precipitate allergic reactions. We encourage careful review of the manufacturer’s product insert. Supplementary surgical techniques have been described to gain additional fascial advancement to the traditional component separation procedure. If there is inadequate coverage over the xiphoid and subxiphoid region with excessive tension on the closure, removal of the xiphoid process, excision of any neo-ossiﬁcations in the upper wound, or taking the external oblique fascia up on the costal margin 6 to 8 cm can provide some additional

mobility of the upper fascia.10 Release of the posterior rectus sheath 1.0 to 1.5 cm from the linea alba has been described in the literature in order to gain additional advancement of composite tissue ﬂaps.1,17 This maneuver can result in injury to the neurovascular pedicle to the rectus abdominis muscle. Such a vascular injury could result in partial or total ﬂap loss. Partial ischemia of the muscle ﬂap can lead to atrophy, at best, presenting with pseudohernia or eventration. Total ﬂap loss results in hernia recurrence requiring immediate revision. Failure to

55 COMPONENT SEPARATION FOR COMPLEX ABDOMINAL WALL

F2

563

F3

Figure 55–9, cont’d.

diagnose total muscle ﬂap necrosis can lead to signiﬁcant soft tissue infection and a more complex staged reconstruction. Given the risk of total ﬂap loss in the hands of the inexperienced surgeon, we discourage this supplemental aspect of component separation procedures. Other “partition” methods are considered at high risk for such a complication and should be avoided (Fig. 55–13).6 ● Prevention Careful preoperative planning can prevent an unexpected failure of fascial closure. Abdominal CT scanning can deﬁne fascial boundaries in morbidly obese patients. Interdisciplinary teams including general and plastic surgeons dedicated to complex abdominal wall reconstruction can foster an environment to address the more difﬁcult cases hallmarked by prior resistant soft tissue infections, radiation, profound loss of domain, and in particular, unstable skin.18 An additional approach to aid in obtaining closure, although invasive and requiring several weeks to perform, is the placement of inﬂatable tissue expanders between the external and the internal oblique muscles, parallel to the abdominal wall defect, to expand the lateral abdominal wall.7,8 Tissue expanders are inﬂated gradually, allowing for an expansion of the abdominal domain and possible closure of larger defects (see Fig. 55–1). The use of vacuum-assisted devices to help achieve early fascial closure is a promising new advance that may help facilitate closure of the fascia or aid in overall management of large abdominal wounds, although more experience is needed.19,20

Recurrent Hernia, Dehiscence, Evisceration ● Consequence The rate of recurrent incisional hernia after component separation closure of the abdominal wall defect varies between 0% and 32%, with most studies having recurrence rates in the range of 2% to 12%.1,3,16,21–23 Rates of acute dehiscence and/or evisceration have been reported as high as 43%.13 Grade 3/4 complication ● Repair Acute dehiscence/evisceration and recurrent hernia in the setting of prior component separation often require the addition of synthetic mesh, acellular dermis, or more complex rotational autologous ﬂaps in the setting of a secondary reconstructive operation (see Figs. 55– 10 to 55–12). ● Prevention Dehiscence, evisceration, and hernia recurrence occurs more frequently in the morbidly obese population (mean body mass index [BMI] >30 kg/m2).16,24 Some consideration of weight loss prior to hernia surgery should be discussed with all overweight patients. Combined panniculectomy procedures may be beneﬁcial to patients with more urgent surgical requirements (see Fig. 55–9). Prevention of excessive tension on the fascial closure by placement of either synthetic mesh or AlloDerm at the initial repair can reduce complication rates such as these. The difﬁculty lies in the common desire to avoid

564

SECTION VIII: HERNIA

B1

A

B3

B2

B4

Figure 55–10 Rotational TFL ﬂap for rectus abdominis resection and irradiation for sarcoma. A, A 26-year-old woman presents with a midline abdominal wound secondary to a sarcoma resection and postoperative irradiation. A portion of her right rectus abdominis muscle and overlying fascia was previously resected. B, A right TFL ﬂap was used as an autologous method of reconstruction, given her history of irradiation and chronicity of her open wound.

55 COMPONENT SEPARATION FOR COMPLEX ABDOMINAL WALL

P1

P2

P3

P4

Figure 55–11 Abdominal wall reconstruction with TFL rotational ﬂap in an infected ﬁeld and history of failed synthetic mesh. A 56year-old man presents with infected Surgisis (COOK Biotech Inc., Indianapolis, IN) placed for an acute wound dehiscence in the setting of an intraperitoneal cadaveric renal transplant. An ipsilateral TFL ﬂap is utilized for an immediate autologous reconstruction with complete removal of the infected synthetic mesh.

synthetic materials in many patients requiring component separation. This desire to avoid mesh materials and lengthy autologous ﬂap reconstructions in these high-risk patients subjects them to tight wound closures that places them further at risk for dehiscence and recurrence. A subtotal autologous reconstruction including a component separation and acellular dermis with minimal tension fares better for an obese patient with signiﬁcant loss of

565

P5

domain over a component separation closed under undue tension. Some attention should be focused on the techniques of ﬂap approximation. A recent meta-analysis looking at suture material and type of stitch for closure of abdominal hernias suggests that the use of a nonabsorbable suture in a running fashion may reduce the relative risk of incisional hernia by up to 32%.25

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SECTION VIII: HERNIA

Respiratory Insufﬁciency ● Consequence The loss-of-domain phenomenon can cause decreased total lung capacity, vital capacity, and functional residual capacity. This may be evidenced by difﬁculty with ventilation.3 Loss of domain causing respiratory insufﬁciency is likely the cause for an average stay of 2.7 days in a surgical intensive care unit.13 Grade 3/4/5 complication

Figure 55–12 Alternative method of reconstruction for failed component separation. AlloDerm acellular dermal regenerative tissue matrix is used for a recurrent hernia repair for a failed component separation. The need for a multiple-sheet “quilting” technique places the patient at risk for hernia recurrence.

● Repair If respiratory insufﬁciency or difﬁculty ventilating the patient is noted intraoperatively, the tension from the closure can be released by taking down the midline fascial repair and interposing synthetic mesh or AlloDerm. This will increase the intra-abdominal volume and should resolve any acute surgically induced respiratory insufﬁciency. ● Prevention Preoperative pulmonary function testing may be indicated to identify patients at risk for the respiratory

A External oblique fascia

Transverse abdominis fascia

RA EO IO TA

Partitioning method

B Figure 55–13 Additional component separation fascial partition method. A, Hernia defect and abdominal wall anatomy superior to the umbilicus after elevation of bilateral adipocutaneous ﬂaps. B, Component separation with addition of partition method. See text for full description and technical warning.

55 COMPONENT SEPARATION FOR COMPLEX ABDOMINAL WALL failure secondary to the loss-of-domain phenomenon.9 Patients should be screened for preexisting pulmonary insufﬁciency. Intraoperative observation of peak airway pressures should be routine throughout the surgical procedure. Aggressive pulmonary toilet postoperatively is mandatory in this population of patients to prevent perioperative pneumonia. Attention to alternative pain management protocols may be required for more complex hernia repairs to aid in early ambulation and pulmonary toilet.

Adipocutaneous Flap Advancement and Approximation Seroma, Hematoma ● Consequence Fluid collections in between the fascia and the overlying adipocutaneous ﬂaps place patients at risk for superinfection, skin ﬂap dehiscence, and prolonged wound healing problems. Grade 1/2/3 complication ● Repair Watchful waiting, needle aspiration, percutaneous drain placement, or reoperation are all options, depending on the clinical situation. ● Prevention Strategic closed suction wound drain placement intraoperatively in combination with meticulous adipocutaneous ﬂap planning and development is the key to prevention of seroma formation. Drains must be cleared of occlusive exudates by “stripping” the drains every 4 hours for conventional component separation procedures and every 2 hours for those reconstructions including AlloDerm. The exudate from wounds containing AlloDerm are more viscous, the etiology of which is currently unknown. Drains are kept in place for up to 21 days for AlloDerm-independent reconstructions, with shorter durations for AlloDerm reconstructions in the range of 10 to 14 days. Drains are removed when outputs are less than 30 ml/day per drain. Prophylactic antibiotics for wound drains are controversial, but this is a common practice in our patients not requiring a preoperative bowel preparation. Subjectively, we have observed higher rates of Clostridium difﬁcile colitis in patients who have received a bowel preparation and are maintained on postoperative prophylactic antibiotics. This association is currently under investigation at our institution. We look forward to the potential use of antibiotic-coated closed suction drains currently under development in order to alleviate the need for oral antibiotics (Bacterin International, Belgrade, MT). Closed suction drains do not prevent hematomas. Given the risk of deep vein thrombosis (DVT) and pulmonary embolism (PE) in obese patients undergoing hernia repair,

567

all patients are aggressively treated with subcutaneous heparin or enoxaparin.26,27 Care should be taken to alert the nursing staff not to inject anticoagulants into the abdominal adipocutaneous ﬂaps to avoid a local effect predisposing a patient to a focal bleed. Acute resolution of drain output should alert one to the possibility of a compressive hematoma preventing ﬂuid egress. Ultrasound can be a helpful diagnostic tool in the obese patient.

Wound Infection ● Consequence Superﬁcial wound infections and focal incisional dehiscence can reﬂect poor surgical technique or lack of adherence to “best practices.” Grade 1/2 complication ● Repair Bedside débridement and local wound care typically result in the resolution of simple wound healing problems. ● Prevention Preoperative intravenous antibiotics are administered to all patients at least 30 minutes prior to incision. Maintaining standard principles of surgical sterility yields comparable infection rates according to the surgical contamination grade. Adipocutaneous ﬂap development should reﬂect as limited a dissection as possible in an attempt to prevent ischemia and to promote a lower rate of wound infection. Smoking should be eliminated preoperatively, if at all possible.28 Interrupted dermal monoﬁlament sutures (e.g., 3-0 Monocryl [Ethicon, Inc., Cornelia, GA]) followed by running subcuticular monoﬁlament suture (e.g., 4-0 Monocryl) are used whenever possible. Deep sutures within the fat and surgical staples are avoided. We further reenforce our closures with DERMABOND (Ethicon, Inc., Cornelia, GA) as a barrier method to ﬁght infection. Use of DERMABOND avoids the use of tape on delicate skin ﬂaps, thereby avoiding tension bullae formation. In addition, it promotes early showering to keep skin bacterial counts low.

Assimilation of Postoperative Secrets to Success Skin Flap Bullae and Partial-Thickness Loss ● Consequence Use of abdominal binders and tape is discouraged owing to the potential for injury to skin ﬂaps. Grade 1/2 complication ● Repair Shear and/or tension bullae and partial-thickness skin loss requires serial débridement and local dressing changes. It is important to provide a moist environ-

568

SECTION VIII: HERNIA

ment to promote rapid healing should they occur. Antibiotic ointments covered by nonadherent dressings occasionally result in allergic reactions. Duoderm (ConvaTec, Ltd., Deeside, UK) semipermeable hydrocolloid dressing is an acceptable alternative. ● Prevention Once skin ﬂap ischemia is no longer a concern, liposuction garments are preferred for abdominal wall compression owing to their inherent design to protect the skin (zippers, labels, and seams on the outside of the garment). Compressive liposuction garments may prevent seroma formation and should be encouraged for 3 to 6 months postoperatively. Liposuction garments can hold absorbent dressings in place without tape, should they be required. They are adequate in holding dressings over open wounds should extended would care be required. Many patients are more comfortable in some form of compression garment, therefore facilitating early ambulation.

DVT, PE ● Consequence Many hernia repair patients are at risk for perioperative venous thromboembolic complications. Risk factors include patient age, duration of general anesthetic, concomitant acute trauma or active malignancy, and elevated BMI.27 Grade 1/2/3/4 complication ● Repair Systemic anticoagulation with heparin or enoxaparin and potential for inferior vena cava ﬁlter placement according to accepted practice guidelines are recommended.27 ● Prevention Patients participate in an active postoperative ambulation protocol. Our patients walk in the hallway on the evening of surgery and seven times daily thereafter. They record their walking on a chart, which they subsequently use at home after discharge. Each walking chart is reviewed with the patient on their ﬁrst postoperative visit to ensure continued ambulation and DVT/ PE prevention. Elastic compressive stockings, sequential compressive devices, and perioperative subcutaneous heparin or enoxaparin are aggressively applied.29 Consideration of home prophylaxis is important for patients with active malignancies, obesity, or conditions that predispose them to inactivity.29

CONCLUSIONS Component separation is a useful surgical technique to address the repair of complex abdominal wall hernias. Used alone or in combination with other ancillary techniques, it promotes maximal innervated musculofascial

coverage of the abdominal wall and improved function for the individual patient. Complications can be avoided by appropriate preoperative planning, familiarity of the essential abdominal wall anatomy, meticulous surgical technique, and attentive postoperative surveillance of the surgical wound.

REFERENCES 1. Ramirez OM, Ruas E, Dellon AL. “Components separation” method for closure of abdominal-wall defects: an anatomic and clinical study. Plast Reconstr Surg 1990;86:519–526. 2. Kolker AR, Brown DJ, Redstone JS, et al. Multilayer reconstruction of abdominal wall defects with acellular dermal allograft (AlloDerm) and component separation. Ann Plast Surg 2005;55:36–41. 3. Shestak KC, Edington HJ, Johnson RR. The separation of anatomic components technique for the reconstruction of massive midline abdominal wall defects: anatomy, surgical technique, applications, and limitations revisited. Plast Reconstr Surg 2000;105:731–738. 4. DiBello JN Jr, Moore JH Jr. Sliding myofascial ﬂap of the rectus abdominus muscles for the closure of recurrent ventral hernias. Plast Reconstr Surg 1996;98:464– 469. 5. Ennis LS, Young JS, Gampper TJ, Drake DB. The “openbook” variation of component separation for repair of massive midline abdominal wall hernia. Am Surg 2003;69: 733–742. 6. Lindsey JT. Abdominal wall partitioning (the accordion effect) for reconstruction of major defects: a retrospective review of 10 patients. Plast Reconstr Surg 2003;112:477– 485. 7. Jacobsen WM, Petty PM, Bite U, Johnson CH. Massive abdominal-wall hernia reconstruction with expanded external/internal oblique and transversalis musculofascia. Plast Reconstr Surg 1997;100:326–335. 8. Hobar PC, Rohrich RJ, Byrd HS. Abdominal-wall reconstruction with expanded musculofascial tissue in posttraumatic defect. Plast Reconstr Surg 1994;94:379– 383. 9. Rohrich RJ, Lowe JB, Hackney FL, et al. An algorithm for abdominal wall reconstruction. Plast Reconstr Surg 2000;105:202–216. 10. Jernigan TW, Fabian TC, Croce MA, et al. Staged management of giant abdominal wall defects: acute and long-term results. Ann Surg 2003;238:349–355. 11. Core GB, Grotting JC. Reoperative surgery of the abdominal wall. In Grotting J (ed). Aesthetic and Reconstructive Plastic Surgery. St. Louis: Quality Medical, 1995; pp 1327–1375. 12. Hurwitz DJ, Hollins RR. Reconstruction of the abdominal wall and groin. In Cohen M (ed): Mastery of Plastic and Reconstructive Surgery. Boston: Little, Brown, 1994; pp 1349–1359. 13. Lowe JB 3rd, Lowe JB, Baty JD, Garza JR. Risks associated with “components separation” for closure of complex abdominal wall defects. Plast Reconstr Surg 2003;111:1276–1283.

55 COMPONENT SEPARATION FOR COMPLEX ABDOMINAL WALL 14. Sigurdsson GH. Perioperative ﬂuid management in microvascular surgery. J Reconstr Microsurg 1995;11:57– 65. 15. Joshi GP. Intraoperative ﬂuid restriction improves outcome after major elective gastrointestinal surgery. Anesth Analg 2005;101:601–605. 16. de Vries Reilingh TS, van Goor H, Rosman C, et al. “Components separation technique” for the repair of large abdominal wall hernias. J Am Coll Surg 2003;196: 32–37. 17. Losanoff JE, Richman BW, Jones JW. Endoscopically assisted “component separation” method for abdominal wall reconstruction. J Am Coll Surg 2002;194:388–390. 18. Mathes SJ, Steinwald PM, Foster RD, et al. Complex abdominal wall reconstruction: a comparison of ﬂap and mesh closure. Ann Surg 2000;232:586–596. 19. Suliburk JW, Ware DN, Balogh Z, et al. Vacuum-assisted wound closure achieves early fascial closure of open abdomens after severe trauma. J Trauma 2003;55:1155– 1160; discussion 1160–1161. 20. Miller PR, Meredith JW, Johnson JC, Chang MC. Prospective evaluation of vacuum-assisted fascial closure after open abdomen: planned ventral hernia rate is substantially reduced. Ann Surg 2004;239:608–614. 21. Saulis AS, Dumanian GA. Periumbilical rectus abdominis perforator preservation signiﬁcantly reduces superﬁcial wound complications in “separation of parts” hernia repairs. Plast Reconstr Surg 2002;109:2275–2280.

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22. van Geffen HJ, Simmermacher RK, van Vroonhoven TJ, van der Werken C. Surgical treatment of large contaminated abdominal wall defects. J Am Coll Surg 2005;201: 206–212. 23. Lowe JB, Garza JR, Bowman JL, et al. Endoscopically assisted “components separation” for closure of abdominal wall defects. Plast Reconstr Surg 2000;105:720–729. 24. Langer C, Schaper A, Liersch T, et al. Prognosis factors in incisional hernia surgery: 25 years of experience. Hernia 2005;9:16–21. 25. Hodgson NCF, Malthaner RA, Ostbye T. The search for an ideal method of abdominal fascial closure: a metaanalysis. Ann Surg 2000;231:436–442. 26. Prystowsky JB, Morasch MD, Eskandari MK, et al. Prospective analysis of the incidence of deep venous thrombosis in bariatric surgery patients. Surgery 2005; 138:759–763. 27. Buller HR, Agnelli G, Hull RD, et al. Antithrombotic therapy for venous thromboembolic disease: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126(3 suppl):401S–428S. 28. Ewart CJ, Lankford AB, Gamboa MG. Successful closure of abdominal wall hernia using the components separation technique. Ann Plast Surg 2003;50:269–273. 29. Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:338S–400S.

Section IX

HEMATOPOIETIC Stephen R. T. Evans, MD It is a mistake to suppose that men succeed through success; they much oftener succeed through failures. Precept, study, advice, and example could never have taught them so well as failure has done.—Samuel Smiles

56

Laparoscopic Splenectomy Diana M. Weber, MD and Aarti Mathur, MD INTRODUCTION The birth of the laparoscopic era has revolutionized the surgical approach to the abdomen. Since Delaitre’s performance of the ﬁrst laparoscopic splenectomy (LS) in 1991, LS has come to replace open splenectomy (OS), and it is now the standard procedure for patients with hematologic disorders.1 LS is associated with a lower complication rate than that of OS, primarily owing to the greater visualization of anatomic structures and the less invasive nature of laparoscopy.2 However, because of the fragile parenchyma, rich blood supply, and intimate relation to intra-abdominal organs such as the stomach, colon, and pancreas, LS, even when performed by experienced surgeons, is not without complications.3–5 Multivariate analyses show that these parameters increase the risk of complications associated with LS: learning curve of the surgeon, patient age, degree of hematologic malignancy, and extent of splenomegaly deﬁned as splenic weight greater than 1000 g or craniocaudal length greater than 20 cm.6–8 Splenomegaly may compromise the surgeon’s ability to manipulate the spleen, achieve hemostasis, and retrieve the specimen.9 Malignant spleens also tend to weigh more than benign spleens.10,11 Large splenic size of greater than 2 kg has been shown to have a complication rate of 63% versus 25% for a normal-sized spleen.11 Complications are also greater in elderly patients (53% vs. 13%).7,12 Because LS has a steep learning curve,

performance of more than 10 cases has been recommended to achieve competency.12–16

INDICATIONS 17 ● Red blood cell disorders: sphereocytosis, elliptocytosis,

autoimmune hemolytic anemia, thalassemias, sickle cell ● White blood cell disorders: lymphoma (staging), myelo-

ﬁbrosis, chronic lymphocytic leukemia, chronic myelogenous leukemia, hairy cell leukemia ● Platelet disorders: idiopathic thrombocytopenic purpura, thrombotic thrombocytopenic purpura, Evans’ syndrome ● Secondary hypersplenism: cirrhosis, cystic ﬁbrosis ● Miscellaneous: splenic trauma, abscess, cyst, tumor, angiomatosis, splenic artery aneurysms, Gaucher’s disease, sarcoidosis

CONTRAINDICATIONS 18 ● Severe coagulopathy or thrombocytopenia (platelet

<20 K)

● Severe splenomegaly deﬁned as a craniocaudal access

greater than 30 cm. ● Pregnancy ● Calciﬁed splenic artery

572

SECTION IX: HEMATOPOIETIC

Figure 56–1 splenectomy.

● Relative contraindication exists in patients with portal

hypertension secondary to the potential of lifethreatening hemorrhage and difﬁculty achieving hemostasis19

INSTRUMENTATION Preparation for the procedure with the appropriate equipment aids in performing a smooth operation and minimizes complications. The essential equipment for LS is as follows: ● ● ● ● ● ● ● ●

Angled laparoscope (30°) 5 to 10 mm 5-mm graspers and dissector Curved laparoscopic scissors Linear laparoscopic stapling device—two should be readily available Ultrasonic dissector (harmonic) Nylon extraction sac (500–750 ml capacity) Clip appliers Suction cannula

PREOPERATIVE PREPARATION All patients should be immunized against encapsulated bacteria, and coagulopathies should be corrected. Polyvalent pneumococcal, Haemophilus inﬂuenzae, and Neisseria meningitidis vaccines should be administered 1 to 2 weeks prior to surgery to allow time for an adequate antibody response.1,10,20 Patients who have received corticosteroids within the previous year should be treated with a stress dose to prevent acute adrenocortical insufﬁciency.20 Splenic artery embolization is generally not indicated unless the spleen is larger than 30 cm.21

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5

Position patient Trocar placement Abdominal exploration and search for accessory spleens Mobilization of inferior pole of spleen Incision of lateral attachments to spleen

Step 6 Step 7 Step 8 Step 9 Step 10 Step 11 Step 12 Step 13

Ideal patient positioning for laparoscopic

Division of lower pole vessels Entrance to lesser sac and division of short gastrics Dissection and ligation of splenic artery and vein Place spleen into sac Division of remaining splenophrenic ligament and closure of sac Morcellate and extract spleen Irrigation and hemostasis Trocar removal

OPERATIVE PROCEDURE Positioning (Fig. 56–1) In the earliest reports of LS, the procedure was performed almost exclusively with the patient in the supine position. The gradual evolution of this procedure has led surgeons to perform the majority of LS using the hanging spleen technique, with the patient in the right lateral decubitus position with a kidney rest and about 30° of reverse Trendelenburg.20 The peritoneal attachments of the spleen are used to suspend it in place. Gravity facilitates retraction of the stomach, omentum, and colon and allows slightly easier access and better visualization of the posterior aspect of the hilum, reducing the frequency of complications.20

Trocar Insertion1,20 (Fig. 56–2) Life-threatening and less serious complications can occur with trocar insertion. Complications, repair, and prevention are discussed in Section I, Chapter 7, Laparoscopic Surgery. A standard three- or four-trocar technique is used, placing the working ports along the left subcostal border. The camera port site accommodating a 30° scope is placed at the rim of the umbilicus in pediatric and slender patients; for larger patients, this may need to be moved to the left upper quadrant. A 5- to 12-mm port placed either cranially or caudally in the medioclavicular line is used as a working port as well as for the endovascular stapler. A paramedial epigastric 5- to 12-mm port is used as a second working port for the grasper and suction. An optional fourth 5-mm trochar may be placed in the left anterior

56 LAPAROSCOPIC SPLENECTOMY

Spleen Kidney

573

Pancreas Colon

Stomach

Figure 56–2 Trocar positioning for laparoscopic splenectomy.

subcostal or subxiphoid space for retraction. If a handassisted technique is to be used, the hand is introduced through either a Pfannenstiel incision or a lower right or left 5- to 6-cm abdominal incision.16,21–25 Consequences, repair, and prevention are discussed in Section I, Chapter 7, Laparoscopic Surgery.

Abdominal Exploration and Search for an Accessory Spleen (Fig. 56–3) Accessory spleens are present in about 25% of patients and can cause recurrence of the hematologic disease after splenectomy.10,19,26,27

Recurrent Thrombocytopenia ● Consequence Recurrent thrombocytopenia may occur, especially in patients with idiopathic thrombocytopenic purpura, secondary to failure to remove accessory spleens.25,28,29 Although most recurrences happen within the ﬁrst 2 years after splenectomy, they have been reported up to 18 years later.10 Grade 2/3 complication ● Repair If disease recurrence is identiﬁed, a denatured red blood cell scintigraphy or sulfur colloid scan may be performed to identify the accessory spleen. Reoperation may be necessary for symptomatic disease.25,26

● Prevention Laparoscopic magniﬁcation may improve detection of accessory splenic tissue.6 Careful and systematic dissection of splenic hilum, lateral lesser sac, pancreatic tail, splenocolic, and gastrosplenic ligaments allows accurate identiﬁcation.17 This area is explored by gently retracting the spleen laterally and opening the gastrosplenic ligaments with endoshears. Once detected, an accessory spleen should be resected because it may later be mistaken for hematoma as the operation progresses, and it can cause disease recurrence or treatment failure.19 Accessory spleens can be found in a variety of locations with the following frequencies18: ● ● ● ● ● ● ●

Hilar region 54% Pedicle 25% Greater omentum 12% Tail of pancreas 6% Splenocolic ligament 2% Mesentery 0.5% Left ovary 0.5%

Mobilize Inferior Pole of the Spleen/Splenic Flexure Colonic Injury ● Consequence INJURY may result in spillage of colonic contents into the abdominal cavity and resultant peritonitis. Grade 1/3 complication

574

SECTION IX: HEMATOPOIETIC

2 Spleen 1

Stomach

5 Pancreas

3 4

Colon

Accessory Spleen Locations 1. Hilar region 2. Greater omentum 3. Tail of pancreas 4. Splenocolic ligament 5. Pedicle

● Repair Early identiﬁcation of the perforation and laparoscopic repair with primary closure are essential.28 ● Prevention Dissection of the splenic ﬂexure can be accomplished by a combination of sharp dissection and the ultrasonic dissector. Knowledge of the anatomy, gently rotating the colon medially and inferiorly out of the ﬁeld, and the placement of the patient in the appropriate position will minimize this injury.30

Capsular Bleeding ● Consequence Hemorrhage originating in the parenchyma is usually less dangerous than vascular bleeding, but it impairs visualization for further dissection.19 Grade 1 complication ● Repair Hemorrhage originating from the parenchyma can be managed by clamping the artery and vein, by applying slight pressure with gauze, or using either collagen ﬂeece or ﬁbrin adhesive.1,19 If signiﬁcant bleeding occurs, conversion to an open procedure may be required. ● Prevention Capsular bleeding, which is seen more frequently in patients with splenomegaly, may occur at any time

Figure 56–3 sory spleens.

Locations of acces-

during LS, mostly from excessive manipulation or grasping of the spleen.31 Appropriate gentle traction of structures away from the spleen and clear visualization of the spleen minimize capsular injury.

Incise Lateral Attachments to the Spleen (Splenorenal and Splenophrenic) (Fig. 56–4) Diaphragmatic Injury ● Consequence A small puncture/cautery injury in the diaphragm, especially of the muscled part, may be ampliﬁed by the presence of pneumoperitoneum, causing a pneumothorax.19,26 Grade 2/3 complication ● Repair Increased peak airway pressures along with paradoxical diaphragmatic motion indicate diaphragmatic injury. Once identiﬁed, immediate intraoperative needle decompression followed by tube thoracostomy after completion of the procedure reexpands the lung.26 It is not always necessary to repair the diaphragmatic perforation. ● Prevention Knowledge of anatomy and meticulous dissection help to avoid this complication. In addition, appropriately positioning the patient in reverse Trendelenburg allows for greater visualization of this space and increases the distance to the diaphragm. The right lateral decubitus

56 LAPAROSCOPIC SPLENECTOMY

575

Diaphragm

Spleen

Figure 56–4 Incising the attachments to the spleen.

lateral

position, which takes advantage of gravity to expose retroperitoneal attachments even in the presence of dense diaphragmatic adhesions, reduces the frequency of potential diaphragmatic injury.31

Divide the Lower Pole Vessels Bleeding Inferior polar arteries, usually originating from the left gastroepiploic arteries, occur in approximately 80% of patients, numbering from one to ﬁve vessels. These vessels are relatively simple to dissect and are typically ligated with the ultrasonic dissector. ● Consequence Bleeding from the inferior polar vessels may be a life-threatening hemorrhage or may just become a hindrance to the operation because rapidly accumulating blood can impair visualization.19 Grade 1/3 complication ● Repair Bleeding that impairs visualization can be stopped with clips, electrocoagulation, or the ultrasonic dissector.3 Bleeding resulting in life-threatening hemorrhage requires conversion to laparotomy and further control. ● Prevention Appropriate traction allows for visualization of tissues prior to dissection. It is crucial to identify larger vessels that may need to be clipped prior to division with the ultrasonic dissector. The ultrasonic dissector should completely envelop all visible vessels within its grasp

to avoid incomplete division of a vessel, resulting in bleeding. Excessive traction during ligation may tear the tissue and prevent achievement of complete hemostasis.

Enter the Lesser Sac and Divide the Short Gastrics (Fig. 56–5) Bleeding ● Consequence Although not life threatening, bleeding from the short gastrics can become a hindrance to the operation because rapidly accumulating blood can impair visualization.19 Grade 1 complication ● Repair Bleeding can be stopped with clips, electrocoagulation, ultrasonic dissector, or bipolar cautery.3 Sponges and Gelfoam may aid in control of the bleeding. If bleeding persists or is uncontrollable, conversion to an open procedure may be required. ● Prevention The appropriate use of the harmonic shears has greatly reduced the incidence of bleeding from the short gastrics. The entire circumference of the vessel should be placed within the harmonic scalpel to avoid incomplete ligation, resulting in bleeding. During ligation, excess traction may result in tearing of tissue and incomplete hemostasis. Undue retraction on the stomach to tent and isolate these vessels may also result in shearing and premature release of tissues, causing bleeding.

576

SECTION IX: HEMATOPOIETIC

Spleen Stomach

Transverse colon

Gastric Perforation (Gastrotomy)/Necrosis ● Consequence Gastrotomy results in the spillage of gastric contents into the abdominal cavity, resulting in peritonitis. This can present immediately in the operating room from direct penetrating injury to the stomach during dissection, or it may present later with a delayed perforation from thermal injury or serosal tears during dissection. Use of a harmonic scalpel near the stomach can contribute to thermal or serosal injuries that may result in delayed perforation. Grade 1/3/5 complication ● Repair If recognized during the procedure, primary repair of a gastric perforation may be attempted laparoscopically; however, it is recommended to convert to laparotomy.24 A delayed perforation requires laparotomy for repair. ● Prevention It is not uncommon for the proximal greater curve of the stomach to directly abut the spleen. Therefore, appropriate traction and clear visualization of tissues during division of the short gastrics are essential. Care must also be taken to appreciate the structures that the heated portion of the dissector may touch. The ultrasonic dissector allows for less dissection around the

Figure 56–5 Entering the lesser sac and dividing the short gastric vessels.

vessels close to the stomach and spleen, reducing the incidence of gastric perforation.

Dissect and Ligate the Splenic Artery and Vein (Figs. 56–6 and 56–7) Hilar Bleeding/Hemorrhage This remains the surgeon’s key concern, because the need for transfusions in some series has exceeded 25%.7,9 ● Consequence Hemorrhage and associated shock may result from massive blood loss. Grade 3/5 complication ● Repair Bleeding from the main artery and vein mandates conversion to open laparotomy via a left subcostal incision and hemorrhage control. Intraoperative staple line bleeding can be managed with individual clips or sutures placed along that portion of the staple line. Postoperative bleeding from the staple line may be managed by splenic artery embolization.19 ● Prevention Clear understanding of splenic anatomy is crucial. Gentle retraction of the inferior pole exposes the hilar groove and allows evaluation of the vascular anatomy. The splenic vasculature has two common variations, the

56 LAPAROSCOPIC SPLENECTOMY

Spleen Stomach Kidney

Pancreas

Hilus

Figure 56–6 Dissection and ligation of the splenic artery and vein–anterior view.

Spleen

Splenic a., v. Pancreas

Figure 56–7 Dissection and ligation of the splenic artery and vein– posterior view.

577

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SECTION IX: HEMATOPOIETIC

magistral and the distributive pattern.32 In the distributive pattern, multiple branches arise from the main trunks approximately 2 to 3 cm from the hilum, and each terminal branch should be divided between clips. In the magistral pattern, the pedicle formed by the artery and vein enters the hilum as a compact bundle and should be transected en bloc with a single application of a vascular linear stapler. A window can be created above the hilar pedicle in the splenorenal ligament so that all structures are included within the markings of the linear stapler under direct vision. Looking at the internal surface of the spleen will aid in differentiating between these two vascular patterns. If the splenic vessels entering the spleen cover only 25% of the internal surface, a magistral pattern is present. Conversely, if the splenic vessels cover greater than 75% of the internal surface, a distributive pattern is present.32 The number of splenic branches is also related to the presence of the number of notches on the spleen. The number of notches have been found to correlate with the distributive anatomy and may be used as a helpful indicator at the beginning of the dissection.16,32 Proper positioning of the stapling device around the entire splenic hilum, facilitated by hilar dissection and splenic elevation, decreases the risk of perioperative bleeding and minimizes potential instrument failures.5,31 Prominent splenic vessels, perihilar fat, and the relatively narrow jaw opening of currently available staplers may lead to increased difﬁculty in encompassing the entire hilum. Therefore, clean and delicate dissection of the artery and vein helps exclude extraneous tissue and prevent “wedging” of the stapler into place, which would promote rupture of smaller pancreatic and splenic blood vessels.5,33,34 The ends of the stapling device on both sides should be visualized prior to ﬁring. Placement of metallic endoclips near the hilum may interfere with the gastrointestinal anastomosis (GIA) stapler. Inclusion of a clip in the GIA stapler may result in massive bleeding because the stapler will cut but not ligate. Prior to stapling, another stapler should be readily available in the case of equipment failure or partial transaction of the hilum. In the case of splenomegaly, the perisplenic ligaments are relatively shorter and the splenic hilum is deeply hidden, increasing the risk of bleeding.31 Hand-assisted laparoscopic surgery has shown to decrease rates of bleeding by providing increased exposure.21–23 Preoperative splenic artery embolization has not been proved to decrease morbidity, but it may be considered for postoperative splenic artery staple line bleeding.19

Pancreatic Injury This is the most common morbidity associated with LS.35 ● Consequence Injury to the pancreas may result in a wide array of manifestations from asymptomatic hyperamylasemia

to pancreatitis, peripancreatic ﬂuid collection, abscess, pancreatic ﬁstula, and pancreatic tail necrosis.4,19,35–37 Grade 1/2 complication ● Repair If an intraoperative injury is suspected, a closed suction drain should be placed and exited through a trocar site. Amylase levels should be checked on the drains postoperatively, and if elevated, the diet should be advanced more slowly. The drain may be removed when the output is less than 50 ml/24 hr. A ﬂuid collection may be managed by percutaneous drainage.35 ● Prevention Knowledge of anatomy can guide the surgeon to identify landmarks and apply the stapler in close proximity to the hilum on a site beyond the tip of the pancreas.30 In 75% of patients, the tail of the pancreas is less than 1 cm from the splenic hilum, and in 30% of patients, the tail is in direct contact with the hilum.25 Therefore, great care must be taken during hilar dissection. Ironically, the incidence of pancreatic injury may be increased as a result of the same factors that have facilitated the success of this procedure. The lateral positioning of the patient alters the orientation between the spleen and the pancreatic tail by allowing the hilum to lengthen.19 Limited exposure to the splenic hilum, especially in patients with splenomegaly, increases the risk of pancreatic injury. Therefore, meticulous skeletonization of the artery and vein as well as application of the stapler in close proximity to the hilum minimizes the risk of transection or injury to the pancreatic tail.35 Multiple applications of the GIA stapler to prevent hilar bleeding may increase the risk of pancreatic injury.36 In patients with splenomegaly, the hilar structures can pose a serious challenge because they are deeply hidden. Early use of hand-assisted devices in the course of LS for large spleens may help to minimize this occurrence.38 Some institutions routinely place Jackson-Pratt drains in the splenic fossa after hand assisted laparoscopic splenectomy (HALS) and check amylase on postoperative day 1.39

Place the Spleen into the Sac, Morcellate, and Extract (Fig. 56–8) Splenosis ● Consequence Residual splenic tissue present in abnormal locations usually remains asymptomatic and can be an incidental ﬁnding on imaging many years later, mimicking a tumor. In symptomatic patients, it may cause pain or disease recurrence.29 Grade 1/2/3 complication

56 LAPAROSCOPIC SPLENECTOMY

579

Spleen

Figure 56–8 Placing the spleen into a bag.

● Repair Laparoscopic excision is indicated for symptomatic disease, occasionally with the aid of an argon beam coagulator.40 ● Prevention Gentle and minimal manipulation of the spleen to avoid capsular tears resulting in splenic spillage aids in preventing this complication.41 The quality of dissection, absence of hemorrhage, copious irrigation, and use of a large specimen bag to extract the spleen all minimize the risk of splenosis.20,24,25 Morcellation should be performed inside the specimen bag with either ﬁngers or atraumatic forceps.32

Irrigate and Achieve Hemostasis Intra-abdominal/Subphrenic Abscess ● Consequence Development of an abscess typically occurs within the ﬁrst 30 days and is associated with abdominal pain, nausea, vomiting, fever, and rarely, death.4,17 Grade 2/3/5 complication ● Repair Intra-abdominal and subphrenic abscesses require a drainage procedure, most commonly, a percutaneous drain performed by interventional radiology.10,16,28 A small percentage may not easily be accessed via radiographic guidance and may require reoperation. ● Prevention Copious irrigation and suction until the irrigant ﬂuid is clear and assurance that hemostasis has been achieved

minimize the risk of abscess formation. Preoperative exposure to chemotherapy or steroids increases the risk of infectious complications.

Retroperitoneal Hematoma ● Consequence Retroperitoneal hematoma is usually discovered in the ﬁrst several postoperative days with a dropping hematocrit, pain, and symptomatic anemia.26,41 Grade 2/3 complication ● Repair If the hematocrit does not stabilize, intervention is required in the form of reexploration or laparoscopic drainage.10,26 ● Prevention Adequate hemostasis and copious irrigation reduce the risk of a hematoma.

Trocar Removal Wound Site Complications Wound site complications include port site hernias, wound infections, and abdominal wall hematomas.7,28 All of these complications can occur with any form of laparoscopic surgery and are discussed in Section I, Chapter 7, Laparoscopic Surgery. In general, ports should be removed under direct vision and fascia of all ports of 10 mm or larger should be closed to avoid port site herniation.37 Morbidity at the surgical site is minimized by hemostasis prior to closure.26

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Other Complications Portal/Splenic Vein Thrombosis Thrombosis of the portal venous system has been reported as a possible cause of death after splenectomy. The reported incidence of portal/splenic vein thrombosis (PSVT) after LS from routine postoperative surveillance ultrasound is as high as 55% in some series.42,43 Although most patients are asymptomatic, some may present with fever of unknown origin, intestinal infarction, variceal hemorrhage, and hepatic failure in the short term.43,44 Preexisting coagulation abnormalities and a large splenic mass may be risk factors for postsplenectomy PSVT.43 Transient thrombocytosis develops after splenectomy in 60% to 75% of patients.45 In addition to the coagulation abnormalities that these patients may have, it has been postulated that the surgical technique itself may inﬂuence the incidence of this complication. Pneumoperitoneum causes a hypercoagulable state during laparoscopic surgery.46 In patients with splenomegaly, the large stump of splenic vessels causes turbulence that may enhance coagulation.44–46 Routine surveillance imaging is not warranted; however, high-risk patients may have postoperative surveillance. Treatment for symptomatic patients ranges from anticoagulation and/or systemic thrombolytics to local, via the superior mesenteric artery, or percutaneous transhepatic thrombolysis. Variceal hemorrhage requires endoscopic control.46 Grade 1/2 complication Overwhelming Postsplenectomy Infection Removal of the spleen, which functions as a ﬁlter for encapsulated bacteria, puts the patient at risk for developing a life-threatening fulminant infection with a mortality rate greater than 50%.47–50 Risk factors include younger patient age and hematologic malignancy. The syndrome typically occurs within the ﬁrst 6 months postoperatively. It begins with nonspeciﬁc symptoms that rapidly progress in 24 to 48 hours to progressive hypotension, disseminated intravascular coagulation, purpuric lesions in the extremities, acute respiratory insufﬁciency, metabolic acidosis, and coma.47,48 Immediate high-dose pencillin is the initial treatment, and vancomycin and ceftriaxone are reserved for patients in areas where penicillin resistant Streptococcus pneumoniae is present. Preventive strategies fall into three major categories including chemoprophylaxis, immunoprophylaxis, and patient education. Pneumococcal, meningococcal, and H. inﬂuenzae type B vaccines should be administered at least 14 days prior to or soon after splenectomy. Booster injections of the pneumococcal vaccine should be considered every 5 to 6 years. Annual inﬂuenza immunization is advisable. Penicillin prophylaxis is indicated in the ﬁrst 5 years of life or the ﬁrst 2 years postoperatively in high-risk adults, such as those with hematologic malignancies, severe liver disease, or immunocompromised states. A lack of consensus exists among experts regarding lifelong prophylaxis;

however, it may be considered in immunocompromised patients.50 Grade 1/5 complication

REFERENCES 1. Uranues S, Alimoglu O. Laparoscopic surgery of the spleen. Surg Clin North Am 2005;85:75–90. 2. Winslow ER, Brunt ML. Perioperative outcomes of laparoscopic versus open splenectomy: a meta-analysis with an emphasis on complications. Surgery 2003;134:647– 655. 3. Brodsky JA, Brody FJ, Walsh RM, et al. Laparoscopic splenectomy. Surg Endosc 2002;16:851–854. 4. Glasgow RE, Mulvihill SJ. Laparoscopic splenectomy. World J Surg 1999;23:384–388. 5. Kercher KW, Novitsky YW, Czerniach DR, Litwin DEM. Staple line bleeding following laparoscopic splenectomy: intraoperative prevention and postoperative management. Surg Laparosc Endosc Percutan Tech 2003;13:353– 356. 6. Rosen M, Brody F, Walsh M, et al. Outcome of laparoscopic splenectomy based on hematologic indication. Surg Endosc 2002;16:272–279. 7. Tagarona EM, Espert JJ, Bombuy E, et al. Complications of laparoscopic splenectomy. Arch Surg 2000;135:1137– 1140. 8. Duperier T, Brody F, Felsher J, et al. Predictive factors for successful laparoscopic splenectomy in patients with immune thrombocytopenic purpura. Arch Surg 2004;139: 61–66. 9. Patel AG, Parker JE, Wallwork B, et al. Massive splenomegaly is associated with signiﬁcant morbidity after lap splenectomy. Ann Surg 2003;238:235–240. 10. Rosen M, Brody F, Walsh RM, et al. Outcome of laparoscopic splenectomy based on hematological indication. Surg Endosc 2002;16:272–279. 11. Horowitz J, Smith JL, Weber TK, et al. Postoperative complications after splenectomy for hematologic malignancies. Ann Surg 1996;233:290–296. 12. Kavic SM, Segan RD, Park AE. Laparoscopic splenectomy in the elderly: a morbid procedure? Surg Endosc 2005; 19:1561–1564. 13. Peters MB, Camacho D, Ojeda H, et al. Deﬁning the learning curve for laparoscopic splenectomy for immune thrombocytopenic purpura. Am J Surg 2004;188:522– 525. 14. Pace DE, Chiasson M, Schlachta M, et al. Laparoscopic splenectomy: does the training of minimally invasive surgical fellows affect outcomes? Surg Endosc 2002;16:954–956. 15. Rege RV, Joehl RJ. A learning curve for laparoscopic splenectomy at an academic institution. J Surg Res 1999;81:27–32. 16. Kathkhouda N, Manhas S, Umbach TW, et al. Laparoscopic splenectomy. J Laparosc Adv Surg Tech 2001;11: 383–390. 17. Glasgow RE, Yee LF, Mulvihill SJ. Laparoscopic splenectomy: the emerging standard. Surg Endosc 1997;11:108– 112.

56 LAPAROSCOPIC SPLENECTOMY 18. Park A. Laparoscopic splenectomy. In Cameron J (ed): Current Surgical Therapy, 8th ed. Philadelphia: Elsevier Mosby, 2004; pp 1254–1257. 19. Park A, Taragona EM, Trias M. Laparoscopic surgery of the spleen: state of the art. Arch Surg 2001;386:230– 239. 20. Schlinkert RT, Teotia SS. Laparoscopic splenectomy. Arch Surg 1999;134:99–103. 21. Taragona EM, Balague C, Cerdan G, et al. Hand-assisted laparoscopic splenectomy in cases of splenomegaly. Surg Endosc 2002;16:426–430. 22. Taragona EM, Gracia E, Rodriguez M, et al. Handassisted laparoscopic surgery. Arch Surg 2003;138:133– 141. 23. Rosen M, Brody F, Walsh M, Ponsky J. Hand-assisted laparoscopic splenectomy vs conventional laparoscopic splenectomy in cases of splenomegaly. Arch Surg 2002; 137:1348–1352. 24. Poulin EC, Mamazza J. Laparoscopic splenectomy: lessons from the learning curve. Can J Surg 1998;41:28–36. 25. Delaitre B, Blezel E, Samana G, et al. Laparoscopic splenectomy for idiopathic thrombocytopenic purpura. Surg Laparosc Endosc Percut Tech 2002;12:413–419. 26. Brodsky JA, Brody FJ, Walsh RM, et al. Laparoscopic splenectomy: experience with 100 cases. Surg Endosc 2002;16:851–854. 27. Gigot JF, Jamar F, Ferrant A, et al. Inadequate detection of accessory spleens and splenosis with laparoscopic splenectomy. Surg Endosc 1998;12:101–106. 28. Pomp A, Gagner M, Salky B, et al. Laparoscopic splenectomy: a selected retrospective review. Surg Laparosc Endosc Percutan Tech 2005;15:139–143. 29. Schwartz J, Eldor A, Szold A. Laparoscopic splenectomy in patients with refractory or relapsing thrombotic thrombocytopenic purpura. Arch Surg 2001;136:1236– 1238. 30. Laparoscopic splenectomy. In Scott-Conner CEH, Dawson DL (eds): Operative Anatomy, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2003; pp 362–366. 31. Tan M, Zheng C, Whu Z, et al. Laparoscopic splenectomy: the latest technical evaluation. World J Gastroenterol 2003;9:1086–1089. 32. Poulin EC, Schlachta CM, Mamazza J. Laparoscopic splenectomy. In Souba WW (ed): American College of Surgeons ACS Surgery: Principles and Practice. New York: Web MD Inc, 2004; pp 520–534. 33. Miles WFA, Greig JD, Wilson RG, Nixon SJ. Technique of laparoscopic splenectomy with a powered vascular linear stapler. Br J Surg 1996;83:1212–1214. 34. Machado MAC, Makdissi FF, Herman P, et al. Exposure of splenic hilum increases safety of laparoscopic splenec-

35.

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tomy. Surg Laparosc Endosc Percutan Tech 2004;14: 23–25. Chand B, Walsh RM, Ponsky J, Brody F. Pancreatic complications following laparoscopic splenectomy. Surg Endosc 2001;15:1273–1276. Klinger PJ, Tsiotos GG, Glaser KS, Hinder RA. Laparoscopic splenectomy: evolution and current status. Surg Laparosc Endosc Percutan Tech 1999;9:1–8. Chan SW, Hensman C, Waxman BP, et al. Technical developments and a team approach leads to an improved outcome: lessons learnt implementing laparoscopic splenectomy. Aust N Z J Surg 2002;72:523–527. Terrosu G, Baccarani U, Bresadola M, et al. The impact of splenic weight on laparoscopic splenectomy for splenomegaly. Surg Endosc 2002;16:103–107. Smith L, Luna G, Merg A, et al. Laparoscopic splenectomy for treatment of splenomegaly. Am J Surg 2004; 187:618–620. Serur E, Sadana N, Rockwell A. Laparoscopic management of abdominal pelvic splenosis. Obstet Gynecol 2005;106:1170–1171. Corcione F, Esposito C, Cuccurullo D, et al. Technical standardization of laparoscopic splenectomy: experience with 105 cases. Surg Endosc 2002;16:972–974. Winslow ER, Brunt LM, Drebin JA, et al. Portal vein thrombosis after splenectomy. Am J Surg 2002;184:631– 636. Ikeda M, Sekimoto M, Takiguchi S, et al. High incidence of thrombosis of the portal venous system after laparoscopic splenectomy. Ann Surg 2005;241:208–216. Brink JS, Brown AK, Palmer BA, et al. Portal vein thrombosis after laparoscopy-assisted splenectomy and cholecystectomy. J Pediatr Surg 2003;38:644–647. Fransciosi C, Romano F, Caprotti R, et al. Splenoportal thrombosis as a complication after laparoscopic splenectomy. J Laparoendosc Adv Surg Tech 2002;12:273–276. Kercher KW, Sing RF, Watson KW, et al. Transhepatic thrombolysis in acute portal vein thrombosis after laparoscopic splenectomy. Surg Laparosc Endosc 2002;12: 131–136. Opal SM. Splenectomy and splenic dysfunction. In Cohen J, Powderly WG (eds): Infectious Diseases, 2nd ed. Philadelphia: Mosby, 2004; pp 1145–1149. Bridgen ML, Pattullo AL. Prevention and management of overwhelming postsplenectomy infection: an update. Crit Care Med 1999;27:836–842. El-Alfy MS. Overwhelming postsplenectomy infection: is quality of patient knowledge enough for prevention? Hematol J 2004;5:77–80. Newland A, Provan D, Myint S. Preventing severe infection after splenectomy. BMJ 2005;331:417–418.

57

Supraclavicular Lymph Node Biopsy Diana M. Weber, MD and Eleanor Faherty, MD INTRODUCTION

OPERATIVE STEPS

The supraclavicular lymph node biopsy was ﬁrst described in the literature in 1949 by Daniels.1 It has remained a diagnostic tool for intrathoracic and/or metastatic disease, even with the development of more noninvasive procedures such as ultrasound-guided biopsy and scalene biopsy during mediastinoscopy.2–4 The supraclavicular lymph nodes are also called the scalene nodes because of their close proximity with the scalene muscles. The supraclavicular fossa or scalene triangle is bounded medially by the sternal head of the stenocleidomastoid, laterally by the clavicular head of the same muscle, and inferiorly by the clavicle. The lymph nodes are invested in a fat pad that lies directly over the anterior scalene muscle, just lateral to the carotid sheath. The phrenic nerve and the transverse cervical and suprascapular arteries run through this region, as does the thoracic duct on the left.5 In experienced hands, the procedure is very simple; however, a lack of understanding of the anatomy may result in complications including bleeding, thoracic duct injury, and phrenic or recurrent laryngeal nerve injury. Studies have reported an 8% morbidity rate and a 3% mortality rate.6,7 The scalene lymph nodes are a common location for metastasis of several cancers, the most common of which is lung cancer.8 In the United States, lung cancer has the highest mortality of all cancers, and disease spread to the scalene lymph nodes (N3) may contraindicate surgical therapy.4 Esophageal cancer studies have also demonstrated that 15% of patients have positive scalene nodes at presentation.9 Sarcoidosis, a benign but debilitating condition, has also been shown to present with supraclavicular lymphadenopathy.10

Step Step Step Step Step

INDICATIONS ● ● ● ● ●

Lung cancer Esophageal cancer Cervical cancer Testicular cancer Sarcoidosis

1 2 3 4 5

Skin incision Incise platysma Retract heads of sternocleidomastoid muscles Dissection of scalene fat pad Closure

OPERATIVE PROCEDURE Dissection of the Scalene Fat Pad Vessel Injury The carotid sheath, containing the carotid artery and internal jugular vein, lies medial to the scalene fat pad and may be injured during dissection. Branches of the thyrocervical trunk, the transverse cervical and suprascapular arteries, also run through the fat pad and may be injured and result in bleeding. ● Consequence Bleeding may occur if vessels are injured or transected. If the carotid artery is involved, bleeding may be massive. There may also be neurologic compromise if there is contralateral carotid disease. Grade 1 or 3 complication ● Repair Ligation may be performed of the transverse cervical and suprascapular arteries if injured. Primary repair should be completed for any injury or transection of the carotid artery or internal jugular vein. ● Prevention The carotid sheath runs in the medial supraclavicular fossa, close to the sternal head of the sternocleidomastroid muscle. Gentle medial retraction of the sheath during dissection should protect these structures.

Phrenic Nerve Injury ● Consequence The phrenic nerve innervates the diaphragm and is important in respiration. Patients with severe respiratory disease may have worsening symptoms if the

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phrenic nerve is compromised. Unilateral phrenic nerve injury is generally tolerated in most patients. Grade 4 complication ● Prevention The phrenic nerve runs along the anterior scalene muscle in the same direction as its ﬁbers. It runs deep in the scalene fat pad. Careful identiﬁcation of the nerve should occur during sharp dissection to prevent injury.

Chylous Fistula ● Consequence A chyle leak from a thoracic duct injury may result in a failure to thrive in patients owing to weight loss and debility from the loss of triglycerides. Grade 2/3 complication ● Repair Conservative management is possible in some patients. Parenteral nutrition or feeding with only medium-chain fatty acids may help to decrease chyle production and allow spontaneous closure. In patients with chronic cough or those in whom conservative treatment has failed, primary surgical repair or ligation of the thoracic duct should occur.11 ● Prevention If lymph nodes are nonpalpable, or whenever possible, the scalene lymph node biopsy should be done on the right to avoid possible thoracic duct injury. The duct can be visualized in the medial side of the supraclavicular fossa where it joins the subclavian vein. Careful identiﬁcation of the duct should occur during dissection to prevent injury. In patients who are awake for biopsy, the surgeon may ask the patient to cough at the completion of the procedure to check for a jet of chyle (milky, white ﬂuid), which would indicate a ductal injury.

REFERENCES 1. Daniels AC. A method of biopsy useful in diagnosing certain intrathoracic diseases. Dis Chest 1949;16:360. 2. Fultz PJ, Harrow AR, Elvey SP, et al. Sonographically guided biopsy of supraclavicular lymph nodes: a simple alternative to lung biopsy and more invasive procedures. AJR Am J Roentgenol 2003;180:1403–1409. 3. Fultz PJ, Feins RH, Strang JG, et al. Detection and diagnosis of nonpalpable supraclavicular lymph nodes in lung cancer at CT and US. Radiology 2002;222:245– 251. 4. Lee JD, Ginsberg RJ. Lung cancer staging: the value of ipsilateral scalene lymph node biopsy performed at mediastinoscopy. Ann Thorac Surg 1996;62:338–341. 5. Cervical lymph node biopsy and scalene node biopsy. In Scott-Conner CEH, Dawson DL (eds): Operative Anatomy, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2003; pp 69–73. 6. Ketcham AS, Sindelar WF, Feliz EL, Bagley DH. Diagnostic scalene node biopsy in the preoperative evaluation of the surgical cancer patient: a 5 year experience with 108 cases and literature review. Cancer 1976;38:948– 952. 7. Skinner DB. Scalene lymph node biopsy: Reappraisal of risks and indicators. N Engl J Med 1963;268:1324– 1329. 8. Lynch DF, Richie JP. Supraclavicular node biopsy in staging testis tumors. J Urol 1980;123:39–40. 9. Van Overhagen H, Lameris JS, Berger MY, et al. Supraclavicular lymph node metastases in carcinoma of the esophagus and gastroesophageal junction: assessment with CT, US and US-guided ﬁne-needle aspiration biopsy. Radiology 1991;179:155–158. 10. Lohela P, Tikkakoski T, Strengell L, et al. Ultrasoundguided ﬁne-needle aspiration cytology of non-palpable supraclavicular lymph nodes in sarcoidosis. Acta Radiol 1996;37:896–899. 11. Wertheimer M, Hughes RK. Scalene lymph node biopsy; prevention of postoperative chylous ﬁstula. Am J Surg 1971;122:121–122.

Section X

VASCULAR SURGERY Richard F. Neville, MD I have not failed. I’ve just found 10,000 ways that won’t work.—Thomas A. Edison

58

Carotid Endarterectomy Dahlia Plummer, MD and Richard F. Neville, MD INTRODUCTION In the United States, the incidence of new and recurrent stroke is estimated at approximately 700,000 per year, with over 80% attributable to an ischemic etiology.1 Surgery for the prevention of ischemic stroke from atherosclerotic extracranial vascular disease was ﬁrst performed by Eastcott, Pickering and Rob in 1954. A carotid endarterectomy (CEA) was performed for symptomatic atheroembolic disease. The procedure fell into disfavor by many in the ensuing years until two prospective, randomized trials (North American Symptomatic Carotid Endarterectomy Trial [NASCET] and Asymptomatic Carotid Atherosclerosis Study [ACAS]) as well as numerous corollary trials demonstrated CEA to be effective for symptomatic and asymptomatic patients with appropriate degrees of stenosis.2–5 CEA is a procedure heavily dependent on the experience and technique of the operating surgeon. The actual surgical technique that is the foundation of CEA has changed little, but patient selection, intraoperative care, and postprocedural follow-up have been greatly reﬁned. The CEA has long maintained a prominent position in stroke prevention, and its efﬁcacy has been borne out in a number of landmark trials. Nationally, between 180,000 and 200,000 CEAs are performed each year.4 NASCET and the European Carotid Stenosis Trial (ECST) both demonstrated decreased stroke risk in symptomatic patients undergoing CEA. Symptomatic patients, in a medically treated cohort, with 70% or greater arterial ste-

nosis were shown to have a cumulative 2-year risk of ipsilateral stroke of 26% versus 9% in those treated surgically; the absolute risk reduction was 17%.2 In the ACAS, a lower risk of stroke and death was seen in patients managed with surgery over matched controls receiving medical management. The 5-year risk of stroke was 5.1% in patients treated with surgery versus 11% in those treated medically, with an absolute risk reduction of 5.9%.3 These ﬁndings accounted for a 53% relative risk reduction in the surgical cohort over the 5-year study period.3 Unlike therapy for coronary and most other peripheral vascular occlusive disease, the critical clinical aspect of extracranial cerebrovascular disease is not chronic ischemia and lack of blood ﬂow, but embolic events. Although we continue to use the degree of stenosis as a primary factor in the evaluation of appropriate candidates for therapy, symptoms are the most predictive ﬁnding. Much remains to be done to determine the nature of plaque stability and to develop an understanding of the critical events that transform a “dormant” lesion into an “active” lesion with acute changes and embolic phenomena. Open surgical exposure of the carotid bifurcation results in a small physiologic insult to the patient. Subcutaneous exposure of the carotid bifurcation can be done with the patient under either local or general anesthesia. The procedure requires a maximum amount of control through employing distal control of the internal carotid, reversal of ﬂow in the internal carotid prior to restoring antegrade ﬂow, visual inspection and débridement of the plaque site, and control of the proximal and distal endpoints of

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the endarterectomy. CEA is based on ﬁve fundamental principles: 1. Minimal physiologic insult—predictable location and subcutaneous exposure. 2. Arterial control—reliably achieved without additional manipulation. 3. Maintenance of cerebral perfusion. 4. Plaque removal—complete removal of embolic lesion. 5. Lumen enlargement—endarterectomized vessel greater than 100% of native vessel diameter, especially with patch angioplasty providing prevention of restenosis.

KEY DECISION POINTS ● Anesthesia: local/regional versus general ● Intraoperative shunting: selective versus routine ● Arterial closure: primary versus patch

INDICATIONS ● ● ● ●

Symptomatic stenosis greater than 50% Asymptomatic stenosis greater than 60% to 80% Symptomatic ulcerated plaque type B/C Asymptomatic ulcerated plaque type C

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5

Step 6

Step 7 Step 8

Step 9

Patient positioning Skin incision Dissection and exposure of extracranial carotid artery Arterial control—proximal and distal Evaluation of intracranial circulation a. Routine shunting b. Selective shunting c. Operation in awake patient d. Stump pressures e. Electroencephalography f. Cerebral infrared oximetery Arteriotomy a. Longitudinal b. Everson technique Endarterectomy Arteriotomy closure a. Primary closure b. Patch closure Wound closure

OPERATIVE PROCEDURE Patient Positioning During CEA, the patient assumes a supine position with extension of the neck and contralateral rotation of the

head toward the opposite side. The arms should be tucked to the sides and the table slightly ﬂexed at the waist. Proper positioning affords maximal exposure of the carotid triangle. The geometry of the neck may also be enhanced by using a shoulder roll to optimize neck extension. Caution is exercised to avoid hyperextension because this may place excessive tension on the vessels of the neck. The patient should be prepared widely and draped in a manner that allows exposure of the anterior cervical triangle. The operative table may be rotated to provide the optimum visibility for the operator.

Improper Positioning ● Consequence Loss of orientation. There is no substitute for caution and attention to detail during surgery. Notwithstanding, exposure of the earlobe and chin serves to orient the operator in left versus right side procedures. The angle of the mandible, the anterior border of the sternocleidomastoid muscle, and the sternal notch should be clearly visible. Grade 1 complication ● Consequence Hyperextension of the neck. It has been shown that excessive angulation of the neck may result in mechanical compression of the posterior cerebral circulation, and prolonged hyperextension could predispose a patient to stroke and should be avoided. The pathophysiology of stroke, in this instance, is based on the combined effects of endothelial injury in the presence of atherosclerosis. These features lead to up-regulation of the inﬂammatory cascade, vasoconstriction, and subsequent thrombosis and/or arterial occlusion. Arterial dissection secondary to hyperextension has also been described. Individuals identiﬁed with the biologic markers of hypoplasia, carotid and vertebral occlusion, severe stenosis, or prior ischemic vascular disease may be at increased risk and should receive special attention to neck position in the perioperative period.5 Another consequence of hyperextension is loss of the normal orientation of the neurovascular structures in the neck. Grade 1 complication ● Prevention Careful positioning by the operating surgeon is of paramount importance. A thin roll should be placed under the shoulders posteriorly. The head should be supported so as to not hang free and/or move during the procedure and turned carefully away from the operative side. The operating room table should be placed in slightly reversed Trendelenburg position and tilted slightly away from the operative side to allow adequate distal exposure.

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Skin Incision The length of the skin incision is often governed by the morphology of the neck. A vertical skin incision extending from the mastoid process to just above the sternoclavicular junction coursing along the anteromedial margin of the sternocleidomastoid muscle represents the classic skin incision utilized during exposure of the cervical carotid artery (Fig. 58–1). Preprocedure duplex-assisted localization of the carotid bifurcation may be used in order to limit the length of the traditional skin incision to one that may be more esthetically pleasing.6 Alternatively, a transverse cervical incision made along Langer’s lines may be used to gain access to the carotid artery. There is no demonstrable difference in results when comparing the longitudinal and the transverse incisions with similar efﬁcacy and incidence of cranial nerve deﬁcits.7

Limited Exposure ● Consequence Inadequate surgical exposure leading to incomplete hemostasis and inappropriate management of the target lesion are primary concerns when the surgical ﬁeld is limited by the length of the skin incision. In patients with high bifurcations and otherwise challenging anatomy, an abbreviated incision may render the patient at increased risk for intraoperative complication (Fig. 58–2). Grade 1 complication

Figure 58–1 Classic vertical skin incision.

● Repair Additional exposure can be obtained by extension of the incision. Distal exposure is most commonly the

Figure 58–2 Carotid kink: example of challenging anatomy for exposure.

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problem. Care must be taken not to violate the substance of the parotid gland during this maneuver so as to avoid injury to the facial nerve or create a sialocutaneous ﬁstula. Subluxation of the mandible can also aid in very high distal exposure. ● Prevention Whereas preoperative duplex localization may facilitate identiﬁcation of the carotid bifurcation prior to skin incision, these incisions may necessitate the use of excessive amounts of traction in order to adequately mobilize the distal internal carotid artery. Ideally, adequate exposure should include the diseased portion of the common and internal carotid arteries as well as a region on the normal-appearing distal internal carotid artery where vascular clamps may be applied. By compromising adequate exposure, the operator may experience difﬁculty securing an adequate dissection endpoint or may cause inadvertent neurovascular injury, leading to increased patient morbidity.

Dissection and Exposure of the Carotid Artery The skin incision is deepened through to the platysma muscle, and the dissection is carried along the anteromedial border of the sternocleidomastoid muscle until the carotid sheath is reached. Division of the facial vein allows lateral retraction of the internal jugular vein and visualization of the carotid artery. The vagus nerve should be identiﬁed as it courses deep and posterolateral to the common and internal carotid arteries (Fig. 58–3). In a small subset of patients, the vagus nerve may assume an anterior position within the carotid sheath. This must be recognized and the nerve carefully retracted to complete the arterial exposure. During the arterial dissection, caution should be taken to avoid manipulation of the vessels by “dissecting the patient away form the artery.” Mobilization of the internal carotid artery should be extended distally just beyond the region of disease. Anticoagulation is administered prior to obtaining proximal and distal arterial control, beginning with the distal internal carotid artery, followed by the common and external carotid arteries.

Perturbation of the Carotid Baroreceptor ● Consequence The carotid sinus region is an important baroreceptor area involved in blood pressure regulation.8 During dissection of the carotid artery, caution should be exercised to avoid disruption of the carotid sinus nerves (Fig. 58–4). Sinus bradycardia and hypotension may occur owing to baroreceptor stimulation with the possibility of a new setpoint established in the perioperative period. Grade 1 complication

Figure 58–3 Intraoperative dissection with vagus nerve (arrow).

Figure 58–4 (arrow).

Intraoperative dissection with carotid body

● Repair Inject the carotid bulb or control hemodynamic changes with intravenous medications. ● Prevention The efﬁcacy of prophylactic treatment with local anesthetic remains controversial. Maher and coworkers9 showed that injection of lidocaine into the carotid sinus at the time of CEA is not associated with a signiﬁcant improvement in any hemodynamic factor.9 Al-Rawi and colleagues10 also questioned whether application of

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a local anesthetic in the region of the carotid sinus could simulate denervation, thereby validating a neural basis for baroreceptor denervation. They concluded that the baroreceptor response could be abolished by the application of local anesthesia to the carotid sinus and recommended selective usage in patients demonstrating severe sinus sensitivity during CEA.

Cranial Nerve Injury Most nerve injuries that occur during CEA are associated with retraction and are usually self-limiting. In order to minimize the risk of permanent injury, a thorough understanding of the neurovascular anatomy in the vicinity of the carotid artery is mandatory. In the NASCET and ACAS trials, the incidence of cranial nerve injury was 8.6%2 and 4.9%,3 respectively. Both studies showed complete resolution of symptoms in the overwhelming majority of their respective participants. Vagus Nerve Injury ● Consequence The anatomic location of the vagal trunk may vary because approximately 5% of patients may present with a nerve lying anterior to the common carotid artery. Complete vagal transection or ipsilateral recurrent nerve injury results in hoarseness and vocal cord paralysis. Other vagal branches, which are susceptible to injury, include the superior laryngeal and recurrent laryngeal nerves. The superior laryngeal nerve courses posteriorly and just superior to the carotid bifurcation in a tangential plane adjacent to the superior thyroid artery. Injury results in voice fatigue and an inability to reach high-pitched notes. Damage to its internal, sensory, branch may result in aspiration due to a loss of sensory input to the supraglottic mucosa of the larynx. Grade 4 complication ● Repair Ipsilateral nerve injury may go undetected or produce mild postoperative symptomatology. In the published literature, the reported frequency of nerve injury ranges between 3% and 23%.11 Whenever these injuries are suspected, close follow-up and direct laryngoscopy should be used to further clarify the degree of impediment, especially if a contralateral procedure is contemplated. ● Prevention Careful dissection in the carotid sheath while gaining access to the artery with awareness of the anterior vagus anomaly.

Hypoglossal Nerve Injury ● Consequence Upon exiting the skull, the hypoglossal nerve descends posterior to the internal and external carotid arteries

Figure 58–5 (arrows).

Intraoperative dissection with hypoglossal nerve

before coursing in an oblique fashion anteriorly and medially to provide motor innervations to the tongue (Fig. 58–5). Injury to this structure results in ipsilateral tongue deviation. Dysarthria and biting of the tongue have been described in cases of profound dysfunction.11 Exposure of a high-lying plaque in the internal carotid artery often necessitates cephalad retraction, which may result in undue tension being placed on the nerve. Neuropraxia results from such traction injuries and may lead to difﬁculty with speech, mastication, and swallowing. Grade 4 complication ● Repair If an injury to the hypoglossal nerve is recognized intraoperatively, direct repair should be considered often in consultation with otolaryngology or plastic surgery. ● Prevention Injury may be avoided by careful dissection. The hypoglossal can be localized by following the ansa hypoglossi to its junction with the main nerve. The ansa may be ligated along with small vessels providing arterial supply and the venous drainage from the sternocleidomastoid muscle to mobilize the hypoglossal nerve, allowing distal exposure of the internal carotid artery.12 Bilateral nerve injury may result in upper airway obstruction and death.

Marginal Mandibular Nerve Injury ● Consequence This superﬁcial branch of the facial nerve exits from the parotid gland to supply motor innervations to the angle of the mouth. Its usual course is along the inferior ramus of the mandible, but it can be found in more distal locations depending on the patient’s anatomy or neck position. Hyperextension with contralateral neck rotation may lead to injury because the nerve moves caudally when this position is assumed. Most commonly, injury to the marginal mandible nerve is due to

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retraction and results in drooping of the ipsilateral lower lip. Grade 2 complication ● Repair None, as these injuries are often self-limiting. ● Prevention Patients with high carotid bifurcations or extensive distal internal carotid disease who require proximal extension of the skin incision are at increased risk for injury. In these cases, a posterior curving incision may avoid direct nerve injury. Additional self-retaining retractors should be positioned superﬁcial to the platysma muscle, thus avoiding direct contact with the nerve.

Cutaneous Innervation ● Consequence These structures are quite vulnerable to injury during CEA. The greater auricular nerve provides sensory innervation to the earlobe and the angle of the mandible. Injury results in paresthesia in the region of innervation. The transverse cervical nerve provides sensory innervation in the region of the anterior cervical triangle. When this nerve is injured, some men may complain of numbness with shaving in the area of their skin incision. Grade 1 complication ● Prevention There are no speciﬁc therapeutic recommendations for management of cutaneous nerve injuries. Patients should, however, be made aware of these sensory deﬁcits, and appropriate caution must be exercised, for example, while shaving. These lesions are often self-limiting.

Arterial Control Beginning with the internal carotid artery, vascular control should be obtained in a stepwise fashion. This technique serves to reduce the opportunity for distal embolization of atheromatous debris. Occlusion of the common and external carotid arteries should follow sequentially (Fig. 58–6).

Stroke ● Consequence Stroke, the most feared complication of CEA, may occur owing to distal embolization of atheromatous debris or thrombus. Stroke may also occur owing to thrombotic occlusion of the artery. However, neurologic deﬁcits are most frequently due to technical error resulting in cerebral thromboembolization.13 Grade 4 complication

Figure 58–6 Proper vascular control of arteries prior to arteriotomy and endarterectomy.

● Repair Contemporary management remains the subject of debate. Many advocate immediate operative exploration to reestablish ﬂow; others argue that only those patients with suspected thrombosis should be reexplored because this group are the only ones who may stand to beneﬁt from operative intervention.14 Immediate duplex ultrasound imaging can determine whether thrombosis has occurred. If the ultrasound shows normal ﬂow in the carotid circulation, urgent arteriography should be considered to better deﬁne the endarterectomy site and reveal intracranial abnormalities. If imaging reveals any abnormalities, management options include correction of any technical defects such as intimal ﬂaps, irregularities associated with the anastomotic site, removal of platelet aggregates and thrombus, or limited thrombectomy with caution exercised owing to the risk of creating a carotid-cavernous sinus ﬁstula.

58 CAROTID ENDARTERECTOMY ● Prevention Prevention relies on adequate surgical exposure, generous arteriotomies beyond the disease endpoint, meticulous endarterectomy, and patch angioplasty to reduce technical error.15

Evaluation of Intracranial Circulation Whereas many reports attribute postoperative cerebral ischemia to thromboembolic events, cerebral perfusion abnormalities are a cause of stroke during CEA. The intracranial circulation must be assessed and managed by either prophylactic arterial shunting or intraoperative monitoring.

Stroke ● Consequence Stroke. Grade 4 complication ● Prevention Whereas many surgeons routinely use interarterial shunting, thereby avoiding the need to assess distal perfusion, intraoperative monitoring and selective shunting avoid the risks associated with shunt placement. Numerous techniques have been described for the evaluation, monitoring, and prevention of cerebral malperfusion during carotid surgery. Mechanical shunts (Sundt, Plainsboro, NJ; Javid, Tempe, AZ; Inahara-Pruitt, Burlington, MA) are placed in the internal carotid artery, allowing uninterrupted ﬂow from the distal common carotid to the proximal internal carotid artery (Fig. 58–7). The major argument against the use of shunts is the increased risk of dislodging atheromatous debris and subsequent distal embolization leading to stroke. The operation can be performed in the awake patient allowing real-time monitoring of consciousness as a surrogate marker for the adequacy of cerebral perfusion. Stump pressures measure internal carotid artery backpressure. This is an inferred value derived after occlu-

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sion of the common and external carotid arteries. This technique attempts to equate backpressure at the proximal internal carotid artery with the cerebral perfusion pressure. Whereas some report internal carotid artery clamping at mean stump pressures higher than 25 mm Hg, Calligaro and associates16 suggest that stump pressures less than 40 mm Hg systolic should be used as a threshold for carotid shunting when the operation is performed under general anesthesia. In patients with a previous history of stroke or in those with ﬂuctuating systolic blood pressures, stump pressures may not be reliable. Electroencephalography is a noninvasive neuromonitoring technique. It correlates neuronal dysfunction, as seen with cerebral ischemia, as changes in electrical frequency. A diminution in amplitude on electroencephalographic tracings is observed during times of cerebral ischemia. Criticisms offered include the need for continuous monitoring, expert interpretation, and increased cost. Notwithstanding, its use has been well established in the literature.17 Cerebral infrared oximetery is an indirect method used to measure brain oxygen tension. It uses near-infrared spectroscopy through the scalp and skull for continuous noninvasive monitoring of cerebral oxygen saturation (rSO2).18 During CEA, changes in cerebral oxygen saturation may serve as a monitor of oxygenation trends. With carotid cross-clamping, however, an absolute value cannot be recommended.

Arteriotomy There are two types of incisions commonly used during CEA: the longitudinal and the oblique arteriotomies. The longitudinal incision begins at the posterolateral aspect of the distal common carotid artery and extends into the proximal internal carotid artery to include the region of disease. The length of this incision depends on the extent of disease. An oblique arteriotomy is used when the eversion technique is contemplated for exposure of the internal carotid artery. This incision is made in an oblique plane though the junction of the internal and common carotid arteries.

Arterial Injury ● Consequence Arterial injury may occur secondary to inadvertent damage to the back wall of the carotid artery. Grade 2 complication ● Repair Standard arterial repair. Should injury occur, primary repair with interrupted double-armed Prolene sutures is indicated.

Figure 58–7 Shunt in place during endarterectomy.

● Prevention It is important to maintain a bloodless ﬁeld as the arteriotomy is lengthened under direct visualization. These injuries may be avoided if complete vascular control is obtained prior to arteriotomy.

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SECTION X: VASCULAR SURGERY When eversion CEA is chosen, an oblique incision is used, and the endarterectomy endpoint is achieved in a similar fashion. First, the proximal internal carotid artery is transected. A dissection plane is established in the transected internal carotid artery, followed by gentle peeling away of the remaining media and adventitia from the atheroma until an endpoint is reached.

High Carotid Bifurcation ● Consequence Need for additional distal exposure. Grade 1 complication

Figure 58–8 Shunt in place and arrows show the endpoint of plaque where the dissection plane will be developed for endarterectomy.

● Repair One of the current indications for carotid artery stenting is a surgically inaccessible lesion; those appearing at or above C2 or inferior to the clavicle are considered at high surgical risk and may be treated with catheterbased endovascular techniques.20 Adjunctive techniques used to gain access to distal lesions may include division of the posterior belly of the digastric muscle and subluxation of the mandible, which may provide an additional 1.5 cm of distal exposure.

Difﬁcult Endpoint ● Consequence Need for additional distal exposure or extended arteriotomy to safely perform the CEA. Grade 1 complication

Figure 58–9 Completion endarterectomy with all plaque and medial ﬁbers removed from the wall of the carotid artery.

Endarterectomy Removal of atheromatous debris from the internal carotid artery should be done in a careful and methodical fashion. A dissection plane is developed, either in the common carotid artery or at the level of the endpoint in the distal internal carotid, that ensures the proper plane. This plane is established between the diseased intima and the circular ﬁbers of the arterial media19 (Fig. 58–8). The plaque is removed and can be divided if necessary in an area where there is a smooth transition to normal-appearing intima. Tacking sutures are required in 25% to 30% of cases to ensure a smooth endpoint that does not lift up when prograde arterial ﬂow is established. Residual plaque involving the external carotid artery is removed using the eversion technique. Great care must be taken to remove all residual medial ﬁbers from the endarterectomy surface (Fig. 58–9).

● Prevention Selecting the proper dissection plane is crucial to establishing a smooth distal transition point. The ideal plane is achieved when there is a gradual feathering of the atheromatous intima/media from the remaining artery. In some instances, this plane may be illusive, if not impossible, to establish owing to plaque morphology, which may include ruptured or ulcerated debris with and without thrombus. In these instances, tacking sutures may be necessary in order to secure any step-off created during dissection and to minimize the risk of distal propagation of the dissection plane.

Patch Angioplasty The efﬁcacy of patch angioplasty for arteriotomy closure after CEA is well established in the literature. Patch closure has been demonstrated to be superior to primary closure in prospective randomized comparisons. AbuRahma and colleagues21 reported lower incidence of perioperative morbidity; stroke, early restenosis, and acute postoperative thrombosis when patch closure was utilized. In an analysis of patch angioplasty, Bond and coworkers22 showed no obvious differences in the risk of stroke or death in patients receiving synthetic versus venous patches.22 Commonly used prosthetic materials include

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of suture line bleeding, attention to blood pressure control cannot be overemphasized.

Wound Closure Hemorrhage ● Consequence Systemic heparinization and widespread usage of antiplatelet agents singularly or in combination may contribute to incomplete hemostasis and hematoma formation in patients undergoing CEA. Hematomas may be benign or potentially life threatening if airway compromise ensues. Grade 4 complication

Figure 58–10 Patch angioplasty with Dacron patch (above) and vein patch (below).

autogenous vein, polytetraﬂuoroethylene (PTFE), Dacron, and bovine pericardium (Fig. 58–10).

Long Arteriotomy ● Consequence Suture line folds and kinks. Grade 3 complication ● Repair Repeat anastomosis properly. ● Prevention Patch angioplasty should be applied in a manner that avoids suture line folds and kinks. The length of the arteriotomy should be limited to that which is necessary to safely remove the endarterectomized plaque burden. Long arteriotomies may cause suture line kinking and subsequent disruption of ﬂow patterns. Suture line irregularities may also result in generation and adhesion of microthrombi, leading to an increased incidence of thromboembolism.

Suture Line Bleeding ● Consequence Most frequently associated with PTFE prosthetic patches and suboptimal surgical technique. Grade 3 complication ● Repair Careful anastomotic technique. ● Prevention Bleeding may be successfully treated with the application of topical hemostatic agents. In the management

● Repair Careful surgical hemostasis. Surgical reexploration and evacuation of symptomatic hematomas should always be considered. The incision should be reopened in the operating room, if possible, where airway management is critical. Consideration should be given to tracheostomy at the time in the setting of a large hematoma and subsequent neck tissue edema. ● Prevention Whereas most surgeons do not reverse systemic anticoagulation because of the risk of potentially deleterious neurologic events, there is no substitute for good surgical technique. To reduce the potential for perioperative bleeding and subsequent hematoma formation, blood pressure control and utilization of temporary suction drains are adjuncts toward reducing the morbidity associated with hematoma formation.

CAROTID STENT—SUPPORTED ANGIOPLASTY Application of minimally invasive endovascular techniques to carotid artery disease represents an alternative management option in the treatment of the extracranial internal carotid artery. Carotid artery stenting with cerebral protection has emerged as an alternative for some patients possessing signiﬁcant extracranial carotid stenosis but who are considered at increased surgical risk. During this procedure, access to the carotid artery is obtained percutaneously through a puncture site in the femoral artery. Under direct visualization, guidewires and catheters are used to negotiate the aortic arch and to traverse the internal carotid artery. An appropriately sized metal stent is introduced and deployed across the diseased portion of the artery, excluding this region from the circulating blood ﬂow, thus creating a new unobstructed lumen. Although this procedure is performed while the patient is awake, both groups receive similar postprocedure monitoring. There is a large amount of enthusiasm for carotid stent– supported angioplasty often supported by physicians who

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have no prior experience in the evaluation, treatment, or follow-up of patients with extracranial cerebrovascular disease. The same principles crucial to carotid surgery certainly apply to carotid intervention: careful patient evaluation and selection, specialized clinical training and practice, and careful follow-up and outcomes analysis. Interventional techniques for carotid therapy continue to develop, although typically they are compared with the most unfavorable ﬁgures available in the medical literature for CEA. There are several published series with over 100 consecutive cases of elective CEA or statewide registries that demonstrate perioperative stroke rates less than 3%.23,24 There are surgical series with acute stroke rates less than 1% and 5-year follow-up documenting lower than 1% ipsilateral stroke rate per year during follow-up.25 Whereas proponents of interventional therapies are quick to note cranial nerve palsy, they fail to note that this small group of patients usually experiences only a very mild and transient palsy from operative nerve retraction and protection. The case for endovascular approaches to coronary occlusive disease or aortic aneurysms is far more compelling because the open surgical alternative is a more invasive and morbid option. This is not the case for carotid intervention. Carotid surgery is less invasive with respect to the diseased vascular tissue manipulated than is the transfemoral approach. Time to discharge and intensive care unit stay are often less for carotid endarterectomy than for carotid stenting. The cost of CEA is stable and low, whereas the costs associated with carotid stenting continue to grow with the addition of distal protection devices and the advent of drug-coated stent technology. One must also consider the complications unique to a remote approach to the carotid bifurcation. These include femoral access site complications, lower extremity ischemic and embolic events, renal and visceral embolic events, cerebrovascular emboli via the nonoperated carotid and vertebral vessels, and the arrhythmias induced by stenting the baroreceptor at the carotid bifurcation. These complications are rarely reported because they are unique to carotid stenting and are, therefore, not characterized in the literature of CEA, which is used as the predicate for carotid stenting. Stenting of the baroreceptor at the carotid bifurcation alone results in a signiﬁcant incidence of bradycardia requiring intravenous medications and intensive care unit admission. Indeed, most series have a higher rate of intensive care unit admission and multiday admission for stenting than is typical for CEA. The primary method of intervention (i.e., dilation and plaque disruption) produces emboli known to be responsible for cerebral events in patients with carotid bifurcation disease. Studies with transcranial Doppler have documented an eightfold increase in emboli during angioplasty and stenting procedures versus CEA.26 There has been a proliferation of “protection devices” to prevent periprocedural emboli; however, the addition of each new device and

technical aspect to the procedure adds risks and additional cost. The rate of restenosis also remains a long-term issue, although in the carotid, the expectation of a low restenosis rate is good: high ﬂow, large lumen, short diameter. However, there are factors that would affect the rate of restenosis, such as stent design and construction (i.e., rigidity, cell size, metal composition), with an often tortuous artery in a mobile and compressible location. We also know that stent apposition is often poor at a bifurcation where there is a sudden and dramatic change in lumen diameter (common carotid to the internal carotid). There is well-recognized restenosis at the end of stents (“edge effect”) that has not been characterized in the distal internal carotid near the skull base. When restenosis occurs, the options can be limited compared with options for restenosis after CEA. Repeat interventional therapy involves attempts at redilation with additional stenting. Surgical exposure requires a more extensive exposure of the carotid vasculature, particularly the more difﬁcult cephalad portion near the skull base.27

SUMMARY CEA is one of the most highly scrutinized, studied, and ultimately successful operative procedures available. At this time, carotid stenting is most applicable to patients with higher risk factors for surgical exposure of the carotid (e.g., prior radiation, prior carotid surgery, adjacent stomas, skull base lesions). Clinical trials in groups without those risk factors will ultimately determine the role of stenting in those patients. Other distinct patient groups will likely be delineated as reasonable candidates for primary carotid stenting but we are also likely to ﬁnd those who are at distinctly higher risk for carotid stenting (e.g., tortuous carotids, bulky irregular lesions, longer lesions, certain calciﬁc lesions). The efﬁcacy of CEA in stroke prevention is well established in the literature. A thorough understanding of the local anatomy, anatomic variances, meticulous surgical technique, and innovations in intraoperative monitoring will allow CEA to preserve its position as the reigning “gold standard” in the treatment of carotid disease.

REFERENCES 1. American Heart Association. Heart and stroke facts. Available at http://www.americanheart.org (assess veriﬁed 1/25/07). 2. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneﬁcial effects of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325:445–453. 3. Endarterectomy for asymptomatic carotid artery stenosis. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. JAMA 1995;273:1421–1428.

58 CAROTID ENDARTERECTOMY 4. Department of Health and Human Services, Center for Medicare and Medicaid Services. Summary report, ICD-9CM Coordination and Maintenance Committee, April 1–2, 2004. Available at http://www.cms.hhs.gov/ paymentsystems/icd9 (access veriﬁed 1/25/07). 5. Weintraub MI, Khoury A. Cerebral hemodynamic changes induced by simulated tracheal intubation: a possible role in perioperative stroke?: magnetic resonance angiography and ﬂow analysis in 160 cases. Stroke 1998;29:1644– 1649. 6. Ascher E, Hingorani A, Marks N, et al. Mini skin incision for carotid endarterectomy (CEA): a new and safe alternative to the standard approach. J Vasc Surg 2005;42: 1089–1093. 7. Skillman JJ, Kent KC, Anninos E. Do neck incisions inﬂuence nerve deﬁcits after carotid endarterectomy? Arch Surg 1994;129:748–752. 8. Eckberg DL, Sleight P. Human baroreﬂexes in health and disease. In Baroreﬂex Anatomy. Oxford, England: Clarendon, 1992; pp 19–31. 9. Maher CO, Wetjen NM, Friedman JA, et al: Intraoperative lidocaine injection into the carotid sinus during endarterectomy. J Neurosurg 2002;97:80–83. 10. Al-Rawi PG, Sigaudo-Roussel D, Gaunt ME. Effect of lignocaine injection in carotid sinus on baroreceptor sensitivity during carotid endarterectomy. J Vasc Surg 2004;39:1288–1294. 11. Schauber MD, Fontenelle LJ, Solomon JW, et al. Cranial/cervical nerve dysfunction after carotid endarterectomy. J Vasc Surg 1997;25:481–487. 12. Knight FW, Yeager RM, Morris DM. Cranial nerve injuries during carotid endarterectomy. Am J Surg 1987; 154:529–532. 13. Riles TS, Imparato AM, Jacobowitz GR, et al. The cause of perioperative stroke after carotid endarterectomy. J Vasc Surg 1994;19:206–216. 14. Aburahma AF, Robinson PA, Short YS. Management options for post carotid endarterectomy stroke. J Cardiovasc Surg 1996;37:331–336. 15. Rockman CB, Jacobowitz GR, Lamparello PJ. Immediate reexploration for the perioperative neurologic event after carotid endarterectomy: is it worthwile? J Vasc Surg 2000; 32:1062–1070. 16. Calligaro KD, Dougherty MJ. Correlation of carotid stump pressure and neurologic changes during 474 carotid

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endarterectomies performed in awake patients. J Vasc Surg 2005;42:684–689. Reuter NP, Charette SD, Sticca RP. Cerebral protection during carotid endarterectomy. Am J Surg 2004;188:772– 777. Casati A, Spreaﬁco E, Putzu M, et al. New technology for noninvasive brain monitoring: continuous cerebral oximetry. Minerva Anestesiol 2006;72:605–625. Moore WS, Quiñones-Boldrich WJ, Krupski WC. Indications, surgical technique and results for repair of extracranial occlusive lesions. In Rutherford RB (ed): Vascular Surgery, 6th ed. Philadelphia: Elsevier Saunders, 2005; pp 1789–1822. Yadav JS, Wholey MH, Kuntz RE, et al, and the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy Investigators. Protected carotid artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004;351:1493–1501. AbuRahma AF, Khan JH, Robinson PA, et al. Prospective randomized trial of carotid endarterectomy with primary closure and patch angioplasty with saphenous vein, jugular vein, and polytetraﬂuoroethylene: perioperative (30-day) results. J Vasc Surg 1996;24:998–1007. Bond R, Rerkasem K, Naylor R, et al. Patches of different types for carotid patch angioplasty. Cochrane Database Syst Rev 2004;(2):CD000071. Yates GN, Bergamini TM, George SM, et al. Carotid endarterectomy results from a state vascular society. Am J Surg 1997;173:342–344. Mayo SW, Eldrup-Jorgenson J, Lucas FL, et al. Carotid endarterectomy after NASCET and ACAS: a statewide study. J Vasc Surg 1998;27:1017–1023. Hallet JW, Pietropaoli JA, Ilstrup DM, et al. A comparison of NASCET trial and population based outcomes for carotid endarterectomy. J Vasc Surg 1998;27:845– 851. Jordan WD, Voellinger DC, Doblar DD, et al. Microemboli detected by transcranial Doppler monitoring in patients during carotid angioplasty versus carotid endarterectomy. Cardiovasc Surg 1999;7:33–38. Vale FL, Fisher WS, Jordan WD, et al. Carotid endarterectomy performed after progressive carotid stenosis following angioplasty and stent placement. J Neurosurg 1997;87:940–943.

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Aortic Surgery John Byrne, MB and R. Clement Darling III, MD INTRODUCTION Aortic reconstruction is an index operation, one whose outcome is used to compare surgeons and centers. With validated tools, the surgeon can be made the statistical variable.1 In an era of ranking and league tables, there are obvious implications. For patients, the implications are more critical. But aortic surgery is difﬁcult. Even in the best hands, complications occur. Despite the advent of endovascular procedures, there are still those who are unsuitable for, or unwilling to undergo, stent grafting, and even this procedure is not without complications. Infrarenal aortic surgery can be divided into three areas: (1) aortobifemoral bypass for occlusive disease, (2) elective abdominal aortic aneurysm (AAA) repair, and (3) repair of ruptured AAAs. There are two approaches to the aorta: transabdominal and retroperitoneal. In this chapter, we describe how we do aortic surgery at Albany Medical Center, by the retroperitoneal approach. We share the strategies we use to minimize complications. More pertinently, we describe what we do when complications arise. Young surgeons will read of these and doubt their relevance. Older surgeons will read them and empathize. In the surgical literature, papers detailing success outnumber those documenting failure. Therefore, much of this chapter is based on our own complications or dealing with the aftermath of others’. We use the retroperitoneal approach for all aortic repairs including ruptured aneurysms.2 We accept this is a minority practice. Most aortic surgery is performed via a transperitoneal approach. Despite our bias, we still employ the transabdominal approach when other pathology needs to be addressed at the same operation. However, before describing techniques in detail, it is worthwhile addressing some recurring arguments.

CONTINUING CONTROVERSIES End-to-Side or End-to-End Anastomosis in Aortobifemoral Bypass? (Fig. 59–1) In Europe, the end-to-side anastomosis is favored. In North America, end-to-end is preferred. It is argued that

an end-to-end anastomosis is easier to perform. It is more anatomic and avoids competitive ﬂow between the graft and the native arteries. Therefore, it ought to have better patency and carry low risk for duodenal ﬁstulas. The argument in favor of the end-to-side approach is that it preserves anterograde ﬂow to the pelvic viscera, and in the event of graft occlusion, the patient’s status reverts to that prior to surgery rather than being profoundly worse, as might be the case if an end-to-end anastomosis occluded. Both opinions steer clear of the facts. There have been randomized, controlled studies comparing both approaches. An initial study of 79 patients in 1982 from Chicago showed small but signiﬁcant advantages for endto-end anastomoses over end-to-side.3 However, a larger study from Becquemin’s group4 in Paris in 1990 of 158 patients refuted this, as did a study from Toronto of 120 patients.5 The most impressive statistic, however, was just how durable aortic bypasses were, regardless of the means used to sew them together. Actuarial primary 5-year patency rates were 90%. Secondary patency rates were 98%. So there is really little to choose between either approach. The best advice came from the French who suggested that “as we could not ﬁnd any difference between the results in the two groups, we suggest choosing the simplest procedure which maintains adequate pelvic and colonic blood supply, according to angiographic ﬁndings.”

Polytetraﬂuoroethylene or Dacron? Most centers use Dacron for aortic surgery. These grafts are either knitted collagen-coated or knitted gelatincoated. Woven Dacron grafts are not widely used now. The alternative is expanded stretch polytetraﬂuoroethylene (PTFE). Since 1991, we have used stretch Gore-Tex grafts for all our aortic anastomoses. Concerns about needle hole bleeding are unfounded. We ﬁnd that stretch PTFE has handling characteristics that are at least as good as those of Dacron. Theoretically, PTFE is also less likely to dilate over time. Again, there are good randomized, controlled data comparing the various materials. A well-performed prospective study from Cornell in 1995 compared PTFE and

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Figure 59–1 End-to-side aortobifemoral bypass with Dacron.

Dacron and showed no difference in outcomes.6 A large multicenter, prospective, randomized, controlled trial of gelatin-impregnated Dacron, collagen-impregnated Dacron, and PTFE involving 315 patients from Vienna in 2001 also failed to show a difference.7

Clamp the Aneurysm Neck or the Common Iliacs First? The sequence of applying clamps to AAAs has exercised some of the better minds in vascular surgery. Whether to clamp the proximal neck prior to the iliacs or vice versa? At the outset, we should declare an interest—we always clamp the iliacs ﬁrst in elective cases. There are two questions: (1) Does clamping the iliacs ﬁrst protect against emboli traveling down the leg? (2) Does clamping the aortic neck ﬁrst protect against embolization to the renal and visceral arteries from the aortic sac? A study from Leicester in the United Kingdom in 2004 examined the ﬁrst question by comparing the rate of embolization down the superﬁcial femoral arteries of patients undergoing aortic surgery using a transcranial Doppler.8 They showed no difference between the “aortaﬁrst” group and the “iliacs-ﬁrst” group. The second question was most recently addressed by the Monteﬁore Medical Center study in 1999.9 Although this was an animal study in nonatherosclerotic aortas, they suggested that clamping the aorta ﬁrst could protect against embolization to the renal arteries.

Retroperitoneal or Transperitoneal? (Fig. 59–2) Why do we favor the retroperitoneal approach? Aside from the theoretical considerations of quicker return of bowel and respiratory function, we feel it is more versatile. It provides easy access to the left common iliac and internal iliac arteries. Once mastered, it also provides easier access to the left renal artery and the aortic neck. It avoids the left renal vein, which is reﬂected anteriorly out of the operative ﬁeld, and also avoids the gonadal veins, which

Figure 59–2 Transperitoneal exposure of an abdominal aortic aneurysm (AAA).

can be a problem when the aorta is approached from the front. Many of the aneurysm repairs we perform are those rejected for endovascular repair and are really juxtarenal or suprarenal aneurysms. Suprarenal clamping, therefore, becomes an important issue. Once the lumbar branch of the left renal vein is ligated and the peritoneal contents and kidney are retracted cephalad and medial, access to the infradiaphragmatic aorta can easily be obtained by incising the left crus. This allows the proximal aortic clamps to be placed above, below, or between the renals as well as on the supraceliac aorta. However, the procedure has a deﬁnite learning curve. Using a left ﬂank incision, access to the right common and internal iliac arteries is difﬁcult and, in many cases, impossible. To access these vessels, we perform a separate right counterincision. Reimplantation or bypass of the right renal artery, when required, is also technically difﬁcult but can be performed with experience.10 The retroperitoneal approach is more time-consuming when performing a straightforward infrarenal tube graft. The areolar tissue around the aorta is also vascular and can result in blood loss that is usually not encountered in the conventional approach. There are randomized, controlled data. Initial reports were equivocal. In 1990, the Massachusetts General Hospital group showed little difference in outcomes between the two techniques.11 However, in 1995, Sicard and coworkers12 reported the results of a randomized, controlled trial of 145 patients. Whereas there was no difference in mortality rates, the retroperitoneal approach was associated with fewer postoperative complications, shorter hospital and intensive care stays in the hospital, and lower cost. In 1999, Kirby and colleagues13 from Atlanta reported on 92 high-risk American Society of Anesthesiologists Class IV (ASA IV) patients randomized to either transabdominal or retroperitoneal aortic repair. Complications were signiﬁcantly lower in the retroperitoneal group. So, it would seem that proponents of the retroperitoneal approach, including ourselves, are vindicated by the literature. Unfortunately, in the interests of balance, we must also include Lawrence-Brown and associates’ trial

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from Perth in 199714 involving 100 patients that showed no difference at all between the two techniques. In the end, it seems that either approach is justiﬁed as long as outcomes are acceptable and pitfalls avoided.

Aortobifemoral Bypass by the Retroperitoneal Approach INDICATIONS Severe aortoiliac occlusive disease resulting in ● Limiting claudication in a young patient ● Rest pain or nonhealing wounds ● Leriche’s syndrome

Figure 59–3 Patient positioning for an aortobifemoral bypass with the incisions marked.

In higher-risk patients unsuitable for endovascular procedures, consideration should be given to iliofemoral bypass or extra-anatomic bypasses: femorofemoral, iliofemoral crossover, or axillofemoral bypass.

OPERATIVE STEPS The left ﬂank approach was ﬁrst described by Williams and coworkers at Johns Hopkins in 1980.15 They described an incision through the 11th intercostal space with division of the left crus of the diaphragm. Our technique is based on this original description. We do not use the so-called anterior retroperitoneal approach of Schumacker, whereby the retroperitoneal space is developed using a vertical midline incision.16 Step Step Step Step

1 2 3 4

Step 5 Step 6 Step 7 Step 8

Patient positioning Exposure of both femoral arteries Left ﬂank skin incision Reﬂection of peritoneum and creation of retroperitoneal space Dissection of aorta Fashioning of proximal anastomosis Tunneling of graft limbs and performing femoral anastomoses Inspection of peritoneal cavity and closure of ﬂank incision

Figure 59–4

Skin markings for an aortobifemoral bypass.

shoulders angled at 45o. The trunk is supported in this position using a beanbag that extends from the hips to the shoulder. This is made ﬁrm once the patient’s position is correct. Care is taken to place the hips over the break in the table. The left hip is ﬂexed, and the knee and lower leg are supported on a beanbag. The right hip is externally rotated and the knee is ﬂexed (frog-legged). The table is broken. An indelible marker is used to draw the incision. The landmarks are the 10th intercostal space (just above the last ﬂoating rib) and a point midway between the symphysis pubis and the umbilicus along the lateral margin of the rectus abdominis muscle.

OPERATIVE PROCEDURE Incision Too Low

Patient Positioning (Figs. 59–3 and 59–4) This may seem pedantic. However, poor positioning for the retroperitoneal approach can transform a relatively straightforward operation into a miserable experience for all concerned. The patient is placed in the left lateral position with the hips angled at 30o to the horizontal and the

● Consequence Placing an incision too low makes access to the aortic neck difﬁcult, if not impossible. Time spent marking the incision is time well spent, especially when learning this approach. Grade 1 complication

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SECTION X: VASCULAR SURGERY femoral fascia and then dissect medially, lifting the inguinal nodes medially until the common femoral artery is encountered. The superﬁcial epigastric artery is frequently encountered coming anteriorly off the common femoral artery 1 to 2 cm below the inguinal ligament.

Femoral Neuropathy

Figure 59–5 Exposure of both femoral arteries followed by exposure of the aorta.

● Repair Taking the incision more posterior will allow for more upward exposure. ● Prevention Attention to anatomic landmarks and careful marking of the incisions preoperatively.

● Consequence The femoral nerve supplies sensory branches to the skin of the anterior thigh and also via the saphenous nerve to the lateral aspect of the lower leg. More importantly, it also supplies motor branches to the quadriceps femoris. Damage results in signiﬁcant loss of knee ﬂexion. Grade 4 complication ● Prevention Careful placement of the skin incision. The position of the incision is as already described. The femoral nerve has already divided into several branches at this level. All major branches are lateral to the artery and deep to the lymph nodes. Judicious use of electrocautery at this level will also reduce the risk of inadvertent nerve injury.

Left Flank Skin Incision (See Fig. 59–5) Exposure of Both Femoral Arteries (Fig. 59–5; see also Fig. 59–4) We also mark the position of the femoral arteries on the skin prior to draping. The exaggerated position of the patient for this procedure can obscure the normal surface anatomy and result in unnecessarily large groin incisions. We perform a node-sparing femoral incision to reduce the risk of postoperative lymphatic ﬁstulas.

Lymphatic Leak ● Consequence Many lymphatic ﬁstulas are self-limiting and eventually seal spontaneously. However, particularly persistent leaks may require intervention. Grade 2/3 complication ● Repair Persistent leaks can be explored. We inject disulfan blue into the lower thigh just prior to surgery. This enables us to identify the leak. We then oversew the leaking lymphatic with a Vicryl suture. ● Prevention Careful placement of the skin incision. The position of the incision is the junction of the lateral two thirds and the medial one third of the inguinal ligament (identiﬁed by the pubic tubercle medially and the anterior superior iliac spine laterally). We identify the superﬁcial

The skin is incised and the subcutaneous fat divided using electrocautery. The ﬂank muscles (external oblique, internal oblique, and transversus abdominis) and the transversalis fascia are divided using electrocautery to minimize bleeding. The peritoneum is exposed laterally. Medially, it is fused to the overlying muscle layers and can be more easily breached. All efforts are made to gently dissect the peritoneum off the overlying muscle and the tissues of the abdominal wall without tearing it. When dividing the muscle layers medially, the rectus sheath is not usually divided.

A Tear in the Peritoneum ● Consequence A small opening in the peritoneum can quickly develop into a large one with herniation of the small bowel into the operative ﬁeld, requiring extensive manipulation of the bowel to reduce it back into the peritoneal cavity. This defect can then be extremely difﬁcult to close. Grade 1 complication ● Repair Any breach in the peritoneum can usually be repaired with 2-0 or 3-0 Vicryl. ● Prevention Start dissecting the peritoneum laterally. Frequently, the peritoneum is more adherent to the overlying

59 AORTIC SURGERY muscles medially. Immediately repair any small tear in the peritoneum because, as the operation proceeds, these can quickly develop into larger holes.

Reﬂection of the Peritoneum and Creation of the Retroperitoneal Space (Figs. 59–6 and 59–7) The peritoneum usually can be swept off the underlying adipose tissue and the lateral abdominal wall muscles fairly easily. It is easier to sweep the peritoneum from the iliac vessels ﬁrst and then move superiorly and laterally. The peritoneum is swept off the psoas muscle. Next, the left kidney is displaced anteriorly. The connective tissue strands anchoring the peritoneum to the lateral abdominal wall are sharply divided. Some of these are reasonably vascular and need to be cauterized. We now position our Bookwalter retractor. Others may use an OmniTract or similar self-retaining retraction device. At this stage, the aorta can usually be palpated, although it will be encased in areolar tissue. This is sharply dissected off the underlying aorta. The left ureter is identiﬁed at this stage, although usually it does not impinge on the operative ﬁeld.

601

Splenic Laceration ● Consequence If, at any stage during surgery, an unexplained drop in blood pressure occurs, injury to the spleen should be suspected. Grade 4 complication ● Repair Usually mandates splenectomy, which can be performed via the left ﬂank incision. ● Prevention Careful placement of the retractors is key. We always try to ensure that the blades of the Bookwalter retractor are angled towards the patient’s right shoulder and away from the left upper quadrant of the abdomen where the spleen lies. Thus, direct compression of the spleen is avoided.

Duodenal Injury ● Consequence Duodenal injury. Grade 4 complication ● Repair Duodenal injury will manifest itself by a ﬁstula several days after surgery. Whereas the ﬁstula itself may seal after a few days, the consequence will be an infected graft. ● Prevention We avoid placing the blades of the retractor directly in contact with the underlying tissues, but instead, try to protect them with abdominal swabs. The key, though, is awareness of the possibility of these complications.

Dissection of the Aorta Figure 59–6 The left ureter is always identiﬁed and carefully preserved.

Figure 59–7

Placement of a Bookwalter retractor.

For an aortobifemoral bypass, dissection is conﬁned to the aorta between the inferior mesenteric artery and the renal arteries. As well as avoiding unnecessary dissection, it also reduces the danger of injury to the superior hypogastric plexus with its attendant effects on sexual function in the male. Several lumbar arteries and veins may be encountered at this level, and these are either ligated or surgically clipped. Dissection is carried behind the aorta, and all areolar tissue is also cleared anteriorly. In patients with a total occlusion of the aorta to the level of the renal arteries, one must clamp the aorta and both renal arteries prior to dividing the aorta. Here, it will be necessary to dissect the suprarenal aorta. To do this, the left crus of the diaphragm is divided. With more dissection, it is possible to place a clamp around the aorta. The left renal artery should also be readily apparent at this stage. The right renal artery requires more dissection. With ﬂush occlusions of the aorta to the level of the renals, removal of the plug of atheroma from the aorta has been likened to popping the cork from a bottle of wine. This is not always

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the case. Sometimes, it can be removed only in piecemeal fashion.

Inferior Vena Cava Injury ● Consequence Life-threatening hemorrhage. Grade 4 complication ● Repair The traditional teaching, often forgotten in the heat of battle, is to use two spongesticks: one proximal to the injury and one distal. The inferior vena cava (IVC) is then repaired using a Prolene suture. However, it is also useful to have an experienced helper with two large suctions who realizes the gravity of the situation. If the posterior wall has also been penetrated, it may be necessary to mobilize a segment of the IVC. ● Prevention Careful dissection is again key in this situation.

Fashioning of the Proximal Anastomosis Following administration of heparin (usually in the range of 3000 IU), the aorta is cross-clamped using two Fogarty aortic clamps. The aorta is transected, and any lumbars are sutured or clipped. The distal aorta is oversewn using 3-0 Prolene suture and the clamp removed. A bifurcated Gore-Tex graft is brought into the operating ﬁeld and trimmed. An end-to-end anastomosis is fashioned using a 3-0 running stitch. We then position a clamp distal to the anastomosis and check the anastomosis to ensure that it is hemostatic. Frequently, at this stage, we place thrombin-impregnated Gelfoam around the proximal anastomosis, although this is not of much help if a large leak occurs in the proximal suture line.

Suture Line Bleed ● Consequence The consequence is bleeding, often life-threatening. Grade 1 complication ● Repair Reinforce the suture line with further 3-0 Prolene sutures. Sometimes, it is more useful to use a smaller suture such as a 4-0 or even a 5-0 for particularly troublesome bleeds. Some have also described, albeit anecdotally, placing a tube of Dacron or Gore-Tex over the suture line in bad bleeds in which nothing else has helped. ● Prevention Careful attention to anastomotic technique.

Tunneling of Graft Limbs and Femoral Anastomoses (Fig. 59–8) This is a blind procedure. The initial several centimeters of the tunnels can be performed under direct vision from

Figure 59–8 Tunneling of the aortic graft.

the groin incisions. The tunnels are fashioned in an anatomic fashion, which means staying as close to the native vessels as possible. The femoral anastomoses are then performed using 6–0 Prolene suture in a standard parachute fashion.

Venous Injury ● Consequence The most easily injured vein is the deep circumﬂex iliac vein, which crosses in front of the external iliac artery approximately 2 cm above the inguinal ligament to join the external iliac vein. To avoid this, the ﬁrst 1–2 centimeters of the tunnel from the groin should be completed under direct vision. If this vein is injured, it can result in troublesome bleeding, which needs to be addressed. Grade 1 complication ● Repair If the deep circumﬂex iliac vein is injured, it needs to be repaired. Often, direct suture repair is required, although occasionally the use of large Ligaclips can be effective. ● Prevention The initial several centimeters of the tunnel from the groin should be completed under direct vision. The

59 AORTIC SURGERY tunnel should be made as close to the native artery as possible.

Bleeding from the Tunnel ● Consequence This can be a problem in patients in whom postoperative anticoagulation needs to be reinstigated fairly quickly such as those with prosthetic mitral valves. Very often, it is self-limiting, but it can result in the loss of several units of blood. Grade 1 complication ● Repair If bleeding is noticed at the time of surgery, of course the source of the bleeding should be found and addressed. If found postoperatively in a stable patient (e.g., on computed tomography [CT]), it can be managed conservatively like most retroperitoneal bleeds. ● Prevention See “Prevention” under “Venous Injury,” earlier.

Bowel Injury ● Consequence This is the nightmare scenario of blind tunneling. This was reported in the 1960s,17–19 but has not been admitted to since. Grade 4/5 complication There is little choice but to deal with this in the manner of any infected graft with explantation of the graft and either direct reconstruction with femoral vein or by means of bilateral axilloprofunda bypasses. ● Prevention Ensure that the tunnel remains extraperitoneal and that, in the pelvis, the tunnel is made as posterior as possible, avoiding inadvertent injury to the cecum on the right or the sigmoid colon on the left.

Inspection of the Peritoneal Cavity and Closure of the Flank Incision Inspect the peritoneal cavity. Free blood may alert to a splenic laceration or intra-abdominal catastrophe. Ischemic bowel may alert to the need for reimplantation of the inferior mesenteric artery. Inspect the ureter. It is usually placed under some tension in this exposure. In older patients with less elastic tissue, it can rupture. Sweep the peritoneum away from the muscle layers to prevent peritoneum (and sigmoid colon) being incorporated into the muscle closure. On at least two occasions that the authors know of, this has occurred, resulting in an infected graft in the ﬁrst case and a fecal ﬁstula with need for a Hartmann’s procedure in the second.

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Division of the Ureter ● Consequence Either inadvertent cutting of the ureter or, more likely, a traction injury resulting in the ureter being torn apart. A retrievable situation if recognized immediately, with few immediate implications for the patient or the graft. If not recognized until urine is found leaking from the ﬂank wound several days later, the prognosis is less favorable, with a high risk of graft infection. Grade 1 complication if recognized immediately, grade 3 complication if recognized several days postoperatively ● Repair Call for a urologist. Repair involves insertion of a double-J stent, with suture repair of the ureter over the stent using Vicryl suture. Alternatively, it may be necessary to reimplant the ureter into the bladder or even perform a ureteroureterostomy. ● Prevention Awareness of the condition is key. Also, it is mandatory to inspect the ureter at the end of surgery to ensure the left ureter is intact. This is treatable if identiﬁed in the operating room.

Bowel Injury/Fecal Fistula ● Consequence Fecal peritonitis carries a high mortality rate. Aortic graft infection also has a high morbidity. These two complications in tandem, therefore, have a particularly poor prognosis. Grade 4/5 complication ● Repair Help will be needed from a colorectal surgeon. Usually, the ﬁrst indication of this complication is a fecal ﬁstula or peritonitis several days postoperatively. The patient usually requires a Hartmann’s procedure. If graft contamination has occurred, the infected graft must be removed with either in situ revascularization with femoral vein or extra-anatomic revisualization by axillofemoral bypasses. ● Prevention Closure is best performed after sweeping the peritoneum away from the overlying muscle layers, ensuring that good bites are taken through muscle rather than peritoneum.

Postoperative Small Bowel Obstruction Due to Herniation through the Posterior Sheath of the Rectus Abdominis ● Consequence A rare complication, but one best avoided and easily mistaken for post-operative ileus. If the posterior rectus

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sheath is opened and not adequately closed at the end of surgery, small bowel can herniate through the newly formed oriﬁce and incarcerate. Grade 3 complication ● Repair The incarcerated incisional hernia needs to be repaired in the same manner as any other incisional hernia, using either primary or mesh closure. ● Prevention Awareness of the potential for this to occur and scrupulous attention to abdominal wound closure.

Flank Bulge ● Consequence A minority of patients will notice a bulge in their left ﬂank after their wound heals. This can be uncomfortable for patients. The patient may even be referred to a general surgeon by their primary care doctor for repair of an incision hernia. This is in fact ﬂaccid denervated abdominal wall musculature. Grade 2 complication ● Repair No repair. Avoid the temptation to place a mesh deep to the whole area. It never resolves the problem. Garments are available that will act as binders to improve the cosmetic appearance. ● Prevention Some have suggested that, by not taking the incision beyond the costal margin, this complication may be avoided.

Elective AAA Repair by the Retroperitoneal Approach (Including Repair of Suprarenal and Juxtarenal AAAs) INDICATIONS ● AAA larger than 5.5 cm or larger than 5.0 cm in

differences. We tend to use bifurcated grafts in about 80% of our patients. Therefore, it is important to gain access to the right iliac system. We do this with a small counterincision. Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7 Step 8 Step 9

Patient positioning Left ﬂank skin incision Right suprainguinal incision (in case of bifurcated grafts) Reﬂection of peritoneum and creation of retroperitoneal space Dissection of aorta and iliacs Clamping distally and proximally; suprarenal clamp if needed Opening of aneurysm sac Proximal and distal anastomoses Inspection of peritoneal cavity and closure of ﬂank incision

OPERATIVE PROCEDURE Patient Positioning See “Aortobifemoral Bypass by the Retroperitoneal Approach,” earlier.

Left Flank Skin Incision See “Aortobifemoral Bypass by the Retroperitoneal Approach,” earlier.

Right Suprainguinal Incision (In Case of Bifurcated Grafts) (Fig. 59–9) For patients with signiﬁcant right common iliac artery occlusive disease, the landing zone for the right-sided anastomosis can be the right common femoral artery or the right external iliac artery. We prefer the external iliac artery because it is more deeply placed than the common femoral with less chance of lymphatic leakage and infective complications than the femoral artery. To approach this, a 4- to 5-cm transverse suprainguinal incision is made. The external oblique aponeurosis is divided, and the internal oblique is also divided to approach the peritoneum. The peritoneum is swept superiorly off the underlying external iliac artery. The other scenario is a patient with a large right common iliac artery aneurysm. The options for dealing with this are

females ● Symptomatic nonruptured AAAs ● Rapidly expanding aneurysms ● Saccular AAAs (controversial)

OPERATIVE STEPS The operative steps are very similar to those described for aortobifemoral bypass. However, there are several

1. Ligating the distal common iliac from the left ﬂank incision (see later) with a bypass onto the right external iliac artery. This then perfuses the right internal iliac by retrograde ﬂow. 2. Dissecting superiorly along the anterior wall of the external iliac until the junction of the right internal and external iliac arteries is encountered. The right internal iliac is then encircled with a size 1 or 0 Ethibond or silk suture and ligated. Pelvic blood supply is then

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A Figure 59–10 Dissection of both common iliac arteries and clamping of the left common iliac artery with a single-rubber clamp. Note the areolar tissue encasing the AAA.

B Figure 59–9 A and B, Incisions for an aortobi-iliac bypass for aneurysmal disease and close-up of the right suprainguinal incision for exposure of the right external iliac artery.

dependent on the left internal iliac artery, which must be preserved. The right external iliac is similarly ligated proximally, and the right limb of the graft is sewn either end-to-side or end-to-end onto it. In the case of an obese patient, the skin incision will need to be extended to access the internal iliac artery.

Reﬂection of the Peritoneum and Creation of the Retroperitoneal Space See “Aortobifemoral Bypass by the Retroperitoneal Approach,” earlier (see Figs. 59–5 and 59–7).

Figure 59–11 Ligation of the origin of the right common iliac artery with nonabsorbable suture.

Dissection of the Aorta and Iliacs; Clamping Distally and Proximally, Suprarenal Clamp if needed; Opening of the Aneurysm Sac; Proximal and Distal Anastomoses (Figs. 59–10 to 59–21) The left common and external iliac arteries are usually ﬁrst encountered as the peritoneum is swept forward. With more dissection, the right common iliac artery can also be identiﬁed. Next, the aortic bifurcation is dissected. The

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Figure 59–12 Ligation of the lumbar branch of the left renal vein. This is one of the three markers for the aortic neck; the others being the left crus of the diaphragm and the left renal artery.

patient is heparinized. Clamps are placed on the common iliacs if they are not aneurysmal. If the left common iliac is dilated, it is easy to place clamps on the internal and external iliacs instead. If the right common iliac is aneurysmal, it may be possible, with enough countertraction, to encircle the distal right common iliac and ligate it through the left ﬂank incision. However, it is prudent to place a clamp on the right external iliac before attempting to do this. Excessive traction on the right common iliac can cause embolization down the right leg. If access cannot be obtained, then the right external and internal iliacs should be clamped and ligated from below via a right suprainguinal incision. The next step is to control the aortic neck. The aorta is identiﬁed deep to its investing areolar tissue, and dissection is continued cephalad. The lumbar branch of the left renal vein is encountered and must be ligated. With further dissection, the left renal artery will be seen reﬂected anteriorly. As they are encountered, the lumbar arteries and the inferior mesenteric artery can be ligated. The aorta needs to be freed from its surrounding areolar tissue, both anteriorly and posteriorly. Any lumbar arteries or veins can be ligated. A Fogarty Hydrogrip clamp is now placed across the aorta. The aortic sac is incised and the contents evacuated and any lumbars oversewn with 3–0 Prolene. The aortic neck is transected completely to allow for an

Figure 59–13 Placement of a Fogarty Hydrogrip clamp across the neck of the aneurysm and opening of the aortic sac.

Figure 59–14 The completely transected aortic neck.

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Figure 59–15 Sewing the Gore-Tex graft in place with 3-0 polypropylene suture using the parachute technique.

Figure 59–16 Completed anastomosis demonstrates the left renal artery (arrow).

end-to-end anastomosis. Care must be taken to ensure that a decent rim of aortic neck (at least 1 cm) is left for the proximal anastomosis. If suprarenal control is needed, divide the left crus of the diaphragm. This will always be required for adequate access to the suprarenal aorta. It may also be needed, sometimes, for access to the infrarenal aorta.

rariﬁed atmosphere of the recovery area. If either leg is ischemic, it is important to ensure that there is adequate ﬂow through both iliacs in the case of a tube graft and into the femorals in the case of a bifurcated graft. Once adequacy of inﬂow has been established, the femorals should then be explored and a femoral embolectomy performed. If adequate amounts of clot are retrieved and the Fogarty catheter passes to the ankle, little else may need to be done. However, on occasion, it may also be necessary to explore the infrageniculate popliteal artery and perform selective embolectomies of the crural vessels. This, although tiresome at the end of a long procedure, is preferable to a major limb amputation at a later date.

Distal Embolization ● Consequence This may manifest itself as atheroemboli, which appear as punctate lesions on the toes and are often selflimiting. Occasionally, atheroemboli may appear on the buttocks as a consequence of embolization down the internal iliacs. Rarely, this may manifest itself as lumbosacral plexopathy. If a signiﬁcant embolus has occurred, acute leg ischemia will be the result with a cold, pale, pulseless extremity. Untreated, the ultimate consequence will be limb loss. Grade 3/4 complication ● Repair Recognition that there is a problem is the most important step, especially at the end of a long and taxing operation. It is not enough to hope that a cold, cyanosed limb will start pinking up upon return to the

● Prevention Adequate heparinization is of course important. In the retroperitoneal approach, the iliac clamps should be in place before dissecting the aneurysm sac. There is more manipulation of the sac in this approach, and therefore, the potential for emboli is possibly greater.

Injury to the IVC or the Common Iliac Veins ● Consequence Bleeding, often life-threatening. Grade 4 complication

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Figure 59–19 Inspection of the sigmoid colon for evidence of overt ischemia and inspection of the peritoneal cavity for intraabdominal bleeding.

Figure 59–17 Right limb of graft–to–right external iliac artery bypass.

Figure 59–20 Closure of muscles in three layers.

Figure 59–18 Completed repair of AAA: aorta–to–right external iliac and –left common iliac bypass with Gore-Tex.

● Repair Again the two-spongestick approach is useful. As a general rule in the retroperitoneal approach, dissection around the right common iliac artery should be kept to a minimum owing to the difﬁculty in controlling venous bleeding from the left ﬂank incision. Remember, direct pressure on the bleeding site will contain many problems, until deﬁnitive repair can be performed with 3/0 or 4/0 prolene sutures.

Figure 59–21 Completed skin closure.

59 AORTIC SURGERY ● Prevention Careful dissection. Avoid unnecessary dissection around the right common iliac artery.

Injury to the Ureter ● Consequence See under “Division of the Ureter,” earlier. Grade 1 complication if recognized, Grade 3 complication if unrecognized ● Repair See under “Division of the Ureter,” earlier. ● Prevention See under “Division of the Ureter,” earlier.

Proximal Aortic Neck “Falls Apart” ● Consequence Bleeding, often life-threatening. Grade 4 complication ● Repair Occasionally, the proximal neck may be very friable and may not hold sutures, resulting in disruption of the anastomosis. The answer, in the cold, clear light of day, is to dissect back to healthy tissue. This is easier said than done. If this is not possible and the situation is really grim, there may be little option but to oversew the aortic stump and perform an axillobifemoral bypass. This is not the ideal, but it may be life-saving. Issues of patency can be then argued another day. ● Prevention Dissect back to healthy aorta. Ensure that endarterectomy of the proximal aorta, when necessary, is not too extensive and that a decent amount of aorta is left to sew to. It may also be useful to perform the proximal anastomosis in an interrupted fashion with pledgelets around the Prolene sutures to avoid cheese-wiring through a particularly friable aortic neck.

Inspection of the Peritoneal Cavity and Closure of the Flank Incision See under “Aortobifemoral Bypass by the Retroperitoneal Approach,” earlier.

POSTOPERATIVE COMPLICATIONS Graft Infection/Aortoenteric Fistulas Can occur days to years after the initial operation. The most common site of aortoenteric ﬁstulas is the third part of the duodenum. The cause of melena in a patient with an aortic graft is often an aortoduodenal ﬁstula. These can be difﬁcult to diagnose. The bleeding point is frequently not seen on routine endoscopy owing to its location in

609

the third part of the duodenum. Classic changes can be seen on CT. However, a high index of suspicion is probably the best tool of all. ● Consequence Bleeding, often catastrophic, although the initial herald bleed can be quite small. Grade 4 complication ● Repair Options are (1) bilateral axilloprofunda artery bypass with vein patch angioplasty of the common femoral arteries and subsequent explantation of the graft, (2) in situ replacement of the infected graft with femoral veins (the Claggett procedure), and (3) in-line replacement of an infected transabdominal graft, in which a new graft is inserted retroperitoneally from the proximal aorta above the infection and tunneled to either femoral artery. The infected graft is then removed via a laparotomy. ● Prevention The retroperitoneal approach seems to confer some immunity from this feared complication. An end-toend anastomosis also seems to reduce the likelihood of this because the anastomosis lies more anatomically and away from the duodenum.

Graft Limb Occlusion/Graft Occlusion ● Consequence Early postoperative occlusion usually results in acute ischemia. Late occlusion can result in intermittent claudication or rest pain. Grade 3 complication ● Repair If this occurs early in the postoperative period, the patient should return to the operating room for graft thrombectomy and correction of the underlying technical defect. If this occurs as a late complication, the most frequently employed option is femorofemoral crossover grafting. ● Prevention Careful attention to surgical technique, especially avoiding any kink or undue redundancy in the graft limbs. Also, we feel it is mandatory to employ some form of quality control. We use a handheld Doppler to conﬁrm good outﬂow.

Pseudoaneurysm This can occur months or years after the initial operation. ● Consequence The primary concern is that this is a manifestation of graft infection, and therefore, at the time of surgery, it

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is important to send samples of the graft and aneurysm contents for culture. Small pseudoaneurysms (<2 cm) in frail patients with limited life expectancy can be observed. However, aneurysms in surgically ﬁt patients merit intervention because they can often enlarge impressively over relatively short intervals. Grade 3 complication ● Repair Good preoperative imaging is important. The safest way to manage pseudoaneurysms is to ﬁrst obtain proximal control by a ﬂank incision that starts at McBurney’s point and is continued laterally in line with the 10th intercostal space. After division of the muscle layers, the peritoneum is reﬂected forward to give access to the common and external iliac and the graft. A separate, vertical right groin incision is made, and control of the superﬁcial femoral, profunda femoris, and common femoral proximal to the graft is obtained. After heparinization, the sac is opened. Often, all that remains of the native common femoral is the posterior wall with the oriﬁces of the superﬁcial femoral and profounda femoris arteries. The graft will have retracted above the inguinal ligament. A new 8- or 10-mm graft is brought into the operating ﬁeld and sewn end-to-end onto the proximal graft in the pelvis and end-to-side onto the common femoral remnant. Tackling such aneurysms by means of a single vertical groin incision is possible, but this invites problems if the aneurysm sac is entered and proximal control cannot be established. If infection is a reasonable concern for the etiology of the pseudoaneurysm, routing of the reconstruction extra-anatomically ﬁrst is recommended prior to opening the pseudoaneurysm. ● Prevention Again, attention to surgical technique and use of nonabsorbable monoﬁlament sutures for the anastomosis are key.

AVOIDING PITFALLS IN UNUSUAL CASES Inﬂammatory AAA Inﬂammatory AAAs are difﬁcult, regardless of surgical approach. In patients with suitable anatomy, there is a case for considering endovascular repair, regardless of the patient’s ﬁtness for surgery. However, in patients who need operative intervention, the retroperitoneal approach may be better: The posterolateral aspect is typically spared from the inﬂammatory process compared with the anterior aortic wall; the left renal vein is lifted interiorly and the duodenum is moved away from the operative ﬁeld and does not need to be dissected. This is supported by reports in the literature, albeit involving small numbers of patients.20,21 Our experience is that in patients with severe retroperitoneal ﬁbrosis, the retroperitoneal approach is

still a difﬁcult operation and not quite the panacea portrayed in the literature.

Horseshoe Kidney A horseshoe kidney (or fused renal ectopia) is one of the places in which the retroperitoneal approach has clear advantages over the transabdominal approach.22,23 With horseshoe kidneys, the renal arteries are often multiple, and it is essential to reimplant as many as possible either individually or as a patch. With the kidney lifted forward out of the operative ﬁeld, division of the isthmus is a moot point. It also avoids injury to a ureter in an anomalous position. Retroaortic Left Renal Vein The retroaortic left renal vein is present in 2% of patients, and a circumaortic left renal vein is present in 3%.24 This can make a left retroperitoneal approach difﬁcult if not noted prior to surgery. In order to avoid injury to the renal vein in such circumstances, we “drop the kidney”: place it back in its usual anatomic position rather than in the exaggerated anterior position with the conventional posterolateral retroperitoneal exposure. The kidney is separated from the perinephric fat (this can be reasonably vascular) and replaced on the posterior abdominal wall. Reimplantation of Renal Arteries If it is anticipated in advance that the renal arteries will require reimplantation, we sew 6-mm Gore-Tex limbs onto the aortic graft prior to starting the surgery. Following adequate dissection of the aorta, the suprarenal aorta and renal arteries are clamped. The aorta is transected, and it is only at this stage that adequate access to the right renal artery can be obtained. The proximal aortic anastomosis is performed, and then the renal arteries are sewn in place. Approach to Suprarenal Aneurysms Again the suprarenal aorta is dissected with division of the left crus of the diaphragm. The aorta and renals are clamped. The aorta is divided obliquely, and a graft is sewn end-to-end.

Repair of Ruptured AAA via the Left Retroperitoneal Approach The key in the management of ruptured AAAs is rapid proximal control of the aortic neck. For those unfamiliar with the retroperitoneal approach, it may seem foolhardy to perform a retroperitoneal approach in such circumstances. However, this has been our practice since 1989. Our operative outcomes are reasonable.25

59 AORTIC SURGERY

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7

Patient positioning Left ﬂank skin incision/cross-clamp thoracic aorta Dissection of aortic aneurysm Clamping distally and proximally suprarenal clamp if needed Opening of aneurysm sac Proximal and distal anastomosis Inspection of peritoneal cavity and closure of ﬂank incision.

611

Proximal and Distal Anastomoses See “Elective AAA Repair by the Retroperitoneal Approach (Including Repair of Suprarenal and Juxtarenal AAAs),” earlier.

Inspection of the Peritoneal Cavity and Closure of the Flank Incision Special attention should be paid to inspection of the peritoneal cavity contents at the end of the operation to ensure that there are no signs of colonic ischemia or splenic injury.

Patient Positioning This is no different from that employed in elective aortobifemoral or aneurysm repair cases. Familiarity with the position on the part of the operating room team ensures that the patient can be placed in the left lateral position without delaying surgery.

Left Flank Skin Incision/Cross-clamp Thoracic Aorta We occasionally extend our incision far posterior so that the incision can be deepened through the intercostal muscles to access the lower thorax and allow for cross-clamping of the lower thoracic aorta, which allows time for more detailed dissection of the aortic neck. Once the proximal neck is dissected, the clamp can then be repositioned.

Dissection of AAA With ruptured AAAs, most of the dissection has been done by the rupture itself, as the most common site of rupture is posterior and inferiorly. We always divide the left crus of the diaphragm to facilitate rapid access to the neck. We regard this as crucial in emergency situations. One of the most common problems encountered in the conventional transabdominal approach to ruptured aneurysms is injury to the gonadal and left renal veins in an already coagulopathic patient. The advantage of the retroperitoneal approach is that the gonadal veins and the left renal vein are pushed away from the operative ﬁeld. In contrast to elective surgery, we clamp proximally ﬁrst. As with elective cases, we minimize dissection around the right common iliac artery and vein.

SPECIAL PROBLEMS Ischemic Colitis/Ischemic Bowel Ischemic bowel is a relatively rare occurrence in elective aortic surgery. However, in emergent repair, the incidence of colon ischemia is 5% to 7%. It carries a mortality rate of up to 80%. In order to reduce ischemic complications after emergent AAA repair, we therefore have a policy of colonoscopy within 48 hours of surgery. Our experience shows 42% of patients develop colon ischemia after ruptured AAA repair. Of these patients, almost a quarter had full-thickness necrosis of the bowel wall (grade 3 colonic ischemia). Even with recognition of the problem and prompt resection, the mortality rate in this subgroup of patients was 55%.26 Grade 4/5 complication

CONCLUSIONS Aortic surgery is difﬁcult. It has the highest mortality rate of any elective vascular surgical procedure. Mortality rates in the United States for AAA repair are 5.6%,27 above what is regarded acceptable for coronary artery bypass. They have not altered appreciably since the 1980s, despite advances in critical care and anesthesia. Evidence from most centers suggests that mortality rates for aortoiliac occlusive disease are even higher. These reﬂect the complexity of the surgery and the general health of our patients. In this chapter, we have related problems we have encountered in performing aortic surgery in the hope that many of these experiences can be avoided by others in the future.

Opening of the Aneurysm Sac This is performed in the same manner as elective surgery, with oversewing backbleeding arteries. If the right common iliac cannot be expeditiously controlled, we place a size 14 Foley catheter down the artery to control backbleeding. A right suprainguinal incision can then be made to access the right external iliac artery.

REFERENCES 1. Pearce WH, Parker MA, Feinglass J, et al. The importance of surgeon volume and training in outcomes for vascular surgical procedures. J Vasc Surg 1999;29:768–776; discussion 777–778.

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2. Chang BB, Shah DM, Paty PS, et al. Can the retroperitoneal approach be used for ruptured abdominal aortic aneurysms? J Vasc Surg 1990;11:326–330. 3. Pierce GE, Turrentine M, Stringﬁeld S, et al. Evaluation of end-to-side v end-to-end proximal anastomosis in aortobifemoral bypass. Arch Surg 1982;117:1580–1588. 4. Melliere D, Labastie J, Becquemin JP, et al. Proximal anastomosis in aortobifemoral bypass: end-to-end or endto-side? J Cardiovasc Surg (Torino) 1990;31:77–80. 5. Ameli FM, Stein M, Aro L, et al. End-to-end versus endto-side proximal anastomosis in aortobifemoral bypass surgery: does it matter? Can J Surg 1991;34:243–246. 6. Friedman SG, Lazzaro RS, Spier LN, et al. A prospective randomized comparison of Dacron and polytetraﬂuoroethylene aortic bifurcation grafts. Surgery 1995;117:7–10. 7. Prager M, Polterauer P, Bohmig HJ, et al. Collagen versus gelatin-coated Dacron versus stretch polytetraﬂuoroethylene in abdominal aortic bifurcation graft surgery: results of a seven-year prospective, randomized multicenter trial. Surgery 2001;130:408–414. 8. Webster SE, Smith J, Thompson MM, et al. Does the sequence of clamp application during open abdominal aortic aneurysm surgery inﬂuence distal embolisation? Eur J Vasc Endovasc Surg 2004;27:61–64. 9. Lipsitz EC, Veith FJ, Ohki T, Quintos RT. Should initial clamping for abdominal aortic aneurysm repair be proximal or distal to minimize embolization? Eur J Vasc Endovasc Surg 1999;17:413–418. 10. Shah DM, Darling RC III, Chang BB, et al. Access to the right renal artery from the left retroperitoneal approach. Cardiovasc Surg 1996;4:763–765. 11. Cambria RP, Brewster DC, Abbott WM, et al. Transperitoneal versus retroperitoneal approach for aortic reconstruction: a randomized prospective study. J Vasc Surg 1990;11:314–324; discussion 324–325. 12. Sicard GA, Reilly JM, Rubin BG, et al. Transabdominal versus retroperitoneal incision for abdominal aortic surgery: report of a prospective randomized trial. J Vasc Surg 1995;21:174–181; discussion 181–183. 13. Kirby LB, Rosenthal D, Atkins CP, et al. Comparison between the transabdominal and retroperitoneal approaches for aortic reconstruction in patients at high risk. J Vasc Surg 1999;30:400–405. 14. Sieunarine K, Lawrence-Brown MM, Goodman MA. Comparison of transperitoneal and retroperitoneal

15.

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26.

27.

approaches for infrarenal aortic surgery: early and late results. Cardiovasc Surg 1997;5:71–76. Williams GM, Ricotta J, Zinner M, Burdick J. The extended retroperitoneal approach for treatment of extensive atherosclerosis of the aorta and renal vessels. Surgery 1980;88:846–855. Shumacker HB Jr. Midline extraperitoneal exposure of the abdominal aorta and iliac arteries. Surg Gynecol Obstet 1972;135:791–792. Shucksmith HS. Duodenal, sigmoid, and ureteric ﬁstulas resulting from aorto-iliac grafts or endarterectomy. Br J Surg 1968;55:402–403. Beach PM, Risley TS. Aorticosigmoid ﬁstulization following aortic resection. Arch Surg 1966;92:805–807. Beall AC Jr, Crosthwait RW, De Bakey ME. Injuries of the colon including those incident to surgery upon the aorta. Surg Clin North Am 1965;45:1273–1282. Todd GJ, DeRose JJ Jr. Retroperitoneal approach for repair of inﬂammatory aortic aneurysms. Ann Vasc Surg 1995;9:525–534. Fiorani P, Faraglia V, Speziale F, et al. Extraperitoneal approach for repair of inﬂammatory abdominal aortic aneurysm. J Vasc Surg 1991;13:692–697. Canova G, Masini R, Santoro E, et al. Surgical treatment of abdominal aortic aneurysm in association with horseshoe kidney. Three case reports and a review of technique. Tex Heart Inst J 1998;25:206–210. Stroosma OB, Kootstra G, Schurink GW. Management of aortic aneurysm in the presence of a horseshoe kidney. Br J Surg 2001;88:500–509. Kawamoto S, Lawler LP, Fishman EK. Evaluation of the renal venous system on late arterial and venous phase images with MDCT angiography in potential living laparoscopic renal donors. AJR Am J Roentgenol 2005;184:539–545. Darling RC 3rd, Cordero JA Jr, Chang BB, et al. Advances in the surgical repair of ruptured abdominal aortic aneurysms. Cardiovasc Surg 1996;4:720–723. Champagne BJ, Darling RC 3rd, Daneshmand M, et al. Outcome of aggressive surveillance colonoscopy in ruptured abdominal aortic aneurysm. J Vasc Surg 2004;39:792–796. Heller JA, Weinberg A, Arons R, et al. Two decades of abdominal aortic aneurysm repair: have we made any progress? J Vasc Surg 2000;32:1091–1100.

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Infrainguinal Revascularization Christopher J. Abularrage, MD and Richard F. Neville, MD INTRODUCTION Lower extremity revascularization is being offered to an increasing number of patients. This is due in part to the aging of our population, but the population is also increasingly active and aware of the effects of peripheral arterial disease on lifestyle and mobility. Advances in open and endovascular therapies have allowed an increasingly aggressive approach to revascularization for a patient population that is becoming increasingly older and often sicker. These factors continue to increase the number of prospective patients seeking revascularization to increase mobility and avoid amputation. Although the advent of sophisticated endovascular techniques continues to push the limits of catheter-based revascularization, open bypass will continue to play a major role in the revascularization of the critically ischemic lower extremity. This may prove especially true for those patients who are in need of pulsatile ﬂow directly to a speciﬁc angiosome to prevent tissue loss. The classic indications for revascularization are incapacitating claudication, rest pain, and tissue loss including gangrene and nonhealing ulcerations.1 Patient selection is important in determining the optimal mode of therapy because pain relief and maintenance of function are the goals of revascularization and not the cure of atherosclerosis. Claudication is rarely a limb-threatening situation, and a failed intervention can result in a more complicated revascularization and conversion to the threat of limb loss. Whereas 25% of claudicants have progressive symptoms, fewer than 20% require revascularization for limb salvage after 10 years.2 The majority of infrapopliteal revascularization procedures should be performed for patients in a limb-threatening situation with symptoms manifesting as pain at rest or tissue loss. In these patients, both an aggressive approach to revascularization and proper wound care are essential to maintain limb length and the ambulatory status of the patient. This affects both life and limb. The history and physical examination remain an important tool in management of the vascular patient. The history provides information about the indication for vascular intervention as well as concurrent risk factors in other arterial beds. The physical examination (pulses, skin

envelope) provides an assessment of the extent of vascular involvement. The hand-held Doppler is widely used in the evaluation of ischemia. An experienced examiner can differentiate an acoustically normal from an abnormal Doppler signal. The presence of a Doppler signal indicates that there is blood ﬂow in the examined artery; however, it does not indicate whether this ﬂow is adequate. The severity of ischemic disease should be documented by noninvasive vascular laboratory testing prior to any intervention. These studies conﬁrm the degree of ischemia and serve as a baseline for future postprocedure follow-up. The noninvasive vascular laboratory uses Doppler ultrasound to measure the ankle/brachial index (ABI), segmental pressures, and waveform analysis and to generate duplex images. Other important tests include pulse volume recordings (PVR), transcutaneous oxygen tension (tcPO2) and photoplethysmography (PPG). The ABI is measured as the ankle pressure divided by the brachial pressure, with a normal value of 1.0. In intermittent claudication, an ABI of 0.5 to 0.9 is usually obtained, whereas in severe ischemia, the ABI is usually less than 0.5. Noncompressible arteries lead to falsely high ankle pressures in more than 30% of diabetic patients3; therefore, other noninvasive studies should be added to determine the adequacy of blood ﬂow in diabetics with ischemia.4 Segmental pressures and waveforms can help localize vascular occlusive disease. The tcPO2 measures the partial pressure of oxygen that diffuses through heated skin.5 A tcPO2 can be accurate in predicting healing. Healing is likely if tcPO2 is above 35 to 40 mm Hg, and unlikely if it is below 20 to 26 mm Hg. A tcPO2 regional index can be used to account for changes in systemic arterial oxygen tension.6 To obtain the regional index, the tcPO2 of the leg is divided by the tcPO2 measured at a reference point (chest). Wounds with a tcPO2 index below 0.4 are unlikely to heal, and those with tcPO2 above 0.6 are likely to heal.7 After it has been determined that revascularization is indicated, an imaging study is needed to plan the appropriate procedure. Arteriography remains the most common method for arterial imaging in order to plan revascularization. However, new modalities such as duplex ultrasound, magnetic resonance angiography, and computed tomographic (CT) angiography are being used

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with increasing frequency. These new modalities avoid the complications of arterial puncture and possible renal dysfunction associated with arteriography. However, these newer, noninvasive imaging modalities are still being reﬁned and require the involvement of physicians dedicated to obtaining precise images. The chosen method must allow the surgeon to identify the inﬂow and outﬂow arteries as well as the adequacy of the runoff—all key factors for a successful bypass. A successful bypass depends on careful preoperative planning and meticulous attention to detail during the operation. Preoperative decisions include choice of inﬂow artery, recipient artery, and the conduit for bypass. Error in judgment in any of these decisions is a technical error leading to graft failure. Meticulous dissection, conduit preparation, and suturing of the anastomosis are crucial in preventing intraoperative technical errors leading to early graft failure. There is little margin for error in suturing anastomoses, especially to those small diseased arteries below the knee.

KEY DECISION POINTS ● Bypass anatomy: inﬂow artery, recipient artery ● Conduit: vein, prosthetic, composite

Figure 60–1 Transverse versus groin incision.

minimal tissue manipulation and respect for anatomic tissue planes can avoid the complications associated with this portion of the procedure. There is some support for the use of a transverse groin incision as opposed to a vertical incision in order to avoid lymphoceles and seromas (Fig. 60–1). This decision should not compromise appropriate arterial exposure.

Improper Choice of Inﬂow Artery

INDICATIONS ● Severe disabling claudication ● Rest pain ● Tissue loss or gangrene

OPERATIVE STEPS Step Step Step Step Step Step Step Step Step

1 2 3 4 5 6 7 8 9

Proximal artery exposure Distal artery exposure Preparation of conduit Tunneling of conduit Intraoperative anticoagulation Proximal anastomosis Distal anastomosis Evaluation of bypass Wound closure

OPERATIVE PROCEDURE Proximal Artery Exposure Proximal arterial exposure involves proper choice of the inﬂow artery for bypass. Several methods exist to aid this choice. Presence of a strong, palpable pulse and preoperative imaging should be considered. Any doubt requires measurement of an arterial pressure, which can be performed at the time of surgery.8 Careful dissection with

● Consequence Graft failure. Grade 3 complication ● Repair Improvement of inﬂow—proximal arterial angioplasty, additional revascularization of the inﬂow artery by a jump graft or extension of the existing bypass to an appropriate inﬂow source. ● Prevention Preoperatively, adequate evaluation of the inﬂow artery through multiplanar arteriography is critical. Pre- and postlesion pressure measurements can be made at the time of the arteriogram to delineate the hemodynamic signiﬁcance of an inﬂow stenosis. If any doubt remains at the time of surgery, an arterial pressure can be measured with an intraoperative arterial line at the site of the proximal anastomosis for comparison with the patient’s proximal pressure (brachial, radial). The pressure gradient should not be more than 15 to 20 mm Hg.

Femoral Nerve Injury (Fig. 60–2) ● Consequence Weakness in the extensor muscles of the thigh and paresthesias of the anterior thigh. Chronic pain can be observed in up to 15% of patients.9 Grade 1 complication

60 INFRAINGUINAL REVASCULARIZATION ● Repair Direct repair by peripheral nerve specialist. ● Prevention Nerve injuries occur approximately 4% of the time10 and can be prevented with meticulous surgical technique and an understanding of the injury’s medial position to the femoral artery. The femoral sheath should be opened longitudinally to expose the femoral artery.

615

Care must be taken to avoid transverse dissection because femoral nerve injury may occur at the lateral aspect of the dissection.

Distal Artery Exposure Similar principles apply to the distal dissection as to the proximal exposure. Ideally, distal arteries can be dissected between muscle planes and not through a large mass of muscle. If large amounts of muscle are being transected, reconsider the proper plane of dissection (Fig. 60–3).

Venous Injury (Fig. 60–4) ● Consequence Injury to the corresponding veins that run in the vascular pedicle with the outﬂow artery can lead to intraoperative blood loss and a decreased ﬁeld of vision and limited exposure of the site for distal anastomosis. Grade 3 complication

Figure 60–2 Proximal arterial exposure shows the proximity of the femoral nerve to the inﬂow artery.

A

● Repair A careful repair of the venous injury with ﬁne suture must be performed with extra care given to control of bleeding during the repair. Often, the repair must be performed without formal vascular control through the

B

C

Figure 60–3 A, Incision planning for below-knee popliteal exposure. B, Incision for below-knee popliteal exposure. C, Distal exposure for the dorsalis pedis artery. D, Distal exposure for the plantaris pedis branch of the posterior tibial artery.

D

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SECTION X: VASCULAR SURGERY ● Repair Direct repair by a peripheral nerve specialist. ● Prevention The common peroneal nerve branches into the deep and superﬁcial peroneal nerves. The deep peroneal nerve is most commonly injured during exposure of the anterior tibial artery.

Superﬁcial Peroneal Nerve Injury

Figure 60–4 Distal arterial exposure shows the proximity of the tibial veins to the outﬂow artery.

use of digital pressure and judicious use of ﬁne-tipped suction. Care should also be taken to avoid occlusion of the vein owing to the repair. This can create local venous hypertension and make the remaining venous circulation more difﬁcult to handle. ● Prevention Careful dissection of the outﬂow artery from its corresponding veins, with exposure limited to that minimal portion of the artery necessary for vascular control and the construction of the anastomosis. Consideration can also be given to the use of a proximal external pressure cuff for vascular control. This allows a more minimal dissection of the outﬂow artery, thereby minimizing the chance of venous injury and clamp injury to the artery.

Common Peroneal Nerve Injury ● Consequence Footdrop secondary to loss of the dorsiﬂexor and eversion muscles of the foot as well as paresthesias on the lateral aspect of the leg and the dorsum of the foot. Grade 1 complication ● Repair Direct repair by a peripheral nerve specialist. ● Prevention The common peroneal nerve branches off the sciatic nerve at the superior aspect of the popliteal fossa and heads laterally with the medial border of the biceps femoris muscle. It then passes over the posterior aspect of the ﬁbular head. Care must be taken to avoid injury to this nerve when exposing the below-knee popliteal artery.

Deep Peroneal Nerve Injury ● Consequence Footdrop. Grade 1 complication

● Consequence Paresthesias of the lateral aspect of the leg and the dorsum of the foot. Grade 1 complication ● Repair Direct repair by a peripheral nerve specialist. ● Prevention The superﬁcial peroneal nerve courses along the lateral aspect of the leg and can be injured during division of the ﬁbula when accessing the below-knee popliteal artery or the trifurcation. This can be prevented by dividing the ﬁbular periosteum from distal to proximal in order to identify the superﬁcial peroneal nerve, which courses around the upper ﬁbula. Avoidance of the nerve can be further ensured by staying within the subperiosteal plane.

Tibial Nerve Injury ● Consequence Weakness in plantar ﬂexion of the foot as well as paresthesias on the sole of the foot. Grade 1 complication ● Repair Direct repair by a peripheral nerve specialist. ● Prevention The tibial nerve is a branch of the sciatic nerve that passes through the popliteal fossa superﬁcial to the popliteal artery. It then travels on the posterior aspect of the posterior tibial artery inferiorly to the foot. It is most commonly injured during exposure of the popliteal and posterior tibial arteries.

Preparation of Conduit Preparation of the conduit is obviously most important if autogenous vein is available to use for the bypass. Sources for venous conduit include the greater saphenous, lesser saphenous, and arm veins. If vein is not available, prosthetic materials can be used prior to the choice of primary amputation. However, every effort should be made to use an autogenous reconstruction. In this case, the avoidance of venous spasm and injury demands meticulous dissection and gentle vein handling. This is a crucial part of the

60 INFRAINGUINAL REVASCULARIZATION

617

nous vein. The saphenous nerve is a cutaneous branch of the femoral nerve. It travels with the superﬁcial femoral artery through the adductor canal and then exits distal to the hiatus between the sartorius and the gracilis muscles to join the course of the greater saphenous vein. It may also be injured during medial exposure of the above-knee popliteal artery. A

Vein Spasm, Vein Injury, Poor Vein Quality (Fig. 60–7) ● Consequence Graft thrombosis. Grade 3 complication

B Figure 60–5 A, Autogenous vein harvest for bypass conduit. B, Vein harvest shows the vein cannula in place to administer gentle hydrostatic dilation during harvest and a skin bridge for enhancement of wound closure at the knee.

Figure 60–6 Saphenous vein harvest shows dissection of the saphenous nerve in proximity to the vein.

● Repair Veins of adequate quality and diameter can be sutured together to create a composite graft with sufﬁcient length. Otherwise, a prosthetic graft can be considered. ● Prevention Preoperative vein mapping with duplex ultrasound can provide detailed information regarding the quality of a potential vein graft. It can detect constriction of veins secondary to sclerosis, previous manipulation, or thrombophlebitis. It can also assess length and diameter of the vein. These can be particularly important when performing a tibial bypass for which a long segment is necessary. Diameters greater than 3 mm for reverse11 and 2 mm for in situ12 saphenous vein grafts have been recommended to obtain adequate long-term patency; however, judgment is required because the vein may be suitable with intraoperative preparation. Intraoperative preparation involves distal vein exposure with the instillation of premixed vein solution prior to more proximal dissection. This solution should be instilled under enough pressure to gently dilate the vein, but not to overdistend the vein, leading to endothelial injury. Endothelial ischemic time should also be minimized by allowing the vein to remain in place as long as possible whether it is used in a reversed, translocated, or in situ conﬁguration.

Residual Arteriovenous Fistula (Fig. 60–8) operation and not one that should be left to the most junior member of the operating team (Fig. 60–5).

Saphenous Nerve Injury (Fig. 60–6) ● Consequence Paresthesias of the skin on the medial aspect of the lower leg below the knee joint. Grade 1 complication ● Prevention Saphenous nerve injuries can be prevented with an understanding of its anatomy and relation to the saphe-

● Consequence Failure to locate and ligate all side branches from a translocated in situ vein graft. Arteriovenous ﬁstula causing low ﬂow through the bypass with possible thrombosis. Grade 1/2/3 complication ● Repair Patent side branches can be located with manual palpation, Doppler ultrasound, or angiography. Once identiﬁed, these can be ligated with sutures or surgical clips. If identiﬁed postoperatively, a small incision can be made over the side branch with subsequent ligation.

618

SECTION X: VASCULAR SURGERY ● Prevention Three types of ﬁstulas exist: small cutaneous branches usually found in the thigh that do not greatly affect graft ﬂow; perforator branches that increase graft inﬂow but have no effect on distal graft ﬂow; and perforator branches that increase graft inﬂow and decrease graft outﬂow.13 Prevention is aimed at carefully examining the bypass intraoperatively and ligating all branches. 1 2

Failure to Lyse All Venous Valves (Fig. 60–9) ● Consequence Low ﬂow through the bypass thrombosis. Grade 1/2/3 complication

with

possible

● Repair Intraoperative identiﬁcation of untreated valves can be made with Doppler ultrasound or angiography. Proper

RT

GSV

MID

Thigh

4

A

2 1

RT

B

GSV

PROX

Thigh

4

Figure 60–8 Intraoperative completion angiogram shows a patent arteriovenous ﬁstula (arrows) after in situ bypass. This emphasizes the need for some type of completion study after bypass to ensure the desired result.

Figure 60–7 Duplex ultrasound image of the greater saphenous vein taken preoperatively to assess vein quality and suitability for use as a bypass conduit. A, Transverse view. B, Longitudinal view. This technique can also guide the operative exposure and help avoid larger tissue ﬂaps that result in postoperative wound complications.

60 INFRAINGUINAL REVASCULARIZATION

619

B

A

Figure 60–9 A, Intraoperative angiogram with valves properly lysed after vein bypass. B, Intraoperative angiogram with the ﬁrst valve beyond the saphenofemoral junction not properly lysed and impeding ﬂow through the bypass graft.

valve lysis must then be performed with the valvulotome favored by the operating surgeon. ● Prevention The vein conduit can be used in one of three conﬁgurations: reversed, in situ, or translocated. Reversed vein grafts avoid the need for valvulotomy but may lead to size mismatch when performing the anastomoses. The in situ technique is advantageous because there is no size mismatch between artery and vein, but valve lysis is required with the vein often only partially exposed. If care is not taken, the valvulotome can injure the vein, most commonly at the site of a venous side branch. In a recent prospective, randomized study, there were no differences in the number of retained valves between types of valvulotomes.14 Hemodynamically signiﬁcant stenoses due to unlysed valves required revision 2.5% of the time.15 The translocated technique also matches size of the artery and vein and optimizes valve lysis under direct observation, but it does increase venous endothelial ischemic time compared with that of the in situ technique. Translocated vein also allows possible variation in the path of the bypass through the lower extremity in order to avoid infection or heavy scar formation. The operating surgeon should choose the

method with the most comfort and familiarity because patency rates seem to be similar.16

Wound Infection or Dehiscence ● Consequence Wound infections of the vein harvest site can usually be managed nonoperatively. Grade 1 complication ● Repair Treatment typically includes antibiotic therapy with or without local wound incision and drainage. ● Prevention Prevention is aimed at risk factor modiﬁcation because patients with diabetes mellitus and obesity are at increased risk for vein harvest site infections.17 A recent prospective, randomized trial found that endoscopic vein harvest reduced leg wound complications from 7.4% to 19.4% compared with those of open vein harvest.18 The endoscopic harvest time is signiﬁcantly longer than that of the traditional harvesting technique, and care must be taken not to cause venous spasm or injury during endoscopic vein harvest.19 Proper wound closure is also critical in preventing post-

620

SECTION X: VASCULAR SURGERY

A

C B Figure 60–10 A, Subcutaneous tissue should be closed to minimize dead space with monoﬁlament suture without tension. If required, retention-type sutures can be placed through the skin in mattress fashion to take tension off the wound edges. B, Final wound closure. C, Wound closure across a groin skin crease. Care must be taken to approximate the skin edges appropriately to avoid tension and wound complications. The wound is appropriately closed.

operative wound complications. Important principles to consider include closure without tension on the wound edges, use of absorbable suture to minimize soft tissue reactivity and inﬂammation, and approximation of the wound edges (Fig. 60–10). A

Tunneling of Conduit Bypass grafts should be tunneled in away from areas of infection and in such a way as to protect the graft from wounds of future exposure. Vein grafts are often tunneled in a subcutaneous position to allow for ease of follow-up and revision in the future. Prosthetic grafts should be tunneled in an anatomic location under muscular tissue planes. Various tunneling devices are available and should be chosen in order to allow atraumatic graft manipulation with a minimum of tissue displacement (Fig. 60–11).

Graft Kinking ● Consequence Low ﬂow through the bypass with possible thrombosis. Grade 1/2/3 complication

B Figure 60–11 Graft tunneled without kinking or redundancy.

60 INFRAINGUINAL REVASCULARIZATION

621

● Repair Kinking of a graft must be directly ﬁxed by reorienting the graft throughout its course. ● Prevention Kinking of a bypass is rare, occurring 1% of the time.20 Reversed or translocated vein grafts should be marked at their ends to maintain proper orientation and avoid kinking throughout their course. Most polytetraﬂuoroethylene (PTFE) grafts have orientation markers to prevent twisting or kinking of the graft during tunneling. If there is any question as to kinking, the graft should be withdrawn and tunneled again.

Injury to Deep Structures ● Consequence Hemorrhage if a vessel is injured; neuropathy if a nerve is injured. Grade 1/3 complication ● Repair Bleeding vessels must be located and ligated or electrocauterized. Bleeding from the graft tunnel can be difﬁcult to isolate but should not be left untreated.

A

● Prevention After exposure of the proximal and distal arteries, the tunneler must be kept in speciﬁc tissue planes to avoid injury to underlying neurovascular structures.9

Graft Stricture by Fascia or Tendon (Fig. 60–12) ● Consequence If a deep anatomic tissue plane is chosen (especially for above-knee femoral-popliteal bypass with prosthetic), care must be taken not to cross different anatomic compartments and to stay in the anatomic plane of the native artery. Entrance and exit points from the tunnel should be free of any tension. If a lateral course for the graft must be used, the proximal portion of a bypass may be constricted by the tense bands of the tensor fascia lata, resulting in low ﬂow and possible graft thrombosis. Grade 1/2/3 complication ● Repair Constriction of the bypass must be directly repaired by creating a larger window through the fascia lata for the bypass to travel. ● Prevention The fascia lata should be incised in cruciate fashion or partially excised prior to placing the graft through it.

Intraoperative Anticoagulation Intraoperative anticoagulation is used primarily to prevent arterial thrombosis while the native arterial circulation

B Figure 60–12 A, Intraoperative angiogram or bypass graft compression by the tendon during wound closure. B, Intraoperative view of the tendon compressing the distal end of the bypass graft.

is clamped and ﬂow occluded to perform the arterial anastomoses. Although most surgeons use systemic anticoagulation, regional administration can be performed directly into the distal arterial tree.

Inadequate Anticoagulation ● Consequence Arterial thrombosis if anticoagulation is inadequate. Grafts should always be allowed to evidence some prograde bleeding prior to completion of the distal anastomosis in order to ensure that no thrombus has developed in the graft or clamped proximal artery. Excessive bleeding, especially from suture needle holes or raw tissue surfaces, can occur if anticoagulation is overly aggressive. Grade 1 complication

622

SECTION X: VASCULAR SURGERY

● Repair Acute arterial thrombosis can usually be treated with catheter thrombectomy because the thrombus is acute and easily removed. An underlying lesion should be considered as a cause for the thrombosis. If hemostasis is necessary at the end of the procedure, it may be necessary to reverse the effects of heparin by administration of protamine. Protamine sulfate may be given at a dose of 1 mg/100 units of circu-lating heparin if there is excessive bleeding due to over-anticoagulation. ● Prevention Heparinization of the patient should be performed 1 to 2 minutes prior to clamping the vessels to prevent thrombosis. This is done after exposure of the proximal and target vessels and preparation of the conduit in order to minimize blood loss and maintain a hemostatic operating ﬁeld. It also avoids hemorrhage during tunneling of a graft. Heparin has a half-life of 1 to 1.5 hours and lasts approximately 3 to 4 hours. Adequate anticoagulation can be followed with activated clotting time (ACT). For peripheral vascular operations, an ACT in the 250- to 350-second range is adequate.21

Proximal Anastomosis Intimal Dissection ● Consequence Distal arterial thrombosis and ischemia. Grade 1/2/3 complication

plaque rupture and embolization. If the artery is calciﬁed, an attempt should be made to palpate the artery and place the clamp so as not to fracture the plaque.

Anastomotic Dehiscence ● Consequence Anastomotic dehiscence can lead to a pseudoaneurysm, hematoma, or hemorrhage, depending on the severity of the dehiscence. Grade 1/2/3 complication ● Repair Repair can be accomplished with complete revision of the anastomosis using monoﬁlament sutures with or without patch angioplasty. ● Prevention Anastomotic dehiscence was more common with the use of Dacron grafts and absorbable sutures. With the advent of PTFE grafts and synthetic nonabsorbable monoﬁlament sutures, the rate of anastomotic pseudoaneurysm has greatly decreased. Currently, the greatest risk factors are infection of the anastomosis, undue tension, and inadequately placed sutures secondary to technical failure.23,24 Duplex ultrasound may be useful for evaluating the integrity of the anastomosis if the diagnosis is in question.

Distal Anastomosis ● Repair Intimal dissections can be repaired by placing fullthickness tacking sutures through the arterial wall. ● Prevention In almost all circumstances, anastomotic sutures should be placed from outside-to-inside through the conduit and from inside-to-outside through the arterial wall. This avoids dissection and lifting of the plaque from the arterial media. Performance of a local endarterectomy at the anastomotic site can be considered, but this must be performed with care to minimize the risk of intimal dissection and should prompt careful intraoperative evaluation of the anastomosis22 (Fig. 60–13).

Intra-arterial Plaque Embolization ● Consequence Distal arterial thrombosis and ischemia. Grade 2/3 complication ● Repair Catheter embolectomy. ● Prevention When gaining control of an artery, vascular clamps should be placed on a noncalciﬁed portion to avoid

Anastomotic Narrowing ● Consequence Narrowing of the distal anastomosis may lead to disadvantageous anastomotic hemodynamics and graft thrombosis. Grade 3 complication ● Repair If the anastomosis is narrowed, the suture line must be transected and the narrowed portion redone or opened with a patch angioplasty repair. ● Prevention Sutures placed at the toe and heel of the anastomosis are the most important because these are the crucial areas of the anastomosis to ensure good ﬂow and patency. The two best methods of suture placement at the toe involve the “parachute” technique and sequential interrupted sutures at the toe with continuity after the side sutures are placed. Both of these techniques allow suture placement under direct vision at the critical areas of the anastomosis (Fig. 60–14). Careful proximal and distal control of the recipient artery is also important to have a good length of artery to suture under direct vision (Fig. 60–15).

60 INFRAINGUINAL REVASCULARIZATION

A

623

B

D C Figure 60–13 A, Anastomosis with the parachute technique of suture material allowing for precise placement of the sutures at the critical portions of the anastomosis: toe and heel. B, Anastomosis with eversion of the graft material and arterial wall. C, Anastomosis with the graft brought down with the parachute technique. D, Completed anastomosis with the toe carefully constructed.

Figure 60–15 Arterial control prior to the construction of the distal anastomosis. Figure 60–14 Distal anastomosis of a vein graft with the toe carefully constructed.

624

SECTION X: VASCULAR SURGERY

Lumen ⫹

Endothelial cells

Platelets

Migration

*

Subendothelial intima Monocyte Internal Macrophages elastic lamina Media

⫹ Proliferation MIC

n

r

io at

ig

M

⫹

⫹

SMC

A

PTFE grafts have decreased patency compared with autogenous vein bypasses owing to an increased hyperplastic response between the prosthetic material and the native artery.27 In the absence of available vein, PTFE augmented with a distal vein patch provides a larger oriﬁce at the arterial interface, thus increasing the diameter necessary for intimal hyperplasia to stenose the distal anastomosis.28,29 When combined with oral anticoagulation using warfarin sodium, this results in 4-year primary patency and limb salvage rates of 63% and 79%, respectively.30

Intraoperative Evaluation of Bypass Poor Graft Performance ● Consequence After completion of a bypass, the outcome should be evaluated prior to skin closure. Multiple techniques are available including intraoperative Duplex ultrasound or arteriography. Signs of an adequate result include a palpable pulse in the target artery and a strong Doppler signal that decreases with graft occlusion, but intraoperative imaging should be used liberally, if not routinely, to avoid graft thrombosis. Grade 1/2/3 complication

B Figure 60–16 A, Schematic of the biology of myointimal hyperplasia based on vascular smooth muscle cell migration and proliferation. B, Hyperplastic lesion in a vein graft. The lesion was discovered at the site of a venous valve during routine graft surveillance using Duplex ultrasound.

Intimal Hyperplasia (Fig. 60–16) ● Consequence Intimal hyperplasia can lead to midterm graft failure between 30 days and 2 years postoperatively. Grade 3 complication ● Repair Intimal hyperplasia can be repaired with patch angioplasty of the lesion, a jump bypass around the lesion, or angioplasty with a cutting balloon or atherectomy. ● Prevention Signiﬁcant hemodynamic lesions secondary to intimal hyperplasia occur at a rate of 5% per year in vein grafts with a majority in the ﬁrst 2 years and cannot be directly prevented.25 The goal of surveillance protocols is to identify correctable lesions before thrombosis, thus permitting elective revision. Graft failure may be indicated by (1) the recurrence of symptoms, (2) low velocities, or low-ﬂow state, on duplex ultrasound, (3) elevated velocities in an area of stenosis, or (4) a decrease in the ABI.26

● Repair Intraoperative arteriography allows the surgeon to evaluate both anastomoses, the conduit, and the outﬂow arterial tree. If thrombosis has occurred, thrombectomy should precede angiography. Any technical errors noted at either anastomosis or in the conduit must be repaired at the time of surgery. If no technical errors are noted, arterial inﬂow pressures should be measured and conﬁrmed. Hemodynamically signiﬁcant inﬂow gradients requiring inﬂow augmentation may occur after the bypass owing to decreased outﬂow resistance31 (Fig. 60–17). Angioscopy may also be used to evaluate a bypass after completion. In a recent study of 90 grafts with normal completion angiograms, 7 were found to have signiﬁcant pathology on angioscopy.32 The authors concluded angioscopy was superior to angiography for disclosing conduit defects, although it did not provide adequate information about the distal arterial runoff. However, our experience with angioscopy was suboptimal owing to technical difﬁculties and clearing the endoluminal ﬁeld of blood for adequate views. Intraoperative duplex ultrasound has gained increasing favor as the primary method to evaluate a bypass. The entire graft can be easily insonated as well as the anastomoses and proximate arterial tree. Peak systolic velocities higher than 180 cm/sec, spectral broadening, and velocity ratio greater than 3 (suggesting turbulent ﬂow), and peak systolic velocities higher than 30 to 40 cm/sec and high outﬂow resistance with absent diastolic ﬂow (suggesting low ﬂow) predict a failing graft that warrants surgical intervention.33

60 INFRAINGUINAL REVASCULARIZATION

625

● Prevention Poor ﬂow after completion of a bypass can be prevented only with optimal patient selection and meticulous surgical technique. Patients should have adequate runoff because poor runoff scores are an independent predictor of limb loss after revascularization.34

Wound Closure Lymphatic Leak/Seroma ● Consequence Dissection of tissues may lead to lymphatic disruption and leak. This occurs in approximately 0.5% to 4% of patients with groin incisions.35,36 This can be diagnosed by clear ﬂuid drainage and/or a lymphocele on duplex ultrasound. Grade 1/2/3 complication

A

● Repair Conservative treatment with leg elevation and compression stocking therapy may be sufﬁcient, although surgical excision and oversewing of the lymphatic pedicle decreases hospital stay, lowers complication rates, and results in fewer recurrences.37 ● Prevention It is important to prevent lymphatic leaks because they are a risk factor for subsequent infection.38 They can be prevented by electrocauterization or ligation of divided lymphatics at the time of surgery as well as by close approximation of tissue planes.

Wound Hemorrhage ● Consequence Hematoma formation. Grade 1/2/3 complication ● Repair If the cause of hemorrhage is believed to be surgical in nature, wound exploration with ligation of bleeding vessels is warranted (Fig. 60–18). If the cause is medical, cessation of antiplatelet or anticoagulant therapy with possible reversal of anticoagulation with blood products may be necessary. After the anticoagulation has been reversed, hematoma evacuation may be performed. B Figure 60–17 A, Completion angiogram after femoral–to– plantaris pedis branch of the posterior tibial artery bypass using the saphenous vein. B, Completion angiogram after a distal vein patch bypass using polytetraﬂuoroethylene (PTFE) to the anterior tibial artery.

● Prevention Signiﬁcant hemorrhage occurring within 48 hours is infrequent, occurring less than 2% of the time.39 The most common causes are failure to ligate a venous or arterial branch and suture line hemorrhage owing to technical failure. Bleeding may also occur secondary to arterial or venous damage during wound closure with a needle. Many patients are placed on antiplatelet or anticoagulant therapy to prevent graft thrombosis as well as coronary complications. One study found that treating patients at highest risk of major hemorrhage

626

SECTION X: VASCULAR SURGERY

with aspirin instead of oral anticoagulants would result in a reduction of nonfatal hemorrhages, but the reduction was outweighed by an increase in ischemic events and graft occlusions.40

Wound Infection ● Consequence The incidence of wound infections ranges from 5% to 20%.41–43 Two classiﬁcations of wound infections exist (Table 60–1). The Johnson classiﬁcation is more thorough because it recognizes a group of wounds that are not infected but have the possiblity of becoming so. Class 1 and 2 wounds minimally alter a patient’s hospital course, whereas class 4 wound infections could lead to loss of the bypass graft and, possibly, amputation. Grade 1/2/3 complication ● Repair Treatment depends on the type of wound. Class 1 wounds may be observed. Class 2 wounds may need local débridement of the necrotic suture line. Prophy-

Figure 60–18 “Bleeding” of blood through the interstices of a PTFE graft. Direct suture repair or topical hemostatic agents such as thrombin-soaked Gelfoam can be used to prevent surgical bleeding from resulting in postoperative hematoma. Table 60–1

lactic antibiotic therapy may be used for class 1 and 2 wounds in order to prevent conversion to class 3 or 4 and possible involvement of the bypass. Class 3 wounds require more extensive débridement of devitalized tissue. Class 4 wounds represent a treatment dilemma. Infection of the anastomotic segment typically requires excision of the graft secondary to the higher incidence of anastomotic dehiscence. If the infection of the graft does not involve the anastomosis and there is no evidence of systemic sepsis, graft thrombosis, or septic emboli, graft-preserving therapy can be undertaken with aggressive local wound débridement and administration of broad-spectrum antibiotics, with or without muscle ﬂap coverage44 (Fig. 60–19). Infected prosthetic grafts are more difﬁcult to treat with antibiotic therapy alone because there is a high incidence of recurrent sepsis.45 A large proportion of infected prosthetic grafts managed with incomplete graft removal require subsequent operations. Complete excision of infected graft material results in a signiﬁcant reduction in sepsis, amputation, and early mortality.46 ● Prevention Wound closure is of paramount importance after an infrainguinal bypass. Closure of the proximal groin wound begins by closing the femoral sheath. The subcutaneous tissue is then closed in layers, ensuring adequate coverage of the bypass. A layered closure decreases the risk of postoperative complications. A similar layered closure of the distal (and saphenectomy) incision is performed. Care must be taken to avoid compression of the graft during closure of the wounds (Fig. 60–20). The deeper layer closure should be performed with monoﬁlament absorbable suture to reduce the inﬂammatory response in the wound. Skin closure can be completed with permanent suture or staples or a subcuticular absorbable suture. The skin should not be closed with a running permanent suture line because this can lead to ischemia of the wound edges. Risk factors for wound infection include poorly controlled diabetes,47 end-stage renal disease,48 obesity,49 and intraoperative hypothermia.50 Wound infections can be

Classiﬁcation of Wound Complications Szilagyi Classiﬁcation74

Johnson Classiﬁcation45

Treatment

Erythema and seroma without infection

Class 1

Observation ± Antibiotics

Ischemic necrosis of the incision without infection

Class 2

Observation ± Débridement ± Antibiotics

Ischemic necrosis and wound breakdown with infection

Grade I (dermis only) Grade II (subcutaneous)

Class 3

Débridement Antibiotics

Open, infected wound with involvement of bypass graft

Grade III

Class 4

Débridement Antibiotics ± Graft excision ± Muscle ﬂap

60 INFRAINGUINAL REVASCULARIZATION

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prevented with the use of preoperative antibiotics,51 skin cleansing with povidine-iodine or chlorhexadine,52 and meticulous surgical technique. Finally, continuous wound incisions for saphenectomy have a higher risk of infection (27%–42%) than incisions interrupted with skin bridges (9%–20%).53,54

Other Complications

A

B Figure 60–19 A, Exposed graft after aggressive débridement for infection. The anastomosis is not involved. B, Sartorius muscle ﬂap coverage of the exposed graft.

Figure 60–20 Wound closure. Primary closure over the graft (arrow) with relaxing incision and xenograft closure.

Graft Thrombosis Graft failure can be divided into early, midterm, and late thrombosis. Early graft thrombosis occurs within 30 days approximately 10% of the time43 and is typically caused by technical failure, postoperative hypotension, hypercoagulability, or poor distal runoff.55 All are avoidable by careful preoperative planning, meticulous intraoperative execution, and close postoperative monitoring. Hypercoagulable states occur in approximately 13% of patients undergoing infrainguinal bypass and should be suspected in any graft thrombosis that is recurrent or for which no other cause can be identiﬁed.56 In two prospective studies, treatment of patients with acute ischemia (0–14 days) with thrombolysis had improved amputation-free survival and shorter hospital stays. However, for patients with chronic ischemia (>14 days), surgical revascularization was more effective and safer than thrombolysis.57,58 Midterm graft failures occur between 30 days and 2 years and are discussed under “Distal Anastomosis,” earlier. Late graft failures are most likely related to recurrent atherosclerosis and occur beyond 2 years. Grade 2/3 complication Myocardial Infarction Clinical risk assessment is a key aspect of the preoperative work-up for infrainguinal revascularization. Mild to moderate coronary artery disease (CAD) is present in 92% of patients with peripheral occlusive disease, and severe CAD in present in 25%.59 In fact, perioperative myocardial infarction occurs in 2% to 6.5% of patients after infrainguinal revascularization.60 Two frequently used CAD scoring systems are the Eagle criteria61 and the American College of Cardiology/American Heart Association (ACC/AHA) guidelines.62 Clinical assessment by combined Eagle criteria and ACC/AHA guidelines accurately estimates patients at higher risk for myocardial infarction and cardiac-related mortality after vascular surgery.63,64 Multiple studies have been performed examining the utility of preoperative cardiac risk testing. In the past, reversible perfusion defects found on stress tests were an indication for coronary angiography. More recent studies have shown that coronary revascularization in patients with stable symptoms undergoing peripheral vascular procedures does not improve outcomes.65 Furthermore, preoperative stress tests do not predict survival in diabetic patients.66 Based on these studies, coronary angiography

628

SECTION X: VASCULAR SURGERY

and possible coronary revascularization should be reserved for those patients with unstable angina. For the remainder of patients, risk factor modiﬁcation including βblockade,67,68 antiplatelet agents,69 and statin therapy70 remains the mainstay of cardiac optimization prior to infrainguinal bypass. Grade 1–5 complication

Pneumonia/Respiratory Failure The high incidence of tobacco use and chronic obstructive pulmonary disease (COPD) in patients undergoing lower extremity revascularization places them at increased risk for pulmonary complications, including pneumonia and respiratory failure. In a recent study, advanced age, American Society of Anesthesiologists class 2 or higher, functional dependence, COPD, and congestive heart failure placed patients at risk for pulmonary compli-cations after infrainguinal bypass.71 There was insufﬁcient evidence to support preoperative spirometry as a tool to stratify risk. Preoperative smoking cessation, exercise regimen, bronchodilators, and inhaled steroids may all reduce the incidence of postoperative pulmonary complications. Grade 1/4/5 complication Renal Failure Acute renal failure occurs in approximately 1% to 2% of patients undergoing lower extremity revascularization.72 This is most commonly caused by contrast nephropathy and prerenal acute tubular necrosis. The incidence of acute renal failure has decreased owing to advances in critical care. Grade 1/4/5 complication Deep Venous Thrombosis Lower extremity edema is a common occurrence after infrainguinal bypass. Although typically asymptomatic in nature, untreated edema can lead to an increased incidence of wound infection. Edema is most likely caused by venous or lymphatic disruption during dissection.73 It can also be due to impaired venous return after years of chronic ischemia. In each of these cases, treatment entails leg elevation and possibly compression stocking therapy. Deep venous thrombosis is a less common cause of postoperative edema, but it must be ruled out to avoid pulmonary embolism. In a patient with a history of multiple graft thromboses and deep venous thrombosis, a hypercoagulable state must be considered. Grade 1/2/5 complication

REFERENCES 1. Kempczinski RF, Bernhard VM. Management of chronic ischemia of the lower extremities: introduction and general considerations. In Rutherford RB (ed): Vascular Surgery, 3rd ed. Philadelphia, Saunders, 1989; p 643.

2. Johnston KW. The chronically ischemic leg: an overview. In Rutherford RB (ed): Vascular Surgery, 6th ed. Philadelphia: Elsevier Saunders; 2005; pp 1077–1082. 3. Jager KA, Langlois Y, Roederer GO, Strandness DE. Non-invasive assessment of upper and lower extremity ischemia. In Bergan JJ, Yao JST (eds): Evaluation and Treatment of Upper and Lower Extremity Circulatory Disorders. Orlando, FL: Grune and Stratton, 1984; p 97. 4. Christensen T, Neubauer B. Increased arterial wall stiffness and thickness in medium-sized arteries in patients with insulin-dependent diabetes mellitus. Acta Radiol 1988;29:299. 5. Clark LC. Monitor and control of blood and tissue oxygen tensions. Trans Am Soc Artif Intern Organs 1956; 2:41. 6. White RA, Nolan L, Harley D, et al. Non-invasive evaluation of peripheral vascular disease using transcutaneous oxygen tension. Am J Surg 1982;144:68. 7. Hauser CJ, Shoemaker WC: Use of transcutaneous PO2 regional perfusion index to quantify tissue perfusion in peripheral vascular disease. Ann Surg 1983;197:337. 8. Gupta SK, Veith FJ, Kram HB, Wengerter KA. Signiﬁcance and management of inﬂow gradients unexpectedly generated after femorofemoral, femoropopliteal, and femoroinfrapopliteal bypass grafting. J Vasc Surg 1990;12: 278–283. 9. Greiner A, Rantner B, Greiner K, et al. Neuropathic pain after femoropopliteal bypass surgery. J Vasc Surg 2004;39: 1284–1287. 10. Busch T, Strauch J, Aleksic I, et al. Incidence and importance of lower extremity nerve lesions after infrainguinal vascular surgical interventions. Eur J Vasc Endovasc Surg 1999;17:290–293. 11. Wengerter KR, Veith FJ, Gupta SK, et al. Inﬂuence of vein size (diameter) on infrapopliteal reversed vein graft patency. J Vasc Surg 1990;11:525–531. 12. Bergamini TM, Towne JB, Bandyk DF, et al. Experience with in situ saphenous vein bypasses during 1981 to 1989: determinant factors of long-term patency. J Vasc Surg 1991;13:137–147. 13. Gwynn BR, Shearman CP, Simms MH. The inﬂuence of patent branches on in situ vein graft haemodynamics. Eur J Vasc Surg 1987;1:169–172. 14. Malmstedt J, Takolander R, Wahlberg E. A randomized prospective study of valvulotome efﬁcacy in in situ reconstructions. Eur J Vasc Endovasc Surg 2005;30:52– 56. 15. Vesti BR, Primozich J, Bergelin RO, Strandness E Jr. Follow-up of valves in saphenous vein bypass grafts with duplex ultrasonography. J Vasc Surg 2001;33:369–374. 16. Wengerter KR, Veith FJ, Gupta SK, et al. Prospective randomized multicenter comparison of in situ and reversed vein infrapopliteal bypasses. J Vasc Surg 1991;13: 189–197. 17. Allen KB, Heimansohn DA, Robison RJ, et al. Risk factors for leg wound complications following endoscopic versus traditional saphenous vein harvesting. Heart Surg Forum 2000;3:325–330. 18. Yun KL, Wu Y, Aharonian V, et al. Randomized trial of endoscopic versus open vein harvest for coronary artery bypass grafting: six-month patency rates. J Thorac Cardiovasc Surg 2005;129:496–503.

60 INFRAINGUINAL REVASCULARIZATION 19. Schurr UP, Lachat ML, Reuthebuch O, et al. Endoscopic saphenous vein harvesting for CABG—a randomized, prospective trial. Thorac Cardiovasc Surg 2002;50:160–163. 20. Mills JL, Fujitani RM, Taylor SM. Contribution of routine intraoperative completion arteriography to early infrainguinal bypass patency. Am J Surg 1992;164:506–510. 21. Belkin M, Whittemore AD, Donaldson MC, et al. Peripheral arterial occlusive disease. In Townsend CM, Beauchamp RD, Evers BM, Mattox KL (eds): Textbook of Surgery, 18th ed. Philadelphia: WB Saunders, 2004; p 1989. 22. Ameli FM, Provan JL, Williamson C, Keuchler PM. Etiology and management of aorto-femoral bypass graft failure. J Cardiovasc Surg (Torino) 1987;28:695–700. 23. Bandyk DF, Bergamini TM, Kinney EV, et al. In situ replacement of vascular prostheses infected by bacterial bioﬁlms. J Vasc Surg 1991;13:575–583. 24. Seabrook GR, Schmitt DD, Bandyk DF, et al. Anastomotic femoral pseudoaneurysm: an investigation of occult infection as an etiologic factor. J Vasc Surg 1990;11:629– 634. 25. Bandyk DF, Kaebnick HW, Stewart GW, Towne JB. Durability of the in situ saphenous vein arterial bypass: a comparison of primary and secondary patency. J Vasc Surg 1987;5:256–268. 26. Bandyk DF, Schmitt DD, Seabrook GR, et al. Monitoring functional patency of in situ saphenous vein bypasses: the impact of a surveillance protocol and elective revision. J Vasc Surg 1989;9:286–296. 27. Parsons RE, Suggs WD, Veith FJ, et al. Polytetraﬂuoroethylene bypasses to infrapopliteal arteries without cuffs or patches: a better option than amputation in patients without autologous vein. J Vasc Surg 1996;23:347–354. 28. Norberto JJ, Sidawy AN, Trad KS, et al. The protective effect of vein cuffed anastomoses is not mechanical in origin. J Vasc Surg 1995;21:558–564. 29. Trubel W, Schima H, Czerny M, et al. Experimental comparison of four methods of end-to-side anastomosis with expanded polytetraﬂuoroethylene. Br J Surg 2004; 91:159–167. 30. Neville RF, Tempesta B, Sidway AN. Tibial bypass for limb salvage using polytetraﬂuoroethylene and a distal vein patch. J Vasc Surg 2001;33:266–271. 31. Gupta SK, Veith FJ, Kram HB, Wengerter KA. Signiﬁcance and management of inﬂow gradients unexpectedly generated after femorofemoral, femoropopliteal, and femoroinfrapopliteal bypass grafting. J Vasc Surg 1990;12: 278–283. 32. Woelﬂe KD, Kugelmann U, Bruijnen H, et al. Intraoperative imaging techniques in infrainguinal arterial bypass grafting: completion angiography versus vascular endoscopy. Eur J Vasc Surg 1994;8:556–561. 33. Johnson BL, Bandyk DF, Back MR, et al. Intraoperative duplex monitoring of infrainguinal vein bypass procedures. J Vasc Surg 2000;31:678–690. 34. Seeger JM, Pretus HA, Carlton LC, et al. Potential predictors of outcome in patients with tissue loss who undergo infrainguinal vein bypass grafting. J Vasc Surg 1999;30:427–435. 35. Tyndall SH, Shepard AD, Wilczewski JM, et al. Groin lymphatic complications after arterial reconstruction. J Vasc Surg 1994;19:858–863.

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36. Roberts JR, Walters GK, Zenilman ME, Jones CE. Groin lymphorrhea complicating revascularization involving the femoral vessels. Am J Surg 1993;165:341–344. 37. Schwartz MA, Schanzer H, Skladany M, et al. A comparison of conservative therapy and early selective ligation in the treatment of lymphatic complications following vascular procedures. Am J Surg 1995;170:206–208. 38. Reifsnyder T, Bandyk D, Seabrook G, et al. Wound complications of the in situ saphenous vein bypass technique. J Vasc Surg 1992;15:843–848. 39. Taylor LM Jr, Edwards JM, Porter JM. Present status of reversed vein bypass grafting: ﬁve-year results of a modern series. J Vasc Surg 1990;11:193–205. 40. Ariesen MJ, Tangelder MJ, Lawson JA, et al, and the Dutch Bypass Oral Anticoagulants or Aspirin Study Group. Risk of major haemorrhage in patients after infrainguinal venous bypass surgery: therapeutic consequences? The Dutch BOA (Bypass Oral Anticoagulants or Aspirin) Study. Eur J Vasc Endovasc Surg 2005;30:154– 159. 41. Donaldson MC, Mannick JA, Whittemore AD. Femoraldistal bypass with in situ greater saphenous vein. Longterm results using the Mills valvulotome. Ann Surg 1991; 213:457–464. 42. Prendiville EJ, Yeager A, O’Donnell TF Jr, et al. Longterm results with the above-knee popliteal expanded polytetraﬂuoroethylene graft. J Vasc Surg 1990;11:517– 524. 43. Schepers A, Klinkert P, Vrancken Peeters MP, Breslau PJ. Complication registration in patients after peripheral arterial bypass surgery. Ann Vasc Surg 2003;17:198– 202. 44. Dosluoglu HH, Schimpf DK, Schultz R, Cherr GS. Preservation of infected and exposed vascular grafts using vacuum assisted closure without muscle ﬂap coverage. J Vasc Surg 2005;42:989–992. 45. Johnson JA, Cogbill TH, Strutt PJ, Gundersen AL. Wound complications after infrainguinal bypass. Classiﬁcation, predisposing factors, and management. Arch Surg 1988;123:859–862. 46. Mertens RA, O’Hara PJ, Hertzer NR, et al. Surgical management of infrainguinal arterial prosthetic graft infections: review of a thirty-ﬁve-year experience. J Vasc Surg 1995;21:782–790. 47. Goodson WH 3rd, Hunt TK. Wound healing in experimental diabetes mellitus: importance of early insulin therapy. Surg Forum 1978;29:95–98. 48. O’Hare AM, Sidawy AN, Feinglass J, et al. Inﬂuence of renal insufﬁciency on limb loss and mortality after initial lower extremity surgical revascularization. J Vasc Surg 2004;39:709–716. 49. Kent KC, Bartek S, Kuntz KM, et al. Prospective study of wound complications in continuous infrainguinal incisions after lower limb arterial reconstruction: incidence, risk factors, and cost. Surgery 1996;119:378–383. 50. Kurz A, Sessler DI, Lenhardt R. Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. Study of Wound Infection and Temperature Group. N Engl J Med 1996;334:1209– 1215. 51. Bandyk DF. Vascular graft infections: epidemiology, microbiology, pathogenesis and prevention. In Bernhard

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52.

53.

54.

55.

56.

57.

58.

59.

60.

61. 62.

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VM, Towne JB (eds): Complications in Vascular Surgery. St. Louis: Quality Medical, 1991; pp 223–234. Berry AR, Watt B, Goldacre MJ, et al. A comparison of the use of povidone-iodine and chlorhexidine in the prophylaxis of postoperative wound infection. J Hosp Infect 1982;3:55–63. Schwartz ME, Harrington EB, Schanzer H. Wound complications after in situ bypass. J Vasc Surg 1988;7: 802–807. Wengrovitz M, Atnip RG, Gifford RR, et al. Wound complications of autogenous subcutaneous infrainguinal arterial bypass surgery: predisposing factors and management. J Vasc Surg 1990;11:156–161. Donaldson MC, Mannick JA, Whittemore AD. Causes of primary graft failure after in situ saphenous vein bypass grafting. J Vasc Surg 1992;15:113–118. Curi MA, Skelly CL, Baldwin ZK, et al. Long-term outcome of infrainguinal bypass grafting in patients with serologically proven hypercoagulability. J Vasc Surg 2003; 37:301–306. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity. The STILE trial. Ann Surg 1994;220:251–266. Comerota AJ, Weaver FA, Hosking JD, et al. Results of a prospective, randomized trial of surgery versus thrombolysis for occluded lower extremity bypass grafts. Am J Surg 1996;172:105–112. Hertzer NR, Beven EG, Young JR, et al. Coronary artery disease in peripheral vascular patients. A classiﬁcation of 1000 coronary angiograms and results of surgical management. Ann Surg 1984;199:223–233. Marek JM, Mills JL. Risk factor assessment and indications for reconstruction. In Management of Chronic Lower Limb Ischemia. London: Arnold, 2000; pp 30–44. Eagle KA, Boucher CA. Cardiac risk of noncardiac surgery. N Engl J Med 1989;321:1330–1332. Eagle KA, Berger PB, Calkins H, et al. ACC/AHA guideline update for perioperative cardiovascular evaluation for noncardiac surgery—executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Anesth Analg 2002;94:1052–1064.

63. Back MR, Schmacht DC, Bowser AN, et al. Critical appraisal of cardiac risk stratiﬁcation before elective vascular surgery. Vasc Endovascular Surg 2003;37:387– 397. 64. Back MR, Leo F, Cuthbertson D, et al. Long-term survival after vascular surgery: speciﬁc inﬂuence of cardiac factors and implications for preoperative evaluation. J Vasc Surg 2004;40:752–760. 65. McFalls EO, Ward HB, Moritz TE, et al. Coronary-artery revascularization before elective major vascular surgery. N Engl J Med 2004;351:2795–2804. 66. Monahan TS, Shrikhande GV, Pomposelli FB, et al. Preoperative cardiac evaluation does not improve or predict perioperative or late survival in asymptomatic diabetic patients undergoing elective infrainguinal arterial reconstruction. J Vasc Surg 2005;41:38–45. 67. 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. 68. Wallace A, Layug B, Tateo I, et al. Prophylactic atenolol reduces postoperative myocardial ischemia. McSPI Research Group. Anesthesiology 1998;88:7–17. 69. Hackam DG. Cardiovascular risk prevention in peripheral artery disease. J Vasc Surg 2005;41:1070–1073. 70. Parker Ward R, Leeper NJ, Kirkpatrick JN, et al. The effect of preoperative statin therapy on cardiovascular outcomes in patients undergoing infrainguinal vascular surgery. Int J Cardiol 2005;104:264–268. 71. Smetana GW, Lawrence VA, Cornell JE, and the American College of Physicians. Preoperative pulmonary risk stratiﬁcation for noncardiothoracic surgery: systematic review for the American College of Physicians. Ann Intern Med 2006;144:581–595. 72. Faries PL, LoGerfo FW, Hook SC, et al. The impact of diabetes on arterial reconstructions for multilevel arterial occlusive disease. Am J Surg 2001;181:251–255. 73. AbuRahma AF, Woodruff BA, Lucente FC. Edema after femoropopliteal bypass surgery: lymphatic and venous theories of causation. J Vasc Surg 1990;11:461–467. 74. Szilagyi DE, Smith RF, Elliott JP, Vrandecic MP. Infection in arterial reconstruction with synthetic grafts. Ann Surg 1972;176:321–333.

61

Arteriovenous Hemodialysis Access Robyn A. Macsata, MD and Anton N. Sidawy, MD INTRODUCTION Currently, over 325,000 patients are on dialysis in the United States, and more than 100,000 new patients begin dialysis each year.1 Medicare spends over $18 billion dollars annually in the care of these patients; a large portion of the expenses is dedicated to dialysis access and its complications.2 With these numbers, it is no surprise that vascular access is a prevalent part of many surgeons’ practices. With the ever-increasing numbers and cost of care of these patients, it is imperative that surgeons provide the most reliable dialysis access with the lowest possible risk of complications. Autogenous arteriovenous accesses have consistently been shown to have excellent patency rates and low risk of complications when compared with prosthetic arteriovenous accesses. Two-year primary patency rates of autogenous access range between 34% to 69%, which is clearly superior to the 2-year primary patency rates of prosthetic access, which averages 25%.3–6 Complications of infection, pseudoaneursyms, and seromas are rarely seen in autogenous access. With these beneﬁts, the disadvantages of autogenous access, including a long maturation time, failure to mature, and acute thrombosis, are acceptable. In consideration of these data, the current Dialysis Outcomes Quality Initiative (DOQI) recommendation is to place autogenous access in at least 50% of all patients requiring long-term access.7 In order to place long-term autogenous access with the lowest risk of complications, preoperative evaluation is essential. A thorough patient history is taken, documenting the patient’s dominant extremity, recent history of peripheral intravenous lines, site of indwelling or previous central lines, all previous access procedures, any history of trauma or previous surgery to the extremity, and all comorbid conditions. On physical examination, the patient’s arm is evaluated for edema and varicosities. With an upper arm tourniquet in place, the arm is inspected for visible cephalic and basilic veins. Indications for preoperative venography are listed in Box 61–1; venography may be substituted with a venous duplex scan as long as the surgeon recognizes the limitations of evaluating the central venous system. To assess for adequate arterial inﬂow, a thorough pulse examination including Allen’s test is done.

Abnormal pulses in the planned operative extremity are further evaluated with arteriogram.7,8 Box 61–2 lists the multiple access conﬁgurations possible in the upper and lower extremities as well as the body wall.9 An autogenous access is always attempted before prosthetic access, including use of basilic vein transpositions. One-year primary patency rates of basilic vein transpositions range between 35% and 84% with an acceptably low complication rate and are, therefore, an excellent alternative to cephalic vein access.6,10–13 Preference is given to the nondominant arm over the dominant arm, followed by distal location over proximal location. Controversy still exists whether a prosthetic forearm access should be placed before an upper arm autogenous access. The autogenous access will likely offer longer patency but eliminates the placement of subsequent forearm prosthetic access. Therefore, this decision remains surgeon and patient dependent. Lower extremity and body wall access are used only once both upper extremity uses have been exhausted.7

INDICATIONS ● Creatinine clearance less than 25 ml/min ● Serum creatinine greater than 4 mg/dl ● Patient within 1 year of anticipated need for dialysis

OPERATIVE STEPS Autogenous Posterior Radial Branch–Cephalic Direct Wrist Access (Fig. 61–1) Step Step Step Step Step

1 2 3 4 5

Cephalic vein exposure and evaluation Posterior radial branch artery exposure Radial artery–to–cephalic vein anastomosis Ligation of venous branches Wound closure

Autogenous Brachial-Basilic Upper Arm Transposition (Fig. 61–2) Step 1 Step 2

Basilic vein exposure and evaluation Basilic vein harvest with ligation of all side branches (see Fig. 61–2A)

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Box 61–1 Indications for Venous Imaging before Access Insertion

Box 61–2

●

●

● ● ● ● ●

Edema in the extremity in which an access is planned Collateral vein development in any planned access site Differential extremity size of the considered limb Current or previous transvenous catheter, of any type, in the ipsilateral limb Previous arm, neck, or chest trauma or surgery in venous drainage of the planned access site Multiple previous accesses in the ipsilateral extremity

Arteriovenous Access Conﬁguration

Forearm Autogenous Autogenous posterior radial branch–cephalic direct access ● Autogenous radial-cephalic direct wrist access ● Autogenous radial-cephalic forearm transposition ● Autogenous brachial-cephalic forearm looped transposition ● Autogenous radial-basilic forearm transposition ● Autogenous ulnar-basilic forearm transposition ● Autogenous brachial-basilic forearm looped transposition ● Autogenous radial-brachial indirect saphenous vein translocation ● Autogenous brachial-antecubital forearm looped saphenous vein translocation Prosthetic ● Prosthetic radial-antecubital forearm straight access ● Prosthetic brachial-antecubital forearm loop access ●

Adapted from NKF-K/DOQI Clinical practice guidelines for vascular access: update 2000. Am J Kidney Dis 2001;37(suppl):S137–S181.

●

Upper Arm ●

Autogenous Autogenous brachial-cephalic upper arm direct access ● Autogenous brachial-cephalic upper arm transposition ● Autogenous brachial-basilic upper arm transposition ● Autogenous brachial-brachial (vein) upper arm transposition ● Autogenous brachial-axillary indirect saphenous vein translocation Prosthetic ● Prosthetic brachial-axillary access ●

●

Lower Extremity ●

Autogenous Autogenous femoral–greater saphenous looped access transposition ● Autogenous femoral–superﬁcial femoral vein looped access transposition Prosthetic ● Prosthetic femoral-femoral looped inguinal access ●

●

Figure 61–1 Autogenous posterior radial branch-cephalic direct wrist access. (Adapted from Weiswasser JM, Sidawy AN. Strategies of arteriovenous dialysis access. In Rutherford RB (ed): Vascular Surgery, 6th ed. Philadelphia: Elsevier Saunders, 2005; p 1671.)

Step 3 Step 4 Step 5 Step 6

Brachial artery exposure (see Fig. 61–2B) Tunneling of basilic vein Brachial artery–to–basilic vein anastomosis (see Fig. 61–2C) Wound closure

Prosthetic Brachial-Antecubital Forearm Loop Access (Fig. 61–3) Step Step Step Step Step Step

1 2 3 4 5 6

Antecubital vein exposure and evaluation Brachial artery exposure Tunneling of graft Arterial graft anastomosis Venous graft anastomosis Wound closure

Body Wall ●

Prosthetic Prosthetic ● Prosthetic ● Prosthetic ● Prosthetic ● Prosthetic ●

axillary-axillary chest access axillary-axillary chest loop access axillary–internal jugular chest loop access axillary-femoral body wall access femoral-femoral suprainguinal access

Adapted from Sidawy AN, Gray R, Besarab A, et al. Recommended standards for reports dealing with arteriovenous hemodialysis accesses. J Vasc Surg 2002;35:603–610.

OPERATIVE PROCEDURE Venous Exposure Early Autogenous Arteriovenous Access Thrombosis ● Consequence Access thrombosis and inability to dialyze. The major disadvantage of autogenous arteriovenous access is

61 ARTERIOVENOUS HEMODIALYSIS ACCESS

633

A

Figure 61–3 Prosthetic brachial-antecubital forearm loop access. (Reproduced with permission from Weiswasser JM, Sidawy AN. Strategies of arteriovenous dialysis access. In Rutherford RB (ed): Vascular Surgery, 6th ed. Philadelphia: Elsevier Saunders, 2005; p 1674.)

B

publication of the DOQI guidelines in 1997, surgeons have become more aggressive in attempting to place autogenous accesses, with use of smaller-caliber veins, possibly increasing early thrombosis rates.16 This is believed to be an acceptable risk for the potential beneﬁts of autogenous access.7 Other less common causes include poor arterial inﬂow and anastomotic stenosis. Grade 3 complication

C Figure 61–2 Autogenous brachial-basilic upper arm transposition. A, Basilic vein harvest with ligation of all side branches. B, Brachial artery exposure. C, Brachial artery–to–basilic vein anastomosis.

primary failure rates that range from 3% to 33%.13–15 Early access thrombosis is due to technical failure and most commonly is associated with inadequate venous outﬂow, which may be secondary to inadequate caliber of the outﬂow vein or central venous stenosis. With the

● Repair Thrombectomies and thrombolysis are rarely successful for autogenous accesses. If early thrombosis is secondary to small caliber of the outﬂow vein, the autogenous arteriovenous access is redone using a different vein (e.g., conversion of an autogenous radial-cephalic direct wrist access to an autogenous radial-basilic forearm transposition) or, if no vein is available, a prosthetic arteriovenous access. Central venous stenosis (Fig. 61–4) is treated with angioplasty and/or stenting or venous bypass (e.g., subclavian vein–to–internal jugular vein bypass [Fig. 61–5]), followed by a new autogenous or prosthetic arteriovenous access. An arterial inﬂow stenosis is treated with angioplasty and/or

634

A

SECTION X: VASCULAR SURGERY

C

Figure 61–4 Central venous stenosis. A, Upper extremity varicosities associated with central venous stenosis. B, Upper extremity edema associated with central venous stenosis. C, Venogram of the patient in Figure 61–4A demonstrates subclavian vein stenosis. (A and C, Reproduced with permission from Adams ED, Sidawy AN. Nonthrombotic complications of arteriovenous access for hemodialysis. In Rutherford RB (ed): Vascular Surgery, 6th ed. Philadelphia: Elsevier Saunders, 2005; p 1700.)

B stenting or proximal arterial bypass to restore adequate arterial inﬂow followed by a new autogenous or prosthetic arteriovenous access. An alternative approach is to move the ﬁstula either proximally or to another extremity where arterial inﬂow is adequate. Anastomotic stenosis is a primary technical failure and is redone with close attention to surgical technique. ● Prevention Preoperative evaluation with a thorough history and physical examination is imperative to place functional autogenous arteriovenous accesses. We perform a preoperative venous duplex scan on all patients with the indications listed in Box 61–1 and any patient whose superﬁcial veins cannot be visualized on physical examination. The cephalic or basilic veins are used for autogenous access only if they are a minimum of 2.0 mm in diameter.17 Preoperative venography is completed in any patient with high clinical suspicion for central venous stenosis or with abnormal ﬁndings on venous duplex scan. Occurrence of central venous stenosis is decreased by keeping use of central venous lines to a

minimum. If they are required, the internal jugular approach is preferable. Central venous stenosis is treated before placement of arteriovenous ﬁstula with angioplasty and/or stenting or proximal venous bypass. Any patient with an abnormal pulse examination is further evaluated with upper extremity pulse volume recordings and segmental pressures. Any drop in pressure greater than 30 mm Hg is believed to be abnormal, and if possible, we place the arteriovenous access in an alternate extremity or proximal to the area of stenosis. If an arteriovenous access must be placed in an area of abnormal arterial inﬂow, the patient is further evaluated with arteriogram, and any stenosis is treated with angioplasty and/or stenting or arterial bypass. To avoid anastomotic stenosis, care must be taken intraoperatively to ensure patency of this small anastomosis.7,8

Late Arteriovenous Access Thrombosis ● Consequence Access thrombosis and inability to dialyze. Primary patency rates of autogenous accesses range between

61 ARTERIOVENOUS HEMODIALYSIS ACCESS

Int. juglar v.

A

Axillary v.

B Figure 61–5 Subclavian vein–to–internal jugular bypass. A, Subclavian vein–to–internal jugular bypass using a 6-mm expanded polytetraﬂuoroethylene (ePTFE) prosthetic graft. B, Postoperative venogram of subclavian vein–to–internal jugular bypass using a 6mm ePTFE prosthetic graft. (A, Reproduced with permission from Adams ED, Sidawy AN. Nonthrombotic complications of arteriovenous access for hemodialysis. In Rutherford RB (ed): Vascular Surgery, 6th ed. Philadelphia: Elsevier Saunders, 2005; p 1701.)

43% and 84% at 1 year and 34% and 69% at 2 years and are superior to primary patency rates of prosthetic accesses of 41% to 54% at 1 year and 24% to 25% at 2 years.3–6,10,11,13–15 Late arteriovenous access thrombosis is most commonly due to intimal hyperplasia (Fig. 61–6A). In an autogenous access, this usually occurs just distal to the anastomosis; however, it may occur anywhere along the venous outﬂow tract. In a prosthetic access, intimal hyperplasia occurs at the graft– venous anastomosis. Central venous stenosis is a second common cause of late autogenous and prosthetic arteriovenous access failure. Grade 2/3 complication ● Repair Thrombectomies and thrombolysis are rarely successful in autogenous ﬁstulas. If late thrombosis is due to intimal hyperplasia in the outﬂow vein, the autogenous arteriovenous access is redone using a different outﬂow

635

vein (e.g., converting an autogenous radial-cephalic direct wrist access to an autogenous radial-basilic forearm transposition) or using a proximal site of access (e.g., converting an autogenous radial-cephalic direct wrist access to an autogenous brachial-cephalic upper arm direct access). Central venous stenosis (see Fig. 61–4) is treated with angioplasty and/or stent placement or proximal venous bypass (e.g., subclavian–to– internal jugular bypass [see Fig. 61–5]), followed by placement of a new arteriovenous access. Thrombectomies and thrombolysis may be successful in acutely thrombosed prosthetic accesses and are attempted before abandoning the access for a new site. Because the inciting lesion is most often located in the graft–venous anastomosis, surgical thrombectomy is performed by exposing this anastomosis and opening it longitudinally. The thrombectomy is performed with a Fogarty catheter, taking care to identify the arterial plug to ensure complete clot removal (see Fig. 61–6B). A patch angioplasty of the distal anastomosis is performed to alleviate the outﬂow stenosis and prevent recurrent thrombosis. Alternatively, a jump graft using autogenous vein or prosthetic graft may be performed around the distal anastomosis (see Fig. 61–6C). Percutaneous mechanical thrombectomy has recently been popularized as an alternative to open surgical thrombectomy. Another minimally invasive option is thrombolysis with urokinase or tissue-type plasminogen activator (t-PA). Both percutaneous mechanical thrombectomy and thrombolysis must be followed by a contrast study and repair of the inciting stenosis with angioplasty and/or stent placement to prevent recurrent thrombosis of the access.18 ● Prevention Dialysis access surveillance and preemptive correction of subclinical stenosis have been shown to prolong access survival.19 Therefore, nephrologists monitor dialysis access using multiple different techniques including physical examination, dialysis venous pressure measurements, access blood ﬂow assessment, and urea recirculation.19,20 Any abnormalities noted are further assessed by duplex ultrasound. Any increase in peak systolic velocity greater than 4 : 1 or any peak systolic velocity less than 200 ml/min is believed to be abnormal, and a ﬁstulogram is obtained.21 Any abnormalities are treated with venous angioplasty and/or stenting or open surgical techniques including patch angioplasty or proximal venous bypass.22

Venous Hypertension ● Consequence Patients may be clinically asymptomatic with only increased dialysis venous pressures or may present with clinical symptoms including prolonged puncture site bleeding, extremity edema, and varicosities. In severe cases, bluish discoloration of the skin, ulceration of the ﬁngertips, and neuralgias may occur23–25 (see Fig. 61–

636

SECTION X: VASCULAR SURGERY

A

C

B

Figure 61–6 Later arteriovenous access thrombosis due to intimal hyperplasia. A, Cross-section of intimal hyperplasia at the prosthetic graft–venous anastomosis. B, Arterial plug seen with complete thrombus removal performed with a Fogarty catheter. C, Jump graft placed around the prosthetic graft–venous anastomosis to prevent future thrombosis.

4A and B). Both groups of patients are at risk for access thrombosis. Venous hypertension occurs irrespective of whether an autogenous or a prosthetic access is placed and is secondary to central venous stenosis (see Fig. 61–4C) with or without venous valvular incompetence. Approximately 50%26 of patients on dialysis will develop a central venous stenosis, but only 15% to 20% will be clinically symptomatic.27 Grade 2/3/4 complication ● Repair Central venous stenosis is initially treated with angioplasty and/or stenting and, if unsuccessful, open surgical repair. Open surgical repair techniques include internal jugular–to–subclavian vein turndown with direct anastomosis of the internal jugular vein to the subclavian vein distal to the subclavian vein occlusion or subclavian vein–to–internal jugular vein bypass28–30 (see Fig. 61–5). Valvular incompetence is treated with ligation of all veins distal to the outﬂow anastomosis noted to have reﬂux. Patients in whom the central venous stenosis is not amenable to endovascular or open surgical techniques require access ligation. Unfortunately, these patients will require a new access in a different location.

● Prevention Preoperative evaluation with a thorough history and physical examination is important to detect possible central venous stenosis. We perform a preoperative venous duplex scan on all patients with the indications listed in Box 61–1. Preoperative venography is completed in any patient with a high clinical suspicion for central venous stenosis or with abnormal ﬁndings on venous duplex scan. To prevent occurrence of central venous stenosis, placement of central venous lines are kept to a minimum, and if required, an internal jugular approach is preferred. All central venous stenoses are treated before placement of arteriovenous access with angioplasty and/or stenting or proximal venous bypass. To decrease the incidence of venous reﬂux intraoperatively, the distal vein being used for the ﬁstula is ligated and an end vein–to–side artery anastomosis is performed.

Failure to Mature ● Consequence Inability to access graft for dialysis. Failure to mature is the second major disadvantage of autogenous access. Rates vary widely in the literature, ranging from 3% to

61 ARTERIOVENOUS HEMODIALYSIS ACCESS

637

steal occurs secondarily to low access tract resistance, creating a reversal of blood ﬂow in the arterial outﬂow tract toward the access and away from the hand. Arterial occlusive disease increases resistance in the distal outﬂow of the arteriovenous access, which also contributes to the pathophysiology.31 Arterial steal occurs in both prosthetic and autogenous access and is seen in approximately 10% of all accesses placed. However, only in 1% of distal forearm accesses and 3% to 6% of upper arm accesses are clinical symptoms severe enough to warrant surgical intervention.32–37 Grade 3/4 complication Figure 61–7 Ligation of large side branches after completion of an autogenous radial-cephalic direct wrist access to improve access maturation.

38%; however, average maturation times are consistent at 3 months.4–6,10–12,15 This occurs secondary to either inadequate venous dilation associated with venous side branches or a deep location of the venous outﬂow tract. Grade 3 complication ● Repair Any large side branches of the outﬂow vein are ligated (Fig. 61–7). If the vein is located too deep, which is seen most commonly with radial cephalic direct wrist access, an incision is made overlying the venous outﬂow tract, and the vein is transposed superﬁcially and placed directly underneath the skin. ● Prevention Patients are examined preoperatively, and the superﬁcial veins with their major side branches are marked. If the veins are not easily visualized, a venous duplex scan is used to evaluate patency and size of both cephalic and basilic veins as well as any side branches. The cephalic vein, basilic vein, and all side branches are marked. Intraoperatively, before the anastomosis, the venous outﬂow is distended with heparinized saline and the vein is reassessed. All side branches not previously visualized are marked. If a thrill cannot easily be felt through the skin, the vein is believed to be too deep. Before performing the arteriovenous anastomosis, the vein is transposed superﬁcially for adequate cannulation in the future. After completing the anastomosis, all side branches are ligated to allow for adequate distention of the vein.

Arterial Dissection Arterial Steal ● Consequence Symptoms vary from mild coolness and paresthesias, which occur only on dialysis, to severe rest pain, paralysis, and gangrene and may appear immediately or be delayed after arteriovenous ﬁstula placement. Arterial

● Repair Mild cases with minimal clinical symptoms usually resolve spontaneously after several weeks. Cases that do not resolve and those with severe symptoms require surgical treatment; multiple surgical techniques have been reported. Ligation of the access will instantly resolve the symptoms but leaves the patient without a dialysis access. Banding of the access tract (Fig. 61–8A) creates a stenosis that increases the resistance to the blood ﬂow in the access and reverses arterial ﬂow in the distal artery. However, it is difﬁcult to judge the degree of stenosis required to alleviate the steal without causing thrombosis of the access. Ligation of the distal outﬂow artery has been reported as a successful technique in patients with distal access and a patent palmer arch; however, this approach does not restore possible required inﬂow to the hand. Distal revascularization with interval ligation (DRIL) (see Fig. 61–8B) entails ligation of the arterial outﬂow tract just distal to the takeoff of the access followed by placement of a bypass from the artery proximal to the takeoff of the access to the artery distal to the area of ligation. This procedure eliminates reversal of ﬂow in the distal outﬂow artery while keeping the access patent and perfusion pressures to the hand constant. Complete relief of symptoms has been reported in greater than 90% of patients. Primary 1-year patency rates range from 86% to 100% for the arterial bypass and from 69% to 86% for the arteriovenous access.38–40 ● Prevention Preoperative pulse examination should reveal equal and normal pulses bilaterally. Any patient with an abnormal pulse examination is further evaluated with upper extremity pulse volume recordings and segmental pressures. Any drop in pressure greater than 30 mm Hg is believed to be abnormal, and if possible, the arteriovenous access is placed in an alternate extremity or proximal to the area of stenosis. If an arteriovenous access must be placed in an area of abnormal arterial inﬂow, the patient is further evaluated with an arteriogram, and any stenosis is treated with angioplasty and/or stenting or arterial bypass. Intraoperatively, with autogenous access, care is taken to make the arteriovenous

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638

the anastomosis is not critical with prosthetic access; the outﬂow is limited by the size of the graft.

Ischemic Monomelic Neuropathy

A

Cephalic vein

Brachial artery

Reverse saphenous vein graft

● Consequence Acute pain, parasthesias, and weakness or paralysis of the hand and forearm immediately after placement of arteriovenous access. On physical examination, the patient’s hand remains warm with palpable radial and ulnar pulses. Ischemic monomelic neuropathy (IMN) occurs secondary to arterial steal, leading to ischemia of the nerves, which produces neurologic deﬁcits of the median, radial, and ulnar nerves but is not sufﬁcient to cause muscle or skin necrosis. IMN occurs only rarely with both autogenous and prosthetic accesses originating at or proximal to the brachial artery.41–43 Grade 3/4 complication ● Repair Early treatment is imperative to prevent hand paralysis; therefore, access surgeons should have a high index of suspicion. Because IMN is a form of arterial steal, the treatment options are similar. See “Treatment” under “Arterial Steal,” earlier. ● Prevention IMN may be completely avoided by placement of access using arterial inﬂow distal to the brachial artery. Because IMN is a form of arterial steal, preoperative evaluation and prevention are similar. See “Prevention” under “Arterial Steal,” earlier.

Anastomosis Congestive Heart Failure

Figure 61–8 Treatment options of arterial steal. A, Banding of arteriovenous access. B, Distal revascularization with interval ligation (DRIL) entails ligation of the arterial outﬂow tract just distal to the takeoff of the access followed by placement of a bypass from the artery proximal to the takeoff of the access to the artery distal to the area of ligation. (A and B, Reproduced with permission from Adams ED, Sidawy AN. Nonthrombotic complications of arteriovenous access for hemodialysis. In Rutherford RB (ed): Vascular Surgery, 6th ed. Philadelphia: Elsevier Saunders, 2005; pp 1698– 1699.)

● Consequence Dyspnea and bilateral lower extremity edema. Highoutput cardiac failure is a rare complication of both autogenous and prosthetic accesses, occurring in 2% to 4% of accesses placed.44,45 High-output congestive heart failure occurs secondary to decreased total peripheral resistance, which is compensated for by an increase in total cardiac output. Cardiac output may increase to over 8.0 L/min with access ﬂow accounting for over 50% of the cardiac output.46,47 To maintain such a high output, myocardial contractility and heart rate must relatively increase, which ultimately leads to cardiac failure.48,49 Grade 3/4/5 complication

anastomosis as small as possible, 6 to 8 mm at the largest. Also, interrupted sutures, which allow the anastomosis to enlarge with time, are avoided. These techniques will prevent subsequent dilation of the outﬂow tract creating increased ﬂow in the access and an increased propensity toward arterial steal. The size of

● Repair Ligation of the access will reverse the high-output cardiac failure but leaves the patient without dialysis access. Banding of the arteriovenous access tract is an alternative approach; however, similar to arterial steal, it is hard to judge the amount of stenosis required to reduce the cardiac output without thrombosis of the access.

B

61 ARTERIOVENOUS HEMODIALYSIS ACCESS ● Prevention When placing autogenous access, the anastomosis is kept between 6 and 8 mm in maximum diameter. Also, interrupted sutures, which allow the anastomosis to enlarge with time, are avoided. These techniques will prevent subsequent dilation of the outﬂow tract creating increased ﬂow in the access, which ultimately leads to high-output cardiac failure. With prosthetic accesses, a graft with a maximum diameter of 6 mm is placed, to avoid a similar low-resistance circuit.

Wound Closure Infection ● Consequence Diffuse cellulitis or focal abscess (Fig. 61–9) overlying the access. One of the biggest advantages of autogenous access is average infection rates of 5%, which are clearly superior to infection rates of 20% seen with prosthetic accesses.50 Infectious organisms appear to be independent of type of access. There is usually a predominance of gram-positive organisms, most commonly Staphylococcus aureus. However, up to 25% of infections may involve gram-negative organisms or be polymicrobial.51,52 Grade 1/3 complication ● Repair Autogenous access infection usually responds to 2 to 4 weeks of broad-spectrum antibiotics. Any associated abscess is drained with preservation of the access. A trial of broad-spectrum antibiotics is attempted in prosthetic

639

accesses presenting with only a mild cellulitis. However, most prosthetic infections require abscess drainage with removal of the infected portion of the graft. If either anastomosis is involved, the entire graft is removed to prevent anastomotic disruption. ● Prevention With such a lower risk of infection associated with autogenous arteriovenous access, autogenous access is placed when at all possible. If a graft is required, close attention to sterile surgical technique is mandatory. Dialysis technologists must also practice sterile technique in the routine cannulation of all types of access.

Hemorrhage ● Consequence Intraoperative diffuse bleeding. Postoperative incisional bleeding or hematoma formation. This occurs secondary to uremia-associated platelet dysfunction. Grade 1/3 complication ● Repair Diffuse hemorrhage is treated with 1-deamino-8-Darginine vasopressin (DDAVP).53,54 Other options include cryoprecipitate54 and activated factor VII.55 Patients with large hematomas are taken back to the operating room for drainage. ● Prevention If possible, anticoagulants and antiplatelet agents are stopped 1 week prior to access placement. Surgery is performed 24 hours after dialysis to allow for adequate recovery of platelet function. Recombinant human erythropoietin (rHuEPO) is given on dialysis, which increases hematocrit and improves platelet function. Other options include preoperative transdermal estrogen56 and vitamin K.57

Seroma ● Consequence Slowly increasing ﬂuid collection surrounding the arteriovenous access (Fig. 61–10), which usually occurs within 1 month of access placement. This complication affects only prosthetic access and occurs in 0.5% to 4% of these patients.58,59 The exact etiology is unknown, but it is presumed to occur from transudation of serous ﬂuid from porous grafts.60 Grade 2/3 complication

Figure 61–9 Abscess cavity surrounding the prosthetic graft.

● Repair Multiple surgical treatments have been reported including serial aspiration, incision and drainage, cyst removal, and graft replacement. Graft replacement is shown to be most successful, with a 92% cure rate.61 When replacing the graft, a new graft made of different material is placed through a new tunnel.

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SECTION X: VASCULAR SURGERY ysis is continued by accessing the uninvolved portion of the access; however, temporary access is sometimes required. An alternative approach recently being developed is endovascular treatment with covered stent grafts. Current studies show initial success rates up to 100% and primary patency rates at 6 months that range from 29% to 70%.65–67

Figure 61–10 Seroma cavity overlying the prosthetic graft.

● Prevention With a clearly lower pseudoaneursym occurrence rate, autogenous arteriovenous anastomoses are placed when at all possible. Dialysis technologists are encouraged to routinely rotate dialysis access puncture sites.

REFERENCES

Figure 61–11 Multiple asymptomatic pseudoaneurysms that developed several years after placement of an autogenous radialcephalic direct wrist access. (Reproduced with permission from Adams ED, Sidawy AN. Nonthrombotic complications of arteriovenous access for hemodialysis. In Rutherford RB (ed): Vascular Surgery, 6th ed. Philadelphia: Elsevier Saunders, 2005; p 1696.)

● Prevention With essentially no occurrence of seroma, autogenous arteriovenous accesses are placed when at all possible.

Other Complications Pseudoaneurysms ● Consequence Increased risk of hemorrhage, thrombosis, pain, and cosmetic issues. Pseudoaneurysms (Fig. 61–11) are seen much more frequently in prosthetic accesses, with an occurrence rate of 5% to 11% compared with an average rate of 3% seen with autogenous accesses.36,62–64 Pseudoaneurysms occur secondary to continuous puncturing of the access in the same site by dialysis unit personnel. Grade 1/2/3 complication ● Repair Most pseudoaneurysms may be safely monitored without intervention; however, if the pseudoaneursym size is signiﬁcantly increasing over time or the skin overlying the pseudoaneurysm is very thin or ulcerated, intervention is indicated. Traditional open surgical treatment is to excise the involved portion of autogenous or prosthetic access and replace it with either transposed vein or prosthetic graft. In most cases, dial-

1. Incidence and prevalence. In: U.S. Renal Data System, USRDS 2007 Annual Data Report: Atlas of End-Stage Renal Disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, 2007. Accessed at www.usrds.org/2007/view/02_incid_prev.asp 2. Costs of CKD and ESRD. In: U.S. Renal Data System, USRDS 2007 Annual Data Report: Atlas of End-Stage Renal Disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, 2007. Accessed at www.usrds.org/2007/view/11_econ.asp 3. Gibson KD, Gillen DL, Caps MT, et al. Vascular access survival and incidence of revisions: a comparison of prosthetic grafts, simple autogenous ﬁstulas, and venous transposition ﬁstulas from the United States Renal Data System Dialysis Morbidity and Mortality Study. J Vasc Surg 2001;34:694–700. 4. Hodges TC, Fillinger MF, Zwolak RM, et al. Longitudinal comparison of dialysis access methods: risk factors for failure. J Vasc Surg 1997;26:1009–1019. 5. Ascher E, Gade P, Hingorani A, et al. Changes in the practice of angioaccess surgery: impact of dialysis outcome and quality initiative recommendations. J Vasc Surg 2000; 31:84–92. 6. Choe MH, Lal BK, Cerveira JJ, et al. Durability and cumulative functional patency of transposed and nontransposed arteriovenous ﬁstulas. J Vasc Surg 2003;38:1206– 1211. 7. NKF-K/DOQI Clinical practice guidelines for vascular access: update 2000. Am J Kidney Dis 2001;37(suppl): S137–S181. 8. Huber TS, Ozaki CK, Flynn TC, et al. Prospective validation of an algorithm to maximize native arteriovenous ﬁstulae for chronic hemodialysis access. J Vasc Surg 2002;36:452–459. 9. Sidawy AN, Gray R, Besarab A, et al. Recommended standards for reports dealing with arteriovenous hemodialysis accesses. J Vasc Surg 2002;35:603–610. 10. Silva MB, Hobson RW, Pappas PJ, et al. Vein transposition in the forearm for autogenous hemodialysis access. J Vasc Surg 1997;26:981–988. 11. Rao RK, Azin GD, Hood DB, et al. Basilic vein transposition ﬁstula: a good option for maintaining hemodialysis access site options? J Vasc Surg 2004;39:1043–1047.

61 ARTERIOVENOUS HEMODIALYSIS ACCESS 12. Hakaim AG, Nalbandian M, Scott T. Superior maturation and patency of primary brachiocephalic and transposed basilic vein arteriovenous ﬁstulae in patients with diabetes. J Vasc Surg 1998;27:154–157. 13. Keuter XH, van der Sande FM, Kessels AG, et al. Excellent performance of one-stage brachial-basilic arteriovenous ﬁstula. Nephrol Dial Transplant 2005;20: 2168–2171. 14. Rooijens PP, Tordoir JH, Stijnen T, et al. Radiocephalic wrist arteriovenous ﬁstula for hemodialysis: meta-analysis indicates a high primary failure rate. Eur J Vasc Endovasc Surg 2004;28:583–589. 15. Obialo CI, Tagoe AT, Martine PC, Asche-Crowe PE. Adequacy and survival of autogenous arteriovenous ﬁstula in African American hemodialysis patients. ASAIO J 2003; 49:435–439. 16. Patel ST, Hughes J, Mills JL. Failure of arteriovenous ﬁstula maturation: an unintended consequence of exceeding Dialysis Outcome Quality Initiative guidelines for hemodialysis access. J Vasc Surg 2003;38:439–445. 17. Mendes RR, Farber MA, Marston WA, et al. Prediction of wrist arteriovenous ﬁstula maturation with preoperative vein mapping with ultrasonography. J Vasc Surg 2002;36: 460–463. 18. Lumsden AB, Bush RL, Lin PH, Peden EK. Management of thrombosed dialysis access. In Rutherford RB (ed): Vascular Surgery, 6th ed. Philadelphia: Elsevier Saunders, 2005; pp 1684–1692. 19. Tessitore N, Lipari G, Poli A, et al. Can blood ﬂow surveillance and pre-emptive repair of subclinical stenosis prolong the useful life of arteriovenous ﬁstulae? A randomized controlled study. Nephrol Dial Transplant 2004;19:2325–2333. 20. Quarello F, Forneris G, Pozzato M. Clinical and instrumental surveillance of the arteriovenous ﬁstula. G Ital Nefrol 2004;21:317–330. 21. Doelman C, Duijm LEM, Liem YS, et al. Stenosis detection in failing hemodialysis access ﬁstulas and grafts: comparison of color Doppler ultrasonography, contrast enhanced magnetic resonance angiography, and digital subtraction angiography. J Vasc Surg 2005;42:739–746. 22. Hingorani A, Ascher E, Kallakuri S, et al. Impact of reintervention for failing upper extremity arteriovenous autogenous access for hemodialysis. J Vasc Surg 2001;34: 1004–1009. 23. Bennjon RS, Wilson SE. Hemodialysis and vascular access. In Moore WS (ed): Vascular Surgery: A Comprehensive Review, 6th ed. Philadelphia: WB Saunders, 2002; pp 656–676. 24. Wood ML, Reilly GD, Smith GT. Ulceration of the hand secondary to a radial arteriovenous ﬁstula: a model for varicose ulceration. BJM 1983;287:1167–1168. 25. Knezevic W, Mastaglia FL. Neuropathy associated with Brescia-Cimmino arteriovenous ﬁstulas. Arch Neurol 1984;41:1184–1186. 26. Barrett N, Spencer S, McIvor J, Brown EA. Subclavian stenosis: a major complication of subclavian dialysis catheters. Nephrol Dial Transplant 1988;3:423–425. 27. Vanherweghem JL, Yassine T, Goldman M, et al. Subclavian vein thrombosis: a frequent complication of subclavian vein cannulation for hemodialysis. Clin Nephrol 1986;26:235–238.

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28. Puskas JD, Gertler JP. Internal jugular to axillary vein bypass for subclavian vein thrombosis in the setting of brachial arteriovenous ﬁstula. J Vasc Surg 1994;19:939– 942. 29. Currier CB, Widder S, Ali A, et al. Surgical management of subclavian and axillary vein thrombosis in patients with a functioning arteriovenous ﬁstula. Surgery 1986;100:25– 28. 30. Brown L, McLarent JT. Subclavian to jugular bypass for relief of intractable venous hypertension and salvage of hemodialysis access. JVS 1993;18:537. 31. Murphy GJ, White SA, Nicholson ML. Vascular access for haemodialysis. Br J Surg 2000;87:1300–1315. 32. Schanzer H, Schwartz M, Harrington E, Haimov M. Treatment of ischemia due to “steal” by arteriovenous ﬁstula with distal artery ligation and revascularization. J Vasc Surg 1988;7:770–773. 33. Duncan H, Ferguson L, Faris I. Incidence of the radial steal syndrome in patients with Brescia ﬁstula for hemodialysis: its clinical signiﬁcance. J Vasc Surg 1986;4:144– 147. 34. Haimov M, Burrown L, Schanzer H, et al. Experience with arterial substitutes in the construction of vascular access for hemodialysis. J Cardiovasc Surg 1980;21:149– 154. 35. Porter JA, Sharp WV, Walsh EJ. Complications of vascular access in a dialysis population. Curr Surg 1985;42:298– 300. 36. Zibari GB, Rohr MS, Landreneau MD. Complications from permanent hemodialysis vascular access. Surgery 1988;104:681–686. 37. Winsett OE, Wolma FJ. Complications of vascular access for hemodialysis. South Med J 1985;78:513–517. 38. Lin PH, Chen C, Suroweic SM, et al. Management of hand ischemia in patients with hemodialysis access by distal arterial ligation and revascularization. Vasc Surg 1999;33:481–488. 39. Lazrides MK, Staramos DN, Kopadis G, et al. Onset of arterial “steal” following proximal angioaccess: immediate and delayed types. Nephrol Dial Transplant 2003;18: 2387–2390. 40. Knox RC, Berman SS, Hughes JK, et al. Distal revascularization-interval ligation: a durable and effective treatment for ischemic steal syndrome after hemodialysis access. J Vasc Surg 2002;36:250–256. 41. Lazarides MK, Staramos DN, Panagopoulos GN, et al. Indications for surgical treatment of angioaccessinduced arterial “steal.” J Am Coll Surg 1998;187:422– 426. 42. Wilbourn AJ, Furlan AJ, Hulley W, Ruschhaupt W. Ischemic monomelic neuropathy. Neurology 1983;33: 447–451. 43. Miles AM. Upper limb ischemia after vascular access surgery: differential diagnosis and management. Semin Dial 2000;132:312–315. 44. Taylor SM, Eaves FL, Weatherford DA, et al. Results and complications of arteriovenous access dialysis grafts in the lower extremity: a ﬁve year review. Am Surg 1996;62: 188–191. 45. Murphy GJ, White SA, Knight AJ, et al. Long-term results of arteriovenous ﬁstulas using transposed autologous basilic vein. Br J Surg 2000;87:819–823.

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46. Bednarek-Skublewska A, Jozwiak L, et al. Acute cardiac failure secondary to brachiocephalic arteriovenous ﬁstula in patients on chronic haemodialysis. Pol Arch Med Wewn 2004;112:1221–1227. 47. Isoda S, Kajiwara H, Kondo J, Matsumoto A. Banding a hemodialysis arteriovenous ﬁstula to decrease blood ﬂow and resolve high output cardiac failure: report of a case. Surg Today 1994;24:734–736. 48. Murray BM, Rajczak S, Herman A, Leary K. Effect of surgical banding of a high-ﬂow ﬁstula on access ﬂow and cardiac output: intraoperative and long-term measurements. Am J Kidney Dis 2004;44:1090–1096. 49. Savage MT, Ferro CJ, Sassano A, Tomson CRV. The impact of arteriovenous ﬁstula formation on central hemodynamic pressures in chronic renal failure patients: a prospective study. Am J Kidney Dis 2002;40:753– 759. 50. Churchill K, Taylor KW, Cook RJ. Canadian hemodialysis morbidity study. Am J Kidney Dis 1992;19:214–234. 51. Marr KA, Sexton DJ, Conlon PJ. Catheter-related bacteremia and outcome of attempted catheter salvage in patients undergoing hemodialysis. Ann Intern Med 1997; 127:275–280. 52. Saad TF. Bacteremia associated with tunneled, cuff hemodialysis catheters. Am J Kidney Dis 1999;34:1114– 1124. 53. Andrassy K, Ritz E. Uremia as a cause of bleeding. Am J Nephrol 1985;5:313–319. 54. Wolfson AB, Singer I. Hemodialysis-related emergencies: II. J Emerg Med 1987;6:61–70. 55. Ng HJ, Koh LP, Lee LH. Successful control of postsurgical bleeding by recombinant factor VIIa in a renal failure patient given low molecular weight heparin and aspirin. Ann Hematol 2003;82:257–258.

56. Sloand JA, Schiff MJ. Beneﬁcial effect of low-dose transdermal estrogen on bleeding time and clinical bleeding in uremia. Am J Kidney Dis 1995;26:22–26. 57. Dember LM. Critical care issues in the patient with chronic renal failure. Crit Care Clin 2002;18:421–440. 58. Borrero E, Doscher W. Chronic perigraft seromas in PTFE grafts. J Cardiovasc Surg 1988;29:46–49. 59. Ahn SS, Machleder HI, Gupta R. Perigraft seroma: clinical, histologic, and serologic correlates. Am J Surg 1987;154:173–178. 60. Szilagyi DE. In discussion of Kaupp et al. Graft infection or graft rejection? Arch Surg 1979;114:1422. 61. Blumenberg RM, Galfand ML, Dale WA. Perigraft seromas complicating arterial grafts. Surgery 1985;97:194– 203. 62. Rivers SP, Scher LA, Sheehan E, et al. Basilic vein transposition: an underused autologous alternative to prosthetic dialysis angioaccess. J Vasc Surg 2002;36:202. 63. Chia KH, Ong HS, Teoh MK, et al. Chronic haemodialysis with PTFE arteriovenous grafts. Singapore Med J 1999;40:685–690. 64. Lenz BJ, Veldenz HC, Dennis JW, et al. A three-year follow-up on standard versus thin wall ePTFE grafts for hemodialysis. J Vasc Surg 1998;28:464–470. 65. Najibi S, Bush RL, Terramani TT, et al. Covered stent exclusion of dialysis access pseudoaneurysms. J Surg Res 2002;106:15–19. 66. Silas AM, Bettmann MA. Utility of covered stents for revision of aging failing synthetic hemodialysis grafts: a report of three cases. Cardiovasc Intervent Radiol 2003;26:550–553. 67. Sapoval MR, Turmel-Rodrigues LA, Raynaud AC, et al. Cragg covered stents in hemodialysis access: initial and midterm results. J Vasc Interv Radiol 1996;7:335–342.

62

Venous Surgical Pitfalls Niten Singh, MD and James Laredo, MD INTRODUCTION Surgery on the superﬁcial venous system is typically performed to address two speciﬁc conditions of the lower extremities: (1) symptomatic varicose veins and (2) superﬁcial venous insufﬁciency. Varicose veins of the lower extremity are dilated superﬁcial veins that are classiﬁed according to their size: small telangiectatic veins (“spider veins”); larger (1–3 mm) intradermal veins, which are not usually tortuous, called reticular veins; and ﬁnally, true varicose veins, which are greater than 3 mm and tortuous.1,2 These veins can cause cosmetic problems as well as pain. The overlying skin can darken as hemosiderin from the static blood is deposited in the area.3 Also, with the surrounding nerves, a sensation of dull aching is often described by the patient. The vast majority of patients with symptomatic varicose veins also have superﬁcial venous insufﬁciency. Superﬁcial venous insufﬁciency is a condition in which the valves present in the superﬁcial veins are incompetent, which results in reﬂux of blood within the vein. Reﬂux of blood within the superﬁcial veins—namely, the greater and lesser saphenous veins— results in elevated venous pressure. Venous hypertension leads to lower extremity edema, pigmentation, stasis dermatitis, lipodermatosclerosis, and venous ulceration of the lower extremities. The objective of surgical intervention in patients with both symptomatic varicose veins and superﬁcial venous insufﬁciency is twofold: removal of the symptomatic varicose veins and treatment of the superﬁcial venous insufﬁciency.4

INDICATIONS ● Symptomatic varicose veins ● Superﬁcial venous insufﬁciency

OPERATIVE PROCEDURE Stripping of the GSV The procedure is performed with the patient under general or regional anesthesia. A transverse incision in the groin is performed one to two ﬁngerbreadths from the pubic tubercle. The saphenofemoral junction (SFJ) is identiﬁed (Fig. 62–1), and all of the tributaries of the GSV are ligated. The GSV is then divided at the SFJ and the stump is suture-ligated. A stripping device (Fig. 62–2) is then introduced into the GSV via a small incision in the lower thigh. The device is passed proximal to the groin incision, and the divided GSV at the SFJ is secured to the stripper and removed via the thigh incision5 (Fig. 62–3). The vein is usually removed above the knee only to avoid injury to the saphenous nerve, which is within the proximity of the GSV below the knee.

Injury to the Saphenous Nerve ● Consequence Owing to its proximity especially below the knee, saphenous nerve injury may occur and result in chronic neuropathic pain in the region of the saphenous nerve. Grade 1 complication ● Repair Conservative therapy with pain control and observation may sufﬁce if there is a traction-type injury. However, persistent pain may require local injection and possible neurolysis.6 ● Prevention If the GSV is to be stripped, many advocate stripping only the thigh portion of the GSV. Nerve injuries are less likely if stripping is carried out only in this segment.

OPERATIVE STEPS Step Step Step Step

1 2 3 4

Stripping of GSV Ligation of GSV Laser or radiofrequency ablation of GSV Stab avulsion of varicose veins

Hematoma within the Saphenous Vein Tract ● Consequence As the GSV is stripped, its tributaries are avulsed in the thigh, and bleeding from these may lead to

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Incision Common femoral, v. Superficial epigastric v. Saphenofemoral junction

Inguinal ligament

Superficial circumflex iliac v. Anterior femoral cutaneous v.

Sup. external pudendal v. Accessory saphenous v.

Greater saphenous n. Greater saphenous v. Incision

Figure 62–1

Saphenofemoral junction (SFJ).

Common fermoral v. Common femoral v.

Olive tip

Olive tip

Greater saphenous v. Greater saphenous v.

Figure 62–2 Vein stripper.

Accessory saphenous v.

Figure 62–3 Stripping of the greater saphenous vein (GSV).

62 VENOUS SURGICAL PITFALLS ecchymosis, hematoma, and possible permanent skin discoloration. Grade 1 complication ● Repair Conservative measures are employed initially, using compression and warm compresses. If the overlying skin becomes threatened owing to a tense hematoma, evacuation of the hematoma should be carried out. ● Prevention Leg elevation immediately after stripping and pressure over the stripping site in the thigh are usually sufﬁcient. Other techniques that have been described are the use of a tourniquet and internal packing of the stripping site as well as tumescent anesthesia.1

Ligation of the GSV The procedure is performed with the patient under general or regional anesthesia. A transverse incision in the groin is performed one to two ﬁngerbreadths from the pubic tubercle. The SFJ is identiﬁed, and all of the tributaries of the GSV are ligated. The GSV is then divided at the SFJ and suture-ligated.7

Misidentiﬁcation of the SFJ ● Consequence If the SFJ is misidentiﬁed, the femoral vein may be mistaken for the GSV and ligated, which would result in massive limb swelling that could lead to limb threat. Grade 4 complication ● Repair Repair/reestablish continuity of the femoral vein with likely anticoagulation. ● Prevention Visualization of the GSV at the SFJ and clear identiﬁcation are the keys to prevention of this injury. If needed, further dissection may be done around the femoral vein to ensure that the junction is visualized.

Incomplete Ligation of the Tributaries of the GSV

645

● Prevention Dissecting the SFJ and ligating all tributaries of the GSV can obviate recurrence.

GSV Ablation The procedure is performed with the patient under local anesthetic with sedation (oral or intravenous) and requires vascular duplex ultrasound imaging. The patient is positioned supine, the ipsilateral thigh is externally rotated, and the knee is ﬂexed with a bump placed under the distal thigh. This position allows complete duplex imaging of the common femoral vessels and GSV. Next, the ipsilateral common femoral vessels are imaged and identiﬁed. The GSV is then imaged from the SFJ to the knee. Local anesthetic is used to anesthetize the skin overlying the GSV at the knee/distal thigh. Under ultrasound guidance, the GSV is punctured with a micropuncture needle, followed by placement of a 0.014″ guidewire through the needle. A small 4-Fr catheter is placed into the GSV over the 0.014″ guidewire. The 0.014″ guidewire is removed, and a 0.035″ J or Bentson guidewire is placed into the GSV and advanced into the common femoral vein. The laser catheter or radiofrequency catheter is advanced into the GSV over the 0.035″ guidewire and positioned at the SFJ under ultrasound guidance (Fig. 62–4A). The guidewire is removed, and the laser or radiofrequency catheter is pulled 2 cm distal to the SFJ (see Fig. 62–4B). The laser ﬁber or radiofrequency probe is then inserted into the catheter. Tumescent anesthesia (200–400 ml) is inﬁltrated into the perivenous tissues under ultrasound guidance. The laser ﬁber or radiofrequency probe is then armed, and laser energy or radiofrequency energy is delivered to the GSV during pullback of the laser ﬁber or radiofrequency probe. Energy delivered to the GSV results in ablation of the vein. Based on the less invasive nature and comparable results, ablation of the GSV using laser or radiofrequency energy is now becoming the preferred method of treating GSV incompetence.8,9 Assessment of the common femoral vein and SFJ to document preservation of ﬂow is then performed prior to wrapping the leg with an Ace bandage.

Injury to the Common Femoral Vein

● Consequence Incomplete identiﬁcation of the tributaries of the GSV may lead to continued ﬂow and reﬂux through the GSV and recurrence of varicosities in the leg.7 Grade 1 complication

● Consequence Because the procedure is performed with ultrasound guidance, this complication is exceedingly rare. Guidewire or catheter injury to the common femoral vein may result in bleeding and hematoma formation. Grade 1 or 3 complication

● Repair Exploration and identiﬁcation of the GSV and its tributaries and likely stripping the vein.

● Repair Guidewire injury or catheter injury may require exploration and repair of the injury.

646

SECTION X: VASCULAR SURGERY

Laser Stenotic common femoral v.

Common femoral v.

Greater saphenous v.

A

B

Figure 62–4 Position of the laser catheter in the GSV. A, Catheter tip at the SFJ. B, Catheter tip advanced 2 cm distal to the SFJ.

● Prevention Ultrasound guidance will prevent guidewire or catheter injuries.

● Repair Most burn injuries often require only local wound care. However, for extensive burn injuries, local débridement and skin grafting may be required.

Thermal Injury to the Common Femoral Vein

● Prevention Liberal use of perivenous tumescent anesthesia and cessation of energy delivery before removing the laser ﬁber or radiofrequency probe from the GSV and skin insertion site.

● Consequence Thermal injury to the common femoral vein can occur if the laser ﬁber or radiofrequency probe is present within the common femoral vein at the time of energy delivery. Grade 1 or 3 complication ● Repair Thermal injury to the common femoral vein may require operation and reconstruction of the vein. ● Prevention Careful ultrasound imaging and positioning of the laser or radiofrequency catheter, prior to insertion of the laser ﬁber or radiofrequency probe, will prevent thermal injury to the common femoral vein.

Skin Burns ● Consequence Burn injury is often at or near the insertion site of the laser catheter or radiofrequency probe and is caused by delivery of energy to a superﬁcial portion of the GSV or at the skin insertion site. Thermal injury can also occur from energy traveling through superﬁcial tributaries of the GSV. Grade 1 or 3 complication

Deep Vein Thrombosis ● Consequence Thrombus may form within the proximal stump of the ablated GSV and may propagate up into the common femoral vein. This is more likely to occur with radiofrequency ablation than with laser ablation. Grade 1 complication ● Repair Anticoagulation with warfarin sodium (Coumadin) is indicated when there is thrombus protruding into or propagation of thrombus into the common femoral vein. Vena cava ﬁlter placement may be indicated in cases of free-ﬂoating thrombus within the common femoral vein. ● Prevention The incidence of deep vein thrombosis (DVT) has been reported to be 0.3% with laser ablation and 2.1% with radiofrequency ablation of the GSV. Postoperative venous duplex scanning may be indicated in

62 VENOUS SURGICAL PITFALLS high-risk patients (patients with a history of DVT or thrombophilia).

Superﬁcial Thrombophlebitis ● Consequence Superﬁcial thrombophlebitis may develop in the ablated GSV or in the superﬁcial tributaries of the GSV. Grade 1 complication ● Repair The majority of cases of superﬁcial thrombophlebitis will resolve with nonsteroidal anti-inﬂammatory agents, leg elevation, and warm compresses. ● Prevention Perioperative antibiotic administration and meticulous aseptic surgical technique.

647

allow unidirectional ﬂow from the superﬁcial to the deep venous system.10 The incompetence of these perforating veins can lead to venous ulcerations of the skin overlying the perforating vein. The Linton procedure for incompetent perforating veins was a radical operation in which perforating veins were directly ligated through a longitudinal incision made over the medial leg, posterior to the medial border of the tibia. This technique was complicated by wound problems secondary to the overlying unhealthy skin that would often fail to heal.11 More recently, a less invasive technique—subfascial endoscopic perforator surgery (SEPS)—has been developed to address the incompetent perforating veins.

INDICATION ● Venous ulcerations of skin overlying perforating vein

Stab Avulsion of Varicose Veins The varicose veins are marked preoperatively, usually just before bringing the patient to the operating room. Small stab incisions overlying the marked varicose veins are made, and the varicose veins are elevated into the incisions and avulsed and/or ligated. The varicose veins are removed, and the small incisions are closed with a buried absorbable suture or Steri-Strips. Use of a thigh tourniquet may minimize blood loss.

Injury to the Saphenous Nerve ● Consequence Nerve injury may occur during stab avulsion of varicose veins in close proximity to the saphenous vein and the saphenous nerve below the knee. Injury may result in chronic neuropathic pain in the region of the saphenous nerve. Grade 1 complication

OPERATIVE STEPS Step 1 Step 2

Step 3

Step 4 Step 5 Step 6

Step 7

● Repair Conservative therapy with pain control and observation may sufﬁce if there is a traction-type injury. However, if this does not improve, local injection with longacting local anesthetic and possible neurolysis may be required.9

Step 8

● Prevention Stab avulsion of varicose veins in the area of the GSV below the knee should be carefully performed.

DVT

Mark incompetent perforating vein on skin preoperatively under duplex guidance Exsanguinate affected limb using Esmarch bandage and thigh tourniquet inﬂated to 300 mm Hg to create bloodless ﬁeld Place 10-mm endoscope in medial aspect of calf 10 cm distal to tibial tuberosity and medical to anterior edge of tibia Inﬂate endoscopic balloon to dissect subfascial space Remove balloon and insufﬂate with 30 mm Hg of CO2 to visualize space Place second 5-mm port distal to ﬁrst, near but well above ankle, to perform clipping and division of perforators Use standard laparoscopic surgery clips to clip and divide all visualized perforaters Wound closure

Exsanguinate the Affected Limb Using an Esmarch Bandage and a Thigh Tourniquet Inﬂated to 300 mm Hg to Create a Bloodless Field

Subfascial Endoscopic Perforator Surgery

● Consequence Patients with an unknown hypercoagulable disorder or prolonged placement of the tourniquet may develop a DVT, which could lead to worsening of the chronic venous insufﬁciency symptoms and potential pulmonary embolism (PE). Grade 1 complication

Perforating veins connect the superﬁcial to the deep venous system. Venous valves within these perforators

● Repair Anticoagulation is the mainstay of therapy for DVT.

648

SECTION X: VASCULAR SURGERY

● Prevention Avoidance of the tourniquet as well as administering heparin prior to tourniquet placement may alleviate this problem. Postoperatively, early ambulation and compression stockings, if tolerated, may decrease the incidence.

Step 2 Step 3 Step 4

Perform cavagram to note diameter of IVC and level of renal veins Deploy ﬁlter below level of renal veins Obtain hemostasis over insertion site with manual compression for 5 to 10 minutes

Wound Closure Wound Complications ● Consequence Many of these patients have nonhealing ulcers in the lower extremity as a consequence of chronic venous insufﬁciency and have fragile skin, which can lead to wound breakdown/infection, which can become a chronic problem in this patient population. Grade 1 complication ● Repair Local wound care and antibiotics are the mainstays of treatment. ● Prevention Administration of perioperative antibiotics and meticulous care in closure of these wounds.

Inferior Vena Cava Filter Placement

A

Placement of inferior vena cava (IVC) ﬁlters is indicated when anticoagulation is contraindicated or has failed in patients with DVT. In addition, placement of IVC ﬁlters is indicated in patients with severe head injuries and with spinal cord injuries that may make these high-risk trauma patients prone to PE.12 As technology has evolved the delivery system has become lower proﬁle in size compared with the initial percutaneous Greenﬁeld ﬁlter, which required a 28-Fr sheath. Currently, some devices require a 6-Fr delivery system, which can reduce the length of compression of the insertion site and local thrombosis of the insertion site.13

INDICATIONS ● Anticoagulation contraindicated or has failed in patients

with DVT ● Severe head injuries and spinal cord injuries in patients

prone to PE

OPERATIVE STEPS Step 1

Obtain venous access via internal jugular or femoral approach

B Figure 62–5 A, Filter placed over right renal vein. B, Migration of ﬁlter over bifurcation of iliac veins.

62 VENOUS SURGICAL PITFALLS

Venous Access Hematoma, Arterial Puncture, Creation of an Arteriovenous Fistula ● Consequence Often, in the obese or edematous patient, the venous access site is not readily apparent and numerous attempts may be employed to gain access, which could lead to any of the common access complications. Grade 1 complication ● Repair If the artery is entered and recognized, removal of the needle and manual compression are all that are required. Hematomas can usually be managed conservatively unless overlying skin necrosis is noted. If an arteriovenous ﬁstula (AVF) is noted, conservative management is usually the initial management. However, if the limb is compromised, the AVF can be ligated. ● Prevention The use of anatomic landmarks is usually sufﬁcient in nonobese patients (i.e., using the pulsation of the femoral artery and puncturing the medially located femoral vein). With portable ultrasound machines more readily available, image-guided access should be performed whenever possible.

Filter Deployment Filter Misplacement and Migration ● Consequence Not sizing the IVC properly (the majority of ﬁlters are designed for an IVC < 30 mm) may lead to migration of the ﬁlter, which could enter the right atrium; placement over the renal veins may cause thrombosis of the renal veins (Fig. 62–5). Grade 2 complication ● Repair Endovascular snares and retrieval devices often obviate the need for operative retrieval. However, if these fail, direct surgical retrieval may be necessary. ● Prevention Performing a cavagram and proper sizing of the IVC to ensure that the ﬁlter is properly sized and below the level of the renal veins.

649

REFERENCES 1. Bergen JJ. Varicose veins: treatment by interventional including sclerotherapy. In Rutherford RB (ed): Vascular Surgery, 6th ed. Philadelphia: Elsevier Saunders, 2005; pp 2251–2267. 2. Allegra C, Antiganani P, Bergan JJ. The “C” of CEAP: suggested deﬁnitions and reﬁnements. An International Union of Phlebology conference of experts. J Vasc Surg 2003;37:129. 3. Georgiev M. Post sclerotherapy hyperpigmentations: a one year followup. J Dermatol Surg Oncol 1989;15:214– 219. 4. Goldman MP, Weiss MA, Beren JJ. Diagnosis and treatment of varicose veins: a review. J Am Acad Dermatol 1994;31:393–398. 5. Goren G, Yellin AE. Invaginated axial saphenectomy by a semirigid stripper: perforate-invaginate stripping. J Vasc Surg 1994;20:970–977. 6. Morrison C, Dalsing MC. Signs and symptoms of saphenous nerve injury after greater saphenous vein stripping: prevalence, severity, and relevance for modern practice. J Vasc Surg 2003;38:886–890. 7. Rutherford RB, Sawyer JD, Jones DN. The fate of residual saphenous vein after partial removal or ligation. J Vasc Surg 1990;12:422–428. 8. Manfrini S, Gasbarro V, Danielsson G. Endovenous management of saphenous vein reﬂux. J Vasc Surg 2000; 32:330–342. 9. Proebstle TM, Gül D, Lehr HA, et al. Infrequent early recanalization of greater saphenous vein after endovenous laser treatment. J Vasc Surg 2003;38:511–516. 10. Mozes G, Gloviczki P, Menawat SS, et al. Surgical anatomy for endoscopic subfascial division of perforating veins. J Vasc Surg 1996;24:800–808. 11. Kalra M, Gloviczki P. Management of perforator vein incompetence. In Rutherford RB (ed): Vascular Surgery, 6th ed. Philadelphia: Elsevier Saunders, 2005; pp 2268– 2286. 12. Rodriguez JL, Lopez JM, Proctor MC. Early placement of prophylactic vena caval ﬁlters in injured patients at high risk for pulmonary embolism. J Trauma 1996;40:797– 802. 13. Ascher E, Hingorani A, Yorkovich WR. Complications of vena cava ﬁlters. In Towne JB, Hollier LH (eds): Complications in Vascular Surgery, 2nd ed. New York: Marcel Dekker, 2004; pp 569–579.

63

Endovascular Interventions Niten Singh, MD and David Deaton, MD INTRODUCTION Endovascular therapy has changed the spectrum of vascular care that a surgeon can offer a patient. In the past, procedures such as angioplasty were believed to be reserved for short-segment stenosis and for patients in whom a bypass was not an option. The advent of stents and the technological advances made in this area have allowed endovascular options to be offered in every vascular bed. In high-risk patients in whom an open abdominal aortic aneurysm (AAA) repair was believed to be too dangerous, a stent graft can be placed with very low procedural risk. Although believed by many to have few complications because procedures are performed through sheaths in the femoral artery, endovascular procedures are still an operative procedure in the vascular system and can be associated with similar complications as well a new variety of complications unique to catheter-based interventions. Some of these complications are described in this chapter.

INDICATIONS ● Peripheral arterial disease

OPERATIVE STEPS Step 1 Step 2 Step 3

Access and contrast Angioplasty and stenting Endovascular AAA repair

Operative Procedure Contrast Toxicity Performance of catheter-based techniques requires the use of contrast agents and digital subtraction imagery. Contrast toxicity can affect many organs and have a profound detrimental effect. Many minor reactions of contrast have been reduced with the lower-osmolality agents now available.1 One of the major adverse effects of contrast agents is nephrotoxicity, which is generally deﬁned as a rise in the creatinine of greater than 25% above baseline in the

absence of other inciting events2 (grade 1 complication). The event usually occurs within 48 hours of the procedure. For most patients, it is nonoliguric and resolves over time. The most important risk factor for the development of contrast-induced nephropathy is preexisting renal insufﬁciency. Other contributing factors are dehydration, diabetes, and the amount of contrast used. The treatment for contrast-induced nephrotoxicity is hydration, with less than 1% of patients progressing on to the need for dialysis. Prevention of nephrotoxicity is accomplished via the following methods: hydration, especially in patients with renal insufﬁciency, has been shown to be the most effective preventive measure; Nacetylcysteine has been shown to reduce the risk of contrast-induced nephropathy in patients with renal insufﬁciency3; and alkalinization of the urine has also been found to be beneﬁcial in patients with renal insufﬁciency.4

Access Site Complications Although simplistic in nature, the puncture and access of the arterial system can lead to serious complications. In infrainguinal procedures, the common femoral artery is accessed above the bifurcation of the superﬁcial femoral artery (SFA) and the profunda femoris artery (PFA) and below the inferior epigastric artery. The access site is identiﬁed via ﬂuoroscopic imaging and palpation of the femoral artery.5 The ideal location is over the femoral head6 (Fig. 63–1). After the procedure, manual pressure is applied to achieve hemostasis of the puncture site or a closure device is used to mechanically seal the area. Numerous complications can occur during this part of the procedure.

High Arterial Puncture (Fig. 63–2) ● Consequence Uncontrolled bleeding and retroperitoneal bleeding can occur because ineffective pressure can be applied to this area. A signiﬁcant amount of blood can be lost, especially if the patient has received heparin or antiplatelet agents. Grade 1/3 complication

652

A

SECTION X: VASCULAR SURGERY

Figure 63–1 Proper position of femoral access site. A, Subtracted view displays access below the inferior epigastric artery and above the bifurcation. B, View with landmarks displays access in the common femoral artery over the femoral head.

B

unstable, the need for direct surgical repair of the artery is necessary. ● Prevention Using anatomic imaging.

landmarks

and

preprocedural

Low Arterial Puncture ● Consequence Pseudoaneurysm (PSA) formation and potential distal ischemia can occur with a low puncture. Grade 1/2/3 complication ● Repair PSA can be monitored if it is small, and many will spontaneously regress. More recently, duplex-guided thrombin injection has been used to treat this complication. If the patient has distal ischemia from injury to the SFA or the PFA, surgical exploration and repair are mandated. Figure 63–2 High arterial puncture. Note the entrance of the sheath near the upper border of the femoral head.

● Repair The retroperitoneum will often tamponade the bleeding, but the patient will have pain and likely require blood transfusions. In some instances, if the patient is

● Prevention As described earlier and recognizing the problem prior to removing the sheath.

Poorly Angled Puncture ● Consequence If the angle of the access needle is greater than 60 degrees, the guidewire and sheath may not pass easily.

63 ENDOVASCULAR INTERVENTIONS This can cause injury to the back wall of the artery and hematoma formation as well as potential dissection of the artery. Grade 1/2 complication ● Repair Removing the needle and manual compression and thorough pulse examination after compression. ● Prevention The needle should not be angled at greater than 60 degrees during the access.

Access Site Thrombosis ● Consequence Development of acute ischemia of the involved limb. Grade 3/4 complication ● Repair Immediate surgical exploration and repair of the affected artery. ● Prevention When applying manual pressure, excessive force should be avoided to allow blood ﬂow to continue and deposit platelets over the access site. If a closure device is used, the artery should be inspected ﬂuoroscopically for the presence of disease and adequate caliber.

Angioplasty and Stenting

653

● Repair If the perforation is noted in an extremity vessel, placement of the balloon over the site and inﬂated to the lowest pressure to allow sealing of the injury usually resolves the issue. Anticoagulation should be reversed as well. If this is not the case, placement of a covered stent is necessary. In vascular beds such as the iliac artery, control of the bleeding with a balloon will not likely control the perforation; therefore, placement of a covered stent is the treatment.8 In a renal angioplasty, distal perforation can be controlled with coil embolization. If these methods fail, surgery is mandated. ● Prevention Attempt to properly size vessels; if the patient experiences discomfort during the procedure, deﬂate the balloon and evaluate. To prevent guidewire perforation, the tip of the wire should always be visualized.

Arterial Dissection ● Consequence Passing a guidewire (particularly a hydrophilic wire) into the subintimal plane and failure to reenter the true lumen can lead to dissection of the artery, as can angioplasty of a severely diseased vessel. If not recognized, this can lead to thrombosis of the treated vessel.9 Grade 1/2 complication ● Repair Placement of a stent over the dissected area effectively treats most dissections.

The technological advances such as the lower-proﬁle devices have allowed this procedure to become a fairly routine practice in vascular surgery. The insertion of a balloon into a diseased artery allows for expansion of the lumen. However, this lesion may recoil; therefore, placing a stent to prevent recoil may be advantageous in certain vascular beds. The procedure is conducted after obtaining access, as described previously. The guidewire is then passed through the lesion and maintained in this position as the angioplasty balloon is passed and expanded. Stents are balloon-expandable (stent premounted on a balloon) or self-expanding (may require postdeployment angioplasty) and are placed over the diseased area.7

● Prevention Dissections are frequent occurrences and can be prevented and treated adequately by placement of stents. The key element is recognizing a dissection.

Arterial Perforation

● Repair Fundamentally, there are two options: (1) removing the embolized material or (2) deploying, or “trapping,” it in a safe location. If the embolic material is from a diseased vessel or thrombus, the use of large ﬂush catheter to aspirate the material or, if necessary, a mechanical thrombectomy device can usually be successful. The use of snares to capture free balloons or guidewires is often effective. If a stent is free, attempts to cannulate it and expand it in a more peripheral

● Consequence Arterial perforation can occur during balloon angioplasty and distally as well with the guidewire perforating the wall of the vessel. Depending on the vascular bed, this may lead to minor discomfort or lifethreatening hemorrhage. Grade 2 or possibly 4 complication depending on vascular bed (i.e., aortoiliac artery) or if not recognized

Embolization ● Consequence Embolization of calciﬁc plaque or an endovascular device (e.g., a stent) is always a potential hazard with any intervention. The potential for ischemia is present, particularly in the case of severely diseased run-off for the lower extremity or end-organ ischemia in organs such as the kidney. Grade 1/2 complication

654

SECTION X: VASCULAR SURGERY

location such as the iliac artery or placing a larger stent to trap it is a useful technique. Ultimately, it may be necessary to perform an open surgical procedure to remove the device directly from the vessel if the prior endovascular salvage techniques are unsuccessful and the device is impeding critical blood ﬂow. ● Prevention Attention to the devices and inspecting balloons and stents prior to using them as well as careful endovascular techniques can usually prevent this uncommon occurrence.

Endovascular AAA Repair Endovascular AAA (EVAR) has been a major advance in vascular surgery since its approval by the U.S. Food and Drug Administration in 1999. It has allowed for treatment of AAA in patients who would not likely have been offered an open repair owing to other comorbidities. It is also a minimally invasive approach to aortic reconstruction that offers signiﬁcantly fewer acute complications and a much speedier recovery. Because several devices are now available, the volume of EVAR has increased and patients with anatomic characteristics that earlier would have been prohibitive are now offered the option of EVAR using adjunctive techniques to facilitate its use.10 The basic procedure for the modular devices is as follows: access via bilateral femoral arteries; delivery of the main body and ipsilateral limb of the device below the renal arteries; cannulation of the contralateral limb and delivery and deployment of this limb; placement of iliac extensions if necessary; and angioplasty of the proximal and distal seal zones. Although much less invasive than traditional open repair, EVAR still constitutes an operation on the aorta and its complications can be devastating.

should be placed to occlude the aorta as well as within the iliac artery portion and open repair performed. ● Prevention As with any case, but in particular, with EVAR, preoperative planning is the key, and careful examination of the access sites can prevent this problem.

Device Fatigue ● Consequence Fracture of the stent or material fatigue can lead to devastating problems and endoleaks that can result in perfusion of the aortic sac that was previously excluded by the endovascular graft. This acute repressurization of the old AAA sac can lead to acute rupture. Grade 2/3 complication ● Repair Recognition and detailed evaluation with high-deﬁnition computed tomography with reconstruction and an arteriogram to identify the source of failure, which can potentially be treated with another stent graft. If endovascular option is not possible, explanting the device and proceeding with open repair. ● Prevention This problem is difﬁcult to prevent and requires ongoing surveillance of patients with endografts.

Endoleaks Classiﬁcation of endoleaks is as follows: Type I: ﬂow into the aneurysm sac via the proximal or distal attachment site (Fig. 63–3)

Access Failure ● Complication As opposed to the standard sheaths for peripheral interventions, the EVAR devices are much larger, with sheaths ranging from 22 to 26 Fr for the main body and 12 to 20 Fr for the contralateral limb. If the iliac artery is less than 7.5 mm, there may be difﬁculty in delivering the device, which may lead to iliac artery injury (e.g., perforation, occlusion, dissection) or avulsion. Grade 2/3/4 complication ● Repair If the device will not pass easily, the alternative is to use an iliac conduit in which a retroperitoneal incision is made and a 10-mm Dacron graft is then sewn to the iliac bifurcation and the device delivered through this. If a portion of the artery has a focal stenosis, angioplasty may be sufﬁcient. If iliac avulsion is noted, a balloon

Figure 63–3 Type I endoleak from distal migration of endografts. Note the large aneurysm sac on angiography.

63 ENDOVASCULAR INTERVENTIONS

655

● Consequence Type I and III endoleaks represent continued aneurysm sac exposure to aortic pulsatility and pressure. Aneurysm rupture is likely if untreated. Grade 2/3/5 complication Type II endoleaks are generally self-limiting and most close spontaneously. Close follow-up is necessary, and intervention is indicated for evidence of aneurysm growth. Grade 1/2 complication Type IV endoleaks are rare and most disappear in the early follow-up period. Grade 1/2 complication12

Figure 63–4 Type II endoleaks likely emanating from a patent lumbar. Note that there is only a small amount of contrast within the sac that is predominantly thrombosed.

● Repair For type I endoleaks, immediate repair at the time of the initial procedure is warranted if the defect can be accurately identiﬁed and treated with endovascular means. This is usually accomplished via balloon expansion of the proximal and distal attachment sites, placement of additional cuffs over this area, or placement of a balloon-expandable stent to seal the area. Type II endoleaks can be monitored, but if the AAA enlarges during follow-up, treatment is necessary. This can include transarterial coil embolization or direct translumbar aortic embolization.13 Type III endoleaks, if at graft attachment sites, are treated with additional endograft coverage of the graft defect. ● Prevention Recognition of the problem at the time of the completion arteriogram and during follow-up, as well as preoperative planning and accurate sizing particularly of the proximal and distal seal zones, are the most important methods of preventing this.

REFERENCES

Figure 63–5 Type III endoleaks from displacement of the left iliac limb. This area was subsequently treated with a covered stent with resolution of the endoleaks.

Type II: circulation within the sac from aortic branches such as the lumbar arteries or inferior mesenteric artery (Fig. 63–4) Type III: reperfusion of the aneurysm sac from either a hole in the fabric of the graft or disjunction of modular components (Fig. 63–5) Type IV: ﬂow through porous fabric material11

1. Barrett BJ, Carlisle EJ. Meta-analysis of the relative nephrotoxicity of high- and low-osmalality iodinated contrast media. Radiology 1993;188:171–178. 2. Murphy SW, Barrett BJ, Parfrey PS. Contrast nephropathy. J Am Soc Nephrol 2000;11:171–182. 3. Tepel M, Van Ger Giet M, Schwarzﬁeld C, et al. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med 2003;343: 180–184. 4. Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate. JAMA 2004;291:2328–2334. 5. Schneider PA (ed). How to get in: percutaneous vascular access. In Endovascular Skills: Guidewire and Catheter Skills for Endovascular Surgery, 2nd ed. New York: Marcel Dekker, 2003; pp 5–30. 6. Rupp SB, Vogelzang RL, Nemeck AA, et al. Relationship of the inguinal ligament to pelvic radiographic landmarks: anatomic correlations and its role in femoral arteriography. J Vasc Interv Radiol 1993;4:409–413.

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7. Schneider PA (ed). Balloon angioplasty: minimally invasive autologous revascularization. In Endovascular Skills: Guidewire and Catheter Skills for Endovascular Surgery, 2nd ed. New York: Marcel Dekker, 2003; pp 201–216. 8. Scheinert D, Ludwig J, Steinkamp. Treatment of cath induced iliac artery injuries with self-expanding endografts. J Endovasc Ther 2000;7:213–220. 9. Ansel GH. Endovascular complications of angioplasty and stenting. In Complications in Vascular Surgery. New York: Marcel Dekker; 2004; pp 597–614. 10. Fairman RM, Velazquez O, Baum R, et al. Endovascular repair of aortic aneurysms: critical events and

adjunctive procedures. J Vasc Surg 2001;33:1226– 1232. 11. Deaton DH, Makaroun MS, Fairman RM. Endoloeak: predictive value for aneurysm growth at 3 years. Ann Vasc Surg 2002;16:37–42. 12. Beebe HG. Endoleak. In Towne JB, Hollier LH (eds). Complications in Vascular Surgery. New York: Marcel Dekker, 2004; pp 659–682. 13. Baum RA, Carpenter JP, Golden MA, et al. Treatment of type 2 endoleaks after endovascular repair of abdominal aortic aneurysms: comparison of transarterial and translumbar techniques. J Vasc Surg 2002;35:23–29.

Section XI

THORACIC SURGERY M. Blair Marshall, MD Good people are good because they’ve come to wisdom through failure. We get very little wisdom from success, you know—William Saroyan

64

Bronchoscopy: Flexible and Rigid; Esophagoscopy: Flexible and Rigid; Mediastinoscopy; and Anterior Mediastinotomy John C. Kucharczuk, MD Bronchoscopy: Flexible and Rigid INTRODUCTION In the late 1890s, Gustav Killian used a rigid tube to remove an impacted piece of bone from the right main stem of an awake 63-year-old man. Twenty years later in Philadelphia, Chevalier Jackson popularized extensive examination of the airways using rigid bronchoscopy. Jackson’s techniques were effective, however, they required specialized training; only a few physicians possessed the skills required to perform the procedure safely. Today, awake rigid bronchoscopy is rarely practiced. Nevertheless, rigid bronchoscopy performed with the patient under general anesthesia remains a valuable diagnostic and therapeutic tool for the modern thoracic surgeon. It is irreplaceable in certain circumstances. The advent of the ﬂexible bronchoscope in the 1970s revolutionized the ﬁeld of bronchoscopy. Flexible bron-

choscopy can be easily performed in awake patients as well as in those who are anesthetized. Flexible bronchoscopes can be used for both diagnostic and therapeutic interventions and are available in a number of sizes and specialized conﬁgurations designed for particular applications. Working channels from 1.2 mm up to 3.2 mm allow for aspiration of secretions as well as deployment of a number of instruments into the airway under direct vision. The modern thoracic surgeon must be an expert bronchoscopist comfortable with both ﬂexible and rigid bronchoscopy. He or she must be able to choose the approach and instrument most appropriate to a given clinical situation.

BRONCHOSCOPY STEPS Step 1 Step 2 Step 3

Select procedure (rigid vs. ﬂexible) Select appropriate anesthesia (topical general) Institute monitoring

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Fiberoptic connection

Distal ventilation holes

Ventilation side port

Figure 64–1 The most commonly used rigid bronchoscopes of varying sizes. Note the ventilatory attachment and the side ports.

Step 4 Step 5 Step 6

Supply supplemental oxygen Perform procedure Recover patient

BRONCHOSCOPY PROCEDURE Select the Appropriate Bronchoscopy Technique The greatest pitfall in bronchoscopy is the inappropriate choice of one technique (ﬂexible or rigid) over another. Currently, rigid bronchoscopy is performed exclusively in anesthetized patients and allows for the examination of the trachea and proximal airway only. Flexible bronchoscopy, conversely, can be performed in awake or anesthetized patients and allows for examination of the airway down to the subsegmental level.

RIGID BRONCHOSCOPY Rigid bronchoscopy should be performed in the operating room with the patient under general anesthesia. Speciﬁc applications for rigid bronchoscopy are listed later. Rigid bronchoscopes come in a variety of diameters and lengths, as shown in Figure 64–1. They are sized according to the outside diameter. Figure 64–2 shows the computed tomography (CT) scan of a patient with a tracheal mass and impending respiratory obstruction. This patient is an ideal candidate for rigid bronchoscopy for diagnosis and palliative relief of the airway obstruction using a “coring” technique. The ﬁnal pathology is this case was a tracheal chondrosarcoma.

INDICATIONS Removal of foreign bodies Evacuation of tracheal stenosis Placement of nonexpandable stents Control of massive hemoptysis Evaluation of tracheobronchial mobility

Figure 64–2 Computed tomography (CT) image of impending airway obstruction from a chondrosarcoma (arrow) of the trachea.

Evaluation of airway invasion or adherence by esophageal tumors Palliation of airway obstruction by tumor (“coring out”)

Inappropriate Patient for Rigid Bronchoscopy The preoperative assessment of patients undergoing rigid bronchoscopy includes examination of the neck and oral cavity. Severe cervical arthritis with a contracted neck makes rigid bronchoscopy difﬁcult. Poor dentition and loose teeth are at risk during rigid bronchoscopy, and removable dental work such as bridges and dentures should be taken out prior to the procedure. The presence of a mature tracheostomy, conversely, is not a contraindication to rigid bronchoscopy. The tracheostomy device can be removed and the patient intubated with the rigid scope from above or, in some circumstances, directly through the stoma, with particular care being taken to avoid injury to the posterior membranous portion of the trachea. Likewise, rigid bronchoscopy can be performed through the mature stoma in patients who have undergone total laryngectomy. ● Consequence Inability to position the patient appropriately, resulting in an inability to safely perform the procedure. Complications can range from minor damage to the dentition to life-threatening perforation of the pharynx or airway. Grade 1–5 complication ● Repair Select an alternative method for airway visualization and intervention.

64 BRONCHOSCOPY: FLEXIBLE AND RIGID ● Prevention Adequately evaluate the patient preoperatively. Do not attempt rigid bronchoscopy on patients with a ﬁxed cervical spine or an inability to be positioned appropriately.

Inadequate Cooperation between Surgeon and Anesthesiologist The performance of rigid bronchoscopy with the patient under general anesthesia requires close coordination between the anesthesiologist and the surgeon. While the anesthesiologist institutes the appropriate monitoring and intravenous access, the surgeon should prepare the rigid bronchoscope along with its light source and supporting hardware. During “routine” rigid bronchoscopy, general anesthesia is induced with a combination of intravenous and inhalation anesthetics. Secretions are aspirated from the posterior pharynx, and the patient is mask-ventilated. A muscle relaxant is then administered to allow easier placement of the rigid bronchoscope. Patients with large mediastinal masses or near-complete obstructing tracheal tumors represent a particular challenge and, as such, require special anesthetic consideration. Placement of these patients in a supine position or administration of general anesthesia with a muscle relaxant can lead to complete airway obstruction and life-threatening hypoxemia. In these patients, the airway should ﬁrst be anesthetized with local agents. Patients should remain in a somewhat upright position while general anesthesia is slowly induced with intravenous agents. During this phase, the anesthesiologist assists the patient’s spontaneous ventilation. Use of muscle relaxants should be avoided until the airway is secure. Once anesthetized, the patient should be quickly positioned and intubated with the rigid scope. Ventilation through the anesthesia circuit connected to the side port of the ventilating scope can then begin. If a nonventilating scope is used, insufﬂation of oxygen via a Venturi apparatus can be used to maintain oxygenation. ● Consequence Inadequate control of the airway resulting in hypercarbia, hypoxemia, and death. Grade 3/4/5 complication ● Repair Both the surgeon and the anesthesiologist must understand the conduct of the procedure and work together as a team. It is helpful to review the planned procedure with the entire operating room team as well as to have a contingency plan in case of a loss of the airway. ● Prevention The procedure should be performed by a cohesive group of anesthesiologists, surgeons, and nurses. The entire team must understand the procedure before starting.

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Inability to Place the Rigid Bronchoscope When the surgeon is ready to introduce the rigid bronchoscope, the patient should be positioned supine with the neck slightly ﬂexed (“snifﬁng position”). The surgeon stands behind the patient’s head, secretions are suctioned from the posterior pharynx, and tooth guards are placed. The surgeon controls the patient’s head by gripping the maxilla with the middle and ring ﬁngers of the left hand. The index ﬁnger and thumb of this same hand hold the scope in the manner in which one holds a pool stick. The right hand grasps the scope at the level of the eyepiece. The instrument is introduced with the bevel down and advanced until the epiglottis is visualized. The scope is placed just under the leading edge of the epiglottis, which is then gently elevated to reveal the vocal cords. Elevation is achieved by the use of the left thumb. Use of the patient’s teeth or gums as a fulcrum to elevate the epiglottis results in damage to the teeth and must be avoided. One should avoid advancing the scope further than 1 cm beyond the tip of the epiglottis because this places the scope beyond the larynx. When the vocal cords are visualized, the scope is rotated 90° to the right and advanced into the trachea. Once in the trachea, the scope is rotated back to its original position. The supporting pillow can then be removed from behind the head and the table headboard can be lowered to extend the neck. Ventilation is begun either through the side port with an eyepiece in place or via the Venturi apparatus if a nonventilating scope is being used. ● Consequence Inability to insert the rigid bronchoscope can result from a number of causes: inadequate training, inability to position the patient appropriately, and inadequate visualization owing to secretions or blood. Complications can range from having to convert to an alternative technique, minor damage to dentition, life-threatening perforation of the pharynx or airway, and even loss of airway control and death. Grade 1–5 complication ● Repair If the patient is an inappropriate candidate for rigid bronchoscopy or the operator is not sufﬁciently trained, an alternative method for airway visualization and intervention should be selected. ● Prevention Adequately evaluate the patient preoperatively.

Inadequate Visualization of the Airway The patient’s head should be turned to the side opposite that which you wish to examine. When passing the scope into the right main stem, for example, the patient’s head should be turned slightly to the left. We typically hold ventilation and remove the eyepiece when advancing the scope. If closer inspection of the airway is required, a

1

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Hopkins rod telescope is passed through an adapter on the main channel of the rigid scope. These telescopes provide magniﬁcation as well as a variety of angled views. If telescopes are not available, a ﬂexible bronchoscope can be passed through the rigid scope. ● Consequence Advancing a rigid bronchoscope with inadequate visualization of the airway will likely result in airway perforation, necessitating thoracotomy and complex reconstruction. Grade 3–5 complication ● Repair The best strategy is not to advance a rigid bronchoscope in the airway unless a clear lumen can be seen ahead. ● Prevention The patient’s head is manipulated to align the long axis of the airway with the scope, allowing the scope to be passed with clear visualization of the distal lumen.

Recover the Patient After rigid bronchoscopy, the patient is recovered from general anesthesia in a postanesthesia care unit. Those patients undergoing laser ablation of an obstructing lesion or relief of airway obstruction by a “coring technique” utilizing the rigid bronchoscope should be hospitalized and observed overnight to ensure that an adequate airway has been achieved.

FLEXIBLE BRONCHOSCOPY Unlike rigid bronchoscopy, awake ﬂexible bronchoscopy can be performed in the outpatient setting for a variety of diagnostic and therapeutic indications, as listed later. Unfortunately, ﬁberoptic bronchoscopes are delicate instruments; they require specialized training for cleaning, maintenance, and storage, as shown in Figure 64–3.

INDICATIONS Examination of airway to subsegmental level Aspiration of secretions Mucosal brushings Biopsy of endobronchial lesions Deployment of expandable airway stents Removal of small foreign bodies Transbronchial needle biopsy Outpatient awake ﬂexible bronchoscopy is performed in a specially designed endoscopy suite. The suite must include a supplemental oxygen supply, pulse oximetry, cardiac monitoring, and intubation equipment to be used in the event of an airway emergency. Supplemental oxygen—via either nasal cannula or face mask with a specially designed opening to allow for the passage of the

Figure 64–3 Storage unit for ﬂexible bronchoscopes to prevent damage.

bronchoscope—should be provided to all patients undergoing bronchoscopy. Adequate monitoring of the awake patient includes pulse oximetry and heart rate monitoring. Most patients have an intravenous line in place; however, with properly administered topical anesthesia, intravenous sedation is rarely required. Figure 64–4 shows the bronchoscopic view of a patient with an endobronchial lesion. This patient is an ideal candidate for outpatient diagnostic ﬂexible bronchoscopy with endobronchial biopsy prior to embarking on deﬁnitive management. Awake bronchoscopy during the postoperative period is frequently performed on the thoracic surgery ward. The most common indication for postoperative bronchoscopy is atelectasis due to mucus plugging. Well-timed therapeutic bronchoscopy in these patients can often prevent more serious complications such as pneumonia and reintubation. To facilitate the bedside procedure, bronchoscopy carts stocked with a ﬂexible bronchoscope, a light source, suction tubing, bite blocks, oxygen masks, local anesthetics, pulse oximetry, and emergency airway equipment should be readily available. Carts should be inventoried and maintained daily by an adequately trained respiratory therapist. Having this simple cart available will minimize the frustration encountered when attempting a procedure on an awake patient without appropriate equipment. At our institution, we typically use a standard adult bronchoscope with an external diameter of 5.9 mm for awake procedures.

64 BRONCHOSCOPY: FLEXIBLE AND RIGID

Figure 64–4 Obstruction of the right upper lobe oriﬁce by tumor.

Flexible bronchoscopy with the patient under general anesthesia should be performed in the operating room under the supervision of an anesthesiologist. Monitoring should include pulse oximetry, noninvasive blood pressure monitoring, and three-lead electrocardiographic monitoring. Following the induction of general anesthesia, direct laryngoscopy is performed and an endotracheal tube is placed. Tube position is conﬁrmed by auscultation, observation of the chest, and end-tidal CO2 monitoring. In the adult patient, an 8.0-mm endotracheal tube should be used. This tube size allows ventilation via a bronchoscopy adapter during the use of a standard 5.9-mm outside diameter (OD) ﬂexible bronchoscope. The 5.9-mm OD ﬂexible bronchoscope is preferred because its working channel of 2.8 mm is large enough to allow aspiration of thick secretions without becoming clogged. The use of smaller endotracheal tubes with smaller bronchoscopes is often frustrating because of difﬁculty in clearing secretions in order to obtain an adequate view. The “pediatric bronchoscope” has an OD of 3.5 mm and a working channel of only 1.2 mm. In the case of laser bronchoscopy and other specialized uses, a 6.2-mm OD scope with a 3.2-mm working channel can be used. If possible, a 9.0-mm endotracheal tube should be used in these patients.

Select Appropriate Anesthesia Inadequate Topical Anesthesia for Awake Flexible Bronchoscopy Adequate topical anesthesia is paramount to the performance of awake ﬂexible bronchoscopy. Anesthesia should begin with the administration of nebulized lidocaine (5 ml

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of 1% lidocaine solution) by a respiratory therapist. The posterior pharynx, tonsillar pillars, and soft palate are then sprayed with 1% lidocaine. Next, 2 to 5 ml of a 2% lidocaine solution is injected transtracheally through the cricothyroid membrane with a 21-gauge needle. This maneuver causes the patient to cough but results in topical anesthesia of the airway. Finally, a bite block is placed in the mouth, and the bronchoscope is introduced through the mouth and advanced down to the level of the vocal cords. One milliliter of a 4% lidocaine solution is then sprayed through the working channel of the bronchoscope onto each vocal cord under direct vision. The scope is removed and the patient is encouraged to cough. At this point, local anesthesia is complete and awake bronchoscopy can be easily performed with satisfactory patient comfort. Intravenous sedation can lead to hypoxemia, hypercarbia, and hypotension and should thus be avoided. With properly administered local anesthesia, patients remain comfortable throughout the procedure and subsequent intravenous sedation is rarely required. After awake ﬂexible bronchoscopy, patients should be monitored with pulse oximetry for a short period to ensure that oxygenation is satisfactory. A chest x-ray should be obtained to rule out pneumothorax, lobar collapse, and novel inﬁltrates. Because the posterior pharynx and vocal cords remain anesthetized, patients should remain on nothing by mouth for 3 to 4 hours after the procedure to minimize the risk of aspiration. ● Consequence Inability to complete the procedure owing to patient discomfort. Grade 1/2 complication ● Repair Suspend the procedure and provide adequate topical anesthesia. ● Prevention Generous topical analgesia for all patients undergoing awake bronchoscopy. Avoid intravenous sedation, which can contribute to secretion-management difﬁculties.

PROCEDURE OUTCOMES Complication rates for both rigid and ﬂexible bronchoscopy should be low. Bleeding dyscrasias should be addressed prior to the procedure, particularly if biopsy is planned. The majority of complications surrounding awake ﬂexible bronchoscopy are related to preprocedural intravenous sedation. As discussed previously, this issue can be avoided altogether with the proper application of local anesthesia and avoidance or minimal use of intravenous sedation. This cannot be stressed enough when dealing with frail or elderly patients, in whom signiﬁcant hypoxemia must be avoided. Particularly tenuous patients

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are probably better off undergoing elective intubation followed by therapeutic bronchoscopy rather than struggling through a difﬁcult awake bronchoscopy. Avoiding hypoxemia during rigid bronchoscopy requires teamwork and coordination between the anesthesiologist and the surgeon.

CONCLUSIONS Both rigid and ﬂexible bronchoscopy are invaluable tools for the thoracic surgeon. Whereas ﬂexible bronchoscopy has become the norm, situations arise that demand the use of rigid bronchoscopy. As such, thoracic surgeons must obtain sufﬁcient training so that they can perform both procedures with conﬁdence.

Esophagoscopy: Flexible and Rigid INTRODUCTION Esophagoscopy has developed along lines similar to those of bronchoscopy. Initial examinations of the esophagus were performed with rigid metal tubes, the forerunners of the current rigid esophagoscope. The advent of ﬁberoptic technology revolutionized the ﬁeld of diagnostic esophagoscopy. The ﬂexible esophagoscope is easy to insert in the sedated or anesthetized patient, and minimal training is required to become quite proﬁcient in its use. Conversely, rigid esophagoscopy requires an anesthetized patient along with specialized insertion skills. Improper insertion of a rigid esophagoscope can result in esophageal perforation, a highly morbid event.

ESOPHAGOSCOPY STEPS Step 1 Step 2 Step 3 Step 4 Step 5

Select technique (ﬂexible vs. rigid) Select appropriate anesthesia (sedation vs. general) Institute monitoring Perform procedure Recover patient

channel: biopsy forceps, snares, brushes, cautery wires, dilation balloons, and laser ﬁbers. Conversely, rigid esophagoscopy must be performed in the operating room on an intubated patient under general anesthesia. Because of its large lumen, the rigid esophagoscope is ideally suited for the visualization and extraction of impacted foreign bodies. Its superior suction capacity makes it extremely useful in the case of severe esophageal bleeding; conversely, ﬂexible scopes can easily be overcome by signiﬁcant bleeding. The rigid esophagoscope also allows for better visualization of the difﬁcult to view masses located just below the cricopharyngeus. Finally, compared with the ﬂexible ﬁberoptic esophagoscope, the rigid esophagoscope is inexpensive and durable. The improperly inserted esophagoscope, whether ﬂexible or rigid, can result in pharyngeal or esophageal perforation. Insertion of a ﬂexible scope in the sedated patient requires only placement of a bite block to protect the scope, a simple forward jaw lift, and smooth insertion of the esophagoscope into the cervical esophagus with gentle air insufﬂation. The rigid esophagoscope is a rigid metal tube with a ﬂared tip and a thin ﬁberoptic rod for illumination. These are available in a number of lengths, as shown in Figure 64–5. Inserting a rigid esophagoscope is signiﬁcantly more challenging than inserting a ﬂexible esophagoscope. The patient should be intubated and tooth guards placed to protect dentition. If dentures or dental bridges are present, they should be removed prior to the procedure. The patient’s head should be positioned in the snifﬁng position with slight neck extension. Because of the positioning requirements, rigid esophagoscopy is contraindicated in patients with unstable cervical spines, restricted jaw movement, or severe kyphoscoliosis. The presence of thoracic arch aneurysms is a relative contraindication to rigid esophagoscopy. Once the patient is properly positioned, the scope is placed through the open mouth and passed through the posterior pharynx into the proximal esophagus. The esophagus must be entered gently because the cervical esophagus is at high risk for perforation during this phase. If resistance is encountered after passing through the cricopharyngeus, deﬂation of the endotracheal tube cuff, which sits just anterior in the tracheal lumen, can often provide easier passage. Once the scope

ESOPHAGOSCOPY PROCEDURE Select the Appropriate Technique Flexible ﬁberoptic esophagoscopy is ideal for outpatient diagnostic procedures because it can be performed safely in an outpatient endoscopy suite on a sedated patient. The procedure allows for examination of the entire esophagus, stomach, and proximal duodenum. A variety of instruments are available for deployment via the working

Figure 64–5 diameters.

Rigid esophagoscopes of varying lengths and luminal

64 BRONCHOSCOPY: FLEXIBLE AND RIGID has been inserted into the cervical esophagus, the patient’s neck should be fully extended to align the rigid scope with the longitudinal axis of the esophagus. In order to avoid perforation, forward advancement of the rigid scope must be done gently with the distal lumen always in sight.

Inability to Insert the Scope ● Consequence Insertion of an esophagoscope, either ﬂexible or rigid, must be done with the utmost care. Because of the high-pressure zone at the upper esophageal sphincter, the cervical esophagus is at high risk for perforation during incorrect scope insertion. Grade 1–5 complication ● Repair Select the appropriate method for esophageal visualization and intervention. ● Prevention Adequately evaluate patients preoperatively. Do not attempt rigid esophagoscopy on patients with a ﬁxed cervical spine or an inability to be positioned appropriately. Always advance the esophagoscope with a clear view of the distal lumen.

PROCEDURE OUTCOMES Both rigid and ﬂexible esophagoscopy should have low complication rates. This being said, patients with severe chest pain, subcutaneous emphysema, pneumothorax, pleural effusion, or fever after either rigid or ﬂexible esophagoscopy must be suspected of having an iatrogenic perforation. An immediate esophagogram should be performed in each and every one of these patients to determine the site and extent of the damage and to guide the subsequent management of these injuries.

CONCLUSIONS Both rigid and ﬂexible esophagoscopy are invaluable tools for the esophageal surgeon. Whereas ﬂexible esophagoscopy has become the norm, situations arise that demand the use of rigid esophagoscopy. As such, the practicing esophageal surgeon should be conﬁdent with the use of both procedures.

Mediastinoscopy INTRODUCTION Mediastinoscopy was ﬁrst described in the late 1950s. Since that time, it has become a routine diagnostic procedure for patients with lung cancer. It is currently widely

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used as a diagnostic tool for a variety of other mediastinal abnormalities occurring in the paratracheal and subcarinal regions. By its very nature, mediastinoscopy violates all of the basic surgical tenets. The procedure is performed with limited exposure, around the great vessels with no vascular control. Nevertheless, in competent hands, it can be performed safely, providing invaluable diagnostic information.

MEDIASTINOSCOPY STEPS Step Step Step Step Step

1 2 3 4 5

Patient selection General anesthesia Positioning Perform procedure/conﬁrm pathology Recover patient

MEDIASTINOSCOPY PROCEDURE Selecting the Appropriate Patient for Mediastinoscopy Many patients are referred for mediastinoscopy inappropriately. Patients present with a variety of anterior mediastinal, aortopulmonary window, and posterior mediastinal abnormalities. It is vital that the surgeon performing mediastinoscopy understand the limitations of the procedure and the relationship of vital vascular structures to the mediastinoscopy plane. Standard cervical mediastinoscopy can assess both the right and the left paratracheal areas as well as the subcarinal space. Figure 64–6A shows a CT scan of the chest from a patient with paratracheal, subcarinal, and hilar adenopathy. The paratracheal and subcarinal nodes are accessible by mediastinoscopy (see Fig. 64–6B). The hilar nodes are not accessible (see Fig. 64–6C), and an attempt at biopsy via cervical mediastinoscopy will result in lifethreatening hemorrhage owing to azygous vein and/or pulmonary artery injury. Mediastinoscopy is performed under general anesthesia with the patient’s neck fully extended. Proper positioning is critical. An inﬂatable bag placed under the patient’s shoulders will provide adequate extension (Fig. 64–7A). The patient shown in Figure 64–7B is properly positioned and ready for the procedure. An inability to ﬂex the neck is a contraindication to the procedure. Prior cardiac surgery does not affect the procedure because the mediastinoscopy plane descends posterior to the pericardium. A history of a prior tracheostomy may make cervical dissection more difﬁcult but is not a contraindication. Mediastinoscopy cannot be performed in patients with a current tracheostomy device in place or in those with tracheal stomas due to laryngectomy. Prior neck and anterior mediastinal radiation are relative contraindications to the procedure because the mediastinal plane may or may not be obliterated.

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Neck extended

Inflatable bag

A A

B B Figure 64–6 A, Paratracheal adenopathy (arrow) accessible by mediastinoscopy. B, Subcarinal adenopathy accessible with the mediastinoscope (single arrow). Right hilar adenopathy (arrowheads) not accessible with the mediastinoscope.

Inappropriate Patient Selection ● Consequence Inappropriate patient selection for mediastinoscopy can have disastrous consequences. Patients must have cervical neck ﬂexibility in order to be properly positioned for the procedure to be performed safely. Prior mediastinal surgery is a relative contraindication and must be evaluated on a case-by-case basis. Grade 2–5 complication ● Repair In patients who are not candidates for mediastinoscopy but require mediastinal sampling, alternative techniques such as transbronchial needle aspiration should be considered. ● Prevention Adequately evaluate patients preoperatively. Do not attempt mediastinoscopy on patients with a ﬁxed cervical spine or an inability to be positioned appropriately.

Figure 64–7 A, Proper patient positioning for cervical mediastinoscopy with the patient’s shoulders resting on an inﬂatable bag and the neck extended. B, The patient has been prepared and draped for cervical mediastinoscopy.

Perform the Procedure/Conﬁrm the Pathology Bleeding A standard cervical mediastinoscope is illustrated in Figure 64–8. Light is supplied to the tip of the scope via a ﬁberoptic cable. As such, any signiﬁcant bleeding results in “lights out” with total loss of visualization. Clearly, the best method for dealing with bleeding during mediastinoscopy is avoidance. The mediastinum is replete with small perinodal vessels that can cause problematic bleeding. A special insulated suction/cautery device (Fig. 64–9) is used to coagulate small bronchial vessels. Lack of insulation at the distal tip of the device allows for conduction of current to the tip of the device only. Suction allows for aspiration of blood to clear the ﬁeld. Cautery should not be used in the left paratracheal space because it can result in damage to the left recurrent nerve, which courses through the left tracheal esophageal groove. A specialized aspirating needle (Fig. 64–10) should be used to avoid biopsy of vascular structures such as the aorta, pulmonary

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● Consequence Bleeding during mediastinoscopy ranges from minor to life threatening, depending upon the bleeding site. Small bleeding bronchial vessels can obscure visualization but are usually easily controlled with cautery. Major vascular injuries can lead to exsanguination. Grade 3–5 complication

Figure 64–8 Standard scope used for cervical mediastinoscopy.

Non-insulated tip Cautery connection

Suction port

Figure 64–9 Insulated suction cautery device used for dissection through the mediastinoscope as well as to control hemorrhage for small vessels.

Biopsy forceps

Aspirating needle

● Repair Should major bleeding occur during mediastinoscopy, the mediastinum should be packed immediately. A long E-tape or vaginal packing can be inserted directly into the scope. The scope can then be slowly withdrawn as the packing is advanced. Once the scope is removed, digital compression should be applied. Because bleeding most commonly results from injury to the azygous vein or pulmonary artery, packing easily controls these low-pressure systems. Once successful packing is achieved, blood should be ordered and adequate largebore venous access conﬁrmed. Having a functioning arterial line is helpful. When these safeguards are in place, median sternotomy is performed and the injury is identiﬁed and repaired under direct visualization. Always resist the urge to convert to a thoracotomy; all vascular injuries caused by mediastinoscopy can be repaired via sternotomy, some are not reparable via a thoracotomy approach. Once the injury is repaired, staging can be completed by obtaining the appropriate additional lymph node biopsies. In the event that a lung resection was planned for the same sitting and the patient is found to be stage-appropriate, the resection can be performed through the sternotomy. ● Prevention The best method for dealing with bleeding during mediastinoscopy is avoidance.

Pneumothorax Occasionally, the right pleural space is inadvertently breached during mediastinoscopy. Typically, the incision can be closed over a red rubber tube; the anesthesiologist then applies a Valsalva breath to the ventilatory circuit as the tube is removed. In cases in which the lung has been damaged or biopsied and an ongoing air leak exists, a chest tube is required.

Figure 64–10 A variety of biopsy forceps used through the mediastinoscope, as well as the long aspiration needle. The latter is useful for differentiating nodal tissue from blood vessels.

● Consequence A small pneumothorax caused by entrance into the pleural space is inconsequential. Parenchymal lung damage with ongoing air leak requires placement of a chest tube. Grade 1–3 complication

artery, superior vena cava, and azygous vein. The nodes themselves should be sampled with a gentle “twisting” of the biopsy forceps. Forceful “pulling” of nodal tissue will result in disruption of major associated vascular structures.

● Repair When the pleura is entered with no lung injury, the pleural air can be evacuated by closing the incision around a small red rubber tube, giving a large positivepressure breath on the anesthesia circuit and then removing the tube. In this case, a small, stable

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pneumothorax on a postoperative ﬁlm is of no signiﬁcance. Conversely, if there has been lung injury with an ongoing air leak, a chest tube must be placed and remain in place until the air leak resolves. ● Prevention Careful attention to detail and knowledge of the anatomy should allow one to avoid inadvertent entrance into the pleural space.

ANTERIOR MEDIASTINOTOMY STEPS Step Step Step Step

1 2 3 4

Step 5

Patient selection Select anesthesia (general vs. local) Perform procedure Intraoperative conﬁrmation of diagnostic material (working with pathologist) Recover patient

ANTERIOR MEDIASTINOTOMY PROCEDURE

PROCEDURE OUTCOMES Mediastinoscopy continues to be the single best method for staging the mediastinum in patients with lung cancer. In well-trained hands, the procedure can be performed safely with very accurate results. The overall complication rate for mediastinoscopy should be less than 1%.

Anterior Mediastinotomy INTRODUCTION The anterior mediastinotomy or Chamberlain procedure, as originally described, provides access to the aortopulmonary lymph nodes. These nodes are not assessable with standard cervical mediastinoscopy. In our current understanding of lung cancer, however, patients with left-sided lung cancers and aortopulmonary window nodal metastasis (stations 5 and 6) enjoy a much better outcome with surgical resection than those patients with stage IIIa disease based on left paratracheal metastasis. Thus, anterior mediastinotomy is infrequently performed at present in the staging of lung cancer. However, it remains a very useful technique to sample anterior mediastinal masses. Figure 64–11 shows the CT scan of a patient with a large anterior mediastinal mass. This lesion is appropriate for sampling by anterior mediastinotomy.

Left mammary vessels Mass

There are very few contraindications to anterior mediastinotomy in patients with anterior mediastinal masses. Signiﬁcant experience and cooperation with the anesthesiologist is required in patients with very large anterior mediastinal masses and airway compression. Controversy has always surrounded the biopsy of a well-deﬁned mass believed to be an encapsulated thymoma because of the concern for pleural dissemination. When conﬁdent on clinical and radiographic grounds that the lesion is a wellencaspsulated thymoma, it should be resected without a biopsy. In less-clear cases or in cases in which lymphoma is a consideration, biopsy via anterior mediastinotomy is performed. In general, we avoid needle biopsies of anterior mediastinal masses because our pathologist and hematopathologist prefer large amounts of tissue for histology and special studies. This practice, however, is largely institution-dependent. An important subset of patients are those with mediastinal germ cell tumors. They do not require biopsy for diagnosis; the diagnosis is made by serum markers including β-human chorionic gonadotropin and αfetoprotein levels. Surgery in this cohort of patients is reserved for resection of residual masses following systemic treatment.

Anesthesia (General vs. Local) The anterior mediastinotomy procedure can be performed with the patient under local or general anesthesia. In patients with very large masses, the major concern is airway compression with muscle paralysis; in difﬁcult cases, spontaneous ventilation is maintained throughout the procedure. A rigid bronchoscope should be available in case it is required to emergently establish an airway. Obviously, both the surgeon and the anesthesiologist must cooperate and have signiﬁcant experience to safely perform the procedure on patients with very large masses.

Loss of Airway

Figure 64–11 CT scan demonstrates an anterior mediastinal mass appropriate for a Chamberlain procedure.

● Consequence Loss of airway during anesthesia. Grade 2–5 complication

induction

of

general

64 BRONCHOSCOPY: FLEXIBLE AND RIGID ● Repair Have a rigid bronchoscope available and assembled in the operating room to establish an airway in an emergent situation. ● Prevention Adequately evaluate the patient preoperatively with the anesthesia team. Maintain spontaneous respirations in a somewhat upright position until the airway has been secured.

Perform the Procedure Incorrect Incision The standard incision is made overlying the second costal cartilage. This incision is 3 cm in length and starts at the sternal boarder. The angle of Louis (sternal angle) is the palpable landmark on the sternum that marks the level of the second costal cartilage. This position corresponds to the narrowing of the sternum seen on consecutive axial CT scan images as the manubrium transitions to the body of the sternum. The incision can be made over any costal cartilage that overlies the abnormality. However, the second costal cartilage always serves as the landmark and is used as a reference point for locating masses that occur lower in the mediastinum. Figure 64–12 shows a patient being readied for anterior mediastinotomy; the intent is to enter the superior mediastinum through the bed of the left second intercostal cartilage. The sternal notch and angle of Louis are marked for reference. If the mass is very large, the intercostal muscles are divided and the biopsy is performed between the ribs. In situations in which better exposure is required, the anterior perichondrium is scored with cautery and a periosteal elevator is used to perform an extraperichondrial resection of a 3-cm segment of costal cartilage. The posterior perichondrium

667

is opened with a scalpel, allowing direct access to the anterior mediastinum. ● Consequence Inability to locate and biopsy the lesion. Grade 1–3 complication ● Repair In difﬁcult situations, a lighted mediastinoscope can be placed through the incision to help visualize the target lesion. ● Prevention Correlate the location of the incision with the preoperative chest CT scan and known anatomic landmarks, especially the sternal angle

Bleeding The most common cause of bleeding during anterior mediastinotomy is inadvertent damage to the mammary artery. The mammary arteries run close to the sternal border. Knowing the anatomy allows the surgeon to identify and protect the vessels by gently sweeping them laterally. If the mammary artery is injured, bleeding is controlled with ligation. Complete transaction of the artery may be difﬁcult to control because the cut ends have a tendency to retract. In these cases, the ends must be located and ligated or clipped; cautery is not sufﬁcient. ● Consequence Signiﬁcant blood loss. Grade 1–4 complication ● Repair Locate and ligate both ends of a transected mammary artery. ● Prevention Mobilize and “sweep” the mammary artery laterally to avoid injury.

Figure 64–12 Patient being readied for a Chamberlain procedure (anterior mediastinotomy); the sternal notch and angle of Louis have been highlighted and the bed of the left second costal cartilage is marked (2).

Pneumothorax The causes of pneumothorax during anterior mediastinotomy are (1) inadvertent entrance into the pleural cavity and (2) injury to the lung with creation of an air leak. Distinguishing between the two mechanisms is crucial because the management is quite different. During dissection, the pleural membrane should be swept laterally with the mammary vessels. If the pleural cavity is inadvertently entered, the incision is closed over a red rubber catheter (Fig. 64–13) and a Valsalva breath is used to evacuate the air. The tube is removed while the positive-pressure breath is held by the anesthesiologist. The ﬁnal stitch is tied to create an airtight seal. In the case of injury to the underlying lung with a persistent air leak, a chest tube is placed. Although the tube can be placed through the incision, this is generally uncomfortable and cumbersome for a chest

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Intraoperative Conﬁrmation of Diagnostic Material Nondiagnostic Material Intraoperative review of the biopsy material with a pathologist familiar with mediastinal pathology is mandatory. Several of the lymphomas generate a brisk tissue reaction, and initial samples may show only ﬁbrosis whereas deeper samples conﬁrm the pathology. I usually review a touch preparation and frozen section on the portion of the initial biopsy specimen with the pathologist. The pathologist cannot make the ﬁnal diagnosis based on these initial studies. She or he must, however, conﬁrm the presence of an abnormality (not just ﬁbrous tissues or necrosis) and the adequacy of tissue for appropriate studies to obtain a diagnosis. Nothing is more frustrating than ﬁnding out 3 days after the procedure that more tissue is needed. ● Consequence A nondiagnostic procedure and need for additional invasive procedures. Grade 1–3 complication ● Repair Do not conclude the procedure until adequate diagnostic material has been obtained.

Figure 64–13 Red rubber catheter placed though the skin incision evacuating an iatrogenic pneumothorax during anterior mediastinotomy.

tube. When a chest tube is required, I recommend placing it through a separate incision in a traditional site. ● Consequence A small pneumothorax caused by entrance into the pleural space is inconsequential. Parenchymal lung damage with ongoing air leak requires placement of a chest tube. Grade 1–3 complication ● Repair When the pleura is entered with no lung injury, the pleural air can be evacuated by closing the incision around a small red rubber tube, giving a large positivepressure breath on the anesthesia circuit and then removing the tube. In this case, a small, pneumothorax on a postoperative ﬁlm is of no signiﬁcance. Conversely, if there has been lung injury with an ongoing air leak, a chest tube must be placed and remain in place until the air leak resolves. ● Prevention The pleural membrane should be swept laterally with the mammary vessels to avoid entering the pleural cavity and/or inadvertent lung injury.

● Prevention Mandatory intraoperative review of touch preparations and frozen sections with a qualiﬁed pathologist or hematopathologist to conﬁrm adequate diagnostic tissue.

PROCEDURE OUTCOMES The anterior mediastinotomy procedure is a safe and effective way to sample anterior mediastinal masses. The complication rate is low, and the diagnostic rate should be high. In stable patients, the procedure is performed on an outpatient basis. Patients with large masses and concern for airway compression are admitted and their pathology rushed so that treatment may begin within 36 hours.

SUGGESTED READINGS Bronchoscopy: Flexible and Rigid 1. Alvarez F, Burger C, Grinton S, et al. Competencies in pulmonary procedures. Chest 2004;125:800–801. 2. British Thoracic Society guidelines on diagnostic ﬂexible bronchoscopy. Thorax 2001;56(suppl 1):i1–i21. 3. Lukomsky GI, Ovchinnikov AA, Bilal A. Complications of bronchoscopy: comparison of rigid bronchoscopy under general anesthesia and ﬂexible ﬁberoptic bronchoscopy under topical anesthesia. Chest 1981;79:316–321. Esophagoscopy: Flexible and Rigid 4. Gaer JA, Blauth C, Townsend ER, Fountain SW. Method of endoscopic esophageal intubation using a rigid esophagoscopy. Ann Thorac Surg 1990;49:152–153.

64 BRONCHOSCOPY: FLEXIBLE AND RIGID 5. Glaws WR, Etzkorn KP, Wenig BL, et al. Comparison of rigid and ﬂexible esophagoscopy in the diagnosis of esophageal disease: diagnostic accuracy, complications, and cost. Ann Otol Rhinol Laryngol 1996;105:262–266. 6. Brinster CJ, Singhal S, Lawrence L, et al. Evolving options in the management of esophageal perforation. Ann Thorac Surg 2004;77:1475–1483. Mediastinoscopy 7. Hammoud ZT, Anderson RC, Meyers BF, et al. The current role of mediastinoscopy in the evaluation of thoracic disease. J Thorac Cardiovasc Surg 1999;118:894– 899. 8. Lemaire A, Nikolic I, Petersen T, et al. Nine-year single center experience with cervical mediastinoscopy: complications and false negative rate. Ann Thorac Surg 2006;82:1185–1189; discussion 1189–1190.

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9. Kumar P, Yamada K, Ladas GP, Goldstraw P. Mediastinoscopy and mediastinotomy after cardiac surgery: are safety and efﬁcacy affected by prior sternotomy? Ann Thorac Surg 2003;76:872–876; discussion 876–877. Anterior Mediastinotomy 10. McNeill TM, Chamberlin JM. Diagnostic anterior mediastinotomy. Ann Thorac Surg 1966;2(4):532–539. 11. Patterson GA, Piazza D, Pearson FG, et al. Signiﬁcance of metastatic disease in subaortic lymph nodes. Ann Thorac Surg 1987;43:155–159. 12. Watanabe M, Takagi K, Aoli T, et al. A comparison of biopsy through a parasternal anterior mediastinotomy under local anesthesia and percutaneous needle biopsy for malignant anterior mediastinal tumors. Surg Today 1998;28:1022–1026.

65

Lobar Resections Todd S. Weiser, MD and Scott J. Swanson, MD

INTRODUCTION Lung cancer remains the most common cause of cancer death in the United States for both men and women. Approximately 170,000 deaths each year are attributable to lung cancer, surpassing the number of deaths due to the next four most common cancers combined.1 The majority of these cases are due to non–small cell lung carcinoma (NSCLC). Most patients present with advanced locoregional or disseminated disease, and despite advances in multimodality treatment of this disease, the 5-year survival remains 10% to 12%. However, when patients with lung cancer are diagnosed at an early stage, the overall 5-year survival may exceed 70% to 80%.2 Complete surgical resection remains the cornerstone for curative therapy of NSCLC.3,4 The ﬁrst successful resection for lung cancer, a pneumonectomy, was performed by Evarts Graham in 1933. An anatomic resection, preferably a lobectomy or pneumonectomy and, in some instances, segmentectomy, is the standard treatment for stage I or II NSCLC.5 Between 20% and 30% of all patients with new lung cancers have disease that is amenable to surgical treatment. The remainder of patients present with locally unresectable disease or with distant metastases. Neoadjuvant strategies involving chemotherapy, thoracic radiation, or both can render some of these patients subsequently resectable. Nonanatomic wedge resections are used for diagnostic purposes and, in rare instances, for the local control of lung cancer. The ﬁrst description of thoracoscopy appeared in 1910, when pleural adhesions were lysed with the use of a cystoscope.6 With the advent of selective bronchial intubation, the use of thoracoscopy expanded from addressing pleural processes to performing bullectomies and wedge resections, and it is now utilized in the surgical treatment of lung cancer with anatomic lung resections. Video-assisted thoracic surgery (VATS) lobectomy has been employed in the treatment of lung cancer since 1993.7,8 No large, prospective, randomized studies have been reported comparing video-assisted lobectomy with those performed via the traditional open approach. There are, however, some small, nonrandomized studies comparing

outcomes with these two surgical approaches.9,10 Data from these series, as well as others,7,8,11–13 demonstrate that in experienced hands, lobectomy by either approach is associated with minimal morbidity and mortality. The perioperative mortality rate associated with a VATS lobectomy is less than 1%, which compares favorably with the open approach. Video-assisted thoracoscopic anatomic resections are certainly more technically demanding than those carried out via a conventional approach. There have been no prognostic variables identiﬁed to date that are able to predict intraoperative complications in patients undergoing pulmonary lobectomy. The VATS operation consists of individual hilar ligation via three to four small incisions without rib spreading. This anatomic lobectomy should replicate the identical oncologic principles as those achieved via traditional thoracotomy.14 That is, the surgeon resects the tumor with negative margins performing individual vascular and bronchial ligation and division, with a complete hilar node dissection. Furthermore, a mediastinal lymph node dissection, or sampling, is performed, as appropriate. Certain aspects in VATS lobectomies, such as avoiding rib spreading and/or the use of a rib retractor, are emphasized with the goal of improving the patient’s postoperative experience. Cosmetic aspects such as smaller scars (the largest incision is usually 5 to 8 cm) are also important. One variant, the video-assisted simultaneously stapled lobectomy, does not employ individual hilar ligation. In essence, it is a different operation and is not discussed in this chapter. Nevertheless, some surgeons have achieved excellent results with this technique.15

INDICATIONS ● Primary lung neoplasms ● Pulmonary metastases not amenable to wedge resec-

tion owing to anatomic considerations ● Benign lung tumors not amenable to wedge resection

owing to anatomic considerations ● Congenital anomalies such as arteriovenous malforma-

tions and pulmonary sequestrations ● Infectious or inﬂammatory pathology

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OPERATIVE STEPS Step 1 Step 2 Step 3 Step Step Step Step

4 5 6 7

Positioning and incision/thoracoscopic port placement Lung mobilization Isolation and division of pulmonary arterial and venous branches Fissure completion Bronchial division Lymph node dissection Closure

OPERATIVE PROCEDURE Incision/Thoracoscopic Port Placement Intercostal Bundle Injuries After the patient is placed in a lateral decubitus position, the chest is typically entered through a serratus-sparing, limited posterolateral thoracotomy in either the fourth or the ﬁfth interspace for traditional open lobectomies. To facilitate exposure and avoid unintentional rib fracture with retraction, we routinely remove a small segment of posterior rib in a subperiosteal fashion with a rib cutter. To perform a thoracoscopic lobectomy, two ports and an access incision are usually required (Fig. 65–1). This is an incision 5 cm or less that aids in the hilar dissection and through which the specimen is extracted via an endoscopic bag. Avoiding rib spreading is the key element in VATS lobectomy to prevent postoperative pain and trauma to the intercostal nerve bundles responsible for the postthoracotomy pain syndrome. Port placement may vary slightly owing to patient body habitus, location of the tumor, and surgeon preference. However, optimal port placement is important for safe and successful resection. The ﬁrst port is the camera port, and it is usually placed within the seventh or eighth intercostal space. Whether it is in the anterior, middle, or posterior axillary line depends on the level of the diaphragm as seen from a review of a preoperative chest x-ray, on the location of the pathology, and on left- versus rightsided procedures. Ideally, this port should provide views of the anterior and posterior hilum and should align with the major ﬁssure. We almost exclusively use a 30° thoracoscope. It provides optimal views, not afforded by a 0° scope, particularly during the difﬁcult dissection around the superior hilum. The anterior port should be placed right over the hilum because this will be used as the access/utility port. Dissection of both the hilum and the ﬁssure will be performed through this port. This incision is initially 1 to 2 cm. It is not extended to 5 centimeters in length until we have decided to proceed with the VATS lobectomy. The port is usually created anterior to the latissimus dorsi in the fourth intercostal space for upper lobectomies and in the ﬁfth intercostal space for lower lobectomies. The third port is usually in the fourth or ﬁfth intercostal space, either inferior or posterior to the scapu-

5th or 6th interspace 4th interspace 5 cm incision

7th interspace

Figure 65–1 The three thoracoscopic port incisions for completion of a video-assisted thoracic surgery (VATS) right upper lobectomy. The 5-cm access incision is placed in the fourth intercostal space and in the anterior axillary line. The camera port is placed in the seventh interspace, and the posterior port is located in the fourth intercostals space, posterior to the tip of the scapula. (From Nicastri DG, Yun J, Swanson SJ. VATS lobectomy. In Sugarbaker DS, Bueno R, Zellos L (eds): Adult Chest Surgery: Concepts and Procedures. New York: McGraw-Hill, Inc., 2006. Reprinted with permission.)

lar tip. This port usually serves as the lung retraction port. Hemostasis is very important when creating the ports because bleeding from the port sites onto the camera, and onto the surgical ﬁeld, during the procedure is a nuisance and can signiﬁcantly prolong the operation. Post-thoracotomy pain is believed to be caused by rib spreading with resultant trauma to the intercostal nerve. Benedetti and coworkers16 analyzed superﬁcial abdominal reﬂexes in patients after posterolateral thoracotomy and concluded that increased incisional pain intensity may be due to intercostal nerve impairment. Many studies evaluated the intensity of acute pain after minimally invasive thoracic surgery. In particular, Landreneau and associates17 performed a study comparing 165 patients who had a lung resection through a posterolateral thoracotomy with 178 patients who had a VATS resection.17 At 1-year follow-up, there was a signiﬁcant difference in overall pain, pain intensity scores, and shoulder function between the two groups, favoring a VATS approach.

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● Consequence Intercostal nerve trauma may be associated with chronic pain syndromes such as intercostal neuralgias. Grade 1/2 complication ● Repair Once the intercostal nerve has been injured, little can be done to repair it. Usually, such an injury is not recognized until subsequent postoperative visits. At this time, the patient complains of a chronic pain syndrome that does not improve with healing. ● Prevention Avoiding pressure on the intercostal bundle while using the thorascopic instruments is the best way to prevent injury to these structures.

Lung Mobilization Phrenic Nerve Injury Once access to the chest cavity is obtained, a thorough exploration is performed. The pleural surface is inspected for tumor implants and any adhesions are lysed sharply with cautery or with an ultrasonic cutting and coagulation device. Extensive pleural adhesions are not a contraindication to proceed with a VATS lobectomy. Careful and complete adhesiolysis allows full mobility of the lung. Retraction of the lung is critical to being able to complete the resection. The discovery of tumor invasion into the chest wall is a contraindication to a VATS approach because it requires en-bloc chest wall resection. Digital palpation of the tumor and lung is performed through the anterior/access port to conﬁrm the location and presence of the tumor and also to rule out additional unsuspected nodules or pathology not identiﬁed on preoperative studies. In VATS resections, ipsilateral mediastinal lymph node sampling is performed, especially if mediastinoscopy was not performed earlier. If N2 disease is discovered on frozen section, the VATS resection is aborted and the patient is treated with neoadjuvant therapy. If a preoperative tissue diagnosis has not been determined, a wedge or core biopsy is performed initially, followed by lobectomy if frozen section reveals carcinoma. ● Consequence Circumferential evaluation of the hilar structures should then be performed to determine lung resectability. The salient goal of lobectomy is to ligate and divide the major vessels and bronchus with clear margins. To achieve this, the hilar pleura is opened. Anteriorly, the course of the phrenic nerve should be identiﬁed and the pleura should be opened posterior to this structure (Fig. 65–2). Inadvertent injury of the phrenic nerve leads to paralysis of the ipsilateral hemidiaphragm. This complication has not been adequately described in the literature for patients undergoing pulmonary lobectomy. The effects of unilateral phrenic nerve transection have been studied in young patients with normal

A

B Figure 65–2 A, The right upper lobe is retracted posteriorly, exposing the superior pulmonary vein (thin arrow). The right phrenic nerve is visualized (thick arrow) as it lies anterior to the pulmonary hilum. The nerve should be carefully mobilized away from the anterior hilum to avoid inadvertent injury. B, The left upper lobe is retracted posteriorly. The left phrenic nerve (thin arrow) is visualized and dissected anteriorly during isolation of the left superior pulmonary vein (thick arrow).

preoperative respiratory function who have undergone phrenic nerve transfer for brachial plexus injuries.18 In these patients with normal lung function, there was no evidence of diminished pulmonary function parameters within 1 year. One could anticipate signiﬁcant pulmonary compromise and complications with phrenic nerve injuries in patients undergoing pulmonary lobectomy. Most of these patients have baseline pulmonary dys-

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function and will also have reduced pulmonary capacity associated with lung resection. Grade 2/3 complication ● Repair Direct neural repair is not recommended. If signiﬁcant postoperative respiratory insufﬁciency exists, potential surgical interventions can be performed to improve respiratory function. Diaphragmatic plications via thoracoscopic and open techniques have been developed to achieve this goal.19,20 In a recent study of 22 patients with unilateral diaphragm paralysis, VATS diaphragmatic plication resulted in signiﬁcant improvements in patients’ functional status, pulmonary spirometry, and dyspnea scores.19 There was no operative mortality, and the mean length of hospital stay was 3.7 days. Longterm follow-up in a similar group of patients undergoing plication via a thoracotomy found durable results exceeding 10 years.20 Phrenic nerve pacing with diaphragmatic electrodes has also resulted in clinical improvements in ventilator-dependent, quadriplegic patients.21 This technique has not been employed for patients with unilateral phrenic nerve dysfunction. ● Prevention Early identiﬁcation and preservation of the phrenic nerve should allow the surgeon to avoid this potentially devastating injury.

Esophageal Injury The inferior pulmonary ligament is typically divided in all pulmonary lobectomies. This is performed during upper lobectomies, allowing the lower lobe to potentially decrease the amount of intrathoracic space associated with lung resection. Access to the inferior pulmonary vein for lower lobectomies is facilitated by division of the pulmonary ligament. This structure is a remnant of the embryologic pleural fold and lies in close proximity to the inferior pulmonary vein and esophagus. ● Consequence Unrecognized esophageal injury can lead to a delayed presentation of esophageal perforation and sepsis. Esophagopleural ﬁstulas, although uncommon, have been most frequently described after pneumonectomy for both benign and malignant diseases.22 This can be secondary to injury directly onto the esophagus or to its vascular supply from extensive dissection. Grade 3/4/5 complication ● Repair If recognized intraoperatively, esophageal injuries from electrocautery or sharp dissection can be repaired with layered repair and vascularized tissue buttress. Delayed recognition of esophageal injuries often requires control of infection, hyperalimentation, and either closure of the injury or possibly esophagectomy. Covered esoph-

Figure 65–3 The right lower lobe is retracted anteriorly, placing the right inferior pulmonary ligament in tension. This maneuver allows proper visualization of the esophagus (arrow) and avoids esophageal injury during division of the pulmonary ligament.

ageal stent placement can be considered as an alternative approach in selected cases. ● Prevention The lower lobe is gently grasped and retracted cephalad. The pulmonary ligament is placed on adequate tension and then divided with electrocautery. Care must be taken to identify the underlying esophagus and inferior pulmonary vein (Fig. 65–3). Adequate exposure should prevent esophageal injury as well as possible life-threatening hemorrhage associated with damage to the inferior pulmonary vein.

Technical Aspects of Speciﬁc Lobectomies Performed utilizing Thoracotomy An intimate understanding of the anatomy of the hilar structures is crucial to avoid the surgical pitfalls of pulmonary lobectomy. Speciﬁcally, one must have a comprehensive mastery of the course of the main pulmonary artery and its branches. These are delicate, thin-walled vessels requiring meticulous dissection to avoid life-threatening injury.

Right Upper Lobectomy The sequence in dissection and ligation is based on the anatomic setting and convenience. Initial dissection is undertaken at the anterior hilum. The mediastinal pleura is opened posterior to the phrenic nerve, and this plane is continued superiorly and posteriorly between the lung and the azygous vein. The lung is retracted anteriorly to expose the right main stem bronchus at the bifurcation of the upper lobe bronchus and bronchus intermedius. The plane between these two structures is developed bluntly. The upper lobe branches of the superior pulmonary vein are identiﬁed and ligated. The draining veins of the

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the lower lobe arises posteriorly and across from the corresponding middle lobe branch. Division of the superior segmental branch is followed with ligation of the arterial branches to the basilar segments. The inferior pulmonary vein is identiﬁed after the inferior pulmonary ligament is divided using electocautery. Level 9 lymph nodes should be swept up into the specimen. The posterior mediastinal pleura is opened to allow effective clearance of the inferior pulmonary vein from the lower lobe bronchus. A vascular stapler is used to divide the inferior pulmonary vein once preservation of middle lobe venous drainage is ensured. Fissure completion is performed, leaving the lower lobe attached only by its bronchus. Care must be taken not to compromise the airway to the middle lobe when dividing the lower lobe bronchus. Figure 65–4 When performing a right upper lobectomy, care must be taken to identify and preserve the middle lobe of the pulmonary vein (arrow).

middle lobe must be identiﬁed as well to prevent unintentional division (Fig. 65–4). In the anterior hilum, the main pulmonary artery is then dissected as it exits the mediastinum inferior to the azygous vein. The truncus anterior artery, with its apical and anterior branches, is isolated and divided with a vascular stapler or suture ligature. The upper lobe bronchus is then divided. This can be performed either with a stapling device using a thick tissue staple load or with a scalpel and subsequent absorbable suture closure. With the truncus anterior branch of the pulmonary artery already divided, pulmonary arterial injury is avoided. Attention must be given during retraction of the upper lobe at this point because the posterior recurrent pulmonary artery branch remains. Avulsion injuries can occur if excessive tension is exerted in this area. The remaining ﬁssures are then completed with stapling devices. The bronchial stump is tested for its integrity under saline immersion.

Left Upper Lobectomy Dissection is initially undertaken at the anterior hilum with the lung retracted posteriorly. The mediastinal pleura is incised over the left main pulmonary artery after it courses beneath the aortic arch. Care is taken to identify and preserve the phrenic nerve anteromedially and the vagus nerve with its recurrent laryngeal branch, which courses under the aortic arch. Attention is then given to exposing the interlobar pulmonary artery within the major ﬁssure. Once this is achieved, careful isolation of the upper lobe pulmonary arterial branches is undertaken. There is considerable anatomic variability in the number of separate arterial branches to the left upper lobe. It may be necessary to isolate and divide the superior pulmonary vein to the upper lobe in order to safely gain access to the ﬁrst pulmonary artery branch. The left upper lobe bronchus is divided once all of the pulmonary arterial branches have been addressed.

Left Lower Lobectomy Right Middle Lobectomy The dissection begins at the intersection of the oblique and horizontal ﬁssures to expose the interlobar pulmonary artery. The parenchyma of the middle lobe is then retracted anteriorly with the identiﬁcation of the middle lobe pulmonary artery, which may be present as a single trunk or as two separate vessels. After pulmonary artery division, the middle lobe pulmonary venous supply is isolated in the anterior hilum. The middle lobe bronchus is the remaining structure after the division of pulmonary venous outﬂow. Draining lymphatics are swept up toward the specimen, and the bronchus is divided.

Right Lower Lobectomy Attention is initially given to identifying and exposing the interlobar pulmonary artery at the junction of the oblique and horizontal ﬁssures. The superior segmental artery to

The posterior hilum is approached initially with exposure of the interlobar pulmonary artery in the ﬁssure. Dissection, isolation, and subsequent division of the arterial branch to the superior segment are performed. Next, the basilar trunk arterial branches are identiﬁed and divided. Attention must be given to preserving the lingular segmental arterial branches that arise in close proximity to those supplying the basilar segments (Fig. 65–5). The ﬁssure can now be safely completed with a stapler. The inferior pulmonary ligament is then divided, exposing the lower border of the inferior pulmonary vein. The mediastinal pleura is opened to the anterior and posterior hila, enabling isolation of the inferior vein. This must be meticulously freed from the membranous wall of the lower lobe bronchus. Once mobilized, the vein is divided with the use of a stapling device. Occasionally, the left superior and inferior veins will join to form a common trunk before draining into the left atrium. This rarely occurs in the

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Figure 65–5 Attention must be given to identifying the pulmonary arterial branches to the lingular segments (thin arrow) when performing a left lower lobectomy. These lingular branches lie in close proximity to those supplying the basilar segments (thick arrows).

A

pulmonary venous system of the right lung. One must ensure preservation of the superior pulmonary vein when performing a left lower lobectomy (Fig. 65–6). The lobe is now attached only by the lower lobe bronchus, which is then transected after nodal tissue is swept up into the specimen. The upper lobe bronchial oriﬁce should not be narrowed with the application of the stapler. Patency of the upper lobe bronchus can be ensured by having the anesthesiologist gently inﬂate the left lung prior to ﬁring the stapling device.

Technical Aspects of Speciﬁc Lobectomies Performed utilizing the VATS Approach The principles of video-assisted thoracoscopic lobectomies do not differ from those that pertain to traditional open procedures. Pulmonary arteries, veins, and bronchi must be separately isolated and divided. Standard lymph node dissection practices are also adhered to with VATS techniques. All resected specimens are placed in a heavy laparoscopic extraction sac to prevent tumor seeding of the port and are removed through the anterior access incision without any rib spreading. The conduct of the operation for the different lobes is essentially the same and is described later with some caveats.

Right Upper Lobectomy We usually place our camera port in the seventh intercostal space and the anterior axillary line. This provides good visualization of the anterior and superior hilum, the area

B Figure 65–6 A, The left inferior pulmonary ligament has been divided and circumferential dissection performed around the inferior pulmonary vein (arrow). B, Further inspection reveals that what had been previously identiﬁed as the inferior pulmonary vein was, in fact, a common venous trunk (thin arrow) emptying into the left atrium. Dissection and isolation of the left inferior pulmonary vein (thick arrow) was completed, followed by vascular division.

of most hazardous dissection. The access port is usually located in the fourth intercostal space anteriorly, with care taken not to injure the long thoracic nerve and avoiding breast tissue in women. The posterior working/utility port is placed inferior or posterior to the scapula tip. The orientation of this port should provide a right-angle conﬁguration between instruments in the access and working ports. After the initial exploration, dissection is begun in the anterior hilum. The right upper lobe is grasped gently

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A

677

C

Stapler

Camera

Retractor

B Figure 65–7 A, The right superior pulmonary vein (thin arrow) has been dissected off of the underlying right pulmonary artery (thick arrow). Care must be taken during this aspect of right upper lobectomy to avoid catastrophic bleeding from an injured proximal pulmonary artery. B, Placement of the thoracoscopic vascular stapler through the posterior working port for division of the right superior pulmonary vein. The pulmonary artery lies underneath this structure. Attention must be given to minimizing torsion of the stapler to prevent injury to the underlying artery. C, The endoleader is attached to the stapling device to gently guide this instrument across the vein. The red rubber catheter must be dislodged from the stapler before it is closed and ﬁred. This maneuver can be performed with an endo-Kitner or ring forceps. (B, From Nicastri DG, Yun J, Swanson SJ. VATS lobectomy. In Sugarbaker DS, Bueno R, Zellos L [eds]: Adult Chest Surgery: Concepts and Procedures. New York: McGraw-Hill, Inc., 2006. Reprinted with permission.)

with ring forceps and retracted posteriorly. This maneuver creates excellent exposure to the anterior hilum. The superior pulmonary vein is isolated ﬁrst by dividing its pleural covering with a harmonic scalpel, Pearson scissors, and/or endo-Kitners. The plane between the vein and the under-

lying pulmonary artery must be carefully developed (Fig. 65–7A). An oiled 2-0 silk tie is then looped around the superior pulmonary vein. The “endo-leader,” an 8-Fr red rubber catheter, may be utilized to enable safe passage of the vascular stapler around the vein (see Fig. 65–7B and

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A

C

Retractor

Stapler Camera

B 7C).23 The stapler is introduced through the posterior port, providing the most effective angle for stapler application and division of the vein. Once this is completed, the truncus anterior branch of the right pulmonary artery and its variable number of segmental branches are exposed

(Fig. 65–8A). These are isolated individually or as one trunk, depending on their conﬁguration and accessibility. They are then divided individually or as one trunk, using an endovascular stapler. The endoleader can be used to safely guide the stapler around the fragile arterial branches

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Figure 65–8 A, The right superior pulmonary vein has been divided. Careful dissection exposes the anterior truncus branch of the right pulmonary artery. This view is achieved by placing the camera through the anterior thoracoscopic port as we then bring the stapling device through the camera port for division of this pulmonary arterial structure. B, Optimal instrument placement for division of the anterior truncus branch of the right pulmonary artery. The camera is moved anteriorly, while the vascular stapler is brought through the thoracoscopic camera port. An endoleader may be utilized to guide the stapler across these delicate arterial branches. C, The red rubber catheter has been disengaged from the vascular stapler and the stapler is then ready for closure and division. The azygous vein (arrow) lies in close proximity and must be protected to avoid enclosure within the stapling device. (B, From Nicastri DG, Yun J, Swanson SJ. VATS lobectomy. In Sugarbaker DS, Bueno R, Zellos L [eds]: Adult Chest Surgery: Concepts and Procedures. New York: McGraw-Hill, Inc., 2006. Reprinted with permission.)

Once all of the arterial branches are divided, the right upper lobe bronchus is dissected free by sweeping all nodal tissue on the bronchus toward the specimen. An endoscopic stapler is then introduced through the camera port to divide the bronchus (Fig. 65–10). The ﬁssure is completed with serial ﬁrings of the endoscopic stapler and the specimen is placed in a heavy laparoscopic extraction sac and removed through the access incision without rib spreading.

Right Middle Lobectomy

Figure 65–9 An anterior hilar approach is useful for identifying and dividing the posterior recurrent arterial branch to the right upper lobe. Utilizing this method usually obviates the need to perform tedious ﬁssural dissection for exposure of the interlobar pulmonary artery. Here, anterior dissection reveals the origin of the posterior recurrent artery (arrow) to the right upper lobe. This can then be divided with a vascular stapler brought through the camera port incision.

(see Fig. 65–8B and 8C). This division is best accomplished with the stapler introduced through the camera port, with the camera switched to viewing from the access port. The next step is to gain access to the recurrent posterior segmental arterial branch. Thoracoscopically, the most straightforward and preferred approach is via the anterior hilum (Fig. 65–9). This avoids the tedious and often challenging dissection that can be encountered when exposing the interlobar pulmonary artery at the conﬂuence of the horizontal and oblique ﬁssures, especially when the ﬁssures are incomplete. If the posterior recurrent branch is not well visualized from the anterior hilum and the major ﬁssure is incomplete, one can partially, but carefully, divide the ﬁssure with a stapler or harmonic scalpel. This provides better exposure of the interlobar pulmonary artery for dissection. The goal is to identify the space between the recurrent ascending arterial branch to the upper lobe and the superior segmental artery of the lower lobe. This allows safe division of the recurrent ascending branch and completion of the posterior ﬁssure.

For right middle lobectomies, the camera port is placed in the seventh intercostal space in the midaxillary line. This provides an excellent view of both the anterior hilum and the major ﬁssure. The anterior access port is usually in the ﬁfth intercostal space, one interspace below the location utilized for right upper lobectomy. The working port is usually posterior to the scapular tip in the sixth or seventh intercostal space. The right middle lobe is retracted laterally, and the middle lobe venous drainage is dissected free and divided using the endovascular stapler. Care must be taken in dissecting the posterior aspect of the middle lobe veins off of the underlying pulmonary artery. The middle lobe bronchus is then exposed. We divide the bronchus ﬁrst because the bronchus is anterior to the middle lobe artery. One must be careful not to injure the arterial branches to the middle lobe when dissecting around the bronchus (Fig. 65–11). The arterial branches to the middle lobe are then isolated and divided with the endovascular stapler. The endoleader technique may be helpful to guide the stapler around these branches. The ﬁssure is completed, and the middle lobe is removed in a specimen sac through the access incision.

Right and Left Lower Lobectomy The camera port is placed in the eighth interspace in the posterior axillary line to provide improved exposure to the posterior hilum and to avoid crowding of the instruments. The access port is placed anteriorly in the ﬁfth intercostal space. The posterior working port is usually posterior to the scapular tip in the sixth or seventh interspace. We ﬁrst divide the inferior pulmonary ligament and sample level 9 lymph nodes. The lower lobe is retracted superiorly with a ring forceps through the posterior port so that the liga-

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Retractor

Stapler Camera

A

B

Figure 65–10 A and B, The technique to effectively divide the right upper lobe bronchus. As with division of the anterior truncus branch of the pulmonary artery, the stapler is brought through the camera port as the camera is moved to the access incision. Care must again be taken to avoid injury to the azygous vein (arrow). (A, From Nicastri DG, Yun J, Swanson SJ. VATS lobectomy. In Sugarbaker DS, Bueno R, Zellos L [eds]: Adult Chest Surgery: Concepts and Procedures. New York: McGraw-Hill, Inc., 2006. Reprinted with permission.)

65 LOBAR RESECTIONS

Figure 65–11 The middle lobe veins have been divided for this right middle lobectomy. The right middle lobe bronchus (arrow) lies anterior to the middle lobe arterial branches. Circumferential dissection around the bronchus must be performed with care because the pulmonary artery lies immediately posterior. The middle lobe arterial branch cannot be seen because it lies just behind the bronchus.

ment is under tension. A long-tipped electrocautery, or ultrasonic scalpel, divides the ligament through the access port. The interlobar pulmonary artery is then isolated within the ﬁssure. The basilar trunk and the artery to the superior segment are identiﬁed, dissected, and divided with the endovascular stapler. Usually, the superior segmental artery is divided ﬁrst and basilar trunk division follows. This sequence avoids injury to the superior segmental branch with the stapler used to divide the basilar arterial branches. Next, the inferior pulmonary vein is dissected free and divided with an endovascular stapler. Finally, the bronchus to the lower lobe is dissected and divided with an endoscopic stapler. As in the open technique, care must be observed on the right side to not impinge on the middle lobe bronchus. The ﬁssure is completed, and the lobe is removed in a specimen sac.

Left Upper Lobectomy In our opinion, the left upper lobectomy is technically the most difﬁcult because of the variability in the pulmonary arterial circulation. The order of division of the hilar structures is the same as with the right upper lobe—vein, artery, bronchus. The position of the inferior camera port is placed more posteriorly to avoid obstruction of the camera view by the heart and the pericardial fat pad. In patients with marginal pulmonary function and a small tumor, a lingula-sparing left upper lobectomy or lingulec-

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Figure 65–12 When isolating and dividing the venous drainage of the left upper lobe, attention must be focused on mobilizing the back of the superior venous branches off of the upper lobe bronchus. The area between the venous branches of the upper division (thick arrow) and the lingula (thin arrow) is cleared to provide exposure to the underlying upper lobe bronchus (thick arrow). The back of the venous tributaries must be cleared from the airway prior to vascular division.

tomy, as appropriate, should be considered. When isolating the superior pulmonary vein, care must be taken when mobilizing it from the anterior aspect of the upper lobe bronchus. These two structures can be quite adherent to one another, and precautions should be made to avoid injury to the back wall of the vein when dissecting this off of the airway (Fig. 65–12).

Isolation and Division of Pulmonary Arterial and Venous Branches Vascular Injury ● Consequence A feared complication of lobectomy is an uncontrolled vascular injury. Scant data is available regarding division of intrathoracic vessels during pulmonary resection. Asamura and colleagues24 reported on 842 mechanical vascular divisions in 603 consecutive pulmonary resections. Endostaplers were used for all applications except 2. There was an overall stapling failure rate of 0.1%. One superior pulmonary vein was divided during a VATS case without the formation of staples. This hemorrhage was controlled with suture ligation after conversion to thoracotomy. In this series, reexploration for bleeding complications was never due to vascular staple line issues.

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In the largest series of VATS lobectomies, McKenna and coworkers11 described their results with 1100 operations.11 There were 9 deaths in this series, for a perioperative mortality rate of 0.8%. No intraoperative deaths were encountered. Only 28 cases (2.5%) were converted to a thoracotomy, and of these, 7 were due to bleeding. No deaths occurred among these 7 patients. In a separate survey of 1578 VATS lobectomies, only 1 intraoperative death was reported—secondary to a myocardial infarction.25 Grade 2/3/4/5 complication ● Repair A sponge stick or a dental pledget on a clamp should always be readily available to tamponade bleeding from stapler malfunction or avulsion of vascular branches. In thoracoscopic resections, this single maneuver allows time for adequate control and conversion to an open thoracotomy, if needed. Minor vascular avulsion injuries during VATS resections can be adequately repaired utilizing direct suture repair of the vessel through the access incision. More signiﬁcant injuries, difﬁculties in exposure, and cases in which patients exhibit hemodynamic compromise from vascular injuries should be converted to a thoracotomy for effective vascular control. ● Prevention Having a thorough understanding of the vascular anatomy is crucial to preventing vascular injury during pulmonary lobectomy. The relatively thin walls of pulmonary arterial branches make these structures more prone to injury than their venous counterparts. We advocate that pulmonary arterial vessels are never directly grasped with any instrument. Extra care must be directed to isolating and dividing these vessels. During VATS resections, optimization of exposure with angled thoracoscopes along with correct port placement while adhering to standard thoracic surgical principles minimizes the risk of vascular complications.

Lymph Node Dissection Because the prognosis of lung cancer is directly related to the presence or absence of lymph node metastases, accurate surgical lymph node staging is paramount. Complete mediastinal lymph node dissection of levels 2, 4, 7, and 9 is performed on all right-sided lobar resections. Left-sided mediastinal lymph node dissection is performed on all lobar resections and should include levels 5, 6, 7, and 9. The American College of Surgery Oncology Group Z0030 study sought to determine whether long-term lung cancer survival is effected by mediastinal lymph node sampling versus complete dissection. This was a prospective, randomized, multi-institutional study whose secondary purpose was to ascertain whether perioperative morbidity or mortality varied between the two groups. While we await the effects on survival between the two

surgical groups, the study’s initial results found no statistically signiﬁcant differences in the incidence of chylothorax, recurrent laryngeal nerve injuries, reoperation for bleeding, or median length of hospital stay between the two groups.26

Chylothorax ● Consequence Postoperative chylothorax is a rare, but occasionally morbid, complication after pulmonary resection. The incidence of pulmonary resections has been reported from 0.26% to as high as 2.5%.27,28 It is often diagnosed by the presence of chylous drainage from the chest tube. Chemical analysis of efﬂuent with elevated triglycerides (>110 mg/dl) conﬁrms the diagnosis. Often, this complication is self-limited and resolves with dietary modiﬁcations, but occasionally, reoperation with thoracic duct ligation is required. Patients with chylothorax are prone to infectious complications and may develop a postoperative empyema.28 Residual intrapleural chylous collections may be addressed with imageguided percutaneous drainage techniques. Grade 2/3/4 complication ● Repair Appreciation of excessive lymphatic leakage intraoperatively after lymph node dissection can be addressed with direct suture or clip ligation. This, however, is not the usual occurrence, and chylothorax is often diagnosed postoperatively with increased chest tube drainage. Patients should be started on a medium-chain triglyceride diet, and if this is not effective, complete cessation of oral intake should be considered. All attempts should be taken to minimize residual postoperative pleural spaces. These maneuvers are usually successful in ameliorating this complication. However, when drainage exceeds 1 L per day for 7 days, most surgeons advocate operative exploration with thoracic duct ligation.29 ● Prevention Knowledge of the anatomic course of the thoracic duct may assist the surgeon in avoiding this potential complication. However, this may not be preventable owing to the proximity of the duct to the trachea, its often variable location, and the frequent existence of large collateral channels among mediastinal lymph nodes. Intraoperative realization and ligation of signiﬁcant lymphatic injury may prevent chylothoraces from occurring. Careful lymphatic ligation with electrocautery or ultrasonic shears should minimize postoperative lymphatic leaks.

Recurrent Laryngeal Nerve Injury ● Consequence Unilateral recurrent laryngeal nerve dysfunction is usually well tolerated by most patients, but life-

65 LOBAR RESECTIONS threatening consequences are possible because patients are prone to aspiration events. Many patients undergoing pulmonary resections have compromised lung function owing to longstanding cigarette use. With the diminished ability to clear pulmonary secretions associated with vocal cord dysfunction secondary to recurrent nerve injury, the potential for signiﬁcant morbidity exists. The diagnosis is usually fairly easy to make by physical examination at the bedside and can be conﬁrmed with ﬁberoscopy. Watanabe and colleagues30 described their experience with lymph node dissection for clinical stage I lung cancer and reported on the incidence of recurrent laryngeal nerve injury. In this review of 221 VATS resections and 190 open resections via thoracotomy, there were 5 (2.3%) and 3 (1.6%) recurrent nerve injuries, respectively, in the two surgical groups. No mention was made regarding the consequence of this complication in these patients, nor is this complication expounded further elsewhere in the literature. Grade 2/3 complication ● Repair Direct repair is not advised, but several techniques have been devised to minimize the morbidity associated with this complication in regards to both improving voice quality and eliminating aspiration. Early treatment includes involvement of speech pathologists who can instruct patients on maneuvers to minimize aspiration events. Temporary unilateral vocal cord dysfunction can be remedied by injection of material into the cord for augmentation purposes.31 Medialization thyroplasty remains a deﬁnitive, yet more invasive, approach toward managing this complication.32 ● Prevention It is important for the surgeon to have a full understanding of the anatomy of the recurrent laryngeal nerves to avoid this complication. During mediastinal lymph node dissections of levels 5 and 6, care must be taken to isolate and protect both the vagus and the phrenic nerves in this region.

REFERENCES 1. Jemal A, Tiwari RC, Murray T, et al. Cancer statistics, 2004. CA Cancer J Clin 2004;528–529. 2. Nesbitt JC, Putnam JB, Walsh GL, et al. Survival in earlystage lung cancer. Ann Thorac Surg 1995;60:466–472. 3. Ginsberg R, Rubernstein L. Randomized trial of lobectomy versus limited resection for T1N0 non-small cell lung cancer. Ann Thorac Surg 1995;60:615–623. 4. Landreneau RJ, Sugarbaker DJ, Mack MJ, et al. Wedge resection versus lobectomy for stage I (T1N0M0) nonsmall cell lung cancer. J Thorac Cardiovasc Surg 1997; 113:691–700. 5. Warren WH, Faber LP. Segmentectomy versus lobectomy in patients with stage I pulmonary carcinoma. J Thorac Cardiovasc Surg 1994;107:1087–1094.

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6. Jacobeus HC. Ueber die moglichkeit de zystoskopie bei untersuchung seroser hohlungen anzuwenden. Munchen Med Wochenschur 1910;57:2090–2092. 7. Kirby TJ, Rice TW. Thoracoscopic lobectomy. Ann Thorac Surg 1993;56:784–786. 8. Walker WS, Carnochan FM, Pugh GC. Thoracoscopic pulmonary lobectomy. Early operative experience and preliminary clinical results. J Thorac Cardiovasc Surg 1993;106:1111–1117. 9. Demmy TL, Curtis JJ. Minimally invasive lobectomy directed toward frail and high-risk patients: a case-control study. Ann Thorac Surg 1999;68:194–200. 10. Nagahiro I, Andou A, Aoe M, et al. Pulmonary function, postoperative pain, and serum cytokine level after lobectomy: a comparison of VATS and conventional procedure. Ann Thorac Surg 2001;72:362–365. 11. McKenna RJ, Houck W, Fuller CB, et al. Video-assisted thoracic surgery lobectomy: experience with 1,100 cases. Ann Thorac Surg 2006;81:421–426. 12. Sagawa M, Sato M, Sakurada A, et al. A prospective trial of systematic nodal dissection for lung cancer by videoassisted thoracic surgery: can it be perfect? Ann Thorac Surg 2002;73:900–904. 13. Landreneau RJ, Hazelrigg SR, Mack MJ, et al. Postoperative pain-related morbidity: video-assisted thoracic surgery versus thoracotomy. Ann Thorac Surg 1993;56:1285– 1289. 14. Swanson SJ, Batirel HF. Video-assisted thoracic surgery (VATS) resection for lung cancer. Surg Clin North Am 2002;82:541–559. 15. Lewis RJ, Caccavale RJ, Bocage JP, et al. Video-assisted thoracic surgical non-rib spreading simultaneously stapled lobectomy: a more patient-friendly oncologic resection. Chest 1999;116:1119–1124. 16. Benedetti F, Amanzio M, Casadio C, et al. Postoperative pain and superﬁcial abdominal reﬂexes after posterolateral thoracotomy. Ann Thorac Surg 1997;64:207–210. 17. Landreneau RJ, Mack MJ, Hazelrigg SR, et al. Prevalence of chronic pain after pulmonary resection by thoracotomy or video-assisted thoracic surgery. J Thorac Cardiovasc Surg 1994;107:1079–1089. 18. Xu WD, Gu YD, Lu JB, et al. Pulmonary function after complete unilateral phrenic nerve transaction. J Neurosurg 2005;103:464–467. 19. Freeman RK, Wozniak TC, Fitzgerald EB. Functional and physiologic results of video-assisted thoracoscopic diaphragm placation in adult patients with unilateral diaphragm paralysis. Ann Thorac Surg 2006;81:1853– 1857. 20. Higgs SM, Hussain A, Jackson M, et al. Long-term results of diaphragmatic placation for unilateral diaphragm paralysis. Eur J Cardiothoacr Surg 2002;21:294–297. 21. DiMarco AF, Onders RP, Ignagni A, et al. Phrenic nerve pacing via intramuscular diaphragm electrodes in tetraplegic subjects. Chest 2005;127:671–678. 22. Massard G, Wihlm JM. Early complications: esophagopleural ﬁstula. Chest Surg Clin North Am 1999;9:617– 631. 23. Garcia JP, Richards WG, Sugarbaker DJ. Surgical treatment of malignant mesothelioma. In Kaiser L, Kron I, Spray T (eds): Mastery of Cardiothoracic Surgery. Philadelphia: Lippincott-Raven, 1997; p 683.

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24. Asamura H, Suzuki K, Kondo H, et al. Mechanical vascular division in lung resection. Eur J Cardiothorac Surg 2002;21:879–882. 25. Mackinlay TA. VATS lobectomy: an international survey. Presented at the IVth International Symposium on Thoracoscopy and Video-Assisted Thoracic Surgery, May 1997, Sao Paulo, Brazil. 26. Allen MS, Darling GE, Pechet TT, et al. Morbidity and mortality of major pulmonary resections in patients with early-stage lung cancer: initial results of the randomized, prospective ACOSOG Z0030 trial. Ann Thorac Surg 2006;81:1013–1020. 27. Cerfolio RJ, Allen MS, Deschamps C, et al. Postoperative chylothorax. J Thorac Cardiovasc Surg 1996;112:1361– 1365. 28. Schimizu K, Yoshida J, Nishimura M, et al. Treatment strategy for chylothorax after pulmonary resection and

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lymph node dissection for lung cancer. J Thorac Cardiovasc Surg 2002;124:499–502. Patterson GA, Todd TR, Delarue NC, et al. Supradiaphragmatic ligation of the thoracic duct in intractable chylous ﬁstula. Ann Thorac Surg 1981;32:44–49. Watanabe A, Koyanagi T, Obama T, et al. Assessment of node dissection for clinical stage I primary lung cancer by VATS. Eur J Cardiothorac Surg 2005;27:745– 752. Hartl DM, Travagli JP, Leboulleux S, et al. Clinical review: concepts in the management of unilateral recurrent laryngeal nerve injury after thyroid surgery. J Clin Endocrinol Metab 2005;90:3084–3088. Bielamowicz S. Perspectives on medialization laryngoplasty. Otolaryngol Clin North Am 2004;31:139– 160.

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Bronchial and Vascular Sleeve Lobectomy M. Blair Marshall, MD and Fabio May da Silva, MD INTRODUCTION Bronchial and vascular sleeve resections have come to replace pneumonectomy in the management of central disease of the airway and pulmonary artery (PA). Sleeve resection is performed in approximately 5% of patients undergoing resection for lung cancer.1 Although this technique was initially reserved for patients with inadequate pulmonary reserve, it is now considered the optimal technique in all patients, regardless of pulmonary status. Bronchial sleeve resection was introduced by Price Thomas in 1947 at the Brompton Hospital in London. In this case, sleeve lobectomy was carried out for a carcinoid tumor located in the right main bronchus.2 Following this, bronchial sleeve resection became the standard procedure for benign lesions of the central airway. In lung cancer patients, much of the credit for popularizing bronchial sleeve resection as an alternative to pneumonectomy has to be given to Paulson and coworkers.3,4 Initial reports of postoperative morbidity and mortality prohibited routine use of sleeve resection in patients with adequate pulmonary reserve. However, the increased morbidity in patients undergoing sleeve resection reﬂected the decreased pulmonary reserve, which required a sleeve resection in these early reports of sleeve lobectomy.5 Sleeve resection may be appropriate with any lobectomy but is most frequently performed in a right upper lobectomy (Fig. 66–1). Combined bronchovascular sleeve resections are most common on the left owing to the position of the PA (Fig. 66–2). Again, the most commonly performed sleeve resection on the left is the upper lobe. Bronchial and bronchovascular sleeve resections are complex, technically demanding procedures. Operative mortality ranges from 0% to 6.2%,6,7 with postoperative morbidity ranging from 10% to 50%.8,9 Some data demonstrate that the perioperative risks of bronchial and bronchovascular sleeve resection are comparable with those of standard lobectomy.1,10–12 Although concerns have been raised over the adequacy of oncologic clearance with this technique, the literature demonstrates equivalent local recurrence and long-term survival in patients under-

going sleeve resection compared with those receiving pneumonectomy.13–15 The advantages of sleeve resection have been clearly demonstrated. As the preoperative management strategy of patients with advanced lung cancer has shifted over the past two decades, additional data demonstrate that bronchial and bronchovascular sleeve resection may be performed safely after neoadjuvant therapy.13 Factors affecting survival include the presence of nodal disease, the type of bronchoplastic procedure, impaired lung function, and the presence of cardiovascular risk.16,17 An additional important consideration is the postoperative quality of life in patients who undergo pneumonectomy compared with sleeve lobectomy. Pneumonectomy, “a disease,” is associated with long-term sequelae of pulmonary hypertension and respiratory failure. Also, one must not forget that patients may go on to develop a second primary tumor.

INDICATIONS ● Tumors with involvement of lobar bronchus preclud-

● ● ● ●

●

ing lobectomy, but not inﬁltrating so far as to require pneumonectomy (Fig. 66–3) Patients with compromised pulmonary reserve who cannot tolerate pneumonectomy N1 Nodal disease with involvement of lobar bronchus and/or PA Metastatic malignancies with lobar extension to main bronchus Major bronchial disruption as result of penetrating or blunt chest trauma requiring débridement and reapproximation Benign bronchial stricture related to trauma or inﬂammatory disease

OPERATIVE STEPS Step 1

Bronchoscopy to evaluate extent of disease within airway by operating surgeon (Fig. 66–4)

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Figure 66–1 Tumor involving the right upper lobe bronchus with lines of transection demonstrate an adequate resection margin on the proximal and distal bronchus with reanastomosis.

Figure 66–2 Bronchial and vascular sleeve lobectomy specimen demonstrates the proximity of the left upper lobe bronchus and left pulmonary artery.

Figure 66–4 Bronchoscopic image demonstrates a right upper lobe tumor extending into the right main stem oriﬁce.

Figure 66–3 Computed tomography (CT) images of a left upper lobe tumor that would suggest a potential for sleeve lobectomy.

66 BRONCHIAL AND VASCULAR SLEEVE LOBECTOMY

Figure 66–5 Intraoperative photograph of the tumor in Figure 66–4 with the proximal right main stem divided and stay sutures on the proximal and distal airway.

Step 2

Step 3 Step 4 Step 5 Step 6 Step 7 Step 8 Step 9 Step 10

Step 11 Step 12 Step 13 Step 14 Step 15

Step 16 Step Step Step Step Step

17 18 19 20 21

General anesthesia with double-lumen tube placed in bronchus opposite planned side of resection Lateral decubitus position Thoracotomy (posterolateral and anterior approaches both adequate) Thoracic exploration (visual and manual) Assess resectability prior to irreversible maneuvers Mediastinal lymphadenectomy Obtain proximal and distal control of PA, ligate and divide vein to lobe being resected Venous control if unable to get distal control of PA Circumferential dissection of main stem and distal bronchus. Place umbilical tapes to facilitate division Complete ﬁssures around disease when possible Stay sutures on proximal and distal airway to orient anastomosis Harvest pericardium for vascular repair when needed Notify anesthesiologist when preparing for resection and clamping PA Heparin 30 units/kg intravenously when planning on vascular sleeve resection prior to clamping main PA Divide proximal airway and artery once vessels have been controlled (stay sutures) (Fig. 66–5) Frozen section margins (Fig. 66–6) Bronchial anastomosis (Fig. 66–7) Vascular anastomosis or patch angioplasty Wrap bronchial anastomosis with viable ﬂap Closure

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Figure 66–6 Intraoperative photograph of a right upper lobe sleeve resection with both the proximal and the distal airways divided. Forceps are holding the lobectomy specimen.

Figure 66–7 Bronchial anastomosis being performed with the interrupted suture technique.

Step 22 Fiberoptic bronchoscopy Step 23 Extubate patient in operating room

Bronchoscopy The foundation of bronchial evaluation is bronchoscopy. This deﬁnes the extent of pathology in the bronchus. Rigid or ﬂexible bronchoscopes can be used, although we routinely use ﬂexible bronchoscopy. It is important that the operating surgeons perform the examination. Pertinent ﬁndings indicating a probable sleeve resection include endobronchial tumor, submucosal vascularity, and thickening. Careful evaluation of bronchial motion is important to infer the state of tissues outside the bronchus. It may be difﬁcult to determine a need for pulmonary arterial reconstruction preoperatively; however, one should always be prepared, especially with central tumors or N1 disease. If there is a question about the extent of

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disease, multiple biopsies may be performed at the time of bronchoscopy. Sleeve lobectomy can be planned, but the surgeon must also prepare the patient and family for the possibility that a pneumonectomy may be required because of technical issues or tumor extension Complications of bronchoscopy are discussed in Section XI, Chapter 64.

Double-Lumen Tube Placement Misplacement of the double-lumen tube can lead to hypoxia and hypoventilation. Preoperative bronchoscopy ensures appropriate positioning, although the tube can become dislodged during the procedure when manipulating the airway. The endobronchial tube should be placed in the bronchus opposite the side of resection.

Intraoperative Displacement (Fig. 66–8) ● Consequence Hypoxia and hypoventilation during single lung ventilation. Grade 1–5 complication ● Repair Bronchoscopy is used to check the position of the bronchial cuff and to ensure that the oriﬁce of the bronchial or tracheal lumen is neither pressed against the bronchial or tracheal walls nor blocking the oriﬁce to the left upper lobe. For right-side tubes, the position of the slit in the bronchial cuff with respect to the oriﬁce to the right upper lobe must be rechecked, as well as the patency of the right middle and lower lobes. During the dissection or once the airway has been divided, the double-lumen tube can herniate out of its appropriate position and result in occlusion of the bron-

Figure 66–8 Double-lumen tube correctly positioned in the airway initially, followed by mechanism for hypoxia when the doublelumen tube moves proximally and the balloon herniates, preventing the nonoperative lung from being adequately ventilated.

chus to the ventilated lung. Usually, one may simply inﬂate the operative lung in order to ventilate while the problem is identiﬁed and resolved. If, however, the airway has already been divided, this may not be possible. Deﬂation of the bronchial balloon eliminates the occlusion and allows the patient to be ventilated while the problem is investigated. ● Prevention During the operation, one must be aware of the pulse oximetry in order to intervene early if there has been a change in the ability of the patient to be ventilated.

Exposure Complications associated with the various exposures are covered in Section XI, Chapter 64.

Dissection of the Hilum Vascular Injury ● Consequence Bleeding that occurs as a result of PA injury ranges from minimal, which is controlled and resolved with direct pressure, to excessive and life-threatening; the latter is rare. Grade 1–5 complication ● Repair If injury to the vessel occurs, the bleeding should be controlled initially by direct pressure with a folded gauze sponge, speciﬁcally guarding against any maneuver that might further tear the vessel. Adequate exposure is obtained and both proximal and, when possible, distal control of the artery is obtained. The artery may be clamped without heparinization for short periods. If distal control cannot be obtained, control of the pulmonary veins is helpful to minimize blood loss during repair of large injuries or later during arterioplasty if necessary. Primary repair is usually all that is necessary. Vascular clamps may be applied to the area of injury when feasible with subsequent direct repair, although one should be careful when using this technique. When a tear in the artery extends proximally, cardiopulmonary bypass may be required for repair. ● Prevention One must be cautious when working with central tumors. Excessive traction on the mass, especially with left upper lobe tumors or bulky N1 disease, can result in arterial disruption. It is important to routinely obtain proximal control of the main PA trunk as well as the pulmonary veins prior to proceeding with the central dissection or resection to avoid devastating consequences. Because the veins are located more anterior, they are not commonly involved when performing a sleeve resection.

66 BRONCHIAL AND VASCULAR SLEEVE LOBECTOMY

Bronchial Anastomosis Anastomotic Torsion or Kinking ● Consequence Failure to orient the bronchial anastomosis properly can result in kinking of the airway or torsion. This is usually identiﬁed during the postoperative bronchoscopy and can be directly repaired by taking down the anastomosis. Retained secretions and pneumonia are suggestive of this in the postoperative setting. Grade 3/4 complication ● Repair When mild, retained secretions can be managed with aggressive pulmonary toilet and repeat therapeutic bronchoscopy. Stenting of the anastomosis can be effective in the management of luminal compromise. For those refractory to conservative techniques, reoperation is necessary with either revision of the anastomosis or completion pneumonectomy. ● Prevention Placing stay sutures prior to division of the airway helps to maintain proper orientation to prevent torsion. Liberal use of ﬁberoptic bronchoscopy and minitracheostomy in the postoperative setting aids in pulmonary toilet.

Leak/Dehiscence/Bronchovascular Fistula Circumferential dissection of the bronchus is performed prior to division of the airway when performing the resection. In performing a lymphadenectomy, much of the blood supply to the bronchus is compromised. This places the anastomosis at risk for complications. ● Consequence Although small air leaks may heal spontaneously, one should never leave the operating room with a leak from the bronchial anastomosis. Persistent postoperative air leaks, new air leaks, postoperative fever, or an elevated white blood cell count should alert one to the possibility of an anastomotic complication. Flexible bronchoscopy should be done to assess the bronchial anastomosis. In this setting, the morbidity can range from minimal, with the development of fever and leukocytosis, to empyema or bronchovascular ﬁstula. The latter is rarely salvageable. Grade 2–5 complication ● Repair One should have a very low threshold for ﬁberoptic bronchoscopy during the postoperative period. Most thoracic surgeons advocate the routine use of bronchoscopy prior to discharge.1,10 A small persistent leak may be managed conservatively if clinically indicated, with some authors reporting the success of ﬁbrin glue in this setting.12 Dehiscence requires a more aggressive

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approach with reoperation and repair of the bronchus, if viable, or completion pneumonectomy. One should remain clinically suspicious and intervene early because infections from bronchial dehiscence are associated with complications ranging from empyema and bronchopleural ﬁstula to bronchovascular ﬁstula, usually a fatal event. Anastomotic strictures occur late and can usually be managed with bronchoscopic interventions including dilation and stenting. ● Prevention When mobilizing the airway, the operating surgeon must pay close attention to the dissection of the bronchus itself and the corresponding bronchial vessels. Excessive dissection or failure to maintain an adequate blood supply to the airway may result in poor healing with dehiscence or stricture formation.18,19 The bronchial anastomosis may be performed in an interrupted, continuous, or combined fashion with no particular technique demonstrating superiority. When there is a size discrepancy between the proximal and the distal bronchi, an interrupted technique may allow for better approximation. If the size discrepancy is excessive, telescoping of the distal bronchus into the proximal, as with a lung transplant anastomosis, can be performed (Fig. 66–9).20 Stay sutures placed during the time of dissection may be tied together to help alleviate tension on the anastomosis. Division of the inferior pulmonary ligament will relieve some tension, but if not completely successful, a pericardial release will allow for greater mobilization of the lower lobe. The anastomosis should be tested at the time of the initial operation, and any air leaks should be primarily repaired. A ﬂap of well-vascularized tissue should be used to wrap the anastomosis21 and, in particular, to separate the bronchial anastomosis from the PA. Most commonly, intercostal muscle, pleura, or pericardial fat is used. For the intercostal muscle, one must be careful not to wrap the bronchus circumferentially because ossiﬁcation of the muscle with bronchial stricture may result.22 At the completion of the operation, prior to extubation, ﬁberoptic bronchoscopy should be performed to ensure that there is no luminal compromise or torsion.

Atelectasis ● Consequence Persistent atelectasis is one of the most common morbidities reported after bronchoplasty. It may be due to the interruption of the ciliary epithelium and lymphatics or to anastomotic edema. Grade 2 complication ● Repair Aggressive pulmonary toilet during the postoperative period is usually effective. However, if it is due to anastomotic compromise related to technical issues, these should be addressed as previously discussed.

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Figure 66–9 The intussusception technique for the bronchial anastomosis when size discrepancy is an issue.

● Prevention Anastomotic edema will resolve on its own, although some authors advocate the use of perioperative steroids.13

Pedicled Flaps Devascularization of the Flap ● Consequence If the vascular supply is not protected, the ﬂap will be nonviable and can contribute to postoperative anastomotic complications. Grade 2/3 complication ● Repair Poor blood supply to the ﬂap can be identiﬁed in the operating room. If this occurs, another ﬂap should be used as an alternative. ● Prevention If planning on an intercostal ﬂap, it should be harvested prior to placing the retractor against the ribs, thus avoiding trauma to the ﬂap. For pericardial ﬂaps, the dissection is begun at the base of the pericardium and the chest wall. As the ﬂap is mobilized cephalad, one must be constantly conscious of the vascular supply to the pedicle. As the pedicle thins out, it is possible to inadvertently divide the vascular pedicle.

PA Reconstruction PA Thrombosis ● Consequence When PA thrombosis occurs, the remaining lobe necroses. This results in infectious symptoms with fever and

Figure 66–10 Intraoperative photograph demonstrates a pericardial patch arterioplasty on the left main pulmonary artery.

an elevated white blood cell count. One must have a high index of suspicion in any patient with a fever or elevated white blood cell count following vascular tangential or sleeve resection. Oligemia may suggest this on the postoperative chest ﬁlm. The diagnosis is usually made with a perfusion scan or pulmonary arteriogram. Grade 3/4 complication ● Repair If a compromise in the lumen of the artery is identiﬁed at the initial operation, the anastomosis may be revised by either converting a tangential resection with reconstruction to a circumferential resection with end-to-end

66 BRONCHIAL AND VASCULAR SLEEVE LOBECTOMY

691

circumference is involved, a circumferential resection with an end-to-end anastomosis may be preferable (Fig. 66–11). Torsion or kinking can occur when the arterial anastomosis is performed before the bronchial anastomosis. One must pay careful attention to the course of the artery once the lobe is reexpanded to identify this before leaving the operating room.

Lymphadenectomy It is preferable to accomplish the lymphadenectomy prior to the bronchial sleeve procedure to avoid traction on or manipulation of the anastomosis.

A

POSTOPERATIVE COMPLICATIONS ASSOCIATED WITH PULMONARY SURGERY ● ● ● ● ● ● ● ● ●

Bleeding Pneumonia Atelectasis Atrial ﬁbrillation Esophageal injury Chyle leak Phrenic nerve injury Recurrent nerve injury Post-thoracotomy pain syndrome

REFERENCES B Figure 66–11 Intraoperative photographs demonstrate the technique for an end-to-end pulmonary artery sleeve resection. A, Both the proximal and the distal pulmonary arteries are clamped. B, The completed anastomosis.

anastomosis or revision of the primary anastomosis. If a sleeve resection of the artery was performed without need for a bronchial sleeve, the distal artery may not be able to be directly reconstructed to the proximal artery. In this setting, a tube graft can be fashioned from pericardium.23 Some authors advocate a sleeve resection of the bronchus to shorten the main stem and allow for the arterial ends to come together.24 ● Prevention Pulmonary arterial thrombosis occurs as a result of technical failure. Either the repair is too narrow or the artery is under torsion or kinked. When performing a tangential resection, if the resection exceeds over 25% of the arterial circumference, a patch angioplasty should be performed (Fig. 66–10).25 When more of the arterial

1. Suen HC, Myers BF, Guthrie T, et al. Favorable results after sleeve lobectomy or bronchoplasty for bronchial malignancies. Ann Thor Surg 1999;67:1557–1562. 2. Thomas CP. Conservative resection of the bronchial tree. J R Coll Surg Edinb 1955;1:169–186. 3. Paulson DL, Shaw RR. Preservation of lung tissue by means of bronchoplastic procedures. Am J Surg 1955;89: 347–355. 4. Paulson DL, Urschel HC, McNamara JJ, Shaw RR. Bronchoplastic procedures for bronchogenic carcinoma. J Thorac Cardiovasc Surg 1970;59:38–47. 5. Faber LP, Jensik RJ, Kittle CF. Results of sleeve lobectomy for bronchogenic carcinoma in 101 patients. Ann Thorac Surg 1984;37:279–285. 6. Okada M, Yamagishi H, Satake S, et al. Survival related to lymph node involvement in lung cancer after sleeve lobectomy compared with pneumonectomy. J Thorac Cardiovasc Surg 2000;119(4 pt 1):814–819. 7. Hollaus PH, Wilﬁng G, Wurnig PN, Pridun NS. Risk factors for the development of postoperative complications after bronchial sleeve resection for malignancy: a univariate and multivariate analysis. Ann Thorac Surg 2003;75:966– 972. 8. Mezzetti M, Panigalli T, Giuliani L, et al. Personal experience in lung cancer sleeve lobectomy and sleeve pneumonectomy. Ann Thorac Surg 2002;73:1736–1739.

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9. Icard P, Regnard JF, Guibert L, et al. Survival and prognostic factors in patients undergoing parenchymal saving bronchoplastic operation for primary lung cancer: a series of 110 consecutive cases. Eur J Cardiothorac Surg 1999;15:426–432. 10. Ludwig C, Stoelben E, Olschewski M, Hasse J. Comparison of morbidity, 30-day mortality, and long-term survival after pneumonectomy and sleeve lobectomy for non–small cell lung carcinoma. Ann Thorac Surg 2005;79:968–973. 11. Yoshino I, Yokoyama H, Yano T, et al. Comparison of surgical results of lobectomy with bronchoplasty and pneumonectomy for lung cancer. J Surg Oncol 1997;64: 32–35. 12. Lausberg HF, Graeter TP, Tscholl D, et al. Bronchovascular versus bronchial sleeve resection for central lung tumors. Ann Thorac Surg 2005;79:1147–1152. 13. Redina E, Venuta F, Giacomo T, et al. Safety and efﬁcacy of bronchovascular reconstruction after induction chemotherapy for lung cancer. J Thorac Cardiovasc Surg 1997; 114:830–837. 14. Tronc F, Grégoire J, Rouleau J, Deslauriers J. Long-term results of sleeve lobectomy for lung cancer. Eur J Cardiothorac Surg 2000;17:550–556. 15. Deslauriers J, Gregoire J, Jacques LF, et al. Sleeve lobectomy versus pneumonectomy for lung cancer: a comparative analysis of survival and sites of recurrences. Ann Thorac Surg 2004;77:1152–1156. 16. Fadel E, Yildizeli B, Chapelier AR, et al. Sleeve lobectomy for bronchogenic cancers: factors affecting survival. Ann Thorac Surg 2002;74:851–858. 17. End A, Hollaus P, Pentsch A, et al. Bronchoplastic procedures in malignant and nonmalignant disease: multivariable analysis of 144 cases. J Thorac Cardiovasc Surg 2000;120:119–127.

18. Vildizeli B, Fadel E, Mussot S, et al. Morbidity, mortality and long-term survival after sleeve lobectomy for nonsmall cell lung cancer. Eur J Cardiothorac Surg 2007;31: 95–102. 19. Kutlu CA, Goldstraw P. Tracheobronchial sleeve resection with the use of a continuous anastomosis: results of one hundred consecutive cases. J Thorac Cardiovasc Surg 1999;117:1112–1117. 20. Teddler M, Anstadt MP, Teddler SD, Lowe JE. Current morbidity and mortality after bronchoplastic procedures for malignancy. Ann Thorac Surg 1992;54:387–391. 21. Hollaus PH, Janakiev D, Pridun NS. Telescope anastomosis in bronchial sleeve resections with high-caliber mismatch. Ann Thorac Surg 2001;72:357–361. 22. Turrentine MW, Kesler KA, Wright CD, et al. Effect of omental, intercostal, and internal mammary artery pedicle wraps on bronchial healing. Ann Thorac Surg 1990;49: 574–578. 23. Deeb ME, Sterman DH, Shrager JB, Kaiser LR. Bronchial anastomotic stricture caused by ossiﬁcation of an intercostal muscle ﬂap. Ann Thorac Surg 2001;71:1700– 1702. 24. Rendina EA, Venuta F, De Giacomo T, et al. Sleeve resection and prosthetic reconstruction of the pulmonary artery for lung cancer. Ann Thorac Surg 1999;68:995– 1001. 25. Dartevalle P. How I do it: sleeve lobectomy. General Thoracic Symposium at Annual Meeting, American Association for Thoracic Surgery. Accessible at www. conferencearchives.com/aats2006/index.html 26. Shrager JB, Lambright ES, McGrath CM, et al. Lobectomy with tangential pulmonary artery resection without regard to pulmonary function. Ann Thorac Surg 2000;70: 234–239.

67

Pneumonectomy James E. Davies, MD and Mark S. Allen, MD

INTRODUCTION

INDICATIONS

The ﬁrst successful pneumonectomy was performed by Rudolph Nissen in 1931 in Berlin, Germany. His patient was a 12-year-old girl with severe bronchiectasis of the entire left lung. This was a staged procedure with a cervical phrenic crush performed initially, followed by a left thoracotomy. The pneumonectomy was performed by placing a rubber tube ligature around the hilum of the left lung. The chest was packed, and 2 weeks later, the lung sloughed off. A small bronchial ﬁstula developed but closed spontaneously 2 months later.1 On April 5, 1933, Everts Graham,2 Chair of Surgery at Washington School of Medicine, performed the ﬁrst successful single-stage pneumonectomy. The patient was a 48-year-old gynecologist with a squamous cell carcinoma of the left lung that could be removed only with a pneumonectomy. Since these early reports, the number of pneumonectomies has steadily increased and mortality rates have improved. These improvements are probably secondary to a combination of better surgical approaches, patient selection, anesthesia, and postoperative care. Wilkins and coworkers3 showed a decrease in operative mortality, from 56% to 11%, over a period of 4 decades (1931–1970) at the Massachusetts General Hospital. Numerous reports since 1980 have shown mortality rates from 3% to 12%.3–6 Certain risk factors associated with higher mortality rates have been identiﬁed. Right-sided pneumonectomies have a higher morbidity and mortality than left-sided pneumonectomies. Reports by Nagasaki and associates4 and Wahi and colleagues5 conﬁrmed signiﬁcantly higher mortality rates with right- versus left-sided pneumonectomies. Wahi and colleagues reported in 19895 that right-sided pneumonectomy had a 12% mortality versus only 1% with left pneumonectomy. In 2001, Martin and coworkers,7 from Memorial Sloan-Kettering Cancer Center, reported a 24% mortality for right-sided pneumonectomy versus 2.4% for left-sided pneumonectomy. Other risk factors shown to be associated with higher mortality include age greater than 70 years, neoadjuvant therapy, completion pneumonectomy, and resection for inﬂammatory or infectious disease.8–14

● Carcinoma of lung (centrally located) ● Inﬂammatory/infectious lung disease with destroyed

lung ● Proximal

bronchial stricture/obstruction with destroyed lung ● Completion pneumonectomy ● Extrapleural pneumonectomy for malignant mesothelioma ● Trauma

OPERATIVE STEPS Step 1 Step Step Step Step Step Step Step Step

2 3 4 5 6 7 8 9

Anesthesia (double-lumen endotracheal tube and epidural catheter) Posterolateral thoracotomy Exploration of pleural cavity Mediastinal lymphadenectomy Mobilization of pulmonary hilum Ligation of pulmonary veins Ligation of pulmonary artery Transection of bronchus Closure

Mediastinal Lymphadenectomy Chylothorax Chylothorax is a rare complication after pneumonectomy. In 1993, Vallieres and associates15 published a review of the literature that showed a total of only 27 cases. Since that time, other series have shown an incidence of 0.37% to 0.5% of pneumonectomies.16,17 Cerfolio and colleagues17 reviewed the Mayo Clinic experience from 1987 to 1995 (315 patients) and found an incidence of 0.37%. ● Consequence Initially, chylothorax is difﬁcult to diagnose in the pneumonectomy patient because normally all chest tubes are removed within 24 hours. This leads to a delay in the diagnosis and a potentially extended hospital stay. The diagnosis should be suspected when

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there is rapid accumulation of ﬂuid within the pleural cavity. In the series by Sarsam and coworkers,16 nine patients had a rapid accumulation of ﬂuid but only four were symptomatic. These symptoms are normally increased respiratory difﬁculty or compromise. Tension chylothorax requiring emergency drainage was described by Karwande and associates in 1986.18 Chylothorax can lead to serious metabolic defects secondary to the composition of chyle. The loss of protein, fat, and fat-soluble vitamins requires increased nutritional support, and the immunologic status of the patient can be affected by the loss of chyle. Grade 2/3 complication ● Repair The initial treatment for a chylothorax is conservative management with external drainage, nutritional support, and observation. The diagnosis is suggested by the presence of milky white drainage and conﬁrmed by an elevated triglyceride level of the ﬂuid (>110 mg/ dl). The patient should be placed on total parental nutrition or a medium-chain triglyceride diet, and the volume of the ﬂuid should be observed and recorded accurately. If it is greater than 500 ml/day, it is less likely to resolve with conservative therapy and surgical intervention should be performed. The leak can be isolated by giving 100 to 200 ml of olive oil or cream to the patient by nasogastric tube 2 to 3 hours prior to the surgical exploration.19 This will increase the output of the milky ﬂuid from the duct and make it easier to identify intraoperatively. The chest should be reopened on the side of the pneumonectomy and the thoracic duct ligated. This can be done by direct closure on the leak, mass ligation of the ductal tissue, or supradiaphragmatic ligation of the duct on the right side. Other techniques that have been described include pleuroperitoneal shunting with double-valve Denver peritoneal shunts and the use of ﬁbrin glue.20,21 ● Prevention The best way to prevent an injury to the thoracic duct during a pneumonectomy or any thoracic procedure is through knowledge of the anatomy of the duct (Fig. 67–1). It originates from the cisterna chyli at the level of the second lumbar vertebrae and ascends through the aortic hiatus into the chest. The duct continues superiorly on the anterior surface of the vertebral column behind the esophagus and between the aorta and the azygos vein. At the level of T4 or T5, it crosses the midline behind the aorta into the left side of the chest. The duct continues superiorly adjacent to the esophagus and drains into the left subclavian–jugular junction.22

Recurrent Laryngeal Nerve Injuries Recurrent laryngeal nerve injuries are not common with pneumonectomy or any pulmonary resection. They can be intentional (sacriﬁcing the nerve for a complete onco-

Left jugular vein

Superior vena cava

Thoracic duct Aorta

Azygos vein

Diaphragm

Cisterna chyli

Figure 67–1 Anatomy of the thoracic duct.

logic resection) or unintentional (secondary to traction or direct injury). Mediastinal lymphadenectomy can lead to more injuries, especially on the left. Bollen and colleagues23 reported that 3 out of 62 patients undergoing complete mediastinal lymphadenectomy suffered unintentional injury. Conversely, in the American College of Surgical Oncology Group’s (ACOSOG) study24 of lymphadenectomy versus lymph node sampling, no increase was observed in the incidence of recurrent nerve injuries with mediastinal lymph node dissection. ● Consequence Injury to recurrent laryngeal nerve leads to unilateral vocal cord paralysis. The degree of dysfunction is variable, but it may cause inadequate cough, inability to clear secretions, or aspiration in the postoperative setting. Patient age, recent weight loss, and overall

67 PNEUMONECTOMY 3p

3a Vagus nerve 6

5

Phrenic nerve

Figure 67–2 Anatomy of the left aortopulmonary window with levels V and VI lymph nodes.

pulmonary function prior to resection correlate with the patient’s ability to compensate postoperatively. Grade 3 complication ● Repair The treatment and timing for recurrent laryngeal nerve injuries depend on the status and condition of the patient. Deﬁnitive treatment is with medialization of the vocal cords, normally performed by an otolaryngologist. Three techniques described include vocal cord injection, neuromuscular transfer, and vocal cord implant.25 ● Prevention Injury to the recurrent laryngeal nerve is most common on the left during resection of stations 5 and 6 lymph nodes. Care must be taken during this portion of the procedure to avoid direct injury or excessive traction on the recurrent laryngeal nerve. If needed, sharp dissection rather than cautery should be used. A vessel loop can also be placed around the nerve for gentle traction. This decreases the crushing effect of picking up the nerve directly. Figure 67–2 shows the anatomy of the nerve in relation to levels V and VI lymph nodes.

Mobilization of the Pulmonary Hilum Esophagopleural Fistula Esophagopleural ﬁstula (EPF) occurs in 0.5% to 0.65% of patients undergoing pneumonectomy.26–28 EPFs are more

695

common of the right side, and the incidence is increased in patients undergoing pneumonectomy for inﬂammatory or infectious diseases. This is most likely secondary to the difﬁculty in the dissection of the pulmonary hilum in these patients. Massard and Wihlm29 divided EPFs into two groups: early and late (>3 mo). The etiology in the early group was direct operative trauma or devascularization/ necrosis versus recurrent cancer or chronic infectious/ inﬂammatory disorder in the late group. The diagnosis can be difﬁcult to make in either group because EPFs tend to present in the same way as a bronchopleural ﬁstula (BPF). Therefore, the work-up tends to be directed at ruling out a BPF with a ﬂexible bronchoscopy. If this is negative, a water-soluble swallow study should be performed immediately to rule out an EPF. ● Consequence EPF presents with an associated empyema in both the early and the late groups. Early reports cited a mortality of 50% in these patients.28,30 More recent reports, including one from the Mayo Clinic by Deschamps and coworkers in 2001,31 showed a mortality of approximately 7.5% in patients with empyemas after pneumonectomy. The increased mortality depends on the etiology of the ﬁstula; the late group has a higher incidence of recurrent malignancy. Grade 3 complication ● Repair The initial treatment of empyema with EPF is drainage of the empyema, appropriate antibiotics, and nutritional support with nasogastric tube or parenteral nutrition. Deﬁnitive treatment depends on the etiology of the ﬁstula, but EPF is treated in the same way as a BPF, which is discussed in detail later in this section. ● Prevention If a difﬁcult dissection of the mediastinum is suspected or found during the operation, a large bougie may be inserted to aid in identifying the esophagus. This may help avoid but will not prevent direct injury to the esophagus. If an injury is suspected, methylene blue or air may be injected into the nasogastric tube to help identify the injury. Once the injury is located, it can be closed in two layers of ﬁne nonabsorbable suture and buttressed with a pleural ﬂap or other viable tissue.30

Cardiac Herniation Cardiac herniation or torsion is a rare complication after pneumonectomy, but it is associated with a mortality rate of 40% to 50%.32,33 It is associated with opening the pericardial sac for intrapericardial pneumonectomy. On the left, herniation results in strangulation of the left ventricle with decreased ﬁlling and ejection. There is also decreased or no coronary blood ﬂow, leading to myocardial ischemia. The right-sided herniation leads to a counterclockwise rotation of the heart and obstruction of the superior and inferior vena cava (Fig. 67–3). These normally present

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Figure 67–4 Intraoperative large pericardial defect after intrapericardial pneumonectomy.

Ligation of the Pulmonary Veins Peripheral Tumor Embolus

Figure 67–3 Chest radiograph of right-sided cardiac herniation.

within 24 hours but have been reported up to 72 hours postoperatively. ● Consequence The patient will develop abrupt hypotension, tachycardia, increased venous pressure, and progressive cardiovascular collapse. If the diagnosis and treatment are not instituted immediately, fatality will result.32,33 Grade 3/5 complication ● Repair After diagnosis, the patient should be placed immediately with the operative side up and taken back to the operating room. Upon reopening of the thoracotomy, the cardiac herniation should be reduced and the pericardium reconstructed, usually with a synthetic patch. ● Prevention Closure of all but very small pericardial defects should be performed intraoperatively. If the pericardium cannot be closed without causing cardiac restriction, a synthetic patch should be used. This does not fully eliminate postoperative herniation, as reported by Veronesi and associates in 2001.34 Also, the pleural cavity should not be placed or kept on excessive suction. Figure 67–4 shows a large pericardial defect after a left extrapleural pneumonectomy.

● Consequence Peripheral tumor embolus during a pneumonectomy is a rare but potentially lethal complication.35 It was ﬁrst described by Taber36 and Senderoff and Kirschner37 in the early 1960s. Whyte and colleagues38 reported that the distribution of the emboli were most commonly major arterial sites: the aortic bifurcation and femoral arteries (50%), the carotid and cerebral arteries (32%), and the visceral arteries (18%). Grade 3/4 complication ● Repair If a tumor embolus is suspected in the perioperative period, an angiogram should be performed. Once the diagnosis is conﬁrmed, removal by an embolectomy is done if the patient is clinically stable enough to return to the operating room. ● Prevention If a tumor is suspected pre- or intraoperatively within the pulmonary vein, a transesophageal echocardiogram is performed to assess intra-atrial involvement.35,39 At the time of surgery, the intrapericardial portion of the pulmonary hilum is explored and assessed for resectability. Another technique described by Taber36 is placement of a pursestring suture in the left atrium and transatrial digital palpation. If the tumor involves the left atrium or distal pulmonary vein, it may be removed with or without cardiopulmonary bypass.35,38,39 Figure 67–5 shows a management algorithm described by Whyte and colleagues in 1992.38

Ligation of the Pulmonary Artery Pulmonary Artery Embolism/Thrombosis In 1966, Chuang and coworkers40 reported that approximately 1% of all pneumonectomy patients had a pulmonary embolus originating from the pulmonary arterial

67 PNEUMONECTOMY

697

Palpable tumor within pulmonary vein (consider intracardiac tumor)

Intraoperative transesophageal ECHO digital palpation through left atrial pursestring suture

Intracardiac tumor Yes

No

Wedge resection of left atrium using endo stapling device Resection of CPB Unresectable

Intrapericardial ligation of vein

Tumor within line of transection

Yes

Peripheral vascular exam

Neurological exam

Normal

Abnormal

No change from preop

Carotid duplex scan

Head CT Medical management

No

EKG

Visceral angiography for any abdominal symptoms

Acute ischemia

Embolectomy

Possible carotid embolectomy if tumor lodged in extracranial carotid artery

Embolus

Negative

No change

Acute ischemia

Embolectomy or abdominal exploration

Coronary angiography

Medical management of MI

Coronary revascularization

Figure 67–5 Peripheral tumor embolus algorithm. (From Whyte RI, Starkey TD, Orringer MB. Tumor emboli from lung neoplasms involving the pulmonary vein. J Thorac Cardiovasc Surg 1992;104:421–425.)

stump. It occurs more commonly on the right, possibly secondary to the longer arterial stump.41 ● Consequence Overall, pulmonary artery embolus is the fourth leading cause of death in pneumonectomy patients.42 Grade 1/3 complication

● Repair Initial treatment of pulmonary arterial thrombosis is the same as with any postoperative patient with a pulmonary embolus, including supportive care and anticoagulation. If the patient is hemodynamically unstable, either a pulmonary embolectomy or a catheter-based treatment may be an option.

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● Prevention The exact etiology of a pulmonary embolus originating from the pulmonary arterial stump is unknown, but it is believed that appropriate arterial closure with a nonabsorbable suture or stapler may decrease the incidence. Also, postoperatively, prevention should include early mobilization, sequential compression devices, and/or subcutaneous anticoagulation.

Closure of the Bronchus Empyema with or without BPF The incidence of empyema after pneumonectomy is between 2% and 16%.4,43 A BPF is commonly but not always associated with empyemas. In a series from the Mayo Clinic in 2001,31 53 (7.5%) of 713 pneumonectomy patients developed postoperative empyemas and 32 (4.5%) had associated BPF. Risk factors for developing BPF include right-sided pneumonectomy, completion pneumonectomy, preoperative radiation therapy, pneumonectomy for inﬂammatory or infectious disease, residual/recurrent tumor, and intraoperative technical factors. A BPF can develop early (1–7 days), secondary to technical factors, or up to years later from multiple different factors.44,45 ● Consequence Mortality in patients with an empyema and BPF has been reported to be between 16% and 72%.46 Signiﬁcant morbidity associated with BPF includes increased hospital stay, long rehabilitation, and recurrent operative procedures. Grade 3/4 complication ● Repair The initial management of patients suspected of having empyema with or without BPF includes stabilization of the patient, accurate diagnosis, and deﬁnitive treatment, including adequate pleural drainage, parental

A Figure 67–6 Débridement of the bronchial stump.

antibiotics, nutritional support, removal of necrotic tissue, and obliteration of the residual pleural space.45 If the patient presents acutely ill with signs of respiratory distress, she or he should be placed in the lateral decubitus position with the operative side down to prevent contamination of the contralateral lung. Once the patient has been stabilized, deﬁnitive treatment options include thoracoplasty, open pleural drainage, anterior transpericardial closure of the ﬁstula, obliteration of the empyema space with ﬂuid or muscle, primary closure of the bronchial stump with vascularized tissue, or the use of a continuous irrigation system.47–52 At the Mayo Clinic, a combination of the original Clagett technique and the use of a well-vascularized extrathoracic muscle is used to cover the bronchial stump.53,54 After initial stabilization, which may include tube thoracostomy, the patient is returned to the operating room and the thoracotomy is reopened. The BPF is identiﬁed by ﬁlling the pleural cavity with ﬂuid and observing for leakage of air bubbles. Once the BPF is identiﬁed, it is débrided and reclosed near the carina with interrupted nonabsorbable sutures to prevent a long stump (Fig. 67– 6). A well-vascularized muscle ﬂap is then used to cover the bronchial stump (Fig. 67–7). Options for the muscle ﬂap include serratus anterior, latissimus dorsi, pectoralis major, or rectus abdominis. If the empyema exists without a BPF, muscle ﬂap is not required but may be used to protect underlying structures. The remainder of the pleural cavity is irrigated, débrided, and packed with wet dressings (Fig. 67–8). Irrigation and débridement are repeated every 48 hours in the operating room until the pleural cavity is clean with good granulation tissue. The cavity is then ﬁlled with débridement antibiotic solution (DABS) (0.5 g neomycin, 0.1 g polymyxin B sulfate, and 80 mg gentamicin per liter of saline) and closed (Fig. 67–9).45 ● Prevention The bronchial stump should be handled gently to avoid devascularization and should not be left excessively

B

67 PNEUMONECTOMY

A

A

699

B

B

Figure 67–7 Serratus anterior muscle ﬂap to cover a bronchopleural ﬁstula (BPF).

Figure 67–8 Débridement and packing of the pleural cavity.

long. No single technique of closure of the bronchial stump has been shown to be superior. The series from the Mayo Clinic31 showed a decrease in BPF with stapled versus hand-sewn closure of the bronchus. al-Kattan and associates55 had a 1.3% BPF rate in 530 pneumonectomies using interrupted nonabsorbable monoﬁlament 2-0 polypropylene sutures. Also, the prophylactic use of a vascularized muscle ﬂap is not clear. Deschamps and coworkers31 showed an increased incidence of BPF with the use of bronchial stump reinforcement in 2001, but this was not a randomized trial and the patients that had prophylactic muscle ﬂaps were believed to be at signiﬁcantly higher risk. It is generally recommended that patients having a pneumonectomy for inﬂammatory of infectious disease or those who received neoadjuvant radiation therapy should have a muscle ﬂap to cover the bronchial stump at the initial procedure.

Postoperative Complications Cardiac Arrhythmias Postoperative cardiac arrhythmias occur in 14% to 40% of pneumonectomy patients.56 The majority of these arrhythmias are atrial in origin, with atrial ﬁbrillation being the

Figure 67–9 Filling of the pleural cavity with débridement antibiotic solution (DABS).

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most common. Predisposing factors include advanced age, coronary artery disease, and more extensive procedures (e.g., extrapleural pneumonectomy). The exact etiology is unclear, but it probably results from a combination of factors including hypoxia, vagal stimulation, electrolyte imbalances, abnormal blood pH, reduced pulmonary vascular reserve, local inﬂammation of the atria, distention of the atria, and general anesthesia.56 ● Consequence Cardiac arrhythmias are associated with an up to 40% increased perioperative mortality.56 They may also lead to an increased length of intensive care unit and overall hospital stay. Grade 1 complication ● Repair Patients should have continuous cardiac monitoring postoperatively to help identify these arrhythmias. Ritchie and colleagues57,58 showed that over half of these arrhythmias occurred in the ﬁrst 24 hours after surgery. Once the diagnosis has been conﬁrmed, the patient should be stabilized and treated appropriately. This may include β-blockers, calcium channel blockers, digoxin, or electrical/chemical cardioversion. ● Prevention Prophylactic treatment of arrhythmias in the postoperative setting has been examined in multiple studies. The early studies using digoxin showed beneﬁt, but this was not conﬁrmed in more recent studies.57–60 Borgeat and coworkers61 looked at the use of ﬂecainide as a continuous infusion and found a decrease in the incidence of arrhythmias, but the regimen was complicated and intravenous ﬂecainide is not available in the United States. Amiodarone has also been studied with conﬂicting results.62,63 Some believe that the pulmonary complications of amiodarone in the setting of a pneumonectomy outweigh the potential beneﬁt. Van Miegham and associates64 and Amar and colleagues65 showed a decrease in postoperative arrhythmias with calcium channel blockers. No single study has been absolutely conclusive; therefore, the prophylactic use of any of these medications is not routine.

Postpneumonectomy Pulmonary Edema Postpneumonectomy pulmonary edema (PPE) is a condition that occurs in the early postoperative period (usually within 72 hours), in which patients develop rapidly progressive hypoxia and inﬁltration of the contralateral lung.66 The incidence is between 3% and 5% of pneumonectomy patients and the mortality approaches 80% to 100%.66,67 Risk factors include right pneumonectomy, duration of surgery, extent of surgery, perioperative ﬂuid overload, and postoperative pleural drainage.66–69 Initially, patients present with dyspnea that rapidly progresses despite optimal treatment, and they require mechanical ventilation within 12 to 24 hours after the

Figure 67–10 Chest radiograph of a right-sided postpneumonectomy pulmonary embolism (PPE).

onset of symptoms. The chest radiograph will quickly develop picture consistent with acute respiratory distress syndrome (ARDS) (Fig. 67–10). ● Consequence Even with early diagnosis and aggressive treatment, the mortality approaches 80% to 100%.66,67 Grade 4/5 complication ● Repair Once the patient begins to develop dyspnea and hypoxia, the differential diagnosis should include cardiogenic pulmonary edema, aspiration pneumonitis, infectious pneumonitis, pneumonia, massive atelectasis, pulmonary embolus, sepsis, and PPE. Normally, the patient is transported to the intensive care unit and supported with mechanical ventilation, but there have been reports of treatment with continuous positive airway pressure (CPAP) masks.70 Bronchoscopy, pulmonary artery catheter monitoring, pan-cultures with the initiation of empirical broad-spectrum antibiotics, and computed tomography (CT) scans of the chest should be performed to rule out other causes of the hypoxia. Normally, the patients require elevated levels of inspired oxygen and higher airway pressures to maintain adequate oxygenation. Pressure control ventilation may aid in decreasing the volutrauma associated with the mechanical ventilation in these patients. Nutritional support should also be started as soon as possible. Other therapies that have been described but have not been shown to have consistent improvement include steroids, extracorporeal membrane oxygenation (ECMO), and inhaled nitrous oxide.66,71,72 ● Prevention The etiology of PPE is not fully understood; therefore, no deﬁnitive prevention is known. In the initial

67 PNEUMONECTOMY

701

Figure 67–11 Preoperative computed tomography (CT) scan of the chest in right-sided postpneumonectomy syndrome (PPS).

postoperative period, ﬂuid restriction with the use of diuretics has been generally accepted. Intravenous ﬂuid rates are kept between 30 and 50 ml/hr.73 Otherwise, standard postoperative care of the thoracic patient should include adequate pain control, early mobilization, and pulmonary rehabilitation.

Postpneumonectomy Syndrome ● Consequence Postpneumonectomy syndrome (PPS) results from major airway compression secondary to progressive mediastinal shift toward the side of the pneumonectomy. This leads to stretching and/or compression of the trachea or main stem bronchus. PPS is more commonly associated with right-sided pneumonectomies, and PPS after a left pneumonectomy is usually associated with a right-sided aortic arch.74,75 Although Shamji and coworkers76 reported a series of patients with PPS after left pneumonectomy and normal aortic arch anatomy. The right-sided PPS is secondary to a counterclockwise rotation of the heart and great vessels, leading to stretching of the left main stem bronchus with compression between the aorta and the pulmonary artery (Fig. 67–11). Left PPS has a clockwise rotation of the heart and mediastinum with compression of the right main stem bronchus over the vertebral body. PPS may present early or several years later. Shepard and associates77 reported a case of right PPS 37 years after resection. Other risk factors associated with PPS are young age and female gender, likely secondary to increased elasticity of the mediastinum in these patients.74 Grade 3 complication ● Repair The presentation of PPS is usually one of a slow progressive increase in dyspnea associated with repeated

Figure 67–12 Bronchoscopic view of a patient after right pneumonectomy with a narrowed left lower lobe oriﬁce.

episodes of respiratory infection, coughing, and stridor.74 Initially, a chest radiograph may suggest the diagnosis, but it is conﬁrmed with bronchoscopy and CT scan. The bronchoscopy may reveal narrowing of the airway or tracheobronchial malacia (Fig. 67–12). Once the diagnosis has been conﬁrmed, treatment consists of stabilization of the patient, dissection of the adhesions on the operative side, placement of a prosthetic device, and correction of the tracheobronchial malacia if present. Many different materials have been described for expansion of the pleural space, but the best results appear to be with an expandable saline prosthesis (Figs. 67–13 and 67–14).75,76,78–81 The tracheobronchial malacia has been treated with expandable metallic stents.82–84

Platypnea—Orthodeoxia Syndrome Platypnea is a very rare complication after pneumonectomy: only 39 cases had been reported in the literature as of 1998.85 The ﬁrst report was in 1956 by Schnabel and colleagues.86 Clinically, the patient presents with dyspnea and hypoxia while sitting upright or standing. In the supine position, the dyspnea and hypoxia are either absent or signiﬁcantly decreased. The etiology is increased rightto-left shunting at the atrial level secondary to a patent foramen ovale (PFO) or atrial septal defect (ASD), which may or may not have been present preoperatively.85 Possible causative factors include increased pulmonary vascular resistance, decreased right ventricular compliance, or rotation of the heart with distortion of ﬂow from the

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Figure 67–13 Intraoperative photograph after placement of a saline implant in a patient with right-sided PPS. Figure 67–15 Intraoperative transesophageal echocardiogram of a patent foramen ovale (PFO).

REFERENCES

Figure 67–14 Postoperative CT scan of the chest in a patient with right-sided PPS.

inferior vena cava.85 This leads to right-to-left shunting associated with increased intrathoracic pressures during sitting or standing. ● Consequence Platypnea is usually insidious in presentation and may be quite complex to diagnose because most pneumonectomy patients have some degree of dyspnea. Therefore, the diagnosis may be delayed along with the patient’s recovery. Repair of the PFO/ASD corrects the problem and is associated with limited mortality. Grade 2/3 complication ● Repair The diagnosis can usually be made with transthoracic echocardiography (Fig. 67–15), but occasionally, a right heart catheterization is required to demonstrate the defect. The PFO is then repaired surgically or with a percutaneous closure device.85–88

1. Nissen R, Wilson R. In History of Chest Surgery. Springﬁeld, IL: Charles C Thomas, 1960; pp 41–43. 2. Graham EA, Singer JJ. Successful removal of an entire lung for carcinoma of the bronchus. JAMA 1933;101: 1371. 3. Wilkins EW, Scannell JG, Craver JG. Four decades of experience with resections for bronchogenic carcinoma at the Massachusetts General Hospital. J Thorac Cardiovasc Surg 1978;76:364–368. 4. Nagasaki F, Flehinger BJ, Martini N. Complications of surgery in treatment of carcinoma of the lung. Chest 1982;1:25–29. 5. Wahi R, McMurtrey MJ, DeCaro LF, et al. Determinants of perioperative morbidity and mortality after pneumonectomy. Ann Thorac Surg 1989;48:33–37. 6. Ginsberg RJ, Hill LD, Eagan RT, et al. Modern thirty-day operative mortality for surgical resections in lung cancer. J Thorac Cardiovasc Surg 1983;86:654–658. 7. Martin J, Ginsberg RJ, Abolhoda A, et al. Morbidity and mortality after neoadjuvant therapy for lung cancer: the risks of right pneumonectomy. Ann Thorac Surg 2001;72: 1149–1154. 8. Hepper NG, Bernatz PE. Thoracic surgery in the aged. Dis Chest 1960;37:298–303. 9. Dyszkiewicz W, Pawlak K, Gasiorowski L. Early postpneumonectomy complications in the elderly. Eur J Cardiothorac Surg 2000;17:246–250. 10. Rusch VW, Albain KS, Crowley JJ, et al. Surgical resection of stage IIIA and IIIB non-small-cell lung cancer after concurrent induction chemoradiotherapy. A Southwest Oncology Group Trial. J Thorac Cardiovasc Surg 1993;105:97–104. 11. McGovern EM, Trastek VF, Pairolero PC, Payne WS. Completion pneumonectomy: indications, complications, and results. Ann Thorac Surg 1988;46:141–146. 12. Pomerantz M, Madsen L, Goble M, Iseman M. Surgical management of resistant mycobacterial tuberculosis and

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33. Arndt RD, Frank CG, Schmitz AL, Haveson SB. Cardiac herniation with volvulus after pneumonectomy. AJR Am J Roentgenol 1978;130:155–156. 34. Veronesi G, Spaggiari L, Solli PG, Pastorino U. Cardiac dislocation after extended pneumonectomy with pericardioplasty. Eur J Cardiothorac Surg 2001;19:89–91. 35. Zwischenberger JB, Alpard SK, Bidani A. Early complications: respiratory failure. Chest Surg Clin North Am 1999;9:543–564. 36. Taber RE. Massive systemic tumor embolization during pneumonectomy: a case report with comments on routine primary pulmonary vein ligation. Ann Surg 1961;154: 263–268. 37. Senderoff E, Kirschner PA. Massive tumor embolism during pulmonary surgery. J Thorac Cardiovasc Surg 1962;44:528–535. 38. Whyte RI, Starkey TD, Orringer MB. Tumor emboli from lung neoplasms involving the pulmonary vein. J Thorac Cardiovasc Surg 1992;104:421–425. 39. Mansour KA, Malone CE, Craver JM. Left atrial tumor embolization during pulmonary resection: review of literature and report of two cases. Ann Thorac Surg 1988; 46:455–456. 40. Chuang TH, Dooling JA, Connolly JM, Shefts LM. Pulmonary embolization from vascular stump thrombosis following pneumonectomy. Ann Thorac Surg 1966;2:290–298. 41. Takahashi T, Yokoi K, Mori K, Miyazawa N. Clot in the pulmonary artery after pneumonectomy. AJR Am J Roentgenol 1993;161:744–745. 42. Goodman LR, Curtin JJ, Mewissen MW, et al. Detection of pulmonary embolism in patients with unresolved clinical and scintigraphic diagnosis: helical CT versus angiography. AJR Am J Roentgenol 1995;164:1369–1374. 43. Pairolero PC, Deschamps C, Allen MS, et al. Postoperative empyema. Chest Surg Clin North Am 1992;2:813– 822. 44. Kerr WF. Late-onset post-pneumonectomy empyema. Thorax 1977;32:149–154. 45. Deschamps C, Pairolero PC, Allen MS, et al. Early complications: bronchopleural ﬁstula and empyema. Chest Surg Clin North Am 1999;9:587–595. 46. Ponn RB. Complications of pulmonary resection. In Shields TW, Locicero J III, Ponn RB, Rusch VW (eds): General Thoracic Surgery, 6th ed. Philadelphia: Lippincott Williams & Wilkins, 2005; pp 568–572. 47. Pairolero PC, Trastek VF. Surgical management of chronic empyema: the role of thoracoplasty. Ann Thorac Surg 1990;50:584–585. 48. Shamji FM, Ginsberg RJ, Cooper JD, et al. Open window thoracostomy in the management of postpneumonectomy empyema with or without bronchopleural ﬁstula. J Thorac Cardiovasc Surg 1983;86:818–822. 49. Ginsberg RJ, Pearson FG, Cooper JD, et al. Closure of chronic postpneumonectomy bronchopleural ﬁstula using the transsternal transpericardial approach. Ann Thorac Surg 1989;47:231–235. 50. Miller JI, Mansour KA, Nahai F, et al. Single-stage complete muscle ﬂap closure of the postpneumonectomy empyema space: a new method and possible solution to a disturbing complication. Ann Thorac Surg 1984;38:227– 231.

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51. Puskas JD, Mathisen DJ, Grillo HC, et al. Treatment strategies for bronchopleural ﬁstula. J Thorac Cardiovasc Surg 1995;109:989–996. 52. Gharagozloo F, Trachiotis G, Wolfe A, et al. Pleural space irrigation and modiﬁed Clagett procedure for the treatment of early postpneumonectomy empyema. J Thorac Cardiovasc Surg 1998;116:943–948. 53. Clagett OT, Geraci JE. A procedure for the management of postpneumenectomy empyema. J Thorac Cardiovasc Surg 1963;45:141–145. 54. Pairolero PC, Arnold PG, Piehler JM. Intrathoracic transposition of extrathoracic skeletal muscle. J Thorac Cardiovasc Surg 1983;86:809–817. 55. al-Kattan K, Cattalani L, Goldstraw P. Bronchopleural ﬁstula after pneumonectomy with a hand suture technique. Ann Thorac Surg 1994;58:1433–1436. 56. Asamura H. Early complications: cardiac complications. Chest Surg Clin North Am 1999;9:527–541. 57. Ritchie AJ, Bowe P, Gibbons JR. Prophylactic digitalization for thoracotomy: a reassessment. Ann Thorac Surg 1990;50:86–88. 58. Ritchie AJ, Danton M, Gibbons JR. Prophylactic digitalisation in pulmonary surgery. Thorax 1992;47:41–43. 59. Shields TW, Ujiki GT. Digitalization for prevention of arrhythmias following pulmonary surgery. Surg Gynecol Obstet 1968;126:743–746. 60. Patel RL, Townsend ER, Fountain SW. Elective pneumonectomy: factors associated with morbidity and operative mortality. Ann Thorac Surg 1992;54:84–88. 61. Borgeat A, Petropoulos P, Cavin R, et al. Prevention of arrhythmias after noncardiac thoracic operations: ﬂecainide versus digoxin. Ann Thorac Surg 1991;51:964–967. 62. Van Mieghem W, Coolen L, Malysse I, et al. Amiodarone and the development of ARDS after lung surgery. Chest 1994;105:1642–1645. 63. Lanza LA, Visbal AI, DeValeria PA, et al. Low-dose amiodarone prophylaxis reduces atrial ﬁbrillation after pulmonary resection. Ann Thorac Surg 2003;75:223–230. 64. Van Miegham W, Titis G, Demuynck K, et al. Verapamil as prophylactic treatment for atrial ﬁbrillation after lung operations. Ann Thorac Surg 1996;61:1083–1085. 65. Amar D, Roistacher N, Rusch VW, et al. Effects of diltiazem prophylaxis on the incidence and clinical outcome of atrial arrhythmias after thoracic surgery. J Thorac Cardiovasc Surg 2000;120:790–798. 66. Deslauriers J, Aucoin A, Gregoire J. Early complications: postpneumonectomy edema. Chest Surg Clin North Am 1999;9:565–585. 67. Zeldin RA, Normandin D, Landtwing D, Peters RM. Postpneumonectomy pulmonary edema. J Thorac Cardiovasc Surg 1984;87:359–365. 68. Waller DA, Keavey P, Woodﬁne L, Dark JH. Pulmonary endothelial permeability changes after major lung resection. Ann Thorac Surg 1996;61:1435–1440. 69. Turnage WS, Lum JJ. Postpneumonectomy pulmonary edema. a retrospective analysis of associated variables. Chest 1993;103:1646–1650. 70. Nabers J, Hoogsteden HC, Hilvering C. Postpneumonectomy pulmonary edema treated with a continuous positive airway pressure face mask. Crit Care Med 1989;17:102– 103.

71. Mathisen DJ, Kuo EY, Hahn C, et al. Inhaled nitric oxide for adult respiratory distress syndrome after pulmonary resection. Ann Thorac Surg 1998;66:1984–1992. 72. Gattinoni L, Presenti A, Mascheroni D, et al. Lowfrequency positive-pressure ventilation with extracorporeal CO2 removal in severe acute respiratory failure. JAMA 1986;256:881–886. 73. Slinger PD. Perioperative ﬂuid management for thoracic surgery: the puzzle of postpneumonectomy pulmonary edema. J Cardiothorac Vasc Anesth 1995;9:442–451. 74. Mehran RJ, Deslauriers J. Late complications: postpneumonectomy syndrome. Chest Surg Clin North Am 1999; 9:655–673. 75. Grillo HC, Shepard JA, Mathisen DJ, Kanarek DJ. Postpneumonectomy syndrome: diagnosis, management, and results. Ann Thorac Surg 1992;54:638–650. 76. Shamji FM, Deslauriers J, Daniel TM, et al. Postpneumonectomy syndrome with an ipsilateral aortic arch after left pneumonectomy. Ann Thorac Surg 1996;62:1627– 1631. 77. Shepard JA, Grillo HC, Mcloud TC, et al. Rightpneumonectomy syndrome: radiologic ﬁndings and CT correlation. Radiology 1986;161:661–664. 78. Adams HD, Junod F, Aberdeen E, Johnson J. Severe airway obstruction caused by mediastinal displacement after right pneumonectomy in a child. a case report. J Thorac Cardiovasc Surg 1972;63:534–539. 79. Powell RW, Luck SR, Raffensperger JG. Pneumonectomy in infants and children: the use of a prosthesis to prevent mediastinal shift and its complications. J Pediatr Surg 1979;14:231–237. 80. Wasserman K, Jamplis RW, Lash H, et al. Post-pneumonectomy syndrome. Surgical correction using Silastic implants. Chest 1979;75:78–81. 81. Audry G, Balquet P, Vazquez MP, et al. Expandable prosthesis in right postpneumonectomy syndrome in childhood and adolescence. Ann Thorac Surg 1993;56: 323–327. 82. Evans GH, Clark RJ. Management of life threatening adult postpneumonectomy syndrome. Anaethesia 1995; 50:148–150. 83. Shah R, Sabanathan S, Mearns AJ, Featherstone H. Selfexpanding tracheobronchial stents in the management of major airway problems. J Cardiovasc Surg 1995;36:343– 348. 84. Kelly RF, Hunter DW, Maddaus MA. Postpneumonectomy syndrome after left pneumonectomy. Anaethesia 2001;71:701–703. 85. Wihlm J-M, Massard G. Late complications: late respiratory failure. Chest Surg Clin North Am 1999;9:633– 654. 86. Schnabel TG Jr, Ratto O, Kirby CK, et al. Postural cyanosis and angina pectoris following pneumonectomy: relief by closure of an interatrial septal defect. J Thorac Surg 1956;32:246–250. 87. Rao PS, Sideris EB, Hausdorf G, et al. International experience with secundum atrial septal defect occlusion by the buttoned device. Am Heart J 1994;128:1022–1035. 88. Godart F, Porte HL, Rey C, et al. Postpneumonectomy interatrial right-to-left shunt: successful percutaneous treatment. Ann Thorac Surg 1997;64:834–836.

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Chest Wall Resections Jessica S. Donington, MD INTRODUCTION Indications for chest wall resections are listed below, malignancy is the most common indication today.1 Resections for malignancy are performed for primary chest wall malignancies, metastatic spread to the chest wall from distant sites, or direct extension from lung cancer or breast cancer. Chest wall resections must be discussed hand-inhand with reconstruction. The tenets of chest wall resection and reconstruction are (1) remove all malignant or devitalized tissue, (2) restore rigidity to large chest wall defects to prevent ﬂail chest, and (3) provide healthy soft tissue coverage that will seal the pleural space, protect underlying organs, and prevent infection. Functional reconstruction can often be more difﬁcult than the resection for these cases. These patients are best cared for by a team of physicians, including reconstructive and thoracic surgeons. Appropriate planning is required prior to the start of surgery to ensure that adequate margins are obtained while necessary muscles and soft tissues needed for reconstruction are preserved.

MAJOR INDICATIONS ● Malignancy ● Infection ● Radiation injury

LESS COMMON INDICATIONS ● Congenital abnormalities ● Trauma

PREOPERATIVE PREPARATION Planning and Consultation Poor Planning and Lack of Preoperative Consultation ● Consequence Poor planning and lack of preoperative consultation with a reconstructive surgeon can leave the thoracic

surgeon alone in the operating room with a defect larger than anticipated and inadequate tissue to restore chest wall rigidity and provide soft tissue coverage. Grade 1/2 complication ● Repair Intraoperative consultation is necessary to provide closure, but it may require extensive operating time and tissue manipulation if the patient is not appropriately prepared or positioned. It may necessitate a staged operation to complete reconstruction. ● Prevention Consult a reconstructive surgeon prior to any chest wall resection that may result in a wound larger than 4 cm with concern for soft tissue coverage.

HISTORY The ﬁrst reported chest wall resection was by Aimar in 1778; the next reports are from Parham in 18982 and Lund in 1913.3 Airway control, positive-pressure ventilation, and closed chest drainage systems were introduced at the end of the 19th century. These technologies and the expanded use of antibiotics dramatically advanced the ﬁeld of thoracic surgery. In the 1930s and 1940s, large series of chest wall resections were published by Hedblom,4 Harrington,5 and Zinniger.6 At that time, operative mortality was as high as 29%. In the 1940s, treatment of injuries from World War II brought signiﬁcant advancements in the management of infected pleural spaces, ventilatory mechanics, and reconstructive techniques with soft tissue coverage. Fascia lata grafts for large bony defects and rib grafts for sternal reconstruction were described.7,8 One of the major advancements in chest wall reconstruction has been the use of musculocutaneous ﬂaps. Latissimus dorsi ﬂaps for the reconstruction of chest wall defects after radical mastectomy were ﬁrst described by Tansini as far back as 1906.9 Campbell10 also described use of musculocutaneous ﬂaps in the 1950s, but the frequent use of muscle ﬂaps for chest wall reconstruction did not begin until 1977, when Jurkiewicz and associates11 at Emory University began using them regularly. Their techniques are widely used today, and rotational muscle ﬂaps are the workhorses of chest wall reconstruction. All major tho-

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racic muscles, including the latissimus dorsi, pectoralis major and minor, serratus anterior, rectus abdominis, and external obliques, can be used in chest wall reconstruction. With use of these modern techniques, autologous soft tissue coverage is almost always possible, even for the most aggressive chest wall resections. This chapter speciﬁcally addresses chest wall resections for primary chest wall tumors and chest wall resections performed en bloc with lung resections for direct extension from a bronchogenic carcinoma, with special consideration to Pancoast’s tumors and sternal resections for infection.

Resection of Primary Chest Wall Tumors Chest wall tumors generally present as slowly growing asymptomatic masses. Fifty percent to 80% of primary chest wall tumors are malignant. The most common malignant tumors of the chest wall are malignant ﬁbrous histocytomas (MFH), chondrosarcoma, and rhabdomyosarcomas. The most common benign tumors are chondromas, osteochondromas, and desmoid tumors.1,12 Evaluation of patients with chest wall tumors includes a history and physical examination and conventional x-rays compared with previous x-rays, if available, to document rate of growth. In general, magnetic resonance imaging (MRI) is the preferred method for imaging primary chest wall malignancies. MRI allows visualization of the tumor in multiple planes and is superior to computed tomography (CT) at distinguishing tumor from nerves and vasculature. CT also plays a vital role because it is superior to MRI for evaluation of the pulmonary parenchyma for metastatic involvement. Each resection is unique, but the basic steps of the operation are outlined here.

OPERATIVE STEPS Biopsy Determine necessary resection margin Consider consultation with reconstructive surgeon Step 4 Epidural catheter, double-lumen endotracheal tube, and positioning Step 5 Skin incision Step 6 Dissection to chest wall Step 7 Enter pleural space Step 8 Palpate tumor inside of chest Step 9 Divide intercostal muscles Step 10 Resect ribs Step 11 En-bloc resection of involved underlying structures Step 12 Chest tube insertion Step 1 Step 2 Step 3

Step 13 Mesh reconstruction of bony chest wall Step 14 Soft tissue coverage Step 15 Skin closure

Biopsy Primary chest wall tumors require tissue diagnosis prior to treatment. A well-performed biopsy is one of the keys to the successful management of these tumors. An incorrectly placed biopsy or inadequate tissue sampling can severely compromise treatment. To allow for proper technique and placement, it is best if the surgeon who will perform the deﬁnitive resection also performs the biopsy. The biopsy needs to allow for maximal tissue for pathologic evaluation; small incisional biopsies and needle biopsies obtain limited amounts of tissue and can lead to misdiagnosis of low-grade malignancies. At tertiary cancer centers, core needle biopsy for diagnosis has been advocated, but only with the support of a specialized cytopathologist.13 At most other institutions, excisional biopsies are preferred for tumors smaller than 4 cm. The best chance for cure of low-grade malignancies is wide resection; without an adequate amount of tissue for diagnosis, the opportunity for cure can be missed. For tumors larger than 4 cm, an incisional biopsy is usually necessary. The skin incision for the biopsy needs to be placed so that it can be completely removed at the time of deﬁnitive resection and does not compromise any of the soft tissue or vasculature necessary for reconstruction. Soft tissue dissection should be minimal; tissue ﬂaps should not be raised. The capsule of the mass should be closed after the biopsy to reduce tumor spillage. Careful operative technique is essential. A wound infection can signiﬁcantly delay chemotherapy, radiation therapy, or deﬁnitive surgery, and a hematoma can lead to signiﬁcant soft tissue contamination, resulting in a larger deﬁnitive resection.

Incorrectly Performed Biopsy ● Consequence Incorrectly performed biopsies can result in inadequate tissue for diagnosis, contaminated tissue planes, and unnecessary sacriﬁce of skin and soft tissue. Grade 2/3 complication ● Repair Deﬁnitive diagnosis is imperative, and a repeat biopsy may be needed if only a small tissue sample was obtained at the initial biopsy attempt. Because complete resection with wide margins is essential for cure, an improperly performed biopsy can lead to a signiﬁcantly larger resection in order to encompass all tissue violated by a biopsy or to postbiopsy hematoma or infection. ● Prevention The surgeon who performs the resection should ideally perform the biopsy. In masses smaller than 4 cm, exci-

68 CHEST WALL RESECTIONS sional biopsy should be undertaken with plans to return for wider deﬁnitive resection if a malignant diagnosis is obtained. Incisional biopsy is used for larger tumors. The biopsy should be made as directly over the mass as possible, taking into account that the entire biopsy site will need to be removed with the deﬁnitive resection. Care should be taken to avoid vascular pedicles to musculature, which may be needed for reconstruction. Careful surgical technique and homeostasis are essential to minimize postbiopsy hematoma or infection. If incisional biopsy is needed because of tumor size, it is important that skin ﬂaps are not raised and that the deep plane of the tumor, especially the pleural surface, is not disturbed. This needs to be left intact to prevent dissemination of tumor cells.

Resection When a diagnosis has been made, deﬁnitive resection can be carried out. The surgical approach is dictated by the location, histology, and extent of overlying soft tissue involvement. Preoperative assessment by a reconstructive surgeon is essential for many of these resections. An epidural catheter is recommended for those resections that do not involve the spine. A double-lumen endotracheal tube should be used to selectively deﬂate the ipsilateral lung; this helps to avoid lung injury, facilitates wedge resections, and allows for manual palpation of the lung to rule out metastasis. Decubitus positioning is used for most thoracotomies, but it may need to be modiﬁed in these cases based on the location of the mass. If a muscle ﬂap is needed for closure, it must be considered prior to positioning and draping the patient. Obtaining adequate resection margins is essential to minimize the risk of local recurrence. The extent of resection should not be limited by the size of the resulting defect. The appropriate margin of resection for primary chest wall tumors varies depending on the type of neoplasm. High-grade tumors, such as MFH and osteogenic sarcomas, have the potential to spread within the bone marrow and along the periosteal tissue planes. Therefore, the entire involved rib, the corresponding anterior costal margin for anterior tumors, and partial resection of the ribs above and below the neoplasm should be removed. Resection of the entire sternum and bilateral costal arches is indicated for malignant tumors of the sternum. Less aggressive primary chest wall malignancies should be resected with at least 4-cm margins. In a Mayo Clinic review14 of survival after resection of primary chest wall malignancies, 56% of patients with margins 4-cm or greater were cancer free at 5 years compared with only 29% of those patients with 2-cm margins. Any attached structures including lung, thymus, pericardium, or overlying chest wall musculature, should be resected en bloc with malignant chest wall tumors. If there is any involvement of the overlying skin, at least a 1-cm margin of normal skin is recommended.15

707

Most low-grade lesions and benign tumors can be resected with 2- to 3-cm margins. The exceptions to this are desmoid tumors, which are classiﬁed as low-grade malignancies but are locally very aggressive and have a very high rate of local recurrence. These are, therefore, managed surgically like malignant chest wall lesions, and 4-cm resection margins are recommended.16 When the skin is involved, the incision is dictated by that involvement, and full-thickness resection of skin, muscle, and chest wall is undertaken in a “cookie cutter” fashion. If the mass does not involve the overlying skin and soft tissue, a standard thoracotomy-type incision can be made in the area over the mass and ﬂaps can be carefully raised and used for closure. One normal musculofascial plane should be included in the resection, but uninvolved tissues can be spared.17 The pleural space should be entered one full rib space above or below the involved tumor. The mass should be palpated on the underside of the chest wall to determine margins of resection (4 cm from the mass for malignant tumors and 2–3 cm for benign) (Fig. 68–1). Any attached structures should be resected en bloc. The lung should be palpated to evaluate for pulmonary metastases. Once the margins have been determined, the bony resection is undertaken. Electrocautery or the periosteal elevator can be used to lift the intercostal musculature and neurovascular bundle from the ribs at the superior and inferior margins of resection. At the anterior and posterior margins, cautery is used to clear a 1- to 2-cm length at each rib (Fig. 68–2). The intercostal neurovascular bundle can be divided with cautery or between clips through that space. A guillotine or shear rib cutter is used to divide the ribs. A 1-cm segment of each rib should be removed at the resection margin and submitted for pathologic examination after decalciﬁcation (Fig. 68–3). Any questionable soft tissue margin should be submitted for frozen section evaluation. One cannot overemphasize the importance

Figure 68–1 The surgeon palpates the tumor inside of the chest to determine the margins of resection.

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Figure 68–2 The intercostal muscles and neurovascular bundles are cleared with electrocautery over a 2- to 3-cm length at each rib space.

Figure 68–3 The technique for the division or ribs with rib shear, sending 1-cm margin from each rib for evaluation after decalciﬁcation.

of a wide resection with clear margins at the primary resection.

Reconstruction The goals of reconstruction include restoring the structural stability of the thorax and providing soft tissue coverage. In general, defects smaller than 4 cm do not require reconstruction of the bony portion of the chest wall. Fullthickness defects of the chest wall greater than 4 cm require reconstruction. The exception is high posterior defects, because the overlying scapula provides support. Defects located near the tip of the scapula need to be reconstructed to prevent impingement of the scapula with arm movement, which can be painful. The choice of material for reconstruction remains controversial. Autologous tissues such as fascia lata and ribs have been used,7,8 but

Figure 68–4 Mesh replacement is ﬁxed with large monoﬁlament suture around the ribs at the upper and lower extent of resection and through drilled holes in the cut ribs. The mesh is best ﬁxed to the underside of the chest wall, so it is not pushed away from the chest wall with each breath.

prosthetic meshes are used most commonly today. The prosthetic materials most frequently used are polypropylene mesh (Marlex; Bard, Cranston, RI) and polytetraﬂuoroethylene (PTFE/Gore-Tex; W.L. Gore and Associates, Newark, DE). The Marlex mesh has interstices that allow for ingrowth of ﬁbrin. It can be used in two layers with methyl methacrylate as a sandwich for contoured reconstructions. Marlex is not watertight. Gore-Tex is watertight and required when the skeletal resection accompanies a pneumonectomy, so that the pneumonectomy space can ﬁll with ﬂuid. Otherwise, both work equally well and are used at the surgeon’s discretion. In situations in which infection is present or the viability of soft tissue coverage is questionable, the newly available acellular dermal matrixes (Derma Matrix; Musculoskeletal Transplant Foundation, Edison, NJ), derived from cadaver skin, can be used to provide structural support to the chest wall. The mesh or dermal matrix is sewn in place with heavy monoﬁlament suture. It should be anchored around the ribs at the inferior and superior margins. To facilitate ﬁxation of the anterior and posterior margins without compromise of neurovascular structures, drilled holes in the ribs are recommended. These should be placed at least 1 cm back from the resection margin (Fig. 68–4). A handheld pneumatic drill is preferred to towel clips and rib punches because it creates less crush injury to the bone (Fig. 68–5). If the chest wall musculature has been removed, direct skin closure over the prosthesis is not recommended. Muscle or other soft tissue coverage is necessary and can be provided via a pedicled rotational ﬂap from the pectoralis major or minor, serratus, latissimus, or rectus muscles. If those muscles are inadequate or not available, an omentum or a muscular free ﬂap is used. The majority of large defects do not result in impairment of respiratory mechanics when properly reconstructed. Large anterior defects are most likely to create any risk of respiratory

68 CHEST WALL RESECTIONS

A

B Figure 68–5 A young male with a recurrent desmoid tumor of the right lateral chest wall. A, The resulting chest wall defect after resection. B, Patch reconstruction of the bony chest wall with dermal matrix.

compromise, secondary to the resulting weak cough and retention of secretions. Aggressive postoperative pulmonary toilet and bronchoscopy may be necessary in these patients. There is no advantage to empirically prolonged postoperative intubation; it provides no increase in stability of the reconstruction. Every effort should be made to extubate these patients in the operating room.

Chest Wall Resections for Lung Cancer Lung cancer is the leading cause of cancer death worldwide, with greater than 1 million new cases each year. Five percent to 8% of patients with non–small cell lung cancer (NSCLC) have contiguous chest wall involvement.18 Historically, these tumors were considered unresectable until Coleman’s series in 1947.19 Five patients survived, and two had long-term cure after resection of a lung with

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en-bloc removal of the chest wall for lung cancer. These are currently recognized as T3 tumors. In the absence of lymph node metastasis, survival rates after complete resection are 45%.20 The most common presenting symptom is pain, which occurs in 37% to 75% of patients.19,21,22 Preoperative evaluation includes the standard evaluation for patients undergoing NSCLC operations. This includes staging and metastatic work-up with CT and positron-emission tomography (PET), cardiopulmonary evaluation, and determination of pulmonary reserve with pulmonary function tests. In general, mediastinoscopy is performed at the discretion of the surgeon; however, if there is any suspicion of mediastinal lymph node involvement on CT or PET scan at station 2R, 4R, 2L, 4L, or 7, mediastinoscopy is a necessity prior to resection. Patients who are found to have N2 disease should consider chemoradiotherapy as either induction or deﬁnitive therapy. Appropriate anticipation and preparation for chest wall resection is one of the keys to a successful operation. Signs of chest wall invasion on CT include evidence of rib destruction, obliteration of the extrapleural fat pad, an obtuse angle of interface between the tumor and the chest wall, extended length of the tumor-pleural interface, and the relation between the length of that interface and the size of the tumor.23,24 MRI can be useful, as in primary chest wall tumors; it is superior to CT at delineating soft tissue invasion (Fig. 68–6).

OPERATIVE PROCEDURE Once the preoperative staging work-up is complete, the patient can move to thoracotomy. Some surgeons advocate thoracoscopy to evaluate for chest wall invasion.25 This step is largely unnecessary unless the tumor is so large that there is concern about where to safely enter the chest cavity. Thoracoscopy is an inadequate tool to assess chest wall invasion or to resect these aggressive tumors. Standard thoracotomy can be performed with care taken to enter the chest away from the area of chest wall involvement. Once inside the pleural space, evaluation for chest wall invasion is the ﬁrst step and vital to good outcome. If only ﬂimsy, inﬂammatory-type adhesions are present, they can be gently taken down or removed by extrapleural dissection. If there is any concern of invasion into the chest wall, an en-bloc resection should be performed. Numerous studies have demonstrated that an extrapleural dissection in this situation is inadequate.26–28 Inappropriate evaluation at this point can be costly, because frozen section evaluation of the chest wall margin is not very useful. There is typically a large tissue plane, and signiﬁcant sampling error can occur. Complete resection is one of the main determinants of long-term survival29; therefore, this initial assessment is extremely important and should be performed with great care.

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A

C

B

Figure 68–6 The computed tomography (CT) scan (A), positron-emission tomography (PET) scan (B), and magnetic resonance imaging (MRI) (C) from a 65-year-old man with a T3N0M0 bronchogenic carcinoma of the right upper lobe involving the posterior aspects of ribs 3, 4, and 5. The patient presented with right-sided back pain.

Determine Necessary Resection Margin Inaccurate Evaluation and Incomplete Resection ● Consequence Inaccurate evaluation of chest wall invasion can lead to an incomplete resection that is typically not detected until the ﬁnal pathologic evaluation. Incomplete resection is one of the main determinants of poor survival. Grade 4 complication ● Repair If, while taking down ﬁlmy adhesions or performing extrapleural dissection, there is any signiﬁcant resistance from the tissues, the dissection should be aborted and en-bloc chest wall and lung resection performed, including wide resection of the chest wall around the area of dissection. ● Prevention The surgeon should have a low threshold for removal of the chest wall en bloc with a closely adherent lung cancer because of the overwhelming importance of negative surgical margins for long-term survival.

Dissection to the Chest Wall Once the determination for the need of a chest wall resection is made, the procedure starts; this includes formal lobectomy with complete hilar and mediastinal dissection and chest wall resection. The extent and location of chest wall involvement dictate the order of the procedure. Often, the chest wall resection is done ﬁrst and dropped into the chest to provide hilar exposure. If the tumor is very large and its bulk hinders exposure to the hilum, a stapler can be ﬁred through the normal lung to wedge the mass out and provide exposure for the lobectomy. Most of these operations are best approached through a standard posterolateral thoracotomy to allow maximal exposure to the hilum of the lung for the lobectomy and mediastinal lymph node dissection. Exposure for the chest wall resection may require extension of that incision and division of both the latissimus and the serratus muscles. The rib spreader can provide exposure to the chest wall by placing one blade in the rib space and the other under the chest wall musculature. For upper lobe tumors, the inferior blade is placed in the rib space and the cephalad blade is placed under the tip of the scapula (Fig. 68–7).

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anterior Pancoast’s tumors, which often require two incisions.

Enter the Pleural Space

Figure 68–7 Rib spreader placed with the inferior blade in the rib space and the cephalad blade retracting the scapula upward to expose the chest wall for resection of an upper lobe tumor invading the chest wall.

As the retractor is opened, it lifts the scapula and chest wall musculature off the chest wall, similar to opening the hood of a car. For lower lobe tumors that involve the chest wall below the thoracotomy, the upper blade of the rib spreader is placed in the rib space and the more caudal blade is used to retract back the skin and the overlying chest wall muscles. Without the scapula there, perforating towel clips can be used to keep the rib spreader from slipping.

Inappropriate Placement of the Skin Incision and Thoracotomy ● Consequence Placing the skin incision and thoracotomy over the area of chest wall involvement may facilitate the rib resection, but it will make the lobectomy and mediastinal lymphadenectomy technically challenging. Grade 1/2 complication ● Repair If the entrance into the pleural space is too high or too low to allow for safe and complete hilar dissection for the lobectomy, a second thoracotomy can be made through the same skin incision at the ﬁfth intercostal space to facilitate the lobectomy and mediastinal lymph node dissection. ● Prevention A better approach is to perform a generous, standard posterolateral thoracotomy, which provides the best exposure to the hilum for the lobectomy, and use the rib spreader with one blade in the rib space and the other under the chest wall musculature to provide exposure for the chest wall resection. The exception is

The chest wall is removed with at least a 2-cm margin. Margins do not need to be as wide as those for primary chest wall tumors. The resection of the bony chest wall proceeds as described in the previous section. The overlying chest wall musculature does not need to be resected unless it is directly involved with the tumor. The principles of reconstruction are also similar to those described in the previous section. Small bony defects and those under the protection of the scapula do not require reconstruction; others are reconstructed with a mesh or dermal matrix patch. Tumors near the spine require special attention. Tumors that invade the spine are T4 and require consultation with a spinal surgeon. For tumors that approach the spine but do not invade it, the rib can be disarticulated from its transverse process or the head of the rib can be resected en bloc with the transverse process using an osteotome. To perform either maneuver, the paraspinous muscles, costotransverse ligaments, and costovertebral ligaments are lifted off the exterior of the chest wall with cautery past the midline to expose the joints. Inside the chest, the parietal pleura is elevated off of the anterior spinal column and resected with the tumor. The joint is disarticulated or resected ﬂush against the vertebral body, and the rib is pushed anterior into the chest. This will expose the nerve root, which is clipped and divided close to where it exits the canal. Inappropriate traction at this location or mismanagement of the nerve root can result in an iatrogenic subarachnoid pleural ﬁstula. This can result in a large pleural effusion as a result of cerebrospinal ﬂuid (CSF) leak, tension pneumocephalus, or meningitis.

Excessive Traction and Avulsion of the Dorsal Nerve Roots ● Consequence Excessive traction and avulsion of the dorsal nerve roots as they exit the spinal canal can result in a dural tear and a communication between the intracranial vault and the pleural space. This can result in a postoperative CSF leak, tension pneumocephalus, or meningitis. Grade 2/3 complication ● Repair Subarachnoid pleural ﬁstulas that are not recognized in the operating room are usually discovered in the ﬁrst postoperative week,30 when patients present with excessive chest tube output or neurologic symptoms. Conservative management involves antibiotics, bedrest with a ﬂat head position, and placement of a chest tube to water seal.31 Suction on the chest tube should be avoided when possible to prevent CSF extravasation,

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but resolution of pneumothorax is an important part of treatment. Therefore, low suction may be necessary if the air leak is signiﬁcant.30 These maneuvers usually result in an improvement in symptoms within 48 hours. Fistulas that persist for longer than 2 weeks require surgical intervention.31 Surgical strategies for repair include laminectomy with placement of an intradural or extradural patch32 or thoracoplasty with proximal nerve ligation.33 Others advocate the use of ﬁbrin sealant.34 ● Prevention Care should be taken to avoid undo traction on the dorsal nerve roots. They should be carefully identiﬁed as the rib is separated from the spine and ligated between vascular clips. If a ﬁstula is recognized in the operating room, the neural foramen can be packed with muscle and conservative management initiated postoperatively.

Bleeding from the Intercostal Artery Bleeding from the intercostal artery can be bothersome at this location, and care needs to be taken to properly identify and ligate or clip these vessels prior to transecting. Again, undo traction on the ribs can result in avulsion. Cautery in this area should be performed with bipolar or between pickups to avoid thermal injury. The routine use of radiation therapy either preoperatively or postoperatively in patients with chest wall involvement but without N2 disease remains controversial. Preoperative therapy has the potential beneﬁt of downstaging tumors and making an unresectable tumor resectable, but the majority of tumors invading the chest wall are resectable at presentation. Preoperative chemoradiotherapy has been shown to be very useful in the management of Pancoast’s tumors,35 but this approach has not been investigated for other patients with chest wall involvement. To date, preoperative therapy in patients who have resectable tumors that invade the chest wall has no proven beneﬁt. In the face of negative surgical margins, postoperative radiation therapy to the area of chest wall resection is not recommended.

Pancoast’s Tumors The classic deﬁnition of a Pancoast tumor is that of a carcinoma involving the apex of the chest that causes pain down the medial aspect of the arm and Horner’s syndrome owing to involvement of the nerve roots in the lower part of the brachial plexus and the stellate ganglion.36 Biologically, Pancoast’s tumors are not different from other NSCLCs; they are unique owing to their location. They involve structures that are technically difﬁcult to approach with surgery, and the extent of resection is limited by the risk for long-term disability. Therefore, wide local excision with negative margins can be challeng-

ing. Resection of a Pancoast tumor should include a lobectomy and removal of the affected chest wall. The importance of a complete resection with negative margins cannot be overemphasized. In up to one third of resections for Pancoast’s tumors, a complete resection is not achieved,37 and survival is no better than if surgery had not been performed.37–39 The use of neoadjuvant chemoradiation has signiﬁcantly improved the rate of R0 resection for Pancoast’s tumors, as demonstrated in the North American Intergroup Trial 0160.35 In that trial, complete resection resulted in a 5-year survival rate of 53% and a local recurrence rate of only 12%.40 Induction chemoradiotherapy resulted in a pathologic complete response rate of 66%, a signiﬁcant improvement over historic controls. No randomized, controlled trial has been done on tumors of the superior sulcus, and because of their rarity (<5% of lung cancers), completion of such a trial is unlikely. The results of the Intergroup Trial form the basis for our treatment today. It demonstrated that induction chemoradiation is safe and well tolerated and results in a high rate of tumor sterilization, a high rate of complete resection, and improved local control compared with surgery alone or preoperative radiation therapy. All patients with superior sulcus tumors, regardless of symptoms, should be considered for neoadjuvant chemoradiotherapy prior to resection. A complete understanding of the anatomy of the thoracic inlet is essential to planning a resection of a superior sulcus tumor. The thoracic inlet can be divided into three compartments based on the insertion of the anterior and middle scalene muscles (Fig. 68–8). The anterior compartment, which is anterior to the anterior scalene muscle, contains the internal jugular and subclavian veins. The middle compartment lies between the anterior and the middle scalene muscles and contains the subclavian artery and brachial plexus. The posterior compartment is behind the middle scalene and contains the nerve roots to the brachial plexus, the stellate ganglion, and the vertebrae. In general, vascular structures are anterior, and neural structures are posterior. Recognizing these differences is key to deciding on the surgical approach. Thorough preoperative evaluation of the thoracic inlet and the extent of tumor involvement is vital in planning this operation. It is essential to determine whether the tumor is resectable and the approach that will provide the best chance for a complete resection. MRI is superior to CT for evaluation of tumors in this location.41 It allows for evaluation of the tumor in the sagittal and coronal planes and is superior in determination of neurovascular involvement. Vascular involvement was once considered a contraindication to resection, but in newer series, using the anterior approach and improved surgical techniques demonstrates that good survival can be obtained in cases with vascular involvement, as long as R0 resection is obtained.42,43 Resection and reconstruction of vascular structures are technically easier from the anterior approach. Spinal involvement was also considered a contraindication to resection, but with

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OPERATIVE PROCEDURE Preoperative Evaluation Inappropriate Preoperative Evaluation ● Consequence Inappropriate preoperative evaluation of the thoracic outlet and extent of tumor involvement can result in a poor decision regarding approach and can leave the surgeon in the operating room with inadequate exposure for either vascular resection and reconstruction or spinal resection. Complete resection of the structures is possible and recommended if it will allow for an R0 resection. Negative margins have a signiﬁcant impact on survival. Grade 4 complication Figure 68–8 Schematic representation of the thoracic inlet with attention to the anterior, middle, and posterior compartments. Compartments are deﬁned by the insertion of the anterior and middle scalene muscles. The anterior compartment is anterior to the anterior scalene and contains the jugular and subclavian veins. The middle compartment lies between the anterior and the middle scalene muscle and contains the brachial plexus and subclavian artery. The posterior compartment lies behind the middle scalene muscle and contains the dorsal nerve roots, stellate ganglion, and vertebrae.

● Repair If the tumor invades more structures than originally anticipated and more extensive resection is needed, the surgeon should consider a second incision from the other side if it would make an R0 resection possible. ● Prevention Thorough preparation and evaluation of the inlet is essential in these procedures. The surgeon needs to be comfortable with both approaches, and preoperative consultation with a spine surgeon or vascular surgeon should be anticipated preoperatively.

Posterior Approach newer orthopedic techniques for vertebral resection and stabilization, long-term survival is also possible in this group of patients.44 Nerve involvement is still an important part of determining resectability. Resection of the T1 nerve root is well tolerated, but resection of the C8 nerve root or lower trunk of the brachial plexus will lead to loss of function of intrinsic musculature of the hand and is discouraged. This type of complex resection is contraindicated in any patient with N2 disease. Five-year survival is less than 10% in patients with N2 disease.38 Thorough evaluation of the mediastinal lymph nodes is vital, and most surgeons recommend mediastinoscopy. There are two basic surgical approaches to Pancoast’s tumors, the posterior approach described by Shaw and coworkers in 196145 and the anterior transclavicularthoracic or transclavicular approach described by Dartevelle and colleagues.42 There have been several modiﬁcations to the anterior approach, but all with the same goal: improved exposure to the anterior aspect of the thoracic inlet. In general, tumors in the anterior and middle compartments are best treated from an anterior approach because it allows for better exposure to the vasculature, whereas tumors involving the posterior compartment are best treated via the posterior approach. This decision as to which approach needs to be made preoperatively because positioning is signiﬁcantly different.

The posterior approach is performed with the patient in the lateral decubitus position. The incision is an extended posterolateral thoracotomy. The posterior extension runs halfway between the scapula and the spine up to the level of the seventh cervical vertebrae. Chest wall exposure is achieved by completely dividing the trapezius and rhomboid muscles. As with other chest wall tumors, the superior blade of the rib spreader is placed under the scapula to expose the chest wall. Alternatively, an internal mammary retractor can also be placed under the tip of the scapula to elevate it off the chest wall. Dissection begins by removing the scalene muscles from the upper surface of the ﬁrst and second ribs, making sure to come above any involved tumor. The inlet can now be evaluated for invasion of subclavian vessels or brachial plexus. The posterior rib dissection is performed by disarticulating the rib from the transverse spinal process or by en-bloc resection of the joint, as discussed in the previous section. This begins at the inferior aspect of the resection and proceeds toward the apex. Special care needs to be taken with the dorsal nerve roots; iatrogenic subarachnoid pleural ﬁstulas occur in up to 1% of apical lung resections.31 The anterior ribs are also approached inferiorly and moving toward the apex. The ribs and bony chest wall are divided in the manner discussed in the ﬁrst section. The ﬁrst rib is difﬁcult to take with rib shears, and a Gigli saw or oscillating

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saw is recommended. The T1 dorsal nerve root can be taken with the tumor, but sacriﬁce of higher portions of the brachial plexus will result in functional loss in the hand. Once the tumor is freed from the apex, the hilar dissection for the lobectomy proceeds as normal. Reconstruction of the chest wall defect is rarely necessary because it is all under the scapula.

Anterior Approach The anterior approach is performed with the patient supine with the neck hyperextended and the head turned away from the involved side. A bolster or roll is placed under the operative shoulder to elevate the ﬁeld. An Lshaped incision is made along the anterior border of the sternocleidomastoid and then out horizontally below the clavicle in the second intercostal space. The sternocleidomastoid and pectoralis muscles are dissected off the clavicle. The myocutaneous ﬂap is folded back to expose the anterior portion of the thoracic inlet. The omohyhoid is divided. The scalene fat pad is resected and inspected for lymph node involvement. The anterior chest is entered in a rib space below the tumor to allow palpation for further evaluation of the tumor involvement. If the tumor is believed to be resectable, the clavicle needs to be removed from the ﬁeld. The medial half of the clavicle can be resected or the sternoclavicular joint can be divided and the clavicle reﬂected laterally. The venous conﬂuence is then the most superﬁcial structure and is dissected ﬁrst. The internal jugular vein can be ligated to provide exposure, and the subclavian vein can be resected if it is involved with tumor. On the left side, care needs to be taken to identify and ligate the thoracic duct as it enters the venous conﬂuence to avoid a chylothorax. The anterior scalene muscle is divided off the ﬁrst rib, above any tumor involvement. The phrenic nerve needs to be identiﬁed as it courses over the anterior surface of the anterior scalene and protected. Unnecessary division can lead to a paralyzed hemidiaphragm and unwanted respiratory complications. The subclavian artery will now be visible. If it is involved with tumor, it needs to be resected. Dissection is undertaken to achieve good proximal and distal control away form the tumor. The vessel is cross-clamped and divided; reconstruction is usually performed with a ringed Gore-Tex vascular graft when the resection is complete. The middle and posterior scalene muscles are now divided above the tumor to expose the C8 and T1 nerve roots. The T1 nerve root is divided just lateral to the intervertebral foramen. Division of the C8 nerve should be avoided if possible. Through the transclavicular approach, the chest wall is resected anterior to posterior and superior to inferior. The ﬁrst rib is divided from the sternum at the costochondral junction, and the second rib is resected free of involved tumor. The dissection is carried down the superior surface of the ﬁrst uninvolved rib, usually the third or fourth. Cautery is used to dissect along the superior border of the uninvolved rib to the costovertebral angle. The posterior aspect of resection also starts at the top. The ﬁrst rib is then disarticulated from its vertebral

attachments, followed by ribs two and three, again taking care to identify and clip the dorsal nerve roots prior to division. At the completion of the posterior chest wall resection, the specimen should be free from the inlet with a resulting defect into the chest cavity. It is possible to perform the hilar dissection for the lobectomy through the hole, but this can be technically challenging. The surgeon needs to have a low threshold to close the anterior incision and perform a separate posterolateral thoracotomy to complete the resection rather than compromise any oncologic aspect of the lobectomy and lymph node dissection.

Infection The most common infectious indication for chest wall resection is infected sternal wounds after cardiac surgery. Sternal wound infection is a rare but devastating complication of cardiac surgery. These infections can carry signiﬁcant mortality if they are not recognized early and treated with aggressive débridement. When the median sternotomy was introduced for cardiac surgery in 1957, infection rates were 5%. Infection inevitably led to sternal dehiscence, which was associated with a 50% mortality rate.46 Early treatment protocols involved débridement and wound packing. Healing with this technique was slow, and patients frequently died from cardiac rupture or rupture of a vein graft secondary to continued infection or desiccation. The introduction of antibiotic irrigation systems with indwelling catheters was a major advancement that decreased mortality to 20%.47–49 Hospital stays remained unacceptably long, and the risk of vein graft rupture was still an issue. In the mid 1970s, the concept of wide débridement with immediate ﬂap closure was introduced. Lee and associates50 described the successful use of an omental ﬂap. Jurkiewicz and colleagues51,52 at Emory University described the use of pectoralis major muscle ﬂaps; this technique is most widely used today. This procedure has signiﬁcantly decreased the hospital stay and mortality associated with sternal wound infections.53 With the risk of mediastinitis and cardiac rupture, the morbidity and mortality associated with infected sternal wounds are higher than those of many other chest wall infections, but the principles of management are the same. The wound should be aggressively débrided of devitalized and infected bone and soft tissue and covered early with healthy, well-vascularized soft tissue. Early detection and treatment are fundamental to successful treatment of sternal wound infections. The patients who undergo coronary artery bypass grafting continue to get older and sicker. Therefore, the risk for these types of infection persist and the risk for resulting multisystem organ failure remains great. Clinical signs of infection include exposed wires, sternal instability, wound drainage, and elevated leukocyte count. Renal function needs to be carefully evaluated because renal deterioration is often the ﬁrst sign of impending multisystem organ failure.

68 CHEST WALL RESECTIONS Treatment begins with wound exploration with the patient under general anesthesia. The sternotomy wound is completely reopened. Wound cultures are taken, and all wires are removed. If infection is found, the sternal edges are resected until healthy bone with brisk bleeding is encountered. If the bone is necrotic and oozing pus, radical removal of the entire sternum is recommended.54,55 Survival with radical sternectomy is superior to débridement and reﬁxation, with or without an irrigation system.55 Costal cartilages should also be resected if they are necrotic. This aggressive approach is essential to clearing the infection and improving survival. As in chest wall resections performed for cancer, one should not let the magnitude of the resulting defect limit the extent of an appropriate resection. Adequate débridement is the hallmark of a successful outcome. Without the sternum to reafﬁx, patients are left with paradoxical chest wall motion with breathing and coughing. Muscle ﬂap coverage provides sufﬁcient stability for normal activity. Pulmonary function does not differ from that in controls, and there is no added difﬁculty with extubation.56 In the past, muscle ﬂap closure was delayed by several days to weeks, but now, immediate ﬂap closure is advocated by most. This step has signiﬁcantly shortened hospital stays and decreased mortality.54 Options for soft tissue coverage include bilateral pectoralis major ﬂaps, latissimus dorsi ﬂaps, omentum, or rectus abdominis ﬂaps. Most surgeons favor bilateral pectoralis major ﬂaps; these are large muscles that lie in the operating ﬁeld and are easy to dissect. Rectus abdominis ﬂaps are a frequent second choice. Omentum is very useful and can conform to the deepest recesses of these wounds but requires a laparotomy for harvesting. Latissimus dorsi ﬂaps can provide extensive tissue including skin, but they need to be placed as a free ﬂap.55

CONCLUSION The most frequent indications for chest wall resection are cancer, radiation injury, and infection. The basic principles of successful resection are the same for all indications: 1. Prompt and appropriate diagnosis is essential. 2. Preoperative consultation with a reconstructive surgeon is necessary for any chest wall resection that may result in a signiﬁcant loss of soft tissue. 3. Adequate margins of resection cannot be overemphasized—4 cm margins for high-grade sarcomas or resection of any and all devitalized tissue in the case of infection or radiation injury. Margins of resection should not be compromised by the size of the resulting defect. Adequate resection is the key to cure for each of these conditions. 4. The ideal reconstruction will seal the pleural space, restore rigidity to the chest wall, protect underlying organs, and be covered with well-vascularized soft tissue.

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22. Allen MS, Mathisen DJ, Grillo HC, et al. Bronchogenic carcinoma with chest wall invasion. Ann Thorac Surg 1991;51:948–951. 23. Ratto GB, Piacenza G, Frola C, et al. Chest wall involvement by lung cancer: computed tomographic detection and results of operation. Ann Thorac Surg 1991;51:182– 188. 24. Rendina EA, Bognolo DA, Mineo TC, et al. Computed tomography for the evaluation of intrathoracic invasion by lung cancer. J Thorac Cardiovasc Surg 1987;94:57–63. 25. Waller D, Clarke S, Tsang G, Rajesh P. Is there a role for video-assisted thoracoscopy in the staging of non-small cell lung cancer? Eur J Cardiothorac Surg 1997;12:214– 217. 26. Grillo HC, Greenberg JJ, Wilkins EW Jr. Resection of bronchogenic carcinoma involving thoracic wall. J Thorac Cardiovasc Surg 1966;51:417–421. 27. McCaughan BC, Martini N, Bains MS, McCormack PM. Chest wall invasion in carcinoma of the lung. Therapeutic and prognostic implications. J Thorac Cardiovasc Surg 1985;89:836–841. 28. Piehler JM, Pairolero PC, Weiland LH, et al. Bronchogenic carcinoma with chest wall invasion: factors affecting survival following en bloc resection. Ann Thorac Surg 1982;34:684–691. 29. Downey RJ, Martini N, Rusch VW, et al. Extent of chest wall invasion and survival in patients with lung cancer. Ann Thorac Surg 1999;68:188–193. 30. Reddy HV, Queen S, Prakash D, Jilaihawi AN. Tension pneumocephalus: an unusual complication after lung resection. Eur J Cardiothorac Surg 2003;24:171–173. 31. Bilsky MH, Downey RJ, Kaplitt MG, et al. Tension pneumocephalus resulting from iatrogenic subarachnoidpleural ﬁstulae: report of three cases. Ann Thorac Surg 2001;71:455–457. 32. Qureshi MM, Roble DC, Gindin RA, Scudamore HH. Subarachnoid-pleural ﬁstula. Case report and review of the literature. J Thorac Cardiovasc Surg 1986;91:238–241. 33. Hofstetter KR, Bjelland JC, Patton DD, et al. Detection of bronchopleural-subarachnoid ﬁstula by radionuclide myelography: case report. J Nucl Med 1977;18:981–983. 34. Morgan JA. Closure of subarachnoid-pleural ﬁstulae with ﬁbrin sealant. Eur J Cardiothorac Surg 1988;2:56–57. 35. Rusch VW, Giroux DJ, Kraut MJ, et al. Induction chemoradiation and surgical resection for non-small cell lung carcinomas of the superior sulcus: initial results of Southwest Oncology Group Trial 9416 (Intergroup Trial 0160). J Thorac Cardiovasc Surg 2001;121:472–483. 36. Pancoast HK. Superior pulmonary sulcus tumor: tumor characterized by pain, Horner’s syndrome, destruction of bone and atrophy of hand muscles. JAMA 1932;99:1391– 1396. 37. Detterbeck FC. Pancoast (superior sulcus) tumors. Ann Thorac Surg 1997;63:1810–1818. 38. Ginsberg RJ, Martini N, Zaman M, et al. Inﬂuence of surgical resection and brachytherapy in the management of superior sulcus tumor. Ann Thorac Surg 1994;57: 1440–1445. 39. Niwa H, Masaoka A, Yamakawa Y, et al. Surgical therapy for apical invasive lung cancer: different approaches according to tumor location. Lung Cancer 1993;10:63– 71.

40. Rusch VW, Giroux DJ, Kraut MJ, et al. Induction chemoradiotherapy and surgical resection for non-small cell lung carcinomas of the superior sulcus: prediction and impact of pathologic complete response. Lung Cancer 2003;41(suppl 2):S78. 41. Heelan RT, Demas BE, Caravelli JF, et al. Superior sulcus tumors: CT and MR imaging. Radiology 1989;170(3 pt 1):637–641. 42. Dartevelle PG, Chapelier AR, Macchiarini P, et al. Anterior transcervical-thoracic approach for radical resection of lung tumors invading the thoracic inlet. J Thorac Cardiovasc Surg 1993;105:1025–1034. 43. Martinod E, D’Audiffret A, Thomas P, et al. Management of superior sulcus tumors: experience with 139 cases treated by surgical resection. Ann Thorac Surg 2002;73: 1534–1539. 44. Fadel E, Missenard G, Chapelier A, et al. En bloc resection of non-small cell lung cancer invading the thoracic inlet and intervertebral foramina. J Thorac Cardiovasc Surg 2002;123:676–685. 45. Shaw RR, Paulson DL, Kee JL. Treatment of superior sulcus tumors by irradiation followed by resection. Ann Surg 1961;154:29–40. 46. Sarr MG, Gott VL, Townsend TR. Mediastinal infection after cardiac surgery. Ann Thorac Surg 1984;38:415– 423. 47. Shumacker HB Jr., Mandelbaum I. Continuous antibiotic irrigation in the treatment of infection. Arch Surg 1963; 86:384–387. 48. Bryant LR, Spencer FC, Trinkle JK. Treatment of median sternotomy infection by mediastinal irrigation with an antibiotic solution. Ann Surg 1969;169:914–920. 49. Bjerno T, Arendrup HC, Alstrup P. [Mediastinal infection following open heart surgery]. Ugeskr Laeger 1990;152: 3699–3702. 50. Lee AB Jr, Schimert G, Shaktin S, Seigel JH. Total excision of the sternum and thoracic pedicle transposition of the greater omentum; useful strategems in managing severe mediastinal infection following open heart surgery. Surgery 1976;80:433–436. 51. Jurkiewicz MJ, Arnold PG. The omentum: an account of its use in the reconstruction of the chest wall. Ann Surg 1977;185:548–554. 52. Jurkiewicz MJ, Bostwick J III, Hester TR, et al. Infected median sternotomy wound. Successful treatment by muscle ﬂaps. Ann Surg 1980;191:738–744. 53. Nahai F, Rand RP, Hester TR, et al. Primary treatment of the infected sternotomy wound with muscle ﬂaps: a review of 211 consecutive cases. Plast Reconstr Surg 1989;84: 434–441. 54. Jones G, Jurkiewicz MJ, Bostwick J, et al. Management of the infected median sternotomy wound with muscle ﬂaps. The Emory 20-year experience. Ann Surg 1997;225:766– 776. 55. Wettstein R, Erni D, Berdat P, et al. Radical sternectomy and primary musculocutaneous ﬂap reconstruction to control sternal osteitis. J Thorac Cardiovasc Surg 2002; 123:1185–1190. 56. Larson DL, McMurtrey MJ. Musculocutaneous ﬂap reconstruction of chest-wall defects: an experience with 50 patients. Plast Reconstr Surg 1984;73:734–740.

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Thymectomy and Resection of Mediastinal Masses Felix G. Fernandez, MD and Daniel Kreisel, MD, PhD INTRODUCTION The mediastinum can be divided into separate anatomic compartments, the anterior, middle or visceral, and posterior mediastinum.1 Tumors requiring surgical attention generally originate in the anterior and posterior compartments in this three-compartment model. Common anterior mediastinal tumors include thymic tumors, thyroid tumors, lymphomas, and tumors of germ cell origin. Thymic tumors are the most frequently seen among this group. Posterior mediastinal tumors are most often neurogenic in origin, arising from intercostal nerves, sympathetic ganglia cells, or paraganglia cells. This chapter therefore examines complications of mediastinal surgery in the context of thymectomy and resection of posterior mediastinal neurogenic tumors.

● Encapsulated or invasive thymomas ● Thymic carcinoma

OPERATIVE STEPS OF RADICAL TRANSSTERNAL THYMECTOMY 4 Step 1 Step 2 Step 3 Step 4 Step 5 Step 6

Median sternotomy Dissection of thymus off pericardium and encircling in midline Dissection of thymus off right pleura and pericardium Dissection of cervical extent of right thymic lobe from carotid artery and strap muscles Left lateral and cervical thymic dissections Dissection of inferior thymus from phrenic nerve to phrenic nerve Sternal closure

Thymectomy

Step 7

Although it has not been evaluated prospectively, thymectomy has become standard therapy for myasthenia gravis based on signiﬁcant retrospective data.2,3 Two major surgical approaches for thymectomy have evolved, transsternal and transcervical thymectomies, with video-assisted thoracic surgery (VATS) resection of the thymus also a viable alternative. All procedures allow for extracapsular resection of the thymus but vary in the extent of mediastinal fat removed, which may contain ectopic foci of thymic tissue. Transcervical thymectomy has been shown to be less morbid and costly than the transsternal approach. Controversy exists as to whether response rates are similar with each procedure. For thymomas or thymic carcinomas, however, a transsternal approach is indicated. Major indications for thymectomy include thymic hyperplasia associated with myasthenia gravis, encapsulated or invasive thymomas, and thymic carcinoma.

OPERATIVE STEPS OF TRANSCERVICAL THYMECTOMY 5

INDICATIONS

Sternal Disruption and Mediastinitis

● Myasthenia gravis ● Thymic hyperplasia

Step 1 Step 2 Step 3 Step Step Step Step

4 5 6 7

Low cervical incision and splitting and elevation of strap muscles in midline to expose thymus Mobilization of superior poles of thymus and ligation near inferior thyroid vein Thymic dissection continued inferiorly into thoracic inlet Thymic veins divided posteriorly Inferior thymic poles dissected along pleura Inferior thymic poles swept off pericardium Cervical wound closure

OPERATIVE PROCEDURE Median Sternotomy ● Consequence Sternal disruption impairs the respiratory mechanics of the patient and may result in respiratory embarrassment

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requiring mechanical ventilation. Underlying mediastinal infection may produce sepsis including fevers, rigors, and hypotension. The incidence of sternal disruption is reported to be between 1% and 4%.3,6,7 Grade 3/4 complication ● Repair If a sternal disruption with underlying mediastinitis is detected early, the wound may be débrided and drained with primary sternal closure. For lateral weakness or fractures in the sternum, a lateral longitudinal wire support as described by Robicsek8 may be used. Muscle transposition ﬂaps are generally the preferred option, however, especially in the setting of extensive mediastinitis or sternal disruption.9

● Prevention Visualization of this thymic vessel is essential to prevent injury. As one dissects under the thymus from an inferior-to-superior direction, one must anticipate the position of the brachiocephalic vein and look for the thymic vein entering, typically, the inferior surface of this vessel (Figs. 69–1 and 69–2). Typically, there are two veins. The dissection should not stray from the surface of the pericardium. When using a transcervical approach, the thymus is dissected off the anterior surface of the brachiocephalic vein and the thymic veins

Brachiocephalic vein Thymic vein divided

● Prevention Preoperative antibiotics covering typical skin ﬂora should be administered prior to skin incision. The surgeon should ensure that the sternum is divided in the midline. There is no evidence that the use of closed suction drains reduces the incidence of mediastinitis or sternal wound infections.

Dissection of the Thymus off the Pericardium and Encircling in the Midline Injury to the Thymic Veins or the Brachiocephalic Vein As the thymus is dissected off the pericardium in a caudalto-cephalad direction in order to encircle it with a tape, the thymic vein draining thymic blood into the brachiocephalic vein is invariably encountered. This vein is typically located near the midline originating off the inferior border of the brachiocephalic vein. Failure to recognize this vein or too vigorous retraction of the thymic tissue may result in injury to either the thymic or the brachiocephalic veins.

Figure 69–1 Dissection on the inferior border of the brachiocephalic vein reveals the thymic vein near the midline. This vein can be transected between ligatures. (Reproduced with permission from Elsevier from Mason D. Radical transsternal thymectomy. Oper Tech Thorac Cardiovasc Surg 2005;10:231–243.)

● Consequence Injury to these veins results in bleeding with uncontrolled transection, which can be signiﬁcant if the brachiocephalic vein is injured. If a transcervical approach is used, a median sternotomy may be necessary to provide exposure to control hemorrhage. Ligation of the brachiocephalic vein may result in edema of the left upper extremity, although reports indicate that the edema will eventually resolve.10 If the pleural spaces are open, blood may drain into a hemothorax. Thrombosis of the subclavian vein has also been reported.11 Grade 1 complication ● Repair Thymic vein injuries may be simply ligated or oversewn. Injuries to the brachiocephalic vein may require lateral venorrhaphy, end-to-end anastomosis, or ligation. Tube thoracostomy may be required if a hemothorax develops. Subclavian vein thrombosis must be treated with anticoagulation.

Figure 69–2 Operative photograph demonstrates the thymic vein ligated on the inferior border of the brachiocephalic vein.

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719

are visualized and controlled posteriorly. Ventilatory volume and rate may be reduced to facilitate exposure of the mediastinum. Occasionally, the upper poles of the thymus are located posterior to the innominate vein, and this variant should be recognized.

Dissection of the Thymus off the Right Pleura and the Pericardium Phrenic Nerve Injury As the thymus is dissected off the pleura and pericardium, the phrenic nerve may be contused or divided. Phrenic nerve injuries during thymectomies are reported to occur in 0% to 4.5% of cases.6,7,12,13 ● Consequence Injury to the phrenic nerve can result in paralysis of the ipsilateral diaphragm, which may be transient in the setting of a neurapraxia or permanent if the nerve has been transected. This may result in respiratory insufﬁciency with prolonged mechanical ventilation, increased intensive care unit stay and development of respiratory infections.14 Forced vital capacity has been shown to be reduced after phrenic nerve injury.15 Spontaneous recovery of phrenic nerve function may be anticipated in about two thirds of patients in whom the injury is identiﬁed postoperatively.15 Most patients, however, are asymptomatic. Grade 1/2/3 complication ● Repair A primary repair of the phrenic nerve may be attempted, but function is generally not restored. In cases of respiratory impairment, transthoracic diaphragmatic plication to ﬂatten the diaphragm may be an effective means of treatment.14 ● Prevention The surgeon must visualize both phrenic nerves during dissection of the thymic lobes off of the pleura and pericardium. The phrenic nerves are less obvious in the superior part of the mediastinum and thymus, and adipose tissue must be dissected carefully without excessive traction in this area to avoid injury. Dissection of the left side may be more challenging because the phrenic nerve may follow a more intimate course with the lateral portion of the thymus. The pleura may be incised to facilitate visualization of the phrenic nerves from within the thoracic cavities (Fig. 69–3). The pleura may be incorporated into the thymic specimen if dense adhesions are present. Dissection with cautery at low power in a patient who is free of muscle relaxants should allow one to see or feel the diaphragm move, indicating proximity to the phrenic nerve. The artery accompanying the phrenic nerve provides some blood supply to the thymus, and these small vessels should be divided with hemoclips not cautery to avoid thermal injury to the nerve. Thymomas occasionally extend into

Figure 69–3 With the pleural reﬂection opened, the phrenic nerve is easily visible.

Vagus nerve Aorta AP window thymoma Pulmonary artery

Phrenic nerve

Figure 69–4 Extension of the thymus into the aortopulmonary window. Thymic tumors may come in close proximity to or invade the phrenic nerve in this location. (Reproduced with permission from Elsevier from Mason D. Radical transsternal thymectomy. Oper Tech Thorac Cardiovasc Surg 2005;10:231–243.)

the aortopulmonary window, and this is the most frequent site of phrenic nerve involvement (Fig. 69–4). A hemi-clamshell incision or left thoracoscopy may improve exposure in these instances.

Recurrent Laryngeal Nerve Injury ● Consequence The incidence of damage to the recurrent laryngeal nerve is reported to be between 0% and 4.5%.6,7,12 Injury to the recurrent laryngeal nerve results in ipsilateral vocal cord paralysis with the cord generally in an abducted paramedian position preventing adequate airway sealing. Recurrent laryngeal nerve palsy may be devastating in the early postoperative period owing to

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an inability to cough and clear secretions. Aspiration is also a risk, especially in older patients. Long-term disabilities may include hoarseness, shortness of breath, swallowing difﬁculties, and chronic aspiration. Older patients and those with lung disease are less tolerant of vocal cord paralysis. Patients with bilateral injuries can potentially have compromise of their airway. Spontaneous recovery of nerve function is expected in the majority of patients. Grade 2/3/4 complication ● Repair None. Medialization of the paralyzed vocal cord with autologous fat, Teﬂon, gelatin, or collagen may be attempted to palliate symptoms. These substances create a rigid structure against which the normal vocal cord apposes during cough, thereby sealing the airway.16 ● Prevention Surgeons should be aware of the intrathoracic anatomy of the recurrent laryngeal nerves. The recurrent nerves should never be handled directly or encircled for retraction purposes. A common site of injury during thymectomy is in the subaortic region near the ligamentum arteriosum. When thymic or mediastinal tumors are present in the aortopulmonary window, a hemiclamshell incision or left thoracoscopy may be incorporated to improve exposure, as previously mentioned. In addition, accessory thymic lobules may be present posterior to the superior lobe of the thyroid, and the recurrent laryngeal nerves must be identiﬁed and preserved when dissecting in this area6 (Fig. 69–5).

Pneumothorax and Hydrothorax Opening of the pleural spaces during thymectomy may result in the accumulation of air or ﬂuid. The incidence of these complications ranges from 2% to 4.5%.11,12 ● Consequence The accumulation of air or ﬂuid in the pleural spaces can result in collapse of pulmonary parenchyma and lead to impairments of ventilation and/or oxygenation. In extreme cases, a tension pneumothorax may result. Grade 2 complication ● Repair The large majority of small pneumothoraces will resolve on their own. Large pneumothoraces and hydrothoraces should be evacuated with a thoracostomy tube. ● Prevention As the thymic lobes are dissected off the right and left pleural surfaces, entry into the pleural spaces is common. If the pleural spaces have been entered, air may be evacuated with a small rubber catheter prior to wound closure. If, during the pleural dissection, the pulmonary parenchyma has been injured producing an air leak, a chest tube should be left in that pleural cavity.

3

2

4

1

Figure 69–5 The anatomic relationship of the cervical thymus and its variations and the recurrent laryngeal nerves (arrow). (1) Cervical portion of the left cervical-mediastinal lobe; (2) the thymus superior to the ﬁbrous cord, which may be continuous or discontinuous; (3) an accessory thymic lobule behind the superior lobe of the thyroid; (4) an accessory lateral cervical thymic lobe. (1–4, Reproduced with permission from Elsevier from Jaretzki A 3rd, Wolff M. “Maximal” thymectomy for myasthenia gravis. Surgical anatomy and operative technique. J Thorac Cardiovasc Surg 1988;96:711–716.)

Myasthenic Crisis Myasthenic crisis is deﬁned by the need for mechanical ventilatory support. The incidence of this complication after thymectomy for myasthenia gravis is reported to range between 6% and 33%.13,17,18 Crisis is preceded by progressive weakness, oropharyngeal symptoms, refractoriness to anticholinergic medication, and intercurrent infection in most patients. One study reported that risk of postoperative myasthenic crisis was affected by the presence of preoperative bulbar symptoms, a previous history of myasthenic crisis, antiacetylcholinesterase antibody greater than 100 nmol/ml and intraoperative blood loss greater than 1000 ml.19 Myasthenic crisis is a temporary exacerbation, and the goal is to keep the patient stable until the transient stress of the surgery has passed and

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721

responsiveness to anticholinesterase medications returns. Aggressive pulmonary toilet and ambulation should be initiated postoperatively. Some groups advocate withholding anticholinesterase medications for 48 hours postoperatively to increase the sensitivity of the receptors to these drugs.20 Grade 1 complication

INDICATION

Resection of Posterior Mediastinal Masses

Step 1 Prone or semi-lateral prone position Step 2 Midline incision over spinous process of involved vertebrae Step 3 Muscles and fascia elevated off spinous process Step 4 Hemilaminectomy and foraminectomy at appropriate level, tumor exposed and neurosurgically resected Step 5 Rib overlying tumor resected subperiosteally along with transverse process Step 6 Intrathoracic portion of tumor generally resectable through the costotransversectomy Step 7 Appropriate neurovascular bundle ligated Step 8 Layered wound closure

Complications of surgery in the posterior mediastinum are best considered by examining the resection of hourglass tumors of the posterior mediastinum. An hourglass (or dumbbell) tumor refers to a tumor with both intraspinal and intrathoracic components connected by a narrow waist traversing the bony intervertebral foramen. These tumors are most often neurogenic in origin. The complexity of the bony, vascular, and neural anatomy in the posterior mediastinum complicates the removal of these tumors. Figure 69–6 illustrates the proximity of these various structures in the posterior mediastinum. Surgery for hourglass tumors requires entry into two anatomic regions: the thorax and the spinal canal. Hourglass tumors can generally be resected through one of two approaches: a single-stage approach or a combined anteroposterior approach involving both a laminectomy and a thoracotomy. VATS is often substituted for thoracotomy for the thoracic phase of the operation.

Vertebral body Intercostal vessels Enlarged foramen Displaced spinal cord

Head of thoracic rib Dumbbell-shaped neurogenic tumor

Intercostal nerve Pedicle

Facet Spinous process

Lamina

Transverse process

Intercostal nerves and vessels

Figure 69–6 A large neurogenic hourglass tumor is demonstrated with a compressed spinal cord, enlarged intervertebral foramen, and large posterior mediastinal tumor component. Note the proximity of the surrounding structures. (Reproduced with permission from Lippincott Williams & Wilkins from Kern JA, Daniel TM. Resection of posterior mediastinal tumors. In Kaiser LR, Kron IL, Spray TL [eds]: Mastery of Cardiothoracic Surgery. Philadelphia: Lippincott-Raven, 1998; p 112.)

● Hourglass or dumbbell tumor of posterior mediastinum

Resection of Intraspinal Component of Tumor Operative steps of a single stage approach for resection of an hourglass tumor of posterior mediastinum

Operative steps for two stage resection of an hourglass tumor of posterior mediastinum Step 1 Posterior neurosurgical resection of intraspinal component of tumor as detailed above Step 2 Costotransversectomy avoided Step 3 Separate posterolateral thoracotomy or videoassisted resection of intrathoracic portion of tumor performed

Spinal Cord Injury Paralysis as a complication of resection of a posterior mediastinal hourglass tumor is rare but devastating. Injury to the spinal cord may occur in several different ways. The spinal cord is typically supplied by a large nutritive vessel in the lower thoracic spine, commonly known as the artery of Ademkiewicz.21 Ligation of this blood vessel may render the spinal cord ischemic, resulting in paralysis, as has been reported.22 Inadvertently cutting across the narrow foraminal tumor neck can result in tumor hemorrhage and spinal cord compression. Finally, bleeding from the small radicular arteries that originate from the posterior branches of the intercostal arteries and supply the spinal cord may also result in an epidural hematoma and cord compression. ● Consequence Injury to the spinal cord results in paralysis, with the deﬁcit being variable depending on the level and extent of injury to the cord. Grade 4 complication ● Prevention Proper imaging, typically with magnetic resonance (MRI), to determine whether a posterior mediastinal tumor has an intraspinal component is essential to

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avoid inadvertent spinal cord injury from excessive traction on the tumor or hemorrhage at the neural foramina. Intraoperatively, involvement of the neural foramina can be detected by the widening of the foramen with visualization of the tumor entering along the nerve root.23 Some groups advocate the use of magnetic resonance angiography to identify the artery of Adamkiewicz preoperatively because its position is extremely variable.24 Finally, care should be taken in identifying and controlling the small radicular arteries originating from the intercostal vessels that supply the spinal cord. These radicular vessels originate close to the vertebral column; however, the presence of tumor may signiﬁcantly distort the anatomy. Finally, absorbable gelatin sponges should not be left in the neural foramina because they may swell and could compress the cord.

Cerebrospinal Fluid Leak Hourglass tumors may follow a nerve root intradurally. In these circumstances, the dura must be opened and partially resected in order to remove the tumor. The dura is subsequently closed, and breakdown of this closure can result in the development of CSF leak, generally draining into the pleural space. ● Consequence The most signiﬁcant consequence of a CSF leak is seeding of the dural space with bacteria and the development of meningitis. A CSF leak may result in the development of a pseudomeningocele in the thoracic cavity.25 CSF leaks also decrease intradural pressure, which may result in severe headaches. Grade 2/3/4 complication ● Repair Signiﬁcant CSF leaks may be repaired in a variety of manners, including pleural ﬂaps, pericardial fat, intercostal muscle, or a large piece of thrombin-soaked gelatin sponge.21 Another treatment option is the insertion of a lumbar drain to divert ﬂow from the CSF ﬁstula, allowing it to heal.26 ● Prevention When the dura is violated, it should be closed meticulously to avoid development of a ﬁstula. Some surgeons have advocated covering the dural repair with ﬁbrin glue or some other biologic sealant.21 When the dura cannot be closed primarily without tension, pleura, pericardial fat, or intercostal muscle may be used to bridge the gap. These options are also available to buttress a dural closure. Dural closure may be tested intraoperatively with a Valsalva maneuver. If a patient is believed to be at high risk for the development of a CSF leak, a lumbar drain may be placed prophylactically. Excessive chest tube suction has also been impli-

cated in perpetuating CSF leaks, and placing chest tubes to water-seal as soon as feasible is advocated.27

Resection of Intrathoracic Component of Tumor Sympathetic Nerve Injury The sympathetic chain is located on the heads of the ribs from the thoracic inlet to the diaphragm. Neurogenic tumors often arise from the sympathetic chain, and therefore, the resultant deﬁcit after resection of the tumor cannot be considered a surgical complication but rather a consequence of the operation. Injury to the sympathetic ganglia is most frequently seen during thoracoscopic sympathetectomy. ● Consequence Injury to the stellate ganglion results in Horner’s syndrome with the typical ﬁnding of ptosis, miosis, and anhidrosis. Injury to the sympathetic chain below the stellate ganglion may also produce signiﬁcant symptoms. These patients may experience hyperhydrosis, tingling, and differences in skin color and temperature in the affected areas.28 Grade 1 complication ● Repair Rarely, intercostal or sural nerve grafts have been used with limited results to reverse Horner’s syndrome.29 A blepharoplasty is generally performed for cosmetic purposes, and the miosis can be treated with eyedrops. ● Prevention Often, sympathetic nerve injury is unavoidable because the tumor may be originating from this structure. However, one must be careful when dividing the sympathetic chain at the appropriate level and use cautery at low settings, especially when near the stellate ganglia.

Injury to the Thoracic Nerve Roots ● Consequence Injury to a thoracic nerve root generally results in little discernible deﬁcit except for numbness in a dermatomal distribution. The exception is injury to the T1 or T2 levels where injury can result in compromise of ipsilateral hand function, resulting in an ulnar hand with clawing of the fourth and ﬁfth digits due to lumbrical muscle weakness. Grade 1 complication ● Repair Interposition nerve grafts with the intercostal and other nerves have been attempted for injuries affecting hand function with mixed results. ● Prevention Surgeons should be aware of the thoracic nerve roots exiting the intervertebral neural foramina. Sacriﬁce of

69 THYMECTOMY AND RESECTION OF MEDIASTINAL MASSES a nerve root may be unavoidable if the tumor originates from that particular nerve.

Thoracic Aortic Injury ● Consequence Injury to the thoracic aorta can result in life-threatening hemorrhage. Grade 5 complication ● Repair Emergent primary vascular repair. ● Prevention Neurogenic hourglass tumors commonly receive their nutritive blood supply from the intercostal arteries or radicular braches from the intercostal vessels. The proximity of these small vessels to the thoracic aorta must be recognized to avoid avulsing them off the aorta. Anatomic distortion by the tumor may make these small vessels originating from the aorta difﬁcult to identify and place the aorta at risk for injury.

Esophageal Injury ● Consequence Transmural injury to the esophagus can result in leak of esophageal contents with mediastinitis and/or empyema. An esophageal leak in patients undergoing resection of hourglass tumors may also result in meningitis if the dura of the spinal cord has been violated and a cerebrospinal ﬂuid (CSF) leak is present. Contamination of the mediastinum will result in infection that can become a diffuse necrotizing mediastinitis with systemic sepsis and multisystem organ failure. Grade 2/3/4 complication

723

Chylothorax The thoracic duct enters the chest through the aortic hiatus and is located to the right of the vertebral bodies until it crosses to the left, typically at the level of T5 or T6. The thoracic duct may be injured at any point along its course in the posterior mediastinum. ● Consequence Presentation is typically delayed until the patient has resumed oral intake. Chest x-rays will demonstrate a rapid accumulation of a pleural effusion. The amount of pleural drainage can be as high as 1.5 to 2 liters a day. Patients may become hypovolemic from excessive ﬂuid losses and develop signiﬁcant electrolyte abnormalities. Owing to the high protein content of chyle, protein depletion occurs quickly, accompanied by weight loss. Decreases in peripheral lymphocyte counts also result in a state of immunosuppression. Grade 2/3/4 complication ● Repair None. Intraoperatively recognized thoracic duct injuries should be suture-ligated to prevent a leak. Chyle leaks may be managed conservatively with chest tube drainage, cessation of oral intake, and total parenteral nutrition. In the setting of persistent high-output thoracic duct ﬁstulas or nutritional or metabolic complications, reoperation is necessary. Options include direct ligation of the ﬁstula through reopening of the previous incision. Heavy cream may be given to the patient preoperatively to help in identiﬁcation of the ﬁstula. A second option is interruption of the thoracic duct above the diaphragm.30 Interventional radiology techniques may also be attempted to embolize the ﬁstula with some reported success.31

● Repair Perforations of the esophagus may generally be repaired primarily. The esophageal muscle is incised to visualize the entire mucosal defect, and the tissue is débrided to healthy edges. The esophagus is then closed in two layers. Vascularized tissue should be used to reinforce the repair. Options include parietal pleural, intercostal muscle, and pericardial fat pad. A nasogastric tube is placed past the repair, and several chest tubes are left in the thorax.

● Prevention Thorough knowledge of the course of the thoracic duct is essential when operating in the mediastinum. If copious drainage of milky ﬂuid is encountered when operating in the posterior mediastinum, injury to the thoracic duct should be expected and aggressively searched for.

● Prevention Mobilization of the esophagus to access posterior mediastinal tumors should be done away from the esophagus to minimize the risk of injury or devascularization if possible from an oncologic standpoint. Retraction of the esophagus should be performed gently, either bluntly or by encircling it with a Penrose retractor. Aggressive grasping of the esophagus should be avoided, as should the use of thermal energy in close proximity to it.

● Consequence If only one vagus nerve is injured, there is generally no consequence unless the injury occurs high in the mediastinum proximal to the origin of the recurrent laryngeal nerve, which would result in ipsilateral vocal cord paralysis, as discussed previously. If both vagus nerves are injured, gastrointestinal complications may result, namely, delayed gastric emptying and postvagotomy diarrhea. Grade 1 complication

Vagus Nerve Injury

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Figure 69–7 The azygos vein is being divided over the thoracic esophagus in the posterior mediastinum. Visible is an esophageal leiomyoma within the esophageal wall, which was enucleated.

● Repair None. Medialization of the ipsilateral vocal cord is required if the injury occurs proximal to the origin of the recurrent laryngeal nerve. ● Prevention The surgeon must have an understanding of the mediastinal course of the vagus nerves. In particular, its position high in the thorax should be appreciated in order to avoid recurrent nerve palsy.

Azygos Vein Injury ● Consequence Signiﬁcant intraoperative hemorrhage may occur if the azygos vein is inadvertently injured. Grade 3 complication ● Repair Primary vascular repair or ligation. ● Prevention The surgeon must be aware that the venous outﬂow of a posterior mediastinal tumor may be in close proximity to or directly into the azygos vein (Fig. 69–7). In addition, the tumor mass may distort the anatomy and make this difﬁcult to identify. The azygos vein can usually be divided with impunity, and early ligation of this vessel may protect it from injury and improve exposure.

REFERENCES 1. Shields T. Primary tumors and cysts of the mediastinum. In Shields T (ed): General Thoracic Surgery. Philadelphia: Lea & Febiger, 1972; p 908.

2. Busch C, Machens A, Pichlmeier U, et al. Long-term outcome and quality of life after thymectomy for myasthenia gravis. Ann Surg 1996;224:225–232. 3. Stern L, Nussbaum M, Quinlan J, Fischer J. Long-term evaluation of extended thymectomy with anterior mediastinal dissection for myasthenia gravis. Surgery 2001;130: 774–780. 4. Mason D. Radical transsternal thymectomy. Oper Tech Thorac Cardiovasc Surg 2005;10:231–243. 5. de Perrott M, Keshavjee S. Video-assisted transcervical thymectomy. Oper Tech Thorac Cardiovasc Surg 2005; 10:220–230. 6. Jaretzki A 3rd, Penn AS, Younger DS, et al. “Maximal” thymectomy for myasthenia gravis. Results. J Thorac Cardiovasc Surg 1988;95:747–757. 7. Spath G, Brinkmann A, Huth C, Wietholter H. Complications and efﬁcacy of transsternal thymectomy in myasthenia gravis. Thorac Cardiovasc Surg 1987;35:283–289. 8. Robicsek F. Postoperative sterno-mediastinitis. Am Surg 2000;66:184–192. 9. Losanoff JE, Richman BW, Jones JW. Disruption and infection of median sternotomy: a comprehensive review. Eur J Cardiothorac Surg 2002;21:831–839. 10. Sudhakar CB, Elefteraides JA. Safety of left innominate vein division during aortic arch surgery. Ann Thorac Surg 2000;70:856–858. 11. Detterbeck FC, Scott WW, Howard JF Jr, et al. One hundred consecutive thymectomies for myasthenia gravis. Ann Thorac Surg 1996;62:242–245. 12. Bulkley GB, Bass KN, Stephenson GR, et al. Extended cervicomediastinal thymectomy in management of myasthenia gravis. Ann Surg 1997;226:324–334. 13. Hatton PD, Diehl JT, Daly BD, et al. Transsternal radical thymectomy for myasthenia gravis: a 15-year review. Ann Thorac Surg 1989;47:838–840. 14. Lemmer J, Stiller B, Heise G, et al. Postoperative phrenic nerve palsy: early clinical implications and management. Intensive Care Med 2006;32:1227–1233. 15. Deng Y, Byth K, Paterson HS. Phrenic nerve injury associated with high free right internal mammary artery harvesting. Ann Thorac Surg 2003;76:459–463. 16. Kraus DH, Ali MK, Ginsberg RJ, et al. Vocal cord medialization for unilateral paralysis associated with intrathoracic malignancies. J Thorac Cardiovasc Surg 1996;111:334–341. 17. Cohn HE, Solit RW, Schatz NJ, Schlezinger N. Surgical treatment in myasthenia gravis. A 27 year experience. J Thorac Cardiovasc Surg 1974;68:876–885. 18. Leventhal SR, Orkin FK, Hirsh RA. Prediction of the need for postoperative mechanical ventilation in myasthenia gravis. Anesthesiology 1980;53:26–30. 19. Watanabe A, Watanabe T, Obama T, et al. Prognostic factors for myasthenic crisis after transsternal thymectomy in patients with myasthenia gravis. J Thorac Cardiovasc Surg 2004;127:868–876. 20. Kas J, Kiss D, Simon V, et al. Decade-long experience with surgical therapy of myasthenia gravis: early complications of 324 transsternal thymectomies. Ann Thorac Surg 2001;72:1691–1697. 21. Shadmehr M, Gaissert H, Wain J, et al. The surgical approach to “dumbbell tumors” of the mediastinum. Ann Thorac Surg 2003;76:1650–1654.

69 THYMECTOMY AND RESECTION OF MEDIASTINAL MASSES 22. Takamori A, Hayashi K, Tayama M, et al. Resection of a malignant ﬁbrous histiocytoma invading the thoracic aorta. Jpn J Thorac Cardiovasc Surg 1998;46:825– 828. 23. Singhal D, Kaiser L. The posterior mediastinum. In Sellke F, del Nido P, Swanson S (eds): Sabiston & Spencer Surgery of the Chest, Vol 1. Philadelphia: Elsevier Saunders, 2005; pp 689–702. 24. Maruki S, Tanaka A, Miyajima M, et al. Ademkiewicz artery demonstrated by MRA for operated posterior mediastinal tumors. Ann Thorac Cardiovasc Surg 2006; 12:270–272. 25. Cammisa F, Girardi F, Sangani P, et al. Incidental durotomy in spine surgery. Spine 2000;25:2663– 2667. 26. Shapiro S, Scully T. Closed continuous drainage of cerebrospinal ﬂuid via a lumbar subarachnoid catheter for treatment or prevention of cranial/cerebrospinal ﬂuid ﬁstula. Neurosurgery 1992;30:241–245.

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27. Citow JS, Macdonald RL, Ferguson MK. Combined laminectomy and thoracoscopic resection of a dumbbell neuroﬁbroma: technical case report. Neurosurgery 1999;45:1263–1265; discussion 1265–1266. 28. Krasna M, Forti G. Nerve injury: injury to the recurrent laryngeal, phrenic, vagus, long thoracic, and sympathetic nerves during thoracic surgery. Thorac Surg Clin 2006; 16:267–275. 29. Miura J, Doita M, Miyata K, et al. Horner’s syndrome caused by a thoracic dumbbell-shaped schwannoma: sympathetic chain reconstruction after a one-stage removal of the tumor. Spine 2003;28:E33–E36. 30. Fahimi H, Casselman FP, Mariani MA, et al. Current management of postoperative chylothorax. Ann Thorac Surg 2001;71:448–450; discussion 450–451. 31. Binkert C, Yucel E, Davison B, et al. Percutaneous treatment of high-output chylothorax with embolization or needle disruption technique. J Vasc Interv Radiol 2005;16:1257–1262.

70

Esophageal Surgery Angela M. Mislowsky, MD and Richard F. Heitmiller, MD INTRODUCTION

OPERATIVE PROCEDURE

Esophagectomy is a complex surgery associated with signiﬁcant morbidity and mortality. Complications can lead to lengthy hospital stay and can negatively affect postsurgical quality of life by altering or interrupting the ability to swallow. Understanding the complications that are possible with this surgery is vital to their prevention. The two key principles for performing esophagectomy successfully are (1) to prevent complications to begin with, if possible, and (2) to have safeguards in place to manage complications if they do occur. The objective of this chapter is to review both principles.

The technique of esophagectomy can be broken down into three parts, as summarized in Box 70–1. The ﬁrst is the step of gastric mobilization; the second, esophageal dissection along with at least single-ﬁeld lymphatic dissection for patients with cancer; and the third is the reconstructive esophageal anastomosis. We have advocated routine use of an adjuvant jejunostomy feeding tube.1 When used, this would be the fourth surgical step. The several different incisional approaches to performing esophagectomy include transhiatal (midline laparotomy, left cervical incision), Ivor Lewis (right thoracotomy and midline laparotomy), three-incision (cervical, right thoracotomy, midline laparotomy), and left thoracoabdominal methods. Despite their widely variant incisions, all utilize the three-part surgical steps stated previously. Selection of the speciﬁc approach is based on location of the esophageal tumor or disease, reconstruction plans, and surgical preference. In experienced hands, there is no difference in morbidity, mortality, and survival as a function of surgical approach. The majority of surgeons prefer to use the mobilized stomach to replace the resected esophagus. Advantages of the stomach as a replacement conduit include easy mobilization and superb blood supply that minimizes the incidence of conduit ischemia and results in only one anastomosis. Colon or jejunum may also be used as replacement conduits. Doing so results in more operative time, a higher risk of conduit ischemia, and more reconstructive anastomosis. For the purposes of this chapter, the discussion of complications largely focuses on the technique of esophagectomy when the stomach is used for esophageal replacement.

INDICATIONS ● ● ● ● ●

Esophageal cancer Barrett’s mucosa with high-grade epithelial dysplasia Advanced functional disorders Multiple failed previous antireﬂux procedures Strictures

OPERATIVE STEPS Positioning: supine with head turned to right Incision: supraumbilical incision from xyphoid to umbilicus Step 3 Divide triangular ligament and retraction of left lateral segment of liver Step 4 Separate greater omentum from stomach Step 5 Divide short gastric vessels Step 6 Incise peritoneum overlying hiatus, encircle esophagogastric junction Step 7 Divide gastrohepatic omentum Step 8 Divide left gastric vessels Step 9 Mobilize distal greater curve of stomach Step 10 Perform Kocher’s maneuver Step 11 Perform pyloroplasty or pyloromyotomy Step 1 Step 2

Complications Complications are listed in the same order as they might arise during the surgery and postoperative management of a patient undergoing esophagectomy. Therefore, complications include operative complications, those that occur early and late during the initial hospital stay, and

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Box 70–1 ●

●

Step 1

●

Step 2 Step 3

●

Step 4

Box 70–2

● Divide platysma and omohyoid ● Retract sternocleidomastoid and carotid sheath later-

Esophagectomy Technique: Overview Gastric mobilization. If jejunum or colon is used instead of stomach, assess conduit options before proceeding with esophageal resection Esophageal dissection Reconstructive anastomosis; most commonly, esophagogastric anastomosis Adjuvant jejunostomy

ally and larynx and trachea medially Dissect esophagus posterior along prevertebral fascia Incise areolar tissue overlying lateral esophageal wall Dissect esophagus circumferentially Continue circumferential mobilization of esophagus down to carina ● Divide cervical esophagus and deliver into abdomen with umbilical tape tied to esophagus to maintain posterior mediastinal route ● ● ● ●

Esophagectomy Complications

Operative ● ● ● ●

●

Abdominal Phase Part II

Bleeding Splenic injury Airway injury Esophageal conduit issues ● Transmural opening ● Ischemia ● Insufﬁcient length Chyle leak

● Tubularize gastric conduit ● Bring gastric conduit through posterior mediastinal ● ● ● ●

tunnel and out cervical incision Esophagogastric anastomosis Place cervical drain Feeding jejunostomy Close incisions

Early Inpatient Complications (<72 hr) ●

● ● ●

Surgical Resection of the Esophagus

Respiratory complications ● Atelectasis ● Pleural effusion ● Respiratory failure ● Pneumonia Hoarseness (recurrent laryngeal nerve injury) Conduit ischemia Arrhythmia

Late Inpatient Complications (>72 hr) ● ● ● ●

Aspiration pneumonia Anastomotic leak Wound infection Chyle leak

Postdischarge Complications ● ●

Anastomotic stricture Diaphragmatic hernia

ﬁnally those encountered after discharge. The complications to be discussed are listed in Box 70–2.

Transhiatal Phase ● Blunt dissection of esophagus away from surrounding

pleura and aorta with downward traction maintained on gastroesophageal junction ● Small vessels and lymphatics are clipped and divided ● Dissection progresses cephalad, staying on esophagus ● Proximal small vessels and lymphatics are avulsed when unable to clip

Cervical Phase ● Oblique

incision sternocleidomastoid

along

anterior

border

of

Operative Bleeding The esophagus has a diverse and robust blood supply and lies in close proximity to many prominent vascular structures. Therefore, surgical resection of the esophagus always carries a risk of signiﬁcant bleeding. The reported rate of perioperative hemorrhage complicating esophagectomy ranges from 0.3% to 4%.2–4 The risk and consequences of bleeding vary depending on the technique of esophagectomy. The risk of bleeding related to preparing the stomach for esophageal conduit is shared by all incisional techniques. Open thoracotomy approaches minimize the risk of unexpected vascular injury because these methods give direct visual exposure of the operative ﬁeld. In addition, vascular injuries can be promptly identiﬁed and repaired, generally through the same exposure. Conversely, these approaches add a thoracotomy incision and open the mediastinal pleura. Diffuse, small mediastinal bleeding vessels, likely to thrombose if contained to the mediastinum, may result in greater blood loss if they can drain into the opened pleural space. Risk of chest wall bleeding from the thoracotomy incision is also introduced. Transhiatal esophagectomy is associated with very real and signiﬁcant bleeding during the intrathoracic, “blunt,” or transhiatal phase of esophageal dissection. Bleeding may result from large esophageal arteries originating from the aorta, inferior pulmonary vein, or pulmonary artery, as illustrated in Figure 70–1. Bleeding is usually immediately apparent as brisk blood ﬂow exiting from the lower mediastinum or from the neck. However, if the mediastinal pleura has been opened during transhiatal dissection, then the bleeding event, or at least its severity, can be masked. When this happens, the ﬁrst sign of trouble is an unexpected volume requirement or unstable hemodynamics. It

70 ESOPHAGEAL SURGERY

729

● Bleeding from any vessel source that requires re-

exploration for repair with or without transfusion. ● Bleeding that is abnormal but self-limited. This may

result in hematoma or hemothorax with resultant fevers, potential for infection, or respiratory compromise. ● Bleeding from the right gastroepiploic vessels whose repair compromises the use of the stomach as a replacement conduit. ● Massive bleeding that jeopardizes the patient’s life, may require additional incisions for exposure and repair, and signiﬁcantly alters the patient’s planned clinical care. Grade 2–5 complication

Figure 70–1 The proximity of the esophagus to major intrathoracic vascular structures such as the pulmonary artery, superior and inferior pulmonary veins, aorta, and esophageal arteries and the juxtaposition of the airway and esophagus.

is essential that the surgeon and anesthesiologist remain in communication during this phase of the operation. The abdominal phase of esophagectomy involves mobilizing the stomach based on the right gastroepiploic arcade and adding a Kocher maneuver. Bleeding may occur from any of the divided vessels including the short gastric, right and left gastric, and paraduodenal vessels. Bleeding is most likely to occur in regions where exposure is most compromised. Most commonly, this means the short gastric vessels and the left gastric vessels. Splenic injury is discussed separately. ● Consequence The consequence of bleeding varies greatly depending on the vessel injured, what esophagectomy technique is being used, and how rapidly the problem is diagnosed and repaired. Outcomes range from bleeding that increases the estimated blood loss but does not require transfusion or change a patient’s clinical course to exsanguination and death. From least to most severe, consequences include ● Bleeding from any vessel source that is controlled

but results in a need for transfusion.

● Repair For open surgical techniques, bleeding vessels are directly exposed and bleeding is controlled by standard methods. Smaller vessels are ligated or coagulated; larger vessels may require proximal and distal control prior to suture repair. Use of prosthetic material, such as patches or pledgets, is to be avoided whenever possible because of the potential for infection from the esophagus. Intrathoracic bleeding during transhiatal surgery is one of the most feared complications. Bleeding from esophageal feeding arteries emanating from the aorta can lead to a sizeable blood loss before it can be visualized and controlled. If the vessel can be visualized easily in the lower mediastinum, it should be ligated, clipped, or coagulated promptly. If not, pack the mediastinum with a lap pad. This will greatly reduce the bleeding and make ﬁnding and controlling the vessel easier. Narrow handheld malleable retractors often help greatly to see up into the mediastinum to ﬁnd the bleeding vessel. Liberal use of suctioning and a surgeon’s headlight are also beneﬁcial. Massive bleeding from the aorta, inferior pulmonary vein, or pulmonary artery is immediately life-threatening. Once bleeding is identiﬁed, it is essential that the surgeon have an idea which vessel was injured. Even without seeing into the chest, the surgeon should have an idea what was injured based on where the dissection had been just before injury. Pack the mediastinum. Notify your anesthesia colleague. Get blood into the room. Consider calling for vascular or cardiac surgery assistance. Almost invariably, another incision will be needed to get exposure for repair. A median sternotomy is not the best incision to use to ﬁx the vessels injured during transhiatal dissection. A separate thoracotomy is most appropriate. Choose left or right based on what you think is injured. Rapidly close the abdominal incision or leave it covered, turn the patient, and get exposure. Then identify and control the bleeding using standard methods. If the inferior pulmonary vein is injured, it cannot simply be ligated because this will destroy the lower lobe. In addition, an open pulmonary vein risks serious air embolism. Position the patient’s head down until the injury site is controlled. As mentioned

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previously, intraoperative consultation with cardiothoracic surgery may be needed. ● Prevention Prevention is key to prevent bleeding complications. For open cases, an understanding of the anatomy, careful dissection, and prophylactic proximal and distal control of vessels potentially at risk during esophageal dissection or gastric mobilization will minimize bleeding complications. Within the abdomen, use of mechanical retraction devices, nasogastric decompression of the stomach, and coagulating devices adapted from laparoscopic surgery both optimize exposure and help to safely coagulate and divide difﬁcult exposure vessels like the short gastrics. During transhiatal dissection, the surgeon must stay in the immediate paraesophageal plane, as shown in Figure 70–2. A nasogastric tube within the esophagus and downward countertraction to keep the esophagus straight are both very helpful. Alert your anesthesia colleague that you are starting the chest dissection. Begin the dissection posteriorly because this is often the easiest side of the esophagus to clear. Never persist with transhiatal dissection if the pathology forces you off the juxtaesophageal plane. If this is the case, convert to a thoracotomy approach. It will make for a longer case but will prevent disastrous consequences.

Penrose drain encircles cervical esophagus Trachea L. bronchus Thoracic esophagus

Hiatus (enlarged at midline) Liver

Fundus of stomach

Figure 70–2 Safe transhiatal esophageal dissection in the immediate paraesophageal plane and the proximity of the trachea and left main stem bronchus to the esophagus.

Splenic Injury Injury to the spleen during esophagectomy requiring incidental splenectomy occurs with a reported incidence of 4.1% to 8.4%.5,6 Most commonly, the spleen is injured by traction on short gastric vessels during gastric mobilization that secondarily tear the splenic capsule. Occasionally, the spleen is directly injured by retraction. There are no data to support routine inclusion of the spleen as part of an esophageal resection for cancer. Although there are no data that splenectomy inﬂuences cancer recurrence rates,5 adverse consequences of splenectomy are well-described. It is, therefore, a complication that should be avoided. ● Consequence Splenectomy increases a patient’s susceptibility to overwhelming sepsis secondary to encapsulated organisms. Grade 4 complication ● Repair The spleen is salvaged, if possible, using standard methods of packing or suturing. If not, it is resected keeping the dissection close to its hilum. ● Prevention Achieve optimal exposure of the upper abdomen using assistants or mechanical devices for retraction. Keep the stomach decompressed with a nasogastric tube. Avoid unnecessary traction on the stomach and short gastric vessels because this could result in secondary splenic capsular tearing. Many coagulation or surgical clipping devices originally designed for use in laparoscopy are now in mainstream use with open surgeries. These permit much easier control of the deep short gastric vessels that were considerably more difﬁcult to control by standard ligation techniques.

Airway Injury The trachea, carina, and main stem bronchi are in close proximity to the esophagus and are at risk for injury during esophageal resection (see Figs. 70–1 and 70–2). The trachea is oriented so that its weakest feature, its soft membranous wall, is immediately adjacent to the esophagus. The defenses of the membranous wall are further compromised when it is thinned and distended over an indwelling endotracheal balloon cuff. The reported rate of airway injury is unclear. Intraoperative injuries are identiﬁed and managed immediately. There is no reported series to indicate rate of injuries. The membranous wall of the trachea is at risk for injury when encircling the esophagus in the neck during transhiatal cases (Fig. 70–3). The trachea and carina are at risk for injury while mobilizing proximal third esophageal tumors in the chest. The main stem bronchus, especially on the left side, is at risk for injury during transhiatal esophageal dissection. If the airway opening is proximal to the endotracheal tube (ETT) cuff, the surgeon will see the open airway; however, there should be no change in the patient’s cardiorespiratory status. If, however, the

70 ESOPHAGEAL SURGERY

Thyroid

Esophagus

Carotid sheath

Trachea Recurrent laryngeal n.

Figure 70–3 The membranous wall of the trachea is at risk for injury during mobilization of the cervical esophagus.

airway is opened distal to the ETT cuff, air escapes during positive-pressure ventilation leading to an urgently unstable situation. ● Consequence The consequence of the airway opening depends on its orientation with regard to the endotracheal cuff. An airway injury proximal to the balloon cuff merely opens the airway. This can be repaired as described later. Both the initial injury and the closure risk injuring the ipsilateral recurrent laryngeal nerve (RLN). Failure to buttress the repair site with some tissue patch risks later development of an esophagorespiratory ﬁstula. An airway injury distal to the ETT cuff results in an immediate escape of air and anesthetic gas, especially with positive-pressure ventilation. Patients may become rapidly unstable with limited ability to ventilate them and with associated ﬁre risk if the electrocautery is used. During transhiatal dissection, in addition to difﬁculty with ventilation, signiﬁcant pneumomediastinum and even tension pneumothorax may result if there is communication with the pleural space. Grade 2/4/5 complication ● Repair Airway injury proximal to the ETT cuff should be closed primarily with interrupted 4-0 Vicryl sutures. The suture line needs to be secondarily covered with a soft tissue patch such as a regional rotational muscle ﬂap, pericardial fat pad, or intercostal muscle pedicle

731

ﬂap. The patient’s airway is then managed as per routine postoperatively. An airway injury distal to the ETT cuff requires more urgent action. If the hole is accessible, it can be temporarily occluded with one’s ﬁnger. The best way to repair these injuries, whenever possible, is to direct the ETT distal to the hole to convert a distal airway hole into a proximal one. If this cannot be done, have the anesthesiologist manually ventilate the patient with more rapid, lowvolume breaths, then close the hole between breaths, as described previously. This leaves the airway injury site exposed to positive-pressure ventilation. In the short term, this is acceptable; however, patients should be extubated as early as possible postoperatively. During transhiatal esophagectomy, if an airway injury is created in the cervical trachea, it should be repaired primarily. An intrathoracic injury requires repositioning the patient for a thoracotomy. A right thoracotomy is preferred. Not only will this provide exposure to the trachea and carina, but the left posterior aspect of the left mainstem bronchus is easily seen as well. ● Prevention Avoid blunt dissection methods when encircling the esophagus. Doing so places the adjacent tracheal membranous wall at risk for injury. When performing transhiatal dissection of the esophagus, stay on the esophageal wall.

Esophageal Replacement Conduit Complications A healthy and properly functioning esophageal replacement conduit is essential to a successful outcome after esophagectomy. Many of the complications regarding conduit use can be prevented during the operative procedure. This section refers speciﬁcally to the use of stomach as a replacement conduit. However, the principles involved could be applied to the use of colon or jejunal conduits. The incidence of conduit ischemia for stomach, colon, and jejunal grafts is 3.2%, 5.1%, and 4.2%, respectively.7 Three speciﬁc gastric conduit complications are discussed—gastrotomy, ischemia, and insufﬁcient length. Gastrotomy results either from preoperative feeding tube placement or from intraoperative injury. Ischemia is largely an iatrogenic complication related to the technique of gastric mobilization. The stomach is a versatile esophageal replacement conduit that, once fully mobilized, should reach to the neck. There are times during transhiatal esophagectomy when this is difﬁcult without excessive tension. ● Consequence When stomach is used as a replacement conduit, it functionally becomes the new esophagus. Therefore, postoperative leakage from the stomach is as deadly a complication as a primary esophageal leak. A virulent mediastinitis develops that drains into the pleural space if the mediastinal pleura has been opened at surgery. Systemic sepsis rapidly develops with the

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potential for hemodynamic instability, multisystem failure, and death. A good clinical outcome after esophagectomy is greatly dependent on the viability and function of the esophageal replacement conduit. Nonnecrotic ischemia of the stomach is believed to increase the risk of both anastomotic leak and stricture formation. If the stomach becomes frankly necrotic, it must be emergently removed, the cervical esophagus is diverted, the patient is unable to eat or drink by mouth, and further surgery is needed in the future to complete the esophageal reconstruction. When the stomach conduit does not reach to the neck during transhiatal esophagectomy, the temptation is to try to pull the stomach tip more forcefully to get it to reach. Doing so can result in progressive tearing of the fundus tip or ischemia of the fundus secondary to disruption of ﬁne submucosal vascular arcades. Both circumstances may render the stomach graft unusable. Grade 3/4/5 complication ● Repair All seromuscular stomach wall injuries should be closed with ﬁne silk Lembert sutures. Gastrotomies need to be closed in two layers. Conduit ischemia is largely iatrogenic. Prevention is essential. Details are discussed later. During the procedure, the surgeon must determine whether the conduit is viable or not. If it is not, there are no data to support the use of medication (such as steroids) or anticoagulation to “salvage” the ischemic conduit. Nonviable conduits need to be resected and another conduit chosen. A properly mobilized stomach tube should reach to the neck without tension. Preservation of the fundus, multiple staple ﬁrings to create the stomach tube, and a generous Kocher maneuver all contribute to optimal conduit length. If the stomach still does not reach to the neck without tension, or because the thoracic outlet is too tight, two options can handle this problem, illustrated in Figure 70–4. 8 The ﬁrst is to extend the cervical incision onto the upper sternum in the midline to the angle of Louis. The left cervical strap muscles are divided, thus opening the thoracic outlet region and permitting a slightly lower cervical anastomosis. The second approach is as listed previously plus adding a partial upper sternotomy. This “cervicomediastinal” exposure greatly opens the thoracic outlet and permits esophagogastric anastomosis several centimeters lower than could be accomplished by standard cervical exposure. ● Prevention It may not be possible to avoid gastrotomy. Use of jejunostomy instead of gastrostomy feeding tubes protects the stomach but is not always possible. The stomach is mobilized based on the right gastroepiploic arcade. There are no data demonstrating an additional beneﬁt to preserving the right gastric artery. Greater curvature–based gastric tubes are fashioned by multiple linear stapler application, as shown in Figure 70–5.9 Evi-

Optional collar incision

Angle of Louis

Figure 70–4 If the stomach conduit will not easily reach to the neck during transhiatal esophagectomy, extend the cervical incision inferiorly and divide the upper sternum. This permits a lower esophageal anastomosis and widens the thoracic outlet. (Adapted from Heitmiller RF, Heitmiller ES: Surgery for myasthenia gravis. In Franco KL, Putnam JB Jr [eds]: Advanced Therapy in Thoracic Surgery, 2nd ed. Hamilton, London, Ontario: BC Decker, 2005; p 413.)

1 Fundus divided in 3 firings of stapler

Level of cross section Minimal post-op compression of airway

2 3 Tr.

Ao.

Gastric tube

Figure 70–5 The stomach tube is fashioned by multiple ﬁrings of a linear stapler. This optimizes stomach length. (Adapted from Heitmiller RF. Impact of gastric tube diameter on upper mediastinal anatomy. Dis Esophagus 2000;13:288–292, with permission.)

dence demonstrates that the width of the gastric tube, especially toward the fundus, is important to minimizing ischemic complications. A stomach tube measuring 4 to 5 cm in diameter seems to be the optimal width. A tube narrower than this will result in fundal tip necrosis; a gastric tube too wide risks ischemia and leakage along the lesser curvature staple line and is too bulky a conduit to

70 ESOPHAGEAL SURGERY pass through the upper mediastinum. The blood supply to the tip of the gastric tube comes from ﬁne submucosal vessels. Unnecessary traction on this portion of the stomach tube will disrupt these ﬁne vessels and risk fundal tip ischemia. Proper mobilization of the stomach with a Kocher maneuver usually yields excellent length. When it does not, extend the cervical incision inferiorly and proceed with a lower reconstructive anastomosis.

Chyle Leak Intraoperative chyle leak is usually only seen when using right thoracotomy esophagectomy techniques. The thoracic duct may be injured anywhere along the intrathoracic esophagus during its dissection from the mediastinum. However, it is most prone to injury at the level of the carina where the duct begins to cross from the right side of the mediastinum to the left (Fig. 70–6).10 Identiﬁcation of a chylous leak may be difﬁcult at times. Esophagectomy patients often have trouble eating and have not eaten prior to surgery. The chyle, therefore, may be low volume and clear.

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● Consequence Failure to diagnose a signiﬁcant chyle leak leads to postoperative chylothorax. This requires drainage, delay in eating, nonenteric feeding, lengthened hospital stay, and often, operative intervention for repair. Prior to parenteral alimentation and recommendations for early surgical repair for large leaks, the mortality of this complication was signiﬁcant. It still is a serious complication. Grade 1 complication (if discovered and repaired at surgery) ● Repair Postoperative chylothorax is discussed later under “Postdischarge Complications.” ● Prevention It is often not feasible to prevent intraoperative thoracic duct injury. For patients with esophageal cancers, complete resection with wide lymphatic dissection supersedes thoracic duct protection. Whenever a right thoracotomy approach is used for esophagectomy, it is prudent to consider thoracic duct ligation as close to the diaphragm as possible. This will prevent postoperative chylothorax.

Subclavian vein

Early Inpatient Complications (<72 Hr) Superior vena cava Ribs

Azygos vein Aorta Thoracic duct

Diaphragm

Cisterna chyli

Figure 70–6 The course of the thoracic duct from the abdomen to the neck and its proximity to the azygos vein. The point at which the duct moves from the right to the left side of the chest is approximately at the level of the carina. (Adapted from Rodgers BM. The thoracic duct and the management of chylothorax. In Kaiser LR, Kron IL, Spray TL [eds]: Mastery of Cardiothoracic Surgery. Philadelphia, New York: Lippincott-Raven, 1998; pp 212– 220.)

Respiratory Complications Respiratory complications, including atelectasis, pleural effusion, respiratory failure, and pneumonia, are both some of the most common and some of the most serious of the postoperative complications. At least some basilar atelectasis and small pleural effusions are common after esophagectomy. Gillinov and Heitmiller11 reported rates of atelectasis and effusion of 97% and 85%, respectively. Most of the time, this presents only as a radiographic ﬁnding in a patient who is progressing as expected. Conversely, pneumonia leads to increased intensive care time, lengthened hospital stays, and a greatly increased mortality. Many respiratory complications can be anticipated12 or even prevented with adequate preoperative medical evaluation and risk assessment.13 Respiratory complications are discussed in order of their severity from least to most serious. Atelectasis results from low lung volumes associated with general anesthesia, incisional pain, and bedrest. Pleural effusions are mostly transudates and result from perioperative intravenous ﬂuid infusion especially in the setting of poor nutrition status (low albumin). In addition, there is the potential for transhiatal transit of peritioneal ﬂuid into the chest after esophagectomy. ● Consequence Atelectasis is the collapse of alveoli in the dependent portions of the lung associated with decreased lung compliance, impairment of oxygenation, and increased pulmonary vascular resistance. Radiographically, some degree of basilar atelectasis is expected after esophagec-

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tomy. In its mildest form, patients develop fevers, a cough, and perhaps, continued need for supplemental oxygen. In its more severe form, or if left untreated, it may progress to respiratory failure and pneumonia.14 Small, asymptomatic pleural effusions are commonly identiﬁed on chest ﬁlms after esophagectomy and are of little consequence. Larger effusions can lead to atelectasis, increasing respiratory failure, and possibly, pneumonia. Respiratory failure is more a consequence itself of atelectasis, pleural effusion, pneumonia, or underlying respiratory disease. However, once respiratory failure occurs, it leads to prolonged intensive care and hospital stays. Patients generally require prolonged invasive monitoring with risk of line complications. Patients are immobile and at increased risk for deep venous thrombosis and pulmonary embolic episodes. Prolonged tracheal and esophageal intubations increase the risk for tracheal injury and esophagorespiratory ﬁstula formation. Oral feedings are delayed pending extubation. Given that many patients present with nutritional deﬁcits, a delay in enteral feeding (if adjuvant jejunostomy has not been used) could ensue. Pneumonia is one of the most severe postesophagectomy complications and is associated with reported mortality rates of 2.9% to 50%.11,12,15–17 Pneumonia requires antibiotic use, prolongs intensive care time, generally lengthens overall hospital stay, and is associated with a markedly increased chance of dying. Increased coughing needed to clear pneumonia increases intrathoracic pressure, jeopardizing the healing of the esophagogastric anastomosis. Finally, because postesophagectomy pneumonias are considered aspiration events, oral feedings are generally delayed until the pneumonia clinically resolves. Grade 1/4/5 complication ● Repair Lung expansion maneuvers can help to expand collapsed areas of the lung that can lead to the development of atelectasis and pneumonia. These maneuvers include incentive spirometry, chest physiotherapy, deepbreathing exercises, postural changes, and coughing.11 The use of both bi-level positive airway pressure (BiPAP) ventilation and nasotracheal suctioning must be avoided or used with caution because they may potentially injure the esophagogastric anastomosis and result in a leak. If patients need airway suctioning, ﬂexible bronchoscopy or reintubation should be considered. The size of the pleural effusion dictates the treatment regimen. Smaller effusions may be watched and managed conservatively. Larger effusions, leading to symptoms and lung compression, should be drained by thoracentesis or chest catheter.18 Pneumonia is managed with antibiotics and respiratory care per routine. Patients who need suctioning should undergo bronchoscopy. If respiratory secretions are prominent, consider reintubation for suctioning. Hold oral feedings to minimize the likelihood of aspiration. Always treat postesophagectomy pneumonia aggressively. It is potentially life-threatening.

● Prevention As mentioned previously, some degree of basilar atelectasis and small pleural effusions is a near certainty after esophagectomy. With regards to atelectasis and pneumonia, there are two postesophagectomy management strategies. The ﬁrst believes that early (in the operating room) extubation, optimal use of regional anesthesia for pain control, and early patient mobilization will reduce respiratory complications after esophagectomy. The second strategy involves leaving patients intubated at the end of the surgery and sending them to the intensive care unit. Patients are extubated the next day (or later, as clinical course dictates), once it is clear that they are stable and chest ﬁlms are clear.11 Both strategies have their advocates. We believe that the early postoperative period should focus on systemic care and ﬂuid management while protecting the airway from aspiration (with the ETT cuff), minimizing secretions (with ETT suctioning), and atelectasis (with positive-pressure ventilation). Preventing complications, especially respiratory ones, after esophagectomy is key to a good outcome and short hospital stay. Appropriate ﬂuid management will minimize the risk of signiﬁcant pleural effusion. Many patients are taking diuretics preoperatively. When appropriate, these should be restarted after surgery. If a thoracotomy approach is used, a chest drain is placed at surgery. This should be left in place until approximately postoperative day 4 or 5. If a transhiatal approach is used, care should be taken not to open the pleural space. This will minimize the risk of transhiatal passage of peritoneal ﬂuid. Anticipate postoperative respiratory complications in patients with cardiorespiratory risk factors such as asthma, chronic obstructive pulmonary disease, and ischemic coronary artery disease. Optimize the patient’s status before surgery if possible.

Hoarseness (Ipsilateral RLN Injury) The ipsilateral RLN is at risk for injury during upper thoracic and especially cervical esophageal dissections. The reported rate of RLN injury ranges from 9% to 16%.4,16,19–21 ● Consequence The consequence of RLN injury depends on the severity of the injury and the position of the affected vocal fold. Hoarseness is the most common consequence of RLN injury. Signiﬁcant hoarseness results in a very “breathy” voice requiring a great deal of effort to communicate. Patients get winded quickly, which adds further frustration to the recovery effort. The vocal fold is one of the last and most effective defenses for airway protection against aspiration. Studies have shown that 50% of patients with unilateral RLN injury have documented aspiration22,23 and are therefore at increased risk for pneumonia. Grade 3 complication

70 ESOPHAGEAL SURGERY

735

cause, who develops an elevated serum potassium, signiﬁcant leukocytosis, or fever should be suspected of having conduit ischemia. As bad as this complication is, it is far worse to miss the diagnosis and let the patient develop a possible intrathoracic esophageal leak.7 ● Consequence Nonnecrotic cases present with high fever and leukocytosis that ultimately resolves with supportive therapy. Often, it is not clear what is wrong with the patient. The clinical instability resolves spontaneously. Most of the time, patients are systemically sick in a sepsis-like state. Failure to make the diagnosis and treat patients may result in multisystem failure, esophageal leakage, esophagorespiratory or esophagovascular ﬁstula formation, and death. Grade 3/4/5 complication

Figure 70–7 The anatomy of the recurrent laryngeal nerves.

● Repair Most affected RLNs are injured, not divided, and will recover with time. Heitmiller and Jones23 showed that patients prone to aspiration after transhiatal esophagectomy will spontaneously recover airway protection signiﬁcantly or completely within 1 month after surgery. During this time, enteral feeding via jejunostomy avoids aspiration pneumonia. More severe deﬁcits may be managed by vocal fold medialization transiently (by injections) or permanently (by surgery). ● Prevention The risk of RLN injury can be minimized by an understanding of its anatomy (Fig. 70–7), careful dissection around the nerve avoiding use of electrocautery, and especially, avoiding traction on the nerve when encircling the cervical esophagus.18 Although the goal is zero nerve injury, this is not always possible, especially in cancer patients.

Conduit Ischemia The success of esophagectomy is largely dependent on the viability and function of the esophageal conduit. Often, the risk of graft ischemia can be detected at surgery. Many times, however, the operative procedure progresses well and ischemic complications develop without warning. Arterial insufﬁciency will present early after surgery. The rates of conduit ischemia have been listed previously. Any patient early after surgery who is unstable without obvious

● Repair Prevention is the rule. There are no data to demonstrate that treatment with steroids, anticoagulants, antibiotics, or pressors will prevent the development of necrotic ischemia once the process has started. If there is ischemia of the entire conduit, the patient must return to the operating room for re-resection and esophageal diversion (cervical esophagostomy and jejunostomy). Reconstruction is planned as a second stage once the patient has had the opportunity to recover fully. ● Prevention Prevention of ischemia by careful operative technique is the best way to avoid ischemic complications. This has been covered earlier in this chapter.

Arrhythmia Cardiac arrhythmias, especially atrial ﬁbrillation and supraventricular tachycardia, can be a postoperative complication of esophagectomies. This is especially found in patients who are over the age of 70 or have a history of cardiac disease.24 Intraoperative risk factors include blood loss and extensive thoracic dissection. The patients who develop atrial ﬁbrillation have a higher risk for other postoperative complications. Aspiration, pneumonia, myocardial infarction, anastomotic leak, and sepsis are the most common.25 ● Consequence The consequence of this complication is hemodynamic instability, myocardial ischemia, and respiratory failure. Long-term atrial arrhythmias may increase the possibility of systemic embolic episodes. Grade 1 complication ● Repair The management involves conﬁrmation of the diagnosis and standard arrhythmia treatment using medical or electrical cardioversion. At this time, the patient should undergo a full work-up to determine the underlying cause of the arrhythmia.

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● Prevention Again, prevention lies in medically optimizing the patient before surgery. A full cardiac work-up should be performed if the patient has any history of cardiac disease. Preoperative medications can be administered as prophylaxis against postoperative atrial ﬁbrillation. These include digoxin, calcium channel blockers, βblockers, and amiodarone. To date, no standard of care has been developed to prevent atrial ﬁbrillation in esophagectomy patients.

Late Inpatient Complications (>72 Hr) Aspiration (Pneumonia) The risk of postesophagectomy aspiration and pneumonia is not uniform. Patients are at greatest risk early after surgery when they are sedated and supine and later when they resume oral feedings. ● Consequence The consequence of aspiration is risk of pneumonia. The signiﬁcance of this complication has previously been covered. Just because a patient appears to be progressing well toward discharge does not mean that a life-threatening pneumonia cannot occur late in the hospital course. Grade 1/4/5 complication ● Repair The treatment has been previously discussed. ● Prevention Clinical evaluation of swallowing function is not sensitive at identifying aspiration. The best way to screen for aspiration is with contrast video esophagogram studies.23 The consistency of the contrast can be altered to mimic different foods. If signiﬁcant aspiration is identiﬁed, oral feedings should be held, patients should continue enteral jejunostomy feedings, should be discharged home, and should undergo a repeat swallowing study in approximately 4 weeks.

Anastomotic Leak An esophageal anastomotic leak can be a potentially lifethreatening complication that may result in extended mechanical ventilation, respiratory failure, or septic shock. The reported leak rate for esophagogastric anastomosis ranges from 0% to 14% in most series.16,20,21,26–30 By deﬁnition, scheduled plans to have a patient resume swallowing are placed on hold. Most leaks occur around postoperative day 4 or 5; however, leaks may occur earlier or up to a week or two after surgery. If a leak is suspected, the diagnosis is best conﬁrmed by contrast esophagogram. If a patient is unable to swallow contrast, a tube study—contrast infused through a nasogastric tube—may be employed.

● Consequence The consequence of leak depends primarily on its location. As mentioned previously, scheduled plans to resume swallowing are placed on hold pending leak management. A cervical leak, if suspected early and managed, has the least adverse consequences. These include a messy neck wound, usually some delay in hospital discharge, a delay in swallowing, and an increased risk of later anastomotic stricture formation. An intrathoracic leak is a potentially life-threatening problem. If the leak is large and drains into the mediastinum or pleural space, patients will rapidly develop signs of systemic sepsis. Plans to resume swallowing are on hold indeﬁnitely. Hospital stays are lengthened, and the objective of therapy shifts to saving the patient’s life without, if possible, jeopardizing the esophageal reconstruction. This is not always possible. Grade 3 complication ● Repair Cervical leaks are the easiest to manage. Neck wounds must be widely opened to permit free transcervical drainage. Neck wounds should be opened, viability of the conduit conﬁrmed, and the wound irrigated and left open with packing.18 The better the drainage, the faster the closure of the leak, and the less chance for inferior extension of infection into the mediastinum. If an adjuvant jejunostomy is in place, continue to advance enteral feedings to goal. Once stable, patients may even conclude treatment as outpatients. When cervical leaks close, drainage from the wound abruptly ends and the wound closes very fast. Intrathoracic leaks are much more challenging.18 If the leak is small and contained, it may be followed closely. Keep the patient on nothing by mouth, use nasogastric drainage if it is already in place, and advance enteral feedings to goal. If it is not contained, the ﬁrst option is wide drainage (nasogastric tube and chest drains) with intravenous antibiotics and enteral feedings. Some patients will weather this storm, but they will be sick, in intensive care, with long hospital stays. The second option is to divert the cervical esophagus, drain the chest and mediastinum, and advance enteral feedings. The third option is to take down the reconstructive conduit and divert the esophagus. Obviously, this last option must be used if the conduit is necrotic. With the last two options, reconstruction later becomes a challenge. ● Prevention Prevention may not always be possible. Optimize preoperative nutrition and cardiorespiratory function. Avoid operating on patients who are catabolic or on steroids.30 Carefully mobilize esophageal conduits to avoid ischemia. Perform anastomosis carefully, without tension. Secondarily reinforce anastomoses when possible.26 Consider esophagectomy approaches that use

70 ESOPHAGEAL SURGERY neck anastomoses. Several reports indicate that leak rates are affected by anastomotic technique.31

Wound Infection Many esophagectomy patients have lost weight preoperatively, and the midline abdominal incision is potentially exposed to contamination from the esophagus. As a result, superﬁcial wound infection is seen in approximately 5% to 10% of esophagectomy patients. The main bacterial contaminants are Staphylococcus aureus, coagulase-negative Staphylococcus, Enterobacter species, Escherichia coli, and group D Enterococcus. ● Consequence Wound infections, diagnosed early and treated, should have little consequence. Patients may develop fever and leukocytosis, which resolves quickly with treatment. Antibiotics may be needed if cellulitis is present. Wound packing will be required, but this should not delay discharge or enteral feedings. Grade 1/2 complication ● Repair An infected wound should be gently explored with a sterile cotton swab and the loculations broken apart. If the infection has not caused the fascial layers to separate, the wound can be cleaned with sterile saline followed by bedside débridement of nonviable tissue and packed with saline-moistened gauze to allow healing by secondary intention from the base. A course of antibiotics is needed only if there is associated cellulitis. ● Prevention Optimized preoperative nutritional status, preoperative antibiotics, intraoperative wound irrigation, and interrupted wound closure will minimize the risk of abdominal wound infection.

Chyle Leak Chyle leakage secondary to thoracic duct injury has been discussed previously. The reported rate of postesophagectomy chlye leak is 3.7%; however, the risk of chlye leak varies according to the location of esophageal disease. Rao and coworkers32 reported rates of 0.8% for lower third and 5.8% for middle third esophageal diseases. Although sometimes suspected at surgery, chyle leakage is more commonly seen around postoperative days 3 to 5 when enteral feeding is started. At that time, the patient develops a large pleural effusion, usually on the right side but it can occur on either side. If a chest drain is in place, the characteristic high-volume, milky white drainage is noted. Characteristic laboratory studies for chylous ﬂuid are listed in Box 70–3. Prior to intravenous alimentation and current strategies for early intervention, this complication was associated with a high mortality.

Box 70–3

737

Appearance and Composition of Chyle

Appearance ● ●

Turbid, milky white Layers upon standing into ● Upper (chylomicrons) ● Intermediate (milky) ● Dependent (cellular)

Speciﬁc Gravity ●

1.020–1.030

Protein Content ●

3–4 g/100 ml

Fat Content ●

1–4 g/100 ml

Triglycerides ●

>110 mg/dl

● Consequence Chyle is rich in protein, fat, and white blood cells. Prolonged high-volume loss of chyle leads to nutritional failure and immunosuppression. Wound healing problems, anastomotic leakage, and infectious complications are all possible. Hospital stays are extended, pending resolution of this problem. Grade 2/3 complication ● Repair After diagnosis, enteral feedings are held to put the gastrointestinal tract at rest and reduce chyle ﬂow through the thoracic duct. Intravenous feedings are initiated. Treatment plans are largely based on chyle drainage volume. Leaks less than 500 ml/day generally resolve with drainage. Leaks with greater than 1000 ml/ day invariably need operative intervention for resolution. If drainage is high, a time period should be set during which the leak should lessen quickly or operative intervention will proceed. Generally, this time period is 5 to 7 days. If daily drainage is 500 to 1000 ml/day, it is hard to predict the clinical course. Start with drainage and intravenous feedings, follow output, and wait for 5 to 7 days to see the trend. Operative repair involves low right thoracotomy or thoracoscopy with thoracic duct ligation just above the right hemidiaphragm (Fig. 70–8).10 Chylous leaks should promptly resolve with surgery. ● Prevention Understanding thoracic duct anatomy during surgery and prophylactically ligating the duct at surgery are the best and only methods of prevention.

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SECTION XI: THORACIC SURGERY Azygos vein

Lung (retracted)

Injured thoracic duct IVC

Aorta Esophagus (retracted) Diaphragm

Figure 70–8 Operative ligation of the thoracic duct is performed through the right chest. The thoracic duct is identiﬁed and ligated low in the chest, close to the diaphragm. A right thoracotomy is shown; however, the procedure could also be performed by thoracoscopy. (Adapted from Rodgers BM. The thoracic duct and the management of chylothorax. In Kaiser LR, Kron IL, Spray TL [eds]: Mastery of Cardiothoracic Surgery. Philadelphia, New York: Lippincott-Raven, 1998; pp 212–220.)

● Repair Progressive solid food dysphagia within 2 to 6 months of esophagectomy, especially when a patient’s swallowing was initially not restricted, is a sure sign of anastomotic narrowing. The diagnosis can be conﬁrmed by contrast esophagogram, but this is not always needed. Flexible esophagoscopy will also make the diagnosis of anastomotic stricture. It is essential that early endoscopy be performed for later strictures to rule out recurrent tumor. Treatment is dilation. Our experience has been that these are “soft” strictures that dilate easily but have a tendency to recur unless they are dilated slowly, in stages.26 Generally, two to three dilations are needed to open the stricture in steps so that, once open, it will stay open. Recurrence is then uncommon. ● Prevention It may not be possible to prevent strictures. Careful preoperative patient selection and preparation, mobilization of the esophageal conduit without ischemia, and creation of a tension-free anastomosis will help to reduce the chance of stricture. Some data suggest that avoiding neck anastomosis will reduce the incidence of strictures. However, a cervical anastomosis prevents the risk associated with leakage—a much more serious problem. Some believe that a stapled anastomosis reduces stricture formation, whereas others have demonstrated good results with hand-sewn methods.

OTHER COMPLICATIONS Additional speciﬁc complications associated with a thoracoabdominal approach or Ivor Lewis approach to esophagectomy are predominantly associated with the thoracotomy incision.

Postdischarge Complications Anastomotic Stricture Anastomotic narrowing with healing may occur after surgery. Most anastomotic strictures occur between 2 and 6 months after surgery. Risk factors for stricture include location of anastomosis, conduit ischemia, early postoperative anastomotic leakage, preexisting low cardiac output, and anastomotic technique. Factors believed to be associated with a high risk of stricture include cervical anastomosis, leakage, low preoperative cardiac output, and hand-sewn anastomosis.30 Strictures may occur even without these risk factors. Late anastomotic strictures (>1 yr postoperative) must raise the suspicion of recurrent cancer. ● Consequence Signiﬁcant anastomotic narrowing results in poor swallowing, reduced quality of life, reduced oral intake with potential for weight loss, and increased risk of “overﬂow” aspiration. Grade 1/2 complication

Diaphragmatic Hernia/Paraesophageal Hernia The esophageal hiatus is widened during esophagectomy to permit passage of the replacement esophageal conduit up into the chest. Postoperative herniation of abdominal structures through the hiatus, alongside the conduit, has been reported. This complication presents in two ways. The ﬁrst is an acute presentation early in the postoperative course. The second is as a late ﬁnding on surveillance ﬁlms.33 ● Consequence Early herniation is generally an acute event, with signiﬁcant herniation of transverse colon and omentum into the right chest. It is associated with acute respiratory symptoms and requires operative repair. Late herniation usually involves a section of the transverse colon, is a radiographic ﬁnding, is asymptomatic, and does not require intervention. Grade 3 complication ● Repair Early herniation presents as an acute event with prominent respiratory symptoms. Early transabdominal exploration is indicated. The herniated contents are reduced and the hiatus narrowed. Abdominopexy of abdominal contents may sometimes be needed. Late herniation is invariably an asymptomatic radiographic ﬁnding and does not require intervention.

70 ESOPHAGEAL SURGERY ● Prevention At the initial surgery, open the hiatus only as much as needed for intrathoracic dissection and passage of the stomach conduit. If needed, narrow the hiatus anteriorly before closing the abdomen.

REFERENCES 1. Brock MV, Venbrux AC, Heitmiller RF. Percutaneous replacement jejunostomy after esophagectomy. J Gastrointest Surg 2004;4:407–411. 2. Matory YL, Burt M. Esophagogastrectomy: reoperation for complications. J Surg Oncol 1993;54:29–33. 3. Postlethwaite RW (ed). Surgery of the Esophagus, 2nd ed. Norwalk, CT: Appleton-Century-Crofts, 1986; p 410. 4. Baue AE, Geha AS, Hammond GL, et al. Surgical options for esophageal resection and reconstruction with stomach. In Orringer MB (ed): Glenn’s Thoracic and Cardiovascular Surgery, 6th ed. Stamford, CT: Appleton & Lange, 1996; pp 899–922. 5. Black E, Niamat J, et al. Unplanned splenectomy during oesophagectomy does not affect survival. Eur J Cardiothoracic Surg 2006;29:244–247. 6. Gockel I, Kneist W, Junginer T. Inﬂuence of splenectomy on perioperative morbidity and long-term survival after esophagectomy in patients with esophageal carcinoma. Dis Esophagus 2005;18:311–315. 7. Wormuth J, Heitmiller RF. Esophageal conduit necrosis. Thorac Surg Clin 2006;16:11–22. 8. Heitmiller RF, Heitmiller ES. Surgery for myasthenia gravis. In Franco KL, Putnam JB Jr (eds): Advanced Therapy in Thoracic Surgery, 2nd ed. Hamilton, London, Ontario: BC Decker, 2005; p 413. 9. Heitmiller RF. Impact of gastric tube diameter on upper mediastinal anatomy. Dis Esophagus 2000;13:288–292. 10. Rodgers BM. The thoracic duct and the management of chylothorax. In Kaiser LR, Kron IL, Spray TL (eds): Mastery of Cardiothoracic Surgery. Philadelphia, New York: Lippincott-Raven, 1998, pp 212–220. 11. Gillinov AM, Heitmiller RF. Strategies to reduce pulmonary complications after transhiatal esophagectomy. Dis Esophagus 1998;11:43–47. 12. Law S, Wong KH, Kwok KF, et al. Predictive factors for postoperative pulmonary complications and mortality after esophagectomy for cancer. Ann Surg 2004;240:791–800. 13. Arozullah AM, Conde MV, Lawrence VA. Preoperative evaluation for postoperative pulmonary complications. Med Clin North Am 2003;87:153–173. 14. Duggan M, Kavanagh BP. Pulmonary atelectasis: a pathogenic perioperative entity. Anesthesiology 2005;102: 838–854. 15. Kita T, Mammoto T, Kishi Y. Fluid management and postoperative respiratory disturbances in patients with transthoracic esophagectomy for carcinoma. J Clin Anesth 2002;14:252–256.

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16. Orringer MB, Marshall B, Iannettoni MD. Transhiatal esophagestomy: clinical experience and reﬁnements. Ann Surg 1999;230:392–400. 17. Avendano CE, Flume PA, et al. Pulmonary complications after esophagectomy. Ann Thorac Surg 2002;73:922– 926. 18. Lin J, Iannettoni MD. Transhiatal esophagectomy. Surg Clin North Am 2005;85:593–610. 19. Gockel I, Kneist W, Keilmann A, Junginger T. Recurrent laryngeal nerve paralysis (RLNP) following esophagectomy for carcinoma. Eur J Surg Oncol 2005;31:277–281. 20. Katariya K, Harvey JC, Pina E, et al. Complications of transhiatal esophagectomy. J Surg Oncol 1994;57:157– 163. 21. Gandhi SK, Naunheim KS. Complications of transhiatal esophagectomy. Chest Surg Clin North Am 1997;7:601– 610. 22. Heitmiller RF, Tseng E, Jones B. Prevalence of aspiration and laryngeal penetration in patients with unilateral vocal fold motion impairment. Dysphagia 2000;15:184–187. 23. Heitmiller RF, Jones B. Transient diminished airway protection after transhiatal esophagectomy. Am J Surg 1991;162:442–446. 24. Loran DB. Thoracic surgery in the elderly. J Am Coll Surg 2004;199:773–784. 25. Murthy SC. Atrial ﬁbrillation after esophagectomy is a marker for postoperative morbidity and mortality. J Thorac Cardiovasc Surg 2003;126:1162–1167. 26. Heitmiller RF, Fischer A, Liddicoat JR. Cervical esophagogastric anastomosis: results following esophagectomy for carcinoma. Dis Esophagus 2000;12:264–270. 27. Atkins BZ, Shah AS, et al. Reducing hospital morbidity and mortality following esophagectomy. Ann Thorac Surg 2004;78:1170–1176. 28. Crestallano JA, Deschamps C, Cassivi SD, et al. Selective management of intrathoracic anastomotic leak after esophagectomy. J Thorac Cardiovasc Surg 2005;129:254– 260. 29. Michlet P, D’Journo XB, Roch A, et al. Perioperative risk factors for anastomotic leakage after esophagectomy: inﬂuence of thoracic epidural anesthesia. Chest 2005;128: 3461–3466. 30. Briel JW. Prevalence and risk factors for ischemia, leak, and stricture of esophageal anastomosis: gastric pull-up versus colon interposition. J Am Coll Surg 2004;198:536– 541. 31. Ercan S, Rice TW, Murthy SC, et al. Does esophagogastric anastomotic technique inﬂuence the outcome of patients with esophageal cancer? J Thorac Cardiovasc Surg 2005;129:623–631. 32. Rao DV, Chava SP, Sahni P, Chattopadhyay TK. Thoracic duct injury during esophagectomy: 20 years experience at a tertiary care center in a developing country. Dis Esophagus 2004;17:141–145. 33. Heitmiller RF, Gillinov AM, Jones B. Transhiatal herniation of colon after esophagectomy and gastric pull-up. Ann Thorac Surg 1997;63:554–556.

71

Cervical Tracheal Resection and Reconstruction Joseph B. Shrager, MD INTRODUCTION

INDICATION

A wide variety of conditions cause anatomic or functional narrowing of the trachea. The most efﬁcient and effective treatment for most of these conditions is tracheal resection with subsequent end-to-end anastomosis (TR). Techniques have been standardized since the 1960s to allow these procedures to be performed with excellent results and low morbidity and mortality. Release techniques have been developed that frequently allow even long segments to be resected with the creation of a tension-free anastomosis that will usually heal without incident. However, even in the most experienced hands, TR can engender a variety of complications—some of which are emergent and life threatening. This chapter reviews the basic operative steps of TR and the complications that can be encountered as they relate to each step. The management of each complication is presented as well as technical details that can be followed in order to try to prevent the complication from occurring. I focus upon “simple cervical tracheal resection”—the excision of a segment of the upper trachea, not including the cricoid cartilage or higher, carried out through a curvilinear neck incision just above the jugular notch. More complex resections including the larynx or the distal trachea approaching the carina, though utilizing many of the same basic principles, require somewhat different and more advanced techniques that are beyond the scope of this chapter. Further, it has been established that as the anastomotic level ascends, a progressive increase in complication rate occurs: failure rates rise from 2.2% for trachea-trachea anastomosis to 6.0% for trachea-cricoid anastomosis to 8.1% for trachea–thyroid cartilage anatomosis.1 Two centers pioneered the techniques of TR that are now in standard use around the world: these are the groups formerly headed by Hermes Grillo at the Massachusetts General Hospital (MGH) and by Grifﬁth Pearson at the Toronto General Hospital. Because I am more familiar with the methods and results of the MGH group, having trained with Grillo, I focus upon their techniques and their published results in reporting the incidences of the various complications.

● Tracheal stenosis in upper third of trachea caused by

prior tracheostomy or endotracheal intubation, inﬂammatory disorders, or tumors

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7 Step 8

Rigid bronchoscopy with or without dilation Circumferential dissection of involved portion of trachea Tension-releasing maneuvers Airway division Cross-table or high-frequency jet ventilation (HFJV) Anastomosis “Chin stitch” Extubation

OPERATIVE PROCEDURE AND COMPLICATIONS Rigid Bronchoscopy with or without Dilation Rigid bronchoscopy is nearly always performed immediately prior to TR for a variety of reasons. First, the view of the mucosa with a Hopkins lens system passed via a rigid bronchoscope is superior to that obtained through a ﬂexible bronchoscope, therefore, decisions regarding whether acute inﬂammation has resolved and whether or not there is any need to delay the procedure can be made most accurately. Second, measurements of the length of the stenosis, the distance from the distal end of the stenosis to the carina, and the distance from the proximal edge of the stenosis to the vocal cords can be made most accurately with a rigid scope. The most important reason for carrying out rigid bronchoscopy immediately preoperatively, however, is the frequent need for tracheal dilation immediately prior to the procedure. One would like to pass at least a size-5 and preferably a size-6 endotracheal tube (ETT) beyond the

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SECTION XI: THORACIC SURGERY the eventual TR. Patients who are salvaged may suffer varying degrees of anoxic brain injury. Grade 2–5 complication

Figure 71–1 Bronchoscopic view of a postintubation tracheal stenosis just prior to dilation with the rigid bronchoscope through which the stenosis is seen. Dilation is performed to allow placement of an endotracheal tube (ETT) prior to resection. It is done by stretching the stenosis with serially larger rigid bronchoscopes.

stenosis prior to positioning and operation so that the airway is secure and the dissection can proceed without undue haste up to the point of initial airway division. In situations in which a size-6 tube cannot be passed because of the tight nature of the stenosis, progressive dilation with rigid scopes will generally allow passage of such a tube. The technique of dilation involves beginning with a scope with a diameter only slightly larger than the visible tracheal lumen (Fig. 71–1). This bronchoscope is passed through the stenosis and deeply into the airway, and it is held there for at least 1 minute as the stenosis is stretched, maintaining ventilation through the bronchoscope. A scope that is 0.5 to 1 mm larger is passed next, and the procedure is repeated until the lumen is sufﬁciently large to pass the ETT. For a critically tight stenosis, one can use Jackson dilators passed through the bronchoscope initially until the lumen is large enough to pass the tip of the scope itself.

Preoperative Loss of Airway ● Consequence If not rapidly salvaged, this complication can lead to death. Its occurrence requires the rapid and focused application of all of the knowledge and abilities of a team consisting of surgeon, anesthesiologist, and nurses. Often, tracheostomy is necessary, complicating

● Repair The onus is clearly upon the surgeon to reestablish an airway. If edema at the site of stenosis and prior dilation is the cause of the loss of airway, a single attempt to reintroduce a smaller rigid bronchoscope is the initial maneuver. One can then ventilate via this scope as a more detailed plan is formulated. If one is unable to pass the scope into the trachea because of an unusually large epiglottis or other supraglottic abnormalities, visualization of the cords with use of a Miller blade on the laryngoscope may be useful, followed by passage of the rigid bronchoscope through cords that have been directly visualized in this manner. If the patient is persistently desaturated to less than 75% and an airway cannot be reestablished from above, emergent tracheostomy is necessary. Typically a size-6 tracheostomy is selected. The opening in the trachea is made directly through the area of stenosis, if at all possible. This will preserve the length of remaining healthy trachea and will not increase the length of the ultimate tracheal resection that will be required. If, for some reason, an actual tracheostomy cannot be performed or if it cannot be performed expeditiously, and if HFJV is available, a needle may be passed into the airway through or below the stenosis and HFJV instituted. ● Prevention A surgical set sufﬁcient to perform tracheostomy must always be fully opened before the performance of rigid bronchoscopy with dilation, and a variety of endotracheal and tracheostomy tubes must be immediately available should they be needed. Ideally, HFJV will also be available. The surgeon and anesthesiologist need to discuss in detail before the induction of anesthesia the anesthetic and bronchoscopy plan, the likelihood of an untoward event, and the plan in case of an untoward event. During dilation, one should hyperventilate and superoxygenate the patient through the scope each time a scope is passed beyond the stenosis. This will allow a greater period of time to pass the next larger scope before desaturation or hypercarbia ensues. One should never attempt to pass a ﬂexible bronchoscope, which does not allow ventilation through a tight stenosis—particularly not outside of an operating room where rigid scopes, ETTs, and tracheostomies are available. This may precipitate airway occlusion without the ability to salvage the situation.

Circumferential Dissection of the Involved Portion of the Trachea After the curvilinear cervical skin incision has been made, subplatysmal ﬂaps are mobilized down to the jugular

71 CERVICAL TRACHEAL RESECTION AND RECONSTRUCTION

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Figure 71–2 Typically, one ﬁrst dissects the trachea circumferentially only at the distal end of the diseased area. A Penrose or red rubber drain is then passed around the trachea in this location.

notch and up to the thyroid cartilage, and the anterior wall of the trachea is exposed by division of the thyroid isthmus. The critical portions of the operation are then begun. In many cases, the distal extent of the internal stenosis can be seen by thickening and scar tissue visible on the external surface noted during mobilization. When this line is unclear, a ﬂexible bronchoscope can be introduced from above, and its light or visualization of a needle passed into the lumen from without can be used to demonstrate the distal extent to the operating surgeon. A ﬁne suture is placed on the external tracheal surface at this level to indicate the extent of mobilization required and the ultimate point of distal division. The involved region of trachea is then mobilized ﬁrst from its lateral, vascular attachments, then from the posterolaterally placed recurrent laryngeal nerves, and ﬁnally from the esophagus, which is closely apposed to the posterior, membranous tracheal wall. A Penrose or red rubber drain can then be placed around the trachea (Fig. 71–2). Almost all of the circumferential dissection is carried out sharply. In some cases, when there is little scarring or inﬂammation, circumferential dissection of virtually the entire involved segment can be done prior to airway division. In most situations, however, I mobilize only the most distal portion of the involved airway circumferentially, leaving the posterior dissection of the more proximal portion from the underlying esophagus for after the division of the airway distally. After this distal division has been carried out, the proximal segment to be resected can be progressively lifted up, facilitating its dissection away from the nerves and esophagus (Fig. 71–3). It is critical that circumferential dissection be taken only about 5 mm beyond what will become the margins of resection in order to maximally preserve blood supply to the anastomosis (see the section on “Anastomosis,” later).

Figure 71–3 After placing distal, midlateral stay sutures of 0-0 Vicryl and withdrawing the ETT, sharp division is carried out with a scalpel. From this point on, cross-table ventilation is carried out. Next, the proximal involved segment of trachea is dissected more proximally away from the esophagus and recurrent nerves until the proximal point of division is reached. (From Grillo HC. Surgery of the Trachea and Bronchi. United States, BC Decker, Inc; 2004.)

Recurrent Nerve Injury ● Consequence Injury to one recurrent laryngeal nerve will cause hoarseness, but it may also cause incomplete airway compromise and swallowing dysfunction that can lead to aspiration. A nerve is sometimes injured or stretched but not actually divided; in this case, its function may return over several weeks. In addition, the opposite vocal cord may adapt over time, coming across the midline to improve voice and prevent aspiration. However, function will not be restored in the case of complete division. If a nerve becomes paralyzed in a medial position, it may serve as an obstruction to airﬂow but aspiration is less likely. If it becomes paralyzed in a lateral position, it will not obstruct airﬂow, but voice will be weak and coughing difﬁcult. Further, with a cord in the lateral position, aspiration is more likely. Injury to both recurrent laryngeal nerves usually creates an airway emergency, with the patient being unable to spontaneously ventilate adequately after extubation. This will require urgent placement of a tracheostomy if one has not been placed prophylactically after TR. It will also typically cause severe aspiration difﬁculties requiring the establishment of long-term enteral feeding. Out of a total of 521 TRs for postintubation stenosis reported by the MGH group since 1986, 25 patients (5%) had varying degrees of postoperative laryngeal dysfunc-

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tion.1–3 This included 62 patients who required complete resection of the anterior cricoid (higher than a “simple” TR). The laryngeal dysfunction was considered minor or temporary in 14, but 11 patients had more severe dysfunction. Of these, 7 required tracheostomy (3 permanent), 1 required a permanent T-tube, and 1 required a subglottic stent. Two patients required tube feedings for persistent aspiration. TRs for tumors of the upper trachea, as one might expect given the greater extent of lateral dissection often required to allow complete tumor excision, likely lead to a greater incidence of recurrent nerve injury and laryngeal dysfunction. The MGH group reported 26 cervical TRs for tumor in a series of 126 primary tracheal tumors reported in 1990.4 Among the 126, 11 (8.7%) suffered vocal cord paralysis. Six (4.7%) suffered aspiration. Because this number includes patients who underwent more extensive resections and even carinal resections, the incidences of these complications after simple cervical TR for tumor are difﬁcult to glean, but I believe it is fair to say that resections for tumor have a higher rate of nerve injury than those for postintubation lesions. Grade 2–4 complication ● Repair Bilateral recurrent nerve injury requires emergent tracheostomy and will almost certainly require prolonged enteral feeding owing to chronic aspiration. Unilateral recurrent nerve injury, if it is not associated with signiﬁcant aspiration and if the patient has an adequate airway, can generally be monitored for improvement over approximately 6 months. If, after that period of time, an acceptable voice has not returned owing to a persistently lateralized cord, that cord can be medial-

ized by a minor procedure performed by an experienced otorhinolaryngologist. If a unilateral recurrent nerve injury is associated in the early postoperative period with aspiration and/or difﬁculty generating a sufﬁciently strong cough owing to lack of cord apposition, medialization can be performed early. If aspiration persists, enteral feeds must be begun, but this is almost always a temporary necessity in unilateral nerve injury. ● Prevention Careful operative technique minimizes the risks of recurrent nerve injury. When circumferentially dissecting the trachea, one should not try to identify the recurrent nerves. Rather, one hopes not to see them whatsoever. The dissection is maintained directly on the wall of the tracheal cartilage at all times. If this rule is adhered to, only very rarely (e.g., in cases which a vigorous inﬂammatory process has destroyed that cartilage and/or drawn the nerve into a matted mass of inﬂammatory tissue) that a nerve will be injured. If the wall of the trachea is not clearly visualized, it is far better to cut into what will ultimately be the resected specimen while dissecting the trachea out than to try to stay outside of it and risk injuring the nerve(s). It must be understood by the tracheal surgeon that as one more closely approaches the larynx, the recurrent nerves (particularly on the right) are increasingly at risk because their position becomes progressively more medial and closer to the trachea until they ﬁnally disappear behind the posterior cricoid plate (Fig. 71–4). It is, therefore, at the upper end of the dissection and during true subglottic resections that one must be most careful to stay directly on the trachea.

Right vagus nerve Right subclavian artery

Left common carotid artery Left subclavian artery

Right recurrent laryngeal nerve Right and left brachiocephalic veins Brachiocephalic artery Superior vena cava

Right common carotid artery Left vagus nerve Aorta

Left recurrent laryngeal nerve Pulmonary trunk

Figure 71–4 Demonstration of how the recurrent nerves become closer to the trachea and, thus, are at greater risk of injury, as the dissection ascends cephalad toward the larynx. (From Grillo HC. Surgery of the Trachea and Bronchi. United States, BC Decker, Inc; 2004.)

71 CERVICAL TRACHEAL RESECTION AND RECONSTRUCTION In addition, cautery should be used extremely judiciously as one approaches the posterior one half of the trachea. The best technique is simply not to use cautery whatsoever in this region because the punctuate bleeders that develop here almost always seal spontaneously. However, if cautery is necessary, only the exact point of bleeding should be cauterized, and the device should be set on an extremely low setting, preferably using the bipolar cautery. Because nerve injury does occasionally occur, these patients should always be begun initially on thickened liquids rather than clear liquids by mouth because thickened liquids are less easily aspirated. The initial feeding should be carefully monitored for signs of aspiration. Only after thickened liquids have been tolerated for about 2 days should clear liquids be attempted.

Esophageal Injury Esophageal injury is very rare and often recognized intraoperatively. It is most likely to occur either as one encircles the trachea prior to distal tracheal division or as one proceeds with cephalad dissection of the membranous wall of the trachea off of the underlying esophagus. ● Consequence If discovered and repaired immediately, as is usually the case, a small injury to the esophagus rarely leads to any postoperative problems. An undiscovered esophageal injury, or a repair that breaks down, may lead to wound infection and neck cellulitis or tracheoesophageal ﬁstula. The latter results from development of a communication between the area of esophageal injury and the membranous wall portion of the tracheal anastomosis. Grade 1–4 complication ● Repair If discovered intraoperatively, the esophagus should be closed in two layers, and a strap muscle should be mobilized based upon its inferior vascular pedicle and interposed between the esophagus and the posterior portion of the tracheal anastomosis (Fig. 71–5). I prefer to tack the muscle circumferentially onto the area of injury prior to creating the tracheal anastomosis. An esophageal injury that is discovered late postoperatively is more problematic and involves complex management options beyond the constraints of this chapter. ● Prevention Esophageal injury, like recurrent nerve injury, can generally be prevented by staying directly on the wall of the trachea. This is somewhat more difﬁcult on the membranous than the cartilaginous wall because the former is often less well deﬁned. There have been cases of resection of benign tracheal stenoses during which I have left some of the posterior tracheal scar (remnant of the membranous wall) in place on the esophagus in order to avoid any possibility of creating an esophageal

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Esophagus

Figure 71–5 Technique of mobilizing strap muscle for placement between the esophagus and the trachea in the event of an esophageal injury. The larger and more superﬁcial of the strap muscles, the sternohyoid, is divided at the upper end of the operative ﬁeld and rotated into the space between the trachea and the esophagus. It is tacked circumferentially around the injury with interrupted horizontal mattress 00-00 Vicryl sutures taken into the esophageal muscularis only. This type of muscle ﬂap can also be used to isolate the anastomosis from a tracheostomy tube on the rare occasion in which a small tracheostomy is left in place at the completion of the procedure. (From Reed MF, Mathisen DJ. Tracheoesophageal ﬁstula. Chest Surg Clin North Am 2003;13:271–290.)

injury. The technique mentioned previously of initially mobilizing only the most distal portion of the involved trachea circumferentially, then dividing at this level before trying to dissect the trachea off of the esophagus more proximally (see Fig. 71–3), is generally successful at allowing safe dissection in this plane.

Tension-Releasing Maneuvers Maximal reduction of tension on the tracheal anastomosis is probably the most important single technical aspect of these operations. The basic tension-releasing maneuvers are preferably performed prior to airway division. In every patient, the avascular, pretracheal plane is dissected all the way down to the level of the carina to allow the distal trachea to slide easily upward into the neck. In resections of 4 cm or greater in length, a suprahyoid laryngeal release (SLR) will often be required to create a tension-free anastomosis; this can be performed at this point as well. Alternatively, one can save this last maneuver to be carried out after one has carried out the resection. At that point, one can test the anticipated tension on the anastomosis by bringing the cut edges together as the neck is ﬂexed by the anesthesiologists. If this demonstrates that tension will

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Figure 71–7 With the traditional technique of distal intubation with an ETT, seen here, intermittent removal of the ETT from the distal airway is required to allow placement of the anastomotic sutures. Note the silk suture that emerges from the proximal segment. This has been sutured to the end of the withdrawn ETT to ensure that it can be relocated distally just prior to completing the anastomosis.

Figure 71–6 The longer, more caudal incision pictured here is the primary incision through which the tracheal resection with subsequent end-to-end anastomosis (TR) is carried out.The smaller, more cephalad incision is at the level of the hyoid bone for performance of suprahyoid laryngeal release. Through this incision, the muscles attached to superior margin of the middle two thirds of the hyoid are divided, and the bone itself is divided at either end of this mobilized portion. This allows the larynx to descend toward the trachea, providing signiﬁcant tension relief for more extensive TRs. The image here is taken after the release has been performed. The forceps are spread to denote the distance that the hyoid has descended after the release.

be present, the SLR can be performed at that time (Fig. 71–6). It is highly unusual for release maneuvers other than dissection in the pretracheal plane or SLR to be required for a standard cervical tracheal resection. When a more extensive tracheal resection that requires median sternotomy is being performed, infrahilar pericardial releases are often added. In what also might be considered a tension-releasing maneuver, a 0-0 polyglactin suture is placed in most cases in a midlateral location on each side of the proximal and distal tracheal segments. These sutures ultimately take tension off of the anastomosis when they are tied to one another prior to tying the actual anastomotic sutures, which have a less deep and thus less strong bite of tissue (see the section on “Anastomosis,” later).

Anastomotic Dehiscence or Restenosis See discussion under “Anastomosis,” later. The two most important technical features in avoiding anastomotic complications are creation of a tension-free anastomosis with the release procedures described here and maintenance of the blood supply to the anastomosis by limiting circumferential dissection of the trachea to no more than 5 mm beyond the limits of resection. Grade 3–5 complication

Airway Division The most distal end of the segment to be resected is divided ﬁrst, and cross-table ventilation is instituted through a second ETT (Fig. 71–7; see also Fig. 71–3) or HFJV passed through the original ETT into the distal trachea (Fig. 71–8). The entire tracheal segment to be resected is then dissected circumferentially as proximally as necessary. The proximal point of division is then created, and the resected segment is removed from the operative ﬁeld.

Cross-table or HFJV Both cross-table and HFJV have their advocates. The former has the advantage of being readily available, but it requires frequent removal and replacement of the tube in order to allow placement of the posterior wall of sutures. This can lead to hypoxia or hypoventilation occasionally, but it should not be a problem if it is appropriately attended to. HFJV allows a better, continuous view of the operative ﬁeld without frequent manipulations (see Fig. 71–8), but it may have a somewhat higher incidence of

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Figure 71–9 The classic Massachusetts General Hospital (MGH) anastomotic technique wherein all 00-00 polyglactin sutures are placed prior to being tied down, with the knots situated on the outside of the tracheal lumen. The sutures are placed approximately 4 mm apart and 4 mm deep into the cut tracheal margin. (From Grillo HC. Surgery of the Trachea and Bronchi. United States, BC Decker, Inc; 2004.) Figure 71–8 The high-frequency jet ventilator cannula seen here passing through the anastomosis from above allows placement of all sutures without serially withdrawing and reinserting a distally placed ETT.

hypoventilation and requires more careful monitoring by the anesthesiology team.

Anastomosis Many technical methods of anastomotic creation have been described. Historically, interrupted silk or polyester sutures were used, but this led to an unacceptably high rate of granulation formation.1 Since then, high rates of success have been reported with interrupted polyglactin, running monoﬁlament absorbable or nonabsorbable sutures, and combinations of these. My preference is for the MGH technique of interrupted 00-00 polyglactin. The detailed MGH method involves placing all of the sutures circumferentially beginning posteriorly, prior to securing them down (Fig. 71–9). They are then tied from front (cartilaginous wall) to back (membranous wall) after having tied the midlateral 0-0 tensionreleasing sutures (Fig. 71–10) to one another. Before these sutures are tied, the inﬂatable bag that has kept the neck extended until this point in the case is now deﬂated, and the anesthesiologist ﬂexes the neck and then maintains this moderately ﬂexed position until the end of the operation when the “chin stitch” can be placed.

With the MGH anastomotic technique, all knots are placed on the outside of the lumen. However, in relatively straightforward situations in which the lumen is of normal caliber after resection of a short involved tracheal segment, some have found that it is more convenient and appears to be equally successful to place the posterior half of the anastomotic sutures ﬁrst with the knots within the lumen. These can then be tied without the use of midlateral stay sutures after having tied down at least two of the most posterior cartilaginous wall sutures in order to take off the initial tension. The anterior wall sutures can then be placed and tied last (Fig. 71–11). The two sides of thyroid isthmus can be reapproximated to provide some soft tissue coverage to the anterior portion of the anastomosis.

Anastomotic Granulation Formation ● Consequence Prior to the change from silk or Tevdek to polyglactin suture at MGH in 1978, 23.6% of patients had this problem.2 It leads to partial or, in rare cases, complete airway obstruction at the level of the anastomosis. Grade 2–4 complication ● Repair Granulations can generally be managed by bronchoscopic removal either mechanically or with careful use of the laser. The offending suture(s) should also be removed. This may require repeated bronchoscopic

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Figure 71–10 Midlateral stay sutures of 0-0 Vicryl are placed as shown here for the distal segment, in both the distal and the proximal segments to be brought together. These are tied down to one another as the shoulder bag is deﬂated and the neck ﬂexed, immediately before tying the actual anastomotic sutures. This serves to take tension off of the anastomotic sutures. (From Grillo HC. Surgery of the Trachea and Bronchi. United States, BC Decker, Inc; 2004.)

that is most proved to avoid the formation of granulation tissue.

Anastomotic Dehiscence/Restenosis

Figure 71–11 An alternative anastomotic technique that can be used in simpler cases, in which the posterior half of the anastomotic sutures have at this point been placed and tied with the knots within the lumen. The anterior half-sutures have been placed and are about to be tied down.

débridement. Local steroid injections may prevent reformation of granulations. Severe cases may require temporary or permanent T-tube placement or even tracheostomy when the granulations cannot be controlled. ● Prevention After 1978, when the suture material used at MGH was changed to polyglactin, only 1.6% of patients have had a problem with granulation tissue formed at the site of anastomosis.2 Use of absorbable monoﬁlament or even nonabsorbable monoﬁlament suture also appears to virtually eliminate this problem. However, because the MGH series are the largest and most deﬁnitive, I believe polyglactin to be the anastomotic suture

● Consequence The failure rate after anastomosis for all postintubation stenoses was 5.8% in the MGH series. However, for simple lesions requiring only trachea-to-trachea anastomosis, the failure rate was only 2.2%.2 A 2004 review of all 901 patients who had undergone tracheal resection in all locations and for all types of lesions found on multivariate analysis that reoperation (odds ratio [OR] 3.03), diabetes (OR 3.32), greater than 4 cm resection length (OR 2.01), laryngotracheal resection (OR 1.80), age younger than 17 (OR 2.26), and need for preoperative tracheostomy (OR 1.79) were signiﬁcant predictors of anastomotic complications.5 Early, complete dehiscence may lead to airway obstruction and death and is an emergency that may require Ttube placement6 or tracheostomy. Incomplete dehiscence or partial separation may not be noted clinically early on but may lead to healing with a cicatrizing circumferential scar that leads to restenosis. Either complete or incomplete dehiscence may, in rare cases, result in tracheoinnominate ﬁstula (TIF) or even tracheoesophageal ﬁstula. Seven of 29 patients in the MGH series with complete dehiscence died of this complication. Two of the deaths were due to TIF. Grade 3–5 complication ● Repair If early dehiscence is suspected, the patient is taken urgently back to the operating room for rapid and careful bronchoscopic evaluation. If a correctable technical error (such as lack of a needed release procedure)

71 CERVICAL TRACHEAL RESECTION AND RECONSTRUCTION is suspected, reanastomosis with a protective size-4 tracheostomy tube placed two rings below the anastomosis or reanastomosis over a T-tube is reasonable. Alternatives include T-tube placement6 alone or fullsized tracheostomy placement alone. Patients with TIF create among the most difﬁcult surgical emergencies. The airway in this situation must be secured by endotracheal intubation with a cuffed tube and the patient taken emergently to the operating room. Via a median sternotomy, the innominate artery must be divided before exsanguination or drowning occurs, the involved segment is resected, and the remaining ends of the artery are covered with surrounding muscle. In patients without major preexisting cerebrovascular disease, this will not lead to stroke. However, if intraoperative electrocardiographic monitoring can be rapidly arranged, a vein graft can be used for reinstitution of ﬂow if signiﬁcant changes are identiﬁed with clamping. The anastomosis can then be managed as described in the preceding paragraph. Late anastomotic stenosis that occurs during healing of an ischemic or partially separated anastomosis will present with the typical symptoms of upper tracheal stenosis: dyspnea and stridor. The MGH group published a series of 75 reoperations for tracheal stenosis occurring after an initial failed attempt at resection.7 Complications occurred

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in 39% of patients, but 79% had an outcome considered to be “good,” and another 13.3% had an outcome considered to be “satisfactory.” The repair was unsuccessful in only 5.3% of patients, and 2.6% died perioperatively. Options other than reoperation again include T-tube6 or tracheostomy. ● Prevention There are two critical technical issues that must be attended to in order to prevent anastomotic failure: (1) minimizing devascularization of the tissue to be anastomosed and (2) creating a tension-free anastomosis. To minimize devascularization, it is critical to maintain the blood supply to the tracheal segments to be anastomosed by leaving their lateral tissue attachments intact (Fig. 71–12), because these contain the major blood supply. The airways to be anastomosed should be mobilized circumferentially for no more than 5 mm beyond the cut margin, and the cut margin should be handled as little as possible to avoid tissue injury. Because the anastomotic sutures are placed 3 to 4 mm deep, 5 mm of mobilization is sufﬁcient. To create a tension-free anastomosis, the tensionreleasing maneuvers utilized in TRs include

Coronal section of tracheal wall... Anterior transverse intercartilaginous artery

Lumen Trachea

Lateral longitudinal anastomosis

Submucosal capillary plexus Transverse intercartilaginous artery

Primary tracheal artery Posterior transverse intercartilaginous artery

Pattern of microvasculature of mucosa

Tracheoesophageal artery Primary esophageal artery

Esophagus

Muscular posterior wall of trachea

Secondary tracheal twig to posterior wall

Figure 71–12 Demonstration of the lateral tissue pedicles that contain the main blood supply to the trachea and thus must be left intact beyond 5 mm from the cut margin of the tracheal resection. Because the anterior, pretracheal plane is avascular, it is bluntly dissected as far as possible into the mediastinum as part of the routine tension-relieving procedures. (From Salassa JR, Pearson BX, Payne WS. Gross and microscopical blood supply of the trachea. Ann Thorac Surg 1977;24,100–107.)

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1. Dissection of the pretracheal plane to the level of the carina (described previously). 2. Suprahyoid laryngeal release (described previously). 3. 2-0 Vicryl lateral “stay” sutures tied to one another prior to tying anastomotic sutures (described previously). 4. Taking down the inﬂatable bag beneath the shoulders and using neck ﬂexion during the tying down of the anastomotic sutures (described previously). 5. The “chin stitch” (described later). Numbers 1, 3, 4, and 5 are used in essentially all TRs, while SLR is used only for longer resections or when tension is noted upon the initial attempt to bring the cut margins toward one another. It is critical that the cut ends of the airway come together easily and with no more than minimal tension. If they do not, the anastomosis will not heal soundly. A third important point in avoiding anastomotic complications is to be sure not to operate upon a trachea that is in the acute phase of inﬂammation. If, upon preoperative bronchoscopy, the airway remains edematous or erythematous, it is best to postpone surgery until this inﬂammation subsides, even if this requires temporary stenting with a T-tube6 or even tracheostomy. Finally, if a patient has been on chronic steroids, these should be weaned preoperatively to as low a dose as possible, preferably to the point of having been stopped completely for a month or longer. Although preoperative steroid use did not fall out as a signiﬁcant predictor in the MGH multivariate analysis described previously,5 common sense and experience dictate that weaning steroids is prudent if feasible. It may also be useful to administer vitamin A perioperatively in patients who remain on steroids to mitigate the known effects of steroids upon healing. With regard speciﬁcally to TIF, one means of avoiding this is always keeping the dissection plane directly on the trachea when separating the innominate artery from the airway. This leaves some investing soft tissue around the innominate artery that will generally prevent subsequent erosion. In situations in which there is reason to think that this investing tissue is not present, a ﬂap of strap muscle should be interposed between the innominate and the anastomosis.

Chin Stitch Once the anastomosis has been completed and the wound closed over a Jackson-Pratt drain, a size 2 suture of Tevdek or polypropylene is placed between the submental skin and the skin over the angle of Louis (Fig. 71–13). It is important to note that the neck is to be held in only modest ﬂexion. The intention of the skin stitch is more to prevent the patient from suddenly hyperextending and

Figure 71–13 The “chin stitch” shown here is intended not to maximally ﬂex the neck but only to hold it in no more than 45° of ﬂexion and, more importantly, prevent sudden extension. Note that this patient, who had a subglottic resection, has also had a small tracheostomy placed below the anastomosis as a precaution.

thus stressing the anastomosis than it is to maintain dramatic ﬂexion.

Paraplegia ● Consequence Several case reports8 have described disastrous spinal infarcts believed to have resulted from severe neck ﬂexion after TR. I am aware of one other unreported case of this terrible complication. Grade 4/5 complication ● Repair If lower extremity weakness is noted, the chin stitch should be immediately cut and the patient allowed to return his or her neck to a neutral position. Elevation of blood pressure to increase spinal perfusion might be helpful. ● Prevention The neck should generally be ﬂexed to more than 45°. In the rare situation in which more than 45° of ﬂexion is required to create a tension-free anastomosis, careful monitoring of neurological function should be carried out and the previously described maneuvers carried out urgently if any deﬁcits are noted.

71 CERVICAL TRACHEAL RESECTION AND RECONSTRUCTION

Extubation Extubation is performed immediately after TR in the operating room, if at all possible. This is facilitated by avoidance of paralytic agents in the anesthetic. Occasionally, one is sufﬁciently worried about the anastomosis that one “protects” it by placing a small, size-5, uncuffed tracheostomy two rings below the anastomosis. Another alternative after difﬁcult resections, high laryngotracheal resections, or resections in children in whom a small amount of edema can reduce the smaller lumen signiﬁcantly is to maintain intubation for 2 to 3 days postoperatively as a rapidly tapering course of steroids is given to reduce edema.

Postoperative Airway Edema ● Consequence Most TR patients have some degree of airway edema postoperatively, either at the level of the vocal cords or at the anastomosis itself. However, this generally becomes a problem only in those patients with anastomoses in the subglottic region or in children with smaller airways. In these patients, stridor may develop 12 to 48 hours postoperatively that was not present immediately postoperatively. Grade 1–3 complication ● Repair Symptomatic airway edema can usually be managed with head elevation, racemic epinephrine nebulizers, diuretics, and a rapidly tapering 24-hour cycle of steroids, if this was not already instituted. Heliox is also a useful adjunct because its use reduces the resistance to ﬂow in the airways.9 In rare cases, the patient must be taken back to the operating room for placement of a small tracheostomy below the anastomosis or for very careful reintubation from above with an uncuffed ETT. ● Prevention A rapidly tapering 24-hour cycle of steroids is appropriate for those with subglottic resections, children, and those in whom more than the usual amount of cord trauma was believed to have occurred during intubation or rigid bronchoscopy. All TR patients should have minimal ﬂuid replacement postoperatively and be managed with the head of the bed elevated. For those considered to be at highest risk, a small tracheostomy

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placed at the time of surgery or a planned, 2- to 3-day postoperative period of intubation with an uncuffed ETT can be considered.

SUMMARY With careful attention to the details of surgery and postoperative management, cervical tracheal resection can be performed with anastomotic failure rates as low as 2.2% and all other complications together totaling less than 5%. The incidence of complications rises, however, as the proximal point of resection enters the larynx. This chapter has reviewed the management and prevention of all complications of tracheal resection that occur in substantial numbers.

REFERENCES 1. Grillo HC, Zannini P, Michelassi F. Complications of tracheal reconstruction: incidence, treatment and prevention. J Thorac Cardiovasc Surg 1986;91:322–328. 2. Grillo HC, Donahue DM, Mathisen DJ, et al. Post intubation tracheal stenosis; treatment and results. J Thorac Cardiovasc Surg 1995;109:486–493. 3. Lanuti M, Mathisen DJ. Management of complications of tracheal surgery. Chest Surg Clin North Am 2003;13:385– 397. 4. Grillo HC, Mathisen DJ. Primary tracheal tumors: treatment and results. Ann Thorac Surg 1990;49:69–77. 5. Wright CD, Grillo HC, Wain JC, et al. Anastomotic complications after tracheal resection: prognostic factors and management. J Thorac Cardiovasc Surg 2004;128: 731–739. 6. Gaissert H, Grillo HC, Mathisen DJ, Wain JC. Temporary and permanent restoration of airway continuity with the tracheal T-tube. J Thorac Cardiovasc Surg 1994;107:600– 606. 7. Donahue DM, Grillo HC, Wain JC, et al. Reoperative tracheal resection and reconstruction for unsuccessful repair of postintubation stenosis. J Thorac Cardiovasc Surg 1997;114:934–938. 8. Silver JR. Paraplegia as a result of tracheal resection in a 17-year-old male. Spinal Cord 2007;45:576–578. 9. Ho AM, Dion PW, Karmakar MK, et al. Use of heliox in critical upper airway obstruction: physical and physiologic considerations in choosing the optimal helium:oxygen mix. Resuscitation 2002;52:297–300.

Section XII

TRAUMA SURGERY Edward E. Cornwell III, MD The only real mistake is the one from which we learn nothing.—John Powell

72

Evaluating Trauma Literature David C. Chang, MD INTRODUCTION In some surgical specialties, new procedures and guidelines are frequently developed and adopted based on uncontrolled case series, despite the fact that selection bias often appears in these series (to select the “best” possible surgical candidate patients to demonstrate the feasibility of the new procedure). This bias makes the results difﬁcult to generalize to the “average patient.” In contrast, conclusions based on carefully analyzed evidence in the literature have played an ever-increasing role in the development of clinical guidelines in trauma care. The most prominent early example of evidence-based guidelines in trauma grew out of important work performed by the Brain Trauma Foundation, in collaboration with the American Association of Neurologic Surgeons.1 Guidelines were developed around 13 speciﬁc clinical issues in patients with severe traumatic brain injuries. In highlighting the importance of evidence-based surgical practice in trauma, this chapter emphasizes speciﬁc pitfalls to be avoided in evaluating the trauma literature. The example of the evolution of management of traumatic colon injuries are utilized to illustrate the pitfalls.

PITFALL 1: GENERATING A CLASS I RECOMMENDATION BASED ON CLASS III DATA In 1943, the Surgeon General of the United States issued guidelines that all colon injuries sustained by soldiers in

the North African theater during World War II be managed by colostomy either at or proximal to the site of injury, rather than by primary repair or resection and anastomosis.2 Retrospective analysis of this recommendation included the observations that colon injuries during the Civil War carried an associated 90% mortality, whereas those experienced during World Wars I and II carried a 60% and a 30% mortality, respectively. The reduced mortality of injuries experienced during World War II was attributed to the policy of mandatory colostomies, ignoring the contribution of advances in ﬂuid resuscitation, plasma preservation, blood-banking techniques, the availability of antimicrobial agents, and superior military triage and evacuation. ● Consequence For the two decades after World War II, the military mandate led to the assumption in civilian practice that colostomy should be the standard of care for traumatic colon injuries. This led to thousands of patients receiving colostomies and the need for subsequent operations with their associated morbidity. Tradition and intuition would play a large role in the choice of management until Stone and Fabian published a report in 19793 comparing the outcomes of colostomies versus primary repair in patients with less severe injuries. ● Repair/Prevention The prevention of future misassumption is hopefully feasible with the development of the principles of evidence-based medicine. These principles dictate that

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class II (prospective nonrandomized) and class III (retrospective) data should generate questions rather than answers. Once the feasibility and estimated complication rates of two possible treatment arms (colostomy/ diversion versus primary repairs/anastomosis) are established, the development of clinical guidelines should ideally be derived from well-designed prospective, randomized trials. In retrospect, attributing the decreased mortality from colon injuries in World War II to the policy of mandatory colostomy was probably unfairly indicting primary repair and unduly promoting colostomies.

PITFALL 2: INAPPROPRIATE COMPARISON OF COMPLICATION RATES BETWEEN RETROSPECTIVE AND PROSPECTIVE SERIES When a clinical researcher and a study nurse formally deﬁne complications (such as intra-abdominal abscess after colon repairs) and prospectively compile them, the magnitude of the complication rates will almost always be higher than the complication rates generated by chart reviews and retrospective recall. An example of a remarkably low complication rate generated by retrospective methodology is seen in a 1984 study of traumatic colon injuries at an urban trauma center.4 In this series of 56 patients over a 6-year period, none developed an intraabdominal abscess. These incredible results raise the question as to whether more severely injured patients who developed complications somehow eluded the investigators’ chart reviews. Subsequent retrospective series published over the ensuing decade would echo a near 0% septic complication rate among patients undergoing primary repair of penetrating colon injuries.5,6 Interestingly, these excellent outcomes are unattainable when the same patients are evaluated prospectively.7,8 ● Consequence Patients, malpractice attorneys, hospitals, and performance-improvement committees may well develop the unreasonable expectation that the management of traumatic colon injuries carries a 0% septic complication rate.

PITFALL 3: GENERATING A CLASS I RECOMMENDATION FROM CLASS II DATA When surgeons began to appreciate the difference between high-velocity military injuries and low-velocity injuries seen in the civilian setting, the wartime practice of routine colostomy would gradually come under challenge. A report in 1951 identiﬁed a 9% mortality rate when primary repair of selected colon injuries was used.9 American surgeons trained from the 1950s through the 1980s developed the ability to identify patients who have extremely severe injuries and pronounced physiologic derangement. These sicker patients with predictably higher complication rates have generally been managed with colostomies. Not surprisingly, virtually every retrospective or prospective, nonrandomized study analyzing intraabdominal septic complications found that patients who received primary repair had complication rates equal to or less than those who received colostomy. This culminated in a paper in 1997 entitled, “Primary repair of 58 consecutive penetrating injuries of the colon: should colostomy be abandoned?”10 ● Consequence Surgeons initially credited colostomy and impugned primary repair in the 1950s based primarily on class III data (i.e., retrospective review of data) from World Wars I and II. Subsequently, surgeons impugned colostomy in the 1980s based on primarily class II data (prospective but nonrandomized trials), ignoring the trend that colostomy was becoming reserved for a progressively severely injured subset of patients. ● Repair/Prevention Clearly septic complications can be predicted to occur in patients with penetrating colon injuries. The question remained whether colostomy decreases that risk, which can only be answered by prospective, randomized analyses in which patients are equally likely to receive one treatment mode or the other, without regard to the severity of their injuries. There are four such trials in the literature.11–14 In all four trials, primary repair patients had outcomes that were as good as those of colostomy patients.

FUTURE DIRECTIONS ● Repair/Prevention Unlike other ﬁelds of medicine, the development of many surgical treatment modalities remains unregulated; therefore, each new advance in treatment requires some form of self-regulation. Only by insisting upon proper interpretation of clinical data and the avoidance of unsupported conclusions can we guard against the unrealistic expectation described previously.

A question arises of whether there are enough severely injured patients in the prospective randomized trials who require resection and anastomosis under physiologically compromised situations to routinely recommend primary repair in every circumstance. There has been a total of only 37 patients described in the prospective, randomized studies discussed earlier who underwent resection and anastomosis; and in three of those four trials, the severity

72 EVALUATING TRAUMA LITERATURE of injuries were represented by the groups’ average Penetrating Abdominal Trauma Index (PATI). Therefore, it was unclear how many of the 37 patients were at actual high risk for septic complications. Although none of the 37 patients had identiﬁed suture line disruption, there appears to be an inadequate number of patients with destructive colon injuries and other major risk factors to recommend that colostomies to be abandoned altogether. Guidelines developed by the Eastern Association for the Surgery of Trauma (EAST) reﬂect these concerns, reserving colostomy as a level II recommendation for patients with destructive colon injuries that require resection in a setting of shock, underlying disease, or severe associated injury.15

REFERENCES 1. Brain Trauma Foundation. The integration of brainspeciﬁc treatment to the initial resuscitation of the severe head injury patient. J Neurotrauma 1996;13:653–659. 2. Circular Letter No. 178. Washington, DC: Ofﬁce of the Surgeon General of the United States. October 23, 1943. 3. Stone HH, Fabian TC. Management of perforating colon trauma: randomization between primary closure and exteriorization. Ann Surg 1979;190:430–435. 4. Adkins RB Jr, Zirkle PK, Waterhouse G. Penetrating colon trauma. J Trauma 1984;24:491–499. 5. Nallathambi MN, Ivatury RR, Shah PM, et al. Aggressive deﬁnitive management of penetrating colon injuries: 136 cases with 3.7 per cent mortality. J Trauma 1984;24:500– 505.

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6. Levison MA, Thomas DD, Wiencek RG, Wilson RF. Management of the injured colon: evolving practice at an urban trauma center. J Trauma 1990;30:247–251; discussion 251–253. 7. George SM Jr, Fabian TC, Voeller GR, et al. Primary repair of colon wounds. A prospective trial in nonselected patients. Ann Surg 1989;209:728–733; discussion 733– 734. 8. Demetriades D, Charalambides D, Pantanowitz D. Gunshot wounds of the colon: role of primary repair. Ann R Coll Surg Engl 1992;74:381–384. 9. Woodhall JP, Ochsner A. The management of perforating injuries of the colon and rectum in civilian practice. Surgery 1951;29:305–320. 10. Jacobson LE, Gomez GA, Broadie TA. Primary repair of 58 consecutive penetrating injuries of the colon: should colostomy be abandoned? Am Surg 1997;63:170– 177. 11. Chappuis CW, Frey DJ, Dietzen CD, et al. Management of penetrating colon injuries: a prospective randomized trial. Ann Surg 1991;213:492–498. 12. Falcone RE, Wanamaker SR, Santanello SA, Carey LC. Colorectal trauma: primary repair or anastomosis with intracolonic bypass vs ostomy. Dis Colon Rectum 1992; 35:957–963. 13. Sasaki LS, Allaben RD, Golwala R, Mittal VK. Primary repair of colon injuries: a prospective randomized study. J Trauma 1995;39:895–901. 14. Gonzalez RP, Merlotti GJ, Holevar MR. Colostomy in penetrating colon injuries: is it necessary? J Trauma 1996; 41:271–275. 15. Eastern Association for the Surgery of Trauma. Trauma practice guidelines. 1998. Accessed at www.east.org

73

Evaluation and Acute Resuscitation of the Trauma Patient Elliott R. Haut, MD INTRODUCTION Although not all trauma patients need surgical intervention, they do require immediate evaluation and resuscitation. Therefore, trauma continues to be a surgical disease. Early intervention in critically injured patients can signiﬁcantly inﬂuence mortality, morbidity, and disability after major trauma. Patients have improved outcomes when treated at these specialized centers1–3 and when additional resources and commitment are dedicated to trauma care.4–6 The Advanced Trauma Life Support (ATLS) course sponsored by the American College of Surgeons Committee on Trauma is the “gold standard” for teaching trauma management and heavily emphasizes the importance of the initial trauma resuscitation.7 This chapter utilizes the ATLS framework to highlight the essentials and potential pitfalls in the evaluation and resuscitation of the injured patient.

PRIMARY SURVEY Upon arrival at the trauma center, rapid primary survey should include evaluation of the Airway (with cervical spine protection considered), Breathing and ventilation, Circulation with hemorrhage control, Disability (neurologic status) and Exposure/Environmental control. These ABCDEs are the basic initial management emphasized by ATLS. Major pitfalls at this point can rapidly cause death. It is ideal to strictly adhere to systematic performance of the primary survey and focus on the ABCDEs to ensure that the most life-threatening injuries are dealt with ﬁrst. Do not be distracted by major external injuries. Although these obvious injuries are often quite impressive and gruesome, they are not immediately life threatening. If a major ﬁnding is identiﬁed on the primary survey, it should be treated immediately before moving on to the next step.

Airway Airway management is always the ﬁrst step in trauma evaluation. When in doubt, the safest route is often to intubate the patient and completely control the airway.

Loss of Airway ● Consequence Loss of airway during trauma resuscitation can rapidly lead to respiratory and then cardiopulmonary arrest and death. Grade 5 complication ● Repair If an airway problem is found, it needs to be deﬁnitively remedied before moving on to breathing and circulation. If at any time during the evaluation the need for airway control is recognized, start back at airway evaluation and reconsider performing standard endotracheal intubation. ● Prevention All potential alternatives must be anticipated. Do not assume that the ﬁrst attempt at endotracheal intubation will be immediately successful. If endotracheal intubation cannot be done expeditiously, advanced airway manipulation (e.g., ﬁberoptic intubation, laryngeal mask airway) may be the next attempted maneuver. The ultimate backup is surgical airway by cricothyrotomy, which should be in the armamentarium of every surgeon treating trauma patients (Fig. 73–1). Occasional providers still attempt to achieve emergency surgical airway by means of a tracheostomy. This dangerous practice ignores the anatomic fact that the cricothyroid membrane is the most superﬁcial access point to the airway and the trachea immediately dives deep into the mediastinum.

Allowing an Episode of Hypoxia ● Consequence Even short periods of hypoxia are known to worsen outcomes after traumatic brain injury (TBI). Grade 4/5 complication

758

SECTION XII: TRAUMA SURGERY

Hyoid bone

Thyrohyoid m.

Sternohyoid m.

Omohyoid m.

Anterior jugular v.

Thyroid cartilage

Cricoid cartilage

Cricothyroid membrane Sternocleidomastoid muscle

Thyroid gland isthmus

Trachea

MC

A

Skin incision over cricothyroid membrane

B Figure 73–1 Cricothyrotomy. A, The cricothyroid membrane is located between the thyroid cartilage above and the cricoid ring below. B, The operator’s nondominant hand holds the thyroid cartilage while the other hand performs the procedure. A vertical skin incision avoids the anterior jugular veins to minimize bleeding.

73 EVALUATION AND ACUTE RESUSCITATION OF THE TRAUMA PATIENT

759

Cricothyroid membrane

C

Cricothyroid membrane

D

Cricoid cartilage

Thyroid gland

Figure 73–1, cont’d C, The cricothyroid membrane is incised transversely. D, The opening is widened with a small hemostat.

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SECTION XII: TRAUMA SURGERY

Tracheostomy tube

Tracheostomy tube

E

Figure 73–1, cont’d E, The tracheostomy tube is placed into the airway and the cuff is inﬂated.

● Repair If hypoxia is noted, urgent attention should be paid to airway management. High-ﬂow oxygen should be given. If endotracheal intubation is not successful, surgical airway (cricothyrotomy) should be rapidly performed. ● Prevention Delays in obtaining a deﬁnitive airway can lead to hypoxia, which has signiﬁcant negative impact on outcomes in head-injured patients. This is yet another reason why airway management is the ﬁrst critical step in trauma evaluation.

Conversion of a Metastable Airway to an Unstable Airway ● Consequence Conversion of a metastable airway to an unstable airway can rapidly change a difﬁcult situation into an impossible one. Death from airway loss is never a pretty sight. Grade 5 complication ● Repair Often, this error leads to emergent cricothyrotomy instead of a smoother, controlled airway management scheme.

73 EVALUATION AND ACUTE RESUSCITATION OF THE TRAUMA PATIENT

761

● Prevention Before dosing a patient with paralytics for rapidsequence intubation, consider the potential consequences in a patient with a metastable airway. Paralytics may convert a patient who is protecting her or his own airway and able to oxygenate and ventilate to a patient who is no longer breathing and is unable to be intubated. Consider letting the patient sit up to help clear blood and secretions, rather than making her or him lay ﬂat and possibly inducing aspiration.

● Prevention Decreased breath sounds on one side should lead to an immediate chest tube before radiographic evaluation in patients with signiﬁcant respiratory distress or shock. In this case, treatment of a tension pneumothorax can be life saving. Tension pneumothorax should be a clinical diagnosis made by physical examination, not radiographically. Tracheal deviation (away from the tension pneumothorax) helps conﬁrm the diagnosis in patients with decreased breath sounds and hypotension.

Causing Worse Neurologic Injury with Spine Manipulation

Placing an Unnecessary Chest Tube

● Consequence Exacerbating neurologic deﬁcits by not immobilizing the cervical spine can have long-lasting devastating consequences. Patients with spinal column injuries may have no neurologic deﬁcit or only an incomplete spinal cord injury. It is incredibly tragic when patients such as this have worsening of their injury from inappropriate cervical spine immobilization. Grade 4/5 complication ● Prevention Cervical spine stabilization is emphasized during airway management by ensuring that the head stays in neutral position. Hyperextending the neck in a patient with an unstable cercival spine injury may change a patient’s functional outcome signiﬁcantly by exacerbating neurologic injury. A patient may be rendered permanently quadriplegic with even small manipulations of the neck.

Breathing The next step of evaluation during the trauma resuscitation is breathing and ventilation. Often, it is quite difﬁcult to differentiate a breathing problem from an airway issue. In this situation, if the airway is controlled and the problem continues, there is most likely a lung or breathing problem. Physical examination is the key ﬁrst maneuver to making the appropriate diagnosis.

● Consequence Tube thoracostomy is not a benign procedure. It is associated with injury to structures within the chest and abdomen and has the potential to cause infection. Appropriate tube thoracostomy placement can be necessary; however, if a patient does not need a chest tube, we should not place one. Grade 2 complication ● Prevention In the hemodynamically stable patient who is physiologically normal from a respiratory standpoint (e.g., no hypoxia, shortness of breath, use of accessory muscles), consider getting an early chest x-ray to clearly deﬁne whether a hemo- and/or pneumothorax is present before intervention. Providers must always be cognizant of the beneﬁt of listening very closely with an unbiased stethoscope. Often, when there is a wound over one hemithorax, we expect (and subsequently believe we ﬁnd) decreased breath sounds when there may be no anatomic pathology. An early chest x-ray can save the patient a potentially unnecessary chest tube placed for “unequal breath sounds” in the physiologically normal trauma patient. However, this recommendation should not be taken as a suggestion to wait for a chest x-ray in an unstable patient with signs of respiratory distress or tension pneumothorax.

Conversion of Simple Pneumothorax to Tension Pneumothorax with Positive-Pressure Ventilation

● Consequence Missing tension pneumothorax on physical examination or waiting for a conﬁrmatory chest x-ray can lead to an unnecessary prolonged period of hypotension, shock, hypoperfusion, anoxic brain injury, and/or death. Grade 5 complication

● Consequence Trauma patients may have a small pneumothorax, which may be too small to see on chest x-ray or computed tomography (CT) scan. These may be of no consequence and heal on their own without intervention. However, if there is a hole in the visceral pleura over the lung, this simple pneumothorax can be converted to a tension pneumothorax with positivepressure ventilation. Grade 5 complication

● Repair Immediate chest decompression (by needle) followed by tube thoracostomy.

● Repair Immediate chest decompression (by needle) followed by tube thoracostomy.

Missed Tension Pneumothorax on Physical Examination

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SECTION XII: TRAUMA SURGERY

● Prevention Ventilation may rapidly deteriorate with endotracheal intubation and positive-pressure ventilation owing to a worsening pneumothorax. In patients with known pneumothorax, consider placing a chest tube as soon as the patient is intubated, rather than waiting until a conﬁrmatory chest x-ray is performed.

Main Stem Intubation Leading to Unnecessary Chest Tube ● Consequence Straightforward successful intubation is the expected outcome after plans for controlling the airway. Main stem intubation is a common minor complication of endotracheal intubation. In and of itself, it does not cause major problems. However, if unrecognized, it may lead the team to perform further procedures (e.g., tube thoracostomy for presumed hemo- or pneumothorax owing to decreased or absent breath sounds) before the simple diagnosis is made. Grade 2 complication ● Repair Pull the endotracheal tube back to the appropriate position and reconﬁrm by chest x-ray or ﬁberoptic bronchoscopy. ● Prevention Main stem intubation (more commonly into the right main stem bronchus) can give the appearance of chest pathology owing to absent or decreased breath sounds. Always consider this possibility rather than assuming another lung pathology (such as hemo- or pneumothorax). Conﬁrming endotracheal tube placement by early chest x-ray or pulling the endotracheal tube back may avoid an unnecessary tube thoracostomy.

Air Embolism ● Consequence Intubation and positive-pressure ventilation may cause air embolism. Hypovolemic patients whose penetrating injuries produce direct communications between the small airways and the pulmonary venous tributaries are at particularly high risk. When positive pressure is applied to the bronchial tree, air may go through these abnormal connections and eventually enter the left side of the heart. Air can then ﬂow to the brain causing stroke or the coronary arteries causing myocardial infarction. Grade 4/5 complication ● Repair Initial treatment includes increasing the fraction of inspired oxygen (FIO ). Hyperbaric oxygen therapy may have a role, but there are no large studies to prove its beneﬁt. 2

● Prevention Air embolism is difﬁcult to prevent. Key maneuvers include minimizing the time of positive-pressure ventilation before attempting surgical control of a penetrating lung injury. Prompt hydration and ﬂuid resuscitation will also help ensure a full venous system, which may help prevent air embolism as well.

Circulation Uncontrolled External Hemorrhage ● Consequence Ongoing external hemorrhage can rapidly lead to shock, exsanguination, and death. Grade 5 complication ● Repair Control of external hemorrhage during the early phase (circulation) of resuscitation is imperative. ● Prevention External bleeding is best controlled by direct digital pressure. Frequently, a patient with a small head laceration presents to the trauma center with a large, loosely wrapped, bulky gauze dressing saturated with blood. When the trauma team removes this dressing and sees a 2-cm laceration, digital pressure from one ﬁnger can completely stop this external hemorrhage and save multiple units of blood transfusions for this patient.

Exacerbating a Vascular Injury by Blind Clamping ● Consequence Blindly placing a clamp into a bleeding wound has considerable potential to enlarge a small arterial or venous injury. This may change the necessary surgical procedure signiﬁcantly. What may have taken one or two simple sutures may now require a complex vascular repair. Grade 3/4 complication ● Repair Surgical repair of major vascular injury as indicated will be the only way to correct this injury. These more complex injuries may require an interposition vein or prosthetic conduit placement to restore ﬂow to the injured extremity. ● Prevention In the extremities, external bleeding is often best controlled with digital pressure directly on the bleeding wound. Blind clamping should be avoided to prevent further major vascular injury. Imprecise clamp placement can convert a small partial-thickness arterial injury to a complete transaction requiring a larger, more complex arterial reconstruction. Although there is con-

73 EVALUATION AND ACUTE RESUSCITATION OF THE TRAUMA PATIENT troversy about their use, tourniquets may be considered if direct pressure does not stop the ongoing hemorrhage.8 A blood pressure cuff placed directly over the wound and inﬂated to above the arterial blood pressure should temporize the situation and control external hemorrhage while the rest of the ABCDEs are addressed. The primary and secondary surveys can be ﬁnished expeditiously while a deﬁnitive plan (surgical exploration) for hemorrhage control is undertaken.

Assuming that a Normal Heart Rate or Blood Pressure Ensures that a Patient Is Not in Shock ● Consequence Making a false assumption such as this will ultimately delay the diagnosis of shock. This may allow a patient enough time to continue to exsanguinate. Hemorrhage is a major cause of death after trauma. In a recent review of 2594 deaths at a large regional trauma center, delayed intervention for hemorrhage accounted for the largest percentage of preventable death.9 Grade 5 complication ● Repair As soon as the diagnosis of shock is made, work-up directed at the differential diagnosis of bleeding sites is imperative. Ongoing active ﬂuid resuscitation should be performed simultaneously during this evaluation. ● Prevention Early consideration of control of internal hemorrhage is important, although this often falls into the secondary survey in hemodynamically stable patients. Pitfalls during this portion of resuscitation can occur in speciﬁc patient populations. Young, well-trained athletes and patients who are well β-blocked will continue with a normal heart rate (or bradycardia), even after signiﬁcant blood loss has occurred. Patients in class II hemorrhagic shock (blood loss of 15%–30% of blood volume or 750–1500 ml) will compensate with tachycardia and vasoconstriction but may still have “normal” vital signs. The only physical examination ﬁnding may be a narrow pulse pressure. Take the example of a patient whose baseline blood pressure is 120/80 mm Hg and heart rate is 60. His or her vital signs after trauma (blood pressure 110/90 mm Hg and pulse 90) may be in the overall “normal” range but represent a 50% decrease in pulse pressure and a 50% increase in heart rate. Elderly patients also may not exhibit typical signs and symptoms of hemorrhage and shock (e.g., tachycardia, hypotension) after major trauma. These patients may not have the physiologic reserve that their younger counterparts do. Extra vigilance must be used in elderly trauma patients to ensure timely diagnosis and treatment because elderly patient may not be able to recover if the therapy is delayed. Trauma team activation and early intensive monitoring may improve outcomes in trauma patients older than 70 years.10,11

763

Assuming Hemodynamic “Stability” Excludes Signiﬁcant Hemorrhage after Penetrating Abdominal Trauma ● Consequence Delay in laparotomy once the diagnosis of peritonitis is made can allow a longer period of bleeding and abdominal contamination. This may lead to the need for more extensive surgery, higher rates of abdominal sepsis, and death. Grade 3–5 complication ● Repair Early laparotomy should be undertaken as soon as signs of bleeding (i.e., dropping hemoglobin or hematocrit, hypotension) or peritonitis occur. ● Prevention In the modern era of selective management of penetrating abdominal trauma, not all patients with stab or gunshot wounds require mandatory laparotomy, as was the practice pattern for many years. Patients with a completely benign abdominal examination and normal vital signs may be safely treated expectantly, but the trauma team should be ready and willing to operate immediately at the ﬁrst sign of clinical deterioration. Even patients who are stable at initial presentation may have signiﬁcant injury. A recent review of 139 hemodynamically stable patients with penetrating abdominal trauma in whom peritonitis was the sole indication for laparotomy highlighted this point. In this large series from a busy trauma center in Los Angeles, major vascular injury (11%), intraoperative hypotension (25%), and blood transfusion (39%) were common. Nearly half of the patients required intensive care, 25% had at least one complication and 3 died (including 2 from exsanguination).12 Peritonitis should triage patients for emergent operation regardless of vital signs.

Disability Not Intubating a Patient with a Glasgow Coma Scale Score of 8 or Lower ● Consequence Failure to intubate a patient with a Glascow Coma Score (GCS) of 8 or lower may lead to hypoxia and cause secondary brain injury and worsen functional outcomes after TBI.13 Grade 4 complication Delay in intubation can also lead to aspiration in the patient who is unable to control her or his airway. Grade 3 complication ● Repair Intubate as soon as possible when a GCS of 8 or lower is noted.

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SECTION XII: TRAUMA SURGERY

Table 73–1 Glasgow Coma Scale Score Motor

Verbal

Eye Opening

6 Obeys commands

5 Oriented

4 Spontaneous

5 Localizes pain

4 Confused

3 To voice

4 Withdraws to pain

3 Inappropriate words

2 To pain

3 Flexion to pain (decorticate posturing)

2 Incomprehensible sounds

1 None

2 Extension to pain (decerebrate posturing)

1 None

1 None

● Prevention It is often difﬁcult to determine which patients have a TBI and which patients are confused or agitated for different reasons. The signs and symptoms of acute mental status change have a long list of differential diagnoses. Patients can have altered mental status owing to intoxication with alcohol and/or other drugs. Other causes such as hypoglycemia, hypoxia, hypercarbia, and hypotension resulting in shock must be considered and not missed or attributed to head injury, drugs, or alcohol. In the belligerent, aggressive patient, the entire list must be considered and each item should be ruled out before assuming that intoxication is the only signiﬁcant cause of behavioral problems.

Missing a Subtle Spinal Cord Injury ● Prevention Use the GCS, which is the standard tool and a quick reliable score, to determine eventual outcome after a head injury (Table 73–1). All trauma patients should have the GCS completed even if there is no obvious/ overt head injury. If the GCS is 8 or lower, the patient should be immediately intubated owing to the risk of not being able to control or protect his or her own airway.

Hypotension ● Consequence Even a single episode of hypotension can worsen a patient’s functional status after TBI.13 Grade 4 complication ● Repair Aggressively treat hypotension in the setting of TBI. Aggressive ﬂuid resuscitation, blood transfusion, and vasopressors are often part of the treatment algorithm. ● Prevention Patients with TBI have already suffered their primary insult. The most important thing we can do for them is to prevent secondary brain injury. Hypotension is a well-described cause of secondary brain injury and should be avoided.13

Attributing Mental Status Change to Drug Intoxication ● Consequence Delay in diagnosis of TBI can have dire consequences ranging from permanent neurologic disability to death. Grade 4/5 complication ● Repair Immediate appropriate work-up to rule out anatomic or physiologic brain injury is indicated.

● Consequence Early diagnosis of spinal cord injury with neurologic deﬁcit may give the patient the best possible outcome by preserving any remaining neurologic function and potentially reversing the cause and allowing improvement. Grade 4 complication ● Repair As soon as the spinal cord syndrome is identiﬁed, appropriate neurosurgical consultation and intervention have the best chance to improve outcome. ● Prevention The disability evaluation must include a gross motor examination of both the upper and the lower extremities to avoid missing a clinically signiﬁcant spinal cord injury. The motor component of the GCS is scored, paying ca reful attention to the ability to follow commands. A patient with a spinal cord injury and complete extremity paralysis may still potentially have a GCS of 15. As long as the patient can follow any motor command, for example, with her or his eyes, she or he can still have a normal GCS. Never perform the motor examination of the lower extremities only and assume that if the lower extremities are intact, the patient has no chance of having a spinal cord injury. This premise is incorrect. Patients with cervical spine stenosis may have a central cord syndrome and have physical ﬁndings only in the upper extremities with normal lower extremities. Frequent, neurologic reevaluation is critical to ensure early identiﬁcation of any decrement in function.

Exposure/Environmental Hypothermia ● Consequence Hypothermia can lead to many downstream effects such as confusion, mental status changes, electrolyte abnormalities, cardiac arrhythmias, and death. Grade 4/5 complication

73 EVALUATION AND ACUTE RESUSCITATION OF THE TRAUMA PATIENT ● Repair Immediate active warming of the patient should begin when the diagnosis of hypothermia is made. ● Prevention The exact steps in exposure and environmental evaluation depend on the patient’s speciﬁc situation. In the hospital setting (e.g., in the trauma bay), the patient should be fully disrobed and all wounds should be evaluated along with the rest of the patient’s physical examination. However, every effort must be made to avoid hypothermia, which has deleterious effects on most organ systems. Warming blankets, heat lamps, and warm intravenous (IV) ﬂuids are utilized as soon as practically possible. Patients can get severely hypothermic in a room that is “not that cold.” Even on a warm, sunny, 80° day, a trauma patient may lose the ability to autoregulate temperature and can become severely hypothermic.

EARLY INTERVENTIONS Venous Access Placement of Insufﬁcient IV Access ● Consequence Using the wrong size of IV catheter for ﬂuid resuscitation can lead to signiﬁcant underresuscitation of the severely injured trauma patient. This can lead to ongoing shock, multiple organ failure, and death if not rapidly remedied. Grade 4/5 complication ● Repair Place at least two appropriate large-bore IV lines. A short, large-bore catheter is the preferred line of choice. ● Prevention One of the most important early adjuncts to the primary resuscitation is adequate venous access for ﬂuid resuscitation and medication administration. Optimal venous access is often obtained in the prehospital setting with a peripheral IV in the forearm or antecubital fossa. For patients in whom peripheral IV access cannot be obtained, the next step is placement of a central venous line via the Seldinger technique. A short, large-bore catheter will have optimal ﬂow rates and is best to enable rapid ﬂuid administration. Placement of a longer, narrow-gauge (e.g., triple-lumen) catheter in this situation would be inappropriate because the smaller diameter and longer length signiﬁcantly impede ﬂow. Emergent central venous access placement can be performed in the internal jugular, subclavian, or femoral vein. The anatomic location of choice will depend on the patient’s injury pattern. Trauma patients often have a cervical collar blocking access to the jugular vein and ruling

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out this site. The femoral position gives the easiest access when multiple other procedures are being performed simultaneously on the patient’s airway and chest. However, femoral access has signiﬁcant drawbacks. Femoral cannulation is more difﬁcult to place based on anatomic landmarks alone, has a higher rate of deep vein thrombosis, and is relatively contraindicated in patients with pelvic and/or extremity injuries. The subclavian vein probably has the most constant anatomic position, making it ideally suited for placement by anatomic landmarks. However, it does pose the risk of hemo- and pneumothorax.

Central Venous Access Complications These are discussed in Section I, Chapter 7, Laparoscopic Surgery.

Inability to Obtain Venous Access ● Consequence Inability to obtain venous access can cause signiﬁcant morbidity and mortality. Life-saving ﬂuids, blood, and medications are necessary to further an ongoing resuscitation. Grade 4/5 complication ● Repair Consider intraosseous needle placement (even in adults) as an alternative for ﬂuid, blood, and drug administration. Use the endotracheal or intramuscular (IM) routes as appropriate. ● Prevention Other potential sources of venous access exist for difﬁcult cases. Intraosseous needle placement (e.g, proximal tibia) has been a standard alternative IV access in children under 6 years of age. More recently, the intraosseous route has been found to be acceptable in older children and adults as well.14 Venous cutdown is still an option, but it has been replaced by the more commonly performed percutaneous route. Some medications can be given down the endotracheal tube (if the patient is intubated). These medications can be remembered by the simple mnemonic NAVEL (naloxone, atropine, vasopressin, epinephrine, lidocaine). Use the IM route for medications needed to enable intubation of a combative trauma patient in whom IV access is not obtainable. Ketamine and succinylcholine can be given intramuscularly for sedation and paralysis to allow intubation.

Resuscitation through a Femoral Venous Cannula in Cases of Major Abdominal Venous Injury ● Consequence If ﬂuids, blood, or blood products are given through a femoral venous central line but bleed out into the abdominal cavity from a major venous injury (e.g., vena cava, iliac, hepatic), the patient will not get any

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SECTION XII: TRAUMA SURGERY

beneﬁt of the attempted resuscitation. This will lead to ongoing shock, hemorrhage, and death. Grade 5 complication ● Repair Venous access should be obtained in the antecubital fossa or a central vein above the diaphragm (internal jugular or subclavian). ● Prevention In certain situations, venous access above the diaphragm is more important than venous access below the diaphragm. The pitfall of placing the line in the femoral position begins with assuming that resuscitative ﬂuids (or blood) given through a femoral vein reach the heart and central circulation. This assumption may be incorrect in the case of iliac vein, inferior vena cava, or hepatic vein injuries. Large amounts of blood and ﬂuid resuscitation given through the groin may not stay intravascular, but rather end up pouring out of the venous hole and not helping the patient’s hemodynamics as expected.

Gastric and Urinary Decompression Adjuncts such as gastric and urinary decompression can be performed simultaneously with the rest of the evaluation and play an important role in the early resuscitation. ATLS suggests that these should be adjuncts to the primary survey,7 although in many instances, these commonly wait until after the secondary survey is performed.

Placing a Nasogastric Tube outside Its Normal Anatomic Pathway ● Consequence Gastric catheters can be necessary for gastric decompression, but they have associated risks. The most devastating complication is seen when the nasal route is chosen in a patient with a basilar skull or cribriform plate fracture. The nasogastric tube easily passes through the nares and directly into the brain. Grade 4/5 complication ● Prevention In patients with known (or suspected) skull base fractures, the nasal route is contraindicated for both gastric decompression and endotracheal intubation. In intubated patients, the orogastric route is preferred.

Exacerbation of a Minor Urethral Tear into a Complete Transaction ● Consequence Foley catheter insertion is important to measure urine output (as a marker of adequate resuscitation) and look for blood (gross and microscopic) in the urine. However, there is a risk of urethral injury when the

catheter is placed. In patients with incomplete urethral injuries, blind placement is contraindicated. This blind attempt at placement may convert a small, partial urethral tear into a complete transaction. Grade 2/3 complication ● Repair Urologic consultation will most likely be helpful in these situations. Repair will often necessitate suprapubic tube placement, cystoscopy for Foley catheter placement, and possibly, direct surgical repair of the torn urethra. ● Prevention There is a potential hazard in placing these urinary catheters, especially in patients with complex pelvic fractures and urethral injury. These injuries occur in men with some regularity. They are rare in women; however, the notion that they never occur is incorrect.15 Thorough physical examination should be performed to rule out the urethral injury before placement of a Foley catheter. Identiﬁcation of blood at the penile meatus (or introitus), perineal ecchymosis, scrotal hematoma, a high-riding or nonpalpable prostate, gross hematuria, or complex pelvic fracture should serve notice of potential urethral injury. In this case, a retrograde urethrogram is warranted to rule out urethral injury before placement of a Foley catheter blindly. Skipping this crucial step can convert a minor urethral tear into a complete transaction.

Assessment of the Need for Transfer Delaying Transfer ● Consequence Delayed recognition of the patient who needs to be transferred potentially inﬂuences eventual morbidity and mortality. Grade 1–5 complication ● Repair Arrange for transfer (if appropriate) as soon as possible after immediate stabilization of the patient. ● Prevention Transfers of trauma patients are common when an additional higher level of care is necessary. Early consideration of the need to transfer should be entertained, but it should not delay resuscitative measures. Often, basic measures and procedures (e.g., intubation, tube thoracostomy, venous access) must be performed just to stabilize the patient enough for a safe transfer. A small, nontrauma hospital may not have the resources (e.g., operating room, radiology, intensive care unit, blood bank) to handle a patient, even though an individual trauma surgeon working there may be comfortable doing so.

73 EVALUATION AND ACUTE RESUSCITATION OF THE TRAUMA PATIENT

SECONDARY SURVEY Missed Injury ● Consequence Grade 1–5 complication ● Repair Treatment for any injury should be performed (or planned for) as soon as the injury is identiﬁed. ● Prevention The secondary survey immediately follows the primary survey and associated adjuncts to resuscitation. This secondary survey consists of a thorough, systematic, head-to-toe physical examination. This examination should be done in the same order on every patient, reducing the potential pitfall of missing any injury, however small it may be. Abnormal physical examination ﬁndings may direct one toward further evaluation and work-up. Certain physical ﬁndings are hallmarks of traumatic injuries and, when recognized, prompt further diagnostic evaluation. “Seat belt signs” are severely bruised areas where a shoulder belt or lap belt crosses the body. When found over the neck, blunt cerebrovascular injury (BCVI) and cervical spine injury should be considered. A seat belt sign over the torso prompts concern of sternal fracture, hollow viscus injury, and lumbar spine fracture (Chance fracture). The handlebar of a bicycle can cause a classic circular injury pattern that should prompt consideration of hollow viscus and solid organ injury.

Incorrect Assessment of Patients with Gunshot Wounds ● Consequence Incorrect assessment of patients with gunshot wounds can lead to missed injuries and delays in diagnosis. Some complications may be insigniﬁcant, but others may have major implications. Delayed diagnoses may lengthen hospital stay and lead to worse clinical outcomes, organ failure, amputation, and death, depending on the injuries. Inappropriate judgment may also lead to unnecessary operations and/or procedures, which could be avoided by correct assessment. Grade 1–5 complication ● Repair The situation can be remedied by careful reevaluation and assessment (making sure the number of holes plus the number of bullets is an even number). As soon as a potential injury is identiﬁed, appropriate work-up and evaluation should be performed. ● Prevention In patients with gunshot wounds, it is imperative to count the number of gunshot wounds and identify all

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bullets retained in the patient’s body. When added together, this number must be even. Every bullet either makes an entrance and an exit wound or leaves a retained bullet. If the initial count is an odd number, the trauma surgeon may have made a mistake and must correct it immediately. Inadequate physical examination may miss holes within the hairlines, axilla, soft tissue folds, mouth, rectum, or vagina. Retained bullets are commonly missed on x-rays when the area between the chest and the pelvis ﬁlms is not adequately interrogated radiographically or the soft tissues are not included on a chest x-ray of an obese patient. CT scan can be beneﬁcial, even if only the scout ﬁlm is used to look for retained bullets. You may count up to an odd number erroneously if an old bullet (from a prior gunshot wound) is counted. Ask patients if they have been shot before; speciﬁcally question where they have retained bullets and subtract these from the count.

TREATMENT OF SPECIFIC INJURIES Pelvic Injury Although suggested by ATLS, not every trauma patient needs a plain pelvic x-ray.7 The pelvic x-ray has limited sensitivity (68% in adults and 54% in children) for detecting pelvic fractures compared with CT scanning. Patients who are hemodynamically stable and are going to get an abdominopelvic CT scan during their immediate resuscitation do not need a plain pelvic x-ray. Early pelvic x-ray may be helpful in hemodynamically unstable patients, those with signiﬁcant physical ﬁndings, and those who will not undergo immediate abdominopelvic CT scanning because of other clinical priorities.16

Ongoing Pelvic Hemorrhage ● Consequence Ongoing bleeding within the pelvis can have the same complications of bleeding as in all other patients (exsanguination, death). However, more commonly, it will lead to unnecessary blood transfusions, ongoing shock with hypotension and hypoperfusion, and further searches for possible bleeding sites. Grade 2–5 complication ● Repair Placement of a pelvic binder or external ﬁxator to close down pelvic volume should be done as soon as an unstable pelvis at high bleeding risk is found. ● Prevention Clinical assessment of the pelvis early in resuscitation is important because pelvic hemorrhage is a common cause for shock after blunt trauma.17 The pelvis is ﬁrst examined by lateral compression, looking for an unstable pelvic fracture. If the pelvis can be compressed, the examination should stop. Although this may seem like

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an ideal teaching case for every resident and student to examine the grossly unstable pelvis, this should not be done; only one person should examine the unstable pelvis. Every manipulation causes more arterial and venous bleeding from the pelvic fractures, only worsening the situation. A pelvic binder should be placed to close down the pelvic volume to control hemorrhage. External binding for pelvic stabilization is accomplished by using either a tightly wrapped bed sheet or a commercially available device (e.g., PelvicBinder) (Fig. 73–2).

Getting a Pelvic CT Scan without IV Contrast ● Consequence A pelvic CT scan without IV contrast cannot fully evaluate for contrast blush in the pelvis. This can lead to missing pelvic bleeding as a source of ongoing hemorrhage that may lead to shock, necessitate more blood transfusion, and possibly, lead to death. Grade 2–5 complication

A

● Repair Always order a CT scan of the pelvis with IV contrast administration. The same contrast bolus can be used to evaluate the rest of the torso (chest and abdomen) to screen for blunt aortic and/or solid organ injury, which is commonly associated with complex pelvic fractures. ● Prevention Abdominopelvic CT scan with IV contrast is critical to deﬁne the pelvic fracture and to evaluate for pelvic hematoma and arterial contrast blush (extravasation).18,19 The ﬁnding of arterial extravasation warrants immediate arteriography with therapeutic angioembolization. Angiographic embolization has rapidly become the standard of care for hemorrhage control after pelvic injury because operative attempts to control such bleeding are often unsuccessful. Pelvic vessel embolization has been shown to be safe and effective to control hemorrhage.20 Its application should be applied liberally. Older age (>60 yr) is associated with a higher risk of bleeding requiring intervention.21 Some trauma surgeons have suggested that certain speciﬁc anatomic injuries are associated with higher rates of bleeding.22,23 However, others have shown that the fracture pattern may not reliably predict which patients will beneﬁt from intervention.24 Repeat angiography is warranted in cases of ongoing hemorrhage and shock, even after initially normal angiography.25

Blunt Cerebrovascular Injury (BCVI) Delayed Diagnosis of BCVI in a Neurologically Normal Patient ● Consequence BCVI is a rare but devastating injury seen in trauma patients. BCVI is most often associated with a highspeed deceleration mechanism or a direct blow to the

B

C Figure 73–2 A, Pelvic x-ray of a patient with a complex pelvic fracture and pubic symphysis diastasis. B, Pelvic x-ray of the same patient after placement of the PelvicBinder. C, A patient with the PelvicBinder in place. (A–C, Courtesy of and reproduced with permission of PelvicBinder, Inc., Dallas, TX.)

cervical area. The ﬁrst sign or symptom of BCVI can be a massive stroke, after which clinical outcome is often poor. Grade 4/5 complication ● Prevention Aggressive screening practices are suggested to prevent this dreaded complication.26–28 Patients with signiﬁcant

73 EVALUATION AND ACUTE RESUSCITATION OF THE TRAUMA PATIENT

Box 73–1 Proposed Criteria for Screening for Blunt Cerebral Vascular Injury (BCVI) ●

●

●

History ● Injury mechanism consistent with severe neck hyperextension, rotation, or hyperﬂexion ● Hanging ● Amaurosis fugax Physical Examination ● Arterial hemorrhage from the head or face from the mouth, nose, ears, or wounds ● Massive epistaxis ● Expanding cervical hematoma ● Bruit in the neck of a young patient (<50 yr) ● Complex facial or mandible fractures ● Severe closed head injury ● Seat belt sign across the neck ● Anisocoria ● Unexplained mono- or hemiparesis ● Neurologic examination unexplained by head computed tomography (CT) scan ● Glasgow Coma Scale score ≤8 (in the ﬁeld or in the emergency department) ● Lateralizing neurologic signs ● Cerebrovascular accident (CVA) ● Transient ischemic attack (TIA) ● Horner’s syndrome Radiographic ﬁndings ● Complex facial or mandible fractures ● Cervical spine fracture ● Basilar skull fracture through or near the carotid canal ● Fracture through the foramen transversarium ● Cerebral infarction on CT scan

risk factors for BCVI should have liberal screening to avoid the potential pitfall of delayed stroke that can be prevented by earlier injury identiﬁcation and treatment with anticoagulation (e.g., heparin, antiplatelet agents). Although deﬁnitive criteria for screening are not clearly deﬁned, many signs and symptoms have been suggested to predict a high risk of BCVI26,29 (Box 73–1). The gold standard for screening these patients has been conventional catheter-based angiography. Newer data have suggested that multi-lanar CT angiography is a promising screening modality.30–34

Hypotensive Blunt Trauma Patient The hypotensive blunt trauma patient presents many potential areas to make mistakes with dire consequences. These patients need immediate, rapid evaluation with concurrent resuscitation in an attempt to stay alive.

Not Rapidly Identifying the Site of Bleeding ● Consequence Delayed diagnosis of the source and site of bleeding in a hypotensive blunt trauma patient can rapidly lead to hypotension, shock, and death from exsanguination. Grade 4/5 complication

769

● Repair Rapidly search for or rule out bleeding from all potential sites including the chest, abdomen, pelvis, retroperitoneum, and extremities and observe for external blood loss. ● Prevention Hemorrhage is the number-one potential cause of shock in these patients, and it must be ruled out quickly. Only a ﬁnite number of places exist in which an adult patient can bleed enough to go into hemorrhagic shock. These include the chest, abdomen, pelvis, retroperitoneum, extremities, and external blood loss. Most of these areas are rapidly assessed with physical examination, two plain x-rays (chest and pelvis) and focused abdominal sonography for trauma (FAST). Provider-performed FAST is a quick, reliable, noninvasive ultrasound designed to identify hemopericardium and/or hemoperitoneum. It has almost universally replaced diagnostic peritoneal lavage for identifying intra-abdominal hemorrhage in hypotensive blunt trauma patients. If enough blood is lost into the abdomen to cause hemorrhagic shock, this should be clearly apparent on FAST (Fig. 73–3). In the ﬁrst major series, FAST was 100% sensitive and speciﬁc for identifying or ruling out intra-abdominal bleeding as the source of hypotension in blunt trauma patients.35 Other series have also shown that abdominal ﬂuid is nearly always identiﬁed when present.36,37 If positive, rapid exploratory laparotomy is indicated to control bleeding. If the FAST is unavailable, diagnostic peritoneal lavage can still be used to determine whether abdominal bleeding is the cause of hypotension.

Missed Cause of Shock ● Consequence Although hemorrhage is the most common cause of shock in these patients, it is not the only one. Other causes do occur including obstructive (tension pneumothorax or cardiac tamponade), neurogenic, cardiogenic, and anaphylactic shock. Grade 4/5 complication ● Repair If all potential sites of bleeding have been ruled out, consider other possible causes of post-traumatic shock. ● Prevention If the FAST and radiographs are negative, consider the other rare causes of post-traumatic shock in patients who are persistently hypotensive. Obstructive shock (cardiac tamponade and/or tension pneumothorax) should be reconsidered, and if any doubt remains, steps should be taken to correct this. Neurogenic shock is rare, and its diagnosis is commonly delayed. Neurogenic shock is ruled out quickly by observing patients moving all their extremities. Physical examination

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SECTION XII: TRAUMA SURGERY artery thrombosis, (4) cardiac failure, (5) minor electrocardiographic cardiac enzyme abnormality, or (6) complex arrhythmia with cardiac failure. Formal echocardiography is necessary to identify wall motion abnormalities and anatomic defects.39–41 Anaphylaxis and sepsis are exceedingly uncommon causes of shock after trauma, but if all other causes have been ruled out, these possibilities must be considered.

Normal

Kidney Liver

REFERENCES

A Diaphragm Hemoperitoneum

Fluid

Liver

Kidney

B Diaphragm

Figure 73–3 Focused abdominal sonography examination. A, Normal right upper quadrant right upper quadrant view shows ﬂuid between liver. (A and B, Reproduced with permission MD.)

for trauma (FAST) view. B, Abnormal the kidney and the of Thomas Scalea,

ﬁndings consistent with neurogenic shock include hypotension, bradycardia, and warm skin (as opposed to the patient in hemorrhagic shock who is hypotensive and tachycardic with cool skin). In the obtunded or intubated patient, an early lateral cervical spine ﬁlm is imperative to identify cervical spine fracture and help identify neurogenic shock early. A recently reported case highlighted the major pitfall of delay in diagnosis of neurogenic shock.38 Neurogenic shock went unrecognized, resulting in an unnecessary (and negative) laparotomy for presumed bleeding. Although the death was not preventable, the laparotomy was avoidable.38 Cardiogenic shock from blunt cardiac injury (BCI) is a rare ﬁnding in an alive trauma patient. BCI is always deﬁned by its physiologic effect and can include (1) septal rupture, (2) free wall rupture, (3) coronary

1. MacKenzie EJ, Rivara FP, Jurkovich GJ, et al. A national evaluation of the effect of trauma-center care on mortality. N Engl J Med 2006;354:366–378. 2. Demetriades D, Martin M, Salim A, et al. Relationship between American College of Surgeons trauma center designation and mortality in patients with severe trauma (injury severity score >15). J Am Coll Surg 2006;202: 212–215; quiz A45. 3. Demetriades D, Martin M, Salim A, et al. The effect of trauma center designation and trauma volume on outcome in speciﬁc severe injuries. Ann Surg 2005;242:512–517; discussion 517–519. 4. Demetriades D, Berne TV, Belzberg H, et al. The impact of a dedicated trauma program on outcome in severely injured patients. Arch Surg 1995;130:216–220. 5. Cornwell EE 3rd, Chang DC, Phillips J, Campbell KA. Enhanced trauma program commitment at a level I trauma center: effect on the process and outcome of care. Arch Surg 2003;138:838–843. 6. Scarborough K, Slone DS, Uribe P, et al. Reduced mortality at a community hospital trauma center: the impact of changing trauma level designation from II to I. Arch Surg 2008;143:22–27; discussion 27–28. 7. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support (ATLS) Student Course Manual, 7th ed. Chicago: American College of Surgeons, 2004, p 73. 8. Welling DR, Burris DG, Hutton JE, et al. A balanced approach to tourniquet use: lessons learned and relearned. J Am Coll Surg 2006;203:106–115. 9. Gruen RL, Jurkovich GJ, McIntyre LK, et al. Patterns of errors contributing to trauma mortality: lessons learned from 2,594 deaths. Ann Surg 2006;244:371–380. 10. Demetriades D, Karaiskakis M, Velmahos G, et al. Effect on outcome of early intensive management of geriatric trauma patients. Br J Surg 2002;89:1319–1322. 11. Demetriades D, Sava J, Alo K, et al. Old age as a criterion for trauma team activation. J Trauma 2001;51:754–756; discussion 756–757. 12. Brown CV, Velmahos GC, Neville AL, et al. Hemodynamically “stable” patients with peritonitis after penetrating abdominal trauma: identifying those who are bleeding. Arch Surg 2005;140:767–772. 13. Brain Trauma Foundation and American Association of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care. Management and Prognosis of Severe Traumatic Brain Injury. Available at http://www2. braintrauma.org/guidelines/ (accessed June 16, 2006).

73 EVALUATION AND ACUTE RESUSCITATION OF THE TRAUMA PATIENT 14. Davidoff J, Fowler R, Gordon D, et al. Clinical evaluation of a novel intraosseous device for adults: prospective, 250patient, multi-center trial. JEMS 2005;30(10 suppl):20– 23. 15. Black PC, Miller EA, Porter JR, Wessells H. Urethral and bladder neck injury associated with pelvic fracture in 25 female patients. J Urol 2006;175:2140–2144; discussion 2144. 16. Guillamondegui OD, Pryor JP, Gracias VH, et al. Pelvic radiography in blunt trauma resuscitation: a diminishing role. J Trauma 2002;53:1043–1047. 17. DiGiacomo JC, Bonadies JA, Cole FJ, et al. Practice Management Guidelines for Hemorrhage in Pelvic Fracture. The Eastern Association for the Surgery of Trauma. Available at http://www.east.org/tpg 18. Pereira SJ, O’Brien DP, Luchette FA, et al. Dynamic helical computed tomography scan accurately detects hemorrhage in patients with pelvic fracture. Surgery 2000;128:678–685. 19. Ryan MF, Hamilton PA, Chu P, Hanaghan J. Active extravasation of arterial contrast agent on post-traumatic abdominal computed tomography. Can Assoc Radiol J 2004;55:160–169. 20. Velmahos GC, Toutouzas KG, Vassiliu P, et al. A prospective study on the safety and efﬁcacy of angiographic embolization for pelvic and visceral injuries. J Trauma 2002;53:303–308; discussion 308. 21. Kimbrell BJ, Velmahos GC, Chan LS, Demetriades D. Angiographic embolization for pelvic fractures in older patients. Arch Surg 2004;139:728–732. 22. Hamill J, Holden A, Paice R, Civil I. Pelvic fracture pattern predicts pelvic arterial haemorrhage. Aust N Z J Surg 2000;70:338–343. 23. Eastridge BJ, Starr A, Minei JP, et al. The importance of fracture pattern in guiding therapeutic decision-making in patients with hemorrhagic shock and pelvic ring disruptions. J Trauma 2002;53:446–450; discussion 450– 451. 24. Sarin EL, Moore JB, Moore EE, et al. Pelvic fracture pattern does not always predict the need for urgent embolization. J Trauma 2005;58:973–977. 25. Shapiro M, McDonald AA, Knight D, et al. The role of repeat angiography in the management of pelvic fractures. J Trauma 2005;58:227–231. 26. Bifﬂ WL, Moore EE, Offner PJ, et al. Optimizing screening for blunt cerebrovascular injuries. Am J Surg 1999;178:517–522. 27. Cothren CC, Moore EE, Ray CE Jr, et al. Screening for blunt cerebrovascular injuries is cost-effective. Am J Surg 2005;190:845–849.

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28. Kerwin AJ, Bynoe RP, Murray J, et al. Liberalized screening for blunt carotid and vertebral artery injuries is justiﬁed. J Trauma 2001;51:308–314. 29. Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Surg 2002;236: 386–393. 30. Mutze S, Rademacher G, Matthes G, et al. Blunt cerebrovascular injury in patients with blunt multiple trauma: diagnostic accuracy of duplex Doppler US and early CT angiography. Radiology 2005;237:884–892. 31. Bub LD, Hollingworth W, Jarvik JG, Hallam DK. Screening for blunt cerebrovascular injury: evaluating the accuracy of multidetector computed tomographic angiography. J Trauma 2005;59:691–697. 32. Bifﬂ WL, Egglin T, Benedetto B, et al. Sixteen-slice computed tomographic angiography is a reliable noninvasive screening test for clinically signiﬁcant blunt cerebrovascular injuries. J Trauma 2006;60:745–751; discussion 751–752. 33. Berne JD, Norwood SH, McAuley CE, Villareal DH. Helical computed tomographic angiography: an excellent screening test for blunt cerebrovascular injury. J Trauma 2004;57:11–17; discussion 17–19. 34. Eastman AL, Chason DP, Perez CL, et al. Computed tomographic angiography for the diagnosis of blunt cervical vascular injury: is it ready for primetime? J Trauma 2006;60:925–959. 35. Rozycki GS, Ballard RB, Feliciano DV, et al. Surgeonperformed ultrasound for the assessment of truncal injuries: lessons learned from 1540 patients. Ann Surg 1998;228:557–567. 36. Holmes JF, Harris D, Battistella FD. Performance of abdominal ultrasonography in blunt trauma patients with out-of-hospital or emergency department hypotension. Ann Emerg Med 2004;43:354–361. 37. Farahmand N, Sirlin CB, Brown MA, et al. Hypotensive patients with blunt abdominal trauma: performance of screening US. Radiology 2005;235:436–443. Epub 2005; March 29. 38. McMonagle MP. Images in clinical medicine. The importance of early cervical-spine radiography. N Engl J Med 2006;354(4):e4. 39. Schultz JM, Trunkey DD. Blunt cardiac injury. Crit Care Clin 2004;20:57–70. 40. Elie MC. Blunt cardiac injury. Mt Sinai J Med 2006;73: 542–552. 41. Haut ER. Blunt cardiac injury. In Cameron JL (ed): Current Surgical Therapy, 9th ed. Philadelphia: Elsevier, 2008; pp 1063–1066.

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Management of Thoracic Trauma David T. Efron, MD and Edward E. Cornwell III, MD INTRODUCTION As with all traumatic injury, the management of thoracic trauma is centered on both the rapid diagnosis and the correction of the insult. Particular to injuries to the chest is the possible simultaneous disruption of two of the three life-sustaining physiologic processes (namely, breathing and circulation). Therefore, life-saving treatment and diagnosis often must occur in congruity. Many of the pitfalls that present themselves in the management of thoracic trauma are mistakes of omission and carry the risk of extreme morbidity and mortality. Many of the physiologic principles apply in the management of both blunt and penetrating injuries. As such, speciﬁc injuries are addressed in this chapter rather than mechanism. The steps followed in the care of the traumatically injured patient are well described and outlined by the Advanced Trauma Life Support training put forth by the Committee on Trauma of the American College of Surgeons.1 Ensuring an airway and conﬁrming effective breathing and circulation are prime goals and permit appropriate diagnosis and guide treatment options.

INDICATIONS ● Hypotension ● Chest wall defects (open or closed) ● Injury mechanism

MANAGEMENT OF THORACIC TRAUMA STEPS Step Step Step Step Step

1 2 3 4 5

Airway Breathing Circulation Disability Exposure

On arrival at the trauma bay, once an airway is deemed secure, the lung ﬁelds are auscultated with a stethoscope. Absence of breath sounds suggests loss of pulmonary

aeration and is likely due to collapse of the pulmonary parenchyma and replacement with air, blood, or abdominal contents owing to diaphragmatic rupture (very rare on the right). Adjunctive physical examination ﬁndings may aid in the cause of pulmonary collapse such as tracheal shift from midline, hyperresonance (pneumothorax), or dullness (hemothorax) to percussion. However, in a busy, loud trauma room, these are rarely discernible. Victims of penetrating trauma will have wounds that will aid in identiﬁcation of potential injury and that must be sealed as a source of pleural air. Accompanying hypotension may suggest tension physiology, which requires immediate decompression either by placement of a large-bore intravenous catheter into the pleural space (via the second intercostal space in the midclavicular line) or by immediate chest tube placement if it is readily available. Chest radiograph as an adjunct to the primary survey is often helpful in identifying hemo- or pneumothorax in the hemodynamically stable patient.

Incomplete Pleural Decompression of a Pneumothorax ● Consequence Because victims of thoracic trauma are at risk of multiple injuries contributing to the overall picture, accurate diagnosis and treatment are vital. An inadequately performed decompression of a tension pneumothorax not only continues the circulatory embarrassment of the patient but also confuses the picture and may delay vital diagnostic and therapeutic decision making. The thoracic cavity may be entered in the initial attempt at tube placement, thereby relieving the immediate tension pneumothorax. However, if the tube is subsequently left in the subcutaneous space, the tension may reaccumulate owing to ongoing leak from the pulmonary parenchyma. Grade 4/5 complication ● Repair Replacement of the intravenous catheter. Replacement of a subcutaneous chest tube.

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● Prevention Intravenous decompression: The apex of the thoracic cavity at the level of the second rib slopes posteriorly, though the chest wall in most patients remains parallel to the ﬂoor in the supine patient. To properly position this catheter, it is angled in a caudal direction and passed over the third rib. Chest tubes: This is often identiﬁed at postprocedure chest x-ray. Making the skin directly over the sixth rib at the point at which the tube is intended to enter the thoracic cavity and not trying to tunnel the chest tube helps avoid subcutaneous placement and ensure correct positioning. Obese patients are particularly at risk.

Incomplete Decompression of a Hemothorax ● Consequence Persistent hypotension after appropriate treatment of tension pneumothorax suggests an alternative ongoing source of shock. Massive hemothorax with ongoing bleeding is a well-recognized indication for operative intervention. Unrecognized persistent hemothorax at minimum hinders respiratory status, but more worrisome is the failure to recognize the source of ongoing hemorrhage and basing decision making on incomplete or faulty data (i.e., unnecessary laparotomy or delayed thoracotomy). This may be due to ongoing thoracic bleeding or improper positioning or kinking of the chest tube. Grade 3/4 complication

Figure 74–1 This patient suffered multiple rib fractures on the left after a motor vehicle collision. Initial chest tube placed for a pneumothorax was kinked at the most distal hole. Persistent pneumothorax is evident at the left apex on the chest x-ray.

● Repair A postinsertion chest radiograph conﬁrms positioning of the chest tube. Recognition of a kinked chest tube on x-ray leads the surgeon to reposition it appropriately (Fig. 74–1). Clotted chest tubes can occur; however, this scenario is often associated with massive hemothorax and ongoing blood loss (Fig. 74–2). ● Prevention Insertion of a large-bore chest tube (36, 38, or 40 Fr) allows for maximal drainage of blood in patients with hemothorax. By twirling the chest tube around its longitudinal axis while inserting it through the chest wall, one ensures that it is not kinked. This maneuver should be performed whether the tube is inserted for hemothorax or pneumothorax.

Unrecognized Aortic Tear In the absence of hemothorax, the approach to the management in this scenario depends upon whether the mechanism of injury is blunt or penetrating. Patients suffering blunt injury of signiﬁcant force are at elevated risk for aortic tear, most frequently seen just distal to the left subclavian oriﬁce. Frequently, chest x-ray evidence suggests signs of great vessel injury including widened mediastinum, loss of the aortic knob, and pleural capping.2 Other signs that indicate heightened energy

Figure 74–2 This patient suffered a gunshot wound to the right chest and presented with a hemopneumothorax. The persistent massive hemothorax can be seen despite the excellent position of two chest tubes.

transfer include high rib fractures and sternal or scapular fractures. ● Consequence The ultimate consequences of unrecognized aortic injury include rupture and death. In addition, if the rupture remains contained, subsequent thoracic aortic aneurysm may develop. Grade 4/5 complication

74 MANAGEMENT OF THORACIC TRAUMA ● Repair Acute thoracic aortic disruption requires repair, most frequently with short segment graft interposition. Despite some case reports, there is not consistent enough experience to recommend an attempt at endovascular repair outside major study centers.3,4 ● Prevention Aggressive work-up and recognition of these injuries are mandatory. The “gold standard” has traditionally been conventional aortography. However, thoracic computed tomography (CT) scan has been shown to be reliable. Transesophageal echocardiography, when available, is another potential alternative.

Unrecognized Abdominal Injury ● Complication Hypotension in the setting of blunt aortic injury must be ascribed to another source of shock. Noncontained aortic tears result in rapid demise from exsanguinating hemorrhage. The blood found in the periaortic tissue from a contained tear in and of itself is usually not enough to cause global shock. Patients suffering sufﬁcient blunt injury to incur aortic tear are also at risk for multiple injuries including fractures and abdominal injuries such as liver and splenic fractures. These injuries are much more likely to be exsanguinating, especially in the time it takes to work up and treat the aortic tear. Missed abdominal injury in this setting is potentially lethal. Grade 4/5 complication

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warranted. The prime goals are to (1) release a tamponade by opening the pericardium, (2) potentially control the hemorrhagic source by direct pressure, and (3) ensure adequate blood ﬂow to the brain and coronary vessels by applying an aortic cross-clamp. This is achieved via a left anterolateral thoracotomy in the ﬁfth intercostal space. When access to the thoracic cavity is gained, the pericardium is opened.7,8

Delayed Transport to the Operating Room to Allow Intubation ● Consequence In the setting of penetrating injury to the pulmonary parenchyma, the relatively low-pressure pulmonary vasculature is directly exposed to the aerated regions owing to the disruption of the architecture of each. In the nonintubated patient, the bronchial tree is also a low pressure system. When the patient is intubated, positive-pressure ventilation often causes the bronchial tree to become the higher-pressure system, especially in the setting of deep hemorrhagic shock. This raises the risk of air embolus. Grade 4/5 complication ● Prevention Rapid transport to and intubation in the operating room minimize the exposure time of the injured pulmonary vessels to the potentially high positive-pressure ventilation transmitted across injured airways. This also minimizes the time to deﬁnitive surgical therapy.

Phrenic Nerve Injury

● Repair Rapid exploratory laparotomy is the only solution if the injury is recognized late.

● Consequence Left hemidiaphragm paralysis. Grade 2/3 complication

● Prevention Aggressive screening is vital. In the hemodynamically stable patient, CT scanning of the chest and abdomen is integral to accurate injury diagnosis. Patients who are hemodynamically unstable may undergo focused abdominal ultrasound for trauma (FAST) or diagnostic peritoneal lavage (DPL).5,6 The ﬁnding of intraabdominal ﬂuid in this setting necessitates immediate laparotomy prior to the deﬁnitive work-up for aortic tear (which is undertaken immediately after the abdominal injuries are stabilized).

● Prevention As the phrenic nerve courses longitudinally along the anterior aspect of the pericardium in the left hemithorax, the nerve is identiﬁed and the opening in the pericardium is made in a longitudinal manner parallel to the course of the nerve.

Hypotension in the Setting of Penetrating Thoracic Injury Hypotension in the setting of penetrating thoracic injury is due to bleeding, tension physiology, or cardiac tamponade. Ongoing bleeding often requires immediate operative repair. Tamponade often results in patient arrest en route to or immediately after arrival at the trauma bay. When this occurs, emergency department thoracotomy is

Unrecognized Right Thoracic Injury at Left Thoracotomy ● Consequence Missed thoracic injury in the right hemithorax signiﬁcantly delays appropriate management and may lead to a lethal delay. Grade 4/5 complication ● Prevention For penetrating injuries to the chest, especially in the case of multiple injuries and suspected transmediastinal trajectory, simultaneous right chest tube placement at the time of left thoracotomy is advisable.

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Figure 74–4 Laparoscopic view of a diaphragmatic injury in a patient suffering an isolated stab wound to the left lower chest posteriorly. The Kelly clamp has been passed through the external defect and deﬁnes the track of the injury.

It should be noted that up to 20% of diaphragmatic injuries are present in the setting of a normal chest radiograph.10

Inadequate Analgesia for Rib Fractures Figure 74–3 Barium enema study of a patient with herniation of his colon through the left diaphragm. The defect is a result of a stab wound to the left lower chest several years prior.

Other Issues Unrecognized Diaphragm Injury ● Consequence Forty percent of penetrating thoracoabdominal wounds demonstrate associated diaphragm injury.9 Over time, left hemidiaphragm lacerations are at risk for developing into diaphragmatic hernias (Fig. 74–3). The right side is well protected by adhesion to the dome of the liver. Grade 2/3 complication ● Repair Subsequent operative takedown of a transdiaphragm hernia and repair are required. ● Prevention We favor an aggressive approach to penetrating injuries to this region. Any patient suffering a penetrating injury to the left thoracoabdominal region (from the sternum at or below the level of the nipple around to the scapular tip posteriorly and inferiorly to the costal margins) is taken for exploratory laparoscopy to inspect the diaphragm (Fig. 74–4). Injuries may be repaired in an open manner or laparoscopically if the surgeon is conﬁdent that other intraperitoneal injury can be excluded.

● Consequence The force sustained during blunt injury required to cause multiple rib fractures is often transmitted to the underlying pulmonary parenchyma and results in pulmonary contusion. This combination of pathology can lead to severe respiratory embarrassment. The area of contusion behaves as an intrapulmonary shunt demonstrating perfusion without aeration. Early on postinjury, this physiology worsens as the contusion matures. In addition, the patient will ineffectively breathe to utilize the remaining pulmonary tissue because of the pain associated with rib fractures. Analgesia is vital to successful pulmonary toilet and maintenance of pulmonary function. Inadequate analgesia can result in respiratory failure with subsequent mechanical ventilation and potential development of pneumonia. Grade 2/3 complication ● Prevention Accurate recognition of the extent of the injury is key. Patients may require intravenous patient-controlled analgesia with narcotics combined with oral nonsteroidal anti-inﬂammatory agents. The Eastern Association for the Surgery of Trauma guidelines recommend that epidural anesthesia is the preferred method of pain control for rib fractures from blunt injury (level 1 recommendation), that all patients over 65 with four or more rib fractures should undergo placement of a thoracic epidural for pain control, and consideration of thoracic epidural anesthesia should be given to

74 MANAGEMENT OF THORACIC TRAUMA any patient with four or more rib fractures (level 2 recommendations).11

Retained Hemothorax ● Consequence Entrapped lung from ﬁbrin peal formation and empyema. Grade 2/3 complication ● Repair Open thoracotomy for excision of ﬁbrin peal and release of entrapped lung. This is often a difﬁcult procedure, given the inﬂammation, and is frequently accompanied by moderate blood loss.12 ● Prevention Plain chest radiographic imaging has a poor sensitivity in predicting the absence or presence of a signiﬁcant volume of retained pleural blood. The pulmonary parenchyma is often contused, and this can suggest ﬂuid where there is none or mask a signiﬁcant volume of retained blood. A CT scan of the thorax enables quantiﬁcation of retained ﬂuid.13 If done within the ﬁrst 4 days postinjury (prior to the formation of the ﬁbrin peal), a video-assisted thoracoscopic drainage of the retained blood is usually successful and avoids the need for thoracotomy and empyemectomy.14

REFERENCES 1. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support (ATLS) Student Course Manual, 7th ed. Chicago: American College of Surgeons, 2004. 2. Nagy K, Fabian T, Rodman G, et al. Guidelines for the diagnosis and management of blunt aortic injury. Eastern Association for the Surgery of Trauma: Trauma Practice Guidelines, 2001. Available at http://www.east.org/tpg/ chap8.pdf

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3. Tehrani HY, Peterson BG, Katariya K, et al. Endovascular repair of thoracic aortic tears. Ann Thorac Surg 2006;82: 873–877. 4. Hoornweg LL, Dinkelman MK, Goslings JC, et al. Endovascular management of traumatic ruptures of the thoracic aorta: a retrospective multicenter analysis of 28 cases in The Netherlands. J Vasc Surg 2006;43:1096– 1102. 5. Ma OJ, Gaddis G, Steele MT, et al. Prospective analysis of the effect of physician experience with the FAST examination in reducing the use of CT scans. Emerg Med Australas 2005;17:24–30. 6. Von Kuenssberg Jehle D, Stiller G, Wagner D. Sensitivity in detecting free intraperitoneal ﬂuid with the pelvic views of the FAST exam. Am J Emerg Med 2003;21:476– 478. 7. Branney SW, Moore EE, Feldhaus KM, Wolfe RE. Critical analysis of two decades of experience with postinjury emergency department thoracotomy in a regional trauma center. J Trauma 1998;45:87–94. 8. Hunt PA, Greaves I, Owens WA. Emergency thoracotomy in thoracic trauma—a review. Injury 2006;37:1–19. 9. Murray JA, Demetriades D, Asensio JA, et al. Occult injuries to the diaphragm: prospective evaluation of laparoscopy in penetrating injuries to the left lower chest. J Am Coll Surg 1998;187:626–630. 10. 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. 11. Pain management in blunt thoracic trauma (btt)—an evidence-based outcome evaluation. Eastern Association for the Surgery of Trauma: Trauma Practice Guidelines 2004. Available at http://www.east.org/tpg/painchest.pdf 12. Navsaria PH, Vogel RJ, Nicol AJ. Thoracoscopic evacuation of retained posttraumatic hemothorax. Ann Thorac Surg 2004;78:282–285. 13. Velmahos GC, Demetriades D. Early thoracoscopy for the evacuation of undrained haemothorax. Eur J Surg 1999; 165:924–929. 14. Ahmed N, Jones D. Video-assisted thoracic surgery: state of the art in trauma care. Injury 2004;35:479–489.

75

Management of Pancreatic and Duodenal Injuries David T. Efron, MD and Edward E. Cornwell III, MD

INTRODUCTION The management of pancreatic and duodenal injuries is often difﬁcult, primarily owing to the unforgiving nature of injured tissues in these organs. Damage to these structures is often associated with a high mortality, especially with a penetrating mechanism, because of simultaneous injury to major vascular and other intra-abdominal structures.1–5 Appropriate management requires accurate diagnosis of the injuries, a clear understanding of gastrointestinal physiology (with a plan for restoring disrupted continuity), and acute attention to the ongoing status and stability of the patient.

MANAGEMENT OF PANCREATIC AND DUODENAL INJURIES STEPS Step 1 Step 2

Step 3 Step 4

Stabilization and diagnosis Complete exposure of duodenum and pancreas (Kocher’s maneuver, exploration of lesser sac, mobilization of spleen and pancreatic tail) Determination of resection, repair, drainage Repair (dependent upon injuries present)

OPERATIVE PROCEDURE Stabilization and Diagnosis Patients presenting with penetrating injuries that result in pancreatic or duodenal injuries almost uniformly demonstrate signs requiring immediate laparotomy. Hypotension and abdominal distention indicative of excessive blood loss are suggestive of major associated vascular injury. This is the setting in which most patients are explored for and

the pancreatic and duodenal injuries must be suspected and ruled out. To accomplish this, the entire trajectory of the penetrating object must be assessed. Central retroperitoneal hematomas must be explored. In the hemodynamically stable patient, peritonitis is often identiﬁed on presentation and also warrants immediate exploration. Victims of blunt abdominal trauma are often hemodynamically stable, allowing for more substantial work-up and diagnosis of injuries. Many patients present with multiple injuries, the result of high-energy transfer, such as motor vehicle collisions, pedestrians struck, or falls from height. Other blunt mechanisms include focused-point blows to the epigastrium with transmitted force directly over the duodenum and pancreas (such as falling onto a bicycle handle).6 Admission and serial serum amylase measurements can be useful to guide a more focused investigation of pancreatic injury. However, serum amylase at presentation is a poor predictor of pancreatic injury requiring operative repair.7,8 Computed tomography scanning is useful because it provides the most anatomic information with regards to these injuries and can easily diagnose duodenal wall hematomas, pancreatic fracture, peripancreatic edema or hematoma, free extravasation of contrast from duodenal disruption as well as associated trauma such as splenic or hepatic fractures.4,5,9,10 However, isolated pancreatic injury may not be evident at the time of initial scanning when inﬂammation may still be minimal. Focused abdominal sonography for trauma (the FAST scan) clearly demonstrates free intra-abdominal ﬂuid but cannot delineate a speciﬁc source and is not useful for the diagnosis of retroperitoneal injuries. In the stable patient without peritonitis, more speciﬁc diagnostic modalities are useful to assess for suspected pancreatic and duodenal injuries. An upper gastrointestinal contrast study with Gastrograﬁn can identify both luminal narrowing (the result of a duodenal mural hematoma) and contrast extravasation.9 Esophagogastro-

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duodenoscopy (EGD) with endoscopic retrograde cholangiopancreatography (ERCP) allows nonoperative assessment of the integrity of both the main pancreatic and the common bile ducts.11,12

Inappropriate Radiographic Work-up Delaying Operative Intervention ● Consequence Delayed operative intervention for a patient with major intra-abdominal hemorrhage is potentially life threatening and can have highly morbid sequelae owing to the need for resuscitation, excessive blood transfusion, and risk of coagulopathy. Grade 4/5 complication ● Prevention Adherence to the principles of trauma management with recognition of the hard indications for abdominal exploration facilitates rapid transport to the operating room. Pancreatic and duodenal injuries in and of themselves are rarely a cause of hemodynamic instability. When present, this is the result of other injuries, which must be immediately addressed.

Complete Exposure of the Duodenum and Pancreas (Kocher’s Maneuver, Exploration of the Lesser Sac, Mobilization of the Spleen and the Pancreatic Tail) The entire trajectory of the penetrating object must be assessed, and central retroperitoneal hematomas must be explored. Complete mobilization of the duodenum and the head of the pancreas allows inspection and palpation of the posterior aspect of these organs and the potential injuries that may have resulted from a through-andthrough trajectory to this region. When the track of the bullet traverses to the right of the superior mesenteric artery and vein, complete mobilization of the second portion of the duodenum and the head of the pancreas is accomplished via an extensive Kocher maneuver. By retracting the hepatic ﬂexure of the colon inferomedially, the avascular connective tissue along the left lateral and posterior borders of the duodenum is easily divided (Fig. 75–1). Often, the right colon must be mobilized from the retroperitoneum along the line of Toldt to allow access to this region. Care must be taken to remain close to the duodenum and posterior pancreatic head because the inferior vena cava, right renal veins, and Gerota’s fascia are just deep to this dissection. The mobilization is taken to the lateral (right) edge of the superior mesenteric artery and vein. The anterior surface of the body and tail of the pancreas is explored through the lesser sac. Access to the lesser sac is best achieved through the gastrocolic ligament, initially via the relatively avascular area to the left of the midline toward the splenic ﬂexure. This provides a clear view of the anterior surface of the pancreas (Fig. 75–2). A hematoma overlying the pancreas is explored (Fig. 75–3).

Figure 75–1 Division of the connective tissue along the lateral edge of the duodenum as the beginning of the Kocher maneuver.

Figure 75–2 Exploration of the lesser sac demonstrates the length of the anterior surface of the pancreas. A central hematoma is shown.

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Figure 75–3 Hematoma overlying the pancreas is explored. The inferior border of the gland is safely mobilized so that the posterior aspect of the gland may be explored for injury.

The posterior aspect of the body and tail of the pancreas is visualized either by dissection along the relatively avascular plane at the lower border of the pancreas (see Fig. 75–3) or by the complete mobilization of the spleen and pancreas medially out of the retroperitoneum (Fig. 75–4). This aspect of medial visceral rotation is accomplished by freeing the retroperitoneal attachments of the spleen from along the diaphragm and Gerota’s fascia and subsequently elevating the pancreas from the retroperitoneum with the splenic artery and veins intact. This allows inspection of the posterior border of the pancreas for through-andthrough injury. The pancreas can be mobilized to the level of the superior mesenteric vessels. The Kocher maneuver allows inspection of the entire C-loop of the duodenum. The ﬁrst, third, and fourth portions are more easily directly inspected. If an anterior injury is noted as a result of penetrating injury, a posterior exit should be sought.

Missed Pancreatic or Duodenal Injury ● Consequence Failure to identify pancreatic injury may result in pancreatic leak, peripancreatic abscess, pancreatic ﬁstula, pancreatitis, pseudoaneurysm formation, sepsis, and pseudocyst formation.2–5,13 Similarly, failure to identify duodenal perforation can result in local abscess, duodenocutaneous ﬁstula, and severe sepsis.13–15 Each carries elevated morbidity and mortality. Grade 4/5 complication

Figure 75–4 Medial rotation of the spleen and pancreas from the left retroperitoneum also allows access to the posterior aspect of the gland and is the principal maneuver in completing a distal pancreatectomy and splenectomy.

● Repair Control of leakage and wide drainage are the governing principles to treatment of missed injuries. In all but a very few stable patients, this includes reexploration for appropriate treatment. Isolated pancreatic duct injuries identiﬁed endoscopically may be treated with placement of a pancreatic duct stent (Fig. 75–5). ● Prevention Complete mobilization of the duodenum and the head of the pancreas allows inspection and palpation of the posterior aspect of these organs and the potential injuries that may have resulted from a through-and-through penetrating trajectory to this region. Complete mobilization of both the duodenum and the pancreas at the time of laparotomy is also important in blunt trauma in which there is suspicion of pancreatic or retroperitoneal duodenal injury.

Injury to a Replaced Right Hepatic Artery during Kocherization ● Consequence In 10% to 15% of patients, a replaced right hepatic artery is identiﬁed at the superior edge of the dissection.16 The difﬁculty of this dissection is at times

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Figure 75–5 Endoscopically placed pancreatic duct stent for successful isolation of traumatic pancreatic duct disruption.

increased by tissue hematoma from bleeding vessel branches. If this is injured in the dissection, signiﬁcant hepatic ischemia may ensue, especially if there is concomitant injury to the portal vein. Grade 2/3 complication

The decision to proceed with a complex gastrointestinal reconstruction in this acute setting will invariably lead to exacerbation of the lethal triad of hypothermia, coagulopathy, and acidosis with subsequent patient demise.18

pancreatic duct is not easily identiﬁed in a normal gland, this is not always easily accomplished by inspection alone. Intraoperative ﬂuoroscopic pancreatography (either endoscopic or transduodenal) aids in identifying duct disruption for the hemodynamically stable patient. Because neither the pancreatic duct nor the pancreatic parenchyma are well managed with primary repair, pancreatic duct disruption often necessitates pancreatic resection. Injury to the duct at the neck, body, and tail of the pancreas is well treated with a distal pancreatectomy. In patients with a normal gland prior to injury, up to an 80% distal pancreatectomy may be well tolerated without subsequent endocrine or exocrine insufﬁciency.19 This may be performed either with or without splenic preservation. If splenic preservation is opted for, careful dissection is necessary to ligate the numerous splenic arterial and venous branches found along the superior border of the pancreas (Fig. 75–6). Injury to the pancreatic parenchyma in the absence of main duct injury is best treated with wide drainage with closed suction drains placed at the time of exploration. These serve well to control the pancreatic ﬁstulas reported in as many as 15% of cases.2–5

Hemodynamic Instability, Acidosis, Hypothermia, Coagulopathy

Failure to Identify the Pancreatic Duct

● Repair If the right lobe of the liver demonstrates critical vascular compromise owing to interrupted ﬂow, arterial bypass emergent may be necessary.17 ● Prevention Careful palpation of a pulse in this vessel (if present) deﬁnes the superior limit of the Kocherization and avoids injury to this vessel.

Determination of Drainage, Repair, or Resection

● Consequence Death. Grade 4/5 complication ● Prevention Control of hemorrhage and intestinal spillage and temporary abdominal closure with transport to the intensive care unit for correction of the previously described physiologic perturbations are the only life-sustaining options. Interval return to the operating room to reestablish gastrointestinal continuity is undertaken when the patient is more stable.1,2

Pancreas Complete exposure of the injury to the pancreas allows assessment for main pancreatic duct injury. The integrity of this duct guides operative decision making. Because the

● Consequence High-output pancreatic ﬁstula, metabolic acidosis, exocrine insufﬁciency. Grade 2/3 complication ● Repair Although consistent data are lacking for the deﬁnitive treatment of pancreatic ﬁstulas, a number of options exist for control of the ﬁstula. Strict nothing-by-mouth status with total parenteral nutrition decreases the stimulus of pancreatic exocrine function. The addition of subcutaneous octreotide (100 mcg three times per day) may also help, although prospective, randomized, controlled studies of octreotide use in elective pancreatic surgery provide conﬂicting evidence.20–24 ERCP may be useful in identifying a proximal pancreatic duct stricture the stenting of which may improve appropriate enteric

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783

may also be necessary to achieve hemorrhage control. As previously noted, in hemodynamically unstable patients, reconstruction of gastrointestinal continuity can be delayed until the patient is adequately resuscitated.

Failure to Identify the Course of the Common Bile Duct in the Head of the Pancreas or the Ampulla at the Duodeum ● Consequence Suture ligation of the common bile duct with complete biliary obstruction. Grade 3/4 complication

Figure 75–6 Careful dissection and ligation of the multiple vascular branches along the superior edge of the pancreas allow the option of splenic preservation in the course of distal pancreatectomy for signiﬁcant injury to the distal body and tail of the gland.

ﬂow of pancreatic juice. Occasionally, persistent ﬁstula necessitates distal pancreatectomy (or revision distal pancreatectomy), or roux-en-Y pancreatoenterostomy (to the leaking distal pancreas) to control. Exocrine insufﬁciency is well treated with oral pancrelipase supplementation, whereas bicarbonate replacement for severe cases may also be provided via the oral route. ● Prevention Identiﬁcation of the pancreatic duct and directed ligation at the time of distal pancreatectomy reduce the incidence of major leak.

Duodenum The management of penetrating injury to the duodenum is governed by the percentage of bowel wall involvement. Disruption of greater than 50% of the duodenal circumference precludes primary repair. Alternatively, these injuries can be repaired with direct patching via a jejunoduodenostomy (either a loop or a roux). If the patient is hemodynamically unstable, simple control of soilage is achieved as part of a damage control procedure, and deﬁnitive reconstruction is delayed. Extensive tissue destruction or complete disruption of the distal common bile duct resulting from combined pancreaticoduodenal trauma may require resection of the second portion of the duodenum and pancreatic head via a pancreaticoduodenectomy. This

● Repair Endoscopic transampullary imaging with endoscopic stent placement is possible for incomplete transection and incomplete ligation of the common bile duct. This may not be optimal in a patient with a fresh duodenal repair and suture line. A percutaneous transhepatic biliary drain can often be threaded across such a biliary structure. However, in the case of suture ligation, this is technically quite difﬁcult. This may result in complete external drainage of biliary ﬂow. In such cases, delayed choledochoenterostomy or hepaticoenterostomy is undertaken several months after recovery from the acute injury. ● Prevention At the time of initial exploration, the ampulla may be identiﬁed through the duodenal injury and a probe or dilator passed into the bile duct to guide the placement of repair sutures to avoid iatrogenic injury. If the ampulla cannot be identiﬁed in this manner, a cholecystectomy may be performed with passage of a catheter distally into the duodenum to identify both the common bile duct and the ampulla itself, again facilitating repair.

Repair (Dependent upon Injuries Present) The principles in the management of complex combined pancreatic and duodenal injuries include maintenance of enteric, pancreatic, and biliary ﬂow; abundant drainage of all injuries; and repairs and isolation of injured and repaired tissue by diversion of the enteric stream. In addition to repair of the duodenal injury (either primary or patched) and drainage of the pancreatic parenchymal injury, the pylorus is surgically closed (pyloric exclusion), either by suture or by staples applied across the muscle, with additional creation of a gastrojejunostomy. Remarkably, the pylorus is often patent at 4 to 6 weeks regardless of the method of closure. At the time of repair, a feeding jejunostomy is fashioned to assist in postoperative enteral feeding should a pancreatic or proximal duodenal leak form precluding oral-enteral alimentation. Some surgeons add a retrograde intraluminal drainage tube to assist in enteric decompression.2,14,15

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Inadequate Pyloric Exclusion ● Consequence Inadequate isolation of injured duodenal segment. If sutures are placed in a prepyloric location, isolated distal gastric antrum is excluded from exposure to acid-losing feedback inhibition. This results in hypersecretion of gastrin, subsequent hyperacidity and potential for gastritis, and marginal ulceration at the gastrojejunostomy.25 Grade 2/3 complication ● Repair In the short-term, proton pump inhibitors may aid this. Sutures may potentially be cut endoscopically, but stapled exclusion is not amenable to this. Surgical revision is reserved for intractable cases.

11.

12.

13.

14.

15.

● Prevention Appropriate identiﬁcation of the pylorus ensures correct placement of the exclusion. Internal digital palpation of the pylorus via a gastrostomy greatly facilitates correct identiﬁcation.

16.

REFERENCES

18.

1. Rickard MJ, Brohi K, Bautz PC. Pancreatic and duodenal injuries: keep it simple. Aust N Z J Surg 2005;75:581– 586. 2. Lopez PP, Benjamin R, Cockburn M, et al. Recent trends in the management of combined pancreatoduodenal injuries. Am Surg 2005;71:847–852. 3. Vasquez JC, Coimbra R, Hoyt DB, Fortlage D. Management of penetrating pancreatic trauma: an 11-year experience of a level-1 trauma center. Injury 2001;32: 753–759. 4. Patton JH, Fabian TC. Complex pancreatic injuries. Surg Clin North Am 1996;76:783–795. 5. Patton JH Jr, Lyden SP, Croce MA, et al. Pancreatic trauma: a simpliﬁed management guideline. J Trauma 1997;43:234–239. 6. Jacombs AS, Wines M, Holland AJ, et al. Pancreatic trauma in children. J Pediatr Surg 2004;39:96–99. 7. Shilyansky J, Sena LM, Kreller M, et al. Nonoperative management of pancreatic injuries in children. J Pediatr Surg 1998;33:343–349. 8. Jobst MA, Canty TG, Lynch FP. Management of pancreatic injury in pediatric blunt abdominal trauma. J Pediatr Surg 1999;34:818–824. 9. Degiannis E, Boffard K. Duodenal injuries. Br J Surg 2000;87:1473–1479. 10. Cornwell EE, Campbell K. Operative management of pancreatic trauma. In Baker RJ, Fischer JF (eds): Mastery

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24.

25.

of Surgery, 4th ed. Baltimore: Lippincott Williams & Wilkins, 2001; pp 1319–1325. Varadarajulu S, Noone TC, Tutuian R, et al. Predictors of outcome in pancreatic duct disruption managed by endoscopic transpapillary stent placement. Gastrointest Endosc 2005;61:568–575. Wolf A, Bernhardt J, Patrzyk M, Heidecke CD. The value of endoscopic diagnosis and the treatment of pancreas injuries following blunt abdominal trauma. Surg Endosc 2005;19:665–669. Tyburski JG, Dente CJ, Wilson RF, et al. Infectious complications following duodenal and/or pancreatic trauma. Am Surg 2001;67:227–230. Timaran CH, Martinez O, Ospina JA. Prognostic factors and management of civilian penetrating duodenal trauma. J Trauma 1999;47:330–335. Tsuei BJ, Schwartz RW. Management of the difﬁcult duodenum. Curr Surg 2004;61:166–171. Covey AM, Brody LA, Maluccio MA, et al. Variant hepatic arterial anatomy revisited: digital subtraction angiography performed in 600 patients. Radiology 2002; 224:542–547. Samek P, Bober J, Vrzgula A, Mach P. Traumatic hemobilia caused by false aneurysm of replaced right hepatic artery: case report and review. J Trauma 2001;51: 153–158. Loveland JA, Boffard KD. Damage control in the abdomen and beyond. Br J Surg 2004;91:1095–1101. Slezak LA, Andersen DK. Pancreatic resection: effects on glucose metabolism. World J Surg 2001;25:452– 460. Hesse UJ, De Decker C, Houtmeyers P, et al. Prospectively randomized trial using perioperative low dose octreotide to prevent organ related and general complications following pancreatic surgery and pancreaticojejunostomy. Acta Chir Belg 2005;105:383–387. Yeo CJ, Cameron JL, Lillemoe KD, et al. Does prophylactic octreotide decrease the rates of pancreatic ﬁstula and other complications after pancreaticoduodenectomy? Results of a prospective randomized placebo-controlled trial. Ann Surg 2000;232:419–429. Lowy AM, Lee JE, Pisters PW, et al. Prospective, randomized trial of octreotide to prevent pancreatic ﬁstula after pancreaticoduodenectomy for malignant disease. Ann Surg 1997;226:632–641. Montorsi M, Zago M, Mosca F, et al. Efﬁcacy of octreotide in the prevention of pancreatic ﬁstula after elective pancreatic resections: a prospective, controlled, randomized clinical trial. Surgery 1995;117:26–31. Buchler M, Friess H, Klempa I, et al. Role of octreotide in the prevention of postoperative complications following pancreatic resection. Am J Surg 1992;163:125–130. Fang JF, Chen RJ, Lin BC. Controlled reopen suture technique for pyloric exclusion. J Trauma 1998;45:593– 596.

76

Traumatic Brain Injury Adil H. Haider, MD and Edward E. Cornwell III, MD INTRODUCTION Traumatic brain injury (TBI) is one of the most signiﬁcant trauma diseases of our time, with an estimated annual incidence of 1.4 million cases per year in the United States. These injuries result in upward of 50,000 deaths and 80,000 to 90,000 patients with lifelong or long-term disabilities each year.1,2 It is estimated that 5.4 million Americans are disabled owing to TBI, and the direct and indirect costs associated with this problem exceeded $50 billion dollars annually by 1995.3 Little can be done to reverse the initial traumatic insult and the resultant primary brain injury. However, secondary brain injury caused by decreased perfusion of the brain tissue can be prevented and is, therefore, the most important aspect in TBI management. Secondary injury is commonly a consequence of hypotension, hypoxia, or both. In a study of the Trauma Coma Databank,4 mortality rose from 25% to 75% if patients were subjected to both of these factors (Table 76–1). Guidelines for management of TBI have been developed by the Brain Trauma Foundation (BTF) and the American Association for Neurological Surgery (AANS), using the best available evidence.5 These guidelines use the following terminology: “standards” for level 1 recommendations, “guidelines” for level 2, and “options” for level 3. The guidelines have three standards that recommend against the use of certain previously practiced therapeutics including (1) hyperventilation, (2) use of steroids after head injury, and (3) prophylactic use of antiseizure medications to prevent late seizures. This chapter presents common TBI scenarios with management recommendations based on BTF/AANS guidelines.

SCENARIO 1 A 27-year-old man, nonhelmeted rider of a motorcycle is brought to the emergency department after colliding with a stationery vehicle. The paramedics report that the patient initially complained of something “wrong with my head” and now is verbalizing words that do not make any sense. On primary survey, his airway is clear, he has bilateral breath sounds, and his blood pressure is 101/61. Upon

painful stimuli, he opens his eyes and withdraws his extremities, making incomprehensible sounds. The paramedics suspect head injury, so the patient is immediately transported to the computed tomography (CT) scanner. The trauma team is concerned about intracranial hemorrhage, “he may need to be rushed to the OR (operating room),” comments the trauma team leader. Upon arrival at the CT scanner, the patient has agonal breathing— requiring emergent intubation—and suffers several minutes of desaturation.

Did not Intubate a Patient with a Glasgow Coma Score of 8 or Less ● Consequence Emergent airway establishment leading to hypoxemia and further brain injury. Grade 3/4 complication ● Prevention In the ABCDs of resuscitation, D is for disability, or quick neurologic examination with ascertainment of the Glasgow Coma Score (GCS) (Table 76–2). This patient has a GCS of 8 (eye opening [E] 2, verbal [V] 2, motor [M] 4). The two culprits most responsible for secondary brain injury leading to death and disability in TBI patients are hypoxia and hypotension. A patient with GCS of 8 or less must be intubated to protect the airway and prevent hypoxia. If endotracheal intubation proves to be difﬁcult and is not achievable quickly, a cricothyroidotomy should be performed, and there should be no hesitation in establishing a surgical airway in trauma patients. In this scenario, the trauma team had the correct sense of urgency for obtaining the CT scan because the faster the scan the faster the patient can be triaged to the operating room for an operable lesion. Once the airway is secured and the primary survey is completed, a patient with a GCS of 8 should receive a CT scan of the brain as soon as possible to determine the extent of brain injury. In these cases, valuable time should not be wasted performing the secondary survey or doing routine procedures such as placing a Foley catheter (Fig. 76–1).

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Table 76–1 Outcomes after Secondary Brain Insult among Patients with Traumatic Brain Injury Secondary Insult (N)

TBI with GCS 3-8

None to Moderate Disability (%)

Death (%)

Total patients (699)

43

37

Hypoxia (78)

45

33

Hypotension (113)

26

60

Neither (456)

51

27

6

75

Hypotension and hypoxia (52)

Adapted from Trauma Coma Databank: Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993;34:216–222.

Table 76–2 Glasgow Coma Score Score

Secure airway (Intubation vs cricothyroidotomy)

Complete primary survey (Secure IV access, ensure HD stable)

HD stable: Proceed to CT scan Bypass secondary survey

HD unstable: Continue ATLS protocol

Figure 76–1 Initial management of the traumatic brain injury (TBI) patient. HD, hemodynamically.

Criterion

Eye Opening 4

Spontaneous

3

To verbal command

2

To pain

1

None

Motor 6

Obeys commands

5

Localizes pain

4

Withdraws to pain

3

Abnormal ﬂexion to pain (decorticate)

2

Abnormal extension to pain (decerebrate)

1

None

Verbal 5

Oriented and converses

4

Confused conversation

3

Inappropriate words

2

Incomprehensible sounds

1

None

Figure 76–2 Computed tomography (CT) scan shows frontal contusions without a midline shift.

Glascow Coma Score (GCS) = Eye opening + motor + verbal.

SCENARIO 2 A 52-year-old woman, restrained driver of a motor vehicle is brought to the emergency department after a head-on collision with another vehicle. Her heart rate is 65, blood pressure is 97/54, and she has a peripheral oxygen saturation of 97%. She is noted to make incomprehensible sounds, has an abnormal ﬂexion of the limbs upon stimuli, and opens her eyes only after being stimulated. She is appropriately intubated to “protect the airway.” Initial CT

scan of the head reveals frontal contusions without midline shift (Fig. 76–2). No other injuries are noted. Her blood work is also within normal limits except for a mild base deﬁcit on the arterial blood gas. The patient is slated to be transferred to the intensive care unit (ICU) and is to get a repeat CT scan in 8 hours. After a delay owing to bed availability, the patient arrives at the trauma ICU 3 hours later. The admitting nurse notes that the patient has ﬁxed and dilated pupils and now has a heart rate of 54 and blood pressure of 194/107.

76 TRAUMATIC BRAIN INJURY

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Box 76–1 Risk of Intracranial Pressure Elevation and Progression to Coma according to GCS

Box 76–2 Calculation of Cerebral Perfusion Pressure, (CPP)

Mild TBI (GCS 13–15) < 3%

Cerebral perfusion pressure (CPP) = Mean arterial pressure (MAP) − Intracranial pressure (ICP)

Moderate TBI (GCS 9–12) = 10%–20% Routine ICP monitoring in these patients not indicated.

Severe Head Injury (GCS £ 8) and *Abnormal CT Scan = 50%–60% Place ICP monitor.

Severe Head Injury (GCS £ 8) and Normal CT = 13% In a patient with a normal CT, if any two of the following three factors are present: age >40 years; systolic blood pressure <90 mm Hg on admission; posturing then the risk of ICH is similar to that of a patient with an abnormal head CT. In such cases, an ICP monitor should be placed. *Abnormal CT scan includes hematomas, contusions, edema, compressed basal cisterns, and so on. CT, computed tomography; GCS, Glascow Coma Score; ICH, intracranial hemorrhage; ICP, intracranial pressure; TBI, traumatic brain injury.

Did not Insert Intracranial Pressure Monitor for a Patient with a High Risk of Intracranial Hypertension ● Consequence Missed rising intracranial hypertension (ICH) leading to brain herniation. Grade 4/5 complication ● Prevention The BTF/AANS has clear guidelines suggesting insertion of an intracranial pressure (ICP) monitor in patients with increased risk for intracranial hypertension (ICH)5 (Box 76–1). Although a ventriculostomy offers the added therapeutic advantage of being able to drain cerebrospinal ﬂuid, it frequently is technically difﬁcult to place in patients with cerebral edema and compressed ventricles. A ﬁberoptic catheter placed directly into the brain parenchyma provides the most rapid ICP monitoring access.

SCENARIO 3 A 73-year-old man with a past medical history of hypertension, chronic renal insufﬁciency, and alcohol abuse falls off a stool in a bar and suffers a subdural hematoma 6 mm in size without any midline shift. The patient has a GCS of 13 and is admitted to the trauma ICU for close neurologic observation. The patient becomes somewhat belligerent, trying to take off his C-spine collar and moving his legs out of the bed. With the ICU staff suspecting alcohol withdrawal, the patient is given a 2-mg dose of lorazepam. The treating physician also notes that the patient has a blood pressure of 180/80 mm Hg with a

pulse of 53. He treats this hypertension with 10 mg of hydralazine because the heart rate was only in the 50s. The physician returns 2 hours later to assess the patient after being informed that the vital signs had not changed and the patient was now “fast asleep.” He ﬁnds the patient to be unresponsive with a dilated left pupil.

Not Recognizing Changes in Mental Status due to Raised ICP, even when Cushing’s Signs Are Present ● Consequence Missed rising ICH leading to brain herniation. Grade 4/5 complication ● Prevention The cerebral perfusion pressure (CPP) (Box 76–2) is the difference between the mean arterial pressure (MAP) and the ICP. The injured brain has minimal room to expand because it is contained in the cranium, a ﬁxed space. Hemorrhage or space-occupying lesions increase the ICP from its normal value of 1 to 10 mm Hg at the expense of CPP. ICPs above 20 to 25 mm Hg should be treated. As depicted in Box 76– 2, a rise in the ICP results in decreased CPP, which for adults must be maintained over 70 mm Hg. In the previous scenario, initial increases in ICP, manifested by changes in neurologic status, were not noticed. The patient then starts to exhibit Cushing’s triad (hypertension, bradycardia, and widening pulse pressure), an ominous presentation suggesting markedly raised ICPs and impending or concurrent ccerebral herniation (Fig. 76–3).

SCENARIO 4 A 37-year-old woman construction worker falls off a scaffolding to the ground 20 feet below. She is intubated in the ﬁeld and resuscitated in the emergency department, where she is labeled as a transient responder to ﬂuids. Her work-up reveals bilateral open lower extremity fractures, a grade 3 splenic laceration for which her splenic artery is embolized, and a single sided hemopneumothorax for which a chest tube is placed. She has a GCS of 7, and a CT reveals subarachnoid hemorrhage with multiple cerebral contusions, which are nonoperative. An ICP monitor is placed, and her initial ICPs are in the 10 to 12 mm Hg range. In the ICU, the patient’s ICP rises to 24 mm Hg and the CPP is now only 48 mm Hg. To treat this, a 100mg bolus of mannitol is administered and a continuous infusion of mannitol is also started. The patient immedi-

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TBI with GCS ⱕ8

ICP monitor placed

Maintain CPP ⬎70

Elevate head of bed to 30 Reverse Trendelenburg for spinal precaution patients

Raise MAP ⬎90 if adequately volume hydrated

ICP’s still elevated; CPP ⬍70

Mannitol bolus 0.5 mg/kg Q 6 hourly

Hypertonic saline 3% infusion or 26% “bullet”

If ICP still elevated consider using acute hyperventilation for short periods only

If ICP remains high consider secondary methods: Phenobarbitol coma–decreases intracerebral metabolism Decompressive craniectomy

Figure 76–3 pressure.

Schema for treatment of elevated intracranial

ately starts to make a large volume of urine along with further dropping her MAP to 58 mm Hg. In an effort to avoid giving ﬂuids and “minimize the probability of further intracerebral cellular swelling,” she is started on a phenylephrine infusion to elevate her MAPs and keep her CPP in the 70s because that is “where the guidelines need her to be.”

Giving Osmotic Diuretics and Pressors to a Hypovolemic Trauma Patient ● Consequence Decreased perfusion to body tissues, further exacerbating shock. Grade 2/3 complication ● Prevention A CPP of at least 70 mm Hg should always be maintained in TBI patients, according to the BTF/AANS guidelines.5 In some circumstances, this is done by elevating the MAP to above 90 mm Hg with the help of vasopressors. However, this should be done only when hypovolemia has been ruled out. As with any trauma resuscitation, hypovolemia must be alleviated with the judicious use of ﬂuids. (Normal saline is commonly used because glucose-containing solutions are

Figure 76–4 Subdural hematoma with a midline shift.

avoided in TBI.) Similarly, diuretics should be given only to patients with adequate volume on board. Mannitol, an osmotic diuretic, works by decreasing blood viscosity and decreasing the diameter of peripheral blood vessels, which helps maintain cerebral blood ﬂow. It also shifts water from the intracellular to intravascular compartments, preventing cellular edema. This effect lasts 6 hours, which is the reason for redosing at 6 hours. BTF/AANS guidelines also address the use of hypertonic saline in trauma patients with brain injury, identifying it as an option in which the goal is to achieve hyperosmolar euvolemic resuscitation.

SCENARIO 5 A 65-year-old man is a restrained passenger in a minivan that overturns. He suffers a subdural hematoma (Fig. 76–4), which is surgically evacuated. However, he still has increased ICPs, which are treated with mannitol, hypertonic saline, and ventriculostomy drainage. By postoperative day 2, his ICPs are under control but he is still unresponsive. Even though the mannitol infusions have been stopped, the patient continues to make copious amounts of urine, 4 L over 12 hours. He becomes tachycardic and is initiated on β-blockers. In addition, his serum sodium continues to rise, which is ascribed to the previous use of

76 TRAUMATIC BRAIN INJURY hypertonic saline. Subsequently, the patient’s MAP decreases and he starts to have seizures. His serum sodium is found to be 172 mEq/L.

Ignoring the Signs of Diabetes Insipidus ● Consequence Decreased perfusion to body tissues, electrolyte imbalances, and future neurologic impairment. Grade 2/3 complication ● Prevention TBI patients, especially those who have had severe enough injury to warrant an operation, have a signiﬁcantly high incidence of central diabetes insipidus. In this disorder, antidiuretic hormone (ADH) secretion is decreased, leading to excessive, dilute urine production. If not treated, this disorder may lead to hypovolemia and, as in the case described previously, hypernatremic seizures. Treatment is by replacing the ﬂuid losses and administration of desmopressin, a 2amino acid substitute of ADH that has potent antidiuretic but no vasopressor activity.

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REFERENCES 1. Langlois JA, Rutland-Brown W, Wald M. The epidemiology and impact of traumatic brain injury: a brief overview. J Head Trauma Rehab 2006;21:375–378. 2. Thurman D, Alverson C, Dunn K, et al. Traumatic brain injury in the United States: a public health perspective. J Head Trauma Rehabil 1999;14:602–615. 3. Thurman D. The epidemiology and economics of head trauma. In Miller L, Hayes R (eds): Head Trauma: Basic, Preclinical, and Clinical Directions. New York: Wiley & Sons, 2001; pp 376–388. 4. Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993;34:216–222. 5. Bullock MR, Chesnut R, Ghajar J, et al. Guidelines for the surgical management of traumatic brain injury. Neurosurgery 2006;58(3 suppl):S2-1–S2-3.

77

Managing Injuries to the Spleen Adil H. Haider, MD and Edward E. Cornwell III, MD INTRODUCTION Management of splenic injuries, whether iatrogenic or traumatic, has one common principle: Never jeopardize a patient’s life in an attempt to preserve the spleen; some patients with splenic injury are best served by an expeditious splenectomy. This chapter describes common pitfalls in the operative management of the injured spleen along with a discussion about nonoperative management (NOM) of traumatic splenic injuries. The decision to save rather than remove an injured spleen requires consideration of the clinical presentation of the patient. Splenic salvage should not be attempted in an unstable patient with signiﬁcant injuries. Similarly, a patient who has an iatrogenic injury to the spleen during a complex abdominal surgery for cancer may not be a candidate for splenorrhaphy. If splenic repair inordinately prolongs the trauma laparotomy or requires the transfusion of 2 or more units of packed red blood cells, splenorrhaphy should be aborted and a splenectomy should be performed.

Attempting Splenorrhaphy without Adequate Mobilization/Exposure ● Consequence Attempting to repair an incompletely mobilized spleen is a frustrating exercise for both the surgeon and the assistant. Struggling in the operative ﬁeld usually leads to increased surgical complications; it also may further increase blood loss. Grade 2/3 complication ● Repair/Prevention Division of the avascular ligaments (lienophrenic, lienorenal, and lienocolic) is essential in mobilizing the spleen medially out of its bed and up into the operative ﬁeld close to the midline position of its embryologic origin (Fig. 77–1). Once the spleen is mobilized and assessed, hemostasis may be achieved by a combination of topical hemostatic agents such as microﬁbrillar collagen (e.g., Avitene), methylcellulose (e.g., Surgicel), or mattress sutures (e.g., 3-0 Prolene) placed either directly or over Teﬂon pledgets.

Partial splenectomy may be selected when early ligation of a branch of the splenic artery to a segment of the spleen results in major progress toward hemostasis (Fig. 77–2). Provided that 50% of the splenic parenchyma attached to an identiﬁable vessel is viable, partial splenectomy may be performed and splenic immune function can be expected to be maintained. Early demarcation of the segment of the spleen to be removed with the electrocautery device facilitates exposing intrasplenic vessels for individual suture ligation, which should proceed meticulously. Occasionally, cross-clamping the splenic hilum may be temporarily required if manual compression does not produce adequate hemostasis. The resected margin of the spleen is then oversewn with mattress sutures with or without pledgets (Fig. 77–3). If needed, a blunt liver needle may be used to place such mattress sutures.

ADJUNCTS TO SPLENORRHAPHY Argon Beam Coagulator The argon beam coagulator (ABC) is an electrocoagulation system that should not be confused with the argon laser. No eyewear is required. The instrument achieves hemostasis by using inert gas as a medium to conduct radiofrequency energy (Fig. 77–4). The gas is emitted as a constant ﬂow at room temperature from a handpiece and nozzle, which blows away blood and debris to optimize visualization. The ﬁrst large clinical series utilizing the ABC for splenic salvage was published in 1991.1 This report concluded that most spleens with superﬁcial lacerations are easily salvaged with standard topical maneuvers and that the ABC offers a technical advantage in patients with deep parenchymal injuries. In the ensuing decade, the ABC achieved wide acceptance in the management of both spleen and other solid organ injuries.

Absorbable Mesh Wrap Polyglycolic mesh wrap is another modality reported to be useful in splenic salvage. The injured spleen is passed through an enlarged hole in the mesh fashioned for this purpose. The mesh is then wrapped around the spleen and

792

SECTION XII: TRAUMA SURGERY

Lower pole resected

Figure 77–1 After division of avascular ligaments, the spleen can be mobilized medially, up into the operative ﬁeld, close to the midline position. (Adapted from Trunkey DD. Spleen. In Blaisdell FW, Trunkey DD [eds]: Trauma Management, Vol 1: Abdominal Trauma. New York: Thieme, 1982; pp 149–163.)

Figure 77–2 To achieve hemostasis, the splenic artery branch to the lower pole of the spleen is ligated. Subsequently, an anatomic resection of the lower pole of the spleen is performed. (Courtesy of Corrine Sandone, MA, CMI 2007.) Mattress sutures placed through pledgets

sutured to itself to provide tamponade (Figs. 77–5 and 77–6).2,3 More recent reports also suggested incorporating methylcellulose into the mesh to help “bulk it up.” In this technique, multiple layers of methylcellulose are placed directly onto the injured surfaces, after which the mesh is secured around the spleen, enhancing the tamponade effect. Previous concerns of possible mesh infection, especially in the setting of hollow viscus injury, have proved to be unfounded based on large series of patients.4

Fibrin Glue Early impressive laboratory experience with ﬁbrin glue, which consists of ﬁbrinogen, dried thrombin, and calcium chloride, prompted its emergence in the clinical area. Commonly available ﬁbrin sealants like Tisseal and Crosseal may be applied directly to the injured surfaces of the spleen to achieve immediate hemostasis, especially on linear tears and cracks. Recent reports have demonstrated application of ﬁbrin sealants to “glue together” massively injured spleens and then performing mesh splenorrhaphy. Using this approach, grade 3 and 4 injured spleens have been salvaged.5

Figure 77–3 Manual compression and, if necessary, clamping of the splenic artery provide the hemostasis required to oversew the margin of the retained spleen. Teﬂon pledgets are employed to prevent suture from cutting through the otherwise friable tissue. (Courtesy of Corrine Sandone, MA, CMI 2007.)

77 MANAGING INJURIES TO THE SPLEEN

Argon beam coagulation of fractured surface

793

Figure 77–6 Mesh splenorrhaphy in situ with Surgicel placed directly over the injured portion of the spleen, prior to suturesecuring the mesh. (Courtesy of Horacio A. Massotto, MD, Costa Rica; reproduced with permission from www.trauma.org.)

Pancreatic Injury Figure 77–4 Argon beam coagulator (ABC). (Courtesy of Corrine Sandone, MA, CMI 2007.)

Spleen passed through hole in mesh

Mesh gathered posteriorly

Figure 77–5 Mesh splenorrhaphy. The injured spleen is passed through an enlarged hole in the mesh. The mesh is then wrapped around the spleen and sutured to itself. (Courtesy of Corrine Sandone, MA, CMI 2007.)

● Consequence The pancreatic tail is in close proximity to the splenic hilum and is particularly prone to iatrogenic injury during splenectomy, which may lead to a pancreatic ﬁstula. Grade 3/4 complication ● Repair/Prevention The pancreatic tail is in close proximity to the splenic hilum and is particularly prone to iatrogenic injury during splenectomy. The splenic hilum and its vessels should not be clamped until the spleen is completely mobilized. After the splenic ligaments and the necessary short gastric vessels are divided, the spleen is brought upward and toward the midline, as described in Figure 77–1. Upward traction elevates the spleen away from the tail of the pancreas. In this position, the spleen is attached only by the splenic artery and vein. The artery should be taken ﬁrst by clamping it and then dividing it close to the hilum. The splenic vein is very delicate and should not be clamped. It is easier to just tie it off in continuity as a ﬁnal step and then transect it at the hilum, delivering the spleen. If the procedure is unusually difﬁcult or if pancreatic injury is considered, a drain should be left at the tail of the pancreas to aid with long-term management of this injury.

Gastric Injury during Splenectomy ● Consequence Gastrocutaneous ﬁstula. Grade 2/3 complication

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SECTION XII: TRAUMA SURGERY

● Repair/Prevention During splenectomy, the short gastric vessels must be individually identiﬁed, isolated, and ligated toward the spleen. Avoidance of injury to the stomach’s fundus and greater curvature is essential during this step. After the short gastrics are taken, the greater curvature should be inspected, and if there is any suspicion of compromise, it must be repaired. This is commonly done by inverting the suspect area and placing seromuscular sutures with 2-0 or 3-0 silk. Ischemia or even a partialthickness gastric wall injury (e.g., owing to an electrocautery burn or by catching a portion of the gastric wall while clamping the short gastrics) may lead to a gastrocutaneous ﬁstula.

Table 77–1 American Association for the Surgery of Trauma—Organ Injury Scale for the Spleen Grade*

Injury Type

Description of Injury

1

Hematoma

Subcapsular, <10% surface area

Laceration

Capsular tear, <1 cm parenchymal depth

Hematoma

Subcapsular, 10%–50% surface area; intraparenchymal, <5 cm in diameter

Laceration

Capsular tear, 1–3 cm parenchymal depth that does not involve a trabecular vessel

Hematoma

Subcapsular, >50% surface area or expanding; ruptured subcapsular or parenchymal hematoma; intraparenchymal hematoma ≥5 cm or expanding

Laceration

>3 cm parenchymal depth or involving trabecular vessels

4

Laceration

Laceration involving segmental or hilar vessels producing major devascularization (>25% of spleen)

5

Laceration Vascular

Completely shattered spleen Hilar vascular injury with devascularized spleen

2

3

LONG-TERM SEQUELAE OF SPLENECTOMY Not Administering Immunizations after Splenectomy ● Consequence Overwhelming postsplenectomy infection. Grade 3/4 complication ● Prevention The widespread acceptance of splenic salvage grows from concerns for the physiologic risk of the asplenic state, which includes possible susceptibility to nonfatal infections as well as overwhelming postsplenectomy infection (OPSI). OPSI is rare, with a reported prevalence of less than 0.5% in asplenic patients6; however, it is lethal in adults, with a reported mortality in excess of 50%. As a precautionary measure, patients who get an elective splenectomy should be vaccinated against three major encapsulated bacteria—Streptococcus pneumoniae, Haemophilus inﬂuenzae, and Neisseria meningitides—prior to the procedure. Emergent splenectomy patients should ideally recieve vaccines 2 weeks after the procedure to obtain the most substantial immunological response. However, many trauma surgeons, who fear losing a patient to follow-up, administer vaccines just prior to discharge from the hospital.

NOM OF SPLENIC TRAUMA Continuing NOM in a Patient Requiring Multiple Blood Transfusions ● Consequence Increased blood transfusions are independently associated with increased complications (especially infectious complications) in trauma patients. Grade 2/3 complication

*Advance one grade for multiple injuries up to grade 3. From Moore EE, Cogbill TH, Jurkovich GJ, et al. Organ injury scaling: spleen and liver (1994 revision). J Trauma 1995;38;323–324.

● Repair/Prevention At present, the proportion of patients with splenic injuries managed nonoperatively has grown to over 70%, owing to improvements in computed tomography (CT) scanning technology as well as advancing techniques in angioembolization of the spleen. The art of NOM has been enhanced by the utility of the American Association for the Surgery of Trauma (AAST)—Organ Injury Scale.7 The scale enables researchers and clinicians to make comparisons according to a standard approach, aiding in therapeutic and research decisions (Table 77–1).

Criteria for Patient Inclusion Patients with blunt splenic injuries must meet the following criteria to be considered candidates for NOM: (1) hemodynamic stability, (2) CT documentation and classiﬁcation of the injury, (3) absence on CT scan of intra-abdominal (hollow viscus) or retroperitoneal (duodenum, pancreas, kidney) injuries mandating operative intervention, and (4) transfusion of less than 2 units of packed red blood cells (PRBCs) (Box 77–1). Restricting transfusions to less than 2 units of PRBCs is extremely important along with the known infectious risks associated with blood transfusions. Compelling evidence now identi-

77 MANAGING INJURIES TO THE SPLEEN

Box 77–1 Criterion for Nonoperative Management of Blunt Splenic Injury 1 2 3 4

Hemodynamic stability Documented computed tomography (CT) classiﬁcation of injury Absence of additional injuries requiring operative intervention Transfusion of <2 units of packed red blood cells

ﬁes blood product transfusion as an independent risk factor for complications in the injured patient.8 Other exclusion criteria for NOM are patients in whom coagulopathy cannot be reversed or those who need to be anticoagulated urgently (e.g., a patient with an artiﬁcial heart valve or a trauma victim with blunt carotid injury requiring anticoagulation).

795

Association (WTA)12 showed that grade of injury best predicts the need for a vascular embolization procedure (placement of coils or Gelfoam) and outcomes. In this study with the adjunctive use of angioembolization procedures, more than 90% of patients with grade 3 splenic injuries and 80% of patients with grade 4 and 5 splenic injuries were successfully managed without an operation. The study did not detect any differences between the types of embolization material used (coils versus Gelfoam); neither did it show any difference in success rates between main splenic artery embolization and superselective embolization techniques, in which the more distal splenic artery segments are embolized. It also determined that the main predictor of failure of angioembolization is the presence of an arteriovenous ﬁstula on the initial CT scan. The study also suggested that hemodynamically unstable patients and older patients (age >55 yr) had a higher likelihood of failure of angioembolization.

The Particulars of NOM In 2003, the Eastern Association for the Surgery of Trauma (EAST)9 published practice management guidelines for patients with blunt liver or spleen injuries based on best available evidence. Their level-two recommendations suggest that age, neurologic status, or associated injuries do not preclude NOM in a hemodynamically stable patient and that an abdominal CT scan is the most reliable method to assess the severity of organ injury. Level-three evidence suggests that this initial CT scan be obtained with intravenous and oral contrast to enhance its ability to delineate associated injuries. The optimal success rate with NOM is obtained when CT scanning is combined with careful serial clinical examinations. Patients should be observed in a setting in which serial physical examinations, vital sign readings, and hematocrit determinations can be performed, and there should be immediate operating availability in case clinical examination reveals an acute change. A suggested NOM scheme for blunt splenic injury is depicted in Figure 77–7.

Angioembolization of the Splenic Artery Initially described in 1995, angiography and embolization of the splenic artery have become accepted adjuncts for NOM in patients with blunt splenic injury.10 Routine performance of an angiogram on all patients with splenic injury has been found to be unnecessary, because very few patients with grade 1 or 2 splenic injury require an interventional procedure. Earlier recommendations of performing splenic angiography on all patients with “contrast pooling” or a “contrast blush” on the initial CT scan have given way to greater emphasis on the grade of injury.11 Angiography of the splenic artery should be considered in patients with grade 3 splenic injuries (Fig. 77–8) and above and in patients with frank splenic artery hemorrhage delineated on the initial CT scan. A multicenter study performed under the auspices of the Western Trauma

Progression of Care Studies are currently being performed to determine the optimal time a patient receiving NOM should be kept on nothing by mouth or on bedrest and when they should be initiated on deep venous thromboembolism prophylaxis. Other questions under study are when such patients can be safely discharged home and resume normal activity, and whether or not they need follow-up radiographic imaging for their splenic injury. In the meantime, surgical intuition has been surveyed; a poll of EAST members published in 200513 revealed that approximately 50% of surgeons would recommend a patient with a grade 1 to 2 splenic injury return to light, normal activity at 2 weeks and that they would not order a routine follow-up CT scan for such patients. However, the same groups of surgeons responded that they would recommend that a patient with a higher-grade injury wait at least 4 to 6 weeks before resuming normal activities and would obtain a follow-up CT scan. The physicians surveyed seemed to be in agreement with level-three guidelines from EAST that recommend obtaining a follow-up CT scan in patients with grade 3 or higher splenic injuries, and in those with high-risk occupations (e.g., athletes, construction workers) before granting them medical clearance for normal activity.

Success of NOM A multi-institutional trial sponsored by EAST and published in 200014 revealed a NOM success rate of 89% (1488 patients in 27 centers). In 2004, the AAST spleen study group15 reported a 96% success rate with NOM (300+ patients). In children, the reported failure rate for NOM is less than 2%. The most common cause for failure of NOM is bleeding in the ﬁrst 96 hours. If the patient becomes hemodynamically unstable, emergent splenectomy is indicated. If the patient remains stable, a repeat

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Abdominal trauma PRBC = packed red blood cells Hemodynamically unstable

Hemodynamically stable

CT scan revealing splenic injury

Isolated low grade splenic injury

Contrast “blush” or grade ≥ III injury

Success

24–48 hour observation • Monitor • Serial hemoglobins • Bedrest

Injury requiring repair/resection

Fails

Consider arterial embolization

Peritonitis Requires ≥ 2 units PRBC Hemoglobin fails

Operative intervention

Hemodynamically unstable

Stable

Continue observation

<2 units PRBC transfused and hemodynamically stable

Repeat CT

Hemoperitoneum larger and/or active bleeding present

Splenic injury stable

Treatment for other sources of blood loss

Figure 77–7 Algorithm for nonoperative management of blunt splenic injuries.

Figure 77–8 Computed tomography (CT) scan depicts grade III splenic injury. (Courtesy of Eduardo Bastos, General Surgeon, Marilia, Brazil; reproduced with permission from www.trauma.org.)

77 MANAGING INJURIES TO THE SPLEEN CT scan may be performed with intravenous contrast. On occasion, the initial CT scan may not reveal the true grade of splenic injury or an injured vessel that was previously in spasm that may now have relaxed and started to hemorrhage. Patients with such ﬁndings may beneﬁt from angioembolization. However, if the patient has required 2 or more units of blood or has undergone prior angioembolization, operative intervention is indicated. Other causes for NOM failure include late bleeding (before or after discharge), abscess formation, and splenic artery pseudoaneurysm.

CONCLUSION Careful selection, CT scanning, and serial clinical examinations are crucial to the successful NOM of patients with blunt splenic injuries. Angioembolization has enhanced our ability to salvage a patient’s spleen without an operation. Patients requiring splenorrhaphy are best managed with adequate exposure and mobilization. ABC, ﬁbrin glue, and absorbable mesh wrap appear to have advanced the art of splenic salvage beyond the level achieved by topical hemostatic agents, suturing, and partial splenectomy. Finally, patients who are unstable or who do not meet the selection criteria for splenic salvage should receive a splenectomy with careful avoidance of the pitfalls described in this chapter.

REFERENCES 1. Dunham CM, Cornwell EE, Militello P. The role of argon beam coagulator in splenic salvage. Surg Gynecol Obstet 1991;173:179. 2. Fingerhut A, Oberlin P, Cotte JL, et al. Splenic salvage using an absorbable mesh: feasibility, reliability and safety. Br J Surg 1992;79:325–327. 3. Delany HM, Rudavsky AZ, Lan S. Preliminary clinical experience with the use of absorbable mesh splenorrhaphy. J Trauma 1985;25:909–913. 4. Berry MF, Rosato EF, Williams NN. Dexon mesh splenorrhaphy for intraoperative splenic injuries. Am Surg 2003; 69:176–180.

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5. Bohicchio GV, Arciero C, Scalea TM. “The hemostatic wrap”: a new technique in splenorrhaphy. J Trauma 2005; 59:1003–1006. 6. Styrt B. Infection associated with asplenia: risks, mechanisms, and prevention. Am J Med 1990;88:33N. 7. Moore EE, Cogbill TH, Jurkovich GJ, et al. Organ injury scaling: spleen and liver (1994 revision). J Trauma 1995; 38:323–324. 8. Duke BJ, Modin GW, Schecter WP, Horn JK. Transfusion signiﬁcantly increases the risk of infection after splenic injury. Arch Surg 1993;128:1125–1130; discussion 1131– 1132. 9. EAST Practice Management Guidelines Work Group. Practice Management Guidelines for the Non-Operative Management of Blunt Injury to the Liver and Spleen. Eastern Association for the Surgery of Trauma, 2003. Available at http://www.east.org/tpg/livspleen.pdf (accessed June 14, 2006). 10. Schurr MJ, Fabian TC, Gavant M, et al. Management of blunt splenic trauma: computed tomographic contrast blush predicts failure of non-operative management. J Trauma 1995;39:507–513. 11. Cooney R, Ku J, Cherry R, et al. Limitations of splenic angio-embolization in treating blunt splenic injury. J Trauma 2005;59:926–932. 12. Haan HM, for the Western Trauma Association MultiInstitutional Trials Committee. Splenic embolization revisited: a multi-center review. J Trauma 2004;56: 542. 13. Fata P, Robinson L, Fakhry S. A survey of EAST member practices in blunt splenic injury: a description of current trends and opportunities for improvement. J Trauma 2005;59:836–842. 14. Peitzman AB, Heil B, Rivera L, et al. Blunt splenic injury in adults. Multi-institutional study of the Eastern Association for the surgery of trauma. J Trauma 2000;49:177– 189. 15. Feliciano D, for the AAST Spleen Study Group. Nonoperative management of the injured spleen: a prospective study from the AAST Multi-institutional trial committee. Presented at the American Association for the Surgery of Trauma 2004, Annual Meeting. September 29 to October 2, 2004, Grand Wailea Resort Hotel & Spa, Maui, HA.

78

Damage Control: Abdominal Closures Benjamin Braslow, MD, Bruno Molino, MD, and Vicente H. Gracias, MD INTRODUCTION Massive hemorrhage ranks second only to central nervous system injuries as the leading cause of prehospital traumarelated mortality.1 Moreover, uncontrolled bleeding stands atop the list of early in-hospital mortality due to major trauma.2 Regarding penetrating trauma patients, increasing use of newer, more powerful automatic ﬁrearms, now common in the civilian population, have resulted in more frequent multiple penetrations (often multicavity) with more severe degrees of tissue destruction and bleeding.3 This is even more pronounced in injuries sustained from high-velocity military weaponry now being experienced all too frequently in the global theater of war and terrorism. Advances in prehospital care and trauma bay resuscitations since the mid 1980s has resulted in a greater number of these severely injured patients surviving to the point of necessitating operative intervention. Such patients usually present nearing physiologic exhaustion with profound acidosis, hypothermia, and coagulopathy, the so-called lethal triad of hemorrhage. The “traditional surgical approach” to such patients, in which surgeons would deﬁnitively repair all identiﬁed injuries at the initial operation, proved inadequate with extremely high mortality despite control of anatomic bleeding. During the peak of gun violence in the late 1980s into the early 1990s, urban American trauma centers gained extensive experience in treating these patients and the concept of “Damage Control” (DC) surgery was born. Borrowed from the Navy, the term “damage control” referred to any and all methods used to keep a badly damaged ship aﬂoat to maintain mission integrity.4 For the trauma surgeon, DC describes the process of abbreviated laparotomy and expedient control of hemorrhage and contamination followed by intra-abdominal packing and temporary coverage. From the operating room (OR), the patient is taken to the surgical intensive care unit (SICU) for physiologic resuscitation. Finally, the patient returns to the OR, after physiologic capture, for deﬁnitive repair of all injuries and, if possible, abdominal wall closure. To the uninformed

observer, the increased morbidity associated with this multistep process might seem like surgical failure or abandonment of proper technique. Despite the associated high morbidity, the DC sequence has proved to be an aggressive and effective strategy to combat the lethal pattern of physiologic failure associated with severe blunt and penetrating injury.5–8

INDICATIONS Because of the associated morbidity that accompanies the DC process, patient selection and proper timing are crucial. Although major liver injury and progressive coagulopathy remain the most frequent indications, the list continues to expand. In 1997, Rotundo and Zonies9 organized the “key” factors in patient selection for DC into three categories: conditions, complexes, and critical factors. In 1998, Moore and coworkers10 offered their six major indications for abbreviated laparotomy with consideration for institutional available resources and expertise. Ultimately, the decision to proceed with DC principles rests on the surgeon present and is based on the physiology of the patient. ● Inability to achieve hemostasis due to coagulopathy ● Inaccessible major venous injury (pelvis, liver, etc.) ● Time-consuming procedure in a patient with sub-

optimal response to resuscitaton ● Management of extra-abdominal life-threatening injury ● Reassessment of intra-abdominal contents ● Inability to reapproximate abdominal fascia due to

visual or abdominal wall edema

THE DC SEQUENCE DC 0 Once a patient’s injury pattern and physiology are assessed as critical and DC principles are initiated, time becomes critical.

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● Consequence Failure to recognize a patient necessitating early application of DC principles. Aoki and associates in 200111 reported on 68 patients who underwent DC surgery at Ben Taub Hospital. Failure to correct pH above 7.21 by the conclusion of DC I and a PTT greater than 78.7 were predictive of 100% mortality. Likewise, in their review of iliac vascular injuries in 1997, Cushman and colleagues12 reported a fourfold greater risk of dying for the hypothermic patient (preoperative core temperature of ≤34°C). This stresses the importance of early implementation of DC principles to avoid reaching this level of physiologic demise. Grade 5 complication

DC I The primary objectives of the initial laparotomy are control of hemorrhage, limiting contamination (and the subsequent inﬂammatory response), and temporary abdominal wall closure to protect viscera and limit heat loss. All of this ideally is accomplished in under 2 hours (about the length of a music CD).

DC I STEPS Positioning and incision Manual abdominal wall retraction and fourquadrant abdominal packing 3 Division of falciform ligament 4 Placement of large self-retaining retractor 5 Sequential removal of packs; abdominal inspection 6 Exposure and control of vascular or solid organ hemorrhage (pack, ligate, shunt, resect) 7 Control of contamination from hollow viscus injury (isolation, resection, repair) 8 Repacking of abdomen 9 Temporary abdominal closure 10 Transport to SICU

Step 1 Step 2

● Repair Truncated scene times for emergency medical services and rapid trauma bay throughput are essential to get the patient to the OR, where hemorrhage control can be best addressed.

Step Step Step

● Prevention Important steps during this phase include obtaining large-bore intravenous (IV) access, rapid-sequence intubation for airway control, gastric decompression (nasogastric tube placement is contraindicated in the presence of facial trauma or basilar skull fractures), chest tube placement (if indicated by absent breath sounds or crepitus), early rewarming maneuvers, and early blood product resuscitation. Large-volume crystalloid resuscitation increases the risk of subsequent edema and dilutional coagulopathy.13 Minimal diagnostic x-rays are required. A chest x-ray after rapidsequence intubation is useful to conﬁrm tube position and identify immediately treatable hemo- and/or pneumothorax. In the unstable blunt trauma patient, a pelvic x-ray can identify signiﬁcant pelvic fractures that must be temporarily stabilized to reduce pelvic volume and help tamponade bleeding. Also, for suspected blunt trauma, spinal precautions including a cervical collar must be continued until deﬁnitive injury can be excluded. A focused abdominal sonography in trauma (FAST) examination can be helpful in rapidly conﬁrming intraperitoneal bleeding when the physical examination is equivocal and multicavitary trauma is suspected. This technique has supplanted diagnostic peritoneal lavage in many institutions for this purpose. Communication with the blood bank is essential to keep them abreast of the potential for massive transfusion requirements. Likewise, early communication with the anesthesia service is paramount to hasten their preparation for this complicated patient and to initiate prewarming of the OR. A Cell Saver device should be mobilized to the OR for collection and reinfusion of shed autologous blood. Before incision, broad-spectrum antibiotics and tetanus prophylaxis should be administered and a Foley catheter placed.

Step

Step

Step Step Step

Positioning and Incision Failure to Gain Access to Injured Body Cavities ● Consequence Failure to adequately prepare and position the patient can result in failure to gain access to injured body cavities and limit the ability to diagnose and treat hemorrhage. Grade 5 complication ● Repair The patient is placed supine on the OR table with the right upper extremity extended at a right angle from the torso. The left arm is placed on an arm board with the elbow partially ﬂexed and the arm extended above the level of the head (a modiﬁed “taxi-hailing” position). This leaves the left chest widely accessible for emergent thoracotomy if necessary. The patient is prepared from the chin to the knees anteriorly and down to the level of the bed laterally. A vertical midline incision from the xyphoid process to the pubis is ideal. In the setting of a suspected severe pelvic fracture, the inferior limit of this incision can be curtailed to just below the umbilicus. This will prevent loss of tamponade of a retroperitoneal pelvic hematoma. ● Prevention In anticipation of the potential need for a median sternotomy, resuscitative left thoracotomy, or bilateral tube thoracostomy, no leads or tubing should be

78 DAMAGE CONTROL: ABDOMINAL CLOSURES present on the anterior or lateral chest wall. Incision should not be delayed while waiting for insertion of invasive monitoring devices (arterial lines and central venous catheters). A posterior heating pad is ideal because a convection warm air blanket becomes impractical. If the patient has had a previous midline laparotomy, a bilateral subcostal incision can be used. This allows for rapid access to the peritoneal cavity away from the anticipated midline adhesions. These adhesions can then be lysed quickly under direct vision.

Division of the Falciform Ligament and Placement of a Large, Self-retaining Retractor Iatrogenic Injury to the Abdominal Contents ● Consequence Once in the abdomen, a large hand-held abdominal wall retractor is used circumferentially to create space for extensive packing of all four quadrants. Iatrogenic injury to the abdominal contents can occur during this rapid, forceful maneuver. Often, bowel loops are compressed between the retractor and the abdominal wall and are bruised or torn or traction injury to the liver occurs. Grade 2 complication ● Prevention The hand-held body wall retractor must be initially placed under direct vision as the surgeon or assistant widely pushes down on the abdominal contents to create an area of separation between the abdominal contents and the abdominal wall. The retractor is then slid along the abdominal wall, maintaining the zone of separation. Packs (laparotomy pads) are carefully placed into the gutters and pelvis as the bowels are swept in the opposite direction. Surgeons on opposite sides of the table trade retracting and packing duties as appropriate. The falciform ligament is rapidly divided all the way to the dome of the liver to prevent iatrogenic traction injury to the liver during suprahepatic pack placement. Next, a large self-retaining retractor is placed to liberate all surgical hands available and maximize exposure. Next, packs are removed in a sequential fashion, beginning in the areas least likely to harbor the source of major hemorrhage. This provides space to pack the bowels away from areas of bleeding and create maximal exposure.

Hypotension ● Consequence Once the peritoneum is opened, any tamponade effect that had been provided by the abdominal wall is immediately lost. This may induce abrupt and severe hypotension. Sometimes, the patient remains profoundly hypotensive after four-quadrant packing is complete. Grade 5 complication

801

● Repair Control of aortic inﬂow should be obtained. Manual occlusion of the aorta at the diaphragmatic hiatus can be performed quickly by passing one’s hand anterior to the stomach underneath the left hepatic lobe. The aorta can be palpated immediately to the right and posterior to the esophagus. Here, it can be compressed posteriorly against the vertebral body either manually or with an aortic occlusion device. This maneuver has been shown to not only slow intra-abdominal bleeding but also augment cerebral and myocardial perfusion while anesthesia catches up on volume replacement and the source of bleeding is identiﬁed and controlled.14 If, for some reason, control of aortic inﬂow cannot be controlled from within the abdomen, an emergent left thoracotomy can be performed and the descending aorta cross-clamped from within the thorax. This adds morbidity to the procedure but, for some surgeons, allows for more rapid control of the aorta.

Sequential Removal of Packs; Abdominal Inspection Retroperitoneal Hematoma ● Consequence A centrally located retroperitoneal hematoma is encountered. Injury to a major vascular structure is anticipated. Grade 5 complication ● Repair As is true in all vascular surgery, exposure is the key ﬁrst step. The small bowel is initially eviscerated. This is followed by left and/or right medial visceral rotation to expose centrally located vessels. Often, packing alone is adequate for some vascular injuries, speciﬁcally venous. If an injury is amenable to rapid arteriorrhaphy or venorrhaphy, this is the treatment of choice. Of note, almost every vessel in the abdomen can be ligated with limited morbidity.15 However, ligation of the main aorta, external iliac arteries, and proximal superior mesenteric artery are associated with devastating tissue and/or bowel ischemia potentially necessitating limb amputation or extensive small bowel resection. Temporary intraluminal shunts are relatively easy to place and maintain end-organ perfusion. They are secured in place using silk ties or Rumel tourniquets. The largest shunt that ﬁts easily within the vessel should be used. Argyle carotid shunts and Javid shunts work well on medium-sized vessels, whereas chest tubes may be used when larger conduits are required (aorta or inferior vena cava). Literature on DC shunting of abdominal vessels is sparse and mostly limited to case reports; nevertheless results are encouraging.16,17 The feasibility of major abdominal and pelvic vein shunting in critically injured patients is controversial because published

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patency rates are low. However, it has been proposed that temporary shunting may help control short-term edema during acute high-volume resuscitation. In the context of DC surgery, there is no justiﬁcation for wasting time with pelvic vein shunting or reconstruction.18 When ligation is performed, the clinically signiﬁcant edema rate does not appear to be different from that of repaired veins if leg elevation, compression stockings, and liberal use of fasciotomies are utilized.19 Tense laparotomy pad packing and/or inﬂatable balloon catheters (e.g., Foley or Fogarty catheters) can be utilized for persistent hemorrhage from inaccessible locations or uncontrollable vessels. They may be placed directly into the missile or knife tract or directly into the defect in the injured vessel.

Solid Organ Injury ● Consequence Ongoing bleeding from solid organ injury. Grade 4 complication ● Repair With respect to solid organ injuries, prolonged repair for bleeding must be avoided. Splenic and renal hemorrhage is best managed with prompt resection, especially when the patient is approaching physiologic exhaustion. Tight packing anteriorly and posteriorly initially controls bleeding from liver parenchyma. Ongoing deep parenchymal bleeding is then controlled by compression of the porta hepatis (Pringle’s maneuver), followed by a ﬁnger fracture technique to expose deep vessels for suture ligation or clip application.20 More complex injuries (e.g., transhepatic gunshot wounds with long narrow columns of injury and active bleeding) require more innovative techniques like the insertion of a Penrose drain ligated distally, secured to and inﬂated over a red rubber catheter.21 Any and all topical hemostatic agents can be applied as well including ﬁbrin glue. A “liver tampon” made up of several sausage-sized pieces of absorbable gelatin sponge (Gelfoam) soaked in thrombin solution and wrapped loosely in a sheet of oxidized cellulose (Surgicel) is a recommended hemostatic modality. This device is then stuffed into the parenchymal defect followed by additional packing. This effectively tamponades bleeding and creates a hemostatic milieu.22 Tampons composed of other absorbable hemostatic materials available to the surgeon are also feasible. ● Prevention After the completion of DC I, all cases of complex hepatic injury should be interrogated with angiography. Even in those cases in which hemostasis is seemingly achieved, there can be a high incidence of ongoing intrahepatic arterial bleeding or traumatic arteriovenous ﬁstula, which requires therapeutic embolization.

Control of Contamination from a Hollow Viscus Injury (Isolation, Resection, Repair) Ongoing Intra-abdominal Contamination ● Consequence Ongoing intra-abdominal contamination from a hollow viscus injury. Grade 3 complication ● Repair After cessation of hemorrhage, limiting contamination becomes the next highest priority. This is done by controlling spillage of intestinal contents and urine from hollow viscus injuries. Simple bowel injuries, limited in size and number, are initially controlled with Babcock clamps and repaired using simple, single-layer continuous suture and tagged for reinspection later. More extensive injured bowel segments can either be isolated with proximal and distal circumferential umbilical tape or be divided with gastrointestinal anastomosis stapling devices. Formal resection can be postponed, and deﬁnitive reconstruction or ostomy creation is avoided at this time. This concept is very important when dealing with high-velocity penetrating wounds because the extent of bowel wall edema and blast injury is often underappreciated at the initial operation. This can cause delayed bowel ischemia and threaten anastamoses and stomas. Options for the management of ureteral injuries during DC include ligation and exteriorization. Ligation will require temporary percutaneous or open nephrostomy after several days if deﬁnitive repair is delayed for a prolonged period of time. Temporary percutaneous ureterostomy avoids this complication. Here, a tube is inserted into the proximal ureter and brought out laterally through the skin. Most bladder injuries can be rapidly closed with a single-layer running suture for initial management.23 Biliary tract and pancreatic injuries can be temporarily controlled by intra- or extraluminal tube drainage to temporarily diminish the damaging effects of pancreatic enzymes and bile on surrounding tissues. Again, all drains must be placed laterally so as not to interfere with temporary abdominal wall closure options. ● Prevention Meticulous inspection of the entire intra-abdominal and retroperitoneal digestive and urinary tract is paramount. The extent of intervention is based upon patient physiology.

Repacking of the Abdomen Ongoing Bleeding ● Consequence Ongoing bleeding from raw surface areas created during extensive retroperitoneal or pelvic dissection. In

78 DAMAGE CONTROL: ABDOMINAL CLOSURES the coagulopathic patient, these areas can be responsible for massive blood loss. Grade 3 complication ● Repair Correction of coagulopathy and adequate repacking at the conclusion of DC I. Once all vascular and bowel injuries have been controlled, diffuse intra-abdominal packing is performed. This technique is especially important when coagulopathy is noticed and extensive retroperitoneal or pelvic dissection has been performed.24,25 Folded laparotomy pads are ﬁrst placed over any solid organ injuries as well as over all dissected areas. ● Prevention Packing should be tight enough to provide adequate tamponade without compromising venous return to the heart or distal arterial supply.26

Temporary Abdominal Closure Increased Risk of Abdominal Compartment Syndrome ● Consequence Formal closure of the abdominal fascia after DC laparotomy has been associated with increased risk of abdominal compartment syndrome (ACS), acute respiratory distress syndrome, and multisystem organ failure. These conditions result from postoperative reperfusion injury and ongoing capillary leakage during DC II, causing intestinal and abdominal wall edema. Grade 4 complication ● Prevention Temporary abdominal closure is the ﬁnal step in the initial laparotomy prior to transport to the SICU. The goals of temporary closure include containment of abdominal viscera, thermoprotection, control of abdominal secretions, and maintenance of intraabdominal pressure tamponade. The simplest option for temporary closure includes skin-only closure using towel clips or a running nonabsorbable suture. This allows for considerable abdominal domain expansion while maintaining an insulating, protective shield. Note that towel clips, although the quickest method to deploy, can interfere with postoperative imaging studies (e.g., arteriography). If bowel edema prevents skin approximation, a temporary silo device is an option. The Bogotá bag is a 3 L IV ﬂuid bag sewn to the skin along the perimeter of the incision. This rapid, cheap closure technique, however, allows the abdominal fascia to retract considerably, potentially complicating deﬁnitive closure later. The vacuum dressing has evolved as the alternative of choice. This device can be placed quickly and allows for considerable increase in abdominal volume while maintaining some inward traction on the fascia.

803

Controlled egress of ﬂuid from the abdomen is permitted while maintaining a sterile, secure barrier, suitable for prone positioning ventilation if necessary. This dressing is composed of a surgical towel wrapped in Ioban and tucked subfascially over the bowel and omentum, which, if present, should be used to drape the small bowel and should be spread caudally and laterally to act as an abdominal apron. Two closed suction drains are then placed atop this dressing and are kept to high wall suction. Several laparotomy pads are placed over these drains, followed by a ﬁnal external Ioban sheet over the entire abdomen. To ensure that the Ioban sticks securely to the skin, all abdominal wall hair, especially in the groin and the suprapubic areas, is shaved and the skin is painted with a thin layer of benzoin. The dressing collapses down under suction and becomes semiﬁrm if placed properly.

Failure to Control Surgical Bleeding ● Consequence Failure to control surgical bleeding from a source in an anatomic location not amenable to deﬁnitive rapid surgical control. This is particularly true for complex hepatic, retroperitoneal, and pelvic or deep muscle injuries that would require lengthy surgical exploration often in the setting of coagulopathy. Grade 4 complication ● Repair DC I is not complete until all surgical bleeding is controlled. Although venous bleeding from these sources is often controlled with packing alone, an arterial bleeding source will often require an interventional radiology (IR) procedure to achieve or prolong hemodynamic stability.27 ● Prevention The IR team should be contacted and mobilized early in DC I if it is suspected that they will be needed. It is imperative that DC II strategies be initiated and maintained while the patient is in IR. SICU personnel and resources might need to be mobilized to the IR suite for this purpose.

DC II The goal of DC II is to reverse the sequelae of shock, speciﬁcally the lethal triad of hypothermia,28,29 acidosis,30 and coagulopathy, and support physiologic and biochemical restoration. Accordingly, any and all measures available for core rewarming should be utilized including raising the ambient temperature of the room and warming IV ﬂuids and the ventilator circuit. A convection hot air blanket is reapplied anteriorly, and if available, a ﬂuid circulating heating pad is placed posteriorly on the back and thighs. Other, more aggressive measures include pleural, gastric, and bladder lavage with warmed ﬂuids. Occasionally, extracorporeal circulation devices like venovenous or arteriovenous bypass via femoral vessel

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cannulation are necessary for rapid correction of severe hypothermia (core temperature 28°C–32°C). Use of venovenous bypass is limited by its requirement for systemic anticoagulation.31 Coagulopathy, a direct result of both hypothermia and resuscitative dilution of clotting factors, is treated by aggressive administration of fresh frozen plasma, platelets, and cryoprecipitate if ﬁbrinogen levels fall. Recombinant activated factor VII is a relatively new product available to combat clinical coagulopathy that does not correct with standard measures.32,33 The metabolic acidosis that results from hypovolemic shock and tissue ischemia causes an uncoupling of βadrenergic receptors. This diminishes the body’s response to endogenous and exogenous catecholamines and manifests primarily in lowered cardiac output and hypotension. This is treated by a predominant biologically active colloid (packed red blood cells, fresh frozen plasma, platelet) resuscitation to optimize oxygen delivery, cardiac output, and coagulation parameters. This resuscitation should be guided by at least central venous and invasive arterial pressure monitoring. In elderly patients with other comorbidities, a pulmonary artery catheter may be necessary. Crystalloid administration should be limited (<10 L) to control bowel edema and pulmonary third spacing.34

High Packed Cell Transfusion Requirement ● Consequence Patient maintains a high packed cell transfusion requirement despite normalization of temperature and coagulation factors. This is due to continued surgical bleeding either not identiﬁed at the conclusion of DC I or new-onset hemorrhage secondary to clot disruption or vasodilation. Grade 3 complication ● Repair Once recognized, immediate operative reexploration or IR reinterrogation to localize and stop the bleeding must occur. ● Prevention Throughout DC II, the patient should remain sedated on complete ventilation support. Chemical paralysis is used to promote synchrony with the ventilator and prevent disruption of clot formed in the packed open abdomen. Also, care must be taken to ensure that the patient does not become signiﬁcantly hypertensive during the DC II resuscitative phase because this can have deleterious effects on clot stability and hemostasis.

Development of ACS Injuries Sustained during Trauma ● Consequence Other injuries sustained during trauma remain undetected during DC sequence. Grade 3 complication ● Repair Injury speciﬁc by appropriate consulting service. ● Prevention During DC II, a complete physical examination or “tertiary survey” of the patient should occur. Appropriate radiographs should be obtained to evaluate for additional skeletal injuries based on physical ﬁndings that induce suspicion such as gross deformity or bruising. Immobilization and/or traction devices are applied when indicated. In the case of associated blunt mechanism, completion of the spine survey is imperative. Peripheral wounds are addressed, and vascular integrity of all injured limbs is frequently assessed. Adjunctive studies such as computed tomography scanning should be obtained at this time unless the patient is too unstable for travel. Recruitment of consultants for all deﬁnitive repairs should occur early in this phase, and both the extent and the priority of repairs must be established. Two subgroups of patients emerge who require premature reoperation during DC II prior to achieving physiologic restoration.

● Consequence Patient develops ACS, usually from bowel edema. ACS is deﬁned as an intra-abdominal pressure (bladder pressure measured via a Foley catheter) of greater than 25 mm Hg associated with one or all of the following physiologic sequelae: elevated peak airway pressures, impaired ventilation associated with hypoxia and hypercarbia, decreased urine output, increased systemic vascular resistance, and decreased cardiac output.35 This occurs in approximately 6% of patients after DC laparotomy for severe abdominal and/or pelvic injuries.36 These patients are at high risk for the development of intra-abdominal hypertension (IAH) from several causes: the use of bulky abdominal packs, continued bleeding into the abdominal cavity from uncorrected coagulopathy or failed and/or unrecognized mesenteric vascular injuries, bowel distention and edema from extensive resuscitation volumes (>10 L), and abdominal wall edema. A vacuum pack closure does not eliminate the possibility of ACS.37 This may be due to the efﬁciency with which the vacuum pack dressing is able to contain the abdominal volume and allow subsequent rises in abdominal pressures as visceral and abdominal wall edema worsens. Grade 4 complication ● Repair Treatment consists of immediately opening the patient’s abdomen to relieve the pressure. If ongoing blood loss

78 DAMAGE CONTROL: ABDOMINAL CLOSURES is suspected as the cause of the increased intra-abdominal pressure, this is best performed in the OR where lighting and equipment availability are maximized, if the patient can tolerate the necessary transport. The emergency alternative is to open the abdomen at the bedside in the intensive care unit (ICU) under sterile conditions. Occasionally, adequate decompression can be achieved without extensive operative intervention by incising the external Ioban drape of the vacuum pack to allow for further expansion of the neoabdominal wall and more eventration of abdominal viscera prior to placement of a new sterile Ioban cover. Failure to treat immediately is associated with extreme mortality.

DC III The primary objectives of DC III are deﬁnitive organ repair and fascial closure, if possible. Physiologic capture usually takes 24 to 36 hours to achieve, even with aggressive ICU management. In the OR, all packs are copiously irrigated and carefully teased off raw surfaces to avoid clot disruption. If diffuse bleeding is encountered, the surgeon must be prepared to abort the procedure, repack, and return after further resuscitation. After successful pack removal, the abdomen is reexplored to assess repairs made during DC I and to identify missed injuries. Formal vascular repairs are performed, and intestinal continuity is restored. Any bowel anastamoses should be covered with omentum and/or tucked under mesentery to promote sealing without ﬁstula formation. Stoma creation and percutaneous feeding tubes are avoided if fascial closure does not seem possible. Ideally, a nasogastric decompression tube and nasojejeunal feeding tube should be positioned intraoperatively. If a stoma is necessary (and fascial closure is to be delayed), it should be placed as laterally as possible to allow subsequent mobilization and separation of the abdominal wall components when deﬁnitive closure is performed. Once all of the repairs are completed, formal abdominal closure without tension is the ﬁnal step in the planned reoperation sequence.

Deﬁnitive Closure Techniques Primary Closure This is the most preferable closure. Maneuvers to temporarily approximate the fascial edges should be performed with clamps. If gentle abduction allows the fascial edges to approximate, a standard fascial closure should be possible. The risk of infection, enterocutaneous ﬁstula (ECF), and recurrent wound problems appears to be lower. This may be delayed days to weeks as physiology improves and edema lessens.

Persistent Edema ● Consequence Persistent edema within the retroperitoneum, bowel wall, and abdominal wall often renders primary fascial

805

closure impossible at the time of the original take-back operation after DC I and II. Attempting to close too large a defect can lead to ACS and its associated physiologic sequelae. Grade 3 complication ● Repair Patients who develop ACS will require reoperation to release and reopen the abdomen. ● Prevention A determination will need to be made at the time of closure as to the tension that will be placed on the abdomen and whether it can be close primarily or not. The surgeon’s judgment is most important here. In general, if, when the abdomen is viewed from across the OR table, the bowels are visualized above the level of the skin, then a low-tension primary closure is unlikely. Generally, a gap larger than 4 cm between fascial edges cannot be successfully closed primarily.38 Another good rule to follow is that if the peak airway pressure rises more than 10 cm H2O during temporary fascial approximation, the fascia should be left open and the aforementioned vacuum pack closure replaced. The patient is then returned to the ICU, and aggressive diuresis is implemented over the next several days if hemodynamically tolerated. This helps to decrease bowel and body wall edema. During this period, the patient undergoes a daily abdominal washout, reinspection, and meticulous replacement of the vacuum pack dressing so as not to promote ﬁstula formation. This can occur at the bedside if personnel and resources are readily available. The majority of damage controlled open abdomens can be primarily closed within 7 to 10 days, especially if there is no sign of intra-abdominal infection.

Retained Foreign Body after Closure of the Abdomen ● Consequence All sponges and instruments are not removed prior to closure. The emergent nature of the trauma of DC laparotomy increases the likelihood of retained foreign body.39 Multiple sponges used for packing as well as certain instruments are initially intentionally left in the abdomen. These may be unrecognized and left behind after deﬁnitive closure. Grade 3 complication ● Repair Retained foreign body will require reexploration and removal. ● Prevention Do not rely on sponge counts at the time of deﬁnitive closure. Obtain an intraoperative abdominal radiograph to ensure that no retained foreign bodies are present

806

SECTION XII: TRAUMA SURGERY

prior to proceeding with closure. Be sure that the radiograph displays the entire abdominal cavity. For obese patients, multiple radiographs might be necessary to properly view all four abdominal quadrants. Approximately 20% of DC patients fail primary fascial closure and are managed as open abdominal wounds or large ventral hernias. If fascial closure is still not achieved after 7 to 10 days, the surgeon faces a number of alternatives that will cover the abdominal defect but leave the patient with a large ventral hernia. The ﬁrst of these involves closing the skin with no attempt at fascial reapproximation. The patient would then undergo repair of the abdominal wall defect several months later. Often, this is not possible because the gap is too wide and, despite skin ﬂap mobilization, the edges cannot be approximated. In a second option, a Vicryl (polyglycolic acid) mesh is placed over the entire abdominal wall defect and sutured to the fascial edges. The Vicryl mesh is then covered with saline-soaked wet-to-dry dressings. It is always advisable to drape the greater omentum, if still available, over the bowel so that frequent dressing changes do not promote formation of enteric ﬁstulas. Careful daily dressing changes are performed over this mesh, and the wound is allowed to granulate through the material. Once a smooth bed of granulation tissue is established (2–3 wk), a sponge vacuum dressing can then be applied to promote faster granulation.

Enteroatmospheric Fistula ● Consequence Exposed suture lines, anastomoses, or bowel wall exposed to the mesh or fascial edges may result in enteroatmospheric ﬁstulae. Frequent manipulation (i.e., dressing or vacuum pack changes) of the granulating wound compounds this risk. These can be even more challenging to manage than ECF owing to the lack of skin to apply an appliance to control drainage. Grade 4 complication ● Repair The same principles apply here as to ECF, with the addition of the necessity to provide skin coverage around the ﬁstula site. It is most important not to attempt a split-thickness skin graft (STSG) until the ﬁstula drainage is controlled so as to not jeopardize the chance for a successful take. It may be necessary to stage the STSG. By allowing the ﬁstula output to drain opposite the side of grafting, half of the wound area can be covered before proceeding with grafting the remainder of the wound and allowing the output to drain out the grafted side. This can be accomplished by temporarily positioning the patient in ways that allow gravity to determine the direction of drainage. ● Prevention The same principles apply here as to ECF. Next, an STSG is applied once the granulation bed matures. Over the next 6 to 12 months, this skin graft will

mature, separate, and develop a thin layer of connective tissue or fat between the underlying viscera. At this point, the patient is ready for excision of the skin graft and deﬁnitive reconstruction. Many reconstructive techniques have been described in the literature, including the use of preoperative tissue expanders40 and abdominal wall component separation with bilateral rectus release to achieve primary component closure with extrafascial mesh support.41 Here, the external oblique aponeurosis is incised approximately 2 cm lateral to the rectus sheath and separated from the internal oblique. This allows the rectus muscle to be approximated medially and sutured. Various modiﬁcations of this technique have been described.42 The involvement of a plastic surgeon at this step is advisable to lend additional expertise at this delayed setting.

Dense Abdominal Adhesions ● Consequence Dense abdominal adhesions will make the dissection of the skin graft off of the intestines very difﬁcult. This may lead to prolonged operative times and incur many enterotomies, thus contaminating the operative ﬁeld. Grade 3 complication ● Repair Standard enterotomy closures or bowel resection. ● Prevention Wait at least 6 months to a year before scheduling a patient for reconstruction. All acute processes of the original pathology must be resolved, nutritional status must be satisfactory, and the abdomen must pass the “pinch test” (the skin graft is pinched and is able to be elevated off of the abdominal contents without palpable adhesions).

ALTERNATIVES TO COMPLEX ABDOMINAL WALL RECONSTRUCTIONS Permanent Prosthesis Nonabsorbable mesh is often used to bridge the gap between fascial edges. Unfortunately, this is associated with high recurrence and ﬁstula rates.43,44 The main advantage of permanent mesh closure is avoidance of complex abdominal wall reconstruction. Options for permanent prosthesis include polypropylene, expanded polytetraﬂuoroethylene (ePTFE), composite material, and biologic material. Polypropylene mesh incorporates well (usually within 2 wk) secondary to ﬁbroblastic reaction but can have problems with shrinkage, adhesion formation, seroma and infection (5%), and late recurrence. The ECF rate is approximately 3%. ePTFE has less ﬁbroblastic reaction and adhesions than polypropylene and, thus, an increased recurrence rate. Although ePTFE can be placed adjacent to bowel, ECF remains a problem. This material is also more expensive than polypropylene. A composite

78 DAMAGE CONTROL: ABDOMINAL CLOSURES material is available made up as a “sandwich” of ePTFE placed down on the bowel and polypropylene facing up. This allows an intraperitoneal placement and combines the advantages of both materials while minimizing complications.

ECF ● Consequence ECF appears to be a particularly challenging complication to manage and is due to bowel dessication and adherence of bowel to the mesh and exposed fascial edges. The bowel ﬁstulizes with the anterior abdominal wall and its contents drain through the skin. Grade 4 complication ● Repair ECF remains the Achilles heel of the general surgeon. The management here is no different than traditional teaching. The anatomy of the ﬁstula needs to be determined and output should be classiﬁed as high or low. Nothing-by-mouth status and total parenteral nutrition are instituted. If the ﬁstula fails to close spontaneously, operation is required. ● Prevention Every attempt should be made to protect the bowel from adhering to permanent mesh and fascial edges. Suture lines and anastomoses are particularly vulnerable to ﬁstulization. These should be buried if possible, so as to minimize exposure to the rough surface. The omentum can be used and is quite helpful in serving as a barrier between the bowel and the anterior abdominal wall. Nutrition should be optimized.

Biologic Material Derived from the extracellular matrix from animal or human tissue or cadaveric fascia, these materials have a decreased incidence of infection and ECF. Their use is preferred in contaminated wounds. Surgisis (Cook) is derived from porcine small intestinal submucosa. It is composed mostly of type I collagen from the extracellular matrix and is acellular. It has been used successfully in contaminated wounds.45,46 Alloderm (Lifecell) is human acellular dermis from processed cadaveric skin. It consists of the basement membrane and a dermal collagen matrix. There is no antigenic response, and Alloderm has been shown to be effective in abdominal wall reconstruction in patients at increased risk for mesh-related complications.47 One drawback is its signiﬁcant expense ($25/cm2). Permacol, a porcine dermal collagen, is another biologic material that has been on the market since 2001.

Recurrent Herniation ● Consequence As with all hernias, recurrences will occur at variable times after repair. Grade 3 complication

807

● Repair Reoperation is required. This may be accomplished by the open or the laparoscopic method. ● Prevention A pitfall here is not overlapping enough mesh over the defect edges. Laparoscopic experience indicates that at least a 4-cm overlap should be used to avoid failure.

REFERENCES 1. MacKenzie EJ, Fowler CJ. Epidemiology. In Mattox KL, Feliciano DV, Moore EE (eds): Trauma, 5th ed. New York: McGraw-Hill, 2004; pp 21–39. 2. Sauaia A, Moore FA, Moore EE, et al. Epidemiology of trauma deaths: a reassessment. J Trauma 1995;38:185– 193. 3. McGonigal MD, Cole J, Schwab CW, et al. Urban ﬁrearm deaths: a ﬁve year perspective. J Trauma 1993;35:532– 537. 4. Surface Ship Survivability. Naval War Publication 3–20.31. Washington, DC: Department of Defense, 1996. 5. Shapiro MB, Jenkins DH, Schwab CW, et al. Damage control: collective review. J Trauma 2000;49:969–978. 6. Stone H, Strom P, Mullins R. Management of the major coagulopathy with onset during laparotomy. Ann Surg 1983;197:532. 7. Rotondo MF, Schwab CW, McGonigal MD, et al. Damage control: an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma 1993;35:373–383. 8. Johnson JW, Gracias VH, Schwab CW, et al. Evolution in damage control for exsanguinating penetrating abdominal injury. J Trauma 2001;51:261–271. 9. Rotondo MF, Zonies DN. The damage control sequence and underlying logic. Surg Clin North Am 1997;77:761– 777. 10. Moore EE, Burch JM, Franciose RJ, et al. Staged physiologic restoration and damage control surgery. World J Surg 1998;22:1184–1190. 11. Aoki N, Wall M, Demsar J, et al. Predictive model for survival at the conclusion of a damage control laparotomy. Am J Surg 2001;180:540–545. 12. Cushman JG, Feliciano DV, Renz BM, et al. Iliac vascular injury: operative physiology related to outcome. J Trauma 1997;42:1033. 13. Moore FA, McKinley BA, Moore EE. The next generation in shock resuscitation. Lancet 2004;363:1988–1996. 14. Garcia-Rinaldi R, Defore WW, Mattox KL, et al. Unimpaired renal, myocardial, and neurologic function after cross clamping of the thoracic aorta. Surg Gynecol Obstet 1976;143:243. 15. Feliciano DV. Abdominal vascular injury. In Mattox KL, Feliciano DV, Moore EE (eds): Trauma, 5th ed. New York, McGraw-Hill, 2004; pp 755–777. 16. Reilly PM, Rotondo MF, Carpenter JP, et al. Temporary vascular continuity during damage control: intraluminal shunting for proximal superior mesenteric artery injury. J Trauma 1995;39:757–760. 17. Aldridge SD, Badellino MM, Malaspina PJ, et al. Extended intravascular shunting in an experimental model of vascular injury. J Cardiovasc Surg 1997;38:183–186.

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18. Aucar JA, Hirshberg A. Damage control for vascular injuries. Surg Clin North Am 1997;77:853–862. 19. Arrillaga A, Nagy K, Frykberg ER, et al. Practice management guidelines for penetrating trauma to the lower extremity. EAST Practice Management Guidelines. Accessed January 2008 at http://www.east.org/tpg/ lepene.pdf 20. Pachter HL, Spencer FC, Hofstetter SR, et al. Signiﬁcant trends in the treatment of hepatic trauma. Experience with 411 injuries. Ann Surg 1992;215:492. 21. Demetriades D. Balloon tamponade for bleeding control in penetrating liver injuries. J Trauma 1998;44:538–539. 22. Braslow B, Brooks AJ, Schwab CW. Damage control. In Mahoney PF, Ryan JM, Brooks AJ, Schwab CW (eds): Ballistic Trauma: A Practical Guide, 2nd ed. London: Springer, 2005; pp 180–208. 23. Schreiber MA: Damage control surgery. Crit Care Clin 2004;20:101–118. 24. Feliciano DV, Mattox KL, Burch JM, et al. Packing for control of hepatic hemorrhage. J Trauma 1986;26:738. 25. Saiﬁ J, Fortune JB, Graca L, et al. Beneﬁts of intraabdominal pack placement for the management of nonmechanical hemorrhage. Arch Surg 1990;125:119. 26. Feliciano DV, Mattox KL, Burch JM, et al. Packing for control of hepatic hemorrhage. J Trauma 1986;26:738. 27. Kushimoto S, Arai M, Aiboshi J, et al. The role of interventional radiology in patients requiring damage control laparotomy. J Trauma 2003;54:171. 28. Cushman JG, Feliciano DV, Renz BM, et al. Iliac vascular injury: operative physiology related to outcome. J Trauma 1997;42:1033. 29. Gentilello LM. Practical approaches to hypothermia. In Maull KI, Cleveland HC, Feliciano DV, et al (eds): Advances in Trauma and Critical Care, vol 9. St. Louis: Mosby, 1994; p 39. 30. Abramson D, Scalea TM, Hitchcock R, et al. Lactate clearance and survival following injury. J Trauma 1993;35: 584–589. 31. Gentilello LM, Cobean RA, Offner PJ, et al. Continuous arteriovenous rewarming: rapid reversal of hypothermia in critically ill patients. J Trauma 1992;32:316. 32. Martinowitz U, Kenet G, Segal E, et al. Recombinant activated factor VII for adjunctive hemorrhage control in trauma. J Trauma 2001;51:431–439. 33. Lynn M, Jeroukhimov I, Klein Y, et al. Updates in the management of severe coagulopathy in trauma patients. Intensive Care Med 2002;28(suppl):s241–s247.

34. Bifﬂ WL, Moore EE, Burch JM, et al. Secondary abdominal compartment syndrome is a highly lethal event. Am J Surg 2001;182:645–648. 35. Ivatury RR, Sugerman HJ. Abdominal compartment syndrome: a century later, isn’t it time to pay attention? Crit Care Med 2000;28:2137–2138. 36. Ertel W, Oberholzer A, Platz A, et al. Incidence and clinical pattern of the abdominal compartment syndrome after “damage control” laparotomy in 311 patients with severe abdominal and/or pelvic trauma. Crit Care Med 2000;28:1747–1753. 37. Gracias VH, Braslow B, Johnson J, et al. Abdominal compartment syndrome in the open abdomen. Arch Surg 2002;137:1298–1300. 38. Ciofﬁ WG (Moderator), Bifﬂ WL, Croce MA, Feliciano DV (Panelists). Component separation for the open abdomen (Symposium). Contemp Surg 2006;62:216–220. 39. Gawande AA, Studert DM, Orav EJ, et al. Risk factors for retained instruments and sponges after surgery. N Engl J Med 2003;348:229–235. 40. Livingston DH, Sharma PK, Glantz AI. Tissue expanders for abdominal wall reconstruction following severe trauma: technical note and case reports. J Trauma 1992;32:82. 41. Ramirez OM, Raus E, Dellon AL. “Components separation” method for closure of abdominal-wall defects: an anatomic and clinical study. Plast Reconstr Surg 1990;86: 519–526. 42. 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. 43. Fabian TC, Croce MA, Pritchard FE, et al. Planned ventral hernia. Staged management for acute abdominal wall defects. Ann Surg 1994;219:643–650. 44. Rutherford EJ, Skeete DA, Brasel KJ. Management of the patient with an open abdomen: techniques in temporary and deﬁnitive closure. Curr Probl Surg 2004;41:821–876. 45. Franklin ME Jr, Gonzalez JJ Jr, Glass JL. Use of porcine small intestinal mucosa as a prosthetic device for laparoscopic repair of hernias in contaminated ﬁelds: 2-year follow-up. Hernia 2004;8:186–189. 46. Helton WS, Fisichella PM, Berger R, et al. Short-term outcomes with small intestinal submucosa for ventral abdominal hernia. Arch Surg 2005;140:549–562. 47. Butler CE, Langstein HN, Kronowitz SJ. Pelvic, abdominal, and chest wall reconstruction with AlloDerm in patients at increased risk for mesh related complications. Plast Reconstr Surg 2005;116:1263–1277.

79

Management of Penetrating Neck Injury Ali Salim, MD and Demetrios Demetriades, MD INTRODUCTION Penetrating neck injuries (PNIs) are notoriously difﬁcult to evaluate and manage because of the complex anatomy and the dense concentration of numerous vital structures in a small anatomic area. The clinical evaluation can be challenging, and signiﬁcant injuries may easily be missed. The radiologic evaluation of these injuries has undergone major changes since the early 2000s and shifted from invasive diagnostic procedures to noninvasive methods. The selection of the most appropriate investigation remains a controversial issue. The surgical exposure of some neck structures such as the distal carotid artery, the subclavian vessels, and the vertebral artery can challenge the surgical skills of even the most experienced trauma or vascular surgeons and require excellent knowledge of the local anatomy. The advancement of interventional radiology has revolutionized many aspects of the management of some complex vascular injuries that are difﬁcult to manage operatively.

EPIDEMIOLOGY Firearms are responsible for about 43%, stab wounds for about 40%, shotguns for about 4%, and other weapons for about 12% of all PNIs in urban trauma centers in the United States.1 Gunshot wounds (GSWs) are signiﬁcantly more likely to be associated with large neck hematomas, hypotension on admission, and vascular or aerodigestive injuries than are knife wounds.1,2 Overall, about 35% of all GSWs and 20% of stab wounds to the neck are associated with signiﬁcant injuries to vital structures, but only 16.5% of GSWs and 10.1% of stab wounds require a therapeutic operation. Transcervical GSWs are associated with signiﬁcant injuries to vital structures in 73% of victims, although only 21% require a therapeutic operation.3 Shotgun injuries account for about 4% of civilian PNIs, often cause injuries to multiple structures, and pose major evaluation and management problems. Overall, the most commonly injured structures in the neck are the vessels, followed by the spinal cord, the aerodigestive tracts, and

nerves.1 The incidence of injury to the various neck structures according to mechanism of injury is shown in Table 79–1.

ANATOMY In penetrating trauma, the neck is divided into three anatomic zones for evaluation and therapeutic strategy purposes (Fig. 79–1): Zone I comprises the area between the clavicle and the cricoid cartilage. This zone includes the innominate vessels, the origin of the common carotid artery, the subclavian vessels and the vertebral artery, the brachial plexus, the trachea, the esophagus, the apex of the lung, and the thoracic duct. The surgical exposure of the vascular structures in Zone I is difﬁcult because of the presence of the clavicle. Zone II comprises the area between the cricoid cartilage and the angle of the mandible and contains the carotid and vertebral arteries, the internal jugular vein, the trachea, and the esophagus. This zone is more accessible to clinical examination and surgical exploration than the other zones. Zone III extends between the angle of the mandible and the base of the skull and includes the distal carotid and vertebral arteries and the pharynx. Zone III is not amenable to easy physical examination or surgical exploration.

MANAGEMENT The initial evaluation and management should follow the Advanced Trauma Life Support (ATLS) protocols. During the primary survey, the following life-threatening conditions from the neck should be identiﬁed and treated as soon as possible: 1. Airway obstruction due to laryngotracheal trauma or external compression by a large hematoma. 2. Tension pneumothorax. 3. Major active bleeding, externally or in the thoracic cavity.

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SECTION XII: TRAUMA SURGERY

Zone III

Zone III

Zone II

Zone II

Zone I

Zone I

Figure 79–1 Surgical zones of the neck: zone I is between the clavicle and the cricoid; zone II is between the cricoid and the angle of the mandible; and zone III is between the angle of the mandible and the base of the skull. Table 79–1 Incidence and Type of Injuries according to Mechanism of Injury (N = 223 Patients)1 Injury

All Mechanisms (%)

GSW (%)

SW (%)

21.5

26.8

14.6

Aerodigestive

6.3

7.2

3.4

Spinal cord

6.7

13.4

1.1

Peripheral or cranial nerves or sympathetic

9.0

12.4

4.5

Hemo- or pneumothorax

17.9

15.5

13.5

Vascular

GSW, gunshot wounds; SW, stab wounds. From Demetriades D, Theodorou D, Cornwell EE, et al. Evaluation of penetrating injuries of the neck: prospective study of 223 patients. World J Surg 1997;21:41–48.

4. Spinal cord injury or ischemic brain damage due to carotid artery occlusion. During the secondary survey the following neck injuries should be identiﬁed: 1. Occult vascular injuries.

Figure 79–2 Patient with a large hematoma in zone I of the neck, secondary to subclavian artery injury.

cheal intubation difﬁcult and dangerous, even in an ideal environment. Inability to secure the airway in such a patient can lead to severe respiratory distress and, ultimately, cardiac arrest. Grade 4/5 complication

2. Occult laryngotracheal injuries. 3. Pharyngoesophageal injuries. 4. Cranial or peripheral nerve injuries. 5. Small pneumothoraces. The more common pitfalls initially encountered when dealing with patients with PNI follow.

Failure to Secure the Airway ● Consequence The presence of a large hematoma (Fig. 79–2) or edema or laryngotracheal trauma makes the endotra-

● Repair Cricothyroidotomy in the emergency room may be necessary in about 6% of all PNIs4 or about 12% of laryngotracheal injuries.5 In the presence of large midline hematomas, the procedure is difﬁcult and may be associated with severe bleeding. On rare occasions with visible large laryngotracheal wounds, the endotracheal tube can be inserted under direct view into the distal transected segment through the neck wound. The distal larynx or trachea should be grasped and secured with a tissue forceps before insertion of the tube in order to avoid complete transection or retraction into the mediastinum.

79 MANAGEMENT OF PENETRATING NECK INJURY

811

● Prevention Early recognition of the need for surgical airway is key. Air bubbling through a neck wound is pathognomonic of laryngotracheal injury. Firm manual compression over the wound reduces the air leak and usually improves oxygenation. Emergency room endotracheal intubation should be considered only in patients who fail to improve after ﬁrm occlusion of the wound with the air leak. Orotracheal intubation in the emergency room should be performed by the most experienced physician present, with a surgeon ready to perform a surgical airway.

Active Hemorrhage More than 20% of patients who sustain a PNI have evidence of vascular injury (see Table 79–1). Patients may present with a moderate to large hematoma or active bleeding, either externally or into the thoracic cavity. ● Consequence Major active bleeding, externally or into the thoracic cavity, is potentially life threatening and needs to be addressed immediately after the airway has been secured. In addition, venous injuries may lead to air embolism. Without prompt attention, patients will suffer cardiovascular collapse. Grade 3/4 complication ● Repair On arrival at the hospital, patients with active bleeding should be placed in the Trendelenberg position to reduce the risk of air embolism in cases with venous injuries. In cases of suspected subclavian venous injuries, the intravenous line should be inserted in the opposite arm in order to avoid extravasation of infused ﬂuids or medications from a proximal venous injury. External bleeding can successfully be controlled by direct pressure in most cases. However, bleeding from the vessels behind the clavicle or near the base of the skull or the vertebral artery is often difﬁcult to control by external pressure. In these cases, digital compression with a gloved index ﬁnger through the wound should be attempted. For these situations, we have successfully used balloon tamponade.6–8 The technique involves insertion of a Foley catheter into the wound and advancement as far as it can go. The balloon is then inﬂated with water until the bleeding stops or moderate resistance is felt. If the bleeding continues after this maneuver, the balloon is deﬂated and the catheter is slightly withdrawn and reinﬂated. Signiﬁcant bleeding through the catheter is suggestive of bleeding distal to the balloon and repositioning should be attempted. In periclavicular injuries, the bleeding may occur in both the intrathoracic cavity and externally. In these cases, a Foley catheter is advanced into the chest cavity through the neck wound, the balloon is then inﬂated, and the catheter is pulled back until some resistance is felt.

Balloon compressing bleeder

Figure 79–3 Balloon tamponade for bleeding control from the subclavian vessels. It can also be used for bleeding control from other zones in the neck.

In this position, the balloon compresses the bleeding vessels against the ﬁrst rib or the clavicle (Fig. 79–3). The traction is maintained by application of a Kelly forceps on the catheter, just above the skin. If external bleeding continues, a second Foley is inserted and inﬂated in the wound tract.7 Blind clamping of suspected bleeding should be avoided because it is rarely effective and the risk of further vascular or nerve damage is very high. Many patients with major injuries to the neck vessels reach the hospital in cardiac arrest or imminent cardiac arrest. These patients may beneﬁt from a resuscitative thoracotomy. Bleeding from the left subclavian vessels can be controlled with a vascular clamp applied under direct view through the thoracotomy. Besides the usual resuscitation measures, the right ventricle should be aspirated for air embolism. In our experience, survival after resuscitative thoracotomy for PNI is very poor.9 ● Prevention The sequelae of hemorrhage can be minimized only by digital pressure and early recognition.

Diagnostic Work-up Impaired by a Cervical Collar Cervical spine protection by means of a neck collar remains a common practice during the prehospital transportation of patients with PNIs. The value of this practice is questionable and may be harmful in some patients. ● Consequence Spinal immobilization may complicate the evaluation and diagnostic work-up, and most importantly; the application of a cervical collar in the presence of a large or expanding hematoma may cause respiratory obstruction (see Fig. 79–2). Grade 1/2 complication

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SECTION XII: TRAUMA SURGERY

● Repair Removal of the collar. ● Prevention Cervical spine protection has absolutely no role in patients with stab wounds to the neck. Its value in cases with GSWs is limited. It is rare that low-velocity GSWs result in spinal instability. In a series of 1300 patients with GSWs of the spine, Meyer and coworkers10 found no unstable fractures. However, it has been reported and it is also our experience, that in rare occasions, a low-velocity GSW can cause unstable spinal fractures without cord injury.11 In high-velocity wounds, massive destruction of the bone and ligament structures of the cervical spine may cause instability. However, these injuries are always associated with irreversible cord destruction, making spinal immobilization of limited practical value. It is recommended that in knife injuries, no cervical collar is applied. In GSWs, a collar may be applied, always monitoring for expanding hematoma or respiratory distress. In these cases, the collar should be loosened to relieve the airway obstruction.

Inadequate Selection of Patients for Surgical Intervention ● Consequence Only about 17% of GSWs and 10% of stab wounds to the neck require a therapeutic operation. Subjecting the remaining 83% to 90% of patients to an unnecessary operation is not an acceptable practice. At the same time, failure to follow written protocols and algorithms, especially in low-volume trauma centers or by an inexperienced surgeon, may result in missing signiﬁcant injuries Grade 2/3 complication ● Prevention/Repair The selection of patients for operation or observation is based on clinical examination and appropriate investigations. It is essential that clinical examination is performed systematically, preferably according to a written protocol (Box 79–1), and investigations are selected with the help of an algorithm, which takes into account the experience and resources of the individual trauma center. Figure 79–4 demonstrates the algorithms that have been in use at the Los Angeles County and University of Southern California trauma center since 1997.

INVESTIGATIONS The mechanism of injury and clinical examination should determine the need and type of speciﬁc investigations in the evaluation of PNIs. Patients with hard signs of major vascular or laryngotracheal injuries should undergo an operation without any delay for deﬁnitive investigations.

Box 79–1 Protocol for Clinical Examination in Penetrating Injuries of the Neck Systemic Examination 1 Dyspnea: 䊐 Yes 䊐 No 2 Blood pressure: 3 Pulse:

Local Examination Vessels 1 Active bleeding: 䊐 Minor 䊐 Severe 䊐 No bleeding 2 Hematoma: 䊐 Small 䊐 Large 䊐 No bleeding 䊐 Expanding 3 Pulsatile hematoma: 䊐 Yes 䊐 No 4 Peripheral pulses (compare with normal side): 䊐 Normal 䊐 Diminished 䊐 Absent 5 Bruit: 䊐 Yes 䊐 No 6 Ankle-brachial index (ABI): Larynx-Trachea-Esophagus 1 Hemoptysis: 䊐 Yes 䊐 No 2 Air bubbling through wound (ask the patient to cough): 䊐 Yes 䊐 No 3 Subcutaneous emphysema: 䊐 Yes 䊐 No 4 Pain on swallowing sputum: 䊐 Yes 䊐 No Nervous System 1 Glasgow Coma Scale (GCS): 2 Localizing signs (describe): 3 Cranial nerve injury: ● Facial nerve: 䊐 Yes 䊐 No ● Glossopharyngeal nerve: 䊐 Yes 䊐 No ● Recurrent laryngeal nerve: 䊐 Yes 䊐 No ● Accessory nerve: 䊐 Yes 䊐 No 4 Spinal cord: 䊐 Normal 䊐 Abnormal (describe): 5 Brachial plexus injury: ● Median nerve: 䊐 Yes 䊐 No ● Ulnar nerve: 䊐 Yes 䊐 No ● Radial nerve: 䊐 Yes 䊐 No ● Musculocutaneous nerve: 䊐 Yes 䊐 No ● Axillary nerve: 䊐 Yes 䊐 No 6 Horner’s syndrome: 䊐 Yes 䊐 No

If time permits, chest and neck ﬁlms may be helpful in locating foreign bodies (Fig. 79–5) or diagnosing an associated hemopneumothorax, which requires treatment. There is good evidence from large prospective studies that patients with no signs or symptoms of vascular or aerodigestive injuries do not have signiﬁcant injuries requiring treatment, and they are very unlikely to beneﬁt from routine angiography or esophageal studies.1,12

Plain Chest and Neck Films Chest ﬁlms should be obtained in all fairly stable patients with PNIs in zone I or any other wounds that could have violated the chest cavity. About 16% of GSWs and 14% of stab wounds to the neck are associated with a hemo/ pneumothorax.1 Other important radiologic ﬁndings include a widened upper mediastinum (Fig. 79–6), which is suspicious of a thoracic inlet vascular injury, subcutaneous emphysema, fractures, and missiles.

79 MANAGEMENT OF PENETRATING NECK INJURY

813

ALGORITHM FOR EVALUATION OF PENETRATING NECK INJURIES Clinical examination according to protocol

Obvious significant injuries? Severe active bleeding Shock not responding to fluids Absent radial pulse Air bubbling through wound Respiratory distress Yes Operation

No

No

Diminished peripheral pulse Bruit Widened mediastinum Shotgun injuries Yes

No

No Gunshot wounds

Hemoptysis Hoarseness Painful swallowing Subcutaneous emphysema Hematemesis Proximity in obtunded patient

CT scan with IV contrast

Hematoma Shock responding to fluids Proximity injury

Angio

Suspicious tract Yes

Yes Color flow Doppler

Observation (color flow Doppler optional)

Definitely normal vessels

Indeterminate CFD or poor visualization

Observe

Angiogram

No

Yes

No

Esophagography Endoscopy

Angio/ swallow

Observe

Figure 79–4 Algorithm for the evaluation of penetrating injuries to the neck.

Angiography Angiographic evaluation of the neck vessels after PNI remained a standard practice in many centers for many years.13–15 Sclafani and associates13 in a review of 72 asymptomatic patients with proximity PNIs who underwent routine angiography reported a high incidence of vascular injuries. The authors suggested that routine angiography, in asymptomatic patients with PNIs which violate the platysma, should be the standard of care until additional data are available.13 Since then, numerous publications have suggested that routine angiography in asymptomatic patients is unnecessary, has a low yield, and does not offer any beneﬁt over physical examination and other noninvasive investigations.1,6,12,16–19 Clinical examination alone may miss minor injuries to the neck vessels not requiring treatment.1,17 Many studies have suggested that clinically occult, angiographically detected injuries have a benign prognosis and do not require treatment.19,20 However, there is concern that

minor carotid injuries may be different from extremity minor vascular injuries, and it might be prudent to monitor them until complete healing. In order to address this concern, we suggest that asymptomatic patients be evaluated with a combination of clinical examination according to a written protocol and color ﬂow Doppler (CFD).1 Although the absence of clinical signs suggestive of vascular trauma reliably excludes signiﬁcant injuries requiring treatment (negative predictive value [NPV] 100%),1,17 the presence of soft clinical signs does not reliably identify patients who will require an operation. It is obvious that angiography in this group of patients has a low yield. However, clinical examination according to a written protocol combined with CFD studies reliably diagnosed all vascular injuries.1,17 Some surgeons suggested a policy of routine angiography only for injuries in zones I and III, irrespective of clinical ﬁndings.21 Such a policy still has a very low yield at considerable costs and patient discomfort. In summary, angiography for PNIs should be reserved only for selected

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Box 79–2 Indications for Conventional Angiography Diagnostic Indications ● ● ● ●

Inconclusive color ﬂow Doppler (CFD) or computed tomography (CT) angiogram Shotgun injuries Gunshot wounds involving the transverse foramen of the spine Widened upper mediastinum in zone I injuries

Therapeutic Indications (Possible Stenting or Embolization) ● ● ●

Bruit on auscultation Diminished upper extremity pulse Persistent slow bleeding from suspected vertebral artery injury

cases with speciﬁc diagnostic or therapeutic indications (Box 79–2).

CFD

Figure 79–5 Chest and neck ﬁlms may be helpful in locating foreign bodies. This patient has retained bullets in zones I and III.

CFD has been suggested as a reliable alternative to angiography in the evaluation of PNIs.1,6,8,17,22–26 In a prospective study from Los Angeles, 82 hemodynamically stable patients were clinically examined according to a written protocol and subsequently had angiographic and CFD evaluation. CFD diagnosed 10 of the 11 angiographically detected injuries and missed 1 small intimal tear that did not require treatment.17 The study concluded that the combination of a careful clinical examination and CFD imaging is a safe and cost-effective alternative to routine angiography. CFD has the disadvantage of being operator dependent and has some limitations in the visualization of the proximal left subclavian artery, especially in obese patients; the internal carotid artery near the base of the skull; and the segments of the vertebral artery under the bony part of the vertebral canal.8,24

Computed Tomography

Figure 79–6 Chest x-ray in a zone I penetrating injury shows a widened upper mediastinum, which is suspicious of a thoracic inlet vascular injury. This patient needs angiographic evaluation.

Computed tomography (CT) has become a very useful tool in the evaluation of PNIs, especially in GSWs. At our center, it has become the ﬁrst-line investigation in all hemodynamically stable patients with GSWs to the neck. The entry and exit of the bullet should be marked with radiopaque markers and 3-mm CT cuts should be obtained between the markers or between the entry and the retained bullet. Identiﬁcation of the bullet trajectory is very helpful in determining the need for further invasive investigations, such as angiography or endoscopy. Patients with trajectories away from the major vessels or the aerodigestive structures do not need further evaluation.8 Gracias and colleagues27 in a study of 19 patients with PNIs found

79 MANAGEMENT OF PENETRATING NECK INJURY

815

that in 13 cases (68%), the CT scan showed trajectories away from vital structures and no further evaluation was required. In addition to the missile trajectory, the CT scan may provide information about the site and nature of any spinal fractures, involvement of the spinal cord, the presence of fragments in the spinal canal, and the presence of any hematomas compressing the cord.8 Helical CT angiography has been used since the early 2000s for the evaluation of the major neck vessels after PNI. The reported results are very encouraging, and CT angiography has become an excellent initial investigation for suspected vascular injuries.28–30 Munera and coworkers28 in a prospective study of 60 patients with PNIs compared conventional angiography and helical CT angiography. The performance of CT angiography was very good, with a sensitivity of 90%, speciﬁcity 100%, positive predictive value (PPV) 100% and NPV 98%. In another study of 175 patients, Munera and associates29 reported excellent results with CT angiography and suggested that it is a valuable investigation for evaluation of suspected arterial injuries of the neck. The study may have some limitations owing to artifacts from metallic fragments or excessive air in the soft tissues.30 In these cases, conventional angiography may be necessary for accurate evaluation. A brain CT scan is indicated in patients with PNIs and unexplained central neurologic deﬁcits in order to evaluate for a possible anemic infarction secondary to a carotid artery injury or an associated direct brain injury due to a missile fragment.8

Esophageal Studies Esophageal studies are recommended in stable patients with suspicious clinical signs, such as painful swallowing, hemotemesis, or subcutaneous emphysema and in cases with a CT scan bullet trajectory toward the esophagus (Fig. 79–7). Contrast esophagography is the most commonly used study for the evaluation of the esophagus after PNIs. There has been some concern that esophagography may miss small esophageal injuries. In a retrospective review of 23 cervical esophageal injuries, Armstrong and colleagues31 reported that contrast esophagography diagnosed only 62% of perforations, compared with 100% with rigid esophagoscopy. This is not our experience and at our trauma center, where we have not seen any missed esophageal injuries by esophagography since 1995. The technique of esophagography is important in avoiding false-negative studies. The study is ﬁrst performed with a water-soluble contrast, such as Gastrograﬁn. If no leak is identiﬁed the study is repeated with thin barium. Gastrograﬁn alone may miss small injuries.32 Esophagoscopy, if performed by an experienced endoscopist, may be a useful investigation in the evaluation of the cervical esophagus. Flexible endoscopy has been shown to have an NPV of 100% but a PPV of up to

Figure 79–7 Esophageal studies are recommended in stable patients with suspicious clinical signs, such as painful swallowing, hemotemesis, or subcutaneous emphysema and in cases with a computed tomography (CT) scan showing bullet trajectory toward the esophagus. This patient has a signiﬁcant leak in the cervical esophagus.

33%.33,34 We reserve ﬂexible endoscopy only for patients who cannot undergo esophagogram because of a depressed level of consciousness or intraoperatively. Rigid esophagoscopy may be superior to ﬂexible endoscopy in the evaluation of the upper esophagus and is the investigation of choice of some authors after esophagography.35 However, rigid esophagoscopy can be performed only with the patient under general anesthesia, and many surgeons are not experienced with the technique. We reserve this procedure only for intraoperative evaluation of the esophagus.

Studies for Laryngotracheal Evaluation Indications for laryngotracheal evaluation include proximity injury with soft clinical signs suspicious of airway injuries (minor hemoptysis, hoarseness, subcutaneous emphysema) or CT scan ﬁndings showing a bullet track near the larynx or trachea.

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Flexible ﬁberoptic endoscopy is the investigation of choice, and it can be performed early in the emergency room. The most common abnormal ﬁndings are blood or edema in the laryngotracheal tract and vocal cord dyskinesia.1 However, only 20% of patients with abnormal ﬁndings require an operation.1,36

CONCLUSION There have been some signiﬁcant advances in the evaluation and management of PNIs. Selective nonoperative management of penetrating injuries, including transcervical GSWs, is an important advancement. The replacement of angiography with CFD or CT angiography is a major diagnostic advancement. The introduction of angiographic stenting in selected cases with carotid or subclavian artery injuries may revolutionize the management of these injuries and eliminate the need for complex surgery in many patients.

REFERENCES 1. Demetriades D, Theodorou D, Cornwell EE, et al. Evaluation of penetrating injuries of the neck: prospective study of 223 patients. World J Surg 1997;21:41–48. 2. Demetriades D, Velmahos GC, Asensio JA. Penetrating injuries of the neck. In Shoemaker W (ed): Textbook of Critical Care, 4th ed. Philadelphia: WB Saunders, 2000; pp 330–337. 3. Demetriades D, Theodorou D, Cornwell E, et al. Transcervical gunshot injuries: mandatory operation is not necessary. J Trauma 1995;40:758–760. 4. Shearer VE, Giesecke AH. Airway management for patients with penetrating neck trauma: a retrospective study. Anesth Analg 1993;77:1135–1138. 5. Vassiliu P, Baker J, Henderson S, et al. Aerodigestive injuries of the neck. Am Surg 2001;67:75–79. 6. Demetriades D, Asensio JA, Velmahos GC, Thal E. Complex problems in penetrating neck trauma. Surg Clin North Am 1996;76:661–683. 7. Gilroy D, Lakhoo M, Charalambides D, Demetriades D. Control of life-threatening hemorrhage from the neck: a new indication for balloon tamponade. Injury 1992;23: 557–559. 8. Demetriades D. Neck injury. In Mondavia DP, Newton EJ, Demetriades D (eds): Color Atlas of Emergency Trauma. Cambridge, England: Cambridge University Press, 2003; pp 59–81. 9. Demetriades D, Rabinowitz B, Soﬁanos C. Emergency room thoracotomy for stab wounds to the chest and neck. J Trauma 1987;27:483–485. 10. Meyer PR, Apple DF, Bohlman HH, et al. Symposium: management of fractures of the thoracolumbar spine. Contemp Orthop 1988;27:90. 11. Applebaum ID, Cantrill SV, Waldman N. Unstable cervical spine without spinal cord injury in penetrating neck trauma. Am J Emerg Med 2000;18:55–57.

12. Demetriades D, Charalambides D, Lakhoo M. Physical examination and selective conservative management in patients with penetrating injuries of the neck. Br J Surg 1993;80:1534–1536. 13. Sclafani SJ, Cavaliere G, Atnweh N, et al. The role of angiography in penetrating neck trauma. J Trauma 1991; 31:557–562. 14. Hiatt JR, Busuttil RW, Wilson SE. Impact of routine arteriography on management of penetrating neck injuries. J Vasc Surg 1984;1:860–866. 15. Weigelt JA, Thal ER, Snyder WH, et al. Diagnosis of penetrating cervical esophageal injuries. Am J Surg 1987; 154:619–622. 16. Eddy VA. Is routine arteriography mandatory for penetrating injury to zone I of the neck? Zone I Penetrating Neck Injury Study Group. J Trauma 2000;48:208–213. 17. Demetriades D, Theodorou D, Cornwell EE, et al. Penetrating injuries of the neck in patients in stable condition. Physical examination, angiography, or color ﬂow Doppler imaging. Arch Surg 1995;130:971–975. 18. Beitsch P, Weigelt JA, Flynn E, Easley S. Physical examination and arteriography in patients with penetrating zone II neck wounds. Arch Surg 1994;129:577–581. 19. Stain S, Yellin A, Weaver F, Pentecost M. Selective management of nonocclusive arterial injuries. Arch Surg 1989;124:1136–1140. 20. Frykberg ER, Crump JM, Vines FS, et al. A reassessment of the role of arteriography in penetrating proximity trauma: a prospective study. J Trauma 1989;29:1041– 1050. 21. Rao PM, Ivatury RR, Sharma P, et al. Cervical vascular injury: a trauma center experience. Surgery 1993;114: 527–531. 22. Fry WR, Dort JA, Smith RS, et al. Duplex scanning replaces arteriography and operative exploration in the diagnosis of potential cervical vascular injury. Am J Surg 1994;168:693–696. 23. Carr P, Abdoel CA, Robbs J. Colour-ﬂow ultrasound in the detection of penetrating vascular injuries of the neck. S Afr Med J 1999;899:644–646. 24. Montalvo BM, Leblang SD, Nunez DB, et al. Color Doppler sonography in penetrating injuries of the neck. AJNR Am J Neuroradiol 1996;17:943–951. 25. Ginzburg E, Montalvo B, Leblang S, et al. The use of duplex ultrasonography in penetrating neck trauma. Arch Surg 1996;131:691–693. 26. Kuzniec S, Kauffman P, Molnar LJ, et al. Diagnosis of limbs and neck arterial trauma using duplex ultrasonography. Cardiovasc Surg 1998;6:358–366. 27. Gracias V, Reilly P, Philpott J, et al. Computed tomography in the evaluation of penetrating neck trauma: a preliminary study. Arch Surg 2001;136:1231–1235. 28. Munera F, Soto JA, Palacio D, et al. Diagnosis of arterial injuries caused by penetrating trauma to the neck: comparison of helical CT angiography and conventional angiography. Radiology 2000;216:356–362. 29. Munera F, Soto JA, Palacio DM, et al. Penetrating neck injuries: helical CT angiography for initial evaluation. Radiology 2002;224:366–372. 30. Nunez DB, Torres-Leon M, Munera F. Vascular injuries of the neck and thoracic inlet: helical CT-angiographic correlation. Radiographic 2004;24:1087–1098.

79 MANAGEMENT OF PENETRATING NECK INJURY 31. Armstrong WB, Detar TR, Standley RB. Diagnosis and management of external penetrating cervical esophageal injuries. Ann Otol Rhinol Laryngol 1994;103:863–871. 32. Fan ST, Lau WY, Yip WC, et al. Limitations and dangers of Gastrograﬁn swallow after esophageal and upper gastric operations. Am J Surg 1988;153:495–497. 33. Srinivasan R, Haywood T, Horwitz B, et al. Role of ﬂexible endoscopy in the evaluation of possible esophageal trauma after penetrating injuries. Am J Gastroenterol 2000;95:1725–1729.

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34. Flowers JL, Graham SM, Ugarte MA, et al. Flexible endoscopy for the diagnosis of esophageal trauma. J Trauma 1996;40:261–265. 35. Weigelt JA, Thal ER, Snyder WH, et al. Diagnosis of penetrating cervical esophageal injuries. Am J Surg 1987; 154:619–622. 36. Demetriades D, Velmahos G, Asensio J. Cervical pharyngoesophageal and laryngotracheal injuries. World J Surg 2001;1044–1048.

Section XIII

PEDIATRIC SURGERY A. Alfred Chahine, MD Mishaps are like knives, that either serve us or cut us, as we grasp them by the blade or the handle.—James Russell Lowell

80

Malrotation, Volvulus, and Bowel Obstruction Philip C. Guzzetta, Jr., MD Malrotation and Volvulus INTRODUCTION Intestinal malrotation is the result of abnormal rotation of the intestinal tract and resultant abnormal ﬁxation of the intestine. The normal embryologic process of intestinal lengthening begins at approximately 5 weeks of gestation when the gastrointestinal (GI) tract is essentially a short straight tube with vascular supply from the superior mesenteric artery (SMA) and the superior mesenteric vein (SMV) (Fig. 80–1). As the GI tract rapidly lengthens over the next 7 weeks, the duodenum makes its C-loop conﬁguration posterior to the SMA, and the distal small bowel and cecum lengthen and reenter the abdomen anterior to the SMA, after a short time within the umbilical stalk, at about the 10th week of gestation. The cecum enters in the left upper quadrant and then rotates 270° counterclockwise to reach its ﬁnal destination in the right lower quadrant. Once the rotation is completed, the intestine should be ﬁxed in an inverted N arrangement with the ascending colon attached to the right retroperitoneal area, the small intestinal mesentery ﬁxed at the terminal ileum in the right lower quadrant to the ligament of Treitz in

the left upper quadrant, and ﬁnally, the descending colon attached to the left retroperitoneal area (Fig. 80–2). When this normal rotation and ﬁxation do not occur, the cecum typically remains in the midabdomen or left upper quadrant, attempted cecal ﬁxation results in band formation across the ﬁrst and second portion of the duodenum (Ladd’s bands), and the entire midgut is attached by only a narrow band of tissue around the SMA, predisposing it to twisting (midgut volvulus) (Fig. 80–3). Certain patients, such as children with congenital heart disease and heterotaxia syndrome, are at increased risk for intestinal malrotation.1 Other children with “nonrotation” of the intestine are those with congenital diaphragmatic hernia, gastroschisis, and omphalocele. However, these children rarely need operative intervention for the nonrotation because they are rarely symptomatic and volvulus almost never occurs in them. It must be emphasized that, although the previous description of intestinal malrotation is the most common type, variations of the anomaly occur. Some patients with radiographic ﬁndings of malrotation may have normal ﬁxation and little risk of volvulus, whereas ileal volvulus can occur with normal rotation, although that is rare.2 The classic clinical presentation of a child with intestinal malrotation is one with bilious vomiting. If the child also has midgut volvulus, hematemesis, hematochezia, and peritonitis may be present as late signs, but within the

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SECTION XIII: PEDIATRIC SURGERY

Ao.

0°

Duodenumjejunum S.M.A.

Figure 80–1 Schematic ventrolateral view of a 5-mm embryo. (Reprinted with permission from Smith SD. Disorders of intestinal rotation and ﬁxation. In Grosfeld JL, O’Neill JA, Fonkalsrud EW, Coran AG (eds): Pediatric Surgery, 6th ed. Philadelphia: Mosby Elsevier, 2006; p 1343.)

Figure 80–2 Normal ﬁxation of the midgut, shaped as an inverted N that prevents midgut volvulus. (Reprinted with permission from Smith SD. Disorders of intestinal rotation and ﬁxation. In Grosfeld JL, O’Neill JA, Fonkalsrud EW, Coran AG (eds): Pediatric Surgery, 6th ed. Philadelphia: Mosby Elsevier, 2006; p 1346.)

A

B

C

ﬁrst hours of midgut volvulus, the abdominal examination may be deceptively benign. Approximately 60% of patients with intestinal malrotation present in the ﬁrst week of life, 80% in the ﬁrst month of life, and 90% in the ﬁrst year of life, but the patient may be asymptomatic until adulthood.3

Figure 80–3 Pathophysiology of midgut volvulus with malrotation. The narrow mesenteric attachment in nonrotation (A) or incomplete rotation (B) predisposes the patient to midgut volvulus (C). (A–C, Reprinted with permission from Smith SD. Disorders of intestinal rotation and ﬁxation. In Grosfeld JL, O’Neill JA, Fonkalsrud EW, Coran AG (eds): Pediatric Surgery, 6th ed. Philadelphia: Mosby Elsevier, 2006; p 1347.)

The diagnosis of intestinal malrotation is best made by emergent upper gastrointestinal (UGI) study when the diagnosis is considered. A normal examination, thus ruling out malrotation, requires that the fourth portion of the duodenum crosses the midline to the left of the vertebra and ascends to the level of the greater curvature of the

80 MALROTATION, VOLVULUS, AND BOWEL OBSTRUCTION Step 2

Step 3

Step 4

Step 5

821

If there is volvulus, it is untwisted ﬁrst, in counterclockwise direction, and viability of intestine is conﬁrmed. Ladd’s bands are excised to free duodenum; if duodenum is “accordionated” by bands, duodenum should be straightened. Anterior peritoneum of small intestinal mesentery should be scored, taking care to avoid injuring vessels and not going completely through mesentery. This allows base of mesentery to be widened by placing proximal small bowel into right lower quadrant and cecum and rest of colon into left lower quadrant. No suture ﬁxation of these newly positioned intestinal segments is done. Most pediatric surgeons remove the appendix prior to placing cecum into left lower quadrant, because future diagnosis of appendicitis would be difﬁcult, although Ladd originally described procedure without appendectomy.4

COMPLICATIONS OF THE OPERATIVE PROCEDURE Delay in Diagnosis with Intestinal Ischemia

Figure 80–4 Lateral view of an upper gastrointestinal study shows intestinal malrotation with midgut volvulus. Note the “corkscrew” appearance of the contrast in the duodenum.

stomach. Volvulus may be diagnosed by UGI if the contrast forms a sharp “beak” at the third portion of the duodenum without contrast passing distally, or rarely, a corkscrew appearance of the contrast is seen at the duodenal-jejunal junction4 (Fig. 80–4). Malrotation may also be diagnosed by abdominal ultrasound or computed tomography (CT) scan with intravenous contrast because of an abnormal relationship between the SMA and the SMV. However, UGI remains the most commonly used examination.

INDICATIONS In the symptomatic patient with malrotation, urgent operation to correct the condition is indicated. In asymptomatic patients with malrotation, elective operation to prevent midgut volvulus is also indicated.

OPERATIVE STEPS (THE LADD PROCEDURE) (FIG. 80–5) Step 1

Procedure may laparoscopically.

be

done

open

or

● Consequence The greatest risk with intestinal malrotation is that the diagnosis will be delayed, resulting in volvulus and ischemia of some or all of the midgut, a catastrophic result of a correctable condition. Grade 4/5 complication ● Repair If there is obvious ischemia of the midgut at exploration, but no perforation of the intestine, most surgeons would untwist the volvulus, release Ladd’s bands, and loosely close the abdomen with a plan to reassess the intestine with a second-look laparotomy within 24 hours. At the second procedure, all frankly necrotic intestines should be resected and, depending upon the overall condition of the child and the appearance of the “viable” intestine, a primary anastomosis or enterostomies created. Development of short gut syndrome and all its sequelae commonly results in a full-term infant with less than 40 cm of small intestine, particularly if the viable intestine is predominantly jejunum without an ileocecal valve, and 25 cm with an intact ileocecal valve. ● Prevention Any child with bilious emesis unexplained by another condition, especially in the ﬁrst month of life, must have an urgent UGI to rule out intestinal malrotation.

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A

B

E C

D Figure 80–5 Operative correction of intestinal malrotation with midgut volvulus. A, The appearance of the viscera upon entering the abdomen. B, The intestinal mass is delivered out of the wound and pulled downward. C, The volvulus is corrected by untwisting the midgut in a counterclockwise direction. D, Ladd’s bands are lysed. E, The mesentery is widened, and the intestine is returned to the abdomen with the duodenum straightened and coming down the right side, and the cecum (after appendectomy) is placed into the left lower quadrant. (A–E, Reprinted with permission from Smith SD. Disorders of intestinal rotation and ﬁxation. In Grosfeld JL, O’Neill JA, Fonkalsrud EW, Coran AG (eds): Pediatric Surgery, 6th ed. Philadelphia: Mosby Elsevier, 2006; p 1355.)

● Repair Same as for “Delay in Diagnosis with Intestinal Ischemia,” earlier.

Recurrent Volvulus ● Consequence Intestinal infarction and possible syndrome. Grade 3/4/5 complication

short

bowel

● Prevention If the Ladd procedure is done properly and all the preduodenal and intermesenteric bands are taken down

80 MALROTATION, VOLVULUS, AND BOWEL OBSTRUCTION and the mesentery widened, the incidence of recurrent volvulus is less than 5%. Fixation of the intestine with sutures does not decrease this risk, but this may slightly increase the risk of small intestinal obstruction.5

Small Intestinal Obstruction Because an important part of the Ladd procedure is to widen the mesentery and encourage adhesion formation to this area to prevent volvulus, it is no surprise that future intestinal obstruction may occur in 5% to 10% of patients. Small intestinal dysmotility symptoms may persist after the Ladd procedure, especially when the procedure is done in children older than 1 year of age who have had chronic symptoms (>2 mo) preoperatively.6 ● Consequence Intestinal ischemia and perforation. Grade 2/3/4 complication ● Repair Standard nonoperative and potentially operative management of small intestinal obstruction. ● Prevention Avoiding placing sutures to ﬁx the intestines.

823

obstruction have had the condition diagnosed by fetal ultrasound and/or fetal magnetic resonance imaging. For example, the baby with duodenal atresia is usually identiﬁed prenatally because of fetal ultrasound done in a mother with polyhydramnios. If the intestinal obstruction was not determined prenatally, the baby is usually diagnosed within the ﬁrst day of life because of abdominal distention, bilious vomiting, and/or failure to pass meconium stool. When intestinal obstruction is suspected in a neonate, the ﬁrst diagnostic test should be plain x-ray ﬁlms of the abdomen as kidney, ureter, and bladder (KUB) and lateral decubitus views. Air is an excellent contrast agent, and often, the probable cause of the obstruction may be determined by plain ﬁlms alone. When the obstruction is due to atresia in the duodenum or proximal jejunum, the proximal bowel is very dilated and there is no gas distally. If gas is in the distal bowel with duodenal and gastric distention, there may be duodenal stenosis or malrotation with midgut volvulus. Distal intestinal atresia is characterized by plain x-rays showing diffuse dilated intestinal loops (Fig. 80–6) and must be evaluated by contrast enema to determine the cause of the distal obstruction. Other causes of congenital bowel obstruction include malrotation, prenatal intestinal perforation, meconium ileus, congenital intra-abdominal bands

Injury of the Mesentery During the division of the intermesenteric Ladd bands, the mesenteric vessels can be damaged. ● Consequence Bleeding and intestinal ischemia. Grade 2/3/4 complication ● Repair Repair of the mesenteric arteries could be attempted if the child is of appropriate size. ● Prevention The anterior peritoneum of the small intestinal mesentery should be scored, taking care to avoid injuring the vessels and not going completely through the mesentery.

Bowel Obstruction INTRODUCTION Intestinal obstruction in children is either congenital or acquired, and the evaluation and treatment depend greatly upon which of these etiologies is the cause of the obstruction. If the obstruction is acquired, management is dictated by whether the child has previously had an abdominal operation and, if so, what that operation was.

Congenital Bowel Obstruction With many of the pregnancies in the United States being monitored by ultrasound, many neonates with intestinal

Figure 80–6 Plain abdominal x-ray of a newborn with distal obstruction shows multiple diffuse dilated intestinal loops.

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(most often mesodiverticular bands), meconium plug syndrome, Hirschsprung’s disease, and imperforate anus. Treatment for all neonatal bowel obstruction is operative, with the exception of meconium plug syndrome and meconium ileus, which may be successfully treated with contrast enemas. The operative procedure obviously depends upon the cause of the obstruction, but atresia is repaired primarily with either tapering or partial resection of the dilated proximal intestine. Because multiple atresias occur in 15% of patients, a potential complication is to miss a distal atresia that has no mesenteric defect (type I atresia), which would lead to continued obstruction postoperatively. Congenital bands are treated by operative lysis of the bands.

Acquired intestinal obstruction can be due to infectious or mechanical causes.

In children between the ages of 6 months and 3 years, a common cause of intestinal obstruction is intussusception. Likely, the hypertrophic Peyer patches that act as the lead point in intussusception are caused by a viral gastroenteritis, which is why the children frequently have a several-day history of diarrhea with or without vomiting as a prodrome to the triad of symptoms of intussusception: (1) intermittent crampy abdominal pain, (2) bilious vomiting, and (3) bloody stools. An obstructive gas pattern in a child of the proper age is enough to warrant a contrast or air enema even if not all of the triad of symptoms of intussusception are present. Another cause of obstruction in children older than 3 years is perforated appendicitis. One should be alert to that possibility because the diagnostic evaluation is either ultrasound or abdominal CT when appendicitis is considered likely rather than proceeding with air or contrast enema, which would be indicated if intussusception was suspected.

Infectious Bowel Obstruction

Recurrent Obstruction

In the neonate, a common cause of abdominal distention and an obstructive gas pattern on plain x-rays is generalized sepsis. Another common cause in the premature neonate is necrotizing enterocolitis (NEC); frequently, it is difﬁcult to differentiate between sepsis without NEC and sepsis due to NEC unless pneumatosis intestinalis (Fig. 80–7) or free intraperitoneal is present on plain abdominal x-rays, implying that the cause of the obstruction is NEC. In patients with NEC successfully treated medically, approximately 15% will develop a stricture 3 to 6 weeks after the onset of the NEC,7 which presents as feeding intolerance and an obstructive gas pattern on plain x-rays. Although most patients with NEC have the disease primarily in the ileum, most post-NEC strictures occur in the colon.

● Consequence Intussusception has a 5% to 10% incidence of recurrence. Any disease that requires either an open or a laparoscopic procedure carries some risk of mechanical intestinal obstruction in the future, as is discussed next. Grade 3/4 complication

Acquired Bowel Obstruction

Figure 80–7 Cross-table left lateral decubitus plain abdominal x-ray shows pneumatosis intestinalis in a premature infant with necrotizing enterocolitis (NEC).

Mechanical Bowel Obstruction The most common cause of mechanical intestinal obstruction in children, as in adults, is adhesions secondary to previous abdominal surgery. There is some hope that minimally invasive procedures will induce fewer adhesions than their open counterparts, but that has not been conclusively determined. Two procedures that traditionally have fairly high incidences of intestinal obstruction after an open procedure are the Ladd procedure for intestinal malrotation, as discussed previously, and Nissen fundoplication for gastroesophageal reﬂux. Intestinal obstruction after a Nissen fundoplication can be devastating because many of those procedures are done in neurologically impaired children who cannot communicate early symptoms of obstruction to the parents and an intact fundoplication prevents them from vomiting. This “closed on both ends” arrangement can rapidly lead to closed loop obstruction, intestinal ischemia, and patient death. Another cause of mechanical intestinal obstruction is congenital bands, mentioned under “Congenital Bowel Obstruction,” earlier, but that is a rare condition. If a child with previous abdominal surgery presents with vomiting (especially if the emesis is bilious) and no stool output and has air ﬂuid levels on plain x-ray, the child should undergo prompt volume resuscitation and abdominal exploration because the risk of intestinal ischemia is

80 MALROTATION, VOLVULUS, AND BOWEL OBSTRUCTION high, particularly after a fundoplication. As laparoscopic techniques have improved, minimally invasive lysis of adhesions is being performed more frequently, but massive intestinal distention proximal to an obstruction continues to limit routine use of this technique in advanced mechanical bowel obstruction.

Recurrent Intestinal Obstruction due to Adhesions ● Consequence Depending upon the extensiveness of the previous lysis of adhesions, there is about a 15% lifetime incidence of recurrent obstruction owing to adhesions. Grade 3 complication

Intestinal Ischemia and Intestinal Resection ● Consequence As mentioned previously, patients after open fundoplication are at risk for this complication, but in anyone, intestinal strangulation beneath an adhesive band may lead to loss of a signiﬁcant length of intestine, resulting in short bowel syndrome. When recognition of intestinal ischemia is delayed, sepsis and death may result. Grade 4/5 complication

825

REFERENCES 1. Choi M, Borenstein SH, Hornberger L, Langer JC. Heterotaxia syndrome: the role of screening for intestinal rotation abnormalities. Arch Dis Child 2005;90:813– 815. 2. Kitano Y, Hashizume K, Ohkura M. Segmental smallbowel volvulus not associated with malrotation in childhood. Pediatr Surg Int 1995;19:335–338. 3. Ford EG, Senac MO, Srikanth MS, Weitzman JJ. Malrotation of the intestine in children. Ann Surg 1992;215:172– 178. 4. Ladd WE. Surgical diseases of the alimentary tract in infants. N Engl J Med 1936;215:705–708. 5. Stauffer UG, Herrmann P. Comparison of late results in patients with corrected intestinal malrotation with and without ﬁxation of the mesentery. J Pediatr Surg 1980;15: 9–12. 6. Coombs RC, Buick RG, Gornall PG, et al. Intestinal malrotation: the role of small intestinal dysmotility in the cause of persistent symptoms. J Pediatr Surg 1991;26:553– 556. 7. Horowitz JR, Lally KP, Cheu HW, et al. Complications after surgical intervention for necrotizing enterocolitis: a multicenter review. J Pediatr Surg 1995;30:994– 999.

81

Imperforate Anus and Hirschsprung’s Disease A. Alfred Chahine, MD Imperforate Anus and Anorectal Malformations INTRODUCTION Anorectal malformations (ARMs) are a complex set of anomalies involving the development of the anorectal region. They manifest themselves along a spectrum from the simple membrane covering a well-formed anorectal canal to the cloaca and other complex defects that present a considerable challenge for reconstruction. The etiology of ARMs is unknown. The reported incidence is about 1 in 5000 live births, with a slight male preponderance.1 Associated anomalies are common, occurring in about 50% or 60% of the patients.2 They include cardiovascular, genitourinary, gastrointestinal, gynecologic, spinal, and vertebral anomalies. They have been associated with other syndromes and have been described to occur in families.3,4

CLASSIFICATION There are multiple historical classiﬁcation schemes but the most widely used system is currently that proposed by Peña5,6 (Table 81–1). The scheme is based on a description of the anatomy and the presence or absence of a ﬁstula from the rectum to the urinary system. It is different for males and females and has prognostic and therapeutic implications. Most defects with a perineal ﬁstula are considered “low” and are usually amenable to primary repair in the newborn period if the baby is stable and has no other underlying major issues. If no perineal ﬁstula is detected, it usually indicates a “high” defect that is best managed with a colostomy ﬁrst followed by repair.

CLINICAL PRESENTATION AND PREOPERATIVE PREPARATION Some ARMs are suspected prenatally because of the presence of polyhydramnios and dilated echogenic intestinal loops on a fetal ultrasound. The majority are detected at birth. A careful physical examination including the anorectal and genitourinary systems is essential to classify the defect and guide the next step in management. Perineal ﬁstulas are sometimes subepithelial in the midline raphe of the scrotum or perineal body and not always evident initially. In addition, because meconium is viscous, it takes a signiﬁcant pressure within the rectum to force the meconium through the small diameter of the ﬁstula.7 That pressure usually builds up in the ﬁrst 24 hours after birth. Therefore, unless the newborn is massively distended and at risk for perforation, there should be a systematic search for the ﬁstula in the ﬁrst 24 hours after birth. A small gauze should be placed at the tip of the urethra to collect any meconium in the urine. The perineal body should be inspected again a few hours after birth to detect any subepithelial accumulation of meconium. Concurrently, a search for associated anomalies should be undertaken with an echocardiogram to rule out cardiac defects, a renal ultrasound to rule out hydronephrosis, vertebral radiographs to detect spinal defects, and a spinal ultrasound to rule out a tethered cord. In addition, esophageal atresia should be ruled out. Just like with any other intestinal obstruction, intravenous hydration and nasogastric decompression should be initiated. Antibiotics are necessary to prevent contamination of the urinary tract by a rectourinary ﬁstula.

INDICATIONS The mere presence of an ARM is an indication to repair it.

CHOICE OF OPERATION The three operations available to the surgeon in the newborn period are (1) a primary anoplasty, also called a

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Figure 81–1 A male newborn with a perineal ﬁstula behind a “bucket-handle” skin deformity. (Courtesy of Dr. Richard Ricketts, Emory University, Atlanta.) Table 81–1

Classiﬁcation of Anorectal Malformations

Males

Females

Perineal ﬁstula

Perineal ﬁstula

Rectourethral ﬁstula

Vestibular ﬁstula

Rectovesical ﬁstula

Persistent cloaca

No ﬁstula

No ﬁstula

Rectal atresia

Rectal atresia

Complex defects

Complex defects

Modiﬁed from Peña A. Anorectal malformations. Semin Pediatr Surg 1995;4:35–47.

limited posterior sagittal anorectoplasty; (2) a deﬁnitive repair of the ARM with a pull through of the rectum, called posterior sagittal anorectoplasty (PSARP); and (3) a protective colostomy. The decision of which operation to perform depends on the sex of the patient and the complexity of the defect.7 Laparoscopic techniques have been reported in the management of high ARMs.8–10 The principles are the same as for PSARP with laparoscopic mobilization of the rectum and division of the ﬁstula. The short-term results seem to be equivalent to those of PSARP, but long-term results are not yet mature enough to allow an evidence-based comparison with PSARP.11,12

Male Patients A male newborn with a perineal ﬁstula and no other serious anomalies and no prematurity is a good candidate to have a primary anoplasty without a protective colostomy (Fig. 81–1). If a perineal ﬁstula is not detected, a cross-table lateral radiograph with the patient in the prone position is obtained to determine the level of the rectum. If the rectum is above the coccyx, it is best to perform a protective colostomy followed by an elective repair. If the rectum ends below the coccyx, a primary PSARP could

Figure 81–2 A female newborn with a rectovestibular ﬁstula. The clamp is in the ﬁstula. (Courtesy of Dr. Richard Ricketts, Emory University, Atlanta.)

be contemplated if the patient is stable without any other associated problems and if the surgeon is experienced. Otherwise, it is always safest to perform a colostomy in the newborn period, then do the deﬁnitive PSARP later. The repair of high ARMs in the newborn period without a protective colostomy has been reported but should be limited to surgeons with extensive experience.13

Female Patients Just like for males, a female newborn with a perineal ﬁstula and no other issues is a good candidate for a primary anoplasty. If a vestibular ﬁstula is present, a colostomy followed by deﬁnitive repair is recommended even though there is a recent trend of performing primary PSARP in these situations, depending on the surgeon’s experience level (Fig. 81–2). If the baby has only one perineal opening visible and no separate opening for the vagina and urethra, that patient has a cloaca and a colostomy should be performed (Fig. 81–3). A detailed evaluation of the urinary and gynecologic systems should be performed to rule out severe hydronephrosis and hydrometrocolpos caused by obstruction secondary to the small size of the common channel. If the baby has separate openings for the urethra and vagina and no perineal ﬁstula, a cross-table lateral radiograph with the patient in the prone position is

81 IMPERFORATE ANUS AND HIRSCHSPRUNG’S DISEASE

Figure 81–3 A female newborn with a cloaca. Note the small external genitalia. (Courtesy of Dr. Richard Ricketts, Emory University, Atlanta.)

obtained to determine the level of the rectum. The same algorithm as in males, as discussed earlier, would apply.

OPERATIONS Because of the wide spectrum of ARMs, the actual operation has to be tailored to the speciﬁc defect and associated anomalies. Therefore, we discuss only the pitfalls of the three most common operations performed for ARMs.

ANOPLASTY Step 1 Step 2 Step Step Step Step

3 4 5 6

Step 7

OR

829

Figure 81–4 Stimulation of the sphincter muscles with a ﬁnetip electrical nerve stimulator is essential to divide the muscles in the midline and allow for symmetrical reconstruction. (Courtesy of Dr. Phillip Guzzetta, Children’s National Medical Center, Washington, DC.)

● Prevention Prior to making the incision, the actual boundaries of the sphincter should be delineated with electrical stimulation (Fig. 81–4). The incision should be made in the middle of the delineated area, and division of the muscle should be guided by intraoperative stimulation of the muscle.

LIMITED PSARP

Patient is placed in prone jackknife position Multiple ﬁne sutures are placed around ﬁstula at mucocutaneous junction Sphincter is divided in midline Rectum is dissected circumferentially Rectum is positioned in middle of sphincter Rectum is attached to skin with multiple sutures Perineal body is reconstructed

The Sphincter Is Divided in the Midline Asymmetrical Division of the Sphincter ● Consequence If the muscles are not divided in the midline during the dissection, the rectum is not surrounded by symmetrical amounts of muscle in its new position. This might lead to either incontinence because of ineffective contractions or constipation because of abnormal angulation of the rectum. Grade 2/3 complication ● Repair A reoperation via a posterior sagittal approach is required to reposition the rectum in the middle of the muscles.14,15

The Rectum Is Dissected Circumferentially Injury to the Urethra or the Vagina ● Consequence Some anterior perineal ﬁstulas will have very intimate contact with the urethra in males and the vagina in females and even share a common wall with them. During the course of the dissection of the rectum, an injury can occur to either the urethra or the vagina. Grade 2/3 complication ● Repair If detected intraoperatively, primary repair of the defect is undertaken with ﬁne absorbable sutures and the perineal body is reconstructed to completely cover the repair and separate it completely from the rectum. If not detected at the time of the operation, the patient will present with a rectourethral or rectovaginal ﬁstula. This will need to be repaired via a reoperation. ● Prevention Placing a catheter in the urethra of a male (or the vagina of a female) helps in its identiﬁcation during the dissection of the rectum. Meticulous dissection along the anterior wall of the rectum will avoid an injury to the intimately attached urethra or vagina.

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SECTION XIII: PEDIATRIC SURGERY

The Perineal Body Is Reconstructed Mucosal Prolapse ● Consequence After the anoplasty, the mucosa can prolapse into the perineum, causing local irritation and staining of the underwear owing to excess mucus secretion. Sometimes, it interferes with anal sensation.16,17 Grade 1–3 complication ● Repair If minor, the prolapse does not need to be repaired. If signiﬁcant, a local operation to trim the excess mucosa is performed. ● Prevention During the anoplasty, the rectum should be under slight tension so that, at the end of the operation, no mucosa is visible.16

Dehiscence ● Consequence After an anoplasty, a dehiscence of the repair can be superﬁcial or deep. A superﬁcial breakdown is usually secondary to infection. A deep dehiscence is a breakdown of the entire rectal repair, usually secondary to excessive tension or ischemia. Dehiscence can lead to strictures of the neorectum or acquired atresia in the case of a complete breakdown.17,18 Grade 2–4 complication ● Repair A superﬁcial dehiscence can be treated with local wound care and allowed to heal by secondary intention. Strictures could be dilated. Acquired atresia will need to be reoperated on. ● Prevention Complete mobilization of the rectum off the perineal body, urethra, and/or vagina is essential to avoid tension on the repair. The rectum depends on its intramural blood supply for survival; therefore, the integrity of the rectal wall has to be preserved as much as possible during the dissection. By not grabbing the actual rectum and rather using the ﬁne sutures placed at the mucocutaneous junction to achieve uniform traction on the rectum can achieve this. In addition, the blood supply of the rectum has to be preserved at the time of the colostomy formation, if a colostomy was created previously.

Strictures ● Consequence Strictures can develop after an anorectoplasty from ischemia, tension, or pressure from the surrounding muscles. They usually lead to a partial intestinal obstruction. Grade 3/4 complication

● Repair Mild strictures might respond to dilations. Severe ones will need to be addressed operatively. ● Prevention The rectum should be completely dissected from all surrounding structures including the vagina or the urinary tract to minimize tension on it. Avoiding injury to the rectal wall during the mobilization should preserve the intramural rectal blood supply. Placing multiple ﬁne sutures at the tip of the rectum to achieve uniform traction on it rather than grabbing the wall and damaging it can achieve this. Finally, a rigorous regimen of daily sequential dilation should be taught to the parents to counteract the natural pressure of the sphincter muscles on the neorectum.18

COLOSTOMY Step Step Step Step Step Step

1 2 3 4 5 6

Left lower quadrant incision Identifying sigmoid colon Mobilizing sigmoid colon Dividing colon Maturing colostomy and mucous ﬁstula Irrigation of mucous ﬁstula

Dividing the Colon Prolapse ● Consequence If minor, the prolapse can be managed nonoperatively. But if it is severe, the colostomy will need to be revised. Grade 1–3 complication ● Repair The colostomy needs to be taken down and rematured. ● Prevention Prolapse can be essentially avoided if the colon is divided at a spot just distal to the junction of the descending and sigmoid colon as the sigmoid colon becomes mobile from the retroperitoneal attachments of the descending colon.19 In addition, the colostomy has to be carefully matured to the edges of the fascia circumferentially.

Maturing the Colostomy and the Mucous Fistula Ischemia ● Consequence Because the rectum mobilized during the anorectoplasty depends on its intramural blood supply, the cephalad rectal blood supply has to be preserved while constructing the colostomy. Otherwise, the rectum

81 IMPERFORATE ANUS AND HIRSCHSPRUNG’S DISEASE is susceptible to ischemia and necrosis, leading to strictures and dehiscence.17,18 Grade 2–4 complication

mucous ﬁstula will allow the colostomy appliance to be placed over the colostomy only, leaving the mucous ﬁstula out of the fecal stream altogether.

● Repair Ischemic strictures require dilations. A dehiscence of the rectum will require a reoperation and mobilization of the descending colon.

PSARP

● Prevention During the construction of the colostomy, care has to be taken to avoid dividing the arcade supplying the distal sigmoid colon. The dissection has to remain close to the wall of the sigmoid colon to avoid injuring the blood supply.

Step Step Step Step

Irrigation of the Mucous Fistula Dilatation of the Rectum ● Consequence If the rectum becomes very dilated prior to the actual anorectoplasty, it will be difﬁcult for it to ﬁt in the middle of the levator and sphincter muscles and will need to be tapered. In addition, a megarectum will exacerbate the constipation that patients with ARMs are prone to. Grade 2–4 complication ● Repair The rectum will need to be tapered at a separate operation. ● Prevention Thoroughly irrigating the mucous ﬁstula during the colostomy construction will allow the rectum to remain decompressed until the anorectoplasty. In addition, choosing to construct the colostomy at the sigmoid level rather than at the transverse colon will make it easier to decompress the rectum through the mucous ﬁstula.

Urinary Tract Contamination ● Consequence If there is a rectourinary ﬁstula, the urinary tract can be contaminated by the fecal stream, putting the patient at risk for urinary tract infections. Grade 1–3 complication ● Repair If there is persistent contamination of the urinary tract, the patient might require an earlier anorectoplasty or a revision of the colostomy. ● Prevention A divided colostomy provides the best protection against spillage of fecal contents into the distal rectum. In addition, creating a signiﬁcant bridge of skin and subcutaneous tissues between the colostomy and the

831

Step 1 Step 2 3 4 5 6

Step 7 Step 8

Patient is placed in prone jackknife position Sphincter and levator muscles are divided in midline Rectum is dissected circumferentially Rectum is divided in midline Rectum and ﬁstula are separated Rectum is positioned in middle of sphincter and levator muscles Rectum is attached to skin with multiple sutures Perineal body is reconstructed

The same pitfalls discussed under the limited PSARP, earlier, apply to a full PSARP. In addition, there are speciﬁc problems to avoid.

The Rectum and the Fistula Are Separated Urethral Diverticulum ● Consequence If the ﬁstula is divided too far from the urethra, leaving a remnant of rectum, a urethral diverticulum will develop, leading to repeated urinary tract infections, orchidoepididymitis, urinary pseudoincontinence, and even rectal adenocarcinoma developing 30 years after repair.17,18 Grade 1–4 complication ● Repair The diverticulum will need to be repaired at a separate operation. ● Prevention The ﬁstula should be divided and closed with absorbable sutures as close as possible to the urethra without narrowing it.

Inability to Find the Rectum ● Consequence If the rectum is really high as in the case of a rectovesical ﬁstula, it would be unlikely to be reached from a posterior sagittal approach. Persistent dissection to try to ﬁnd the rectum could result in injury to the seminal vesicles, urethra, or intestines.17,20 Grade 2–4 complication ● Repair A laparotomy will be required to locate the rectum in the abdomen. ● Prevention Prior to anorectoplasty, the anatomy of the rectum should be delineated by obtaining a colostogram

832

SECTION XIII: PEDIATRIC SURGERY

Figure 81–5 A colostogram through the mucous ﬁstula delineates the position of the rectal tip. In this patient, a rectovesical ﬁstula is discovered. This should prompt planning of an abdominal approach in combination with the sacral approach for the anorectoplasty. The metallic pellet is placed at the skin level where the anal dimple is. (Courtesy of Dr. Clifton Leftridge, Georgetown University Medical Center, Washington, DC.)

through the mucous ﬁstula to help locate the rectal end. If a rectovesical ﬁstula is present (Fig. 81–5), an abdominal approach to locate the rectum and divide the ﬁstula should be planned and combined with a posterior sagittal sacral approach for the anorectoplasty.

Hirschsprung’s Disease INTRODUCTION Hirschsprung’s disease (HD) is caused by the congenital absence of ganglion cells in the myenteric and submucosal plexuses of the intestines. Its incidence varies from 1 in 4400 to 1 in 700 live births.21,22 The aganglionosis usually starts just proximal to the dentate line and extends in continuity to the transition line, which is usually in the rectosigmoid colon. There is a 4 : 1 male-to-female preponderance, except for long-segment HD in which the ratio is reversed.23

Figure 81–6 A barium enema in a newborn with intestinal obstruction shows the classic reversal of the R/S (rectum-tosigmoid) ratio: The sigmoid colon is larger than the rectum, and the transition zone is at the level of the rectosigmoid junction. (Courtesy of Dr. Clifton Leftridge, Georgetown University Medical Center, Washington, DC.)

CLINICAL PRESENTATION AND PREOPERATIVE PREPARATION The classic presentation is that of a newborn with intestinal obstruction: feeding intolerance, abdominal distention, failure to pass meconium spontaneously, and evidence of a low intestinal obstruction on abdominal radiographs. The diagnosis is initially suspected by a barium enema, which reveals the characteristic transition zone with reversal of the rectum-to-sigmoid (R/S) ratio: The rectum should always be larger than the sigmoid. If aganglionic, the rectum will not distend and will be smaller than the sigmoid (Fig. 81–6). The diagnosis is conﬁrmed with a suction biopsy of the mucosa and submucosa, which shows the aganglionosis and compensatory neuronal hypertrophy in Meissner’s plexus. The initial treatment is decompression with rectal washouts performed at the bedside. If the washouts are successful in decompressing the obstruction, an elective repair is contemplated. If the transition zone is higher than can be reached by the washouts, the decompression is going to be unsuccessful and the patient will require a formal leveling colostomy, in which intraoperative biopsies are serially obtained to determine the level of ganglionosis. A divided colostomy is then constructed at that level.

81 IMPERFORATE ANUS AND HIRSCHSPRUNG’S DISEASE

INDICATION The presence of HD is an indication to repair it.

OPERATION There are three classic operations to repair HD.23 They all utilize the same principles: resecting the aganglionic intestines, resecting or bypassing the rectum, maintaining continence by preserving the internal sphincter, which is also aganglionic in HD patients. The Swenson operation resects the aganglionic intestines and rectum almost all the way to the dentate line. The ganglionic intestine is then anastomosed to the anus just proximal to the dentate line. The Soave-Boley operation is an endorectal pullthrough of the ganglionic bowel. The aganglionic intestine is resected to the level of the rectum below the peritoneal reﬂection. A submucosal dissection from both the pelvic side and the anal side removes the rectal mucosa and creates a muscular cuff. The ganglionic intestine is then pulled through the cuff, and the anastomosis is created just proximal to the anorectal verge. The Duhamel operation leaves the rectal stump intact after the resection of the aganglionic intestines. A retrorectal space is created for the ganglionic intestine. An incision is made in the posterior rectal wall just proximal to the dentate line, and an anastomosis is created between the rectum and the ganglionic intestine. All the operations just discussed have been performed laparoscopically with good results.24–30 In addition, a transanal approach to the pull-through has emerged and has probably become the most commonly performed procedure for HD today.31–37 Therefore, we limit the discussion of the operation and its pitfalls to this procedure, even though all the other available operations are safe and effective.

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5

Step 6 Step 7 Step 8

Patient is placed in lithotomy position Anal verge is retracted circumferentially with either sutures or retractors Mucosa is incised circumferentially a few millimeters proximal to dentate line Submucosal dissection proceeds, leaving muscular cuff At peritoneal reﬂection, rectal cuff is divided circumferentially to transition from submucosal to full-thickness dissection Cuff is divided in midline posteriorly Mesentery of rectum and colon is divided sequentially Full-thickness biopsies are obtained at various levels to determine level of ganglionosis on frozen sections.

833

Once level is found, aganglionic bowel is resected and ganglionic segment is pulled through cuff Step 10 Ganglionic intestine is anastomosed in fullthickness fashion to anorectal verge Step 11 Laparoscopy can be performed to help with mobilization of proximal colon and to obtain level of ganglionosis prior to transanal dissection Step 9

A Submucosal Dissection Proceeds, Leaving a Muscular Cuff Injury to the Nervi Erigentes ● Consequence While mobilizing the rectum, the nervi erigentes can be injured, creating sexual dysfunction, including impotence and absence of ejaculation,38 and constipation.39 Grade 4 complication ● Repair The nervi erigentes cannot be repaired. ● Prevention Keeping the dissection very close to the muscle of the rectum and pushing the mesorectal tissues away gently with minimal force, as originally advocated by Swenson and associates, will preserve the nervi erigentes.40–42

The Aganglionic Bowel Is Resected and the Ganglionic Segment Is Pulled through the Cuff Twisting of the Pulled-through Intestines ● Consequence During the transanal mobilization of the ganglionic bowel, a twist can occur, leading to an obstruction. Grade 3/4 complication ● Repair A redo pull-through will be needed to straighten out the intestines. ● Prevention During the transanal mobilization of the rectum and colon, marking the posterior and anterior parts of the colon sequentially will ensure that the pull-through is straight and not twisted (Fig. 81–7). In addition, laparoscopy can be used to conﬁrm that the pull-through is straight and not kinked.

Anastomotic Leak ● Consequence The incidence of leaks after pull-throughs for HD is around 2%.36,40,43,44 Leaks will predispose to pelvic sepsis and the late development of strictures. Grade 2–4 complication

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SECTION XIII: PEDIATRIC SURGERY

General Pitfalls Incontinence ● Consequence The incidence of incontinence after a pull-through varies widely and is more common in patients with trisomy 21.47–52 Obviously, it contributes to a decline in the quality of life of the patients and their parents. Grade 4 complication

Sutures in anterior midline of intestine

Figure 81–7 Hidden anatomy: During a transanal pull-through, marking the intestines with sequential sutures will prevent the twisting of the intestines.

● Repair Most leaks are best treated with a diverting colostomy. A major disruption of the anastomosis will require a redo pull-through, especially if it is early after the initial operation.45 ● Prevention Meticulous technique during the dissection to preserve as much of the blood supply of the pull-through as possible is imperative. The anastomosis should be constructed without tension.

Stricture ● Consequence There is a widely reported (0%–20%) range of stricture formation after a pull-through for HD.23 Strictures lead to persistent obstruction and predispose the patient to recurrent bouts of enterocolitis.36,44 Grade 2–4 complication ● Repair Most strictures will respond to anal dilations. Recalcitrant strictures need to be addressed with stricturoplasty via a posterior sagittal approach or a redo pull-through.46 ● Prevention Avoiding leaks should decrease the rate of stricture formation. Routine postoperative dilations in the immediate postoperative period are being used more frequently because the transanal pull-through is being performed at an earlier stage when the anal canal is smaller. Whether this will prevent stricture formation is yet to be seen.

● Repair The majority of patients with incontinence issues after an HD pull-through improve with time and bowel management programs.53,54 ● Prevention No speciﬁc factor has been identiﬁed in the pathogenesis of incontinence after pull-through, so its prevention remains elusive.

Enterocolitis ● Consequence Hirschsprung’s enterocolitis is a poorly understood phenomenon causing fevers, stool retention or diarrhea, abdominal distention, leukocytosis, and a sepsis-like picture.23 If untreated, it carries a signiﬁcant mortality. Grade 2–4 complication ● Repair Enterocolitis is treated with antibiotics and rectal washouts. Anal dilations and injection of botulinum toxin to relax the aganglionic anal sphincter have also been helpful.55 Most patients with enterocolitis will eventually outgrow it without any further interventions. Patients with recurrent recalcitrant bouts of enterocolitis may beneﬁt from a posterior myomectomy.56 ● Prevention Rectal washouts after a pull-though have been suggested as a way to decrease the incidence of enterocolitis.57

Total Colonic HD ● Consequence If total colonic HD is not suspected before a transanal dissection is undertaken, one might be forced to commit to a choice of pull-through in the neonatal period that is suboptimal for this very difﬁcult problem. Grade 3/4 complication ● Repair Multiple operations have been devised for the treatment of total colonic HD, including the Kimura right colonic patch,58,59 the Martin modiﬁcation of the Duhamel procedure,60 and the straight ileoanal pull-through.61

81 IMPERFORATE ANUS AND HIRSCHSPRUNG’S DISEASE

835

tomosis is not in the transition zone where ganglion cells could be present but sparse.

REFERENCES

Figure 81–8 Barium enema in a patient with total colonic Hirschsprung’s disease shows the characteristic “lead piping” with blunting of both splenic and hepatic ﬂexures.

● Prevention Total colonic HD should be suspected preoperatively and an appropriate choice of operation selected prior to transanal dissection. Females and patients with hereditary HD have a higher incidence of total colonic HD. The barium enema shows a characteristic “lead piping” with blunting and rounding of both splenic and hepatic ﬂexures (Fig. 81–8). These patients do not usually respond well to rectal washouts. Therefore, a period of observation in the neonatal period with rectal washouts to ascertain that the baby is going to thrive and remain decompressed might be wise prior to transanal pull-through.

Residual Aganglionosis ● Consequence Performing the anastomosis at a level at which the ganglion cells are still absent will result in persistent obstruction. Grade 3/4 complication ● Repair A redo pull-through will need to be performed. ● Prevention The availability of reliable pathologists to recognize ganglionic segments on frozen section is imperative. Once a level is detected, performing the anastomosis a few centimeters proximal to that ensures that the anas-

1. Stephens FD. Malformations of the anus. Aust N Z J Surg 1953;23:9–24. 2. Boocock GR, Donnai D. Anorectal malformation: familial aspects and associated anomalies. Arch Dis Child 1987;62: 576–579. 3. Pinsky L. The syndromology of anorectal malformation (atresia, stenosis, ectopia). Am J Med Genet 1978;1:461– 474. 4. Shimada K, Hosokawa S, Matsumoto F, et al. Urological management of cloacal anomalies. Int J Urol 2001;8:282– 289. 5. Peña A. Important basic considerations. In Peña A (ed): Atlas of Surgical Management of Anorectal Malformations. New York: Springer-Verlag, 1990; pp 1–14. 6. Peña A. Anorectal malformations. Semin Pediatr Surg 1995;4:35–47. 7. Peña A, Levitt M. Anorectal malformations. In Grosfeld JL, O’Neill JA Jr, Fonkalsrud EW, Coran AG (eds): Pediatric Surgery, vol. 2. Philadelphia: Mosby Elsevier, 2006; pp 1566–1589. 8. Georgeson KE, Inge TH, Albanese CT. Laparoscopically assisted anorectal pull-through for high imperforate anus—a new technique. J Pediatr Surg 2000;35:927–930; discussion 930–931. 9. Yamataka A, Segawa O, Yoshida R, et al. Laparoscopic muscle electrostimulation during laparoscopy-assisted anorectal pull-through for high imperforate anus. J Pediatr Surg 2001;36:1659–1661. 10. Sydorak RM, Albanese CT. Laparoscopic repair of high imperforate anus. Semin Pediatr Surg 2002;11:217– 225. 11. Lima M, Tursini S, Ruggeri G, et al. Laparoscopically assisted anorectal pull-through for high imperforate anus: three years’ experience. J Laparoendosc Adv Surg Tech A 2006;16:63–66. 12. Wong KK, Khong PL, Lin SC, et al. Post-operative magnetic resonance evaluation of children after laparoscopic anorectoplasty for imperforate anus. Int J Colorectal Dis 2005;20:33–37. 13. Albanese CT, Jennings RW, Lopoo JB, et al. One-stage correction of high imperforate anus in the male neonate. J Pediatr Surg 1999;34:834–836. 14. Brain AJ, Kiely EM. Posterior sagittal anorectoplasty for reoperation in children with anorectal malformations. Br J Surg 1989;76:57–59. 15. Peña A. Advances in the management of fecal incontinence secondary to anorectal malformations. Surg Annu 1990;22:143–167. 16. Belizon A, Levitt M, Shoshany G, et al. Rectal prolapse following posterior sagittal anorectoplasty for anorectal malformations. J Pediatr Surg 2005;40:192–196. 17. Peña A, Grasshoff S, Levitt M. Reoperations in anorectal malformations. J Pediatr Surg 2007;42:318–325. 18. Peña A, Hong AR, Midulla P, Levitt M. Reoperative surgery for anorectal anomalies. Semin Pediatr Surg 2003; 12:118–123.

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19. Peña A, Migotto-Krieger M, Levitt MA. Colostomy in anorectal malformations: a procedure with serious but preventable complications. J Pediatr Surg 2006;41:748– 756. 20. Hong AR, Acuna MF, Peña A, et al. Urologic injuries associated with repair of anorectal malformations in male patients. J Pediatr Surg 2002;37:339–344. 21. Orr JD, Scobie WG. Presentation and incidence of Hirschsprung’s disease. Br Med J (Clin Res Ed) 1983;287(6406):1671. 22. Spouge D, Baird PA. Hirschsprung disease in a large birth cohort. Teratology 1985;32:171–177. 23. Teitelbaum DH, Coran AG. Hirschsprung’s disease and related neuromuscular disorders of the intestine. In Grosfeld JL, O’Neill JA Jr, Fonkalsrud EW, Coran AG (eds): Pediatric Surgery, Vol 2. Philadelphia: Mosby Elsevier, 2006; pp 1514–1559. 24. Georgeson KE, Fuenfer MM, Hardin WD. Primary laparoscopic pull-through for Hirschsprung’s disease in infants and children. J Pediatr Surg 1995;30:1017– 1022. 25. Smith BM, Steiner RB, Lobe TE. Laparoscopic Duhamel pull-through procedure for Hirschsprung’s disease in childhood. J Laparoendosc Surg 1994;4:273–276. 26. Curran TJ, Raffensperger JG. The feasibility of laparoscopic swenson pull-through. J Pediatr Surg 1994;29:1273–1275. 27. Bufo AJ, Chen MK, Shah R, et al. Analysis of the costs of surgery for Hirschsprung’s disease: one-stage laparoscopic pull-through versus two-stage Duhamel procedure. Clin Pediatr (Phila) 1999;38:593–596. 28. de Lagausie P, Bruneau B, Besnard M, et al. Deﬁnitive treatment of Hirschsprung’s disease with a laparoscopic Duhamel pull-through procedure in childhood. Surg Laparosc Endosc 1998;8:55–57. 29. Ghirardo V, Betalli P, Mognato G, Gamba P. Laparotomic versus laparoscopic Duhamel pull-through for Hirschsprung disease in infants and children. J Laparoendosc Adv Surg Tech A 2007;17:119–123. 30. Kumar R, Mackay A, Borzi P. Laparoscopic Swenson procedure—an optimal approach for both primary and secondary pull-through for Hirschsprung’s disease. J Pediatr Surg 2003;38:1440–1443. 31. Berrebi D, Fouquet V, de Lagausie P, et al. Duhamel operation vs neonatal transanal endorectal pull-through procedure for Hirschsprung disease: which are the changes for pathologists? J Pediatr Surg 2007;42:688–691. 32. El-Sawaf MI, Drongowski RA, Chamberlain JN, et al. Are the long-term results of the transanal pull-through equal to those of the transabdominal pull-through? A comparison of the 2 approaches for Hirschsprung disease. J Pediatr Surg 2007;42:41–47; discussion 47. 33. Yamataka A, Kobayashi H, Hirai S, et al. Laparoscopyassisted transanal pull-through at the time of suction rectal biopsy: a new approach to treating selected cases of Hirschsprung disease. J Pediatr Surg 2006;41:2052–2055. 34. Zhang SC, Bai YZ, Wang W, Wang WL. Clinical outcome in children after transanal 1-stage endorectal pull-through operation for Hirschsprung disease. J Pediatr Surg 2005;40:1307–1311. 35. Dasgupta R, Langer JC. Transanal pull-through for Hirschsprung disease. Semin Pediatr Surg 2005;14:64–71.

36. Langer JC, Durrant AC, de la Torre L, et al. One-stage transanal Soave pull-through for Hirschsprung disease: a multicenter experience with 141 children. Ann Surg 2003; 238:569–583; discussion 583–585. 37. Langer JC, Fitzgerald PG, Winthrop AL, et al. One-stage versus two-stage Soave pull-through for Hirschsprung’s disease in the ﬁrst year of life. J Pediatr Surg 1996;31:33– 37. 38. Puri P, Nixon HH. Long-term results of Swenson’s operation for Hirschsprung’s disease. Prog Pediatr Surg 1977; 10:87–96. 39. Devroede G, Arhan P, Duguay C, et al. Traumatic constipation. Gastroenterology 1979;77:1258–1267. 40. Sherman JO, Snyder ME, Weitzman JJ, et al. A 40-year multinational retrospective study of 880 Swenson procedures. J Pediatr Surg 1989;24:833–838. 41. Swenson O, Sherman JO, Fisher JH, Cohen E. The treatment and postoperative complications of congenital megacolon: A 25 year follow-up. Ann Surg 1975;182: 266–273. 42. Swenson O, Sherman JO, Fisher JH. Diagnosis of congenital megacolon: an analysis of 501 patients. J Pediatr Surg 1973;8:587–594. 43. Georgeson KE, Cohen RD, Hebra A, et al. Primary laparoscopic-assisted endorectal colon pull-through for Hirschsprung’s disease: a new gold standard. Ann Surg 1999;229:678–682; discussion 682–683. 44. Teitelbaum DH, Cilley RE, Sherman NJ, et al. A decade of experience with the primary pull-through for Hirschsprung disease in the newborn period: a multicenter analysis of outcomes. Ann Surg 2000;232:372–380. 45. Laberge JM, Adolph VR, Flageole H, Guttman FM. Salvage of Soave-Boley endorectal pull-through by conversion to a classical Soave procedure. Eur J Pediatr Surg 1996;6:362–363. 46. Teitelbaum DH, Coran AG. Reoperative surgery for Hirschsprung’s disease. Semin Pediatr Surg 2003;12:124– 131. 47. Yanchar NL, Soucy P. Long-term outcome after Hirschsprung’s disease: patients’ perspectives. J Pediatr Surg 1999;34:1152–1160. 48. Quinn FM, Surana R, Puri P. The inﬂuence of trisomy 21 on outcome in children with Hirschsprung’s disease. J Pediatr Surg 1994;29:781–783. 49. Hackam DJ, Superina RA, Pearl RH. Single-stage repair of Hirschsprung’s disease: a comparison of 109 patients over 5 years. J Pediatr Surg 1997;32:1028–1031; discussion 1031–1032. 50. Moore SW, Albertyn R, Cywes S. Clinical outcome and long-term quality of life after surgical correction of Hirschsprung’s disease. J Pediatr Surg 1996;31:1496– 1502. 51. Diseth TH, Bjornland K, Novik TS, Emblem R. Bowel function, mental health, and psychosocial function in adolescents with Hirschsprung’s disease. Arch Dis Child 1997;76:100–106. 52. Bai Y, Chen H, Hao J, et al. Long-term outcome and quality of life after the Swenson procedure for Hirschsprung’s disease. J Pediatr Surg 2002;37:639–642. 53. Heikkinen M, Rintala R, Luukkonen P. Long-term anal sphincter performance after surgery for Hirschsprung’s disease. J Pediatr Surg 1997;32:1443–1446.

81 IMPERFORATE ANUS AND HIRSCHSPRUNG’S DISEASE 54. Rescorla FJ, Morrison AM, Engles D, et al. Hirschsprung’s disease. Evaluation of mortality and longterm function in 260 cases. Arch Surg 1992;127:934–941; discussion 941–942. 55. Minkes RK, Langer JC. A prospective study of botulinum toxin for internal anal sphincter hypertonicity in children with Hirschsprung’s disease. J Pediatr Surg 2000;35:1733–1736. 56. Wildhaber BE, Pakarinen M, Rintala RJ, et al. Posterior myotomy/myectomy for persistent stooling problems in Hirschsprung’s disease. J Pediatr Surg 2004;39:920–926. 57. Mir E, Karaca I, Gunsar C, et al. Primary DuhamelMartin operations in neonates and infants. Pediatr Int 2001;43:405–408.

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58. Kimura K, Nishijima E, Muraji T, et al. A new surgical approach to extensive aganglionosis. J Pediatr Surg 1981;16:840–843. 59. Kimura K, Nishijima E, Muraji T, et al. Extensive aganglionosis: further experience with the colonic patch graft procedure and long-term results. J Pediatr Surg 1988;23(1 pt 2):52–56. 60. Martin LW. Surgical management of Hirschsprung’s disease involving the small intestine. Arch Surg 1968;97:183–189. 61. Sandegard E. Hirschsprung’s disease with ganglion cell aplasia of the colon and terminal ileum; report of a case treated with total colectomy and ileo-anostomy. Acta Chir Scand 1953;106:369–376.

82

Pectus Excavatum Brian J. Duffy, MD, David M. Powell, MD, and Martin R. Eichelberger, MD INTRODUCTION Pectus excavatum is the most common congenital anterior chest wall deformity, occurring in approximately 1 in 700 live births. It is characterized by depression of the sternum and lower costal cartilages, resulting in a funnel-shaped appearance of the anterior chest wall. The exact etiology is unknown. Early investigators attributed the defect to abnormal development of the diaphragm, but there has been little evidence to support this hypothesis except for the rare occurrence of pectus excavatum in association with congenital diaphragmatic hernia. There is frequent association with Marfan’s syndrome, an inherited disorder that affects cartilage and other connective tissue. Approximately 26% of children with pectus excavatum have thoracic scoliosis, and 37% have a family history of an anterior thoracic deformity.1 In the majority of children, the abnormality becomes apparent in the ﬁrst year of life. As the child grows, the deformity may become progressively worse. Typical symptoms are chest pain and exercise intolerance, attributable to the restrictive effect of the deformity on the cardiopulmonary system. Occasionally, children experience palpitations or syncope related to an underlying cardiac abnormality, such as mitral valve prolapse. As children become older, they become self-conscious about their physical appearance, often prompting a surgical evaluation. In the early 1900s, Meyer and Sauerbrach reported the ﬁrst operative repairs for pectus excavatum.1 In 1949, Ravitch2 reported his technique consisting of excision of all deformed cartilages within the perichondrium, division of the xiphoid from the sternum, division of the intercostal bundles from the sternum, and a transverse sternal osteotomy. Since the original description by Ravitch, several modiﬁcations of the open technique have been used successfully. In 1998, Nuss and coworkers3 reported their technique for the minimally invasive repair of pectus excavatum. Currently, the minimally invasive technique is widely accepted as an alternative to the open approach. In this chapter, both the open and the minimally invasive repairs are discussed separately. Selection of an

approach should be based not only on the ultimate results and long-term recurrence rates but also on the potential complications. Factors inﬂuencing the decision to perform an open versus a minimally invasive pectus excavatum repair include the severity of the defect, symmetry of the deformity, prior failed operation, and prior cardiac or thoracic surgery. Long-term results and recurrence rates have yet to be reported for the minimally invasive technique.

INDICATIONS ● Chest pain, especially in area of deformed cartilages or

after sustained exercise ● Palpitations, tachycardia, or syncope related to cardiac

arrhythmia ● Exercise intolerance secondary to cardiopulmonary

insufﬁciency ● Prevention or correction of postural deformity ● Improvement of self-image based on abnormal physical

appearance Note: Cardiac and pulmonary insufﬁciency in children with pectus excavatum is controversial and difﬁcult to measure with current diagnostic testing, but many clinicians and patients report increased stamina after surgical repair.1

Open Repair (Modiﬁed Ravitch) OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4

Midline incision—nipple to xiphoid Skin and pectoralis muscle ﬂaps to expose deformed costal cartilages Subperichondrial resection of the abnormal costal cartilages (usually ribs two to six) Transverse anterior wedge osteotomy at cephalad transition from normal to posteriorly

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Step Step Step Step Step Step

SECTION XIII: PEDIATRIC SURGERY

displaced sternum (to facilitate elevation of sternum) 5 Division of rectus muscle from xiphoid process 6 Strut ﬁxation of sternum using retrosternal approach (Adkins strut) 7 Advancement of pectoralis muscle ﬂaps to cover sternum 8 Reattachment of rectus muscle to lower sternum 9 Evacuation of air from chest cavity with red rubber catheter 10 Closure of skin incision over closed suction drain

Subperichondral Resection of Abnormal Costal Cartilages (Figs. 82–1 to 82–4) Damage to the Perichondrium

Figure 82–2 Elevation of the cartilage with a towel clip facilitates circumferential dissection.

● Consequence Remodeling of the anterior chest wall after operation depends upon regeneration of cartilage from the perichondrium. Damage to the perichondrium impairs its regenerative capacity. Grade 4 complication ● Repair Simple suture repair. ● Prevention Careful dissection of the costal cartilage from its perichondrium using specially designed perichondrial elevators.

Damage to the Costochondral Junction ● Consequence Misalignment of the bone and cartilage during healing, leading to chest wall asymmetry and protuberance of the chest wall. Grade 4 complication

Figure 82–1 Using a perichondrial elevator separates the perichondrium from the costal cartilage.

Figure 82–3 Circumferential dissection of the perichondrium from the cartilage.

Figure 82–4 Dividing the cartilage facilitates separation at the costochondral junction.

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● Repair Simple suture repair of perichondrium to bone. ● Prevention Excise only the amount of deformed cartilage necessary for elevation of the chest wall. Minimize dissection at the costochondral junction.

Strut Placement for Fixation of the Sternum (Figs. 82–5 to 82–9) Damage to the Intercostal or Internal Mammary Vessels ● Consequence Severe bleeding, hemothorax, or hemomediastinum. Delayed-onset thoracodystrophy can result from ischemia to the sternum. Grade 2–5 complication

Figure 82–7 space.

Passing the strut through the contralateral rib

Figure 82–5 Metal strut used for elevation and ﬁxation of the sternum.

Figure 82–8

Elevation of the sternum into the ﬁnal position.

Figure 82–6 Using a ﬁnger to guide the strut under the sternum.

Figure 82–9 Wire ﬁxation of the strut.

● Repair Simple ligation.

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● Prevention Avoid detaching the perichondrium from the sternum to help preserve the intercostal vessels. Dissect directly adjacent to the sternum when creating the retrosternal space for strut placement to avoid injury to the internal mammary vessels located slightly more lateral to the sternum.

Damage to the Heart ● Consequence Cardiac perforation, pericardial tamponade, pericarditis. Grade 5 complication ● Repair Cardiac perforation requires emergent median sternotomy for relief of tamponade and repair of cardiac injury. Pericarditis can occur postoperatively and often resolves with nonsteroidal anti-inﬂammatory medication. Percutaneous drainage is usually required for a large or persistent effusion. ● Prevention Careful blunt dissection in the retrosternal space while passing the strut, especially in a patient who has had prior cardiothoracic surgery.

Dissection around the Pleura (Fig. 82–10) ● Consequence Pneumothorax from lung or pleural injury. Injury to the lung can result in persistent air leak and expanding pneumothorax after operation. Isolated injury to the parietal pleura causes pneumothorax resulting from air trapping from the external environment, but this should not continue to expand after closure. Grade 1/2 complication ● Repair If there is suspicion of lung injury, insert a chest tube. If a small injury is made to the pleura, widen the hole

to prevent a tension pneumothorax during the operation. At the end of operation, evacuate air from the pleural cavity using a red rubber catheter and Valsalva maneuver followed by suture repair of the pleura. ● Prevention Careful dissection when mobilizing the perichondrium, detaching the rectus muscle, dissecting around the sternum, and placing the strut.

POSTOPERATIVE COMPLICATIONS Wound Complications and Infection Seroma formation beneath the skin ﬂaps of the anterior chest wall can be prevented with closed suction drainage catheters placed at the time of operation. Perioperative antibiotic therapy helps reduce the incidence of wound infection. Wound infection or dehiscence may lead to infection of the metal strut, requiring long-term antibiotic therapy. Failure of antibiotic therapy for strut infection necessitates bar removal and delayed chest wall reconstruction. Postoperative analgesia and pulmonary toilet help prevent atelectasis and pneumonia. Recurrence If the metal strut is left in place for at least 1 year to allow for adequate formation of new cartilage, there is a low incidence of recurrence. Children with Marfan’s syndrome are more likely to recur early, so the strut is often left in place for longer than 1 year. Premature removal results in depression of the sternum and recurrence of the excavatum. A second reconstructive procedure may be indicated, depending on symptoms and cosmetic appearance. Acquired Asphyxiating Thoracic Dystrophy Abnormal growth of the chest wall can occur years after repair and may cause severe respiratory symptoms. Haller4 report a series of 12 children who underwent open repair at less than 4 years of age and subsequently developed severe chest wall constriction from growth retardation. Proposed mechanisms for limited chest wall growth are disruption of the growth center at the costochondral junction and disruption of the vascular supply to the sternum.1 As a result, most surgeons strongly advise against repairing a pectus deformity too early (before 4 years of age).

Minimally Invasive Repair (Nuss) OPERATIVE STEPS Step 1 Figure 82–10 catheter.

Evacuating air from the chest using a red rubber

Width of chest is measured and correct length bar is selected and bent to conform to desired curvature of anterior chest wall

82 PECTUS EXCAVATUM Small transverse lateral thoracic skin incisions are made bilaterally 3 Skin tunnel is raised, and selected intercostal space is entered from right under direct visualization with thoracoscopy 4 Introducer is passed through tunnel, posterior to sternum and anterior to heart, to emerge through contralateral intercostal space 5 Two strands of umbilical tape are tied to end of introducer, and introducer and strands are then pulled back through tract 6 Introducer is removed and umbilical tape is transferred to pectus bar 7 Bar is pulled through tract in a concave conﬁguration 8 Bar is rotated 180°, elevating sternum and chest wall into normal position 9 Each end of bar is secured to stabilizer plate or chest wall (or both) 10 Pneumothorax is evacuated before closing incisions

Step 2 Step

Step

Step

Step Step Step Step Step

Epidural Catheter Placement (by Anesthesiologist) (Fig. 82–11) Transient Horner’s Syndrome ● Consequence Acute mechanical stress is applied to the deformed costal cartilages and depressed sternum during operative positioning of the pectus bar. A thoracic epidural catheter provides excellent postoperative analgesia.5 Adequate pain control with oral and intravenous medication alone can be difﬁcult to achieve in the immediate postoperative period. Inadequately controlled chest pain impairs the ability to perform incentive spirometry and thereby predisposes to atelectasis and pneumonia. Use of the epidural can also cause transient Horner’s syndrome.5 Grade 1 complication

Figure 82–11 Epidural catheter placed by the anesthesiology team.

843

● Repair If the epidural does not provide adequate analgesia, a combination of oral, intravenous, and transdermal medication (e.g., fentanyl patch) may be necessary. Horner’s syndrome is transient and resolves spontaneously with discontinuation of the epidural medication. No cases of permanent Horner’s syndrome after this operation have been reported in the literature. ● Prevention Proper placement of the epidural by a skilled anesthesiologist.

Inserting the Introducer and Pectus Bar (Figs. 82–12 to 82–15) Injury to the Pericardium Resulting in Pericarditis ● Consequence In a multi-institutional review of 251 cases by Hebra and associates,6 the incidence of pericarditis was 0.4%. Even with the use of thoracoscopy, the injury may not be recognized at the time of operation. Signs and symptoms include chest pain, dyspnea, malaise, fever, lethargy, and a pericardial friction rub. Low voltage may be present on electrocardiogram, and a pericardial effusion may be apparent on echocardiogram. In a series of patients by Miller and colleagues,7 one child (1.2%) presented 1 month after repair with noninfectious pericarditis requiring anti-inﬂammatory medication and pericardiocentesis. In a more severe case, bacterial pericarditis occurred in association with bilateral empyema, ultimately requiring bar removal and open débridement of the pericardium.8 No deaths have been reported from pericarditis. Grade 1 complication

Figure 82–12 Using thoracoscopy helps guide placement of the introducer and bar.

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A

A

B

B Figure 82–13 A, Entering the right chest with the introducer. Note the pectus deformity protruding inward from the anterior chest wall. B, Passing the introducer between the heart and the sternum.

A

Figure 82–14 A and B, Transthoracic placement of the introducer elevates the chest wall deformity in preparation for bar placement.

B

Figure 82–15 A and B, Placement of the bar using thoracoscopic guidance. Note that the bar is placed initially in a concave position, then rotated 180° into the ﬁnal position.

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● Repair Repair of the torn pericardium should not be attempted at operation. Similar to the postpericardiotomy syndrome seen commonly after cardiac surgery, most cases of pericarditis are transient and resolve with nonsteroidal anti-inﬂammatory medication.5 Persistent symptoms may respond to methylprednisolone.9 A large or persistent pericardial effusion usually requires percutaneous drainage. ● Prevention Careful dissection in the retrosternal space minimizes trauma to the pericardium. The current shape of the introducer has helped to facilitate the dissection, thereby decreasing the incidence of pericarditis.10

Injury to the Heart and Blood Vessels ● Consequence Cardiac perforation has been reported only once in the literature, and it occurred while the introducer clamp was being passed blindly across the mediastinum.10 Emergency median sternotomy, cardiac bypass, and repair of the tricuspid valve were performed, followed by open repair of the pectus excavatum. Injury to major blood vessels is rare, but it includes laceration of the internal mammary artery11 and pseudoaneurysm of the anterior thoracic artery.6 Grade 5 complication ● Repair Emergency median sternotomy is recommended for any cardiac injury. Intraoperative echocardiography helps delineate concomitant valve injury. Primary repair or ligation is the recommended treatment for blood vessel injury. ● Prevention Careful dissection when passing the introducer and pectus bar beneath the sternum and across the mediastinum. Thoracoscopy improves visualization when passing the introducer and pectus bar between the heart and the sternum. Jacobs and coworkers12 reported success with the tunnel device normally used for endoscopic saphenous vein removal to help create the retrosternal tunnel. A small subxiphoid incision7 and external traction to the sternum can help facilitate passage of the introducer and pectus bar.

Securing the Bar and Lateral Stabilizers (Figs. 82–16 to 82–18) Bar displacement ● Consequence Rotation of the bar (known as “ﬂipping”) is a complication unique to the minimally invasive procedure. Recurrence of the deformity and chest pain are the two most common presenting features. In their original paper, Nuss and coworkers3 reported bar displacement

Figure 82–16 Proper initial measurement from midaxillary to midaxillary line allows for correct sizing of the bar, minimizing postoperative bar displacement.

Figure 82–17 Pectus bar, pictured with two different types of stabilizers.

in 2 of 42 children (4.8%), requiring revision. In a questionnaire survey of pediatric surgeons, bar displacement was reported as the most common complication requiring reoperation (9.2%).6 Grade 3/4 complication ● Repair Numerous reports have clearly documented the need for reoperation for bar repositioning or removal after displacement.7,13–16 Early bar displacement is corrected in the operating room by repositioning and ﬁxing the bar more securely to the chest wall. Late displacement may require removal of the bar and may necessitate repeat operation to correct the resultant deformity. ● Prevention Selection of a bar that ﬁts the desired contour of the chest wall and use of the lateral stabilizer signiﬁcantly reduce bar displacement. Since the introduction of the lateral stabilizer, the incidence of bar displacement has decreased from 16% to 5%.10 The following recommendations from Hebra and associates6 may help prevent bar displacement: 1. Proper initial measurement from midaxillary to midaxillary line, realizing that the distance will be slightly longer (1 to 2 cm) than the bar required.

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SECTION XIII: PEDIATRIC SURGERY pain and irritation of the overlying skin. Also, the stabilizer can cause pressure on the skin with seroma formation and aseptic dermatitis.17 Grade 3/4 complication ● Repair Resecure the stabilizer.

A

● Prevention Wiring the bar to the stabilizer has helped decrease the incidence of bar displacement.5 Currently, the system recommended by Nuss16 of wiring a stabilizer to the bar and applying several polydioxanone (PDS) sutures to the bar and underlying ribs on the opposite side under thoracoscopic guidance has a very low displacement rate (0.8%).

Pneumothorax ● Consequence Through the incisions and thoracoscopy, air can be trapped in the thoracic cavity, resulting in postoperative pneumothorax. Injury to the lung is a rare cause of pneumothorax. In a survey of pediatric surgeons by Hebra and associates,6 pneumothorax requiring chest tube was the second most common complication of the procedure (4.8%). In a single-center experience by Miller and colleagues,7 the most common complication was pneumothorax (40%), but only 2 patients (2.4%) required chest tube. Grade 1/2 complication B Figure 82–18 A and B, Wire ﬁxation of the pectus bar and stabilizer. Additional sutures are placed through the holes of the stabilizer to improve ﬁxation.

2. Placing the transverse lateral thoracic incisions at the midaxillary line. 3. Placing the bar at the deepest point of the excavatum deformity with the bar crossing the sternum at a 90° angle. 4. Placement of a second bar (also with stabilizer) in older or more active patients or those with severe deformity. 5. Securing the bar itself to the chest wall muscles (in addition to securing the stabilizer). 6. Smooth transition from general anesthesia to conscious sedation with minimal agitation. 7. Good posture and maintenance of a straight spine position in the ﬁrst 30 days after operation to allow ﬁbrous tissue integration and bar stabilization.

Improper Fixation of the Stabilizer ● Consequence Increased probability of displacement. Chronic movement and instability of the stabilizer cause persistent

● Repair Because postoperative from air entering the lung injury, most will tomatic or enlarging thoracostomy.

pneumothorax mainly occurs chest cavity rather than from resolve spontaneously. Symppneumothorax requires tube

● Prevention A water-seal system using a rubber catheter and positive pressure prior to closing the last incision has minimized the incidence of pneumothorax.10 A chest radiograph is performed immediately after operation, and again as needed at the discretion of the surgeon to rule out expanding pneumothorax.

POSTOPERATIVE COMPLICATIONS Noninfectious Complications Noninfectious complications include seroma formation, dermatitis, and pleural effusion. Seroma or dermatitis usually occurs at the lateral thoracic incisions from mechanical irritation from the stabilizer and often resolve spontaneously. If the seroma is very large, or there is suspicion of infection, needle aspiration may be diagnostic and therapeutic. Simple pleural effusion may occur immediately after operation or in delayed fashion, but it usually resolves spontaneously.

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Infectious Complications

Asymmetry, Overcorrection, and Recurrence

Perioperative antibiotic therapy should always be used because a foreign body is being inserted into the chest. Although infectious complications occur with low incidence (2%),6 they can have serious sequelae. Superﬁcial wound infection, bar or stabilizer infection, pneumonia, empyema, mediastinitis, and bacterial pericarditis have all been documented in the literature. Superﬁcial wound infection often resolves with antibiotic therapy and does not require bar removal. Bar infection is minimized by sterile technique and applying povidone-iodine (Betadine) to the incisions during insertion.10 Abscess around the stabilizer or bar can be treated with local drainage and intravenous antibiotic, but the stabilizer or bar may ultimately require removal.7 Contact dermatitis with fungal superinfection has occurred at the epidural insertion site and resolved with topical therapy.14 Pneumonia is minimized by use of perioperative antibiotics, vigorous pulmonary toilet, and early return to ambulation. Bilateral empyema and bacterial pericarditis have been reported, requiring bar removal, pericardiocentesis, and open débridement of the pericardium.8 If mediastinitis is present, bar removal is indicated to clear the infection. Reoperation should be deferred for 6 to 12 months.

Chest asymmetry prior to operation can result in a less than optimal cosmetic result. Some surgeons recommend against the minimally invasive repair for an asymmetrical deformity. Overcorrection of the deformity may lead to pectus carinatum. Mild overcorrection or carinatum has resolved with bar removal or orthotic treatment.5 Severe chest wall asymmetry and progressive carinatum may require bar removal and open carinatum repair.13,14 Although short-term follow-up results after bar removal appear promising, long-term results and recurrence rates are not yet available for the minimally invasive operation.

Rare Complications Rare complications include cardiac arrhythmia, thoracic outlet syndrome, acquired thoracic scoliosis, and metal allergy. Cardiac arrhythmias presumably result from mechanical irritation of the heart during the retrosternal dissection and passage of the introducer and pectus bar. Thoracic outlet syndrome has been reported in three adolescent males who experienced persistent paresthesias in an upper extremity after operation.8 Two resolved spontaneously 4 weeks after operation, and one required bar removal for persistent symptoms and bar instability. Acquired thoracic scoliosis has been reported in two children after the minimally invasive repair.18 In the ﬁrst child, mild preoperative scoliosis became markedly pronounced after surgery. Moderate improvement was achieved with an exercise regimen and physical therapy. In the second child, there was no preoperative scoliosis. Scoliosis occurred after operation and showed improvement with exercise and physical therapy. Asymmetrical pneumatic pressure in the thoracic cavity and paraspinal muscle imbalance probably contribute to acquired scoliosis. Metal allergy is manifest by an unrelenting skin rash with hyperesthesia over the distribution of the bar. Nickel allergy has been documented in the literature, but this should be conﬁrmed with formal allergy testing prior to bar removal. A trial of topical steroids is appropriate, but if bar removal becomes necessary, replacement should be with a custom-made nonallergenic alloy such as titanium.10

REFERENCES 1. Shamberger RC. Pectus excavatum. In Ziegler M, Azizkhan R, Weber TR (eds): Operative Pediatric Surgery. New York: McGraw-Hill, 2003; pp 255–267. 2. Ravitch MM. The operative treatment of pectus excavatum. Ann Surg 1949;129:429–444. 3. Nuss D, Kelly RE, Croitoru DP, Katz ME. A 10-year review of a minimally invasive technique for the correction of pectus excavatum. J Pediatr Surg 1998;33:545–552. 4. Haller JA Jr. Severe chest wall constriction from growth retardation after too extensive and too early (<4 years) pectus excavatum repair: an alert. Ann Thorac Surg 1995; 60:1857–1858. 5. Croitoru DP, Kelly RE, Goretsky MJ, et al. Experience and modiﬁcation update for the minimally invasive Nuss technique for pectus excavatum repair in 303 patients. J Pediatr Surg 2002;37:437–445. 6. Hebra A, Swoveland B, Egbert M, et al. Outcome analysis of minimally invasive repair of pectus excavatum: review of 251 cases. J Pediatr Surg 2000;35:252–258. 7. Miller KA, Woods RK, Sharp RJ, et al. Minimally invasive repair of pectus excavatum: a single institution experience. Surgery 2001;130:652–659. 8. Moss RL, Albanese CT, Reynolds M. Major complications after minimally invasive repair of pectus excavatum: case reports. J Pediatr Surg 2001;36:155–158. 9. Muensterer OJ, Schenk DS, Praun M, et al. Postpericardiotomy syndrome after minimally invasive pectus excavatum repair unresponsive to nonsteroidal anti-inﬂammatory treatment. Eur J Pediatr Surg 2003;13:206–208. 10. Nuss D, Croitoru DP, Kelly RE, et al. Review and discussion of the complications of minimally invasive pectus excavatum repair. Eur J Pediatr Surg 2002;12: 230–234. 11. Willekes CL, Backer CL, Mavroudis C. A 26-year review of pectus deformity repairs, including simultaneous intracardiac repair. Ann Thorac Surg 1999;67:511– 518. 12. Jacobs JP, Quintessenza JA, Morell VO, et al. Minimally invasive endoscopic repair of pectus excavatum. Eur J Cardiothorac Surg 2002;21:869–873. 13. Engum S, Rescorla F, West K, et al. Is the grass greener? Early results of the Nuss procedure. J Pediatr Surg 2000; 35:246–251.

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14. Molik KA, Engum SA, Rescorla FJ, et al. Pectus excavatum repair: experience with standard and minimal invasive techniques. J Pediatr Surg 2001;36:324–328. 15. Fonkalsrud EW, Beanes S, Hebra A, et al. Comparison of minimally invasive and modiﬁed Ravitch pectus excavatum repair. J Pediatr Surg 2002;37:413–417. 16. Nuss D. Recent experiences with minimally invasive pectus excavatum repair: “Nuss procedure.” Jpn J Thorac Cardiovasc Surg 2005;53:338–344.

17. Watanabe A, Watanabe T, Obama T, et al. The use of a lateral stabilizer increases the incidence of wound trouble following the Nuss procedure. Ann Thorac Surg 2004;77: 296–300. 18. Niedbala A, Adams M, Boswell W, Considine J. Acquired thoracic scoliosis following minimally invasive repair of pectus excavatum. Am Surg 2003;69:530–533.

83

Tracheoesophageal Fistula and Esophageal Atresia Repair Shawn D. Safford, MD and Jeffrey Lukish, MD INTRODUCTION

INDICATIONS

Esophageal atresia (EA) occurs in approximately 1 in every 3000 to 4500 live births and has no described sex predilection. EAs with and without tracheal ﬁstulas have been classiﬁed into ﬁve types: (1) EA with distal tracheoesophageal ﬁstula (TEF), (2) EA without TEF, (3) EA with proximal TEF, (4) EA with proximal and distal ﬁstula, and (5) isolated TEF (H type). EA with a TEF between the distal esophagus and the trachea occurs in approximately 86% of cases.1–3 EA occurs with other signiﬁcant congenital anomalies in 30% to 76% of children.2,4 Importantly, these associated congenital anomalies are the major source of morbidity and mortality associated with EA repair.1 The most common congenital anomaly is congenital heart disease, which is found in up to 20% of children.5 The acronym VACTERL groups associated defects into vertebral, anal, cardiac, tracheoesophageal, renal, and limb abnormalities. Children present at various times depending on the type of anomaly. EA prevents the child from swallowing amniotic ﬂuid, with a resultant polyhydramnios. Prenatal ultrasound can demonstrate polyhydramnios, absent or small stomach bubble, and an esophageal pouch.6,7 Those not detected prenatally become symptomatic soon after birth with drooling, choking, and the inability to tolerate feeding. In contrast, patients with an H-type TEF may not be diagnosed until later in life. The diagnosis should be suspected in a child with recurrent episodes of aspiration pneumonia, choking, and coughing with feedings. The diagnosis of EA is demonstrated on chest radiograph showing a curved catheter in the proximal esophageal pouch. In patients with an isolated EA, other ﬁndings include a gasless abdomen. Other studies in the work-up may include contrast esophagogram and bronchoscopy. Evaluation should also include echocardiogram, renal ultrasound, and vertebral ﬁlms to rule out major cardiac, renal, and vertebral anomalies. In addition, the echocardiogram will evaluate for the location of the aortic arch to aid in planning the operation.

● Newborn with blind ending upper esophageal pouch ● Newborn with a gasless abdomen on plain x-ray

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4

Position patient for posterolateral thoracotomy opposite aortic arch Division of ﬁstula tract Dissection of proximal esophageal pouch End-to-end anastomosis of proximal and distal esophagus

OPERATIVE PROCEDURE Posterolateral Thoracotomy Right-sided Aortic Arch ● Consequence With the signiﬁcant association with congenital cardiac anomalies, the location of the aortic arch is right-sided in up to 5.4% of children.8–10 The location in the opposite chest makes the already challenging anastomosis more difﬁcult.8 The aorta obscures the esophagus and ﬁstula when approaching from the right chest. Proceeding with the operation through the right chest leads to a higher leak rate (42%) and higher morbidity and mortality.9 Of signiﬁcance, the ﬁnding of a rightsided aortic arch (RAA) should raise the suspicion for the ﬁnding of a long-gap atresia. Long-gap atresias are found in up to 42% of patients with RAA.8 Grade 3 complication ● Repair Babu and coworkers8 proposed the approach to management of RAA tracheoesophageal repairs. All infants

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should have a preoperative echocardiogram, and if RAA is suspected, the echocardiogram should be repeated; alternatively, magnetic resonance imaging (MRI) is performed. When an unsuspected RAA is found at the time of the initial exploration, the decision to proceed is based on the anatomy and the ease of dissection. If the dissection is difﬁcult, a delayed left thoracotomy should be performed after a complete evaluation of the vascular anatomy. ● Prevention Preoperatively, all patients should undergo an extensive work-up to diagnose an RAA including echocardiogram. If identiﬁed, a repeat echocardiogram or MRI should be performed to conﬁrm the diagnosis. The alternate vascular abnormality of a double aortic arch would not change the approach on the right side.

Division of the Fistula Missed Upper Pouch Fistula ● Consequence If an upper pouch ﬁstula is missed during the dissection of the esophageal pouch, the patient is susceptible to recurrent aspirations. Grade 3 complication ● Repair A missed upper pouch ﬁstula will require a reoperation to close it via a repeat thoracotomy or a cervical incision if it is high enough. ● Prevention A rigid bronchoscopy at the beginning of the operation will identify the presence of an upper pouch ﬁstula and help identify the location of the TEF (Fig. 83–1).

Ligation of the Fistula Too Close or Too Far from the Trachea Long Thoracic Nerve Injury ● Consequence In 89 patients undergoing thoracotomy for TEF repair, 29 (33%) had signiﬁcant musculoskeletal abnormalities, and 24% demonstrated long thoracic nerve injury.11 The long thoracic nerve is purely motor and originates from the ﬁfth to seventh cervical roots and supplies the serratus anterior. The serratus anterior is responsible for the abduction and elevation of the superior limb and can act as an accessory muscle during inspiration. Paralysis of the muscle causes “winged scapula,” in which the scapula moves away from the thoracic wall, the shoulder falls down, and the arm cannot be lifted higher than 90° when stretched outward. Grade 4 complication

● Consequence Ligation of the TEF too close to the trachea may lead to tracheal stenosis, which may result in recurrent pneumonias or difﬁculty with breathing. In contrast, dividing the ﬁstula too far from the trachea may lead to respiratory symptoms secondary to recurrent aspirations from the resultant esophageal diverticulum.16 Grade 3 complication

● Repair In most cases, serratus anterior paralysis secondary to thoracotomy will resolve over 6 months.8 If conservative treatment is unsuccessful, the scapula will require loose ﬁxation to the chest wall.12 ● Prevention Bianchi and associates13 proposed the use of an axillary skin crease muscle-sparing incision through the third or fourth intercostal space. Exposure was not restricted, scar aesthetic was excellent, and no signiﬁcant difference was found regarding duration of operation, postoperative ventilation, or the incidence of anastomotic stricture.14 Thoracoscopic repair has been shown to be a safe alternative when performed by experienced surgeons.15 The thoracoscopic approach decreases the morbidity associated with the thoracotomy with no subsequent increase in morbidity and/or mortality.

Figure 83–1 Rigid bronchoscopy at the beginning of the operation would help locate the location of the tracheoesophageal ﬁstula (TEF) (here proximal to the carina) and rule out the presence of an upper pouch second ﬁstula. (Courtesy of Dr. David Powell, Children’s National Medical Center, Washington, DC.)

83 TRACHEOESOPHAGEAL FISTULA AND ESOPHAGEAL ATRESIA REPAIR

851

Proximal esophagus

B

Membraneous trachea

Tracheoesophageal fistula

C

A

D Figure 83–2 During dissection of the TEF, the ﬁstula should be circumferentially controlled and occluded. Once dissected free of surrounding tissue, the ﬁstula should be ligated with a 1-mm cuff on the tracheal side (A). Ligation of the TEF too close or too far may lead to tracheal stenosis (B) or an esophageal diverticulum (C), respectively.

● Repair If the patient develops recurrent aspirations in the setting of an esophageal pouch, an exploration of the chest and excision of the pouch should be performed. For tracheal stenosis, depending on the location of the stenosis, treatment options include resection, costal cartilage grafting, and stenting.17 ● Prevention During dissection, the ﬁstula should be circumferentially controlled and occluded. Once dissected free of

surrounding tissue, the ﬁstula should be ligated with a 1-mm cuff on the tracheal side (Fig. 83–2).

Dissection of the Proximal and Distal Esophageal Pouch Esophageal/Tracheal Injury ● Consequence Esophageal stricture is discussed in the section on “Esophageal Stenosis,” later.

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Esophageal disruption/anastomotic leak are discussed in the section on “Esophageal Leak,” later. Grade 3/4/5 complication ● Repair Special care must be taken during the dissection to minimize the amount of damage to the normal esophagus. If an injury occurs, primary repair should be performed to conserve native esophagus. ● Prevention The distal esophagus is particularly susceptible to injury during dissection. Dissection should involve locating the proximal portion of the distal esophagus and encircling it with a vessel loop just distal to the ﬁstula in order to control the passage of further contents. No further dissection of the distal esophagus should be performed to minimize the tenuous blood supply from segmental branches of the aorta. In order to carry out the dissection of the proximal esophagus and aid in its identiﬁcation, the anesthesiologist pushes against a 20-Fr catheter in the proximal esophageal pouch. A transmural stitch placed through the ﬁstula and incorporating the catheter also makes manipulation of the proximal esophagus less traumatic.

Long Gap Atresia ● Consequence The ﬁnding of a long gap atresia signiﬁcantly alters the options for repair (Fig. 83–3). Grade 2/3/4 complication ● Repair Current techniques of correcting long gap atresia include cervical esophagostomy with eventual esophageal replacement, circular esophagomyotomy, bouginage, esophageal reconstruction using a ﬂap from the proximal stump, and extrathoracic traction stitches.18–21 Every effort should be made to maintain the native esophagus because children whose native esophagus is preserved have better swallowing function and less gastroesophageal reﬂux.22 If the ends of the proximal and distal esophagus cannot be brought together, the initial maneuver would include careful dissection of the distal end. Classic teaching discourages dissection of the distal esophageal dissection, but the risks of this have been a subject of debate. In studies by Lessin and colleagues,23 distal esophageal dissection allowed for primary closure without signiﬁcant morbidity. If dissection of the distal esophageal pouch is unsuccessful, an attempt should be made at closing the anastomosis primarily under tension. In previous studies with ultra– long gap atresias measuring greater than 3.5 cm, none of eight children developed anastomotic leaks, disruptions, recurrent TEFs or deaths; however, tension did lead to a signiﬁcant stricture rate (50%), and major gastroesophageal reﬂux disease (GERD) (63%) requiring Nissen funduplication.24 Three of the strictures responded to dilation

Figure 83–3 Radiograph represents an infant with long gap esophageal atresia. A nasogastric tube represents the extent of the proximal esophageal pouch. Note the biliary dilator in the distal esophagus representing the extent of the distal esophagus. This child has a gap of the esophagus of 3.5 vertebral bodies. (Courtesy of Dr. Jeff Lukish, National Naval Medical Center, Bethesda, MD.)

and one required resection. These data compare favorably with esophagomyotomies and esophageal replacement. When these maneuvers are unsuccessful, Livaditis circular myotomies can be performed.25 The timing for the myotomies has ranged from the initial operation to 2 months esophageal stretching.26,27 To create length, up to three circular myotomies can be performed. Previous studies in six children with myotomies reported no anastomotic leak or disruption in patients.27 However, one patient did develop a stricture that was amenable to dilation. Esophageal motility and swallowing were no different from children with EA who did not undergo myotomy. Delayed complications of circular myotomies include delayed ballooning and esophageal diverticulum formation.28,29 If the anastomosis is still unable to be performed, the distal esophagus should be oversewn and tacked to the prevertebral fascia to prevent retraction. Classically, a feeding gastrostomy and cervical esophagostomy is created for the neonatal period; however, this invariably leads to esophageal replacement using the colon or stomach. Another option includes delaying the deﬁnitive surgery until the esophagus lengthens to permit primary anasto-

83 TRACHEOESOPHAGEAL FISTULA AND ESOPHAGEAL ATRESIA REPAIR mosis by proximal pouch suction.30 Most clinicians recommend continuous proximal pouch suction to reduce the risk of aspiration, but more recently, investigators demonstrated the safety and efﬁcacy of intermittent suction every 10 to 30 minutes.31 Alternatively, Foker and coworkers19 described placing two sutures through the ends of the pouches and bringing these through the thoracic wall to be sequentially tightened to create length. Postoperatively, the sutures are lengthened approximately 1 to 2 mm daily until the esophageal ends are in close proximity. This method has been used to bridge gaps measuring 5.3 to 6.8 cm and could be performed in children weighing between 3.5 and 4 kg. Finally, a last option for a long gap atresia is replacement with a colon interposition, gastric tube, or gastric pull-up. The isoperistaltic gastric tube has been demonstrated to have better results than the colonic transposition.32 In a series of 173 children undergoing gastric tube transposition (127 with EA), the mortality rate was 5.2%. The anastomotic leak rate was 12%, and only 1 of these children did not close spontaneously. Anastomotic strictures developed in 20% and only 3 of 34 children did not respond to dilation, requiring resection. Swallowing difﬁculties were common (31%) and long lasting (16%). A late complication of the procedure included delayed gastric emptying. These data are in comparison with the colonic interposition, which has a mortality of 13.4%, a failure of graft rate of 14.3%, a leak rate of 30.3%, and stricture in 30.3%.33

End-to-end Anastomosis Esophageal Leak ● Consequence The incidence of postoperative anastomotic leak ranges from 10% to 21%.4,34–36 Leaks are usually evident by saliva or feedings appearing in the chest tube. The leaks are usually small and asymptomatic secondary to the extrapleural approach. If the leak is major, sepsis may ensue and surgical intervention is required. Grade 3/4/5 complication ● Repair In the setting of a minor leak, one may treat nonoperatively with broad-spectrum antibiotics and chest tube drainage. In contrast, a major leak usually requires prompt repair. The esophageal repair should involve primary closure with intercostal muscle with or without pleural patch and/or thoracic drainage.37 In seven patients with a major esophageal disruption, circumferential disruptions ranged from 15% to 85%. In follow up of their gastrointestinal function, ﬁve of the seven children were tolerating oral feedings, one had severe neurologic impairment of eating, and only one demonstrated a recurrent lead with associated mediastinitis. If attempted esophageal repair is unsuccessful, a divert-

853

Figure 83–4 Because the esophagus lacks serosa, the surgeon needs to take signiﬁcant bites of the mucosa to reduce the chances of leak. The mucosa has a characteristic whitish, heaped-up look that should be sought for with each bite.

ing cervical esophagostomy with gastrostomy should be performed with a planned esophageal replacement in the future. ● Prevention The rate of esophageal anastomotic leak is reduced by using a double-layer closure (17% vs. 6.2%)34; however, this lower leak rate comes at the cost of an increased stricture rate. The minor nature of most leaks makes the leak the lesser of complications; therefore, most surgeons favor a single-layered closure with higher leak and lower stricture rates. The surgeon needs to take signiﬁcant bites of the mucosa to reduce the chances of leak (Fig. 83–4). An additional protective step to reduce the signiﬁcance of a leak is to perform the repair via an extrapleural approach.

Esophageal Stenosis ● Consequence Children with strictures usually present with gastrointestinal symptoms such as dysphasia, poor feeding, and emesis in 80% of cases; 8% of children present with foreign body obstruction with food; and 12% present with recurrent pneumonias secondary to aspirations.38 The rate of esophageal stricture ranges widely from 18% to 50%.34,39 In order to qualify as a stricture, the narrow segment of esophagus must be obstructing.

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SECTION XIII: PEDIATRIC SURGERY and repeated two or three times per intervention.41 The size of the balloon should be 2 to 5 mm larger than the stricture, and if dilation is easily accomplished, the balloon may be increased in size by 2 mm per step. The procedure should be repeated weekly until the SI is less than 10%. ● Prevention Strictures result from anastomotic ischemia, leaks, and gastroesophageal reﬂux. The risk of anastomotic leak increases with tension and local ischemia at the suture line. Anastomotic strictures are more common after repair of a gap larger than 2.5 cm, which is believed to be secondary to the tension.38 In a subjective estimate of the degree of tension in the end-to-end anastomosis, surgeons reported moderate to severe tension in 60% of cases.42 In addition to anastomotic ischemia, GERD may play a role in the development of esophageal strictures. Gastroesophageal reﬂux was present in 52% of children with strictures versus only 22% of children without strictures.43 Management of GERD is, therefore, an important part of the treatment of esophageal strictures.11

Recurrent TEF

Figure 83–5 Radiograph represents a barium swallow after esophageal atresia repair. Note the esophagus is nearly obstructed at the site of the anastomosis, representing a severe stricture. (Courtesy of Dr. Jeff Lukish, National Naval Medical Center, Bethesda, MD.)

● Consequence A recurrent TEF occurs in 3% to 12% of children between 2 to 18 months after repair.4,34,35 Recurrent TEF usually presents with cough, choking, recurrent pneumonia, or cyanosis with feeding.11 Grade 3/4/5 complication

Frequently, the proximal pouch is baggy compared with the distal esophagus and requires a barium swallow to establish whether the narrowing is functionally obstructing (Fig. 83–5). Grade 2/3/4 complication

● Repair The location of the ﬁstula is usually at the location of the original ﬁstula. These recurrences usually never close spontaneously and will require some intervention. Novel, less aggressive techniques for closure include endoscopic application of ﬁbrin glue.44

● Repair Most strictures will respond to dilation and usually present after 6 months. Those strictures that present prior to 6 months generally require surgical intervention. Multiple dilations have been shown to be necessary in 26% of children during the ﬁrst 5 years of life.40 If the strictures are resistant to repeated dilations, resection or stricturoplasty is the best option to preserve the esophagus. To guide the surgeon in performing balloon dilation, the stricture index (SI) may be used39: A −a A where A is the diameter of the lower pouch of the esophagus and a is the stricture diameter. Balloon dilation is performed for strictures that are greater than 50% of the esophageal lumen. These can be performed under radiographic assistance with the balloon applying pressure to 3 atmospheres over 1 to 2 minutes, SI =

● Prevention Previous studies demonstrated less recurrence in patients who have had minimal mobilization of the esophagus, one-layer closure, and end-to-end anastomosis using absorbable sutures.45 Recurrent TEFs form more frequently when the tracheal closure and the esophageal ﬁstula are in close proximity and in the setting of a previous esophageal leak.46 Techniques to reduce the chances of a TEF include pleura, intercostal muscles, or pericardial interposition graft with minimal mobilization of the distal esophagus and careful dissection of the esophagus from the posterior tracheal wall.

Other Complications GERD ● Consequence Postoperative GERD occurs in 35% to 58% of patients.4,34,40,43 Furthermore, using an esophageal pH

83 TRACHEOESOPHAGEAL FISTULA AND ESOPHAGEAL ATRESIA REPAIR probe, pathologic GERD may be observed in two thirds of children after repair.47 The presence of GERD has been implicated in contributing to leaks, strictures, aspiration leading to pneumonia, bronchial hyperreactivity, lung damage, cyanotic spells, and failure to thrive.4,11,43,48 Grade 2/3/4 complication ● Repair One third of patients fail medical therapy and will require surgical correction.40 The indications for surgical repair include failure of medical management as evidenced by persistent reﬂux symptoms, Barrett’s esophagitis, failure to thrive, stricture formation, or aspiration secondary to reﬂux. Options for correction include the Toupet (a 270° wrap) or a Thal (a partial anterior wrap). These should be considered for patients with severe dysmotility or small stomachs. The operation should take place from 6 to 21 months after the initial surgery.11 ● Prevention GERD is the result of delayed gastric emptying, displacement of the gastroesophageal junction owing to tension, and decreased esophageal clearance in the dysmotile esophagus.49 The surgical repair should not be compromised for the risk of developing GERD. Aggressive medical management should be pursued in the setting of GERD to reduce the rate of associated complications.

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9. Harrison M, Hanson B, Mahour G, et al. The signiﬁcance of right aortic arch in repair of esophageal atresia and tracheoesophageal ﬁstula. J Pediatr Surg 1977;12:861– 869. 10. Canty T, Boyle E, Linden B, et al. Aortic arch anomalies associated with long gap esophageal atresia and tracheoesophageal ﬁstula. J Pediatr Surg 1997;32:1587–1591. 11. Kovesi T, Rubin S. Long-term complications of congenital esophageal atresia and/or tracheoesophageal ﬁstula. Chest 2004;126:915–925. 12. Vukov B, Ukropina D, Bumbasirevic M, et al. Isolated serratus anterior paralysis: a simple surgical procedure to reestablish scapulo-humeral dynamics. J Orthop Trauma 1996;10:341–347. 13. Bianchi A, Sowande O, Alizai N, Rampersad B. Aesthetics and lateral thoracotomy in the neonate. J Pediatr Surg 1998;33:1798–1800. 14. Kalman A, Verebely T. The use of axillary skin crease incision for thoracotomies of neonates and children. Eur J Pediatr Surg 2002;12:226–229. 15. Holcomb G, Rothenberg S, Bax K, et al. Thoracoscopic repair of esophageal atresia and tracheoesophageal ﬁstula: a multi-institutional analysis. Ann Surg 2005;242:422– 430. 16. Gaissert H, Grillo H. Complications of the tracheal diverticulum after division of congenital tracheoesophageal ﬁstula. J Pediatr Surg 2006;41:842–844. 17. Kamata S, Usui N, Ishikawa S, et al. Experience in tracheobronchial reconstruction with a costal cartilage graft for congenital tracheal stenosis. J Pediatr Surg 1997; 32:54–57. 18. Al-Qahtani A, Yazbeck S, Rosen N, et al. Lengthening technique for long gap esophageal atresia and early anastomosis. J Pediatr Surg 2003;38:737–739. 19. Foker J, Linden B, Boyle E, Marquardt C. Development of a true primary repair for the full spectrum of esophageal atresia. Ann Surg 1997;226:533–541. 20. Hendren W, Hale J. Esophageal atresia treated by electromagnetic bouginage and subsequent repair. J Pediatr Surg 1976;11:712–722. 21. Eraklis A, Rosello P, Ballantine T. Circular esophagomyotomy of upper pouch in primary repair of long-segment esophageal atresia. J Pediatr Surg 1976;11:709–712. 22. Puri P, Ninan G, Blake N, et al. Delayed primary anastomosis for esophageal atresia: 18 months’ to 11 years’ follow-up. J Pediatr Surg 1992;27:1127–1130. 23. Lessin M, Wesselhoeft C, Luks F, DeLuca FG. Primary repair of long-gap esophageal atresia by mobilization of the distal esophagus. Eur J Pediatr Surg 1999;9:369–372. 24. Boyle E, Irwin E, Foker J. Primary repair of ultra-longgap esophageal atresia: results without a lengthening procedure. Ann Thorac Surg 1994;57:576–579. 25. Livaditis A, Radberg L, Odensjo G. Esophageal end to end anastomosis: reduction of anastomotic tension by circular myotomy. Scand J Thorac Cardiovasc Surg 1972;6:206–214. 26. Kimura K, Nishimima E, Tsugawa C, et al. Multistaged extrathoracic esophageal elongation procedure for long gap esophageal atresia: experience with 12 patients. J Pediatr Surg 2001;36:1725–1727. 27. Giacomoni M, Tresoldi M, Zamana C, Giacomoni A. Circular myotomy of the distal esophagus stump for long gap esophageal atresia. J Pediatr Surg 2001;36:855–857.

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28. Otte J, Gianello P, Wese F, et al. Diverticulum formation after circular myotomy for esophageal atresia. J Pediatr Surg 1984;19:68–71. 29. Janik J, Filler R, Ein S, Simpson J. Long-term follow-up circular myotomy for esophageal atresia. J Pediatr Surg 1980;15:835–841. 30. Rescorla F, West K, Scherer LR, Grosfeld J. The complex nature of type A (long-gap) esophageal atresia. Surgery 1994;116:658–664. 31. Aziz D, Schiller D, Gerstle J, et al. Can “long-gap” esophageal atresia be safely managed at home while awaiting anastomosis? J Pediatr Surg 2003;38:705–708. 32. Spitz L, Kiely E, Pierro A. Gastric transposition in children—a 21-year experience. J Pediatr Surg 2004;39: 276–281. 33. Ahmed A, Spitz L. The outcome of colonic replacement of the esophagus in children. Prog Pediatr Surg 1986;19: 37–54. 34. Manning P, Morgan R, Coran A, et al. Fifty years’ experience with esophageal atresia and tracheoesophageal ﬁstula. Beginning with Cameron Haight’s ﬁrst operation in 1935. Ann Surg 1986;204:446–453. 35. Spitz L, Kiely E, Brereton R. Esophageal atresia: ﬁve-year experience with 148 cases. J Pediatr Surg 1987;22:103– 108. 36. Randolph J, Newman K, Anderson K. Current results in repair of esophageal atresia with tracheoesophageal ﬁstula using physiologic status as a guide to therapy. Ann Surg 1989;209:526–530. 37. Chavin K, Field G, Chandler J, et al. Save the child’s esophagus: management of major disruption after repair of esophageal atresia. J Pediatr Surg 1996;31:48–51. 38. McKinnon L, Kosloske A. Prediction and prevention of anastomotic complications of esophageal atresia and tracheoesophageal ﬁstula. J Pediatr Surg 1990;25:778– 781.

39. Chetcuti P, Phelan P. Gastrointestinal morbidity and growth after repair of oesophageal atresia and tracheooesophageal ﬁstula. Arch Dis Child 1993;68:163–166. 40. Little D, Rescorla F, Grosfeld J, et al. Long-term analysis of children with esophageal atresia and tracheoesophageal ﬁstula. J Pediatr Surg 2003;38:852–856. 41. Said M, Mekki M, Golli M, et al. Balloon dilation of anastomotic strictures secondary to surgical repair of oesophageal atresia. Br J Radiol 2003;76:26–31. 42. Yanchar NL, Gordon R, Cooper M, et al. Signiﬁcance of the clinical course and early upper gastrointestinal studies in predicting complications associated with repair of the esophageal atresia. J Pediatr Surg 2001;36:813–822. 43. Chittmittrapap S, Spitz L, Kiely E, Brereton R. Anastomotic stricture following repair of esophageal atresia. J Pediatr Surg 1990;25:508–511. 44. Ng W, Luk H, Lau C. Endoscopic treatment of recurrent tracheoesophageal ﬁstulae: the optimal technique. Pediatr Surg Int 1999;15:449–450. 45. Myers N, Beasley S, Auldist A. Secondary esophageal surgery following repair of esophageal atresia with distal tracheoesophageal ﬁstula. J Pediatr Surg 1990;25:773– 777. 46. Ein S, Stringer D, Stephens C, et al. Recurrent tracheoesophageal ﬁstulas: seventeen-year review. J Pediatr Surg 1983;18:436–441. 47. Biller J, Allen J, Schuster S, et al. Long-term evaluation of esophageal and pulmonary function in patients with repaired esophageal atresia and tracheoesophageal ﬁstula. Dig Dis Sci 1987;32:985–990. 48. Chetcuti P, Phelan P. Respiratory morbidity after repair of oesophageal atresia and tracheo-esophageal ﬁstula. Arch Dis Child 1993;68:167–170. 49. Koch A, Rohr S, Plaschkes J, Bettex M. Incidence of gastroesophageal reﬂux following repair of the esophageal atresia. Prog Pediatr Surg 1986;19:103–113.

84

Congenital Diaphragmatic Hernia T. A. Rothenbach, MD and A. Alfred Chahine, MD INTRODUCTION Congenital diaphragmatic hernias (CDHs) occur in approximately 1 out of every 2500 live births. The true incidence is likely higher because some fetuses do not survive to birth. The two most common types of CDH are Bochdalek (posterolateral) and Morgagni (anterior). The development of the diaphragm defect is ﬁrst noticeable in the 8th week of gestation. Bochdalek-type defects tend to occur more commonly on the left than the right. The actual pathophysiology of the CDH lies not in the physical defect, but in the resultant pulmonary hypoplasia and hypertension that occur. The exact mechanism of these physiologic responses to the CDH remains poorly understood. CDH can be diagnosed by fetal sonogram. Once diagnosed, a work-up should ensue to rule out concomitant anomalies. This should include a chromosomal analysis as well as evaluation of the cardiac, gastrointestinal, and genitourinary systems. Most infants present shortly after birth with respiratory distress. Immediate care includes endotracheal intubation and placement of a nasogastric tube and central access. Diagnosis is conﬁrmed by plain ﬁlm. Depending on the degree of physiologic compromise caused by the pulmonary hypoplasia and hypertension, interventions such as nitric oxide administration, high-frequency oscillating ventilation, and extracorporeal membrane oxygenation (ECMO) may be necessary. Timing for repair is determined by the infant’s physiologic condition and response to interventions. As previously stated, the pulmonary hypertension and degree of pulmonary hypoplasia—not the presence of abdominal viscera in the chest—are the source of physiologic derangement. These realizations have led to a shift from urgent repair of CDH to delayed repair when the infant is stable from a pulmonary hypertension standpoint. The timing of repair of infants who require ECMO intervention remains controversial. The standard approach for repairing a CDH in neonates remains the open approach. Laparoscopic and thoracoscopic repairs have been reported but have been fraught with high conversion rates, long operative times, and high recurrence rates.1–4 Yang and coworkers2 suggested anatomic (presence of the stomach in the abdomen) and

physiologic (minimal ventilator requirements and no evidence of pulmonary hypertension) criteria for successful thoracoscopic repair in neonates.

INDICATION ● Presence of a CDH

OPERATIVE STEPS Step 1

Step 2 Step 3

Step 4 Step Step Step Step

5 6 7 8

Infant is placed on operating table in supine position under warming lights with small roll placed under infant’s ﬂank on affected side Prepare patient to have access to both thoracic cavities Gentle reduction of abdominal contents from chest to allow visualization of diaphragmatic defect Inspection for extralobar pulmonary sequestration Inspection for, and excision of, hernia sac Creation of tension-free closure Placement of chest tube Monitor pulmonary tidal volume while closing abdominal wall

OPERATIVE PROCEDURE Anesthetic Preparation Small, critically ill patients require close monitoring throughout the procedure. Appropriate presurgical preparation includes increasing the temperature in the operating room, placing overhead warming lights on the infant, placing an arterial line for monitoring of preductal blood gases, nasogastric tube placement, and Foley catheter placement.

Skin Preparation of Both Thoracic Cavities Occasionally, these infants may develop a contralateral pneumothorax, severely compromising pulmonary

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function. This will require rapid placement of the chest tube on the contralateral thorax.

Gentle Reduction of the Abdominal Viscera from the Thoracic Cavity After making a left subcostal incision, gentle downward retraction is placed on the viscera in the thoracic cavity.

Injury to Solid Organs or Hollow Viscus Organ ● Consequence Inappropriate retraction of the small or large intestine can lead to intramural hematomas. More commonly, aggressive reduction of the liver and spleen can lead to hemorrhage. Grade 2–4 complication ● Repair If hematomas of small and large bowel are identiﬁed, they should be closely inspected. If there is concern for a full-thickness injury to the involved intestine, resection should be carried out with a primary anastomosis in cases in which the infant is stable. The larger concern is for potential injury to the liver and spleen. When encountered, control of liver bleeding in a neonate is best achieved with compression of the liver and topical hemostatic agents. Further interventions are often more harmful than helpful. Initial management of splenic or renal lacerations should be handled in a similar fashion. ● Prevention Gentle distraction of the bowel, either manually or with the use of atraumatic forceps, will help prevent bowel or mesenteric injury. When reducing the stomach, care must be taken to avoid excessive stretch on the short gastric vessels. With careful manual reduction of the solid viscera, injury can usually be avoided. In order to maintain the intra-abdominal position of each organ as it is reduced, placement of laparotomy pads under retractors can be helpful in avoiding solid organ injury.

Inspection for Extralobar Pulmonary Sequestration Missed Extralobar Pulmonary Sequestration ● Consequence Two problems can arise from management of an extralobar pulmonary sequestration associated with a CDH. The ﬁrst complication is failure to recognize the lesion. Approximately 10% of patients with CDH will have a concomitant extralobar pulmonary sequestration (Fig. 84–1). These are usually located along the border of the diaphragm. The second complication is inadequate ligation of the blood supply to the sequestration, leading to hemorrhage. Grade 2/3 complication

Figure 84–1 Extralobar pulmonary sequestration presenting in conjunction with a congenital diaphragmatic hernia (CDH). Failure to recognize it intraoperatively might result in a need for a second operation or hemorrhage if its systemic blood supply from the aorta is not adequately controlled.

● Repair Failure to recognize a pulmonary sequestration may result in the patient requiring a second operative procedure later in life when the lesion becomes symptomatic or is discovered under other circumstances. Obviously, inadequate ligation of the blood supply to a pulmonary sequestration will result in blood loss and possible need for reexploration. ● Prevention All patients with CDH should undergo inspection for the presence of an associated pulmonary sequestration. When present, the blood supply should be carefully delineated and ligated.

Inspection for, and Excision of, a Hernia Sac Missed Hernia Sac Up to 20% of patients with a CDH will have an associated hernia sac covering the abdominal viscera and bulging into the thoracic cavity.5 ● Consequence The sac needs to be excised prior to closing the defect. Failure to do so predisposes to a recurrence.6 Grade 3 complication ● Repair A recurrent CDH needs to be repaired, requiring a repeat laparotomy or thoracotomy. ● Prevention Complete excision of the hernia sac will allow a better closure of the defect.

Creation of a Tension-free Repair Closure under Tension ● Consequence After the defect is inspected, the decision is made to close the defect primarily or with a patch. Whenever

84 CONGENITAL DIAPHRAGMATIC HERNIA

859

Posterior remnant of diaphragm

Parietal peritoneum

A

Side view Right angle clamp

B Parietal peritoneum

Figure 84–2 Hidden anatomy. A, Often, the posterior remnant of the diaphragm is rolled up like a shade under a layer of parietal peritoneum. B, It needs to be carefully unrolled to optimize the amount of diaphragm available for repair so that tension is minimized.

possible, primary closure is preferred. When necessary to provide a tension-free repair, placement of a patch may be required. Closure of the defect under tension increases the risk of a recurrent hernia defect.7 The incidence of recurrence has been reported to vary between 5% and 50%.8 Grade 3 complication ● Repair Recurrent CDH will require reoperation. In cases of failed primary repairs, patch closure should be considered. In patients with a failed patch closure, repair of the defect with a latissimus dorsi ﬂap or replacement of the patch can be performed.9

● Prevention When performing primary closure of the CDH, adequate diaphragmatic remnant should be present. Often, the remnant is rolled up like a shade under a layer of parietal peritoneum covering the retroperitoneum5 (Fig. 84–2). Solid bites of tissue should be taken using nonabsorbable suture. If an adequate remnant is not present, closure should proceed with patch materials, which portends a higher rate of recurrence.10 In performing a patch closure, adequate native tissue should be included in each suture. In infants with agenesis of the diaphragm or a large defect, placement of the sutures around the nearest rib may be necessary. Medially, the patch may need to be secured to the crus. The

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patch should not be secured to the aortic adventitia or the esophagus.

Placement of a Chest Tube The use of a chest tube after a CDH repair is not universal. The main beneﬁt of having one postoperatively is in case a pneumothorax develops from the small hypoplastic lung.

Suction on the Chest Tube ● Consequence After repair of a CDH, there is always an empty space in the ipsilateral thorax because the neodiaphragm cannot move up and the hypoplastic lung cannot expand. It slowly ﬁlls up with ﬂuid over the ﬁrst few days. If suction is applied on a chest tube, it will draw the very compliant neonatal mediastinum toward the repair very quickly, potentially causing a cardiovascular collapse. Grade 5 complication ● Repair Suction should be removed immediately to allow the mediastinum to spring back toward the contralateral side. ● Prevention If a chest tube is placed, the suction port should be covered with tape to avoid inadvertent connection to suction.

Monitor Pulmonary Tidal Volume While Closing the Abdominal Wall Creation of Abdominal Compartment Syndrome ● Consequence If tidal volumes are not monitored during abdominal wall closure, an iatrogenic abdominal compartment syndrome could be missed. This circumstance may lead to postoperative ventilatory problems, decreased urinary output, and poor intra-abdominal perfusion. Grade 2/3 complication ● Repair Operative reexploration will be required to examine the intestinal viscera for viability and placement of an abdominal patch. ● Prevention Communication with the anesthesiologist during the ﬁnal stage of the procedure can help prevent this complication. Prior to returning the intestinal viscera to the abdomen, the surgeon should know the peak airway pressure. As the viscera are returned to the abdomen and the abdominal wall is closed, this variable should continue to be checked. If airway pressures jump precipitously or the abdominal wall feels excessively tight, primary closure of the abdominal wall should be aborted and a patch closure undertaken.

Other Complications Chylothorax The occurrence of a chylothorax after the repair of a CDH has been reported.8,11–14 It seems to correlate with the need for ECMO,11 the use of a prosthetic patch,11,12 and the presence of a hernia sac.13 It is probably related to abnormal mediastinal lymphatics rather than to a direct injury during repair.8 Regardless of the pathogenesis of chylothorax, it invariably responds to nonoperative medical therapy.11–14 Grade 1 complication

REFERENCES 1. Knight CG, Gidell KM, Lanning D, et al. Laparoscopic Morgagni hernia repair in children using robotic instruments. J Laparoendosc Adv Surg Tech A 2005;15:482– 486. 2. Yang EY, Allmendinger N, Johnson SM, et al. Neonatal thoracoscopic repair of congenital diaphragmatic hernia: selection criteria for successful outcome. J Pediatr Surg 2005;40:1369–1375. 3. Holcomb GW 3rd, Ostlie DJ, Miller KA. Laparoscopic patch repair of diaphragmatic hernias with Surgisis. J Pediatr Surg 2005;40:E1–E5. 4. Arca MJ, Barnhart DC, Lelli JL Jr., et al. Early experience with minimally invasive repair of congenital diaphragmatic hernias: results and lessons learned. J Pediatr Surg 2003; 38:1563–1568. 5. Stolar CJ, Dillon PW. Congenital diaphragmatic hernia and eventration. In Grosfeld JL, O’Neill JA Jr, Coran AG, et al (eds): Pediatric Surgery, Vol 1. Philadelphia: Mosby Elsevier, 2006; pp 931–954. 6. Puri P. Congenital diaphragmatic hernia. Curr Probl Surg 1994;31:787–846. 7. Rowe DH, Stolar CJ. Recurrent diaphragmatic hernia. Semin Pediatr Surg 2003;12:107–109. 8. Cullen ML. Congenital diaphragmatic hernia: operative considerations. Semin Pediatr Surg 1996;5:243–248. 9. Saltzman DA, Ennis JS, Mehall JR, et al. Recurrent congenital diaphragmatic hernia: a novel repair. J Pediatr Surg 2001;36:1768–1769. 10. Moss RL, Chen CM, Harrison MR. Prosthetic patch durability in congenital diaphragmatic hernia: a long-term follow-up study. J Pediatr Surg 2001;36:152–154. 11. Hanekamp MN, Tjin ADGC, van Hoek-Ottenkamp WG, et al. Does V-A ECMO increase the likelihood of chylothorax after congenital diaphragmatic hernia repair? J Pediatr Surg 2003;38:971–974. 12. Oshio T, Matsumura C. Chylothorax following Bochdalek herniorrhaphy in an infant. J Pediatr Surg 1983;18:298– 299. 13. Kavvadia V, Greenough A, Davenport M, et al. Chylothorax after repair of congenital diaphragmatic hernia—risk factors and morbidity. J Pediatr Surg 1998;33:500–502. 14. Naik S, Greenough A, Zhang YX, Davenport M. Prediction of morbidity during infancy after repair of congenital diaphragmatic hernia. J Pediatr Surg 1996;31:1651–1654.

85

Wilms’ Tumor and Neuroblastoma Todd A. Ponsky, MD Wilms’ Tumor INTRODUCTION Nephroblastoma, also known as Wilms’ tumor after Max Wilms who described seven cases in 1899, is the most common intra-abdominal cancer in children. Wilms’ tumor represents 6% of all pediatric cancers and the incidence is 8 cases per 1 million children younger than 15 years of age or 1 in 10,000 infants.1 Seventy-ﬁve percent of cases occur in children under 5 years of age, and the peak incidence is 2 to 3 years of age.2 Surgical therapy for Wilms’ tumor was ﬁrst described in 1877, with poor outcomes. Over the next 100 years, the operative strategy for Wilms’ tumor was modiﬁed to include the addition of chemotherapy and, occasionally, radiation. Furthermore, a cooperative study of several groups called the National Wilms’ Tumor Study (NWTS) developed treatment standards that have improved overall survival to approximately 95.6% for stage 1 tumors.3 Children suspected of having a renal mass should undergo an abdominal ultrasound (US). Besides conﬁrming the presence of the tumor, abdominal US is necessary to assess contralateral disease and evidence of caval invasion. Chest x-ray should be performed to assess for metastatic disease.

INDICATIONS ● Renal mass on computed tomography (CT) or US

scan

OPERATIVE STEPS Step 1 Step 2 Step 3 Step 4 Step 5 Step 6

Position patient with affected side elevated on roll Transverse abdominal incision Thorough abdominal exploration, reﬂection of colon off of tumor Exploration of contralateral kidney Ligation of hilar vessels Division of lateral attachments

Step Step Step Step

7 8 9 10

Separation of kidney from adjacent organs Perinephric lymph nodes dissection Ureter ligation Removal of kidney and abdominal wall closure

OPERATIVE PROCEDURE Incision Poor Exposure/Tumor Spillage Prior to incision, the involved side should be slightly elevated with a roll. The optimal incision for Wilms’ tumor is a transverse abdominal incision, which offers the best exposure. A large incision is crucial in order to avoid excessive tumor manipulation and potential tumor spill. Flank incisions offer suboptimal exposure. ● Consequence Poor exposure may lead to excessive tumor manipulation, which may lead to tumor rupture and spillage. Spillage of tumor will automatically upgrade the tumor to stage 3, which will require postoperative radiation and the addition of doxorubicin (Adriamycin) to the chemotherapy regimen. Grade 4 complication ● Repair If the initial incision offers poor exposure, it would be prudent to extend the incision rather than struggle. Once spillage occurs, there is no remedy. ● Prevention Poor exposure can be prevented by elevating the affected side with a roll and creating a generous transverse incision.

Exploration of the Contralateral Kidney Contralateral Wilms’ Tumor Identiﬁed Intraoperatively Although controversial, many surgeons will explore the contralateral kidney prior to nephrectomy. Gerota’s fascia is incised, the kidney is palpated and visually inspected on all sides, and any lesions are biopsied.

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● Consequence Occasionally, contralateral tumor that was not visualized on preoperative studies is identiﬁed intraoperatively. This may require a complete change in the anticipated management. Grade 3 complication ● Repair If a mass is identiﬁed in the contralateral kidney intraoperatively, it should be biopsied. If the biopsy conﬁrms Wilms’ tumor, the operation should be aborted and neoadjuvant chemotherapy should be performed. ● Prevention Preoperative US and CT scans should signiﬁcantly reduce the chance of a contralateral tumor being identiﬁed intraoperatively.

Renal Hilum Ligation Ligation of the Contralateral Vessels Sometimes, the large renal mass encroaches on the hilum so much that it thins out the inferior vena cava (IVC) and the ipsilateral renal artery and vein and lifts the contralateral renal vessels up, making them susceptible to injury or ligation (Fig. 85–1).

● Consequence Ischemia of the contralateral normal kidney. Grade 4 complication ● Repair Repair of the injury can be attempted. Bypass of the contralateral renal vessels might be necessary if the injury was crushing or extensive. ● Prevention It is essential to completely identify both sets of renal vessels and their junction with the IVC and aorta to avoid inadvertent injury to the contralateral vessels.

Tumor Spillage Ideally, the renal vein is ligated prior to tumor manipulation. However, large tumors may make early vein ligation prohibitively unsafe. Attempts at early vein ligation in the face of poor exposure may lead to tumor spillage. Although some investigators speculated that delayed vein ligation may increase the chance of pulmonary embolism,4,5 results from the NWTS-1 and -2 showed that delayed renal vein ligation did not lead to a worse outcome when compared with early vein ligation.6

Renal mass

Left renal vein

Superior mesentery artery

Right kidney Abdominal aorta

Right renal vein Inferior vena cava

Figure 85–1 Hidden anatomy. When a right renal mass extends into the hilum, it ﬂattens the short right renal vein and lifts up the longer left renal vein. This puts the latter at risk for being mistaken for the right renal vein and ligated inadvertently.

85 WILMS’ TUMOR AND NEUROBLASTOMA ● Consequence Poor exposure of the renal vein may lead to excessive tumor manipulation and tumor rupture and spillage. Spillage of tumor will automatically upgrade the tumor to stage 3, which will require postoperative radiation and the addition of doxorubicin (Adriamycin) to the chemotherapy regimen. Grade 4 complication ● Repair Once spillage occurs, there is no remedy. ● Prevention If a large renal mass prevents optimal exposure of the renal vein, vein ligation should be delayed until after the mass has been mobilized.

Intravascular Extension Bleeding/Pulmonary Tumor Embolism Occasionally, extension of the tumor into the renal vein or the IVC is identiﬁed on preoperative imaging studies. If the proximal extent of the tumor thrombus can be palpated, proximal and distal control of the IVC is obtained, a venotomy is performed, and the thrombus is removed. If the proximal extent cannot be identiﬁed, an alternative approach is necessary. Some surgeons will perform a venotomy without proximal control and suck the thrombus out of the IVC. Others may remove the thrombus after placing the patient on cardiopulmonary bypass. Tumor thrombectomy may be complicated by bleeding and pulmonary embolism. ● Consequence Care must be taken to ensure that the proximal extent of the tumor thrombus is identiﬁed prior to placing the proximal clamp on the IVC or embolism may occur. Attempts at removing a high thrombus with proximal control may lead to signiﬁcant bleeding. Grade 4/5 complication ● Repair Hypoxia, hypotension, and decreased end-tidal CO2 after placement of the proximal caval clamp are highly suspicious of a pulmonary tumor embolism. If hypoxia and hypotension persist, median sternotomy, cardiopulmonary bypass, and pulmonary artery thrombectomy may be necessary. Some centers may utilize ﬂuoroscopic suction thrombectomy through the IVC. ● Prevention Preoperative Doppler US may help identify renal or IVC involvement. The proximal extent may be visualized, which will help to plan the operative approach. Neoadjuvant chemotherapy is very effective at shrinking or often completely eliminating tumor thrombus.

863

Division of Lateral Renal Attachments/ Perinephric Lymph Node Biopsy/Dissection of the Kidney off of the Surrounding Organs Injury to the Surrounding Organs After control of the renal hilum is achieved, the kidney is separated from its surrounding attachments. First, the lateral attachments are divided, and then the kidney is separated from the surrounding organs. If the tumor is involving a surrounding organ such as the liver or diaphragm, it should be resected en bloc if this can be done safely. ● Consequence En-bloc resection of involved organs may be more hazardous than leaving tumor behind. For example, resection of a major segment of liver may lead to signiﬁcant bleeding, and pancreatic resection may lead to a pancreatic ﬁstula. Grade 3/4 complication ● Repair If there is any question regarding the safety of en-bloc resection, tumor should be left behind and treated with chemotherapy and radiation. ● Prevention Preoperative CT scans may help identify or suggest surrounding organ involvement and help to plan the operation.

Neuroblastoma INTRODUCTION Neuroblastoma is the most common solid malignancy in childhood. Because it is a tumor of neural crest cell origin, the tumor can develop anywhere along the path of neural crest cell migration.7,8 Fifty percent of neuroblastomas are found in the adrenal medulla, 25% in the paraspinal ganglia, 20% in the posterior mediastinum, and 5% in the neck or pelvis.9–11 Most cases of neuroblastoma present as an abdominal mass. Twenty-ﬁve percent of children present with hypertension as a result of the catecholamines secreted from the tumor.9 Forty percent of patients are younger than 1 year, 35% are aged 1 to 2 years, and 25% are older than 2 years. More than 40% of patients present with metastatic disease.8 Children who present with localized disease have a good prognosis (90% 3-year survival), whereas children who present with metastatic disease have 20% 5-year survival. Curative resection is the goal of therapy for children with localized disease. Children with regional spread or metastatic disease will require surgical biopsy, but primary therapy consists of chemotherapy and radiation.

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INDICATIONS Surgical resection is indicated if the mass appears to be resectable on preoperative imaging. If there is evidence that the mass has neurovascular invasion or if it appears that the mass cannot be completely resected, resection should not be attempted. In these situations, open surgical biopsy should be performed for histologic conﬁrmation.

“Claw” sign

OPERATIVE STEPS The steps of the operation vary depending on where the mass is located. In general, however, a generous incision to ensure adequate exposure is performed. Adequate proximal and distal control of any involved vessels should be attained prior to attempts at resection.

OPERATIVE PROCEDURE Pitfalls speciﬁc to neuroblastoma resection are discussed here.

Resection versus Biopsy Alone Preoperative Confusion of a Neuroblastoma with Wilms’ Tumor Unlike Wilms’ tumor, neuroblastoma is frequently adherent to its surrounding structures, making resection prohibitive. Therefore, if a CT scan reveals that the tumor is adherent to blood vessels or spinal components, attempts at resection should be avoided and a simple biopsy should be performed for neoadjuvant chemotherapy. However, Wilms’ tumor is often nonadherent and respectable, even though it may appear to be in close proximity to major vessels. Therefore, the approach to a Wilms’ tumor may be different than that for a neuroblastoma. Therefore, it is important to differentiate neuroblastoma from Wilms’ tumor on CT scan. This can be very difﬁcult, especially in an adrenal-based neuroblastoma. Sometimes, a neuroblastoma may look very similar to the classic “claw sign” seen with Wilms’ tumor. The claw sign is the name given to the CT scan ﬁnding in which the kidney “claws” around the tumor, suggesting that the tumor is arising from the kidney rather than externally compressing it (Fig. 85–2). ● Consequence Excessive bleeding or major injury to surrounding structures when attempts are made at resection because the neuroblastoma was believed to be Wilms’ tumor. Grade 3–5 complication

Figure 85–2 This tumor appears to be emanating from the kidney as a Wilms’ tumor. In fact, this is a neuroblastoma that was believed to be a Wilms’ tumor and attempts were made at resection. Notice the claw shape of the kidney that is classic for a Wilms’ tumor.

● Repair In cases of excessive bleeding, the abdomen can be packed and closed and the patient should be brought to the intensive care unit. ● Prevention Careful examination of the CT looking for signs of neuroblastoma such as calciﬁcations will help distinguish Wilms’ tumor from neuroblastoma. Some may argue that any tumor that appears to be distorting major vessels should be only biopsied at ﬁrst.

Resection Vascular Injury Because neuroblastoma often involves the aortocaval window and the central visceral vessels (celiac and superior and inferior mesenteric arteries), attempts at resecting a tumor that has vascular involvement may lead to critical and sometimes fatal vascular injury. ● Consequence Tissue ischemia or hemorrhage. Grade 3–5 complication ● Repair If vascular injury occurs, primary anastomosis or repair with a polytetraﬂuoroethylene (PTFE) graft may be possible. ● Prevention Any tumor with ANY suggestion of vascular involvement on preoperative imaging should probably be

85 WILMS’ TUMOR AND NEUROBLASTOMA

865

Aorta IVC

Portal vein

Figure 85–3 A large mass on the right is clearly distorting the inferior vena cava (IVC) and portal vein.

Figure 85–5 A large mass is involving the aorta.

REFERENCES SMA

Figure 85–4 A large mass is involving the superior mesenteric artery (SMA).

treated with primary chemotherapy prior to attempts at resection (Figs. 85–3 to 85–5). It is recommended to identify the anterior surface of the aorta away from the tumor and proceed along its adventitia to identify the root of the central visceral arteries. If this cannot be done safely, the resection should be aborted and a simple biopsy performed prior to closure.

1. Bernstein L, Linet M, Smith M. Renal tumors. In Gurney J (ed): Cancer Incidence and Survival among Children and Adolescents: United States SEER Program 1975– 1995. Bethesda, MD: National Cancer Institute, 1999; pp 79–90. 2. Davidoff A, Shochat S. Nephroblastoma (Wilms’ tumor). In Weber TR (ed): Operative Pediatric Surgery. New York: McGraw-Hill Professional, 2003; pp 1169– 1180. 3. D’Angio G, Breslow N, Beckwith J. Treatment of Wilms’ tumor: results of the Third National Wilms’ Tumor Study. Cancer 1989;64:349–360. 4. Shurin S. Fatal intraoperative pulmonary embolism of Wilms’ tumor. J Pediatr 1982;101:559. 5. Akyon M, Arsian G. Pulmonary embolism during surgery for Wilms’ tumour (nephroblastoma). Case report. Br J Anaesth 1981;59:903. 6. Leape L, Breslow N. The surgical treatment of Wilms’ tumor: results of the National Wilms’ Tumor Study. Ann Surg 1978;187:351. 7. Wright J. Neurocytoma or neuroblastoma, a kind of tumor not generally recognized. J Exp Med 1910;12: 556–561. 8. Davidoff A. Neuroblastoma. In Oldham K (ed): Principles and Practice of Pediatric Surgery, Vol 1. Philadelphia: Lippincott Williams & Wilkins, 2005; pp 571–593. 9. Grosfeld JL. Neuroblastoma. In O’Neill J (ed): Pediatric Surgery, Vol 1. St. Louis: Mosby, 1998; pp 405–419. 10. Grosfeld JL, Baehner RL. Neuroblastoma: an analysis of 160 cases. World J Surg 1980;4:29–37. 11. Gerson JM, Chatten J, Eisman S. Familial neuroblastoma: a follow-up. Letter. N Engl J Med 1974;290:1487.

86

Inguinal and Umbilical Hernias Earl Hodin, MD Inguinal Hernia INTRODUCTION Inguinal herniorrhaphy is one of the most common operations performed by the pediatric surgeon. Inguinal hernias in children are indirect, a result of a patent processus vaginalis.

● Repair Once severed, these nerves cannot be repaired in children; if entrapped, reoperation with release or division may be necessary. ● Prevention Lifting up of the aponeurosis during the division and careful identiﬁcation during dissection.

Separation of the Hernia Sac INDICATION ● Presence of inguinal hernia in child

An inguinal hernia in a child warrants repair to avoid the risk of incarceration. Unlike umbilical hernias in children, inguinal hernias do not close spontaneously.

OPERATIVE STEPS Step Step Step Step Step

1 2 3 4 5

Step 6 Step 7 Step 8 Step 9

Inguinal crease incision Division of Scarpa’s fascia Opening of external oblique aponeurosis Isolation of spermatic cord Separation of hernia from cord contents to internal ring Division of sac Contralateral laparoscopic exploration, if warranted (favored in some institutions) High ligation of sac Closure of external oblique aponeurosis and Scarpa’s fascia

External Oblique Aponeurosis Division Ilioinguinal and Iliohypogastric Nerve Injury ● Consequence Although division of these nerves may lead to a small area of anesthesia, entrapment by a suture can lead to signiﬁcant paresthesias, which can be considerably more troublesome. Grade 4 complication

Damage to the Vas Deferens ● Consequence Infertility is unlikely if only one vas has been damaged. Grade 4 complication ● Repair Primary repair should be attempted but, in smaller children, can be challenging. Successful repairs and fertility have been reported after puberty and in adulthood.1–4 ● Prevention When dissecting the hernia sac, the vas must be carefully identiﬁed and protected. A clamp should not be applied to the sac before the vas is identiﬁed. The vas and vessels should be gently teased away from the sac and never grasped with a forceps. Merely picking up the vas with forceps has been shown to lead to ﬁbrotic luminal occlusion in rats.5,6

Damage to the Spermatic Vessels ● Consequence Ischemic orchitis and atrophy of the affected testicle.7 Grade 4 complication ● Repair The spermatic vessels in children are too small to repair. ● Prevention Careful, atraumatic dissection of the cord; the use of magnifying lenses can be helpful.

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High Ligation of the Sac Tear in the Sac ● Consequence Hernia recurrence.7 Grade 3 complication

● Prevention Inspecting the anteromedial wall of the hernia sac prior to high ligation will prevent injuries to sliding organs. If present, the transﬁxion and ligation of the sac should be distal to the sliding organ, and consideration should be given to narrowing the internal ring if needed.

● Repair The sac should be repaired with a ﬁne suture if a tear is discovered.

Laparoscopic Contralateral Exploration

● Prevention Tears are common in the premature or ex-premature infant with a large, thin sac. It is a good idea to open the dissected sac prior to ﬁnal ligation to ascertain that the entire circumference of the sac is being incorporated in the ligature.

Incomplete Evacuation of the Pneumoperitoneum

Injury to Sliding Organs Pelvic organs such as the bladder, cecum, appendix, sigmoid colon, and fallopian tubes can form part of the anteromedial wall of the hernia sac as a sliding component. ● Consequence When the sac is ligated high at the internal ring, these sliding organs can be ligated or lacerated7 (Fig. 86–1). Grade 3/4 complication ● Repair Injuries to sliding organs are usually detected postoperatively and require further procedures.

This technique is employed in some centers as a means for assessing the need for contralateral repair.

● Consequence Subcutaneous emphysema and hernia recurrence.8 Grade 3 complication ● Repair The sac should be reopened and the pneumoperitoneum evacuated. ● Prevention The pneumoperitoneum should be evacuated thoroughly prior to closing the sac with the patient in the Trendelenburg position, a Valsalva maneuver performed by the anesthesiologist, and the internal ring stented open.

Closure of the External Oblique Aponeurosis Entrapment of the Cremaster ● Consequence Iatrogenic or acquired undescended testicle.9 Grade 3 complication ● Repair If an iatrogenic undescended testis occurs, an orchiopexy will be required. ● Prevention If cremaster is incorporated in the aponeurotic closure sutures, the inevitable postoperative scarring may actually serve to withdraw the testis into the canal or ﬁx a testis left in the canal. Therefore, the cremaster should be separated from the undersurface of the external oblique prior to its repair. At the end of the procedure, it should be ascertained that the testis has been replaced in the scrotum.

Other Complications Figure 86–1 Hidden anatomy. The fallopian tube or any other pelvic organs can be incorporated into the anteromedial wall of the hernia sac and injured during the transﬁxion and high ligation. If there is a sliding component, the ligation should be distal to the sliding organ.

Iatrogenic Direct Inguinal Hernia ● Consequence Iatrogenic direct inguinal hernia.7 Grade 3 complication

86 INGUINAL AND UMBILICAL HERNIAS

869

● Repair The direct hernia should be repaired by any of several accepted techniques. ● Prevention Although a direct hernia may rarely be seen in infants and children, a normal posterior inguinal wall may feel weak to the inexperienced operator. If, in a misguided attempt to shore up this structure, one or more sutures are placed in it, they can serve only to weaken what was actually quite normal. Because the only procedure necessary to correct the congenital inguinal hernia is a high ligation of the patent processus vaginalis, an attempt at “repair” of the inguinal ﬂoor is to be condemned.

Umbilical Hernia INTRODUCTION Umbilical hernias are very common in children. Most close spontaneously by age 4 or 5 years. The rate of incarceration is very low.

INDICATION ● Persistence of an umbilical hernia after age 4 or 5

years The persistence of an umbilical hernia after age 4 or 5 years warrants repair to prevent incarceration in the future.

Figure 86–2 Hidden anatomy. Violation of the umbilical hernia sac during dissection can result in injury to loops of intestine residing in the sac.

● Prevention The dissection of the sac should be patient and methodical to ensure that the sac is completely dissected off the surrounding subcutaneous tissues rather than pierced by the dissecting instrument. Despite this, the sac may occasionally still be entered. Therefore, the patient should be completely relaxed during this phase of the procedure, allowing the intestine to drop away. This, in turn, is best ensured by the use of deep, endotracheal general anesthesia.

Closure OPERATIVE STEPS Step Step Step Step Step Step

1 2 3 4 5 6

Infra-umbilical incision Dissection of hernia sac Excision of hernia sac Repair of defect Umbilicoplasty if necessary Skin closure

Dissection of the Hernia Sac Violation of the Sac ● Consequence Intestinal injury. The sac is commonly entered during its blunt dissection. If bowel is present in the sac at the time, particularly bowel under tension, it may be inadvertently pierced (Fig. 86–2). If unrecognized, it can be disastrous. Grade 2/3 complication ● Repair An intestinal injury should be repaired primarily if at all possible.

Hematoma ● Consequence Infection and hernia recurrence. Grade 1/3 complication ● Repair Infected wounds will usually need to be opened; recurrences will require repeat repair. ● Prevention Careful hemostasis should be achieved prior to closure. A carefully constructed pressure dressing should be carefully applied after closure and left in place for at least several days.

REFERENCES 1. Weber CH. Successful restoration of fertility twenty-nine years after bilateral vasal injury in infancy. Urology 1986; 28:299–300. 2. Pryor JL, Fusia T, Mercer M, et al. Injury to the prepubertal vas deferens. II. Experimental repair. J Urol 1991; 146:477–480.

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3. Pryor JL, Mills SE, Howards SS. Injury to the pre-pubertal vas deferens. I. Histological analysis of pre-pubertal human vas. J Urol 1991;146:473–476. 4. Sheynkin YR, Hendin BN, Schlegel PN, Goldstein M. Microsurgical repair of iatrogenic injury to the vas deferens. J Urol 1998;159:139–141. 5. Abasiyanik A, Guvenc H, Yavuzer D, et al. The effect of iatrogenic vas deferens injury on fertility in an experimental rat model. J Pediatr Surg 1997;32:1144–1146. 6. Shandling B, Janik JS. The vulnerability of the vas deferens. J Pediatr Surg 1981;16:461–464.

7. Meier AH, Ricketts RR. Surgical complications of inguinal and abdominal wall hernias. Semin Pediatr Surg 2003;12: 83–88. 8. Benjamin LC, Chahine AA. Forceful evacuation of retained pneumoperitoneum mimics an acute recurrent inguinal hernia. J Laparoendosc Adv Surg Tech A 2005;15:487– 488. 9. Donaldson KM, Tong SY, Hutson JM. Prevalence of late orchidopexy is consistent with some undescended testes being acquired. Indian J Pediatr 1996;63:725–729.

87

Pyloromyotomy Aziz Merchant, MD and Kurt D. Newman, MD INTRODUCTION

INDICATIONS

Infantile hypertrophic pyloric stenosis (HPS) is a common condition of infancy that is easily corrected by surgery. The overall annual incidence ranges from 8.2 to 12.3 cases per 1000 live births.1 The classic presentation is that of nonbilious, projectile vomiting in a 2- to 8-week-old newborn. The vomiting results in a contraction alkalosis secondary to severe dehydration. Sonographic identiﬁcation of a thickened and lengthened pylorus helps to solidify the diagnosis. The “gold standard” of treatment is the open pyloromyotomy described by Fredet in 19082 and modiﬁed by Ramstedt in 1912.3 An overall complication rate of 10% (4% intraoperative and 6% postoperative) has been reported, with complications including duodenal mucosal perforation, wound infection,4 and postoperative vomiting.5 Eighty years after the conventional open procedure was introduced, laparoscopic pyloromyotomy (LPM) was described.6,7 Over the ensuing years, the minimally invasive approach has gained widespread use and acceptance. Complication rates of 3% to 18% have been reported for LPM.8–11 These complications have included mucosal perforation, incomplete pyloromyotomy, serosal laceration, conversion to open pyloromyotomy, and wound complications. Perceived advantages of LPM, including excellent visualization, shorter time to full feeds, shorter length of stay, and superior cosmesis compared with the open surgery, have made LPM a mainstay of the pediatric surgical armamentarium. Preoperatively, patients may present with a hypochloremic, metabolic alkalosis due to vomiting and will generally be dehydrated. Aggressive resuscitation and stabilization with a normalized urine output is important prior to surgical treatment of the disease. The bicarbonate level must be normalized through administration of a saline solution, because infants with a metabolic alkalosis will respond with a respiratory acidosis resulting in postoperative apnea. Postoperatively, patients can be advanced on a feeding regimen or ad libitum. Postoperative emesis with feedings is frequent but self-limiting in most cases. This chapter discusses the preoperative, intraoperative, and postoperative management and pitfalls of both pyloromyotomy procedures.

● Persistent, nonbilious emesis. ● Palpation of thickened pylorus or demonstration of

pyloric stenosis on ultrasound

OPERATIVE STEPS Laparoscopic Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7 Step 8

Position and trocar placement Lateral retraction of stomach Hypertrophied pylorus relative to duodenum visualized Incision made in pylorus Hypertrophied ﬁbers split down to mucosa using the laparoscopic pyloric spreader Pylorus halves tested for independent mobility Check for mucosal perforation Trocar removal and closure

Open Pyloromyotomy Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7 Step 8 Step 9

Incision is made in right upper quadrant or supraumbilical Fascia is opened Stomach and pylorus are delivered gently through wound Hypertrophied pylorus relative to duodenum visualized Incision made in pylorus Hypertrophied ﬁbers split down to mucosa using pyloric spreader and tapered back of knife Pylorus halves tested for independent mobility Check for mucosal perforation Closure

PREOPERATIVE MANAGEMENT A good outcome after pyloromyotomy is predicated upon adequate preoperative resuscitation. Children with HPS will usually present with a hypokalemic, hypochloremic

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metabolic alkalosis. The severity of ﬂuid and electrolyte abnormality is reﬂected by carbon dioxide12 levels, with increased severity correlating with higher levels in the blood. Five percent dextrose and 0.45 normal saline solution sufﬁces in most cases, delivered at 1.5 to 2 times maintenance rate with an initial bolus of 20 ml/kg of the child’s weight. The ﬂuid is supplemented with potassium if the renal function is normal. Approximately 20% to 36% of infants with pyloric stenosis may present with nonclassic hyperkalemia and 12% to 18% with acidosis instead of alkalosis.13 Fluid resuscitation is again paramount.

DIAGNOSIS AND ERRORS Preoperative work-up of projectile nonbilious emesis involves a careful history and physical examination, drawing a basic metabolic blood panel with bicarbonate and chloride values and, in most instances, obtaining an ultrasound. The sensitivity and speciﬁcity of physical examination alone was found to be 72% and 97%, whereas that of ultrasound was 97% and 100%.14 However, false positives on ultrasound resulting in negative laparotomy were reported at an incidence of 0.7% to 5.3%.15,16

OPERATIVE PROCEDURE Trocar Insertion See Section I, Chapter 7, Laparoscopic Surgery.

Retraction of the Stomach and Duodenum Stomach Perforation/Laceration (Laparoscopic and Open) ● Consequence Intra-abdominal sepsis. Grade 3/4/5 complication ● Repair Experienced laparoscopists may choose to repair a laceration or perforation intracorporeally. Otherwise, conversion to an open procedure may be necessary to repair the injury. Postoperative gastric decompression with nasogastric suction, intravenous hydration, and perioperative and postoperative antibiotics are important adjuncts of treatment. Injury during an open pyloromyotomy is less common than with LPM; however, repair of the injury requires a similar approach as outlined previously. ● Prevention Improper grasping of the stomach, including inadequate purchase, forceful retraction, and/or careless maneuvering, may result in serosal laceration or, more dangerously, mucosal perforation. If undetected or with delayed detection, the child may become very ill

from intra-abdominal sepsis. Use of Babcock clamps and atraumatic graspers during this step will minimize untoward complications. In addition, ﬁrm but gentle technique for retraction is required for a successful operation. An analysis of errors during LPM revealed that most hollow viscus injuries are due to movements involving excessive force or depth. Therefore, accurate and precise movements are of utmost importance during laparoscopic surgery in small infants.

Incision of the Pylorus and Spreading of the Muscle Layer Mucosal Pyloric Perforation (Laparoscopic and Open) ● Consequence Hollow viscus injury with leak and peritonitis. Grade 3/4/5 complication ● Repair Repair can be carried out laparoscopically or by conversion to an open procedure depending on surgeon comfort level and experience. There are two approaches to repair. Traditionally, one may repair the injury with mucosal and muscular reapproximation, followed by sufﬁcient rotation of the pylorus and repyloromyotomy. Alternatively, simple mucosal reapproximation, without muscular closure and repyloromyotomy, can be performed to maintain the currently performed myotomy. Both approaches have shown equal efﬁcacy for repair. Rates of hospital stay, time to feeding, and postoperative complications were the same regardless of the type of repair, and both repairs are regarded as widely acceptable.17 ● Prevention A 21-year retrospective study revealed a mucosal perforation rate of 1.7%.17 Excellent visualization of the pylorus is paramount during this step. Stable and effective retraction of the stomach or duodenum will assist in visualization and dissection. During incision of the pylorus, small controlled movements should be performed. An effective incision length of approximately 2 cm was found to be adequate in an analysis of 171 LPMs for pyloric stenosis.18 The incision should stop just before the prepyloric vein of Mayo to avoid injuring the mucosa of the duodenal recess at the distal end of the pylorus (Fig. 87–1). A retractable blade instrument can minimize accidental punctures. Moreover, a guarded electrocautery blade may be used for the incision, which will provide better visualization secondary to better hemostasis. One must be aware of electrocautery thermal injury to bowel, which may manifest postoperatively as a delayed bowel injury and possible perforation. In addition, forceful and deep spreading of the muscle ﬁbers of the pylorus can result in perforation through the mucosa. The tips of the spreader

87 PYLOROMYOTOMY

Figure 87–1 Hidden anatomy. The pyloromyotomy incision should stop just before the prepyloric vein of Mayo to avoid injuring the mucosa of the duodenal recess at the distal end of the pylorus.

should be pushed in just enough to engage the muscle with the serrations on the outside of the jaws (Fig. 87–2). To conﬁrm mucosal integrity after spreading, one insufﬂates the stomach with air (120–180 cc). Green froth at the pyloromyotomy site is a sign of mucosal perforation.

Incomplete Pyloromyotomy (Laparoscopic and Open) ● Consequence Recurrent or persistent postpyloromyotomy vomiting, dehydration, and possible reoperation. Grade 2/3 complication ● Repair Patients present with persistent vomiting after pyloromyotomy. Radiographic studies may show continued obstruction with a thin pyloric channel, except that surrounding muscle layers will be thinned out. Patients can be observed with intravenous hydration in the hospital, and many of these cases will resolve. Alternatively, in the face of persistent vomiting, dehydration, and weight loss, reoperation is necessary. Balloon dilation of failed pyloromyotomies has also been described.19 ● Prevention Most cases of incomplete pyloromyotomy occur secondary to inadequate length of division across the pylorus or inadequate depth through the muscle ﬁbers. One great disadvantage of LPM compared with the

873

Figure 87–2 Hidden anatomy. In order to avoid a mucosal perforation during the spreading of the ﬁbers of the hypertrophied pylorus, the tips of the spreader should be pushed in just enough to engage the muscle with the serrations on the outside of the jaws.

open procedure is the lack of haptic manipulation to judge whether the pylorus has been adequately spread. A length of 2 cm across the pylorus has been found to be adequate according to a recent retrospective study of laparoscopic procedures.18 The pylorus should be divided completely from the pyloroduodenal junction to 1 cm beyond the antral fold proximally. The two halves of the split pylorus should be tested for independent motion. Failed pyloromyotomy can be attributed to the laparoscopic “learning curve,” differences in movement associated with laparoscopic procedures compared with open ones, and inadequate retraction of the stomach and duodenum resulting in poor visualization of the pylorus.

Postoperative Complications Persistent Vomiting Postoperative vomiting after pyloromyotomy is fairly common, ranging from 36% to 90% in certain series.4 However, Campbell and coworkers4 considered postoperative vomiting a complication if hospital stay is extended beyond 48 hours. Using this deﬁnition, only 3.5% of cases in their series had this complication. In rare cases, reoperation is required owing to incomplete surgery in the ﬁrst operation.5,20 Grade 1/2 complication

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Wound Complications Wound complications occur in approximately 1% of cases and include wound infections and hematoma. Technical complications and patient disease (e.g., hemophilia) can affect this outcome. Choice of incision for open surgery has not been shown to make a difference.9 Incisional hernias are rare in pediatric laparoscopy; however, they have been reported with open pyloromyotomy at a rate of 0.5% to 1.5%.21,22 Rates reported in the literature approximate 1.2%.23 Grade 2/3 complication

POSTOPERATIVE CARE AND FEEDING REGIMENS Postoperative feeding regimens vary widely based on local practice and surgeon preference. Traditionally, complex feeding regimens involved a long period of NPO after the operation followed by graded increases or decreases in formula volume and strength based on tolerance or intolerance of feeds. Ad libitum feeding regimens were shown in cohort studies to be cost-effective with shorter length of stays and statistically insigniﬁcant changes in postoperative emesis compared with complex feeding regimens.24 In addition, ad libitum feeds have been shown to decrease the time to full feeds after pyloromyotomy without signiﬁcant increases in rates of readmission for vomiting.25,26 Early feeding (<8 hr after the operation) resulted in signiﬁcant increases in postfeeding emesis and signiﬁcantly longer lengths of stay compared with traditional timing of feeds (>12 hr after the operation).27,28 Randomized clinical trials have not been performed to assess which method of feeding is better, and both strict feeding regimens and ad libitum feeding are successfully used by pediatric surgeons after pyloromyotomy. Persistent postoperative emesis, feeding intolerance, and distress may be associated with complications such as a failed pyloromyotomy, perforation, or other source of intra-abdominal sepsis. One must maintain a high degree of suspicion for these problems to be identiﬁed. Laboratory and radiologic studies, in addition to clinical suspicion, will assist in the diagnosis. Prompt resuscitation along with operative or nonoperative management may be required for resolution. A meta-analysis of 11,003 procedures performed in this country revealed a postoperative complication rate of 2.7%, including perforation, wound infection, and failed procedures with persistent vomiting.1

REFERENCES 1. Safford SD, Pietrobon R, Safford KM, et al. A study of 11,003 patients with hypertrophic pyloric stenosis and the association between surgeon and hospital volume and outcomes. J Pediatr Surg 2005;40:967–972.

2. Dufour H, Freaei P. La stenose hypertrophique du pylore chez le nourisson et son traitement chirurgical. Rev Chir 1908;37:208. 3. Ramstedt C. Zur Operation der angeborenen pylorustenose. Med Klin 1912;8:1702–1705. 4. Rao N, Youngson GG. Wound sepsis following Ramstedt pyloromyotomy. Br J Surg 1989;76:1144–1146. 5. Hulka F, Harrison MW, Campbell TJ, Campbell JR. Complications of pyloromyotomy for infantile hypertrophic pyloric stenosis. Am J Surg 1997;173:450–452. 6. Alain JL, Grousseau D, Terrier G. Extramucosal pyloromyotomy by laparoscopy. Surg Endosc 1991;5:174– 175. 7. Alain JL, Moulies D, Longis B, et al. Pyloric stenosis in infants. New surgical approaches. Ann Pediatr (Paris) 1991;38:630–632. 8. Hendrickson RJ, Yu S, Bruny JL, et al. Early experience with laparoscopic pyloromyotomy in a teaching institution. JSLS 2005;9:386–388. 9. Kim SS, Lau ST, Lee SL, Waldhausen JH. The learning curve associated with laparoscopic pyloromyotomy. J Laparoendosc Adv Surg Tech A 2005;15:474–477. 10. Kim SS, Lau ST, Lee SL, et al. Pyloromyotomy: a comparison of laparoscopic, circumumbilical, and right upper quadrant operative techniques. J Am Coll Surg 2005;201:66–70. 11. Hall NJ, Van Der Zee J, Tan HL, Pierro A. Meta-analysis of laparoscopic versus open pyloromyotomy. Ann Surg 2004;240:774–778. 12. Benson CD, Alpern EB. Preoperative and postoperative care of congenital pyloric stenosis. Arch Surg 1957;75: 877. 13. Schwartz D, Connelly NR, Manikantan P, Nichols JH. Hyperkalemia and pyloric stenosis. Anesth Analg 2003; 97:355–357 14. Misra D, Akhter A, Potts SR, et al. Pyloric stenosis: is over-reliance on ultrasound scans leading to negative explorations? Eur J Pediatr Surg 1997;7:328–330. 15. Godbole P, Sprigg A, Dickson JA, Lin PC. Ultrasound compared with clinical examination in infantile hypertrophic pyloric stenosis. Arch Dis Child 1996;75:335– 337. 16. Neilson D, Hollman AS. The ultrasonic diagnosis of infantile hypertrophic pyloric stenosis: technique and accuracy. Clin Radiol 1994;49:246–247. 17. Royal RE, Linz DN, Gruppo DL, Ziegler MM. Repair of mucosal perforation during pyloromyotomy: surgeon’s choice. J Pediatr Surg 1995;30:1430–1432. 18. Ostlie DJ, Woodall CE, Wade KR, et al. An effective pyloromyotomy length in infants undergoing laparoscopic pyloromyotomy. Surgery 2004;136:827–832. 19. Khoshoo V, Noel RA, LaGarde D, et al. Endoscopic balloon dilatation of failed pyloromyotomy in young infants. J Pediatr Gastroenterol Nutr 1996;23:447– 451. 20. van Heurn LW, Vos P, Sie G. Recurrent vomiting after successful pyloromyotomy. Pediatr Surg Int 1999;15:385– 386. 21. van den Ende ED, Allema JH, Hazebroek FW, Breslau PJ. Can pyloromyotomy for infantile hypertrophic pyloric stenosis be performed in any hospital?: results from two teaching hospitals. Eur J Pediatr 2006:166:553–557.

87 PYLOROMYOTOMY 22. St. Peter SD, Holcomb GW 3rd, Calkins CM, et al. Open versus laparoscopic pyloromyotomy for pyloric stenosis: a prospective, randomized trial. Ann Surg 2006;244:363– 370. 23. Ure BM, Bax NM, van der Zee DC. Laparoscopy in infants and children: a prospective study on feasibility and the impact on routine surgery. J Pediatr Surg 2000;35: 1170–1173. 24. Puapong D, Kahng D, Ko A, Applebaum H. Ad libitum feeding: safely improving the cost-effectiveness of pyloromyotomy. J Pediatr Surg 2002;37:1667– 1668.

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25. Garza JJ, Morash D, Dzakovic A, et al. Ad libitum feeding decreases hospital stay for neonates after pyloromyotomy. J Pediatr Surg 2002;37:493–495. 26. Carpenter RO, Schaffer RL, Maeso CE, et al. Postoperative ad lib feeding for hypertrophic pyloric stenosis. J Pediatr Surg 1999;34:959–961. 27. Van der Bilt JD, Kramer WL, van der Zee DC, Bax NM. Early feeding after laparoscopic pyloromyotomy: the pros and cons. Surg Endosc 2004;18:746–748. 28. Lee AC, Munro FD, MacKinlay GA. An audit of postpyloromyotomy feeding regimens. Eur J Pediatr Surg 2001;11:12–14.

Index Note: Page numbers followed by f refer to ﬁgures; page numbers followed by t refer to tables; page numbers followed by b refer to boxes. A Abdomen chest tube placement in, 139, 140f compartment syndrome of, 803, 805–806 laparotomy and, 89–91, 90f, 91f injury to. See also Damage control surgery femoral venous cannula with, 765–766 gastrostomy and, 148 hemorrhage with, 763 jejunostomy and, 155 thoracic trauma and, 775 postlaparotomy abscess of, 92–94, 93f Abdominal adhesions damage control surgery and, 806 laparoscopic gastric bypass and, 202 laparotomy and, 71–72, 73–74, 74f Abdominal aortic aneurysm elective repair of, 604–610 aortoenteric ﬁstula after, 609 bleeding with, 609 common iliac vein injury with, 607–609 dissection and clamping for, 598, 605– 607, 605f, 606f, 607f, 608f distal embolization with, 607 graft occlusion after, 609 horseshoe kidney and, 610 indications for, 604 infection after, 609 inferior vena cava injury with, 607–609 in inﬂammatory disease, 610 peritoneal reﬂection for, 605 proximal neck friability in, 609 pseudoaneurysm after, 609–610 renal artery reimplantation in, 610 retroaortic left renal vein and, 610 right suprainguinal incision for, 604–605, 605f steps in, 604 in suprarenal disease, 610 ureteral injury with, 609 endovascular therapy for, 654–655 access failure with, 654 device fatigue with, 654 endoleaks with, 654–655, 654f, 655f inﬂammatory, 610 rupture of ischemic colitis with, 611 repair of, 610–611 suprarenal, 610 Abdominal compartment syndrome, 803, 805–806 laparotomy and, 89–91, 90f, 91f Abdominal perineal resection, 291–297 abdominal dissection for, 291–292 colostomy creation for, 295–297, 295f, 296f leakage from, 297 obesity and, 297, 297f parastomal hernia with, 297 stomal necrosis with, 295–296 stomal stenosis with, 297, 297f indications for, 291 perineal dissection for, 292–295, 292f, 293f, 294f perineal wound breakdown with, 294–295 radiation effects on, 294–295

Abdominal perineal resection (Continued) steps in, 291 urethral injury with, 293–294 vaginal injury with, 294 Abdominal wall. See also Abdominal wall reconstruction hematoma of laparoscopic gastric bypass and, 220–221 laparoscopic surgery and, 200–201 hemorrhage from, laparoscopic gastric bypass and, 220–221 hernia of, 76, 77f laparoscopic gastric bypass and, 202 reconstruction for. See Abdominal wall reconstruction, component separation in incisional hernia repair–related loss of, 536 injury to laparoscopic surgery and, 200–201 percutaneous gastrostomy tube placement and, 153 Abdominal wall reconstruction component separation in, 545–568, 546f– 547f adhesiolysis for, 557 adipocutaneous advancement ﬂaps for, 554, 555f–557f, 567 AlloDerm for, 559, 559f bowel injury with, 557 deep venous thrombosis with, 568 dehiscence with, 563, 565 DERMABOND in, 567 drain placement for, 567 evisceration with, 563, 565 external oblique fascia incision for, 559– 560, 560f–562f failure of, 560–567, 564f, 565f, 567f ﬂap ischemia with, 554, 555f–557f ﬂuid therapy in, 554 hernia recurrence after, 563, 565 hernia sac excision for, 554, 556–557 hernia sac preservation for, 556–557, 557f–558f iatrogenic enterotomy with, 551, 553 ileus after, 553–554 indications for, 545, 548 infection and, 554, 557f, 567 liposuction garments after, 568 mesh excision for, 554 muscle ﬂap advancement and approximation for, 560–567, 564f, 565f, 566f obesity and, 548, 549f–550f ostomy and, 548, 550f–551f, 552f–553f partial-thickness loss with, 567–568 partition methods in, 562–563, 564f peritoneal cavity entry for, 551, 553–554 pulmonary embolism with, 568 rectus abdominis denervation with, 560 recurrent hernia after, 563, 565 respiratory insufﬁciency with, 566–567 seroma with, 554, 567 skin ﬂap bullae with, 567–568 skin incision for, 548–550, 549f–551f, 552f–553f skin necrosis with, 548

Abdominal wall reconstruction (Continued) Spigelian hernia with, 559–560 split-thickness skin graft excision for, 551, 553–554, 553f staged, 545, 546f–547f steps in, 548 venous congestion with, 554 tensor fascia lata ﬂaps for, 560–563, 564f, 565f Abortion, spontaneous, 62–63 Abscess appendectomy and, 301–302, 303–305 arteriovenous access and, 639, 639f intra-abdominal epigastric hernia repair and, 527–528 laparoscopic splenectomy and, 579 laparotomy and, 92–94, 93f umbilical hernia repair and, 527–528 paravesical, inguinal hernia repair and, 507 subphrenic, 92, 93f laparoscopic splenectomy and, 579 Absorbable mesh wrap, in splenorrhaphy, 791–792, 793f N-Acetyl cysteine, 36 Achalasia, 187 esophagomyotomy for. See Esophagomyotomy Adenoma adrenal, 421 parathyroid, 410, 411, 411f Adhesiolysis in abdominal wall reconstruction, 557 in incisional hernia repair, 533, 538, 539f, 540f intestinal, 75–76, 75f, 76f Adhesions abdominal damage control surgery and, 806 laparoscopic gastric bypass and, 202 laparotomy and, 71–72, 73–74, 74f intestinal, 75–76, 75f, 76f Adrenal artery, injury to, 426–427 Adrenal gland biochemical evaluation of, 422–423 computed tomography of, 421, 422, 422f, 423f evaluation of, 421–423, 422f, 423f hepatectomy-related injury to, 332–333 long limb variant of, 423f metastasis of, 423f pheochromocytoma of, 423 removal of. See Adrenalectomy Adrenal insufﬁciency, 43 Adrenal vein identiﬁcation of, 426, 427f, 431, 431f injury to adrenalectomy and, 426, 427f pancreatectomy and, 376–377 Adrenalectomy, 421–432 anterior transperitoneal approach to, 423 biochemical evaluation before, 422–423 imaging before, 421–422, 422f, 423f indications for, 421, 422f laparoscopic transperitoneal approach to, 424, 425–428 adrenal vein in, 426, 427f

878

INDEX

Adrenalectomy (Continued) arterial dissection for, 426–427 bowel injury with, 426 diaphragm injury with, 427, 427f dissection for, 426–427 fractures with, 426 gastric injury with, 427 inferior vena cava dissection for, 426 kidney dissection for, 427 liver mobilization for, 426 nerve injury with, 425–426 positioning for, 425–426, 425f solid organ injury with, 426, 428 steps in, 425, 425t trocar insertion for, 426, 426f trocar site closure for, 428 vascular injury with, 426, 427, 427f Nelson’s syndrome after, 423 open anterior approach to abdominal entry for, 428 arterial dissection for, 430 colonic injury with, 428, 429 dissection for, 430 duodenal injury with, 428 hepatic ﬂexure injury with, 428 left, 428–430 lymphatic injury with, 430 pancreatic injury with, 429 pancreatic mobilization for, 428–430 right, 428, 429f small bowel injury with, 428 splenic injury with, 429–430 open posterior approach to, 424, 430–431 arterial dissection for, 431, 431f closure for, 431 incision for, 430 lumbar hernia with, 431, 431f pleural injury with, 430 positioning for, 430 renal dissection for, 430–431 renal hemorrhage with, 430–431 renal vein injury with, 431 rib resection for, 430 steps in, 430 vascular injury with, 430 vena cava injury with, 431 open transperitoneal approach to, 424 partial, 431–432, 432f retroperitoneal posterior approach to, 424, 431–432, 432f thoracoabdominal approach to, 424 Afferent loop syndrome, after Billroth II reconstruction, 230 Aﬁbrinogenemia, 40t Aganglionosis. See Hirschsprung’s disease Air embolism central vein catheterization and, 114 laparoscopic hepatectomy and, 365–366 right hepatectomy and, 331–332 trauma and, 762 Air-ﬂuid level, postlaparotomy, 94 Air leak, bronchial and vascular sleeve lobectomy and, 689 Airway compromise of, 51 edema of, tracheal resection and, 751 esophagectomy-related injury to, 730–731, 731f establishment of, before tracheal resection, 742 loss of in anterior mediastinotomy, 666–667 before tracheal resection, 742 metastable, 760–761 in neck trauma, 810–811, 810f risk assessment for, 33–34, 34f, 35f

Airway (Continued) in thyroid surgery, 398, 398f, 404 in trauma, 757, 758f–760f, 810–811, 810f unstable, 760–761 visualization of, in rigid bronchoscopy, 659–660 Alcohol dependence, 29–30, 29b, 30f CAGE questionnaire for, 30, 30b Aldosterone, adenoma secretion of, 423 Allis clamps, for venous hemorrhage, 84, 85f AlloDerm in component separation procedure, 559, 559f in damage control surgery, 807 in failed component separation procedure, 561–562, 566f Amnesia, inadequate, 51 Amnestic agents, 50t Amputation, in melanoma, 499 Anal ﬁstulotomy, 315–318 anesthesia for, 315 cut for, 317–318, 317f ﬁstula persistence with, 317–318 Goodsall’s rule for, 316, 316f hydrogen peroxide injection for, 316, 316f indications for, 315 opening identiﬁcation for, 315–316, 316f, 317f sphincter assessment for, 316–317, 317f sphincter weakening with, 316–317 steps in, 315 urinary retention with, 315 Anal sphincter division of, 829, 829f ﬁstulotomy-related weakening of, 316–317 hemorrhoidectomy-related injury to, 308– 309 Anal stenosis, hemorrhoidectomy and, 308, 309, 309f Anal stricture, hemorrhoidectomy and, 311, 312 Analgesia, 28–29, 28t, 29t, 50t inadequate, 51 in chest tube insertion, 137–138 in thoracic trauma, 776–777 postoperative narcotic, 28–29, 29t non-narcotic, 28–29, 28t Anastomosis bleeding of gastrectomy and, 229 laparoscopic gastric bypass and, 208 rectal resection and, 285, 285f dehiscence of colectomy and, 263 tracheal resection and, 746, 748–750, 749f granulation formation of, tracheal resection and, 747–748 leakage from biliary resection and, 394–395 colectomy and, 269–270, 269f enterectomy and, 237, 242–243 esophagectomy and, 736–737 gastrectomy and, 227–229, 228b gastric bypass and, 215–216, 215f Hirschsprung’s disease repair and, 833– 834 pancreaticojejunostomy and, 382 pyloroplasty and, 171–172 rectal resection and, 283–285 Roux-en-Y cystjejunostomy and, 384 tracheoesophageal ﬁstula repair and, 853 stricture of enterectomy and, 241–242, 243f, 244f esophagectomy and, 738

Anastomosis (Continued) gastrectomy and, 230–231 rectal resection and, 285–286 Anatomic Complications of General Surgery, 8 Anesthesia in anal ﬁstulotomy, 315 in anterior mediastinotomy, 666–667 in congenital diaphragmatic hernia repair, 857 in ﬂexible bronchoscopy, 661 in greater saphenous vein ablation, 645 in hemorrhoidectomy, 307–308 local, 49–50, 50t in stereotactic image-guided breast biopsy, 438–439 in ultrasound image-guided breast biopsy, 443–444 pitfalls in, 49–64 block-speciﬁc, 53–56, 53t, 54f, 55f, 56f, 57f inpatient, 56–64 aspiration and, 63 cardiovascular system, 59–60 cardioverter-deﬁbrillator–related, 60–61 medications and, 56–58 nausea and vomiting and, 63–64, 64b, 64t neurologic system, 58–59, 58b, 59t pacemaker-related, 60–61 pediatric, 63–64 pregnancy-related, 62–63 pulmonary system, 61–62 outpatient, 49–53, 50t cardiovascular system, 52 hematologic system, 52–53 neurologic system, 49–51, 50t respiratory system, 50t, 51–52 in rigid bronchoscopy, 659 Aneurysm abdominal aorta. See Abdominal aortic aneurysm pulmonary artery, catheter-related, 124– 127, 125f, 126f Angiography in infrainguinal revascularization, 617–618, 618f, 619f, 624, 625f in neck injury, 813–814, 814b Angiolymphoid hyperplasia, of breast, 449 Angioplasty, 653–654 arterial dissection with, 653 arterial perforation with, 653 embolization with, 653–654 patch, in carotid endarterectomy, 592–593, 593f Angioscopy, in infrainguinal revascularization, 624 Ankle block, 53t, 55–56, 57f Ankle/brachial index, 613 Anoplasty, 829–830 asymmetrical sphincter division with, 829 dehiscence after, 830 mucosal prolapse with, 830 perineal body reconstruction for, 830 rectal dissection for, 829 sphincter division for, 829, 829f steps in, 829 stricture after, 830 urethral injury with, 829 vaginal injury with, 829 Anorectal malformations, 827–832 classiﬁcation of, 827, 828t evaluation of, 827 incidence of, 827 repair of, 827–832 anoplasty for, 829–830, 829f colostomy for, 830–832, 831f, 832f

INDEX Anorectal malformations (Continued) in female patient, 828–829, 828f, 829f in male patient, 828, 828f posterior sagittal anorectoplasty for, 831– 832 Anorectoplasty, sagittal, posterior, 831–832, 832f steps in, 831 urethral diverticulum with, 831 Anterior resection syndrome, 287. See also Low anterior resection Antiarrhythmia agents, prophylactic, in pneumonectomy, 700 Antibiotics, preoperative, 37, 38t in mastectomy, 476 Anticoagulation in infrainguinal revascularization, 621–622 preoperative assessment of, 39 in venous thrombosis, 41 Antiemetics, 63–64, 64t Antiplatelet agents, perioperative management of, 39 Anus congenital malformation of. See Anorectal malformations ﬁstula of. See Anal ﬁstulotomy imperforate. See Anorectal malformations resection of. See Abdominal perineal resection Anxiolysis, inadequate, 51 Anxiolytic agents, 50t Aorta aneurysm of. See Abdominal aortic aneurysm dissection of, in aortobifemoral bypass, 601–602 injury to laparoscopic Nissen fundoplication and, 182, 182f trauma and, 774–775 vagotomy and, 172 in neuroblastoma resection, 864–865, 865f surgery on, 597–611. See also Abdominal aortic aneurysm; Aortobifemoral bypass clamping sequence for, 598 polytetraﬂuoroethylene vs. Dacron grafts for, 597–598 transperitoneal vs. retroperitoneal, 598– 599, 598f Aortic arch, right-sided, 849–850 Aortic stenosis, 59–60 Aortobifemoral bypass, 599–604 anastomoses for, 597, 598f end-to-end, 597 end-to-side, 597, 598f femoral, 602–603 proximal, 602 bleeding with, 603 Bookwalter retractor for, 601, 601f bowel injury with, 603 dissection for, 601–602 duodenal injury with, 601 fecal ﬁstula with, 603 femoral artery exposure for, 600, 600f femoral nerve injury with, 600 ﬂank bulge with, 604 graft tunneling for, 602–603, 602f indications for, 599 inferior vena cava injury with, 602 left ﬂank skin incision for, 600–601 lymphatic leak with, 600 peritoneal cavity inspection for, 603–604 peritoneal reﬂection for, 601, 601f peritoneal tear with, 600–601 positioning for, 599, 599f skin markings for, 599–600, 599f

Aortobifemoral bypass (Continued) small intestine obstruction with, 603–604 splenic laceration with, 601 steps in, 599 suture line bleeding with, 602 ureteral division with, 603 venous injury with, 602–603 Aortoenteric ﬁstula, abdominal aortic aneurysm repair and, 609 Appendectomy, laparoscopic, 299–305 abscess after, 304–305 appendiceal stump leak with, 303–304, 304f bladder injury with, 300 colon injury with, 301–302 dissection for, 301–303, 301f, 302f epigastric vessel injury with, 300 indications for, 299 mesenteric bleeding with, 303 mesenteric division for, 303, 303f resection for, 303–305 specimen pouch for, 301, 301f staple line inspection for, 303, 303f staple placement in, 303, 303f steps in, 299 stump infection with, 304 trocar insertion for, 300–301, 300f ureteral injury with, 302–303 wound infection with, 300–301 Appendiceal artery, bleeding from, 303 Appendicitis, 299. See also Appendectomy in children, 824 stump, 304 Argon beam coagulation in splenorrhaphy, 791, 793f in trisectionectomy, 347 Arrhythmias bupivacaine and, 52 central vein catheterization and, 115 esophagectomy and, 735–736 laparoscopic surgery and, 101, 199 pectus excavatum repair and, 847 pneumonectomy and, 699–700 pulmonary artery catheterization and, 123 Arterial catheterization, 129–134 axillary artery, 131 infection with, 131 paresthesias with, 131, 133f, 134 femoral artery, 131 bleeding with, 131, 132f indications for, 129 pulmonary artery. See Pulmonary artery catheterization radial artery, 129–131, 130f infection with, 129–130 ischemia with, 131 pseudoaneurysm with, 130, 130f thrombosis with, 129 Arterial steal, arteriovenous access and, 637– 638, 638f Arteriography in infrainguinal revascularization, 617–618, 618f, 619f, 624, 625f in neck injury, 813–814, 814b Arteriotomy in carotid endarterectomy, 591 long, carotid endarterectomy and, 593 Arteriovenous ﬁstula inferior vena cava ﬁlter placement and, 649 residual, after infrainguinal revascularization, 617–618 Arteriovenous hemodialysis access, 631–640, 632b anastomosis for, 638–639 arterial dissection for, 637–638 arterial steal with, 637–638, 638f

879

Arteriovenous hemodialysis access (Continued) brachial–antecubital vein, 632, 634f brachial–basilic vein, 631–632, 633f central venous stenosis in, 633, 634f, 635f congestive heart failure with, 638–639 early thrombosis with, 632–634 graft maturation failure with, 636–637 hemorrhage with, 639 imaging before, 631, 632b, 634, 636 indications for, 631 infection with, 639, 639f ischemic monomelic neuropathy with, 638 late thrombosis with, 634–635, 636f posterior radial branch–cephalic vein, 631, 632f pseudoaneurysm with, 640, 640f pulse examination for, 637–638 seroma with, 639–640, 640f side branch ligation for, 637, 637f venous exposure for, 632–637 venous hypertension with, 635–636 wound closure for, 639–640 Artery of Ademkiewicz, in posterior mediastinal mass resection, 721 Ascites chylous, postvagotomy, 169 pancreatic, 388–389 paracentesis for, 143–146. See also Paracentesis refractory, umbilical hernia and, 528, 528f Asphyxiating thoracic dystrophy, pectus excavatum repair and, 842 Aspiration esophagectomy and, 736 during induction, 63 Associative phase, of Fitts and Posner skill acquisition model, 6, 6f Asthma, perioperative management of, 61 Atelectasis bronchial and vascular sleeve lobectomy and, 689–690 esophagectomy and, 733–734 Atheroembolism, in abdominal aortic aneurysm repair, 607 Atrial ﬁbrillation, 32–33 Atrioventricular dissociation, laparoscopic surgery and, 101 Atypical intraductal hyperplasia, of breast, 448–449 Autonomous phase, of Fitts and Posner skill acquisition model, 6, 6f Aviation training, 11–12 Axillary artery cannulation of, 131, 133f, 134 dissection-related injury to, 467 Axillary dissection, 465–468, 466f, 467f drain placement for, 468 hemostasis for, 467–468 incision for, 465–466 indications for, 465 lymphedema after, 467 nerve injury with, 466–467, 466f, 467f steps in, 465 technique of, 466–467, 466f vascular injury with, 467 Axillary vein, dissection-related injury to, 467 Azygos vein, resection-related injury to, 724, 724f B Balloon tamponade, in neck injury–related bleeding, 811, 811f Bancroft closure, in gastrectomy, 225, 226f Bariatric surgery. See Gastric bypass, laparoscopic

880

INDEX

Benign papillary lesion, of breast, 446–447, 447f Bicarbonate, with contrast agents, 36 Bile duct. See also Biliary tract common in biliary resection and reconstruction, 394 cholecystectomy-related injury to, 320– 321, 321f, 321t, 322b identiﬁcation of, 783 extrahepatic. See also Biliary tract anatomy of, 392, 392f blood supply to, 391, 392f resection-related stricture of, 394 trisectionectomy-related ischemia of, 349 Bile leak cholecystectomy and, 323, 324, 326–327 laparoscopic hepatectomy and, 365 right hepatectomy and, 337–338 trisectionectomy and, 352–354 Bile reﬂux gastritis, 231–232 Biliary tract damage control surgery for, 802 resection and reconstruction of, 391–396 anastomosis for, 394–395 anastomotic leak with, 394–395 bile duct isolation for, 391–394, 392f, 393f biliary stricture with, 394 common hepatic artery injury with, 392 distal stump leak with, 394 excision for, 394, 394f hepatic artery injury with, 392–393 hepatic duct leak with, 395 incision for, 391 indications for, 391 peribiliary vessel bleeding with, 391–392 portal vein injury with, 393–394 steps in, 391 Biliopancreatic limb, in laparoscopic gastric bypass, 205 Billroth gastrojejunostomy, 227–229, 227t, 228f, 229f cancer after, 233 Biopsy breast. See Breast biopsy chest wall, 706–707 parathyroid gland, 412 sentinel lymph node. See Sentinel lymph node biopsy soft tissue sarcoma, 490–491 supraclavicular lymph node, 583–584 Bladder dysfunction of, after low anterior resection, 282–283 injury to inguinal hernia repair and, 517 laparotomy and, 82–84 paracentesis and, 144, 144f rectal resection and, 274–275, 275f trocar placement and, 300 mesh migration into, in laparoscopic incisional hernia repair, 542 Bleeding abdominal wall, gastric bypass and, 220– 221 adrenalectomy and, 426–427, 427f anastomotic gastrectomy and, 229 laparoscopic gastric bypass and, 208 rectal resection and, 285, 285f anterior gastrotomy and, 383–384 anterior mediastinotomy and, 667 aortobifemoral bypass and, 602, 603 appendectomy and, 303 arteriovenous access and, 639

Bleeding (Continued) bronchial and vascular sleeve lobectomy and, 688 bronchoscopy and, 661 carotid endarterectomy and, 593 cholecystectomy and, 321–322, 324, 326 colectomy and, 261–262 cystgastrostomy and, 383–384 damage control surgery and, 802–803 endovascular intervention and, 651–652 enterectomy and, 240 esophagectomy and, 728–730, 729f esophagomyotomy with Dor fundoplication and, 194 femoral artery cannulation and, 131, 132f gastric bypass and, 200–201, 203, 204– 205, 208–209, 211, 213, 216 hemorrhoidectomy and, 308, 313 hepatectomy and, 330, 336–337, 361, 364–365 incisional hernia repair and, 538 infrainguinal revascularization and, 621, 625–626, 625f inguinal hernia repair and, 502–503, 517, 518 isolated limb perfusion of melphalan and, 499 laparoscopic surgery and, 100 mastectomy and, 479 mediastinoscopy and, 664–665 mesenteric, laparoscopic gastric bypass and, 204–205, 208–209, 213, 219 neck injury and, 811, 811f open gastrostomy and, 149 pancreatectomy and, 375–376, 377 pancreatic débridement and, 385, 387 pancreaticoduodenectomy and, 368, 369– 370, 372 paracentesis and, 145 pelvic trauma and, 767–768 pulmonary artery, 124–127, 125f, 126f rectal resection and, 275–277, 276f, 277f, 279, 281–282, 282f, 285, 285f right hepatectomy and, 330, 336–337 risk assessment for, 39, 40t Roux-en-Y cystjejunostomy and, 384 splenectomy and, 574, 575, 576–578 stereotactic image-guided breast biopsy and, 441 trauma and, 762–763, 769–770, 770f trisectionectomy and, 349–352 ultrasound image-guided breast biopsy and, 445–446, 445f VATS lobectomy and, 681–682 venous, laparotomy and, 84–85, 85f β-Blockers in atrial ﬁbrillation prevention, 33 in myocardial infarction prevention, 31–32, 32b, 57 Blood pressure, trauma-related, 763 Blood transfusion in total mastectomy, 479 in trisectionectomy, 350 Bogota Bag, 90, 91f Bookwalter retractor, in aortobifemoral bypass, 601 Bougie insertion, for laparoscopic Nissen fundoplication, 180–181, 181f Brachial plexus injury adrenalectomy and, 425–426 axillary dissection and, 467 Brachiocephalic vein, thymectomy-related injury to, 718–719 Bracing, 19–20, 20f, 99, 99f Bradyarrhythmias, laparoscopic surgery and, 101

Bradycardia, laparoscopic surgery and, 199 Brain, trauma to. See Traumatic brain injury BRCA, 45t Breast angiolymphoid hyperplasia of, 449 atypical intraductal hyperplasia of, 448–449 benign papillary lesion of, 446–447, 447f biopsy of. See Breast biopsy calciﬁcations of, 450 cyst of, 442 ductal carcinoma in situ of, 449 ﬂat epithelial atypia of, 449–450, 450f radial scar of, 450–451, 451f removal of. See Mastectomy Breast biopsy image-guided, 433–451 indications for, 433–434 infection after, 475–476 pathologic pitfalls with, 446–451 angiolymphoid hyperplasia/lobular carcinoma in situ and, 449 artifacts and, 447 atypical intraductal hyperplasia and, 448–449 benign papillary lesion and, 446–447, 447f calciﬁcations and, 450 ductal carcinoma in situ and, 449 edge artifact and, 447 estrogen receptor immunostain and, 448 ﬂat epithelial atypia and, 449–450, 450f HER-2 assessment and, 447–448, 448f lobular carcinoma in situ and, 449 radial scar and, 450–451, 451f thermal injury and, 447 tissue crush and, 447 tissue retraction and, 447 underﬁxation and, 448 stereotactic, 434–442 anesthetic preparation for, 438–439 bleeding with, 441 clip migration with, 441–442 compression thickness in, 438 device insertion for, 439 device misselection with, 440–441 ﬁne-needle aspiration needle for, 440 inappropriate mammogram lesion with, 434 lesion depth with, 436–437, 437f, 438f lesion mislocation with, 435 lesion mispositioning with, 436 lesion misvisualization with, 435–436 lesion targeting for, 438 lesion window positioning for, 436, 437f mammogram evaluation for, 434–436 mistaken approach with, 435 negative stroke margin with, 436–437, 437f, 438, 438f, 439 patient characteristics in, 434–435 patient positioning for, 436, 436f postprocedure images for, 441–442 sample adequacy for, 440–441 specimen radiograph for, 442 steps in, 434 stroke margin in, 436–437, 437f, 438, 438f, 439 targeting errors with, 439–440, 440f Tru-Cut device for, 440–441 VAB device for, 440–441 ultrasound, 442–446 alignment failure with, 444, 445f anesthesia for, 443–444 bleeding with, 445–446, 445f

INDEX Breast biopsy (Continued) conﬁrmation scans for, 444, 445f cystic lesion on, 442 device insertion for, 444 device selection for, 445 dressing for, 445–446 focal zone for, 443, 443f hematoma with, 445–446, 445f hemothorax with, 444 image optimization for, 443, 443f lesion sampling for, 445 mispositioning with, 442–443 pneumothorax with, 444 poor image optimization with, 443 position for, 442–443 steps in, 442 open, 455–458 cosmetic outcomes of, 457–458 hematoma with, 458 incision placement for, 457–458 indications for, 455 lesion marking for, 456 lesion mislocalization with, 456–457 localization for, 456–457, 457f, 458f radiography for, 458 resection for, 458 steps in, 455 Breathing. See also Airway evaluation of, 761–762 Bronchial and vascular sleeve lobectomy, 685– 691 air leaks with, 689 anastomotic torsion or kinking with, 689 arterial thrombosis with, 690–691 atelectasis with, 689–690 bronchial anastomosis for, 687f, 689–690, 690f bronchoscopy for, 687–688 complications of, 691 double-lumen tube placement for, 688, 688f ﬂap devascularization with, 690 hilar dissection for, 688 historical perspective on, 685 hypoxia with, 688 indications for, 685, 686f lymphadenectomy and, 691 pedicled ﬂaps for, 690 pulmonary artery reconstruction for, 690– 691, 690f, 691f steps in, 685, 687, 687f vascular injury with, 688 Bronchocutaneous ﬁstula, chest tube insertion and, 138–139 Bronchopleural ﬁstula chest tube insertion and, 138–139 pneumonectomy and, 698–699, 698f, 699f Bronchoscopy, 657–662 in bronchial and vascular sleeve lobectomy, 687–688 ﬂexible, 660–662, 660f anesthesia for, 661 complications of, 661–662 indications for, 660, 661f postoperative, 660 steps in, 657–658 rigid, 658–660, 658f airway nonvisualization with, 659–660 complications of, 661–662 inadequate surgeon-anesthesiologist cooperation with, 659 inappropriate patient for, 658–659 indications for, 658, 658f noninsertion with, 659 patient recovery from, 660 positioning for, 659

Bronchoscopy (Continued) steps in, 657–658 for tracheal resection, 741–742, 742f Bupivacaine, 50t arrhythmia with, 52 Burn injury, saphenous vein ablation and, 646 C CAGE questionnaire, 30, 30b Calciﬁcations, breast, 450 Calcium gluconate, in hypoparathyroidism, 400–401 Calcium supplements, in hypoparathyroidism, 400–401 Cancer after Billroth II reconstruction, 233 breast. See Breast biopsy; Mastectomy lung, 671. See also Bronchial and vascular sleeve lobectomy; Pneumonectomy; Video-assisted thoracic surgery (VATS) lobectomy chest wall resection for, 709–712, 710f, 711f supraclavicular lymph node biopsy in, 583–584 parathyroid gland, 419 screening for, 44t–45t, 45 Capnothorax, laparoscopic surgery and, 101– 102 Carcinoma, ileostomy, 254 Cardiac herniation, pneumonectomy and, 695–696, 696f Cardiac output, laparoscopic surgery and, 101 Cardiac tamponade central vein catheterization and, 115–116, 117f laparoscopic Nissen fundoplication and, 184 Cardiovascular disease, risk assessment for, 30–32, 31t, 32b, 32t Cardioversion, 32 Cardioverter-deﬁbrillator, perioperative management of, 60–61 Carotid artery high bifurcation of, 592 node biopsy–related injury to, 583 stent for, 593–594 Carotid artery disease, 27–28, 28f. See also Carotid endarterectomy Carotid body, 588–589, 588f Carotid endarterectomy, 27–28, 28f, 585–594 arterial control for, 590–591, 590f arteriotomy for, 591 baroreceptor perturbation with, 588–589 bleeding with, 593 carotid kink in, 587, 587f closure for, 593 cranial nerve injury with, 589 cutaneous nerve injury with, 590 difﬁcult endpoint in, 592 dissection and exposure for, 588–590, 588f, 589f fundamental principles of, 586 high carotid bifurcation in, 592 hypoglossal nerve injury with, 589, 589f improper positioning with, 586 incision for, 587–588, 587f indications for, 586 intracranial circulation evaluation for, 591, 591f limited exposure with, 587–588 long arteriotomy with, 593 marginal mandibular nerve injury with, 589–590 patch angioplasty for, 592–593, 593f positioning for, 586

881

Carotid endarterectomy (Continued) results of, 585 shunt for, 591, 591f steps in, 586 stroke with, 590–591 suture line bleeding with, 593 technique of, 592, 592f vagus nerve in, 588, 588f, 589 Catell and Braasch maneuver, 67, 69f Catheter(s) arterial, 129–134. See also Arterial catheterization infection of, 129–130, 131 thrombosis with, 129 central vein. See also Central vein catheterization infection of, 116 thrombosis with, 116–117 intravenous, in trauma, 765 pulmonary artery, 122, 122f. See also Pulmonary artery catheterization coiling/knotting of, 123–124, 124f urinary, in trauma, 766 Celiac artery stenosis of, pancreaticoduodenectomy and, 371 thrombosis of laparoscopic Nissen fundoplication and, 184 Cellulitis arteriovenous access and, 639 epigastric hernia repair and, 527 umbilical hernia repair and, 527 Central vein catheterization, 107–117 air embolism with, 114 in anticoagulated patient, 112 arrhythmia with, 115 arterial puncture with, 112–113, 113f body mass index and, 112 cachexia and, 112 cardiac perforation with, 115–116, 116f checklist for, 108–109, 108f coagulation proﬁle before, 112 femoral vein, 110, 111f guidewire loss with, 115, 115f indications for, 107 infection with, 116 internal jugular vein, 109, 111f patient characteristics in, 111–112, 111f pneumothorax with, 113–114, 114f Seldinger technique for, 110 setup for, 108–109, 108f steps in, 107–108 subclavian vein, 109–110, 111f, 112 thoracic duct injury with, 114–115 ultrasound guidance for, 110–111 venous thrombosis with, 116–117 Central venous pressure, in right hepatectomy, 337 Central venous stenosis, in arteriovenous access procedures, 633–635, 634f, 635f Cerebral perfusion pressure, 787, 787b, 788f Cerebrospinal ﬂuid leak, posterior mediastinal mass resection and, 722 Cerebrovascular injury, blunt, 768–769, 769b Cervical collar, in neck injury, 811–812 Cervical spine injury, intubation and, 58 Chest tube insertion, 135–142 analgesia for, 137–138 aseptic technique for, 136–137 after congenital diaphragmatic hernia repair, 860 diaphragmatic perforation with, 135–136, 136f, 137f effusion with, 141 empyema with, 136–137 ﬁngersweep for, 138–139, 139f

882

INDEX

Chest tube insertion (Continued) inadequate analgesia with, 137 incision for, 138 indications for, 135 insertion site selection for, 135–136 intercostal nerve injury with, 138, 138f intercostal vessel injury with, 138 intra-abdominal placement with, 139, 140f lung apex placement with, 140 lung laceration with, 138–139 mediastinum placement with, 140–141 nonfunctional drain with, 141 patient positioning for, 135 pneumothorax with, 141 reexpansion pulmonary edema with, 141– 142 steps in, 135 subcutaneous tissue placement with, 140 tube placement for, 140–141 tube suturing for, 141 unnecessary, in trauma, 761, 762 wound site infection with, 136 Chest wall infection of, 714–715 Pancoast’s tumor of, 712–714, 713f pectus excavatum of. See Pectus excavatum resection of. See Chest wall resection Chest wall resection, 708–715 biopsy before, 706–707 dissection for, 710–711, 711f dorsal nerve root injury with, 711–712 historical perspective on, 708–709 imaging before, 710, 711f incomplete, 710 indications for, 708 for infection, 714–715 intercostal artery bleeding with, 712 for lung cancer, 709–712, 710f, 711f margins for, 707–708, 707f, 710 for Pancoast’s tumor, 712–714, 713f pleural space entry for, 711 poor planning for, 705 preparation for, 708 for primary tumor, 706–709, 707f, 708f, 709f reconstruction after, 708–709, 708f, 709f skin incision misplacement with, 711 spinal consultation for, 711 thoracotomy misplacement with, 711 Child-Pugh classiﬁcation, 35, 35t Children anorectal malformations in, 827–832, 828f, 828t, 829f, 832f appendicitis in, 824 bowel obstruction in, 823–825, 823f, 824f diaphragmatic hernia in, 857–860, 858f, 859f Hirschsprung’s disease in, 832–835, 832f, 834f, 835f hypertrophic pyloric stenosis in, 871–874, 873f inguinal hernia in, 867–869, 868f intestinal malrotation in, 819–823, 820f, 821f, 822f intubation in, 63 neuroblastoma in, 863–865, 864f, 865f pectus excavatum in, 839–847. See also Pectus excavatum tracheoesophageal atresia/ﬁstula, 849–855. See also Tracheoesophageal ﬁstula repair umbilical hernia in, 869, 869f Wilms’ tumor in, 861–863, 862f, 864 Chin stitch, in tracheal resection, 750, 750f Chloroprocaine, 50t Cholangiography, in trisectionectomy, 353, 354

Cholecystectomy, 319–327 laparoscopic, 320–324 bile duct injury with, 319, 320–321, 321f, 321t, 322b bile leak with, 323 cystic artery in, 322, 322f cystic duct in, 322, 322f dissection for, 323 gallbladder perforation with, 323 hemobilia with, 323 hepatic artery injury with, 321–322, 322f indications for, 320 liver injury with, 323 Rouviere’s sulcus in, 321, 321f steps in, 320 trocar insertion for, 320, 320f viscus injury with, 323–324 open, 324–325 bleeding with, 324 closure for, 325 cystic artery ligation for, 324–325 cystic duct ligation for, 324–325 incisional hernia with, 325 indications for, 324 infection with, 325 liver resection and, 325–327, 325f, 326f bile leak with, 326–327 bleeding with, 326 nodal resection for, 327 portal vein injury with, 327 steps in, 324 Chronic obstructive pulmonary disease, 33– 34, 35f Chunking, 5–6 Chvostek’s sign, 400 Chylothorax congenital diaphragmatic hernia repair and, 860 esophagectomy and, 733, 733f, 737, 737b pneumonectomy and, 693–694 posterior mediastinal mass resection and, 723 VATS lobectomy and, 682 Chylous ascites, postvagotomy, 169 Chylous ﬁstula adrenalectomy and, 430 mastectomy and, 485 supraclavicular lymph node biopsy and, 584 Cigarette smoking history of, 37–38 preoperative cessation of, 38 Cirrhosis, laparoscopic gastric bypass and, 201–202 Cisterna chyli, in vagotomy, 169 Clamping in abdominal aortic aneurysm repair, 598, 605–607, 605f, 606f, 607f, 608f in aortic surgery, 598 blind, in trauma, 762–763 in trisectionectomy, 351 Claudication, revascularization for. See Infrainguinal revascularization Claw sign, 864, 864f Coagulation factors, deﬁciency of, 39, 40t Cognitive phase, of Fitts and Posner skill acquisition model, 6, 6f Cognitive remodeling, 7, 7f Colectomy left, 265–270 anastomosis for, 269–270, 269f anastomotic leak with, 269–270 bowel injury with, 270 indications for, 265 laparoscopic, 265–266 open, 265, 270

Colectomy (Continued) peritoneal incision and sigmoid mobilization for, 266–268, 266f, 267f, 268f proximal colon division for, 268–269 splenic injury with, 268–269 steps in, 265–266 ureter injury with, 167f, 266–267 vascular injury with, 267–268 right, 257–264 anastomosis for, 262, 263f, 264f cecum mobilization for, 259–260, 260f deep vein thrombosis with, 263 dissection for, 259–260, 259f, 260f duodenal injury with, 261 exploration for, 258–259 hepatic ﬂexure mobilization for, 260– 261, 261f indications for, 257 small bowel injury with, 259–260 steps for, 257–258 trocar placement for, 258 ureteral injury with, 259–260 vascular control for, 261–262, 262f wound infection with, 263 Colic artery ligation of, in colectomy, 269, 269f middle, ligation of, 387 Colic vein, middle, pancreatectomy and, 375– 376 Colitis ileostomy and, 254 ischemic, ruptured abdominal aortic aneurysm and, 611 Colon injury to adrenalectomy and, 426, 428, 429 aortobifemoral bypass and, 603 appendectomy and, 301–302 cholecystectomy and, 323–324 component separation procedure and, 557 inguinal hernia repair and, 506 laparoscopic gastric bypass and, 213 laparoscopic incisional hernia repair and, 539 laparoscopic splenectomy and, 573–574 laparoscopic surgery and, 97–100, 98f laparotomy and, 74–75, 75f, 76f open gastrostomy tube placement and, 148 paracentesis and, 144, 144f percutaneous gastrostomy tube placement and, 151–152, 152f stoma dissection and, 77–78, 78f ventral hernia repair and, 76, 77f obstruction of, incisional hernia and, 534– 535 splenic ﬂexure of, retraction of, 80–81, 82f Color ﬂow Doppler, in neck injury, 814, 814b Colostomy abdominal perineal resection and, 295–297, 295f, 296f leakage with, 297 obesity and, 197f, 297 parastomal hernia with, 297 stomal necrosis with, 295–296 stomal stenosis with, 297, 297f component separation procedure and, 548, 552f–553f pediatric, 830–831 colon division for, 830 ischemia with, 830–831 mucous ﬁstula for, 830–831 prolapse with, 830 rectal dilatation with, 831

INDEX Colostomy (Continued) steps in, 830 urinary tract contamination with, 831 Common femoral vein, saphenous vein ablation–related injury to, 645–646 Common iliac vein, aortic aneurysm repair– related injury to, 607–609 Common peroneal nerve, infrainguinal revascularization–related injury to, 616 Communication, surgeon-patient, 23–24 Compartment syndrome abdominal, 803, 805–806 laparotomy and, 89–91, 90f, 91f with congenital diaphragmatic hernia repair, 860 Competency, 7 Complications in Surgery, 8 Complications in Surgery and Trauma, 8 Component separation, in abdominal wall reconstruction. See Abdominal wall reconstruction, component separation in Computed tomography of accessory spleen, 422f in adrenal gland evaluation, 421, 422, 422f, 423f in gastric fundus mass, 422f in neck injury, 814–815 in pancreatic injury, 779 in pelvic trauma, 768 in soft tissue sarcoma, 491–492, 491f in splenic injury, 794, 795–797, 796f in traumatic brain injury, 786, 786f in varix, 422f Computed tomography angiography, in neck injury, 815 Congestive heart failure, arteriovenous access and, 638–639 Contiguity, in technical skill learning, 13 Continuous positive airway pressure, in obstructive sleep apnea, 61–62 Contrast media nephrotoxicity of, 36 for pelvic computed tomography, 768 toxicity of, endovascular intervention and, 651 Cooper’s ligament, in laparoscopic inguinal hernia repair, 517 Coronary artery bypass graft, carotid endarterectomy and, 28 Corticosteroids weaning from, 750 wound healing impairment and, 43 Cortisol, tumor secretion of, 423 Costochondral junction, pectus excavatum repair–related injury to, 840–841 Coumadin, perioperative management of, 39, 41f Cowden disease, 44t Cranial nerve, carotid endarterectomy–related injury to, 589 Cremaster entrapment, inguinal hernia repair and, 868 Cricothyroidotomy, in neck injury, 810–811 Cricothyrotomy, 757, 758f–760f Cryopreservation, of parathyroid gland, 418 Cushing’s syndrome, fracture in, 426 Cutaneous nerve, carotid endarterectomy– related injury to, 590 Cyst breast, 442 pancreatic. See Pancreatic cyst Cystgastrostomy, 383–384 Cystic artery in biliary resection and reconstruction, 394, 394f in cholecystectomy, 322, 322f

Cystic duct in biliary resection and reconstruction, 394, 394f in cholecystectomy, 322, 322f Cystjejunostomy, Roux-en-Y, 384 D Dacron graft, vs. polytetraﬂuoroethylene graft, 597–598 Damage control surgery, 799–806 access for, 800–801 adhesions and, 806 AlloDerm for, 807 biliary tract injury with, 802 biologic material for, 807 bleeding with, 802–803 closure for, 803, 805–806 compartment syndrome with, 803, 805– 806 contamination control for, 802 DC 0 steps for, 799–800 DC 1 steps for, 800–803 DC II steps for, 803–805 DC III steps for, 805–806 early implementation of, 799–800 edema with, 805 enteroatmospheric ﬁstula with, 806 enterocutaneous ﬁstula with, 807 falciform ligament division for, 801 foreign body retention with, 805–806 herniation after, 807 high transfusion requirement with, 804 hypotension with, 801 iatrogenic injury with, 801 indications for, 799 inspection for, 801–802 packing for, 802–803 pancreatic injury with, 802 prosthesis for, 806–807 retroperitoneal hematoma with, 801–802 self-retraining retractor placement for, 801 shunting in, 801–802 solid organ injury with, 802 temporary closure for, 803 undetected injuries with, 804 ureteral injury with, 802 Dantrolene, in malignant hyperthermia, 59 Débridement mesentery, in colectomy, 269, 269f in pancreatic necrosis, 386, 387–388 Deep circumﬂex iliac vein, aortobifemoral bypass–related injury to, 602–603 Deep peroneal nerve, infrainguinal revascularization–related injury to, 616 Deep venous thrombosis, 39, 41–42, 42t colectomy and, 263 component separation procedure and, 568 inferior vena cava ﬁlter placement in, 648– 649, 648f infrainguinal revascularization and, 628 laparoscopic surgery and, 103 saphenous vein ablation and, 646–647 subfascial endoscopic perforator surgery and, 647–648 Delayed gastric emptying gastrectomy and, 232–233 left hepatectomy and, 342 pancreaticoduodenectomy and, 371–372 Deliberate practice, 6–7 Delirium tremens, 29–30 DERMABOND, in component separation procedure, 567 Deserosilization, incisional hernia repair and, 533 Dexamethasone, 63–64, 64t

883

Diabetes insipidus, in traumatic brain injury, 789 Diabetes mellitus pancreatic débridement and, 387–388 perioperative management of, 42–43, 43b Diaphragm, injury to adrenalectomy and, 427, 427f chest tube insertion and, 136–137, 136f, 137f right hepatectomy and, 332, 332f splenectomy and, 574–575 thoracic trauma and, 776, 776f Diazepam, 50t Diuretics, in esophagectomy, 734 Diverticulum, urethral, 831 Documentation alteration of, 25–26 completeness of, 25 family history, 43–45, 44t–45t for informed consent, 24 review of, 26 Dog-ear deformity, in total mastectomy, 481, 481f Double-lumen tube, in bronchial and vascular sleeve lobectomy, 688, 688f Double-stapling technique, in laparoscopic gastric bypass, 207, 207f Drain in abdominal wall reconstruction, 567 in axillary dissection, 468 in mastectomy, 478 in tracheal resection, 743, 743f Droperidol, 63–64, 64t Drugs intoxication with, vs. mental status changes, 764 nephrotoxic, 36, 36b preoperative, 56–58 Dumping syndrome, 232 Duodenal injury adrenalectomy and, 428 aortobifemoral bypass and, 601 cholecystectomy and, 323–324 colectomy and, 261 management of, 779–784 bile duct identiﬁcation for, 783 delayed, 780 diagnosis in, 779–780 exposure for, 780–782, 780f, 781f hemodynamic instability with, 782 inadequate pyloric exclusion with, 784 missed injury with, 781 principles of, 783–784 replaced right hepatic injury with, 781– 782 stabilization in, 779–780 steps in, 779 right hepatectomy and, 332, 332f Duodenal stump, blow-out of, in gastrectomy, 225 Duodenal ulcer Helicobacter pylori infection and, 163–164 perforation of enlargement of, 160 after Graham patch repair, 164, 164b nonoperative treatment of, 159, 160b operative treatment of. See Graham patch repair sealed, 159, 160 pyloroplasty for. See Pyloroplasty vagotomy for. See Vagotomy Duodenum injury to. See Duodenal injury stenosis of, Graham patch repair and, 160– 161

884

INDEX

Duodenum (Continued) transection of, for gastrectomy, 224–226, 225f ulcer of. See Duodenal ulcer Dysphagia laparoscopic esophagomyotomy and, 192– 194 laparoscopic Nissen fundoplication and, 182–183 vagotomy and, 169 Dyspnea, pneumonectomy and, 701 E Edema airway, tracheal resection and, 751 anastomotic, laparoscopic gastric bypass and, 208 damage control surgery closure and, 805 pulmonary chest tube insertion and, 141–142 pneumonectomy and, 700–701, 700f Efferent loop syndrome, 230 Electrolyte imbalance, paracentesis and, 145– 146 Embolism air central vein catheterization and, 114 laparoscopic hepatectomy and, 363 trauma and, 762 gas laparoscopic gastric bypass and, 198–199 laparoscopic surgery and, 102 pulmonary artery, pneumonectomy and, 696–698 pulmonary artery catheter, 127 tumor, pneumonectomy and, 696, 697f Embolization endovascular intervention and, 653–654 plaque, infrainguinal revascularization and, 622 Emphysema, subcutaneous, laparoscopic gastric bypass and, 199–200 Empyema chest tube insertion and, 136–137 pneumonectomy and, 698–699, 698f, 699f Endarterectomy, carotid. See Carotid endarterectomy Endoscopic retrograde cholangiopancreatography, in trisectionectomy-related bile leak, 353 Endoscopy, in percutaneous gastrostomy tube placement, 151, 152, 152f, 153, 153f, 154 Endovascular therapy, 651–655 abdominal aortic aneurysm treatment with, 654–655, 654f, 655f access failure with, 654 device fatigue with, 654 endoleaks with, 654–655, 654f, 655f access site for, 651–653, 652f access site thrombosis with, 653 angioplasty for, 653–654 arterial dissection with, 653 arterial perforation with, 653 contrast toxicity with, 651 embolization with, 653–654 high arterial puncture with, 651–652, 652f indications for, 651 low arterial puncture with, 652 poorly angled puncture with, 652–653 stenting for, 653–654 steps in, 651 Enterectomy, 237–245 anastomosis for, 238–244 failure of, 237, 241–243

Enterectomy (Continued) leak from, 237, 242–243 misalignment prevention in, 240, 241 patency check of, 242, 244f staple line for, 240, 242f stricture prevention in, 241–242, 243f, 244f sutures for, 240, 241f technique of, 240–241, 241f, 242f bleeding with, 240 bowel obstruction after, 245 feeding after, 245 hematoma with, 240 ileus after, 245 incision for, 237–238 closure of, 244 indications for, 237 infection with, 239, 239f ischemia identiﬁcation during, 238 lesion identiﬁcation during, 238, 238f ligation imprecision in, 240 mesenteric defect for, 239, 239f closure of, 243–244, 244f missed lesions during, 238 nutritional deﬁciency after, 245 short bowel syndrome after, 244–245 stapler malfunction in, 239–240 steps in, 237 transection sites for, 238 Enteroatmospheric ﬁstula, damage control surgery and, 806 Enterocolitis, Hirschsprung’s disease repair and, 834 Enterocutaneous ﬁstula damage control surgery and, 807 epigastric hernia repair and, 527–528 incisional hernia repair and, 533, 535f, 536, 540 inguinal hernia repair and, 504 laparotomy and, 92–94, 94f umbilical hernia repair and, 527–528 Enteroenterostomy in laparoscopic gastric bypass, 205–208 stenosis of, in laparoscopic gastric bypass, 207–208 Enterotomy component separation and, 551, 553 incisional hernia repair and, 533, 538 Ephedrine, 63–64, 64t Epigastric artery, injury to appendectomy and, 300 cholecystectomy and, 324 jejunostomy and, 156–157 laparoscopic inguinal hernia repair and, 518 right hepatectomy and, 330 Epigastric hernia. See Hernia, epigastric Epigastric vein, inguinal hernia repair–related injury to, 518 Epinephrine, end-organ ischemia with, 52 Epithelial atypia, of breast, 449–450, 450f Equipment familiarization, in technical skills instruction, 16–17 Ericsson, K.A., 6–7 Error, 1–9. See also Technical skills instruction analytical response to, 4 deﬂection of, 4 fear of, 2–3, 4 gifted response to, 5 heuristics and, 3–4 knowledge-based, 3 morbidity and mortality conference for, 2, 4–5 observational detection of, 8 passive acceptance of, 4 rate of, 1–2

Error (Continued) residents’ response to, 4 response to, 4–5 rule-based, 3 skill-based, 3 surgeon’s response to, 24–26 Error training, 7–9, 7f Esophageal atresia, 849–855 diagnosis of, 849 repair of end-to-end anastomosis for, 853–854, 853f esophageal injury with, 851–852 esophageal leak with, 853 esophageal stenosis with, 853–854, 854f ﬁstula division for, 850–851, 850f GERD with, 854–855 indications for, 849 long gap atresia and, 852–853, 852f long thoracic nerve injury with, 850 misligation with, 850–851, 851f missed upper pouch ﬁstula with, 850 posterolateral thoracotomy for, 849–850 proximal and distal pouch dissection for, 851–853 right-sided aortic arch and, 849–850 steps in, 849 tracheal injury with, 851–852 Esophagectomy, 727–739 abdominal phase for, 728 airway injury with, 730–731, 731f anastomotic leak after, 736–737 anastomotic stricture after, 738 arrhythmias after, 735–736 aspiration after, 736 bleeding with, 728–730, 729f, 730f cervical phase for, 728 chyle leak with, 733, 733f, 737, 737b complications of, 728b conduit ischemia after, 735 diaphragmatic hernia after, 738–739 gastric conduit for, 731–732, 732f hoarseness after, 734–735 incisions for, 727 indications for, 727 paraesophageal hernia after, 738–739 phases of, 728 pneumonia after, 736 recurrent laryngeal nerve injury with, 734– 735 replacement conduit complications with, 731–733, 732f respiratory complications after, 733–734 splenic injury with, 730 steps in, 727, 728b transhiatal phase for, 728, 730, 730f wound infection after, 737 Esophagography, in neck injury, 815 Esophagomyotomy, laparoscopic, 187–194 anterior vagal nerve injury with, 194 bleeding with, 194 dissection for, 189, 189f Dor fundoplication with, 193–194, 193f electrocautery in, 190 endoscope placement for, 188, 188f esophageal perforation with, 190 gastric perforation with, 190 gastric vessel ligation for, 189 gastroesophageal reﬂux/dysphagia after, 192–194 incomplete myotomy with, 190–192, 191f, 192f, 193f indications for, 187–188 mediastinal sepsis with, 190 mucosal injury with, 190, 190f, 192f myotomy for, 190–193, 191f, 192f, 193f

INDEX Esophagomyotomy, laparoscopic (Continued) paraesophageal hernia with, 189, 189f splenic injury with, 194 steps in, 188 trocar insertion for, 189 Esophagopleural ﬁstula, pneumonectomy and, 695 Esophagoscopy, 662–663, 662f in neck injury, 815 Esophagus atresia of. See Esophageal atresia excision of. See Esophagectomy injury to laparoscopic Nissen fundoplication and, 176–177, 178f laparotomy and, 81–82, 83f left hepatectomy and, 339–340, 340f mediastinal mass resection and, 723 thyroid surgery and, 403 tracheal resection and, 745, 745f tracheoesophageal ﬁstula repair and, 851– 852 VATS lobectomy and, 674 perforation of laparoscopic esophagomyotomy with Dor fundoplication and, 190, 190f laparoscopic Nissen fundoplication and, 180–181, 181f vagotomy and, 168–169, 168f stenosis of, esophageal atresia repair and, 853–854, 854f in VATS lobectomy, 674, 674f Estrogen receptor immunostain, on breast biopsy, 448 Etilefrine chlorhydrate, in chylous ﬁstula, 430 Etomidate, 60 External iliac artery, inguinal hernia repair– related injury to, 518 External iliac vein, inguinal hernia repair– related injury to, 518 Extubation, after tracheal resection, 751 F Factor V deﬁciency, 40t Factor VII deﬁciency, 40t Factor X deﬁciency, 40t Factor XI deﬁciency, 40t Factor XIII deﬁciency, 40t Falciform ligament, division of in damage control surgery, 801 right hepatectomy and, 330–331, 331f Familial adenomatous polyposis, 44t Familial hypocalciuric hypercalcemia, 407 Family history, documentation of, 43–45, 44t–45t Fatty liver, laparoscopic gastric bypass and, 201–202 Fear, 2–3, 4 Fecal ﬁstula, aortobifemoral bypass and, 603 Fecal incontinence, Hirschsprung’s disease repair and, 834 Feedback, 21–22 Feeding after enterectomy, 245 after pyloromyotomy, 874 tube. See Gastrostomy feeding tube; Jejunostomy feeding tube Femoral artery cannulation of, 131, 132f hernia repair–related injury to, 505–506 Femoral nerve inadvertent block of, 54 injury to aortobifemoral bypass and, 600

Femoral nerve (Continued) infrainguinal revascularization and, 614– 615 rectal resection and, 273–274, 274f Femoral vein catheterization of, 110, 111f injury to greater saphenous vein ablation and, 645–647 inguinal hernia repair and, 505 for pulmonary artery catheterization, 122 Femoral venous cannula, in abdominal venous injury, 765–766 Fentanyl, 29t, 50t Fetus, malformation in, 62–63 Fibrin sealant in splenorrhaphy, 792 in trisectionectomy, 347–348, 354 Finger block, 53t, 54–55, 55f Finney pyloroplasty, 167, 168, 171, 171f Fish-tail plasty, 481, 481f Fistula anorectal. See Anorectal malformations aortoenteric, abdominal aortic aneurysm repair and, 609 arteriovenous inferior vena cava ﬁlter placement and, 649 residual, infrainguinal revascularization and, 617–618 bronchocutaneous, chest tube insertion and, 138–139 bronchopleural chest tube insertion and, 138–139 pneumonectomy and, 698–699, 698f, 699f chylous adrenalectomy and, 430 mastectomy and, 485 supraclavicular lymph node biopsy and, 584 enteroatmospheric, damage control surgery and, 806 enterocutaneous damage control surgery and, 807 epigastric hernia repair and, 527–528 ileostomy and, 253, 253f incisional hernia repair and, 533, 535f, 536, 540 inguinal hernia repair and, 504 laparotomy and, 92–94, 94f umbilical hernia repair and, 527–528 esophagopleural, pneumonectomy and, 695 fecal, aortobifemoral bypass and, 603 gastrocutaneous, splenectomy and, 793–794 ileovaginal, inguinal hernia repair and, 507 lymphatic, aortobifemoral bypass and, 600 mesh to skin, in incisional hernia repair, 533, 534f pancreatic, 782–783 pancreatectomy and, 377–378 pancreaticoduodenectomy and, 367, 370–371 pancreaticocutaneous, 388 perineal, 828, 828f, 828t rectovaginal hemorrhoidectomy and, 311, 312 rectal resection and, 286 rectovesical, 831, 832f rectovestibular, 828, 828f tracheoesophageal. See Tracheoesophageal ﬁstula Fistula-in-ano. See Anal ﬁstulotomy Fitts and Posner, skill acquisition model of, 6– 8, 6f, 7f

885

Flank bulge, aortobifemoral bypass–related, 604 Flat epithelial atypia, of breast, 449–450, 450f Fluid, ascitic, 143–146. See also Paracentesis Fluid imbalance, paracentesis and, 145–146 Fluid therapy in acute renal failure, 36 in component separation procedure, 554 in congestive heart failure, 32 in damage control surgery, 803–804 Flumazenil, 50t, 52 Fluorescence in situ hybridization (FISH), for HER-2 detection, 447–448 Focused abdominal sonography for trauma (FAST), 769, 770f Foley catheter, 84 Foramen ovale, patent, 701–702, 702f Forced expiratory volume in 1 second (FEV1), 34 Foreign body, after damage control surgery closure, 805–806 Fracture, adrenalectomy and, 426 G Gallbladder cholecystectomy-related perforation of, 323 left-sided, in right hepatectomy, 335–336 Gardner syndrome, 44t Gas bloat syndrome, laparoscopic Nissen fundoplication and, 180 Gas embolism laparoscopic gastric bypass and, 198–199 laparoscopic surgery and, 102 Gastrectomy, 223–233 afferent loop syndrome after, 230 anastomotic bleeding with, 229 anastomotic leak with, 227–229, 228b anastomotic stricture after, 230–231 Bancroft closure for, 225, 226f bile reﬂux gastritis after, 231–232, 232f complications for, 229–233 delayed gastric emptying after, 232–233 dumping syndrome after, 232 duodenal stump blow-out with, 225 duodenum transection for, 224–226, 225f efferent loop syndrome after, 230 esophageal transection for, 226 gastric vessel ligation for, 226 gastroesophageal junction exposure for, 226 incision for, 224 indications for, 223 left gastric artery in, 226, 227f left gastroepiploic ligation for, 226 lymphadenectomy for, 226–227 middle colic vessel injury with, 224, 224f Nissen closure for, 225, 226f nutritional deﬁcits after, 233 preoperative considerations in, 223–224 reconstruction after, 227–229, 227t, 228f, 229f retain gastric antrum with, 225 Roux stasis syndrome after, 231, 231f steps in, 223 Gastric antrum, retained, 225 Gastric artery in gastrectomy, 226, 227f injury to gastrostomy tube and, 151–152 splenectomy and, 575 ligation of, 226 Gastric bypass, laparoscopic, 197–221 abdominal wall hernia and, 202 adhesions and, 202 anastomotic hemorrhage with, 216 anastomotic ischemia with, 209

886

INDEX

Gastric bypass, laparoscopic (Continued) anastomotic leak with, 215–216, 215f anastomotic obstruction with, 208 anastomotic stenosis with, 216–217 anastomotic tension with, 216 anastomotic ulcer with, 217 arrhythmia with, 199 biliopancreatic limb misidentiﬁcation with, 205 bowel misalignment with, 205–206 bowel obstruction after, 217–218 bowel stapler perforation with, 206–207, 207f cirrhosis and, 201–202 colon injury with, 213 double-stapling technique for, 207, 207f enteroenterostomy for, 205–208, 207f, 208f enteroenterostomy stenosis with, 207–208, 208f enterolysis for, 202–203 failed mesentery closure with, 209 fatty liver and, 201–202 gas embolism with, 198–199 gastric injury with, 213 gastric pouch creation for, 209–213 gastrojejunostomy for, 215–216, 215f gastrojejunostomy leak in, 215–216 hemorrhage with abdominal wall, 220–221 anastomotic, 216 enterolysis-related, 203 mesenteric, 204–205, 208–209, 213, 219 staple line, 211 trocar-related, 200–201 inadequate gastric division with, 212 indications for, 197 internal hernia with, 217–218 lesser curvature hemorrhage with, 209 marginal anastomotic ulcer with, 217 mesenteric defect closure for, 208–209 mesenteric hemorrhage with, 204–205, 204f, 208–209, 213, 219 missed abdominal lesion with, 201 organ injury with, 200, 202–203 organ survey for, 201–202 Petersen’s space hernia with, 218–219 pneumoperitoneum for, 198–201 port misplacement with, 201 port site closure for, 220–221 pouch creation for, 209–213, 210f proximal jejunum misidentiﬁcation with, 203 proximal pouch ischemia with, 212–213 Richter’s hernia with, 220 Roux-en-Y limb creation for, 203–205 Roux-en-Y limb hematoma with, 219–220 Roux-en-Y limb length inadequency with, 205, 213–214 Roux-en-Y limb misidentiﬁcation with, 205 Roux-en-Y limb obstruction with, 214–215 Roux-en-Y limb passage for, 213–215, 214f Roux-en-Y limb stenosis with, 219 Roux-en-Y limb twisting with, 214 small bowel injury with, 203–204 small bowel ischemia with, 204 staple line hemorrhage with, 211 staple line leak with, 212 stapler defect closure for, 207, 207f stapler misﬁre with, 206, 211, 215 steps in, 197–198 subcutaneous emphysema with, 199–200 too-large pouch with, 210 too-proximal gastric division with, 209–210 triple stitch technique for, 218, 218f trocar-related injury with, 200–201

Gastric bypass, laparoscopic (Continued) tube stapling with, 210–211 twisted Roux-en-Y limb with, 214, 214f vascular injury with, 198, 200–201 Veress needle insertion in, 198 viscus injury with, 198, 202–203 Gastric emptying, delayed gastrectomy and, 232–233 left hepatectomy and, 342 pancreaticoduodenectomy and, 371–372 Gastric vessel ligation in laparoscopic esophagomyotomy with Dor fundoplication, 189 in laparoscopic Nissen fundoplication, 179– 180, 179f, 180f Gastric volvulus, left hepatectomy and, 342– 343 Gastrocutaneous ﬁstula, splenectomy and, 793–794 Gastroduodenal artery, pancreaticoduodenectomy-related division of, 371 Gastroepiploic artery, ligation of, 226 Gastroesophageal junction dissection in gastrectomy, 226 in laparoscopic Nissen fundoplication, 176– 178, 177f Gastroesophageal reﬂux esophageal atresia repair and, 854–855 gastrectomy and, 233 laparoscopic esophagomyotomy with Dor fundoplication and, 192–194, 193f Gastrojejunostomy, stenosis of, laparoscopic gastric bypass and, 216–217 Gastrostomy feeding tube, 147–154 incision for, 148 indications for, 148 open placement of, 148–150 Janeway, 148, 150 stoma maturation for, 150 tract creation for, 150 tube creation for, 150 tube diameter inadequacy with, 150 tube eversion inadequacy with, 150 tube insertion for, 150 tube length inadequacy with, 150 tube position inadequacy with, 150 Stamm, 148–150 bowel perforation with, 148 gastric tearing with, 149 gastric wall injury with, 149 inadequate suture thickness with, 148 intra-abdominal injury with, 148 steps in, 148 tract loss with, 149 tube damage with, 149 tube dislodgement with, 149–150 percutaneous placement of, 150–153 abdominal wall injury with, 153 angiocatheter insertion for, 151–152 bumper placement for, 153 endoscopy for, 151, 152, 152f, 153, 153f, 154 gastric distention inadequacy with, 151 gastric vessel injury with, 151–152 guidewire capture for, 152, 153f guidewire loss with, 152, 153f intestinal injury with, 151 one-to-one position for, 151, 152f steps in, 150–151 tongue laceration with, 152, 152f tract loss with, 152–153 tube pull-through for, 153 visceral perforation with, 151–152 Gastrotomy, anterior, 383–384 Genetic syndromes, 43–45, 44t–45t

Gladwell, Malcolm, 5, 5f Glasgow Coma Score in trauma, 763–764, 764t in traumatic brain injury, 785, 786t Goals, operative, in technical skills instruction, 15–16 Gonadal artery, colectomy-related injury to, 267–268 Goodsall’s rule, in anal ﬁstulotomy, 316, 316f Graham patch repair, 159–164 drainage after, 163 duodenal stenosis and, 160–161 exposure for, 160 fascial closure for, 163 Helicobacter pylori infection and, 163–164 incision for, 160 indications for, 159 irrigation for, 160 laparoscopic, 160 omental insufﬁciency with, 162–163 omental mobilization for, 161–162, 162f omental strangulation with, 162–163 omental tongue necrosis with, 161–162 perforation enlargement in, 160 reperforation and leak risk after, 164, 164b sealed perforation and, 159, 160 skin closure for, 163 steps in, 159–160 sutures for, 160–161, 161f, 162–163, 162f, 163f trocar-related injury with, 160 viscera injury with, 160 Greater omentum deﬁciency of, in Graham patch repair, 162– 163 necrosis of, in Graham patch repair, 161– 162, 162f strangulation of, in Graham patch repair, 162, 162f, 163f Greater saphenous vein ablation of, 645–647, 646f incomplete ligation of, 645 ligation of, 645 stripping of, 643–645, 644f Guidewire loss, with central vein catheterization, 115, 115f Gunshot wound damage control surgery for. See Damage control surgery incorrect assessment of, 767 to neck, 809 H Hand ischemia of, radial artery cannulation and, 131 paresthesia of, axillary artery cannulation and, 131, 133f, 134 Harmonic scalpel, in mastectomy, 479 Heart, injury to central vein catheterization and, 115–116 laparoscopic Nissen fundoplication and, 184 pectus excavatum repair and, 842, 845 Heart failure, congestive, 30–32 Heart rate, trauma-related, 763 Heineke-Mikulicz pyloroplasty, 167–168, 170f, 171 Hematoma abdominal wall laparoscopic gastric bypass and, 220–221 laparoscopic surgery and, 200–201 axillary dissection and, 467–468 breast image-guided biopsy and, 445–446, 445f open biopsy and, 458

INDEX Hematoma (Continued) central vein catheterization and, 112–113, 113f component separation procedure and, 567 enterectomy and, 240 epigastric hernia repair and, 527 hepatic, laparoscopic Nissen fundoplication and, 184 inferior vena cava ﬁlter placement and, 649 infrainguinal revascularization and, 625–626 mastectomy and, 479, 485 mesenteric, jejunostomy and, 156 pyloromyotomy and, 874 retroperitoneal damage control surgery and, 801–802 laparoscopic splenectomy and, 579 laparoscopic surgery and, 99–100, 100f Roux-en-Y limb, laparoscopic gastric bypass and, 219–220 saphenous nerve stripping and, 643, 645 subdural, in traumatic brain injury, 788– 789, 788f thyroid surgery and, 404 umbilical hernia repair and, 527, 869 Hemobilia, cholecystectomy-related, 323 Hemodialysis access. See Arteriovenous hemodialysis access Hemophilia A, 40t Hemophilia B, 40t Hemorrhage. See Bleeding; Hematoma Hemorrhoidectomy, 307–313 stapled, 310–313 hemorrhage after, 313 inadequate excision with, 311–312 incomplete excision with, 312–313 indications for, 310 pain after, 311, 312 pursestring suture for, 311–312, 311f rectovaginal ﬁstula with, 311, 312 stapler ﬁring for, 312, 312f stapler removal for, 312–313, 313f steps in, 310 stricture after, 311, 312 traditional, 307–310 anal stenosis with, 308, 309 anesthesia for, 307–308 anoscopy for, 308 closure for, 310 hemorrhage with, 308, 310 Hill-Ferguson retractor for, 309, 310f inadequate excision with, 309–310 inadequate planning for, 308 indications for, 307 pedicle excision for, 308–310, 309f, 310f pedicle ligation for, 308, 308f pedicle religation for, 310 sphincter injury with, 308–309 steps in, 307 urinary retention after, 307–308 Whitehead deformity after, 310 Hemostasis in axillary dissection, 467–468 in laparoscopic splenectomy, 579 in thyroid surgery, 403–404 Hemothorax thoracic trauma and, 774, 774f, 777 ultrasound image-guided breast biopsy and, 444 Henley procedure, 231, 232 Heparin, for infrainguinal revascularization, 621–622 Hepatectomy cholecystectomy and, 325–327, 325f, 326f bile leak with, 326–327 bleeding with, 326 closure for, 325

Hepatectomy (Continued) cystic artery resection for, 324–325 cystic duct resection for, 324–325 nodal resection for, 327 portal vein injury with, 327 extended. See Trisectionectomy laparoscopic, 359–366 air embolism with, 365–366 bile leak with, 365 bleeding with, 364–365 closure for, 365 hand-assist technique for, 360, 360f hypotension with, 365 inadequate space for, 362 indications for, 359 liver mobilization for, 361–362, 362f parenchymal division for, 362–365, 363f, 364f patient positioning for, 359–360, 360f pneumothorax with, 362 port placement for, 360–361, 360f, 361f steps in, 359 trocar-related bleeding with, 361 ultrasonography for, 362, 363f viscus injury with, 361 left, 339–344 caudate portal vein injury with, 341, 342f delayed gastric emptying with, 342 esophageal injury with, 339–340, 340f extended. See Trisectionectomy falciform ligament division for, 339 gastric perforation with, 341 gastric volvulus with, 342–343 hepatic vein division for, 344 hepatogastric ligament division for, 340– 341, 341f incision for, 339 indications for, 339 inferior vena cava injury with, 339 left coronary ligament division for, 339– 340, 340f left hepatic artery injury with, 340–341, 341f left hepatic artery ligation and division for, 341 left hepatic duct division for, 343, 343f left portal vein ligation and division for, 341, 342f left triangular ligament division for, 339– 340 parenchymal division for, 342–343 right hepatic duct injury with, 343 splenic injury with, 344 steps in, 339 right, 329–338 adrenal gland injury with, 332–333 air embolism with, 331–332 bile leak with, 337–338 blood loss with, 336–337 central venous pressure in, 337 common hepatic duct compromise with, 334 diaphragm injury with, 332 duodenal injury with, 332 epigastric vessel bleeding with, 330 extended. See Trisectionectomy hepatic vein bleeding with, 336 hepatic vein division for, 333, 333f, 334f hepatic vein injury with, 331–332, 336 hernia with, 329–330 incision for, 329–330, 330f inferior vena cava injury with, 331–332, 333 isovolemic hemodilution in, 337 left lobe torsion with, 330–331 left-sided gallbladder in, 335–336

887

Hepatectomy (Continued) ligament division for, 330–333, 331f, 332f parenchymal transection for, 336–337, 337f phrenic vessels in, 333 porta hepatis dissection for, 333–336, 334f, 335f posterior portal vein injury with, 335, 335f, 336f Pringle maneuver in, 337 replaced right hepatic artery in, 334, 335f right hepatic duct division for, 337–338 right hepatic vein division for, 334, 334f, 336 right portal vein division for, 334–335, 335f steps in, 329 suprahepatic inferior vena cava injury with, 331–332 Hepatic artery common, biliary resection–related injury to, 392 injury to, cholecystectomy and, 321–322 left injury to biliary resection and, 392–393 hepatectomy and, 340–341, 341f replaced, 340–341, 341f right division of, 334, 334f injury to biliary resection and, 392–393 pancreaticoduodenectomy and, 368 replaced, 334, 334f, 335f, 368, 393, 393f Kocherization-related injury to, 781– 782 trisectionectomy-related injury to, 348–349 Hepatic duct common, hepatectomy-related compromise of, 334 resection-related leak from, 395 right division of, 337–338 hepatectomy-related injury to, 343 Hepatic ﬂexure adrenalectomy-related injury to, 428 mobilization of, in right colectomy, 260– 261, 261f Hepatic vein(s) left, division of, 344 middle, division of, 344 right, division of, 336 short, in right hepatectomy, 333, 333f trisectionectomy-related injury to, 349–350 Hepatogastric ligament, division of, 175–176, 176f HER-2 immunostain, on breast biopsy, 447– 448, 448f Hereditary nonpolyposis colorectal cancer, 44t Hernia after damage control surgery, 807 diaphragmatic congenital, 857–860 repair of, 857–860 anesthesia for, 857 chest tube for, 860 chylothorax with, 860 compartment syndrome with, 860 extralobar pulmonary sequestration inspection for, 858, 858f sac excision for, 858 skin preparation for, 857–858 solid organ injury with, 858 steps in, 857

888

INDEX

Hernia (Continued) tension-free closure for, 858–860, 859f tidal volume monitoring for, 860 visceral reduction for, 858 postesophagectomy, 738–739 epigastric recurrence of, 525–526 repair of, 523–528 abscess after, 527–528 enterocutaneous ﬁstula with, 527–528 hematoma with, 527 infection with, 527 laparoscopic, 525, 526f mesh for, 523–525, 524f–525f, 526f open, 523, 525f seroma with, 526–527 skin necrosis with, 528 incisional cholecystectomy-related, 325 laparoscopic repair of, 537–542 adhesiolysis for, 538, 539f, 540f bleeding with, 538 contraindications to, 537 enterocutaneous ﬁstula with, 540 ileus after, 541 indications for, 537 infection with, 539–540 intestinal injury with, 539 mesh migration with, 542 mesh placement for, 539–541 reduction for, 539 seroma with, 541 small bowel perforation with, 542, 542f steps in, 537 suture site pain with, 541–542 trocar placement for, 537, 538f misdiagnosis of, 531 off-midline, 534f, 535 open repair of, 531–536 abdominal wall loss with, 536 adhesiolysis for, 533 bowel obstruction and, 534–535 closure for, 534 deserosalization with, 533 domain loss with, 536 enterocutaneous ﬁstula and, 533, 535f, 536 enterotomy with, 533 fascial edge deﬁnition for, 532–533, 533f infection and, 531, 532, 532f mesh placement for, 533–534, 534f contraindications to, 531, 532f ﬁstula with, 533–534, 534f mesh to skin ﬁstula with, 533–534, 534f in off-midline hernia, 534f, 535 preoperative considerations in, 531– 532 seroma with, 534, 534f steps in, 532 timing of, 534–536 recurrence of, 531–533, 533f, 540–541, 541f surgical history and, 531 inguinal, 515, 516f iatrogenic, 868–869 laparoscopic repair in, 515–521 bladder injury with, 517 bleeding with, 517 contraindications to, 515 Cooper’s ligament in, 517, 517f in direct hernia, 517–518, 517f, 518f, 520, 520f

Hernia (Continued) external iliac vessel injury with, 518 indications for, 515 in indirect hernia, 518–519, 519f, 520f inferior epigastric vessel injury with, 518 mesh placement for, 519–520, 520f, 521f nerve injury with, 520, 521f positioning for, 516 pseudosac in, 517–518, 518f pubic bone exposure for, 517 steps in, 515–516 trocar insertion for, 516, 516f open repair in, 501–507 bowel obstruction with, 506 closure for, 506 contraindications to, 501, 502b enterocutaneous ﬁstula with, 504 external oblique fascia incision for, 502, 503f failure of, 504 femoral vessel injury with, 505–506, 506f hemorrhage with, 502–503 ileovaginal ﬁstula with, 507 ilioinguinal nerve block in, 53, 54f ilioinguinal nerve injury with, 502, 505, 505f indications for, 501, 502b ischemic orchitis with, 502 mesh ﬁxation for, 503–506, 504f, 505f, 506f mesh infection with, 503 mesh migration with, 506, 507f pain after, 505 paravesical abscess with, 507 recurrence after, 504 Scarpa’s fascia dissection for, 502 seroma with, 506, 506f spermatic cord mobilization for, 502– 503, 503f steps in, 501–502 subcutaneous layer dissection for, 502 testicular injury with, 502 vas deferens obstruction with, 504– 505 vasogram after, 504 pediatric, repair of, 867–869 contralateral exploration for, 868 cremaster entrapment with, 868 external oblique aponeurosis closure for, 868 external oblique aponeurosis division for, 867 iatrogenic direct inguinal hernia with, 868–869 iliohypogastric nerve injury with, 867 ilioinguinal nerve injury with, 867 incomplete pneumoperitoneum evacuation with, 868 sac ligation for, 868, 868f sac separation for, 867 sac tear with, 868 sliding organ injury with, 868 spermatic vessel injury with, 867 steps in, 867 vas deferens injury with, 867 prolene system in, 509–512, 510f external pocket development for, 510– 511, 511f hernia type conﬁrmation for, 510 incision for, 509–510 indications for, 509 onlay component positioning for, 512, 512f

Hernia (Continued) posterior space preparation for, 511, 511f steps in, 509 suture placement for, 512 underlay patch deployment for, 511– 512, 512f recurrence of, 504 internal, in laparoscopic gastric bypass, 217– 218 lumbar, adrenalectomy and, 431, 431f paraesophageal laparoscopic esophagomyotomy with Dor fundoplication and, 189, 189f postesophagectomy and, 738–739 Petersen’s space, laparoscopic gastric bypass and, 218–219 Richter’s, laparoscopic gastric bypass and, 220 spigelian, 559–560 stomal colostomy and, 297 ileostomy and, 250, 250f umbilical, 523–528 in end-stage liver disease, 528, 528f pediatric, 869, 869f recurrence of, 525–526 repair of, 523–528 abscess after, 527–528 enterocutaneous ﬁstula with, 527–528 hematoma with, 527 infection with, 527 laparoscopic, 525, 526f mesh for, 523–525, 524f–525f, 526f open, 523, 525f seroma with, 526–527 skin necrosis with, 528 ventral (abdominal wall). See also Hernia, incisional hepatectomy-related, 329–330 laparoscopic gastric bypass and, 202 reconstruction for. See Abdominal wall reconstruction, component separation in repair-related visceral injury with, 76, 77f Heuristics, 3–4 Hill-Ferguson retractor, in hemorrhoidectomy, 309, 310f Hirschsprung’s disease, 832–835, 832f clinical presentation of, 832 repair in, 833–835 aganglionic bowel resection for, 833–834 anastomotic leak with, 833–834 Duhamel, 833 enterocolitis with, 834 incontinence with, 834 intestinal twisting with, 833, 834f nervi erigentes injury with, 833 residual aganglionosis after, 835 Soave-Boley, 833 steps in, 833 stricture with, 834 submucosal dissection in, 833 Swenson, 833 in total colonic disease, 834–835, 835f Hoarseness, postesophagectomy, 734–735 Horner’s syndrome, pectus excavatum repair and, 843 Horseshoe kidney, 610 Hourglass tumor, 721, 721f Hydrocodone, 29t Hydrogen peroxide injection, in anal ﬁstulotomy, 316, 316f Hydromorphone, 29t, 50t Hydrothorax, thymectomy and, 720 Hypercoagulable state, 39, 41–42, 42t

INDEX Hyperglycemia, 42–43, 43b Hyperhomocystinemia, 45t Hyperkalemia, after succinylcholine administration, 58–59, 58b Hyperparathyroidism, 407 in cancer, 419 in genetic disease, 418–419 surgery for. See Parathyroidectomy Hyperparathyroid–jaw tumor syndrome, 418, 419 Hypertension intra-abdominal, 805–806 intracranial, traumatic brain injury and, 787, 787b venous, arteriovenous access and, 635–636 Hyperthermia, malignant, 59, 59t Hyperthyroidism, iatrogenic, 404 Hypertrophic pyloric stenosis, 871. See also Pyloromyotomy Hypocalcemia hypoparathyroidism and, 400 parathyroidectomy and, 413 Hypoﬁbrinogenemia, 40t Hypogastric nerve, in low anterior resection, 282–283, 282f Hypoglossal nerve, carotid endarterectomy– related injury to, 589, 589f Hypoparathyroidism iatrogenic, 418 thyroid surgery and, 400–401, 401t Hypotension adrenal insufﬁciency and, 43 in blunt trauma patient, 769–770 damage control surgery and, 801 induction and, 60 intraoperative, in laparoscopic hepatectomy, 365 medication-related, 52 posttraumatic, 764 Hypothermia damage control surgery steps for, 803–804 posttraumatic, 764–765 Hypothyroidism, iatrogenic, 404 Hypovolemia, in traumatic brain injury, 788 Hypoxemia, in pregnancy, 62 Hypoxia, trauma-related, 757, 760 I Ileostomy, 247–254 abdominal wall–fascial incision alignment for, 250, 250f, 251f, 252f bowel injury with, 250, 251 bowel passage for, 251, 253, 253f bowel segment selection for, 247–249 bowel twisting with, 251, 253 carcinoma of, 254 component separation procedure and, 548, 550f–551f diversion colitis with, 254 end-loop, 247, 248f enterocutaneous ﬁstula with, 253, 253f fascial incision for, 250, 250f, 251f, 252f high-output stoma with, 247–248 indications for, 247 inferior epigastric vessel injury with, 250 mucocutaneous separation with, 249 peristomal hernia with, 250, 250f, 251f, 252f pyoderma gangrenosum with, 254 rectus ﬁber separation for, 250, 252f site selection for, 247, 248f skin incision for, 249 steps in, 247 stoma bowel passage for, 251, 253, 253f stoma incision for, 250, 250f

Ileostomy (Continued) stoma maturation for, 253 stoma misplacement with, 247, 248f stoma necrosis/ischemia with, 249, 249f stoma prolapse with, 250 stoma retraction with, 248–249 stoma stenosis with, 249, 249f stoma varices with, 254 Ileovaginal ﬁstula, inguinal hernia repair and, 507 Ileus component separation procedure and, 553– 554 enterectomy and, 245 incisional hernia repair and, 541 Iliac artery, colectomy-related injury to, 267– 268, 268f Iliohypogastric nerve, hernia repair–related injury to, 510, 867 Ilioinguinal nerve in inguinal hernia repair, 502, 503f inguinal hernia repair–related injury to, 502, 505, 505f, 510, 867 Ilioinguinal nerve block, 53, 54f Immunization after splenectomy, 794 before splenectomy, 572, 580 Imperforate anus. See Anorectal malformations Indocyanine green test, in trisectionectomy, 355 Induction aspiration during, 63 hypotension and, 60 Infection abdominal aortic aneurysm repair and, 609 abdominal perineal resection and, 294–295 appendectomy and, 300–302, 303–305 arteriovenous access and, 639, 639f breast biopsy and, 475–476 catheter axillary artery cannulation and, 131 central vein catheterization and, 116 radial artery, 129–130 chest wall, 714–715 cholecystectomy and, 325 colectomy and, 263 component separation procedure and, 554, 567 enterectomy and, 239, 239f epigastric hernia repair and, 527 incisional hernia repair and, 532, 532f infrainguinal revascularization and, 619– 620, 626–627, 626t, 627f laparoscopic incisional hernia repair and, 539–540 laparotomy and, 92–94, 93f, 94f mesh, in open inguinal hernia repair, 503 pancreatic. See Pancreatic necrosis paracentesis and, 145 pectus excavatum repair and, 842, 847 pyloromyotomy and, 874 sentinel lymph node biopsy and, 471 splenectomy and, 580, 794 sternal wound, 714–715 trisectionectomy and, 353 umbilical hernia repair and, 527 wound, 37, 37t appendectomy and, 300–301 chest tube insertion and, 136 colectomy and, 263 esophagectomy and, 737 laparoscopic gastric bypass and, 37, 37t, 220 laparotomy and, 87–88 sternal, 714–715 Inferior epigastric artery, ileostomy-related injury to, 250, 252f

889

Inferior polar arteries, splenctomy-related injury to, 575 Inferior vena cava injury to abdominal aortic aneurysm repair and, 607–609 adrenalectomy and, 426 aortobifemoral bypass and, 602 left hepatectomy and, 339 pancreaticoduodenectomy and, 368 right hepatectomy and, 331–332, 331f, 333, 333f, 334f trisectionectomy and, 349–350 in neuroblastoma resection, 864–865, 865f suprahepatic, hepatectomy-related injury to, 331–332, 331f Inferior vena cava ﬁlter placement, 41, 42, 648–649, 648f Informed consent, 23 documentation of, 24 steps for, 13 Infrainguinal revascularization, 613–628 anastomotic dehiscence with, 622 anastomotic narrowing with, 622 anticoagulation for, 621–622 bleeding with, 621, 625–626, 626f closure for, 625–627, 627f common peroneal nerve injury with, 616 conduit preparation for, 616–620, 617f, 618f, 619f conduit tunneling for, 620–621, 620f deep peroneal nerve injury with, 616 deep venous thrombosis after, 628 distal anastomosis for, 622–624, 623f distal artery exposure for, 615–616, 616f, 617f evaluation for, 613–614 failed venous valve lysis with, 618–619, 619f femoral nerve injury with, 614–615, 615f graft failure with, 624–625, 627 graft kinking with, 620–621 improper inﬂow artery choice with, 614 inadequate anticoagulation for, 621–622 indications for, 613, 614 infection with, 619–620, 626–627, 626t, 627f intimal dissection with, 622 intimal hyperplasia with, 624, 624f intra-arterial plaque embolization with, 622 intraoperative evaluation for, 624–625, 625f lymphatic leak with, 625 myocardial infarction and, 627–628 pneumonia after, 628 proximal anastomosis for, 622, 623f proximal artery exposure for, 614–615, 614f renal failure after, 628 residual arteriovenous ﬁstula with, 617–618, 618f respiratory failure after, 628 saphenous nerve injury with, 617 seroma with, 625 steps in, 614 stricture with, 621, 621f superﬁcial peroneal nerve injury with, 616 thrombosis with, 627 tibial nerve injury with, 616 vein mapping for, 617, 618f vein spasm with, 617 venous injury with, 615–616 wound closure for, 620, 620f Intercostal nerve, injury to chest tube insertion and, 138, 138f component separation procedure and, 560 VATS lobectomy and, 672–673

890

INDEX

Intercostal vessels, injury to chest tube insertion and, 138 chest wall resection and, 712 pectus excavatum repair and, 841–842 Intercostobrachial nerve, dissection-related injury, 466–467, 466f, 467f Internal mammary vessel, pectus excavatum repair–related injury to, 841–842 Intestinal malrotation, 819–825 delayed diagnosis of, 821 development of, 819–820, 820f diagnosis of, 820–821, 821f Ladd procedure for, 821, 822f delayed, 821 mesentery injury with, 823 recurrent volvulus after, 822–823 small intestinal obstruction after, 823 Intestine. See Colon; Small intestine Intimal hyperplasia arteriovenous access and, 635, 636f infrainguinal revascularization and, 624, 624f Intracranial hypertension, traumatic brain injury and, 787, 787b Intraosseous needle placement, in trauma, 765 Intubation. See also Airway in cervical spine injury, 58 in children, 63 main stem, in trauma, 762 in pregnancy, 62 in trauma, 762 in traumatic brain injury, 785, 786t Intussusception, 824 Ischemia anastomotic, in laparoscopic gastric bypass, 209 biliary, trisectionectomy-related, 349 colonic, ruptured abdominal aortic aneurysm and, 611 conduit, esophagectomy and, 735 end-organ, 52 epinephrine-related, 52 extremity, abdominal aortic aneurysm repair and, 607 ﬂap, component separation procedure and, 554, 555f–557f foregut, pancreaticoduodenectomy and, 371, 371f, 372f graft, abdominal aortic aneurysm repair and, 609 hand, radial artery cannulation and, 131 proximal gastric pouch, laparoscopic gastric bypass and, 212–213 rectal, pediatric colostomy and, 830–831 small intestine in children, 825 cholecystectomy and, 323–324 laparoscopic gastric bypass and, 204, 209 malrotation and, 821 stoma, ileostomy and, 249, 249f testicular, inguinal hernia repair and, 502 Ischemic monomelic neuropathy, 638 Isolated limb perfusion. See Melanoma, isolated limb perfusion in Isosulfan blue dye, in sentinel node biopsy, 468, 469, 469f, 470, 470f Isovolemic hemodilution, in right hepatectomy, 337 J Jaboulay pyloroplasty, 167, 168, 171 Janeway gastrostomy feeding tube. See Gastrostomy feeding tube, open placement of, Janeway

Jejunostomy feeding tube, open placement of, 155–157 epigastric vessel injury with, 156–157 hematoma with, 156 incision for, 155 indications for, 155 intra-abdominal injury with, 155 jejunal wall injury with, 156 jejunum identiﬁcation for, 155–156 ligament of Treitz misidentiﬁcation with, 155–156 pursestring suture for, 156 steps in, 155 suture inadequacy with, 156, 157 sutures for, 157 tube dislodgment with, 156, 157 tube placement for, 156–157 Jejunum jejunostomy-related injury to, 156 misidentiﬁcation of, in laparoscopic gastric bypass, 203 Joint Commission on Accreditation of Healthcare Organizations (JCAHO), 2 Jordan, Michael, 6 Jugular vein catheterization of, 109, 111f for pulmonary artery catheterization, 122 Juvenile polyposis syndrome, 44t K Kanizsa triangle, 3, 4f Ketamine, 50t, 60 Ketorolac, 50t Kidneys adrenalectomy-related injury to, 430–431 assessment of, 36–37, 36b drug effects on, 36, 36b horseshoe, 610 infrainguinal revascularization–related failure of, 628 Kocher incision, 70 Kocher’s maneuver, 368, 780–782, 780f, 781f inadequate/incomplete, in pyloroplasty, 172 in lateral pancreaticojejunostomy, 380 Kosslyn, Stephen, 5 L Ladd procedure, 821, 822f bowel obstruction after, 824–825 delayed, 821 mesentery injury with, 823 recurrent volvulus after, 822–823 small intestinal obstruction after, 823 Laparoscopic surgery, 97–103 abdominal entry for, 97–100, 98f arrhythmias with, 101 bowel injury with, 97–99, 98f cardiovascular complications of, 100–101 deep vein thrombosis with, 103 for esophagomyotomy. See Esophagomyotomy, laparoscopic gas embolism with, 102 for gastric bypass. See Gastric bypass, laparoscopic Hasson entry technique for, 97 hemodynamic complications of, 103 macrobracing for, 99, 99f for Nissen fundoplication. See Nissen fundoplication, laparoscopic patient positioning for, 101 pneumothorax with, 101–102 port site bleeding with, 100 renal complications of, 102–103

Laparoscopic surgery (Continued) retroperitoneal hematoma with, 99–100, 100f rhabdomyolysis with, 102–103 splanchnic circulation effects of, 103 steps in, 97 ventilation-perfusion mismatch with, 102 Veress needle insertion for, 97, 98, 98f, 99 Laparotomy, 67–95 abdominal compartment syndrome and, 89– 91, 90f, 91f adhesions during, 71–72, 73–74, 74f, 75– 76, 75f, 76f bladder injury with, 82–84 Catell and Braasch maneuver in, 67, 69f closure for, 67, 69f, 85–89, 87f, 88f, 89f denervation injury with, 70–71, 72f embryology and, 67, 68f enterocutaneous ﬁstula after, 92–94, 94f esophageal injury with, 81–82, 83f facial closure for, 85–89, 87f, 88f, 89f incisional planning for, 67, 70, 71–72 infectious complications of, 87–88, 92–94, 93f, 94f intestinal injury with, 74–75, 75f, 76f intestinal obstruction after, 94–95 intra-abdominal abscess after, 92–94, 93f Kocher incision for, 70 linea alba in, 73, 73f liver injury with, 78 Maddox maneuver in, 67, 69f muscle-splitting appendectomy incision for, 70, 71f needlestick injury with, 89, 89f nerve injury with, 70–71, 72f peritoneal cavity identiﬁcation for, 73–74, 73f, 74f Pfannenstiel incision for, 70, 72f splenic injury with, 78–81, 79f sutures for, 87, 87f, 88–89, 88f ureter injury with, 82 vacuum-assisted closure for, 91, 91f vascular injury with, 70–71, 84–85, 85f, 86f wound dehiscence with, 85–86 wound evisceration with, 85–86 wound infection with, 87–88 Laryngotracheal examination, in neck injury, 815–816 Lateral pectoral nerve, dissection-related injury to, 466–467 Leape, Lucian, 2, 2f Learning needs assessment, in technical skills instruction, 13–14 Left hepatic artery, aberrant, injury to, in Nissen fundoplication, 175–176, 176f Left renal vein, retroaortic, 610 Left triangular ligaments, hepatectomy-related division of, 330–331 Legal considerations, 23–26 Lesser sac, laparotomy-related injury to, 78– 81, 80f Lidocaine, 50t Ligament of Treitz incorrect identiﬁcation of, 155–156 in laparoscopic gastric bypass, 203 Limb perfusion, isolated. See Melanoma, isolated limb perfusion in Line of Toldt, 80–81, 82f Linea alba, 73, 73f Liposuction garments, after component separation procedure, 568 Liver. See also Liver disease caudate lobe of blood ﬂow to, 335–336, 336f ligamentous band of, 333, 333f, 334f venous supply of, 341, 342f

INDEX Liver (Continued) cholecystectomy-related injury to, 323 failure of, after trisectionectomy, 354–356 fatty, laparoscopic gastric bypass and, 201– 202 hematoma of, laparoscopic Nissen fundoplication and, 184 laparotomy-related injury to, 78 left lobe torsion in, hepatectomy-related, 330–331 mobilization of in laparoscopic adrenalectomy, 426 in open adrenalectomy, 428, 429f resection of. See Hepatectomy Liver disease screening for, 34–36, 35t umbilical hernia in, 528, 528f Lobectomy hepatic. See Hepatectomy sleeve. See Bronchial and vascular sleeve lobectomy VATS. See Video-assisted thoracic surgery (VATS) lobectomy Local anesthetics, 50t seizure with, 49–50, 50t in stereotactic image-guided breast biopsy, 438–439 in ultrasound image-guided breast biopsy, 443–444 Long thoracic nerve, injury to axillary dissection and, 466–467, 466f tracheoesophageal ﬁstula repair and, 850 Lorazepam, 50t Low anterior resection, 273–287 anastomosis for, 283–287, 284f bleeding from, 285, 285f leak from, 283–285 stricture of, 285–286 bladder dysfunction after, 282–283 bladder injury with, 274–275 bleeding with, 275–277 bowel dysfunction after, 287 colon mobilization for, 275–278, 276f, 277f, 278f, 284f hemorrhage with, 279, 281–282, 282f hypogastric nerve identiﬁcation for, 282, 282f incision for, 274–275, 275f indications for, 273 mesenteric vessel ligation for, 275–278, 276f, 277f patient positioning for, 273–274 peripheral nerve injury with, 273–274, 274f rectal mobilization for, 278–283, 279f, 280f, 281f rectovaginal ﬁstula with, 286 retractors for, 274, 274f, 279, 279f sexual dysfunction after, 282–283 steps in, 273 ureteral injury with, 277–278, 286–287 vaginal injury with, 286 Lumbar hernia, adrenalectomy and, 431, 431f Lumpectomy. See Mastectomy, partial Lungs apex of, chest tube in, 140 cancer of, 671. See also Bronchial and vascular sleeve lobectomy; Pneumonectomy; Video-assisted thoracic surgery (VATS) lobectomy chest wall resection for, 709–712, 710f, 711f supraclavicular lymph node biopsy in, 583–584 laceration of, chest tube insertion and, 138– 139 soft tissue sarcoma metastasis of, 495

Lymph node biopsy axillary. See Axillary dissection sentinel. See Sentinel lymph node biopsy supraclavicular, 583–584 Lymphadenectomy axillary. See Axillary dissection before bronchial and vascular sleeve lobectomy, 691 in gastrectomy, 226–227 in pneumonectomy, 693–695 at porta hepatis, 327 in VATS lobectomy, 682 Lymphatic leakage aortobifemoral bypass and, 600 infrainguinal revascularization and, 625 pneumonectomy and, 693–694 posterior mediastinal mass resection and, 723 VATS lobectomy and, 682 Lymphedema axillary dissection and, 467 sentinel lymph node biopsy and, 469–470 Lynch syndrome, 44t M Macrobracing, 19, 99, 99f Maddox maneuver, 67, 69f Magnetic resonance imaging, in soft tissue sarcoma, 491–492, 491f, 492f Malignant hyperthermia, 59, 59t Malnutrition, 38–39, 38f after enterectomy, 245 Malrotation. See Intestinal malrotation; Volvulus Marginal mandibular nerve, carotid endarterectomy–related injury to, 589– 590 Mastectomy axillary dissection with, 465–468, 466f, 467f drain placement for, 468 hemostasis for, 467–468 incision for, 465–466 indications for, 465 lymphedema after, 467 nerve injury with, 466–467, 466f, 467f steps in, 465 technique of, 466–467, 466f, 467f partial, 458–462 cosmetic outcomes of, 460, 461f, 462 false-positive margins with, 460 Faxitron for, 461f, 462 inadequate negative margins with, 459– 462 incision for, 459, 460f indications for, 458–459 localization for, 459 resection for, 459–460 specimen orientation for, 460, 462 specimen radiography in, 461f, 462 steps in, 459 sentinel lymph node biopsy with, 468–471 allergic reaction with, 469 contraindications to, 468–469 dissection for, 469–470, 469f, 470f failure of, 470, 471 false-negative, 470–471 indications for, 468 infection after, 471 isosulfan blue dye for, 468, 469, 469f, 470, 470f lymphedema after, 469–470 nerve injury with, 469 palpable nodes in, 471 pulse oximeter reading with, 469

891

Mastectomy (Continued) seroma after, 469–470 steps in, 469 total, 475–485 antibiotics for, 476 biopsy before, 475–476 blood transfusion with, 479 cancer recurrence after, 479–480 chylous ﬁstula after, 485 closure for, 480–484, 481f, 482f, 483f crinkly layer in, 480, 480f dissection extent for, 479–480, 480f drain for, 478 ﬁsh-tail plasty for, 481, 481f ﬂap elevation for, 477–479, 480f ﬂap length measurement for, 482, 483f ﬂap necrosis with, 476–477, 476f ﬂap recurrence after, 479 harmonic scalpel for, 479 hematoma after, 485 incision for, 476–477, 477f, 478f indications for, 475 inframammary fold in, 479, 480, 480f omega incision for, 476, 477f pain after, 479 pectoral fascia preservation in, 479, 480 pectoral nerves in, 484, 484f pectoralis atrophy after, 484 phantom breast syndrome after, 485 pneumothorax after, 485 redundant skin with, 480–482 seroma after, 477–479 skin-sparing incision for, 477 steps in, 475 suture-associated issues in, 482, 484 V-Y advancement ﬂap for, 481–482, 482f Mastery, stages of, 17, 17f Mayo hernioplasty, 523, 524f Median nerve block, 53t, 55, 56f Mediastinal mass, posterior, 721, 721f resection of, 721–724 azygos vein injury with, 724, 724f cerebrospinal ﬂuid leak with, 722 chylothorax with, 723 esophageal injury with, 723 spinal cord injury with, 721–722 steps in, 721 sympathetic nerve injury with, 722 thoracic aortic injury with, 723 thoracic nerve root injury with, 722–723 vagus nerve injury with, 723–724 Mediastinitis, 717–718 Mediastinoscopy, 663–666 bleeding with, 664–665 inappropriate patient selection for, 664 instruments for, 664, 665f patient selection for, 663, 664, 664f pneumothorax with, 665–666 positioning for, 663, 664f steps in, 663 Mediastinotomy, anterior, 666–668 airway loss with, 666–667 anesthesia for, 666–667 bleeding with, 667 incision for, 667, 667f indications for, 666, 666f intraoperative pathology for, 668 pneumothorax with, 667–668, 668f Mediastinum chest tube placement in, 140–141 packing of, 665 Medical records alteration of, 25–26 completeness of, 25 for informed consent, 24

892

INDEX

Medical records (Continued) requests for, 26 review of, 26 Medications, preoperative, 56–58 Melanoma amputation for, 499 isolated limb perfusion in, 497–499 indication for, 497 melphalan for, 497, 498–499, 498b pump oxygenator for, 498 steps in, 497 tourniquet application for, 499 toxic effects with, 498–499 vessel dissection for, 498 Melphalan for isolated limb perfusion, 497, 498–499, 498b nerve injury with, 498, 498b toxicities of, 498–499, 498b Mental status, posttraumatic, 764 Meperidine, 29t, 50t seizure with, 49 Mercedes-Benz sign, 518, 519f Mesenteric artery injury to pancreaticoduodenectomy and, 370 rectal resection and, 275–277, 277f in neuroblastoma resection, 864–865, 865f thrombosis of, laparoscopic Nissen fundoplication and, 184 Mesenteric vein inferior, injury to, 376 superior, injury to, 368–369, 369f, 381 Mesentery bleeding of, laparoscopic gastric bypass and, 204–205, 208–209, 219 débridement of, in colectomy, 269, 269f division of, in laparoscopic gastric bypass, 204–205, 204f hematoma of, jejunostomy and, 156 injury to enterectomy and, 239, 239f, 243–244, 244f Ladd procedure and, 823 transillumination of, in enterectomy, 239, 239f Mesh in damage control surgery, 806–807 in epigastric hernia repair, 523–525, 524f– 525f, 526f in incisional hernia repair, 533–534, 534f, 539–541 in inguinal hernia repair, 503–506, 504f, 505f, 506f, 519–520, 520f, 521f in splenorrhaphy, 791–792, 793f in umbilical hernia repair, 523–525, 524f– 525f, 526f Metabolic acidosis, damage control surgery steps for, 804 Metal allergy, after pectus excavatum repair, 847 Metastasis adrenal gland, 423f pulmonary, 495 Methemoglobinemia, 52–53 Methylene blue testing, 354 Microbracing, 19, 20f Microcalciﬁcations, breast, 450 Midazolam, 50t hypotension with, 60 Middle colic artery, gastrectomy-related injury to, 224, 224f Mitral stenosis, 59–60 Model for end-stage liver disease (MELD) score, 35–36 Monoethylglycinexylidide test, 355

Morbidity and mortality conference, 2, 4–5 Morphine, 29t, 50t Movement simpliﬁcation, 20 Multiple endocrine neoplasia, 45t, 418–419 Murphy’s Law, 24 Muscle, melphalan-induced injury to, 498– 499, 498b Muscle-splitting appendectomy incision, 70, 71f Myasthenic crisis, thymectomy and, 720–721 Myocardial infarction infrainguinal revascularization and, 627–628 postoperative, 30–32 Myotomy, for laparoscopic esophagomyotomy with Dor fundoplication, 190–193, 191f, 192f, 193f N Naloxone, 50t, 52 Nasogastric tube for laparoscopic Nissen fundoplication, 180–181, 181f stapling of, in laparoscopic gastric bypass, 210–211 in trauma, 766 Nausea in isolated limb perfusion of melphalan, 499 postoperative, 63–64, 64b, 64t Neck. See also Neck injury anatomy of, 809, 810f hematoma of, 404 Neck injury, 809–816 anatomy of, 809, 810f epidemiology of, 809, 810t management of, 809–812 airway failure with, 810–811, 810f angiography for, 813–814, 814b balloon tamponade for, 811, 811f brain computed tomography for, 815 cervical collar interference with, 811–812 color ﬂow Doppler for, 814, 814b computed tomography for, 814–815 cricothyroidotomy for, 810–811 esophageal studies for, 815, 815f examination for, 812–816, 812b, 813f hemorrhage with, 811 laryngotracheal studies for, 815–816 patient selection for, 812 radiography for, 812, 814f Necrosis gastric, splenctomy and, 576 omental, Graham patch repair and, 161– 162, 162f pancreatic. See Pancreatic necrosis skin, component separation and, 548 skin ﬂap, mastectomy and, 476–477, 476f stomal colostomy and, 295–296 ileostomy and, 249, 249f Necrotizing enterocolitis, 824, 824f Needle for breast biopsy, 440 intraosseous placement of, 765 for paracentesis, 144 SuturTek, 89, 89f Veress, 97, 98, 98f, 99, 198 retroperitoneal vascular injury with, 99– 100, 100f Needlestick injury, 89, 89f Nelson’s syndrome, 423 Nerve blocks, 53–56 ankle, 53t, 55–56, 57f femoral nerve, inadvertent, 54 ﬁnger, 53t, 54–55, 55f ilioinguinal nerve, 53, 54f

Nerve blocks (Continued) median nerve, 53t, 55, 56f needle misposition with, 56 radial nerve, 53t, 55 ulnar nerve, 53t, 55, 56f Nerve injury. See at speciﬁc nerves Nerve roots, injury to chest wall resection and, 711–712 mediastinal mass resection and, 722–723 Nervi erigentes, injury to, 833 Neuroblastoma, 863–865 biopsy for, 864 resection for, 863–865 steps in, 864 vascular injury with, 864–865, 865f vs. Wilms’ tumor, 864, 864f Neurologic injury, trauma-related, 761 Nissen closure, in gastrectomy, 225, 226f Nissen fundoplication bowel obstruction after, 824 laparoscopic, 175–184 aberrant left hepatic artery injury with, 175–176 aortic injury with, 182, 182f bougie insertion for, 180–181 cardiac injury with, 184 celiac artery thrombosis with, 184 crus closure breakdown with, 183 dysphagia with, 182–183 esophageal hiatus closure for, 182–183, 182f esophageal injury with, 176–177, 178f esophageal perforation with, 180–181, 181f gas bloat syndrome with, 180, 180f gastric injury with, 180, 180f gastric perforation with, 180–181 gastric ulceration with, 183–184 gastric vessel ligation for, 179–180, 179f, 180f gastroesophageal junction dissection for, 176–178, 177f harmonic scalpel for, 180, 180f hepatic hematoma with, 184 hepatogastric ligament division for, 175– 176, 176f herniation of, 183 indications for, 175 intraluminal suture placement with, 183 nasogastric tube insertion for, 180–181, 181f pancreatitis after, 184 pneumomediastinum with, 177–178 pneumopericardium with, 177–178 pneumothorax with, 177–178, 178f slipped, 183 splenic injury with, 179, 179f steps in, 175 superior mesenteric artery thrombosis with, 184 sutures for, 183 trocar insertion injury with, 175 vagus nerve injury with, 176, 177f Nonalcoholic steatotic hepatitis, laparoscopic gastric bypass and, 201–202 NPO guidelines, 63 Nutrition assessment of, 38–39, 38f deﬁciency of, after gastrectomy, 233 O Obesity abdominal perineal resection and, 297, 297f component separation procedure and, 548, 549f–550f

INDEX Obesity (Continued) deﬁnition of, 197 gastric bypass for. See Gastric bypass, laparoscopic Objectives, operative, in technical skills instruction, 15–16 Obstructive sleep apnea, 33, 34f postoperative management of, 61–62 Omental patch, for perforated duodenal ulcer. See Graham patch repair Ondansetron, 63–64, 64t One Minute Manager, The, 21 Opioids, 28–29, 29t vasodilatory effects of, 52 Orchitis, ischemic, inguinal hernia repair and, 502 Osmotic diuretics, in traumatic brain injury, 788 Osteoporosis, in Cushing’s syndrome, 426 Oxycodone, 29t Oxygen tension, transcutaneous, 613 P Pacemaker, perioperative management of, 60– 61 Pain arteriovenous access and, 638 incisional hernia repair and, 541–542 inguinal hernia repair and, 505 low threshold for, 28–29, 28t, 29t mastectomy and, 479 stapled hemorrhoidectomy and, 311, 312 VATS lobectomy and, 672–673 Pancoast’s tumor, 712–714, 713f Pancreas cyst of. See Pancreatic cyst injury to. See Pancreatic injury necrosis of. See Pancreatic necrosis pseudocyst of. See Pancreatic pseudocyst Pancreatectomy, distal, 375–378 adrenal vein injury with, 376–377 bleeding with, 375–376, 377 exposure for, 375–376 incision for, 375 indications for, 375 inferior mesenteric vein injury with, 376 leak/ﬁstula with, 377–378 left renal vein injury with, 376–377, 376f medial reﬂection for, 376–377, 376f middle colic vein injury with, 376 pancreatic tail dissection for, 376 parenchymal division for, 377–378 splenic mobilization with, 376 splenic vessel ligation for, 377, 377f steps in, 375 Pancreatic cyst, drainage of, 383–385 bleeding with, 383–384 endoscopic, 383–384 external, 384–385 Pancreatic duct aspiration of, 380, 380f dilation of, 379, 380f drainage of. See Pancreaticojejunostomy, lateral identiﬁcation of, 782–783, 783f incision of, 381, 381f palpation of, 380 Pancreatic ﬁstula, 782–783 pancreatectomy and, 377–378 pancreaticoduodenectomy and, 367, 370– 371 Pancreatic injury adrenalectomy and, 429 damage control surgery for, 802 laparoscopic splenectomy and, 578

Pancreatic injury (Continued) management of, 779–784 delayed, 780 diagnosis in, 779–780 duct identiﬁcation for, 782–783 exposure for, 780–782, 780f, 781f, 783f ﬁstula formation with, 782–783 hemodynamic instability with, 782 missed injury with, 781, 782f principles of, 783 replaced right hepatic injury with, 781– 782 stabilization in, 779–780 steps in, 779 splenectomy and, 793 Pancreatic necrosis, 385–389, 386f management of, 385–389 ascites with, 388–389 closure for, 389 débridement for, 386, 387–388 delayed débridement for, 386–387 drainage for, 388–389, 388f endocrine insufﬁciency with, 387–388 exocrine insufﬁciency with, 387–388 exposure for, 387 incision for, 386–387, 387f, 389 limited drainage with, 389 middle colic vessel ligation for, 387 pancreaticocutaneous ﬁstula with, 388 pleural effusion with, 388–389 vascular injury with, 387 sterile, 386–387 Pancreatic pseudocyst, drainage for anastomotic leak with, 384 anterior gastrotomy bleeding with, 383–384 cyst mislocation with, 384 endoscopic, 383–384 external, 384–385 mesocolon vessel injury with, 384 Roux-en-Y cystjejunostomy for, 384 sump drains for, 385 Pancreaticocutaneous ﬁstula, 388 Pancreaticoduodenectomy, 367–372 common bile duct transection for, 368 delayed gastric emptying after, 371–372 foregut ischemia with, 371, 371f, 372f hemorrhage with, 372 indications for, 367 Kocher’s maneuver for, 368 morbidity with, 367, 372 mortality from, 367, 372 pancreatic ﬁstula after, 367, 370–371 pancreaticojejunostomy for, 370–371 portal vein dissection for, 369–370, 370f portal vein injury with, 369–370 pseudoaneurysm with, 371, 371f, 372f pylorus-sparing, 367 steps in, 367–368 superior mesenteric artery in, 368–369, 369f, 370 superior mesenteric artery injury with, 370 Pancreaticojejunostomy, 370–371 lateral, 379–382 anastomosis for, 381, 382f aspiration for, 380, 380f drainage for, 381, 381f exploration for, 379–380 exposure for, 380 inadequate exposure for, 380 indications for, 379 insufﬁcient decompression for, 381, 381f Kocher maneuver for, 380 leak with, 382 pancreatic duct identiﬁcation for, 380– 381 Roux-en-Y limb orientation for, 381

893

Pancreaticojejunostomy (Continued) steps in, 379 superior mesenteric vein injury with, 381 unexpected ﬁndings on, 379–380 Pancreatitis, after laparoscopic Nissen fundoplication, 184 Papilloma, of breast, 446–447, 447f Paracentesis, 143–146 ascites leak with, 146 bleeding with, 145 ﬂuid and electrolyte imbalance with, 145– 146 ﬂuid nonlocalization in, 143–144 indications for, 143 infection with, 145 needle selection for, 144 organ perforation with, 144, 144f procedure for, 143–146, 144f steps in, 143 Paraesophageal hernia, laparoscopic esophagomyotomy and, 189, 189f Parallax, 18–19, 18f, 19f Paralysis, 58 Paraplegia, tracheal resection and, 750 Parathyroid glands adenoma of, 410, 411, 411f anatomy of, 409–410, 409f autotransplantation of, 401, 413, 417–419 biopsy of, 412 cancer of, 419 capsule of, 412 cryopreservation of, 418 ectopic, 409–410 hyperplastic, 410, 412–413 iatrogenic injury to, 411 normal appearance of, 410 number of, 410 supernumerary, 412–413 surgery on, 407–419. See also Parathyroidectomy vs. thymic tissue, 410 in thyroid surgery, 398, 398f, 400–401, 401t Parathyroid hormone intraoperative monitoring of, 416–417 pharmacologic, 401 Parathyroid surgery, 407–419, 408f. See also Parathyroidectomy Parathyroidectomy, 408–413, 408f biopsy for, 412 cancer discovery with, 419 capsule disruption with, 412 closure for, 413 cryopreserved normal gland with, 418 directed, 413–417 extension of, 417 false-positive parathyroid hormone level with, 416–417 gamma probe for, 416 imaging for, 414–416, 414f, 415f incision for, 417 indications for, 413 parathyroid hormone monitoring for, 416–417 sestamibi scan for, 414–415, 415f steps in, 414 ultrasonography for, 414, 414f, 416 dissection for, 409–412, 410f, 411f failure of, 409–411 in genetic disease, 418–419 hypocalcemia after, 413 inaccurate closure for, 413 incision for, 409 indications for, 408 multigland disease and, 410 normal gland injury with, 411

894

INDEX

Parathyroidectomy (Continued) recurrent laryngeal nerve injury with, 409f, 411–412 steps in, 409 subtotal, 412–413 supernumerary glands and, 412–413 total, 413 ultrasonography for, 410 Paravesical abscess, inguinal hernia repair and, 507 Paresthesia, axillary artery cannulation and, 131, 133f, 134 Parkinson disease, 59 Patent foramen ovale, 701–702, 702f Patient-surgeon communication, 23–24 Pectoral fascia preservation, in total mastectomy, 479, 480 Pectoral nerves, in mastectomy, 484, 484f Pectoralis muscle, in mastectomy, 484, 484f Pectus excavatum, 839–847 repair of, 839–847 indications for, 839 minimally invasive (Nuss), 842–847 arrhythmias after, 847 bar and lateral stabilizers for, 845–846, 845f, 846f bar displacement with, 845–846 cardiac injury with, 845 cosmetic result of, 847 epidural catheter placement for, 843, 843f infection after, 847 introducer and bar for, 843–845, 843f metal allergy after, 847 pericardial injury with, 843, 845 pleural effusion after, 846 pneumothorax with, 846 scoliosis after, 847 seroma after, 846 stabilizer misﬁxation with, 846 steps in, 842–843 thoracic outlet syndrome after, 847 transient Horner’s syndrome with, 843 open (modiﬁed Ravitch), 839–842 asphyxiating thoracic dystrophy after, 842 cardiac injury with, 842 costochondral junction damage with, 840–841 deformity recurrence after, 842 infection after, 842 intercostal vessel injury with, 841–842 internal mammary vessel injury with, 841–842 perichondral damage with, 840 pleural dissection for, 842 pneumothorax with, 842, 842f seroma after, 842 steps in, 839–840 strut placement for, 841–842, 841f subperichondral resection for, 840– 841, 840f Pelvic binder, 768, 768f Pelvic injury, 767–768 binder for, 768, 768f CT scan with IV contrast with, 768 hemorrhage with, 767–768, 768f Peptic ulcer disease duodenal, perforation with enlargement of, 160 after Graham patch repair, 164, 164b nonoperative treatment of, 159, 160b operative treatment of. See Graham patch repair sealed, 159, 160 Helicobacter pylori infection and, 163–164

Performance knowledge-based, 3 rule-based, 3 skill-based, 3 Pericardial defect, pneumonectomy and, 696, 696f Pericardial injury, pectus excavatum repair and, 843, 845 Pericardial tamponade, central vein catheterization and, 115–116, 117f Perineal ﬁstula, 828, 828f, 828t Perineal resection, abdominal. See Abdominal perineal resection Perineum, reconstruction of, 830 Peripheral motor neuropathy, 58–59 Peritoneal cavity, identiﬁcation of, for laparotomy, 73–74, 73f, 74f Peritoneum, tear in, aortobifemoral bypass and, 600–601 Peritonitis fecal, aortobifemoral bypass and, 603 laparoscopic Nissen fundoplication and, 180, 180f Peroneal nerve, adrenalectomy-related injury to, 425–426 Peutz-Jeghers syndrome, 44t Pfannenstiel incision, 70, 72f Phantom breast syndrome, 485 Pheochromocytoma, 423 Phrenic artery, in right hepatectomy, 333 Phrenic nerve, injury to supraclavicular lymph node biopsy and, 583–584 thoracic trauma and, 775 thymectomy and, 719 VATS lobectomy and, 673–674 Phrenic vein, 431, 431f in right hepatectomy, 333 vagotomy-related injury to, 168 Platelet dysfunction, 39 Platypnea–orthodeoxia syndrome, 701–702, 702f Pleura, adrenalectomy-related injury to, 430 Pleural effusion esophagectomy and, 733–734 pancreatic drainage and, 388–389 pectus excavatum repair and, 846 trisectionectomy and, 347–348 Pneumatosis intestinalis, 824, 824f Pneumomediastinum, laparoscopic Nissen fundoplication and, 177–178 Pneumonectomy, 693–702 airway compression after, 701, 701f, 702f arrhythmias after, 699–700 bronchopleural ﬁstula with, 698–699, 698f, 699f bronchus closure for, 698–699, 698f cardiac herniation with, 695–696, 696f chylothorax with, 693–694 empyema with, 698–699, 698f, 699f esophagopleural ﬁstula with, 695 hilar mobilization for, 695–696, 696f indications for, 693 mediastinal lymphadenectomy for, 693– 695, 694f pericardial defect with, 696, 696f peripheral tumor embolus with, 696, 697f platypnea–orthodeoxia syndrome after, 701–702, 702f pulmonary artery embolism/thrombosis with, 696–698 pulmonary artery ligation for, 696–698 pulmonary edema after, 700–701, 700f pulmonary vein ligation for, 696

Pneumonectomy (Continued) recurrent laryngeal nerve injury with, 694– 695, 695f steps in, 693 Pneumonia esophagectomy and, 734, 736 infrainguinal revascularization and, 628 Pneumopericardium, laparoscopic Nissen fundoplication and, 177–178 Pneumoperitoneum for gastric bypass, 198–201 incomplete evacuation of, 868 Pneumothorax anterior mediastinotomy and, 667–668, 668f central vein catheterization and, 113–114, 114f chest tube insertion and, 140, 141 congenital diaphragmatic hernia repair and, 857–858 laparoscopic hepatectomy and, 362 laparoscopic Nissen fundoplication and, 177–178, 178f laparoscopic surgery and, 101–102 mastectomy and, 485 mediastinoscopy and, 665–666 pectus excavatum repair and, 842, 842f, 846 tension, trauma-related, 761–762 thymectomy and, 720 ultrasound image-guided breast biopsy and, 444 vagotomy and, 172 Polytetraﬂuoroethylene graft, vs. Dacron graft, 597–598 Portal vein, 84, 86f caudate, hepatectomy-related injury to, 341, 342f cholangiocarcinoma of, 393, 393f injury to biliary resection and, 393–394 laparotomy and, 84–85 left hepatectomy and, 341, 342f liver resection and, 327 pancreaticoduodenectomy and, 369–370, 370f right hepatectomy and, 334–335, 335f, 336f trisectionectomy and, 348–349 posterior, right hepatectomy–related injury to, 335f, 336f right, right hepatectomy–related division of, 335f thrombosis of, 580 Portal vein embolization, in trisectionectomy, 356 Positive-pressure ventilation, in trauma, 761– 762 Posterior sagittal anorectoplasty, 831–832, 832f. See also Anoplasty steps in, 831 urethral diverticulum with, 831 Postgastrectomy syndromes, 229–233 Postpneumonectomy syndrome, 701, 701f, 702f Practice, 17–18 deliberate, 6–7 independent, 17–18 Pregnancy bleeding during, 62 intubation in, 62 Preoperative pitfalls, 27–45 in advanced liver disease screening, 34–36, 35t in bleeding risk assessment, 39–42, 40t, 41f

INDEX Preoperative pitfalls (Continued) in cardiac risk assessment, 30–33, 31t, 32b, 32t in endocrine assessment, 42–43, 43b in family history documentation, 43–45, 44t–45t in hypercoagulable state assessment, 39, 41–42, 42t in infection risk assessment, 37–38, 37t in neurologic evaluation, 27–30, 28f, 28t, 29b, 29t, 30b, 30f in nutritional assessment, 38–39, 38f in pulmonary risk assessment, 33–34, 34f, 35f in renal assessment, 36–37, 36b Pringle maneuver in hepatectomy–related bleeding, 337 in trisectionectomy, 348, 351 Progesterone, in pregnancy, 62 Promethazine, 63–64, 64t Propofol, 51 hypotension with, 60 Prothrombin deﬁciency, 40t Pseudoachalasia, 187 Pseudoaneurysm abdominal aortic aneurysm repair and, 609– 610 arteriovenous access and, 640, 640f endovascular intervention and, 652 pancreaticoduodenectomy and, 371, 371f, 372f radial artery, cannulation-related, 130, 130f Puestow procedure. See Pancreaticojejunostomy, lateral Pulmonary artery embolism of, pneumonectomy and, 696– 698 reconstruction of, in bronchial and vascular sleeve lobectomy, 690–691, 690f, 691f rupture of, catheterization and, 124–127, 125f, 126f thrombosis of, pneumonectomy and, 696– 698 Pulmonary artery catheterization, 121–127 arrhythmia with, 123 catheter coiling/knotting with, 123–124, 124f catheter embolism with, 127 external jugular vein for, 122 femoral vein for, 122 indications for, 121 internal jugular vein for, 122 misplacement of, 127 procedure for, 122–123, 122f pulmonary artery rupture with, 124–127, 125f, 126f pulmonary infarction with, 127 pulmonary valve injury with, 127 steps in, 121–122 subclavian vein for, 122 thrombocytopenia with, 127 tricuspid valve injury with, 127 ventricular perforation with, 127 Pulmonary edema chest tube insertion and, 141–142 pneumonectomy and, 700–701, 700f Pulmonary embolism, 39, 41–42, 42t component separation procedure and, 568 Pulmonary infarction, pulmonary artery catheterization and, 127 Pulmonary sequestration, in congenital diaphragmatic hernia repair, 858, 858f Pulmonary shunt, laparoscopic surgery and, 102 Pulmonary valve, catheterization-related injury to, 127

Pulse oximetry, in sentinel node biopsy, 469 Pursestring suture in jejunostomy feeding tube, 156 in stapled hemorrhoidectomy, 311–312, 311f Pyloromyotomy, 871–874 care after, 874 duodenum retraction for, 872 failed, 874 feeding after, 874 incomplete, 873 indications for, 871 laparoscopic, 871 mucosal pyloric perforation with, 872–873 open, 871 preoperative management in, 871–872 pylorus incision for, 872–873, 873f steps in, 871 stomach perforation/laceration with, 872 stomach retraction for, 872 vomiting after, 873 wound complications of, 874 Pyloroplasty, 167–172 anastomotic leak with, 171–172 closure for, 171–172, 171f Finney, 167, 168, 171, 171f Heineke-Mikulicz, 167–168, 170f, 171 inadequate drainage after, 170–171 inadequate/incomplete Kocher maneuver with, 172 indications for, 167 Jaboulay, 167, 168, 171 steps in, 167–168 Pylorus identiﬁcation of, 784 perforation of, 872–873, 873f Pyoderma gangrenosum, 254 Q Quest, Don, 5 Queuing, 8 R Radial artery, cannulation of, 129–131, 130f infection with, 129–130 ischemia with, 131 pseudoaneurysm with, 130, 130f thrombosis with, 129 Radial nerve block, 53t, 55 Radial scar, 450–451, 451f Radiation therapy, in soft tissue sarcoma, 492–493, 494f, 495f Radiography in breast biopsy, 442, 458 in damage control surgery, 800, 804 in neck injury, 812, 814f in partial mastectomy, 461f, 462 postlaparotomy, 94 Ramsey Sedation Score, 29, 29b Rectovaginal ﬁstula, hemorrhoidectomy and, 311, 312 Rectovesical ﬁstula, 831, 832f Rectum See also Posterior sagittal anorectoplasty anatomy of, 278–279 congenital malformation of. See Anorectal malformations dilatation of, in pediatric colostomy, 831 dissection of, in anoplasty, 829 ischemia of, in pediatric colostomy, 830– 831 resection of. See Abdominal perineal resection; Low anterior resection Rectus abdominis muscle, denervation of, 560

895

Recurrent laryngeal nerve anatomy of, 735f injury to esophagectomy and, 734–735 parathyroidectomy and, 411–412 pneumonectomy and, 694–695 thymectomy and, 719–720, 720f thyroid surgery and, 401–402, 401t tracheal resection and, 743–745, 744f VATS lobectomy and, 682–683 in thyroid surgery, 398f, 399f, 402 Refusal of care, documentation of, 24 Renal artery, reimplantation of, 610 Renal failure, 36–37, 36b Renal vein injury to adrenalectomy and, 426, 431 pancreatectomy and, 376–377 pancreaticoduodenectomy and, 368 retroaortic, 610 Respiratory depression, 51–52 Respiratory failure esophagectomy and, 734 infrainguinal revascularization and, 628 Respiratory insufﬁciency component separation procedure and, 566– 567 VATS lobectomy and, 673–674 RET gene, 418–419 Retroperitoneal bleeding, femoral artery cannulation and, 131, 132f Retroperitoneal hematoma damage control surgery and, 801–802 laparoscopic splenectomy and, 579 laparoscopic surgery and, 99–100, 100f Revascularization, infrainguinal. See Infrainguinal revascularization Reverse Trendelenburg position, cardiac output with, 101 Rewarming, in damage control surgery, 803– 804 Rhabdomyolysis, laparoscopic surgery and, 102–103 Rib(s) fracture of, 776–777 resection of in open posterior adrenalectomy, 430 in subphrenic abscess treatment, 92, 93f Richmond Agitation-Sedation Scale, 29, 29b Richter’s hernia, in laparoscopic gastric bypass, 220 Right triangular ligaments, division of, 331– 333, 332f Rouviere’s sulcus, in laparoscopic cholecystectomy, 321, 321f Roux-en-Y cystjejunostomy, 384 Roux-en-Y gastric bypass surgery. See Gastric bypass, laparoscopic Roux stasis syndrome, after gastrectomy, 231, 231f S Sagittal anorectoplasty, posterior, 831–832, 832f. See also Anoplasty steps in, 831 urethral diverticulum with, 831 Sandwich technique, for feedback, 21 Saphenofemoral junction, 644f misidentiﬁcation of, 645 Saphenous nerve, injury to infrainguinal revascularization and, 617 stab avulsion and, 647 vein stripping and, 643 Sarcoma. See Soft tissue sarcoma Satinsky clamp, 84, 85f

896

INDEX

Schumacher, E. F., 8 Scoliosis, pectus excavatum repair and, 847 Scopolamine, 63–64, 64t Sedation. See also Anesthesia Ramsey Sedation Scale for, 29, 29b Richmond Agitation-Sedation Scale for, 29, 29b Seizures, 49–50 Seldinger technique, for central vein catheterization, 110 Sentinel lymph node biopsy, 468–471 allergic reaction with, 469 contraindications to, 468–469 dissection for, 469–470, 469f, 470f failure of, 470, 471 false-negative node with, 470–471 indications for, 468 infection after, 471 isosulfan blue dye for, 468, 469, 469f, 470, 470f lymphedema after, 469–470 palpable nodes in, 471 pulse oximeter reading with, 469 seroma after, 469–470 steps in, 469 Sephraﬁlm (sodium hyaluronate carboxymethylcellulose), 95 Seroma arteriovenous access and, 639–640, 640f axillary dissection and, 468 component separation procedure and, 554, 556–557, 567 epigastric hernia repair and, 526–527 incisional hernia repair and, 534, 534f infrainguinal revascularization and, 625 inguinal hernia repair and, 506, 506f laparoscopic incisional hernia repair and, 541 pectus excavatum repair and, 842, 846 sentinel lymph node biopsy and, 469–470 total mastectomy and, 477–479 umbilical hernia repair and, 526–527 Sestamibi scan, in parathyroidectomy, 414– 415, 415f Sexual dysfunction, after low anterior resection, 282–283 Shock adrenal insufﬁciency and, 43 cardiogenic, 770 neurogenic, 770 trauma-related, 763, 769–770, 770f Short bowel syndrome, after enterectomy, 244–245 Shunt in carotid endarterectomy, 591, 591f in damage control surgery, 801–802 Side-biting clamp, for venous hemorrhage, 84, 85f Skill acquisition, 6–8. See also Technical skills instruction competency and, 7 Fitts and Posner model of, 6–8, 6f, 7f information overload in, 8 queuing in, 8 Skin laser burns of, 646 melphalan-related injury to, 498–499, 498b necrosis of epigastric hernia repair and, 528 umbilical hernia repair and, 528 stoma-related breakdown of, 249 Small intestine injury to adrenalectomy and, 428 component separation procedure and, 557

Small intestine (Continued) inguinal hernia repair and, 506 jejunostomy and, 156 laparoscopic gastric bypass and, 203–204 laparoscopic incisional hernia repair and, 542, 542f laparotomy and, 74–75, 75f, 76f percutaneous gastrostomy tube placement and, 151–152, 152f right colectomy and, 259–260 ischemia of cholecystectomy and, 323–324 identiﬁcation of, 238 laparoscopic gastric bypass and, 204, 209 milking of, 238, 238f obstruction of aortobifemoral bypass and, 603–604 congenital, 823–824, 823f enterectomy and, 245 infectious, in neonate, 824, 824f laparotomy-related, 75, 94–95 mechanical, in children, 824–825 recurrent, in children, 825 resection of. See Enterectomy Sodium hyaluronate carboxymethylcellulose, 95 Sodium thiopental, hypotension with, 60 Soft tissue sarcoma, 489–496 biopsy of, 490–491 computed tomography of, 491–492, 491f diagnosis of, 489, 495 imaging of, 491–492, 491f, 492f limb-sparing surgery for, 492 magnetic resonance imaging of, 491–492, 491f, 492f overaggressive therapy for, 493–495, 494f pseudocapsule of, 493 radiation therapy for, 492–493, 494f, 495f recurrence of, 492–494, 495 staging of, 489–490, 490f, 490t surgical margins in, 493 Spermatic vessel injury, inguinal hernia repair and, 867 Spinal cord injury mediastinal mass resection and, 721–722 missed diagnosis of, 764 Spine, trauma-related manipulation of, 761 Splanchnic circulation, laparoscopic surgery effects on, 130 Spleen accessory, 573, 574f vs. adrenal tumor, 422f injury to. See Splenic injury mobilization of, 79–81, 81f Splenectomy for iatrogenic injury, 79 laparoscopic, 571–580 abdominal exploration for, 573, 574f abscess after, 579 accessory spleens in, 573, 574f bleeding with, 574, 575, 576–578 capsular bleeding with, 574 colonic injury with, 573–574 contraindications to, 571–572 diaphragmatic injury with, 574–575 gastric perforation with, 576 hanging spleen technique in, 572 hilar bleeding with, 576–578 immunization before, 572, 580 indications for, 571 infection after, 580 instrumentation for, 572 irrigation and hemostasis for, 579 lateral attachment incisions for, 574–575, 575f lower pole vessel division for, 575

Splenectomy (Continued) pancreatic injury with, 578 portal vein thrombosis after, 580 positioning for, 572, 572f retroperitoneal hematoma after, 579 short gastrics division for, 575–576, 576f splenic mobilization for, 573–574 splenic vein thrombosis after, 580 splenic vessel dissection and ligation for, 576–578, 577f splenosis after, 578–579 steps in, 572 thrombocytopenia after, 573 thrombosis after, 580 tissue removal for, 578–579, 579f trocar insertion for, 572–573, 573f trocar removal for, 579 open gastric injury with, 793–794 infection after, 794 pancreatic injury with, 793 partial, 791, 792f Splenic artery angioembolization of, 794 dissection and ligation of, 576–578, 577f Splenic ﬂexure, retraction of, 80–81, 82f Splenic injury adrenalectomy and, 429–430 aortobifemoral bypass and, 601 colectomy and, 268–269, 268f computed tomography in, 794, 796f esophagectomy and, 730 laparoscopic esophagomyotomy with Dor fundoplication and, 194 laparoscopic Nissen fundoplication and, 179, 179f laparotomy and, 78–81, 79f left hepatectomy and, 344 management of, 791–797. See also Splenectomy nonoperative, 794–797, 794b algorithm for, 796f angioembolization for, 795, 796f computed tomography for, 795–797, 796f criteria for, 794–795, 795b follow-up for, 795 results of, 795, 797 splenorrhaphy for absorbable mesh wrap in, 791–792, 793f argon beam coagulator in, 791, 793f ﬁbrin glue in, 792 mobilization/exposure for, 791, 792f pancreatectomy and, 376 rectal resection and, 278, 278f vagotomy and, 169 Splenic vein dissection and ligation of, 576–578, 577f pancreatectomy-related injury to, 377 thrombosis of, 580 Splenorrhaphy. See also Splenectomy absorbable mesh wrap for, 791–792, 793f argon beam coagulator for, 791, 793f ﬁbrin glue for, 792 mobilization/exposure for, 791, 792f Splenosis, after splenectomy, 578–579 Sponge sticks, for venous hemorrhage, 84, 85f Spontaneous abortion, 62–63 Stamm gastrostomy feeding tube. See Gastrostomy feeding tube, open placement of, Stamm Stapler/stapling across nasogastric tube, in laparoscopic gastric bypass, 210–211

INDEX Stapler/stapling (Continued) bleeding from, in laparoscopic gastric bypass, 211 bowel perforation by, in laparoscopic gastric bypass, 206–207 for hemorrhoidectomy. See Hemorrhoidectomy, stapled leak from, in laparoscopic gastric bypass, 212 misﬁring of in enterectomy, 239–240 in laparoscopic gastric bypass, 206, 211, 215 in partial adrenalectomy, 432, 432f Stellate ganglion, thyroid surgery–related injury to, 403 Stenosis anal, hemorrhoidectomy and, 308 aortic, 59–60 celiac artery, pancreaticoduodenectomy and, 371 duodenal, Graham patch repair and, 160– 161 enteroenterostomy, laparoscopic gastric bypass and, 207–208 esophageal, atresia repair and, 853–854, 854f gastrojejunostomy, laparoscopic gastric bypass and, 216–217 mitral, 59–60 Roux-en-Y limb, in laparoscopic gastric bypass, 219 stomal colostomy and, 297, 297f ileostomy and, 249, 249f Stent, carotid artery, 593–594 Sternocleidomastoid muscle, parathyroid gland transfer to, 401, 417–419 Sternotomy, 717–718 infection and, 714–715 Stoma. See Colostomy; Ileostomy Stomach conduit of, for esophagectomy, 731–732, 732f feeding tube in. See Gastrostomy feeding tube placement injury to adrenalectomy and, 427 gastrostomy and, 149 laparoscopic esophagomyotomy with Dor fundoplication and, 190, 190f laparoscopic gastric bypass and, 213 laparoscopic Nissen fundoplication and, 180–181, 180f left hepatectomy and, 341 pyloromyotomy and, 872 splenectomy and, 576, 793–794 surgical bypass of. See Gastric bypass, laparoscopic tumor of, vs. adrenal tumor, 422f ulcer of, after laparoscopic Nissen fundoplication, 183–184 volvulus of, left hepatectomy and, 342–343 Stricture anal, hemorrhoidectomy and, 311, 312 anastomotic enterectomy and, 241–242, 243f, 244f gastrectomy and, 230–231 rectal resection and, 285–286 biliary, resection and, 394 Stroke carotid endarterectomy and, 590–591 patient history of, 58–59 Subclavian vein catheterization of, 109–110, 111f, 112 arterial puncture with, 112–113

Subclavian vein (Continued) for pulmonary artery catheterization, 122 stenosis of, in arteriovenous access procedures, 633–635, 634f, 635f Subcostal nerve, adrenalectomy-related injury to, 430 Subcutaneous emphysema, laparoscopic gastric bypass and, 199–200 Subcutaneous tissue, chest tube placement in, 140 Subdural hematoma, in traumatic brain injury, 788–789, 788f Subfascial endoscopic perforator surgery, 647– 648 Subroutines, 12–13 Succinylcholine, 58–59, 58b Superﬁcial peroneal nerve, infrainguinal revascularization–related injury to, 616 Superﬁcial venous insufﬁciency, 643. See also Varicose veins Superior laryngeal nerve, thyroid surgery– related injury to, 402–403 Superior mesenteric artery in neuroblastoma resection, 864–865, 865f thrombosis of, laparoscopic Nissen fundoplication and, 184 Supraclavicular lymph node biopsy, 583–584 Surgical assistants, disclosure of, 24 Sutures in enterectomy anastomosis, 240, 241f in Graham patch repair, 160, 161f, 162– 163, 162f, 163f in laparoscopic Nissen fundoplication, 183 in laparotomy closure, 87, 87f, 88–89, 88f in mastectomy, 482, 484 in open gastrostomy tube placement, 148– 150 pursestring in hemorrhoidectomy, 311–312, 311f in jejunostomy feeding tube, 156 SuturTek needle, 89, 89f Sympathetic nerves, injury to mediastinal mass resection and, 722 thyroid surgery and, 403 T Technical skills instruction, 11–22 feedback for, 21–22 intraoperative, 17–21 bracing and, 19, 20f parallax and, 18–19, 18f, 19f simplifying movement and, 20 visualization and, 20–21 postoperative, 21–22 preoperative, 13–17 equipment familiarization in, 16–17 goals and objectives deﬁnition in, 15–16 learning needs assessment in, 13–15 principles of, 12–13 TENDS pneumonic, 21 Tensor fascia lata ﬂaps, in abdominal wall reconstruction, 560–563, 564f, 565f Testes, inguinal hernia repair–related injury to, 502 Tetracaine, 50t Thoracic aorta, mediastinal mass resection– related injury to, 723 Thoracic duct anatomy of, 694, 694f injury to. See also Chylothorax central vein catheterization and, 114–115 thyroid surgery and, 403 vagotomy and, 169 ligation of, 737, 738f

897

Thoracic dystrophy, asphyxiating, pectus excavatum repair and, 842 Thoracic inlet, anatomy of, 712, 713f Thoracic nerve root, mediastinal mass resection–related injury to, 722–723 Thoracic outlet syndrome, pectus excavatum repair and, 847 Thoracic trauma, 773–777 abdominal injury in, 775 diaphragm injury in, 775, 775f hemothorax in, 774, 774f, 777 hypotension in, 775 management of aortic tear with, 774–775 chest tube for, 774, 774f delayed transport with, 775 hemothorax in, 774, 774f inadequate analgesia with, 776–777 incomplete hemothorax decompression with, 774 incomplete pleural decompression with, 773–774 indications for, 773 missed aortic tear with, 774–775 phrenic nerve injury with, 775 pneumothorax in, 773–774, 774f retained hemothorax with, 777 steps in, 773 unrecognized abdominal injury with, 775 unrecognized diaphragm injury with, 776, 776f unrecognized right thoracic injury with, 775 rib fracture in, 776–777 Thoracodorsal nerve, dissection-related injury to, 466–467, 466f, 467f Thoracotomy, in damage control surgery, 800 Thorax empyema of, chest tube insertion and, 136– 137 trauma to. See Thoracic trauma Thrombectomy, arteriovenous access and, 635, 636f Thrombocytopenia pulmonary artery catheterization and, 127 splenectomy and, 573 Thrombophlebitis, greater saphenous vein ablation and, 647 Thrombosis access site, endovascular intervention and, 653 arterial, bronchial and vascular sleeve lobectomy and, 690–691 arteriovenous access and, 632–635 celiac artery, laparoscopic Nissen fundoplication and, 184 graft, infrainguinal revascularization and, 627 pulmonary artery, pneumonectomy and, 696–698 radial artery, cannulation and, 129 superior mesenteric artery, laparoscopic Nissen fundoplication and, 184 venous, 39, 41–42, 42t central vein catheter and, 116–117 Thymectomy, 717–721 brachiocephalic vein injury with, 718–719 dissection for, 718–721, 718f, 719f hydrothorax with, 720 indications for, 717 median sternotomy for, 717–718 mediastinitis with, 717–718 myasthenic crisis with, 720–721 phrenic nerve injury with, 719, 719f pneumothorax with, 720

898

INDEX

Thymectomy (Continued) recurrent laryngeal nerve injury with, 719– 720, 720f respiratory embarrassment with, 717–718 steps in, 717 thymic vein injury with, 718–719 transcervical, 717 transsternal, 717 Thymic vein, injury to, 718–719 Thymus, vs. parathyroid glands, 410 Thyroid hormone, 404 Thyroid surgery, 397–404 airway management for, 398, 398f cervical dissection for, 398–403, 398f, 400f esophageal injury with, 403 hematoma with, 404 hemostasis for, 403–404 hyperthyroidism after, 404 hypoparathyroidism after, 400–401, 401t hypothyroidism after, 404 indications for, 397 nerve injury with, 401–403, 401t recurrent laryngeal nerve injury with, 401– 402, 401t steps in, 397–398 superior laryngeal nerve injury with, 402– 403 sympathetic chain injury with, 403 thoracic duct injury with, 403 thyroid hormone management after, 404 tracheal injury with, 403 Tibial nerve, infrainguinal revascularization– related injury to, 616 Tibial vein, infrainguinal revascularization– related injury to, 615–616 Tidal volume monitoring, in congenital diaphragmatic hernia repair, 860 To Err Is Human, 1 Total parenteral nutrition, preoperative, 38– 39, 38f Tourniquet, for isolated limb perfusion, 499 Trachea compression of, thyroid surgery and, 398, 398f injury to thyroid surgery and, 403 tracheoesophageal ﬁstula repair and, 851– 852 Tracheal resection, 741–751 airway division for, 746, 746f, 747f airway edema after, 751 airway loss before, 742 anastomosis for, 747–750, 747f, 748f anastomotic dehiscence with, 746, 748– 750, 749f chin stitch for, 750, 750f circumferential dissection for, 742–745, 743f cross-table ventilation for, 746–747 drain placement for, 743, 743f esophageal injury with, 745, 745f extubation for, 751 feeding after, 745 granulation formation with, 747–748 high-frequency jet ventilator cannula for, 746–747, 747f indication for, 741 paraplegia after, 750 recurrent laryngeal nerve injury with, 743– 745, 744f restenosis after, 746, 748–750 rigid bronchoscopy for, 741–742, 742f steps in, 741 steroid weaning before, 750 suture material for, 747

Tracheal resection (Continued) tension-releasing maneuvers for, 745–746, 746f Tracheoesophageal ﬁstula repair, 849–855 end-to-end anastomosis for, 853–854, 853f esophageal injury with, 851–852 esophageal leak with, 853 esophageal stenosis with, 853–854 ﬁstula division for, 850–851, 850f ﬁstula ligation for, 850–851, 851f GERD after, 854–855 indications for, 849 long gap atresia and, 852–853, 852f long thoracic nerve injury with, 850 posterolateral thoracotomy for, 849–850 pouch dissection for, 851–853 recurrent ﬁstula after, 854 right-sided aortic arch and, 849–850 steps in, 849 tracheal injury with, 851–852 Transcutaneous oxygen tension, 613 Transfer, for trauma, 766, 775 Transfusion therapy, in damage control surgery, 804 Trauma abdominal. See Abdominal injury; Damage control surgery blunt bleeding with, 769, 770f hypotension in, 769–770 shock with, 769–770 brain. See Traumatic brain injury cerebrovascular, 768–769, 769b duodenal. See Duodenal injury evaluation and acute management of, 757– 770 air embolism with, 762 airway in, 757–761, 758f–760f airway loss in, 757, 758f blind clamping with, 762–763 breathing in, 761–762 central venous access complications with, 765–766 circulation in, 762–763 delayed transfer with, 766 disability assessment in, 763–764 early intervention for, 765–766 in elderly patient, 763 exposure/environmental factors in, 764– 765 failure to intubate with, 763–764 femoral venous cannula with, 765–766 gastric decompression for, 766 Glasgow Coma Scale in, 763–764, 764t gunshot wound assessment in, 767 hemorrhage with, 762, 763 hypotension with, 764 hypothermia with, 764–765 hypoxia in, 757, 760 insufﬁcient IV access with, 765 mental status changes in, 764 missed injury with, 767 missed shock diagnosis with, 763 missed spinal cord injury in, 764 missed tension pneumothorax with, 761 nasogastric tube misplacement with, 766 neurologic injury with, 761 primary survey in, 757–765 secondary survey in, 767 spine manipulation in, 761 tension pneumothorax with, 761–762 transfer for, 766 unnecessary chest tube placement with, 761, 762 unstable airway in, 760–761 urethral tear with, 766

Trauma (Continued) vascular injury with, 762–763 venous access for, 765–766 literature evaluation on, 753–755 class II data in, 754 class III data in, 753–754 retrospective vs. prospective series in, 754 neck. See Neck injury pancreatic. See Pancreatic injury pelvic. See Pelvic injury splenic. See Splenic injury thoracic. See Thoracic trauma Traumatic brain injury, 785–789 cerebral perfusion pressure in, 787, 787b, 788f computed tomography in, 786, 786f diabetes insipidus with, 789 Glasgow Coma Score in, 785, 786t guidelines for, 785, 786f, 786t hypovolemia with, 788 intracranial hypertension with, 787, 787b intubation for, 785, 786t mental status changes with, 787 osmotic diuretics in, 788 outcomes of, 785, 786t subdural hematoma with, 788–789, 788f Trendelenburg position, reverse, cardiac output with, 101 Tricuspid valve, catheterization-related injury to, 127 Trisectionectomy, 345–356 argon beam coagulation for, 347 bile duct injury with, 349 bile leak after, 352–354 biliary drainage before, 356 bleeding with, 350–352 blood transfusion for, 350 cholangiography before, 353 cholangiography during, 354 clamp-crushing technique for, 352 clamping techniques for, 351 dissecting sealer device for, 352 endoscopic retrograde cholangiopancreatography after, 353 ﬁbrin sealant for, 347–348, 354 hemorrhage with, 349–352 hepatic artery injury with, 348–349 hepatic insufﬁciency after, 354–356 hepatic vein injury with, 349–350 hepatic volume in, 355–356 Hydrojet for, 352 inadequate exposure with, 346–347 incision for, 346–347 indications for, 345 indocyanine green test in, 355 inferior vena cava injury with, 349–350 inﬂow vessel control for, 348–349, 349f liver mobilization for, 347–348 methylene blue testing during, 354 monoethylglycinexylidide test in, 355 morbidity with, 345 mortality with, 345, 353 necrosis with, 348–349 outﬂow vessel control for, 349–350 parenchymal transection for, 350–354 pleural effusion after, 347–348 portal vein embolization in, 356 portal vein injury with, 348–349 Pringle maneuver for, 348, 351 residual function after, 355 selective hepatic venous exclusion for, 352 steps in, 345–346 total hepatic venous exclusion for, 351– 352 ultrasonic dissector for, 352

INDEX Trocar insertion for adrenalectomy, 426, 426f for appendectomy, 300–301, 300f for cholecystectomy, 320, 320f for esophagomyotomy, 189 for incisional hernia repair, 537, 538f for inguinal hernia repair, 516, 516f for laparoscopic Nissen fundoplication, 175 for laparoscopic surgery, 97–100, 97f, 99f for right colectomy, 258 for splenectomy, 572–573, 573f Trousseau’s sign, 400 Tube. See Gastrostomy feeding tube; Jejunostomy feeding tube; Nasogastric tube Turcot syndrome, 44t U Ulcer duodenal Helicobacter pylori infection and, 163– 164 perforation of enlargement of, 160 after Graham patch repair, 164, 164b nonoperative treatment of, 159, 160b operative treatment of. See Graham patch repair sealed, 159, 160 pyloroplasty for. See Pyloroplasty vagotomy for. See Vagotomy gastric, after laparoscopic Nissen fundoplication, 183–184 Ulceration, venous, subfascial endoscopic perforator surgery for, 647–648 Ulnar nerve block, 53t, 55, 56f Ultrasonography in breast biopsy. See Breast biopsy, imageguided, ultrasound in central vein catheterization, 110–111 in infrainguinal revascularization, 624 in laparoscopic hepatectomy, 362, 362f in parathyroidectomy, 414, 414f, 416 Umbilical hernia. See Hernia, umbilical Ureter, injury to aortobifemoral bypass and, 603 appendectomy and, 302–303 colectomy and, 259–260, 266–267, 266f, 267f damage control surgery for, 802 laparotomy and, 82 rectal resection and, 277–278, 278f, 286– 287 Urethra, injury to abdominal perineal resection and, 293–294 anoplasty and, 829 trauma and, 766 Urethral diverticulum, 831 Urinary catheter, in trauma, 766 Urinary incontinence, anal ﬁstulotomy and, 316–317 Urinary retention anal ﬁstulotomy and, 315 hemorrhoidectomy and, 307–308

Urinary tract infection, after pediatric colostomy, 831 Urinoma, laparotomy and, 82 V V-Y advancement ﬂap, in total mastectomy, 481–482, 482f Vacuum-assisted closure, 91, 91f Vagal trunk, injury to, laparoscopic esophagomyotomy with Dor fundoplication and, 194 Vagina, injury to abdominal perineal resection and, 294 anoplasty and, 829 rectal resection and, 286 Vagotomy, 167–172 aortic injury with, 172 chylous ascites after, 169 dysphagia after, 169 esophageal perforation with, 168–169, 168f inadequate drainage after, 170–171 incomplete, 169–170 division and resection for, 169–170, 170f liver mobilization for, 168 vagus nerve identiﬁcation for, 168–169 indications for, 167 phrenic vein injury with, 168 pneumothorax with, 172 splenic injury with, 169 steps in, 167 thoracic duct injury with, 169 Vagus nerve in carotid endarterectomy, 588, 588f injury to carotid endarterectomy and, 589 laparoscopic Nissen fundoplication and, 176, 177f mediastinal mass resection and, 723–724 Varicose veins, 643–647 stab avulsion of, 647 vein ablation for, 645–647, 646f vein ligation for, 645 vein stripping for, 643–645, 644f Varix (varices) vs. adrenal tumor, 422f ileostomy-related, 254 Vas deferens, hernia repair–related disorders to, 504–505, 867 VATS lobectomy. See Video-assisted thoracic surgery (VATS) lobectomy Venography, in arteriovenous hemodialysis access, 631, 632b, 634, 636 Venous insufﬁciency, superﬁcial, 643. See also Varicose veins subfascial endoscopic perforator surgery for, 647–648 Ventilation-perfusion mismatch, laparoscopic surgery and, 102 Veress needle, 97, 98, 98f, 99, 198 retroperitoneal vascular injury with, 99–100, 100f Vicryl mesh, in damage control surgery closure, 806

899

Video-assisted thoracic surgery (VATS) lobectomy, 671–683 chylothorax with, 682 esophageal injury with, 674, 674f indications for, 671 intercostal bundle injury with, 672–673 left lower, 675–676, 676f, 679, 681 left upper, 675, 681, 681f lung mobilization for, 673–674, 673f lymph node dissection for, 682–683 phrenic nerve injury with, 673–674 port placements for, 672–673, 672f pulmonary vessel isolation and division for, 681–682 recurrent laryngeal nerve injury with, 682– 683 right lower, 675, 679, 681 right middle, 675, 679, 681f right upper, 674–675, 675f, 676–679, 677f–678f, 679f, 680f steps in, 672 vascular injury with, 681–682 Visualization, 5–6, 20–21 Vitamin B12 deﬁciency, after enterectomy, 245 Voice, thyroid surgery–related changes in, 402 Volvulus, 819–825 delayed diagnosis of, 821 development of, 819–820, 820f diagnosis of, 820–821, 821f Ladd procedure for, 821, 822f delayed, 821 mesentery injury with, 823 recurrent volvulus after, 822–823 small intestinal obstruction after, 823 recurrent, 822–823 Vomiting in isolated limb perfusion of melphalan, 499 postoperative, 63–64, 64b, 64t after pyloromyotomy, 873, 874 Von Willebrand disease, 39, 40t W Whipple procedure. See Pancreaticoduodenectomy Whitehead deformity, hemorrhoidectomy and, 310 Wilms’ tumor, 861–863 vs. neuroblastoma, 864, 864f removal of, 861–863 bleeding with, 863 contralateral tumor with, 861–862 contralateral vessel injury with, 862 dissection for, 863 exploration for, 861–862 incision for, 861 liver resection with, 863 pulmonary embolism with, 863 renal hilum ligation for, 862–863, 862f steps in, 861 tumor spillage with, 861, 862–863 Withdrawal syndrome, alcohol, 29–30, 29b, 30f Wound infection. See Infection, wound