Surgical Pitfalls: Prevention and Management

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

Working together to grow libraries in developing countries www.elsevier.com | www.bookaid.org | www.sabre.org

Printed in China Last digit is the print number:

9

8

7

6

5

4

3

2

1

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

3

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.)

5

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

7

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.

9

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.

2

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

21

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

REFERENCES 1. Blacker DJ. The preoperative cerebrovascular consultation: common cerebrovascular questions before general or cardiac surgery. Mayo Clin Proc 2004;79:223– 229. 2. Chalela J, Katzan I, Liebeskind D, et al. Safety of intraarterial thrombolysis in the postoperative period. Stroke 2001;32:1365–1369. 3. Evans BA, Wijdicks FM. High-grade carotid stenosis detected before general surgery. Is endarterectomy indicated? Neurology 2001;57:1328–1330. 4. Brener BJ, Hermans H, Eisenbud D, et al. The management of patients requiring coronary bypass and carotid endarterectomy. In Moore WS (ed): Surgery for Cerebrovascular Disease. Philadelphia: Saunders, 1996; pp 278– 287. 5. Carroll IR, Angst MS, Clark JD. Management of perioperative pain in patients chronically using opioids. Reg Anesthes Pain Med 2004;29:576–591.

46

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.

47

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.

62

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

REFERENCES 1. Lapetina E, Armstrong E. Preventing errors in the outpatient setting: a tale of three states. Heath Affairs 2002;21:26–39. 2. Beliveau M, Multach M. Perioperative care for the elderly patient. Med Clin North Am 2003;87:273–289. 3. Najjar S, Devinsky O, Rosenberg A. Procedures in epilepsy patients. In Ettinger A, Devinsky O (eds): Managing Epilepsy and Co-existing Disorders. Boston: Butterworth-Heinemann, 2002; pp 499–513.

5 ANESTHESIA FOR THE SURGEON 4. Tesniere A, Servin F. Intravenous techniques in ambulatory anesthesia. Anesthesiol Clin North Am 2003;21:273– 288. 5. Guarracino F, Lapolla F, Cariello C, et al. Target controlled infusion: TCI. Minerva Anestesiol 2005;71:335–337. 6. Coates D. “Diprifusor” for general and day-case surgery. Anaesthesia 1998;53(suppl 1):46–48. 7. Rodrigo MR, Irwin MG, Tong CK, Yan SY. A randomised crossover comparison of patient-controlled sedation and patient-maintained sedation using propofol. Anaesthesia 2003;58:333–338. 8. Jastak JT, Peskin RM. Major morbidity or mortality from office anesthetic procedures: a closed-claim analysis of 13 cases. Anesth Prog 1991;38:39–44. 9. Merah NA, Wong DT, Ffoulkes-Crabbe DJ, et al. Modified Mallampati test, thyromental distance and interincisor gap are the best predictors of difficult laryngoscopy in West Africans. Can J Anaesth 2005;52:291–296. 10. Byrne MF, Mitchell RM, Gerke H, et al. The need for caution with topical anesthesia during endoscopic procedures, as liberal use may result in methemoglobinemia. J Clin Gastroenterol 2004;38:225–229. 11. O’Donohue WJ Jr, Moss LM, Angelillo VA. Acute methemoglobinemia induced by topical benzocaine and lidocaine. Arch Intern Med 1980;140:1508–1509. 12. Wright RO, Lewander WJ, Woolf AD. Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med 1999;34:646–656. 13. Salam GA. Regional anesthesia for office procedures: part II. Extremity and inguinal area surgeries. Am Fam Physician 2004;69:896–900. 14. Song D, Greilich NB, White PF, et al. Recovery profiles and costs of anesthesia for outpatient unilateral inguinal herniorrhaphy. Anesth Analg 2000;91:876–881. 15. Bugedo GJ, Carcamo CR, Mertens RA, et al. Preoperative percutaneous ilioinguinal and iliohypogastric nerve block with 0.5% bupivacaine for post-herniorrhaphy pain management in adults. Reg Anesth 1990;15:130–133. 16. Ghani KR, McMillan R, Paterson-Brown S. Transient femoral nerve palsy following ilio-inguinal nerve blockade for day case inguinal hernia repair. J R Coll Surg Edinb 2002;47:626–629. 17. Lipp AK, Woodcock J, Hensman B, Wilkinson K. Leg weakness is a complication of ilio-inguinal nerve block in children. Br J Anaesth 2004;92:273–274. 18. Rosario DJ, Jacob S, Luntley J, et al. Mechanism of femoral nerve palsy complicating percutaneous ilioinguinal field block. Br J Anaesth 1997;78:314–316. 19. Eagle KA, Froehlich JB. Reducing cardiovascular risk in patients undergoing noncardiac surgery. N Engl J Med 1996;335:1761–1763. 20. Lindenauer PK, Pekow P, Wang K, et al. Perioperative beta-blocker therapy and mortality after major noncardiac surgery. N Engl J Med 2005;353:349–361. 21. 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. 22. Poldermans D, Boersma E, Bax JJ, et al. The effect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

33.

34.

35.

36. 37.

38.

65

surgery. Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography Study Group. N Engl J Med 1999;341:1789–1794. 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). J Am Coll Cardiol 2002;39:542–553. Fleisher LA, Eagle KA. Clinical practice. Lowering cardiac risk in noncardiac surgery. N Engl J Med 2001;345:1677– 1682. Salem M, Tainsh RE Jr, Bromberg J, et al. Perioperative glucocorticoid coverage. A reassessment 42 years after emergence of a problem. Ann Surg 1994;219:416–425. Centers for Medicare and Medicaid, Division of Quality, Evaluation, and Health Outcomes. Guide to quality measures: a compendium, Vol 1. 2006. Available at http://www.cms.hhs.gov/MedicaidSCHIPQualPrac/ downloads/pmfinalaugust06.pdf (accessed November 1, 2006). Roth W, Kling J, Gockel I, et al. Dissatisfaction with postoperative pain management—a prospective analysis of 1071 patients. Acute Pain 2005;7:75–83. Pasternak L, Arens J, Caplan C, et al. Practice advisory for preanesthetic evaluation. 2003. Avail-able at http://www. asahq.org/publicationsAndServices/preeval.pdf (accessed March 1, 2006). Mcleod A, Calder I. Spinal cord injury and direct laryngoscopy—the legend lives on. Br J Anaesth 2000;84: 705–709. Hastings R, Marks JD. Airway management for trauma patients with potential cervical spine injuries. Anesth Analg 1991;73:471–482. Hastings R, Wood PR. Head extension and laryngeal view during laryngoscopy with cervical spine stabilization maneuvers. Anesthesiology 1994;81:1081–1082. Lambert D, Deane R, Mazuzan J. Anesthesia and the control of systemic blood pressure in patients with spinal cord injury. Anesth Analg 1982;61:344–348. Martyn J, White D, Gronert G, et al. Up-and-down regulation of skeletal muscle acetylcholine receptors. Anesthesiology 1992;76:822–831. Carson JM, Van Sickels JE. Preoperative determination of susceptibility to malignant hyperthermia. J Oral Maxillofac Surg 1982;40:432–435. Litman RS, Rosenberg H. Malignant hyperthermia: update on susceptibility testing. JAMA 2005;293:2918– 2924. Nicholson G, Pieriera A, Hall G. Parkinson’s disease and anesthesia. Br J Anaesth 2003;90:524–525. Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation 1999;100:1043–1049. Eagle KA, Guyton RA, Davidoff R, et al. ACC/AHA 2004 guideline update for coronary artery bypass graft surgery: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee to Update the 1999 Guidelines

66

39.

40.

41. 42.

43.

44.

45. 46.

47.

48.

49.

50.

51.

SECTION I: GENERAL CONSIDERATIONS

for Coronary Artery Bypass Graft Surgery). Circulation 2004;110:e340–e437. Wagner R, White P. Etomidate inhibits adrenocortical function in surgical patients. Anesthesiology 1984;61:647– 651. Zed PJ, Abu-Laban RB, Harrison DW. Intubating conditions and hemodynamic effects of etomidate for rapid sequence intubation in the emergency department: an observational cohort study. Acad Emerg Med 2006;13: 378–383. Epub 2006; Mar 10. Preziosi P, Vacca M. Adrenocortical suppression and other endocrine effects of etomidate. Life Sci 1988;42:477–489. Wanscher M, Tonnesen E, Huttel M, Larsen K. Etomidate infusion and adrenocortical function. A study in elective surgery. Acta Anaesthesiol Scand 1985;29:483– 485. Duthie DJ, Fraser R, Nimmo WS. Effect of induction of anaesthesia with etomidate on corticosteroid synthesis in man. Br J Anaesth 1985;57:156–159. Fragen RJ, Shanks CA, Molteni A, Avram MJ. Effects of etomidate on hormonal responses to surgical stress. Anesthesiology 1984;61:652–656. Himmelseher S, Durieux M. Ketamine for perioperative pain management. Anesthesiology 2005;102:211–220. Atlee J, Bernstein A. Cardiac rhythm management devices (part II): perioperative management. Anesthesiology 2001; 95:1492–1506. Wong D, Middleton W. Electrocautery-induced tachycardia in a rate-responsive pacemaker. Anesthesiology 2001; 94:710–711. Biavati MJ, Manning SC, Phillips DL. Predictive factors for respiratory complications after tonsillectomy and adenoidectomy in children. Arch Otolaryngol Head Neck Surg 1997;123:517–521. Cohen MM, Cameron CB. Should you cancel the operation when a child has an upper respiratory tract infection? Anesth Analg 1991;72:282–288. Duncan PG, Cohen MM. Postoperative complications: factors of significance to anaesthetic practice. Can J Anaesth 1987;34:2–8. Lawrence VA, Dhanda R, Hilsenbeck SG, Page CP. Risk of pulmonary complications after elective abdominal surgery. Chest 1996;110:744–750.

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

88

SECTION I: GENERAL CONSIDERATIONS

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.

92

SECTION I: GENERAL CONSIDERATIONS

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

94

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.

96

SECTION I: GENERAL CONSIDERATIONS

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).

98

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.

99

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

100

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

102

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

104

SECTION I: GENERAL CONSIDERATIONS

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-

35.

36.

37.

38.

39.

40. 41.

42.

43.

44. 45.

46.

47.

48.

49.

50.

51.

neal insufflation. An experimenal study. Surg Endosc 1997;11:911–914. Dexter SP, Vucevic M, Gibson J, et al. Hemodynamic consequences of high and low pressure capnoperitoneum during laparoscopic cholecystectomy. Surg Endosc 1999; 13:376–381. Alishahi S, Francis N, Crofts S, et al. Central and peripheral adverse hemodynamic changes during laparoscopic surgery and their reversal with a novel intermittent sequential pneumatic compression device. Ann Surg 2001; 233:176–182. Safran D, Sgambati S, Orlando R. Laparoscopy in high risk cardiac patients. Surg Gynecol Obstet 1993;176:548– 554. Girish P, Joshi MB. Anesthesia for minimally invasive surgery: laparoscopy, thoracoscopy, hysteroscopy. Anesthesiol Clin North Am 2001;19:1. Henry CP, Hofland J. Laparoscopic surgery: pitfalls due to anesthesia, positioning and pneumoperitoneum. Surg Endosc 2005;19:1163–1171. Magrina JF. Complications of laparoscopic surgery. Clin Obstet Gynecol 2002;45:469–480. Bickel A, Kukuev E, Popov O, et al. Power spectral analysis of heart rate variability during helium pneumoperitoneum: the mechanism of increased cardiac sympathetic activity and its clinical significance. Surg Endosc 2005;19:71–76. Epub 2004;November 11. Myles PS. Bradyarrhythmias and laparoscopy: a prospective study of heart rate changes with laparoscopy. Aust N Z J Obstet Gynaecol 1991;31:171–173. Bickel A, Yahalom M, Roguin N, et al. Improving the adverse changes in cardiac autonomic nervous control during laparoscopic surgery, using an intermittent sequential pneumatic compression device. Am J Surg 2004;187:124–127. Heddle RM, Platt AJ. Tension pnemothorax during laparoscopic cholecystectomy. Br J Surg 1992;79:374. Prystowsky JB, Jericho BG, Epstein HM. Spontaneous bilateral pneumothorax—complication of laparoscopic cholecystectomy. Surgery 1993;114:988–992. Andersson L, Lagerstrand L, Thorne A, et al. Effect of CO(2) pneumoperitoneum on ventilation-perfusion relationships during laparoscopic cholecystectomy. Acta Anaesthesiol Scand 2002;46:552–560. Mutoh T, Lamm WJ, Embree LJ, et al. Volume infusion produces abdominal distension, lung compression, and chest wall stiffening in pigs. J Appl Physiol 1992;72:575. Meininger D, Byhahn C, Mierdl S, et al. Positive endexpiratory pressure improves arterial oxygenation during prolonged pneumoperitoneum. Acta Anaesthesiol Scand 2005;49:778–783. Haroun-Bizri S, ElRassi T. Successful resuscitation after catastrophic carbon dioxide embolism during laparoscopic cholecystectomy. Eur J Anaesthesiol 2001;18:118–121. Zhang W, Ho KS, Han HJ, et al. Successful resuscitation after carbon dioxide embolism during laparoscopic-assisted abdomino-perineal resection. Singapore Med J 2005;46: 347–348. Cobb WS, Fleishman HA, Kercher KW, et al. Gas embolism during laparoscopic cholecystectomy. J Laparoendosc Adv Surg Tech A 2005;15:387–390.

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:

105

diagnosis and treatment. Urology 2005;66(5 suppl):29– 35. 57. Morrison CA, Schreiber MA, Olsen SB, et al. Femoral venous flow dynamics during intraperitoneal and preperitoneal laparoscopic insufflation. Surg Endosc 1998;12: 1213. 58. Schwenk W, Bohm B, Junghans T, et al: Intermittent sequential compression of the lower limbs prevents venous stasis in laparoscopic and conventional colorectal surgery. Dis Colon Rectum 1997;40:1056. 59. Hasukic S. Postoperative changes in liver function tests: randomized comparison of low and high pressure laparoscopic cholecystectomy. Surg Endosc 2005;19:1451– 1455.

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

108

SECTION II: BEDSIDE PROCEDURES

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.

112

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

114

SECTION II: BEDSIDE PROCEDURES

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.

115

● 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.

116

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.

117

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.

118

SECTION II: BEDSIDE PROCEDURES

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

68.

69.

70.

71.

72.

73.

74.

75.

76.

77.

78.

79.

119

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

122

SECTION II: BEDSIDE PROCEDURES

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

124

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.

9 PULMONARY ARTERY CATHETERIZATION

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.)

126

SECTION II: BEDSIDE PROCEDURES

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.

128

SECTION II: BEDSIDE PROCEDURES

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

130

SECTION II: BEDSIDE PROCEDURES

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

132

SECTION II: BEDSIDE PROCEDURES

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

134

SECTION II: BEDSIDE PROCEDURES

● 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

136

SECTION II: BEDSIDE PROCEDURES

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

138

SECTION II: BEDSIDE PROCEDURES

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

140

SECTION II: BEDSIDE PROCEDURES

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

142

SECTION II: BEDSIDE PROCEDURES

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

144

SECTION II: BEDSIDE PROCEDURES

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.

146

SECTION II: BEDSIDE PROCEDURES

● 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

148

SECTION III: GASTROINTESTINAL SURGERY

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

150

SECTION III: GASTROINTESTINAL SURGERY

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

152

SECTION III: GASTROINTESTINAL SURGERY

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.

154

SECTION III: GASTROINTESTINAL SURGERY

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.

156

SECTION III: GASTROINTESTINAL SURGERY

● 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

160

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.

165

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

170

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

172

SECTION III: GASTROINTESTINAL SURGERY

(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.

173

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

176

SECTION III: GASTROINTESTINAL SURGERY

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

178

SECTION III: GASTROINTESTINAL SURGERY

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.

180

SECTION III: GASTROINTESTINAL SURGERY

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

182

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

184

SECTION III: GASTROINTESTINAL SURGERY

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-

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

33.

34.

35.

185

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

188

SECTION III: GASTROINTESTINAL SURGERY

● 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.

190

SECTION III: GASTROINTESTINAL SURGERY

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.

191

192

SECTION III: GASTROINTESTINAL SURGERY

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

194

SECTION III: GASTROINTESTINAL SURGERY

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.

195

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

198

SECTION III: GASTROINTESTINAL SURGERY

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

200

SECTION III: GASTROINTESTINAL SURGERY

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.

201

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

202

SECTION III: GASTROINTESTINAL SURGERY

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

203

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

204

SECTION III: GASTROINTESTINAL SURGERY

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-

205

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

206

SECTION III: GASTROINTESTINAL SURGERY

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.

207

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-

208

SECTION III: GASTROINTESTINAL SURGERY

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

209

● 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

210

SECTION III: GASTROINTESTINAL SURGERY

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

211

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.

212

SECTION III: GASTROINTESTINAL SURGERY

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

213

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

214

SECTION III: GASTROINTESTINAL SURGERY

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.

215

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.

216

SECTION III: GASTROINTESTINAL SURGERY

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

SECTION III: GASTROINTESTINAL SURGERY

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

220

SECTION III: GASTROINTESTINAL SURGERY

● 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.

Hemorrh