Improved Outcomes in Colon and Rectal Surgery

Improved Outcomes in

Colon and Rectal Surgery

Edited by

Charles B Whitlow David E Beck David A Margolin Terry C Hicks Alan E Timmcke

Improved Outcomes in Colon and Rectal Surgery Edited by Charles B Whitlow MD Program Director Colon and Rectal Surgery Ochsner Clinic Foundation New Orleans, Louisiana USA David E Beck MD Chairman Colon and Rectal Surgery Ochsner Clinic Foundation New Orleans, Louisiana USA David A Margolin MD Research Director Colon and Rectal Surgery Ochsner Clinic Foundation New Orleans, Louisiana USA Terry C Hicks MD Associate Chairman Colon and Rectal Surgery Ochsner Clinic Foundation New Orleans, Louisiana USA Alan E Timmcke MD Staff Surgeon Colon and Rectal Surgery Ochsner Clinic Foundation New Orleans, Louisiana USA

© 2010 Informa UK First published in 2010 by Informa Healthcare, Telephone House, 69-77 Paul Street, London EC2A 4LQ. Informa Healthcare is a trading division of Informa UK Ltd. Registered Office: 37/41 Mortimer Street, London W1T 3JH. Registered in England and Wales number 1072954. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of the publisher or in accordance with the provisions of the Copyright, Designs and Patents Act 1988 or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London W1P 0LP. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. A CIP record for this book is available from the British Library. Library of Congress Cataloging-in-Publication Data Data available on application ISBN-13: 9781920071528 Orders Informa Healthcare Sheepen Place Colchester Essex CO3 3LP UK Telephone: +44 (0)20 7017 5540 Email: [email protected] Typeset by C&M Digitals (P) Ltd, Chennai, India Printed and bound in Great Britain by CPI, Antony Rowe, Chippenham, Wiltshire

Contents

List of Contributors Preface Foreword

v ix xi

  1 Preexisting conditions Eric L Marderstein, Siyamek Neragi-Miandoab, and Conor P Delaney

1

  2 Preoperative bowel preparation David A Margolin and Sean Mayfield

14

  3 Anesthesia and intraoperative positioning Lebron Cooper and Larry R Hutson

19

  4 Sepsis Steven Mills and Michael J Stamos

27

  5 Intraoperative anastomotic challenges David E Beck

33

  6 Other intraoperative challenges James T McCormick and Sharon G Gregorcyk

44

  7 Postoperative anastomotic complications Daniel L Feingold

56

  8 General postoperative complications Scott R Steele and Clifford L Simmang

67

  9 Care paths and optimal postop management Surya P M Nalamati and Eric J Szilagy

79

10 Limitations of anorectal physiology testing Thomas E Cataldo and Syed G Husain

87

11 Limitations of colorectal imaging studies Travis J Blanchard, Wilson B Altmeyer, and Charles C Matthews

97

12 Transanal endoscopy Terry C Hicks

132

13 Laparoscopic colorectal surgery James W Fleshman and Jonathan S Chun

140

14 Medical legal issues Charles F Gay Jr and Terry C Hicks

148

15 Miscellanous conditions M Benjamin Hopkins and Alan E Timmcke

154

16 Quality and outcome measures Janak A Parikh, Sushma Jain, Marcia L McGory, and Clifford Y Ko

159

17 Hemorrhoidal surgery Dan R Metcalf and Anthony J Senagore

168

18 Nonoperative therapy for hemorrhoid disease Kerry Hammond and Charles B Whitlow

178

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contents 19 Surgery and nonoperative therapy of perirectal abscesses and anal fistulas Brian R Kann and Charles B Whitlow

183

20 Surgery and nonoperative therapy of anal fissure Jaime L Bohl and Alan J Herline

199

21 Surgery for pilonidal disease and hidradenitis suppurativa Paula I Denoya and Eric G Weiss

215

22 Surgical treatment of fecal incontinence Ann C Lowry and Dimitrios Christoforidis

226

23 Surgery for rectal prolapse Steven R Hunt

239

24 Operative and nonoperative therapy for diverticular disease R Scott Nelson and Alan G Thorson

249

25 Abdominal surgery for colorectal cancer Jason Hall and Rocco Ricciardi

263

26 Transanal approaches to rectal cancer Sachin S Kukreja and Theodore J Saclarides

271

27 Abdominoperineal resection W Brian Perry, Fia Yi, Clarence Clark, and Danny Kim

278

28 Indications and outcomes for treatment of recurrent rectal cancer and colorectal liver and lung metastasis Harry L Reynolds Jr, Christopher T Siegel, and Jason Robke

286

29 Chemotherapy for colon and rectal cancer Liliana Bordeianou and Judith L Trudel

300

30 Radiation therapy: Acute and late toxicity Roland Hawkins

306

31 Surgery for ulcerative colitis Patricia L Roberts

318

32 Surgery for Crohn’s disease Jorge Canedo, Tolga Erim, and Steven D Wexner

331

33 Ostomies Vance Y Sohn and Scott R Steele

349

34 Operative and nonoperative therapy for chronic constipation Harry T Papaconstantinou

361

35 Colorectal trauma S David Cho, Sharon L Wright, and Martin A Schreiber

375

36 Urologic complications of colorectal surgery Scott Delacroix Jr and J Christian Winters

395

Index

405

List of Contributors

Wilson B Altmeyer MD Department of Radiology Ochsner Clinic Foundation New Orleans, Louisiana USA David E Beck MD Colon and Rectal Surgery Ochsner Clinic Foundation New Orleans, Louisiana USA Travis J Blanchard md Department of Radiology Ochsner Clinic Foundation New Orleans, Louisiana USA Jaime L Bohl MD Department of Surgery Vanderbilt University Nashville, Tennessee USA Liliana Bordeianou MD Department of Surgery Division of General and Gastrointestinal Surgery Massachusetts General Hospital Boston, Massachusetts USA Jorge Canedo MD Department of Colorectal Surgery Cleveland Clinic Florida Weston, Florida USA

Dimitrios Christoforidis MD Department of Visceral Surgery, CHUV-University of Lausanne Lausanne, Switzerland Jonathan S Chun MD Section of Colon and Rectal Surgery Washington University School of Medicine St Louis, Missouri USA Clarence Clark MD Department of General Surgery Wilford Hall Medical Center and the University of Texas Health Science Center, San Antonio Lackland AFB, Texas USA Lebron Cooper MD Department of Anesthiology Ochsner Clinic Foundation New Orleans, Louisiana USA Scott E Delacroix, Jr., MD Department of Urology Louisiana State University Health Sciences Center New Orleans, Louisiana University of Texas, MD Anderson Cancer Center Houston, Texas USA Conor P Delaney MD MCh PhD Department of Surgery Division of Colorectal Surgery University Hospitals Case Medical Center Cleveland, Ohio USA

Thomas E Cataldo MD Warren Alpert Medical School of Brown University Brown Program in Colon and Rectal Surgery Rhode Island Hospital/Lifespan Health System Providence, Rhode Island USA

Paula I Denoya MD Department of Colorectal Surgery Cleveland Clinic Florida Weston, Florida USA

S David Cho MD Department of Surgery Oregon Health and Science University Portland, Oregon USA

Tolga Erim MD Department of Colorectal Surgery Cleveland Clinic Florida Weston, Florida USA

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list of contributors Daniel L Feingold MD Section of Colorectal Surgery Columbia University New York, New York USA James W Fleshman MD Section of Colon and Rectal Surgery Washington University School of Medicine St Louis, Missouri USA Charles F Gay Jr Adams and Reeds Attorneys and Counselors at Law New Orleans, Louisiana USA Sharon G Gregorcyk MD Texas Colon and Rectal Specialists Dallas, Texas USA Jason Hall MD Department of Colon and Rectal Surgery Lahey Clinic Tufts University Burlington, Massachusetts USA Roland Hawkins MD Radiation Oncology Ochsner Cancer Institute New Orleans, Louisiana USA Kerry Hammond MD Division of General Surgery Medical University of South Carolina Charleston, South Carolina USA Alan J Herline MD Department of Surgery Vanderbilt University Nashville, Tennessee USA Terry C Hicks MD Colon and Rectal Surgery Ochsner Clinic Foundation New Orleans, Louisiana USA M Benjamin Hopkins MD Department of Colon and Rectal Surgery Ochsner Clinic Foundation New Orleans, Louisiana USA



Steven R Hunt MD Colon and Rectal Surgery Section Division of General Surgery Washington University St. Louis, Missouri USA Syed G Husain MD Brown Program in Colon and Rectal Surgery Warren Alpert Medical School of Brown University Rhode Island Hospital/Lifespan Health System Providence, Rhode Island USA Larry R Hutson MD Department of Anesthiology Ochsner Clinic Foundation New Orleans, Louisiana USA Sushma Jain MBBS MPH David Geffen School of Medicine at UCLA Department of Surgery Los Angeles, California USA Brian R Kann MD Cooper University Hospital UMDNJ-Robert Wood Johnson Medical School-Camden Department of Surgery Camden, New Jersey USA Danny Kim MD Department of General Surgery Wilford Hall Medical Center and the University of Texas Health Science Center, San Antonio Lackland AFB, Texas USA Clifford Y Ko MD MS MSHS David Geffen School of Medicine at UCLA Department of Surgery Los Angeles, California USA Sachin S Kukreja MD Section of Colon and Rectal Surgery Department of General Surgery Rush University Medical Center Chicago, Illinois USA Ann C Lowry MD Colon & Rectal Surgery Associates Ltd St Paul, Minnesota USA

list of contributors James T McCormick DO Department of Surgery Division of Colon and Rectal Surgery Western Pennsylvania Hospital and the Forbes Regional Campus Temple University School of Medicine Philadelphia, Pennsylvania USA Marcia L McGory MD PhD David Geffen School of Medicine at UCLA Department of Surgery Los Angeles, California USA Eric L Marderstein MD MPH Division of Colorectal Surgery, Department of Surgery, University Hospitals Case Medical Center, Cleveland, Ohio USA David A Margolin MD Colon and Rectal Surgery The Ochsner Clinic Foundation New Orleans, Louisiana USA Charles C Matthews MD Department of Radiology Ochsner Clinic Foundation New Orleans, Louisiana USA Sean Mayfield MD Colon and Rectal Surgery The Ochsner Clinic Foundation New Orleans, Louisiana USA Dan R Metcalf MD SMDC Health System Department of Surgery Duluth, Minnesota USA Steven Mills MD University of California Irvine, California USA Surya PM Nalamati Division of Colon and Rectal Surgery Henry Ford Health System Department of Surgery/Colon & Rectal Group Detroit, Michigan USA

R Scott Nelson DO Colon & Rectal Surgery, Inc Omaha, Nebraska USA Siyamek Neragi-Miandoab MD Division of Colorectal Surgery, Department of Surgery, University Hospitals Case Medical Center, Cleveland, Ohio USA Harry T Papaconstantinou MD Department of Surgery Scott & White Hospital and Clinic Texas A&M University System Health Science Center Temple, Texas USA Janak A Parikh MD David Geffen School of Medicine at UCLA Department of Surgery Los Angeles, California USA W Brian Perry MD Department of General Surgery Wilford Hall Medical Center and the University of Texas Health Science Center, San Antonio Lackland AFB, Texas USA Harry L Reynolds Jr MD University Hospital of Cleveland Cleveland, Ohio USA Rocco Ricciardi MD MPH Department of Colon and Rectal Surgery Lahey Clinic Tufts University Burlington, Massachusetts USA Patricia L Roberts MD Department of Colon and Rectal Surgery Lahey Clinic Medical Center Burlington, and Tufts University School of Medicine Boston, Massachusetts USA J Robke MD University Hospital of Cleveland Cleveland, Ohio USA



list of contributors Theodore J Saclarides MD Section of Colon and Rectal Surgery Department of General Surgery Rush University Medical Center Chicago, Illinois USA Martin A Schreiber MD Division of Trauma and Critical Care Oregon Health and Science University Portland, Oregon USA Christopher T Siegel MD University Hospital of Cleveland Cleveland, Ohio USA Anthony J Senagore MD MS MBA Spectrum Health System Grand Rapids, Michigan USA Clifford L Simmang MD Texas Colon and Rectal Surgeons Dallas, Texas USA Vance Y Sohn MD Department of Surgery Madigan Army Medical Center Tacoma, Washington USA

Alan E Timmcke MD Colon and Rectal Surgery Ochsner Clinic Foundation New Orleans, Louisiana USA Judith L Trudel MD, MSc, MHPE University of Minnesota St Paul, Minnesota USA Eric G Weiss MD Department of Colorectal Surgery Cleveland Clinic Florida Weston, Florida USA Steven D Wexner MD Department of Colorectal Surgery Ohio State University and Department of Surgery, Division of General Surgery University of South Florida College of Medicine Cleveland Clinic Florida Weston, Florida USA Charles B Whitlow MD Colon and Rectal Surgery Ochsner Clinic Foundation New Orleans, Louisiana USA

Michael J Stamos MD University of California Irvine, California USA

J Christian Winters MD FACS Department of Urology Female Pelvic Medicine and Reconstructive Surgery Louisiana State University Health Sciences Center New Orleans, Louisiana USA

Scott R Steele MD Department of Surgery Madigan Army Medical Center Tacoma, Washington USA

Sharon L Wright MD Department of Surgery Oregon Health and Science University Portland, Oregon USA

Eric J Szilagy MD Department of Surgery/Colon & Rectal Group Division of Colon and Rectal Surgery Henry Ford Health System Detroit, Michigan USA

Fia Yi MD Department of General Surgery Wilford Hall Medical Center and the University of Texas Health Science Center, San Antonio Lackland AFB, Texas USA

Alan G Thorson MD Colon & Rectal Surgery, Inc Omaha, Nebraska USA

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Preface

Quality measures and outcomes are receiving greater attention by the lay and medical communities. The occurrence or mis­ management of complications often results in poor outcomes, increased cost, and significant morbidity. Answering the call for transparency and improvement requires action by all involved in the care of patients. Collection of objective data and quality measures allows documentation of optimal care and desired out­ comes while identifying areas for improvement. The goal of this text is to present the current knowledge of outcomes, as well as the techniques for minimizing and managing complications from the common diseases and procedures of this specialty. This information will aid providers in optimizing care and encourage research in outcome and quality measurement. Improved Outcomes of Colon and Rectal Surgery represents the collaborative efforts of many individuals. The contributing authors were selected for their knowledge of colorectal surgery and ability to present their surgical judgment and experience in written form. They represent a spectrum of experienced providers who have made significant contributions to younger individuals who

will shape the future of their specialty. In addition to reviewing the available literature, they have described their personal approach to complications in colorectal surgery. Numerous technical descriptions and highlights from multiple discussions held in surgical locker rooms, morbidity and mortality conferences, and the hallways of conferences and symposiums have been included. Using this approach, we hope this text will provide initial guidance to the less experienced provider and stimulate additional thought and research to the more experienced provider. The editors gratefully acknowledge the efforts of the many individuals who made this book possible. This text carries on the vision of previous editors and contributors to the first two editions of Complications in Colon and Rectal Surgery. Charles B Whitlow, MD David E Beck, MD David A Margolin, MD Terry C Hicks, MD Alan E Timmcke, MD



Foreword

In Improved Outcomes in Colon and Rectal Surgery, Drs. Whitlow, Beck, Margolin, Hicks, and Timmcke have assembled a knowledgeable, expert, and distinguished group of contributors who additionally have flavored their contributions with their practical experience and “how I do it” approaches. This volume is the third in a series dealing with improving outcomes, avoiding complications, and in general improving the lot of patients who require surgery for conditions of the large bowel, rectum, and anus. The stated objective of guiding less experienced surgeons in avoiding the pitfalls of both commonly encountered complications and those of rarer occurrence is well met in this volume. It should be in the library of all neophyte surgeons and deserves to be read even by experienced practitioners.

The field of colon and rectal surgery is a dynamic one with endoscopic and open surgery procedures at a mature stage. With constantly improving laparoscopic techniques, robotic surgery and other modalities only dreamed about in the past requiring every surgeon to continue to learn and improve this book fills a visible need. I congratulate the editors and contributors for assembling an extremely useable and timely text. J Byron Gathright, Jr. MD Chairman Emeritus Department of Colon and Rectal Surgery Ochsner Clinic New Orleans, Louisiana USA

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1

Preexisting conditions Eric L Marderstein, Siyamek Neragi-Miandoab, and Conor P Delaney

challenging case A 65-year-old hypertensive male smoker requires a low anterior resection for treatment of an upper rectal cancer. A CT scan of the chest, abdomen, and pelvis does not show any distant metastatic spread and his carcinoembryonic antigen is normal. What additional preoperative laboratory studies and adjunctive testing are indicated? case management A complete history and physical examination is perhaps the single most important step for guiding preoperative preparation. If a cardiac review of systems indicates no symptoms of ischemia at a high workload, and an electrocardiogram is ­normal then no further cardiac testing is necessary. A complete blood count is indicated because the underlying disease can cause anemia and serum chemistries are indicated because of the patient’s hypertension. Although routine laboratory testing is not indicated for most procedures, for patients older than 60 due to undergo major surgery, they are reasonable in many situations. If there is no suggestion of bleeding abnormalities or liver disease on history and physical examination then coagulation studies are not required. Pulmonary function testing, unless the patient has significant pulmonary-attributable shortness of breath or extreme oxygen dependence, is not necessary. The patient should be counseled to stop smoking because it may prevent postoperative pulmonary complications, although several weeks of smoking cessation is required to obtain measurable benefit. introduction Part of the attraction of colorectal surgery is the diversity of diseases, patients, and procedures that the surgeon sees on a routine basis. On one day a surgeon can perform several small outpatient anorectal procedures on relatively healthy patients, followed the next day by several major complex intraabdominal operations on frail elderly patient with significant comorbidities. Such variety underscores the importance of the preoperative evaluation in identifying preexisting medical conditions and determining their effect of the proposed procedure. Knowledge of how preexisting medical conditions can result in certain patterns of postoperative complications helps to guide the preoperative evaluation. This chapter’s recommendations regarding laboratory investigation and additional testing are, when possible, based on published evidence of their clinical efficacy and cost-effectiveness. As a general rule, ordering a myriad of specialized tests or routine laboratory batteries is expensive and provides low yield. Instead, testing is designed to quantify the magnitude of the preexisting medical conditions so they can be optimized in the pre-, intraand postoperative period to maximize the chance of a successful outcome.

history and physical examination A thorough history includes past and current medical and ­surgical history, medications, allergies, family history, functional ­history, and review of systems. History and physical examination are generally more important than laboratory data in the development of a treatment plan for anesthesia. Young healthy patients with an unremarkable history and examination may not need any anesthesia evaluation for moderate size procedures. The overall risk of surgery is extremely low in healthy individuals and no additional benefit is gained from more complex evaluations.(1) If major surgery is planned, or if patients are elderly or have high levels of comorbidity, a preoperative anesthesia consult is warranted and appropriately required at many institutions. While the surgeon needs to play an active role in preoperative risk assessment, it is often very helpful to have an anesthesia consultation to evaluate the patient solely from the standpoint of surgical risk. Coordination and cooperation between surgeons and anesthesiologist is essential to avoid unnecessary delays and surprises before the surgery. A patient self-administered questionnaire on the complexity of their past medical history can act as an effective primary screening tool to stratify patients for further assessment before surgery.(2) Evaluation is performed with a combination of history, physical examination, and selected investigations. In a large prospective clinical-epidemiological study, Arvidsson and colleagues found that a standardized assessment before surgery, by a combination of questionnaires, interview, physical examination, and selected laboratory testing identified a high proportion of patients who were likely to suffer an adverse event in the ­postoperative period.(3) preoperative tests Thorough preoperative assessment of patients can minimize or prevent postoperative complications.(4) Selective laboratory studies can be useful, but routine laboratory tests are often unnecessary.(5, 6) Ordering a battery of routine preoperative laboratory studies leads to inefficient clinical practice and is not cost-effective.(7). In one large study, only 0.22% of routine preoperative laboratory studies revealed abnormalities that might influence peroperative management.(8) Tests ordered in screening panels are frequently not acted upon before surgery, thereby creating additional medicolegal risk.(8) When laboratory tests are felt to be necessary, it is probably safe to use test results that were performed and were normal within the past 4 months as preoperative tests unless there has been an interim change in clinical status. Anemia is present in approximately 1% of asymptomatic patients.(8) However, anemia is common following major surgery and the preoperative hemoglobin level predicts postoperative mortality.(9) A baseline hemoglobin level in patients who are undergoing major surgery that is expected to result in significant blood loss is useful in postoperative management to differentiate

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improved outcomes in colon and rectal surgery between acute or chronic blood loss. The frequency of significant unsuspected white blood cell or platelet abnormalities is also low. (10) Unexpected electrolyte abnormalities are uncommon and routine electrolyte determinations are not recommended unless the patient has a history that increases the likelihood of an abnormality.(8) Premenopausal females at risk should undergo a urine or blood test for beta-HCG to determine if they are pregnant so that appropriate precautions are taken during surgery if still indicated. This practice is codified at many institutions to improve safety and reduce medical liability. Nonetheless, it is all too common for a lapse in obtaining a pregnancy test to result in a lengthy delay in the start of ­surgery. Routine urinalysis to detect disease (proteinuria, glucosuria, bacteruria), however, is not indicated. preoperative risk assessment using scoring systems Scoring systems assess the patients’ risk for morbidity and mortality taking into account the kind of planned surgical procedure and the type of anesthesia.(11) These systems generally use data acquired during prehospital and in-hospital care, while inclusion of the severity of the planned procedure might improve the predictive value of these systems.(12, 13) Others have tried to predict the risk anecdotally, suggesting that a surgeon’s general feeling and personal experience are a good indicator of subsequent outcome.(14) Scoring systems can be helpful in counseling the patient and setting their expectations preoperatively beyond clinical intuition. In addition, well-constructed scoring systems can be used to compare hospitals and surgeons while controlling for the known influence of preoperative risk factors for poor outcome.(15) American Society of Anesthesiologists (ASA) Classification The ASA classification system (Table 1.1) has been developed by anesthesiologists to evaluate patients’ preexisting morbidities and operative risk. The system is easy to use and is based on history, physical examination, and the physician’s experience and it requires no tests.(16, 17) ASA class has been shown to correlate with perioperative mortality and morbidity, as well as with perioperative variables such as intraoperative blood loss, duration of postoperative ventilation, and duration of intensive care unit stay.(18–20) The severity of operative ­procedure, higher ASA class, symptoms of respiratory disease and malignancy are ­predictive of postoperative morbidity.(13) Disadvantages to use of the ASA score is that its accuracy depends on the subjective clinical ­judgment and experience of the attending anesthesiologist. Table 1.1  American Society of Anesthesia (ASA) classification scheme. I II III IV V ‘E’

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Normal healthy patient Mild systemic disease Severe, noncapacitating systemic disease Incapacitating systemic disease, threatening life Moribund, not expected to survive 24 hours Emergency

POSSUM (Physiologic and Operative Severity Score for enUmeration of Mortality and morbidity) POSSUM was developed through multivariate analysis primarily to permit surgical audit for assessment of quality of care.(21) It calculates expected death and expected morbidity rates based on 12 physiological variables and six operative variables each of which are scored 1, 2, 4, or 8 (Table 1.2).(22) POSSUM was developed as a scoring system for audit, so other factors may need to be considered when using POSSUM for risk assessment of patients for surgery. One concern with POSSUM has been that it may over predict mortality and morbidity rates by up to six times with a minimum mortality of 1.1%. POSSUM was modified by Portsmouth to P-POSSUM using a different calculation to reduce the overprediciting bias.(23) While some studies found that both scoring systems overpredicted mortality rates for vascular surgery patients (24, 25), others found that P-POSSUM was a better predictor of mortality and morbidity than POSSUM for vascular (26) gastrointestinal surgery (27), and laparoscopic colorectal surgery (28). The CR-POSSUM (Table 1.3) was a modification of POSSUM designed to assess risk of colorectal procedures. A retrospective multivariate analysis was performed on more than 6,000 patients operated on in the United Kingdom between 1993 and 2001.(29) The overall mortality for the series was 5.7% and the CR-POSSUM was more accurate than POSSUM in their validation patient set. The advent of laparoscopic colorectal procedures may result in CR-POSSUM also overestimating mortality. A recent report noted that CR-POSSUM overestimated mortality in patients undergoing laparoscopic colectomy, but accurately predicted mortality in the subset of patients requiring conversion.(30) When these ­scoring systems were applied

Table 1.2  Parameters for calculation of the POSSUM score. Physiological Parameters

Operative Parameters

Age (years) Cardiac signs/chest x-ray Respiratory signs/chest x-ray Pulse rate Systolic blood pressure (mm Hg) Glasgow Coma Score Hemoglobin (g/dl) White cell count (×1012/l) Urea concentration (mmol/l) Na+ and K+ levels (mmol/l) Electrocardiogram

Operative severity Multiple procedures Total blood loss (ml) Peritoneal soiling Presence of malignancy Mode of surgery

Table 1.3  Parameters for calculation of the CR-POSSUM score. Physiological Parameters

Operative Parameters

Age (years) Cardiac signs/ chest x-ray Pulse rate Systolic blood pressure (mm Hg) Urea concentration (mmol/l)

Operative severity Urgency of surgery Peritoneal soiling Presence of malignancy Hemoglobin (g/dl)

preexisting conditions to data from a series of U.S. hospitals; the CR-POSSUM was the most accurate variant, but overestimated mortality by more than twofold.(31) National Surgery Quality Improvement Project (NSQIP) NSQIP was initially started as a way to measure quality of surgical care at Veteran’s Administration hospitals but the methodology has spread to the private sector and is embraced by the American College of Surgeons (ACS-NSQIP). It is a nationally validated, risk-adjusted, outcomes-based program to measure and improve the quality of surgical care.(32) The program employs a prospective, peer-controlled, validated database to quantify 30-day ­risk-adjusted surgical outcomes, which allows valid comparison of outcomes among all hospitals in the program. Participating hospitals and their surgical staff are provided with the tools, reports, analysis, and support necessary to make informed decisions about improving quality of care. A key lesson from NSQIP was determining what key preoperative variables influence morbidity and mortality. By risk-adjusting the outcomes, morbidity and mortality can be compared between hospitals without the common argument “my patients are sicker.” The initial studies were performed on huge numbers of patients with multivariate analysis ranking certain preoperative conditions/variables as particularly influential on postoperative complications and mortality. Albumin, ASA class, disseminated cancer, emergency surgery, age, blood urea nitrogen, functional status, weight loss, and “do not resuscitate” order are consistently the most important variables in the analysis. (33) The program was initially validated using a range of surgical procedures, but subsequent publications have used the same methodology to study particular types of operations. For example, complications and mortality after colectomy for colorectal cancer depends on identical preoperative variables as the initial validation set.(34) The program is well respected because a great emphasis is placed on data integrity and follow-up to identify preoperative and postoperative events. documentation As an increased emphasis is placed on tracking and reporting of complications it is critically important to the surgeon to document well. For risk-adjusted complications to be valid, preoperative comorbidities must be identified and noted in the medical record. Without this, the surgeon will not have justification for elevated complication rates based on preoperative illness. This will become more important as DRG classification, and therefore institutional technical reimbursement, becomes dependent on diagnosis documented at the time of admission in the near future. cardiovascular disease Perioperative cardiac complications are among the most feared of surgical complications because they can result in death. Their severity spans a wide range from asymptomatic increase in cardiac enzymes to fatal massive myocardial infarctions. The goal of preoperative cardiac evaluation is to quantify the likelihood of a perioperative cardiac event taking into account patient factors and the proposed operative procedure. The concept of “cardiac clearance” is flawed and should not be used. In reality, a patient

with a very low cardiac risk is not immune to perioperative cardiac events and a patient with known severe coronary artery disease is by no means guaranteed to have a fatal myocardial infarction. Even in the highest risk patients undergoing complex vascular surgery, the risk of postoperative cardiac events is only 34%.(35) The risk of the proposed procedure must be weighed against the proposed benefit and urgency to be derived from the operation to permit the surgeon and patient decide about the appropriateness of proceeding with surgery. Multiple models have been devised to estimate perioperative cardiac risk. The Goldman risk model was an early and well­accepted model for pure determination of cardiac risk for ­surgery. (36) The system is easy to use and utilizes relative weighting of risk factors; however, it was designed several decades ago and has not been updated for modern practice. Two more modern predictive models include those proposed by Detsky et al. (37) and Lee et al. (38). The Lee index identified six independent predictors of cardiac complications: high-risk surgery (procedures with a 5% or higher risk of cardiac complications—including prolonged intraperitoneal operations), history of ischemic heart disease, history of congestive heart failure, history of cerebrovascular disease, diabetes, and preoperative serum creatinine >2.0 mg/dL. Patients with 0, 1, 2, or 3 or more criteria were found to have a rate of major cardiac complications of 0.5%, 1.3%, 4%, and 9% respectively. The receiver operating curve generated on a validation cohort of patients was higher for the Lee index versus the Goldman index and Detsky’s model, indicating higher predictive power.(38) The American College of Cardiology (ACC) and American Heart Association have issued evidence-based guidelines for the evaluation of patients for noncardiac surgery. They are available at their website (www.acc.org), the National Guideline Clearinghouse (www.guidelines.gov), and in print.(39) A cardiac history and physical exam is designed to identify unstable coronary syndromes, prior angina, recent or past myocardial infarction, severe valvular disease, decompensated heart failure, and significant arrhythmias. Presence of a pacemaker or implantable cardioverter defibrillator should be noted. Hypertension should be identified and controlled pre-, intra-, and postoperatively. Elevated blood pressure increases myocardial work, stress and oxygen demand. Interestingly, a randomized trial was unable to demonstrate a benefit to delay of surgery for the purpose of control of severe hypertension.(40) Volatile anesthetics and intravenous medications can remedy the hypertension quickly. Antihypertensive medications should be taken with a sip of water on the morning of surgery and resumed postoperatively as soon as possible. Symptomatic aortic or mitral stenosis should be identified and evaluated preoperatively. In certain cases, a valve replacement or percutaneous valvuloplasty will greatly reduce the risk of surgery. A history of orthopnea, dyspnea on exertion, and paroxysmal nocturnal dyspnea are suggestive of congestive heart failure. Pitting ankle edema, rales on auscultation of the chest, jugular venous distention, and an S3 gallop on physical examination all support the diagnosis of heart failure. A chest radiograph showing cardiomegaly and prominent pulmonary vascularity is supportive. Noninvasive evaluation of ventricular function and optimization of the congestive heart failure should be achieved before surgery in such patients.

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improved outcomes in colon and rectal surgery In patients with existing cardiac disease, recent changes in symptoms must be identified. Assessment of functional status is important to determination of preoperative risk. If the patient cannot or does not achieve an adequate level of activity in their daily life it may hide the angina or symptoms they would experience should they reach that level. The surgical stress can cause cardiac complications in these patients who would appear to be asymptomatic based on preoperative questioning if their functional ­status is poor. The Duke Activity Status Index was developed as a way to correlate a patient’s exercise tolerance with activities that they can perform in daily life.(41) Peak oxygen uptake on exercise ­testing correlates very well with the determination by this self- or physician-administered questions. The scale defines these daily activities in terms of metabolic equivalents (METs). Patients who cannot reach four METs (equivalent to light housework, climbing a flight of stairs or walk on level ground at 4 mph) would require additional investigation if it is necessary to determine whether they are really asymptomatic or not. Patients who can exercise at a very high MET without symptoms are less likely to harbor significant cardiac disease. The ACC has defined a stepwise algorithm to preoperative evaluation of the patient requiring noncardiac surgery. Surgery should be cancelled or delayed unless emergent in patients with unstable or severe angina, myocardial infarction <1 month prior, decompensated heart failure, significant arrhythmias or severe valvular disease.(39) Risk stratification for the type of surgical procedure includes high (>5% reported cardiac risk), intermediate (1–5%), or low risk. Intraperitoneal procedures are considered intermediate risk while ambulatory procedures are considered low risk. Laparoscopic intraperitoneal surgery, although associated with less pain and postoperative fluid shifts, should be considered intermediate risk because of the potential need for use of an open approach depending on intraoperative circumstances. In patients undergoing low-risk surgery, no further cardiac assessment is necessary. For patients undergoing intermediate risk surgery, evidence of good functional capacity without symptoms indicates no further testing is neededbefore surgery. If the functional status is poor or unknown, presence of one or more clinical risk factors as defined by Lee (history of coronary artery disease, history of heart failure, history of cerebrovascular disease, diabetes or renal insufficiency) then options include noninvasive cardiac testing to further stratify risk if it will change management. Alternatively, the operation can proceed with heart rate control pre-, intra-, and postoperatively. Patients without symptoms and with a normal cardiac stress test within past 2 years or revascularization in the past 5 years do not require further evaluation. If no clinical risk factors are present, the operation can proceed. The preoperative electrocardiogram (ECG) is not as indispensable as it once was. The prevalence of abnormal ECGs increases with age.(42) However, multiple studies seem to indicate that the electrocardiogram alone is a poor independent predictor of postoperative cardiac complications.(43–45) While ECG abnormalities indicate an elevated cardiac risk, it loses its independent predictive power when analyzed with patient clinical characteristics. One of these studies did indicate particular risk for patients with left or right bundle branch blocks on their ECG.(46) In certain cases, the ECG may contribute to an incomplete history as previous silent

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myocardial infarction is common.(47) A preoperative baseline ECG can be important as a baseline, since it can be of significant importance in identifying postoperative ECG changes.(36) Preoperative dysrhythmias (>5 premature ventricular contractions/min) and P-wave abnormalities are predictive of postoperative dysrhythmias. (48) The recommendations of the ACC are less clear on the value of a preoperative ECG than other clinical issues. A preoperative resting 12-lead ECG is recommended for patients with at least one clinical risk factor who are undergoing intermediate risk procedures or patients with no clinical risk factors who are undergoing high-risk surgery. Additionally, a preoperative and postoperative ECG is not recommended for asymptomatic patients undergoing low risk ­surgery. The quandary lies with the asymptomatic patient planned for intermediate risk surgery. If there is any question about the functional status, an ECG is indicated. By contrast, if the functional status is outstanding and no symptoms are present it could be argued to omit the test. Lee’s Revised Cardiac Risk Index was derived in patients 50 years and older so an arbitrary age cutoff here may be reasonable. Noninvasive evaluation of ventricular function with echocardiography is indicated in patients with dyspnea of unknown origin, current or prior heart failure with change in symptoms.(37) Routine evaluation of ventricular function is not recommended. Preoperative revascularization is generally not indicated before surgery unless it would have been recommended for the patient based on their cardiac evaluation, regardless of whether they had surgery planned. The Coronary Artery Revascularization Prophylaxis (CARP) trial randomized patients with known coronary artery disease by cardiac catheterization to revascularization ­versus medical management before elective vascular surgery.(49) The Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echo­ cardio­graphy (DECREASE-V) trial also randomized patients to revascularization or best medical therapy before ­vascular surgery. (50) Both randomized trials failed to show a benefit to revascularization before surgery when optimal medical treatment was applied. If percutanous coronary intervention is indicated and performed before surgery, either angioplasty or bare-metal stents should be used and drug-eluting stents avoided. Drug eluting stents have a higher associated restenosis rate when anticoagulation is discontinued early. If possible, waiting 4 to 6 weeks after stent placement is beneficial because the stent with be at least partially endothelialized and clopidogrel (Plavix) can be stopped. If possible, aspirin is to be continued or resumed quickly after surgery. Perioperative treatment with beta-blockers titrated to a heart rate of <70 beats per minute to reduce cardiac risk has been studied in multiple clinical trials. Although some more recent trials have not demonstrated the pronounced benefit of earlier trials on the subject, the aggregate conclusion of the multiple studies ­suggests benefit with small risk. Preoperative beta-blockade is indicated in patients having intermediate risk surgery with one or more clinical risk factors or any patient having vascular surgery. It is not indicated in patients for low-risk surgery or intermediate risk surgery without clinical risk factors. Some authors argue that effective betablockade obviates the need for additional ­cardiac testing in certain intermediate risk patients.(51) Institution of statin-class medication for patients with one or more clinical risk factors undergoing intermediate risk surgery should be considered.(52)

preexisting conditions pulmonary disease Postoperative pulmonary complications (PPCs) are equally prevalent and contribute similarly to morbidity, mortality, and length of stay as cardiac complications.(53) They include atelectasis, pneumonia, bronchospasm, and respiratory failure (mechanical ventilation for >48 hours). The American College of Physicians (ACP) issued guidelines for pulmonary risk stratification available on their website www.acponline.org and www.guidelines.gov. Several risk factors are known to increase the risk of pulmonary complications. Even when controlling for other comorbid conditions, evidence suggests that increasing age is a risk for pulmonary complications.(51) Congestive heart failure, although not a pulmonary condition, increases risk for postoperative pulmonary complications. Functional dependence defined as need for assistance from another person or devices to perform activities of daily living was associated with pulmonary complications.(54) Impaired sensorium is associated with an increased risk of pulmonary complications. While obesity does not seem to be associated with an increased risk of pulmonary complications, sleep apnea does appear to confer increased risk.(53) Cigarette smoking greatly increases the incidence of pulmonary complications compared to nonsmokers. Procedure-related risk factors increase the likelihood of pulmonary complications. Incision location (thoracic, upper abdomen, lower abdomen) has been shown in several heterogeneous studies to correlate with pulmonary risk, as well duration of surgery (>2.5 hours in some studies and >4 in others).(53) General anesthesia and emergency surgery have also been found to be associated with increased postoperative pulmonary complications. The ACP guidelines suggested that a preoperative chest radiograph is indicated in patients with known cardiopulmonary ­disease or those older than 50 years of age who are undergoing upper abdominal or abdominal aortic aneurism surgery. Routine chest radiography in all patients has been shown to be associated in many studies with a very small number of abnormalities that influenced management and an even smaller number in patients under the age of 50.(55, 56) It is reasonable however to have a low threshold to order the test in those patients in whom it is more likely to be abnormal than an unselected population. This includes patients with a positive pulmonary review of systems for conditions such as cough, dyspnea on exertion, or recent pneumonia or the presence of chronic lung conditions such as asthma or pulmonary fibrosis. Pulmonary function testing is an expensive and tricky test to administer. It has a well-established place in the preoperative workup of lung resection patients, but there is no clear indication in the preoperative workup of abdominal surgery patients. Evidence from several studies suggests that segregating patients by forced expiratory volume in 1 s (FEV1) creates groups with differing pulmonary complication rates from 14.6% up to 31% in the highest and lowest group respectively.(53) What is lacking from these studies is the correlation of the spirometry with clinical ­history, physical exam and other findings. The implication is that poor preoperative spirometry can be inferred from these noninvasive means. The few studies that have compared spirometry data with clinical data have not consistently shown spirometry to be superior to history and physical examination.(53) The spirometry data do not demonstrate a threshold below which surgery is

prohibitively dangerous. In a study of patients with FEV1 < 50% predicted only <15% of patients died or experienced a major ­pulmonary complication.(57) Control of acute and chronic pulmonary illness and cessation of smoking can help reduce pulmonary complications.(58) Treatment and clearance of acute pulmonary infection before ­surgery is recommended. Smokers have a four-fold higher risk of pulmonary complications compared to nonsmokers. Several studies demonstrate that a 4 to 8 week period of smoking cessation with greatly decrease this risk.(59–61) Anecdotal evidence suggested that stopping smoking too close to the time of surgery would have a paradoxical increase in pulmonary complications. While the salutary effect of stopping smoking is difficult to demonstrate until 4 weeks, these same studies do not report a higher complication rate in those who have recently quit.(59, 61) Optimization of chronic obstructive pulmonary disease (COPD) and treating any exacerbation with steroids if necessary is advantageous.(56) Laparoscopic surgery, if possible, is recommended as it was shown in meta-analysis to have a trend toward lower pulmonary complications.(62) Asthma can worsen after surgery. Patients with asthma should be identified preoperatively and their medications reviewed. The National Asthma Education and Prevention Program has issued guidelines for management of asthmatics undergoing surgery (available at www.guidelines.gov and in print).(63) Their preoperative lung function should be optimized to their predicted ­values or personal best using a short course of steroids if necessary to achieve this. Patients who received >20 mg of prednisone per day for more than 3 weeks in the 6 months before surgery should be assumed to have suppression of hypothalamic—pituitary— adrenal function and stress dose steroids are indicated. The stress dose depends on physicians’ experience, the patient’s condition requiring chronic steroids, the length and dose of preoperative use of steroids. The stress dose can be tapered to preoperative dose within 3 days postoperatively. Postoperative care techniques can reduce pulmonary complications. Adequate pain control is essential for an effective deep breathing program. Multiple studies have been performed evaluating various techniques but the consensus guideline indicates that no lung expansion intervention has been shown superior to another but any type of prophylaxis is better than none.(58) renal disease The patient with preexisting renal disease presents a special challenge to the surgeon. In patients with preexisting renal dysfunction is important to avoid additional intraoperative or postoperative injury caused by dehydration or toxic agents. Adequate urine output is an indication of adequate renal perfusion. Obtaining a preoperative urinalysis may identify unsuspected urinary tract infection, diabetes, or renal insufficiency. However, routine ­urinalysis is not recommended preoperatively for most surgical procedures. (64) Careful questioning regarding symptoms of dysuria, hesitancy, nocturia, and feelings of incomplete evacuation may diagnose prostatic disease and its complications including early stage renal dysfunction. Normal renal function is necessary for the excretion of the nondepolarizing muscle relaxants used for anesthesia and surgery. Renal function is also a consideration when choosing postoperative analgesic regimens including ­nonsteroidal

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improved outcomes in colon and rectal surgery medications such as ketoralac. Age, hypertension, and diabetes may be indications for preoperative selective renal function testing. Once renal function is compromised, all medications cleared by kidney must be dose adjusted in a timely ­manner and carefully monitored if needed. Nephrotoxic agents should be avoided whenever possible. Angiotensin-converting enzyme inhibitors reduce the renal perfusion and should probably be avoided if possible.(65) Mild to moderate renal impairment is usually asymptomatic; the prevalence of an elevated creatinine among asymptomatic patients with no history of renal disease is only 0.2%.(66) However, it increases with age.(67) Dialysis is necessary in 1% of patients who develop acute renal failure; the 30-day mortality is high in those patients with acute renal failure compared to those with normal renal function.(68, 69) Risk factors for acute renal failure include advanced age, baseline renal dysfunction, left ventricular dysfunction, peripheral ­vascular ­disease, and clinical signs of poor cardiac function such as ­pulmonary rales.(38, 68) Patients with end stage renal failure on dialysis require special attention. Patients in with end stage renal disease often have ­concurrent hypoalbuminemia and anemia resulting in poor wound healing and increased risk of complications. Krysa et al. describe a high instance of anastamotic leak in these patients. (70). Decreased leukocyte and immunologic function result in increased risks of infection and impaired cellular immunity.(71) Pulmonary edema and uremic pneumonitis may compromise respiratory function.(72) Postoperative ileus may be prolonged and patients with diverticulosis are at increased risk for acute infection and perforation.(73) Fluid and electrolyte abnormalities occur rapidly and require intensified scrutiny to maintain balance. It is important to know if the patients make any urine preoperatively, otherwise alternative strategies from postoperative urine volume, such as central venous pressure measurement, will be necessary to ensure adequate tissue perfusion. Dialysis can be scheduled on the preoperative day and again on postoperative day number one. Acute postoperative dialysis can be provided at any time using the same indications for acute dialysis in a nonpostoperative patient. Dialysis can improve abnormalities of hemostasis that are caused by platelet dysfunction. Abnormal bleeding in dialysis patients can be improved by platelet transfusion or administration of desmopressin acetate (DDAVP) increasing the release of von Willebrand factor from the endothelium. hepatic disease Operating on patients with significant liver disease is among the most daunting tasks for the colorectal surgeon. Although the ChildPugh classification was originally described to assess the operative risk in patients undergoing shunt surgery for portal hypertension, it has implications for other abdominal surgery. This classification is a scoring scale designed to quantify liver dysfunction. It utilizes bilirubin, albumin, prothrombin time, presence of ascites, and presence of encephalopathy to assign points and a subsequent classification from A to a maximal dysfunction of C. In a classic review of cirrhotic patients undergoing a variety of elective and emergent general surgical procedures, Child’s A cirrhosis carried a 10% mortality, Child’s B cirrhosis had a 31% mortality, and Child’s C cirrhosis was associated with a 76% mortality.(74) In a study of

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cirrhotic patients undergoing colectomy, the in-­hospital mortality was 24% with highest mortality for patients with encephalopathy, ascites, hypoalbuminemia, and anemia.(75) Suggestion of underlying cirrhosis can be detected at physical examination. Scleral icterus, jaundice, spider telangiectasia, and ­palmar erythema may be present. Early cirrhosis is associated with an enlarged liver while advanced disease will lead to a small shrunken liver. Asterixis, or flapping tremor, is a sign of advanced disease. Ascites can be detected by physical examination. Unexpected liver enzyme abnormalities are uncommon, occurring in only 0.3% of patients in one series.(76) In a pooled data analysis, only 0.1% of all routine preoperative liver function tests changed preoperative management.(77) Severe liver function test abnormalities among patients with cirrhosis or acute liver disease are associated with increased surgical morbidity and mortality, but it is not clear if mild abnormalities among patients with no known liver disease have a similar impact.(78) Clinically significant liver disease would most likely be suspected on the basis of the history and physical examination; thus, routine liver enzyme testing is not recommended.(8) In addition, the relationship between an abnormal result and the risk of perioperative hemorrhage is not well defined.(77, 79) Patients with liver disease often have disordered and abnormal coagulation. Decreased production of clotting factors, especially vitamin K-dependent ones, by the liver will often result in elevated prothrombin times (PT) or partial thromboplastin times (PTT). In some cases fresh frozen plasma or vitamin K administration can correct these abnormalities, at other times the liver disease is so severe that the coagulopathy cannot be corrected. In addition, patients with cirrhosis may have portal hypertension and splenomegaly, resulting in sequestration and a very low platelet count. It is mandatory to monitor platelet count as well as PT, PTT preoperatively so that abnormalities can be corrected. Portal hypertension can result in portosystemic varicies resulting in significant intraoperative bleeding at sites which are technically difficult to manage, such as the splenic flexure and the distal rectum. Use of alternate energy sources (such as Liga-SureTM, Valleylab, Boulder, CO or Enseal®, SurgRX, Redwood City, CA) may assist in reducing intraoperative blood loss in these challenging patients. Abnormal clotting factors may increase the risk of bleeding from hemorrhoidal disease in these patients, or actual rectal varices may be present. Patients with liver disease are often nutritionally depleted and have a very low albumin. They may also have ascites present at surgery. Although the ascites can be drained at operation, it generally reaccumulates rapidly. Our practice is to leave a drain in the abdomen perioperatively to assist the fascia to seal, so that the ascites will not become tense and may be less likely to breach the incision. Fluid and electrolyte disturbances are common in the patient with liver disease including sodium retention, potassium losses, and the development of edema. Fluid and sodium restriction, potassium supplementation, and the judicious use of diuretics (spironolactone and furosemide) may be necessary. malnutrition Malnutrition is a frequent preexisting condition in surgical patients. Identification of malnourished patients is possible by clinical history, physical examination, and laboratory parameters.

preexisting conditions Malnourished patients, who have lost more than 10% of their bodyweight in the past 6 months, and have an albumin below 3 g/ dL, have increased complication rates after surgery.(80) A serum albumin of <3 g/dL, transferrin of <200 mg/dL, and total lymphocyte count of <1,200 are consistent with at least some level of nutritional depletion. The enteral route is the preferred route of improving nutrition as long as there is a functioning gastrointestinal tract. There is moderate evidence that improved preoperative nutritional status can improve the postoperative outcome. (81) Severely malnourished patients might benefit more from nutritional support, although this needs to be provided for approximately 2 weeks to achieve such benefit.(82) Low body mass index (BMI) (<20 kg/m2) and hypoalbuminemia (<2.5 g/ dL) are ­independently associated with increased risk of morbidity and mortality after surgery. Patients with decreased albumin levels are also at increased risk for bleeding, renal failure, ­prolonged ventilatory support, and reoperation.(83, 84) immunocompromise The sources of immunocompromise in potential surgical patients are numerous and may be primary or acquired. Primary immunodeficiencies are relatively rare (1/10,000) and will not be encountered by most practicing surgeons.(85) Acquired immunodeficiencies are very common and range from mild defects to complete loss of immune function. Age, malnutrition, obesity, malignancy, burns, sepsis, trauma, surgery, anesthesia, blood transfusion, diabetes, renal failure, liver disease, splenectomy, radiation, and foreign bodies all modify the body’s response to invasion. Drugs including chemotherapeutic agents are probably the most frequently encountered cause of severe immunocompromise in surgical patients and are associated with profound neutropenia. The use of filgrastim, a granulocyte colony-stimulating ­factor, has been shown to decrease the duration of neutropenia and the incidence of infection versus controls in patients undergoing chemotherapy for small cell carcinoma of the lung and other nonmyeloid malignancy (86, 87) Cook et al. (88) reported that neutrophil—lymphocyte ratio (NLR) is an indicator of postoperative complications in colorectal surgical patients in critical care units. An elevated NLR on the first day after an elective colorectal resection is associated with increased risk of subsequent complications. NLR calculation does not burden the hospital with additional cost and can be used to identify patients at high risk of complications.(88) hiv/aids When evaluating a human immunodeficiency virus (HIV) positive patient for surgery it is important to understand the current state of their disease. This can be obtained by checking for history of autoimmune deficiency syndrome (AIDS) defining illness and measuring a CD4 count and HIV viral load. An absolute CD4 count of <200 or a decreasing ratio of CD4 to CD8 (normal 1.8–2.2) is associated with severe immunocompromise and subsequent risk for viral, fungal, protozoal, and bacterial infections as well as ­prolonged wound healing. Newer drug regimens that include combinations of protease inhibitors and nucleoside analogs have greatly improved the prognosis for HIV-infected patients.(89)

metabolic disease Metabolic diseases represent disorders where altered chemical transformation processes have resulted in abnormal release, storage, synthesis, or degradation of various protein, carbohydrate, lipid, or other products of metabolic activity. Gout is a generic term for a number of genetic and acquired conditions manifested by hyperuricemia and the deposition of uric acid crystals in joints precipitating an acute inflammatory arthritis. Acute gouty arthritis often follows a precipitating event. Acute gout has been commonly described in the postoperative setting.(90, 91) It manifests most commonly on the third to fifth postoperative day. Treatment consists of joint rest and administration of colchicine or ­non-steroidal anti-inflammatory agents.(92) A thorough past medical history including previous attacks of gout will alert the clinician that the patient is at risk postoperatively. At the first early signs of an attack it can be treated quickly. Significant delay can result in impaired ambulation secondary to pain which has the potential to prolong ileus and delay recovery. obesity Obesity has reached epidemic proportions in many areas of the world and obese patients are requiring surgery more and more commonly. The BMI is a commonly used relationship to measure obesity and it represents the bodyweight in kilograms divided by the height in meters squared. A BMI 18–25 is considered normal while >30 is obese. Obesity has been demonstrated to be a risk factor for abdominal surgical wound infection.(93) It has not surprisingly been linked to increased incidence of wound dehiscence (94), hernia (95), stoma complications (96). Some studies indicate a higher anastomotic leak rate for low colorectal or coloanal anastamosis in obese patient.(97) Cardiovascular, pulmonary, and thromboembolic complications are more frequent in obese patients, often attributable to their comorbid diseases.(98) Obesity also causes technical difficulties for the surgeon; operative duration and likelihood for conversion were increased in obese patients undergoing laparoscopic surgery.(99) It is reasonable as part of the informed consent process to counsel patients about their elevated operative risk due to obesity. If possible, they should be encouraged to lose additional weight before certain types of surgery where a delay is safe, and indeed may be beneficial (proctocolectomy with pouch-anal anastamosis, some diverticular resections). The extensive experience with bariatric surgery has taught us that sleep apnea is very common in obese individuals. The patient should be questioned for snoring, apneic episodes, arousals during sleep, or daytime somnolence. Physical exam should focus on evaluation of the airway, neck circumference, tonsil size and tongue volume. The American Society of Anestheiologists Task force recommends that if any of these characteristics are present that suggest sleep apnea then the anesthesiologist and surgeon should jointly decide whether to: manage the patient perioperatively based on clinical criteria alone or obtain sleep studies during the conduct of a more extensive evaluation in advance of surgery.(100) Postoperatively supplemental oxygen should be administered continuously to all patients with sleep apnea until they are able to maintain their baseline oxygen saturation while breathing room air. Sleep apnea patients should have continuous pulse oximetry monitoring until they are no longer at

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improved outcomes in colon and rectal surgery increased risk. Intermittent pulse oximetry with observation does not provide the same level of safety.(100) Continuous positive ­airway pressure ventilation (CPAP) is given to all patients using it preoperatively. diabetes The frequency of glucose abnormalities and type II diabetes increases with age; almost 25% of patients aged more than 60 had an abnormal value in one report.(66) The diabetic patient who is recognized and well managed perioperatively can achieve a surgical mortality which is equal to the nondiabetic patient. Protein catabolism after colorectal surgery is increased in patients with type 2 diabetes mellitus.(101) The preoperative assessment should include any complaints of polyuria, polydypsia, or polyphagia. An associated weight loss with any of these could be a sign of diabetes. A fasting blood glucose >140 mg/dl confirms a diagnosis of diabetes. Control of hyperglycemia should be started preoperatively and continued in the postoperative phase. In contrast to past doctrine that mild hyperglycemia is permissible in the perioperative period, newer studies indicate that there is a benefit in tighter glucose control. These intensive insulin strategies result in less hyperglycemia and as a result appear to improve immune function and reduce infectious complications.(102) These intensive strategies require ­frequent monitoring of blood glucose levels but may result in more hypoglycemia which has serious potential adverse consequences, causing two large scale studies of this method to be stopped.(103) Close monitoring of glucose and avoidance of hyperglycemia has clear benefit, but especially in difficult-to-control diabetics it can be challenging to avoid dangerous hypoglycemia. Renal and cardiovascular disease occurs commonly in diabetics and is a major cause of death in these patients. Compared to the nondiabetic population, cardiovascular disease occurs more frequently at a younger age, and with more severe manifestations. The reasons for this accelerated atherosclerosis are postulated to include the high incidence of hyperlipoproteinemia in diabetic patients, abnormalities of endothelial cell function, increased platelet aggregation, and a high incidence of hypertension in diabetics. age Despite advances in surgery, anesthesia, and perioperative care, increasing age continues to be a risk factor for perioperative ­complications. There is an increased risk of surgery associated with advancing age. In a 1982 review of 50,000 elderly patients, the risk of mortality with elective surgery increased from 1.3% for those under age 60, to 11.3% in the 80–89 year-old age group. (104) A recent review nearly 20 years later demonstrates an inhospital mortality of 0.3% for patients 50–59 and increasing to 2.6% for those patients older than 80.(105) Major perioperative complications increased by decade from 4.3% for 50–59, to 5.7% for 60–69, to 9.6% for 70–79 and 12.5% for 80 or older. Surgical procedures and surgery should not be restricted on the basis of age alone.(106) There is clear evidence that age has an effect on physiologic life processes.(107) Maximum heart rate slowly decreases with age (108) and there is an increasing frequency of arrhythmias (109). There is a decline in maximum oxygen

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­consumption except in very active patients.(110) A decrease in ventilatory threshold with age is predominantly due to an age-related decline of skeletal muscle mass.(111, 112) Chronologic age does not always correlate with the more important estimation of physiologic age. Active athletic individuals can maintain lean body mass equal to that of younger athletes well into their 8th decade.(113) Aging is characterized by a decline in renal function and by a susceptibility to renal diseases. Renal function is preserved with aging in healthy subjects at the expense of a complete reduction of renal functional reserve. Proteinuria (114) and bacteriuria (115) increase with the age. Aging is associated with insulin resistance often attributable to obesity and inactivity. Recent evidence suggests that skeletal muscle insulin resistance in aging is associated with mitochondrial alterations. Aging is associated with both whole body and myocardial insulin resistance, independent of obesity and inactivity.(113) The population is steadily aging and geriatric surgical care is likely to increase. As patients enter their 9th decade it will not be uncommon for them to be acceptable candidates for major surgery. Extremely elderly patients are likely to be poorly tolerant of complications and difficult to salvage once complications occur. “Failure to rescue” is a new quality of care indicator to measure the inability to save a patient once a complication has occurred.(116) It is likely that elderly patients will prove particularly ­difficult to rescue once a problem has occurred, so it is up to the surgeon to be fastidious in his preoperative preparation and risk assessment, intraoperative technique and postoperative care to avoid complications in this fragile patient population. neurologic system The prevalence of occult cerebrovascular disease in elderly patients is a common problem. An asymptomatic carotid bruit indicates the presence of peripheral vascular disease and is an indication for further evaluation by duplex scanning. However, prophylactic endarterectomy is not indicated usually, as the increased risk of a perioperative stroke compared to the unselected population is small.(118) Symptomatic disease should be treated before elective interventions. Aspirin prophylaxis and occasionally endarterectomy might be indicated to reduce the incidence of cerebrovascular accidents (CVA).(119) Patients who have had a stroke in the past are at an estimated 5–15% annual risk of a recurrent event if left untreated. Thus these patients are often maintained on either aspirin or clopidogrel (Plavix) to reduce their risk. While clopidogrel is more effective in high-risk patients, it is associated with a higher incidence of bleeding events. The risk of stroke while stopping the anticoagulation must be weighed against the adverse event of postsurgical bleeding. The decision-making must be tailored to the stroke risk of the individual patient based on their history and the magnitude and bleeding risk of the proposed procedure. For most patients, the interruption in their anticoagulation for 7 days to proceed with surgery is not likely to result in harm. Parkinson’s disease is a progressive degenerative neurologic condition associated with tremor and gait disturbance. In its later stages, aspiration pneumonia is common thus patients with advanced disease having abdominal surgery must have particular attention paid to their postoperative respiratory program. Most anti-Parkinsonian medications are only orally administered so

preexisting conditions they must be withheld after abdominal surgery until oral medications can be given. This can result in rigidity and further worsening of airway protection. One author describes use of rectally administered domperidone to patients with Parkinson’s disease having abdominal surgery in an effort to avoid such problems. (120) We have little experience with this, but it may prove useful in a particularly symptomatic patient. hypercoaguable disorders Management of patients with hypercoaguable syndromes can be especially challenging in the setting where the need to control postoperative bleeding is crucial. Common (factor V Leiden deficiency) and relatively uncommon (antithrombin deficiency, protein C and protein S deficiency) causes of thrombosis have ­different risk associations. For example, the relative risk of venous thrombosis in the Caucasian population can range from 2.5% for the prothrombin gene mutation to 25% in the presence of antithrombin deficiency.(121) Furthermore, approximately 50% of cases of venous thrombosis associated with these hereditary disorders are provoked by known risk factors such as surgery. Therefore, aggressive prophylaxis with subcutaneous heparin or low-molecular heparin is warranted peri- and postoperatively. By contrast, for those on long-term anticoagulation, the decision to continue treatment for thrombosis should be individualized. In general, warfarin therapy can be switched to low-molecular weight or intravenous heparin 3 to 5 days before surgery.(121) Patients with antiphospholipid antibody syndrome (lupus anticoagulant/anticardiolipin antibodies, history of arterial or venous thrombosis, and/or recurrent fetal loss) deserve special mention. Currently available anticoagulants are effective in reducing the recurrence rate of venous thromboembolism (VTE). VTE is a common complication in cancer patients and can lead to delay in cancer therapy and is predictive of a worse prognosis. Prophylaxis with anticoagulants is recommended for patients hospitalized for surgery or medical conditions, but is not routinely administered in the ambulatory setting.(122) However, anticoagulant treatment is associated with an increased risk for bleeding ­complications and needs to be discontinued when benefit of treatment no longer clearly outweigh its risks.(123) The incidence of recurrent VTE can be estimated through a two-step decision algorithm. First, the features of the patient (gender), of the initial event (proximal or distal deep vein thrombosis or pulmonary embolism), and the associated conditions (cancer, surgery, etc) provide essential information on the risk for recurrence after anticoagulant treatment discontinuation. Second, at time of anticoagulant treatment discontinuation, D-dimer levels and residual thrombosis have been indicated as predictors of recurrent VTE. Current evidence suggests that the risk of recurrence after stopping therapy is largely determined by whether the acute episode of VTE has been effectively treated and by the patient’s intrinsic risk of having a new episode of VTE. All patients with acute VTE should receive oral anticoagulant treatment for 3 months. At the end of this treatment period, physicians should decide for withdrawal or indefinite anticoagulation. Based on intrinsic patient’s risk for recurrent VTE and for bleeding complications and on patient preference, selected patients could be allocated to indefinite treatment with scheduled periodic reassessment of the benefit from extending

anticoagulation. Cancer patients should receive low-molecular weight heparin over warfarin in the long-term treatment of VTE. These patients should be considered for extended anticoagulation at least until resolution of underlying disease.(123) conclusion The history and physical examination is the most important part of the preoperative evaluation and can be used to guide further workup and testing. Multiple scoring systems are available to quantify risk of postoperative complications and mortality based on preoperative conditions. Optimization of these conditions will increase the likelihood of a successful outcome. references    1. Wilson ME, NB WI, Baskett PJ, Bennett JA, Skene AM. Assessment of fitness for surgical procedures and the variability of anesthetists’’ judgments. Br Med J 1980; 280(6213): 509–12.    2. Parker BM, Tetzlaff JE, Litaker DL, Maurer WG. Redefining the preoperative evaluation process and the role of the anesthesiologist. J Clin Anesth 2000; 12(5): 350–6.    3. Arvidsson S OJ, Sjostedt L, Svardsudd. Predicting postoperative adverse events. Clinical efficiency of four general classification systems. The project perioperative risk. Acta Anaesthesiol Scand 1996; 40(7): 783–91.    4. Roizen MF. The surgical burden: how to prevent a crisis in perioperative medicine. Cleve Clin J Med 2006; 73(Suppl 1): S8–12.    5. Mancuso CA. Impact of new guidelines on physicians’ ordering of preoperative tests. J Gen Intern Med 1999; 14(3): 166–72.    6. Greer AE, Irwin MG. Implementation and evaluation of guidelines for preoperative testing in a tertiary hospital. Anaesth Intensive Care 2002; 30(3): 326–30.    7. Roizen M. Preoperative patient evaluation. Can J Anaesth 1989; 36: S13–9.    8. Kaplan EB, Sheiner LB, Boeckmann AJ et al. The usefulness of preoperative laboratory screening. JAMA 1985; 253(24): 3576–81.    9. Carson JL, Duff A, Poses RM et al. Effect of anaemia and cardiovascular disease on surgical mortality and morbidity. Lancet 1996; 348(9034): 1055–611.   10. Bushick JB, Eisenberg JM, Kinman J, Cebul RD, Schwartz JS. Pursuit of abnormal coagulation screening tests generates modest hidden preoperative costs. J Gen Intern Med 1989; 4(6): 493–7.   11. Delaney CP, McKeigan J. Pre-operative management – bowel preparation, medical evaluation. ASCRS Textbook of Colorectal Surgery, eds. Fleshman, Beck, Wolff, Pemberton, Wexner. Springer Verlag, New York, NY, 2006.   12. Arvidsson S, Ouchterlony J, Sjostedt L, Svardsudd K. Predicting postoperative adverse events. Clinical efficiency of four general classification systems. The project perioperative risk. Acta Anaesthesiol Scand 1996; 40(7): 783–91.   13. Klotz HP, Candinas D, Platz A et al. Preoperative risk assessment in elective general surgery. Br J Surg 1996; 83(12): 1788–91.

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preexisting conditions   46. van Klei WA, Bryson GL, Yang H et al. The value of routine preoperative electrocardiography in predicting myocardial infarction after noncardiac surgery. Ann Surg 2007; 246(2): 165–70.   47. Kannel WB, Abbott RD. Incidence and prognosis of unrecognized myocardial infarction. An update on the Framingham study. N Engl J Med 1984; 311(18): 1144–7.   48. Velanovich V. Preoperative screening electrocardiography: predictive value for postoperative cardiac complications. South Med J 1994; 87(4): 431–4.   49. McFalls EO, Ward HB, Moritz TE et al. Coronary-artery revascularization before elective major vascular surgery. N Eng J Med 2004; 351: 2795–804.   50. Poldermans D, Schouten O, Vidakovic R et al. A clinical randomized trial to evaluate the safety of a noninvasive approach in high-risk patients undergoing major vascular surgery: the DECREASE-V Pilot Study. J Am Coll Cardiol 2007; 49: 1763–9.   51. Poldermans D, Bax JJ, Schouten O et al. Should major vascular surgery be delayed because of preoperative cardiac testing in intermediate-risk patients receiving beta-blocker therapy with tight heart rate control? J Am Coll Cardiol 2006; 48: 964–9.   52. Hindler K, Shaw AD, Samuels J et al. Improved postoperative outcomes associated with preoperative statin therapy. Anesthesiology 2006; 105: 1260–72.   53. Smetana GW, Lawrence VA, Cornell JE. Preoperative pulmonary risk stratification for noncardiothoracic surgery: systematic review for the American College of Physicians. Ann Int Med 2006; 144: 581–95.   54. Arozullah AM, Daley J, Henderson WG, Khuri SF. Multifactorial risk index for predicting postoperative respiratory failure in men after major noncardiac surgery. Ann Surg 2000; 232: 242–53.   55. Smetana GW, Macpherson DS. The case against routine preoperative laboratory testing. Med Clin North Am 2003; 87: 7–40.   56. Archer C, Levy AR, McGregor M. Value of routine preoperative chest x-rays: a meta-analysis. Can J Anesth 1993; 40: 1022–7.   57. Kroenke K, Lawrence VA, Theroux JF, Tuley MR. Operative risk in patients with severe obstructive pulmonary disease. Arch Intern med 1992; 152: 967–71.   58. Lawrence VA, Cornell JE, Smetana GW. Strategies to reduce postoperative pulmonary complications after noncardiothoracic surgery: systematic review for the American College of Physicians. Ann Intern Med 2006; 144(8): 596–608.   59. Nakagawa M, Tanaka H, Tsukauma H, Kishi Y. Relationship between the duration of the preoperative smoke-free period and the incidence of postoperative pulmonary complications after pulmonary surgery. Chest 2001; 120(3): 705–10.   60. Bluman LG, Mosca L, Newman N, Simon D. Preoperative smoking habits and postoperative pulmonary complications. Chest 1998; 113: 883–9.   61. Barrera R, Shi W, Amar D et al. Smoking and Timing of Cessation: impact on pulmonary complications after thoracotomy. Chest 2005; 127: 1977–83.

  62. Abraham NS, Young J, Solomon M. Meta-analysis of shortterm outcomes after laparoscopic resection for colorectal cancer. Br J Surg 2004; 91: 1111–24.   63. National asthma education and prevention program expert panel report: guidelines for the diagnosis and management of asthma update on selected topics-2002. J Allergy Clin Immunol 2002; 110: S141–219.   64. Lawrence VA, Kroenke K. The unproven utility of preoperative urinalysis. Clinical use. Arch Intern Med 1988; 148(6): 1370–3.   65. Hricik DE, Browning PJ, Kopelman R. Captopril-induced functional renal insufficiency in patients with bilateral renal-artery stenoses or renal-artery stenosis in a solitary kidney. N Engl J Med 1983; 308(7): 373–6.   66. Velanovich V. Preoperative laboratory screening based on age, gender, and concomitant medical diseases. Surgery 1994; 115(1): 56–61.   67. Chertow GM, Lazarus JM, Christiansen CL et al. Preoperative renal risk stratification. Circulation 1997; 95(4): 878–84.   68. Gailiunas P Jr, Chawla R, Lazarus JM et al. Acute renal failure following cardiac operations. J Thorac Cardiovasc Surg 1980; 79(2): 241–3.   69. Abrahamov D, Tamariz M, Fremes S et al. Renal dysfunction after cardiac surgery. Can J Cardiol 2001; 17(5): 565–70.   70. Krysa J, Patel V, Taylor J et al. Outcome of patients on renal replacement therapy after colorectal surgery. Dis Col Rectum 2008; 51(6): 961–5.   71. Touraine JL, Touraine F, Revillard JP, Brochier J, Traeger J. T-lymphocytes and serum inhibitors of cell-mediated immunity in renal insufficiency. Nephron 1975; 14(2): 195–208.   72. Bleyl U, Sander E, Schindler T. The pathology and biology of uremic pneumonitis. J Intensive Care Med 1981; 7(4): 193–202.   73. Adams PL, Rutsky EA, Rostand SG, Han SY. Lower gastrointestinal tract dysfunction in patients receiving long-term hemodialysis. Archives of internal medicine 1982; 142(2): 303–6.   74. Garrison RN, Cryer HM, Howard DA, Polk HC. Clarification of risk factors for abdominal operations in patients with hepatic cirrhosis. Ann Surg 1984; 199(6): 648–54.   75. Metcalf AM, Dozois RR, Wolff BG, Beart RW Jr. The surgical risk of colectomy in patients with cirrhosis. Dis Colon Rectum 1987; 30(7): 529–31.   76. Narr BJ, Hansen TR, Warner MA. Preoperative laboratory screening in healthy Mayo patients: cost-effective elimination of tests and unchanged outcomes. Mayo Clin Proc 1991; 66(2): 155–9.   77. Smetana GW, Macpherson DS. The case against routine preoperative laboratory testing. Med Clin North Am 2003; 87(1): 7–40.   78. Powell-Jackson P, Greenway B, Williams R. Adverse effects of exploratory laparotomy in patients with unsuspected liver disease. Br J Surg 1982; 69(8): 449–51.   79. Suchman AL, Mushlin AI. How well does the activated partial thromboplastin time predict postoperative hemorrhage? JAMA 1986; 256(6): 750–3.

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improved outcomes in colon and rectal surgery   80. Campos AC, Meguid MM. A critical appraisal of the usefulness of perioperative nutritional support. Am J Clin Nutr 1992; 55(1): 117–30.   81. Thompson BR, Julian TB, Stremple JF. Perioperative total parenteral nutrition in patients with gastrointestinal cancer. J Surg Res 1981; 30(5): 497–500.   82. Vitello JM. Nutritional assessment and the role of preoperative parenteral nutrition in the colon cancer patient. Semin Surg Oncol 1994; 10(3): 183–94.   83. Cook JW, Pierson LM, Herbert WG et al. The influence of patient strength, aerobic capacity and body composition upon outcomes after coronary artery bypass grafting. Thorac Cardiovasc Surg 2001; 49(2): 89–93.   84. Engelman DT, Adams DH, Byrne JG et al. Impact of body mass index and albumin on morbidity and mortality after cardiac surgery. J Thorac Cardiovasc Surg 1999; 118(5): 866–73.   85. Rosen FS, Cooper MD, Wedgwood RJ. The primary immunodeficiencies. (2). N Engl J Med 1984; 311(5): 300–10.   86. Morstyn G, Campbell L, Souza LM et al. Effect of granulocyte colony stimulating factor on neutropenia induced by cytotoxic chemotherapy. Lancet 1988; 1(8587): 667–72.   87. Bronchud M, Scarffe JH, Thatcher N et al. Phase I/II study of recombinant human granulocyte colony-stimulating factor in patients receiving intensive chemotherapy for small cell lung cancer. Behring Inst Mitt 1988; 83: 327–9.   88. Cook EJ, Walsh SR, Farooq N et al. Post-operative neutrophil-lymphocyte ratio predicts complications following colorectal surgery. Int J Surg (London, England) 2007; 5(1): 27–30.   89. Barrett WL, Callahan TD, Orkin BA. Perianal manifestations of human immunodificiency virus infection: experience with 260 patients. Dis Colon Rectum 1998; 41(5): 606–12.   90. Friedman JE, Dallal RM, Lord JL. Gouty attacks occur ­frequently in postoperative gastric bypass patients. Surg Obes Relat Dis 2008; 4(1): 11–3.   91. Craig MH, Poole GV, Hauser CJ. Postsurgical gout. Am Surg 1995; 61(1): 56–9.   92. Wyngaarden JB. Gout. Philadelphia: Saunders; 1992.   93. Dindo D, Muller MK, Weber M, Clavien PA. Obesity in ­general elective surgery. Lancet 2003; 361: 2032–5.   94. Riou JP, Choen JR, Johnson H. Factors affecting wound dehiscence. Am J Surgery 1992; 163: 324–30.   95. Sugerman HJ, Kellum JM, Reines D et al. Greater risk of incisional hernia with morbidly obese than steroid-dependent patients and low recurrence with incisional prefascial polypropylene mesh. Am J Surg 1996; 171: 80–4.   96. Arumugam PJ, Bevan L, Macdonald L et al. A prospective audit of stomas: analysis of risk factors and complications and their management. Colorectal Dis 2003; 5: 49–52.   97. Rullier R, Laurent C, Garrelon JL et al. Risk factors for anastamotic leakage after resection of rectal cancer. Br J Surg 1998; 85: 355–8.   98. Gendall KA, Raniga S, Kennedy R, Frizelle FA. The impact of obesity on outcome after major colorectal surgery. Dis Colon Rectum 2007; 2223–37.

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  99. Tekkis PP, Senagore AJ, Delaney CP, Fazio VW. Evaluation of the learning curve in laparoscopic colorectal surgery: comparison of right-sided and left-sided resections. Ann Surg 2005; 242: 83–91. 100. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: a report by the American Society of anesthesiologists task force on perioperative management of patients with obstructive sleep apnea. Anesthesiology 2006; 104(5): 1081–93. 101. Schricker T, Gougeon R, Eberhart L et al. Type 2 diabetes mellitus and the catabolic response to surgery. Anesthesiology 2005; 102(2): 320–6. 102. Van den Berghe G, Wouters P, Weekers F et al. Intensive insulin therapy in critically ill patients. NEJM 2001; 345: 1359–67. 103. Blondet JJ, Beilman GJ. Glycemic control and prevention of postoperative infection. Curr Opin Crit Care 2007; 13(4): 421–7. 104. Linn BS, Linn MW, Wallen N. Evaluation of results of surgical procedures in the elderly. Annals of surgery 1982; 195(1): 90–6. 105. Polanczyk C, Marcantonio E, Goldman L et al. Impact of age on perioperative complications and length of stay in patients undergoing noncardiac surgery. Ann Int Med 2001; 134(8): 637–42. 106. Faivre J, Lemmens VE, Quipourt V, Bouvier AM. Management and survival of colorectal cancer in the elderly in population-based studies. Eur J Cancer 2007; 43(15): 2279–84. 107. Leach RE. Aging and physical activity. Der Orthopade 2000; 29(11): 936–40. 108. Helwig BG, Parimi S, Ganta CK et al. Aging alters regulation of visceral sympathetic nerve responses to acute hypothermia. Am J Physiol 2006; 291(3): R573–9. 109. Moller CS, Haggstrom J, Zethelius B et al. Age and followup time affect the prognostic value of the ECG and conventional cardiovascular risk factors for stroke in adult men. J Epidemiol Community Health 2007; 61(8): 704–12. 110. Bogaard HJ, Woltjer HH, Dekker BM et al. Haemodynamic response to exercise in healthy young and elderly subjects. Eur J Appl Physiol Occup Physiol 1997; 75(5): 435–42. 111. Sanada K, Kuchiki T, Miyachi M et al. Effects of age on ventilatory threshold and peak oxygen uptake normalized for regional skeletal muscle mass in Japanese men and women aged 20–80 years. Eur J Appl Physiol 2007; 99(5): 475–83. 112. Galban CJ, Maderwald S, Stock F, Ladd ME. Age-related changes in skeletal muscle as detected by diffusion tensor magnetic resonance imaging. J Gerontol 2007; 62(4): 453–8. 113. Frisard MI, Fabre JM, Russell RD et al. Physical activity level and physical functionality in nonagenarians compared to individuals aged 60–74 years. J Gerontol 2007; 62(7): 783–8. 114. Garg AX, Muirhead N, Knoll G et al. Proteinuria and reduced kidney function in living kidney donors: a systematic review, meta-analysis, and meta-regression. Kidney Int 2006; 70(10): 1801–10.

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120. Galvez-Jimenez N, Lang AE. Perioperative problems in Parkinson’s disease and their management: apomorphine with rectal domperidone. Can J Neurol Sci 1996; 23(3): 198–203. 121 Douketis JD, Berger PB, DunnAS, et al. The perioperative management of antithrombotic therapy: Amercian College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008; 133(6 Suppl): 299S–339S. 122 Lee AY. Cancer and venous thromboembolism: prevention, treatment, and survival. J Thomb Thrombolysis 2008; 25: 33–36. 123 Agnelli G, Becattani C. Treatment of DVT: how long is enough and how do you predict recurrence. J Throm Thrombolysis 2008; 25: 37–44.

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2

Preoperative bowel preparation David A Margolin and Sean Mayfield

challenging case A 57-year-old gentleman with a sigmoid colon cancer found via colonoscopy for a history of anemia and weight loss is awaiting surgery. You stop by the pre-op holding area to see the patient where he tells you, “I tried drinking that prep last night and after only half a glass I got sick and threw up. I just couldn’t take it.” Do you perform elective surgery? case management Yes. Multiple studies have demonstrated the safety of elective bowel surgery in the absence of a mechanical bowel preparation. INtRODUCTION The objectives of preoperative bowel preparation in elective colon and rectal surgery include decreasing the bacterial count in the colon, decreasing the wound infection rate, decreasing the rate of anastomotic leaks, improving interoperative bowel handling, and facilitating interoperative endoscopy if necessary. Aside from the medical reasons for a patient undergoing a bowel prep, there is surgical tradition as well as the medicolegal implications of deviations from the perceived norm. We know that there are a variety of well-documented factors that play a role in infectious compilations in colon and rectal surgery most notably, increased American Society of Anesthesiologists (ASA) classification, obesity, diabetes, prolonged surgical time, interoperative hypotension, excessive blood loss, surgical intervention for bowel obstruction, whether partial or complete, and emergency surgery. (1–5) We as surgeons also try to adhere the dictum of primum non nocere. With those thoughts in mind, preoperative bowl preparation has become the standard before elective colon surgery. Preoperative bowel preparation is divided into two parts: antibiotic prophylaxis and mechanical bowel preparation. The use of antibiotic prophylaxis in elective colon surgery is mandatory to minimize infection complications. Unfortunately the choice antibiotic and rout of antibiotic administration is not as clear. The first principle in prophylactic use of antibiotic administration is to provide coverage for the normal bowel flora. This means choosing antibiotics that cover both aerobic bacteria, especially Escherichia coli and anaerobic species most notably bacteroides sp. Even with appropriately chosen antibiotics the route of antibiotic administration is undergoing a re-evaluation. Oral antibiotics as used in the traditional NicholsCondon antibiotic preparation have been shown to reduce intraluminal and mucosal bacterial count while parenteral antibiotics have been shown to reduce systemic bacterial counts at the tissue level. Colorectal surgery performed before 1970 was fraught with infectious complications which occurred in more than 30–50% of all operations. With a better understanding of bacteriology and the availability of an increasing number of antibiotics, surgeons attempted to improve their outcomes with regards to infections. Garlock and Seley in 1939 gave patients sulfanilamides before surgery; unfortunately, there was no real improvement in infectious

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complications.(6) Dearing in 1951 and Poth in 1960 tied tetracycline and neomycin respectively with only minimal improvement.(7, 8) It was not till the 1970s that a significant improvement in mitigating infectious complications was seen. In a 1977 VA cooperative study, Nichols and Condon showed that by using oral neomycin sulfate and erythromycin base that they were able to decrease the wound infection rate of elective colon resections from 35% to 9%. They also showed that this regimen showed a significant decrease in all septic complications (wound infection, anastomotic leak, and abscess) from 43% to 9%.(9–11) The dosing of 1 g of oral neomycin sulfate and erythromycin base at 2:00 pm, 3:00 pm, and 10:00 pm for an 8:00 am case became and remains a standard oral antibiotic regime for elective surgery. Unfortunately, the Nichols prep has its draw backs. While this antibiotic combination is efficacious, it can cause significant gastrointestinal discomfort severely limiting patient compliance with the remainder of the antibiotic prep and completion of their mechanical preparation. These limitations, along with the significant increase in number and spectrum of paranteral antibiotics, led many investigators to utilize various IV antibiotic combinations to minimize infectious complications. In 1969, Polk demonstrated that cephaloridine versus mechanical prep alone decreased the rate of wound infection in elective colon resections from 30% to 7%.(12) Since that initial study their have been numerous attempts to find the best parenteral antibiotic. From 1983 to 1995 there were more than 150 randomized controlled trials performed (Table 2.1 and 2.2). Finally in 1998, Song and colleagues, in a landmark review in the British Journal of Surgery, codified modern practice and confirmed that parenteral antibiotics alone decrease the rate of wound infection and that no single regimen is superior as long as the antibiotics chosen cover both aerobic and anaerobic bacteria and are given before incision.(13) In 2003, the Surgical Infection Prevention Guideline Writers Workgroup (SIPGWW), a project endorsed by both the American College of Surgeons (ACS) and American Society of Colon and Rectal Surgeons (ASCRS), submitted consensus positions for surgical antimicrobial prophylaxis.(3) They stated that the standard for parenteral antibiotic prophylaxis in elective colon resections should include: 1. Timing: Infusion of the first antimicrobial dose should begin within 60 minutes before surgical incision. 2. Duration: Prophylactic antimicrobials should be discontinued within 24 hours following surgery. 3. Dosing: The initial dose should be adequate based on weight, adjusted dosing weight, or BMI. An additional dose should be administered if the operation continues over two halflives after the initial dose. 4. Selection (Colon Surgery): Cefotetan, cefoxitin, or cefazolin/ metronidazole. – Options for β-lactam allergic patients: – Clindamycin + gentamicin, ciprofloxacin, or aztreonam. – Metronidazole + gentamycin or ciprofloxacin.

preoperative bowel preparation Table 2.1  Intravenous Antibiotics. Author

Wound Infections

No. of Pts.

Antibiotic

403

cefoxitin cefotetan



11.0% 9.0%

Skipper 1992 (15)

 

cefotetan



14.7%

Zanella 2000 (16)

615

cefepime plus metronidazole



7.2%

Mosimann 1998 (17)

440

amoxicillin/ clavulanic



11.1%

Hall 1989 (18)

237

gentamicin plus metronidazole



14.8%

Corman 1993 (19)

907

cefuroxime plus metronidazole



7.3%

Periti 1989 (14)

Table 2.2  Effect of Intravenous Antibiotics. Author

Pts. No.

Antibiotics

Wound Infections

Codon 1983 (20)

1082

neo/erythro neo/erythro + cephalothin



8.0 6.0

Coppa 1983 (21)

241

neo/erythro neo/erythro + cefoxitin



18 7

Portnoy 1983 (22)

104

neo/erythro neo/erythro + cefazolin neo/erythro + ticarcillin



27 4.7 2.3

Lau 1988 (23)

194

neo/erythro metronidazole + gentamicin neo/erythro + metronidazole   + gentamicin

27.4 11.9

Schoetz 1990 (24)

197

neo/erythro neo/erythro + cefoxitin

14.6 5

Stellato 1990 (25)

146

neo/erythro cefoxitin only neo/erythro +cefoxitin

11.4 11.7 7.8

12.3

Since 1887, when Halsted described intestinal anastomosis, the idea of mechanically preparing the bowel has become accepted surgical practice. The rationale for mechanical bowel prep has been to reduce the risk of infectious complications including wound infection and anastomotic leak. At the beginning of the 20th century, morbidity and mortality secondary to septic complications following colon and rectal surgery was high. However, medical innovations including broad-spectrum oral and intravenous antibiotics, improved surgical techniques and instrumentation, improved anesthetic and perioperative care, and presumably mechanical bowel preparation has resulted in decreased infectious complication rates making elective colorectal surgery safe. Mechanical bowel preparation preceding elective colon and rectal surgery has become surgical dogma, and surgeons are trained that primary colonic anastomosis is unsafe in the presence of an unprepared bowel. Proponents argue that the “clean” bowel has a lower bacterial load and is easier to handle thus reducing the chance of fecal spillage and contamination of the wound and peritoneal cavity during surgery. Mechanical bowel prep is also

believed to eliminate the proximal stool column, possibly reducing the chance of anastomotic disruption by the passing stool, and the sequelae should a disruption occur. The merits of this practice however have lacked clear investigational proof and have undergone continued scrutiny over the last decade. In 1973, Hewitt et al. presented whole gut irrigation, using a large volume of isotonic solution, administered via a nasogastric tube.(26) No change in the rate of infection was displayed, although the quality of the prep was improved. A subsequent advance was whole gut lavage using mannitol as an osmotic agent. Mannitol reduced the absorption of water, but was associated with dehydration and loss of electrolytes. Because mannitol is fermented by E. coli into a potentially explosive gas, explosions while using electrocautery were reported. There are two oral preparations routinely used today, polyethylene glycol (PEG) and sodium phosphate (NaP). PEG is an inert osmotically active polymer that is mixed with an electrolyte solution resulting in an isosomotic preparation that acts to lavage stool from the colon lumen. The electrolyte content combined with the osmotic activity of PEG prevents net absorption or excretion or water and electrolytes. Typically, 4 L of PEG is ingested over 2 to 3 hours. This produces good to excellent cleansing in most patients without causing significant fluid or electrolyte derangements. These issues are of particular importance in elderly patients or those with renal insufficiency or congestive heart failure. Nausea, vomiting, and patient compliance are obstacles to achieving adequate results in some patients. This has been addressed by the addition of flavor additives and a reduced volume prep in which patients take 2–4 (10 mg) bisacodyl tablets and ½ the normal volume of PEG (2 L). Some surgeons also prescribe metoclopramide to hasten gastric emptying, or an antiemetic such as promethazine. However, prospective, randomized trials have not confirmed significant benefit from either of these adjuvant medications. NaP is a hypersomolar oral saline laxative. Smaller volumes of hypertonic NaP can produce adequate bowel cleansing with better patient compliance. Patients are instructed to consume 45 ml of sodium phosphate diluted in clear liquids (15 ml NaP in 240 ml) in two doses separated by 10 hours. The timing of this should be such that the patient is not kept awake evacuating the entire night before the procedure. Sodium phosphate tablets are also available and are equally efficacious. Three to four tablets with 8 oz of clear liquid are taken every 15 minutes to a total of 28 tablets. In May 2006, the Federal Drug Administration issued a warning regarding oral NaP for bowel preps in elderly patients or those with underlying kidney disease, dehydration, or those taking medication that affect renal perfusion (diuretics, ACE inhibitors, angiotensin receptor blockers, and NSAIDs).(27) These patients are at increased risk for developing acute renal failure and nephrocalcinosis due to the relatively large phosphate load, fluid shifts, and decreased intravascular volume associated with NaP preps. However, both the avoidance of this complication as well as improved efficacy can be achieved by appropriate patient selection and consumption of large volumes (2–3 L) of clear liquids as part of this prep. A 2003 survey by Zmora et al. of members of the American Society of Colon & Rectum Surgeons displayed that 99% of respondents routinely use mechanical bowel preparation



improved outcomes in colon and rectal surgery although 10% questioned its use.(28) 47% of the surgeons used sodium phosphate, 32% used polyethylene glycol, and 14% alternated between these two options. These results are the same as those reported by Beck et al. in 1990 and are most likely based on surgical tradition rather than evidence-based science.(29) Since 1992, several randomized controlled trials and metaanalyses have studied the influence of mechanical bowel preparation on the outcome of colorectal surgery. Brownson et al. were the first to perform a randomized trial which consisted of 179 patients. Patients were divided into preparation with polyethylene glycol or no mechanical preparation.(30) Interestingly, patients who received a mechanical prep had a higher rate of anastomotic leak and intraabdominal infection. There was no statistically significant difference in wound infection. Burke et al. and Santos et al. in 1994 published similar studies. Neither study showed a significant difference in intraabdominal infection; however, Santos displayed a higher wound infection rate 24% vs. 12% in patients who received mechanical bowel preparation.(31, 32) Miettinen et al. reported the results of a prospective randomized trial in 2000 including patients undergoing rectal surgery. (33) Again, no significant differences in infectious complications were found between the two groups 4% vs. 2% for both wound infections and anastomotic leaks. It was difficult to determine the effect on anastomotic leakage, as this study included patients who did not undergo an anastomosis. Zmora et al. performed the largest study thus far, a randomized prospective trial in 2003 which included 415 patients separated into mechanical bowel prep with polyethylene glycol vs. no bowel prep.(34) Once again surgical infectious complications did not significantly differ between the two groups with the wound infection rate 6.4% for patient who underwent a mechanical bowel prep vs. 5.7 for those who did not. Similar results were seen with regards to anastomotic leak rate 3.7% vs. 2.1%. Fa-Si-Oen et al. performed a well-designed multicenter randomized controlled trial published in 2005.(35) Leftsided colonic resections accounted for approximately half of the procedures. This was distinctive, given the current thinking that

right-sided anastomosis are generally safe. No significant difference in wound infection or anastomotic leak was detected, but the method of determining a wound infection was performed incorrectly in 65 patients which might have therefore affected the validity of the results. Bucher et al. published a randomized control study in 2005 which again compared the outcome of patients who underwent left-sided colorectal surgery with or without mechanical bowel prep.(36) 153 patients were randomized into mechanical bowel preparation (MBP) with polyethylene glycol vs. no prep. The overall rate of abdominal infectious complications was 22% in the prepped group vs. 8% in the unprepped. Anastomotic leak occurred in 6% in the prepped group vs. 1%. Interestingly hospital stay was longer for patient who had MBP, 14.9 days vs. 9.9 in the nonprepped. This was a multicenter trial which the authors agree may partially bias the results. The conclusion was that left-sided colorectal surgery could be performed safely without MBP and that MBP might have a negative impact on the complication rate and hospital stay.(Table 2.3) Additional evidence against the use of mechanical bowel prep has arisen from the literature regarding urgent surgery for traumatic colon injuries. A retrospective review by Conrad et al. was performed in 2000 which evaluated 145 patients with penetrating colon injuries.(33) Two separate time periods were compared, the latter of which included a significantly larger number of primary repairs compared to proximal diversions. The colonic injuries were distributed equally between the right and left colon. Anastomosis of the unprepped bowel appeared safe with only one anastomotic leak in the study. Other infectious complications showed no statistical difference between the two periods. The main focus of this study was to evaluate the safety of primary anastomosis vs. fecal diversion; however it also revealed the safety of an anastomosis in unprepped bowel. A Cochrane review was performed in 2004 as a meta-analysis to analyze the effectiveness and safety of prophylactic mechanical bowel preparation for morbidity and mortality rates in elective colorectal surgery.(39) Out of 1159 patients with anastomoses, 576

Table 2.3  Mechanical Bowel Prep Randomized Controlled Trials. Patients

Zmora 2003 (34)

Fa-Si-Oen 2005 (35)

Ram 2005 (37)

Bucher 2005 (36) Miettinen 2000 (33)

415

250

329

153

267

Patients   (MBP/no MBP)

187/193

125/125

164/165

78/75

138/129

Mean age   (MBP/no MBP)

68/68

68/70

68/68

63/63

61/64

Cancer %   (MBP/no MBP)

78/78

90/92

75/88

32/28

46/55

L colon surgery %   (MBP/no MBP)

68/72

48/58

89/85

100/100

45/47

Type of prep

PEG

PEG

NaPO4

PEG

PEG

Anastomotic leak %   (MBP/no MBP)

3.7/2.1 (NS)

5.6/4.8 (NS)

0.6/1.2 (NS)

6/1 (NS)

4/2 (NS)

Wound infection %   (MBP/no MBP)

6.4/5.7 (NS)

7.2/5.6 (NS)

9.8/6.1 (NS)

13/4 (NS)

4/2 (NS)

1.1/1 (NS)

Not given

0.6/0.6 (NS)

1/3 (NS)

2/3 (NS)

Intraabdominal abscess %   (MBP/no MBP)



preoperative bowel preparation received mechanical bowel prep and 583 underwent no prep. There was no difference in anastomotic leak rates for low anterior resection (12.5 vs. 12%), or colonic surgery (1.2 vs. 6%) in patients with or without MBP. Anastomotic leak rates were significantly lower overall without MBP (5.5 vs. 2.9%). Wound infection, peritonitis, reoperation, mortality, and extra abdominal complications were similar between groups. The authors’ conclusion was no convincing evidence exists that MBP is associated with reduced rates of anastomotic leakage after elective colorectal surgery and that MBP may be associated with an increased rate of anastomotic leakage and wound complications. No definitive conclusion on complication rates was possible due to the clinical heterogeneity of trial inclusion criteria, poor reporting of concealment and allocation, potential performance biases, and failure-to-treat analyses.(39) One other important consideration when evaluating MBP is the patient’s experience. A 2007 study from Sweden performed by Jung et al. evaluated 105 patients who underwent elective colon surgery.(40) 60 patients received MBP with half receiving polyethylene glycol and the remainder receiving sodium phosphate. 52% in the MBP group required assistance via hospital staff or a relative with the prep. Only 30% of the MBP group would consider undergoing the same preoperative procedure. There was no significant difference in postoperative pain and nausea; however, patients in the no MBP group had more pain on postoperative day #4. This was thought to be due to patient’s regaining bowel function earlier compared to the no MBP group. Despite the growing evidence against MBP, there are several benefits unrelated to the risk of infection. A prepped colon is easier to palpate and manipulate, and allows the surgeon to identify smaller tumors and perform intraoperative colonoscopy if required. During laparoscopy, it may reduce the risk of traumatic bowel injury of an otherwise heavy, fecal loaded colon being manipulated by relatively traumatic laparoscopic grasping instruments. However, the overall data from randomized trials and meta-analyses clearly show the safety of performing an anastomosis in unprepared bowel and the lack of benefit of MBP toward infectious complications. references   1. Smith RL, Bohl JK, McElearney ST et al. Wound infection after elective colorectal resection. Ann Surg 2004; 239: 599–605.   2. National Academy of Science NRC. Postoperative wound infections: the influence of ultraviolet irradiation of the operating room and of various other factors. Ann Surg 1964; 160: 1–132.   3. Bratzler DW, Houck PM. Antimicrobial prophylaxis for surgery: An advisory statement from the National Surgical Infection Prevention Project. CID 2004; 38: 1706–15.   4. Forse RA, Karam B, MacLean LD, Christou NV. Antibiotic prophylaxis for surgery in morbidly obese patients. Surgery 1989; 106: 750–6.   5. Perncevich E, Sands K, Cosgrove S et al. Health and economic impact of surgical site infections diagnosed after hospital discharge. Emerg Infect Dis 2003; 9: 196–203.   6. Garlock JH, Seley GP. The use of sulfanilamide in surgery of the colon and rectum. A preliminary report. Surgery 1939; 5: 787.

  7. Dearing WH, Needham GM. The effect of terramycin on the intestinal bacterial flora of patients being prepared for intestinal surgery. Proc Staff Meet Mayo Clin 1951; 26(3): 49–52.   8. Poth EJ. The role of intestinal antisepsis in the preoperative preparation of the colon. Surgery 1960; 47: 1018–28.   9. Clarke JS, Condon RE, Bartlett JG et al. Preoperative oral antibiotics reduce septic complications of colon operations: results of prospective, randomized, double-blind clinical study. Ann Surg 1977; 186: 151. 10. Bartlett JG, Condon RE, Gorbach SL et al. Veterans administration cooperative study on bowel preparation for elective colorectal operations: impact of oral antibiotic regimen on colonic flora, wound irrigation cultures and bacteriology of septic complications. Ann Surg 1978; 188(2): 249–54. 11. Condon RE, Bartlett JG, Nichols RL et al. Preoperative prophylactic cephalothin fails to control septic complications of colorectal operations: results of controlled clinical trial. A Veterans Administration Cooperative Study. Am J Surg 1979; 137: 68. 12. Polk HC, Zeppa R, Warren WD. Surgical significance of differentiation between acute and chronic pancreatic collections. Ann Surg 1969; 169(3): 444–6. 13. Song F, Glenny A. Antimicrobial prophylaxis in colorectal surgery: a systematic review of randomized controlled trials. Br J Surg 1998; 85: 1232–41. 14. Periti P, Mazzei T, Tonelli F. Single-dose cefotetan vs. multiple-dose cefoxitin--antimicrobial prophylaxis in colorectal surgery. Results of a prospective, multicenter, randomized study. Dis Colon Rectum 1989; 32(2): 121–7. 15. Skipper D, Karran SJ. A randomized prospective study to compare cefotetan with cefuroxime plus metronidazole as prophylaxis in elective colorectal surgery. J Hosp Infect 1992; 21(1): 73–7. 16. Zanella E, Rulli F. A multicenter randomized trial of prophylaxis with intravenous cefepime + metronidazole or ceftriaxone + metronidazole in colorectal surgery. The 230 Study Group. J Chemother 2000; 12(1): 63–71. 17. Mosimann F, Cornu P. Are enemas given before abdominal operations useful? A prospective randomised trail. Eur J Surg 1998; 164(7): 527–30. 18. Hall C, Curran F, Burdon DW, Keighley MR. A randomized trial to compare amoxycillin/clavulanate with metronidazole plus gentamicin in prophylaxis in elective colorectal surgery. J Antimicrob Chemother 1989; 24 (Suppl B): 195–202. 19. Corman M, Robertson W, Lewis T et al. A controlled clinical trial. Cefuroxime, metronidazole, and cefoxitin as prophylactic therapy for colorectal surgery. Complications in Surgery 1993; 12: 37–40. 20. Condon RE, Bartlett JG, Greenlee H et al. Efficacy of oral and systemic antibiotic prophylaxis in colorectal operations. Arch Surg 1983; 118(4): 496–502. 21. Coppa GF, Eng K, Gouge TH, Ranson JH, Localio SA. Parenteral and oral antibiotics in elective colon and rectal surgery. A prospective, randomized trial. Am J Surg 1983; 145(1): 62–5. 22. Portnoy J, Kagan E, Gordon PH, Mendelson J. Prophylactic antibiotics in elective colorectal surgery. Dis Colon Rectum 1983; 26(5): 310–13.

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improved outcomes in colon and rectal surgery 23. Lau WY, Chu KW, Poon GP, Ho KK. Prophylactic antibiotics in elective colorectal surgery. Br J Surg 1988; 75(8): 782–5. 24. Schoetz DJ Jr, Roberts PL, Murray JJ, Coller JA, Veidenheimer MC. Addition of parenteral cefoxitin to regimen of oral antibiotics for elective colorectal operations. A randomized prospective study. Ann Surg 1990; 212(2): 209–12. 25. Stellato TA, Danziger LH, Gordon N. Antibiotics in elective colon surgery. A randomized trial of oral, systemic, and oral/ systemic antibiotics for prophylaxis. Am Surg 1990; 56(4): 251–4. 26. Hewitt J, Reeve J, Rigby J, Cox AG. Whole-gut irrigation in preparation for large-bowel surgery. Lancet 1973; 2(7825): 337–40. 27. Food and Drug Administration, HHS. Drug labeling; sodium labeling for over-the-counter drugs. Final rule. Fed Regist 2004; 69(228): 69278–80. 28. Zmora O, Mahajna A, Bar-Zakai B. Colon and rectal surgery without mechanical bowel preparation: a randomized prospective trial. Ann Surg 2003; 237(3): 363–7. 29. Beck DE, Fazio VW. Current preoperative bowel cleansing methods. Results of a survey. Dis Colon Rectum 1990; 33(1): 12–5. 30. Brownson P, Jenkins SA, Nott D, Ellenbogen S. Mechanical bowel preparation before colorectal surgery: results of a prospective randomized trial. Br J Surg 1992; 79: 461–2. 31. Burke P, Mealy K, Gillen P et al. Requirement for bowel preparation in colorectal surgery. Br J Surg 1994; 81(6): 907–10. 32. Santos JC Jr, Batista J, Sirimarco MT, Guimarães AS, Levy CE. Prospective randomized trial of mechanical bowel preparation in patients undergoing elective colorectal surgery. Br J Surg 1994; 81(11): 1673–6.

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33. Miettinen RP, Laitinen ST, Mäkelä JT, Pääkkönen ME. Bowel preparation with oral polyethylene glycol electrolyte solution vs. no preparation in elective open colorectal surgery: prospective, randomized study. Dis Colon Rectum 2000; 43(5): 669–75; discussion 675–7. 34. Zmora O, Mahajna A, Bar-Zakai B et al. Is mechanical bowel preparation mandatory for left-sided colonic anastomosis? Results of a prospective randomized trial. Tech Coloproctol 2006; 10(2): 131–5. 35. Fa-Si-Oen P, Roumen R, Buitenweg J et al. Mechanical bowel preparation or not? Outcome of a multicenter, randomized trial in elective open colon surgery. Dis Colon Rectum 2005; 48(8): 1509–16. 36. Bucher P, Gervaz P, Soravia C et al. Randomized clinical trial of mechanical bowel preparation vs. no preparation before elective left-sided colorectal surgery. Br J Surg 2005; 92(4): 409–14. Erratum in: Br J Surg 2005; 92(8): 1051. 37. Ram E, Sherman Y, Weil R, et al. Is mechanical bowel preparation mandatory for elective colon surgery? A prospective randomized study. Arch Surg 2005; 140: 285–288. 38. Conrad JK, Ferry KM, Foreman ML et al. Changing management trends in penetrating colon trauma. Dis Colon Rectum 2000; 43(4): 466–71. 39. Guenaga KF, Matos D, Castro AA, Atallah AN, WilleJørgensen P. Mechanical bowel preparation for elective colorectal surgery. Cochrane Database Syst Rev. 2003; 2: CD001544. Review. Update in: Cochrane Database Syst Rev 2005; 1: CD001544. 40. Jung B, Påhlman L, Nyström PO, Nilsson E. Mechanical bowel preparation study group. Multicentre randomized clinical trial of mechanical bowel preparation in elective colonic resection. Br J Surg 2007; 94(6): 689–95.

3

Anesthesia and intraoperative positioning Lebron Cooper and Larry R Hutson

challenging case A 47-year-old male is undergoing a transanal excision of a rectal ­villous adenoma under intravenous sedation and local infiltration of xylocaine. During the procedure the patient complains of lightheadedness and numbness of the tongue. The anesthesiologist notices bradycardia and hypotension. case management Xylocaine toxicity is suspected. The patient should be moved to the supine position and supported with supplemental oxygen via mask. The patient’s blood pressure is supported with intravenous fluid and epinephrine. introduction The American Society of Anesthesiologists (ASA) defines anesthesiology as a discipline within the practice of medicine that specializes in the (1) medical management of patients who are rendered unconscious and/or insensible to pain and emotional stress ­during surgical, obstetric, and certain other medical procedures; (2) protection of life functions and vital organs under the stress of anesthetic, surgical, and other medical procedures; and (3) management of problems in pain relief (1). In this chapter, we will be discussing the various kinds of anesthesia used in the operating room for colorectal surgery, including their relative benefits and risks. Additionally, we will be discussing new treatments for postoperative pain relief, as well as one of the more visible risks of anesthesia—awareness under anesthesia. We will also discuss the new Surgical Care Improvement Project (SCIP), including prophylactic antibiotic administration within 1 hour of surgical incision, and the proper positioning and padding of patients for colorectal surgery. anesthesia Local Anesthesia The earliest local anesthetic used was cocaine (prepared in weak solutions and injected in high volumes) for field block at the turn of the 19th century.(2) However, the toxicity of cocaine, its irritant properties, and its strong potential for physical and psychological dependence led to the development of alternative local anesthetics. Many of these—such as lidocaine—are still used today, as much as half a century after their introduction.(3) While there are relatively few instances in colorectal surgery where it is used as the sole anesthetic, local anesthesia still has a place. It requires, however, a cooperative patient who can remain immobile for both the infiltration of the local anesthetic, as well as for the actual procedure itself. It is important to be cognizant of the patient’s underlying health status and the position that the patient will be in for the procedure. A healthy patient in their mid-20s can tolerate the prone jack-knife position much better than an obese geriatric

patient with a pulmonary history who uses supplemental oxygen. Bear in mind that while the patient may only be receiving local anesthesia in an office setting, the patient may be under self-administered mild sedation. Any degree of sedation blunts the body’s response to hypoxia and hypercarbia, and while a restless patient may ­simply be a restless patient, there is always the possibility that the patient is agitated due to relative hypoxia or hypercarbia. One must always keep in mind the possibility of local anesthetic toxicity when using these drugs. The typical doses used for local infiltration in colorectal procedures are far below the threshold needed for systemic toxicity (Table 3.1). However, accidental intravenous or intraarterial injection could result in systemic toxicity. As such, it is important to recognize the signs and symptoms of systemic toxicity when they first appear, as toxicity progresses in a dose-dependent fashion. At lower plasma concentrations, the patient begins to experience central nervous system (CNS) toxicity characterized by lightheadedness, tinnitus, and numbness of the tongue. As plasma concentrations increase, the patient begins to experience CNS excitation, resulting in seizures, followed by unconsciousness, coma, and ­respiratory arrest. At higher plasma concentrations, cardiovascular (CV) toxicity occurs, as the local anesthetic blocks sodium channels of the myocardium. Relative potency of the local anesthetic plays a role here. Lidocaine toxicity will result in bradycardia and hypotension before cardiac arrest, while the longer acting, more potent bupivicaine often results in sudden cardiovascular collapse due to ventricular dysrhythmias. Maintenance of perfusion and ventilation through prolonged cardiopulmonary resuscitation (CPR) is the key, as the patient will not convert into a life-sustaining cardiac rhythm until the local anesthetic has had a chance to completely dissociate from the sodium channels of the conducting system of the heart. Cardiopulmonary bypass may even be considered. Dissociation of local anesthetic from sodium channels has been shown to take a considerable length of time, and prolonged, intensive, and continuous support is warranted. Table 3.1  Local anesthetic drugs. Agent

Onset

Duration

Maximum Dose

Tetracaine

30 seconds

30–60 minutes

400 mg

Lidocaine

2–5 minutes

30–45 minutes

5 mg/kg

Mepivacaine

7–15 minutes

2.5 hours

400 mg

Prilocaine

2 minutes

2.5 hours

80 mg

Bupivicaine

30 minutes

2 hours

2 mg/kg

Procaine

5–10 minutes

15–30 minutes

10 mg/kg

Maximum Dose with Epinephrine

7 mg/kg

4 mg/kg



improved outcomes in colon and rectal surgery Treatment of CNS toxicity, including the cessation of seizure activity, is with the use of benzodiazepines, propofol, or thiopental. Treatment of CV toxicity is supportive in nature, and may require electric cardioversion, epinephrine, and magnesium.(4) Systemic toxicity following local anesthetic administration is thankfully rare. More common, however, is inadequate analgesia following local anesthetic infiltration. This can be multifactorial in nature. Inadequate analgesia resulting from insufficient quantities placed in the correct location is easily resolved with the addition of further local anesthetic at the site. Inadequate analgesia can also result from tachyphylaxis to local anesthetics, which is defined as repeated injection of the same dose of local anesthetic leading to diminishing efficacy. Additionally, inadequate analgesia can be a consequence of the tissue pH into which the local anesthetic is injected. Local anesthetics exist in both an ionized and nonionized state; it is only in the nonionized state that local anesthetics can penetrate the nerve sheath, thus producing analgesia. In an acidic environment (i.e., an infected pilonidal cyst), more of the anesthetic is converted into the ionized state, leading to far less of the nonionized form available to produce analgesia. It is not uncommon for infected tissues to prove nearly impossible to be rendered totally insensitive despite more than adequate amounts of local anesthetic infiltration. A perianal block (Figure 3.1) can be performed with the patient in either the prone or lithotomy position and provides relaxation of the sphincter as well as anesthesia. The anesthetic solution of choice is infiltrated in a fan fashion from the lateral positions to superficially encompass the anal margin. Emphasis should be placed in the posterolateral positions where the greatest concentration of nerves is found. A finger or retractor is placed within the canal. At the anterior, posterior, and lateral positions anesthetic is injected submucosally or intramuscularly through the previously infiltrated tissue. The needle is held parallel to the finger, with care to avoid entering the canal. Monitored Anesthetic Care (MAC) MAC is defined by the ASA as “a procedure in which an anesthesiologist is requested or required to provide anesthetic services,” and includes (1) the diagnosis and treatment of clinical problems during and immediately following the procedure; (2) the support of vital functions; (3) the administration of sedatives, analgesics, hypnotics, anesthetic drugs, or other medications necessary for patient safety; (4) physical and psychological comfort; and (5) the provision of other services as needed to complete the procedure safely (5). When it comes to the care of a patient undergoing MAC, all of the precautions and equipment needed to perform a safe general anesthetic must be present, as it is always possible that an escalation of care will be needed. While uncommon, it is possible that a patient cannot safely undergo a MAC for a specific procedure. Most commonly this is due to the inability to safely prevent a patient from moving in response to painful stimuli without producing oversedation and/or apnea. Some patients, when undergoing MAC, tend to have no middle ground between moving in response to stimuli and airway obstruction or complete apnea, requiring intervention by the anesthesiologist. The same limits of positioning and patient tolerance that were discussed with local anesthetics apply to procedures under MAC



(a)

(b)

Figure 3.1  Technique for anal block. (A) perianal view of submucosal injection. (B) saggital view of injection of anal canal.

as well. While most patients will be able to tolerate a lithotomy or prone position without problem, there are some patients who are unable to tolerate these positions without endotracheal intubation, positive pressure ventilation, and high oxygen concentrations. Additionally, there are those patients who are unable to understand or comply with the requirement that they must remain immobile. Young children, mentally challenged, or extremely ill patients are prime examples of poor candidates for MAC. There is an erroneous perception on the part of patients—and even physicians—that a patient undergoing MAC is at decreased

anesthesia and intraoperative positioning risk for serious anesthesia-related complications when compared to general anesthesia, that MAC is safer. This can best be appreciated by examining the ASA Closed Claims Project database. The ASA Closed Claims Project is a structured evaluation of all adverse anesthetic outcomes obtained from the closed claim files of 35 professional liability insurance companies in the United States. A 2006 review showed more than 40% of claims associated with MAC involved death or permanent brain damage, which was similar to the percentage seen in claims associated with ­general anesthesia. Respiratory depression was the most common (21%) damaging mechanism, nearly half of which were judged to be preventable through better monitoring. Cardiovascular events comprised another 14% of the claims made in patients undergoing MAC, which was similar in frequency to that seen following general anesthesia. The average payment made to a plaintiff in these cases was $159,000 (U.S.).(6) So, while we would like to think that MAC is safer than a general anesthetic for patients, in fact the risk of significant injury and death are ­similar between the two anesthetic types. Regional Anesthesia Central Neuraxial Blockade Regional anesthesia encompasses a wide variety of peripheral and central neuraxial blocks, many of which do not pertain to colorectal surgery. The most common regional anesthesia technique applied in colorectal surgery is the spinal, or intrathecal, blockade. The spinal block is relatively easy to place, has a fast onset of sensory and motor blockade, and has a predictable length of efficacy. This is a very old technique, dating back to the late 1800s, when it was performed using cocaine as the anesthetic agent, to great amazement of surgeons of the day.(2) With the advent of newer local anesthetics, we can now tailor the duration of the spinal blockade to the projected length of the surgery by varying the type and amount of local anesthetic used. The goal is to provide adequate analgesia for the duration of the procedure, yet allowing safe ambulation and encouraging urination within a short time frame after cessation of surgery. There are three different densities of the medications used: hyperbaric, isobaric, and hypobaric. Hypobaric local anesthetics are less dense than normal cerebrospinal fluid (CSF), which allows these medications to rise in the CSF following injection. This is commonly used for perineal procedures that will be performed in the prone jack-knife position. The local anesthetic is injected into the intrathecal space, and the patient is immediately placed in the jack-knife position to allow the hypobaric solution to drift upward, or caudad. After approximately 5 minutes, the spinal anesthetic will have “set up”, meaning the uptake and distribution of the local anesthetic across nerve membranes has occurred. No further migration of the drug should occur at this point. By adding a small amount of glucose to the local anesthetic used, the solution will become hyperbaric. The density of the solution will cause it to sink in relation to the CSF.(7) An alternative approach to perineal analgesia performed in the prone jack-knife position is performing the intrathecal block using a hyperbaric solution, then keeping patients in the sitting position for 5 minutes to allow the spinal anesthetic to sink caudad, thus blocking the ­lumbosacral nerves. Once the block has “set up,” the patient is placed in the

prone jack-knife position. These two techniques have allowed the use of significantly less local anesthetic for the spinal anesthesia, compared to isobaric solutions, which have the same density as CSF. Isobaric solutions require a higher dose of local anesthetic to evenly distribute throughout the CSF, resulting in a larger volume needed to achieve the same blockade of the lumbosacral nerves. The benefits related to reducing the total amount of local anesthetic injected are a decreased risk of toxicity, along with providing adequate analgesia,and allowing faster recovery of motor function. A caudal anesthetic is the placement of a local anesthetic and/ or narcotic into the epidural space from an approach through the sacral hiatus. This is typically performed in either the prone or lateral position. While uncommon in adults, this procedure is used frequently in children, where the caudal space is more easily accessible and a relatively safe and easy approach to infuse local anesthetic and/or narcotic for postoperative analgesia while still under general anesthesia. The third and final type of central neuraxial block is the ­epidural anesthetic. While epidural anesthesia can be used as the sole anesthetic for colorectal procedures, it is more common to place a catheter within the epidural space to provide analgesia during and after the procedure. The location of the block is determined by the anesthesiologist based on several anatomic factors; however, a thoracic approach has been shown to be more effective in reducing postoperative ileus and early return of bowel and bladder function than a lumbar approach.(8) Most commonly, patients will receive a postoperative continuous infusion of a local anesthetic and narcotic mixture through the epidural catheter. In addition, they may be given the opportunity to provide themselves small amounts of analgesia through their epidural catheter on demand. This is termed patient-controlled epidural analgesia (PCEA), and it provides excellent pain control while minimizing the undesirable side effects typically seen with intravenous narcotics. Provided the patient does not manifest signs of systemic infection, the epidural catheter can remain in place for several days following surgery if needed to control pain. This benefit must be weighed against the risk of withholding anticoagulant prophylaxis and a possible resultant thromboembolic event. While initial studies examining PCEA were performed using lumbar epidural, more recent studies have examined the impact of thoracic epidural analgesia on patients undergoing elective colorectal surgery. In a study in 2001, Carli et al. reported 42 patients undergoing open large bowel resection, randomized to receive either an intravenous Patient Controlled Analgesia (ivPCA) morphine or a thoracic (T7-8) epidural with bupivicaine and fentanyl. Patients who received thoracic epidural had distinctly superior analgesia as compared to the ivPCA morphine group; time to first flatus and first bowel movement occurred, on average, 36 hours sooner in the epidural group, and time to readiness to discharge was the same in both groups.(8) In 2007, Taqi et al. examined thoracic epidural analgesia compared to postoperative intravenous morphine for laparoscopic colectomy. Recovery from postoperative ileus occurred sooner in the epidural group by 1 or 2 days, and a full diet was resumed earlier. The epidural group experienced significantly less pain at rest, with coughing, and with ambulation.(9) These studies demonstrate the effectiveness of thoracic epidural analgesia and its superiority in allowing early return of

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improved outcomes in colon and rectal surgery bowel function, ability to resume a full diet, and early ambulation, as compared to intravenous narcotics. All three of these techniques—spinal, caudal, and epidural— have one thing in common: contraindications. Specifically, absolute contraindications to neuraxial techniques include patient refusal, infection at the planned site of needle puncture, elevated intracranial pressure, and bleeding diathesis. There are also several relative contraindications. Bacteremia raises the concern that the needle puncture site of the neuraxial block might allow an epidural abscess or meningitis to develop; however, a clinical scenario may exist where the need to avoid a general anesthetic might outweigh the small risk of such occurring. While chronic back pain is not a contraindication to neuraxial techniques, patients with underlying neurological disease should be considered carefully, as neuraxial blockade might exacerbate their condition, such as in multiple sclerosis. The presence of cardiac disease also indicates that caution should be applied, as patients who receive a neuraxial block typically experience a sudden decrease in lower extremity vascular tone, leading to rapid vasodilation and a significant decrease in systemic vascular resistance. The resultant precipitous drop in systolic and diastolic blood pressure can be extremely dangerous, or even deadly, in patients with severe coronary artery disease, aortic stenosis, and idiopathic hypertrophic subaortic stenosis (IHSS). It is still arguable whether the presence of IHSS or aortic stenosis is an absolute contraindication to neuraxial blockade, and many centers avoid them in the presence of these coexisting morbidities. The final relative contraindication is abnormal coagulation status. Patients with abnormal coagulation—either due to endogenous factors such as liver disease or thrombocytopenia, or due to the administration of anticoagulants—must be considered carefully. Additionally, patients who are receiving or will be receiving anticoagulants postoperatively have different needs than patients who receive a general anesthetic alone. For spinal and caudal anesthesia, the greatest risk of spinal hematoma (a neurosurgical emergency) occurs at the time the block is placed. For epidural anesthesia, the risk of hematoma formation is just as great at the time of epidural catheter removal as during placement. As a result, certain guidelines should be instituted in order to reduce the risk of spinal hematoma formation upon removal of the epidural catheter. Heparin is often administered perioperatively as prophylaxis against deep vein thrombosis formation. While the effect of intravenous heparin administration is immediate, subcutaneous administration requires 1–2 hours to effect a change on coagulation. Small doses of heparin administered before surgery for DVT prophylaxis are not a concern in terms of risk of spinal hematoma formation.(10) Postoperatively, subcutaneous DVT prophylaxis dosing twice daily of heparin while an epidural catheter is in place is acceptable. The catheter is removed 2 hours before the next heparin dosing to maximize safety. Therapeutic heparin, however, is a different matter. Ruff et al. demonstrated that neuraxial procedures performed <1 hour after heparin therapy is discontinued resulted in a 25-fold increase in spinal hematoma.(11) The effect is even more pronounced if the patient also received aspirin. Low-molecular weight heparin (LMWH) was introduced in 1993 as an alternative to heparin prophylaxis for prevention of

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DVT. There have been numerous reports of spinal hematoma in patients receiving LMWH with a neuraxial blockade. For patients receiving low-dose LMWH for thromboprophylaxis preoperatively, it is recommended that neuraxial anesthesia occur at least 12 hours after the last dose. In patients who are receiving highdose LMWH, neuraxial anesthesia should be delayed for 24 hours after the last dose. Postoperatively, the typical prophylactic twicedaily dosing of LMWH should only begin 24 hours after the neuraxial block, and any epidural catheter should be removed before initiation of twice-daily dosing. Once-daily thromboprophylactic dosing, however, can safely occur with an epidural catheter in place, provided that the first dose occurs at least 8 hours following the initial blockade and that any epidural catheter is removed 12 hours after the last dose before its removal.(12) Warfarin therapy is another concern. Warfarin anticoagulation must be stopped 4–5 days before surgery, and the PT/INR assessed before surgery. Anticoagulation with warfarin can be used for thromboprophylaxis in patients with an indwelling ­epidural catheter, though the catheter should be removed while the INR is still <1.5. Typically, this is approximately 36 hours following the initial administration of warfarin. Neurologic and motor testing should be routinely performed on these patients.(12) All three of the neuraxial techniques have possible side effects. Patients can become hypotensive, as their systemic vascular resistance decreases. This is due to the sympathectomy caused by blockade of sympathetic fibers along the thoracic sympathetic chain. Rarely, patients can develop an unintentionally high spinal anesthetic, leading to bradycardia, apnea, and even loss of consciousness. This “high spinal” must be treated as a general anesthetic, with immediate securing of the airway with endotracheal intubation and supportive therapy until the local anesthetic is metabolized. Some patients can experience mild back pain at the site of needle placement, especially when multiple attempts are needed to place the block. Post Dural Puncture Headache (PDPH) can occur, typically following inadvertent dural puncture with an ­epidural needle—a ‘wet tap’. These headaches are characterized by a slow leak of CSF from the puncture, leading to a headache that is strongest when standing and lessened when lying. They are often treated conservatively with oral fluid therapy, oral caffeine, and remaining recumbent. Should there be no relief after a couple of days of conservative treatment, an epidural blood patch can be performed. 20 mL of sterile, autologous blood is injected into the epidural space, resulting in thrombus formation, sealing of the dura, and cessation of CSF leak. If the diagnosis of PDPH is correct, there is typically immediate relief of symptoms. Epidural abscess and meningitis are possible if proper sterile technique is not used, or if systemic infection is present.(7) Transversus Abdominis Plane (TAP) Block The TAP block is a relatively new procedure for blocking the abdominal wall afferent nerves by way of the lumber triangle of Petit. It can be performed using a landmark technique or under ultrasound guidance; 20 mL of 0.375% of bupivicaine or ­levobupivicaine is then injected into the transversus abdominis neurofascial plane.(13, 14, 15) In a prospective, randomized controlled trial, McDonnell et al. reported patients undergoing

anesthesia and intraoperative positioning large bowel resection who received the TAP block required 75% less morphine in the first 24 hours, and had significantly lower pain scores at all time points over the first 24 hours. Additionally, these patients experienced significantly less postoperative nausea and vomiting.(13) This is an excellent block for patients having smaller abdominal procedures, e.g., ventral hernia repair, on an outpatient basis. Ilioinguinal and Iliohypogastric Nerve Block These are field blocks of the terminal branches of the lumbar plexus, primarily from the L1 root. These blocks are relatively simple to perform and provide anesthesia in the inguinal and genital region. A 22-gauge needle is inserted 3 cm medial and 3 cm inferior to the anterior superior iliac spine, in a cephalolateral direction through the abdominal muscles until contact is made with the iliac bone. As the needle is removed, local anesthetic solution is injected. This is repeated 1–2 more times to cover a fan-shaped area, for a total of approximately 10–20 mL of local anesthetic.(16) Awareness Under Anesthesia Awareness under anesthesia is a rare complication of anesthesia, but one which has risen to prominence in the public eye recently. Studies of large numbers of patients in Sweden demonstrated an overall incidence of 0.16%.(17) One can imagine that this would be a distressing event; the frequency of posttraumatic stress disorder (PTSD) in the 2 years following an incident of awareness under anesthesia approached 50%, even if the patient was not initially distressed by the incident. A similarly large study in the United States found an overall incidence rate for confirmed intraoperative awareness of 0.13%, and a rate of 0.24% of possible awareness.(18) It has long been known that awareness occurs with greater frequency in emergent trauma surgery cases, cases involving ­cardiopulmonary bypass, and emergency caesarean sections. These are situations where patients may experience significant hypotension, requiring a reduction in volatile anesthetic agents below the level that ensures amnesia. If there is a question whether a patient has had an episode of awareness under anesthesia, it is imperative the anesthesiologist be contacted, and the patient reassured. Psychiatric evaluation is usually necessary to help the patient deal with the potentially ­distressing nature of this complication. A device available that attempts to determine the depth of consciousness is the bispectral index (BIS), a monitor of anesthetic depth approved by the Food and Drug Administration in the United States. The frontal EEG is measured, processed using proven ­algorithms, and reported on an arbitrary scale of 0–100. A total of 100 equates to completely awake and responsive, and zero represents complete electrical silence of the brain. A BIS of <60 is generally considered a safe level to ensure adequate depth of anesthesia and lack of awareness under anesthesia. In the B-Aware trial, patients at high risk for awareness under anesthesia were randomized to two groups, either routine care or a BIS-guided anesthetic. While the incidence of awareness among even high-risk patients was very low, the BIS-guided group had a reduced risk of awareness by 82%.(19) However, there is controversy surrounding the reliability of the BIS monitor. Use of the BIS monitor and maintenance within the

proper depth of anesthesia (as indicated by the BIS algorithm) is still no assurance that the patient will not have an episode of awareness, as there are numerous reports to the contrary.(20) Additionally, there are numerous conditions that can influence the BIS, causing BIS levels that are paradoxically high, such as ketamine administration or the use of halothane, or paradoxically low, such as following nitrous oxide termination.(21) An analysis of the ASA Close Claims Project database demonstrates that between the years of 1961 and 1995 there were 79 claims for awareness made in the United States; 18 claims for awake paralysis, i.e., the inadvertent administration of a muscle relaxant to an awake patient, and 61 claims for recall under general anesthesia, i.e., recall of events while receiving general anesthesia. Most of the claims for awake paralysis represented substandard care; less than half of the claims for recall were the result of substandard care. The majority of patients experienced temporary emotional distress; 10% of patients were later diagnosed with PTSD. The awareness of sound without pain was the most common intraoperative event; 21% of patients experienced pain while aware under anesthesia.(22) positioning Supine This is the most common surgical position; it results in the least hemodynamic and ventilatory changes and is frequently the best position for surgical exposure. The supine position is not perfect, of course, as it creates certain pressure points that, given time, result in ischemia over certain bony prominences, such as the heels, sacrum, and back of the head. The head should rest on a soft support to spread the pressure, decreasing the incidence of pressure points, thus preventing alopecia. Particular care must be given to the arms, including careful padding of the elbows and wrists. Abduction of the arms must not exceed 90 degrees from the body to prevent compromising blood flow to the distal arm. (23) Trendelenburg positioning while supine has several anesthetic implications, as it causes the diaphragm to move cephalad, causing increased airway pressures and possibly advancing the endotracheal tube into an endobronchial position. Shoulder braces are sometimes used to prevent the patient from sliding off the table during extreme Trendelenburg positioning, though this can cause injury by compressing the brachial plexus. (24) The most common upper extremity injury is to the ulnar nerve, which is 3 times more likely in men who undergo general anesthesia. This seems to occur despite padding of the extremity.(25) Other nerves at risk due to positioning are illustrated in Figure 3.2. Prone Even when a procedure is planned in the prone position, induction of general anesthesia and intubation of the trachea should occur in the supine position. The patient is then turned prone, taking care to keep the cervical spine and head in-line with the rest of the body. There are several different pillow types that allow for proper positioning of the head in a neutral position with the remainder of the body, while keeping the eyes, nose, and chin free from pressure.

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improved outcomes in colon and rectal surgery side of the body in a neutral position, with careful padding of the elbows to prevent injury. Alternatively, the arms can be positioned along side the head, taking care that the arms are not abducted >90 degrees to prevent injury to the brachial plexus.(23, 24) Great care must be taken to not inadvertently dislodge the endotracheal tube while prone, as it is exceedingly difficult to reintubate or mask ventilate a patient in the prone position. Lateral Decubitus Just as with prone positioning, it is imperative that the head be kept in a neutral positioning while turning the patient. Additionally, extra cushioning is needed under the head to keep the cervical and thoracic spines in line. An axillary roll needs to be placed just caudad to the dependent axilla in order to prevent compression injuries to the brachial plexus. It should not be placed in the axilla, as the purpose is for the weight of the thorax to be borne by the chest wall. The dependent arm is extended perpendicular to the body on a padded armboard, while the nondependent arm is similarly extended on an armrest suspended in such a way that the arm is not abducted >90 degrees from the body. Additionally, the arm should not be raised superior to the level of the deltoid. A pillow or cushion should be placed between the knees.(23, 24)

Figure 3.2  Nerves at risk for injury during positioning for a surgical procedure.

There is a low, but significant risk that pressure on the eye or surrounding orbit will lead to increased intraocular pressure, decreased retinal artery blood flow, and resultant blindness, if the intraocular pressure exceeds systemic pressure. Although this is a rare complication associated with the prone position, it is ­nevertheless, devastating. Extreme care must be taken to avoid this life-changing occurrence. The thorax should be supported with chest rolls that extend from the clavicle to the iliac crest. The arms can be placed at the

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Lithotomy The lithotomy position is very common in colorectal surgery. The hips are flexed 80–100 degrees from the trunk, and the legs are abducted 30–45 degrees from midline. It is important that the legs always be moved simultaneously to prevent lumbar spine torsion, and that the legs be carefully padded to reduce the risk of injury. In a retrospective review of patients undergoing surgery in the lithotomy position, Warner et al. found that the most common lower extremity nerve injury was to the common peroneal nerve, accounting for 78% of nerve injuries. It was postulated that the cause was compression of the nerve between the leg support and the lateral head of the fibula.(26) While rare (1 in 8,720), the incidence of compartment ­syndrome of the lower extremities is markedly higher in the lithotomy position than all other surgical positions. Compartment syndrome occurs when high tissue pressure builds within the closed space of the anterior compartment. Ischemia of the tissue in the compartment results in edema of the interstitium, thereby raising compartment pressure. Since perfusion is dependent on compartment pressure being lower than mean arterial pressure to allow tissue perfusion, any situation where increased compartment pressure and/or decreased arterial flow into the tissue can result in ischemia. The result is capillary endothelial damage and even greater interstitial edema. Unfortunately, it is not completely understood why some patients develop a compartment syndrome, while others do not. As a result, no safe maximum time limit can be defined. (27) Early diagnosis and treatment with fasciotomy is imperative. Analysis of closed claims in cases of compartment syndrome due to the lithotomy position during colorectal surgery demonstrated an average indemnity payment of $426,000. Great care must be taken in the positioning and padding, as patients themselves cannot express any pain or discomfort they may be experiencing while under general or regional anesthesia.

anesthesia and intraoperative positioning surgical care improvement project Process and Outcome Measures The Surgical Care Improvement Project (SCIP) of the United States is a national quality initiative involving the American Society of Colorectal Surgeons, the American College of Surgeons, the American Society of Anesthesiologists, the American Hospital Association, the Association of Perioperative Registered Nurses, and a host of governmental agencies dedicated to improvement in healthcare.(28) The goals of the SCIP partnership are to reduce the incidence of surgical complications by 25% by the year 2010, and to promote the use of evidence-based care processes known to reduce surgical complications. Out of approximately 40 million major operations each year, postoperative complications account for up to 22% of preventable deaths among patients, depending on the complication. These complications accounted for 2.4 million additional hospital days and $9.3 billion (USD) in additional charges each year.(29) SCIP focuses on areas where the incidence and cost of the most common and preventable complications are high:

Surgical Site Infections (SSIs) Adverse Cardiac Events Venous Thromboembolism Postoperative Pneumonia

Although not limited to anesthesia care, the anesthesiologist and colorectal surgeon must partner in attempts to meet the expectations set by the national SCIP initiative. One such initiative is the administration of prophylactic antibiotics within 1 hour of surgical incision. Although not typically considered “anesthetic agents”, antibiotics may best be given within 1 hour of incision if administered by the anesthesia provider. Frequent operating room and turnover delays may result in an antibiotic administration well-before the 1 hour limit if given by in the preoperative holding area. Late patient arrivals for same-day admit surgery or administrative paperwork delays may result in inadequate or insufficient time to infuse the antibiotic before going to the operating room (OR), with the result of no antibiotic being given or being given only if the “missed dose” is noticed by someone in the OR. Although no longer reportable as public information, prophylactic antibiotic selection for surgical patients is monitored, as is discontinuation of the antibiotic within 24 hours after the surgery end time (48 hours for cardiac surgery patients). If an antibiotic if felt to be needed beyond the allowed 24 hours, the colorectal surgeon must document, in the medical record, the reason for the continuation of the antibiotic. Another SCIP initiative that is frequently met or monitored by the anesthesiologist is perioperative beta blockade. By having patients see an anesthesiologist preoperatively for assessment and clearance for anesthesia, the anesthesiologist can begin beta blockers on all patients who are not already on them. Venous thromboembolism was discussed above, and involvement of the anesthesiologist and associated regional anesthesia play a significant role here. As previously mentioned, an epidural catheter must be removed at an appropriate time surrounding the initiation and discontinuation of heparin, LMWH, or warfarin.

The risks of inadequate venous thromboembolism prophylaxis must be weighed against the benefits of regional anesthesia for colorectal surgical patients. Postoperative pneumonia is a complication where the cause is multi-factorial. Ventilator management and weaning protocols for patients requiring postoperative mechanical ventilation may fall under the purview of the anesthesiologist. conclusion Although the sum total of anesthesia practice can hardly be related in a textbook chapter, we have attempted in the preceding pages to highlight areas in anesthesia practice of which the colorectal surgeon should be aware. Improved patient satisfaction through reduction of postoperative pain, earlier ambulation, and quicker return of bowel function and diet will have a marked impact on surgical outcomes. Thoracic epidural anesthesia/analgesia is becoming a standard for many colorectal surgical procedures, whether as the sole anesthetic, or in conjunction with general anesthesia. Awareness under anesthesia is a rare, but serious concern, highlighted more recently in the media and receiving much greater appreciation among surgical patients. Supportive care, including psychological counseling may improve outcome and reduce the incidence of posttraumatic stress disorder. Oversedation resulting in hypoventilation, hypoxemia, and hypercarbia can produce devastating results. Extreme caution must be given to the patient who is restless, but sedated. Loss of airway is the ultimate disaster under general anesthesia, and is a surgical, as well as anesthetic, emergency. Proper positioning requires the vigilance of the anesthesia provider, the colorectal surgeon, and the operating room nurses. Severe nerve injuries can generally be avoided with the use of padding. Although even with appropriate padding, there is an increased incidence of neurologic injury with the use of stirrups in the lithotomy position. Extra care must be taken of the patient in the prone position, as neck injuries from improper turning, endotracheal tube dislodgement, or perioperative blindness from periorbital pressure can all result in devastating outcomes. Partnership of the surgeon and the anesthesiologist may help improve outcomes, reduce surgical site infections, improve perioperative cardiac morbidity and mortality, and reduce the incidence of venous thromboembolism. Whether in the office setting, outpatient center, or surgical hospital, safe anesthesia practice is paramount. references   1. Stoelting RK, Miller RD. Scope of Anesthesia Practice in Basics of Anesthesia. Fifth Edition. Philadelphia: Churchill Livingstone Elsevier, 2007: 11.   2. Hutson LR, Vachon CA, Dr. Rudolph M. Innovator and pioneer in anesthesiology. Anesthesiology 2005; 103(4): 885–9.   3. Stoelting RK, Miller RD. Local Anesthetics in Basics of Anesthesia. Fifth Edition. Philadelphia: Churchill Livingstone Elsevier, 2007: 123–34.   4. Barash PG, Cullen BF, Stoelting RK et al. Local Anesthetics in Clinical Anesthesia. Fifth Edition. Philadelphia: Lippincott Williams & Williams, 2006: 449–67.

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improved outcomes in colon and rectal surgery   5. Stoelting RK, Miller RD. Choice of Anesthetic Technique in Basics of Anesthesia. Fifth Edition. Philadelphia: Churchill Livingstone Elsevier, 2007: 178–84.   6. Bhananker SM, Posner KL, Cheney FW et al. Injury and liability associated with monitored anesthesia care: a closed claims analysis. Anesthesiology 2006; 104: 228–34.   7. Stoelting RK, Miller RD. Spinal and Epidural Anesthesia in Basics of Anesthesia. Fifth Edition. Philadelphia: Churchill Livingstone Elsevier, 2007: 241–71.   8. Carli F, Phil M, Trudel JL et al. The effect of intraoperative thoracic epidural anesthesia and postoperative analgesia on bowel function after colorectal surgery. Dis Colon Rectum 2001; 44(8): 1083–9.   9. Taqi A, Hong X, Mistraletti G et al. Thoracic epidural analgesia facilitates the restoration of bowel function and dietary intake in patients undergoing laparoscopic colon resection using a traditional, nonaccelerated, perioperative care program. Surg Endoscopy 2007; 21: 247–52. 10. Liu SS, Mulroy MF. Neuraxial anesthesia and analgesia in the presence of standard heparin. Reg Anesth Pain Med 1998; 23: 157–63. 11. Ruff RL, Dougherty JH. Complications of anticoagulation followed by anticoagulation. Stroke 1981; 12: 879–81. 12. Horlocker TT, Wedel DJ, Benzon H et al. Regional Anesthesia in the Anticoagulated Patient: Defining the Risks (The Second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation) http://www.asra.com/consensus-statements/ RAPM-Anticoagulation.pdf. 13. McDonnell JG, O’Donnell B, Curley G. The analgesic efficacy of transversus abdominis plane block after abdominal surgery: a prospective randomized controlled trial. Anesth Analg 2007; 104(1): 193–7. 14. Rafi AN. Abdominal field block: a new approach via the ­lumbar triangle. Anaesthesia 2001; 56(10): 1021–6. 15. El-dawlatly AA, Thallaj A, Aldohayan A et al. Unilateral US guided TAP block for abdominal surgery. The Internet J Anesthesiology 2006; 16(2). 16. Stoelting RK, Miller RD. Peripheral Nerve Blocks in Basics of Anesthesia. Fifth Edition. Philadelphia: Churchill Livingstone Elsevier, 2007: 273–90.

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17. Sandin RH, Enlund G, Samuelsson P, Lannmarken C. Awareness during anesthesia: a prospective case study. Lancet 2000; 355: 707–11. 18. Sebel PS, Bowdle TA, Ghoneim MM et al. The incidence of awareness during anesthesia: a multicenter United States study. Anesth Analg 2004; 99: 833–9. 19. Myles P, Leslie K, McNeil J, Forbes A, Chan M. Bispectral index monitoring to prevent awareness during anaesthesia: the B-Aware randomised controlled trial. Lancet 2004; 363: 1757–63. 20. Rampersad SE, Mulroy MF. A case of awareness despite an “adequate depth of anesthesia” as indicated by a bispectral index monitor. Anesth Analg 2005; 100: 1363–4. 21. Dahaba AA. Different conditions that could result in the bispectral index indicating an incorrect hypnotic state. Anesth Analg 2005; 101: 765–73. 22. Domino K, Posner KL, Caplain RA, Cheney FW. Awareness during anesthesia: a closed claims analysis. Anesthesiology 1999; 90(4): 1053–61. 23. Barash PG, Cullen BF, Stoelting RK et al. Patient Positioning in Clinical Anesthesia. Fifth Edition. Philadelphia: Lippincott Williams & Williams, 2006: 643–65. 24. Stoelting RK, Miller RD. Positioning and Associated Risks in Basics of Anesthesia. Fifth Edition. Philadelphia: Churchill Livingstone Elsevier, 2007: 291–303. 25. Cheney FW, Domino KB, Caplan RA, Posner KL. Nerve injury associated with anesthesia: a closed claims analysis. Anesthesiology 1999; 90(4): 1062–9. 26. Warner MA, Martin JT, Schroeder DR et al. Lower-extremity motor neuropahty associated with surgery performed on patients in a lithotomy position. Anesthesiology 1994; 81: 6–12. 27. Beraldo S, Dodds SR. Lower limb acute compartment syndrome after colorectal surgery in prolonged lithotomy position. Dis Colon Rectum 2006; 49: 1772–80. 28. “Medicare Quality Improvement Community” website. http://www.medqic.org accessed March 31, 2008. 29. Zhan C, Miller MR. Excess length of stay, charges, and mortality attributable to medical injuries during hospitalization. JAMA 2003; 290: 1868–74.

4

Sepsis Steven Mills and Michael J Stamos

Challenging Case Six days after a low anterior resection with diverting loop ileostomy for rectal cancer, the patient is febrile and has a leukocytosis with a left shift. His vital signs remain stable, but he had a borderline low urine output overnight. case management You increase the patient’s intravenous fluids, start him on broad spectrum antibiotics and obtain a computed tomography scan of the abdomen and pelvis. The study reveals evidence of an anastomotic leak with an associated collection of fluid and gas in the pelvis. After consultation with interventional radiology, the patient undergoes percutaneous drainage with a 7-French pig tail catheter. INTRODUCTION The postoperative patient with sepsis is concerning to any surgeon. There are different causes of sepsis following an operation, from soft tissue infections to intraabdominal infections and pelvic sepsis, not to mention those causes not directly related to the surgical procedure, such as line sepsis, urinary tract infection, or pneumonia. Each can produce a response along a physiologic spectrum, from minimal systemic effects to multisystem organ dysfunction. For the surgeon, knowledge of prevention, identification, and treatment of each type and cause of postoperative sepsis is necessary. Recognizing a postoperative patient in trouble is critical for any surgeon. Changes in certain physiologic parameters may indicate a problem, or may be a normal response to surgery (e.g., tachycardia due to pain). The systemic inflammatory response syndrome (SIRS) is a constellation of findings suggestive of “systemic inflammation” without a defined cause (i.e., either infectious or noninfectious). In contrast, sepsis is this same physiologic response with an identified infectious etiology. A patient with SIRS exhibits two or more of the following: tachycardia, tachypnea, fever, and a leukocytosis.(1) Any patient who qualifies for SIRS by this definition should be carefully evaluated to search for infectious causes of the systemic response, including wound infections, urinary tract infections, pneumonia, abdominal, or pelvic abscesses, etc. As each of these may be treated differently, or indeed, there may be another cause for the patient’s systemic inflammatory response, the surgeon needs to evaluate systematically the patient to determine whether or not any interventions are required. surgical site infections Skin and soft tissue infections are a risk of any operation. The skin functions as a natural barrier to protect our body from invasion by bacteria in the environment. As we violate this protective shield during surgery, a bacterial inoculum occurs at the surgical site, and the host defenses must fight to overcome this bacterial load. Over the past century, surgeons have worked diligently on

methods to decrease the risk of surgical site infections, including improved surgical technique and antimicrobial prophylaxis. If a wound infection does occur, decisions must be made on how appropriately to manage the complication. In an effort to predict the expected risks of infection for a patient before surgery, various scales have been devised to categorize and risk stratify. More recently, some of these same scales have been used to “grade” or trend outcomes. Many of these are based upon a wound classification scale which divides wounds into categories: clean, clean-contaminated, contaminated, and dirty. Predictions of wound infection risk have been based upon this classification. An inclusive classification scheme was devised in 1985 by Haley et al. (2) They described additive factors for wound infection risk which include (in order of importance): abdominal operations, operations >2 hours, contaminated or dirty wounds, and three or more associated medical diagnoses (complicated patients). The lowest risk operations had infection rates of <1% whereas the riskiest procedures carried up to 27% risk of surgical site infection. The National Healthcare Safety Network (NHSN) (formerly known as the National Nosocomial Infections Surveillance (NNIS) System) is regarded as one of the strongest predictors of surgical site infections (SSI).(3) To predict SSI, ASA score, wound class, and surgery duration were evaluated. A “point” is added for each positive category, with cutoffs based upon specific type of surgery being performed (e.g., colon, hepatobiliary, etc.). More recently, the surgical approach has been factored in, with laparoscopic operations having a “point” deducted due to lower risk of infection observed in NHSN’s database. Prophylactic antibiotics given before surgical incision have become standard of care for colon and rectal operations. Most surgeons agree that prophylactic antibiotics will decrease the risk of surgical site infections, though specific choice of agent(s), and their timing and length of use are somewhat more controversial. Nichols et al. described the use of oral antibiotics to decrease the levels of intracolonic bacteria (4) in patients without any intestinal pathology. The same investigative group then followed this with a look at colonic resection and a comparison of mechanical prep alone versus mechanical and oral erythromycin base/neomycin preparation.(5) This study showed a dramatic drop in wound infection rate in the group receiving the oral antibiotics. A followup Veteran’s Administration study (6) showed an improvement from 43% overall septic complications with mechanical bowel prep to 9% with mechanical prep and oral antibiotics. However, with improvements in intravenous antibiotics, the routine use of oral antibiotics has been called into question. In a 2003 survey of members of the American Society of Colon and Rectal Surgeons, 49% felt prophylactic oral antibiotic to be essential, 41% deemed them doubtful and 10% considered oral prophylaxis unnecessary; however, 75% of the surgeons routinely used oral antibiotics, 11% used them selectively and 13% omitted oral prophylaxis. (7) A more recent randomized trial evaluating the efficacy of

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improved outcomes in colon and rectal surgery oral antibiotic prophylaxis in colon surgery (8) compared three oral doses to one oral dose to no oral antibiotics. Patients in all three groups received intravenous cefoxitin before incision and two doses after surgery ended. They found no benefit to the oral antibiotics and indeed found that patients randomized to three doses of oral medications had lower tolerance of the prep. They concluded that there is no benefit to oral antibiotics assuming that appropriate intravenous antibiotics are given. The long-standing practice of mechanical bowel preparations before surgery to decrease the fecal load has also come under closer scrutiny in the past decade. Multiple case series were reported which led to randomized trials in the 1990s and early 2000s. A meta-analysis in 2004 (9) demonstrated in an evaluation of five such randomized trials that mechanical bowel preparation did not improve outcome or decrease the risk of surgical site infection. They concluded that mechanical bowel preparation might be omitted, but that further studies should be performed. A recently published Cochrane Database Review (10) further concluded that there is not good evidence that mechanical bowel preparation reduces the risk of anastomotic and infectious complications. Furthermore, although the data does not support conclusively that mechanical bowel preparation can be deleterious, there is some evidence to that point. All in all, the authors felt that routine mechanical bowel preparation should be reconsidered. A recent multiinstitutional randomized trial also showed similar results, leading the authors to conclude that routine mechanical bowel preparation is unnecessary.(11) Two large multiinstitutional randomized trials recently published also showed similar outcomes between patients receiving bowel preparation and those not receiving one.(12, 13) Close evaluation of the data from these two trials does however raise concern that the lack of a bowel preparation may be deleterious as the rate of abscess and leak (when combined) was higher in the patient group who did not undergo mechanical bowel prep.(14) Further details on bowel preparation are discussed in chapter 2. Some clinicians have advocated using incision protectors to prevent or decrease the amount of contamination of the subcutaneous tissues from both the surrounding skin as well as from enteric organisms during anastomosis formation. One study in the late 1960s gave some hope that draping of the incision with a plastic barrier would decrease wound infection (2.4% vs. 15% without the wound drape).(15) However, subsequent studies over the next decades did not fully support these findings. Nystrom reported a randomized, controlled trial comparing a plastic wound drape to no drape in colorectal surgery patients.(16) They found no improvement in infection rate (9% vs. 10%) by using the wound drape. Indeed, they performed culture swabs of the subcutaneous tissues at the time of surgery in most cases and did not notice any difference in rates of contamination with enteric organisms. Beside preoperative antibiotics and bowel preparation, body temperature and oxygenation may be important in preventing surgical site infection. Kurz et al. showed that in a group of patients undergoing colorectal surgery, there was a higher risk of surgical site infection in patients with lower body temperature (34.7 degrees vs. 36.6 degrees C).(17) However, these findings are somewhat controversial as another group found that there was no relationship between hypothermia and surgical site

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infection in patients undergoing colonic surgery.(18) In terms of tissue oxygenation, many studies have demonstrated lower rates of surgical site infection following colon and rectal surgery in patients receiving inspired oxygen peri- and immediately postoperatively.(19–21) Indeed, in a meta-analysis of randomized trials of immediate postoperative oxygen usage, Chura et al. determined that postoperative oxygen did lower rates of surgical site infection.(22) Despite our best techniques and proper antibiotic prophylaxis, wound infections do still occur. Their exact incidence is hard to gauge given that studies on wound infection incidence have a wide range of results.(6, 23–27) Managing a wound infection properly is important to prevent a relatively small problem from becoming a large, life-threatening problem. Laparoscopic surgery has been postulated by some to result in a lower risk of surgical site infection than does the corresponding open procedure. This has not been shown to be true of all types of surgery. However, it does seem to hold true at least for cholecystectomy and for colonic surgery; laparoscopic colectomy has a lower risk of surgical site infection than does open colectomy.(3) Case selection bias may have affected this result however, as this was an observational study without randomization. Erythema at the surgical incision is often the first sign of a surgical site infection. The incision site should be carefully examined to see if there is any evidence of abscess deep to the skin (e.g., fluctuance). In cases of suspected abscess, the incision should be opened over the area of concern, draining any infection. The rest of the superficial incision should be examined to make sure that all areas of abscess are adequately drained. Routine wound care is then employed, often amounting to “wet-to-dry” dressing changes or negative-pressure dressing device placement. In cases of surrounding skin erythema and in immunocompromised patients, appropriate antibiotics should be employed. The management of open skin and subcutaneous tissue is important. Once nonviable tissue has been debrided and any abscesses drained, the tissue needs to be cared for to promote healing. This often occurs with “wet-to-dry” dressings consisting of gauze dampened with water or saline. Dressing changes occur once or twice daily and the wound closes by secondary intention over time. Another option for closure of a re-opened abdominal incision is with a negative-pressure dressing, for example, the Wound-Vac (KCI). Even in complex wounds, the negative-pressure dressing is a good adjunct for subcutaneous tissue closure.(28) Though uncommon in the postoperative setting, soft tissue necrotizing infections can occur at a surgical site and can be disastrous if not treated aggressively. Wide debridement to healthy, bleeding tissue should be performed urgently and is the mainstay of treatment, along with appropriate antibiotic therapy. The surgeon should have a low threshold to return to the operating room for re-evaluation of the surgical site. Adjunctive treatments of necrotizing soft tissue infections (including Fournier’s gangrene and postoperative soft tissue necrotizing infections) include hyperbaric oxygen (29, 30) and intravenous immunoglobulin administration (31). However, their application is controversial and adherence to surgical treatment at this point is standard of care.

sepsis intraabdominal infections Intraperitoneal anastomoses have a relatively low risk of disruption; nevertheless, abdominal abscess is an all too common complication of abdominal surgery. An abdominal abscess can lead to sepsis and needs to be dealt with in a timely fashion. Again, a spectrum of severity of sepsis and physiologic effect exists. Abscess associated with anastomotic failure can be devastating. Studies have shown mortality rates >20% (32) as well as worse cancer survival (33, 34). In most cases, the intraabdominal abscess is discovered on a CT scan ordered for fever, persistent ileus, leukocytosis, abdominal pain, or other complaint. The surgeon must now decide what steps to take in managing the abscess. One retrospective review showed that many intraabdominal abscesses can be managed with antibiotics alone.(35) Kumar et al. showed a high level of success (55%) with antibiotic treatment alone. There were only two patients who initially succeeded but ultimately required intervention. Most of the abscesses in this study were diverticular or periappendicular, although 11% were postoperative. All patients diagnosed with an abscess were started on parenteral antibiotics. They showed that patients with an abscess >6.5 cm in greatest diameter or in patients presenting with a temperature more than 101.2 were likely to require percutaneous drainage. These authors treated initially with appropriate intravenous antibiotics, and 54% of patients improved with that treatment alone. 44% of patients required percutaneous drainage after 48–72 hours of intravenous antibiotic treatment for failure to improve significantly. Percutaneous drainage of intraabdominal abscesses has become the treatment of choice for intraabdominal abscesses (see Figures 4.1 and 4.2). However, percutaneous drainage is not successful in 100% of patients.(35–37) A patient who is not stable for an attempt of nonoperative management, or one who fails to improve without operation will need to go to the operating room for therapy. Of important note, some studies have indicated a higher mortality for surgical management of intraabdominal abscess after failed percutaneous drainage.(38, 39) Therefore, it is imperative that a surgeon knows the factors which predict failure with nonoperative management. One group looked at 73 patients with abscess in whom attempted percutaneous drainage was performed. They experienced a 19% failure of nonoperative treatment. Using multivariate analysis, they showed that only abscess diameter <5 cm or failure to start the patient on antibiotic therapy before drainage were predictive of failure of percutaneous drainage.(36) Another study examined factors that would predict which patients would fail versus succeed with percutaneous management of intraabdominal abscesses.(40) Of 96 patients prospectively evaluated, they found that 70% of patients were successfully managed with a single percutaneous drainage and that an additional 12% were successful with a second attempt. Further attempts were not often successful. Only 16% of the patients ultimately required surgery. In evaluating their results, success was predicted in postoperative abscess, whereas failure was predicted with pancreatic source of abscess and when yeast was present in the abscess cavity. The following algorithm can be used as a guideline: (Figure 4.3)

Figure 4.1  Computerized tomography of the pelvis showing a large presacral space abscess. Note that staple-line is visible anterior to the large collection.

Figure 4.2  Computerized tomography of pelvic abscess resolved after percutaneous drainage. Note the drain remains in place just anterior and left of the coccyx.

Pelvic Sepsis Postoperatively A surgeon who operates on the rectum needs to know how to deal with pelvic sepsis as the result of an anastomotic leak associated with rectal resection, regardless of the level of anastomosis. One comprehensive study from 2004 looking at which factors related to rectal resection were associated with an increased risk of anastomotic leak showed interesting results.(41) Multivariate analysis of 432 rectal resection patients showed that anastomosis <6 cm from the anal verge, history of preoperative radiation

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improved outcomes in colon and rectal surgery

Figure 4.3  Treatment algorithm for dealing with intraabdominal and pelvic abscesses.

therapy, the presence of adverse intraoperative events, and male sex were independent risk factors for anastomotic leak. Their overall symptomatic leak rate was 12%. In a hemodynamically stable patient with a pelvic abscess (obviously, hemodynamically unstable patients need to be dealt with urgently, often surgically), broad-spectrum antibiotics should be started and a decision about drainage of the abscess needs to be made. In general, the guidelines above for intraabdominal abscesses can be extrapolated to pelvic abscesses. The algorithm above (Figure 4.3) can likewise be used as a guide in management. One common CT-guided approach for pelvic abscesses is via the transgluteal approach. Harisinghani performed a study examining 154 cases of pelvic abscess treated in this manner (42), showing a 96% success rate in completely resolving the abscess via this approach. Complications were uncommon, but did include hemorrhage in 2% (though all had transpiriformis approaches to their abscesses). Two of these patients required angio-embolization for pseudoaneurysm of the inferior gluteal artery while the third patient resolved spontaneously. Endoscopic ultrasound guidance with aspiration and drainage has also been described in treating deep pelvic abscess.(43) They described their first 12 patients in this fashion. 25% of patients required surgical drainage, though eight of nine patients who

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were able to have a stent placed into the cavity were completely treated via this approach. Duration of antibiotic therapy for treating intraabdominal infections is controversial. There is a paucity of good data on length of treatment, and much of the decision is based upon “because that’s how we always do it” logic. Current data and trends are leaning toward shorter duration of treatment. In a review of antibiotic treatment for intraabdominal infections, Mazuski et al. (44) state that two current approaches to duration exist: making decisions based upon intraoperative findings versus tailoring treatment based upon clinical condition and improvement of the patient. One prospective randomized trial looked at minimum length of antibiotic treatment after complicated appendicitis.(45) Appropriate patients were divided into two groups and given IV antibiotics. One group had a minimum of 5 days of antibiotics whereas the other group did not have a minimum number of treatment days. Antibiotic treatment was terminated based upon clinical findings: resolution of fever, improved physical examination, and return of GI function. The group with no minimum number of days of treatment received less doses of antibiotics overall. The authors also determined that stopping antibiotic treatment based upon clinical indices resulted in the same amount of recurrent infections as having a minimum number of days of treatment (i.e., 5 days).

sepsis The decision that nonoperative management has been unsuccessful can be difficult to make. Any hemodynamically unstable patient should return to the operating room. Further, patients who fail to respond to nonoperative management may need surgery. When operating for sepsis secondary to a failed anastomosis, there is some controversy as to whether diversion and washout is adequate or if the anastomosis needs to be resected. One retrospective study of 27 leaks showed that proximal diversion with drainage is adequate and results in a high chance of anastomotic salvage.(46) Knowledge of appropriate treatment of the septic patient following colon and rectal surgery is mandatory for any surgeon operating on these organs. Some patients can be successfully managed with nonoperative techniques. Timely identification of which patients will require intervention, whether it is percutaneous or surgical, is essential as is choosing the most effective treatment plan. Finally, the surgeon must appropriately carry out that plan and know when to switch to another course if failure occurs. References   1. Bone RC, Balk RA, Cerra FB et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM consensus conference committee. American college of chest physicians/society of critical care medicine. Chest 1992; 101(6): 1644–55.   2. Haley RW, Culver DH, Morgan WM et al. Identifying patients at high risk of surgical wound infection. A simple multivariate index of patient susceptibility and wound contamination. Am J Epidemiol 1985; 121(2): 206–15.   3. Gaynes RP, Culver DH, Horan TC et al. Surgical site infection (SSI) rates in the United States, 1992–1998: the National nosocomial infections surveillance system basic SSI risk index. Clin Infect Dis 2001; 33(Suppl 2): S69–77.   4. Nichols RL, Condon RE, Gorbach SL et al. Efficacy of preoperative antimicrobial preparation of the bowel. Ann Surg 1972; 176(2): 227–32.   5. Nichols RL, Broido P, Condon RE et al. Effect of preoperative neomycin-erythromycin intestinal preparation on the incidence of infectious complications following colon surgery. Ann Surg 1973; 178(4): 453–9.   6. Clarke JS, Condon RE, Bartlett JG et al. Preoperative oral antibiotics reduce septic complications of colon operations: results of prospective, randomized, double-blind clinical study. Ann Surg 1977; 186(3): 251–9.   7. Zmora O, Wexner SD, Hajjar L et al. Trends in preparation for colorectal surgery: survey of the members of the American Society of colon and rectal surgeons. Am Surg 2003; 69(2), 150–4.   8. Espin-Basany E, Sanchez-Garcia JL, Lopez-Cano M et al. Prospective, randomized study on antibiotic prophylaxis in colorectal surgery. Is it really necessary to use oral antibiotics? Int J Colorectal Dis 2005; 20(6): 542–6.   9. Bucher P, Gervaz P, Soravia C et al. Randomized clinical trial of mechanical bowel preparation versus no preparation before elective left-sided colorectal surgery. Br J Surg 2005; 92(4): 409–14. 10. Guenaga K, Atallah AN, Castro AA et al. Mechanical bowel preparation for elective colorectal surgery. Cochrane Database Syst Rev 2005; 1: CD001544.

11. Fa-Si-Oen P, Roumen R, Buitenweg J et al. Mechanical bowel preparation or not? Outcome of a multicenter, randomized trial in elective open colon surgery. Dis Colon Rectum 2005, 48(8), 1509–16. 12. Contant CM, Hop WC, van’t Sant HP et al. Mechanical bowel preparation for elective colorectal surgery: a multicentre randomised trial. Lancet 2007; 370(9605): 2112–7. 13. Jung B, Pahlman L, Nystrom PO et al. Multicentre randomized clinical trial of mechanical bowel preparation in elective colonic resection. Br J Surg 2007; 94(6): 689–95. 14. Platell C, Hall J. Mechanical bowel preparation before colorectal surgery? Lancet 2007; 370(9605): 2073–5. 15. Harrower HW. Isolation of incisions into body cavities. Am J Surg 1968; 116(6): 824–6. 16. Nystrom PO, Broome A, Hojer H et al. A controlled trial of a plastic wound ring drape to prevent contamination and infection in colorectal surgery. Dis Colon Rectum 1984; 27(7): 451–3. 17. Kurz A, Sessler DI, Lenhardt R. Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. Study of wound infection and temperature group. N Engl J Med 1996; 334(19): 1209–15. 18. Barone JE, Tucker JB, Cecere J et al. Hypothermia does not result in more complications after colon surgery. Am Surg 1999; 65(4): 356–9. 19. Greif R, Akca O, Horn EP et al. Supplemental perioperative oxygen to reduce the incidence of surgical wound infection. Outcomes Research Group. N Engl J Med 2000; 342(3): 161–7. 20. Belda FJ, Aguilera L, Garica de la Asuncion J et al. Spanish Reduccion de la Tasa de Infeccion Qirirgica Group. Supplemental perioperative oxygen and the risk of surgical wound infection: a randomized controlled trial. JAMA 2005; 294(16): 2035–42. 21. Brasel K, McRitchie D, Dellinger P. EBRS Group. Canadian association of general surgeons and American college of surgeons evidence based reviews in surgery. 21: the risk of surgical site infection is reduced with perioperative oxygen. Can J Surg 2007; 50(3): 214–6. 22. Chura JC, Boyd A, Argenta PA. Surgical site infections and supplemental perioperative oxygen in colorectal surgery patients: a systematic review. Surg Infect (Larchmt) 2007; 8(4): 455–61. 23. Stone HH, Hooper CA, Kolb LD et al. Antibiotic prophylaxis in gastric, biliary and colonic surgery. Ann Surg 1976; 184(4): 443–52. 24. Coppa GF, Eng K, Gouge TH et al. Parenteral and oral antibiotics in elective colon and rectal surgery. A prospective, randomized trial. Am J Surg 1983; 145(1): 62–5. 25. Kaiser AB, Herrington JL Jr, Jacobs JK et al. Cefoxitin versus erythromycin, neomycin, and cefazolin in colorectal operations. Importance of the duration of the surgical procedure. Ann Surg 1983; 198(4): 525–30. 26. Schoetz DJ Jr, Roberts PL, Murray JJ et al. Addition of parenteral cefoxitin to regimen of oral antibiotics for elective colorectal operations. A randomized prospective study. Ann Surg 1990; 212(2): 209–12.

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improved outcomes in colon and rectal surgery 27. Itani KM, Wilson SE, Awad SS et al. Ertapenem versus cefotetan prophylaxis in elective colorectal surgery. N Engl J Med 2006; 355(25): 2640–51. 28. Heller L, Levin SL, Butler CE. Management of abdominal wound dehiscence using vacuum assisted closure in patients with compromised healing. Am J Surg 2006; 191(2): 165–72. 29. Riseman JA, Zamboni WA, Curtis A et al. Hyperbaric oxygen therapy for necrotizing fasciitis reduces mortality and the need for debridements. Surgery 1990; 108(5): 847–50. 30. Jallali N, Withey S, Butler PE. Hyperbaric oxygen as adjuvant therapy in the management of necrotizing fasciitis. Am J Surg 2005; 189(4): 462–6. 31. Norrby-Teglund A, Muller MP, Mcgeer A et al. Successful management of Sever Group A streptococcal soft tissue infections using an aggressive medical regimen including intravenous polyspecific immunoglobulin together with a conservative surgical approach. Scan J Infect Dis 2005; 37(3): 166–72. 32. Kanellos I, Blouhos K, Demetriades H et al. The failed intaperitoneal colon anastomosis after colon surgery. Tech Coloproctol 2004; 8(Suppl 1): s53–5. 33. Walker KG, Bell SW, Rickard MJ et al. Anastomotic leakage is predictive of diminished survival after potentially curative resection for colorectal cancer. Ann Surg 2004; 240(2): 255–9. 34. Law WL, Choi HK, Lee YM et al. Anastomotic leakage is associated with poor long-term outcome in patients after curative colorectal resection for malignancy. J Gastrointest Surg 2007; 11(1): 8–15. 35. Kumar RR, Kim JT, Haukoos JS et al. Factors affecting the successful management of intra-abdominal abscesses with antibiotics and the need for percutaneous drainage. Dis Colon Rectum 2006; 49(2): 183–9. 36. Benoist S, Panis Y, Pannegeon V et al. Can failure of percutaneous drainage of postoperative abdominal abscesses be predicted? Am J Surg 2002; 184(2): 148–53.

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37. Shuler FW, Newman CN, Angood PB et al. Nonoperative management for intra-abdominal abscesses. Am Surg 1996; 62(3): 218–22. 38. Brolin RE, Flancbaum L, Ercoli FR et al. Limitations of percutaneous catheter drainage of abdominal abscesses. Surg Gynecol Obstet 1991; 173(3): 203–10. 39. McLean TR, Simmons K, Svensson LG. Management of postoperative intra-abdominal abscesses by routine percutaneous drainage. Surg Gynecol Obstet 1993; 176(2): 167–71. 40. Cinat ME, Wilson SE, Din AM. Determinants for successful percutaneous image-guided drainage of intra-abdominal abscess. Arch Surg 2002; 137(7): 845–9. 41. Matthiessen P, Hallbook O, Andersson M et al. Risk factors for anastomotic leakage after anterior resection of the rectum. Colorectal Dis 2004; 6(6): 462–9. 42. Harisinghani MG, Gervai DA, Maher MM et al. Transgluteal approach for percutaneous drainage of deep pelvic abscesses: 154 cases. Radiology 2003; 228(3): 701–5. 43. Giovannini M, Bories E, Moutardier V et al. Drainage of deep pelvic abscesses using therapeutic echo endoscopy. Endoscopy 2003; 35(6): 511–4. 44. Mazuki JE, Sawyer RG, Nathens AB et al. Therapeutic agents committee of the surgical infections society. The surgical infection society guidelines on antimicrobial therapy for inta-abdominal infections: an executive summary. Surg Infect (Larchmt) 2002; 3(3): 161–73. 45. Taylor E, Dev V, Shah D et al. Complicated appendicitis: is there a minimus intravenous antibiotic requirement? A prospective randomized trial. Am Surg 2000; 66(9): 887–90. 46. Hedrick TL, Sawyer RG, Foley EF et al. Anastomotic leak and the loop ileostomy: friend or foe? Dis Colon Rectum 2006; 49(8): 1167–76.

5

Intraoperative anastomotic challenges David E Beck

Challenging Case A 28-year-old man is undergoing a restorative proctocolectomy using a double-stapled technique for the ileoanal anastomosis. During insertion of the stapler into the anus, the anal canal distal linear staple line is disrupted. What are your options? case management Initial action is to visualize the distal staple line using retractors. If the ends of the partially closed distal bowel can be visualized and grasped with clamps or traction sutures, the amount of residual bowel can be assessed. If adequate length is present, one option is to reclose the bowel with a linear stapler placed below the disrupted staple line. After the stapler is fired, the residual bowel end can be resected with scissors or a scalpel. A second option is to reclose the disrupted staple line with sutures placed from the abdominal side or placed intralumenally via a retractor (lighted Chelsea-Eaton, Hill-Ferguson, etc.,) placed into the anal canal. If the defect and bowel are successfully closed, the anastomosis can proceed. If the distal segment of bowel is impossible to visualize or close, a musectomy can be performed via the anus and a hand sewn ileo anal anastomosis can be performed, as described in chapter 31. Most surgeons will create a diverting loop ileostomy when the anastomosis has been this challenging. Colon and rectal Surgery is a technique-oriented specialty with many procedures requiring an anastomosis to reestablish bowel continuity. Achievement of a successful anastomosis is related to a number of surgical principles, which can be divided into patient factors and surgeon factors.(1–3) Patient-related factors, such as the patient’s nutritional status and associated medical conditions or medications, are not under the operating surgeon’s control and are discussed in other chapters. This chapter focuses on anastomotic principles and problems (e.g., leakage, ischemia, stenosis, and hemorrhage) that can be identified and managed during the procedure. Preanastomotic Considerations Preoperative Discussion and Planning Before surgery the surgeon should have a plan which includes the expected operative findings or pathology and restoration of intestinal continuity if possible. If the preoperative findings are confirmed, the operation should proceed along an organized pathway. Unexpected findings will obviously require modifications. Before the procedure, the surgeon should also have a discussion with the patient, which includes these considerations with special emphasis on aspects of the anastomosis and the possible need for a temporary or permanent stoma should restoration of intestinal continuity be impossible or ill advised.(4) Proximal diversion will reduce the clinical sequalae from an anastomotic dehiscence. This is more likely in patients receiving preoperative chemotherapy and/or radiation, with poor nutrition, associated infection, or comorbid conditions (steroid use, hypotension,

etc.,). The appropriate site for a potential stoma should be chosen preoperatively, with the assistance of an enterostomal therapist. The selection and marking of a stoma site provides another opportunity for dialogue between the surgeon and patient. Operative Principles The key to uncomplicated healing of an intestinal anastomosis depends on adherence to well-established principles as well as the specifics of the technique. The principles of intestinal anastomosis include: (1) appropriate access and exposure to the two ends of bowel, (2) healthy bowel to be joined, (3) good blood supply, (4) gentle handling of the bowel, and (5) good apposition of ends with no tension on the anastomosis (5). Any compromise of these principles places the anastomosis at risk for complications. Exposure and access to bowel ends can be maximized by taking the time to set up and position retractors and intraabdominal packs. Headlights and lighted retractors minimize the frustration of inadequate overhead lights. Deep pelvic retractors such as the St. Marks retractor or Wiley vein retractors assist the visualization of the distal rectum prior to anastomosis. Extending the mid-line incision to the symphysis pubis likewise, allows maximum exposure of the distal rectum. Operating with poor lighting and inadequate exposure not only jeopardizes the anastomosis but also increases operating room time. Techniques of intestinal anastomosis should also be performed following the principle of gentle bowel handling. Clamps should be used only when absolutely necessary with the least amount of closure required to occlude the lumen. Care should be taken to exclude mesenteric blood vessels within the intestinal clamp. Gingerly inserting appropriately sized intraluminal staplers prevents inadvertent splitting and tearing of bowel ends to be anastomosed. Excessive use of electrocautery at the anastomosis can cause unappreciated tissue necrosis with potential for disruption. Mobilization of intestinal ends is required for exposure, access, and freedom of tension on the anastomosis. However, during mobilization it is important to preserve those blood vessels required for adequate anastomotic healing. For example, excessive skeletonization of the cut intestinal ends may compromise their blood supply. Having two healthy ends of bowel to anastomose is ideal. In some cases (bowel obstruction, diverticular disease, radiation enteritis, Crohn’s disease), this situation may not be possible and the plan to anastomose may be questioned. Optimizing patient nutrition, treating infection, and minimizing inflammation in the preoperative period may improve the bowel status. At operation, all diseased bowel is resected whenever possible to provide soft, pliable bowel ends for anastomosis. Bowel Preparation As described in chapter 2, bowel preparation has undergone major changes over the past 70 years. Until the past decade, mechanical

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improved outcomes in colon and rectal surgery bowel preparation was a standard feature of elective bowel surgery and the lack of a bowel preparation or poor results with a mechanical preparation was in many surgeons view a contraindication to a primary anastomosis. Recent studies have failed to support the accepted view that bowel cleansing, in the presence of appropriate antibiotics, reduced the risk of anastomotic leak or wound infection.(6) Case series and reports from the trauma literature suggested that good or better outcomes could be achieved in unprepared bowel with an anastomosis.(7, 8) A Cochrane review of five randomized trials showed equal or better morbidity or mortality in 576 patients with a mechanical bowel preparation and 583 patients without a mechanical preparation.(9) An additional meta-analysis of seven randomized trials containing 1,454 patients showed no significant differences for wound infection and septic and nonseptic conditions.(10) Certain situations, such as laparoscopic procedures, potential need for intraoperative colonoscopy, or avoidance of spillage from proximal stool loading after a low colorectal anastomosis, still require adequate mechanical bowel preparation. For other situations, many surgeons are minimizing or eliminating a mechanical bowel preparation in elective situations. The current evidence suggests that intralumal contents should not be the primary factor in deciding if an anastomosis should be performed. Other options to consider with unprepareed bowel are to perform a subtotal colectomy with ileocolonic or ileorectal anastomosis. This option has been shown to be a safe option for avoiding a stoma in left colon obstruction.(11) Alternatively, intraoperative colonic lavage in some hands offers the ability to construct an anastomosis in patients with this condition.(11–13) Whatever the bowel preparation used, it is critical that spillage of intralumenal contents be avoided to minimize complications and neoplastic dissemination. Most surgeons agree that a clean, empty colon has less potential for spillage, but cannot compensate for poor technique. An additional protection against spillage of residual intestinal contents is provided by controlling the ends of bowel used in the anastomosis. This can be accomplished by elevating of the ends (with traction sutures) or by occluding the bowel proximal and distal to the anastomosis with tapes or noncrushing clamps.(14) Bowel Status When intestinal surgery is being performed for urgent situations or even during certain elective operations, the first decision is whether or not an anastomosis is appropriate. Healing of an anastomosis is at risk in certain clinical situations. Traditionally, intestine that is unprepared, obstructed, irradiated, inflamed, or ischemic may not be suitable for anastomosis.(15–17) However, other than ischemia, current evidence suggests that constructing an anastomosis is safe in selected cases of obstruction, irradiation, inflammation, and without bowel preparation.(5, 11, 18, 19) In addition to these local factors, patient factors such as malnutrition, diabetes, renal failure, chronic hepatic disease, anemia, shock, steroid use, and other immunocomprised states may place an anastomosis at risk for failure.(4, 5, 6) The safety of intestinal anastomosis in any particular clinical scenario thus depends upon patient and intestinal factors that must be carefully weighed by the operating surgeon.(5) Optimally, the bowel will have a good blood supply, (documented by pink

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color, parastalysis and pulsitile bleeding from the cut edge), lack edema, be free of tension (see later section), and have adequate lumen for the type of anastomosis. The ultimate decision to perform an intestinal anastomosis ultimately depends on surgical judgment derived from an understanding of documented risks as well as knowledge of one’s own ability and experience. Exposure The importance of adequate exposure cannot be overemphasized. Exposure is facilitated by patient position, adequate length of incision, appropriate choice of retractors, and lighting. If the possibility of a left-sided anastamosis exists, the patient should be placed in lithotomy position, using either Lloyd-Davies, Allen or yellow-fin stirrups, after anesthesia is induced. (Figure 5.1) Great care is taken to avoid pressure on the peroneal nerves and hips. (20) The perineum should extend slightly over the end of the operating table to allow easy access for transanal stapled anastamosis, upward pressure on the perineum for exposure of the distal rectum, or a two-surgeon combined approach to hand sewn coloanal anastamosis or abdominoperineal resection. Once the patient is correctly positioned, irrigation of the rectum should be performed to ensure the quality of the bowel preparation and to evacuate any remaining fecal residue. Leaving a large mushroomshaped or Foley catheter in the rectum alerts the surgeon to the level of dissection in the low pelvis, prevents rectal distension and possible enterotomy during mobilization, and allows drainage of rectal contents which minimizes luminal spillage. The trend toward smaller incisions should be critically evaluated when planning a colorectal anastamosis.(4) Pelvic exposure is greatly facilitated by incisions that extend to the pubic bone. The incision may require proximal extension if mobilization of the splenic flexure is required. The extent of this extension will depend on factors such as the patient’s body habitus, disease process, and surgical technique. Adequate exposure with less generous incisions is often possible in thin patients or those with low splenic flexures, mobile colons, or left-sided Crohn’s disease (the splenic flexure that is contracted down into the abdominal cavity). Placement of the operating surgeon between the patient’s legs often improves visualization during splenic flexure mobilization. Adequate visualization is imperative for safe splenic flexure mobilization, and additional retraction or incision extension should be one of the first considerations if mobilization is difficult. Different retractors are available to improve exposure. Those that are fixed to the bed, such as the Bookwalter, “upper hand,” omnitract, or polytract, make life easier for surgical assistants and provide a consistent view throughout the operation.(4) When placing retractor attachments, the surgeon must be aware of the relation of the retractor to the femoral vessels, nerves, and iliac crests. Prolonged constant traction on the bowel may also be a problem, and consideration of relieving the pressure intermittently during long cases may be appropriate. Finally, adequate lighting is extremely important during pelvic dissection as well as to provide a view of the anastomosis, deep in the pelvis. Equipment available to enhance vision includes headlights, lighted retractors, cautery instruments, and suction devices.

intraoperative anastomotic challenges

Figure 5.1  Stirrups for modified lithotomy position.

Obtaining Adequate Length After the appropriate resectional procedure is completed, sufficient proximal and distal mobilization provides tension-free bowel ends for a secure anastomosis. Tension is rarely a problem for small bowel or ileocoioc anastomosis. The small bowel mesentery has an avascular plane anterior to the aorta to the takeoff of the superior mesenteric artery. The right and left colon have a posteriolateral fusion plane anterior to Geroda’a fascia. This avascular plane can be opened using a lateral or medial approach. Difficulty in obtaining tension-free bowel occurs more commonly with a left-sided (e.g., colorectal) anastomosis. Additional left colon length is obtained using the following maneuvers in this order: division of the lateral colonic attachments, division of the splenic flexure, division of the inferior mesenteric artery at its aortic takeoff, and division of the inferior mesenteric vein at the inferior border of the pancreas (Figure 5.2).(4) If these maneuvers do not provide adequate bowel length, branches of the distal middle colic artery and veins may need division. Unfortunately this last action may compromise the blood supply to the remaining colonic end. If this occurs, the ischemic bowel must be resected and additional vessels will need to be divided to provide the required bowel length. In some cases the middle colic vessels will have to be divided proximally and the blood supply of the residual colon will need to be based on the right and/or ileocolic artery. In most patients these vessels will provide adequate blood supply to the proximal transverse colon or hepatic flexure which can be made to reach the rectum with one of two techniques. One method is to open a window in the ileal mesentery medial to the ileocolic artery and vein. The proximal transverse colon is brought through this window to reach the pelvis (Figure 5.3). (21) Another option is to completely mobilize the right colon and then derotate it to the right. This rotates the cecal tip to the right middle abdomen (pointed toward the liver), reverses the direction of the colon, and provides enough length for the hepatic flexure to reach the pelvis (Figure 5.4). As this maneuver moves

Figure 5.2  Operative techniques to obtain left colon length. (1) division of lateral colonic attachments. (2) division of the splenic flexure. (3) division of the inferior mesenteric artery at its aortic takeoff and the inferior mesenteric vein. (4) second division of the inferior mesenteric vein at the inferior border of the pancreas. (5) incision of splenic flexure mesentary. (From Rafferty JF. Obtaining adequate bowel length for colorectal anastomosis. Clin Colon Rectal Surg 2001; 14: 25–31. With permission.)

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improved outcomes in colon and rectal surgery (a)

(b)

Figure 5.3  (A) Window in mesentary is created medial to the ileocolic atrery and vein. (B) Transverse is brought through ileal mesenteric window to reach the pelvis.

(a)

(b)

Figure 5.4  (A) Right colon is mobilized, right colic vessels are divided, and appendix is removed. (B) The right colon is derotated to allow the hepatic flexure to reach the pelvis.

the cecum to an abnormal position, it is important to remove the appendix. Development of appendicitis would produce confusing signs and symptoms. In addition to a lack of tension, it is also critically important that the anastomotic site have a good blood supply. Before the anastomosis is constructed, the bowel should be routinely checked for viability (normal color and peristalsis and a pulsatile blood supply). Well-perfused bowel and its appendages (e.g., appendices epiploicae) will bleed when cut. Dividing an appendices epiploicae at the proximal bowel end intended for the anastomosis is frequently used by the author to objectively confirm an adequate blood supply.

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In addition to the factors described previously, bowel used for an anastomosis must not be edematous, radiated, or ischemic. An appropriate resection should remove ischemic or radiated bowel, while edema of the residual bowel (e.g., associated with peritonitis) may mandate forgoing an anastomosis in favor of a diverting stoma. Anastomotic Technique In performing an anastomosis, surgeons have multiple options. Each technique has associated advantages and disadvantages, and the specific one favored by an individual surgeon depends more on training, personal experience, and perhaps blind faith than on the results of randomized, prospective studies. There has been no

intraoperative anastomotic challenges (a)

(b)

(c)

Figure 5.5  Types of anastomoses. (A) End-to-end anastomosis. (B) Side-to-side functional end-to-end anastomosis. (C) End-to-side anastomosis. (From Beck DE. Malignant lesions. In Beck DE, ed. Handbook of Colorectal Surgery. Quality Medical Publishing, St Louis, MO. 1997, pp 400–430. With permission.).

consistent scientific proof that one intestinal anastomotic technique is superior. Options range from the physical configuration of the anastomosis (end-to-end, side-to-side, end-to-side, side-to-end, etc. Figure 5.5) and the method used to construct it: sutures, staples, a combination of these, and experimental methods such as compression devices or adhesives. Several of these merit discussion.

Staples versus Sutures Suturing has been used since the beginning of intestinal surgery. Different suture materials have shown some experimental differences, but the clinical difference is arguable. In general a stapled anastomosis usually takes less time but is more expensive.(22, 23) Blood flow may be higher with a stapled anastomosis, and in certain situations, such as a low colorectal anastomosis, the use of staples is technically easier.(24) A final consideration is that any device can malfunction and lead to the need for use of additional staplers or conversion to a sutured anastomosis.(5) A meta-analysis of 13 trials comparing hand-sewn with stapled anstomosis showed similar mortality, leak rates, local cancer recurrences, and wound infections.(25) This review did reveal a higher rate of postoperative stricture with the stapled anastomosis, most of which were asymptomatic and easily managed with diltation. Suture techniques such as the number of layers or use of interrupted versus running sutures, have shown some clinical differences. An inverting anastomosis is superior to an everting technique. A number of investigators advocate a single layer anastomosis because they believe it causes less narrowing of the lumen since a smaller amount of tissue is strangulated.(26, 27) A single layer anastomosis is also felt to cause less devascularization, infection, and necrosis, while the continuous suture distributes tension more evenly around the lumen.(27, 28) In clinical practice, however, technical factors such as the correct placement of sutures, correct tension of the suture, and secure knots appear to be more important than the experimental findings discussed previously. Experience, training, clinical judgment, and ability are major factors in a surgeon’s choice of anastomotic technique; however, some of the reported experience with suturing merits additional comment. An extensive experience using a running monofilament technique has been described by Max and colleagues.(28) In a retrospective report of 1,000 single layer continuous polypropylene intestinal anastomoses, the authors believed that this technique was quick, simple, economical, and safe. Although an intraoperative leak rate was not reported, their postoperative leak rate of 1% with the technique compares very favorably with other that in reports using alternate techniques.(28) A Cochrane Database Systemic reviewed six trials with 955 ileocolic participants.(29) The three largest prospective randomized trials comparing stapled versus hand-sewn methods for ileocolic anastomoses conducted between 1970 and 2005 showed fewer leaks with stapled anastomosis. All other outcomes: stricture, anastomotic hemorrhage, anastomotic time, re-operation, mortality, intraabdominal abscess, wound infection, and length of stay, showed no significant difference. End-To-End The use of surgical staplers has advantages in certain situations (e.g., the very low colorectal anastomosis), and they have enjoyed widespread clinical usage. These mechanical devices, however, do not compensate for improper or poor technique. In an early survey of stapler complications by the American Society of Colon and Rectal Surgeons (ASCRS) published in 1981, 243 surgeons responded that they had performed 3,594 end-to-end anastomoses (EEA).(30) Intraoperative complications were reported in 15.1% of patients. These complications

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improved outcomes in colon and rectal surgery included anastomotic leak (9.8%), tear during extraction (1.9%), anvil not extractable (1.2%), complete anastomotic failure that required conversion to another technique (0.9%), instrument failure (0.8%), and bleeding (0.5%). This report represents surgeons’ early experience with the use of staplers, and therefore the results must be evaluated in the proper context. Improvements in the instruments, anastomotic technique, and surgeon experience have resulted in fewer complications. An early experience with 73 consecutive stapled end-to-end colorectal anastomoses by Gordon and Vasilevsky identified intraoperative complications in 19 patients (26%).(31) These included instrument failure (4), incomplete or inadequate doughnuts (5), bleeding (3), bowel injury associated with use of sizers (1), anvil extraction (1), anvil insertion (3), difficulty with stapler extraction (1), and anvil not extractable (1). The relative high incidence of these problems reflects the early learning curve with stapling instruments and the early developmental nature of the instruments used. Increased experience and advances in instruments have minimized the occurrence of these problems. A prospective randomized multicenter study by Dochetry and colleagues described 652 patients who were randomized to a sutured (n = 321) or stapled large bowel anastomosis (n = 331) between 1985 and 1989.(32) During the study, 5 of the 331 patients (1.5%) randomized to a stapled anastomosis had an instrument or technical failure. Intraoperative anastomotic testing was not routinely performed, but postoperative radiologic leaks were identified in 14.4% of the sutured and 5.2% of the stapled colorectal anastomoses. Clinical anastomotic leakage was evident in 4.4% of the sutured patients and 4.5% of the stapled patients. Proper technique is a critical component to obtaining a good anastomosis with a circular intraluminal stapler. To minimize problems, the largest diameter stapler that can be accommodated by both bowel ends should be used.(33) As originally described, an intraluminal stapler entails usage of purse-string sutures to hold the bowel over the stapler cartridge and anvil during stapler closure. This purse-string suture can be placed by hand (with a baseball or in-and-out technique), with a fenestrated purse-string clamp (Purse String Device, Davis & Geck, Wayne, NJ), or with a stapling device (Purse String Instrument-65, U. S Surgical Corp., Norwalk, CT). To work properly, the sutures must be placed correctly (approximately 1–2 mm back from the bowel ends and 2–3 mm apart). If the sutures are placed too close, the bowel will not close tightly around the stapler shaft. This nonconstricting pursestring may be corrected by carefully cutting the bowel overlying the suture in two or more places to release additional suture to bunch up more of the bowel end. If the sutures are placed too far apart or some tear through, gaps in the bowel ends will appear when the suture is tightened. This can be repaired by use of a “Pulley Stitch” (Figure 5.6).(1, 34) These interrupted 4-0 or 3-0 braided sutures (e.g., silk or braided polyester) hold the pursestring suture to the bowel ends and assist in pulling it tightly around the shaft. Finally, placement of sutures, too near the bowel end results in their tearing through the bowel, while placing the sutures too far back from the bowel ends will produce an excessive bulk of tissue around the shaft. If a purse-string clamp is used, it is important that the bowel be divided close to the clamp before the clamp is released. Leaving

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(a)

(b)

Figure 5.6  Repair of pursestring stitch. (A) Gap is identified in pursestring suture. (B) Gap is closed with «pulley» sutures.

excess tissue adjacent to the clamp may result in too much tissue at the purse-string which may prevent the stapler from closing and firing properly. Releasing the clamp before dividing the bowel may result in inadequate tissue to hold the purse-string. Difficulties in using the purse-string clamp low in the pelvis are minimized by the use of a double armed suture (e.g., 2–0 monofilament polypropylene, double-armed TS-9, David & Geck, Wayne, NJ). Both needles are placed through the clamp and the needles can be bent several times while the needle is withdrawn to allow the needles to be removed in the confined pelvis.

intraoperative anastomotic challenges Many surgeons use clamps to hold the bowel ends while placing the purse-string or to hold the bowel open to assist placement of the anvil or stapler. Several problems can occur with use of these clamps. If the clamps are placed too far back from the bowel end and placed too tightly, an injury to the bowel wall can occur which can produce a leak despite a secure anastomosis. If open ended clamps (e.g., Babcock clamps) are used, it is possible for the purse-string to go through the end of the clamp. If this occurs, the clamp or the purse-string suture will need to be cut. Use of solid ended clamps eliminates the chance of this happening. Large clamps increase the difficulty in inserting an anvil in bowel diameter close to the diameter of the anvol. Double Staple Another end-to-end stapling option involves a double staple technique.(35, 36) With this method a linear staple line is placed across the distal bowel and a circular stapler is inserted into this bowel (via the anus for a left-sided anastomosis). To avoid creating an ischemic area, the trocar of the circular stapler should exit adjacent or as close as possible to the linear staples. The anvil is placed in the proximal bowel and secured with a purse-string as described previously. When closed and fired, the circular stapler removes a portion of the crossed linear staple line to create the anastomosis. Concern was initially expressed about these crossing staple lines. However, subsequent experimental and clinical evidence has confirmed the relative safety of this method.(37, 38) The double staple technique is helpful in anastomosing bowel ends of dissimilar size and in ultralow colorectal or coloanal anastomoses. Outside of these situations, the extra cost of using a stapler rather than a sutured purse-string argues more for the use of a purse-string. With low distal staple lines, it can be challenging to insert the stapler into the anus and not disrupt the staple line. Distal staple line disruption can occur if the distal bowel is tenous or under too much traction. It has anecdotically seemed to occur more frequently with the use of a contour stapler (Ethicon). If this occurs, several options are available. Initial action is to visualize the distal staple line. If the ends of the partially closed bowel can be grasped with clamps or traction sutures, the amount of residual bowel can be assessed. If adequate length is present the bowel can be closed with a linear stapler placed below the disrupted staple line. After the stapler is fired, the residual bowel end can be resected with scissors or a scalpel. A second option is to recluse the disrupted staple line with sutures placed from the abdominal side or placed intralumenally via a retractor placed into the anal canal.(39) If the bowel is successfully closed, the anastomosis can proceed. If the distal segment of bowel is impossible to close, a musectomy can be performed via the anus and a hand-sewn coloanal or ileoanal anastomosis can be performed. A serious problem associated with double stapling of the low rectum is the inadvertent creation of a recto-vaginal fistula. This unfortunate complication results from incorporating the posterior wall of the vagina into the staple lines. Maneuvers to reduce this occurrence include an adequate dissection of the rectum off the posterior vagina, careful visualization of the bowel ends during closure of the stapler, and intravaginal palpation of the posterior vaginal wall before firing the stapler.(1)

A variation of double stapling is triple stapling. In this anastomotic method, an extra linear stapler is used to close the bowel end after placement of the anvil into the proximal bowel. The anvil trocar is then advanced through the closed bowel. This technique has been suggested for intracorporeal laparoscopic techniques; however, it is costly and produces another linear suture line that must be incorporated into the final anastomotic staple line. The technique has not gained widespread acceptance due to the relative ease in placing the proximal purse-string. Difficulty with anvil insertion in the proximal bowel lumen usually occurs when the stapler is too large for the diameter of the bowel. Experience or the use of scissors allows accurate selection of the correct size of circular stapler. Additional helpful techniques include the use of dilators to overcome bowel spasm, lubrication of the anvil head (with betadine, saline, or blood), and distraction of the bowel ends with three small-ended forceps or clamps. Use of a recently developed low profile anvil (CDH Ethicon-Endosurgery, Inc. Cincinnati, Ohio) has diminished this occurrence. Detachable Staplers For colorectal anastomosis, the circular stapler is usually placed through the anus. With currently available detachable head staplers, the flat stapler shaft may be difficult to pass atraumatically through the anal sphincter muscles. Khoury and Opelka, in 1995, described a technique to facilitate this maneuver.(40) A Faensler or Chelsey-Eaton anoscope allows a gradual controlled dilation of the sphincters. After removal of the obturator, the stapler shaft can easily be passed through the anoscope (Figure 5.7). Once through the sphincter, the stapler must be inserted up to the resected end of the rectum. Knowledge of rectal anatomy, adequate mobilization of the posterior rectum, and selection of an appropriate size of stapler assist in accomplishing this advancement. Incorrect insertion can tear or split the rectum. Such an injury to the rectum mandates a very low or coloanal anastomosis to reestablish intestinal continuity. A proctoscopic examination of the rectum insures an adequate lumen, confirms an adequate preparation and mobilization, and assists in identifying the apex of a Hartman’s pouch. Once the stapler is closed and fired it must be removed. Stapler extraction from the anastomotic area may be aided with a traction stitch. Bowel spasm or a stapler misfire may cause extraction difficulty. Gentle traction and careful stapler manipulation usually allow it to be removed. If a misfire results in inability to remove the stapler, it may be necessary to excise and reaccomplish the anastomosis. End-To-Side and Side-To-Side (Functional End-To-End) An end-to-side or side-to-end (the proximal bowel is usually listed first) is useful for joining bowel of different diameter. The size of the anastomosis is not limited by the bowel diameter. This configuration is often used for ileocolic or ileorectal anastomoses. A side-to-side anastomosis is frequently used to join bowel with a linear cutting stapler. Use of the bowel ends for a side-to-side anastomosis, serves as a functional end-to-end anastomosis. A surgical atlas should be consulted for additional technical details. A meta-analysis of studies published between 1992 and 2005 of end-to-end versus other anastomotic configurations in

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improved outcomes in colon and rectal surgery (a)

(b)

(c)

Crohn’s disease used eight studies including 661 patients.(41) The authors conclude that a side-to-side anastomosis led to fewer anastomotic leaks and overall complications, a shorter hospital stay, and a perianastomotic recurrence rate comparable to endto-end anastomoses. Anastomotic Testing All surgeons test their anastomoses in some way. At a minimum, the anastomotic site is inspected and in some cases palpated. A visual inspection of a side-to-side anastomosis may be performed before closing the ends of the bowel. Gentle constriction of the bowel proximal or distal to the anastomosis will confirm a patent lumen and the absence of a gross leak. A more sensitive test can easily be performed in the colorectal anastomosis (which is at higher risk for a leak).(42–45) The author prefers to test low colorectal anastomosis with intraluminal instillation of a dilute solution of povidine-iodine (Betadine, Purdue Frederick Co, Norwalk, CT). After the bowel is occluded above the anastomosis with finger pressure, the testing solution is instilled gently with a bulb syringe inserted into the anus. Any leak is readily apparent. Irrigation with this dilute providine-iodine solution also provides antimicrobial and tumorcidal activity. Others have suggested testing with a dilute solution of methylene blue.(46) Larger volumes are infused via a rectal tube, and with care even ileocolic anastomosis can be tested for leaks with this technique. The optimal pressure recommended for detecting intraopeartive leaks with air/water testing is 25–30 cm H2O.(47, 48) If an infusion system is used, the pressure can be controlled by the height of the infusion bag. Some surgeons prefer to test their anastomosis with air.(45) The pelvis is first filled with saline and the distal bowel (containing the anastomosis) is distended with air (instilled transanally). Any anastomotic defect will produce air bubbles. Unfortunately, with this method it is often difficult to accurately identify the location of the leak if any blood has mixed with the saline. The saline must also be removed before any identified leak can be repaired. Testing with air may be preferable for higher colorectal anastomosis as infused intralumenal fluid may not reach a higher anastomosis. A proctoscope can also be used to inspect the colorectal anastomosis. Sufficient lumen size is usually confirmed by the lack of stenosis, hemostasis is confirmed, and the bowel can easily be distended with air. Finally, some surgeons inspect the intraluminal stapler “doughnuts.” The author has not found this to be helpful as complete “dough-nuts” do not ensure the absence of a leak at the anastomotic site (e.g., due to a tear of the bowel or staple lines during stapler removal). Also, an incomplete “dough-nut” may be produced with an intact anastomosis. Intraoperative testing as described above is more sensitive and specific. Whatever method is used to inspect or test an anastomosis, it is important to act on any defect or leak identified. Options include suture reinforcement, reconstruction, or proximal diversion. Challenges

Figure 5.7  Anoscopic assisted stapler insertion. (A) Faensler anoscope is inserted after gentle anal dilation. (B) The anoscope obturator is removed and the circular stapler is inserted through the anoscope. (C) The anoscope is withdrawn and taken off the shaft of the stapler.

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Inadequate Anastomotic Lumen Adequate lumenal patency is important for several reasons. Bowel edema occurs in the perioperative period, and a marginal lumen

intraoperative anastomotic challenges line has the potential to transfer the electrical energy to adjacent portions of the bowel. Reduction or stoppage of the bleeding may also be helped by digital compression or intraluminal instillation of an epinephrine solution (1 to 100,000 or 1 to 200,000 u/mL). Another option is submucosal injection of an epinephrine solution.(50)

Figure 5.8  Isoparastaltic side-to-side functional end-to-end anastomotic technique.

may lead to a partial obstruction. The anastomotic lumen can be sized by palpation or visually inspected. The ability to remove the anvil of a circular stapler confirms a lumen corresponding to the size of the stapler, while distal rectal anastomosis can be evaluated by a proctoscope. An alternative technique for colorectral anastomosis is an isoparastaltic side-to-side anastomosis (Figure 5.8). Leakage An accurate incidence of anastomotic leakage is difficult to determine. Few studies have reported the incidence of intraoperatively identified anastomotic problems. The incidence of leaks identified in the postoperative period is described in chapter 6. If a defective anastomosis is identified, it may be repaired in several ways. Additional sutures can approximate a small gap, or the anastomosis can be resected and completely redone using a stapler or hand-sewn technique. Another option is to replace purse-string sutures around the defective anastomosis and reinsert a new stapler through the lumen. The purse-string sutures are tightened, which should close the defect and hold the previously placed staples toward the stapler shaft. After closure and firing of the new stapler, the new donuts (which should also contain the old staples) are removed with the stapler.(49) If the anastomosis is very low, the defect may also be repaired transanally. Anastomotic Hemorrhage Hemorrhage can occur at both a staple and a suture line. Proper size staple height and correct tension of sutures minimize the occurrence of this problem. Techniques to stop hemorrhage include cautery of the bleeding vessels or placement of a suture at the site of bleeding. Excessive cautery is to be avoided as the staple

Proximal Protection (Stomas) For high-risk anastomosis, a proximal diverting stoma is often used. A diverting stoma will not prevent an anastomotic leak but will reduce the septic morbidity and mortality associated with the leakage. A properly constructed loop stoma is almost totally diverting.(51) However, if absolute total diversion is desired, a Prasad type of end loop stoma may be constructed.(52) If diversion is needed, the author and editors prefer an ileostomy over a colostomy. A diverting colostomy following a colonic resection has several problems. A colostomy includes a larger stoma, and due to its proximal location, the ostomy output is loose or liquid and very odorous. If a significant colonic resection has been performed, the remaining colon length is often insufficient to easily reach the abdominal wall at a preferred stomal location. A loop ileostomy has several advantages.(53) First, it is easy to construct and close. As it is usually created in bowel removed from the anastomotic site, tension and blood supply are rarely a problem. Ileostomy output is liquid, has little odor, and unless the mesentery is abnormally shortened, an ileostomy will reach almost any site on the abdominal wall. Adjuvants and Drains Due to the morbidity associated with leaks, several adjuvants have been used in high risk of potential compromised anastomoses. Wrapping the anastomosis with omentum is a popular adjunct that is felt by many surgeons to prevent disruption. Unfortunately, there is no evidence to support this practice in humans.(54, 55) The use of foreign materials around the anastomosis has been shown to be harmful.(56, 57) Reinforcing sutures positioned around a stapled anastomosis, while not routinely necessary, may provide security especially for low rectal anastomoses. Controversy continues regarding the use of drains as an adjunct to intestinal anastomosis. The abdominal cavity cannot be adequately drained, but in cavities like the low pelvis it is possible. Proponents believe that the drain removes contaminated fluid and blood and, should a leak occur, it would be controlled. Opponents argue that the drain is dangerous as it allows bacteria a portal of entry and it may erode the anastomosis. Trials have clearly shown no benefit from drainage of intestinal anastomoses. (58, 59) Despite evidence to the contrary, the practice of closed suction drainage for low pelvic anastomoses the first few days postoperatively continues due to individual surgeon’s beliefs.(5) Summary Adherence to established surgical principles and techniques should minimize anastomotic problems. Mechanical devices cannot overcome limitations in experience, skill, or judgment. Intraoperative identification of problems that occur permits correction with minimal morbidity.

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improved outcomes in colon and rectal surgery References   1. Beck DE. Intraoperative anastomotic complications. In Hicks TC, Beck DE, Opelka FG. Timmcke AE, eds. Complications of Colon and Rectal Surgery. Williams & Wilkins, Baltimore, 1996: 70–81.   2. Goligher JC. Surgery of the Anus, Rectum, and Colon. 5th ed. London: Balliere Tindall; 1984.   3. Steichen FM, Ravitch MM. Contemporary stapling instruments and basic mechanical suture techniques. Surg Clin North Am 1984; 64: 425–40.   4. Rafferty JF. Obtaining adequate bowel length for colorectal anastomosis. Clin Colon Rectal Surg 2001; 14: 25–31.   5. Sweeney WB. Intra-abdominal anastomotic techniques. Clin Colon Rectal Surg 2001; 14: 15–23.   6. Delaney CP, Mackeiggan JM. Preoperative management – risk assessment, medical evaluation, and bowel preparation. In Wolff BG, Fleshman JW, Beck DE, Pemberton JH, Wexner SD, eds. ASCRS Textbook of Colorectal Surgery. SpringerVerlag, New York, 2007: 116–29.   7. Demetriades D, Murray JA, Chan L et al. Penetrating colon injuries requiring resection: diversion or primary anastomosis? An AAST prospective multicenter study. J Traum 2001; 50: 765–75.   8. van Geldere D, Fa-Si-Oen P, Noach LA et al. Complicatons after colorectal surgery without mechanical bowel preparation. J Am Coll Surg 2002; 194: 40–7.   9. Guenga KF, Matos D, Castro AA, Atallah AN, Wille-Jorgensen P. Mechanical bowel preparation for elective colorectal surgery. Cochrane Database Syst Rev 2003; 2: CD001544. 10. Slim K, Vicaut E, Panis Y et al. Meta-analysis of randomized clinical trials of colorectal surgery with or without mechanical bowel preparation. Br J Surg 2004; 91: 1125–30. 11. Torralba JA, Robles R, Parrilla P et al. Subtotal colectomy vs. intraoperative colonic irrigation in the management of obstructed left colon carcinoma. Dis Colon Rectum 1998; 41: 18–22. 12. Kressner U, Antonsson J, Ejerblad S et al. Intraoperative colonic lavage and primary anastomosis – an alternative to Hartmann procedure in emergency surgery of the left colon. Eur J Surg 1994; 160: 287–92. 13. Forloni B, Reduzzi R, Paludetti A et al. Intraoperative colonic lavage in emergency surgical treatment of left-sided colonic obstruction. Dis Colon Rectum 1998; 41: 23–7. 14. Wexner SD, Beck DE. Sepsis prevention in colorectal surgery. In Fielding LP, Goldnerg SM, eds. Operative Surgery 5th Ed. Butterworth-Heineman, Ltd. London, 1993: 41–6. 15. Irvin TT, Goliger JC. Etiology of disruption of intestinal anastamosis Br J Surg 1973; 60: 461–4. 16. Schrock TR, Deveney CW, Dunphy JE. Factors contributing to leakage of colonic anastomoses. Ann Surg 1973; 177: 513–8. 17. Khoury GA, Waxman BP. Large bowel anastomosis. The healing process and sutured anastomosis: a review. Br J Surg 1983; 70: 61–3. 18. Hsu T-C. One-stage resection and anastomosis for acute obstruction of the left colon. Dis Colon Rectum 1998; 41: 28–32.

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19. Weiber S, Jiborn H, Zederfeldt B. Preoperative irradiation and colonic healing. Eur J Surg 1994; 160: 47–51. 20. Karulf R. Anesthesia and intraoperative positioning. In Hicks TC, Beck DE, Opelka FG, Timmcke AE. eds, Complications of colorectal surgery. Baltimore: Williams & Wilkins, 1996: 34–9. 21. Le TH, Gathright JB, Jr. Reconsitution of intestinal continuity after extended left colectomy. Dis Colon Rectum 1993; 36: 197–8. 22. Graffner H, Andersson L, Lowenhielm P, Walther B. The healing process of anastomoses of the colon: a comparative study using single, double-layer or stapled anastomosis. Dis Colon Rectum 1984; 27: 767–71. 23. Fingerhut A, Hay JM, Elhadad A et al. Supraperitoneal colorectal anastomoses: hand-sewn versus circular staples - a controlled clinical trial. Surgery 1995; 118: 479–85. 24. Wheeless CR Jr, Smith JJ. A comparison of the flow of iodine 125 through three different intestinal anastomoses: standard, Gambee, and stapler. Obstet Gynecol 1983; 62: 513–8. 25. MacRae HM, McLeod RS. Handsewn vs. stapled anastomoses in colon and rectal surgery: a meta-analysis. Dis Colon Rectum 1998; 41: 180–9. 26. Gambee LP, Garnjobst W, Hardwisk CE. Ten years’ experience with a single layer anastomosis in colon surgery. Am J Surg 1956; 92: 222–7. 27. Templeton JL, McKelvey ST. Low colorectal anastomoses: an experimental assessment of two sutured and two stapled techniques. Dis Colon Rectum 1985; 28: 38–41. 28. Max E, Sweeney WB, Baily HR et al. Results of 1,000 singlelayer continuous polypropylene intestinal anastomoses. Am J Surg 1991; 162: 461–7. 29. Choy PY, Bissett IP, Docherty JG, Parry BR, Merrie AE. Stapld versus handsewn methods for ileocolic anastomoses. Cochrane Database Syst Rev 2007; 3: CD004320. 30. Smith LE. Anastomosis with EEA stapler after colonic resection. Dis Colon Rectum 1981; 24: 236–42. 31. Gordon PH, Vasilevsky CA. Experience with stapling in rectal surgery. Surg Clin North Am 1984; 64: 555–66. 32. Dochetry JG, McGregor JR, Akyol AM, Murray GD, Galloway DJ. Comparison of manually constructed and stapled anastomoses in colorectal surgery. Ann Surg 1995; 221: 176–84. 33. Fazio VW. Cancer of the rectum-sphincter-saving operation. Stapling techniques. Surg Clin North Am 1988; 68: 1367–82. 34. Last MD, Fazio VW. The rational use of the purse-string device in constructing anastomoses with the circular stapler. Dis Colon Rectum 1985; 28: 979–80. 35. Cohen Z, Myers E, Langer B et al. Double stapling technique for low anterior resection. Dis Colon Rectum 1983; 26: 231–5. 36. Griffen FD, Knight CD. Stapling technique for primary and secondary rectal anastomoses. Surg Clin North Am 1984; 64: 579–90. 37. Julian TB, Ravitch MM. Evaluation of the safety of endto-end (EEA) stapling anastomoses across linear stapled closures. Surg Clin North Am 1984; 64: 567–78. 38. Ravitch MM. Varieties of stapled anastomosis in rectal resection. Surg Clin North Am 1984; 64: 543–54.

intraoperative anastomotic challenges 39. Tan WS, Ng KH, Eu KW. Salvaging a linear staple line defect in ultra-low anterior resection. Tech Coloproctol 2007; 11: 266–7. 40. Khoury DA, Opelka FG. Anoscopic-assisted insertion of eneto-end anastomosing staplers. Dis Colon Rectum 1995; 38: 553–4. 41. Simillis C, Purkayastha S, Yamato T et al. A meta-analysis comparing conventional end-to-end anastomosis vs. other aastomotic configurations after resection in Crohn’s disease. Dis Colon Rectum 2007; 50: 1674–87. 42. Beard JD, Nicholson ML, Sayers RD, Lloyd D, Everson NW. Intraoperative air testing of colorectal anastomoses: a prospective tandomized trial. Br J Surg 1990; 77: 1095–7. 43. Griffith JM, Trapnell JE. Intraoperative testing of anastomotic integrity after stapled anterior resection for cancer. J R Coll Surg Edinb 1990; 35: 35–6. 44. Yalin R, Aktan AO, Yeg en C, Döslüog lu H, Okboy N. Importance of testing stapled rectal anastomoses with air. Eur J Surg 1993; 159: 49–51. 45. Davies AH, Bartolo DC, Richards AE, Johnson CD, McC Mortensen NJ. Intra-operative air testing: an audit on rectal anastomosis. Ann R Coll Surg Engl 1988; 70: 345–7. 46. Smith S, McGeehin W, Kozol RA, Giles D. The efficacy of intraoperative methylene blue enemas to assess the integrity of a colonic anastomosis. BMC Surg 2007; 7: 15. 47. Gilbert JM, Trapnell JE. Intraoperative testng of the integrity of left-sided colorectal anastomosis: a technique of value to the surgeon in training. Ann R Coll Surg Engl 1988; 70: 158–60. 48. Wheeler JM, Gilbert JM. Controlled intraoperative water testing of left-sided colorectal anastomosis: are ileostomies avoidable. Ann R Coll Surg Engl 1999; 81: 105–818.

49. Makabeli G, Williams LG. Repair of defective EEA anastomosis. Dis Colon Rectum 1984; 27: 490–1. 50. Perez RO, Sousa A Jr, Bresciani C et al. Endoscopic management of postoperative stapled colorectal anastomosis hemorrhage. Tech Coloproctol 2007; 11: 64–6. 51. Pearl RK, Abcarian H. Diverting stomas. In MacKeigan JM, Cataldo PA. Intestinal Stomas: Principles, Techniques, and Management. St. Louis, MO: Quality Medical Publishing, Inc 1993: 107–26. 52. Prasad ML, Pearl RK, Orsay CP. End-loop ileocolostomy for massive trauma to the right side of the colon. Arch Surg 1984; 119: 975–6. 53. Williams NS, Nasmyth DG, Jones D et al. De-functioning stomas: A prospective controlled trial comparing loop ileostomy with transverse colostomy. Br J Surg 1986: 73: 566–70. 54. Carter DC, Jenkins DHR, Whitfield HN. Omental reinforcement of intestinal anastomoses. Br J Surg 1972; 129–33. 55. McLachlin AD, Denton DW. Omental protection of intestinal anastomoses. Am J Surg 1973; 125: 134–40. 56. Trowbridge PR, Howes EL. Reinforcement of colon anastomoses using polyurethane foam treated with neomycin: an experiemental study. Am J Surg 1967; 113: 236–40. 57. Laufman H, Method H. Effects of absorbable foreign substance on bowel anastomosis. Surg Gynecol Obstet 1948; 86: 669. 58. Hoffmann J, Shokouh-Amiri MH, Damm P, Jensen R. A prospective, controlled study of prophylactic drainage after colonic anastomoses. Dis Colon Rectum 1987; 30: 449–52. 59. Sagar PM, Couse N, Kerin M, et al. Randomized trial of drainage of colorectal anastomoses. Br J Surg 1993; 80: 769–71.

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6

Other intraoperative challenges James T McCormick and Sharon G Gregorcyk

challenging case You are operating on 64-year-old man with a locally advanced rectal cancer that has been treated with neoadjuvant chemoradiation. The mass is large, the dissection is difficult and the tissue is edematous and friable. As you are dissecting along the right pelvic sidewall your assistant adjusts the retractor and there is an immediate, brisk rush of blood into the field. You attempt to pack the area but the blood soaks the lap immediately. Your patient is bleeding. You also note significant edema and are already ­concerned about closing the abdomen.

should be stopped 1 week before surgery. The same is true for aspirin, NSAIDs, and clopidogrel bisulfate, while warfarin is held 3 to 5 days before surgery.(3) For patients at a higher risk for a thromboembolic event, such as those with recent coronary stent, a recent (<3 mo) history of venous thromboembolism, or mechanical ­cardiac valve in the mitral position, a discussion with the patients treating physician or cardiologist is advised and the risks and benefits weighed.(4) In the emergency setting, platelets and fresh frozen plasma may be necessary to immediately address bleeding disorders, iatrogenic or otherwise.

case management You alert the anesthesia personnel of the occurrence of ongoing blood loss. Various intraoperative challenges exist and can occur on any given case. Some challenges may be predictable while ­others may not. One must be prepared to address any number of events during any given case. All of these challenges should be approached with calm reason and sound surgical principles to optimize the outcome.

intraoperative hemorrhage Intraoperative bleeding ranges from a small amount of oozing to major hemorrhage. Even small, pesky bleeding can be an issue laparoscopically by absorbing light and obscuring the view. Using cautery or devices such as the Harmonic scalpel™ (Johnson and Johnson) or Ligasure™ (Covidien) may help minimize this obstacle. Dividing major vessels can always result in significant bleeding if the vessel is not adequately ligated. For the open case, simply regrasping the vessel and tying it off takes care of the problem. Laparoscopically, one can quickly lose visualization and lose track of the vessel. Being prepared can help avert this problem. One technique is to hold on to the proximal portion of the vessel being divided so it can be quickly occluded. A surgical clip or Endoloop™ (Johnson and Johnson) can then be applied if needed. Having those supplies in the room where they can be easily and quickly accessed is advantageous. Most important is wisely choosing the device with which to divide the vessel. Older patients may have atherosclerotic disease in their vessels with calcification, which may cause devices such as the Ligasure™ (Covidien) to be less effective. In these cases, stapling, clipping, or tying the vessels may be more prudent. The spleen can be a source of profound bleeding. Its anatomic relationship to the colon and omentum makes it vulnerable to injury, especially during mobilization of the splenic flexure. Dividing these attachments without retracting too vigorously is key to avoid a splenic capsular tear/avulsion. This can be achieved by approaching the splenic flexure from different angles—medially through the lesser sac, inferiorly coming over top of Gerota’s fascia, and laterally by dissecting along the white line of Toldt. If an injury does occur to the spleen, it is most commonly a capsular tear that can be controlled by electrocautery. If the bleeding is brisk, the spleen should be packed off and preparations made to address the bleeding. The anesthesiologist should be alerted to the potential ensuing blood loss. Once the anesthesiologist is prepared, having given adequate fluids, and with blood products available, the packs can be removed. Topical hemostatic agents, such as microfibular collagen, methylcellulose, or fibrin glue may be necessary and should be available. An argon beam coagulator can also be beneficial in this setting. Other key preparatory points

preoperative evaluation The preoperative evaluation is useful to anticipate and in some cases minimize intraoperative challenges. As always, one should start with a thorough history and physical examination. The surgical history including indications and complications is important in predicting intraabdominal adhesive disease. Multiple abdominal surgeries, intraabdominal abscess, perforation, hernia repairs with mesh, and enterocutaneous fistulae are all concerning for significant adhesive disease. On examination, a stiff, noncompliant, scarred abdominal wall adds to the concern. With regards to bleeding risk, you should question the patient about any prior bleeding problems with surgery, easy bruising, bleeding gums when brushing teeth, heavy menses, or a family history of hemorrhagic complications. Any of these may indicate an underlying coagulation disorder. Medical problems such as renal failure, hepatic failure, and portal hypertension should likewise raise a red flag with regards to bleeding risk. If there is no indication by history of a bleeding problem, routine blood work to further assess this issue is not indicated as the yield is very low. (1) When further evaluation is needed, a bleeding time is the most effective single test covering all aspects of the coagulation system. If it is prolonged, then further testing is necessary. Another important component of the history is the patient’s medication list. Easy to identify medications that increase the risk for bleeding are warfarin, aspirin, non-steroidal anti-inflammatory drugs (NSAIDs), clopidogrel bisulfate, and ticlopidine hydrochloride. More subtle, often missed and increasingly popular are herbs, vitamins, and dietary supplements. Some of the more common agents that can prolong bleeding time include garlic, ginkgo, ginseng, capsaicin, fish oil, ginger, and vitamin E.(2) In general, these agents

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other intraoperative challenges are adequate exposure, working suction, and appropriate length instruments. Laparoscopic splenic injuries may require conversion to an open procedure to control the bleeding. However, the risk of splenic injury is actually reported to be lower in laparoscopic versus open cases with one series revealing no splenic injuries in almost 2,000 laparoscopic colectomies compared to 0.24% in over 5,000 open colectomies.(5) Once the packs are removed, if the bleeding cannot swiftly be stopped by simple means, the spleen should be mobilized into the operative field dividing its avascular ligaments with electrocautery. While mobilizing the spleen, pressure is held directly on the spleen or the splenic hilum to slow down the bleeding. The decision now must be made as to whether splenic salvage or splenectomy should be performed. While one should be aggressive in attempting to save the spleen, these attempts should not continue in the face of ongoing bleeding or if the patient is unstable. A splenectomy may be necessary and is very affective in stopping the bleeding. Splenectomy carries a 5% lifetime risk of postsplenectomy sepsis syndrome, primarily from encapsulated bacteria such as Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis. Vaccinations for pneumococcal, meningococcal and H. influenza are recommended following splenectomy to curtail this incidence.(6–8) Additionally, antibiotic prophylaxis and aggressive treatment of infections may be advocated. Early complications associated with a splenectomy include pneumonia, pancreatitis, and subphrenic abscess. Attempts to preserve the spleen include partial splenectomy, mattress suture repair, and mesh wrap. The mesh wrap is performed with a polyglycolic mesh. A keyhole is cut in the mesh and the spleen is passed through the defect such that the hole is encircling the splenic hilum. The mesh is then wrapped around the spleen and sutured to itself resulting in compression on the spleen.(9) Hemorrhage in the pelvis is a particularly difficult challenge. In addition to the vessels themselves being difficult to control, the ­confines of the pelvis limit the exposure and space in which to work. A bulky tumor, inflammation, or radiation changes can magnify the complexity. Portal hypertension which results in enlargement of numerous pelvic collaterals can complicate matters further. While bleeding associated with the posterior vaginal wall or prostate can be frustrating, it does not compare to the potentially exsanguinating hemorrhage that can occur from the pelvic side wall or presacral region. Once again, immediate packing of the region should be performed in an attempt to slow bleeding while preparing to definitively control it. Long instruments, an extra suction device, and any necessary equipment should be gathered. Anesthesiologists should adequately resuscitate the patient and be ready to give blood products. The walls and floor of the pelvis are lined by the endopelvic fascia. If this fascia is not violated, then bleeding is not typically an issue. Deep to this endopelvic fascia on the side walls are the internal iliac veins. Injury to one of these veins results in profuse bleeding. The vessels are large and thin walled which can make suturing difficult. Suture ligation is the best option. Compressing the iliac artery to decrease the inflow may be of benefit but will not stop the bleeding. If a vascular surgeon is readily available, this expertise can prove very helpful. They routinely suture vessels and are less likely to tear thin-walled vessel while attempting repair.

They will need assistance with exposure and help keeping the blood suctioned out. This double-team approach with two skilled surgeons is most advantageous. Other tools that may be useful are clip appliers. The laparoscopic instruments, even in an open case, can give extra length that may be necessary deep in the pelvis. Presacral hemorrhage can also result from violation of the endopelvic fascia over the sacrum and injuring the underlying presacral vein. These avalvular veins communicate with the internal vertebral venous system through the basivertebral vein. This system can attain high pressures and result in profuse bleeding. The veins retract into the sacral foramen, which is problematic. In contrast to injury to the iliac vein, packing the pelvis in the case of presacral vein injury may be sufficient to stop the bleeding. When possible, the specimen should be resected to optimize access. The packing may need to be left in place for 10 minutes or more to be effective and patience is needed. Once again, having resources ready to control the bleeding once the packs are removed is paramount. The electrocautery should be turned up to high levels (up to 60–80 watts) and at times it alone can control the bleeding. Clips or suture ligation can work, but are limited secondary to the retraction of the vessels and the lack of mobility of the presacral tissue. Titanium thumb tacks are commercially available and can be placed directly into the sacrum to occlude the vessels. Multiple thumb tacks may have to be placed. If the bleeding does not stop but is sufficiently retarded, then topical agents or repacking the pelvis may achieve complete hemostasis. In severe cases of pelvic hemorrhage, when all else fails, the pelvis should be tightly packed and the patient taken to the ICU for resuscitation and correction of any coagulopathies. In the rare case of an arterial injury, angiographic embolization may be useful. Typically, the patient is taken back to the operating room in 24–36 hours after having been optimized. At this time, most bleeding will have stopped or at least become manageable. With any massive hemorrhage, consideration should be given to using a cell-saver to allow autotransfusion. In addition to transfusing blood, FFP and platelets may be necessary. The patient should be warmed to ­further improve their clotting ability. Another issue to be addressed, in the pelvis especially, is to whether to proceed with an anastomosis. The patient’s hemodynamic status dictates this decision. Poor perfusion to an anastomosis would result in a high risk of a leak, while a pelvis full of blood clots would increase the risk of infection. Both are deterrent to a successful anastomosis. Additionally, the actual time to do the anastomosis may be a consideration, as this may contribute to hypothermia and blood loss. With laparoscopic surgery, an additional bleeding risk occurs at each trocar site. A vessel can be injured during placement of the port within the abdominal wall. The most commonly injured abdominal wall vessels during laparoscopy are the inferior epigastric vessels, with an average incidence of approximately 0.1%.(10) As the ports themselves will often tamponade a vessel injured during insertion, it is wise to remove as many ports as possible under direct laparoscopic visualization. Recognizing and dealing with the injury at this point will prevent an untimely return the operating room and/or the morbidity related to hematoma. The majority of time this is a small vessel and can be controlled with pressure or cautery alone. In the case of continued bleeding, the incisions may need to be extended and suture ligation of the vessel performed. Alternatively, bleeding

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improved outcomes in colon and rectal surgery from the abdominal wall can be addressed by placing a stitch across the port site defect. This can be accomplished with use of a Keith needle or an Endo Close™ (Covidien) device. The stitch is passed externally through full thickness abdominal wall into the peritoneal cavity, grasped within the peritoneum, and laparoscopically passed back out and tied. This can repeated as necessary. damage control The term damage-control laparotomy refers to a management strategy first described for use in the unstable multiple organ trauma patient.(11–14) The goal is to stop hemorrhage, curtail contamination, and remove or debride any frankly necrotic tissue. Reconstruction, definitive therapy, and abdominal wall closure are deferred in favor of correction of metabolic derangements, hypothermia, and coagulopathy, with the plan, ultimately, to return to the operating room for completion of surgical therapy and abdominal wall closure. This usually involves some sort of temporary containment of the viscera and packing of the open wound. It is not hard to imagine that these basic concepts and principles may be applied to any patient who may benefit from an abbreviated initial operation followed by stabilization and optimization before definitive management.(15, 16) As there is potential morbidity associated with leaving the abdominal wall open and multiple trips to the operating room, indications must be carefully considered and proper patient selection is critical. Patients with poorly controlled metabolic derangements and acidosis, significant hypothermia, and clinical evidence of coagulopathy may be considered appropriate candidates. Selection criteria have been summarized as follows: inability to achieve hemostasis due to coagulopathy, time-consuming procedure in an appropriate patient (>90 min), inaccessible major venous injury, associated life-threatening injury in a second anatomical location, planned reassessment (in 24–72 hours) of abdominal contents (as in a patient with questionable bowel viability), inability to close fascia due to visceral edema, or concern for development of abdominal compartment syndrome.(17, 18) The most common indication is related to hemorrhage and massive resuscitation. This may be accompanied by hemodynamic instability, coagulopathy, cardiac ischemia and often, massive bowel edema. In the nontrauma venue this may be the patient who has received large volume resuscitation for lower gastrointestinal or intraoperative hemorrhage or who has returned to the operating room for postoperative hemorrhage. During the course of the operation previously hemostatic sites may begin to bleed signaling coagulopathy—dilutional, consumptive, and/or hypothermia related. In this bleak scenario, it may be reasonable to pack the abdomen, apply an occlusive dressing, and take the patient to ICU for aggressive rewarming, ongoing resuscitation, and optimization, followed by a return to the operating room in 24–72 hours when these variables have been minimized. Likewise, a patient may escape the coagulopathic and hypothermic effects of large volume resuscitation but massive edema may manifest as increased pulmonary pressures or hemodynamic compromise from abdominal compartment syndrome when the fascia is closed.(19) Occasionally, massive bowel edema can preclude closure of the fascia and forcing the issue can lead to abdominal compartment syndrome or at the very least compromise pulmonary

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function. This can be seen when operating for bowel obstruction but can be worsened further when septic complications accompany the obstruction. Even after the obstruction is relieved, the bowel remains edematous from both the obstruction and from the resuscitation. Serosal compromise is not uncommon, in sometimesdramatic fashion, when longitudinal tears occur secondary to massive dilation. The integrity of the bowel is in question but resection would be too extensive and anastomosis dubious. Protecting the bowel and applying a suction dressing would allow for resolution of the systemic inflammatory response and diuresis, followed by reoperation, reassessment, and definitive abdominal closure. Abdominal compartment syndrome can be caused by increased retroperitoneal volume, increased intraabdominal volume, and/ or restriction of abdominal wall expansion. When intraabdominal pressure (IAP) increases rapidly, physiologic derangement can be seen. This pressure can be measured directly by intraabdominal catheter or indirectly by gastric, urinary, or inferior vena cava catheterization, but urinary bladder pressure has been shown to best correlate with IAP. Physiologic derangements seen in the course of abdominal compartment syndrome occur in multiple systems. Pulmonary changes are usually the most prominent with diaphragmatic elevation leading to decreased pulmonary compliance with decreased lung capacity, decreased residual capacity, and decreased volumes. Cardiovascular changes include decreased filling secondary to venous compression, decreased ventricular end-diastolic volumes, increased afterload, decreased contractility, and loss of cardiac output. Prerenal azotemia unresponsive to volume is a characteristic finding, with oliguria leading to anuria due to decreased renal perfusion, decreased glomerular filtration rate, and increased retention of sodium and water with renin production. Compression of splanchnic vasculature leads to ischemia and translocation of bacteria. Hepatic insufficiency can also result. Intracranial pressure is seen to increase with decreased cerebral perfusion and decreased venous outflow.(20) Abdominal compartment syndrome is generally noted in patients with a urinary bladder pressure of more than 20 mmHg. Patients with high pressure will require decompression if any of the aforementioned signs are noted. If when attempting to close the abdomen pressure becomes unacceptably high, as evidenced by impairment of respiratory mechanics and an increase in the peak airway pressures, the diagnosis should be considered and routine closure should be avoided. The objectives of the temporary closure are containment of viscera, control of abdominal secretions, maintenance of tamponade, and facilitation of future closure.(21) A polyethylene sheet (or a large occlusive dressing folded in half on itself) is perforated multiple times and placed over the peritoneal viscera but beneath the abdominal wall peritoneum. Then, sterile surgical towels are placed atop the protective sheet and the edges tucked below the skin, fascia, and peritoneum. Jackson-Pratt or similar suction drains are positioned on the towels and tunneled beneath the skin to exit away from the wound edge. The skin is prepared with tincture of benzoin and covered with a plastic drape backed with iodophor-impregnated adhesive.(22) The drains are kept to continuous wall suction. Alternatively, a vacuum-assisted closure device, such as V.A.C.® (KCI) may be applied over the polyethylene sheet and may be associated with a higher rate of primary delayed fascial closure (23) (See Figures 6.1 and 6.2).

other intraoperative challenges Careful planning, technique, and patient selection should minimize the colorectal surgeon’s encounters with damage control situations. However, when confronted by a scenario with suspect options and dubious outcome, a damage-control laparotomy can turn an uncontrolled situation into a controlled second-look operation with potentially more desirable options and outcomes.

Figures 6.1  Example of a damage control laparotomy: before placement of temporary closure device.

adhesive disease Adhesions result from prior abdominal surgeries or infections. One would expect adhesions to be worse in a patient with multiple prior abdominal surgeries or a history of a bowel perforation. Particularly concerning for adhesions are those patients with enterocutaneous fistulas and a history of intraperitoneally placed mesh. Sometimes the adhesions encountered are much less than anticipated and other times they are, without warning, much worse than anticipated. Adhesions can be categorized as demonstrated in the grading system in Table 6.1. With surgery, one of the first objectives is to enter the peritoneal cavity without causing a bowel injury. With heightened concern about adhesions, more caution is exercised and, if possible, the abdomen is entered in virgin territory. With laparoscopic surgery, adhesions can be prohibitive. Some patients are obviously not laparoscopic candidates, such as the patient with a stiff abdominal wall with extensive scarring and/ or multiple enterocutaneous fistulas. Other patients may be borderline candidates for laparoscopy. In these cases, an attempt can be made to look in the abdomen with the laparoscope and then make a decision whether to proceed laparoscopically or not. A limited number of laparoscopic instruments can initially be opened to save resources until this decision is made. One may access the peritoneal cavity using the Hasson technique. Alternatively, pneumoperitoneum can be established with a veress needle at a site remote from previous surgery and the insufflated peritoneal cavity accessed using a Visiport™ (USS/TYCO) or a clear optic tip port (Ethicon). The author prefers the later technique most commonly at a left upper quadrant site.(25, 26) Others have advocated the use of a “peek-port” where an approximately 7 cm incision is made and the abdomen assessed. If the abdomen appears hostile, the incision is lengthened and a laparotomy preformed. If favorable, hand-assisted laparoscopic surgery (HALS) can be employed.(27) For open cases, again, entering the abdomen in virgin territory is advantageous. Exposure and visualization are important to avoid bowel injury, so frequent suctioning or dabbing with a laparotomy sponge is used. Different techniques for dividing adhesions exist, but most will be taken sharply with scissors or scalpel. Electrocautery is employed cautiously and judiciously, as collateral damage may occur to adjacent bowel and go unrecognized until the patient becomes sick postoperatively. A scalpel is especially ­useful in the very dense adhesions of bowel to the abdominal wall. Table 6.1  Grading system for bowel adhesions.

Figure 6.2  Example of a damage control laparotomy: after placement of temporary closure device, with application of the V.A.C.® (KCI) system. (Courtesy of Richard Fortunato, DO, Pittsburgh, PA).

Optimal timing of return to the OR is poorly defined but it is felt that patients who are returned to the OR after more than 72 hours experience greater morbidity and mortality.(24)

Grade Description 1 2 3 4

Thin filmy adhesions. Adhesions that can be divided by blunt dissection. Dense adhesions that require sharp division. Dense adhesions, the division of which results in bowel injury.

Source: Adapted from Fazio VW. Personal communication, 1998.

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improved outcomes in colon and rectal surgery A more difficult or dense adhesion can be approached from different angles to help define the appropriate plane. Oftentimes, ­simpler adhesions can be taken down on either side or even behind the dense adhesion to help delineate the proper path of dissection. Placing one’s fingers on either side of the adhesion and palpating can be of assistance to feel the plane and also sometimes stretch out the adhesion for easier division. Of course, one of the biggest keys to success is proper traction and counter-traction. If the traction is too forceful though, tearing of the bowel may occur. If an enterotomy does occur, it should be repaired immediately with absorbable sutures to minimize contamination. If the case is difficult and more injuries are predicted, temporary closure can be employed until all adhesiolysis is complete. A segment of bowel with extensive injuries may be best resected. Waiting until all injuries have been identified and a plan made can save significant time on unnecessary repairs. Sometimes dissection can be performed in an extraperitoneal plane to avoid bowel injury, leaving peritoneum adherent to the bowel wall. Other times a small piece of bowel wall may be left behind, adherent to a more critical structure, such as the ureter or iliac vessels, in order to avoid morbid injury at these crucial sites. Leaving devascularized bowel serosa or muscularis in-situ is not a problem. Any mucosa left behind, however, should be desiccated with electrocautery to prevent formation of mucoceles or malignancy. Consideration should be given in each case to preventing adhesions, which lowers the risk of bowel obstruction and makes any future surgeries easier. Adhesion formation is a local response of the peritoneum and pertonealized structures to ischemia, ­desiccation, or trauma and may form as result of the primary ­disease process or due to contact with surgical instruments, staples, suture, gloves, sponges, and other irritants introduced at the time of surgery. It is assumed that laparoscopy can minimize some of these insults by limiting bowel manipulation and exposure of the peritoneal surface to potential irritants.(28–30) Preliminary evidence in this regard can be found by noting that laparoscopic assisted ileocolic resection is associated with reduced rate of bowel obstruction when compared to open surgery.(31, 32) Adhesions to the anterior abdominal wall are minimal or absent.(33) (See Figures 6.3 and 6.4) (34) Additionally, the CO2 pneumoperitoneum is felt to be protective of certain types of injury.(35, 36) Initial hope for elimination of adhesive disease with the advent of laparoscopy (37) has been replaced by the realization that adhesions do indeed form and reform after laparoscopy, ­primarily in the operative field, (38, 39) but to a lesser extent than with open surgery. Despite these advantages, bowel obstruction continues to occur frequently in patients following laparoscopic surgery. The mechanism, severity, and risk of obstruction have shifted however. In a report for the French Association for Surgical Research, Duron (39) and colleagues noted that only 33% of postoperative bowel obstructions following various laparoscopic surgeries were due to multiple adhesions, while an additional 17% were due to a single band. Intestinal incarceration (in abdominal wall defect or port site) (See Figures 6.5 and 6.6) was responsible for another 46%. All told, 25% of patients required resection. A report from the Western Pennsylvania Hospital describes unique mechanisms of bowel obstruction, such as internal hernia, are common after laparoscopic bariatric surgery.(40) The reason for

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Figure 6.3  Laparoscopic images demonstrating lack of adhesions in a patient undergoing laparoscopic appendectomy for appendicitis 2 years after hand-assisted laparoscopic anterior resection for recurrent sigmoid diverticulitis. (Courtesy of Thomas E. Read, MD, Pittsburgh, PA).

this is assumed to be the result of a laparoscopy-related decrease in scar formation between newly apposed peritoneal surfaces which leaves defects open.(41) One can imagine this same phenomenon following laparoscopic colon resection. Obstructions due to internal hernias are associated with a high incidence of bowel threatening ischemia and therefore require a high index of suspicion and prompt surgical management. The authors’ experience is that relaparoscopy, in this patient population, is an excellent technique for diagnosing and managing these obstructions and other complications.(40) General principles to minimize adhesions include gentle handling of the tissue, hemostasis, and avoidance of infection and ischemia. Products such as SeprafilmTM (Genzyme), a bioabsorbable membrane of sodium hyaluronate, and carboxymethylcellulose, can be placed at the time of surgery to reduce the incidence of adhesions.(42–44) It should be noted that these products should not be placed adjacent to a fresh anastomosis.(45) A qualification must be maintained in the case of adhesions encountered when operating on a patient with a malignancy. If the adhesions are between a cancer and another structure, they

other intraoperative challenges

Figure 6.6  A port site hernia causing a bowel obstruction and injury to the bowel.

should be treated as an extension of the malignancy. In other words, they should not be divided, but instead resected with the specimen. This process might require partial resection of another structure such as another limb of bowel or abdominal wall. Not all adhesions encountered during surgery for malignancy are malignant adhesions however. Attention should be paid to the extent of the tumor such as growth through the full-thickness bowel wall and its relationship to the adhesions as well as the characteristic of the adhesion.

Figure 6.4  Laparoscopic images demonstrating lack of adhesions in a patient undergoing laparoscopic appendectomy for appendicitis 2 years after hand-assisted laparoscopic anterior resection for recurrent sigmoid diverticulitis. (Courtesy of Thomas E. Read, MD, Pittsburgh, PA).

Figure 6.5   A port site hernia causing a bowel obstruction and injury to the bowel.

lesion localization Up to 22% of endoscopically unresectable colorectal neoplasms with benign histology on initial biopsy harbor invasive adenocarcinoma. Adhering to oncologically sound principles for these neoplasms is advised.(46) Many of these will not be easily palpable during surgery and even more difficult to localize laparoscopically. For operative planning, particularly when considering a laparoscopic approach, accurate localization of the tumor is imperative to avoid removal of the wrong segment of intestine.(47) Colonoscopy alone as a localizing technique is inaccurate (48) unless the tumor is clearly noted to be in the direct proximity of to an unmistakable landmark such as the rectum or cecum. As such, localization should be more definitively accomplished preoperatively. Endoscopic injection of India ink in three or four quadrants of bowel adjacent to and distal to, but not through the tumor, is safe and reliable, and preferred in most centers (49, 50) (See Figure 6.7). Other adjuncts for localization include endoscopic placement of clips and subsequent plain film of the abdomen (See Figure 6.8). Alternatively, barium enema or CT colography can be employed. (51) Though more costly than India ink injection and associated with radiation exposure, these modalities offer the additional advantage of preoperative planning for room set up and patient positioning for left vs. transverse vs. right colectomy. One disadvantage of these approaches is they offer no direct intraoperative evidence of the lesion localization. Therefore they may be most effectively used in conjunction with India ink marking. Some centers have reported success with preoperative endoscopic clip placement followed by intraoperative laparoscopic

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improved outcomes in colon and rectal surgery

Figure 6.7  India ink injected endoscopically before laparoscopy provides excellent lesion localization.

Figure 6.8  A plain film of the abdomen after endoscopic placement of clip (arrow) can provide valuable information about the location of the lesion and aid in preoperative planning.

ultrasonography or intraoperative fluoroscopy.(52) These intraoperative imaging modalities, though effective, tend to be cumbersome, resource intensive, and operator dependent. Due to the flexible nature of the colonoscope, the distance of the tumor from the anal verge cannot be accurately measured on colonoscopy. When the tumor is obviously within the colon or is palpable within the rectum, this limitation of the colonoscope is not an issue. Unfortunately, not uncommonly, a tumor reported to be in the sigmoid colon by colonoscopy is actually much lower and represents rectal cancer. A rigid proctoscope is very useful to accurately measure the distance of the tumor from the anal verge, which not only helps in planning surgery but also determines if the tumor is in a location that its stage might warrant preoperative neoadjuvant therapy.(53)

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Careful preoperative assessment and planning is the best way to ensure that the appropriate segment of the intestine is removed. The most notable preventable cause includes assumptions made based on colonoscopic determination of a site that is not within the direct proximity to an unmistakable landmark such as the rectum or cecum. Occasionally, however, despite our best efforts, localization attempts fail to identify lesions intraoperatively in up to 12% of cases.(54) Failure to visualize a tattoo can result from disappearance of the tattoo compound, particularly when products other than India ink are used.(55) Additionally, failure to inject the ink compound into the submucosal tissue plane can result in dissemination of the ink and imprecise localization or intraperitoneal injection. Although this presents little direct risk to the patient, it does present a problem with definitive intraoperative localization. Techniques that have been described to minimize this occurrence include injecting saline to develop the submucosal plane before injection of ink.(56) The surgeon must be prepared to deal with the case where localization efforts have failed. Blind resection is not advised unless confidently guided by preoperative imaging. Mobilization of the flexures and dissection of the omentum off the transverse colon may reveal a hidden tattoo mark. During laparoscopy, palpation cannot be performed well but a hand assist device can be used to overcome this limitation. Still there are cases where the lesion is too small to palpate and remains unfound. Under such circumstances, intraoperative colonoscopy can permit localization.(57) Use of CO2 insufflation during the colonoscopy will minimize bowel distention. This is critical if laparoscopic assisted surgery is planned. Requiring equipment, expertise, and time, this is best reserved as a back-up rather than a primary localization modality. Regardless of the technique of localization, opening the specimen after resection to confirm the presence of the lesion is recommended. abdominal wall closure Abdominal wall closure is required following laparotomy and at the specimen retrieval site for laparoscopic colectomy. Woundrelated complications such as acute wound failure (dehiscence), infection, and incisional hernia can result in significant morbidity. Malnutrition, tobacco abuse, and/or requirement for systemic corticosteroids or chemotherapy will increase risk. Ideally, these factors should be modified preoperatively whenever possible. Intraoperatively, proper technique minimizes the risk of wound complication and will be the focus of this discussion. Acute wound failure, defined as an early separation of the abdominal musculoaponeurotic layers, occurs at an incidence of approximately 1.2% (range 0–2.3%), (58–62) with the majority occurring between the 6th and 9th postoperative days.(63, 64) The most common cause is felt to be suture tearing through the fascia but may also occur as a result of abdominal wall rupture away from the incision or excessive suture interval. Suture breakage and knot slippage are rare.(58, 6, 65–70) An incisional hernia is failure of complete abdominal wall healing following abdominal surgery, resulting in a myofascial defect. The reported incidence of incisional hernias in the literature varies from 9–19%. They often require repair, with recurrence rates as high as 45%, causing further complications. The ideal abdominal wound closure should minimize this complication.

other intraoperative challenges technique Numerous studies have demonstrated mass closure to be superior to layered closure in clinical practice (71–73), since incorporating large bites of tissue reduces the pressure per unit area caused by the suture and decreases the risk of suture cut-through (74, 75). Although a randomized trial of mass versus layered closure showed no significant difference in wound rupture, (76) and most clinical studies comparing mass closure to layered abdominal closure have not revealed a difference in the incidence of incisional hernia formation, (73, 77) mass closure of the abdominal wall is currently favored because of its safety, efficacy, and speed. It is important to note that peritoneum heals by regeneration of the layer over the entire defect, and not in incremental advancement from the wound edge.(78, 79) Randomized studies revealed no difference between a one-layered closure (peritoneum not sutured) and a two-layered closure (peritoneum sutured) in midline and paramedian incisions.(73, 80) Peritoneal closure is therefore not vital in abdominal closures and may contribute to adhesion formation. Experimental models and cadaveric studies have shown that continuous abdominal wall closure provides the greatest wound security in terms of abdominal dehiscence.(81, 82) Continuous suturing is thought to equalize the tension differences between individual stitches and distributes the tension along the suture line, thus reducing the risk of tissue strangulation and late cutthrough.(65, 81, 83, 84) The number of knots and therefore the likelihood of knot slippage may be minimized. A meta-analysis comparing six randomized controlled trials of continuous versus interrupted closure (irrespective of suture type) found the incidence of incisional hernias to be significantly less with continuous closure.(85) There is a zone of collagenolysis and matrix degradation that extends out 0.75 cm from each wound edge.(86, 87) Further, fascia strength near its cut edge decreases by 50% during the first 48 hours after an operation.(88) Experimental models have demonstrated a continuous closure while maintaining a 1 cm stitch interval and a 1 cm tissue bite reduces dehiscence rate as compared to smaller tissue bites by minimizing the risk of suture cut-through.(89)

retention sutures Retention sutures are thought to aid abdominal closure by preventing wound necrosis and avoiding evisceration. However, problems associated with retention sutures are several and include exacerbation of the intraabdominal hypertension when the ­viscera are forcibly contained, and abdominal wall ischemia when the sutures become too tight. Furthermore, several studies have implicated retention sutures in the development of enterocutaneous fistulae even when they are placed extraperitoneally. With caution, retention sutures may be considered in abdominal wall closure in the patient with multiple risk factors for delayed wound healing; they are not recommended for those at risk for development of abdominal compartment syndrome. If loss of abdominal domain does not permit a tension free ­fascial closure, one can consider relaxing incisions to permit medial mobilization of the rectus. This requires dissection above the fascia laterally to the lateral edge of the anterior rectus sheath, which is then incised in the sagittal plane, similar to the technique for separation of parts. This technique should be used cautiously in patients at risk for abdominal compartment syndrome and those at above average risk for wound infection.

suture material Slowly resorbed monofilaments (polydioxanone: PDS® and polyglyconate: Maxon®) are the strongest sutures in the fresh state, ­followed by the nonresorbable monofilaments (nylon: Ethilon® and polypropylene: Prolene®), and then the braided sutures (polyglactin: Vicryl®, polyglycolic acid: Dexon®).(90) Silk and chromic catgut, are not appropriate.(91, 66, 92, 93) With regard to incisional hernia formation, it is known from experimental studies that the abdominal fascia continues to gain strength up to 3 months after surgery.(94) Nylon (Ethilon®) loses approximately 20% strength per year while Polypropylene, Surgilene®, Ethibond®, Tevdek®, and polybutester (Novafil®) seem to retain their strength indefinitely.(95) Catgut, Dexon®, and Vicryl® have tensile strength half-lives in the range of 1–4 weeks, and are not suitable for fascial closure. Vicryl®, compared with ­nonresorbable sutures (Prolene®), is associated with an increased rate of wound failure and incisional hernias (85). This is in contradistinction to more slowly resorbed materials, such as polydioxanone (PDS®), that do not appear to increase the rate of

synthetic prostheses The use of synthetic mesh has been a popular technique in abdominal wall closures and reconstructions for many years and the most extensive experience is with polypropylene mesh (Prolene® and Marlex®).(102) Multiple reports in the literature cite the advantages of this permanent material, which include availability, ease of use, high tensile strength and durability, maintenance of abdominal wall compliance, potential avoidance of future reconstruction, and permeability allowing for peritoneal drainage. However, several investigators have pointed out the many long-term complications related to polypropylene mesh. Most notably, the mesh acts as a nidus of infection and is associated with severe foreign body reactions leading to mesh extrusion and enterocutaneous fistulae with an incidence on the order of 23%.(103) The placement of omentum between the mesh and the viscera has been shown to reduce the early fistula rate to 1–4%.(104) Recently mesh with an adhesion preventative film bonded to it (e.g., Sepramesh® (Genzyme)) has been introduced. The adhesive reductive film may reduce the problem of

incisional hernia (85). Multiple randomized trials have failed to demonstrate a difference in dehiscence rates between resorbable and nonresorbable sutures.(58, 96, 97) Additionally, persistent sinus formation and chronic wound infection can be virtually eliminated with the use of resorbable suture.(73, 98) Multiple clinical studies implicate wound sepsis as the most important factor associated with incisional herniation. Multifilament sutures provide a better growth environment for bacteria and are associated with a higher incidence of wound infection compared to monofilament sutures.(77, 99, 100) In summary, a continuous, mass closure using slowly-resorbable monofilament suture with a 1 cm tissue bite and a 1 cm interval is likely the best technique for primary abdominal wall closure.(101) It is assumed that minimizing abdominal wall trauma vis-à-vis laparoscopic approaches may minimize wound related morbidity.

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improved outcomes in colon and rectal surgery small bowel adherence to the underside of the mesh, which may reduce complications such as enterocutaneous fistulae and allow for an easier re-exploration or mesh removal. Use of polytetrafluoroethylene mesh (PTFE, Gore-Tex®) decreases the incidence of fistulization and mesh extrusion. However, PTFE impedes the free egress of abdominal fluid and may contribute to abdominal compartment syndrome and seroma formation. After appropriate consideration, polypropylene, or polytetrafluoroethylene mesh may be considered for abdominal wall reconstruction when there is tissue loss. Resorbable meshes, polyglactin acid (Vicryl®) and polyglycolic acid (Dexon®), may provide a temporary solution in the management of the difficult abdominal wall. In experimental studies, Dexon® is 50–70% absorbed and Vicryl® is almost fully absorbed by 10 weeks. Resorbable mesh offers the early advantages of permanent mesh without the late complications and allows for egress of fluid reducing the chances of intraabdominal hypertension. However, not surprisingly, the reported incidence of hernia is unacceptably high with the use of resorbable synthetic mesh.(105) biologic meshes There are several commercially available meshes (either allografts or xenografts) that are derived from naturally occurring sources of collagen and related connective tissues. The most extensively studied of these is Alloderm (Lifecell) (acellular dermal matrix derived from donated human skin) (106–109) and Permacol (Tissue Science Laboratories) (intact porcine dermal collagen) (110). Other variations on the theme include Collamend (Bard) (cross-linked acellular porcine dermal collagen and its constituent elastin fibers), Allomax® (Bard) (human dermal collagen), and Strattice® (Lifecell) (acellular dermal matrix derived from porcine skin). The purported advantage of all of these agents is a low risk of mesh infectious complication in contaminated fields. In the case of acellular dermal matrix, extracellular material provides a signal for fibroblast incorporation, collagen deposition, and maturation resulting in tissue that cannot be differentiated from fascia. (111–113) Long-term data are lacking. conclusions The colorectal surgeon can be faced with any number of potential disasters. Proper preparation and maintenance of a diverse toolbox of solutions can help avert or salvage even the most dramatic of these. references    1. Chee YL, Crawford JC, Watson HG, Greaves M. Guidelines on the assessment of bleeding risk prior to surgery or invasive procedures. British Committee for standards in haematology. Br J Haematol 2008; 140(5): 496–504.    2. Ang-Lee MK, Moss J, Yuan CS. Herbal medicines and perioperative care. JAMA 2001; 286(2): 208–16.    3. Spell NO. Stopping and restarting medications in the perioperative period. Med Clin N Am 2001; 85(5): 1117–28.    4. Ansell J, Hirsh J, Poller L et al. The pharmacology and management of the Vitamin K antagonists: The seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest 2004; 126(3 Suppl): 204S–33S.

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  40. Papasavas PK, Caushaj PF, McCormick JT et al. Laparoscopic management of complications following laparoscopic Rouxen-Y gastric bypass for morbid obesity. Surg Endosc 2003; 17: 610–4.   41. Higa K, Ho T, Boone K. Internal Hernias after laparoscopic Roux-en-Y gastric bypass: incidence, treatment and prevention. Obes Surg 2003; 13: 350–4.   42. Becker JM, Dayton MT, Fazio VW et al. Prevention of postoperative abdominal adhesions by a sodium hyaluronatebased bioresorbable membrane: a prospective, randomized, double-blind multicenter study. J Am Coll Surg 1996; 183: 297–306.   43. Diamond MP. Reduction of adhesions after uterine ­myomectomy by Seprafilm membrane (HAL-F): a blinded, prospective, randomized, multicenter clinical study. Fert Steril 1996; 66(6): 904–10.   44. Nordic Adhesion Prevention Study Group. The efficacy of INTERCEED (TC7) for prevention of reformation of postoperative adhesions on ovaries, fallopian tubes, and fimbriae in microsurgical operations for fertility: a multicenter study. Fertil Steril 1995; 63(4): 709–14.   45. Beck DE, Cohen Z, Fleshman JW et al. Adhesion Study Group Steering Committee. A prospective, randomized, multicenter, controlled study of the safety of seprafilm adhesion barrier in abdominopelvic surgery of the intestine. Dis Colon Rectum 2003; 46(10): 1310–9.   46. Brozovich M, Read TE, Salgado J et al. Laparoscopic Colectomy for “Benign” Colorectal Neoplasia: A Word of Caution. Surg Endosc 2007; [Epub ahead of print]   47. Larach SW, Patankar SK, Ferrara A et al. Complications of laparoscopic colorectal surgery: analysis and comparison of early vs. latter experience. Dis Colon Rectum 1997; 40: 592–6.   48. Piscatelli N, Hyman N, Osler T. Localizing colorectal cancer by colonoscopy. Arch Surg 2005; 140(10): 932–5.   49. McArthur CS, Roayaie S, Waye JD. Safety of preoperation endoscopic tattoo with india ink for identification of colonic lesions. Surg Endosc 1999; 13(4): 397–400.   50. Nizam R, Siddiqi N, Landas SK, Kaplan DS, Holtzapple PG. Colonic tattooing with India ink: benefits, risks, and alternatives. Am J Gastroenterol 1996; 91(9): 1804–8.   51. Cho YB, Lee WY, Yun HR et al. Tumor localization for laparoscopic colorectal surgery. World J Surg 2007; 31(7): 1491–5.   52. Nagata K, Endo S, Tatsukawa K, Kudo SE. Intraoperative fluoroscopy vs. intraoperative laparoscopic ultrasonography for early colorectal cancer localization in laparoscopic surgery. Surg Endosc 2008; 22(2): 379–85.   53. McCormick JT, Gregorcyk SG. Preoperative Evaluation of Colorectal Cancer. Surgical Oncology Clinics of North America. Surg Oncol Clin N Am 2006; 15(1): 39–49.   54. Feingold DL, Addona T, Forde KA et al. Safety and reliability of tattooing colorectal neoplasms prior to laparoscopic resection. J Gastrointest Surg 2004; 8(5): 543–6.   55. Price N, Gottfried MR, Clary E et al. Safety and efficacy of India ink and indocyanine green as colonic tattooing agents. Gastrointest Endosc 2000; 51: 438–42.

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improved outcomes in colon and rectal surgery   56. Park JW, Sohn DK, Hong CW et al. The usefulness of preoperative colonoscopic tattooing using a saline test injection method with prepackaged sterile India ink for localization in laparoscopic colorectal surgery. Surg Endosc 2008; 22(2): 501–5.   57. Zmora O, Dinnewitzer AJ, Pikarsky AJ et al. Intraoperative endoscopy in laparoscopic colectomy. Surg Endosc 2002; 16: 808–11.   58. Carlson M. Acute wound failure. Surg Clin North Am 1997; 77: 607–36.   59. Wissing J, van Vroonhoven TJMV, Schattenkerk ME et al. Fascia closure after midline laparotomy: results of a randomized trial. Br J Surg 1987; 74: 738.   60. Trimbos JB, Smit IB, Holm JP et al. A randomized clinical trial comparing two methods of fascia closure following midline laparotomy. Arch Surg 1992; 127: 1232.   61. Niggebrugge AHP, Hansen BE, Trimbos JB et al. Mechanical factors influencing the incidence of burst abdomen. Eur J Surg 1995; 161: 655.   62. Riou JO, Cohen JR, Johnson H Jr. Factors influencing wound dehiscence. Am J Surg 1992; 163: 324.   63. Miles RM, Moore M, Fitzgerald D et al. The etiology and prevention of abdominal wound disruption. Am Surg 1964; 30: 566–73.   64. Reitamo J, Moller C. Abdominal wound dehiscence. Acta Chir Scand 1972; 138: 170–5.   65. Bowen A. Postoperative wound disruption and evisceration: an analysis of thirty four cases with a review of the literature. Am J Surg 1940; 47: 3.   66. Alexander HC, Prudden JF. The causes of abdominal wound disruption. Surg Gynecol Obstet 1966; 122: 1223–9.   67. Gisalson H, Gronbech JE, Soreide O. Burst abdomen and incisional hernia after major gastrointestinal operation—comparison of three closure techniques. Eur J Surg 1995; 161: 349.   68. Greenburg AG, Saik RP, Peskin GW. Wound dehiscence: Pathophysiology and prevention. Arch Surg 1979; 114: 143.   69. Lythgoe JP. Burst Abdomen. Postgrad Med J 1960; 36: 388.   70. Poole GV, Meredith JW, Kon ND et al. Suture technique and wound bursting strength. Am Surg 1984; 50: 569–72.   71. Marsh RL, Coxe JW, Ross WL et al. Factors involving wound dehiscence. JAMA 1954; 155: 1197–200.   72. Ellis H, Heddle R. Closure of the Abdominal Wound. J Royal Soc Med 1979; 72: 17–8.   73. Humphries Al, Corley WS, Moretz WH. Massive closure vs. layer closure for abdominal incisions. Am Surg 1964; 30: 700–5.   74. Dudley HAF. Layered and mass closure of the abdominal wall. Brit J Surg 1970; 57: 664–7.   75. DeBruin ThR. Prevention of abdominal disruption and postoperative hernia. Int Surg 1973; 58: 408–11.   76. Ausobsky JR, Evans M, Pollock AV. Does mass closure of midline laparotomies stand the test of time? A random ­control clinical trial. Ann R Coll Surg Engl 1985; 67: 159.   77. Bucknall TE, Cox PJ, Ellis H. Burst abdomen and incisional hernia: a prospective study of 1129 major laparotomies. Br Med J 1982; 284: 931.

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  78. Ellis H, Harrison W, Hugh TB. The healing of peritoneum under normal and pathologic conditions. Br J Surg 1965; 52: 471.   79. Hubbard TB Jr, Khan MZ, Carag VR et al. The pathology of peritoneal repair: its relation to the formation of adhesions. Ann Surg 1967; 165: 908.   80. Hugh TB, Nankivell C, Meagher AP et al. Is closure of the peritoneal layer necessary in the repair of midline surgical abdominal wounds? World J Surg 1990; 14: 231.   81. Rodeheaver GT, Nesbit WS, Edlich RF. Novafil. A dynamic suture for wound closure. Ann Surg 1986; 204: 193–9.   82. Haxton H. The influence of suture materials and methods on the healing of abdominal wounds. Br J Surg 1965; 52: 372.   83. McNeill PM, Sugerman HJ. Continuous absorbable vs. interrupted non-absorbable fascial closure. Arch Surg 1986; 121: 821–3.   84. Richards PC, Balch CM, Aldrete JS. Abdominal wound ­closure. A randomized prospective study of 571 patients comparing continuous vs. interrupted suture techniques. Ann Surg 1983; 197: 238–43.   85. Hodgson NC. The search for an ideal method of abdominal fascial closure: a meta-analysis. Ann Surg 2000; 231(3): 436–42.   86. Adamsons RJ, Musco F, Enquist IF. The chemical dimensions of a healing incision. Surg Gynecol Obstet 1966; 123: 515.   87. Hogstrom H, Haglund U. Neutropenia prevents decrease in strength of rat intestinal anastomosis: partial effect of oxygen free radical scavengers and allopurinol. Surgery 1986; 99: 716–20.   88. Hogstrom H, Haglund U, Zederfeldt B. Suture technique and early breaking strength of intestinal anastomoses and laparotomy wounds. Acta Chir Scand 1985; 151: 441.   89. Jenkins TPN. The burst abdominal wound: a mechanical approach. Br J Surg 1976; 63: 873.   90. Greenwald D, Shumway S, Albear P et al. Mechanical comparison of 10 suture materials before and after in vivo incubation. J Surg Res 1994; 56: 372.   91. Kronborg O. Polyglycolic acid (Dexon) vs. silk for fascial closure of abdominal incisions. Acta Chir Scand 1976; 143: 9.   92. Goligher JC, Irvin TT, Johnston D et al. A controlled trial of three methods of closure of laparotomy wounds. Br J Surg 1975; 62: 823–92.   93. Postlethwait RW, Schauble JF, Dillon ML et al. Wound healing II. An evaluation of surgical suture material. Surg Gynecol Obstet 1959; 108: 555.   94. Douglas DM. The healing of aponeurotic incisions. Br J Surg 1952; 40: 79–84.   95. Mathes SJ, Abouljoud M. Wound Healing. In Davis JH, Drucker WR, Foster RS Jr, et al. eds. Clinical Surgery. St. Louis, CV Mosby Company, 1987: 493.   96. Lewis RT, Wiegand FM. Natural history of vertical abdominal parietal closure: Prolene versus Dexon. Can J Surg 1989; 32: 196.   97. Krukowski ZH, Cusick EL, Engeset J et al. Polydioxanone or polypropylene for closure of midline abdominal incisions: A prospective comparative trial. Br J Surg 1987; 74: 828.

other intraoperative challenges   98. Irvin TT, Kofman CG, Duthie HL. Layer closure of laparotomy wounds with absorbable and non-absorbable suture materials. Brit J Surg 1976; 63: 793–6.   99. Alexander JW, Kaplan JZ, Altemeier WA. Role of suture materials in the development of wound infection. Ann Surg 1967; 165: 192–9. 100. Sharp WV, Belden TA, King PH et al. Suture resistance to infection. Surgery 1982; 91: 61–3. 101. Ceydeli A, Rucinski J, Wise L. Finding the best abdominal closure: an evidence-based review of the literature. Curr Surg 2005; 62(2): 220–5. 102. Morris-Stiff GJ, Hughes LE. The outcomes of nonabsorbable mesh placed within the abdominal cavity: literature review and clinical experience. J Am Coll Surg 1998; 352–67. 103. Jones JW, Jurkovich GJ. Polypropylene mesh closure of infected abdominal wounds. Am J Surg 1989; 55: 73–6. 104. Mayberry JC, Mullins RJ, Crass RC et al. Prevention of abdominal compartment syndrome by absorbable mesh prosthesis closure. Arch Surg 1997; 132: 957–62. 105. Dayton MT, Buchele BA, Shirazi SS et al. Use of an absorbable mesh to repair contaminated abdominal wall defects. Arch Surg 1986; 121: 954–60. 106. Kim H, Bruen K, Vargo D. Acellular dermal matrix in the management of high-risk abdominal wall defects. Am J Surg 2006; 192(6): 705–9.

107. Butler MD, Langstein MD, Kronowitz MD. Pelvic, abdominal, and chest wall reconstruction with alloderm in patients at increased risk for mesh-related complications. Plast Reconstr Surg 2005; 116(5): 1263–74. 108. Patton MD, Berry MD, Kralovich MD. Use of human acellular dermal matrix in complex and contaminated abdominal wall reconstructions. Am J Surg 2007; 193: 360–3. 109. Diaz JJ Jr, Guy J, Berkes MB, Guillamondegui O, Miller RS. Acellular dermal allograft for ventral hernia repair in the compromised surgical field. Am Surg 2006; 72(12): 1181–8. 110. Catena F, Ansaloni L, Gazzotti F et al. Use of porcine dermal collagen graft (permacol) for hernia repair in contaminated fields. Hernia 2007; 11: 57–60. 111. Silverman RP, Li EN, Holton LH 3rd et al. Ventral hernia repair using allogenic acellular dermal matrix in a swine model. Hernia 2004; 8: 336–42. 112. Sclafani AP, McCormick SA, Cocker R. Biophysical and microscopic analysis of homologous dermal and fascial materials for facial aesthetic and reconstructive uses. Arch Facial Plast Surg 2002; 4: 164–71. 113. An G, Walter RJ, Nagy K. Closure of abdominal wall defects using acellular dermal matrix. J Trauma 2004; 56: 1266–75.

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7

Postoperative anastomotic complications Daniel L Feingold

challenging case A 64-year-old man is 10 days status postlow anterior resection. He complains of pelvic pressure and pain. His abdominal exam demonstrates mild suprapubic tenderness, but no peritoneal signs. He has a low-grade fever and a white blood count of 15,000. case management A CT scan with oral, rectal, and intravenous contrast demonstrates a contained anastomotic leak. The patient is managed with pecutaneous drainage and intravenous antibiotics. INTRODUCTION Surgical research over the past three decades has vastly enhanced our technical abilities and knowledge with respect to creating colorectal anastomoses. The Miles operation, considered state of the art for many years after its description in 1908, has been supplanted by sphincter-saving operations which are now considered the gold standard for the majority of patients with rectal cancer. The era of anal sphincter salvage was ushered in with the commercialization of mechanical staplers that permitted colorectal surgeons to resect cancers even in the distal rectum and maintain intestinal continuity.(1) In 1979, Heald articulated the concept of total mesorectal excision for rectal cancer resection which was subsequently validated and popularized adding a new dimension to our understanding of curative rectal cancer surgery.(2) In addition, appreciation of the distal mural spread of rectal cancer allowed for closer distal margins without compromising oncologic adequacy. Concomitantly, chemoradiation was demonstrated to be an effective adjuvant therapy and became part of the armamentarium routinely used to treat patients with rectal cancer. With the ushering in of the era of low, stapled colorectal anastomoses, and sphincter preservation, experience was gained diagnosing and treating patients in whom complications of these operations arise. The most common complications related to colorectal anastomosis are dehiscence and stricture. The following chapter reviews the relevant surgical literature with emphasis on diagnosis, treatment, and prevention of these complications. Less-common complications such as anastomotic cancer recurrence and anastomotic hemorrhage and other forms of intestinal anastomoses (ileorectal, ileal pouch anal) will not be reviewed. Leaks and strictures are uncommon events and many of the studies describing these complications present conflicting results, are not definitive, or are statistically under-powered. For a more thorough understanding of the literature, this chapter relies frequently on meta-analysis that combines independent clinical trials to come to a statistical consensus supporting evidence-based practice. While meta-analysis is not an infallible tool, a well conducted meta-analysis can allow for more objective appraisal of the evidence, which may lead to resolution of uncertainty and disagreement and may reduce the probability of false negative results (i.e., lower the rate of a type II error).

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anastomotic dehiscence Anastomotic leak is the most serious complication of colorectal operations as the clinical outcome due to anastomotic disruption can be catastrophic. The risk of death within 30 days of colorectal resection is significantly higher in patients who suffered a leak and mortality has been reported as high as 36% in some series.(3, 4) For patients who survive the acute physiologic trespass of an anastomotic leak, there may be formidable, far-reaching implications in terms of long-term survival, quality of life, and function.(5–7) general considerations The incidence of anastomotic dehiscence is about 10% for colorectal anastomoses within 7 cm of the anal verge.(8) The lack of a standardized definition of what actually constitutes a leak makes it difficult to compare series and draw meaningful conclusions.(9) Absence of a universal definition and the low frequency of leak events may explain why the surgical literature has so many similarly constructed trials with contradictory results supporting conflicting conclusions with regard to leaks. Common definitions include leaks identified by reoperation for peritonitis, demonstration of extraluminal contrast during an imaging study or observation of colonic contents through a pelvic drain or through the vagina. When reviewing the literature, it is important to differentiate between patients with clinically relevant leaks and asymptomatic patients who have only radiologic evidence of leak as they have different clinical consequences and are treated differently. Due to the potentially devastating consequences of anastomotic leak, there has been significant research investigating the causes of leaks as well as techniques to reduce the likelihood of anastomotic failure. A number of technical factors considered to contribute to the occurrence of anastomotic leak are subjective assessments made at the time of surgery and are difficult, if not impossible, to quantify objectively. Adequate blood supply to the ends of the bowel to be anastomosed is of critical importance. The mesentery and epiploic appendages should be stripped only enough to allow adequate visualization to permit anastomosis. Overzealous cleaning of the bowel compromises the blood supply to the anastomosis and must be avoided. In terms of the blood supply to the colon proximal to the anastomosis, preserving the left colic artery by transecting the main sigmoidal artery versus ligating the actual inferior mesenteric artery before the takeoff of the left colic (i.e., a high ligation) is oncologically sound but has not been shown to decrease the risk of leak.(8, 10) Rather than dogmatically coming across a specific named blood vessel, the level of transection along the mesenteric blood supply in a particular operation should be chosen to allow a tension-free anastomosis.(11) In cases where a colostomy is created for proximal diversion, care should be taken to preserve the

postoperative anastomotic complications marginal artery blood supply to the distal colon; this is especially important if the inferior mesenteric artery is transected. Although a variety of methods can be used to assess the blood supply to the anastomosis including Doppler ultrasound and intravenous fluorescein visualized with a Wood’s lamp, in the vast majority of cases, straightforward clinical assessment by inspection and palpation is sufficient for this determination. In an effort to improve the blood supply to the rectal side of the anastomosis (and to potentially better protect the hypogastric nerves), it is possible to spare the superior hemorrhoidal artery. Preserving the inferior mesenteric arterial supply to the rectum by transecting the individual sigmoidal branches mid-mesentery may be useful in cases of diverticulitis but would be wholly inappropriate in cancer cases where mesenteric clearance and lymph node harvest are paramount. While sparing the superior hemorrhoidal artery, there may be a tendency to avoid dissecting out the proximal presacral space in order to prevent injury to the artery. In operations for diverticulitis, the proximal rectum must be mobilized in order to ensure complete resection of the sigmoid colon and to facilitate passage of the trans-anal circular stapler to the stapled end of the rectum. In theory, sparing the superior hemorrhoidal artery may preserve blood supply to a colorectal anastomosis but data regarding a potential reduction in the leak rate is lacking. Tension across the anastomosis can decrease blood supply and physically disrupt the anastomosis. Care must be taken to sufficiently mobilize the bowel to eliminate or minimize any tension at the anastomosis. Technically, this may require division of the inferior mesenteric vein at the level of the pancreas to adequately release the descending colon mesentery to permit the colon to reach to the low pelvis. Similarly, the inferior mesenteric artery may be divided proximal to the takeoff of the left colic artery so that the left colic does not tether the colon up in the abdomen. In addition, splenic flexure release should be performed to afford tension-free reach of the colon to the pelvis when required, as is most commonly the case. Although not mandatory from an oncologic perspective, splenic flexure takedown is only omitted from curative resections when patient anatomy and tumor location permit.(12) To further reduce the chance of leak, the bowel to be anastomosed should be healthy. Inflammation, edema, radiation changes, and thickened bowel wall due to chronic obstruction each influence the risk of leak. Under these suboptimal conditions, the bowel should be resected to normal, healthy tissue to allow safe anastomosis; otherwise, a primary anastomosis should be avoided. If unhealthy tissue precludes safe stapled anastomosis, then the anastomosis should not be handsewn; tissue unfit for staples is unfit for sutures. When preparing the colon for anastomosis, it is important to note the presence of any diverticula as incorporating a diverticulum into the staple line jeopardizes the anastomosis. To avoid this, it is helpful to suture the diverticulum in toward the anvil of the stapler so that the diverticulum ends up in the tissue donuts. Alternatively, the diverticulum can be eliminated by resecting additional colon. When marrying the circular stapler, it is important to prevent any extraneous tissue (i.e., vagina, adnexa, bladder, epiploic

appendages, etc.) from catching in the stapler. This tissue can interfere with the firing mechanism of the stapler and increases the risk of anastomotic failure. Once the anastomosis is created, air testing with the pelvis under saline should be performed routinely to identify occult defects requiring repair. Once a defect demonstrated by a leak test has been repaired, as evidenced by a negative repeat on-table leak test, the risk of postoperative anastomotic leak is not increased.(13) Similarly, in situations where the anastomotic donuts are incomplete but the leak test is negative, the risk of anastomotic leak is not increased.(14) proximal diversion Many surgeons divert patients undergoing low anterior resection with total mesorectal excision in the hopes of influencing the leak rate and/or the clinical consequences of a leak.(15, 16) Given the low frequency of anastomotic leak, in order to determine whether fecal diversion protects patients from leaking, large, welldesigned, multiinstitution trials with homogenous study populations are required. Nonrandomized studies testing the hypothesis that diversion decreases anastomotic failure are inherently biased because of patient selection as surgeons are more likely to divert patients in whom complications are anticipated. The Rectal Cancer Trial On Defunctioning Stoma in Sweden, a large, prospective trial including 234 patients, randomly assigned patients undergoing stapled colorectal anastomosis within 7 cm of the anal verge to have proximal fecal diversion.(17) The clinical leak rate in the diverted and nondiverted groups was 10.3% and 28%, respectively (p < 0.001). In addition, the need for urgent re-operation in the diverted and nondiverted groups was 8.6% and 25.4%, respectively (p < 0.0001). To further evaluate the possible utility of a proximal stoma, a meta-analysis was performed evaluating the role of a defunctioning stoma in low rectal cancer surgery including the Swedish trial and three other smaller randomized, controlled trials.(18) The odds ratios for clinical leak and for re-operation due to a leak in diverted patients were 0.32 and 0.27, respectively (p < 0.001). While this meta-analysis and a few other studies demonstrate significant benefits in terms of decreasing the occurrence of leak, much of the remaining literature only supports the concept that proximal diversion ameliorates the septic consequences of leak but does not influence the actual rate of leak.(14, 19–22) Temporary fecal diversion is not without its own ramifications. It is difficult to predict which individual patients will develop a leak and routine stoma creation will reduce the quality of life in patients in whom no anastomotic complication would have occurred. Moreover, a certain percentage of diverted patients will, inevitably, never have intestinal continuity restored; although, a “temporary” diversion is more likely to become permanent in patients who have experienced a leak.(17, 23) Finally, stoma creation carries its own morbidity rate (i.e., increased wound infection rate at the original operation, stoma complications, morbidity of the reversal operation, etc.) and consumes significant healthcare resources.(20) Although there is no consensus regarding which patients should undergo proximal fecal diversion at the time of colorectal anastomosis, many surgeons routinely consider diversion in the setting of low pelvic anastomoses as these are more likely to leak.(5, 24)

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improved outcomes in colon and rectal surgery The specific type of fecal diversion, ileostomy versus colostomy, does not influence anastomotic related outcomes.(25) mechanical bowel preparation Mechanical bowel preparation before elective resection has been surgical dogma since Halsted’s description of intestinal anastomosis in 1887. Empiric-based practice relies on mechanical bowel preparation together with oral antibiotics to reduce the bacterial load of the bowel and, in theory, to decrease the risks of anastomotic leak and surgical site infection. Bowel preparation, far from innocuous, is inconvenient and unpleasant for patients and is associated with potentially harmful metabolic and fluid disturbances. For these reasons, and because the purported benefits of bowel preparation remain unproven, the utility of mechanical preparation has been questioned. A Cochrane review evaluating the efficacy of bowel preparation in its ability to reduce postoperative complications included 1,592 patients from nine randomized, controlled trials stratified to a colectomy group and a low anterior resection group.(26) The clinical leak rate in the colectomy group with and without bowel preparation was 2.9% and 1.6%, respectively (p value not significant). The clinical leak rate in the low anterior resection group with and without bowel preparation was 9.8% and 7.5%, respectively (p value not significant). When the surgical groups were combined, the 6.2% clinical leak rate in the prepared group was significantly higher than the 3.2% rate in the unprepared group (p = 0.003). Meta-analysis of all other infectious complication rates, including surgical site infection, demonstrated no protective effect of mechanical bowel preparation. Despite significant evidence that bowel preparation before elective colorectal resection does not influence infectious complications (and may actually increase the anastomotic leak rate) surgical tradition and medico-legal pressure continue to heavily influence the practice of colorectal surgery with respect to mechanical bowel preparation. anastomotic technique Stapled techniques for low pelvic anastomosis have been rigorously evaluated since their introduction into the armamentarium of colorectal surgery. A systematic Cochrane review comparing the outcomes of straight, end-to-end stapled and handsewn colorectal anastomoses pooled data on 1,233 patients from nine randomized, controlled trials.(27) This comprehensive meta-analysis found no statistically significant difference with regard to clinical leaks (stapled 6.3% vs. handsewn 7.1%, p value not significant) or radiologic anastomotic dehiscence (stapled 7.8% vs. handsewn 7.2%, p value not significant). A similarly conducted Cochrane review of four randomized, controlled trials comparing stapled versus handsewn ileocolic anastomoses during colon cancer resection demonstrated significantly fewer clinical leaks in the stapled group (1%) compared to the handsewn group (4.2%, p = 0.04).(28) Given the fundamental differences between ileocolic and colorectal anastomoses, it is not surprising that they each may have unique technical requirements to reduce the risks of complications. In addition to evaluating the mechanics of forming the anastomosis, the configuration of the anastomosis has been studied

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with regard to possible reduction in the risk of leak. Of the most common stapled colorectal anastomotic configurations (end-toend, side-to-end Baker, colonic “J” pouch) there is no optimal configuration that consistently confers a risk reduction benefit. (8, 10, 15, 17, 19, 29) It has also been shown that the size of the circular stapler does not contribute to the leak rate.(14) omental pedicle In an effort to quarantine an anastomosis in the event of a leak and to mitigate the consequences of a leak, many surgeons utilize an omental pedicle. To reach a pelvic anastomosis, the omentum is typically mobilized to survive off the left gastroepiploic artery. The influence of an omental pedicle on anastomotic outcomes was evaluated in a prospective, randomized study of 705 patients undergoing bowel anastomosis and no statistically significant influence on the rate or severity of leak was observed.(30) Another smaller, randomized, controlled trial of 126 patients demonstrated a protective effect of an omental pedicle; though, this study could be criticized for a rather high leak rate (22%) in the group of patients without an omentoplasty.(31) Both of these studies reported overall leak rates including clinical and radiologic leaks. The discrepancy between these two trials is characteristic of many of the studies investigating anastomotic complications. Leaks are low frequency events requiring large, homogenous study populations for accurate evaluation. No firm evidence-based recommendation can be made with regard to omentoplasty and its potential effects on colorectal anastomotic outcomes; bringing an omental pedicle to the pelvis should be done according to the surgeon’s preference. radiation Neoadjuvant radiotherapy has been evaluated in terms of potentially increasing the risk of dehiscence of pelvic anastomoses. The proposed mechanism of increasing the leak rate is that pelvic radiation may interfere with healing of the anastomosis due to toxicity in the pelvis. Radiation changes to the colon side of the anastomosis are usually not an issue as the irradiated colon is resected at the time of the proctectomy to ensure that healthy colon is used to form the anastomosis. The Dutch Total Mesorectal Excision (TME) trial randomized 1,414 rectal cancer patients to neoadjuvant short-course radiation therapy followed by low anterior resection versus resection alone and demonstrated no significant difference between the two groups with respect to clinical anastomotic leak (neoadjuvant group leak rate 11% versus surgery alone leak rate 12%, p value not significant). However, these results were difficult to interpret because patients in the radiotherapy group were more likely to have a diverting stoma.(19, 22) The Swedish rectal cancer trial randomized 1,168 patients to short-course neoadjuvant radiation followed by surgery versus surgery alone and also demonstrated no significant difference in leak rates between the two study arms.(32) A nonrandomized study comparing 150 patients who received long-course chemoradiation (5,040 cGy) followed by surgery to 531 patients who underwent surgery alone demonstrated similar results with 4% overall leak rate in each group (p = 0.86).(10) The notion that neoadjuvant radiotherapy increases the risk of leak is not supported by the majority of the

postoperative anastomotic complications literature and may be incorrectly based on the fact that low pelvic anastomoses in the setting of total mesorectal excision are more likely to leak.(33, 34) pelvic drains Pelvic drains are placed by some surgeons to prevent colorectal anastomotic leaks and to diagnose leaks sooner with the hope of initiating treatment before leaking patients clinically decompensate. The possible mechanism whereby pelvic drains, theoretically, may protect against colorectal anastomotic leak relies on the characteristics of the extra-peritoneal low pelvis in that the peritoneum is absent. Violation of the presacral space during proctectomy leaves a significant raw surface and without the absorptive abilities of the peritoneum fluid can collect in the dependent dead space created by total excision of the mesorectum. Further complicating the matter is the potential for negative pressure in the low pelvis that promotes the accumulation of fluid that can possibly disrupt the anastomosis. A pelvic drain can, possibly, prevent accumulation of fluid behind the anastomosis. These theoretical benefits of pelvic drainage together with results of statistically under-powered trials may explain why many surgeons continue to drain pelvic anastomoses. Routine pelvic drainage has been evaluated in retrospective fashion as well as with randomized, controlled trials with regard to a possible influence on the occurrence and diagnosis of colorectal anastomotic leak. For example, the data collected in the prospective, randomized Dutch TME trial was studied after-thefact in retrospective fashion to determine the utility of pelvic drainage during low anterior resection.(19) Patients in this trial were randomly assigned whether or not to receive neoadjuvant radiation therapy before TME. At the time of operation, placement of pelvic drains was decided at the discretion of the operating surgeon. Multiple regression analysis demonstrated that pelvic drainage was strongly associated with a lower clinical leak rate (leaks occurred in 9.6% of patients with drains compared with 23.5% of patients without drains, p < 0.001). Moreover, the need for re-operation in leaking patients was significantly more likely in patients without preexisting pelvic drainage (97% of leaking patients without drains were re-operated versus 74% of leaking patients with drains, p = 0.006). Other reviews and randomized trials regarding the use of drains have been published with contradicting results and conclusions; some attributed an increase in the leak rate to pelvic drainage.(14, 29, 35, 36) Like the retrospective study reviewed above, many of these papers may not have accurately evaluated the utility of drains due to lack of statistical power or suboptimal methodology. To better evaluate the utility of pelvic drainage after colorectal anastomosis, a Cochrane review tested the hypothesis that anastomotic drainage after elective colorectal surgery does not prevent the development of complications.(37) This exhaustive meta-analysis pooled data on 1,140 patients from six randomized, controlled trials. The clinical anastomotic leak rate for patients with drains versus without drains was 2% and 1%, respectively (p value not significant). Stratification of the data according to the height of the anastomosis also showed no benefit of drainage even for low pelvic anastomoses. In addition, the re-operation rates between patient groups with and without

drains were comparable. This review does not support the practice of routinely draining colorectal anastomoses. The practice of routinely draining colorectal anastomoses is not supported by strong scientific evidence. In addition, there is no compelling literature supporting the notion that pelvic drains facilitate earlier diagnosis of a leak. miscellaneous Other factors shown to increase the colorectal anastomotic leak rate include total mesorectal excision (8, 15, 16), height of the anastomosis from the anal verge (5, 20, 33), male gender (5, 20), and prolonged operating time (20). Each of these factors is either difficult or impossible to influence. Due to the large numbers of patients required to study anastomotic complications, many variables may never be studied sufficiently in terms of possibly contributing to anastomotic leak (Table 7.1). Total mesorectal excision, as it was originally described, left a relatively ischemic distal rectum after resection for proximal rectal cancer. Tumor specific mesorectal excision for proximal rectal cancer has become popular as it preserves the distal mesorectum without compromising oncologic adequacy and decreases the risk of leak compared with total mesorectal excision.(10, 15, 33, 38) The height of an anastomosis can influence tension across the tissues and, together with prolonged operating time, is likely a surrogate marker for more difficult operations especially in the narrow, male pelvis. It is also postulated that, in low pelvic anastomoses, the proximate anal sphincter increases the intraluminal pressure across the anastomosis jeopardizing its integrity. In terms of the surgical approach, the Clinical Outcomes of Surgical Therapy (COST) trial and others have not demonstrated an increased anastomotic failure rate with regard to laparoscopic versus conventional open colectomy.(39–41) Trials evaluating laparoscopic versus open rectal cancer resection with colorectal anastomosis are underway. clinical presentation The clinical manifestations of anastomotic dehiscence vary depending on the location of the leaking anastomosis, the severity of the leak and whether or not the leak is contained or walled-off. For these reasons, while many patients with anastomotic dehiscence present acutely with signs and symptoms of sepsis and an abdominal catastrophe, a subset of patients have Table 7.1  Factors with conflicting evidence in the literature that may or may not impact anastomotic leak rates. Smoking or alcohol abuse (33, 46, 59) Obesity (8) Hospital operative caseload (24) Surgeon subspecialty training and volume (33, 60, 61) Diabetes (48) Cardiovascular disease (48) Steroid use (46, 48) Malnutrition (46, 62) Anemia (48) Blood transfusions (46) Intraoperative rectal irrigation ASA score (33) Field contamination

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improved outcomes in colon and rectal surgery Table 7.2  The time interval between colorectal anastomosis and diagnosis of a leak. Study N Rullier 1998 (8) Carlsen 1998 (16) Alves 2002 (47) Mäkelä 2003 (46) Hedrick 2006 (4) Matthiessen 2007 (17) Nicksa 2007 (45) Jung 2008 (6)

32 11 43 44 14 27 36 35

Post Op Day of Diagnosisa

Range (days)

11 8 8.1 8 9b 8b 10.1 5.5b

2–41 4–15 4–25 3–25 3–137 3–18 2–50 2–15

a. Mean. b. Median.

a more sub-acute, insidious presentation. This is more typical of walled-off infections and leaks that have sealed on their own. Possibly contributing to a sub-acute presentation of a leak is the use of antibiotics during recovery from colorectal surgery (for pneumonia, urinary tract infection, etc.) that can mask the signs and symptoms of an occult leak. While the majority of patients with colorectal anastomotic leak are diagnosed within a week of operation, a significant proportion of patients are diagnosed well beyond this timeframe (Table 7.2). Patients with a more delayed presentation of a leak have often been released from the hospital only to be diagnosed upon re-admission.(42) Patients with feculent peritonitis or diffuse purulent peritonitis typically become acutely ill, often in dramatic fashion, with classic signs and symptoms of peritonitis, hemodynamic instability and rapid progression to multisystem organ dysfunction. Meanwhile, in a considerable number of patients, recognition of an anastomotic leak may be difficult due to the significant overlap between the signs and symptoms of a leaking patient and those of a typical patient recovering from major abdominal surgery. Patients may present with any combination of fever, tachycardia, varying degrees of abdominal pain and distension, ileus, diarrhea, malaise, failure to thrive, bowel obstruction, and septic shock. Some patients present with symptoms mimicking cardiac complications such as respiratory failure and chest pain. Leaking patients may also fail to clinically progress or recover within a usual timeframe, have increasing narcotic demands, or have decreased urine output requiring fluid boluses. The physical exam of a leaking patient may include focal or diffuse abdominal tenderness, rigidity, guarding, abdominal distension, and evidence of varying degrees of hemodynamic collapse. Patients may have leukocytosis, typically with a left shift, leukopenia, metabolic acidosis, or thrombocytopenia. After any intestinal anastomosis, the surgeon must maintain a high index of suspicion when evaluating patients with unusual signs of sepsis or patients who fail to meet the clinical milestones of normal recovery within a typical timeframe. The potential for delay in diagnosis is significant; delays may impact patient outcomes and have medicolegal ramifications. diagnosis Patients with generalized peritonitis consistent with a leak require urgent return to the operating room with concomitant intravenous fluid resuscitation and broad-spectrum antibiotics. In this

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setting, the time to re-operation is critical and a diagnostic journey with imaging studies will only delay potentially life-saving abdominal exploration. Meanwhile, patients with a more subtle clinical presentation do not mandate immediate exploration and may benefit from imaging studies to confirm the diagnosis and direct appropriate management. Although no single radiologic study is ideal for investigating a possible leak, computed tomography (CT) and contrast enemas are the tests of choice in this setting. The advantage of triple contrast CT scanning with intravenous, oral, and rectal contrast is that it may identify other potential underlying pathologies like ileus, abscess, hematoma, and bowel obstruction. CT scan findings consistent with anastomotic leak include extravasation of luminal contrast, perianastomotic fluid, ascites, and varying amounts of extra-luminal gas. With the exception of contrast extravasation, many of the CT findings in leaking patients are not specific and overlap considerably with CT scans of nonleaking patients in the postoperative setting. The mere presence of free air in the postoperative period is not specific for a leak and has been demonstrated by CT in control patients without anastomoses up to 9 days after operation and even later.(43, 44) Depending on the clinical circumstances, inconclusive CT findings can be followed up with a contrast enema study, repeat CT or abdominal exploration to exclude anastomotic leak. According to some of the literature, CT may be superior to contrast enema when determining the integrity of an anastomosis.(42) Potential shortcomings of enema studies in this setting are that the water-soluble contrast can dilute out and compromise resolution of a contrast enema and that clinicians may be reluctant, in the early postoperative period, to introduce a sufficient column of enema contrast to adequately fill the rectum. On the other hand, some of the retrospective literature strongly favors contrast enema over CT in terms of diagnosing a pelvic anastomotic leak outright as well as after a CT scan fails to demonstrate a leak.(9, 45) Extravasation or pooling of rectal contrast outside of the bowel lumen during an enema study is pathognomonic of leak (Figures 7.1 and 7.2). Water-soluble contrast must be used when evaluating for a possible anastomotic dehiscence as extravasated barium increases the severity of a leak by adding to the inflammatory response in the abdomen. In reality, the choice of imaging study in a particular patient is influenced by the clinical presentation, institutional expertise, and available resources. management The management of anastomotic dehiscence in a particular patient depends on the clinical manifestations of the leak and the condition of the patient (Figure 7.3). Common manifestations of a leak from a colorectal anastomosis are asymptomatic, leak without abscess, leak with associated abscess, peritonitis, and colocutaneous fistula. Asymptomatic Early in the experience with circular staplers, routine watersoluble contrast enemas demonstrated that as many as half of patients with pelvic anastomoses demonstrated a radiologic leak during the first postoperative week. Often these are short, simple sinus tracts originating from the anastomosis. In otherwise

postoperative anastomotic complications

Figure 7.1  Gastrografin enema demonstrating anastomotic leak (black arrows) from colorectal anastomosis (anterior-posterior view).

Figure 7.2  Gastrografin enema demonstrating leak with contained abscess (white arrows) from colorectal anastomosis (lateral view).

Anastomotic Leak

Peritonitis

Laparotomy Antibiotics Resuscitation

Colocutaneous Fistula

Address any collections

Antibiotics Bowel rest Nutrition

Resolution

Fistula

No resolution

No further treatment

Abscess

No abscess No peritonitis

Drainage Antibiotics

Antibiotics Bowel rest

Worsens

Leak resolves

No resolution or Patient worsens

No further treatment

Laparotomy

Figure 7.3  Management algorithm for patients with anastomotic leak.

asymptomatic patients with an anastomotic leak discovered incidentally, no intervention is required as the leak is not likely of clinical consequence and will seal spontaneously. Leak without abscess Stable patients with mild symptoms, focal abdominal tenderness, and radiologic evidence of anastomotic leak without abscess may be initially treated nonoperatively with bowel rest and intravenous fluids and broad-spectrum antibiotics. These are often minor leaks that can, potentially, seal spontaneously. The duration of treatment is empiric and is based on the clinical response, the patient’s condition, and the surgeon’s judgment. An initial

treatment period of several days is reasonable after which parenteral nutrition or re-operation often need to be addressed. Clearly, failure to improve or clinical deterioration requires surgical intervention. It is difficult to predict which patients will successfully recover without re-operation in the setting of a leak; this treatment pathway requires dedicated attention on the part of the surgeon with frequent hands-on re-evaluation. Leak with associated abscess Stable patients with CT evidence of a contained leak with an abdominopelvic abscess should, initially, be treated with drainage and appropriate antibiotic therapy (Figures 7.4 and 7.5). Drainage

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improved outcomes in colon and rectal surgery

Figure 7.4  Abdominal CT scan demonstrating a large abdominal abscess (arrows mark cavity).

Figure 7.5  CT scan of a percutaneous drain in an abscess.

is usually performed percutaneously or trans-anally through the anastomotic defect. There are situations where operative drainage is required due to inaccessibility of an abscess by less invasive routes, but these are quite uncommon. As before, patients who fail nonoperative treatment require exploration. A contained leak can rupture freely into the abdomen; depending on the clinical circumstances, repeat imaging, or urgent exploration would be required in this situation.

There are a number of options available to the surgeon returning a patient to the operating room to address a leaking anastomosis and the particular procedure performed is decided at the time of exploration based on clinical judgment and the unique presentation of the patient on the table. As most patients undergoing reoperation for suspected leak require some form of fecal diversion that may be permanent, potential sites for stoma formation should be marked preoperatively. In the operating room, it is helpful to have the patient in either split leg position or in lithotomy stirrups to facilitate access in case proctoscopy is required. In terms of the surgical approach to re-operation in the setting of a leak, the quickest approach is likely conventional laparotomy. Laparoscopic exploration has potential benefits, especially if the original operation was performed laparoscopically or if the diagnosis of anastomotic leak is not clear, but a minimal-access approach to anastomotic leak should only be performed by surgeons with expertise in advanced laparoscopic techniques. Microbial cultures of the peritoneal fluid encountered during re-operation for anastomotic leak most often demonstrate polymicrobial flora and are of questionable benefit in terms of directing patient management.(23)

Peritonitis Patients with generalized peritonitis consistent with a leak require urgent exploration with aggressive fluid resuscitation and intravenous antibiotic administration on the way to the operating room. Typically, these patients decompensate quickly and become unstable and must be treated in urgent fashion. As reviewed earlier, in these situations, there is no benefit to pursuing diagnostic studies as the consequences of delaying operative intervention may be dire. Colocutaneous fistula Fistulization to the skin, typically through a drain site or skin incision, may be a late manifestation of anastomotic leak. Once a fistula is observed clinically, a CT scan is helpful to evaluate for any undrained collection which would need to be addressed. In general, once the local sepsis has been controlled, most anastomotic fistulae will close with bowel rest. Optimizing nutritional status and attention to wound care are important in these patients. Specific circumstances that may preclude spontaneous resolution of a fistula are distal obstruction, associated anastomotic stricture, radiation, and steroid therapy. Patients who fail nonoperative treatment may benefit from operative intervention. operative intervention The goals of re-operation for anastomotic leak are to control the source of sepsis, remove any purulence or contamination and prevent ongoing leak. While preservation of function is important, it must be emphasized that these are life-saving operations.

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Resection of the leaking anastomosis and colostomy creation Traditionally, the surgical approach for a colorectal anastomotic leak has been to dismantle the anastomosis, bring out the colon as an end stoma, close the rectum as a Hartmann pouch, washout the abdomen, and place drains.(12) This modified Hartmann procedure is very effective at removing the septic source and alleviating the abdominal sepsis. A major drawback of this operation is that end colostomy reversal is technically challenging and carries its own risk of morbidity. It is not surprising that these end colostomies become permanent in a substantial proportion of patients.(4, 23, 46) Exteriorization of the rectal stump as a mucus fistula (typically described in staged resections for fulminant proctocolitis) can be considered in the rare circumstance of a difficult to control rectum.(47)

postoperative anastomotic complications Leaving the leaking anastomosis in place An alternative to end stoma creation in many instances consists of abdominal washout, proximal fecal diversion via loop stoma, and drainage of the anastomotic leak.(19, 23, 45, 46) The benefits of this approach are that it effectively controls the septic source and allows the majority of patients to undergo stoma reversal in the future.(4, 6, 17) The main criticism of leaving a leaking anastomosis in place is that luminal contents proximal to the anastomosis may provide an ongoing source of contamination and that the anastomosis may stricture or fistulize.(23) Review of the literature does not substantiate the concern of ongoing contamination and demonstrates that proximal diversion is safe and has a high rate of anastomotic salvage. The use of a colostomy versus ileostomy for diversion does not impact anastomotic outcomes but meta-analysis of 1,204 patients demonstrated significantly fewer stoma related complications and postreversal hernias with loop ileostomy.(25) Some advocate lavage of the proximal colon to eliminate whatever stool is proximal to the anastomosis and some surgeons describe suturing closed the anastomotic defect in an effort to contain the leak; the utility of these maneuvers remains empiric. Deciding whether or not to resect or preserve a leaking anastomosis depends on the surgeon’s experience, the size of the anastomotic defect, and the viability of the colon. Repeat anastomosis after resection of the leaking anastomosis In certain situations, it may be possible to resect a leaking anastomosis and perform a new anastomosis with or without proximal diversion. This may be technically possible when dealing with a leak from an ileocolic anastomosis. Colorectal anastomoses are unlikely to be amenable to immediate reconstruction given the limitations of reach, especially in a hostile abdomen. Exteriorization of the leaking anastomosis Another surgical option for treating a patient with anastomotic dehiscence is to exteriorize the leaking anastomosis as a stoma. This removes the septic source from the abdomen and may be performed rapidly. The potential problems with this damage control approach are that the anastomosis rarely can reach out to allow exteriorization and that even if the leaking segment can reach out, it will make for a very bulky and difficult to manage stoma. In addition, this form of stoma may be fraught with wound-related complications. The utility and practicality of this approach are questionable. short and long-term implications of leak The short-term consequences of an anastomotic leak requiring operative intervention are substantial. The 30-day mortality rate associated with anastomotic leak is typically documented in the 10% to 15% range and has been reported to be as high as 36% (3, 5, 42, 46, 47). Indeed, the most common cause of death after colorectal cancer resection is due to anastomotic leak.(4) In comparison to patients who recover uneventfully, patients who suffer anastomotic leak consume significantly more healthcare resources. After reoperation for leak, roughly 50% of patients require intensive care and a number of patients go on to require additional percutaneous drainage procedures or operations.(4, 17) Also, the average length of stay of patients with anastomotic leak is considerably prolonged compared with patients who recover normally from colorectal resection.(3, 48) In terms of overall morbidity rates, patients who experience an anastomotic leak are much more likely to experience further complications than patients who did not leak.(47) It is for

these reasons that anastomotic leak is the most dreaded complication of colorectal surgery. Anastomotic leak also carries significant long-term consequences. The quality of life of patients with permanent fecal diversion after a leak and bowel function after experiencing a leak are significantly impaired.(49) In comparison with patients who did not leak, patients who undergo stoma reversal after resolution of a leak have decreased rectal capacity and compliance and more difficulties evacuating.(7) In addition, in a review of nearly 1,400 surgical patients treated for rectal cancer, patients who leaked were less likely to receive adjuvant chemotherapy and when they did receive chemotherapy, it was more likely after a substantial delay.(6) In a multicenter Scottish study of 2,235 patients who underwent curative resection for colorectal cancer, the 5-year overall survival rate, excluding mortalities within 30-days of operation, for patients who leaked compared with patients who did not leak was 42% and 55%, respectively (p < 0.01) (3). The 5-year cancer-specific survival rate, also excluding postoperative deaths, for patients who leaked compared with patients who did not leak was 50% and 68%, respectively (p < 0.001). The increased risk of cancer-specific death in patients with an anastomotic leak was most apparent between 2 and 4 years after surgery. Similarly, other studies have demonstrated increased local recurrence rates (5) as well as decreased overall and cancer-specific survival (50) after anastomotic leak. The etiology of these inferior long-term outcomes in patients who suffer a leak remains speculative. anastomotic stricture Colorectal anastomotic stricture may occur in up to 10% of patients depending on how a stricture is defined.(51, 52) From a clinical standpoint, stricture may be defined as a symptomatic narrowing of the anastomosis that obstructs the flow of intestinal contents. (53) Alternatively, a stricture may be defined by the inability to pass a particular size of proctoscope through an anastomotic narrowing. The vast majority of anastomotic strictures tend to be short segment stenoses less than a centimeter in length (Figure 7.6).

Figure 7.6  Contrast enema demonstrating colorectal anastomotic stricture.



improved outcomes in colon and rectal surgery (a)

(b)

(c)

(d)

Figure 7.7  (A) Colonoscopic view of a strictured colorectal anastomosis. (B) Passage of a through-the-scope balloon dilator. (C) Hydrostatic dilation of the stricture. (D) The dilated anastomosis.

Factors predisposing to anastomotic stricture include anastomotic leak, postoperative pelvic infection, and proximal diversion. In addition, two meta-analyses concluded that stapling the colorectal anastomosis increases the risk of stricture formation compared with hand sewing the anastomosis.(27, 54) It is hypothesized that strictures develop due to an inflammatory response or, possibly, from mucosal gaps within a staple line that heal by secondary intention. Although ischemia is commonly included as a potential etiology of stricture formation, the pathophysiology remains speculative. Whether or not a smaller diameter circular stapler increases the risk of stricture formation is not clear; nonetheless, the convention remains to use the largest diameter stapler that the bowel can accommodate. Late anastomotic stricture formation is associated with recurrent cancer, inflammatory bowel disease, and radiation injury and must be thoroughly investigated.



diagnosis and treatment While most strictures are likely incidental findings, certain patients have symptoms such as mechanical obstruction or impaction at the level of the stricture, constipation, tenesmus, frequent bowel movements, or diarrhea. In general, asymptomatic strictures in patients with intestinal continuity are not clinically relevant and do not require treatment. Meanwhile, symptomatic patients and asymptomatic patients undergoing evaluation before reversal of a diverting stoma who demonstrate stenosis require intervention. Stoma reversal in the face of a stricture risks anastomotic disruption at the site of the stoma takedown and should be avoided. The majority of colorectal anastomotic strictures that require intervention are readily salvaged using endoluminal dilating techniques.(55) Typically, dilation is postponed until the anastomosis has healed and become more pliable; waiting over 4–6

postoperative anastomotic complications weeks is prudent. Simple methods used to dilate a low anastomosis include gentle digital rectal exam or sequentially sized dilators (i.e., bougie, Hegar, etc.). Strictures out of reach for these modalities or that require controlled dilation under direct observation are usually treated with commercially available through-the-scope (TTS) hydrostatic balloon dilators that control radial expansion using a pressure gauge (Figure 7.7). Sequential dilation to a diameter >20 mm is usually accomplished under conscious sedation with or without empiric antibiotic coverage and has a low complication rate.(56) Balloon dilation is successful in the majority of cases although repeat dilations may be required. Injecting triamcinolone, a long-acting corticosteroid, into the stricture or releasing the stricture using electrocautery or laser in combination with balloon dilation may decrease the need for repeat dilations without significantly increasing the complication rate.(57) Larger diameter, over-the-wire balloons may require fewer repeat dilations than TTS devices.(55) The few patients with short anastomotic strictures who do not respond to repeated dilation and patients with long, irregular strictures may be candidates for resection with repeat anastomosis. Depending on the height of the stricture, the anastomosis can be resected and intestinal continuity may be restored with either colorectal or coloanal anastomosis. To avoid dissecting out the distal rectum in a reoperative pelvis consideration could be given to resecting the anastomosis and reconstructing with rectal mucosectomy and a pull-through operation.(51, 53) Alternatives to resection to correct an anastomotic stricture include a number of creative stricturoplasty techniques using transanal endoscopic microsurgery, conventional staplers, or a special mechanical anastomotic staple cutting device.(58) Individual cases of endorectal stenting have been reported in the literature but the utility and long-term outcomes of stenting in the setting of a benign stricture remain questionable and require further evaluation. conclusion Anastomotic complications are difficult to predict and carry significant risks of morbidity and mortality. Attention to detail while forming a colorectal anastomosis is paramount to reducing the risk of complications. Tissue sealants, novel compression anastomosis devices, anastomotic buttressing materials, and alternatives to conventional fecal diversion may each contribute to reducing anastomotic complications in the future. references   1. Knight CD, Griffin FD. An improved technique for low anterior resection of the rectum using the EEA stapler. Surgery 1980; 88: 710–4.   2. Heald RJ. A new approach to rectal cancer. Br J Hosp Med 1979; 22: 277–81.   3. McArdle CS, McMillan DC, Hole DJ. Impact of anastomotic leakage on long-term survival of patients undergoing curative resection for colorectal cancer. Br J Surg 2005; 92: 1150–4.   4. Hedrick TL, Sawyer RG, Foley EF et al. Anastomotic leak and the loop ileostomy: friend or foe? Dis Colon Rectum 2006; 49: 1167–76.   5. Branagan G, Finnis D. Prognosis after anastomotic leakage in colorectal surgery. Dis Colon Rectum 2005; 48: 1021–6.

  6. Jung SH, Yu CS, Choi PW et al. Risk factors and oncologic impact of anastomotic leakage after rectal cancer surgery. Dis Colon Rectum 2008; 51: 902–8.   7. Nesbakken A, Nygaard K, Lunde OC. Outcome and late functional results after anastomotic leakage following mesorectal excision for rectal cancer. Br J Surg 2001; 88: 400–4.   8. Rullier E, Laurent C, Garrelon JL et al. Risk factors for anastomotic leakage after resection of rectal cancer. Br J Surg 1998; 85: 355–8.   9. Bruce J, Krukowski ZH, Al-Khairy G et al. Systematic review of the definition and measurement of anastomotic leak after gastrointestinal surgery. Br J Surg 2001; 88: 1157–68. 10. Enker WE, Merchant N, Cohen AM et al. Safety and efficacy of low anterior resection for rectal cancer: 681 consecutive cases from a specialty service. Ann Surg 1999; 230: 544–54. 11. Lange MM, Buunen M, van de Velde CJ et al. Level of arterial ligation in rectal cancer surgery. Dis Colon Rectum 2008; 51: 1139–45. 12. Brennan J, Moynagh M, Brannigan AE et al. Routine mobilization of the splenic flexure is not necessary during anterior resection for rectal cancer. Dis Colon Rectum 2007; 50: 302–7. 13. Beard JD, Nicholson ML, Sayers RD et al. Intra-operative air testing of colorectal anastomoses: a prospective, randomized trial. Br J Surg 1990; 77: 1095–7. 14. Vignali A, Fazio VW, Lavery IC et al. Factors associated with the occurrence of leaks in stapled rectal anastomoses: a review of 1,014 patients. J Am Coll Surg 1997; 185: 105–13. 15. Law WL, Chu KW. Anterior resection for rectal cancer with mesorectal excision: a prospective evaluation of 622 patients. Ann Surg 2004; 240: 260–8. 16. Carlsen E, Schlichting E, Guldvog I et al. Effect of the introduction of total mesorectal excision for the treatment of rectal cancer. Br J Surg 1998; 85: 526–9. 17. Matthiessen P, Hallböök O, Rutegård J et al. Defunctioning stoma reduces symptomatic anastomotic leakage after low anterior resection of the rectum for cancer. Ann Surg 2007; 246: 207–14. 18. Hüser N, Michalski CW, Erkan M et al. Systematic review and meta-analysis of the role of defunctioning stoma in low rectal cancer surgery. Ann Surg 2008; 248: 52–60. 19. Peeters KC, Tollenaar RA, Marijnen CA et al. Risk factors for anastomotic failure after total mesorectal excision of rectal cancer. Br J Surg 2005; 92: 211–6. 20. Marusch F, Koch A, Schmidt U et al. Value of a protective stoma in low anterior resections for rectal cancer. Dis Colon Rectum 2002; 45: 1164–71. 21. Karanjia ND, Corder AP, Holdsworth PJ et al. Risk of peritonitis and fatal septicemia and the need to defunction the low anastomosis, Br J Surg 1991; 78: 196–8. 22. Marijnen CA, Kapiteijn E, van de Velde CJ et al. Acute side effects and complications after short-term preoperative radiotherapy combined with total mesorectal excision in primary rectal cancer: report of a multicenter randomized trial. J Clin Oncol 2002; 20: 817–25. 23. Parc Y, Frileux P, Schmitt G et al. Management of post-operative peritonitis after anterior resection. Dis Colon Rectum 2000; 43: 579–89.

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improved outcomes in colon and rectal surgery 24. Marusch F, Koch A, Schmidt U et al. Hospital caseload and the results achieved in patients with rectal cancer. Br J Surg 2001; 88: 1397–402. 25. Tilney HS, Sains PS, Lovegrove RE et al. Comparison of outcomes following ileostomy versus colostomy for defunctioning colorectal anastomoses. World J Surg 2007; 31: 1141–51. 26. Guenaga K, Atallah AN, Castro AA et al. Mechanical bowel preparation for elective colorectal surgery. Cochrane Database Syst Rev 2005, 1: CD001544. 27. Matos DDM, Atallah A, Castro A et al. Stapled versus handsewn methods for colorectal anastomosis surgery. Cochrane Database Syst Rev 2001, 3: CD003144. 28. Choy PY, Bissett IP, Docherty JG et al. Stapled versus handsewn methods for ileocolic anastomoses. Cochrane Database Syst Rev 2007, 3: CD004321. 29. Yeh CY, Changchien CR, Wang J et al. Pelvic drainage and other risk factors for leakage after elective anterior resection in rectal cancer patients: a prospective study of 978 patients. Ann Surg 2005; 241: 9–13. 30. Merad F, Hay JM, Fingerhut A et al. Omentoplasty in the prevention of anastomotic leakage after colonic or rectal resection. Ann Surg 1998; 227: 179–86. 31. Agnifili A, Schietroma M, Carloni A et al. The value of omentoplasty in protecting colorectal anastomosis from leakage. Hepatogastroenterology 2004; 51: 1694–7. 32. Swedish Rectal Cancer Study. Initial report from a Swedish multicentre study examining the role of preoperative irradiation in the treatment of patients with resectable rectal carcinoma. Br J Surg 1993; 80: 1333–6. 33. Martel G, Al-Suhaibani Y, Moloo H et al. Neoadjuvant therapy and anastomotic leak after tumor-specific mesorectal excision for rectal cancer. Dis Colon Rectum 2008; 51: 1195–201. 34. Buie WD, MacLean AR, Attard JP et al. Neoadjuvant chemoradiation increases the risk of pelvic sepsis after radical excision of rectal cancer. Dis Colon Rectum 2005; 48: 1868–74. 35. Merad F, Hay JM, Fingerhut A et al. Is prophylactic pelvic drainage useful after elective rectal or anal anastomosis? Surgery 1999; 125: 529–35. 36. Merad F, Yahchouchi E, Hay JM et al. Prophylactic abdominal drainage after elective colonic resection. Arch Surg 1998; 133: 309–14. 37. Jesus EC, Karliczek A, Matos D et al. Prophylactic anastomotic drainage for colorectal surgery. Cochrane Database Syst Rev 2004, 2: CD002100. 38. Zaheer S, Pemberton JH, Farouk R et al. Surgical treatment of adenocarcinoma of the rectum. Ann Surg 1998; 227: 800–11. 39. Nelson H, Sargent DJ, Wieand HS et al. A comparison of laparoscopically assisted and open colectomy for colon cancer. N Engl J Med 2004; 350: 2050–9. 40. Lacy AM, Garcia-Valdecasas JC, Delgado S et al. Laparoscopyassisted colectomy versus open colectomy for treatment of non-metastatic colon cancer. Lancet 2002; 359: 2224–9. 41. Schwenk W, Haase O, Neudecker J et al. Short terms benefits for laparoscopic colorectal resection. Cochrane Database Syst Rev 2005, 2: CD003145. 42. Hyman N, Manchester TL, Osler T et al. Anastomotic leaks after intestinal anastomosis: it’s later than you think. Ann Surg 2007; 245: 254–8.

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43. Power N, Atri M, Haddad R et al. CT assessment of anastomotic bowel leak. Clin Rad 2007; 62: 37–42. 44. Feingold DL, Widmann WD, Calhoun SK et al. Persistent post-laparoscopy pneumoperitoneum: expected or cause for alarm. Surg Endosc 2003; 17: 296–9. 45. Nicksa GA, Dring RV, Johnson KH et al. Anastomotic leaks: what is the best diagnostic imaging study? Dis Colon Rectum 2007; 50: 197–203. 46. Mäkelä JT, Kiviniemi H, Laitinen S. Risk factors for anastomotic leakage after left-sided colorectal resection with rectal anastomosis. Dis Colon Rectum 2003; 46: 653–60. 47. Alves A, Panis Y, Trancart D et al. Factors associated with clinically significant anastomotic leakage after large bowel resection: multivariate analysis of 707 patients. World J Surg 2002; 26: 499–502. 48. Pickleman J, Watson W, Cunningham J. The failed gastrointestinal anastomosis. J Am Coll Surg 1999; 188: 473–82. 49. Lim M, Akhtar S, Sasapu K et al. Clinical and subclinical leaks after low colorectal anastomosis: a clinical and radiologic study. Dis Colon Rectum 2006; 49: 1611–9. 50. Walker KG, Bell SW, Rickard MJ et al. Anastomotic leakage is predictive of diminished survival after potentially curative resection for colorectal cancer. Ann Surg 2004; 240: 255–9. 51. Garcea G, Sutton CD, Lloyd TD et al. Management of benign rectal strictures. Dis Colon Rectum 2003; 46: 1451–60. 52. Bannura GC, Cumsille MA, Barrera AE et al. Predictive factors of stenosis after stapled colorectal anastomosis. World J Surg 2004; 28: 921–5. 53. Schlegel RD, Dehni N, Parc R et al. Results of reoperations in colorectal anastomotic strictures. Dis Colon Rectum 2001; 44: 1464–8. 54. MacRae HM, McLeod RS. Handsewn versus stapled anastomoses in colon and rectal surgery. Dis Colon Rectum 1998; 41: 180–9. 55. Giorgio PD, Luca LD, Rivellini G et al. Endoscopic dilation of benign colorectal anastomotic stricture after low anterior resection. Gastrointest Endosc 2004; 60: 347–50. 56. Nguyen-Tang T, Huber O, Gervaz P et al. Long-term quality of life after endoscopic dilation of strictured colorectal or colocolonic anastomoses. Surg Endosc 2008; 22: 1660–6. 57. Lucha PA, Fticsar JE, Francis MJ. The strictured anastomosis: successful treatment by corticosteroid injectors. Dis Colon Rectum 2005; 48: 862–5. 58. Shimada S, Matsuda M, Uno K et al. A new device for the treatment of coloproctostomic stricture after double stapling anastomoses. Ann Surg 1996; 224: 603–8. 59. Sorensen LT, Jorgensen T, Kirkeby LT et al. Smoking and alcohol abuse are major risk factors for anastomotic leakage in colorectal surgery. Br J Surg 1999; 86: 927–31. 60. Borowski DW, Kelly SB, Bradburn DM et al. Impact of surgeon volume and specialization on short-term outcomes in colorectal cancer surgery. Br J Surg 2007; 94: 880–9. 61. Smith JA, King PM, Lane RH et al. Evidence of the effect of specialization on the management, surgical outcome and survival from colorectal cancer in Wessex. Br J Surg 2003; 90: 583–92. 62. Golub R, Golub RW, Cantu R et al. A multivariate analysis of factors contributing to leakage of intestinal anastomoses. J Am Coll Surg 1997; 184: 364–72.

8

General postoperative complications Scott R Steele and Clifford L Simmang

Financial Disclosure: No outside financial support or provision of supplies was solicited or received in connection with this work. Disclosure and Proprietary Statement: This is an original work by the above author. The opinions expressed are the author’s and author’s alone. They do not necessarily reflect the opinion of the U.S. Government, the U.S. Department of Defense, or Madigan Army Medical Center. challenging case A 72-year-old female is scheduled to undergo a low anterior resection for T3N0M0 rectal cancer. She has been confined to a wheelchair for the last month due to a fibular fracture. Her comorbidities include diabetes, hypertension, hyperlipidemia, and she has a 50 pack-year smoking history. Describe the optimal management for deep venous thrombosis prophylaxis. case management The patient falls into a high risk classification as evidenced by her older age, recent immobility, smoking history, comorbidities, malignancy, and need for pelvic surgery. In addition to the mechanical measures (e.g., graduated compression stockings or intermittent pneumatic compression devices and early ambulation) this patient should receive either subcutaneous unfractionated heparin (typically 5,000 IU two or three times per day) or low molecular weight heparin (~0.5 IU/kg), with higher doses reserved for those patients within the most at risk group. The first dose of unfractionated subcutaneous heparin should be given before induction, preferably 1–2 hours before incision, as some evidence indicates that venous thrombotic events occur more commonly during the time of anesthesia induction. Perioperative use should continue until the patient is fully ambulatory. This may require patient education on self-injection to continue after discharge, for up to 10–14 days. introduction Despite ever-evolving advancements aimed at improving surgical outcomes, which have included technological innovations, comprehension of perioperative physiology, and implementation of clinical pathways, postoperative complications continue to account for significant health care costs. Highlighting this, in a study evaluating the financial impact on surgical site infections alone, development of one single preventable surgical site infection was associated with an increased length of stay of almost 11 days, at a resultant cost of $27,000 for each patient.(1) In addition, lost work days, delayed functional recovery, and resultant physical deficits are oftentimes not as easily quantifiable in monetary amounts, yet create an even larger impact on both patient and society alike. Thus, emphasis needs to be placed not only on the identification and treatment of these complications, but also prevention as a major focus in order

to optimize outcomes. In this chapter we will review the ­current status of a variety of perioperative parameters surrounding complications encountered with colon and rectal surgery as well as explore the most recent measures employed for prevention. More detailed treatment options are found in specific chapters elsewhere within this text. pain Although it may seem intuitive that adequate control of postoperative pain is a mandatory and rather easy standard to achieve, in practice this oftentimes remains a far more difficult objective to attain. In part, this may be secondary to the lack of having an accurate way to predict those patients that will have difficulty with postoperative pain control. In addition, we frequently use primitive measures to quantify pain, relying heavily on devices such as visual analogue scales and verbal pain scales commonly employed in the recovery phase, which, due to language and cultural barriers, often do not have adequate correlation amongst patients. This is especially evident when trying to accurately detect and record changes in pain level over time, evaluate which pain dimension the patient is being asked to report (i.e., intensity versus relief), or to which interval does the pain level correspond (i.e., current level versus average over a time period).(2) Despite these difficulties, adequate pain control remains such an important component to the overall care of the postoperative patient, it is often referred to as the fifth vital sign. Optimal control of pain continues to be pursued through a multifactorial and multifaceted approach. Emphasis in recent years has been toward adequate preoperative and thus preemptive pain control. Medications such as ketorolac, COX-2 inhibitors, and local anesthesia before the incision have all been used in attempt to lessen postoperative pain, as well as decrease reliance on more traditional methods such as narcotics. Sim and colleagues in a prospective randomized blinded study of 40 patients undergoing elective colorectal surgery found the perioperative use of COX-2 inhibitors, which included a single dose 1 hour before surgery, was associated with a significant decrease in both postoperative narcotic use as well as shorter recovery of bowel function and earlier discharge.(3) Lack of widespread use of these agents has, in part, been centered on surgeon concerns regarding the potential for increased bleeding felt to be associated with use of these medications. Yet this appears to be unfounded. As narcotics are plagued by side effects such as respiratory depression, constipation, and ileus, which hinder gastrointestinal recovery following colorectal surgery, methods to decrease their usage seem beneficial in this patient population. This is not to say that patients following both colorectal and anal surgery do not require narcotics; However, other classes of medications may improve pain control, while minimizing the dependency on them. Other Nonsteroidal Antiinflammatory Drugs (NSAIDS) have also been evaluated in the postoperative period as independent pain-controlling agents, yet appear to work better in

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improved outcomes in colon and rectal surgery a narcotic-sparing role. In a study of over 1,000 patients, the addition of ketorolac to standard intravenous morphine significantly reduced the overall postoperative morphine requirements, and lowered side effects both directly attributable to the narcotic (mental status, pulmonary) as well as gastrointestinal function (ileus, nausea, vomiting).(4) The anti-inflammatory action of these agents, especially when used on a set schedule, may be most beneficial for the pain associated with the musculoskeletal trauma of the incision, allowing a significant reduction in pain without the untoward side effects associated with narcotic use. Pain following anorectal surgery can be quite debilitating and is often cited by patients as a primary deterrent toward undergoing needed procedures such as hemorrhoidectomy.(5) In addition to the local trauma associated with resection, pain following anal canal procedures is often attributed to anal sphincter spasm. This, in combination with the constipation and hard stools often associated with narcotic use, results in additional pain and suffering once return of bowel function commences. As in the laparotomy literature, recent trials have shown a marked decrease in the narcotic requirements using ketorolac and other NSAIDs perioperatively for anorectal surgery.(6) Local anesthesia, which has been commonly employed in the field of anorectal surgery, has recently been expanded to continued use postoperatively following abdominal procedures. As a primary modality during anorectal procedures, it has been shown to be effective and safe, with or without the addition of deep intravenous sedation, and provides the additional benefit of less time in the recovery room.(7, 8) As an adjunct following laparotomy, a local anesthetic agent is applied via continuous infusion to the midline wound through a set of subcutaneous catheters placed at the time of surgery. (9) Despite mixed results, some prospective data does demonstrate a decreased narcotic requirement and improved perioperative recovery, including earlier ambulation, in the absence of significant overall postoperative pain score differences.(10, 11) As increased experience is gathered using this modality, further data may determine its appropriate place in the analgesia armamentarium. Another method commonly employed is epidural anesthesia, which works through inhibiting ascending neural pathways as well as the sympathetic output from the spinal cord. This dual action provides the beneficial effects of not only improved pain control, but also has been shown to aid with earlier return of bowel function through its sympathectomy. Various agents have been described for use in epidurals, with the mainstays being local anesthetics and narcotics. In a meta-analysis of sixteen randomized controlled trials from 1987 to 2005 comparing the use of epidurals to parenteral controlled analgesia, Marret and colleagues found epidurals were associated with improved analgesia and overall decreased ileus, with only side effects such as pruritis and labile blood pressure significantly associated with epidural use.(12) Gendall and colleagues confirmed these findings in a recent review of the literature, again demonstrating that epidural anesthesia improves functional recovery and pain relief, while potentially decreasing pulmonary complications.(13) While the epidural is in place, the anesthesiologist often manages all of the pain medications, performing comprehensive pain management. When the epidural is removed, the management returns to the surgeon. The use of anticoagulation for deep venous thrombosis (DVT) prophylaxis

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Figure 8.1  Thumbtack occlusion of a bleeding basivertebral vein.

and epidural placement/removal must be coordinated between the surgeon and anesthesiologist. Downsides to epidurals have consistently been their potential for increasing urinary retention and hypotension, higher costs, and perhaps decreased patient satisfaction, with no change in length of stay.(14) Despite these negative attributes, epidural use for colorectal surgery provides the potential for outcome improvement in analgesia and functional recovery, and is a very useful alternative for pain control following abdominal and large pelvic procedures. Furthermore, gabapentin, a medication that was originally designed for the treatment of epilepsy, has evolved as a treatment for mainly neuropathic pain, and has been studied extensively in both the pre- and postoperative settings. Although the exact mechanism of action is unknown, it is believed to act through N-gated calcium channels, and focus has been on both providing improved perioperative analgesia as well as narcotic-reducing effects.(15) Unfortunately, its use as an independent entity has been less efficacious, and it has not been extensively studied for either colorectal or anorectal surgery.(16) Both it, and a newer analog pregabalin, have been shown to decrease the need for opioids and thus reduce side effects such as nausea, vomiting, and urinary retention in other surgical arenas. While further study awaits recommendations specifically for use in the realm of colon and rectal surgery, these medications, along with standard postoperative regimen of increased oral fluid intake, fiber, stool softeners, sitz baths, and avoidance of constipation all aid in recovery from anorectal surgery. Most importantly, these varying agents all operating through different mechanisms convey the needed concept for the surgeon to use a multimodality approach to ensure successful perioperative pain management.

general postoperative complications bleeding Bleeding complications with any operation can be categorized by many different methods including intraoperative, postoperative, anastomotic bleeding, and gastrointestinal bleeding, such as stress-related ulcers. One of the most important factors for the surgeon is to preoperatively assess and determine the risk of bleeding. A thorough history and physical examination with emphasis on a personal or family history of bleeding tendency is crucial to identification and subsequent evaluation of those patients at risk, and should be completed before embarking on surgery. Questions should focus on any predisposition for easy bleeding or bruising, inability to clot even with mild cuts, or history of prior transfusions following surgeries, to identify certain patients that require further evaluation. Preoperative laboratory evaluation should include a complete blood count, coagulation panel (PT, PTT, INR), and platelet count. For those patients at increased risk, a more detailed analysis of platelet and clotting cascade function to include bleeding times, mixing studies, or evaluation by a hematologist may be appropriate. Perioperative bleeding with colorectal surgery depends in many aspects on the surgical procedure performed. Whereas bleeding rates following hemorrhoidectomy range from 2% to 6%, those following major abdominal operations such as total mesorectal excision (TME) for rectal cancer have been shown to have much higher blood loss estimates, with transfusion requirements reported in up to 43–73% of patients.(17–20) The most common causes for postoperative hemorrhoidal bleeding are technical failure (failed knot) within the first 24 hours, and infection with erosion at 7 days. Despite this, bleeding following hemorrhoidectomy is often able to be controlled either without surgical intervention or with simple suture ligation in the outpatient setting. In contrast, bleeding following major abdominal or pelvic procedures can mandate return to the operating room with corresponding physiological changes that may lead to cardiopulmonary complications. Yet, with the emergence of emphasis on decreased mandatory transfusion requirements, and technological advancements such as improved minimally invasive techniques, transfusion rates are decreasing and blood loss has also decreased. In a study of 147 patients in a case-matched comparative analysis between open and laparoscopic colectomies, Kiran and colleagues found that both estimated blood loss and perioperative transfusion rates were significantly higher in the open group.(21) Timing of the onset of bleeding also provides some insight as to its etiology. Early postoperative bleeding is typically from a technical error at the time of operation.(22) Late bleeding, which tends to present days to weeks after surgery, (though not outside the realm of technical problems) is more commonly secondary to patient factors such as an underlying bleeding tendency, concomitant coagulopathy, or spontaneous rupture or hemorrhage. It is worth noting that the risk of severe bleeding such as after a two or three quadrant hemorrhoidectomy, despite being small (2–6%), can be catastrophic.(5, 19) Therefore, it is imperative that the possibility of bleeding is discussed with all patients preoperatively, no matter how minor of a surgical procedure the patient is undergoing. Although uncommon, massive presacral bleeding during ­pelvic dissection can result in hemodynamic instability and even death.

Injury is secondary to dissection outside the avascular plane. Initial management includes packing and leveling the patient on the operating room table, along with continued resuscitation. This is effective for most patients within 20–30 minutes. Multiple other methods have described including electrocautery, suture ligation, sacral thumbtacks (Figure 8-1), muscle fragment welding, placement of tissue expanders or cyanoacrylate adhesives, topical hemostatic agents, and endoscopic tacking devices.(23–28) Although the presacral veins may be injured, continued bleeding nonresponsive to initial management is most commonly from the basivertebral veins through the sacral foramina.(24, 29, 30) When all else fails, pelvic packing, peritoneal closure, warming, and resuscitation in the ICU with return to the operating room 24–48 hours later may be required. Thus, emphasis on proper technique, knowledge of the pertinent anatomy, and comprehension of options to immediately consider when things do go awry are all important to decrease perioperative bleeding complications and subsequent clinical complications. infection Surgical-Site Infection (SSI) Surgical site infections continue to be a major source of cost and morbidity despite a strong emphasis on proper selection, timing and duration of perioperative antibiotics. Infections can be classified as surgical site infections, general postoperative infections such as pneumonia and urinary tract (which will be covered in separate sections), and infectious processes that deal specifically with the operation itself (i.e., anastomotic leaks, abscesses). Although multiple different patient and surgical factors contribute to the development of postoperative infections, development of any infectious complication results in increased patient suffering, length of stay, and delayed recovery. Additionally, hospital costs encompassing antibiotics, interventional procedures, nursing support, and surgical intervention contribute to driving up overall healthcare system costs. In simple terms, our skin and mucosal lining remain the ­primary defense mechanisms against infectious sources. With surgery, the breach in these protective layers, along with manipulation of the bowel and potential spillage of stool from various colorectal procedures lead to increased rate of infections. Those patients with an extensive component of cellulitis, characterized by leukocytic infiltration of the dermis, bacterial presence, and localized inflammatory response, typically require the addition of antibiotics, especially in patients with immunosuppresion, diabetes mellitus and the elderly. With the emergence of methicillinresistant Staphylococcus aureus (MRSA) and other multiresistant bacteria, it is imperative for the surgeon to help control the emergence of these more virulent pathogens by avoiding prolonged usage of antibiotics and changing antibiotics once the pathogens are cultured and appropriate sensitivity to antibiotics is known. With such a drastic rise in the incidence of MRSA, some hospitals are performing preadmission screening cultures for this pathogen. Thus, if there is an emergence of an active MRSA infection in the postoperative period, the patient most likely brought the infection into the hospital with them. Its presence then is not a result of failure of the surgeon or hospital personnel to follow protocol prevention. From a surgical perspective, proper wound

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improved outcomes in colon and rectal surgery care, drainage of abscesses, and debridement of any necrotic tissue, where appropriate, remain important adjuncts to the medical management of infections. Aspiration and drainage under imaging can often be used to convert an urgent reexploration to either an elective procedure or provide the ability to avoid a reoperation altogether. In addition to proper surgical technique that avoids converting a clean contaminated to a dirty case, identification of at-risk patients can aid in early identification and treatment of infectious complications. In a review of 428 patients specifically undergoing colorectal operations, surgical site infections were independently associated with increased body mass index (BMI) (odds ratio [OR] 1.07), and those in which a revision/ creation/or takedown of a stoma was involved (OR = 2.2).(31) In addition, with the emerging pandemic of obesity throughout the world, increased BMI has been found to be associated with not only higher rate of surgical site infections, but also is an independent predictor of wound dehiscence, herniation, and anastomotic leak.(32) Different methods have been employed to attempt to decrease the incidence of surgical site infections. There is some debate in the literature regarding the duration of antibiotic use for elective colon and rectal surgery. Although preoperative use of intravenous antibiotics to ensure adequate tissue concentrations at the time of incision has become standard of care, there is some controversy regarding the use of a single dose versus multiple doses. Fujita and colleagues performed a study including almost 400 patients undergoing elective resection of colorectal cancer and found that the three dose regimen of an every 8 hour, second generation cephalosporin (i.e., 24-hour perioperative ­coverage) significantly decreased the incidence of surgical site infections over a single preoperative dose (4.3% vs. 14.2%, p = 0.009).(33) However, organ or space SSI and other postoperative infectious ­complications did not differ between the two groups, and has similarly been not significantly different in many other studies. The practice of adding oral antibiotics has similarly contradictory evidence, with large prospective randomized trials demonstrating no decrease in infectious complications, while increasing the rates of nausea, pain, and noncompliance.(34, 35) Yet, other authors including a large prospective randomized trial and metaanalysis of 13 studies demonstrated the addition of oral antibiotics to systemic antibiotics was associated with a higher rate of prevention of surgical site infections.(36, 37) Proponents cite the ability of the oral antibiotics to decrease the bacterial load in the colon, as well as the marked increase of colonic bacterial isolates from the infected surgical wounds as evidence and rationale for its use. With such varying opinions, it is up to the individual ­surgeon to evaluate the literature and determine the best approach as it applies to their patient population. Finally, besides the proper use and timing of preoperative antibiotics, supplemental postoperative high dose oxygen (80%) has been shown to reduce ­surgical site infections by approximately 6–40%.(38, 39) Through ­suggested mechanisms, including more efficient electrontransport chain off-loading and improved neutrophil function, postoperative high-flow oxygen in the immediate recovery period has become part of a standardized postoperative pathway for many institutions. Finally, fewer complications may be associated with

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maintaining perioperative normothermia in patients undergoing colorectal surgery. Employing methods such as preoperative warming with bear-hugger devices, use of warm blankets and fluids, and avoiding prolonged or unnecessary exposure, may all result in less SSI. urinary tract infection and retention Urinary tract infections are the leading cause of nosocomial infections, accounting for ~40% of all infections, of which 80% are associated with transurethral catheter placement.(40) The dilemma remains how to significantly reduce this rate, especially in light of the chronic use of urinary catheters during colorectal procedures. A recent Cochrane review evaluating the use of antibiotics during short-term catheter use demonstrated there was a paucity of evidence that antibiotic prophylaxis was any better than treating patients when clinically symptomatic. While it did show some weaker evidence that bacteriuria, pyuria, and gramnegative bacteria are all reduced following antibiotic use over 24 hours or until catheter removal, none of these studies specifically focused on the colon and rectal patient. In addition, there was limited data on cost or subsequent development of multiresistant organisms, and most patients undergoing colorectal surgery receive perioperative antibiotics to cover bowel flora. Thus, caution needs to be taken when determining the applicability of these results to colorectal surgical patients. Following rectal surgery, urinary tract infection in part depends on the clinical practice of the surgeon regarding length of time of bladder catheter drainage. In a study comparing catheter removal at 1 and 5 days following rectal resection, Benoist and colleagues found urinary tract infections to be increased in those patients with catheters in for 5 days versus those who removed after 1 day (42% vs. 20%, p < 0.01).(41) Increases in urinary tract infection with prolonged drainage must be balanced with voiding dysfunction with early catheter removal. Unfortunately, urinary retention remains a well-known complication of colorectal and anorectal surgery, as well as a result of the spinal anesthesia commonly used during these operations.(42) In the Benoist study, urinary retention was significantly increased in those with the catheter present for only 1 day of postoperative drainage over the 5-day cohort (25% vs. 10%, p < 0.05), especially amongst those with tumors of the low rectum.(41) Following pelvic surgery, this may be, in part, secondary to third spacing and edema around the urethra following disruption of these tissue planes. Thus, in abdominal surgery, where the dissection does not proceed below the peritoneal reflection, this may lower the rate of dysfunction. The authors concluded that 1 day of drainage is adequate for most patients, although for patients undergoing lower resections, longer periods of drainage may be optimal. Changchien and associates in a review of 2,355 patients with colorectal cancer found urinary retention to be significantly associated with multiple factors to include older age, history of lung disease, rectal cancer, longer operations, and additional pelvic procedures such as hysterectomy or cystectomy.(43) Additionally, male gender, American Society of Anesthesiologists’ (ASA) score of 2 or 3, rectal cancer, use of a pelvic drain, and pelvic infection were independently associated with prolonged urinary dysfunction, defined as continued problems over one month postoperatively. To lessen

general postoperative complications the higher rates associated with transurethral catheter placement, some authors have also advocated suprapubic catheter drainage. In patients undergoing pelvic surgery, this has been associated with similar voiding dysfunction rates, but fewer infectious complications than the traditional transurethral route.(44, 45) Following anorectal surgery, urinary retention rates have been reported to be up to 50%.(46) Multiple methods that have attempted to decrease this rate have limited perioperative fluid, use of local versus spinal anesthesia, and even use of alpha-adrenergic blockade preemptively.(46) Although the latter did not seem to significantly affect rates of voiding dysfunction, both fluid restriction and adequate pain control have consistently been shown to have a positive effect at decreasing this difficult problem.(47, 48) Toyonaga and associates, in a prospective study of over 2000, patients found independent predictors significantly associated with the development of urinary retention following anorectal surgery were female sex, prior urinary difficulties, diabetes mellitus, intraoperative fluids over 1 L, and prolonged need for postoperative analgesics.(48) Although ­urinary retention is known to increase overall length of hospital stay, (42) careful patient education and strict fluid control have allowed most anorectal surgeries to be performed in an ambulatory setting with a low rate of return for urinary catheterization. (49) Additional use of agents such as NSAIDs and Ketorolac may minimize narcotic use and increase the success rate by avoiding this complication in an outpatient setting.(6) Surgeons therefore need to be in constant ­communication with their anesthesia counterparts to discuss excessive fluids and proper analgesia, as many are unaware of the potential downfall of these common practices. atelectasis Prevention Basic principles of airway clearance, avoidance of splinting and alveolar collapse, while preserving functional residual capacity and pulmonary reserve remain important components of proper postoperative pulmonary toilet. As a part of the “5 W’s” of the postoperative fever, “wind” as it relates to atelectasis reminds physicians that optimizing ventilation and oxygenation are keys to successful recovery, and are subsequently passed down to successive generations of training surgeons (as much as absolute truth as ancient lore). The fundamental principle behind avoidance of atelectasis has been shown to be successful in pulmonary processes ranging from cystic fibrosis and acute spinal cord injury to postoperative esophagectomy.(50–52) As such, factors such as head of bed elevation, early ambulation, and the ever-present incentive spirometer have become the mainstays of postoperative inpatient care. However, a recent Cochrane review of incentive spirometry use in the postcoronary artery bypass graft population with 443 participants in 4 trials found no difference in pulmonary complications amongst incentive spirometry, positive pressure use continuous positive airway pressure (CPAP), bilevel positive airway pressure (BIPAP), or simple preoperative patient education.(53) Furthermore, a meta-analysis with 14 trials over a 26-year period evaluating the use of incentive spirometry, positive pressure, and deep breathing following upper abdominal surgery to prevent postoperative pulmonary complications, also demonstrated no statistically significant difference between these modalities and no

therapy alone.(54) Pasquina and colleagues performed a review of 35 ­trials evaluating the use of respiratory physiotherapy after abdominal surgery and found that only in one study was the incidence of pneumonia decreased. In another study atelectasis decreased from 77% to 59% using pulmonary toilet methods of deep breathing, cough, and postural drainage.(55) They concluded that there are only a few trials that support its use, and the routine use of respiratory physiotherapy does not seem warranted based on data alone. Despite these large reviews, atelectasis is known to be present in anesthetized patients in the dependent portions of the lungs and has been shown to contribute to decreased lung compliance, worse oxygenation, increased pulmonary vascular resistance, and shunting.(56) It seems at worst that the practice of employing methods to decrease atelectasis is not harmful, and at best, may help out to a small degree with avoidance of pulmonary complications, and therefore, it is our continued practice. Pneumonia There is little data in the literature that directly addresses the development of pneumonia following colorectal or anorectal surgery. As stated above, the degree to which atelectasis and proper pulmonary toilet corresponds to the development of pneumonia is debatable. One thing that is clear is that development of postoperative pneumonia is independently associated with worse outcomes. Therefore, both prevention and early ­recognition and treatment, are key components to ensuring optimal outcomes. Johnson and colleagues found in a study of 180,359 patients that postoperative respiratory failure (defined as mechanical ventilation for longer than 48 hours after ­initial surgery or unanticipated reintubation) was found in 5,389 (3.0%) of patients and was associated with an increased in hospital morbidity, cost, and late mortality.(57) Additionally, factors that were found to be independently associated with the development of this was higher ASA classification, emergency operations, more complex surgery, sepsis, older age, congestive heart failure (CHF), chronic obstructive pulmonary disease (COPD), and smoking. These, along with a history of obesity and obstructive sleep apnea, mandate a need for careful postoperative monitoring and aggressive pulmonary toilet. Many of the patients, especially with underlying malignancy, have these comorbidities, and speak to the complexity of operations and need for close surveillance to avoid this feared complication. deep venous thrombosis Deep venous thrombosis (DVT) and its embolic corollary, pulmonary embolism (PE), are a significant source of morbidity and mortality in the perioperative period. Due to the predominance of abdominal and pelvic surgery, colorectal surgery carries a higher risk of these postoperative complications than other ­general ­surgical procedures. Yet, despite so much emphasis, DVT and PE continue to be the most common cause of preventable deaths during in-hospital admission, accounting for 1 out of every 4 hospitalized patients deaths.(58, 59) More concerning, over 50% of all DVTs are asymptomatic, while the vast majority of PEs are detected only after death (58). Since Virchow’s original description of stasis, hypercoaguability, and endothelial damage as risk factors, large epidemiological studies have found an increase in the development of symptomatic venous

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improved outcomes in colon and rectal surgery thromboembolism in the perioperative period to be associated with male gender, malignancy, trauma, immobility, COPD, sepsis, low hematocrit, low albumin, and major surgery.(60) One of the major problems with development of a DVT is the lack of initial clinical signs. Patient complaints of pain, swelling, edema, warmth, and tenderness of the affected limb are often absent.(61) Those patients that progress onto pulmonary embolism present many times in the late stages with cardiopulmonary shock and collapse, though often heralded by symptoms such as acute shortness of breath, dyspnea, pleuritic chest pain, along with tachycardia and an increasing oxygen requirement. Thus, emphasis has been placed on both prevention and screening. Despite its very high sensitivity and specificity of over 95%, screening with duplex and color Doppler sonography, even in high risk patients, in the absence of symptoms, has been questioned as to its cost-effectiveness.(62, 63) Part of this may be that although the lower extremities are the most common site of origin, approximately one-third of patients have proximal (above popliteal) veins as the site of origin, which are not visualized well by duplex.(59) Venous ultrasonography remains the mainstay for diagnosis of deep venous thrombosis, especially when combined with elevated d-dimer levels. The hallmarks of DVT via ultrasound are both visualization of the clot and more commonly the inability to compress the venous system under direct pressure. (64) Similarly with the advent of multidetector row helical CT scanners, this has essentially ­supplanted the pulmonary angiogram as the procedure of choice for diagnosis of pulmonary embolism, with sensitivity, specificity, and negative predictive value over 90%, even for subsegmental ­pulmonary emboli.(65) Prophylaxis of venous thrombotic events centers on both mechanical and medical means. The current mainstays for chemical thromboprophylaxis are unfractionated and low-­molecular weight heparin. Unfractionated heparin works through antithrombin III to deactivate thrombin and other factors in the ­clotting cascade. Concerns about increased bleeding events as well as its dose-effect relationship have led many to be wary of its use. Low-molecular weight heparin has enhanced antifactor Xa activity and more predictable dose-effect relationships.(66) In a recent Cochrane review addressing the prevention of thromboembolic complications, the combined use of mechanical graduated stockings with either unfractionated or low molecular heparin was identified as the optimal prophylaxis.(67) Interestingly, despite the extensive search, only 3 studies meeting inclusion criteria focused specifically on colon and rectal surgery. That same group evaluated 558 studies, of which 19 met the inclusion criteria, and again found that unfractionated and fractionated heparin were equally effective, and the addition of either to compression stockings was superior to either alone.(68) As pointed out in the opening challenging case, risk stratification continues to be a mainstay for determining the extent of prophylaxis in these patients. Young, healthy patients undergoing routine anorectal surgery, with minimal patient-specific risk factors, do not require any therapy other than mechanical means via graduated compression stockings and/or intermittent pneumatic compression boots and early ambulation. Those patients with multiple risk factors and undergoing high risk surgery, such as pelvic operations, warrant more aggressive means like unfractionated or low-molecular weight heparin, in addition to the

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mechanical devices. Timing has been somewhat controversial with some studies demonstrating higher bleeding without undue increase in thrombotic events when given after the surgery and others stating that dosing should begin preoperatively. Although this question has yet to be definitively answered based on current literature, it is well accepted that some form of perioperative, including intraoperative means, has become the standard of care. The risk of bleeding with thromboprophylaxis dosing is small, with the majority revolving around injection site ecchymoses or hematoma in up to 7% of cases.(69) More clinically significant bleeding, such as gastrointestinal or intraabdominal bleeding, occurs in <0.5%, and is rarely the cause for cessation of therapy. One potential concern that arises frequently in the realm of colorectal surgery is how to treat the patient receiving anticoagulation for colonoscopy. Recent guidelines have shown that aspirin and other NSAIDs do not need to be withheld, with the rate of postpolypectomy bleeding around 2%.(70) On the other hand, coumadin and other more potent antiplatelet medications (i.e., clopidogrel) are commonly held for 5 to 7 days before the procedure, especially when it is known that a polypectomy or other procedure is likely. There is some evidence that the application of endoclips with polypectomy in anticoagulated patients is safe; however, small sample sizes hinder ability to make broad recommendations.(71) Thus, most of the practice is based on guidelines and less on an abundance of available evidence ­supporting or dissuading this practice.(72, 73) nausea and vomiting Though often not deemed as significant or crucial to overall ­success of an operation by surgeons, postoperative nausea and vomiting (PONV) can be extremely bothersome for the patient. Clearly, the etiology is multifactorial—with surgical, anesthetic, medication, and patient-related factors all contributing significantly. Head of bed elevation and early ambulation are minor modifications that may be somewhat helpful. More useful, anesthesia providers have found increasing success through prophylaxis for this phenomenon. As a part of that process, identification of those patients at risk is imperative, as universal prophylaxis has not been shown to be cost-effective.(74) A thorough review of prior surgeries and response to anesthetics may help in identification of these individuals. Intravenous use of ondansetron, a selective serotonin 5HT3 receptor antagonist, has been shown in multiple randomized trials to be effective in complete prevention of postoperative emesis in up to 60–85%, when given before the induction of general anesthesia. (75–77) Finally, routine decompression with nasogastric tubes has demonstrated no impact on PONV and has fallen out of favor.(78) prolonged ileus In general, postoperative obstruction can be divided into two broad categories—early and late. Early postoperative bowel obstruction is defined as onset of symptoms within thirty days of surgery. The majority of early postoperative bowel obstructions are due to paralytic ileus or adhesions—up to 90 percent in some series, with the remaining possible etiologies including phlegmon, intraabdominal abscess, Crohn’s disease, hernia, volvulus, intussusceptions, and malignancy.(79, 80) Late obstructions are those presenting at any point >30 days following surgery. The management of bowel

general postoperative complications obstruction including ileus remains a significant burden to healthcare costs. In 1994, according to Beck and colleagues, there were 303,836 hospitalizations during which adhesiolysis was performed, accounting for 846,415 inpatient days and an estimated $1.3 billion in expenditures.(81) In addition, reoperative surgery in the setting of early bowel obstruction can prove to be significantly challenging, as abdominal inflammation and early adhesions create a hostile environment marked by densely adhered bowel and ­friable tissues. In order to safely and effectively manage these patients, one must have an extensive understanding of the various conditions which may result in prolonged ileus. Like many of the complications discussed in this chapter, the development of a prolonged ileus has multiple potential causative factors including hormones, medications and surgical stress. Postoperative ileus clinically manifests itself with abdominal distension, bloating, failure to pass stool or gas, nausea, emesis, and pain. Even more concerning, Senagore found that in addition to the symptoms experienced as a result of the ileus, delayed surgical wound healing and ambulation, atelectasis, pneumonia, and deep vein thrombosis are all potentially increased by the development of a postoperative ileus, which increases ­hospitalization length of stay and overall costs.(82) The definition of what constitutes a prolonged ileus widely varies in the literature and contributes to discrepancies between different studies. In general, when the symptom complex continues for over 7 days following abdominal surgery, most consider this ­prolonged and should raise concern for more extensive evaluation. Return of bowel function has multiple parameters that can be controlled by the provider in the perioperative period. For example, limiting the amount of intraoperative and postoperative fluid and sodium has been shown to improve time to passage of flatus and stool, and result in earlier hospital discharge.(83) In addition, clinical pathways that include the use of restricted perioperative intravenous fluids, early oral intake, early ambulation, and epidural anesthesia, have been shown to significantly decrease length of stay and perioperative cardiopulmonary complications, although readmissions are slightly higher.(84) Thus, working through optimization of all components of postoperative care may contribute more to a successful recovery than primary emphasis on one factor alone. Through entry into a standardized program, the avoidance of certain variables that negatively affect recovery for both the intraoperative and postoperative settings can provide improved reproducible results.(85) A bonus of implementation of pathways is the ability to help all healthcare providers, including nursing personnel, to become accustomed to a routine postbowel resection course. Therefore, any deviations from this can be ­recognized more readily, allowing intervention before the patient enters a more severe or septic state. A thorough history and physical examination help distinguish some of the benign causes of obstruction and aid in differentiating this from a prolonged ileus. For example, the history in a patient with Crohn’s disease or prior radiation therapy can ­provide just as many clues as to the etiology of the obstruction, such as possible stricture, or an obvious hernia detected on physical examination. As patients often present with concomitant dehydration and electrolyte abnormalities, placement of a nasogastric tube, with appropriate fluid resuscitation, and correction of electrolyte

abnormalities should occur while the work-up is in progress. Plain film radiographs may confirm dilated small bowel loops with stair-stepping air-fluid levels, but usually do not assist in defining the underlying etiology. Despite their frequent use, numerous studies quote a poor sensitivity for plain abdominal radiographs in diagnosis of small bowel obstruction, ranging from 13% for low grade obstruction to 50–60% for high grade obstructions. (86) CT may give anatomical information outside of the bowel wall itself that may help with accurate diagnosis. Caution should be used in giving oral contrast for the patient with high grade ileus or obstruction, and in general, should be avoided. Newer pharmacotherapeutic endeavors, such as the peripherally acting mu-opioid receptor antagonist, alvimopan, have been shown to reduce the incidence of postoperative ileus, nasogastric tube insertion, time to gastrointestinal recovery, and overall hospital length of stay.(87–89) Further studies are still ongoing to evaluate whether its safety profile is acceptable for wide-scale clinical use. Other methods that have been studied in attempt to shorten bowel function return include prokinetic agents such as erythromycin and cisapride, although the results have been mixed. Erythromycin, a motilin agonist, has been shown in the past to be effective for upper gastric and pancreatic surgery, especially with regard to promotion of gastric emptying. In a randomized doubleblind placebo study of 134 patients, erythromycin was not shown to affect clinically relevant outcomes such as time to intake of solid foods, nausea rate, or length of stay.(90, 91) Similarly, cisapride, before its removal from the market secondary to cardiac toxicity, did show some, albeit limited, clinically significant improvements. (92–94) Thus, for hindgut surgery, prokinetic agents have not yet been shown to make a clinically relevant difference. Probably the most important factor that has been shown to make a difference in reducing ileus is postoperative clinical pathways that include early oral feeding.(95) A recent Cochrane review by Andersen et al. including 13 randomized controlled ­trials and over 1,100 patients, evaluated the use of early feeding and the development of complications and found early feeding is safe, may reduce postsurgical complications, and concluded there is no advantage to withholding oral intake.(96) Opponents of this practice cite a lack of a consistent definition of what early feeding encompasses. As such, although many surgeons prefer to advance the postoperative diet slowly, it does seem clear that the recovery of gastrointestinal function as evidenced by first bowel movement or flatus and tolerance of an oral diet in the early postoperative setting are independent of each other, and the practice of early resumption of diet is safe.(97) retained foreign bodies In any complex surgical procedure there exists a potential for items to be unknowingly left in body cavities.(98) To minimize this risk, current standards require all sponges, needles, surgical instruments, equipment, and items small enough to be misplaced be counted before the procedure and one or two times after the completion of the procedure to confirm that all items are accounted for. These activities are usually performed and documented by the operating room nurses and technicians; however, the surgeon is ultimately responsible and should conduct each operation so as to minimize the risk of misplaced foreign bodies. In accordance with

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improved outcomes in colon and rectal surgery (A)

(B)

Figure 8.2  Radiograph demonstrating radoopaque markers. Left to right. Laparotomy sponge, Ray-tec sponge. The upper image is flattened, whereas the lower image demonstrates the radiologic view when the item is crumpled.

Figure 8.4  (A) CT scan of patient with a retained Ray-tec sponge. Image is the inferior cut of the study. The upper edge of the Ray-tec marker is demonstrated as white dots lines between the bladder (filled with contrast) and the sacrum. (B) Pelvic radiograph of the same patient demonstrating Ray-tec marker in pelvis.

Figure 8.3  Radiograph of (left to right) Jackson-Pratt drain, Penrose drain, nasogastric tube.

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this goal, most surgeons, avoid using small Ray-tec sponges in the abdomen and avoid placing laparotomy sponges in areas that are hard to visualize. If sponges must be used to pack areas, the sponge marker should be left in an obvious area, or a ring or clamp may be attached to the sponge. Most important is a through exploration of the entire operative field, which should be performed ­routinely before closing the incision. Items used during the operation that have the potential to be easily lost should be radiopaque or contain a radiopaque marker (e.g., Ray-tec sponges and Silastic drains). Figures 8.2 and 8.3 demonstrate the radiologic view of several common surgical items. Plain radiographs are often the best for identifying the radiopaque markers incorporated into these items; The markers may be much less obvious on studies such as CT scans (Figures 8.4a and b). If an instrument, sponge, or needle count is not correct, several actions are indicated. All the sponge wrappers and suture packages should be counted to confirm the accuracy of the original count. The entire operating room, and especially the trash bags and floor under the operating table, should be searched for the misplaced item. Simultaneously, the surgeon should inspect the operative field thoroughly for the missing item. If the missing item cannot be located, a radiograph of the entire operating field

general postoperative complications should be obtained before closure of the body cavity to identify any radiopaque object and minimize the morbidity of locating the missing item. Because of the potential for human error, a “correct” instrument, needle, or sponge count does not absolutely exclude the presence of a foreign body. Therefore, each member of the team must maintain a high index of suspicion. A sponge or other foreign body left in a body cavity can present or be identified in a number of ways. The foreign body may be seen on a radiograph obtained for other reasons, or the patient may develop symptoms that lead to the need for radiographs or an exploratory procedure. Symptoms may be infectious (fever, elevated white cell count, wound infection, or abscess) or inflammatory (ileus, tenderness, mass effect). For any postoperative patient with unusual or unexplained symptoms, radiographs should be included in the evaluation. Finding a retained foreign body is unusually an indication for an urgent exploratory procedure. The exception may be asymptomatic patient with a retained small needle. The morbidity associated with localizing and removing a small needle must be weighed against the potential risk of leaving it alone, and the patient can assist in this decision. Review of biplanar radiographs may assist in localizing a retained item, and early identification will minimize the morbidity associated with the object’s removal. Retention of operative foreign bodies is uncommon, and a surgical team that adheres to careful practices should avert its occurrence. “time out” and sided surgery concerns Wrong-side/wrong site, wrong-procedure, wrong-patient adverse events (WSPEs) constitute some of the worst medical errors that clinicians and patients experience. These events often result in patient harm and litigation, but literature on frequency and root causes is limited.(99) The Institute of Medicine report To Err Is Human painted a broad picture of the magnitude of medical errors in the United States and gave directions for safety improvements.(100) While, sided surgery is less of a concern in colorectal patients, incorrect surgery due to inadequate lesion location remains a challenge. In July 2004, the Joint Commission on the Accreditation of Healthcare Organizations (JCAHO) implemented the universal protocol for the prevention of WSPEs.(101) The protocol uses preoperative verification of patient, site, and procedure, marking the operative site, and a time-out immediately before starting the procedure. Prevention of WSPEs requires new and innovative technologies, reporting of case occurrence, and learning from successful safety initiatives (such as in transfusion medicine and other high-risk nonmedical industries), while reducing the shame associated with these events. future directions As the push to not only prevent complications but detect them earlier continues to expand, molecular markers may become an increasingly utilized component. Welsch and associates evaluated the use of C-reactive protein (CRP) in the postoperative course of 383 rectal resections with primary anastomosis in patients with rectal cancer and found that using a cutoff of levels above 140 mg/dl on postoperative days 3 and 4 was associated with a sensitivity of 80 and 54% respectively and specificities of 81 and 92%, respectively, for the presence of all infectious complications. (102) Although this is just one example of a vast field, it highlights

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improved outcomes in colon and rectal surgery   78. Petrelli NJ, Stulc JP, Rodriguez-Bigas M, Blumenson L. Nasogastric decompression following elective colorectal surgery: a prospective randomized study. Am Surg 1993; 59(10): 632–5.   79. Pickleman J, Lee RM. The management of patients with suspected early postoperative small bowel obstruction. Ann Surg 1989; 210(2): 216–9.   80. Miller G, Boman J, Shrier I, Gordon PH. Readmission for small-bowel obstruction in the early postoperative period: etiology and outcome. Can J Surg 2002; 45(4): 255–8.   81. Beck DE, Opelka FG, Bailey HR, Rauh SM, Pashos CL. Incidence of small-bowel obstruction and adhesiolysis after open colorectal and general surgery. Dis Colon Rectum 1999; 42(2): 241–8.   82. Senagore AJ. Pathogenesis and clinical and economic consequences of postoperative ileus. Am J Health Syst Pharm 2007; 64(20 Suppl 13): S3–7.   83. Lobo DN, Bostock KA, Neal KR et al. Effect of salt and water balance on recovery of gastrointestinal function after elective colonic resection: a randomized controlled trial. Lancet 2002; 359(9320): 1812–8.   84. Khoo CK, Vickery CJ, Forsyth N, Vinall NS, Eyre-Brook IA. A prospective randomized controlled trial of multimodal perioperative management protocol in patients undergoing elective colorectal resection for cancer. Ann Surg 2007; 245(6): 867–72.   85. Bradshaw BG, Liu SS, Thirlby RC. Standardized perioperative care protocols and reduced length of stay after colon surgery. J Am Coll Surg 1998; 186(5): 501–6.   86. Fukuya T, Hawes DR, Lu CC, Chang PJ, Barloon TJ. CT diagnosis of small-bowel obstruction: efficacy in 60 patients. Am J Roentgenol 1992; 158(4): 765–9.   87. Wolff BG, Weese JL, Ludwig KA et al. Postoperative ileusrelated morbidity profile in patients treated with alvimopan after bowel resection. J Am Coll Surg 2007; 204(4): 609–16.   88. Viscusi ER, Goldstein S, Witkowski T et al. Alvimopan, a peripherally acting mu-opioid receptor antagonist, compared with placebo in postoperative ileus after major abdominal surgery: results of a randomized, double-blind, controlled study. Surg Endosc 2006; 20(1): 64–70.   89. Senagore AJ, Bauer JJ, Du W, Techner L. Alvimopan accelerates gastrointestinal recovery after bowel resection regardless of age, gender, race, or concomitant medication use. Surgery 2007; 142(4): 478–86.   90. Smith AJ, Nissan A, Lanouette NM et al. Prokinetic effect of erythromycin after colorectal surgery: randomized, placebo-controlled, double-blind study. Dis Colon Rectum 2000; 43(3): 333–7.

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  91. Bonacini M, Quiason S, Reynolds M et al. Effect of intravenous erythromycin on postoperative ileus. Am J Gastroenterol 1993; 88(2): 208–11.   92. Roberts JP, Benson MJ, Rogers J et al. Effect of cisapride on distal colonic motility in the early postoperative period ­following left colonic anastomosis. Dis Colon Rectum 1995; 38(2): 139–45.   93. Tollesson PO, Cassuto J, Rimbäck G et al. Treatment of postoperative paralytic ileus with cisapride. Scand J Gastroenterol 1991; 26(5): 477–82.   94. Brown TA, McDonald J, Williard W. A prospective, randomized, double-blinded, placebo-controlled trial of cisapride after colorectal surgery. Am J Surg 1999; 177(5): 399–401.   95. Reissman P, Teoh TA, Cohen SM et al. Is early oral feeding safe after elective colorectal surgery? A prospective randomized trial. Ann Surg 1995; 222(1): 73–7.   96. Andersen HK, Lewis SJ, Thomas S. Early enteral nutrition within 24 hours of colorectal surgery versus later commencement of feeding for postoperative complications. Cochrane Database Syst Rev 2006; (4): CD004080.   97. Han-Geurts IJ, Hop WC, Kok NF et al. Randomized clinical trial of the impact of early enteral feeding on postoperative ileus and recovery. Br J Surg 2007; 94(5): 555–61.   98. Stamos MJ, Theuer CP, Headrick CN. General postoperative complications. In Hicks TC, Beck DE, Opelka FG, Timmcke AE. eds, Complications of Colon & Rectal Surgery. Baltimore: Williams & Wilkins, 1996: 118–39.   99. Kohn LT, Corrigan JM, Donaldson MS. To Err Is Human: Building a Safer Health System. Washington, DC: Institute of Medicine, National Academy Press; 2000. 100. Seiden SC, Barach P. Wrong-side/wrong site, wrong­procedure, wrong-patient adverse events. Are they preventable? Arch Surg 2006; 141: 931–9. 101. Joint Commission on Accreditation of Healthcare Organizations. Guidelines for implementing the universal protocol for preventing wrong site, wrong procedure, wrong person surgery. JCAHO Web site. http://www.jointcommission.org/PatientSafety/UniversalProtocol/. Accessed June 15, 2006. 102. Welsch T, Muller SA, Ulrich A et al. C-reactive protein as early predictor for infectious postoperative complications in rectal surgery. Int J Colorectal Dis 2007; 22(12): 1499–507.

9

Care paths and optimal postop management Surya P M Nalamati and Eric J Szilagy

challenging case A 45-year-old man undergoes an open sigmoid colectomy for diverticular disease and is placed on a postoperative care path. On postoperative day three, the patient is ambulating, has mild nausea, and has not passed flatus. case management The care path is modified to continue intravenous fluids. The patient-controlled analgesia is stopped and the patient is started on small doses of intravenous narcotics. Ambulation is continued. INTRODUCTION The constant endeavor of modern medicine has been to improve the quality of patient care. Over the past century there have been tremendous technological advances in medicine and surgery. The pattern of care has evolved from being a single physician managing one patient’s care to team care involving one or more physicians from same or different fields of specialization, residents, nurses, physician assistants, social workers, and case managers. However, these advances have increased health care delivery costs, which in turn demanded a system of care to be developed that is more efficient without compromising patient safety and the quality of health care. Care paths are one of the most wide spread tools used to enhance outcomes and contain costs.(1) Introduced in early1990s in the United Kingdom and United States, they have rapidly gained acceptance and are now being used all over the world. Care paths are structured, multidisciplinary plans of anticipated care, set in an appropriate time frame, to help patients with specific conditions or sets of symptoms, move progressively through a clinical experience to a positive outcome. Numerous synonyms exist for care paths including clinical pathways, critical care pathways, integrated care pathways, critical paths, multidisciplinary pathways of care, and care maps.(2, 3) Fast-track surgery and ERAS (enhanced recovery after surgery) programs are recent evolutions of the care paths concept.(4–6) Critical pathways, successfully utilized in several different business sectors, including construction and automotive industries, have been adapted and applied to medical field.(7–11) They are designed to support the implementation and translation of national guidelines, or an evidence-based standard of care, into local protocols. The anticipated result is the subsequent application of pathways to clinical practice, clinical and nonclinical resource management, clinical audit, and financial management.(2) They provide detailed guidance for each stage in the management of a patient (diagnosis, treatment, interventions etc.,) for a specific, given condition over a period of time. They encompass the progress of patient care and document details of outcome.(12) Clinical pathways have four main components: a time line, the categories of care or activities and their interventions, intermediate and long-term outcome criteria, and the variance records, which allows deviations to be documented and analyzed.(2)

Care paths differ substantially from clinical guidelines, protocols, and algorithms. Clinical guidelines are consensus statements that are systemically developed to assist practitioners in making patient management decisions related to particular clinical circumstance.(13) Protocols are treatment guidelines that are developed based on clinical guidelines.(14) Although anchored in clinical guidelines, care paths are designed to be used by multidisciplinary teams and focus on details of the process of care and highlight inefficiencies. Care paths in contrast to guidelines contain a continuous monitoring and data evaluation component. This helps in identifying the rate limiting steps and to make any evidence-based changes in the care path to improve the overall process of care. care paths in colon and rectal surgery Care paths in surgery are used in the management of patients undergoing commonly performed surgical procedures.(15) In colon and rectal surgery, care paths have been successfully initiated since the early1990s. Care paths have been used in the management of perioperative care where they were more procedure specific. They have been successfully used in management of standard colon resection, laparoscopic colon resections, complex cases such as restorative proctocolectomy, and complex anorectal reconstructions.(16–20) The objectives of care paths, as reviewed by Pearson et al., were to select the best demonstrated practice when practice varied unnecessarily.(21) He outlined the process guidelines as follows: Define the standards for the expected duration of hospital stay and for the use of tests and treatments. These standards are evidence-based or based on guidelines for the specific clinical circumstance. For example, Stephen et al. noted in their article, that before implementation of pathways patients had their nasogastric tubes removed after they passed flatus.(22) During development of their care path for colonic resection, evidence for the routine use of nasogastric tube which was a rate-limiting step for early recovery was reviewed. Evidence showed that routine prophylactic decompression with nasogastric tube decompression is of no use and should be abandoned.(23) This led to incorporating the step to remove the nasogastric tube on the day of the surgery, which has become now widely accepted clinical practice. •• To examine the interrelations among the different steps in the care process and find ways to coordinate or decrease the time in the rate-limiting step. •• To give all the care providers a common plan from which to view and understand their various roles in overall care process. •• To provide a framework for collecting data on the care process so that providers can learn and analyze how often and why patients do not follow an expected course. •• To decrease documentation burdens and improve patient satisfaction with care by educating patients and their families about the plan of care.

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improved outcomes in colon and rectal surgery defining and improving outcome measures Surgical care outcomes have been defined by a variety of measures. Complication rates relating to abnormal outcomes, such as infection, hemorrhage, organ system dysfunction, and reconstruction failure, are common benchmarks for surgical performance. These rates have been the targets of quality improvement because they have impact not only on morbidity but also mortality. However, these outcome measures, although significant, do not necessarily reflect the effort of the entire surgical team or the efficiency of the care process. Length of stay, rate of return of physiologic function, and quality of life measures are cumulative standards that also take into account the impact of multiple caregivers. They may not only correlate with lower morbidity and mortality, but provide additional metrics for the result of a multidisciplinary team approach.(24) The cumulative effect of introducing efficiency in the multidisciplinary effort is improved utilization of resources, with higher quality, using fewer resources at a lower cost. Traditionally, the hospital stay after colonic resection varied be­­ tween 5 and 10 days with a median of 7 days and a complication rate of 10–20%.(25, 26) Implementation of care paths has significantly reduced this number. Archer et al. reported a mean length of stay decrease from 10.3 to 7.5 days, and average hospital charges from $21,650 to $17,958 (20) whereas Billingham et al., in their series of 263 patients, reported stay of 5.5 vs. 8.2 days and hospital charges $12,672 vs. $16,665 (19). Even though the decreased length of stay and cost benefits appear to be obvious, it is not clear in these studies if there is significant shifting of costs from hospital care to home care. benefits of care paths Care paths provide explicit and well-defined standards for care. They support introduction of evidence-based medicine and use of clinical guidelines thus reducing variations in patient care and improving clinical outcomes.(27) They improve multidisciplinary communication, interprofessional collaboration, teamwork, and care planning. (28) Care paths implement continuous clinical audit, providing a means of continuous quality improvement, thus providing a baseline for future initiatives to modify the pathway. Care paths reduce risk, support training, optimize resources, and reduce costs, which contribute to shortening the hospital stay. Care paths are not prescriptive; they do not override clinical judgment. On the contrary, the surgeon can at any time elect not to follow the pathway based on his clinical judgment. One of the most useful characteristic of care paths is that they provide a visual overview of each patient’s care with specific outcomes stated. This can be reviewed and acted on by every one caring for the patients, as well as by patients themselves.(20) Using care paths designed around evidence-based data and standards of practice, one could expect a decrease in overall malpractice risk.(29) development of care path The development and implementation of care paths consist of the following steps as reviewed in numerous publications.(1, 14, 19, 21, 22, 30, 31) Select a Topic Topic selection for formulating a care path could be either disease or procedure specific. High volume, high-cost diagnoses or procedures are ideal. Critical pathways development in colorectal ­surgery

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concentrated on high volume and high cost procedures like colectomies, restorative total proctocolectomies, and complex anorectal reconstructions.(5, 16, 19, 20, 22) Most of the care paths developed in colon and rectal surgery are procedure specific and aimed at perioperative management. These procedures are more suitable for pathway development because of the predictable course of events before and after hospitalization, and variations in care associated with them. Development of care paths makes the goal of decreased variation and improved resource utilization possible. Select a Team A multidisciplinary team is the most critical element of any care path. Historically, care paths were developed by and for nurses and other nonphysician hospital-based workers. However, the lack of physician participation led to failure of that model of care pathway.(32, 33) The active role of surgeons in a leadership role is crucial to development and implementation of pathways. In addition, it is vital to involve representatives from all groups that will play a role in implementation of pathway. The team should discuss all the elements of the pathways. The team should meet regularly to develop the pathway and after implementation to discuss variances and make appropriate revisions to it. Colon and rectal care path teams consist of surgeons, house staff, physician assistants, stoma nurses, office nurses for preoperative care planning, ward nurses, physical therapists, and social workers to plan the home care needs and arrange them in a timely fashion. Timely intervention by each of the team members is essential for success of the care path. Evaluate the Current Process of Care A careful review of the medical records should be performed to identify the critical intermediate outcome, rate limiting steps, and high cost areas on which to focus. Evaluation can be automated where electronic medical systems are available. This should include review of the preop process (preanesthesia work up, obtaining necessary consults, stoma training if needed, antibiotics, anti coagulation) and the postop process. In our initial review process, during the development of care pathways, we found that nasogastric intubation, postoperative feeding, GI function recovery time, and mobilization to be the important rate limiting steps. Further development will be based on intraoperative anesthesia care, and postoperative pain management. Evaluate Medical Evidence and External Practices After defining the rate limiting steps, the team should evaluate literature for evidence of the best-demonstrated practice. For most of the rate limiting steps in colon rectal surgery there is data available. In the absence of evidence, comparison with other institutes to set up a benchmark is the most reliable method. These steps should be then incorporated into the care path. Establish Goals and Endpoints A reasonable objective should be established as a goal, which serves as an endpoint for the care path. Multiple goals can be established involving each aspect of care in the pathway, and the successful achievement of each of these landmarks would define the success of care path. For example, in our care path for colon surgery (see Figures 9.1 and 9.2), the goal of the pathway is to

Analgesia: PCA____ Epidural_____ Other_____ Resume pre-hospitalization meds

Bowel prep day before surgery Routine meds as DVT prophylaxis indicated by MD

Sign/title_______

Eves

Nights

Figure 9.1 Care Path for Colon Surgery.

PATH WAY

Initials_______

Days

Pre-op education re:bowel prep, post op pre-op teaching activities, pain management_____

TEACHING

REVIEW

Consult CRM: confirm discharge plan

Consult CRM if needs identified Consult CRM by nurse screen or MD

DISCHARGE PLAN

Initials:___Sign/title:____

Initials:___Sign/title:____

Initials:___Sign/title:____

Initials:___Sign/title:____

Initials:___Sign/title:____

Initials:___Sign/title:____

Post-op education, C&DB, SED, Incentive spirometry, early Introduce ostomy ambulation education

Initials:___Sign/title:____

Initials:___Sign/title:____

Initials:___Sign/title:____

Ostomy education

Clear Liquids when tolerating 800cc clear liquid advance to PO#1 diet_____

DIET Clear fluids per MD NPO after midnight NPO/Ice chips Sips of clear liquids Consult CRM: estabilish discharge dispositional needs

I&O dc Foley______ (leave in if fluid status problem or Epidural Bladder scan post vaid straight cath

Analgesia: PCA____ Epidural_____ dc___ Other_____ All routine meds PO if tolerated

NG_______ IV, de dressing, SED Spirometry Incentive

Ambuiate X 4 1. 2. 3. 4 Increase freq & distance 50ft to 100ft

POST_OP/DAY 2 Date________

Bowel prep day ELIMINATION before surgery Confirm bowel prep Monitor I & O Foley Monitor I & O Foley

Analgesia: PCA____ Epidural_____ Other_____ Resume meds

No NG unless obstructed. NG_____ IV, Dressing SED NG_______ Incentive spirometry IV, Dressing, Pulse Ok Wean O2 Incentive spirometry, Pulse Ok

Ambuiate X 4 1. 2. 3. 4 Increase freq & distance 50ft to 100ft

Bed rest, Reposition q 2-4 hr ACTIVITY Increase Dangle Post-op eve______ Ankle Pumps, C&DB

Spirometry TREATMENTS

CBS,chem 7 (only if blood loss or metabolic issue)

CBS,chem 7, Platelets EKG & CXR, as Type and Screen needed only

TESTS

ostomy/ET consult

ET for elective stoma

POST_OP/DAY 1 Date________



POST_OP/DAY OF SURGERY Date_____

Surgery/PCP Anesthesia class3 Anesthesia

PRE-OP/DAY OF SURGERY Date_____

CONSULTS

Aspect of Care PRE-HOSPITAL

care paths and optimal postop management

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Analgesia: change to PO pain medication if tolerating fluids

Monitor I&O Monitor bowel function: Flatus__________

PO # 1 diet Dietary consult if needed

Consult CRM: Finalize discharge plan obtain supplies and equipment. Complete discharge, W-10. Consider discharge if tolerating PO & Passing flatus if needs identified by nurse screen or MD

Reinforce ostomy education. Incerase Review diet, activity patient participation. Review diet, meicaton and home care activity and medication.

Initials:___Sign/title:____

Eves

Nights



ELIMINATION

DIET



DISCHARGE PLAN

Days



TEACHING

REVIEW

PATH

WAY

Figure 9.2  Care Path for Colon Surgery (Continued).

Initials:___Sign/title:____

Initials:___Sign/title:____

Transfer IV to saline lock

TREATMENTS

Initials:___Sign/title:____

Initials:___Sign/title:____

Initials:___Sign/title:____

Initials:___Sign/title:____

Initials:___Sign/title:____

Initials:___Sign/title:____

Consult CRM: review finalize Discharge plan

Diet/Low Residue

Monitor I&O Monitor bowel function: Flatus__________

PO analgesia

Monitor

Ambulate in atleast 4 times(50 ft —100 ft) Ambulate independently, Progressively increase or with aids as required distance/frequency

ACTIVITY



TESTS

Clear discharge with consulting MD

COMMENTS

CONSULTS

POSTE-OP/DAY 4 Date____________

POST-OP/DAY 3 Date____________

Aspect of Care

Patient/Family will understand and participate in plan

Discharge by post-op day #4

Adequate nutritional intake

Effective bowel and bladder functon re-estabilished

Effective pain management

No post-op infections

Elimination of post-op complications related to immobility

Appropriate referrais pre-op

OUTCOMES

improved outcomes in colon and rectal surgery

care paths and optimal postop management ­discharge the patient on postoperative day 4, and if possible on day 3. The subgoals that were established were based on the aspect of care such as to ambulate on day 1 after surgery, remove the Foley catheter on day 2, etc. Goals should also be established for achieving patient satisfaction, as measured by survey tools such as those used by Press Ganey Associates.(34) Determine Critical Pathway Format There are multiple formats, which can be used; most of them have a task-time matrix in which specific tasks are specified along a time line. Care paths range from different kinds of manual ­formats to electronic format, where electronic charting, and pathway compliance are obtained simultaneously.(31, 35) Implement the Care Path Education of all the involved caregivers, patients, and their families is the key to successful implementation of a care path. In-service education should be given to all the involved groups, especially if electronic care paths are used.(36) Different individuals in the care path should be assigned specific functions such as collection of data, analyzing variance etc. Document and Analyze Variance Implementation of the pathway is only the first action of care path. This must be followed by data collection analysis and then process improvement to achieve the set goals. A good tool suited for this purpose is the analysis of variance grids.(27) By examining the variance sheets that record variances in implementation of pathway regularly, it will be easier to identify common reasons for noncompliance. These issues can be discussed with the team to see if any changes can be made for full implementation of care path. our institutional experience Care pathways for colon surgery were initiated in 1995 at our institute. This was used for both standard and laparoscopic colon resections. The care path was designed with an aim of providing optimal care in a cost effective manner. The goal of the pathway is to discharge patients by postoperative day 4 and when possible on day 3. The endpoint of the pathway is to discharge the patient home when tolerating diet and passing flatus. The documentation for the pathways was of paper format and had boxes to check and spaces for writing notes to document the progress. The pathway starts with preoperative patient teaching during their office visit. Patients are informed about the procedure, the length of stay and anticipated days for landmarks of progress, such as ambulation, advancement of diet and return of bowel function, and discharge. They are also provided with a printed copy of the care path guide, which is especially designed for patients, that details preoperative preparation, what to expect on arrival to hospital, and postoperative care scenario. Patients are encouraged to call if they have any doubts regarding the care path. A complete blood count, chemistries are ordered for every patient. Electrocardiogram and chest x-rays are ordered for patients if needed. Patients undergo bowel preparation at home the day before surgery, using Golytely. On the day of surgery the patients receive Heparin 5000 units subcutaneously, and antibiotics in the preoperative period.

Antibiotics are administered for 24 hours and heparin is given throughout their hospital stay. Antiembolism devices such as Venodynes are put on preoperatively. The anesthesiologist places an epidural catheter if the patient consents to it. Postoperatively, the patient is admitted to a regular surgical unit, and vitals monitored every 4 hours during the entire length of hospitalization. The patient is given an incentive spirometer and its use demonstrated. On postoperative day 1 they are ambulated. Patients are given sips of clear liquids and if tolerated given a clear liquid tray. Stoma education is introduced on day 2 if indicated. Patients on postop day 2 are given unrestricted clear liquids and advanced to regular diet if tolerating 800 cc of clear liquids. Foley catheter is also removed. In addition, the epidural or patient controlled anesthesia (PCA) are discontinued and the patient is started on oral pain medications. Discharge disposition needs are established. On postoperative day 3, patients are given a regular diet; discharge paperwork is completed and kept ready. If the patient tolerates diet and passes flatus they are discharged; if not, the patient is discharged on postoperative day 4 after meeting the discharge criteria. Before discharge, the diet, activity, medication, and homecare instructions are reviewed with the patient and follow up appointments are set up. The Care path was routinely analyzed at interdisciplinary conferences. (Refer to Figures 9.1 & 9.2). challenges and concerns Many surgeons believe that their responsibility to practice medicine economically is becoming secondary to their responsibility of practicing medicine effectively.(37) Common reluctance to accept care paths arises from a prejudice in viewing them as a form of “cookbook” medicine.(38, 39) Some consider them to be intrusive, decreasing the physician’s autonomy, and lack the element of individualized care for each patient. However, although care paths encourage standardization as a strategy to improve quality and efficiency, physicians, by helping define these standards, actually would gain greater control over the patient care rather than losing their autonomy. Physicians also need to be free to write orders to change the pathway or to remove the patient from the pathway if needed. Documenting the reasons to do so would help in analyzing the pathway processes and lead to improvement in the pathway. This would increase the acceptance of care paths and also counter the criticism of deficiency of individual care. Although many studies report cost savings in implementation of care paths, most of these do not address the issue of cost of development of care paths. Macario et al. estimated the cost of development of the care path for patients undergoing knee replacement surgery at $21,000.(40) However these did not take into account the time staff physicians spent on the project. There is a concern among the academic faculty that the care paths when used in resident training environments may discourage experimentation, independent thinking, and application of appropriate clinical judgment to individual cases. Those responsible for house staff education may feel care paths might stifle the questioning through which residents learn. However medical training might be well served by incorporating methods such as critical pathways to teach students evidence-based and cost-effective practice.(21)

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improved outcomes in colon and rectal surgery Care pathways may serve to frame the educational process. They are based on expected physiological outcomes, but are monitored so that variances (i.e., complications) can be addressed with the use of clinical judgment. The clinical judgment is, in effect, the implementation of an expanded path or alternate pathway. The alternate pathway, for example, may be for postoperative myocardial infarction management. Pathways are structured but dynamic. There is also a concern that care paths might create an atmosphere in which patients will be steered away from clinical research studies into treatment according to critical pathways. Including a step in the care path can offset this. If set criteria are met, the patient should be considered for the appropriate clinical trial and the research team would be contacted. This would actually yield in improved recruitment to clinical studies. Research questions can themselves be embedded in care paths and answers be obtained on analysis of the care paths. Another frequently voiced concern is that physicians may be more vulnerable to malpractice suits if they do not comply with a care path and a patient has a complication. In essence, litigation is more likely to occur when there is a failure to follow a pathway based on standards of care. Careful documentation as to reason for deviation from the pathway could potentially decrease the chance of litigation. realistic expectations Despite the successful use of care paths for optimal management of postoperative patients undergoing colon and rectal surgeries, it should be noted that the pathways are oriented towards ideal patients with predictable course of care. Enthusiasm to manage every patient with the care path without paying attention to individual circumstance could be counterproductive. Hence, care paths should be designed to recognize patients with special needs or comorbidities. Perioperative pathways that consider the needs of diabetics, cardiac patients, pulmonary patients, or stroke patients for example, would be a proactive way to institute riskreducing strategies that would have a positive impact in reducing perioperative morbidity and mortality. Tremendous scope for improvement still exists in implementation of evidence-based management. In a recent article, Kehlet et al. reviewed the care after colonic surgery in Europe and the United states and analyzed the use of evidence-based care in the perioperative period.(41) They identified mechanical bowel preparation, operative techniques, nasogastric intubation, time frame for postoperative food, and fluid intake, time to recovery from GI function, and mobilization as the important variables, which have positive evidence-based practices. They noted preoperative bowel preparation was used in >85% of patients. The nasogastric tube was left in situ postoperatively in 40% vs. 66% of patients in the United States and Europe, respectively. It took 3–4 days for 50% of patients tolerating liquids. This suggests that clinical practice does not optimally reflect published evidence and indicates a potential for major improvement. fast track colon and rectal surgery Fast track surgery is an evolution in the care path approach that involves rapid progress from perioperative preparation, through surgery, and discharge from hospital. Synonyms used for this

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include accelerated postoperative recovery programs and enhanced recovery programs. Critical elements of fast track colon surgery paths include use of the following: extensive preoperative counseling, no bowel preparation, no premedication, administration of short acting anesthetic drugs, standardized surgical procedure, minimal access techniques, restriction of drains, and catheters, early extubation, rewarming and sustained postoperative normothermia, optimal pain control, avoiding opiates for pain control, early ambulation and discharge, and follow up after discharge. (2, 5, 16, 17, 42–44) Factors that limit early discharge include pain, nausea, vomiting, prolonged ileus, mechanical factors such as drains, indwelling catheters, and stress-induced organ dysfunction.(6, 45) Kehlet and Mogensen, in their study involving 18 patients who underwent open sigmoid colectomy, addressed these factors by implementing a multimodal rehabilitation program.(43) It involved a highly scripted preoperative and postoperative care path regulating the introduction of epidural analgesia, diet, and ambulation. The pathway involved mobilization of patients on the day of surgery, administering cisapride and magnesium, and allowing free fluid intake on evening of surgery, among numerous other inter­ventions instituted. They described a median postoperative stay of 2 days, mobilization of patients for 5 hours on second postoperative day and 10 hours on third postoperative day. They also showed decreased pain and fatigue scores.(43) Delaney et al. studied 60 patients undergoing major abdominal and pelvic surgeries without administration of preemptive epidurals, oral cathartics, and prokinetic agents. They have described shorter length of stay than patients having traditional care.(46) Recent developments of laparoscopic colon surgery showed significant improvements in average length of stay after colectomy and also better patient satisfaction in terms of pain control. This further catalyzed the interest in fast track pathways in colon and rectal surgery. Several authors described in their studies, multimodal care plans involving different strategies to optimize preoperative, intraoperative, and postoperative limiting factors, to achieve an early discharge with no difference in readmission rate or mortality.(16, 17, 24, 42, 46–48) Wind et al. published a review of all randomized controlled and controlled clinical trial on fast track colon surgery. This meta-analysis showed that the average hospital stay (2.61 days) and morbidity were significantly lower for fast track programs.(44) The strategies adapted in these studies included the following: extensive preoperative counseling, no bowel preparation, no premedication, antibiotics administration before surgery, no preoperative fasting, administration of carbohydrate loaded liquids until 2 hrs before surgery, tailored anesthesia encompassing thoracic epidural anesthesia, and short-acting anesthetics, perioperative high inspired oxygen concentrations, avoidance of perioperative fluid load, short incisions, minimally invasive surgery, nonopiod pain management, no ­routine use of drains and nasogastric tubes, early removal of bladder catheters, standard laxatives and prokinetics, and early and enhanced postoperative feeding and mobilization. There are no randomized controlled trails comparing laparoscopic, fast track, and standard approaches. However, recently LAFA (laparoscopic and or fast track multimodal management versus standard care) trial was instituted, which was conceived

care paths and optimal postop management to determine whether laparoscopic surgery, fast track surgery, or a combination of both is to be preferred over open surgery with standard care in patients having segmental colectomy for malignant disease.(49) summary Care paths are tools which promote evidence-based standard care, improve efficiency, and reduce hospital stay without compromising the quality of final outcome of care. Care paths can be used as either disease specific or processspecific tools to manage patients throughout the complete ­disease cycle. Care path development requires a dedicated multidisciplinary team. With increasing popularity of laparoscopic colon surgeries and other techniques to decrease perioperative stress response, care paths in colon and rectal surgery are evolving ­continuously, into new programs, such as fast-track surgery. references   1. Campbell H, Hotchkiss R, Bradshaw N, Porteous M. Integrated care pathways. BMJ 1998; 316: 133–7.   2. Napolitano LM. Standardization of perioperative management: clinical pathways. Surg Clin North Am 2005; 85: 1321–7, xiii.   3. Renholm M, Leino-Kilpi H, Suominen T. Critical pathways. A systematic review. J Nurs Adm 2002; 32: 196–202.   4. Delaney CP, Fazio VW, Senagore AJ et al. ‘Fast track’ postoperative management protocol for patients with high co-morbidity undergoing complex abdominal and pelvic colorectal surgery. Br J Surg 2001; 88: 1533–8.   5. Hendry P, Fearon KCH. Intraoperative surgical considerations for enhanced recovery after elective colonic surgery. Transfus Altern Transfus Med 2007; 9: 61–5.   6. Wilmore DW. From Cuthbertson to fast-track surgery: 70 years of progress in reducing stress in surgical patients. Ann Surg 2002; 236: 643–8.   7. Wagner HM. Principles of Operations Research. 2nd ed. Englewood Cliffs, NJ: Prentice-Hall; 1975.   8. Buffa E. Modern Production Management. 3rd ed. New York: John Wiley & sons; 1969.   9. Critical Path Software Smoothness Road for Automotive supplier. Industria Engineering 1992: 28–9. 10. Kallo G. The reliability of critical path method (CPM) techniques in the analysis and evaluation of delay claims. Cost Engineering 1996; 38: 35–7. 11. Hatfield M. The case for critical path. Cost Engineering 1998; 40: 17–8. 12. Clinical Pathways: multidisciplinary plans of best clinical practice. www.openclinical.org. 13. Field MJ LK. Clinical Practice Guidelines: Directions for a New Program. Washington, DC: National Academy Press; 1990. 14. Nathan R. Critical pathways: a review. AHA Scientific Statement; 2000. 15. Gadacz TR, Adkins RB Jr, O’Leary JP. General surgical clinical pathways: an introduction. Am Surg 1997; 63: 107–10. 16. Basse L, Hjort Jakobsen D, Billesbolle P, Werner M, Kehlet H. A clinical pathway to accelerate recovery after colonic resection. Ann Surg 2000; 232: 51–7.

17. Basse L, Raskov HH, Hjort Jakobsen D et al. Accelerated postoperative recovery programme after colonic resection improves physical performance, pulmonary function and body composition. Br J Surg 2002; 89: 446–53. 18. Edwards SG, Thompson AJ, Playford ED et al. Integrated care pathways: disease-specific or process-specific? Clin Med 2004; 4: 132–5. 19. Melbert RB, Kimmins MH, Isler JT et al. Use of a critical pathway for colon resections. J Gastrointest Surg 2002; 6: 745–52. 20. Archer SB, Burnett RJ, Flesch LV et al. Implementation of a clinical pathway decreases length of stay and hospital charges for patients undergoing total colectomy and ileal pouch/anal anastomosis. Surgery 1997; 122: 699–703. 21. Pearson SD, Goulart-Fisher D, Lee TH. Critical pathways as a strategy for improving care: problems and potential. Ann Intern Med 1995; 123: 941–8. 22. Stephen AE, Berger DL. Shortened length of stay and hospital cost reduction with implementation of an accelerated clinical care pathway after elective colon resection. Surgery 2003; 133: 277–82. 23. Cheatham MLMD, Chapman WCMD, Key SPMDa, Sawyers JLMD. A meta-analysis of selective versus routine nasogastric decompression after elective laparotomy. Annals of Surgery 1995; 221: 469–78. 24. Khoo CK, Vickery CJ, Forsyth N, Vinall NS, Eyre-Brook IA. A prospective randomized controlled trial of multimodal perioperative management protocol in patients undergoing elective colorectal resection for cancer. Ann Surg 2007; 245: 867–72. 25. Bokey EL, Chapuis PH, Fung C et al. Postoperative morbidity and mortality following resection of the colon and rectum for cancer. Dis Colon Rectum 1995; 38: 480–6. 26. Schoetz DJ Jr, Bockler M, Rosenblatt MS et al. “Ideal” length of stay after colectomy: whose ideal? Dis Colon Rectum 1997; 40: 806–10. 27. Panella M, Marchisio S, Di Stanislao F. Reducing clinical variations with clinical pathways: do pathways work? Int J Qual Health Care 2003; 15: 509–21. 28. Atwal A, Caldwell K, Atwal A, Caldwell K. Do multidisciplinary integrated care pathways improve interprofessional collaboration? Scand J Caring Sci 2002; 16: 360–7. 29. Garnick DW, Hendricks AM, Brennan TA. Can practice guidelines reduce the number and costs of malpractice claims? JAMA 1991; 266: 2856–60. 30. Downey LM, Ireson CL, Slavova S, McKee G. Defining elements of success: a critical pathway of coalition development. Health Promot Pract 2008; 9: 130–9. 31. Ramos MC, Ratliff C. The development and implementation of an integrated multidisciplinary clinical pathway. J Wound Ostomy Continence Nurs 1997; 24: 66–71. 32. Hampton DC. Implementing a managed care framework through care maps. J Nurs Adm 1993; 23: 21–7. 33. Yandell B. Critical paths at alliant health system. Qual Manag Health Care 1995; 3: 55–64. 34. Press Ganey Associates, http://www.pressganey.com/. 35. Kopec D, Shagas G, Reinharth D, Tamang S. Development of a clinical pathways analysis system with adaptive Bayesian

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36. 37. 38.

39. 40.

41.

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nets and data mining techniques. Stud Health Technol Inform 2004; 103: 70–80. Clarke A. Implementing electronic integrated care pathways: learning from experience. Nurs Manag (Harrow) 2005; 12: 28–31. Jones JW, McCullough LB, Richman BW. The ethics of clinical pathways and cost control. J Vasc Surg 2003; 37: 1341–2. Audet AM, Greenfield S, Field M. Medical practice guidelines: current activities and future directions. Ann Intern Med 1990; 113: 709–14. Holoweiko M. What cookbook medicine will mean for you. Med Econ 1989; 66: 118–20, 25–7, 30–3. Macario A, Horne M, Goodman S et al. The effect of a perioperative clinical pathway for knee replacement surgery on hospital costs. Anesth Analg 1998; 86: 978–84. Kehlet H, Buchler MW, Beart RW Jr, Billingham RP, Williamson R. Care after colonic operation–is it evidence-based? Results from a multinational survey in Europe and the United States. J Am Coll Surg 2006; 202: 45–54. Gatt M, Anderson AD, Reddy BS et al. Randomized clinical trial of multimodal optimization of surgical care in patients undergoing major colonic resection. Br J Surg 2005; 92: 1354–62. Kehlet H, Mogensen T. Hospital stay of 2 days after open sigmoidectomy with a multimodal rehabilitation programme. Br J Surg 1999; 86: 227–30.

44. Wind J, Polle SW, Fung Kon Jin PH et al. Systematic review of enhanced recovery programmes in colonic surgery. Br J Surg 2006; 93: 800–9. 45. Kehlet. Multimodal approach to control postoperative pathophysiology and rehabilitation. Br J Anaesth 1997; 78: 606–17. 46. Delaney CP, Zutshi M, Senagore AJ et al. Prospective, randomized, controlled trial between a pathway of controlled rehabilitation with early ambulation and diet and traditional postoperative care after laparotomy and intestinal resection. Dis Colon Rectum 2003; 46: 851–9. 47. Ortiz H, Armendariz P, Yarnoz C. Early postoperative feeding after elective colorectal surgery is not a benefit unique to laparoscopy-assisted procedures. Int J Colorectal Dis 1996; 11: 246–9. 48. Zutshi M, Delaney CP, Senagore AJ, Fazio VW. Shorter hospital stay associated with fastrack postoperative care pathways and laparoscopic intestinal resection are not associated with increased physical activity. Colorectal Dis 2004; 6: 477–80. 49. Wind J, Hofland J, Preckel B et al. Perioperative strategy in colonic surgery; LAparoscopy and/or FAst track multimodal management versus standard care (LAFA trial). BMC Surg 2006; 6: 16.

10

Limitations of anorectal physiology testing Thomas E Cataldo and Syed G Husain

challenging case A 65-year-old woman and her 30-year-old daughter both present to your office with complaints of fecal incontinence. Both are G3 P3, all vaginal deliveries, and have had at least one delivery of a child of 8 pounds or more. Both have required an assistance device for delivery of one child. Both report fecal soiling for the last year. The older woman reports progressive uncontrolled passage of flatus and occasional identification of stool in her undergarments that she was unaware of having passed. The daughter reports incontinence to moderate amounts of stool despite attempts to delay defecation. There is additional incontinence associated with athletic activity. case management Normal function of the anus and rectum resulting in comfortable passage of stool under voluntary control is a complex balance of a number of competing factors and requires intricate correct ­performance of enteric and colonic physiology, rectal, anal and pelvic sensory and motor nerves, as well as anatomically intact and functioning anal and pelvic musculature. Disruption of any of these factors may result in fecal incontinence. On the other end of the spectrum, the patient may suffer difficult, painful, or incomplete evacuation. Anorectal dysfunction is often devastating to the patient resulting in emotional distress and social isolation. Fecal continence is defined as the ability to defer defecation until a socially appropriate time and place. Incontinence has a number of definitions from simply involuntary passage of stool to inability to control passage of solid, liquid, or gas. In a 2001 ­consensus conference report fecal incontinence is defined as, “recurrent uncontrolled passage of fecal material for at least one month in an individual with a developmental age of at least four years”.(1) Reported prevalence varies from 1.4% to 18%, with rates as high as 45% in elderly, debilitated, or psychiatrically impaired institutionalized adults. These numbers are generally accepted as under reported due to patients’ unwillingness to come forward due to associated social and cultural stigma.(1–3) Constipation is as difficult to define. It may be as subjective as any difficulty or infrequency in passing stool as perceived by the patient. The Rome II criteria define constipation as two or more of the following for at least 3 months: straining more than 25% of the time, hard stools more than 25% of the time, incomplete evacuation more than 25% of the time, two or fewer bowel movements in a 7 day period.(4) A problem inherent to all anorectal physiology testing is the scarcity of “normal” values for comparison. There is relative paucity of literature describing anorectal physiology testing on normal population and almost all of the available studies are comprised of small group of subjects. physiology of fecal continence Normal fecal continence relies on a number of mechanisms. The first of which is normal enteral and colonic motility and fluid

transport physiology resulting in manageable stool consistency. Stool consistency may be the most important characteristic that influences fecal continence.(5) Some patients may be continent to solid stool but not to liquid or gas. The rectum needs to maintain adequate reservoir capacity. In addition the rectum, anus, and pelvic musculature must have adequate ability to sense and differentiate the presence, of solid, liquid, and gas. Additionally, it is postulated that the vascular cushions or hemorrhoids ­create a controllable seal as a rectal “corpus cavernosum”. This is supported by the identification of leakage in some patients after otherwise uncomplicated hemorrhoidectomy.(5) On a mechanical level, defecation occurs when the pressure within the rectum exceeds the pressure or resistance provided by the anus. For normal defecation this relies on the controlled increase in rectal pressure combined with simultaneous relaxation of the anus and straightening of the rectum through relaxation of the pelvic muscles. The rectum must also possess correct mechanical properties of capacity and distensibility. It must be able to sense the need to empty and the qualities of the contents within it. Disease processes or injuries that limit the ability of the rectum to distend to accept stool and air from the sigmoid colon will alter the urge to defecate, and the ability to defer defecation. Conversely, a chronically distended capacious rectum may lose the ability to sense when it is full and thereby overflow. Both cases might present as incontinence. Alternatively, if the body cannot differentiate between solid, liquid, or gas or if the mechanism by which this is sampled is altered, the result is often fecal soiling. the anorectal physiology lab A battery of devices and tests has been developed to investigate many aspects of normal and altered defecation. Many centers have collected the equipment to accomplish these tests. (Figure 10.1). Much work remains to fully elucidate the source and thereby the solutions to disordered defecation. investigations for incontinence Manometry Manometry is a technique to measure the pressures which exist within the anal canal and the pressures that the anus is capable of achieving voluntarily. Over many years a variety of catheters, pressure detectors, and recording apparatuses have been developed. In addition, different operator techniques have been developed making standardization of results difficult. Throughout the 1960s a variety of catheters were developed with different numbers of open tipped channels and microballoons. The number of channels varied and they were arranged radially or in a spiral orientation. Water within the channels was either static or continuously perfused. Initial continuous recordings were made with pen and ink on polygraph devices. Currently, the state of the art manometers contain solid state micropressure transducers mounted within the catheter itself (Figure 10.2a,b). In addition

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improved outcomes in colon and rectal surgery

Figure 10.1 Typical Anorectal Physiology Lab with Manometry, Transanal ultrasound, Pudendal Nerve Terminal Motor Latency testing, Biofeedback, storage and equipment for sterilization.

(a)

to more reliable and reproducible data, these catheters are more easily and reliably cleaned from patient to patient. Pressure data is recorded continuously to computer based software that assists in creating the interpretation and the report. One critical observation of the water perfused systems is that the patient may react to the sensation of water dripping from the anus with increased tone. Scrupulous technique may avoid this. Because various technologies and methods exist for measuring anal canal pressures, no universally accepted set of normal values exist. Simpson et al. addressed this issue in a study comparing five different catheters and techniques of manometry in both normal and incontinent patients.(6) Although their sample size was small, 10 normal and 11 patients with incontinence, the authors found no significant difference between five commonly employed devices. They were; a water perfused end-hole catheter, a catheter water perfused with four radially arranged side holes, water filled microballoon, microtransducer, and an air-filled portable microprocessor controlled device. sphincter pressure measurement Although written consent is not required as the patient is fully awake, at our institution we obtain full informed consent and confirmation of patient identity, condition being evaluated, and their understanding of the tests they are about to undergo. The patients take one or two small volume cleansing enemas at home before the exam. Anal canal pressures are measured with the patient lying comfortably in the left lateral decubitus position with knees as hips flexed 90°. Some emphasis is placed on comfort and relaxation as anxiety, talking and anything that increases the intraabdominal pressure may affect the results. We employ a stationary pull through technique. The catheter is placed transanally with the measuring points (balloons, holes or microtransducers) to a distance of 6 cm above the anal verge. Measurements are taken in the anterior, posterior, left, and right lateral positions. (Figure 10.2c) Pressures are recorded at relaxation and at maximum “squeeze” for 10 seconds. The patient must be instructed to try to isolate squeeze of the anus and not employ the gluteal or any other accessory muscles. The (C)

(b)

Figure 10.2 (A) Manometry Catheter, with balloon. (B) Manometry Catheter, detail microtransducers. (C) Manometry tracing, computer display.

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limitations of anorectal physiology testing catheter is repositioned 1 cm distally and the process is repeated. The process is repeated in step-wise fashion until the entire canal had been tested. An alternative to this “station pull out” technique is recording pressures during a continuous pullout of the catheter at a controlled steady rate. The following parameters are recorded: length of the anal high pressure zone, mean resting tone, maximum squeeze pressure. In an effort to study the symmetry and detailed overall ­pressure profile of the anal sphincter, pressure vectography, a technique that provides graphical representation of radial pressure profile of anal canal, was developed. the recto-anal inhibitory reflex The presence or absence of the Recto-Anal inhibitory reflex (RAIR) is identified by rapid distention of the rectum by insufflation of the balloon at the tip of the catheter with 10 cc of air. Simultaneous recording taken in the middle of the anal canal high pressure zone are made for 10 seconds. If the RAIR is present, a reflex relaxation of internal sphincter and resultant decrease in anal canal pressure should be observed. Balloon insufflation may be repeated with more air at 10 cc increments up to 60 cc until a reflex is observed. rectal capacity and sensation The balloon at the end of the catheter may also be filled with water in an incremental fashion to assess rectal sensation and compliance. Measurements are made at the minimum volume of first rectal sensation, the volume required to produce a sustained feeling of the need to defecate and a maximum volume that creates significant discomfort or an irresistible need to defecate. value and limitations of manometry for incontinence Anal manometry has become a staple in the evaluation of fecal incontinence. Though routinely performed in many centers, manometry lacks standardization of technique, data collection, and methods of interpretation. This makes it extremely difficult to compare data obtained at different centers. The range of accepted normal values is wide varying for gender, parity, age, and numerous other factors. Despite the fact that the newer catheters are more comfortable and easier to maintain, the test remains mildly invasive and uncomfortable for the patient. There are several technical caveats that may lead to considerable alteration in results. Patients with megarectum may require a higher volume to illicit RAIR and may be falsely labeled as RAIR negative if the usual volume of 30–40 cc is used to illicit RAIR.(7) The balloon material can influence the results as latex ­balloons tend to deform along their axis, resulting in a falsely elevated rectal compliance.(8) Rectal compliance testing depends entirely upon patient’s input, thus patient’s psychological status plays a very important role in data acquisition during this test. (7) Furthermore the results of rectal compliance may differ if the test is performed on “prepared”, i.e., after enema evacuation vs. unprepared rectum.(7) The rate at which water is injected into the balloon may also affect the rectal sensitivity testing.(9) Thus, it is recommended that slow filling should be accomplished at a rate of 1 ml/second.(7) Whatever the method used, the same

technique should be applied to all patients in order to obtain reproducible and comparable results. Caution should be exercised while making treatment decisions based on manometric findings as normal or abnormal values in incontinent patients do not necessarily correlate with severity of symptoms. In a large prospective study Lieberman et al. evaluated 90 incontinent patients, including 6 males with a specific goal at determining what impact physiology testing including manometry had on treatment and outcome. After appropriate history and physical exam patients were selected for medical or surgical management. Following this determination they underwent anal physiology testing including manometry, pudendal nerve terminal motor latency (PNTML), and anal ultrasound (AUS). Overall only 9 (10%) had a change in their management plan. Based on the results of these tests, 5 of 45 patients initially assigned to medical management were offered surgery instead. On the other hand, 3 of 45 patients assigned to undergo surgical treatment were switched to the medical group. Almost all of these alterations in management were based on AUS. Manometry was found to be abnormal in one-third of both management groups and there was no correlation between manometric results and change in management plan. There did not appear to be an association between manometry, AUS and PNTML results.(10) In an elaborate study of 350 patients including 80 controls, Felt-Bersma et al. found that the most significant difference between continent and incontinent patients was maximum squeeze pressure.(11) However, the authors surmised that continent function could not be predicted based on anal manometry alone and ­suggested that these results should only be interpreted in conjunction with other tests. Although it creates a rather striking and impressive graphical representation of anal canal pressure profile, pressure vector diagrams have been shown to be of questionable clinical value for sphincter evaluation.(12) A study by Yang et al. could not demonstrate any correlation when vectoral analysis was compared to needle electromyography (EMG) and ultrasonography.(12) With the increased use of AUS the utility of vectogrpahy has been negated. Anorectal manometry remains of value for objective preoperative documentation of anal tone function or muscle weakness. It is also helpful in excluding patients from surgery.(2) Perhaps the biggest merit of manometry is its role as the initial diagnostic test for short segment Hirschsprung’s disease where the presence of an RAIR effectively rules out the disease. electromyography EMG is the measurement of the electrical activity generated by muscle fibers during contraction or at rest. In 1930 Beck first described anal sphincter EMG.(13) Specifically, the EMG measures activity in a motor group or those muscle cells innervated by a single axon. Muscles whose nerves have been damaged will demonstrate altered activity. Myography has been used to map the perianal area for muscular activity and thereby detect sphincter defects. EMG is also used to demonstrate nerve conduction and appropriate activation and relaxation used in biofeedback therapy. Concentric Needle EMG A concentric needle electrode is two insulated electrodes, one within the other. With the needle inserted into the muscle to

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improved outcomes in colon and rectal surgery be observed, in this case the external sphincter or the pelvic floor, the electrical potential from one electrode to the other is recorded. Information collected includes amplitude, duration and frequency, as well as the number of phases. Amplitude is proportional to the number of muscle fibers activated. Normal values are an amplitude of <600 μV and duration <6 μs.(14, 15) Longer duration or spreading of the signal can indicate dispersion of the motor unit potential (MUP). This may represent denervation or demyelination, or simply aging. The sum of the activity of many muscle cells creates a shape to the MUP. Normal MUPs are bi- or triphasic. In general, more phases within the action potential indicated denervation and reinnervation. However four or more phases have been reported in normal muscle in up to ¼ of the time. Single Fiber EMG Individual muscle fiber action potentials can be recorded with a single fiber EMG. The recording area of the needle is much smaller, 25 μm. In normally innervated external anal sphincter muscle only a few fibers will be activated by a single motor group axon. However, when damage occurs denervated muscle fibers are recruited by surviving axons. The number of muscle fibers and thereby signal density within the recording area of the ­needle increases, resulting in a more polyphasic signal. The test is performed by taking multiple readings requiring multiple skin punctures around the anus. Surface EMG/biofeedback Measurement of muscular activity through the insulation of the skin is far more imprecise but less painful than needle EMG. Surface EMG is valuable for documentation of overall activity, especially during attempted voluntary rest, inhibition, or contraction of a muscle. Surface EMG is helpful to document paradoxical sphincter activity as part of the diagnosis of disordered defecation. Two self-adhering surface electrodes can be applied on opposite sides of the anus over the subcutaneous portion of the external sphincter, with a grounding electrode placed at a distance on the patient. Alternatively, a plug electrode is employed within the anal canal (Figure 10.3). Surface measurement of muscle activity is more valuable if the muscle is being artificially activated by stimulating the nerve. When the time of nerve stimulation is known and time of muscle activity measured, nerve conduction velocity can be assessed. A specific application of nerve stimulation and surface EMG is measurement of the PNTML. pudendal nerve terminal motor latency The pudendal nerve arises from the second, third and fourth sacral nerve roots bilaterally and passes along the inferior pubic rami through Alcock’s canal. Prolonged labor or the use of forceps for delivery may injure the pudendal nerve as it exits from the canal. The conduction time of the nerve can be measured by stimulating the nerve transrectally and observing the time to electrical activity of the external anal sphincter. A St. Marks electrode attached to a gloved finger provides both stimulation and measurement (Figure 10.4a,b). An absent trace may indicate injury to the nerve whereas a prolonged PNTML is interpreted to indicate nerve injury and repair.

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Figure 10.3  Surface EMG electrode.

(a)

(b)

Figure 10.4  St. Marks electrode.

limitations of anorectal physiology testing limitations of electomyography in incontinence The EMG delineation of anatomic sphincter defect has been largely supplanted by imaging studies such as ultrasound and pelvic magnetic resonance imaging (MRI). Concentric needle EMG and single fiber EMG testing is uncomfortable, or in some cases, frankly painful for the patient. The equipment is expensive and difficult to master. Results are variable based on the cooperation of the patient, the experience of the examiner, and the patience of both.(16) Surface EMG is mildly uncomfortable to the patient and technically challenging to perform. Identification of the nerve tracing can be subjective. Pudendal nerve latency testing is operator dependent. Since PNTML measures the fastest remaining fibers, a normal latency time does not exclude injury. The latency values obtained are also affected by the distance between the electrode and the pudendal nerve; shortest latencies being obtained by placing the electrode as close to the nerve as possible.(9) This is usually accomplished with subtle movements of the electrode bearing finger inside the anal canal while observing waveforms for the shortest latency thus generated in response to repeated electrical stimuli. This method may result in significant patient discomfort in some cases. There is some bilateral crossover innervation of the sphincter therefore a unilaterally abnormal test does not preclude normal function. Earlier studies indicated that significantly abnormal bilateral results were predictive of poor outcome with sphincter repair.(17–19) However, other authors have not found PNTML to be helpful in this regard. (10, 20) Increased pudendal nerve terminal velocities have been previously associated with patients with idiopathic incontinence. (21) Newer literature, however, suggests that this association might not be entirely true. Ricciardi et al. showed that only a small percentage of patients with idiopathic fecal incontinence had associated pudendal neuropathy.(22) Anal Ultrasonography High quality circumferential images of the anal sphincter complex can be obtained using anal ultrasonography (AUS). Although a number of probes are available, the most commonly used for evaluation of the anal sphincter is a rotating probe that creates a 360°, two-dimensional transverse image. The transducer generally used is a combined 7 or 10 MHz transducer, rotating within a water-filled rigid cap covered with a balloon or condom. Newer probes are fully self-contained. They still require protection with a condom and some type of interface media such as gel or water.(Figure 10.5) In many outpatient anorectal physiology labs the procedure is performed in the left lateral decubitus position in conjunction with anal manometry. For a patient scheduled to undergo multiple anorectal physiology studies the same day, we follow a policy of performing manometry initially followed by other investigations as the sphincter stretch induced by 12 mm sonogram probe may produce erroneous manometric findings. As such, the patient may have had limited preparation with a small volume enema. This is not required for AUS alone. Some authors prefer the prone or lithotomy positions feeling that the lateral position deforms the anatomy.(23) The clinical significance of this is unclear. AUS can distinguish the internal and external sphincters individually, with an intact internal sphincter representing a continuous hypoechoic band. The external

Figure 10.5  St. Marks electrode attached to glove.

sphincter is more heterogenous but distinctly more hyperechoic. Although images can be taken throughout the anal canal, images are traditionally documented and preserved at proximal, mid and, distal anal canal. Defects in either the internal or external sphincters are identified as a disruption in the continuous ring. The external sphincter naturally splits proximally as it extends to the levator sling and the pelvic floor musculature. Disrupted tissue heals with a scar which appears amorphous, more echogenic than internal sphincter, but less so than external. It is seen bridging the gap in the defect between the disrupted ends of the sphincters. The presence of a sphincter defect on AUS correlates well with a history of obstetrical trauma, as well as with physical exam findings and manometric findings.(10, 20, 24) Interobserver agreement is excellent and when an anatomic defect is present AUS sensitivity approaches 100%, specifically for internal anal sphincter defects in the mid anal canal.(25) Different techniques have been employed to either improve or make easier definition of the anal anatomy. Some authors claim anal squeeze, and relaxation improves the yield of sonographic exam while others have no benefit.(23) A finger placed in the posterior wall of the vagina used to measure the thickness of the perineal body has been shown to aid in the evaluation of anterior sphincter defects.(25)

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improved outcomes in colon and rectal surgery Global deficiencies or thinning of the sphincters rather than defects are more difficult to define with AUS. The internal sphincter is normally between 2 to 4 mm. Since it is more distinct on AUS, excessive thickness or thinness can be identified. One elusive objective is to identify atrophy of the external sphincter as this correlates with poor outcome from sphincter repair.(26) Three dimensional axial endosonography is now available. The probe spirals and moves through the sphincter at a fixed rate ­collecting a three dimensional block of echo-data that can be ­represented on a computer screen and evaluated through any plane through the block. In a study involving 33 women with suspected sphincter injury, two different observers compared 2-D AUS with 3-D evaluation. There was an identifiable improvement in the confidence of the examiner in detecting sphincter defects with 3-D evaluation over 2-D images. Interobserver correlation was also improved by 3-D evaluation but not to a significant degree.(27) Nevertheless, 3-D AUS has not been indisputably demonstrated to be more sensitive or specific, than transverse planar AUS. limitations of ultrasound in incontinence Ultrasound is the most important test in the evaluation of fecal incontinence with few limitations. Anorectal ultrasound entails a significant learning curve (28) and results are operator and experience dependent. The external sphincter is less distinct than internal sphincter and smaller, <90°, defects are harder to demonstrate. (29) Patients with minimal symptoms and limited defects may not require surgery; therefore the clinical significance of a defect is determined by the combination of physical exam, anorectal physiology (ARP) testing, and AUS (Figure 10.4). The presence of atrophy of the external sphincter is similarly hard to prove. This is due to the fact that atrophic external sphincter becomes replaced with fat making sonographic delineation of the sphincter from the surrounding fat tissue more difficult.(30) Many investigators believed that 3-D ultrasound, by virtue of its superior resolution, may result in improved identification of external sphincter atrophy. However a comparative study showed no correlation between 3-d AUS and MRI in 18 incontinent women with MRI evidence of sphincter atrophy.(31) Biofeedback for fecal incontinence Biofeedback is a process by which the patient is given an auditory or visual representation of anorectal information, pressure or muscle activity, which they cannot otherwise perceive or correctly interpret. Techniques of biofeedback have successfully used in the treatment of fecal incontinence for over 25 years. The practice parameters of the American Society of Colon and Rectal Surgeons (ASCRS) give a grade “B” recommendation for its use as a first line therapy and in patients that have incomplete success after sphincter repair.(2) limitations of biofeedback for incontinence Despite some encouraging earlier reports describing success of biofeedback in the management of incontinence, the Cochrane system review of treatments for incontinence in 2006 did not support its use.(32) The authors reported, “The 11 trials reviewed were of very limited value because they were generally small, of

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poor or uncertain quality, and compare different combinations of treatments”. Overall success with biofeedback varies from 65% to 89%.(2, 33, 34) Two large randomised controlled trials include more than 100 subjects. Both concluded that biofeedback provided no additional benefit over office counseling therapy such as advice, education, dietary modification, digital guidance, and medication. Despite the lack of demonstrated benefit, both ­trials showed improvement in severity of symptoms, fecal incontinence scores, and quality of life.(35–37) These benefits were seen in both the treatment and control groups indicating the role of patient motivation and ongoing medical involvement in the treatment of fecal incontinence. The most important predictors of success were completion of the program, and age over 60 years. Higher body mass index was associated with a worse outcome. Summary: Value and limitations of ARP testing for evaluation of fecal incontinence The perceived value of ARP testing in the evaluation and management of fecal incontinence varies greatly on the perspective of the examiner and the expectations of the patient. The most frequently employed test include anal manometry, transanal ultrasound, and pudendal nerve terminal motor latency. Techniques and normal values are not universally accepted. Abnormal results do not equate with specific disease, injury, or symptomatology. Transanal ultrasonography and MRI provide excellent anatomic definition to aid in the planning of surgical intervention. At best manometry serves for documentation of preoperative function and may assist in patient selection for surgery. PNTML is still controversial as to its role in the treatment of fecal incontinence. Investigations for constipation and disordered defecation Constipation is one of the common ailments presented to the colorectal surgeon. It usually entails unsatisfactory defecation resulting from decreased frequency of defecation of difficulty in passing stools or both. Prevalence in the general population in United States has been reported to be as high as 2–15%.(38, 39) Women are affected 2–3 times more commonly with incidence increasing with age. As with incontinence, the etiology is multifactorial and complex. Etiological factors associated with constipation include lifestyle issues and medications; especially narcotics, antidepressants, and calcium channel blockers. Pelvic outlet obstruction (puborectalis dysfunction, rectocele) is also a common underlying abnormality. Other causes include neurological or endocrine dysfunction for example, Parkinson’s disease, diabetes mellitus, and hypothyroidism. Finally, dysfunction of enteric nervous ­system seen in Hirschsprung’s and Chagas disease and psychological ­factors may also play an important role in the pathogenesis. Refractory constipation that fails to respond to dietary modification and conservative management warrants a formal work-up. From management perspective, constipation is usually referred to as either slow transit constipation or obstructed defecation. The initial history and physical examination, in most cases, is able to indicate if the patient is experiencing slow transit constipation vs. obstructed defecation. Colonic transit studies are usually the first tests to be ordered in cases where slow transit is suspected to be the underlying etiology whereas in patients

limitations of anorectal physiology testing with obstructed defecation, a defecogram should be offered as the initial diagnostic study. However, studies have shown that there is little, if any, correlation between these two diagnostic modalities and clinical picture does not necessarily reciprocate the radiological findings.(40) defecography Since the 1960s, continuously recorded fluoroscopy has been used to evaluate the dynamic function of the pelvic floor. Defecating proctography or ciné defecography is a method whereby semi-solid radiopaque contrast material is placed retrograde into the rectum and lateral images are obtained in real time. Creating a realistic “pseudo stool” has been a challenge. A commercially available product was available but was transiently taken off the market. Many institutions create there own contrast as needed using a combination of barium and potato starch. At the authors institution we use a unique recipe based on breadcrumbs. The material must be thick enough to simulate stool but able to be passed transanally. Once the enema is administered the subject is seated in a lateral orientation on a radiolucent commode. Before defecation measurements are made of the angles of the proximal and distal rectum. In women the vagina may be delineated with a tampon soaked with water soluble contrast, and in certain circumstances the small bowel is opacified with oral contrast. If further delineation is required sterile water soluble contrast can be placed intraperitoneally to define the lower peritoneal reflection, furthermore, in patients with suspected cystocele, instillation of dye into the bladder may increase the diagnostic yield of the study. The anorectal angle is created in part by the tone and function of the puborectalis muscle. Measurements are taken as the patient is sitting at rest, during forced contraction, straining without ­defecation (Valsalva maneuver), and during defecation. Perineal decent is defined as the change in distance of the line drawn perpendicularly from the anorectal junction to the pubococcygeal line. This line is drawn from the tip of the coccyx to the posterior-inferior margin of the pubic ramus. In addition perianal skin can be marked with a metal marker and the motion or decent of the perineum measured. Normal reported values vary widely. One author offers a broad range, 70°–140° at rest, 100° to 180° defecating, and 75° to 90° squeezing (41, 42), where another is more specific 92° +/- 1.5° resting and 137° +/- 1.5° straining (5). The change in the angle may be more important than the absolute numbers. In our practice the test is of most value if the surgeon reviews the study with the radiologist while the test is being performed. Abnormal findings include perineal descent of more than 3 cm while resting or more than 3 cm while straining. Paradoxical contraction of the puborectalis and disordered defecation is indicated by an observed ascent of the perineum or a static or more acute anorectal angle during attempted defecation. Additional findings may include internal intussusception to frank prolapse, rectocele, or enterocele. Small, <2 cm rectoceles, are commonly seen in asymptomatic patients and are regarded as a normal finding. limitations of defecography in constipation It must be remembered that defecography is not a “physiological” study as the study is not performed in response to a natural desire to defecate, instead patients are asked to evacuate in a rather alien,

uncomfortable environment. Amongst other criticisms regarding defecography are poor interobserver agreement.(43, 44) To complicate issues further, abnormal defecographic findings are common in asymptomatic patients.(45, 46) The significant degree of overlap between defecographic findings in patients with constipation and asymptomatic controls raises questions regarding the cause and effect relationship between clinical symptoms and defecographic findings. One of the radiological signs frequently documented during these studies is contrast retention within the rectoceles. The clinical significance of this “Barium trapping” seen has also been questioned.(47) In a study by Shorvon et al. one half of asymptomatic subjects had some aspect of mucosal prolapse and intussusception, 17 of 21 women demonstrated some degree of rectocele.(48) In addition, before that work, no work had employed normal, healthy volunteers as controls and “normal” was determined retrospectively by lack of anatomic abnormality. Other studies were performed in patients undergoing barium enemas for other, nonanorectal conditions.(48, 45, 49) Anorectal angle assessment and its interpretation should be performed with utmost caution. As alluded to earlier, there is a wide variation in normal values for anorectal angle and many investigators believe that it is the change in angle rather than the absolute values that serves as a useful guide to therapy.(7) Patients with urge incontinence may frequently show increased threshold for urge to defecate. It is unclear if this finding is the result rather than the cause of constipation (9) and the clinical implication of this finding remains uncertain. Abnormal puborectalis function noted at defecography has also been a topic of considerable debate. Many normal individuals have been shown to have puborectalis abnormalities on defecograms (50), thus the clinical relevance of these findings are questionable and therapeutic decisions should be based on clinical rather than mere abnormal findings on radiological studies. colonic transit studies (sitz marker®) Colonic transit studies play a pivotal role in the assessment of constipation. Majority of colorectal surgeons agree that transit studies supply the most pertinent information out of all the physiology testing modalities available for constipation.(51) The most widely accepted technique involves ingestion of 24 radio-opaque rings followed by X-ray at days 1,3 and 5. A normal study entails passage of more than 80% of the rings. A quick way to help evaluate the patient for the presence of gastroparisis as well as small dysmotily is to make sure that they take the sitzmaker pill right before bed and have the day one x-ray as early in the morning as possible. While not useful in evaluating colonic transit, all of the makers should be out of the upper GI tract. The mean colonic time has been shown to 31 hours in males and 39 hours in females.(15) Based on the location of retained rings, abnormal studies may be labeled as “outlet obstruction” if 20% or more rings are retained at day 5 in the rectosigmoid region or “colonic inertia” if more than 20% rings are dispersed throughout entire colon. Clinical efficacy of colonic transit studies to detect segmental bowel motility remains controversial.(9) No bowel prep is administered before the study and patients are directed to avoid using laxatives and promotility agents including dietary fiber for at least a week before the study and during the duration of the study.

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improved outcomes in colon and rectal surgery small bowel transit studies Since it is generally accepted that slow transit constipation is overwhelmingly attributed to colonic dysfunction, small bowel transit studies are infrequently requested. However when clinical suspicion exists, such as patients with gastroparesis and dilated small bowel on plain x-rays, small bowel motility studies should be undertaken before undertaking a surgical intervention. Several techniques are available to assess small bowel transit. Nondigestible carbohydrates are broken down into hydrogen and fatty acids upon reaching the colon. Hydrogen and fatty acids are then absorbed into the blood stream. Therefore interval between ingestion of substrate and increments in exhaled hydrogen levels estimate small bowel transit. Similarly, orally administered sulfasalazine is broken down by colonic bacteria into mesalazine and sulfapyridine and then absorbed. Colonic transit can be measured by serum detection of sulfapyridine. Radio nucleotide scintigraphy has also been used to assess small bowel transit function. However, the clinical application of these tests is limited by their complexity and variation in bacterial flora in different subjects. mri Magnetic Resonance Imaging (MRI) of the pelvic floor is the newest addition to the diagnostic armamentarium available for pelvic floor evaluation. MRI obviates the exposure to radiation. Technique involves filling rectum with ultrasound gel. Images can be obtained in “static” manner or in the form of dynamic pelvic MRI which involves patient to perform maneuvers that are similar to those performed during conventional defecography. During these maneuvers, multiple images are obtained which are then viewed as a cine loop. MRI provides excellent spatial orientation of the sphincter complex and provides superior delineation of the surrounding structures. MRI appears to be superior to ultrasonography in discerning external sphincter abnormalities.(30) Additionally, dynamic MRI defecography appears to be superior to conventional defecography in the evaluation descending perineum syndrome as it provides excellent spatial assessment of ­pelvic floor musculature.(52) Limitations of mri in constipation Dynamic pelvic floor MRI shares similar limitations as conventional MRI: cost, claustrophobia, and availability. There are however, some specific limitations related to the diagnostic modality. Studies comparing dynamic MRI with conventional defecography have yielded conflicting results. Healy et al. (53) found significant correlation between dynamic MRI findings and defecography in ten patients examined employing both techniques. On the contrary, Matsouka et al. (54), in their study of 22 patients, reported defecography to be more sensitive than dynamic MRI and recommended against the routine use of this expensive modality. Most centers perform pelvic floor imaging with patient in supine position. Patients are asked to strain in a position which is far from physiologic and raises concerns regarding the reliability of the test. The influence of patient positioning has been investigated. Bertschinger et al. (55) performed a prospective comparison of 38 patients who underwent closed MRI in supine position followed by open MRI in a sitting position. Four rectal descents, two enteroceles, four small cystoceles, and four small anterior

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rectoceles were missed at supine MRI. The clinical significance of these findings, however, remains questionable. As mentioned earlier, the lack of “normal controls” makes it difficult to assess the efficacy of this test. Balloon Expulsion Test Balloon expulsion test is an infrequently used method to test motor defecatory function of the rectum. There is complete lack of standardization of methods used in various anorectal manometry laboratories.(55A) Various size balloons have been used for this purpose. Commonly 50–100 cc deformable balloons are used. Alternatively, smaller, more rigid balloons may also be employed. The impact of size and compliance of balloon on the final interpretation of test is unclear. In general, it is easier to evacuate larger balloons.(56) Many investigators believe that volume of balloon should be individualized to induce a constant desire to defecate. Consequently, use of lower volumes may result in false positive results.(57) There is a wide variation in what is considered to be a normal test. Inability to expel balloon in a sitting position within 30–60 seconds is considered abnormal in most centers. Balloon expulsion has been shown to be of importance in differentiating between constipation caused by slow transit from that caused by pelvic floor dyssynergia.(57) biofeedback for constipation Biofeedback training is widely utilized to teach relaxation of the pelvic floor in patients with pelvic floor dyssynergia. A critical review of the available literature by Heymen et al. (58) including thirty eight studies showed that mean success rate with pressure biofeedback was 78% compared to mean success rate of 70% seen with electromyography feedback. The authors surmised that despite the reported success rates, quality research is lacking. The most controversial area involving biofeedback training for constipation is questionable longevity/sustainability of the results. Ferrara et al. (59) reported a clear loss of benefits over time despite initial success. patients perspective Inherent to the evaluation of fecal incontinence is patients’ feelings of shame, embarrassment and discomfort. These sensations are felt by the incontinent patient resulting in depression and social isolation. A number of quality of life tools have been developed to quantify the results of evaluation and treatment of fecal incontinence. No one tool is universally accepted and these tools have been difficult to validate.(60, 61) In addition the testing incontinent patients are subjected to may be embarrassing and uncomfortable. Deutekom et al. conducted a cohort study of 240 consecutive patients undergoing evaluation of fecal incontinence in 16 Dutch centers. Each patient underwent manometry, defecography, AUS, PNTML, and MRI. Two hundred forty of the 270 self-administered questionnaires were returned. Patients were asked to evaluate anxiety, discomfort, embarrassment, and pain. Answers were scaled from 1(not 0), none to 5, severe. Results were also summarized as total test burden. Overall test results were surprisingly low, with average scores in each category not exceeding 2. Overall MRI was the most preferred and least uncomfortable test. Defecography

limitations of anorectal physiology testing was the most inconvenient and uncomfortable. Anorectal combined testing; manometry, PNTML, and AUS, also scored low for ­discomfort and overall test burden but more so than MRI.(62) conclusion Physiological studies of anorectal function can provide valuable information in carefully selected cases. While performing these studies, one should be cognizant of the fact that these procedures can be embarrassing, and at best are far from patient’s usual habits. It is unnerving for many patients to perform the act of ­defecation in the presence of an audience and it is conceivable that “performance anxiety” may lead to results which may not be truly representative of actual patient status. Thus, these studies should be interpreted with a grain of salt. Despite the plethora of literature available, the clinical usefulness of these tests remains vague and there is limited evidence that anorectal imagining guides management in pelvic floor disorders.(63) There are multiple welldesigned studies, which unfortunately report conflicting results. We therefore recommend that the most decisive factor governing treatment decisions is history and physical exam. Physiology ­testing should always be used as an adjunct rather than a primary determinant. references   1. Whitehead WE, Wald A, Norton NJ. Treatment options for fecal incontinence. Dis Colon Rectum 2001; 44: 131–42.   2. Tjandra JJ, Dykes SL, Kumar RR et al. Practice parameters for the treatment of fecal incontinence. Dis Colon Rectum 2007; 50: 1497–507.   3. Person B, Kaidar-Person O, Wexner SD. Novel approaches in the treatment of fecal incontinence. Surg Clin N Am 2006; 86(4): 969–86.   4. Thompson WG, Longstreth GF, Drossman A et al. Functional bowel disorders and functional abdominal pain. Gut 1999; 45(Suppl 2): 43–7.   5. Gordon PG. Anatomy and physiology of the anorectum. In Fazio VW, Church JM Delaney CP, eds. Current Therapy in Colon and Rectal Surgery. 2nd edn Philadelphia ElsevierMosby, 2005: 1–9.   6. Simpson RR, Kennedy ML, Nguyen MH, Dinning PG, Lubowski DA. Anal manometry: a comparison of techniques. Dis Colon Rectum 2006; 49: 1033–8.   7. Wexner SD, Sardinha TC, Gilliand R. Setting up a colorectal physiology laboratory. In Corman ML, ed. Colon and Rectal Surgery 5th edn. Philadelphia Lipincot, Williams & Wilkins, 2005: 129–67.   8. Madoff RD, Orrom WJ, Rothenberger DA, Goldberg SM. Rectal compliance: a critical reappraisal. Int J Colorectal Dis 1990; 5(1): 37–40.   9. Barnett JL, Hasler WL, Camilleri M. American Gastro­ enterological Association medical position statement on anorectal testing techniques. American Gastroenterological Association. Gastroenterology 1999; 116(3): 732–60. 10. Liberman H, Faria J, Ternent CA et al. A prospective Evaluation of the value of anorectal physiology in the management of fecal incontinence. Dis Colon Rectum 2001; 44: 1567–74.

11. Felt-Bersma RJ, Klinkenberg-Knol EC, Meuwissen SG. Anorectal function investigations in incontinent and continent patients. Differences and discriminatory value. Dis Colon Rectum 1990; 33(6): 479–85. 12. Yang YK, Wexner SD. Anal pressure vectography is of no apparent benefit for sphincter evaluation. Int J Colorectal Dis 1994; 9(2): 92–5. 13. Beck A. Electromyographische untersuchungen am sphincter ani. Phlugers Arch 1930; 224: 278–92. 14. Ferrara A, Lujan JH, Cebrian J et al. Clinical Manometric and EMG characteristics of patients with fecal incontinence. Tech Coloproctol 2001; 5: 13–8. 15. Smith LE, Blatchford GJ. Physiologic Testing. In: Wolff BG, Fleshman JW, Beck DE et al, eds. The ASCRS Textbook of Colon and Rectal Surgery New York, Springer, 2006: 40–56. 16. Timmcke AE. Limitations of anal physiologic testing. In: Hicks TC, Beck DE, Opelka FG, Timmcke AE, eds. Complications of Colon and Rectal Surgery. Baltimore Williams & Wilkins, 1996: 419–30. 17. Jacobs PPM, Scheuer M, Juijpers JHC Vingerhoets MH. Obstetric fecal incontinence: role of pelvic floor denervation and results of sphincter repair. Dis Colon Rectum 1990; 33(6): 494–7. 18. Laurberg S, Swash M, Henry MM. Delayed external sphincter repair for obstetric tear. Br J Surg 1998; 75: 786–8. 19. Wexner SD, Marchetti F, Jagelman DG. The role of sphincteroplasty for fecal incontinence reevaluated: a prospective physiologic and functional review. Dis Colon Rectum 1991; 34: 22–30. 20. Buie WD, Lowry AC, Rothenberger DA, Madoff RD. Clinical rather than laboratory assessment predicts continence after anterior sphincteroplasty. Dis Colon Rectum 2001; 44: 1255–60. 21. Kiff ES, Swash M. Slowed conduction in the pudendal nerves in idiopathic (neurogenic) faecal incontinence. Br J Surg 1984; 71(8): 614–6. 22. Ricciardi R, Mellgren AF, Madoff RD et al. The utility of pudendal nerve terminal motor latencies in idiopathic incontinence. Dis Colon Rectum 2006; 49(6): 852–7. 23. Frudinger A, Bartram CI, Halligan, Kamm M. Examination techniques for endosonography of the anal canal. Abdom Imaging 1998; 23: 301–3. 24. Nazir M, Carlsen E, Jacobsen AF, Nesheim BI. Is there any correlation between objective anal testing, rupture grade, and bowel symptoms after primary repair of obstetric anal sphincter rupture: an observational cohort study. Dis Colon Rectum 2002; 45: 1325–31. 25. Zetterstrom JP, Mellgren A, Madoff RD, Kim DG, Wong WD. Perineal body measurement improves evaluation of anterior sphincter lesions during endoanal ultrasonography. Dis Colon Rectum 1998; 41: 705–13. 26. Briel JW, Stoker J, Rociu E et al. External anal sphincter atrophy on endoanal magnetic resonance imaging adversely affects continence after sphincteroplasty. Br J Surgery 1999; 86: 1322–7. 27. Christensen AF, Nyhuus B, Nielson MB, Christensen H. Threedimensional anal endosonography may improve diagnostic

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confidence of detecting damage to the anal sphincter complex. Brit J Radiol 2005; 78: 308–11. Badger SA, Devlin PB, Neilly PJ, Gilliland R. Preoperative staging of rectal carcinoma by endorectal ultrasound: is there a learning curve? Int J Colorectal Dis 2007; 22(10): 1261–8. Dobben AC, Terra MP, Duetekom M et al. Anal inspection and digital examination compared to anorectal physiology tests and endoanal ultrasonography in evaluating fecal incontinence. Int J Colorectal Dis 2007; 22: 783–90. Terra MP, Stoker J. The current role of imaging techniques in faecal incontinence. Eur Radiol 2006; 16: 1727–36. West RL, Dwarkasing S, Briel JW et al. Can three-dimensional endoanal ultrasonography detect external anal sphincter atrophy? A comparison with endoanal magnetic resonance imaging. Int J Colorect Dis 2005; 20: 328–33. Norton C, Cody JD, Hosker G. Biofeedback and/or sphincter exercises for the treatment of faecal incontinence in adults. Cochrane Database Syst Rev 2006, 3: CD002111. Jensen L, Lowry A. Biofeedback improves functional outcome after sphincteroplasty. Dis Colon Rectum 1997; 40: 197–200. Heyman S, Jones KR, Ringel Y, Scarlett Y, Whitehead WE. Biofeedback treatment of fecal incontinence: a critical review. Dis Colon Rectum 2001; 44: 728–36. Solomon MJ, Pager CK, Rex J, Roberts R, Manning J. Randomized, controlled trial of biofeedback with anal manometry, transanal ultrasound, or pelvic floor retraining with digital guidance alone in the treatment of mild to moderate fecal incontinence. Dis Colon Rectum 2003; 46: 703–10. Pager CK, Solomon MJ, Rex J, Roberts RA. Long-term outcomes of pelvic floor exercise and biofeedback treatment for patients with fecal incontinence. Dis Colon Rectum 2002; 45: 997–1003. Norton C, Chelvanayagam S, Wilson-Barnett J, Redfern S, Kamm MA. Randomized controlled trial of biofeedback for fecal incontinence. Gastroenterology 2003; 125: 1320–9. Stewart WF, Liberman JN, Sandler RS et al. Epidemiology of constipation (EPOC) study in the United States: relation of clinical subtypes to sociodemographic features. Am J Gastroenterol 1999; 94(12): 3530–40. Sonnenberg A, Koch TR. Epidemiology of constipation in the United States. Dis Colon Rectum 1989; 32(1): 1–8. Infantino A, Masin A, Pianon P et al. Role of proctography in severe constipation. Dis Colon Rectum 1990; 33(8): 707–12. Moieira H, Wexner SD. Anorectal Physiologic testing. In: Beck DE and Wexner SD, eds. Fundamentals of anorectal surgery. 2nd ed Philadephia WB Saunders, 1998: 37–53. Finlay IG, Bartolo DCC, Bartram CI et al. Proctography (symposium). Int J Colorectal Dis 1998; 3: 67–98. Penninckx F, Debruyne C, Lestar B, Kerremans R. Observer variation in the radiological measurement of the anorectal angle. Int J Colorectal Dis 1990; 5(2): 94–7. Ferrante SL, Perry RE, Schreiman JS, Cheng SC, Frick MP. The reproducibility of measuring the anorectal angle in defecography. Dis Colon Rectum 1991; 34(1): 51–5. Bartram CI, Turnbull GK, Lennard-Jones JE. Evacuation proctography: an investigation of rectal expulsion in 20 subjects without defecatory disturbance. Gastrointest Radiol 1988; 13(1): 72–80.

46. Turnbull GK, Bartram CI, Lennard-Jones JE. Radiologic studies of rectal evacuation in adults with ������������������ idiopathic constipation. Dis Colon Rectum 1988; 31(3): 190–7. 47. Halligan S, Bartram CI. Is barium trapping in rectoceles significant? Dis Colon Rectum 1995; 38(7): 764–8. 48. Shorvon PJ, McHugh S, Diamant NE, Somers S, Stevenson GW. Defecography in normal volunteers: results and implications. Gut 1989; 30: 1737–49. 49. Roe AM, Bartolo DCC, Mortensen NJ. Techniques in evacuation proctography in the diagnosis of intractable constipation and related disorders. J Roy Soc Med 1986; 79: 331–3. 50. Jones PN, Lubowski DZ, Swash M, Henry MM. Is paradoxical contraction of puborectalis muscle of functional importance? Dis Colon Rectum 1987; 30(9): 667–70. 51. Karulf RE, Coller JA, Bartolo DC et al. Anorectal physiology testing. A survey of availability and use. Dis Colon Rectum 1991; 34(6): 464–8. 52. Healy JC, Halligan S, Reznek RH et al. Magnetic resonance imaging of the pelvic floor in patients with obstructed defaecation. Br J Surg 1997; 84(11): 1555–8. 53. Healy JC, Halligan S, Reznek RH et al. Dynamic MR imaging compared with evacuation proctography when evaluating anorectal configuration and pelvic floor movement. AJR Am J Roentgenol 1997; 169(3): 775–9. 54. Matsuoka H, Wexner SD, Desai MB et al. A comparison between dynamic pelvic magnetic resonance imaging and videoproctography in patients with constipation. Dis Colon Rectum 2001; 44(4): 571–6. 55. Bertschinger KM, Hetzer FH, Roos JE et al. Dynamic MR imaging of the pelvic floor performed with patient sitting in an open-magnet unit versus with patient supine in a closedmagnet unit. Radiology 2002; 223(2): 501–8. 55A. Beck DE. A simplified balloon expulsion test. Diseases Colon Rectum 1992; 35: 597–8. 56. Azpiroz F, Enck P, Whitehead WE. Anorectal functional testing: review of collective experience. Am J Gastroenterol 2002; 97(2): 232–40. 57. Minguez M, Herreros B, Sanchiz V et al. Predictive value of the balloon expulsion test for excluding the diagnosis of pelvic floor dyssynergia in constipation. Gastroenterology 2004; 126(1): 57–62. 58. Heymen S, Jones KR, Scarlett Y, Whitehead WE. Biofeedback treatment of constipation: a critical review. Dis Colon Rectum 2003; 46(9): 1208–17. 59. Ferrara A, De Jesus S, Gallagher JT et al. Time-related decay of the benefits of biofeedback therapy. Tech Coloproctol 2001; 5(3): 131–5. 60. Wexner SD, Jorge JM, Lee E et al. Etiology and management of fecal incontinence. Dis Colon Rectum 1993; 36: 139–45. 61. Rockwood TH, Church JM, Fleshman JW et al. Fecal incontinence quality of life scale: quality of life instrument for patients with fecal incontinence. Dis Colon Rectum 2000; 43: 9–17. 62. Deutekom M, Terra MP, Dukgraff MGW et al. Patients perception of tests in the assessment of faecal incontinence. Brit J Radiology 2006; 79: 94–100. 63. Bharucha AE, Fletcher JG. Recent advances in assessing anorectal structure and functions. Gastroenterology 2007; 133(4): 1069–74.

11

Limitations of colorectal imaging studies Travis J Blanchard, Wilson B Altmeyer, and Charles C Matthews

challenging case A 53 year-old woman presents to the emergency room with fever, left lower quadrant abdominal pain, and tenderness. Her temperature is 39 degrees Centigrad and her white blood cell count is 17,000 cells per cubic milliliter. What is the best radiologic test to confirm her diagnosis? case management A CT scan of the abdomen and pelvis will evaluate her to confirm the diagnosis of acute diverticulitis. In the absence of acute diverticulitis it may very well provide anothe explanation for her symptoms. Introduction Years of technical developments, organizational changes, and educational advances have inexorably altered the nature and composition of colorectal imaging. Conventional radiology or “plain films” and barium fluoroscopy studies are still important, but the developments of CT, US, MRI, nuclear medicine, and interventional radiology have greatly expanded the scope of radiology. This chapter will discuss the various imaging modalities, focusing on the capabilities and limitations of each modality to diagnose various disease processes important to the colorectal surgeon.

Figure 11.1  Pneumoperitoneum. Upright radiograph of the abdomen demonstrates a collection of air within the peritoneal space between the liver and the diaphragm.

abdominal radiography (plain films) Abdominal radiography typically consists of a single-view abdominal x-ray of the kidneys, ureters, and bladder (KUB) or an acute abdominal series (AAS). An AAS includes an upright chest radiograph, as well as upright and supine radiographs of the abdomen. An AAS can identify large masses, radiopaque foreign bodies, and radiopaque densities (including gallstones and kidney stones). Pneumoperitoneum As little as 1–2 cc of pneumoperitoneum (free intraperitoneal air) can be seen on an upright chest (Figure 11.1) or lateral decubitus film.(1) Postoperative pneumoperitoneum usually resolves in 3 to 7 days. Failure of progressive resolution or an increase in the amount of air present suggests a bowel anastomosis leak or abscess/sepsis. Signs of pneumoperitoneum (Figure 11.2) on supine radiographs include the “Rigler” sign or “double lumen” sign (gas on both sides of the bowel wall), and gas outlining the falciform ligament.(2) Bowel Obstruction and Dilatation The 3, 6, 9 rule can be used to identify bowel dilatation. The small bowel is dilated when its diameter is 3 cm; the colon when it is 6 cm, and the cecum when it is 9 cm. Abdominal plain films can diagnose small bowel obstruction (SBO), in 50–60% of cases with approximately 20% false-negative rate.(3) SBO can be complete/high grade or partial. Dilated loops of small bowel, air-fluid

Figure 11.2  Pneumoperitoneum. Plain radiograph demonstrates the “Rigler” sign or “double lumen” sign (gas on both sides of the bowel wall).

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improved outcomes in colon and rectal surgery

Figure 11.4  Large Bowel Obstruction. Supine radiograph demonstrates dilated colon as well as dilated small bowel in the right lower quadrant, indicating a large bowel obstruction with incompetent ileocecal valve.

Figure 11.3  Small Bowel Obstruction. Plain radiograph demonstrates dilated loops of small bowel with absence of colonic gas indicating a complete/high grade small bowel obstruction. There is air in the right inguinal canal. This patient had a surgery proven incarcerated right inguinal hernia.

levels, and absence of colonic gas indicate a complete/high grade small bowel obstruction. SBO can be simple (blood supply not impaired) or strangulating (blood supply impaired). Most strangulating obstructions are closed-loop obstructions (blocked at both ends), and this occurs typically with incarcerated hernias (Figure 11.3) and volvulus.(4) Plain films are not able to reliably differentiate simple from strangulating obstruction. However, extensive mucosal thickening or edema, portal venous gas, or a closed loop obstruction indicates high risk for strangulating obstruction.(5) Large bowel obstructions (LBO) occur commonly in the sigmoid colon, where stool is more formed and the colon is narrower. Air fluid levels distal to the hepatic flexure are strong evidence of obstruction unless the patient has had an enema. When the ileocecal valve is competent, the small bowel usually contains little gas. When the ileocecal valve is incompetent (Figure 11.4), gaseous distention of the small bowel is often present as the colon decompresses into the ileum.(6) Toxic Megacolon Toxic megacolon is a manifestation of sever colitis with absent peristalsis, and extreme dilation of all or a portions of the colon. A markedly dilated (>6 cm) colon with “thumbprinting” (thickened mucosal folds projecting into the lumen caused by bowel wall edema) is ­concerning for toxic megacolon (Figure 11.5).



Figure 11.5  Toxic Megacolon. Plain radiograph demonstrates a markedly dilated transverse colon with “thumbprinting” (thickened folds projecting into the lumen caused by bowel wall edema – see arrows) in a patient with ulcerative colitis and toxic megacolon.

When the cecum exceeds 10 cm in diameter, it is at risk for perforation. Ulcerative colitis is the most common cause of toxic megacolon and other causes include: Crohn’s colitis and infectious colitis. Barium enema is ­contraindicated because of the perforation risk.(4) Sigmoid and Cecal Volvulus Sigmoid volvulus is a closed loop obstruction that occurs most common in the elderly. On plain films, the sigmoid colon appears as a large gas-filled loop without haustral makings, arising from the pelvis and extending high into the abdomen. The three white

limitations of colorectal imaging studies

Figure 11.8  Limitations of Plain Films. CT of the same patient in Figure 11.IB-2 shows the cause of the large bowel obstruction is an annular constricting sigmoid carcinoma. A dilated loop of small bowel is seen adjacent to the sigmoid colon. Figure 11.6  Sigmoid Volvulus. Radiograph of the abdomen demonstrates the characteristic massive dilation of the sigmoid colon arising from the pelvis and extending to the right diaphragm. Three lines representing the twisted walls of the sigmoid colon converge in the left lower quadrant.

lines formed by the lateral walls of the loop and the summation of the two opposed medial walls of the loop usually converge inferiorly into the left iliac fossa (Figure 11.6). Cecal volvulus on plain films is characterized by a massively dilated cecum folded over into the left upper quadrant (Figure 11.7), usually with distended small bowel.(6) Confirmation of a volvulus can be obtained with CT or contrast enema (See CT scan [sigmoid volvulus] and fluoroscopy [water soluble enemas]). Benefits and Limitations of Acute Abdominal Series (AAS) Plain Films AAS are relatively inexpensive, and can be performed with portable equipment. However, AAS is insensitive, results are often not specific, and other imaging modalities (e.g. CT) (Figure 11.8) are often needed for definitive evaluation.(2–5) computed tomography (ct scan)

Figure 11.7  Cecal Volvulus. Abdominal radiograph demonstrates a massively dilated cecum folded over into the left upper quadrant with distended small bowel.

Unenhanced Multidector Computed Tomography vs. Plain Films Unenhanced spiral/helical Multidetector Computed Tomography (MDCT) is an accurate technique in the evaluation of patients with traumatic or nontraumatic abdominal pain and should be considered as an alternative to plain films as the initial imaging modality.(7–10) MDCT is more expensive and exposes the patient to more radiation. However, given the poor sensitivity of plain films; the radiation, time, and money spent pursuing a plain film examination in all patients may be unnecessary.(10) Additionally, MDCT provides more information to the surgeon for preoperative planning. With the advent of the new 16, 32, and 64 MDCT fast speed scanners, a high quality MDCT can be obtained almost as rapidly as a plain film, but it is not portable.

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improved outcomes in colon and rectal surgery Table 11.1  Premedication for Contrast Allergy. Oral Premedication for Contrast Allergy Prednisone 50 mg orally at 13, 6, and 1 hour prior to IV contrast administration Diphenhydramine 50 mg orally 1 hour prior to IV contrast administration. Emergency Stat Premedication for Contrast Allergy 30 minutes prior to IV contrast: Hydrocortisone 100 mg IV or Solucortef 200 mg IV and Diphenhydramine 50 mg IV.

Figure 11.10  CT Signs of Bowel Injury. MDCT axial section demonstrates pneumoperitoneum, free intraabdominal fluid, an air fluid level, and extravasation of oral contrast material in a patient with blunt abdominal trauma.

Table 11.2  Bowel wall thickening.

Figure 11.9  Pneumoperitoneum. When viewed on lung windows, free air can be seen in the subdiaphragmatic area, along the anterior peritoneal surfaces of the liver.

Contrast Enhanced Multidector Computed Tomography If the patient has no contraindications to oral and IV contrast (allergy, renal insufficiency), a contrast enhanced MDCT has been shown to be sensitive in diagnosing patients with bowel obstruction; as well as inflammatory, infectious, and neoplastic processes.(9, 11–27) Low osmolar, “nonionic,” iodine-based agents are more expensive than the older “ionic” contrast agents, but provide a decreased risk of adverse reactions and renal damage. If the patient has a simple allergy to IV contrast, such as hives; a low osmolar, “nonionic” contrast should be used and the patient can be premedicated with steroids and diphenhydramine (Table 11.1). Prior anaphylaxis to IV contrast is a complete contraindication. Orally administered water soluble contrast and rectal contrast add significant additional diagnostic information as accurate interpretation requires optimal opacification of the GI tract. However, to allow appropriate intraluminal distention with contrast, the patient has to drink contrast 1–2 hours before the CT scan can be performed. Diluted 2% barium mixture can also be used for oral contrast, but if bowel perforation is suspected, barium should be avoided as it can cause severe peritonitis. Pneumatosis, Pneumoperitoneum, and Bowel Trauma Pneumatosis (air in the bowel wall due to ischemia) and pneumoperitoneum from a traumatic or nontraumatic perforated

Benign

Neoplastic

Circumferential thickening Symmetric thickening Thickening <1–2 cm Segmental or diffuse involvement Mesenteric fat thickening

Eccentric thickening Asymmetric thickening Thickening >2 cm Focal soft tissue mass Abrupt transition and lobulated contour Short segments of involvement except lymphoma Spiculated outer contour

Long segments of involvement Wall is homogeneous soft tissue density Stratified enhancement “double halo” or “target” appearance

Luminal narrowing, adenopathy, or liver metastasis.

abdominal viscus, can be identified on MDCT when examined on “lung ­windows” (window level – 400 to -600 H; window width 1000 to 2000 H). Pneumoperitoneum can be seen in the subdiaphragmatic area, along the anterior surfaces of the liver (Figure 11.9). The accuracy of CT in the diagnosis of blunt abdominal trauma has been reported to be as high as 97%.(28–33) The routine use of oral contrast in CT examination of abdominal trauma is controversial. Oral contrast material can aid in the identification of bowel loops, and differentiation of bowel from hematoma or hemorrhage. Disadvantages of oral contrast include risk of aspiration, and additional time requirements which may delay diagnosis.(33–35) Posttraumatic abdominal CT examinations should be performed using IV contrast, which maximizes the difference between contrast-enhancing bowel and nonenhancing hematomas.(36) CT signs of bowel and mesenteric injury include: (1) pneumoperitoneum; (2) extravasation of oral contrast material; (3) free intraabdominal fluid (Figure 11.10); (4) intramural hemorrhage, manifested as luminal narrowing with thickened and/or discontinuous bowel

This section will focus on abdominal trauma to the bowel and mesentery that a colorectal surgeon may encounter. Trauma to the other intraabdominal organs (e.g. liver, spleen, bones) will be omitted.

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limitations of colorectal imaging studies

Figure 11.13  Neoplastic Wall Thickening. MDCT axial image demonstrates abnormal colon wall thickening (>3 cm) that is asymmetric, nodular, and lobulated in contour with narrowing of the intestinal lumen. The combination of a paucity of pericolonic fat stranding with the short segment of involvement is worrisome for malignancy. Surgery confirmed adenocarcinoma.

Table 11.3  Ulcerative colitis versus Crohn Colitis.

Figure 11.11  Benign, Pathologic Wall Thickening. MDCT coronal reformatted image demonstrates colonic wall thickening (<1 cm) that is homogenous, circum­ ferential, symmetric, and segmental in distribution. The long segment of involvement suggests a benign condition.

Figure 11.12  “Double Halo” or “Target” Sign. MDCT axial image of the same patient in Figure 11.II-D-1, demonstrates a stratified enhancement pattern in a thickened segment of descending colon bowel wall.

wall; (5) intense enhancement or high-attenuation clot (sentinel clot) ­adjacent to the involved bowel (30, 37–48). Bowel Wall Thickening When fully distended the bowel wall is 1–2 mm in thickness, and the collapsed bowel wall should not exceed 3–4 mm. MDCT can often differentiate benign from malignant wall thickening (Table

Ulcerative Colitis

Crohn Colitis

Circumferential disease

Eccentric disease

Continuous disease

Skip lesions

Predominantly left-sided

Predominantly right-sided

Rectum usually involved

Rectum normal in 50%

Confluent shallow ulcers

Confluent deep ulcers

No aphthous ulcers

Aphthous ulcer early

Collar button ulcers

Transverse and longitudinal ulcers

Terminal ileum usually normal

Terminal ileum usually diseased

Terminal ileum patulous in backwash ileitis

Terminal ileum narrowed

No pseudodiverticula

Pseudodiverticula

Inflammatory polyps and pseudopolyps

No polyps or pseudopolyps

No fistulas

Fistulas common

High risk of cancer

Low risk of cancer

Risk of toxic megacolon

No toxic megacolon

11.2). Benign, pathologic wall thickening (Figure 11.11) is seen in infectious, inflammatory, and ischemic processes; usually does not exceed 1–2 cm; is homogenous in attenuation; and is circumferential, symmetric, and segmental in distribution.(49) A stratified enhancement pattern in a thickened segment of bowel wall is used to exclude malignant conditions. Such a pattern may have a “double halo” or “target” appearance of the intestine in cross section which is caused by inflammation, edema, and hyperemia (Figure 11.12). Neoplastic wall thickening is thicker (2–3 cm), asymmetric, nodular, lobulated, or spiculated in contour and tends to narrow the intestinal lumen (Figure 11.13). The extent or length of bowel wall involvement aids in narrowing the differential diagnosis. With few exceptions (mainly lymphoma), long segments of involvement indicate a benign condition. When the perienteric fat adjacent to a thickened bowel segment is normal,

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improved outcomes in colon and rectal surgery

Figure 11.14  Crohn’s Disease. Axial MDCT demonstrates circumferential wall thickening of the terminal ileum that results in narrowing of the bowel lumen and formation of a stricture.

Figure 11.17  Ulcerative Colitis. Coronal reformatted CT image of the abdomen and pelvis shows wall thickening and marked irregularity of the remaining mucosa in the ascending and descending colon (arrows).

an acute inflammatory condition is less likely. Fat stranding that is disproportionately more severe than the degree of wall thickening suggests an infectious or inflammatory process.(50) Figure 11.15  “Comb Sign”. Swollen blood vessels produce an appearance like the teeth of a comb extending from the thickened bowel wall into the mesenteric fat. Note the irregular outer wall of the cecum indicating Crohn’s colitis.

Figure 11.16  Crohn’s Abscess. Axial MDCT image demonstrates extraluminal abscess in this patient with Crohn’s disease/colitis.

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Inflammatory Bowel Disease (IBD) Benign, circumferential thickening of the bowel wall is a hallmark of Crohn’s Disease (Table 11.3). Wall thickening (Figure 11.14) can result in strictures that narrow the bowel lumen in advanced disease.(51–52) CT is excellent in documenting the extraluminal manifestations of the disease such as the “comb sign” (Figure 11.15), which is produced by hyperemic thickening of the vasa recta due to active disease. The swollen blood vessels produce an appearance like the teeth of a comb extending from the thickened bowel wall into the mesenteric fat.(53) “Skip areas” of normal bowel intervened between diseased segments are characteristic. Mesenteric abscesses are characteristic and may can contain fluid, air, or contrast material (54–57) (Figure 11.16). Crohn’s Colitis is characterized by transmural inflammation that usually affects the terminal ileum (80%) and proximal colon (50%).(51–52) Bowel wall thickening in Crohn’s colitis is typically 10 to 20 mm compared with the 7 to 8 mm for Ulcerative Colitis (UC). With Crohn’s colitis (Figure 11.15), the outer wall is irregular, whereas with UC the outer wall is smooth.(58) Acute active disease shows layering of the colon wall (“target and halo” signs), whereas chronic disease with fibrosis shows homogeneous enhancement of the colon wall. Fibrous and fat proliferation in the mesentery (“creeping

limitations of colorectal imaging studies

Figure 11.20  Typhilitis. MDCT axial image demonstrates marked wall thickening, low-density edema within the cecal wall, and pericecal fluid and inflammation in a patient with HIV. The wall thickening and inflammation extended from the cecum to the hepatic flexure.

Figure 11.18  Ulcerative Colitis. Coronal reformatted CT image of the abdomen and pelvis shows pseudopolyps (arrow) that extend into the lumen of the transverse colon.

Figure 11.21  Radiation Colitis. Axial MDCT image demonstrates mucosal thickening with prominent stranding in the expanded pericolic fat confined to the radiation port distribution. A lymphomatous mass is noted adjacent to the radiation colitis (large arrow).

Figure 11.19  Psuedomembranous Colitis. Axial MDCT demonstrates pancolitis with irregular wall thickening and submucoal edema resulting in a characteristic “accordion pattern” of disease.

fat”) separates bowel loops with extensive fat-containing fibrous strands. Sinus tracts between bowel loops, enterocutaneous fistulas, and enterovesicular fistulas are also characteristic findings. Ulcerative Colitis (UC) is characterized by inflammation and diffuse ulceration of the colon mucosa (Figure 11.17). The disease

starts in the rectum and extends proximally to involve part or the entire colon. Wall thickening with luminal narrowing and the inflammatory pseudopolyps, that result from mucosal ulceration, are sometimes seen on CT (Figure 11.18). Narrowing of the rectal lumen with thickening of the rectal wall and widening of the presacral space are often seen (51–53, 58). Similar to Crohn’s disease, mesenteric adenopathy can be seen, but it is not specific for IBD. Other Colitides Psuedomembranous colitis results from overgrowth of Clostri­ dium difficile and its enterotoxin, as a complication of antibiotic therapy. A pancolitis with irregular wall thickening (up to 30 mm)

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improved outcomes in colon and rectal surgery intestinal obstruction and visualization of a normal appendix aid in diagnosis.(63–64)

and submucoal edema results in the “accordion pattern” of disease that is characteristic.(58) The edema and thickening of the colon may be greater than that seen with other colitides, and a pancolitis ­suggests pseudomembranous colitis (Figure 11.19). Typhilitis or neutropenic colitis refers to a potentially fatal infection of the cecum and ascending colon in patients who are immunocompromised. CT is the study of choice for making the diagnosis. Typhilitis is characterized by marked wall thickening (10–30 mm), low-density edema in the cecal wall, pericecal fluid, and inflammation (Figure 11.20), which may be confused with the reactive changes of appendicitis.(58–59) The length of the cecum and right colon involved is generally much greater with typhlitis, and the thickening is more asymmetric in appendicitis.(60) The presence of known risk factors favors the diagnosis of typhilitis. Ischemic colitis features include benign, pathologic wall thickening in a vascular distribution watershed segment of colon, usually at the splenic flexure (Figure 11.12). Radiation colitis in the acute phase demonstrates mild wall thickening and pericolic fat stranding confined to the radiation port area. Chronic radiation injury 6 to 24 months after treatment appears as mucosal thickening with prominent stranding in expanded pericolic fat (Figure 11.21). Infectious colitis differentiation is based on clinical findings because CT findings are nonspecific. Infectious terminal ileitis is usually caused by Yersinia, Tuberculosis, Campylobacter, or Salmonella organisms.(61) The diagnosis is made clinically with stool cultures. CT features are benign wall thickening of the terminal ileum and cecum, and moderate or marked enlargement of the mesenteric lymph nodes in the right lower quadrant. (62) Although a Meckel’s diverticulum occurs at some distance (60–100 cm) from the cecum, it may cause complications such as inflammation, whose differential diagnosis includes appendicitis and IBD.(63) The CT diagnosis of an inflamed Meckel’s diverticulum relies on the identification of a blind-ending, tubular, or round pouch-like structure in the right lower quadrant attached to the small intestine with surrounding inflammation. Small

Figure 11.23  Perforated Diverticulitis. Axial MDCT image demonstrates colon wall thickening and extravasation of oral contrast (small arrows), as well as free peritoneal air anteriorly (large arrow).

Figure 11.22  Diverticulitis. Axial MDCT demonstrates benign wall thickening, hyperemic contrast enhancement, and inflammatory change that extend into the pericolic fat, with diverticula in the involved segment.

Figure 11.24  Colon Cancer. Axial MDCT demonstrates a large colonic mass in the descending colon that narrows the lumen. CT cannot differentiate tumor extension through the wall from pericolonic edema or desmoplastic reaction.



Diverticulitis Acute diverticulitis is characterized by benign wall thickening, hyperemic contrast enhancement, inflammatory pericolic fat stranding, and diverticula in the involved segment (Figure 11.22). Perforation or abscess may form, and CT is better suited to demonstrate extraluminal disease than barium enema (Figure 11.23). Sinus tracts and fistulas may extend to adjacent organs or the skin and are represented by linear fluid or air collections. Air in the bladder suggests a colovesicular fistula, unless the patient has had

limitations of colorectal imaging studies bladder catheterization. Obstruction of the colon or urinary tract from the inflammatory process can be seen on CT. Diverticulitis of the right colon may be confused with acute appendicitis or IBD. Visualization of a normal appendix or inflammatory changes involving the ascending colon distal to the ileocecal valve favor the diagnosis of diverticulitis over appendicitis.(58) The extrinsic inflammation from a tubo-ovarian abscess may cause serosal edema and mural thickening of the cecum or sigmoid colon wall. Recognizing that the inflammation is centered in the adnexa and appropriate distention of the colon with oral and rectal contrast agents assist in making the correct diagnosis.(65–66) Colorectal Cancer Detection and Differentiation from Diverticulitis The CT appearance of diverticulitis overlaps that of colon cancer, as bowel wall thickening and pericolonic fat stranding occur in both. Fluid in the sigmoid mesentery and engorgement of mesenteric vessels favors diverticulitis (Table 11.2). Enlarged lymph nodes, asymmetric wall thickening, and the presence of an intraluminal mass (Figure 11.24) favors cancer.(67–73) Prior recent films showing no colonic wall thickening can aid in diagnosis. A biopsy may be required in equivocal cases. Colorectal Cancer Staging Preoperative CT for staging colorectal cancer is performed to detect invasion of adjacent organs, enlargement of local nodes, or evidence of distant metastases. The Tumor, Nodes, Metastasis (TNM) and Dukes classification are both used for preoperative staging (Table 11.4). Squamous cell carcinoma can occur in the anal canal, and it does not have any ­discriminating imaging features from adenocarcinoma. The primary adenocarcinoma may be seen as a polyp larger than 1 cm, or a soft-tissue cancer mass that narrows the lumen of the colon.(74) Flat lesions appear as focal, lobulated thickening of the bowel wall (>3 mm). “Apple core” lesions demonstrate irregular bulky circumferential wall thickening with marked and irregular narrowing of the bowel lumen.(74–75) Adequate luminal distention is essential, and may be achieved with oral and rectal water soluble contrast or water as a negative contrast agent.(76–77) The accuracy of CT in preoperative staging varies from 48% to 77%, and this variability depends on the actual stage of the cancer.(78–82) The accuracy of CT staging ranges from 17% for early lesions (Dukes stage B) to 81% for advanced lesions (Dukes stage D) (75, 80, 83). Inaccuracies arise

from the inability to distinguish tumor from peritumoral desmoplastic reaction or edema, and the inability to detect microscopic extramural tumor extension (Figure 11.24). A major advantage of CT is the ability to demonstrate the local extent of tumor and involvement of adjacent organs, such as the bladder, vagina, peritoneum, and abdominal or pelvic musculature.(84) Also, MDCT can reliably detect enlarged lymph nodes for staging of colorectal cancer.(83) Although the presence of lymph nodes larger than 1–1.5 cm in short-axis diameter is considered pathologic, not all enlarged nodes contain tumor. Conversely, normal-sized nodes may have microscopic tumor involvement.(80) Another factor that poses problems in staging is ischemic bowel associated with an obstructing colon cancer.(85–87) Detecting ischemic change proximal to colonic carcinoma is important because 25% of cases

Figure 11.25  Colon cancer liver metastasis. MDCT performed with IV contrast material during the portal vein phase of enhancement shows heterogeneous, ringenhancing metastases that are hypodense to the liver.

Table 11.4  TNM compared to modified Dukes staging for colorectal carcinoma. TNM Stage

Modified Dukes Stage

I: Submucosa T1, Muscularis, T2 N0M0

A: Limited to wall mucosa or submucosa

II: Muscularis T3, Perirectal T4 N0M0

B: Extension into or through serosa

IIIA: T1–4N1M0 IIIB: T1–4N2–3M0

C: Cancer that extends to lymph nodes

IV: T1–4 N1–3 M1

D: Distant Metastasis

Figure 11.26  Mucinous Adenocarcinoma Metastatic Disease. MDCT axial image shows necrosis and calcification of meatastatic mucinous adenocarcinoma to the liver.



improved outcomes in colon and rectal surgery

Figure 11.27  Colon Cancer Peritoneal Metastasis. Axial MDCT demonstrates thickening of the peritoneal surfaces, ascities, and two large peritoneal nodules in a patient with colon cancer.

with proximal ischemic colitis have been reported to cause postoperative complications such as suture-line disruption.(86–89) Also, an ischemic segment in colonic carcinoma may give a false radiologic impression regarding tumor length or depth of tumor invasion.(85) Ischemia can develop at sites remote from the obstructing cancer, such as the terminal ileum, mimicking synchronous lesions.(85, 89–93) CT can usually distinguish an ischemic segment from a tumoral segment in approximately 75% of the cases by applying the criteria for benign (ischemic) bowel wall thickening, and the “target” or “double halo” sign is the most specific sign.(88–93) This finding must be interpreted with ­caution, as signet ring cell adenocarcinoma can have low-density mural thickening. Colorectal Cancer Metastasis The liver is the predominant organ to be involved with metastases from colorectal cancer, and MDCT has an established role in detection. Hepatic metastases are supplied by the hepatic artery, and two thirds of the liver is supplied by the portal vein. MDCT (performed with IV contrast material during the portal vein phase of enhancement, 60–70 sec after the start of the bolus) typically shows heterogeneous, ring-enhancing metastases that are hypodense to the liver (Figure 11.25). Images obtained after a longer delay may not reveal evidence of disease because lesions become isodense to the liver.(94–95) Small lesions (<1 cm) do not have adequate enhancing properties to be differentiated and are named indeterminate lesions. Necrosis and calcification of metastatic mucinous adenocarcinoma to the liver can be seen on MDCT (Figure 11.26). CT can detect intraperitoneal metastases, which appear as thickening of the peritoneal surfaces or peritoneal nodules (Figure 11.27), but microscopic seeding will not be detected. Careful attention to the peritoneal surfaces and omentum is needed in the setting of unexplained ascites to identify peritoneal metastases. CT arterial portography is a very sensitive technique for detection of liver metastasis. This procedure requires fluoroscopic/



Figure 11.28  Anastomotic Leak. Axial MDCT demonstrates high density ascites representing extravasted oral contrast in this patient status postterminal ileum resection and ileocolic anastomosis. Pneumoperitoneum is also seen.

angiographic guided catheter placement in the superior mesenteric artery using the Seldinger technique through the femoral artery. Intraarterial injection of contrast material results in intense portal vein enhancement of the normal liver. Both metastatic disease and benign perfusion abnormalities manifest as filling defects on CT portography, and therefore the sensitivity of this test is less than perfect. Likewise, intraarterial hepatic artery injection (hepatic arteriography) can aid in identifying liver metastasis as they will enhance brightly. Some studies have suggested that combined CT arterial portography and CT hepatic arteriography significantly improved the detect ability of hepatic metastases.(96) However, these unified CT-angiography systems are not widely available and require an invasive procedure. Furthermore, a recent study (97) showed that the use of portal venous phase enhanced MDCT as the only preoperative imaging technique in the assessment of colorectal cancer metastases allowed accurate preoperative staging (sensitivity, 85.1%; positive predictive value, 96.1%). Colorectal Cancer Recurrence Local recurrent tumor usually appears as a soft-tissue mass in or near the surgical site. Due to the often largely extrinsic component of local recurrence, CT is better than colonoscopy at demonstrating the early, mass like tumor recurrence.(98, 99) This appearance can mimic postoperative fibrosis, although fibrosis usually appears more linear without a discrete mass. Following abdominoperineal resection, it is common to see soft tissue density within the presacral space. When this material remains plaque-like, fibrosis is likely. Often, distinction between postoperative fibrosis and recurrent tumor is not possible unless serial scans are obtained. CT findings clearly indicative of recurrent malignant disease include enlargement of a soft-tissue mass over time, enlarging lymphadenopathy, and invasion of contiguous structures. CT performed with intravenous contrast material is the imaging modality of choice for detection of recurrent tumor within the liver. CT has been shown to be more helpful in diagnosis of recurrent

limitations of colorectal imaging studies (a)

(b) Figure 11.29  Postoperative Abscess. Axial MDCT demonstrates a large air fluid collection (abscess) in the operative field, in this patient status posttotal colectomy and ileorectal anastomosis. The anastomotic suture line can also be seen. The large amount of gas in the abscess suggests communication with the gastrointestinal tract.

hepatic metastases than laboratory studies (liver function tests, measurement of carcinoembryonic antigen level).(80, 100) The importance of abdominal CT is reflected in the surveillance guidelines proposed by the American Society of Clinical Oncology.(101) The guidelines recommend annual CT of the abdomen for 3 years after primary therapy for patients who are at high risk of recurrence. Postoperative Complications MDCT is often used to diagnose postoperative complications such as abscess, anastomotic leak, fistula, small bowel obstruction, ileus, and pulmonary embolus (small bowel obstruction and ileus will be covered later). Before postoperative day five, it is difficult to differentiate normal postoperative intraperitoneal free air and fluid from fluid or air from an anastomotic leak or abscess.(102) Findings suggestive of an anastomotic leak include an inappropriate volume of free air or fluid in the abdomen. The presence of extraluminal oral contrast (Figure 11.28) confirms an anastomotic leak.(102) CT is the most accurate imaging test for diagnosing abscess formation in the postsurgical patient.(103) The combination of water soluble oral contrast and an intravenous contrast agent is essential in differentiating between a fluid-filled bowel loop and an abscess. The CT appearance of an abscess is variable depending on its age and location. Early abscess appears as a mass with an attenuation value near that of soft tissue. As the abscess matures, it undergoes necrosis with a central region of near-water attenuation surrounded by a high attenuation rim that usually enhances.(104) Approximately one third of abscesses contain variable amounts of gas (Figure 11.29).(104–108) Postoperative packing materials used for hemostasis, such as oxidized cellulose and gelatin bioabsorbable sponge, can mimic a gas-containing abscess. Findings that may help differentiate are: linear arrangement of tightly packed gas bubbles, an unchanged appearance on subsequent examinations, and lack of either a gas-fluid level or an

Figure 11.30  A and 11.30B Acute Appendicitis. Axial MDCT demonstrates an obstructing calcified appendicolith with an abnormally dilated, enhancing appendix surrounded by inflammatory fat stranding.

enhancing wall.(109, 110) A low-density mass containing a high density object suggests a foreign body abscess caused by a retained surgical sponge (gossypiboma).(111) Although CT findings are highly suggestive of abscess, they are not specific. Other masses that can have a central low attenuation include a cyst, pseudocyst, hematoma, urinoma, lymphocele, biloma, loculated ascites, thrombosed aneurysm, and necrotic neoplasm. Because a specific diagnosis of abscess based on CT findings alone is not possible, correlation with clinical history is important. Percutaneous needle aspiration may be necessary to make a definitive diagnosis (See interventional radiology). Fistula formation between the bowel and other organs such as the bladder, vagina, or skin can form as complications of surgical or radiation therapy. Fistula can be identified with IV or oral contrast and are demonstrated as extension of contrast from one organ to the other. Oral and IV contrast should not be used simultaneously for a suspected bowel/bladder fistula because contrast in the bladder could be from renal excretion or a bowel/ bladder fistula. Pulmonary embolism can occur in cancer and postoperative patients. Since the introduction of spiral MDCT, CT angiography



improved outcomes in colon and rectal surgery Appendix

Figure 11.31  Appendix Mucocele. Axial MDCT demonstrates distension of the appendix with mucus.

Figure 11.32  Lipoma. Axial MDCT demonstrates a 2–3 cm, round, sharply defined tumor with homogenous fat density (-80 to -120 H) adherent to the sigmoid colon.

(CTA) has become the method of choice for imaging the pulmonary vasculature, and has replaced invasive pulmonary angiography as the reference standard for diagnosis.(112–117) Another advantage of CTA over pulmonary angiography is the ability to identify alternative or additional diagnosis such as: atelectasis, pneumonia, pulmonary edema, pleural, and pericardial effusions, and many others. CT venography (CTV) combined with CTA can be used as a comprehensive examination of the deep venous system to detect both PE and deep vein thrombosis (DVT). CTV is performed by scanning of the pelvis from the iliac crest to the popliteal fossa approximately 120 s after completion of the CTA. CTV could potentially salvage the occasional suboptimal PE study by diagnosing a DVT and guide interventions such as vena cava filter placement. Numerous studies have cited 97% agreement between CTV and US.(118–122) The addition of CTV increases the gonadal radiation exposure, and should be used selectively on the basis of risk-benefit considerations (e.g., avoided in young patients and reproductive female patients).(116)



Acute Appendicitis MDCT has a high sensitivity (91–100%) and specificity (91– 99%) in diagnosing acute appendicitis (123–126). The diagnosis of acute appendicitis is based on finding: an abnormally dilated (>6 mm), enhancing appendix; appendix surrounded by inflammatory periappendiceal fat stranding; focal thickening of the base of the cecum; periappendiceal abscess; or obstructing calcified appendicolith (Figures 11.30A and 11.30B). The most common reason for a false-negative diagnosis is related to a paucity of intraabdominal fat often seen in pediatric patients and patients with a lean body habitus.(127–130) Optimal cecal opacification and distention are important because without cecal opacification a distended appendix can be mistaken for a small-bowel loop.(131, 132) Therefore, intravenous, oral, and rectal contrast should be used. Appendicitis may cause reactive dilatation of the small bowel and mimic a small-bowel obstruction, resulting in a missed diagnosis of the underlying problem. In addition, the dilated small bowel impedes the flow of oral contrast, so that opacification of the cecal region is suboptimal, creating difficulty in diagnosis. Therefore, a small-bowel obstruction in patients who have no history of surgery or cause for obstruction is suspicious for appendicitis, especially in younger patients.(130) Mucocele and Tumors of the Appendix Mucocele refers to distension of all or a portion of the appendix with mucus secondary to obstruction by appendicolith, adhesions, or tumor.(133) Most commonly, this lesion is a retention mucocele and is asymptomatic (Figure 11.31). Some cases are caused by mucinous cystadenomas or cystadenocarcinomas of the appendix.(133, 134) Continued secretion of mucus produces a large (up to 10 cm), well-defined, cystic mass in the right lower quadrant, which may have a thin rim of wall enhancement or calcification.(135) Rupture of the mucocele may result in psuedomyxoma peritonei causing gelatinous implants and mucinous ascites throughout the peritoneal cavity. Although an enhancing nodular component is concerning for malignancy (136), neoplastic and retention mucoceles cannot be reliably distinguished by imaging studies. Adenocarcinoma of the appendix is rare and is usually discovered in the clinical setting of suspected appendicitis in an older adult. Imaging demonstrates a soft tissue mass within or replacing the appendix.(133) Lymphoma of the appendix appears similar to appendicitis, but is typically larger with a diameter of 3 cm or greater.(137) Carcinoid is the most common tumor of the appendix accounting for 85% of all tumors.(133) Carcinoid of the appendix usually appears as a focal enhancing mass in the distal appendix.(133, 138) Carcinoid metastases to mesentery and the liver enhance brightly on arterial phase imaging because of their vascularity.(138–146) Three-dimensional CT angiography is useful to fully appreciate the mesenteric mass and its relationship to the vessels, which is important for surgical planning. (140–147) In addition to the liver, metastases can be seen on CT in the lung and bones. Other Tumors of the Colon CT remains the imaging study of choice for detection of benign and malignant tumors of the colon other than adenoma and

limitations of colorectal imaging studies

Figure 11.33  GIST. Axial MDCT demonstrates a large heterogenous exophytic mass with cystic degeneration and necrosis that communicates with the lumen of adjacent colon and small bowel.

adenocarcinoma. Metastases to the colon can be seen on contrast enhanced MDCT, if they are large enough; but CT cannot differentiate primary tumor from metastasis.(148) One of the most common benign colonic tumors is a lipoma. Lipomas can be easily diagnosed by demonstrating a 2–3 cm, round or ovoid, sharply defined tumor with homogenous fat density (-80 to -120 H) (Figure 11.32). Colonic lymphoma usually appears as either a marked thickening of the bowel wall that often exceeds 4 cm, or a homogeneous soft-tissue mass without calcification. Lymphoma characteristically causes much larger soft-tissue masses than adenocarcinoma. Owing to the softness of the tumor, the lumen is commonly dilated or normal, rather than constricted, and bowel obstruction is uncommon. The absence of desmoplastic reaction and diffuse lymphadenopathy help to differentiate lymphoma from adenocarcinoma.(149–150) Gatrointestinal Stroma Tumors (GIST) can be benign or malignant and cannot be diffentiated on cross sectional imaging without distant metastases to the liver or peritoneum.(151) GISTs can appear as an exophytic or intraluminal mass, and size varies from millimeters to 30 cm. Cystic degeneration, hemorrhage, and necrosis are common in large lesions with calcification rarely noted (Figure 11.33). The tumor cavity may communicate with the colon lumen and contain air or oral contrast. Sarcomas that arise in the bowel, anorectum, or omentum are indistinguishable from malignant GIST.(151) Tissue types include leiomyosarcoma, fibrosarcoma, and liposarcoma. Sigmoid and Cecal Volvulus Diagnosis of large bowel volvulus is usually made by plain radiographs or fluoroscopy, but CT is used to detect evidence of ischemia. Sigmoid volvulus is seen on CT as distended colon with the mesenteric twist appearing as a “whirl.” Cecal volvulus has a similar appearance with the apex of the distended colon pointed toward the right lower quadrant and the “whirl” of cecal mesentery in the

Figure 11.34  Small Bowel Obstruction. Axial MDCT demonstrates multiple dilated loops of small bowel with air fluid levels. Intraluminal fluid distends the bowel and acts as a natural contrast agent.

Figure 11.35  SBO from Adhesions. Axial MDCT of same patient in Figure 11.IIL-1 shows abrupt transition from dilated to nondilated bowel suggests adhesions as the cause. A suture line from the patient’s colonic resection and ileocolonic anastomosis is seen.

right abdomen. The axis of torsion is in the ascending colon above the ileocecal valve. Signs of bowel ischemia include benign wall thickening, “thumbprinting”, inflammation of pericolic fat, and pneumatosis (air in the bowel wall).(152) Small Bowel Obstruction Accuracy of Diagnosis and Causes of SBO CT has gained favor as the initial radiologic examination of patients with SBO because it can often determine the cause, severity, and transition point of obstruction.(153–158) The sensitivity of CT for high-grade SBO is 90–96%, with a specificity of



improved outcomes in colon and rectal surgery Table 11.5  CTC laxative preparations.

Figure 11.36  Ileocecal Intussusception. Axial MDCT CT demonstrates characteristic findings of the distal segment (intussuscipiens) dilated with a thickened wall. Its lumen contains an eccentric, soft-tissue mass (intussusceptum) with an adjacent crescent of fat density that represents the invaginated mesentery.

Laxative Agent

Limitations

Sodium Phosphate

Because of rare reported instances of acute phosphate nephropathy, avoid use in elderly with hypertension, patients taking angiotensin-converting enzyme inhibitors, and patients with renal or cardiac insufficiency (184).

Magnesium Citrate

Avoid in severely compromised patients who cannot tolerate mild fluid or electrolyte shifts.

Polyethylene Glycol (PEG)

Most favorable safety profile but poorest adherence because of the consistency, taste, and large volume (4 L) that must be ingested.

collapsed and this should not be mistaken for evidence of a transition zone. CT is reported to be less accurate in patients with low-grade or partial SBO and it may be difficult to distinguish between a SBO and paralytic or adynamic ileus. In such cases the “small bowel feces” sign, which is gas bubbles mixed with particulate matter in the dilated bowel, is a reliable indicator of a SBO. (161–166) If oral contrast reaches the colon, a complete SBO is not present. CT Enteroclysis CT enteroclysis is useful in the evaluation of equivocal cases, and is performed by placing a tube in the fourth portion of the duodenum with infusion of 1 to 1.5 L of dilute contrast into the small bowel. The addition of coronal reformations is a valuable adjunct to the transverse scans because it improves identification and exclusion of bowel obstruction.(167)

Figure 11.37  Pneumatosis Intestinalis. Small bowel ischemia is suggested by the decreased segmental bowel-wall enhancement and pneumatosis intestinalis.

91–96%.(153, 157, 159–165) The 3, 6, and 9 rule can be used to detect bowel dilatation on CT scans. Oral contrast is not always necessary as the intraluminal fluid distends the bowel and acts as a natural contrast agent (Figure 11.34). Oral contrast should be avoided in patients with a high grade or complete SBO. Adhesions cause 50% to 75% of SBOs, but are often not directly visualized by CT. Beaklike narrowing or abrupt transition from dilated to nondilated bowel suggests adhesions as the cause (Figure 11.35). Obstruction from tumor, abscess, intussusception (Figure 11.36), inflammation, and hernia are readily diagnosed with CT. Paralytic/Adynamic Ileus Paralytic or adynamic ileus appears as dilation of small bowel without a transition zone. The colon may be distended or



Closed Loop Obstruction, Strangulation, and Intestinal Ischemia CT can diagnose closed loop obstruction of the small bowel and bowel ischemia. The “beak” or “whirl” sign may be seen at the obstruction and volvulus.(168) Dilated bowel loops with stretched and prominent mesenteric vessels converging on a site of obstruction suggest a closed loop obstruction. Decreased segmental bowel-wall enhancement and pneumatosis (Figure 11.37) are associated with small-bowel ischemia.(169) The diagnosis of small-bowel ischemia in the presence of obstruction has reported sensitivities varying from 75% to 100%, and specificities of 61%– 93%.(170–174) computed tomographic colonography (ctc) Colorectal Cancer Screening and the Advanced Adenoma Computed tomographic colonography (CTC) or Virtual Colon­ oscopy is an excellent technique for the detection of colorectal polyps and cancer. Because colorectal cancer has an identifiable precursor lesion, the advanced adenoma (polyp), there is a genuine opportunity for prevention rather than detection alone.

limitations of colorectal imaging studies (216, 217) CTC’s sensitivity for polyp detection is similar to (175) or better than (176) double-contrast barium enema. CTC has accuracy similar to that of optical colonoscopy (OC) both in high-risk groups (177–180) and in a low-prevalence screening population (181). Also, CTC has the potential to become an accepted technique for evaluation of the nonvisualized part of the colon after incomplete OC.(182) CT Colonography (CTC) Technique Adequate CTC software is critical for accurate interpretation, but even the best software system will fail if colonic preparation is inadequate. Colonic preparation involves a clear liquid diet the day before the exam and a laxative for catharsis.(183) The laxative for a standard CTC bowel preparation is sodium phosphate, which is used in nearly 90% of cases (Table 11.5).(183) Dilute barium is used to tag residual feces, and water soluble diatrizoate serves the dual purpose of uniform fluid tagging and secondary catharsis. (185) Gaseous distention can be achieved with room air or CO2, and the insufflations can be automated or manually controlled by the patient or the medical staff (technologist or physician). Both supine and prone axial scans are obtained with 3D software reconstructions. At least 8 to 16 detector CT is needed with 1.25 mm collimation (Figures 11.38 and 11.39).

Benefits, Complications, and Limitations of CT Colonography (CTC) CTC does not involve the sedation or recovery time associated with OC. With the short scan time of MDCT scanners, patients must tolerate maximum inflation for only a few seconds, as opposed to OC and barium enema. A survey of patients undergoing colorectal cancer screening found that patients prefer CTC over OC and barium enema.(186) Unlike colonoscopy and barium enema, CTC allows visualization of organs outside the colon. Although nonenhanced CTC (at one-fourth the standard radiation dose) is not adequate for screening, all solid abdominal and pelvic pathology, important disease such as abdominal aortic aneurysm, renal cell carcinoma, ovarian cancer, and other neoplasms can be detected. The most beneficial situation would be the discovery of an asymptomatic early process that could be cured with early treatment. The safety profile of CTC has been extensively reviewed. The largest U.S. study, the combined Working Group on Virtual Colonoscopy (187), found that CTC was a very safe, noninvasive procedure (Table 11.6) By combining the Working Group results with two other large multicenter studies (188–189), the total number of CTC examinations exceeds 50,000. None of the cases of perforation from these three groups resulted in patient death. Many cases of CTC–related perforation have involved high-risk symptomatic patients for whom OC was either incomplete or contraindicated. No cases of symptomatic perforation resulted from patient-controlled insufflations or automated CO2 delivery. Staff-controlled manual insufflations lack the inherent safeguards of the other two methods and have accounted for virtually all known cases

Table 11.6  Working group on virtual colonoscopy experience (187) — (21,923 CTC performed between 1997 and 2005).

Figure 11.38  Normal CTC Supine Axial 2D Images.

Screening CTC (11,707 patients)

Diagnostic CTC (10,216 patients)

No cases of perforation

2 cases of perforation (1 asymptomatic, 1 symptomatic)

Note: Overall complication rate of 0.02% Symptomatic perforation rate of 0.005% (one in 21,923 patients). The 1 patient in 21,923 with a symptomatic perforation was a patient with known annular carcinoma of the sigmoid colon who was already symptomatic prior to CTC, and massive pneumoperitoneum was found after a few puffs of air were delivered.(187)

Figure 11.39  Normal CTC 3D Image of the Colon.



improved outcomes in colon and rectal surgery Table 11.7.  Results from Kim et al.(195) Primary CTC (n = 3,120)

Variable

Primary OC (n = 3,163)

Use of OC



246



3,163

# of Advanced Adenomas >10 mm 6–9 mm <5 mm Invasive Carcinoma



103 5 1 14



103 11 3 4

Note: Only 3 subcentimeter polyps with high-grade dysplasia (0.05%), and there were no subcentimeter cancers. Total of 2,006 polypectomies to remove diminutive polyps (<5 mm), which yielded only 4 advanced lesions (0.2%).

of symptomatic perforation. The risk of perforation with automated or patient-controlled distention methods approaches zero among asymptomatic adults.(190) The automated CO2 delivery is not only safe but also results in improved colonic distention and reduced spasm.(191) Although the capability of CTC to depict polyps is both operator and technique dependent, this modality has a relatively high specificity.(176, 178–181) Some of the inconsistent results in previous studies have been attributed to reader inexperience, inappropriate protocol, and lack of image software technology. CTC trials involving cohorts with protocols restricted to a primary 2D approach fared poorly (192–194), whereas those that relied on 2D and 3D polyp detection performed well (178–181, 195). Primary CT Colonography Screening with Selective Optical Colonoscopy CTC cannot replace optical colonoscopy (OC), as it is an essential diagnostic tool for the nonsurgical removal polyps. As a screening test applied to asymptomatic adults; however, OC is a relatively invasive procedure, with reported perforation rates of 0.1–0.2%. (196–200) Given that a small minority of screening patients actually harbors a clinically relevant lesion (181, 201–206), the high rate of negative screening studies may come into question now that a less invasive alternative, CTC, is becoming widely available and greatly improved from the past. Therefore, primary CTC with selective OC deserves consideration as a preferred screening strategy. In this approach patients are screened with CTC and patients with polyps >10 mm are offered same-day OC with polypectomy. Patients with polyps 6 to 9 mm are given the option of CTC surveillance or OC with polypectomy. To avoid any confusion, or anxiety, potential diminutive lesions (≤5 mm) are not reported. In a large screening study of asymptomatic adults by Kim et al. (195) (Table 11.7) found that CTC and OC screening methods resulted in similar detection rates for advanced neoplasia within the same general population. The results of this study also suggest that a 10 mm threshold for polypectomy at asymptomatic screening would probably capture the vast majority of clinically relevant lesions. The study noted scarcity of small advanced neoplastic lesions and marked decrease in the use of OC and total rates of polypectomies in the CTC group (Table 11.7); which suggests that this screening approach is a safe, clinically



effective, and cost-effective filter for therapeutic OC.(195) Markov modeling of large cohorts has also shown that the strategy of not reporting diminutive polyps (<5 mm) during CTC screening is a cost-effective approach that can substantially reduce the rate of polypectomy and complications without any sacrifice with respect to cancer prevention.(204) However, the clinical management of polyps 6 to 9 mm that are detected during CTC is controversial. One approach is to offer OC for polypectomy to all patients with polyps >6 mm.(207) An option of short-term CTC surveillance for patients with one or two small CTC-detected polyps has also been suggested.(208) Potential benefits include the decreased use of resources, procedural risks, and cost. Potential drawbacks are the possibility of following a polyp that harbors a focus of cancer. Ultimately, more investigation will be needed to determine which strategy is more beneficial for polyps <10 mm that are found during CTC. Furthermore, by combining CTC and OC screening efforts, the overall screening compliance could substantially increase.(192) CT Colonography Follow-Up after Surgery for Colorectal Cancer More than half of colorectal cancer recurrences are distant metastases to the liver and lungs (209, 210) and most local recurrences lack an intraluminal component (210). CTC is usually performed without IV contrast for screening, but CTC performed with IV contrast enhancement could accomplish the dual function of annual CT surveillance of the abdomen and liver, as well as examination of remaining colonic lumen. CTC could also have a role in postsurgical patients in whom optical colonoscopy has failed or in patients with a colostomy. The limitations of CTC in the postoperative patient include extrusion of surgical staples, inflammatory polyps, and benign ulcers. Extruded staples can be clearly distinguished from true polyps on 2D images by their high attenuation.(211) Because inflammatory polyps and benign ulcers are not distinguishable from adenomatous polyps on CTC, follow-up OC and biopsy will be needed.(211) Nevertheless, it would be efficient if CTC could eliminate through screening those patients whose colon is normal, while also performing the dual function of evaluating the entire abdomen for metastatic disease. Also, the ability of IV contrast enhanced CTC to provide images of the bowel wall, extracolonic tissues, lymph nodes, and liver in one setting may provide a more accurate preoperative staging of colorectal cancers.(212, 213) A recent study found that CTC colorectal cancer T staging overall accuracy was 73–83%, and N staging was associated with an overall accuracy of 80%. (214) Thus, contrast-enhanced CTC is a fairly accurate technique for preoperative staging of colorectal tumors.(212, 213) flouroscopy Barium Enema Single and Double Contrast Barium Enema (DCBE) Single Contrast Barium Enema is performed by filling the rectum and colon with barium through an enema catheter after inflating a retention rectal balloon. Double Contrast Barium Enema (DCBE) or Air Contrast Barium Enema (ACBE) is performed similarly, except the colon is partially filled with undiluted

limitations of colorectal imaging studies be evaluated for other synchronous neoplasms. Performance of DCBE should not be performed in patients with large bowel obstruction, acute colitis, or when there is concern for bowel perforation, as barium can cause peritonitis. In these situations, a water-soluble contrast agent should be used.(216)

Figure 11.40  Annular Carcinoma. DCBE demonstrates an annular “apple core” stricture characterized by circumferential narrowing of the bowel with mucosal destruction and shelf-like, overhanging borders.

barium. Once the barium reaches the middle transverse colon, the enema bag is lowered to the floor and the rectum is drained by gravity. Using a pneumatic bulb, room air is insufflated into the colon. The radiologist manipulates the amount of air insufflated; and analyzes the barium-coated mucosal surface to detect abnormalities. Fluoroscopic guidance allows the radiologist to optimize technical components. Afterwards, overhead radiographs are obtained in projections that the radiologist cannot obtain at fluoroscopy. Both single and DCBE can identify malignant strictures, but the double contrast of air and barium provides better visualization of the mucosa and colon polyps.(215) The radiographic appearance of the lesion depends on the profile in which the lesion is imaged and the location of the lesion relative to the barium pool. It is not possible to distinguish between the sporadic adenomatous polyps and polyposis syndromes using contrast studies.(216) The appearance of polyps and early cancers can be sessile, polypoid pedunculated, or carpet lesions. Colorectal carcinomas may manifest as polypoid, semiannular, or annular strictures. Annular strictures are characterized by circumferential narrowing of the bowel, with overhanging borders referred to as “apple core” lesions (Figure 11.40). Benign strictures from ischemic, infectious, and inflammatory processes, in contrast, tend to have smooth, tapering borders. The positive predictive value for malignant strictures on DCBE is 96% (sensitivity, 63–66%) and the positive predictive value for benign strictures is 84–88% (sensitivity, 88–86%, respectively).(217) On occasion, however, the area of narrowing in diverticulitis may have more abrupt borders and may mimic the appearance of tumor. If the barium enema examination reveals equivocal findings, colonoscopy should be performed after treatment for diverticulitis to rule out an underlying carcinoma. When annular carcinomas are nonobstructive, it usually is possible to perform DCBE so that the colon may

Limitations of Double Contrast Barium Enema (DCBE) DCBE is a valuable tool in colorectal cancer screening, but the examination is not without limitations. When lesions are missed, both perceptive/interpretive and technical errors are responsible. (218, 219) Perceptive/interpretive errors occur when lesions are overlooked because of superimposed bowel loops or are hidden by deep haustral folds. Also, polyps that are small and flat or that directly abut a haustral fold may be subtle. Another area that may pose perceptive diagnostic difficulties is the ileocecal valve. While some carcinomas arising at the ileocecal valve may be obvious polypoid lesions, others may manifest as relatively subtle splaying or distortion of the valve.(220) Incompetence of the ileocecal valve can degrade the quality of barium enemas by preventing full colonic distention and allowing the small bowel to obscure segments of the colon. Internal hemorrhoids appear either as thickened, undulating folds that extend 3 cm or less from the anorectal verge or as a cluster of small submucosal nodules that has been likened to the appearance of a bunch of grapes.(221) In many cases, internal hemorrhoids can be diagnosed confidently on the basis of the radiographic findings. On occasion, however, large or thrombosed hemorrhoids can mimic the appearance of tumor, whereas rectal carcinomas that infiltrate the submucosa can mimic the appearance of hemorrhoids.(221, 223) Digital rectal examination and/ or proctoscopy therefore should be performed whenever the radiographic findings are equivocal. Technical errors occur due to poor bowel preparation and adherent stool can be difficult or impossible to differentiate from true polypoid lesions. Regimens to prepare the colon are similar to CTC and OC. Scout images are taken before the study and if stool is seen in the colon a rescheduled barium enema examination may be performed after more rigorous bowel preparation. DCBE are a fairly safe procedure, but the referring physician should state if a recent endoscopic intervention has been performed. There should be a 1-week interval between barium enema examination and performance of large-forceps biopsy through a rigid sigmoidoscope, snare polypectomy, or hot biopsy; because these endoscopic interventions may tear the colonic mucosa and result in a small risk of perforation. Performance of a smallforceps biopsy through a flexible sigmoidoscope or colonoscope does not preclude performance of barium enema examination on the same day.(224, 225) DCBE has been exhaustively reviewed, usually retrospectively. DCBE has a sensitivity of 70% for polyps >7 mm (226–229) and a sensitivity of 81–95% in detecting polyps >1 cm in diameter (226–228). The detection rate for colorectal cancer or malignant stricture ranges from 70% to >96% (230–232). The American Cancer Society guideline for colorectal cancer screening includes DCBE examinations at 5- or 10-year intervals for patients with average risk and older than 50 years of age.(233) In conclusion, DCBE can be used to detect most polyps (>10 mm) that are at



improved outcomes in colon and rectal surgery

Figure 11.41  Ulcerative Colitis Late in the Disease. DCBE demonstrates blunting of the haustral markings with a narrow tubular appearance of the sigmoid colon, referred to as a “lead pipe colon”.

Table 11.8  Small Bowel Studies. Examination

Technique

Benefits and Limitations

Small Bowel Follow Through (SBFT)

Patient drinks barium while a series of supine abdominal films are obtained until the terminal ileum and cecum are filled.

Demonstrates the mucosal surface, but is insensitive; and limited by overlap of bowel loops, poor distension, and intermittent filling.

Small Bowel Enteroclysis

This study provides more uniform distension of the bowel, even distribution of barium, superior anatomic detail, and shorter overall examination time.

risk for malignant degeneration and provides an invaluable public service by helping to lower the mortality rate due to colorectal cancer.(234) Ulcerative Colitis Barium enema can be used to confirm the diagnosis of UC, to differentiate it from Crohn’s disease/colitis, and to assess the extent and severity of disease. The radiographic appearance of UC depends on the state of the disease process.(216) Early in the disease, the mucosa is stippled with barium adhering to the confluent, superficial ulcers. Collar button ulcers are deeper ulcerations of thickened edematous mucosa with crypt abscesses extending



Figure 11.42  Crohn’s Disease “String Sign”. Small bowel follow through demonstrates fibrosis and progressive thickening of the bowel wall that narrows the terminal ileum, producing the “string sign”.

in the submucosa. As the ulcerations enlarge, inflammatory psuedopolyps (islands of residual mucosa) and inflammatory polyps (islands of inflamed mucosa) appear as irregular projections into the bowel lumen. Late in the disease (Figure 11.41), there is blunting of the haustral markings with a narrow tubular appearance to the colon, referred to as a “lead pipe colon”.(216) The terminal ileum is usually normal, but rare backwash ileitis may produce an ulcerated and patulous terminal ileum. Barium contrast studies are not able to distinguish UC associated polyps from adenomatous polyps or dysplasia; and UC associated cancers tend to be flat or infiltrating and do not always appear as typical neoplasms. Therefore, contrast enemas are not recommended for routine surveillance.(216) Crohn’s Disease and Crohn’s Colitis The appearance of Crohn’s disease in the small bowel and the colon is similar (Table 11.8). Shallow, 1 to 2 mm depressions usually surrounded by a well-defined halo, called aphthous ulcerations, are the earliest mucosal lesions seen in Crohn’s disease. (235) Other hallmarks are: (1) thickened and distorted folds; (2) fibrosis with thickened walls, contractures, and stenosis (Table 11.3). Fibrosis and progressive thickening of the bowel wall narrow the lumen producing the “string sign” in the terminal ileum (Figure 11.42). Pseudodiverticula of the colon are formed by symmetric fibrosis on one side of the lumen, causing saccular outpouchings on the other side. Deep ulcerations are larger and often linear, forming fissures between nodules of elevated

limitations of colorectal imaging studies

Figure 11.43  Divertivulitis. Barium enema demonstrates a deformed colon wall with diverticular sacs.

edematous mucosa (“cobblestone pattern”). Contrast enemas are better than colonoscopy at identifying and characterizing fistulas, strictures, and the distribution of d ­ isease.(236) Diverticulosis and Diverticulitis Diverticula are often seen on barium enema examinations, as barium or gas-filled sacs outside the colon lumen. Barium enema examination is considered safe for diverticulitis, except when signs of free intraperitoneal perforation or sepsis are present. Diverticulitis appears as deformation of the colon wall in association with diverticular sacs (Figure 11.43), and occasionally extravasation of barium outside the colon lumen. Abscess can cause extrinsic mass effect on the adjacent colon and barium can leak into the abscess cavities. A colovesical fistula is the most common diverticular associated fistula, but contrast enemas are able to make the diagnosis only 20% of the time.(237) Colonic Lymphoma, Submucosal, and Extracolonic Lesions Lymphoma can appear as small or large nodules, which may ulcerate and perforate. Diffuse infiltration of the bowel wall results in bulbous folds and thickened bowel wall. In contrast to primary colorectal cancer, narrowing of the lumen is uncommon, and dilation occurs when transmural disease destroys innervations. Endometriosis commonly implants on the sigmoid colon and rectum.(238) Defects are frequently multiple and of variable size. Barium studies demonstrate sharply defined defects that compress, but do not usually encircle the lumen. Benign pelvic masses such as ovarian cysts, cystadenomas, teratomas, and uterine fibroids produce smooth extrinsic mass impressions on the colonic wall, which is displaced but not invaded. Malignant pelvic tumors and metastases involved with the colon often cannot be differentiated from primary tumors by imaging methods, and

Figure 11.44  Cecal Volvulus. Water soluble contrast enema demonstrates a beak like termination at the point of obstruction in the ascending colon with a markedly dilated cecum seen high in the abdomen.

Crohn’s disease may look similar. Lipomas appear as a smooth, well-defined, round filling defect, usually 1 to 3 cm in diameter. The tumors are soft and change shape with compression.(239) (CT can confirm. See CT scan: other tumors of the colon). Water-Soluble Contrast Enema Volvulus and Intussusception Sigmoid volvulus appears as obstruction that tapers to a beak at the point of the twist, usually approximately 15 cm above the anal verge. Mucosal folds spiral into the beak at the point of obstruction. Cecal volvulus appears as a beak like or twisted termination at the point of obstruction in the ascending colon with a dilated cecum high in the abdomen (Figure 11.44). Ileocoloc and colocolic intussusception on contrast studies demonstrate barium trapped between the intussusceptum and the receiving bowel, forming a coiled-spring appearance. Postoperative Complications and Anastomotic Assessment Water-soluble contrast enemas are frequently used postoperatively to examine a colocolic, colorectal, coloanal, or ileal— anal anstomosis.(240) The studies are performed by retrograde



improved outcomes in colon and rectal surgery

Figure 11.45  Anastomotic Leak. Water soluble contrast enema shows extravasation of contrast into the presacral space.

Figure 11.46  Anastomotic stricture. Small bowel follow through and water soluble contrast enema demonstrate an ileal pouch–anal anastomotic stricture.



Figure 11.47  Normal Defecogram. Lateral radiograph is obtained with the patient in a neutral position after a thick barium paste is placed into rectum.

Figure 11.48  Anorectal Angle. The anorectal angle is created by the intersection of the long axis of the anal canal and a line drawn along the posterior wall of the rectum.

limitations of colorectal imaging studies administration of a water-soluble contrast under the weight of gravity or by direct hand injection via a catheter inserted into the anal canal. Radiographic findings of an anastomotic leak include the extravasation of contrast freely into the peritoneal cavity or into a contained cavity (Figure 11.45). Water-soluble contrast enema is more sensitive than CT with rectal contrast.(240) Total proctocolectomy and ileal pouch—anal anastomosis (Figure 11.46) complications include anastomotic stricture.(241–244) Some studies have cited an anastomotic diameter of 8 mm or less as the threshold value for diagnosing strictures that may need dilatation procedures before ileostomy closure.(245) Physiologic Examinations Chronic constipation and incontinence are common complaints with many possible etiologies. Multiple examinations are available to assess the physiology of the lower GI tract, including defecography, anorectal manometry, balloon proctography, and colon transit studies. Defecography Defecography (evacuation proctography) is a dynamic evaluation of the anatomy and mechanics of defecation. A thick barium paste is deposited within the rectum. Static lateral images are obtained with the patient in a neutral, anal contraction, and straining position. Fluoroscopic video is then obtained during the act of defecation. The static images allow measurement of the anorectal angle, the angle created by the anal canal, and posterior wall of the rectum (246) (Figure 11.47 and 11.48). As the patient defecates, the anorectal angle should straighten and approach 180 degrees. Abnormally high or low anorectal angles suggest a mechanical cause for the patient’s constipation. The length that the anorectal junction descends during defecation can be measured as well. An abnormal length of descent (>5 cm) of the anorectal junction can be a source of pudendal nerve damage and, if chronic, incontinence.(247) The most common abnormality detected by defecogram is a rectocele. A rectocele is an outpouching of the rectum, usually along the anterior wall. Retained barium in the rectocele can document incomplete rectal evacuation. In severe cases of rectoceles, internal rectal prolapse can be observed by defecogram. A negative defecogram can exclude such conditions as enteroceles, sigmoidoceles, rectal prolapse, rectal intussusception, puborectalis muscle dysfunction, and posterolateral pouches. Colorectal Transit Colorectal transit times can be documented by having the patient ingest a barium meal and obtaining serial abdominal radiographs. All the barium should be cleared in a normal patient in 4 days. Retained barium after 4 days confirms delayed colorectal transit time.(248) An alternative method utilizes radiopaque rings (Sitzmarkers®, Konsyl Pharmaceuticals, Ft Worth, TX) to assess colonic transit time. Twenty four markers are ingested. The patient is instructed not to use enemas, laxatives, or suppositories for 5 days. Radiographs are obtained daily or on days 1, 3, and 5.(249) Eighty percent of the markers should pass in 5 days and all of the markers normally pass by the seventh day.(246, 248) The diagnosis of colonic hypomotility/inertia is suggested if there is delayed transit time and the markers are scattered evenly

throughout the colon. A functional outlet obstruction, such as rectal prolapsed or anismus, is suggested if there is delayed transit time with clustering of the radiopaque markers in the rectosigmoid colon.(246) Anorectal Manometry and Balloon Proctography Anorectal manometry is performed to assess rectal sensation and motor function. The rectum is distended by a balloon. The normal response to rectal distention is contraction of the external anal sphincter and relaxation of the internal anal sphincter. Loss of this reflex can be detected by anorectal manometry and can be seen in Hirschsprung’s disease or severe idiopathic constipation.(249) Balloon proctography is a similar examination where the rectal balloon is filled with a contrast material, allowing visualization of the rectum. Visual assessment of the rectum with calculation of the anorectal angle can be performed in addition to measurement of the anorectal pressure.(248) Some studies suggest that balloon proctography is less sensitive than defecography in detecting certain anatomic abnormalities, including rectoceles. ultrasonography (us) Transabdominal Ultrasound and Intraoperative Ultrasound (IUS) Ultrasonography (US) utilizes sound waves to provide real time imaging of the body. A transducer is placed on the patient that not only generates sound waves (of a single frequency) but also detects the reflected echoes. US can successfully image solid ­visceral organs and fluid filled structures. US is superb at differentiating between cystic and solid structures, and is frequently

Figure 11.49  Appendicitis. Axial view of the appendix reveals a thickened and hypoechoic wall. An appendicolith is represented by the hyperechoic material seen within the lumen (arrow).



improved outcomes in colon and rectal surgery

Figure 11.50  Colon Cancer Liver Metastasis. US of the liver demonstrates an isoechoic mass with a hypoechoic peripheral halo. This “target” appearance can be seen in a variety of disease processes but is a common finding in metastatic colon cancer and hepatocellular carcinoma.

Figure 11.52  Normal Endoluminal Ultrasound.

Figure 11.51  Normal Layers of Colon on Intrarectal ultrasound (Graphic representation of 5 layers).

called to do so. The US beam will be completely reflected by bone and sufficiently scattered by air to thwart imaging distal to these substances. When the transmitted sound wave reflects off a moving target, the returning echo will have a slightly different frequency (the Doppler Effect). Doppler US capitalizes on this principle and allows the determination of direction and velocity of a mobile target.(250) The most frequent application for Doppler US is the detection and quantification of blood flow. Specifically, Doppler US is extremely helpful in evaluating the upper and lower extremities for deep venous thrombosis. US has many advantages. It is an inexpensive, widely available modality that provides real time, multiplanar images with no radiation exposure to the patient. The US equipment is mobile, allowing critically ill patients to be imaged within the ICU. The structures that can be studied by US include arteries, veins, liver, spleen, gallbladder, bile ducts, pancreas, kidneys, bladder, uterus, and ovaries. Transabdominal US is typically limited in its evaluation of the gastrointestinal tract. Intraluminal bowel gas will obscure the surrounding anatomy. Therefore, patients should be NPO for 4 to 8 hours before being imaged to reduce the volume



Figure 11.53  Ultrasound of uT3 rectal mass.

of intraluminal gas.(251) Nonetheless, US can detect abnormal loops of bowel. Wall thickening, hyperemia, fecoliths, bowel distention, wall edema, and noncompressibility all can be detected by ultrasound and suggest intestinal pathology. US can be helpful in diagnosing a wide variety of disease processes including appendicitis (Figure 11.49), intussusception, inflammatory bowel disease, colitis (from numerous causes), and neoplasm (Figure 11.50). Due to the superior sensitivity and specificity of other imaging modalities, US evaluation of the bowel is typically reserved for situations where limitation of radiation exposure is desired (i.e., pediatric and pregnant patients).

limitations of colorectal imaging studies Intraoperative ultrasound (IUS) can provide important information to the surgeon and is commonly used to evaluate the liver for metastatic disease and guide the subsequent metastasectomy. IUS is particularly useful in delineating the relationship between hepatic tumors and adjacent vasculature.(252) Studies have shown that IUS provides vital information to the surgeon during the procedure that will affect surgical decision making in up to 38% hepatic metastasectomy.(251) Endoluminal Ultrasound Endoluminal ultrasound’s (EUS) impact on the workup for colorectal cancer continues to expand. Transrectal US appears to be the most accurate imaging modality in determining the extent of local invasion of rectal cancer.(253) EUS can delineate the components of the intestinal wall. Images typically consist of five rings of different echogenicity (3 hyperechoic and 2 hypoechoic) that allow the localization of the mucosa, muscularis mucosa, submusoca, muscularis propria, and serosa (254)) (Figure 11.51). Colorectal tumors will appear as a hypoechoic mass that distorts the normal bowel architecture (Figure 11.52 and 11.53). EUS can accurately identify the specific layers of the bowel wall invasion, thereby elucidating the tumor stage.(255) Recent studies have shown that transrectal US has difficulty differentiating between tumor and peritumoral inflammation, thereby producing a tendency to over stage a recently diagnosed cancer. EUS is often used in conjunction with traditional endoscopy to allow direct visualization of the mucosa, assess the depth of wall involvement, facilitate biopsy, and evaluate for pericolonic lymphadenopathy. While EUS has the ability to detect local lymph node involvement, cross sectional imaging (CT, MRI, or PET) is still needed to evaluate for regional and distant metastatic disease.(255) Nononcologic applications of EUS include the evaluation of the colon, rectum, and anus for strictures, fistulas, and abscesses. Transanal US is often used in the evaluation of incontinence as it can detect defects within the internal anal sphincter, external anal sphincter, puborectalis sling, and pelvic musculature.(254) magnetic resonance imaging (mri) In magnetic resonance imaging, strong magnetic fields and targeted radiofrequency pulses are harnessed to map the location of protons within the body. Depending on the specific imaging parameters utilized, protons within fat (T1 MRI sequences), or water (T2 MRI sequences) can be selectively displayed. Ionizing radiation and iodinated contrast agents are not used. MRI images are degraded by motion and the combination of bowel peristalsis and diaphragmatic movement has traditionally limited the application of MRI in the evaluation of gastrointestinal pathology. (254) Ferromagnetic metals cannot be taken into the magnetic field and therefore most surgical implanted devices have been transitioned to MRI compatible materials. Care must still be taken with certain implanted devices as the strong magnetic field may cause malfunction. Confirmation of MRI compatibility with the manufacturer is required for implanted devices such as cardiac pacemakers, cochlear implants, spinal cord stimulators, and basal ganglion stimulation devices. Nephrogenic systemic fibrosis (NSF) is a disorder seen exclusively in patients with chronic renal insufficiency that presents with diffuse systemic sclerosis with

(a)

(b)

Figure 11.54  A and 11.54B Terminal Ileitis in Crohn’s Disease. Axial (A) and coronal (B) T1-fat saturated MRI images demonstrate mucosal enhancement within the terminal ileum (arrow) with no enhancement in the adjacent normal ileum (arrow head). The mucosal enhancement indicates active terminal ileitis.

particularly severe cutaneous fibrosis. In 1997, NSF was linked to gadolinium exposure in patients with renal insufficiency. The FDA has recently placed a black box warning on gadolinium ­containing MRI contrast agents.(256) Technological advancement with quicker image acquisition has reduced motion blurring and has allowed the diagnostic assessment of the sigmoid colon and rectum (anatomically fixed structures). (257) While MRI can be useful in the diagnosis of inflammation of the GI tract (for example, appendicitis, Crohn’s disease, and ulcerative colitis) (Figure 11.54), the largest advances have been made in evaluation of colorectal cancer.(254) The effectiveness of MRI is similar to CT for the initial staging of colorectal tumors.(258) MRI is very accurate evaluating the pelvis for local rectal tumor



improved outcomes in colon and rectal surgery (a)

Figure 11.55  Perirectal Mass. Fluid sensitive (STIR) T2 MRI of the pelvis shows a hyperintense mass adjacent to the rectum, worrisome for rectal carcinoma. However, after resection, this mass was found to be a high grade liposarcoma.

extension (Figure 11.55), and has an advantage over CT in the evaluation of tumoral invasion of the levator ani, mesorectal fascia, internal and external sphincter muscles.(258–259) Endorectal MRI is a promising new technique that can help evaluate the depth of local tumor invasion. Endorectal ultrasound has been shown to be equally sensitive and specific as our currently available endorectal MRI and can be performed in a fraction of the time.(258, 260) MRI is also a valuable tool in detecting distant metastatic disease. Metastatic foci within the brain, skeleton, and liver are readily detected with MRI. Local tumor recurrence can be differentiated from mature fibrosis if the surgical resection was at least 1 year prior. Unfortunately, immature fibrosis (<1 year old) cannot be successfully distinguished from recurrent tumor with MRI.(258, 259)

(b)

(c)

nuclear medicine imaging Positron Emission Tomography Positron Emission Tomography (PET) has been approved by Medicare for the diagnosis, staging, and restaging of colorectal cancer since 2001.(261) Unlike other imaging modalities that rely on architectural distortion, PET scans detect neoplasm based on physiologic differences between normal tissue and cancer cells. Malignant cells have a higher baseline metabolic state, increased mitotic activity, and consume more glucose. PET scans utilize the glucose analog F-18 fluorodeoxyglucose (F-18 FDG). F-18 FDG is transported into the cell through transmembrane glucose transporters but, unlike glucose, it does not undergo further metabolism.(261, 262) This causes an accumulation of F-18 FDG within the tumor cell. Fluorine-18 emits positrons that subsequently undergo annihilation when contacted by electrons. This annihilation produces gamma photons that are summated by specialized detectors and allow image generation. The photon count and inferred amount of glucose uptake is reported in standard uptake values (SUVs). The SUV takes into consideration the dose of F-18 FDG injected and body surface



Figure 11.56  A–11.56C Comparison between CT and PET. Figure 11.56A demonstrates multiple discrete areas of hypermetabolism within the liver on PET scan, representing metastatic colon adenocarcinoma. Figure 11.56B shows a noncontrast CT scan of the same patient. The multiple metastatic foci are nearly impossible to detect without contrast. Figure 11.56C. Iodinated contrast helps to delineate between normal hepatic tissue and hypodense metastatic disease.

limitations of colorectal imaging studies

Figure 11.57  PET-CT. PET-CT images show a focal area of hypermetabolic activity in the presacral space, adjacent to the patient’s low anterior resection site for rectal cancer, representing an area of recurrence. Note that this lesion may have been overlooked on the noncontrast CT.

area.(261) In general, a SUV value above 2.5 is suspicious for malignancy but may also be secondary to an inflammatory or infectious process.(262) Care must be taken when relying on SUVs as they are only semi-quantitative and many variables affect the reported numeric value. One particularly strong variable is the serum glucose. A high serum glucose level will reduce tumor uptake of F-18 FDG and lower SUV values. Patients typically fast overnight and avoid carbohydrates before the procedure.(262) Blood glucose levels are checked before the examination with a level below 200 mg/dl desired. PET imaging of the colon is very sensitive (>90%) but lacks specificity (40–60%) due to physiologic bowel glucose uptake and hypermetabolic benign lesions, including colitis and benign polyps.(262) The main advantage of PET is its superiority over CT in the detection of metastatic colorectal cancer. PET will detect increased glucose metabolism in regional lymph nodes or distant metastatic sites (Figure 11.56) that do demonstrate enough architectural distortion to be detected as abnormal by CT examination. PET has also been shown to be superior to CT in the evaluation of colorectal cancer recurrence (Figure 11.57) (263). PET can help monitor response to chemotherapy and radiation treatment but does not have the ability to detect microscopic residual disease (262). One of the main limitations of PET is low spatial resolution. This problem has largely been overcome by a new technique that allows the concurrent acquisition of PET and CT images during a single examination. PET/CT augments the localization of malignancy in contiguous or overlapping structures.(262) Differentiation of tumor from infection is problematic when the standard uptake value is only minimally elevated as regional lymphocytes will metabolize an abundance of F-18 FDG. Likewise, colonic adenomas/polyps can demonstrate hypermetabolism and be misinterpreted as a tumor. Tumors that have a low cell density, small size, or low metabolic activity (including carcinoid and mucinous adenocarcinoma) have a higher likelihood of a false-negative result.(261, 262)

Gastrointestinal Scintigraphy Nuclear medicine scintigraphy is a useful tool for the colorectal surgeon. A biologically significant substance (RBC, leukocyte) is labeled with a radioactive isotope that will subsequently emit gamma radiation. These gamma photons are detected by scintillation cameras and diagnostic images are generated. Nuclear medicine scintigraphy is especially helpful in answering a specific question. The evaluation for intraabdominal abscess, Meckel’s diverticulum, carcinoid tumor, biliary abnormality, pernicious anemia, and colonic transit time can be performed with radioisotope labeled leukocytes, technetium, octreotide, iminodiacetic acid, vitamin B12, and diethylene triamine pentaacetic acid (DTPA), respectively.(264) With the expanding use of fused PET-CT imaging, traditional nuclear medicine scintigraphy has a limited role in the management of colorectal neoplasia. In tumors that are known to have high false negative PET rates (i.e., mucinous adenocarcinoma), radioisotope labeled monoclonal antibodies may help in evaluating for occult metastatic disease or recurrence.(264, 265) While multiple monoclonal antibodies have been approved by the FDA, none are currently in widespread clinical use.(266) Tc-99m red blood cell scintigraphy is a frequently utilized examination for the evaluation of lower gastrointestinal bleeding. The patient’s RBCs are labeled with the radioisotope technetium-99m (employing either an in-vivo or in-vitro method) in an attempt to identify red blood cells within the lumen of the GI tract, thereby localizing the source of bleeding. Three criteria are needed to confirm a gastrointestinal bleed. The radiotracer uptake pattern should conform to bowel anatomy, increase in intensity over time, and propagate in an antegrade or retrograde fashion (Figure 11.58). Multiple intraabominal abnormalities, including hepatic hemangiomas, accessory splenic tissue, or colonic angiodysplasia, can simulate a GI bleed but these abnormalities will not change in location over time. A false negative Tc-99m RBC scintigram can be secondary to a slow intestinal bleeding rate or an intermittent bleed.(266) The reported



improved outcomes in colon and rectal surgery (a)

Figure 11.59  Percutaneous Abscess Drainage. Axial CT image demonstrates needle placement into the large fluid/air filled abscess.

(b)

and is a sensitive tool that can help isolate the vascular territory of a bleed and direct percutaneous or surgical intervention.(266, 267) In an unstable patient, a Tc-99m sulfur colloid can be used to detect GI bleeding. Sulfur colloid scintigraphy requires less time for patient preparation and image acquisition but has a lower sensitivity for detecting gastrointestinal bleeding. interventional radiology

Figure 11.58  A and 11.58B. Lower Gastrointestinal Bleeding. Figure 11.58A shows a single image of a Tc-99m red blood cell scintigram with a GI bleed originating in the transverse colon, near the hepatic flexure. Figure 11.58B is taken 5 minutes later and shows the radiotracer uptake pattern conforming to bowel and moving in an antegrade fashion towards the splenic flexure.

sensitivity and specificity of Tc-99m RBC imaging has been reported as high as 93% and 95%, respectively.(264, 266) Tc-99m RBC scintigraphy can detect GI bleeding rates as low as 0.2 cc/ minute (compared to 1.0 cc/minute for traditional angiography),



Gastrointestinal (GI) Bleeding The angiographic diagnosis of GI bleeding is based upon visualization of extravasation of contrast into the bowel lumen, and a high rate of bleeding (1 cc/min) is required to visualize extravasation.(268) Angiograms are positive in only about 50% of patients, and a positive Tc-99m RBC scintigraphy scan within the first 5–9 minutes, makes angiography more likely to identify extravasation.(269) The two techniques used for lower GI arterial bleeding are vasopressin infusion and embolization. Vasopressin (pitressin) infused into the proximal SMA or IMA causes both smooth muscle constriction and water retention. Vasopressin can control lower GI bleeding in up to 90% of cases, and half of the patients will never bleed again. Vasopressin requires monitoring in an ICU. Rare complications include cardiac or digital ischemia from vasoconstriction, or hyponatremia from water retention.(268–270) Embolization controls GI bleeding by decreasing the arterial pressure and flow to the point that hemostasis can occur, without creating symptomatic ischemia. Large particles, Gelfoam, or microcoils can be used. Embolization is successful in over 90% of cases, with few instances of bowel ischemia. Rebleeding is reported to occur in 20% of patients. Patients should be monitored for bowel ischemia. Delayed ischemic colonic strictures have been reported.(268–270) Percutaneous Abscess Drainage (PAD) Percutaneous abscess drainage (PAD) has played a major role in decreasing the morbidity and mortality associated with surgical

limitations of colorectal imaging studies

Figure 11.60  US Guided Biopsy of Colon Cancer Liver Metastasis. US image demonstrates needle placement into hepatic tumor of uncertain etiology. This was proven to be metastatic colon adenocarcinoma by pathology.

exploration. CT is the most appropriate modality in image guided PAD (Figure 11.59).(271) PAD of an intraabdominal abscess is effective with a single treatment in 70% of patients and increased to 82% if a second drainage is performed.(272) The overall findings from a large series of 2311 PADs report a success rate of 80–85%.(273) Complication rates of PAD are between none and 10%. Vascular laceration may occur and, if the vessel is small, the bleeding will usually stop spontaneously.(274) Percutaneous abscess drainage may be complicated by bowel perforation from the needle or catheter transversing the bowel. If the patient develops signs of peritonitis after catheter penetration of bowel, then surgical intervention may be required.(275) Image-guided Percutaneous Biopsy The majority of image-guided biopsies can be performed on an outpatient basis. All interventional procedures can result in bleeding, but this complication can be reduced by correction of any coagulopathy before the procedure.(276) US offers the advantage of real-time needle visualization, low cost, portable, and no ionizing radiation (Figure 11.60). US guidance can be problematic in obese patients because the echogenic needle can be hard to visualize in echogenic fat. Lesions located deep to bone or bowel cannot be biopsied with US owing to lack of visualization of the lesion. CT can be used to guide biopsy needles to virtually any area of the body. CT provides excellent visualization of lesions and allows accurate identification of organs between the skin and the lesion.(277) Disadvantages of CT include increased cost, ionizing radiation, and longer procedure times. Complications of abdominal, liver, or lung biopsy include bleeding, introducing infection, pneumothorax, and hemoptysis. Postprocedure pneumothorax may occasionally require chest tube placement and observation in the hospital.(276, 277) Radiofrequency ablation (RFA) and Chemoembolization of Hepatic Metastasis Radiofrequency ablations (RFA) of liver metastasis are performed similar to image-guided needle biopsy, with the RF

probe taking the place of the needle. The RF probe is placed in the hepatic tumor and vibrates at a high frequency, conducting heat into and ablating the tumor.(278). Studies show that the overall 5-year survival rate for colorectal liver metastasis treated by RF ablation is similar to surgical series (25–40%). (279) There are no absolute contraindications, and relative contraindications include low platelets and coagulopathy. RFA of hepatic tumors is associated with very low complication rates, generally below 2%. Complications include pain, pleural effusion, bleeding, and abscess formation.(278) The treatment of certain tumors (metastatic hepatic lesions) with intravascular delivery of chemotherapeutic agents can be ­palliative and prolong life, but is not considered curative.(280) A wide variety of chemotherapeutic regimens are used. These chemotherapeutic medications are usually mixed with an embolic agent that slows flow and allows the drugs to remain in the organ. Metastatic disease to the liver can also be embolized by Yttrium-loaded microspheres that emit beta-radiation. Fulminant hepatic failure or liver abscess formation occurs in <1% of patients. Gallbladder infarction due to chemoembolization is rare. (280–282) references    1. Bluth EI, Locascio LF Jr, Head SC, Smetherman D. Diagnostic imaging. In Beck DE, ed. Handbook of colorectal surgery. St. Louis: Quality Medical Publishing, 1997: 39–62.    2. Brant WE, Helms CA. Fundamentals of Diagnostic Radiology, 3rd ed, Vol III. Lippincott Williams & Wilkins, 2006: 737.    3. Maglinte DD, Kelvin FM, Sandrasegaran K et al. Radiology of small bowel obstruction: contemporary approach and controversies. Abdom Imaging 2005; 30: 160–78.    4. Brant WE, Helms CA. Fundamentals of Diagnostic Radiology, 3rd ed, Vol III. Lippincott Williams & Wilkins, 2006: 743.    5. Mutch MG, Birnbaum EH, Menias CO. ASCRS Textbook of Colon and Rectal Surgery, Chapter 6. New York: SpringerVerlag, 2006: 69–70.    6. Brant WE, Helms CA. Fundamentals of Diagnostic Radiology, 3rd ed, Vol III. Lippincott Williams & Wilkins, 2006: 745.    7. Levine MS. Plain film diagnosis of the acute abdomen. Emerg Med Clin North Am 1985; 3: 541–62.    8. McCook TA, Ravin CE, Rice RP. Abdominal radiography in the emergency department: a prospective analysis. Ann Emerg Med 1982; 11: 7–8.    9. Ahn SH, Mayo-Smith WW, Murphy BL, Reinert SE, Cronan JJ. Acute nontraumatic abdominal pain in adult patients: abdominal radiography compared with CT evaluation. Radiology 2002; 225: 159–64.   10. MacKersie AB, Lane MJ, Gerhardt RT et al. Nontraumatic Acute Abdominal Pain: Unenhanced Helical CT Compared with Three-View Acute Abdominal Series. Radiology 2005; 237: 114–22.   11. Birnbaum BA, Jeffrey RB Jr. CT and sonographic evaluation of acute right lower quadrant pain. AJR Am J Roentgenol 1998; 170: 361–71.

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improved outcomes in colon and rectal surgery 221. Levine MS, Kam LW, Rubesin SE, Ekberg O. Internal hemorrhoids: diagnosis with double-contrast barium enema examinations. Radiology 1990; 177: 141–4. 222. MacCarty RL. Colorectal cancer: the case for barium enema. Mayo Clin Proc 1992; 67: 253–7. 223. Kahn S, Rubesin SE, Levine MS, Laufer I, Herlinger H. Polypoid lesions at the anorectal junction: barium enema findings. AJR Am J Roentgenol 1993; 161: 339–42. 224. Harned RK, Consigny PM, Cooper NB. Barium enema examination following biopsy of the rectum or colon. Radiology 1982; 145: 11–6. 225. Maglinte DDT, Strong RC, Strate RW et al. Barium enema after colorectal biopsies: experimental data. AJR Am J Roentgenol 1982; 139: 693–7. 226. Thoeni RF, Menuck L. Comparison of barium enema and colonoscopy in the detection of small colonic polyps. Radiology 1977; 124: 631–5. 227. Ott DJ, Gelfand DW, Wu WC, Kerr RM. Sensitivity of double-contrast barium enema: emphasis on polyp detection. AJR Am J Roentgenol 1980; 135: 327–30. 228. Ott DJ, Chen YM, Gelfand DW, Wu WC, Munitz HA. Singlecontrast vs double-contrast barium enema in the detection of colonic polyps. AJR Am J Roentgenol 1986; 146: 993–6. 229. Glick S, Wagner JL, Johnson CD. Cost-effectiveness of ­double-contrast bariumenema in screening for colorectal cancer. AJR Am J Roentgenol 1998; 170: 629–36. 230. Beggs I, Thomas BM. Diagnosis of carcinoma of the colon by barium enema. Clin Radiol 1983; 34: 423–5. 231. Fork FT. Reliability of routine double contrast examination of the large bowel: a prospective study of 2590 patients. Gut 1983; 24: 672–7. 232. Rex DK, Rahmani EV, Haeman JH. Relative sensitivity of colonoscopy and barium enema for detection of colorectal cancer in clinical practice. Gastroenterology 1997; 112: 17–23. 233. Byers T, Levin B, Rothenberger D, Dodd GD, Smith RA. American Cancer Society guidelines for screening and surveillance for early detection of colorectal polyps and cancer: update 1997. Ca Cancer J Clin 1997; 47: 154–60. 234. Rice RP. Lowering death rates from colorectal cancer: challenge for the 1990s. Radiology 1990; 176: 297–301. 235. Hizawa K, Iida M, Kohrogi N et al. Crohn’s disease: early recognition and progress of aphthous lesions. Radiology 1994; 190: 451–4. 236. Nolan DJ, Traill ZC. The current role of barium examinations of the small intestine. Clin Radiol 1997; 52: 809–20. 237. Najjar SF, Jamal MK, Savas JF et al. The spectrum of colovesical fistula and diagnostic paradigm. Am J surg 2004; 188: 617–21. 238. Szucs RA, Turner MA. Gastrointestinal tract involvement by gynecologic disease. Radiographics 1996; 16: 1251–70. 239. Thompson, WM. Imaging and findings of lipomas of the gastrointestinal tract. AJr Am J Roentgenol 2005; 184: 1163–71. 240. Mutch MG, Birnbaum EH, Menias CO. Diagnostic Evaluations-Radiology. In ASCRS Textbook of Colon and Rectal Surgery, Chapter 6. New York: Springer-Verlag, 2006: 82–3.

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241. Marcello PW, Roberts PL, Schoetz DJ et al. Long-term results of the ileoanal pouch procedure. Arch Surg 1993; 128: 500–3. 242. Fazio VW, Ziv Y, Church JM et al. Ileal pouch–anal anastomoses complications and function in 1005 patients. Ann Surg 1995; 222: 120–7. 243. Alfisher MM, Scholz FJ, Roberts PL, Counihan T. Radiology of ileal pouch–anal anastomosis: normal findings, examination pitfalls, and complications. RadioGraphics 1997; 17: 81–98. 244. Prudhomme M, Dozois RR, Godlewski G, Mathison S, Fabbro-Peray P. Anal canal strictures after ileal pouch–anal anastomosis. Dis Colon Rectum 2003; 46: 20–3. 245. Dolinsky D, Levine MS, Stephen E. Utility of contrast enema for detecting anastomotic strictures after total proctocolectomy and ileal pouch–anal anastomosis. AJR 2007; 189: 25–9. 246. Houston JD, Davis M. Fundamentals of Fluoroscopy. Philadelphia: W.B. Saunders Company, 2001: 88–90. 247. Halper RD. Gastrointestinal Imaging: The Requisites. Philadelphia: Mosby, 2006: 322–4. 248. Hicks HC et al. Complication of Colon & Rectal Surgery. Lippincott Williams & Wilkins, 1996: 71–3. 249. Gore RM, Levine MS. Textbook of Gastrointestinal Radiology, 2nd edition. Philadelphia: W.B. Saunders Company, 2000: 905–13, 112. 250. Middleton WD, Kurtz AB, Hertzberg BS. Ultrasound: The Requisites, 2nd edition. St. Louis: Mosby, 2004: 220–4. 251. Boutkan H, Luth W, Meyer S et al. The impact of intraoperative ultrasonography of the liver on the surgical strategy of patients with gastrointestinal malignancies and hepatic metastases. Eur J Surg Oncol 1992; 18: 342–6. 252. Kruskal JB, Kane RA. Intraperative US of the Liver: Techniques and Clincal Applications. RadioGraphics, 2006: 1067–84. 253. Bipat S, Glas AS, Slors FJ et al. Rectal cancer: local staging and assessment of lymph node involvement with endoluminal US, CT, and MR Imaging – A Meta-Analysis. Radiology 2004; 232(3): 773–83. 254. Yamada T, Alpers DH, Laine L, et al. Textbook of Gastro­ enterology 4th Edition. Philadelphia: Lippincott Williams & Wilkins, 2003: 3139–55, 3184–98. 255. Gore RM, Levine MS. Textbook of Gastrointestinal Radiology, 2nd edition. Philadelphia: W.B. Saunders Company, 2000: 1031–3. 256. MacCarthy EP et al. http://www.fda.gov/medwatch/safety/ 2007/gadolinium_DHCP.pdf. www.fda.gov. 9/12/2007. 257. Haaga JR, Lanzieri CF, Gilkeson RC. CT and MR Imaging of the Whole Body 4th Edition. St. Louis: Mosby, 2003: 1238–58. 258. Gore RM, Levine MS. Textbook of Gastrointestinal Radiology, 2nd edition. Philadelphia: W.B. Saunders Company, 2000: 86–97. 259. Beets-Tan RG, Beets GL. Rectal Cancer: Review with Emphasis on MR Imaging. Radiology 2004; 232(2):335–46. 260. Bipat S, Glas AS, Slors FJ et al. Rectal Cancer: Local Staging and Assessment of Lymph Node Involvement with Endoluminal US, CT, and MR Imaging – A Meta-Analysis. Radiology 2004; 232(3): 773–83.

limitations of colorectal imaging studies 261. Ziessman HA et al. Nuclear Medicine: The Requisites. Philadelphia: Mosby, 2006: 302–45. 262. Mettler FA, Guiberteau MJ. Essentials of Nuclear Medicine Imaging. Philadelphia: Suanders Elsevier, 2006: 359–422. 263. Gore RM, Levine MS. Textbook of Gastrointestinal Radiology, 2nd edition. Philadelphia. W.B. Saunders Company, 2000: 1043. 264. Ziessman HA et al. Nuclear Medicine: The Requisites. Philadelphia: Mosby, 2006: 346–83. 265. Gore RM, Levine MS. Textbook of Gastrointestinal Radiology, 2nd edition. Philadelphia. W.B. Saunders Company, 2000: 1033–34. 266. Mettler FA, Guiberteau MJ. Essentials of Nuclear Medicine Imaging. Philadelphia: Saunders Elsevier, 2006: 215–9, 322. 267. Hicks HC et al. Complication of Colon & Rectal Surgery. Lippincott Williams & Wilkins, 1996: 69–70. 268. Darcy M. Clinical management of gastrointestinal bleeding. In: Murphy TP, Benenati JF, Kaufman JA, eds. Patient Care in Interventional Radiology, SCVIR, Fairfax, VA, 1999. 269. Hastings GS. Angiographic localization and transcatheter treatment of gastrointestinal bleeding. Radiographics 2000; 20: 1160–8. 270. Gomes AS, Lois JF, McCoy RD. Angiographic treatment of gastrointestinal hemorrhage: comparison of vasopressin infusion and embolization. AM J Roentgenol 1986; 146: 1031–7. 271. Lambiase RE. Percutaneous abscss and fluid drainage: a critical review. Cardiovasc Interv Radiol 1991; 14: 143–57.

272. Cinat ME, Wilson SE, Din AM. Determinants for successful percutaneous image-guided drainage of intra-abdominal abscess. Arch Surg 2002; 137: 845–9. 273. Catalano OA, Hahn PF, Hooper DC, Mueller PR. Efficacy of percutaneous abscess drainage in patients with vancomycin-resistant enterococci. AJR 2000; 175: 533–6. 274. Boland GW, Lee MJ, Dawson SI et al. Percutaneous abscess drainage complications. Semin Interv Radiol 1994; 11: 267–75. 275. Lambiase RE, Cronan JJ, Dorfman GS et al. Postoperative abscesses with enteric communication percutaneous treatment. Radiology 1989; 171: 497–500. 276. Bernardino ME. Percutaneous biopsy. Am J Roentgenol 1984; 142: 41–5. 277. Charboneau JW, Reading CC, Welch TJ. CT and sonographically guided needle biopsy: current techniques and new innovations. Am J Roentgenol 1990; 154: 1–10. 278. McGahan JP, Ddd GD. Radiofrequency ablation of the liver current status. Am J Roentgenol 2001; 176: 3–16. 279. Wood BJ, Ramkaransingh JR, Fojo T, Walther MM, Libutti SK. Percutaneous tumor ablation with radiofrequency. Cancer 2002; 94: 443–51. 280. Sullivan KI. Hepatic artery chemoembolization. Semin Oncol 2002; 29: 145–51. 281. Perler BA, Becker GJ eds. Vascular Intervention: a Clinical Approach. Thieme medical Publisher, New York, 1998. 282. Kerr DJ, McArdle CS, Ledermann J et al. Intrahepatic arterial versus intravenous fluorouracil and folinic acid for colorectal cancer liver metastases: a multicenter randomized trial. Lancet 2003; 361: 368–73.

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12

Transanal endoscopy Terry C Hicks

challenging case A 60-year-old woman with a strongly positive family history of colorectal cancer undergoes a colonoscopy. She has a 1.5 cm pedunculated polyp snared from the transverse colon. Five days after the colonoscopy the patient experienced two bloody bowel movements. She presents to the emergency room with a heart rate of 120 and a blood pressure of 100/70. case management You have two large bore intravenous lines started and begin rapid infusion of 2 L of lactated Ringers. Blood is drawn for a CBC, basic metabolic profile, coagulation studies, and type and cross for 4 units of packed RBC. A nasogastric tube is placed and ­billous heme negative fluid is aspirated. A proctoscopy reveals blood and clots in rectum, but no source of bleeding. A tagged RBC scan is obtained which is immediately positive in the cecum. An angiogram of the ileocolic artery reveals active bleeding in the cecum. Using a micro catheter, the interventional radiologist is able to embolize a segmental vessel and the bleeding ceases. The patient is transferred to the ICU for observation. INTRODUCTION Endoscopy is commonly used to evaluate the gastrointestinal (GI) tract. Endoscopy of the lower GI tract may include colonoscopy, flexible sigmoidoscopy, rigid proctoscopy, and anoscopy. While each of these procedures may have associated risks, discussion of colonoscopy will address the other procedures. This chapter will address the technical and nontechnical issues associated with this procedure. Colonoscopy is a procedure commonly used to diagnose and treat colonic conditions. It is a natural extension of the colon and rectal physical exam, and it has significant advantages over other examinations of the lower GI tract. This procedure allows direct inspection of the mucosal surface with the potential to identify and/or treat polyps, neoplasia, vascular lesions, and inflammatory bowel disease. The success of a colonoscopy is dependent on operator experience, patient selection, as well as the timing and extent of the bowel preparation. Although colonoscopy is an invasive procedure, complications are fortunately infrequent. However, major complications associated with colonoscopy can result in significant morbidity or even death. Serious complications can arise with either a diagnostic or therapeutic colonoscopy and include: perforation, hemorrhage, postpolypectomy coagulation syndrome, problems related to mechanical bowel preparation, infections, and anesthetic maladies (intravenous medications).(1) Nontechnical Complications Colonic complications may occur that are essentially unrelated to the actual technical performance of the procedure. These complications include patient selection, method of preparation of the colon, and administration of medication for sedation before

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and during the procedure, as well as the clinical decisions that are made concerning those patients who are on anticoagulation. Minimizing preventable colonoscopic complications begins with the patient selection process. The endoscopist needs to identify those patients who have enhanced risks for endoscopist injury. This can usually be accomplished by obtaining an appropriate medical history and physical examination, along with any necessary laboratory studies. Before performing an endoscopic examination of the colon, the physician must consider the patient’s general condition. The risk of potential injury must be balanced against the anticipated therapeutic gain, and this includes being cognizant of the patient’s ability to tolerate injury. For example, a patient with signs or symptoms suggestive of a colorectal carcinoma who requires a colon evaluation, but who has recently had a myocardial infarction, may be better evaluated with CT colography or barium enema. Consultation with a patient’s obstetrician is appropriate to insure that the test is merited and falls within acceptable safety guidelines for patients in their last two trimesters of pregnancy. Other relative contraindications to a colonoscopy include large abdominal aortic aneurysms or substantial splenomegaly. Colorectal Preparation Every effort should be utilized to cleanse the colon of feces and ­particulate matter before the examination as an adequate bowel preparation is one of the most important factors in avoiding injury and maximizing the quality of the exam. The ultimate success of the colonoscopy depends on operator experience as well as the timing and extent of bowel preparation. Inadequate colon preparation is reported in approx. 25% of cases and leads to lower cecal intubation rates and decreased polyp detection.(2–4) Other potential problems associated with a suboptimal bowel preparation include: increased rate of complications, longer procedural times, or the need to for repeat examination.(4, 5) Among the many factors that lead to inadequate bowel preparations, poor compliance due to incomplete consumption of the preparation is the most frequent etiology.(6) Reports of poor compliance are usually attributed to the patient’s intolerance of the high volume of ingested cleansing solutions.(7) Some preparations are associated with specific adverse effects in some subpopulations, including those who have renal insufficiency, preexisting electrolyte abnormalities, or congestive heart failure. The clinician must be cognizant of the advantages and disadvantages for different bowel preparations in order to obtain not only the best clinical exam but also to protect the patient from complications. The variety of colonoscopy preparations in clinical use involve combinations of diet restriction and laxatives. As an adjunct, most bowel preparations include a period of time during which the patient is restricted to a clear liquid or low residue diet, to reduce the amount of stool in the colon. However, dietary restriction by itself

transanal endoscopy is insufficient to adequately cleanse the colon. Current cleansing preparations include lavage solutions (usually polyethylene glycol— electrolyte lavage solution) and hypertonic electrolyte solutions. Oral Lavage Oral lavage methods have been developed to reduce the time required for mechanical cleansing (usually only 2–4 hours are required). Oral lavage consists of the ingestion of a large volume of osmotically balanced, nonabsorbable solutions that act as a purgative, clearing the colon of stool through mechanical forces. Polyethylene glycol (PEG) containing preparations have become the most preferred method of colonic preparation.(8) A meta-analysis of eight trials reported that PEG preparations were associated with either an adequate or excellent preparation in 70% of patients.(9) Unfortunately, up to 20% of patients are unable to complete the PEG preparation because of the poor palatability of the solution or its required large volumes. Recently, there have been new strategies to increase the efficacy in patient tolerability of PEG containing solutions. Recent studies have evaluated whether or not there is increased tolerability when using flavor versus nonflavor preparations.(10) There are also recent reports of investigations into the use of lower volume PEG solutions (i.e., 2 L rather than the standard 4 L), with or without the utilization of adjunct purgatives.(11) Other variations include the addition of adjunct purgatives (senna, magnesium citrate, or bisacodyl) in an effort to increase the efficacy of PEG solutions.(12, 13) To assist patients with the volume of fluid that must be ingested some endoscopists have tried adding metoclopramide, in the hopes that it would reduce nausea and increasing bowel motility. A study by Brady et al. (14) (a small placebo trial) utilizing metclopramide as an adjunct reported no significant benefits in the terms of bowel preparation or decrease in abdominal discomfort. Contraindication to oral lavage solutions include significant gastric retention, suspected or established mechanical bowel obstru­ ction, severe colitis, or the presence of ileus. Hypertonic Electrolyte Solutions Salt-based agents for bowel preparation are known as saline laxatives and include those containing magnesium cations or phosphate anions. Salt-based agents work by exerting a hyperosmotic effect in the intestines. The poorly absorbed magnesium or phosphate ions within the small intestine result in retention of water that directly stimulates stretched receptors and increases peristalsis. Sodium phosphate (NaP) is one of the more commonly used saline laxatives and is available in liquid or tablet form. This hyperosmotic product draws fluid into the intestinal tract resulting in a purgative action. Proponents of the utilization of NaP refer to studies that show that in healthy individuals the prep is safe, better tolerated, and equally or more effective than PEG. (15, 16) It is imperative to note that the downside of using oral sodium phosphate solutions is the potential for significant fluid shifts which can precipitate intravascular volume depletion. A few cases of nephrocalcinosis with subsequent renal insufficiency have also been reported.(17) The effect seems to be age and dose related. Additional risk factors for this unusual occurrence include underlying renal disease, dehydration, hypercalcemia, or hypertension with the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs).

These issues makes it imperative that (NaP) not be used in patients with congestive heart failure, decompensated cirrhosis, renal failure, or those presenting with baseline electrolyte abnormalities.(18) There is also the current concern for the development of hyperphosphatemia. Patients who have renal insufficiencies (familial filtration rate of <50% of normal) can develop life threatening hyperphosphatemia. Most patients with normal renal function find the sodium phosphate NaP preparation safe. Rejchrt and his colleagues reported on the utilization of NaP preparations and its effects on the colonic lining. They found the preparation induced mucosal lesions, erosions, and aphthous lesions in up to 3% of patients.(19) They concluded that this preparation should not be utilized for patients undergoing diagnostic evaluation for potential inflammatory bowel ­disease because it may lead to misinterpretation secondary to the mucosa lesions induced by the preparation.(20) As discussed previously, multiple studies have indicated the necessity for good bowel cleansing before endoscopic evaluation, as it adds not only to the quality of the examination, but also reduces potential complications. At present, the choice of bowel preparation is dependent on the clinical context, and the presence or absence of associated risk factors. The endoscopist should be cognitive of these issues before prescribing a colonoscopy preparation. Intravenous Sedation Conscious sedation reduces patient symptoms during endoscopy, but accounts for significant risks including vasovagal reactions and cardiopulmonary events. Conscious sedation can in fact cause respiratory depression, hypotension, tachycardia, or brachycardia.(33, 34) Patients who develop severe hypotension or hypoxia associated with sedation are also at risk for myocardial infarction. To reduce these risks and prevent excessive sedation, it is important that the physician and/or nurse providing the medication carefully titrate it throughout the procedure.(35) In the United States, it is standard to monitor blood pressure, pulse, and oxygen saturation on a timely basis throughout the procedure. It is also common to administer supplemental oxygen via nasal cannula. It is interesting to note that a prospective study of private patients (men and women), less than one-third were willing to undergo colonoscopy without sedation.(36) At present, the most commonly utilized agents for colonoscopic sedation are meperidine, fentanyl, and midazolam. Meperidine and fentanyl are used for analgesia. Fentanyl has a shorter time of onset and recovery, while meperdine appears to potentiate the sedative effect of benzodiazepines. Midazolam provides an anterograde amnesia and possesses a short half life, which is a distinct advantage for the safety of the patient. Midazolam also potentiates the narcotic effect and permits the reduction of narcotic doses and their associated complications. The utilization of these agents affects the psycho­motor function of the patient for hours, and thus postprocedure monitoring is necessary before their discharge from endoscopy unit. Some centers are now evaluating the use of propofol (Diprivan). Propofol lacks analgesic effect but is a rapid onset and effective sedative. It also has a shorter recovery time. Propofol’s most serious potential side effect is sudden respiratory depression, which may require intubation in order to control the airway. Therefore, utilization of this drug usually requires

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improved outcomes in colon and rectal surgery administration by an anesthesiologist, a nurse anesthetist, or a dedicated physician. Most endoscopy centers, with an adequate number of procedure rooms and recovery space have not found this drug cost-effective. Hemodynamic depression is managed with increased intravenous fluids, while respiratory depression is treated with supplemental oxygen and sedation reversal. Naloxone (Narcan); 0.4 mg intravenously (or 0.2 mg intravenously and 0.2 mg intramuscularily) will reverse the narcotic effect. Flumazenil (Romazicon); 0.2 to 1.0 milligrams intravenously, will reverse sedation from Midazolam. Excessive colonic distention may produce a vasovagal reaction which responds to increased intravenous fluids and decompression of colon gas. Significant bradycardia, secondary to the sedation may require administration of atropine (0.5 mg IV every 3–5 minutes to a dose of 3 mg). Infectious Disease Complications Colonoscopy can produce infectious complication by transmission of disease from patient to patient, from patient to examiner, or from bacteremia related to the procedure. Current national recommendations for mechanical cleansing of endoscopic equipment, if followed properly, should prevent the transmission of such diseases as HIV and hepatitis. Transmission of disease from patient to examiner can also be prevented by appropriate eye, facial, and hand protection and endoscopic suites should be equipped with goggles, disposable aprons and gloves, or facial splash guards. The incidence of bacteremia associated with colonoscopy has been reported from 1 to 20%. Despite the potential risks of bacteremia, there are presently only five reported cases of endocarditis associated with colonoscopy, despite the millions of colonoscopies performed annually.(37, 38) The American Heart Association (AHA) had previously recommended antibiotic treatment for patients that were described as high-risk (patients with prosthetic heart valves, congenital cardiac malformations, surgically constructed systemic pulmonary shunts, and previous history of endocarditis). More recently, the AHA SBE prophylaxis panel after extensive study, now recommends that the risk of antibiotic

Figure 12.1  Management of postpolypectomy hemorrhage.

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complications greatly outweighs the potential for bacteremia leading to endocarditis. They conclude that no antibiotics should be administered for SBE prophylaxis during colonoscopy.(39) TECHNICAL COMPLICATIONS Hemorrhage Hemorrhage after colonoscopy is most commonly associated with polypectomy, but can occur with diagnostic procedures. Hemorrhage is most frequently associated with intraluminal bleeding, but can also arise from extraluminal sources, such as a mesentery laceration, secondary to mechanical forces produced during instrumentation. Splenic injury or rupture results in intraperitoneal hemorrhage (see miscellaneous complications section for more details). Hemorrhage following colonoscopic polypectomy has a prevalence that ranges between 1–2.5%, and is the most common complication of polypectomy.(21) The hemorrhage may be an immediate or delayed event and has been reported up to 14 days postpolypectomy.(22) Those hemorrhages occurring during the endoscopic procedure represent 1.5% of polypectomies, and those in the delayed setting, after the completion of the procedure represent 2% of polypectomies.(23) Immediate hemorrhage upon transection of the pedicle of a pedunculated polyp occurs because of inadequate coagulation of the feeding vessels. Pedunculated polyps, >1 cm in diameter with fixed stalks have the highest risk for immediate hemorrhage, as they have substantial vessels.(24) The utilization of the cold biopsy technique can result in capillary bleeding, which is usually of no clinical significance. The corollary to this observation is that significant bleeding can occur with cold or hot biopsy techniques if the patient is being treated with anticoagulants or antiplatelet medications. Though most postpolypectomy hemorrhage is selfcontained, the endoscopist must respect the clinical potential of the bleeding to produce enough hypotension as to cause stroke, myocardial infarction, or frank shock. With persistent and significant ongoing bleeding, the endoscopist my have difficulty in locating the residual stalk. This

transanal endoscopy makes it imperative that the source be quickly controlled at the onset of bleeding before the field being obscured by blood and clot. Initially, the endoscopist can utilize the polypectomy snare to regrasp the stalk and hold it taut for approximately 15 minutes without the utilization of any electrocautery. This maneuver if unsuccessful can be performed again and this usually suffices to control the bleeding. Other options are: the placement of clips or detachable snares. If these are not available, the residual stalk can be injected with 1–10,000 solution of epinephrine plus saline, or the base of the residual stalk can be recoagulated without enough energy to transect the stalk. Many endoscopists now suggest that if one identifies a potentially significant polyp that might produce postpolypectomy bleeding (i.e., large in size or patient’s condition mandates they continue anticoagulation), that the utilization of clips or a detachable snare in advance of the resection may be beneficial. It should be noted that if one elects to use electrocautery after initial snaring, that they should be careful to prevent full thickness injury at the site. Delayed hemorrhage occurs when the retained scar from a polyp site separates prematurely from the coagulation bed, leading to hematochezia. This type of bleeding usually occurs within 2–15 days of the after the procedure, typically within the first 7–10 days. Postpolypectomy bleeding can be significant enough to require in-hospital fluid resuscitation and potential therapeutic intervention. These patients usually have arterial bleeding, and pass bright red bloody bowel movements spaced at close intervals (i.e., 30–60 minutes).(25) The active bleeder (after appropriate resuscitation) may benefit from a prompt colonoscopy without bowel prep to identify the site of bleeding. If the bleeding site is located it can be treated with judicious multipolar cautery, injection of epinephrine solution, detachable snare, or placement of hemoclips. Often times, it is clinically difficult to determine if the hemorrhage has ceased because the hematochezia may continue for several hours afterwards. If the hemorrhage appears persistent, despite local efforts or if the patient needs urgent intervention, the location of the active bleeding may be identified with a tagged RBC scan.(26) If the scan is positive, arteriography can confirm the bleeding location and offers potential treatment modalities for either selective arterial vasopressin infusion, or embolization. The choice depends upon the patient’s clinical history and ­presentation as well as the skill and experience of the radiographer. Figure 12.1 describes the authors’ and editors’ management algorithm for postpolypectomy bleeding. Prophylactic techniques during polypectomy may decrease the incidence of postpolypectomy bleeding.(27) During the technique of taking a large polyp, some endoscopists use a saline intermucosal lift or an epinephrine solution injection into the stalk of the polyp in efforts to control hemostasis. Detachable snares and clips have also been used with a similar goal in mind. Although successful, even in skilled hands, clips may slip or transmit current if cautery makes contact with the metal. Detachable snares may slip from their initial position, or if pulled too tight can cut through the base of the polyp, leading to the problem that one is trying to prevent. The absence of national guidelines concerning the prophylactic approaches to postpolypectomy bleeding, makes each endoscopist responsible for evaluating the clinical situation and being cognitive of his level of expertise.

Table 12.1  Anticoagulant recommendations. Drug

Before Procedure

After Diagnostic Procedure

After Therapeutic Procedure

Aspirin

Continued or stopped 7 days prior

Continued or started day of procedure

Restarted 5–7 days after

Clopidogel

Held for > 7 days prior

Restarted day after procedure

Restarted 7 days after

Warfarin

Held for > 3 days prior and check PT

Restarted day after procedure

Restarted 1–5 days after

Note: PT Prothrombin time.

Another factor in postpolypectomy hemorrhage relates to the management of patients on antiplatelet agents or anticoagulants.(28, 29) The American Society for Gastrointestinal Endoscopy has recommended that aspirin need not to be stopped before polypectomy as there is insufficient evidence supporting an increased risk with its utilization.(30) However, many endoscopists will hold a patient’s aspirin for 7 days if their indication for taking aspirin is weak. If the patient can tolerate it, the author and editors withhold clopidogrel (Plavi®, Sanofi-Aventic, Bridgewater, NJ) for a minimum of 7 days before the colonoscopy and hold warfarin for a minimum of 3 days before the procedure and check a prothrombin time (PT) before the colonoscopy.(31) Therapeutic procedures are usually safe with an INR of <2.(32) If the patient’s INR is above this level, the procedure may be delayed until the INR is lower or if the anticipated need for a therapeutic procedure is low (e.g., a screening indication) a diagnostic procedure may be performed with the understanding that if significant lesions are identified, therapeutic maneuvers (i.e., biopsy or polypectomy) will be deferred. Patients who cannot tolerate reversal of anticoagulation (a determination usually made by the patient’s cardiologist or neurologist) can often be managed with a bridging with enoxaparin sodium (Lovenox®, Sanofi-Aventic, Bridgewater, NJ) or considered for alternate procedures such as CT colography. Recommendations for restarting anticoagulation or antiplatelet agents postpolypectomy are difficult clinical decisions that must be based on the patient’s risk-benefit ratio, (i.e., the risk of stroke, or coagulation of cardiac stents versus the risk of postpolypectomy hemorrhage). Unfortunately, there is little prospective data to support recommendations. The author and editors restart these medications at their normal daily dose the day following a diagnostic procedure. Recommendations after a polypectomy depend on the size and number of polyps removed and the level of anticoagulation at the start of the procedure. Warfarin is ­usually started at the normal daily dose, 1–5 days after the procedure, while clopidogrel is restarted 1 week after the procedure.(32) Anticoagulant recommendations are summarized in Table 12.1. Perforation The most serious complication of colonoscopy is overt perforation.(40) Perforation can result from mechanical forces during colonoscopic insertion or from barotrauma during colonic insufflation, or during the process of polyp removal. Perforation



improved outcomes in colon and rectal surgery Table 12.2  Colonoscopy perforation rates. Author, Year (Reference)

Colonoscopies, n

Perforations, n (%)

Setting

Lo and Beaton, 1994 (44)

26,708

12 (0.045)

University, teaching

Farley et al., 1997 (43)

57,028

43 (0.075)

Mayo clinic, teaching

Anderson et al., 2000 (44)

10,486

10 (0.19)

Mayo clinic, teaching

Araghizadeh et al., 2001 (45)

34,620

31 (0.09)

Ochsner Clinic, teaching

Korman, et al., 2003 (46)

116,000

37 (0.03)

ASC, private practice

Cobb et al., 2004 (47)

43,609

14 (0.032)

Teaching

Lqbal et al., 2005 (48)

78,702

66 (0.084)

Mayo clinic, teaching

Levin et al., 2006 (49)

16,318

15 (0.09)

Kaiser Permanente

occurs in 0.6% to 0.8% of diagnostic procedures and 0.5% to 3% (See Table 12.2).(41, 42) Perforation is diagnosed during the procedure by observation of extraluminal fat or other intraabdominal contents (e.g., small bowel, liver) via the colonoscope. These patients usually report immediate pain and demonstrate signs of peritoneal irritation. Patients that develop symptomatology postprocedure vary from, asymptomatic free intraabdominal air, a tense abdomen, or florid peritonitis and sepsis. Patients presenting with localized symptoms can be observed and treated with intravenous fluids, antibiotics, and bowel rest.(43) Patients who present with or develop signs of generalized peritoneal irritation during observation, should receive a laparotomy. Repair or resection of the perforation is performed with or without a diverting ostomy. An algorithm for the management of colonoscopic perforations is presented in Figure 12.2. It is important to remember that a perforation can come from an unsuccessful encounter with the colon wall with the tip, the deflection bend, and/or the shaft of the colonoscope. The inexperienced examiner can drive the tip of the scope through a large diverticulum; or may, while advancing the scope form a

Figure 12.2  Management of colonoscopic perforation.



significant loop, allowing the shaft of the scope to make a laceration in the bowel wall, away from the tip of the scope, which may go on unrecognized. Significant clinical experience, along with judgment and good technique, serve as the best preventative tools against a perforation.(50, 51) Miscellaneous Complications Though the major complications associated with colonoscopy are hemorrhage and perforation, there exists a large body literature that has reported rarely encountered complications. These include incarceration of the colonoscope within an inguinal hernia, (52) cecal volvulus with subsequent perforation, (53) ischemic colitis, (54) aortic thrombosis in a patient with Bechcet’s syndrome, (55) and splenic injury (56). There have been approximately 59 clinical reports which detail 67 cases of splenic injury, following diagnostic or therapeutic colonoscopy.(56, 57) The authors note the most likely etiology of splenic injury is related to the performance of the procedure rather than any therapeutic maneuver. It is theorized that the mechanism of injury is thought to be excessive traction on the splenocolic ligament or adhesions. This theory has been confirmed by laparotomy in several of the reported cases. It is interesting to note that in most of the injuries, the endoscopists felt the procedure had been performed without difficulty. The presentation for these injuries span between 6–24 hours, and vary from vague abdominal pain of the left upper quadrant, with mild orthostatic hypotension, and a decreased hematocrit to severe hypotension and shock. It is suggested that an abdominal CT scan is the most helpful diagnostic test as it may show a splenic laceration, with free intraperitoneal blood or a splenic hematoma. Most of the cases, required surgery, and the patient’s overall condition dictated whether an emergency intervention was necessary. Observation and conservative management was rarely successful. Awareness of the potential for splenic injury during colonoscopy is important as it may help avoid any delay in diagnosis. Unfortunately, these cases are so rare that no identifiable risk factors have been documented that potentially could help prevent this complication. Patients with reducible hernias, merit additional attention by the endoscopist who must consider the benefits of a diagnostic or therapeutic procedure versus the potential for injury or the delay

transanal endoscopy until the hernia is repaired. For patients with reducible inguinal hernias, the procedure can be performed with general pressure on the hernia sac during the colonoscopy or with the utilization of a truss. Should the colonoscope become incarcerated in an inguinal hernia, a “pulley” technique has been described where a relatively large easily graspable colonoscope loop is created within the hernia sac and then is withdrawn over the pulley “hand” one limb at a time.(52) Development of a cecal volvulus, may occur with a hypermobile cecum.(53) Postpolypectomy Syndrome The postpolypectomy syndrome is believed to result from a transmural burn to the colonic wall and usually presents with a syndrome similar to that of diverticulitis.(58) This represents the second most common polypectomy complication with rates ranging from 0.5% to 1%.(59) Usually this complication occurs in the thin right-sided bowel after removal of a sessile polyp or performance of a hot biopsy. It is felt that the factors leading to this syndrome include the utilization of high cumulative quality and longer duration of electrocautery. It is also possible for the electric current to enter the mucosa opposite the polyp if the tip of the polyp is allowed to touch the opposing wall during the application of the cautery. Moving the polyp back-and-forth during cautery may dissipate the current. This syndrome is usually seen in sessile polyps that are >2 cm in diameter.(60) The patients may present within hours of the procedure but some may not show some significant symptomology until 5–6 days postprocedure. Patients usually present with pain which may or may not include fever, an elevated white count, and localized tenderness. Initial studies include plain x-rays or a CT scan, which confirm by definition an absence of free air. Patients are started on broad spectrum antibiotics and bowel rest, then most importantly patients are examined over appropriate intervals to make sure there is no progression from the localized tenderness to frank peritonitis.(61) Fortunately, most of the patients that are properly managed progress to recovery without surgical intervention, and they can be discharged when their pain has resolved, and their white blood cell count has normalized. Prevention of postpolypectomy syndrome aided by adherence to the previously described guidelines for a safe polypectomy. Proctoscopic Perforations Proctoscopic perforations are rare, serious complications of intestinal endoscopy.(62) Nelson et al. reported only three perforations in 16,325 proscopic exams.(63) The injury most commonly occurs when the bowel wall has been weakened by disease such as colitis, a rectal tumor, or constricting lesion. The line of force during insertion guides the scope to the anterior rectal wall where the usual site of injury is located between the peritoneal reflection and the rectosigmoid junction.(64) The perforation is usually recognized as the scope enters the peritoneal cavity or the endoscopist encounters the perirectal fat or local bleeding. (52) Significant rectal trauma with a rectal perforation requires operative treatment. Most authors believe that delayed treatment increases the mortality from 8% to 20%.(65) The major morbidity and mortality are associated with the fact that the proximal colon typically is not mechanically cleansed. The treatment

involves resection of associated pathology, repair of the perforation site, rectal washout, pelvic drainage, and a diverting colostomy (see chapter 35).(66) Summary Training, experience, and conservative technique help to minimize complications associated with endoscopic procedures of the colorectum. Prompt recognition and appropriate management of complications help to minimize the patient’s morbidity. References   1. Rogers BHG Silvis SE, any Bel OT et al. Complications of Flexible Fibroptic Colonoscopy and Polypectomy. Gastropint Endosc 1975; 22: 73–7.   2. Harewood GC, Sharma VK, de Garmop. Impact of Colonoscopy Preparation Quality on Detection of Suspected Colonic Neoplasia. Gastroinest Endosc 2003; 58: 76–9.   3. Aslinia F, Uradomo L, Steele A et al. Quality Assessment of Colonoscopic Cecal Intubation: Analysis of six years of continuous practice at University Hospital. An J Gastrointestal 2006; 101: 721–31.   4. Froehich F, Wietilsbach V, Gonvers JJ et al. Impact of Colon and Colonic Cleansing on Quality and Diagnostic yield of Colonoscopy; The European panel of appropriateness of gastrointestinal endoscopy European Multi-Center Study, Gastroenterol Endosc 2005; 61; 378–84.   5. Rex DK, Imperiale TF, Latinovich DR, Bratcher LL. Impact of bowel preparation on the efficacy and cost of colonoscopy. ANJ Gastroenterol 2002; 97: 1696–700.   6. Hsu CW, Imperiale TF. Meta-analysis and cost comparison of polyethylene glycol lavage vs. sodium phosphate for colonoscopy preparation. Gastrointest Endosc 1998; 48: 276–82.   7. Harewood GC, Wiersema MJ, Melton LJ III. A prospective control assessment of factors influencing the acceptance of screening colonoscopies. An J Gastroenterol 2002; 97: 3186–94.   8. Lieberman DA, Holb J, Eise G et al. Utilization of colonoscopy in the U.S.: Results from a national consortium. Gastroinest Endosc 2005; 62: 875–83.   9. HSU CW, Imperiale TF. Met-analysis and cost comparisons of polyethylene glycol lavage vs. sodium phosphate for colon preparation. Gastro Endosc 1998; 48: 276–82. 10. Diab FH, Marshal JB. The palatability of five colonic lavage solutions that’s in Aliment Pharmacol Ther 1996; 10: 815–19. 11. Hookey LC, Depew WT, Vonner SJ. Combined low volume polyethylene glycol solution plus stimulant laxative vs. standard volume polyethylene glycol solution: A perspective, randomized study of colon cleansing before colonoscopy. Can J Gastroenterol 2006; 20: 101–5. 12. Clarkston WK, Smith RJ. The use of golytely and docolax in combination in outpatient colonoscopy. J Slin Gastroenterol 1993; 17: 146–8. 13. Sharma VK, Steinberg EN et al. Randomized control study of pretreatment with magnesium citrate and the quality of colonic preparation with polyethylene glycol electrolyte lavage solution. Gastrointest Endosc 1997; 46: 541–3. 14. Brady CE, DiPalma JA, Pierson WP. Golytely lavage – Is metoclopramide necessary? AM J Gastroenterol 1985; 80: 180–4.

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improved outcomes in colon and rectal surgery 15. Cohen SM, Wexner SD, Binder SR et al. Prospective randomized endoscopic blinded trial comparing precolonoscopy bowel cleansing methods that’s in the Dis Colon Rectum 1994; 37: 689–96. 16. Kolts BE, Lyles, WE, Achem SR et al. A comparison of the effectiveness and patient tolerance of oil sodium phosphate, castor oil, and standard electrolyte lavage for colonoscopy or sigmoidoscopy preparation. Am J Gastroenterol 1993; 88: 1218–23. 17. Markowitz GS, Stokes MB, Radhakrishnan J, D’Agati VD. Acute phosphate nephropathy following oral sodium phosphate bowel purgative: an under recognized cause of chromic renal failure. Am Soc Nephrol 2005; 16: 3389–96. 18. Clark LE, Dipalma JA. Safety issues regarding colonic cleansing for diagnostic and surgical procedures. Durg Saf 2004; 27: 1235–42. 19. Rejchrt S, Burues J, Siroky M et al. A prospective observation study of colonic mucosa abnormalities associated with oral administered sodium phosphate for colon cleansing before colonoscopy. Gastrointest Endosc 2004; 59: 651–4. 20. Zwas FR, Cirillo NW et al. Colonic mucosa abnormalities associated with oral sodium phosphate solution. Gastrointest Endosc 1996; 43: 463–6. 21. Wayne JD. Colonoscopy, CA Cancer J Clin; 42: 350–65, 1992. 22. Rex DK, Lewis BS, Wayne JD. Colonoscopy and endoscopic for delayed post polypectomy hemorrhage. Gastrointest Endosc 1992; 38(2): 127–9. 23. Wayne JD, Lewis BS, Wessayan S. Colonoscopy: prospective report of complications. J Clin Gatroenterology 1992; 15(4): 347–51. 24. Sorbi D, Norton I, Conio et al. Post polypectomy lower GI bleeding descriptive analysis. Gastrointestest Endosc 2000; 51(6): 690–6. 25. Gossum AV, Cozzsoli A, Adler M et al: Colonoscopic snare polypectomy: analysis of 1,485 resection comparing two types occurring. Gastrointest Endosc 1992; 38: 472–5. 26. Gibbs DH, Opelka FG, Beck DE et al. Post polypectomy colonic hemorrhage. Dis Colon Rectum 1996; 39: 806–10. 27. Fatima H., Rex DK. Minimizing endoscopic complications: colonoscopic polypectomy, Gastrointest Endosc N Am 2007; 17: 145–56; 153–4. 28. Wousy M, Gost CJ, Barrone TH et al. Post-polypectomy lower gastro intestinal bleeding, the role of aspirin. Am J Gastrointerol 2004; 99(9): 1785–9. 29. Zuckerman MJ, Hirta WK, Adler DG et al. ASGE Guidelines: the management of low molecular weight epinepherine and non-aspirin antiplatelet agents for endoscopic procedures. Gastrointest Endosc 2005; 61(2): 189–194. 30. Hui AJ, Wong RM, Ching JY et al. Risks of colonoscopic polypectomy with anticoagulants and antiplatelet agents: analysis of 1,657 cases. Gastrointest Endosc 2004; 59(1): 44–8. 31. Timothy SKC, Timmcke AE, Hicks TC, Beck DE, Opelka FG. Colonoscopy in the anticoagulated patient. Dis Colon Rectum 2001; 44: 1845–9. 32. Zuraff-Perryman LA, Renz BW, Beck DE et al. The risk of bleeding and thromboembolic events in patients undergoing

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33. 34.

35. 36.

37.

38. 39.

40.

41. 42.

43. 44. 45.

46.

47.

48.

49.

50.

51.

52.

colonoscopic evaluation on clopedigrel (Plavix). Dis Colon Rectum; in press. Herman F. Response to the letter entitled Voidance of sedation. Dis Colon Rectum 1990; 33: 540–1. Iber FL, Sutberry M, Gupta R, Kruss D. Evaluation of complications during and after conscious sedation for endoscopy using pulse symmetry Gastrointest Endosc 1993; 39: 620–5. Beck DE, DiPalma JA. Complications of GI procedures. Problems in Critical Care 1989; 3: 261–70. Rex DK, Imperiale T, Portish VL. Patients willing to try colonoscopy without sedation: Associated clinical factors and results of a randomized controlled trial. Gastrointest Endosc 1999; 49: 554–9. Meyer GW. Prophylaxis of infected endocarditis during ­gastrointestinal procedures: Report of a survey. Gastrointest Endosc 1979; 25: 1–2. Rumfield W, Wallace G, Scott BB. Bacteria endocarditis after endoscopy. Lancet 1980; 1083. Wilson W, Taubert K, Gewitz M, et al. Prevention of infected endocarditis: Guidelines for the American Heart Association. Circulation 2007; 8: 115. Habr-gama A, Wayne JD. Complications and hazards of ­gastrointestinal endoscopy. World J Surg 1989; 13: 193–201. Kavin H, Sinicrope F, Esker AH. Management of Perforation of Colonoscopy. Am J Gastroenterol 1992; 87: 161–7. Opelka FG. Transanal endoscopy. In: Hicks TC, Beck DE, Opelka FG, Timmcke AE, eds. Complications of colorectal surgery. Baltimore: Williams and Wilkins, 1996: 143–52. Reickert CA, Beck DE. Complications of Colonoscopy. Clin Colon Rectal Surg 2001; 14: 379–86. Lo AY, Beaton HL. Selective management of colonoscopic perforations. J AM Coll Surg 1994; 179: 333–7. Farley DR, Bannon MP, Zietlow SP et al. Management of colonoscopic perforations. May Clin Proc 1997; 72: 729–33. Anderson MI, Pasha TM, Leighton IA. Endoscopic perforation of the colon: lessons from a 10-year study. Am J Gastroenterol 2000; 95: 3418–22. Araghizadeh FY, Timmcke AE, Opelka FG, Hicks TC, Beck DE. Colonoscopic perforations. Dis Colon Rectum 2001; 44: 713–6. Korman LY, Overholt BF, Box T, Winker CK. Perforation during colonoscopy in endoscopic ambulatory surgical centers. Gastrointest Endosc 2003; 58: 554–7. Cobb WS, Heniford BT, Sigmon LB et al. Colonoscopic perforations incidence, management, and outcomes. AM Surg 2004; 70: 750–7. Lqbal CW, Chun YS, Farley DR. Colonoscopic perforations: a retrospective review. J Gastrointest Surg 2005; 9: 1229–35. Levin TR, Zhao W, Connel C et al. Complications of colonoscopy in an integrated heath care delivery system. Ann Intern Med 2006; 145: 880–6. Koltun WA, Collier JA. Incarceration of the colonoscope in an inguinal hernia. “Pulley” Technique of removal. Dis Colon Rectum 1991; 34: 191–3.

transanal endoscopy 53. Amidon PB, Story RK Jr. Cecal Volvulus after colonoscopy. Gastrointestinal endoscopy 1993; 39: 105. 54. Wheeldon MN, Grumdman MJ. Ischemic colitis as a complication of colonoscopy. BMJ 1990; 301: 1080–1. 55. Gruber HE, Weisman MH. Aortic thrombosis during sigmoidoscopy and Bechcet’s syndrome. Arch Intern Med 1983; 143: 343–5. 56. Gores PH, Sisma LA. Splenic injury during colonoscopy. Arch Surg 1989; 124: 1342. 57. Michetti CP. Splenic injury due to colonoscopy: Review and analysis of the World literature, a new case report, and recommendations for management. J Am Coll Surg; in press. 58. Conio M, Repici A, Demarquay JF et al. EER of large sessile colorectal polyps in Gastrointest Endosc 2004; 16: 234–41. 59. Wayne JB, Lewis BS, Wessayan S. Colonoscopy: A perspective report of complications. J Clin Gastroenterology 1992; 15(4): 347–51.

60. Nivetongs S. Complications in colonoscopic polypectomy: lesson to learn from an experience with 1,576 polyps. Am Surg 1998; 54(2): 61–3. 61. Christie JP, Marrazzo J III. “Many – perforation” of the colon – not all postpolypectomy perforations require laparotomy. Dis Colon Rectum 1991; 34(2): 132–5. 62. Goligher JC. 4th ed. Injuries of the rectum and colon. In Surgery of the Anus Rectum and Colon. London: Bailliere Tindall, 1980: 916–7. 63. Nelson RL, Abcarian H, Prasad ML. Iatrogenic perforation of the colon and rectum. Dis Colon Rectum 1982; 25: 305. 64. Befeler D. Proctoscopic perforation of the large bowel. Dis Colon Rectum 1967; 10: 376. 65. Andresen AFR. Perforations from proctoscopy. Gastroenter­ ology 1947; 9: 32–43. 65. Beck DE, Opelka FG. Pelvic and perineal trauma. Perspectives in Colon and Rectal Surgery 1993; 6: 134–56.

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13

Laparoscopic colorectal surgery James W Fleshman and Jonathan S Chun

CHALLENGING CASE A 28-year-old male is undergoing an ileocolic resection for Crohn’s disease. During insertion of a right lower quadrant (RLQ) trocar, significant bleeding is observed from the right lower retroperitoneum. MANAGEMENT It appears that the right iliac vein has been injured by the trocar. A Babcock clamp is used to temporarily occlude the bleeding using direct pressure. The anesthesia personnel are informed of the possibility of significant blood loss. While pressure is continued by an assistant, the surgeon rapidly opens the abdomen using a vertical midline incision. With a retractor in place, the Babcock is replaced by the surgeon’s hand. With continued tamponade, proximal and distal control of the vessel is obtained. The venotomy can now be repaired using vascular techniques. It is usually not possible to repair a major vascular injury with laparoscopic techniques. If proximal and distal control can be obtained an experienced laparoscopic surgeon may attempt the repair, but the threshold for opening should be low. INTRODUCTION The rising demand for laparoscopic techniques for colorectal surgery arises from a number of purported benefits, including a reduction in postoperative ileus, decreased pain, earlier recovery, fewer adhesions, and smaller incisional hernias. This enthusiasm, however, has been tempered by, among other things, the long learning curve, increased operative times, and concerns about the oncologic outcomes of laparoscopic resection for curable colon cancer. Concern over cancer implants in trocar sites led to a temporary national moratorium on laparoscopic resection for colon cancer from 1994 to 2004, and multiple national surgical societies called for these procedures to be performed only under the ­auspices of controlled trials. A number of prospective, randomized trials, including the Colon carcinoma Laparoscopic or Open (COLOR), Conventional versus Laparoscopic-Assisted Surgery in Colorectal Cancer (CLASICC), and Clinical Outcomes in Surgical Therapy (COST) studies, have helped address some of these concerns and delineate some of these advantages and disadvantages.(1–7) This chapter will address some of these concerns and address how best to optimize outcomes for laparoscopic surgery in various colorectal disease processes. ADVANTAGES Postoperative pain and suppression of pulmonary function are well-known sequelae of abdominal surgery. While physician bias and patient expectations make a truly objective assessment of pain difficult, multiple prospective, randomized trials have found a reduction in narcotic requirements in patients undergoing laparoscopic colectomy.(5, 6, 8) In the COST trial, patients who underwent successful laparoscopic resections had decreased use of both oral and intravenous analgesics.(1) In an attempt to document improved pulmonary function in patients undergoing laparoscopic surgery for colon cancer at

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the Cleveland Clinic, preoperative and postoperative spirometry was performed every 12 hours postoperatively in 55 patients ­randomized to the laparoscopic surgery group and 54 patients in the open surgery group.(5) These measurements consisted of an 80% recovery of baseline forced vital capacity and forced expiratory volume in-second from each patient. The median recovery for the laparoscopic group was 3 days vs. 6 days in the conventional group. Schwenk et al. had similar results in a similarly designed trial.(8) These results suggest a reduction in postoperative pain and quicker recovery of pulmonary function in patients undergoing laparoscopic colectomy. Reduction in postoperative ileus is another proposed major advantage of laparoscopic surgery. Time to recovery of bowel function, either flatus or tolerance of food, and time to bowel movement are surrogate markers for the length of the postoperative ileus most patients experience after abdominal operations. Virtually all publications, whether retrospective or prospective, have shown a statistically significant reduction in the time to recovery of bowel function. The advantage appears to be 1–2 days in these studies. The mechanism by which ileus is reduced is unknown, but may relate to decreased bowel manipulation, decreased intestinal exposure to air, exposure to the protective effects of carbon dioxide pneumoperitoneum, or reduced narcotic demands from a smaller incision. The biases of the treating physician and the higher expectations of patients undergoing laparoscopic surgery make it difficult to accurately and reliably determine the true time to ileus resolution. Investigators have, therefore, sought to more formally evaluate the return of bowel function. Canine and porcine models have looked at intestinal myoelectric activity as well as radionucleotide techniques in animals that underwent laparoscopic resection.(9–11) These studies confirmed a quicker return of bowel function following laparoscopic vs. open resection. The combination of reduced ileus, decreased pain, and quicker recovery of pulmonary function would logically add up to a reduced length of stay for patients following laparoscopic resection. This benefit appears to be a 1–2 day advantage among patients undergoing laparoscopic resection. The introduction of clinical pathways has been particularly effective and more reliable in patients undergoing minimally invasive approaches.(12, 13) Early ambulation, early feeding protocols, and early switch to nonnarcotic oral analgesics have reduced length of stay for laparoscopic and open procedures. “Fast-tracking” has shown that a 2 day stay after laparoscopic or open colectomy is possible.(14) This may be useful, as patients get used to transferring in-hospital care to home care and become invested in the short hospital stay. Though it is widely accepted that laparoscopic surgery results in fewer adhesions than open surgery, this is difficult to quantify in the context of a clinical trial. A recent observational study by Dowson et al. however, looked at 46 patients (13 laparoscopic and 33 open) who underwent laparoscopy after a previous colectomy. They found a statistically significant difference in adhesions between the two groups, with the laparoscopic group having a lower score.(15)

laparoscopic colorectal surgery While this study was limited due to its small sample size, it does confirm long-held beliefs about decreased adhesions after laparoscopic vs. open surgery, which should help to make later reoperations safer. In the past, 3-stage operations for inflammatory bowel disease were felt to be a disadvantage to both the surgeon and the patient. However, laparoscopic total abdominal colectomy and ileostomy to remove the inflamed ulcerative colitis colon, wean steroids, and improve nutrition can be performed without risking increased adhesions at the time of ileal pouch construction and completion proctectomy. The time between these two procedures can also be reduced using laparoscopic approaches. Fertility, especially in females, is an issue after pelvic surgery, particularly restorative proctocolectomy. Multiple studies have suggested that fertility is adversely affected in women undergoing restorative proctocolectomy.(16–18) This is likely related to adhesions in the pelvis causing scarring of the Fallopian tubes. Laparoscopy, with its decreased adhesion formation, may offer benefits in preserving fertility in reproductive-age females. Obesity and a large amount of visceral fat can make laparoscopic colorectal procedures particularly challenging. The associated comorbid illnesses often associated with obesity, however, would seem to make this group of patients the ideal group to benefit from laparoscopy. Delaney et al., in a case-matched comparative study of patients with a body mass index >30, found no difference in median operating time, complications, readmission, or reoperation rates.(19) The median length of stay, however, was significantly shorter (3 vs. 5.5 days) after laparoscopic colectomy. Twenty-eight patients did require conversion, but the lengths of stay, complication, readmission, and reoperative rates were no different than for patients undergoing open colectomy. Senagore et al. studied a series of 260 patients and compared outcomes between patients with a BMI above 30 and those with a BMI below 30 undergoing segmental colectomy.(20) The obese group had a significantly higher rate of conversions (23.7% vs. 10.9%), longer operative times (109 minutes vs. 94 minutes), higher morbidity rate (22% vs. 13%), and a higher anastomotic leak rate (5.1% vs. 1.2%). While this increase in complications paralleled those in obese patients undergoing open colectomy, Senagore et al. concluded that laparoscopic colectomy is feasible and safe, with the main benefit of a shorter hospital stay. While operative times are longer in obese patients, the use of a hand-assist device may offer the surgeon a useful tool to cut down these times, particularly in this challenging group of patients. Marcello et al. found that the use of a hand-assist device allowed for the more efficient completion of technically challenging and complex procedures while preserving the benefits of a laparoscopic approach.(21) The average BMI of patients in their study was only 28.1 in the hand-assist group vs. 26.3 in the straight laparoscopic group. While their results cannot be used to definitively state that a hand-assisted approach is superior in obese patients, they do suggest that it could be a useful tool to overcome the challenge of completing laparoscopic procedures on these patients. DISADVANTAGES A number of challenges have prevented laparoscopic colorectal surgery from becoming more widely accepted and utilized by surgeons. Most general surgeons perform fewer than 50 segmental

colon resections per year. Laparoscopic colectomy, unlike laparoscopic cholecystectomy, requires working in multiple quadrants of the abdomen, making depth perception and proprioception more difficult. Several studies have evaluated the learning curve for laparoscopic colectomy and suggested that this curve ranges from 20–50 cases, but may be as high as 150 before the surgeon is able to handle all eventualities during a laparoscopic colectomy. The standardization of technique required for entry into the COST trial resulted in no detriment in oncologic outcomes even though the study was undertaken during early laparoscopic experience and the conversion rate was 20% (25% first half to 19% second half).(22–24) The CLASICC trial, which was a prospective, randomized trial comparing laparoscopic and open resection of both colon and rectal cancer in the United Kingdom, also required that surgeons perform at least 20 laparoscopic resections in order to enter the study.(2) Even with this level of experience, the rate of conversion decreased from 38% to 16% over the course of the study—July 1996 to July 2002. This suggested that 20 cases were likely not enough to reach the plateau of the learning curve. The COLOR trial also highlighted the value of surgeon volume in improving patient outcomes.(3) In this trial out of Europe, the median operative time for high-volume (>10 cases/year) vs. low-volume (<5 cases/year) hospitals was 188 minutes vs. 241 minutes. Conversion rates were 9% with high-volume groups vs. 24% for low-volume groups. High-volume groups resected more lymph nodes, had fewer complications, and shorter hospital stays, but there was no difference in oncologic outcomes. Operative times are generally longer with a laparoscopic approach. This difference is approximately 40–60 minutes longer for the laparoscopic technique depending on the portion of colon removed (left > right). While operating times decrease with surgeon experience, they do not reliably decrease to the level of an open approach. The use of a hand-assist device may be a viable solution to decrease the operative times while still maintaining the benefits of a laparoscopic approach. A multicenter, prospective, randomized trial by Marcello and colleagues, comparing short-term outcomes of left/sigmoid colectomies and total colectomies with a hand-assisted approach vs. a straight laparoscopic approach showed a statistically significant decrease in operating times with a hand-assisted approach (reduced by 33 minutes for sigmoid colectomy, reduced by 57 minutes for total colectomy).(21) They also found no differences in the time to return of bowel function, tolerance of diet, length of stay, postoperative pain scores, or narcotic usage between the two groups. The MITT Study group did not include right colectomy since this procedure is routinely performed via a straight laparoscopic or laparoscopic-assisted approach in the same time as an open operation.(21) TREATABLE CONDITIONS Colon Cancer The treatment of colorectal cancer has been among the most controversial topics in the discussion surrounding the application of laparoscopic techniques to colorectal surgery. This controversy centered on early reports of cancer implants at trocar and incision sites and the fear of an inadequate oncologic resection. While

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improved outcomes in colon and rectal surgery later studies suggested that the incidence of wound implants was, in fact, no greater than in open surgery when performed by experienced surgeons, the controversy was one of the main factors that resulted in a call for a moratorium on laparoscopic resection for colon cancer outside of the auspices of a randomized, controlled trial.(25, 26) This resulted in a variety of randomized, controlled clinical trials which served to put to rest many of these concerns and help delineate the true advantages and disadvantages of a laparoscopic approach.(1–5, 8, 27) The first large single-center randomized controlled trial was published by Lacy et al. in 2002, with a median follow-up of 39 months.(4) They, in fact, reported a higher cancer-related survival for the laparoscopic group. While there was no difference between the laparoscopic and open groups in Stage II cancers, they reported a significantly improved survival in the laparoscopic group for Stage III cancers. The results of the COST trial, which consisted of nearly 900 patients randomized to open or laparoscopic colon resection, showed no difference in overall or disease-free survival between the two groups.(1, 28) It also did not report the same advantage for Stage III patients that Lacy et al. did. As Fleshman et al. point out, the survival advantage that Lacy and colleagues reported may be the result of an underpowered subset analysis. The theory that the survival advantage was due to some physiologic benefit of laparoscopy is not borne out by the results of the COST trial.(28) Reassuringly, the COST trial reported only two wound recurrences in the laparoscopic group, and one in the open group. The CLASICC trial out of the United Kingdom also showed similarly reassuring results, though the rate of conversions was higher.(2) The meta-analysis of these trials by Bonjer et al. confirms the equivalence of open and laparoscopic treatment of colon cancer.(29) The results of these large, multicenter, randomized trials illustrate a number of important points in maximizing the outcomes for laparoscopic colon resection. The importance of surgeon experience and judgment cannot be overstated. The consequences of using laparoscopic resection for potentially curable malignancies as “learning cases” are potentially devastating to the patient. Strict adherence to oncologic principles, just as in open surgery, is paramount, and the dangers of sacrificing these principles in the name of a minimally invasive approach are obvious. The importance of rigorously testing new techniques under the auspices of a randomized, controlled trial is also highlighted by these results. The controversy and emotion that arose over the initial reports of wound implants following laparoscopic colectomy have been laid to rest by the results of these multiple trials. It is safe to say that laparoscopic colon resection for cancer, when guided by the proper principles, is as safe as open resection, with a number of tangible benefits to the patient. Endoscopically unresectable “benign” polyps, at first glance, would appear to be an ideal case for a laparoscopic resection by a surgeon who is still on their “learning curve.” However, multiple authors have reported that upwards of 18–22% of these “benign” lesions are found to have adenocarcinoma on final pathology. (30–32) Large, flat lesions with high-grade dysplasia are more likely to have cancer present and these criteria should guide the surgeon in their decision making. Thus, a surgeon with little experience with laparoscopic resection should approach these cases with great caution. It is vital that these cases be approached

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as formal cancer operations, with strict adherence to the usual oncologic principles. INFLAMMATORY BOWEL DISEASE While Crohn’s disease presents its own unique set of challenges for a minimally invasive approach, it can also provide a unique opportunity. In severe Crohn’s disease, severe inflammatory changes in the mesentery, the presence of abscesses or fistulae, and the difficulty in assessing bowel involvement are all challenges that need to be overcome by the surgeon. Isolated terminal ileal disease, however, would seem to be an ideal setting for a minimally invasive approach, especially for the relatively inexperienced laparoscopist. The high incidence of reoperation in Crohn’s patients makes laparoscopy for the initial surgery an appealing option. While randomized, controlled trials are scarce, multiple recent studies support laparoscopy as a viable option in many cases.(33–39) The advantages associated with a laparoscopic approach in Crohn’s disease are the same as those seen in the previously described cancer trials. Resolution of ileus, resumption of diet, postoperative pain, and length of stay were all improved with a laparoscopic approach. In a prospective, randomized trial from Milsom et al. of patients undergoing open or laparoscopic ileocolic resection for refractory Crohn’s disease, the pulmonary function, morbidity, and length of stay were all improved in the short-term with a laparoscopic approach.(40) These studies support the use of laparoscopy in Crohn’s disease, even, in the right setting, for the inexperienced laparoscopist. As always, the surgeon’s judgment is paramount, and there should be a low threshold to switch to an alternate approach in the right situation. There is no difference in recurrence of Crohn’s disease between patients treated by a laparoscopic or open surgical approach.(37) Ulcerative Colitis The slow acceptance of laparoscopic total proctocolectomy revolves around a couple of factors. First, the early reports of laparoscopic total colectomy were unfavorable. The Cleveland Clinic Florida group published several reports of their results with laparoscopic proctocolectomy for ulcerative colitis in the early 1990s.(41, 42) They reported longer operative times and higher blood loss than in the open group without the desired benefits. At that time, the authors discouraged the laparoscopic approach to total colectomy. These initial reports highlight the importance of the aforementioned learning curve. As surgeons have gained experience with segmental resection, and as technology has advanced, the role of laparoscopic total colectomy for inflammatory bowel disease is being reevaluated and is gaining wider acceptance. More recent reports support the use of laparoscopy for total colectomy and proctocolectomy with and without ileoanal pouch construction, with the same advantages for laparoscopy for segmental resections. While some groups have performed laparoscopic total colectomy on an urgent basis for patients with refractory colitis, it is not routinely recommended for those patients with toxic colitis. (43) A recent study from Chung et al. (44) compared their results of a laparoscopic or open approach to total abdominal colectomy for severe colitis and its impact on subsequent restorative proctectomy. They found that patients undergoing a laparoscopic approach had a faster resumption of diet, less narcotic usage, shorter hospital

laparoscopic colorectal surgery stays, and a shorter time to subsequent restorative proctectomy and ileostomy takedown. The rate of complications between the laparoscopic and open groups was similar. Stewart et al. showed that accelerating doses of immune suppressants and steroids resulted in higher rates of complications. Thus, utilization of laparoscopoic abdominal colectomy as the initial operation to treat severe ulcerative colitis, with few adhesions and quicker arrival to the final goal of reconstructive surgery, is a good alternative to continued medical therapy in some cases.(45) Laparoscopic total colectomy and proctocolectomy are technically challenging operations with 3 to 5 hour operative times. The use of hand-assisted techniques may be a way to cut down on this time while still realizing the benefits of laparoscopy. Rivadeneira et al. in a comparative study from the Lahey Clinic, compared the hand-assisted approach to conventional laparoscopy in patients undergoing laparoscopic proctocolectomy (10 HAL, 13 standard laparoscopy).(46) The operative times decreased in the HAL group (mean 247 minutes), while remaining constant in the laparoscopic group (mean 300 minutes, p < 0.05) over the course of the study. There was no disadvantage in terms of bowel function, length of stay, or outcome in this study. STOMA CREATION The creation of a stoma can be an ideal scenario in order for a surgeon to gain experience in laparoscopic colorectal surgery. It is an excellent way to achieve the benefits of minimally invasive surgery while not dealing with the same ramifications as ­discussed with surgery for resectable colon cancer. There are studies that have shown that laparoscopic stoma creation is a viable alternative to an open approach, with benefit shown in several studies in both morbidity and mortality.(47, 48) The key, just as in open surgery, is to ensure that the limbs of the stomas are oriented properly and that the fascial opening is adequate in order to preserve the blood supply. Also, adequate mobilization of the bowel in order to eliminate tension on the stoma is critical. In particularly obese patients, the surgeon should give consideration to a divided loop-end stoma. By leaving the stapled closed distal limb within the abdomen and delivering only the proximal functioning end through the fascia, less tissue needs to be brought through the abdominal wall opening. However, when creating an end stoma, it is critical to ensure that the proximal limb is opened. Measures such as marking proximal and distal limbs of bowel with sutures or clips, insuflating air into the distal bowel via the anus, or performing flexible endoscopy of the stoma are routine procedures in many center to minimize this occurence. Potential complications of laparoscopic stoma formation include those related to laparoscopy itself—including insufflation needle or trocar injury, air embolism, arrhythmias, CO2 intolerance, and subcutaneous emphysema—and those related to laparoscopic colorectal surgery in particular. These particular complications mostly relate to unfamiliarity with the anatomy as seen through the laparoscope and include ureter, iliac, and mesenteric vessel injury, as well as improper orientation of the limbs of the stoma. As with all laparoscopic surgery, it is critical not to retract or grasp out of the field of view in order to avoid any collateral injury that is not immediately recognized. If tension is noted on the loop of bowel selected for the stoma site, further mobilization may be of benefit to release the bowel or

colon from the retroperitoneal fixation. This should also reduce the incidence of retraction and stricturing at the stoma site. A particular skill needed in the performance of laparoscopic stoma construction is the knowledge of bowel/colon anatomy and relationships of the intestine to adjacent structures as well as vascular anatomy to provide adequate blood supply even to a stoma pulled through a thick abdominal wall. Thus, even though considered a basic laparoscopic case, a certain level of colorectal surgical skill is needed. DIVERTICULITIS Laparoscopy for diverticulitis, while not fraught with the oncologic ramifications of colorectal cancer, presents its own set of challenges, both in the elective and the acute setting. The fibrosis associated with recurrent disease in the elective setting, and the inflammatory changes in the acute setting present their own set of technical issues, and the inexperienced laparoscopist in particular should proceed with caution and retain a low threshold for conversion to an open approach or a hand-assisted approach. As laparoscopy gains more popularity in the management of acute intraabdominal processes like appendicitis or perforated peptic ulcers, the question arises as to whether it may be of benefit in management of diverticulitis in the acute setting. The mainstay of treatment for generalized peritonitis secondary to diverticulitis remains open sigmoid resection with end-colostomy.(49) The subsequent colostomy reversal, however, can be difficult because of the significant adhesions that result. In an effort to ease some of those difficulties, different groups have experimented with various strategies, including a laparoscopic Hartmann’s procedure, and laparoscopic peritoneal lavage with no resection and subsequent elective, one-stage resection.(50, 51) Bretagnol et al. looked at 24 patients who underwent laparoscopic management of perforated sigmoid diverticulitis, of whom 19 were found to have purulent or fecal (Hinchey III or IV) peritonitis. They noted a morbidity of 8%. Laparoscopic sigmoid resection was ultimately performed on these patients electively, with a conversion rate of 16%.(50) Myers et al. in a prospective study of 100 patients, attempted laparoscopic peritoneal lavage on all consenting patients with generalized peritonitis from perforated diverticulitis.(51) Their primary endpoints were operative success and resolution of symptoms. They were successful in 92 patients, with morbidity and mortality rates of 4 and 3%. Two patients developed postoperative pelvic abscesses requiring drainage while two patients represented with diverticulitis at a mean follow-up of 36 months. While they did not look at later reoperation, their results do suggest that laparoscopic peritoneal lavage in expert hands may be a viable option in the acute setting and allow avoidance of a colostomy. The timing of surgery after an acute attack of diverticulitis also remains a question. Zingg et al. in a retrospective study of 178 patients undergoing laparoscopic-assisted sigmoid resection for diverticulitis found that patients undergoing surgery during the same hospitalization had a significantly higher conversion rate, 37.7% vs. 12.9%.(52) In addition, the converted patients had an increased surgical morbidity, though this was not statistically significant (23.8% vs. 19.1%). Hospitalization was significantly longer at 13.5 vs. 10.5 days. Their results suggest that patients who respond

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improved outcomes in colon and rectal surgery to initial antibiotic therapy and wish to undergo laparoscopicassisted sigmoid resection would be better served by delaying colectomy for 6 or more weeks. Similarly, Reissfelder et al. looked prospectively in 2006 at 210 patients who underwent laparoscopic sigmoid resection for acute diverticulitis.(53) They were divided into two groups, one with an elective resection 5–8 days after initial antibiotic treatment, and the other 4–6 weeks after their initial hospitalization. There was a statistically significant increase in conversions and anastomotic leaks in the early group, again supporting the idea of delayed resection after the initial episode. As noted earlier in this chapter, a hand-assisted approach is a potentially attractive way to preserve the benefits of laparoscopy while cutting down on operative times and conversion rates. These benefits may be applied to surgery for diverticulitis, ­particularly in complicated cases (i.e., abscess or fistula). Lee et al. in 2006 compared operative times and outcomes between patients undergoing hand-assisted laparoscopic sigmoid resections and those undergoing a totally laparoscopic approach.(54) Patients with complicated diverticulitis were found to have significantly shorter operative times and lower conversion rates when compared to those undergoing a totally laparoscopic approach. Ureteral stents should also be considered in patients undergoing laparoscopic surgery for diverticulitis. The indications, however, are the same as in open surgery—reoperation, severe inflammation, or the presence of an abscess. Lighted stents are generally not necessary, as the stents can be felt by the surgeon, even in a totally laparoscopic approach. The surgeon should resist the temptation to utilize stents too liberally, as they carry their own set of risks, including bleeding, ureteral obstruction, and perforation. The existing data suggests that a laparoscopic approach to treatment of sigmoid diverticulitis may offer a number of benefits over an open approach. Case selection and surgeon experience, as with other disease processes, is paramount. Strong consideration should be given to a hand-assisted approach in complicated cases. As a general principle in the treatment of diverticulitis, the use of laparoscopic techniques should not compromise the surgical procedure by reducing the amount of colon removed or failing to resect to the level of soft, normal rectum on the distal resection margin. RECTAL PROLAPSE Abdominal fixation procedures for rectal prolapse may offer an ideal opportunity for a laparoscopic approach. The lack of a specimen or an anastomosis solves two of the most potentially vexing problems in laparoscopic colorectal surgery. Laparoscopically-assisted resection rectopexy, however, also may offer many of the same benefits over the open procedure. Whether a resection is involved or not, abdominal fixation procedures may offer an excellent opportunity to learn how to mobilize the rectum laparoscopically, which can then be applied to more extensive procedures, including proctocolectomy or rectal cancer surgery. Ashari et al. in 2005, looked at ten years’ worth of prospectively collected data of patients undergoing laparoscopicallyassisted resection rectopexy for full-thickness rectal prolapse.(55) A total of 117 patients were included in the study. Operative times decreased from a median of 180 minutes in their early experience, down to 110 minutes in the latter part of their experience. At a median follow-up of 62 months, only 2.5% of patients had

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full-thickness prolapse recurrence. Mucosal prolapse recurred in 18% of patients, while 4% of patients required dilation of an anastomotic stricture. This mucosal prolapse recurrence may be a result of less adhesion formation in the pelvis after a laparoscopic dissection. Solomon et al. in 2002, published the findings of a randomized clinical trial of laparoscopic vs. open abdominal rectopexy for rectal prolapse, with a total of 40 patients with full-thickness rectal prolapse randomized to the laparoscopic and open group.(56) Patients were placed on a clinical pathway, which was designed to result in discharge before postoperative day 5. Not surprisingly, mean surgical time was greater in the laparoscopic group (153 vs. 102 minutes, p < 0.01). Nineteen of twenty patients in the laparoscopic group were discharged by day five, while only nine of nineteen in the open group were able to achieve that goal. Total narcotic usage was less in the laparoscopic group as well. While these results are encouraging, the follow-up on these patients is short. In addition, the 18% mucosal prolapse reported by Ashari et al. is concerning. Long-term follow-up is essential in these patients before laparoscopy for rectal prolapse can be considered the gold standard. Other considerations such as anterior deep pelvis mobilization, preservation of the anterior lateral stalks, and combination of sigmoid resection and rectopexy will need to be evaluated to derive the true place of laparoscopic treatment of rectal prolapse. COLONOSCOPIC PERFORATION Iatrogenic perforation of the colon during colonoscopy is a fortunately rare complication. Treatment has generally consisted of laparotomy and repair vs. resection. Because the colon has usually undergone mechanical bowel preparation, simple oversewing of the defect is generally safe and effective. Just as laparoscopy is being applied more often to the repair of perforated peptic ulcers, it would seem logical that it may offer benefits in the treatment of colonoscopic perforation. Bleier et al. in 2008, looked at a series of 18 patients in a four-year period who underwent surgical treatment of iatrogenic perforation.(57) Eleven patients in the laparoscopic group and seven patients in the open group had similar operative times. The patients in the laparoscopic group, however, had statistically significant shorter lengths of stay, fewer complications, and shorter incision lengths. Laparoscopic repair of colonoscopic perforation may become the next step after conservative therapy fails and avoid major morbidity and prolonged recovery if accomplished in a timely fashion. TECHNICAL CONSIDERATIONS OF GOOD LAPAROSCOPIC PRACTICE IN COLORECTAL SURGERY A significant part of minimizing morbidity and mortality and maximizing outcomes in laparoscopic colorectal surgery centers around a number of technical considerations, including trocar placement, use of instruments, and techniques for vascular control. TROCAR PLACEMENT The most commonly used trocars are 5 or 10 mm, depending on whether a stapler will be used, and the size of the camera. When selecting the sites, it is important to place them far enough apart to avoid “swordfighting.” They must be placed in a position that

laparoscopic colorectal surgery allows the surgeon to reach the extremes of the opposite quadrants with the instruments. It is important that the trocars and the monitors be placed, and the surgeon and assistant positioned such that the surgeon is working in-line with the camera, the intraabdominal pathology, and the monitors. This maximizes the ability of the surgeon to work efficiently while minimizing the potential awkwardness of working against the camera. The trocars should be placed in such a manner that they are inserted above the level of the bowel. This avoids the potential danger of sticking the bowel or other structures with the instruments each time they are inserted through the trocars. The skin incisions should be large enough to allow the trocars to be placed without undue skin trauma, but should be small enough to avoid unnecessary movement of the trocars, air leaks through the skin site, or falling out of the trocars. When inserting the trocars, the surgeon should take care to insert them at right angles to the tangent of the curve of the abdominal wall to avoid tearing the peritoneum and reduce the risk of an oblique insertion. The abdominal wall should always be illuminated to avoid injury to blood vessels, which can cause nuisance bleeding throughout the operation. The trocars should always be inserted under direct vision and the surgeon should always look at the trocar after placement to ensure that any bleeding from the abdominal wall is dealt with early. In addition, the surgeon should make sure the retainer rings are visible on the peritoneum, so that the trocar is fully fixed in place, and will not move unnecessarily. Nonbladed trocars hold a number of advantages over bladed trocars. They may help to avoid bowel injury, and also limits the size of the peritoneal opening. The healing pattern of nonbladed trocars through the peritoneum is also better than that of bladed trocars. The options for insertion of the initial trocar are an open technique and a closed technique using a Veress needle. While both methods have their proponents, it is the opinion of the authors that an open technique should always be utilized in a patient who has undergone previous abdominal surgery. The risk of injury to bowel or blood vessels is significantly higher with a blind insertion in a patient with adhesions. Options for open insertion include the use of a Hasson trocar, or in the case of a hand-assisted laparoscopic operation, direct guidance through the hand-port. In nearly all cases, the bladder should be decompressed with a Foley catheter. This is particularly important in cases where a suprapubic trocar will be placed, so as to avoid any injury to the bladder upon insertion. An oral gastric tube will also insure ­gastric decompression. INSTRUMENTS One of the mantras for open surgery has included avoidance of direct handling of the bowel with instruments, especially forceps. The lack of hands inside the abdomen should not change this dictum, if at all possible. The surgeon should try to avoid unnecessary grasping of the bowel. If needed, the instruments should instead be used to push and retract. Rather than grasp the bowel directly, the surgeon should try to grasp the surrounding fat instead. The use of the most atraumatic graspers possible, such as the “wavy” grasper, is essential. When retracting, the surgeon

should make every effort to retract in a 3-dimensional manner so as to maximize the effectiveness of the retraction. Wound protectors and specimen bags are two ways in which to avoid contamination of the wound by the specimen. This can have particular implications when dealing with a cancerous specimen, or a contaminated specimen, such as the acutely inflamed or perforated appendix. The skirt of the handport used in a handassist case is a very effective wound protector. If the handport is not available, some form of ring drape should be used. Placing a sponge into the abdomen, either through a 10 mm port, or through the handport, can be a very effective technique. It can be used to pack the bowel out of the way, protect the bowel, or reduce free-flowing blood which can impair visualization. It can be a very effective way to protect the bowel during retraction so that the surgeon is pushing on the sponge instead of directly on the bowel. VASCULAR CONTROL Methods for vascular control include monopolar cautery, ultrasonic coagulation, clips, staplers, and bipolar devices. While each method has its advantages and disadvantages, it is important to keep several issues in mind. The monopolar device should never be used on larger vessels (i.e., ileocolic artery, inferior mesenteric artery, inferior mesenteric vein). While the ultrasonic shears are effective for vessels <7 mm in size, they have not been proven to be effective on vessels larger than that. Bipolar devices have been proven to be effective on vessels as large as 7 mm and can be an effective and efficient way to manage vascular pedicles. While staplers are also effective for large vascular pedicles, two caveats should be kept in mind. The stapler requires the use of at least a 10 mm trocar, and the surgeon must beware of bleeding through the staples as well. No matter what the method of control, the surgeon should always make sure to have an alternate means of control available in the operating room. Perhaps the two most common and simplest methods are the Endoloop or surgical clips. CONCLUSION Laparoscopic colorectal surgery offers many potential benefits over traditional open surgery, including quicker return of bowel function, decreased pulmonary morbidity, shorter hospital stays, and improved cosmesis. Its widening use across the spectrum of colorectal diseases, while exciting, is also cause for caution amongst all colorectal surgeons. The key to optimizing outcomes in laparoscopic colorectal surgery lies in following several key principles, including careful patient selection, strict adherence to oncologic principles, meticulous attention to technical details, and a willingness to alter one’s approach when needed. The ­surgeon should not look upon conversion as a failure, but rather as a switch to an alternative approach. The judicious use of a hand-assisted approach may offer a way for the surgeon to preserve the benefits of laparoscopy while providing a means to complete complex and time-consuming cases in a safer and more efficient manner. Ultimately, randomized, controlled trials with long-term ­follow-up will be needed to truly determine the role of laparoscopy in managing colorectal diseases. If the aforementioned ­benefits are maintained in the long run with durable results, then laparoscopy,

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improved outcomes in colon and rectal surgery performed in expert hands, may ultimately become the standardof-care for treating many of these disease processes. REFERENCES   1. A comparison of laparoscopically assisted and open colectomy for colon cancer. N Engl J Med 2004; 350(20): 2050–9.   2. Guillou PJ, Quirke P, Thorpe H, et al. Short-term endpoints of conventional versus laparoscopic-assisted surgery in patients with colorectal cancer (MRC CLASICC trial): multicentre, randomised controlled trial. Lancet 2005; 365(9472): 1718–26.   3. Kuhry E, Schwenk WF, Gaupset R, et al. Impact of hospital case volume on short-term outcome after laparoscopic operation for colonic cancer. Surg Endosc 2005; 19(5): 687–92.   4. Lacy AM, Pera M, Delgado S, et al. Laparoscopy-assisted colectomy versus open colectomy for treatment of nonmetastatic colon cancer: a randomised trial. Lancet 2002; 359(9325): 2224–9.   5. Milsom JW, Bohm B, Hammerhofer KA, et al. A prospective, randomized trial comparing laparoscopic versus conventional techniques in colorectal cancer surgery: a preliminary report. J Am Coll Surg 1998; 187(1): 46–54.   6. Stage JG, Schulze S, Moller P, et al. Prospective randomized study of laparoscopic versus open colonic resection for adenocarcinoma. Br J Surg 1997; 84(3): 391–6.   7. Stocchi L, Nelson H. Laparoscopic colectomy for colon ­cancer: trial update. J Surg Oncol 1998; 68(4): 255–67.   8. Schwenk W, Bohm B, Muller JM. Postoperative pain and fatigue after laparoscopic or conventional colorectal resections. A prospective randomized trial. Surg Endosc 1998; 12(9): 1131–6.   9. Bessler M, Whelan RL, Halverson A, et al. Controlled trial of laparoscopic-assisted vs. open colon resection in a porcine model. Surg Endosc 1996; 10(7): 732–5. 10. Bohm B, Milsom JW, Fazio VW. Postoperative intestinal motility following conventional and laparoscopic intestinal surgery. Arch Surg 1995; 130(4): 415–9. 11. Hotokezaka M, Combs MJ, Schirmer BD. Recovery of gastrointestinal motility following open versus laparoscopic colon resection in dogs. Dig Dis Sci 1996; 41(4): 705–10. 12. Raue W, Haase O, Junghans T, et al. ‘Fast-track’ multimodal rehabilitation program improves outcome after laparoscopic sigmoidectomy: a controlled prospective evaluation. Surg Endosc 2004. 18(10): 1463–8. 13. Senagore AJ, Duepree HJ, Delaney CP, et al. Results of a standardized technique and postoperative care plan for laparoscopic sigmoid colectomy: a 30-month experience. Dis Colon Rectum, 2003; 46(4): 503–9. 14. Basse L, Jakobsen DH, Billesbolle P, et al. A clinical pathway to accelerate recovery after colonic resection. Ann Surg 2000; 232(1): 51–7. 15. Dowson HM, Bong JJ, Lovell DP, et al. Reduced adhesion formation following laparoscopic versus open colorectal surgery. Br J Surg 2008; 95(7): 909–14. 16. Johnson P, Richard C, Ravid A, et al. Female infertility after ileal pouch-anal anastomosis for ulcerative colitis. Dis Colon Rectum 2004; 47(7): 1119–26.

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17. Cornish JA, Tan E, Teare J, et al. The effect of restorative proctocolectomy on sexual function, urinary function, fertility, pregnancy and delivery: a systematic review. Dis Colon Rectum 2007; 50(8): 1128–38. 18. Gorgun E, Remzi FH, Goldberg JM, et al. Fertility is reduced after restorative proctocolectomy with ileal pouch anal anastomosis: a study of 300 patients. Surgery 2004; 136(4): 795–803. 19. Delaney CP, Pokala N, Senagore AJ, et al. Is laparoscopic colectomy applicable to patients with body mass index >30? A case-matched comparative study with open colectomy. Dis Colon Rectum 2005; 48(5): 975–81. 20. Senagore AJ, Delaney CP, Madboulay K, et al. Laparoscopic colectomy in obese and ­nonobese patients. J Gastrointest Surg 2003; 7(4): 558–61. 21. Marcello PW, Fleshman JW, Milsom JW, et al. Hand-assisted laparoscopic vs. laparoscopic colorectal surgery: a multicenter, prospective, randomized trial. Dis Colon Rectum 2008; 51(6): 818–26. 22. Senagore AJ, Luchtefeld MA, Mackeigan JM. What is the learning curve for laparoscopic colectomy? Am Surg 1995; 61(8): 681–5. 23. Simons AJ, Anthone GJ, Ortega AE, et al. Laparoscopicassisted colectomy learning curve. Dis Colon Rectum 1995; 38(6): 600–3. 24. Wishner JD, Baker JW, Hoffman GC, et al. Laparoscopicassisted colectomy. The learning curve. Surg Endosc 1995; 9(11): 1179–83. 25. Reilly WT, Nelson H, Schroeder G, et al. Wound recurrence following conventional treatment of colorectal cancer. A rare but perhaps underestimated problem. Dis Colon Rectum 1996; 39(2): 200–7. 26. Vukasin P, Ortega AE, Green FC, et al. Wound recurrence following laparoscopic colon cancer resection. Results of the American Society of Colon and Rectal Surgeons Laparoscopic Registry. Dis Colon Rectum 1996; 39(10 Suppl): S20–3. 27. Weeks JC, Nelson H, Gelber S, et al. Short-term quality-of-life outcomes following laparoscopic-assisted colectomy vs. open colectomy for colon cancer: a randomized trial. JAMA 2002; 287(3): 321–8. 28. Fleshman J, Sargent DJ, Green E, et al. Laparoscopic colectomy for cancer is not inferior to open surgery based on 5-year data from the COST Study Group trial. Ann Surg 2007; 246(4): 655–62. 29. Bonjer HJ, Hop WC, Nelson H, et al. Laparoscopically assisted vs. open colectomy for colon cancer: a meta-analysis. Arch Surg 2007; 142(3): 298–303. 30. Brozovich M, Read TE, Salgado J, et al. Laparoscopic colectomy for apparently benign colorectal neoplasia: a word of caution. Surg Endosc 2008; 22(2): 506–9. 31. Pokala N, Delaney CP, Kiran RP, et al. Outcome of laparoscopic colectomy for polyps not suitable for endoscopic resection. Surg Endosc 2007; 21(3): 400–3. 32. Ross HM, Li C, Rosenthal J, et al. Laparoscopic colon resection for polyps: a good novice case? Dis Colon Rectum 2006; 49(6): 879–82.

laparoscopic colorectal surgery 33. Edden Y, Ciardullo J, Sherafgan K, et al. Laparoscopicassisted ileocolic resection for Crohn’s disease. JSLS 2008; 12(2): 139–42. 34. Fichera A, Peng Sl, Elisseou NM, et al. Laparoscopy or conventional open surgery for patients with ileocolonic Crohn’s disease? A prospective study. Surgery 2007; 142(4): 566–71. 35. Tan JJ, Tjandra JJ. Laparoscopic surgery for Crohn’s disease: a meta-analysis. Dis Colon Rectum 2007; 50(5): 576–85. 36. Tilney HS, Constantinides VA, Heriot AG, et al. Comparison of laparoscopic and open ileocecal resection for Crohn’s disease: a metaanalysis. Surg Endosc 2006; 20(7): 1036–44. 37. Lowney JK, Dietz DW, Birnbaum EH, et al. Is there any difference in recurrence rates in laparoscopic ileocolic resection for Crohn’s disease compared with conventional surgery? A longterm, follow-up study. Dis Colon Rectum 2006; 49(1): 58–63. 38. Rosman AS, Melis M, Fichera A. Metaanalysis of trials comparing laparoscopic and open surgery for Crohn’s disease. Surg Endosc 2005; 19(12): 1549–55. 39. Casillas S, Delaney CP. Laparoscopic surgery for inflammatory bowel disease. Dig Surg 2005; 22(3): 135–42. 40. Milsom JW, Hammerhofer KA, Bohm B, et al. Prospective, randomized trial comparing laparoscopic vs. conventional surgery for refractory ileocolic Crohn’s disease. Dis Colon Rectum 2001; 44(1): 1–8. 41. Reissman P, Salky BA, Pfeifer J, et al. Laparoscopic surgery in the management of inflammatory bowel disease. Am J Surg 1996; 171(1): 47–50. 42. Schmitt SL, Cohen SM, Wexner SD, et al. Does laparoscopicassisted ileal pouch anal anastomosis reduce the length of hospitalization? Int J Colorectal Dis 1994; 9(3): 134–7. 43. Marcello P, Young-Fadok T. Laparoscopy, in the ASCRS textbook of colon and rectal surgery, B. Wolff, Fleshman J, Beck, D, Pemberton, J, Wexner, S, ed. Springer: New York, 2007: 698. 44. Chung TP, Fleshman JW, Birnbaum EH, et al. Laparoscopic versus open total abdominal colectomy for severe colitis: impact on recovery and subsequent completion restorative proctectomy. Dis Colon Rectum 2009; 52: 4–10. 45. Stewart D, Chao A, Kodner I et al. Subtotal colectomy for toxic and fulminant colitis in the era of immunosuppressive therapy. Colorectal Dis 2009; 11(2): 184–90.

46. Rivadeneira DE, Marcello PW, Roberts PL, et al. Benefits of hand-assisted laparoscopic restorative proctocolectomy: a comparative study. Dis Colon Rectum 2004; 47(8): 1371–6. 47. Scheidbach H, Ptok H, Schubert D, et al. Palliative stoma creation: comparison of laparoscopic vs. conventional procedures. Langenbecks Arch Surg 2009; 394(2): 371–4. 48. Schwandner O, Schiedeck TH, Bruch HP. Stoma creation for fecal diversion: is the laparoscopic technique appropriate? Int J Colorectal Dis 1998; 13(5–6): 251–5. 49. Roberts P, Abel M, Rosen L, et al. Practice parameters for sigmoid diverticulitis. The standards task force American Society of colon and rectal surgeons. Dis Colon Rectum 1995; 38(2): 125–32. 50. Bretagnol F, Pautret K, Mor C, et al. Emergency laparoscopic management of perforated sigmoid diverticulitis: a promising alternative to more radical procedures. J Am Coll Surg 2008; 206(4): 654–7. 51. Myers E, Hurley M, O’Sullivan G, et al. Laparoscopic peritoneal lavage for generalized peritonitis due to perforated diverticulitis. Br J Surg 2008; 95(1): 97–101. 52. Zingg U, Pasternak I, Guertler L, et al. Early vs. delayed elective laparoscopic-assisted colectomy in sigmoid diverticulitis: timing of surgery in relation to the acute attack. Dis Colon Rectum 2007; 50(11): 1911–7. 53. Reissfelder C, Buhr HJ, Ritz JP. What is the optimal time of surgical intervention after an acute attack of sigmoid diverticulitis: early or late elective laparoscopic resection? Dis Colon Rectum 2006; 49(12): 1842–8. 54. Lee SW, Yoo J, Dujovny N, et al. Laparoscopic vs. handassisted laparoscopic sigmoidectomy for diverticulitis. Dis Colon Rectum 2006; 49(4): 464–9. 55. Ashari LH, Lumley JW, Stevenson AR, et al. Laparoscopicallyassisted resection rectopexy for rectal prolapse: ten years’ experience. Dis Colon Rectum 2005; 48(5): 982–7. 56. Solomon MJ, Young CJ, Eyers AA, et al. Randomized clinical trial of laparoscopic versus open abdominal rectopexy for rectal prolapse. Br J Surg 2002; 89(1): 35–9. 57. Bleier JI, Moon V, Feingold D, et al. Initial repair of iatrogenic colon perforation using laparoscopic methods. Surg Endosc 2008; 22(3): 646–9.

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14

Medical legal issues Charles F Gay Jr and Terry C Hicks

Challenging Case A 60-year-old woman with a strongly positive family history of colorectal cancer undergoes a colonoscopy. She has a 1.5 cm pedunculated polyp snared from the transverse colon. Five days after the procedure, she presents to the emergency room with a lower GI bleed. She is hemodynamically stable and you admit her for observation. She remains stable and is discharged 2 days later with no further bleeding episodes. The hospital risk manager calls you to discuss this case. Comments When you meet with the risk manager, you inform her that you had seen the patient in your office before the procedure. During this office visit, you had discussed with the patient, her risk factors, indications for the procedure, details of the procedure, and potential risks. This conversation was documented in your office note and the patient signed a consent for the procedure. The ­procedure was performed in the usual fashion. You feel that you have a good relationship with the patient and the records are well documented. Although any untoward outcome could lead to ­litigation, the risk manager agrees that you have taken the appropriate actions to minimize your risk. INTRODUCTION As surgery enters the next millennium, it finds itself at the crossroads of a serious medical liability crisis. This chapter will briefly review important aspects of the United States medical liability situation and then addresses some risk-prevention techniques for colorectal surgeons. This includes a general overview of the legal process pertaining to medical malpractice issues and tips to help prevent and defend such cases. It is intended to provide practical information that can be used by medical care providers. Magnitude of the Problem A lack of affordable liability insurance is leading some doctors to retire prematurely; relocate their practices to nonlitigious areas, practice without insurance, or drop risky procedures. Some of the specific examples are as follows: ••

••

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Over the past decade, hundreds of emergency rooms have been forced to close their doors at least temporarily even though the number of emergency visits have climbed over 20%.(1) In many areas of the country, pregnant women are finding it more difficult every year to get the care they need. A survey by the American College of Obstetricians and Gynecologists found that one in seven OBGYNs in the United States have stopped practicing obstetrics because of the medical liability crisis, and more than 12% of OBGYNs have decreased their numbers of deliveries for similar reasons.

•• •• •• ••

The American Hospital Association says that more than half of the hospitals are having difficulty recruiting doctors because of the medical liability crisis.(2) More than half of hospitals surveyed in “crisis” states said their local community lost doctors because of the medical liability crisis. 71% of surveyed neurosurgeons said they no longer perform aneurism surgery, 23% no longer treat brain tumors, and 75% no longer operate on children. At one point, in Palm Beach County, Florida, only four neurosurgeons were available to handle emergency calls in the area’s 13 hospitals, leaving most emergency rooms with no coverage.

The evidence is clear that there exist a medical malpractice crisis in the United States, and at present multiple grass route efforts are being undertaken to address this on a local as well as on a national level. The American Medical Association has continued to add states to its liability crisis list, and more and more physicians are finding that insurance premiums are becoming beyond their reach. The most important fallout of this situation is that access to care is being endangered especially in rural areas and among low-income, inner-city populations. By 2003, medical liability cost reached $26 billion—a 2000% increase over 1975. Medical liability costs are rising far more rapidly than the overall medical costs. From 1975 to 2000, medical costs rose 449%, while medical liability costs rose by 1,642%. A study by Blue Cross Blue Shield of “crisis” states found huge jury verdicts where the primary driver for higher liability premiums.(3) Based on comprehensive jury verdict research, there is little doubt that soaring jury verdicts are serious-ongoing problems. At present, half of the jury awards in medical liability cases exceed $1 million, and the average award is $4.7 million.(4) The number of mega awards has skyrocketed especially in states with no limits on noneconomic damages. For the past several years, juries have awarded lottery-size verdicts of $80, $90, or even $100 million.(5) Many physicians feel the medical liability crisis is very straightforward. They note that medical liability costs are soaring faster than the rate of overall healthcare costs and the rate of inflation, leading directly to increasing insurance premiums for doctors. In short, their position is that the litigation system generates too many lottery-size verdicts, and encourages too many meritless cases. As a result, insurance companies are fleeing the market, making it more difficult for doctors to obtain liability coverage at any price. The US Department of Health and Human Services concluded: “The excess of a litigation system raises the cost of healthcare for everyone, threatens Americans access to care, and impedes efforts to improve the quality of care”.(6) Other major impacts of the malpractice crisis are the practice of defensive medicine and a negative impact on the young physicians in training. In a recent AMA survey, 48% of the students

medical legal issues in their 3rd and 4th year of medical school indicated the liability situation was a factor in their specialty choice. It is of interest to note that overall 75% of medical liability claims in 2004 were closed without payment to the plaintiff; and of the 7% of the claims that went to a jury verdict, the defendant won 83% of the time. Unfortunately, physicians that win at trial still have large fees to pay for their defenses. The average cost being $93,559 per case where the defendant prevailed at trial. In all cases where the claim was dropped or dismissed, the cost of the defendants averaged $18,774.(7) Until medical liability issues are resolved, physicians will be forced to continue to deal with the present medical legal climate, and it is our hope that the following information will provide some guidelines to lower their exposure to medical legal risks by utilizing proactive risk management steps. In today’s litigious society, physicians who practice good medicine, exercise effective communications skills, establish rapport with the patient, and accurately document care have the best chance of averting malpractice claims. Even when physicians do all of these, however, a bad outcome may still result in the patient’s filing a claim for malpractice.(8) Research appears to support the position that a patient who perceives the physician as having good interpersonal skills and communication is less likely to sue.(9) There are ways to conduct a medical practice that deter patients from making claims and, even after one is made, can enhance the chances of winning the case. Physician-Patient Relationship Medicine has changed dramatically in the last few decades because of extraordinary technologic advances that have resulted in specialization, such as colorectal surgery. This fragmentation often decreases the opportunity to communicate effectively with patients, who have also become much more demanding consumers, increasingly aware of their “rights” through media and lawyer advertising. Health insurers contribute to the problem, not only by creating incentives that discourage referrals to a specialist but also by placing restrictions on the specialist, once referral is made, that can impede opportunities to establish rapport with the patient. Under such circumstances, it is important to make the most of each opportunity to listen to the patient, remember and use the patient’s name, explain procedures in lay terms (avoid medical terminology), and take the time necessary to answer any and all questions. Remember that listening to a patient’s questions and complaints will be much less time consuming than defending a malpractice claim. Still one of the best books for improving communication and relationships is Dale Carnegie’s How to Win Friends and Influence People.(10) For a more practical guide with a medical orientation one should read Malpractice Prevention and Liability Control for Hospitals, by Orlikoff and Vanagunas.(11) The frequency of medical malpractice claims has been on the rise since the early 1970s.(12) As long as the contingency fee system exists and there is not a loser pay provision, the rise in suits against physicians will likely continue. Accordingly, it is incumbent on the well-educated and well-trained specialist to be aware of areas of treatment in colorectal disease that present an increased risk of malpractice claims.

High-Risk Areas in Colorectal Treatment The following circumstances associated with increased risk for malpractice claims in colorectal disease have been identified.(13)

Delay in diagnosis of colon and rectal cancer and appendicitis Iatrogenic colon injury (e.g., colon perforation) Iatrogenic medical complications during diagnosis or treatment Sphincter injury with fecal incontinence resulting from anorectal surgery Lack of informed consent The colorectal physician who is aware of these potential high-risk conditions can use risk-prevention strategies to avoid litigation. Informed Consent Physicians should be mindful that consent and informed consent are quite different concepts. Consent implies permission. Informed consent is assent given based on information provided or knowledge of the procedure and its inherent risks, benefits, and alternatives. Courts have long recognized that “Every human being of adult years and sound mind has a right to determine what shall be done with his own body.”(14) The law of informed consent may vary to some degree from state to state, but regardless of the law of the state, each patient should be allowed an exchange of information with the physician before a procedure is done. Informed consent is not satisfied by merely having the patient sign a form. It is satisfied when consent was obtained after full disclosure of the risks, benefits, and alternatives, of the procedure. Many states use the “reasonable practitioner standard” to judge whether informed consent was obtained. This standard focuses on what a reasonable physician would disclose. The physician’s duty is not to disclose all risks but primarily those that are significant or material. A risk is material depending on its likelihood of occurrence or the degree of harm it presents. The focus is on whether a reasonable person in the patient’s position probably would attach significance to the specific risk. This is the “reasonable patient standard” that some state courts apply. Moreover, to prevail on a claim for lack of informed consent, in most states the patient must still prove causation (i.e., that he or she would not have consented to the procedure if informed of the risk. As a practical matter, it is difficult for a patient to persuade a judge or jury that even though the surgery was needed to relieve pain or disease, he or she would not have consented if told of the risk of, for example, perforation of the colon. This is particularly true when a patient is told of much more severe risks such as death or paraplegia and agrees to the surgery. In that regard, the question to be answered by the judge or jury on an issue of informed consent is whether a reasonable patient in the plaintiff ’s positions would have consented to the treatment or procedure even if the material information and risks were disclosed. The following points should always be discussed with the patient: •• •• •• ••

The general nature of the proposed treatment or procedure The likely prospects for success of the treatment (but no guarantee) The risks of failing to undergo the treatment The alternative methods of treatment, if any, and their inherent risks

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improved outcomes in colon and rectal surgery Suffice it to say that good rapport with the patient coupled with accurate and complete charting are the best tools to deter suits based on informed consent and to provide a heavy shield in defending them. Documentation The importance of good communication and rapport with patients (i.e., treating patients as you would like to be treated) cannot be overemphasized in deterring lawsuits; however, ­complete and accurate documentation of patient care is invaluable to a defense of claims. In addition, good documentation may well nip in the bud a potential claim when the plaintiff attorney considering filing suit reviews the record and care is fully documented. Plaintiff attorneys are more likely to bring suit when the case is poorly documented, because they can more easily argue that what happened in the care of the patient was sinister and improper. Where documentation is clear and accurate, the plaintiff attorney may be deterred from filing suit because what ­happened is easily proved from the record. Thus judgment becomes the issue when documentation is accurate, and judgment used by physicians in most cases is easier to successfully defend than a vague, evasive, and poorly documented chart. The following are some time-honored rules for charging that help defend against malpractice claims. Charting A. Thorough and accurate charting is your primary shield to liability. B. If an event in which you are involved gives rise to litigation, chances are your testimony will not be taken for 1 or 2 years after the event. Accordingly, your chart will provide the ­content and guidelines for your testimony. C. Most important: If it is not charted, it was not done, nor was it observed, administered, or reported. In Smith v. State through Dept of HHR, (15) the court stated: The experts concluded that decedent’s condition required continued monitoring and that charting should have been done on a regular basis. The experts also agreed that the lack of documentation indicated that no one was properly observing the decedent, based on the standard maximum “not charted, not done.”   …The evidence indicates that the decedent was not adequately monitored in this case. The nurses did not specifically recall the patient, and thus the best evidence of their actions would have been the documentation of the chart (emphasis added). D. General guidelines   1. If you are the treating or primary physician, make a daily entry on the chart.   2. Chart at the earliest possible time.   3. If the situation prevents you from charting until later, state why and that the recorded times are best estimates and not fully accurate.   4. Always record the time (designate AM or PM) and the date of every entry.   5. Chart all consultations.

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  6. Never black out or white out any entry on a chart. Should you make a mistake in charting, place a single line through the erroneous entry and label the entry “error in charting.” However, if a hospital policy exists that governs errors in charting, follow it. An addendum is acceptable if placed ­properly in sequence with the date and time it is made. An addendum squeezed between progress notes is inappropriate.   7. Write legibly.   8. Spell correctly.   9. Chart professionally; do not impugn or insult the patient. 10. Never alter the medical records. 11. Do not insult, impugn, or criticize colleagues, co-workers, or support staff. 12. Always designate the dose, site, route, and time of medication 13. Sign your entries on the chart. 14. Do not chart an incident report in your notes. 15. Chart objectively, not subjectively; do not use ambiguous terms (examples below) Subjective

Objective

Patient doing well.

Patient denies any complaints. Awake, alert, and oriented. Vital signs stable: BP, 100/70: P, 72; R, 18

Breath sounds within normal limits (WNL)

Respirations regular and unlabored. Breath sounds clear and equal bilaterally on auscultation. No rales or rhonchi noted.

Circulation check WNL.

Pedal pulses noted bilaterally. Nail beds blanch quickly and toes warm to touch. Patient denies any pain or tingling.

16. Document use of all restraints and safeguards, and patient positioning (extremely important in surgery). 17. Document all patient noncompliance. 18. Document all patient education and discharge instructions, and patient responses. 19. Always document patient status on transfer or discharge. 20. Record the patient’s name on each page of the medical chart. 21. Use accepted medical abbreviations. 22. Do not chart in advance. E. Guidelines for charting in the ambulatory setting   1. Always chart the return visit date and the date that was provided to the patient.   2. Always chart all cancelled and missed appointments.   3. Document all telephone conservations and their content.   4. Chart all prescriptions and refills, as well as patient teaching regarding prescriptions.   5. Chart all follow-up and discharge instructions. If possible, have the patient or his or her representative cosign these instructions. Anatomy of a Malpractice Suit Initial Phase Once a patient initiates a claim for medical malpractice, the physician should immediately place a call to the risk manager or to the

medical legal issues malpractice insurance carrier. An attorney will usually be selected, and the physician should insist that the appointed counsel be experienced and have a well-established reputation in the ­handling of malpractice cases. Physicians should work closely with the defense attorney to review and analyze the allegations of the suit, with particular focus on the strengths and weakness of the case. This team effort can often substantially enhance the strength of the defense by educating the attorney on the medical aspects of the case. Pretrial Discovery During this stage, each side will discover the facts and opinions in the case. Written questions, or interrogatories, can usually be propounded to obtain written responses. Depositions usually ­follow the written discovery and are important to the overall outcome of the case. Before testifying by deposition or otherwise, it is advisable that the physician be thoroughly familiar with the facts, including previous and subsequent medical care of the patient and the allegations against the physician. This requires careful review of medical records, other depositions, and all medical data related to the case. A conference should be held with the attorney before the physician’s deposition. They physician should allow ample time to confer with the defense attorney before testifying. Remember that the judicial system is adversarial, and the purpose of the deposition is not to convince the plaintiff attorney to understand that the case is frivolous. They physician is there to answer the questions and defend the care administered, not to educate the plaintiff attorney. The deposition is simply the physician’s testimony, given under oath, before a court reporter, in an informal setting. Attorneys for both defendant and plaintiff are present. Any party to the lawsuit may be present, but often the physician is the only party present. The testimony is taken down in question-and-answer form. Under the laws of discovery, the plaintiff attorney has the right to ask the defendant physician proper questions. The physician is present simply to discharge a legal obligation to answer proper questions. The physician’s deposition is most important. A good effort is essential for an effective presentation. Close cooperation with the defense attorney in preparation is fundamental. Above all, a physician must be his or her own person. Thorough preparation will assist physicians in giving a deposition with which they will be perfectly comfortable when they see the printed transcript, that is, one that will be easily defended, should any part of it later be challenged. The following suggestions for giving testimony in depositions can be helpful to the physician:   1. Tell the truth; you must testify accurately.   2. Do not guess or speculate. If you do not know the answer to a question, say so.   3. If you are not certain of what the attorney is asking, ask that the questions be clarified or repeated. Do not attempt to rephrase the question for the interrogator (e.g., “If you mean such and such,”).   4. Keep your answers short and concise. Do not volunteer information. Answer only the question posed.

  5. Be courteous. Avoid jokes and sarcasm.   6. Think about each question that is posed. Listen to each word. Formulate an answer, then give the answer. Do not permit yourself to become hurried.   7. Do not argue with opposing counsel. If an argument is ­necessary, your attorney will do it for you.   8. If you realize that you have given an incorrect answer to a previous question, stop at that moment and say so; then ­correct your answer.   9. Be aware of questions that involve distances and time. If you make an estimate, make sure everyone knows it is an estimate. 10. Do not lose your temper, no matter how hard pressed. This may be a deliberate ploy; do not fall for it. 11. Do not anticipate questions. Be sure to let the attorney ­completely finish the question before you begin to respond. 12. Do not exaggerate or brag. Testing Your Memory of the Case You have the right to refer to the chart or hospital records whenever you wish. Your memory is usually a composite of events you recall as jogged by your records. Watch for generalities, ploys, and tricky questions by the plaintiff attorney during the deposition. Generalities. Often the plaintiff ’s attorney will begin with general questions, such as, “Doctor, how do you treat a patient when you suspect he has X disease?” In all likelihood, the lawsuit to which you are a party involves X disease or involves the plaintiff ’s attorney trying to make it X disease. You really cannot answer this question, and you should say just that. X disease probably occurs in various forms, and you have been given no particular information—no patient complaints, no patient history, no findings on physical examination, no results of laboratory studies, no clinical impression—all factors you must know to diagnose and treat intelligently. The question is simply too general. A similar question might be “Doctor, what are the standards for making a diagnosis of X disease?” Again, you should advise that this question is too broad and defies rational response because no details have been given. You, as a physician, do not immediately diagnose X disease or any other diagnose X disease or any other disease. You evaluate all the data in light of your formal training and clinical experience in considering or making a diagnosis. Patient signs and symptoms are innumerable. You must have ­specifics. For example, in one doubtful clinical presentation, you may have to order a particular set of laboratory studies; in another, the evidence of a certain disease process may be more definitive and clear-cut from the history and clinical examination. A proper question is, “Doctor, what are the characteristics of X disease?” Particularly if your case involves X disease, you should know its characteristics, but you should also point out that they are general characteristics and most certainly will vary in specific instances. The point is, you must avoid generalities. You must demand specifics. Try to make the questioner stick to the specific case. Ploys Question: “Doctor, you have no memory of events independent of your records, do you?” Appropriate response: “I have an excellent recall of the events when I refer to the records.”

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improved outcomes in colon and rectal surgery Ploy: “Doctor, if an event is not noted in your records or in the hospital records, is it fair to say that event did not occur?” Appropriate response: “That is incorrect. It is impossible for a ­physician to note everything that occurs. My records are for my own use, to jog my memory. Thus I note pertinent highlights, which when later reviewed give me the complete picture at the time in question.” Remember that physicians treat patients, not charts. You may properly testify to the following: 1. 2. 3. 4.

What you actually recall What you recall with the assistance of your records What is recorded What your routine or standard procedure is, even when such is not recalled and not recorded

Tricky questions. Many plaintiff attorneys will use questions cleverly phrased to evoke a response that can later be used against the physician. Possibilities. Questions phrased in terms of possibility invite speculation and are improper. The criterion is reasonable medical probability. Question: “Doctor, isn’t such and such possible?” or “Couldn’t such and such have happened?” Appropriate response: “Most improbable.” Doing things differently. Almost all malpractice cases involve the “retrospectroscope” or Monday morning quarterbacking to suggest the physician knew things beforehand that were only learned later or that the physician has 100% control over the ­healing process. Question: “Doctor, is there anything you would do differently now if you had Mrs. White’s case to treat again?” Appropriate response: “My recommendations to Mrs. White were based on her complaints, her history, and findings at the time and on my clinical impression at that time. The course I ­recommended was appropriate on the basis of those factors. Question: “Doctor, you did not intend for Mrs. White to have this complication, did you?” Appropriate response: “Of course, no harm to Mrs. White was intended. At the time of my recommendations, there were good prospects for a good result. The procedure (or regimen) does have known complications, and that is why the risks were explained to her beforehand.” Many other factors are involved in preparing for and ­suc­cessfully testifying by deposition or at trial.(16) Suffice it to say that effective and sincere testimony is critical to a successful defense in malpractice cases. Ineffective testimony can render a defensible case indefensible. Many tricks and ploys may be used by the plaintiff attorney, and the physician who is prepared with a basic understanding of how to answer such questions can substantially enhance the defense. Trial After pretrial discovery, the physician should have a clear understanding of the evidence and witnesses, the experts in particular, to be use against him or her at trial. Working with the defense attorney to rebut this evidence and to assist with selection or

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expert witnesses to testify for the defense is strongly advised and helps the physician to prepare the defense. At the trial, the physician is carefully observed at all times by the judge and jury, and the physician’s trial testimony, mannerisms, and behavior are critical to a favorable verdict. A well-trained and educated physician who portrays a sincere, conscientious, and caring attitude about the patient’s wellbeing greatly increases the chances of a favorable jury verdict, even where severe complications have occurred and there may be questions of the appropriateness of the course of treatment chosen. Conclusion The defense of medical malpractice claims is similar to the defense of criminal cases. The physician stands accused and reputation is usually an issue of great importance. The emotional costs to the physician are sometimes staggering. The physician should recognize that until some meaningful tort reform is enacted, these cases will likely continue to increase and should be dealt with as a regrettable aspect of practice.(17) Under these circumstances, it is best to accept the reality of the medicolegal arena and use the best means available to aggressively defend and win the malpractice case.(18) References   1. The American College of Emergency Room Physician; cited in Federal Medical Liability Reform. Alliance of Specialty Medicine; 2005.   2. The American Hospital Association. Professional Liability Insurance: A Growing Crisis; 2003.   3. Blue Cross Blue Shield Assoc. The Medical Malpractice Insurance Crisis: The Impact of healthcare and access; 2003.   4. Manhattan Institute. Malpractice maladies: Doctors continue to flee states without – of – control medical – injury- verdicts; 2005.   5. U.S. Dept. of Health and Human Services. Addressing the new healthcare crisis: Reforming the medical litigation ­system to improve the quality of healthcare; 2003.   6. U.S. Dept. of Health and Human Services. Addressing the new healthcare crisis; Reforming the medical litigation ­system, improve the quality of healthcare; 2003.   7. The American Medical Association. Medical liability reform; 2006.   8. Entman SS, Glass CA, Hickson GB et al. The relationship between malpractice claims history and subsequent obstetric care. JAMA 1994; 272: 1588–91.   9. Hickson GB, Clayton EW, Githens PB, Sloan FA. Factors that prompted families to file medical malpractice claims following perinatal injuries. JAMA 1992; 267: 1359–63. 10. Carnegie D. How to Win Friends and Influence People. New York: Simon & Schuster; 1936. 11. Orlikoff J. Vanagunas A. Malpractice Prevention and Liability Control for Hospitals. Chicago: American Hospital Association; 1988. 12. Danzon PM. The frequency and severity of medical malpractice claims: New evidence. Law Contemp Probl 1986; 49: 57–84.

medical legal issues 13. Kern K. Medical malpractice involving colon and rectal disease: a 20-year review of United States civil court litigation. Dis Colon Rectum 1993; 36: 531–9. 14. Schloendorff v. Society of New York Hospital, 211 NY 125, 105 NE 92,93; 1914. 15. Smith v. State, through Dept of HHR, 517 SO2d 1072. La App 3d Cir; 1987.

16. Taraska JM. The physician as witness. In Legal Guide for Physicians. New York: Matthew Bender, 1994: 1–56. 17. Taraska JM. Tort reform. In Legal Guide for Physicians. New York: Matthew Bender, 1994: 1–64. 18. Gay CE. Medicolegal issues. In Hicks TC, Beck DE, Opelka FG, Timmcke AE. eds, Complications of Colon and Rectal Surgery. Baltimore: Williams & Wilkins, 1996: 468–77.

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15

Miscellanous conditions M Benjamin Hopkins and Alan E Timmcke

Challenging Case A 26-year-old man has a 2 month history of perianal itching. He has variable bowel movements and no family history of colorectal cancer. Physical exam demonstrates thickened perianal skin with ridges in a circum anal pattern. The sphincter tone is normal and no masses or tenderness is appreciated. Case Management A diagnosis of pruritis ani is made and the patient was placed on additional dietary fiber and instructed on anal hygiene (keeping his perianal area clean and dry). In addition to the management of conditions already discussed, a number of others merit discussion, including pruritis ani, condyloma acuminatum, Human Immunodeficiency Virus, and other sexually transmitted diseases. Pruritus Ani An itching and burning sensation about the anus is referred to as pruritus ani. Frequently mistaken by patients for symptoms of hemorrhoids, the symptoms can be very discouraging and frequently wax and wane. Despite its ubiquity, pruritus ani is an under-diagnosed condition. The majority of patients choose to self medicate and do not seek medical care.(1) It affects males more frequently than females by 4:1.(2) Most patients complain of itching and burning made worse during hot, humid weather or after exercise. The itching sensation can advance to the point of distress, driving some to suicide. On physical exam, the affected area can vary from mild erythema and excoriations to marked skin thickening, cracking, and lichenification (Figure 15.1). Excessive scratching or vigorous cleansing of the afflicted area can exacerbate the condition. The etiology of pruritus ani, like other dermatitides, can range from poor hygiene, poorly absorbent or ventilated clothing, excessive or improper cleansing, and dietary intolerances. Fecal soilage can be a strong irritant to the perianal area leading to skin irritation. Causes of soilage can include incomplete wiping due to skin tags or other anatomic imperfections, loose or tenacious stool consistency, and poor anal sensation or sphincter tone. A small study of 39 males (23 of whom had pruritus ani) demonstrated a greater rise in rectal pressure associated with decreased anal pressure, and longer duration of internal anal sphincter relaxation.(3) Clothing choice has also been associated with ­idiopathic pruritus ani with tight fitting, nonaerating fabrics exacerbating the problem. Additionally, hirsute patients are more prone to episodes of pruritus ani. Foods such as caffeinated beverages, chocolate, tomatoes, and citrus fruits have been shown to cause pruritus ani.(4–6) Coffee in particular has been associated with pruritus ani, with increased amounts of coffee intake being associated with worsening symptoms. One possible etiology for this is a decreased internal anal sphincter tone, similar to that seen in relaxation of the lower esophageal sphincter with gastroesophageal reflux disease.

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Figure 15.1  Priritis ani.

Contact dermatitis should be ruled out as a possible etiology. Clues to this diagnosis include recent use of new creams, toiletry items, or new laundry detergent. After the initial irritation from these agents, itching and pain can be exacerbated by continued scratching and abrasion. Occasionally, home remedies can worsen the condition as well. Often, simple reassurance can be the best treatment for idiopathic pruritus ani. Knowing that there is no underlying disease, such as cancer, can provide just as much benefit as lifestyle changes. Lifestyle changes should include improved cleanliness, changes in clothing, as well as dietary changes. Patients should cleanse themselves several times a day avoiding excessive scrubbing of the affected area. If available, showering after bowel movements can

miscellanous conditions be very effective. Patients should be instructed to dry the area with a hair dryer or with a blotting technique to avoid trauma to the anal area. Dampened toilet paper may assist in gentle cleansing, but Baby wipes or Tucks should be avoided as they may excessively traumatize the perianal area after defecation. Choice of clothing can exacerbate the condition, with loose fitting, soft cotton clothing providing some relief. Dietary changes involve excluding ­possible causative foods for 2 weeks to see if the condition improves. If the symptoms resolve or improve, suspected foods may be reintroduced to ascertain which cause recurrence or worsening of the itching or burning sensation. Occasionally, hydrocortisone cream may be used to overcome severe problems. The cream decreases inflammation and irritation, thus promoting healing. However, prolonged use of a steroid cream may lead to atrophy of the skin with further breakdown and worsening conditions. Due to this concern, hydrocortisone cream should not be used for more than 2 weeks. Other skin protective creams may be used in the initial stages and then transitioned to dry powders for long-term relief. More extreme measures at treating pruritus ani have been attempted. These include injections with alcohol, oil soluble anesthetics, and methylene blue into the perianal skin.(7, 8) While providing some temporary relief, abscess formation, skin breakdown, and skin sloughing can occur. While these outcomes can be treated with local drainage and antibiotics, the morbidity and poor success rate prevents them from being effective treatments. Surgical undercutting of the perianal skin has also been described. (9) While the skin can be made insensate, recurrence of the dermatitis occurs. Additional problems with abscess formation and sepsis have been described. As with injections, the risks of surgical undercutting outweigh the benefits. Other causes of pruritus ani need to be excluded during the workup. Hemorrhoids, anal fissures, psoriasis, rectal and anal cancer, as well as colon cancer have all presented with an itching or burning sensation of the anus.(10) While the relation of cancer to pruritus ani is unknown, patients presenting with itching in their presenting complaints had longer duration of itching than those with benign causes.(10) Additional medical problems such as diabetes, antibiotic use, fungal and parasite infections, and anal intercourse need to be investigated as well. Condyloma Acuminatum Human papillomavirus (HPV) is the causative pathogen in condyloma acuminatum. The condition affects nearly 20 million sexually active adults, with 5.5 million new cases occurring each year.(11) The virus is spread via close contact with an infected individual and autoinoculation to other body surfaces is possible. Anogenital warts from HPV is considered the most common anorectal infection among homosexual men. Anorectal warts are more common than penile warts owing to the moist, warm environment thought to be favorable to their growth. In addition to perianal lesions, intraanal lesions are common among homosexual men.(12) Therefore, in order to successful treat these patients, internal as well as external therapies need to be utilized to ­prevent reinfection. Additionally, the patient and all sexual partners should be treated to prevent repeat inoculation. Treatment options for patients include excision and destruction.

Excision of the condyloma generates a tissue diagnosis as well as typing of the causative papillomavirus.(13) Due to the risk of malignant transformation, histopathologic examination is recommended for all patients undergoing treatment. The technique used involves elevating the lesion with local lidocaine/ epinephrine injection, and excising the lesion; taking great care that the underlying musculature is left intact. One must also be careful to leave as much of the normal skin and mucosa as possible. Complications of intraanal excision can include strictures of the anal canal. Sitz baths are helpful during convalescence to assist in wound healing. Unfortunately, surgical excision has a high recurrence rate ranging from 9% to 46% depending on the study.(14, 15) Destructive techniques used in the treatment of condyloma include electrocautery, cryotherapy, laser therapy, immunotherapy, and various topical agents. Fulguration of the condyloma using electrocautery and curettage of the destroyed tissue is an effective tool in treating condyloma. Care must be taken to prevent deep burns which can damage the surrounding skin and lead to deep wounds and severe scarring. This method can be of particular use within the anal canal if appropriate precautions are taken. Cryotherapy is similar to electrocautery in that the wart and underlying tissues are destroyed, leading to sloughing of the condyloma. Cryotherapy has been reported to lead to a foul smelling and damp slough thought to result in a higher recurrence rate. Again, great care must be taken to ensure that surrounding healthy tissue is not damaged. Laser therapy is another destructive technique to eliminate condyloma. Similar to other destructive techniques, complications include loss of tissue, fibrosis, and anal stenosis.(16) Additionally, aerosolized viral particles generated during laser therapy can inoculate the medical provider and result in respiratory papillomas.(17) Several topical agents are available for treating anal condyloma. They can be applied in the office setting by medical personnel as well at home by the patient. Trichloroacetic acid, podophyllin, and imiquimod are currently available. Trichloroacetic acid is a caustic agent used to chemically burn the anal wart. The acid must be applied to the anal wart after cleansing the perianal area. Liberal application of trichloroacetic acid will lead to burning and necrosis of normal skin and should be avoided. The acid should be applied to the wart only. After application, the wart should have a frosty white appearance. Treatment of anal canal lesions should include blotting the lesion with a swab before removing the anoscope. This prevents burning of the adjacent mucosa. The caustic effects of trichloroacetic acid include skin necrosis, ­fistula in ano, and anal stenosis. Patients should return to the office every 7–10 days for reapplication. Swerdlow and Salvati reported a recurrence rate of 25% using this technique.(18) Podophyllin is a topical agent which can be applied in the office setting or by the patient at home. Podophyllin is applied to the warts themselves, taking care to not apply to uninvolved skin. Podophyllin is a destructive agent which leads to necrosis of the treated areas. Complications of podophyllin treatment can run the gamut of local skin irritation to systemic toxicity. Complications including fistula in ano, anal stenosis, and skin necrosis have been reported.(19) If large doses are applied to the skin, hepatic, renal,

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improved outcomes in colon and rectal surgery gastrointestinal, and neurologic complications have occurred. Pregnancy is an absolute contraindication for the use of topical podophyllin. Treatment with podophyllin has a clearance rate of about 50%, but the recurrence can be as high as 90%. This high recurrence rate necessitates repeat treatments. Imiquimod is a newer agent in the arsenal against anal condyloma. It can be applied in the office setting as well as at home and has been shown to have similar efficacy to podophyllin and other fulguration techniques.(11) As opposed to destructive application creams, imiquimod stimulates the innate and cell mediated immune response to clear papillomavirus infected cells. The cream is applied to the wart and left in place for 8 hours, and then the washed off. Imiquimod is applied 3 times a week for up to 16 weeks of therapy. As imiquimod is not cytodestructive, concerns of skin necrosis and fistula formation seen with other ablative therapies are not realized. Langley and colleagues reviewed the cost-effectiveness of imiquimod therapy and found a combination initial imiquimod treatment followed by second-line therapy for recurrence gave the highest success rate and the lowest total cost of therapy.(20) Second-line therapy included fulguration techniques used in the office. It should be noted that all topical agents have lower success rates when used to treat highly keratinized warts. Due to this ­limitation, intraoperative techniques may better treat these chronic lesions. If other lesions recur, subsequent treatment with topical agents can be considered. Immunotherapy as described by Abcarian et al. has been shown to effect regression of the condyloma lesions.(21) The therapy consisted of an autologous vaccine created from the patient’s wart tissue. Intramuscular injections were given once the vaccine was created. Difficulty and expense in creating this immunotherapy have curtailed its widespread use. Due to the increased risk of papillomavirus lesions leading to anal squamous intraepithelial lesions and an increased risk of cancer, many are advocating screening techniques similar to routine papanicolaou screening in women. Screening should include identifying risk factors such as human immunodeficiency virus (HIV) status, history of anal warts, and history of anal pain and bleeding. Pap testing using a liquid medium allows for the collection of epithelial cells for analysis.(22) The increased incidence of squamous cell carcinoma transformation in the HIV positive population should lead the clinician to screen these patients yearly. Human Immunodeficiency Virus Due the depressed immune system, HIV positive individuals are at increased risk of wound complications following surgery. Of those affected, more severe HIV disease leads to higher morbidity and mortality from minor surgical procedures including hemorrhoidectomy, lateral internal anal sphincterotomy, and transrectal biopsies. Due to the high complication rates, surgical treatment of benign anorectal diseases should be approached carefully. Before surgical intervention, viral load, and immunosuppression should be carefully evaluated.(23) Treatment of anal ulcers involves identification of the causative agent and appropriate medical management. Etiologies of anal

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ulcer in the HIV patient include herpes virus, syphilis, cytomegalovirus, and cryptococcus.(24, 25) Surgical management is reserved for chronic, nonhealing ulcers and includes local debridement, unroofing of ulcerative cavities, and steroid injection into the cavity. Complications of surgery include prolonged drainage, poor wound healing, incontinence, and superinfections. Treatment for fistula in ano and perianal abscesses in an HIVinfected patient remains the same as HIV negative patients. However, abscesses and fistula appear more frequently in the more advanced stages of HIV infections. Surgical therapy is ­warranted for source control of the affected area, but the complication rate is high. Patients should be advised of the increased risk of nonhealing wounds, recurrence, and sepsis. Surgical management should include conservative strategies used in the treatment of anorectal disorders seen in Crohn’s disease. Draining setons and drainage catheters (Malecot and Pezzar drains) should be the initial treatment in those with severe immunodeficiency. Fibrin glue as well as collagen plugs could also prove useful in the treatment of ­perianal fistula. Kaposi’s sarcoma can lead to abdominal pain, lower and upper gastrointestinal bleeding, malabsorption, obstruction, and perforation.(26, 27) The clinician must understand that gastrointestinal disease can occur in the absence of skin manifestations. Surgical treatment for gastrointestinal disease is reserved for bleeding, obstruction, and perforation. Chemotherapy is used to treat the manifestations of Kaposi’s sarcoma. Complications of medical management include paralytic ileus and necrosis or ­perforation of the bowel. As stated previously, the depressed immune system in HIV positive patients yields higher complication rates with surgery. Therefore, any abdominal colorectal procedure will carry higher rates of wound infections, dehiscence, anastomotic leak, bowel obstruction, and fistula formation. If colorectal resections are required, creation of a diversion with stoma formation has been shown to decrease the rate and severity of subsequent complications.(28–30) Colitis secondary to cytomegalovirus (CMV) infection has an increased rate among the HIV population. Autopsies of those infected with HIV have demonstrated CMV coinfections to be present in almost 90% of those studied.(31, 32) All areas of the ­gastrointestinal tract can be involved; however, colonic involvement predominates. Lower gastrointestinal bleeding and ulcer perforation are common causes for surgical intervention. Ileocolitis and proctocolitis can be indications for partial or total colectomy. It should be noted that any indicated colorectal surgery should be approached cautiously and that the most conservative management possible should be pursued. Previously mentioned surgical complications among the immune compromised patients should guide the surgeon’s interventions in treating these patients with the most conservative care.(24, 28) Common Anorectal Sexually Transmitted Diseases Herpes simplex virus (HSV) is transmitted via direct skin contact and results in small, painful vesicles about the perianal skin. Lesions typically last for 2 weeks and remain contagious even in the asymptomatic stage. Vesicles can become secondarily infected

miscellanous conditions and are noted to have erythematous edges. Proctitis can occur and is diagnosed with endoscopic evaluation demonstrating an inflamed and friable mucosa. Swabs taken from the ulcerations are sent for viral culture and polymerase chain reaction (PCR). Treatment involves medical management and local debridement for superimposed infections. Of note, Elsberg syndrome can develop on this patient population. The ­syndrome describes a sacral radiculitis which includes symptoms of ­constipation, urinary retention, lower extremity weakness, and parasthesias. Magnetic resonance imaging and polymerase chain reaction testing of the cerebrospinal fluid (CSF) can aid in the diagnosis. Management includes local analgesic creams for symptomatic relief and good hygiene to prevent secondary infections of the affected area. Antiviral medications are available which can decrease the severity and length of viral recurrences, but does not cure the ­disease. Patients must be counseled that viral shedding can occur at any stage in the disease progression, even when the patient is asymptomatic. Chlamydia trachomatis infections can lead to proctitis, with symptoms of rectal urgency, bleeding, and pain. If the infection progresses proximally, bloody diarrhea can occur. Endoscopic evaluation demonstrates diffuse inflammation and ulcerations. PCR and cultures reveal the diagnosis. Treatment includes antibiotics such as doxycycline and azithromycin. Neisseria gonorrhea is a gram-negative diplococcus which infects the mucous membranes via direct contact. This infection can lead to proctitis, urethritis, cervicitis, pharyngitis, and conjunctivitis. In men, transmission occurs via anal receptive intercourse. Women may become infected by similar means or from autoinoculation secondary to a vaginal infection. After an incubation period ranging 3 days to 2 weeks, proctitis or cryptitis may occur. Symptoms can include pruritus ani, bloody discharge, and pain. Disseminated gonorrhea occurs if the disease is not treated; pericarditis, meningitis, and arthritis are manifestations of disseminated disease. A thick, purulent discharge can be expresses from the anal crypts and is highly suspicious for gonoccal proctitis. This discharge should be collected on Thayer-Martin plates for identification via culture. Management includes systemic antibiotics with ceftriaxone, cefixime, flouroquinolones, or azithromycin. Current treatment of gonorrhea also includes treatment of a presumed Chlamydia infection. Another common sexually transmitted disease is syphilis, caused by the spirochete, Treponema pallidum. Anorectal disease presents much like other sites of inoculation: a chancre represents the first stage of the disease. These ulcerative lesions may be associated with pain and inguinal adenopathy. Rectal symptoms may include discharge or bleeding. If untreated, the first stage of syphilis resolves within 2–4 weeks with subsequent progression to secondary syphilis. A macular rash on the torso and extremities denotes secondary syphilis. Condyloma lata may be present during this time as well as mucosal ulcerations. Without treatment, this condition will spontaneously resolve within a few weeks. Tertiary syphilis with its neurologic and vascular sequelae will eventually develop if left untreated. Serologic testing with Venereal Disease Research Laboratory (VRDL) and rapid plasma regain (RPR) will provide the diagnosis. The treatment of choice remains penicillin G and doxycycline.

References   1. Nelson RL, Abcarian H, Davids FG, Persky V. Prevalence of benign anorectal disease in randomly selected a population. Dis Colon Rectum 1994; 88: 341.   2. Wexner SD, Dailey TH. Pruritis ani: diagnosis and management. Curr Concepts Skin Disorders 1986; 7: 5–7.   3. Farouk R, Duthie GS, Pryde A, Bartolo DC. Abnormal transient internal sphincter relaxation in idiopathic pruritus ani: physiologic evidence from ambulatory monitoring. Br J Surg 1994; 81: 603.   4. Kranke B, Trummer M, Brabek E et al. Etiologic and causative factors in perianal dermatitis: results of a prospective study in 126 patients. Wien Klin Wochenschr 2006; 118: 90.   5. Friend WG. The cause and treatment of idiopathic pruritus ani. Dis Colon Rectum 1977; 20: 40–2.   6. Daniels GL, Longo WE, Vernava AM. Pruritus ani: causes and concerns. Dis Colon Rectum 1994; 37: 670–4.   7. Stone HB. Pruritus ani. Treatment by alcohol injection. Surg Gynecol Obstet 1926; 42: 565–6.   8. Turell R. Tattooing with mercury sulfide for intractable anal pruritis. Surgery 1948; 23: 63.   9. Lockhart-Mummery JP. Diseases of the Rectum and Colon. London: Baillere; 1934. 10. Daniel GL, Longo WE, Vernava AM 3rd. Pruritus ani. Causes and concerns. Dis Colon Rectum 1994; 37: 670. 11. Sauder DN, Skinner RB, Fox TL, Owens ML. Topical imiquimod 5% cream as an effective treatment for external genital and perianal warts in different patient populations. Sex Transm Dis 2003; 30: 124–8. 12. Sohn N, Robilotti JG. The gay bowel syndrome, a review of colonic and rectal conditions in 200 male homosexuals. AM J Gastroenterol 1977; 67: 478–84. 13. Wexner SD. Sexually transmitted diseases of the colon, rectum and anus. Dis Colon Rectum 1990; 12: 1048–62. 14. Thomas JPS, Grace RH. The treatment of perianal and anal condyloma acuminata: a new operative technique. Proc R Soc Med 1978; 71: 180–5. 15. Gollock JM, Slatford K, Hunter JM. Scissor excision of ­anogenital warts. Br J Venereal Dis 1982; 58: 400–1. 16. Krebs HB, Wheelock JB. The CO2 laser for recurrent and therapy resistant condylomata acuminatum. J Reprod Med 1985; 30: 489–92. 17. Volen D. Intact viruses in CO2 Laser plumes spur safety ­concern. Clin Laser Monthly 1987; 5: 101–3. 18. Swerdlow DB, Salvati EP. Condyloma acuminatum. Dis Colon Rectum 1971; 14: 226–9. 19. Boot JM, Stolz E. Intralesional interferon -2b treatment of Condylomata acuminata previously resistant to podophyllin resin application. Genitoruin Med 1983; 65: 50–3. 20. Langley PC, Tyring SK, Smith MH. The cost effectiveness of patient-applied versus provider-administered intervention strategies for the treatment of external genital warts. Am J Managed Care 1999; 5: 69–77. 21. Abcarian H, Sharon N. Long term effectiveness of immunotherapy of anal condyloma acuminatum. Dis Colon Rectum 1982; 10: 648–51.

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improved outcomes in colon and rectal surgery 22. Mathews WC. Screening for anal dysplasia associated with human papillomavirus. Top HIV Med 2003; 11: 45–9. 23. Wexner SD. AIDS: what the colorectal surgeon needs to know. Perspect Colon Rectal Surg 1989; 2: 19–54. 24. Cohen SM, Schmitt SL, Lucas FV, Wexner SD. The diagnosis of anal ulcers in AIDS patients. Int J Colorect Dis 1994; 9: 168–73. 25. Viamonte M, Dailey TH, Gottesman L. Ulcerative disease of the anorectum in the HIV positive patient. Dis Colon Rectum 1993; 36: 801–5. 26. Danzig JB, Brandt LJ, Reinus JF, Klein RS. Gastrointestinal malignancy in patients with AIDS. J Gastroenterol 1991; 86: 715–8. 27. Laine L, Amerian J, Rarick M, Harb M. The response of symptomatic gastrointestinal Kaposi’s sarcoma to chemotherapy:

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28.

29. 30. 31. 32.

a prospective evaluation using an endoscopic method of disease quantification. Am J Gastroenterol 1990; 85: 959–61. Burack JH, Mandel MS, Bizer LS. Emergency abdominal operations in the patient with AIDS. Arch Surg 1989; 124: 285–6. Zelnick R, Poulard JB, Auguste LJ, Vretakis G, Margolis IB. Surgery in the AIDS patient. AIDS Patients 1991; 1: 10–4. Macho JR. Gastrointestinal surgery in the AIDS patient. Gastroenterol Clin NA 1988; 3: 563–71. Welch K, Finkbeiner W, Alpers CE et al. Autopsy findings in AIDS. JAMA 1984; 252: 1152–9. Chachova A, Dietrich D, Krasinski K. 9 (1,3-dihydroxy2-propoxymethyl) quanine (gancylovir) in the treatment of cytomegalovirus gastrointestinal disease in AIDS. Ann Intern Med 1987; 107–33.

16

Quality and outcome measures Janak A Parikh, Sushma Jain, Marcia L McGory, and Clifford Y Ko

Challenging Case A 64-year-old male is scheduled for a left colectomy for a carcinoma. His past medical history is significant for a 3 vessel cardiac bypass. Case Management The patient’s primary care physician has placed the patient on beta-blockers. Prophylactic antibiotics (second generation cephalosporin) are ordered to be given within 1 hour of surgery. Pneumatic compression stockings are ordered for placement in the holding area. Unfractionated heparin (5,000 units subcutaneously) is ordered for 2 hours before start of the operation. The patient’s body hair is removed with a clipper. Efforts are made to keep the patient normothermic during and after surgery. Prophylactic antibiotics are not continued after surgery. Final pathology documents a T3N1M0 adenocarcinoma. The patient is referred to a medical oncologist for consideration of adjuvant chemotherapy. For the first time in its history, the United States is at an impasse in healthcare. Rising healthcare costs, an aging population, and a growing number of uninsured Americans are causing concern among payers and lawmakers. These concerns have led to a largescale effort to assess and improve the quality of healthcare delivered to Americans. A major impetus for quality improvement was the realization that continuing to increase healthcare expenditure was not feasible. In 2007, the United States spent approximately 16% of its gross domestic product, or $2.3 trillion on healthcare, with projections forecasting a rise to 20% of GDP by 2016.(1) While these numbers far exceed what other countries spend on healthcare, they do not ensure that Americans receive better healthcare than other countries. In fact, with over 46 million people who are uninsured, and an infant mortality that is ranked 37th in the world, Americans are arguably not getting the most value out of their healthcare dollar.(2) The focus on quality in healthcare is a reality that current and future physicians will have to acknowledge, as transparency via public reporting of physician performance is likely in the near future. Currently, most efforts remain at the hospital level. In this chapter, we explore the concept of quality, the various methodologies of quality improvement (including the use of performance measures), and examine some of the quality improvement efforts that are currently ongoing. Defining Quality of Care Though interest in healthcare quality is seemingly new, some have long understood the need to measure and improve the quality of healthcare in the United States. In the arena of quality improvement research, the challenges have been how to define quality, how to measure it, and how best to improve it. As defined by the Institute of Medicine (IOM), quality of care is defined as “the degree to which health services for individuals and populations increase the likelihood of desired health outcomes and are ­consistent with current professional knowledge.”(3) A more basic

but equally accurate definition is the delivery of appropriate care at the right time to the right patient, and done right. In the past, the concept of healthcare quality was not at the political and social forefront as it is today. Many probably assumed that healthcare in the United States is of the highest quality and far superior to healthcare elsewhere in the world given our technological advances and expenditures. However, in 1999, this notion visibly began to be challenged in the public eye. The 1999 IOM report “To Err is Human: Building a Safer Health System” was the first report that challenged the perception of a safe high quality healthcare system in the United States.(4) The IOM report pointed out the human errors in the healthcare industry and helped identify potential faulty systems, processes, and ­conditions within our current healthcare system that led healthcare providers to make mistakes. It is estimated that as many as 98,000 people die in hospitals every year as a result of preventable medical errors.(4, 5) Introduction These types of medical errors not only affect patient’s physical and psychological discomfort, but also increase hospital costs and decrease a patient’s societal productivity. Most importantly, the IOM report forced creation of national goals and recommended a fourtiered approach to achieve patient safety—first, to create leadership; second, to have a nationwide public mandatory reporting system to identify and learn from medical errors; third, to raise performance standards and expectations for improvements in safety; and fourth, to implement safety systems in healthcare organizations.(4) Based largely on the results of the 1999 IOM report, the IOM next developed a report entitled “Crossing the Quality Chasm: A New Health System for the 21st Century”, which defined six ­specific aims for improvement: (1) Safety (e.g., avoiding errors in drug administration by simplifying the protocols for drug delivery), (2) Effectiveness (e.g., appropriate chemotherapy for stage II or III colorectal cancer), (3) Patient-Centeredness (e.g., patients having access to their own medical record information and to healthcare providers by email, phone etc.), (4) Timeliness (e.g., reducing waiting time for provider appointments or in the emergency room), (5) Efficiency (e.g., streamlining forms to reduce paperwork so that providers can spend more time on patient care), and (6) Equity (e.g., patients should receive appropriate care regardless of race, age, gender, ethnicity, income, geographic location).(6) The goal of outlining these six specific aims was to help our current healthcare system to cross the chasm that lies between what is currently being delivered by the healthcare system and the quality of care that should be delivered.(3) History of Quality Assessment and Quality Improvement in Surgery The goal of improving quality and outcomes is actually not new to the discipline of surgery. Ernest Amory Codman, M.D. (1869– 1940), a surgeon, was the founder of the “End Result Idea”, and

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improved outcomes in colon and rectal surgery father of the medical quality movement.(7, 8) In 1895, he graduated from Harvard Medical School and interned at Massachusetts General Hospital (MGH). He later joined the surgical staff at MGH and became a member of the Harvard faculty. In 1914, he proposed evaluating surgeon competency at MGH. He believed that “every hospital should follow every patient it treats long enough to determine whether the treatment has been successful, and then to inquire ‘if not, why not’ with a view to preventing similar failures in the future.” In fact, he is quoted as saying: “… I am called eccentric for saying in public that hospitals, if they wish to be sure of improvement, 1. 2. 3. 4.

Must find out what their results are. Must analyze their results, to find their strong and weak points. Must compare their results with those of other hospitals. Must care for what cases they can care for well, and avoid attempting to care for those cases which they are not qualified to care for well…. 5. Must assign cases to the members of the staff (for treatment) for better reasons than seniority, the calendar or temporary convenience 6. Must welcome publicity not only for their successes, but for their errors, so that the Public may give them help when it is needed. 7. Must promote members of the Staff on a basis which gives due consideration to what they can and do accomplish for their patients.”(7) In this regard, Dr. Codman made one of the most important contributions in the history of outcomes research in healthcare. However, his thinking was well before its time. The MGH refused his plan and asked him to resign. Dr. Codman eventually established his own hospital (which he called the “End Result Hospital”) to pursue his performance measurement and improvement objectives. To support his “end results theory,” Dr. Codman publicly reported these data in a book entitled A Study in Hospital Efficiency. Of the 337 patients discharged between 1911 and 1916, Dr. Codman recorded and published 123 errors. He systematically documented errors in diagnosis and treatment for every patient, and followed each patient for years after ­discharge to evaluate the end results of care. Not surprisingly, he was the first to institute the mortality and morbidity conference. Due to his immense interest in the quality of care delivered to patients, Dr. Codman helped lead the founding of the American College of Surgeons’ (ACS) Hospital Standardization program which later became the Joint Commission on Accreditation of Healthcare Organizations.(7, 8) Unfortunately, Dr. Codman’s ideas were probably too revolutionary for that time period and, as a result, were not well received. In point of fact, we are still working today towards implementing many of Dr. Codman’s original concepts with respect to documentation of complications and evaluating the end results of surgical care in our patients. The Donabedian Model of Quality of Care Today, the most commonly used paradigm for quality improvement is the Donabedian model. In 1988, Donabedian developed a framework for assessing quality of care that involved three

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domains: structure, process, and outcomes.(9) The structural components of care refer to the physical characteristics of the institution. In a hospital, these would include the characteristics of the hospital and provider. Examples of structural components would be the hospital’s volume for a particular procedure, board certification of its physicians, or the presence of a computerized order entry system. Process components include interactions that occur between the provider and patient, and are commonly considered the most direct predictors of quality of care because they identify a priori steps to make improvements and are not affected by patient characteristics (i.e., higher mortality rates for surgeons/hospitals with sicker patients). Examples of specific process measures include such things as timely administration of preoperative antibiotic prophylaxsis, use of sequential compression devices and/or heparin to prevent deep venous thrombosis, and the use of postoperative chemotherapy in patients with stages III colon cancer. Finally, outcome components of care are probably most familiar to surgeons, and include morbidity, complications, and mortality. Two important issues to consider when using outcome to judge quality are that in order to be optimally used, outcomes require risk-adjustment to compare different providers or facilities. Additionally, while outcome measures may be used to identify poor care, in and of itself, outcomes might not readily identify how to actually improve care. If a surgeon’s risk-adjusted anastomotic leak rate is high, the cause may not be immediately or readily known, or identifiable. Nevertheless, outcome measurement is an important component of quality improvement because it has great face validity, as well as being the “standard” by which structural and process-based measures are validated. In point of fact, there have been numerous projects that have made comparisons between hospitals and physicians outcomes. Improvement based on Structural Measures Established as a nonprofit organization in 2000 by a small group of large corporations that purchase healthcare for their employees, the Leapfrog Group’s growing consortium of major companies and other large private and public healthcare purchasers provide health benefits to more than 37 million Americans. (10) The mission of the Leapfrog group is to use the purchasing power of its members to influence the quality and affordability of healthcare. In mid-2001, the Leapfrog Group began ­collecting hospital data to evaluate healthcare quality in six regions in the United States. Currently, the Leapfrog data cover over half the U.S. population and 58% of all hospital beds with over 1,300 participating hospitals nationwide.(11) Their efforts to improve the value of healthcare have been important. The Leapfrog Group encourages its member companies to adhere to the following four purchasing principles in buying healthcare for their enrollees: •• Educating and informing enrollees about the safety, quality and affordability of health care and the importance of comparing the care providers give with initial emphasis on the safety and quality practices. •• Recognizing and rewarding healthcare providers for major advances in the safety, quality, and affordability of their care.

quality and outcome measures •• Holding health plans accountable for implementing the Leapfrog purchasing principles. •• Building the support of benefits, consultants and brokers to use and advocate for the Leapfrog purchasing principles with all of their clients.(11) In their quest, the group established measures by which to rate hospitals. Each quality measure had to meet four criteria: •• There is overwhelming scientific evidence that these quality and safety leaps will significantly reduce preventable medical mistakes. •• Their implementation by the health industry is feasible in the near term. •• Consumers can readily appreciate their value. •• Health plans, purchasers, or consumers can easily ascertain their presence or absence in selecting among healthcare providers.(11) Using these criteria, the Leapfrog Group identified four structural measures to improve care. These included the existence of a computer physician order entry system, evidence-based ­hospital referral (EHR), intensive care unit (ICU) staffing by physicians experienced in critical care medicine, and the Leapfrog Safe Practices Score.(11) Of these measures, the one that has probably gained the most attention in surgery is the evidence-based hospital referral. This measure is founded on literature that demonstrates a volume-outcome relationship for certain complex procedures—more specifically, that higher volume hospitals purportedly have better outcomes. The procedures currently with established volume-­outcome relationships and the current EHR procedures include coronary artery bypass grafting (CABG) (≥450/year), percutaneous coronary intervention (AAA) (≥400/year), aortic valve replacement (≥120/year), abdominal aortic aneurysm repair (AAA) (≥50/year), esophagectomy (≥13/year), pancreatic resection (≥11/year), and bariatric surgery (>100/year).(12) Other procedures that have evidence to suggest a volume-outcome relationship include carotid endarterectomy, lower-extremity bypass, mitral valve replacement, gastrectomy, cystectomy, pneumonectomy, lobectomy, and nephrectomy. (13) Relative to this textbook, the volume-outcome relationship in colorectal cancer surgery is varied. While a recent systematic review found a significant surgeon volume-outcome relationship in colorectal cancer surgery, the magnitude of effect on mortality was small (1–2%).(14–17) This is consistent with the analysis by Birkmeyer et al. upon which the Leapfrog criteria are based.(13) Although there are multiple studies to support the volumeoutcome relationship established by The Leapfrog Group, there are several potential issues that warrant further discussion. First, the analyses in most studies do not account for the possibility that surgeons with similar volumes may have very different outcomes because of systematic differences in processes of care. Thus, a high degree of clustering of outcomes may lessen the impact of volume on outcomes.(18) A second concern is the somewhat arbitrary nature of the cutoffs. For example, several recent ­studies exploring the volume-outcome relationship for CABG and AAA have demonstrated similar outcomes at lower volumes than

the Leapfrog cutoffs. Finally, selective referral may potentially increase disparities, as the disenfranchised likely will not be able to participate in the referral process. Still, volume is being used as a proxy for quality of care, and in this regard, volume-based referral is probably a reasonable way to improve quality at this point in time. Improvement Based on Process Measures Compared to both structural and outcome measures, the use of process measures has the advantage of identifying a ­priori steps that lead to improvements in quality. Furthermore, process measures are not affected by patient characteristics and thus do not require risk-adjustment. For these reasons, process measures play an important role in the Centers of Medicare and Medicaid Services (CMS) effort to improve quality of care. In October of 2005, CMS introduced the Surgical Care Improvement Project (SCIP).(19) The goal of SCIP was to reduce surgical complications by 25% by the year 2010.(19) Many national organizations came together to form an expert panel to develop the SCIP measures. At present, there are approximately 20 measures. These measures target four domains of care, namely, prevention of postoperative infection, prevention of postoperative venous thromboembolism, prevention of cardiac events, and prevention of ventilator-associated pneumonia. There are specific process measures in each domain. For example, prevention of postoperative infection involves such things as administration of appropriate prophylactic antibiotics 1 hour before incision, use of clippers to remove hair, maintainence of normoglycemia postoperatively for cardiac surgery patients, and postoperative normothermia for colorectal surgery patients. A full list of measures is provided in Table 16.1. Hospital participation in SCIP is voluntary at the time of this writing, and at present there is financial incentive for hospitals to enroll in the program since there is “pay for participation.” However, the SCIP measures may become pay-for-performance measures in the future. Currently, CMS has several surgical pay-for-participation measures scheduled to be implemented in October 2008 (Table 16.2).(20–22) In December 2007, CMS unveiled its most recent effort to improve healthcare quality by launching the Physician Quality Reporting Initiative (PQRI). Mandated by the 2006 Tax Relief and Health Care Act, PQRI is a provider-level quality improvement project whose initial aim is to have providers submit data on several CMS quality measures.(23) PQRI is another pay-forparticipation program in which physicians who participate will earn an incentive payment of 1.5% of their total allowed charges for the Medicare Physician Fee Schedule covered services. The incentive payments are based on reporting from January 1, 2008 through December 31, 2008 and are scheduled to be disbursed in mid-2009 from Medicare Part B funds. In total, there are 134 reportable measures that span all areas of care. Healthcare professionals that are eligible to participate in the PQRI program include physicians, dentists, optometrists, nurse practioners, and physical therapists to name a few. For surgeons, there are approximately 14 measures, with an additional 7 measures which are ­generally applicable to all physicians (Table 16.3).(24) Outcomes Similar to the ideas of Dr. Codman, knowing one’s outcomes may help drive quality improvement. One of the best examples of this

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improved outcomes in colon and rectal surgery Table 16.1  Surgical Care Improvement Project (SCIP) measures. SCIP Measures Target Areas

Measures

1.   Surgical Site Infection

1.  Prophylactic antibiotic received within 1 hour prior to surgical incision. 2.  Prophylactic antibiotic selection for surgical patients. 3.  Prophylactic antibiotics discontinued within 24 hours after surgery end time (48 hours for cardiac patients). 4.  Cardiac surgery patients with controlled 6 a.m. postoperative serum glucose. 5.  Postoperative wound infection diagnosed during index hospitalization. (OUTCOME) 6.   Surgery patients with appropriate hair removal 7.  Colorectal surgery patients with immediate postoperative normothermia.

2.  Adverse Cardiac Events

1.  S urgery patients on a beta-blocker prior to arrival that received a beta-blocker during the perioperative period. 2.  Intra- or postoperative acute myocardial infarction (AMI) diagnosed during index hospitalization and within 30 days of surgery. (OUTCOME)

3.  Deep Vein Thrombosis

1.  S urgery patients with recommended venous thromboembolism prophylaxis ordered. 2.  Surgery patients who received appropriate venous thromboembolism prophylaxis within 24 hours prior to surgery to 24 hours after surgery. 3.  Intra- or postoperative pulmonary embolism (PE) diagnosed during index hospitalization and within 30 days of surgery. (OUTCOME) 4.  Intra- or postoperative deep vein thrombosis (DVT) diagnosed during index hospitalization and within 30 days of surgery. (OUTCOME)

4.  Postoperative ventilator related pneumonia

1.  Number of days ventilated surgery patients had documentation of the Head of the Bed (HOB) being elevated from recovery end date (day zero) through postoperative day seven. 2.  Patients diagnosed with postoperative ventilator-associated pneumonia (VAP) during index hospitalization. (OUTCOME) 3.  Number of days ventilated surgery patients had documentation of stress ulcer disease (SUD) prophylaxsis from recovery end date (day zero) through postoperative day seven. 4.  Surgery patients whose medical record contained an order for a ventilator weaning program (protocol or clinical pathway).

Miscellaneous

1.   Mortality within 30 days of surgery. 2.   Readmission within 30 days of surgery. 3.  Proportion of permanent hospital end stage renal disese (ESRD) vascular access procedures that are autogenous AV fistula.

Table 16.2  Centers for Medicare and Medicaid Services (CMS) surgical pay-for-participation measures. CABG

1.   Aspirin prescribed at discharge 2.  CABG using internal mammary artery 3.  Prophylactic antibiotic within 1 hour prior to surgical incision 4.  Prophylactic antibiotic selection for isolated CABG patients 5.  Prophylactic antibiotics discontinued within 487 hours after surgery end time 6.   Inpatient mortality rate 7.   Postoperative hemorrhage or hematoma 8.  Postoperative physiologic and metabolic derangement

Hip & Knee Replacement

1.  Prophylactic antibiotic received within 1 hour prior to surgical incision 2.  Prophylactic antibiotic selection for hip and knee replacement patients 3.  Prophylactic antibiotics discontinued within 24 hours after surgery end time 4.   Postoperative hemorrhage or hematoma 5.  Postoperative physiologic and metabolic derangement 6.   Readmissions 30 days postdischarge 7.  Hip/Knee Surgery Patients with Recommended Venous Thromboembolism Prophylaxis Ordered 8.  Hip/Knee surgery patients Who Received Appropriate Venous Thromboembolism Prophylaxis Within 24 Hours Prior to Surgery to 24 Hours After Surgery

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notion is the National Surgical Quality Improvement Program (NSQIP) and its association with the marked improved surgical care in the Veteran Affairs (VA) hospitals. During the mid-to-late 1980s, the VA hospitals came under a great deal of public scrutiny over the quality of surgical care in their 133 VA hospitals. In 1991, Congressional leaders were concerned that the operative mortality at VA hospitals was higher than that at private hospitals for the same procedure. In an effort to address this quality issue, congress passed a law which mandated the VA to report its risk-adjusted surgical outcome annually and to compare them to national averages. In response to this mandate, the VA established the National VA Surgical Risk Study (NVASRS) in 44 VA medical centers.(25) In this study, a dedicated nurse at each site collected preoperative, intraoperative, and 30-day postoperative data on over 95 outcome variables for more that 117,000 major operations. Using this data, researchers developed a risk-adjustment model and were able to determine risk-adjusted 30-day morbidity and mortality rates in nine surgical specialties. Given the feasibility of the study, helped by the nationwide electronic medical record which has been in place in VA hospitals since 1985, the VA established the NSQIP in 1994. Each year, data from 110,000 major surgical cases are added to the database. Most importantly, the program has been highly successful, reducing 30-day mortality rates by 31% and 30-day morbidity rates by 45%.(26) This success was further solidified when, in 2002, the IOM named NSQIP “the best in the nation” for measuring and reporting surgical quality outcomes.(25) Given the success of NSQIP and the increasing focus on healthcare quality, private hospitals questioned whether or not

quality and outcome measures Table 16.3  Surgery-related Physician Quality Reporting Initiative (PQRI) measures. Surgery Specific Measures Perioperative Care: Timing of Antibiotic Prophylaxis—Ordering Physician Description: Percentage of surgical patients aged 18 years and older undergoing procedures with the indications for prophylactic parenteral antibiotics, who have an order for prophylactic antibiotic to be given within 1 hour (if fluoroquinolone or vancomycin, 2 hours), prior to the surgical incision (or start of procedure when no incision is required) Perioperative Care: Selection of Prophylactic Antibiotic—First OR Second Generation Cephalosporin Description: Percentage of surgical patients aged 18 years and older undergoing procedures with the indications for a first OR second generation cephalosporin prophylactic antibiotic, who had an order for cefazolin OR cefuroxime for antimicrobial prophylaxis Perioperative Care: Discontinuation of Prophylactic Antibiotics (Non-Cardiac Procedures) Description: Percentage of noncardiac surgical patients aged 18 years and older undergoing procedures with the indications for prophylactic antibiotics AND who received a prophylactic antibiotic, who have an order for discontinuation of prophylactic antibiotics within 24 hours of surgical end time Perioperative Care: Venous Thromboembolism (VTE) Prophylaxis (When Indicated in ALL Patients) Description: Percentage of patients aged 18 years and older undergoing procedures for which VTE prophylaxis is indicated in all patients, who had an order for Low Molecular Weight Heparin (LMWH), Low-Dose Unfractionated Heparin (LDUH), adjusted-dose warfarin, fondaparinux or mechanical prophylaxis to be given within 24 hours prior to incision time or within 24 hours after surgery end time Perioperative Care: Timing of Prophylactic Antibiotics—Administering Physician Description: Percentage of surgical patients aged 18 and older who have an order for a parenteral antibiotic to be given within 1 hour (if fluoroquinolone or vancomycin, 2 hours) prior to the surgical incision (or start of procedure when no incision is required) for whom administration of prophylactic antibiotic has been initiated within 1 hour (if fluoroquinolone or vancomycin, 2 hours) prior to the surgical incision (or start of procedure when no incision is required) Use of Internal Mammary Artery (IMA) in Coronary Artery Bypass Graft (CABG) Surgery Description: Percentage of patients aged 18 years and older undergoing isolated coronary artery bypass graft (CABG) surgery using an internal mammary artery (IMA) Preoperative Beta-blocker in Patients with Isolated Coronary Artery Bypass Graft (CABG) Surgery Description: Percentage of patients aged 18 years and older undergoing isolated coronary artery bypass (CABG) surgery who received a beta-blocker preoperatively Perioperative Care: Discontinuation of Prophylactic Antibiotics (Cardiac Procedures) Description: Percentage of cardiac surgical patients aged 18 years and older undergoing procedures with the indications for prophylactic antibiotics AND who received a prophylactic antibiotic, who have an order for discontinuation of prophylactic antibiotics within 48 hours of surgical end time Prevention of Ventilator-Associated Pneumonia—Head Elevation Description: Percentage of ICU patients aged 18 years and older who receive mechanical ventilation and who had an order on the first ventilator day for head of bed elevation (30–45 degrees) Prevention of Catheter-Related Bloodstream Infections (CRBSI)—Central Venous Catheter Insertion Protocol Description: Percentage of patients, regardless of age, who undergo central venous catheter (CVC) insertion for whom CVC was inserted with all elements of maximal sterile barrier technique (cap AND mask AND sterile gown AND sterile gloves AND a large sterile sheet AND hand hygiene AND 2% chlorhexidine for cutaneous antisepsis) followed Vascular Access for Patients Undergoing Hemodialysis Description: Percentage of patients aged 18 years and older with a diagnosis of end stage renal disease (ESRD) and receiving hemodialysis who have a functioning AV fistula OR patients who are referred for an AV fistula at least once during the 12-month reporting period HIT- Adoption/Use of Health Information Technology (Electronic Health Records) Description: Documents whether provider has adopted and is using health information technology. To qualify, the provider must have adopted a qualified electronic medical record (EMR). For the purpose of this measure, a qualified EMR can either be a Certification Commission for Healthcare Information Technology (CCHIT) certified EMR or, if not CCHIT certified, the system must be capable of all of the following: • Getnerating a medication list • Generating a problem list • Entering laboratory tests as discrete searchable data elements HIT- Adoption/Use of e-Prescribing Description: Documents whether provider has adopted a qualified e-Prescribing system and the extent of use in the ambulatory setting. To qualify this system must be capable of ALL of the following: • • • •

Generating a complete active medication list incorporating electronic data received from applicable pharmacy drug plan(s) if available Selecting medications, printing prescriptions, electronically transmitting prescriptions, and conducting all safety checks (defined below) Providing information related to the availability of lower cost, therapeutically appropriate alternatives (if any) Providing information on formulary or tiered formulary medications, patient eligibility, and authorization requirements received electronically from the patient’s drug plan

Pain Assessment Prior to Initiation of Patient Treatment Description: Percentage of patients aged 18 years and older with documentation of a pain assessment (if pain is present, including location, intensity and description) through discussion with the patient or through use of a standardized tool on each initial evaluation prior to initiation of therapy Surgery-Related Measures Chemotherapy for Stage III Colon Cancer Patients Description: Percentage of patients aged 18 years and older with Stage IIIA through IIIC colon cancer who are prescribed or who have received adjuvant chemotherapy during the 12-month reporting period (continued)

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improved outcomes in colon and rectal surgery Table 16.3  (continued). Surgery Specific Measures Radiation Therapy Recommended for Invasive Breast Cancer Patients who have Undergone Breast Conserving Surgery Description: Percentage of invasive female breast cancer patients aged 18 through 70 years old who have undergone breast conserving surgery and who have received recommendation for radiation therapy within 12 months of the first office visit Universal Documentation and Verification of Current Medications in the Medical Record Description: Percentage of patients aged 18 years and older with written provider documentation that current medications with dosages (includes prescription, overthe-counter, herbals, vitamin/mineral/dietary [nutritional] supplements) were verified with the patient or authorized representative Patient Co-Development of Treatment Plan/Plan of Care Description: Percentage of patients aged 18 years and older identified as having actively participated in the development of the treatment plan/plan of care. Appropriate documentation includes signature of the practitioner and either co-signature of the patient or documented verbal agreement obtained from the patient or, when necessary, an authorized representative Screening for Cognitive Impairment Description: Percentage of patients aged 65 years and older who have documentation of results of a screening for cognitive impairment using a standardized tool Screening for Future Fall Risk Description: Percentage of patients aged 65 years and older who were screened for future fall risk (patients are considered at risk for future falls if they have had 2 or more falls in the past year or any fall with injury in the past year) at least once within 12 months

a NSQIP-style program could be implemented in non-VA hospitals and if it would have the same benefits. To explore these questions, a pilot study was launched in 1999 at three non-VA hospitals: Emory University, the University of Michigan, and the University of Kentucky.(25) Despite the study being limited to general and vascular surgery cases, the study determined that the data collection and transmission methods, as well as the risk­adjustment models were applicable in the private sector. The success of this pilot study attracted the attention of the American College of Surgeons (ACS) which, in 2001, began to take an active role in developing a NSQIP system for private hospitals by obtaining funding from the Agency for Healthcare Research and Quality (AHRQ) to expand the pilot program to 14 additional hospitals, including several community-based hospitals.(25) Using the AHRQ grant, the ACS developed the infrastructure to make it feasible to roll the NSQIP to private sector hospitals. This included the development of a web-based data collection system, training nurses to abstract and enter data, and to gather a team of analysts to risk-adjust the outcomes and prepare reports of the member hospitals. Once the infrastructure was in place, the ACS opened the ACS NSQIP to all private ­hospitals in October of 2004. The current program has over 200 participating hospitals and has expanded its scope to address over 10 surgical ­specialties, with additional ones being developed.(25) One area of outcomes-based quality improvement that has gained a lot of recent attention is the so-called hospital acquired conditions, or “never events.” These are a list of 27 events first released publicly by the National Quality Forum (NQF) in November of 2006 (Table 16.4).(27) In 2007, The Leapfrog Group recognized hospitals that met certain criteria in the situation of when a “never event” occurred. These criteria included apologizing to the patient and/or family, reporting the event to JCAHO, performing a root cause analysis to prevent future events, and to waive all costs directly related to the adverse event.(10, 27) Recently, CMS has made a push not to reimburse the hospital for costs attributable to a “never event.” This is one of the best examples to date of a payer levying a financial disincentive against a hospital for poor quality.

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Quality of Care in Colorectal Disease There are a number of quality assessment/quality improvement projects in colorectal surgery and colorectal disease. In addition to the already described “performance measures” (e.g., SCIP), a number of investigative projects have been performed that have studied and identified some potential additional quality measures, as well as importantly studied how we might collect such data. A few of these projects are discussed below to offer a feel for the type and variety of projects that have been performed. One important project initiated with the support of the American Society of Colon and Rectal Surgery (ASCRS) is The Vermont Colorectal Cancer Project.(28) This project demonstrated that a statewide quality improvement project that required surgeons to input case data was feasible, with a compliance rate of 78%. Using these principles, the project was expanded to the New England area with the New England Colorectal Society project registry, a prospective, multiinstitutional regional database of patients undergoing surgery for colorectal cancer at 13 participating hospitals.(29) The study importantly found that surgeons were willing to participate in a collaborative, multi-institutional database, and this set the groundwork for successful data collection to evaluate and improve colorectal cancer care. A number of additional studies have addressed colorectal cancer quality of care. For example, the American Society of Clinical Oncology (ASCO) in part established the National Initiative on Cancer Care Quality (NICCQ) to develop quality of care measures for breast and colorectal cancer.(17, 30, 31) The NICCQ project team developed 25 process-based quality measures that spanned four domains of care: (1) diagnostic evaluation (10 measures); (2) surgery (4 measures); (3) adjuvant therapy (10 measures); and (4) surveillance (1 measure). Using a different set of processes and methodologies, the ACS developed a similar set of quality measures for breast and colorectal cancer. Both the NICCQ and the ACS submitted these measures to the NQF for their endorsement. Facilitated by the NQF, the ACS and NICCQ agreed to synchronize their measures (Table 16.5).(32) After development of the NICCQ measures, compliance was determined using multiple sources (e.g., hospital cancer registries,

quality and outcome measures Table 16.4  National Quality Forum (NQF) hospital acquired conditions (never events).  1

Unintended retention of a foreign object in a patient after surgery or other procedure

 2

Patient death or serious disability associated with patient elopement (disappearance)

 3

Patient death or serious disability associated with a medication error (e.g., errors involving the wrong drug, wrong dose, wrong patient, wrong time, wrong rate, wrong preparation or wrong route of administration)

 4

Patient death or serious disability associated with a hemolytic reaction due to the administration of ABO/HLA-incompatible blood or blood products

 5

Patient death or serious disability associated with an electric shock or elective cardioversion while being cared for in a healthcare facility

 6

Patient death or serious disability associated with a fall while being cared for in a healthcare facility

 7

Artificial insemination with the wrong donor sperm or donor egg Surgery performed on the wrong body part Surgery performed on the wrong patient Wrong surgical procedure performed on a patient Intraoperative or immediately postoperative death in an ASA Class I patient Patient death or serious disability associated with the use of contaminated drugs, devices, or biologics provided by the healthcare facility Patient death or serious disability associated with the use or function of a device in patient care, in which the device is used or functions other than as intended Patient death or serious disability associated with intravascular air embolism that occurs while being cared for in a healthcare facility Infant discharged to the wrong person Patient suicide, or attempted suicide resulting in serious disability, while being cared for in a healthcare facility Maternal death or serious disability associated with labor or delivery in a low-risk pregnancy while being cared for in a healthcare facility Patient death or serious disability associated with hypoglycemia, the onset of which occurs while the patient is being cared for in a healthcare facility Death or serious disability (kernicterus) associated with failure to identify and treat hyperbilirubinemia in neonates Stage 3 or 4 pressure ulcers acquired after admission to a healthcare facility Patient death or serious disability due to spinal manipulative therapy Any incident in which a line designated for oxygen or other gas to be delivered to a patient contains the wrong gas or is contaminated by toxic substances Patient death or serious disability associated with a burn incurred from any source while being cared for in a healthcare facility Patient death or serious disability associated with the use of restraints or bedrails while being cared for in a healthcare facility Any instance of care ordered by or provided by someone impersonating a physician, nurse, pharmacist, or other licensed healthcare provider Abduction of a patient of any age Sexual assault on a patient within or on the grounds of the healthcare facility

 8  9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28

Death or significant injury of a patient or staff member resulting from a physical assault (i.e., battery) that occurs within or on the grounds of the healthcare facility

Table 16.5  American Society of Clinical Oncology (ASCO), National Comprehensive Cancer Network (NCCN), Colorectal Quality Measures, and Commission on Cancer (CoC) Joint Quality Measures for Colorectal Cancer. Area Colon

Rectum

1.  Receipt of adjuvant chemotherapy within 4 months of diagnosis for patients <80 years of age with AJCC Stage III (lymph node positive) colon cancer 2.  ≥12 lymph nodes should be removed and pathologically examined for resected colon cancer 3.  Receipt of radiation therapy within 6 months of diagnosis for AJCC stage III colon cancer patients 4.  Receipt of postoperative adjuvant chemotherapy within 9 months for AJCC stage II or III rectal cancer

patient surveys) in a sample of stage II-III colon cancer survivors in 5 metropolitan areas approximately 4 years after diagnosis. Overall compliance was 78% for all 25 measures; by domain, compliance was 87% diagnostic evaluation; 93% surgery; 64% adjuvant therapy; and 50% surveillance.(17, 32) Interestingly,

this is much higher than the 55% compliance rate found for most types of care.(33) Potential reasons for higher compliance may be the urgency of a cancer diagnosis (beyond chronic conditions such as diabetes) and the multidisciplinary approach to cancer treatment. However, selection bias may increase compliance rates since the NICCQ study only examines 4-year survivors and it is possible that those who died received lower quality care. In 2001, the National Cancer Institute (NCI), in collaboration with the VA, launched a project entitled “Cancer Care Outcomes Research and Surveillance Consortium” (CanCORS) to measure the quality of care patients received in colorectal cancer and lung cancer care. This prospective observational cohort study on nearly 10,000 patients (4,921 with colorectal cancer and 5,105 with lung cancer) addressed how patient, provider, and system characteristics affected the care patients received and their outcomes.(34) The goal was to better understand the reasons behind disparities in cancer care. The two central goals of the project were to: 1) Determine how the characteristics and beliefs of cancer patients and providers and the characteristics of health-care organizations influence treatments and outcomes, spanning the continuum of cancer care from diagnosis to recovery or death. 2) Evaluate the effects of specific therapies on patients’ survival, quality of life, and satisfaction with care.(34)

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improved outcomes in colon and rectal surgery Data collection was completed in April 2007, with 15 years of followup data on the initial cohort. The study used surveys of patients, providers, and caregivers to meet the study objectives. Currently, data are being analyzed to understand the regional variation in cancer care. A number of studies have attempted to develop quality ­indicators, which serve to distinguish acceptable from unacceptable care. In 2006, McGory et al. published a comprehensive set of quality ­indicators for patients undergoing colorectal cancer surgery. McGory et al. used the RAND/UCLA Appropriateness Method to determine the validity of the candidate indicators using colorectal cancer experts. (35–39) This method uses an expert panel and a systematic review of the literature to identify candidate quality ­indicators. McGory et al. focused on process and structural measures. The 142 indicators (92 rated as valid) fall under 6 quality domains: surgeon privileging (e.g., credentialing for laparoscopic colectomy), preoperative evaluation (e.g., staging), patient-provider discussions (e.g., informed consent), medications (e.g., antibiotic prophylaxis), intraoperative care (e.g., prevention of ureteral injury), and postoperative management (e.g., control of blood glucose). Similar to McGory et al. Gagliardi et al. used a 3-step modified Delphi approach to identify the 45 key indicators, of which 37 (82%) were considered valid by the panel.(40) This method also used an expert panel and a systematic review of the literature to identify candidate quality indicators. This study reports the top 15 prioritized quality indicators as their final recommendation for improving the quality of colorectal cancer surgery as rated by the expert panel, including 4 outcome measures (e.g., 30-day mortality) and 4 province level measures (e.g., 5-year survival). Putting it together Overall, the development and use of quality and outcome measures still remains a work in progress with the current levels of underuse, overuse, disparities, and inefficiencies. The goal to improve the quality of care is not the issue. What remains the issue is how to improve the quality of care. We have attempted to show how strategies for improvement have been based on structural, process, and outcome components—all with their individual advantages, but also with their recognizable limitations. To date, there doesn’t appear to be one best way to improve care, which probably means that a combination of measures and metrics will be needed. In the field of colon and rectal surgery, the basic quality measures applicable to most every colorectal surgeon are the SCIP measures at the hospital level, and the PQRI measures at the individual (surgeon) level, but more are probably forthcoming. There are some potential “disease related” measures for colorectal cancer, but they generally address chemo and radiation therapies. The only potential surgery-related measure, which is clearly not solely a surgical issue, is the 12-node measure (i.e., evaluation of a minimum of 12 lymph nodes in a colon cancer resection). There has been demonstrable pushback to this measure, and at present, is not endorsed by the NQF as an “accountability” measure. Probably the single most important measure for evaluating and improving care, regardless of strategy, is obtaining accurate data that is actionable. Specifically, the collection, analysis, and ­feedback of data have yielded quality improvement in a variety of environments and fields, including colorectal surgery.

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The future of quality of care evaluation and improvement is difficult to predict. The use of quality and outcome measures as described in this chapter may only be in its infancy. As data systems become increasingly powerful and sophisticated, and as evidence in the literature continues to build, we suspect that increasingly more quality and outcome measures will be developed and used. The developed measures will likely become increasingly actionable and clinically meaningful, which will help to advance the field of quality improvement. For us to improve our outcomes in colorectal surgery at the present time, knowing our own quality is paramount. In this regard, participation in quality improvement programs that collect, feedback, and benchmark data is probably warranted. In addition, participation in studies that advance the levels of evidence is needed. Finally, recognizing that quality improvement is an iterative process is essential. All of this highlights the importance of surgeon involvement to guide quality improvement in surgery in the right direction. References   1. http: www.nchc.org/facts/cost.shtml. Accessed May 30, 2008; Abstract.   2. http:www.geographyiq.com/ranking/ranking_Infant_Mortality _Rate_aall.htm. Accessed May 30, 2008; Abstract.   3. Committee on Quality of Health Care in America. Crossing the Quality Chasm: A New Health System for the 21st Century. 2001; Abstract.   4. Committee on Quality of Health Care in America. To Err is Human: Building a Safer Health System. 2000; Abstract.   5. Hayward RA, Hofer TP. Estimating hospital deaths due to medical errors: preventability is in the eye of the reviewer. JAMA 2001; 286: 415–20.   6. http: www.ihi.org/IHI/Topics/Improvement/Improvement Methods/ImprovementStories/Health+Care+Must+ Be+Safe.htm. Accessed May 30, 2008; Abstract.   7. Codman E. A Study in Hospital Efficiency as Demonstrated by the Case Reports of the First Five Years of a Private Hospital. 1916; Abstract.   8. Donabedian A. The end results of health care: Ernest Codman’s contribution to quality assessment and beyond. Milbank Q 1989; 67: 233–56.   9. Donabedian A. The quality of care. How can it be assessed? JAMA 1988; 260: 1743–8. 10. http: www.leapfroggroup.org/home. Accessed May 30, 2008. Abstract. 11. http: www.leapfroggroup.org/about_us/leapfrog-factsheet. Accessed May 28, 2008. Abstract. 12. http: www.leapfroggroup.org/media/file/Leapfrog-EvidenceBased_Hospital_Referral_Fact_Sheet.pdf. Accessed May 28, 2008; Abstract. 13. Birkmeyer JD, Siewers AE, Finlayson EV et al. Hospital ­volume and surgical mortality in the United States. N Engl J Med 2002; 346: 1128–37. 14. Billingsley KG, Morris AM, Dominitz JA et al. Surgeon and hospital characteristics as predictors of major adverse outcomes following colon cancer surgery: understanding the volume-outcome relationship. Arch Surg 2007; 142: 23–3.

quality and outcome measures 15. Ho V, Heslin MJ, Yun H, Howard L. Trends in hospital and surgeon volume and operative mortality for cancer surgery. Ann Surg Oncol 2006; 13: 851–8. 16. Killeen SD, O’Sullivan MJ, Coffey JC, Kirwan WO, Redmond HP. Provider volume and outcomes for oncological procedures. Br J Surg 2005; 92: 389–402. 17. Schneider EC, Malin JL, Kahn KL et al. Surviving colorectal cancer : patient-reported symptoms 4 years after diagnosis. Cancer 2007; 110: 2075–82. 18. Panageas KS, Schrag D, Riedel E, Bach PB, Begg CB. The effect of clustering of outcomes on the association of procedure volume and surgical outcomes. Ann Intern Med 2003; 139: 658–65. 19. http: www.cfmc.org/hospital/hospital_scip.htm. Accessed May 28, 2008; Abstract. 20. http: www.premierinc.com/quality-safety/tools-services/p4p/ hqi/faqs-year1-3.jsp#Hospital%20Quality. Accessed May 30, 2008; Abstract. 21. http: www.premierinc.com/quality-safety/tools-services/p4p/ hqi/index.jsp. Accessed May 29, 2008; Abstract. 22. http: www.premierinc.com/quality-safety/tools-services/p4p/ hqi/index.jsp. Accessed May 30, 2008; Abstract. 23. http: www.cms.hhs.gov/pqri/. Accessed May 30, 2008. Abstract. 24. http:www.cms.hhs.gov/PQRI/Downloads/2008PQRIMeasures List.pdf?agree=yes&next=Accept. Accessed May 30, 2008; Abstract. 25. https: acsnsqip.org/main/about_history.asp. Accessed May 29, 2008; Abstract. 26. Khuri SF, Daley J, Henderson W et al. The Department of Veterans Affairs’ NSQIP: the first national, validated, outcome-based, risk-adjusted, and peer-controlled program for the measurement and enhancement of the quality of surgical care. National VA Surgical Quality Improvement Program. Ann Surg 1998; 228: 491–507. 27. http: www.qualityforum.org/pdf/news/prSeriousReportableEvents10–15–06.pdf. Accessed May 30, 2008; Abstract. 28. Hyman N, Labow SB. The Vermont colorectal cancer project: self-portrait. Arch Surg 2002; 137: 413–6. Notes: CORPORATE NAME: Vermont Chapter of the American College of Surgeons.

29. Hyman NH, Ko CY, Cataldo PA, Cohen JL, Roberts PL. The New England colorectal cancer quality project: a prospective multi-institutional feasibility study. J Am Coll Surg 2006; 202: 36–44. 30. Malin JL, Schneider EC, Epstein AM et al. Results of the National Initiative for Cancer Care Quality: how can we improve the quality of cancer care in the United States? J Clin Oncol 2006; 24: 626–34. 31. Schneider EC, Malin JL, Kahn KL, Emanuel EJ, Epstein AM. Developing a system to assess the quality of cancer care: ASCO‘s national initiative on cancer care quality. J Clin Oncol 2004; 22: 2985–91. 32. http: www.asco.org/ASCO/Downloads/Cancer%20Policy% 20and%20Clinical%20Affairs/NCCN/ASCO%20 NCCN%20Quality%20Measures%20table%20web%20posting%20with%20CoC%200507.pdf. Accessed May 30, 2008; Abstract. 33. McGlynn EA, Asch SM, Adams J et al. The quality of health care delivered to adults in the United States. N Engl J Med 2003; 348: 2635–45. 34. http: healthservices.cancer.gov/cancors/. Accessed May 30, 2008; Abstract. 35. Brook RH. The RAND/UCLA Appropriateness Method. Clinical practice guideline development: methodology pers­ pectives. Public Health Service: AHCR 1994; Abstract. 36. Leonardi MJ, McGory ML, Ko CY. Quality of care issues in colorectal cancer. Clin Cancer Res 2007; 13: 6897s–902s. 37. McGory ML. Quality indicators for the care of colorectal cancer in vulnerable elders. J Am Geriatr Soc 2007; 55(Suppl 2): S277–84. 38. McGory ML, Shekelle PG, Ko CY. Development of quality indicators for patients undergoing colorectal cancer surgery. J Natl Cancer Inst 2006; 98: 1623–33. 39. McGory ML, Shekelle PG, Rubenstein LZ, Fink A, Ko CY. Developing quality indicators for elderly patients undergoing abdominal operations. J Am Coll Surg 2005; 201: 870–83. 40. Gagliardi AR, Simunovic M, Langer B, Stern H, Brown AD. Development of quality indicators for colorectal cancer surgery, using a 3-step modified Delphi approach. Can J Surg 2005; 48: 441–52.

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17

Hemorrhoidal surgery Dan R Metcalf and Anthony J Senagore

Challenging Case A 38-year-old man presents to your office after receiving an urgent hemorrhoidectomy 1 year previously. He had continued pain and bleeding with bowel movements. He feels his anus is “too tight” and continues to be symptomatic despite attempts at dilatation, daily fiber, and stool softeners. Examination reveals three healed incisions and anal stenosis. The anus will only admit the tip of your finger with discomfort. Case Management The patient has anal stenosis due to removal of an excessive amount of anoderm with his surgery. The management of refractory posthemorrhoidectomy stenosis usually requires some type of flap repair. The choice of flap repair selected will depend on the degree of stenosis and the surgeon’s experience. The editors have found one or multiple house advancement flaps to be the most common option chosen in our practice. Introduction Few diseases are more chronicled in human history than symptomatic hemorrhoidal disease.(1, 2) Citations of hemorrhoidal disease have been noted in historic texts dating back to Babylonian, Egyptian, Greek, and Hebrew cultures.(1, 2) A multitude of treatment regimens have been offered including anal dilation, various topical liniments, and the often feared red hot poker.(3, 4) Although few people have died of hemorrhoidal disease, some patients wish they had particularly after therapy and this fact led to the beatification of St. Fiachre, the patron saint of gardeners and hemorrhoidal sufferers.(5) This chapter will guide the practitioner to a more humane approach to hemorrhoidal disease with the emphasis on cost-effectiveness and obtaining superior short and long-term outcomes. Anatomy/Etiology Hemorrhoidal cushions are located within the submucosa of the upper anal canal and are a normal component of the anorectal anatomy. These cushions are composed of blood vessels, smooth muscle (Treitz’s muscle), connective tissue, and elastic tissue.(6) (Figure 17.1) Anatomically, the hemorrhoidal cushions appear with marked predictability in the right anterior, right posterior, and left lateral positions, although there may be intervening secondary hemorrhoidal complexes which obscure this classic anatomy.(6) The blood supply to the anal cushions is derived from the superior rectal artery, a branch of the inferior mesenteric; the middle rectal arteries arising from the internal iliac arteries; and the inferior rectal arteries arising from the pudendal arteries. The venous drainage transitions from the portal venous system above the level of the dentate line to the systemic venous system below this level.(6) Anal cushions contribute to the maintenance of anal continence and allow the anal canal to dilate during defecation without tearing.



Figure 17.1  Sagital section of anal cushion showing internal and external hemorroids.

(6) Consequently, in some patients hemorrhoidectomy may result in various degrees of incontinence or leakage. Hemorrhoidal ­disease occurs as the result of abnormalities within the connective tissue of these cushions producing bleeding with or without prolapse of the hemorrhoidal tissue.(7) This can occur as the result of excessive straining, chronic constipation, or low dietary fiber.(8) A clear understanding of the pathophysiology is important when considering therapeutic interventions. At the earlier stages of disease, when the major manifestation is transudation of blood through thin walled damaged vascular channels, ablation of the vessels should be adequate. In contrast, when there is significant disruption of the mucosal suspensory ligament in the late stages of the disease, a technique resulting in fixation of the mucosa to the underlying muscular wall is necessary for effective therapy.(9) Internal anal sphincter dysfunction may play a role, as a number of investigators have demonstrated increased internal anal sphincter tone in patients with hemorrhoidal disease.(10–12) In reality, a combination of all of the above factors are important for the ultimate development of large prolapsing hemorrhoids. Hemorrhoids are divided into two groups, external and internal. External hemorrhoids are located distal to the dentate line and are covered by modified squamous epithelium (anoderm). In contrast, internal hemorrhoids are covered by columnar or transitional epithelium and are located proximal to the dentate line. Internal hemorrhoids are further divided into grades based on size and clinical

hemorrhoidal surgery symptoms. Grade I internal hemorrhoids bulge into the lumen and produce bleeding; Grade II internal hemorrhoids protrude with bowel movements and reduce spontaneously; Grade III internal hemorrhoids protrude spontaneously or with bowel movements and require manual reduction: Grade IV internal hemorrhoids are permanently prolapsed and irreducible.(13) Mixed hemorrhoids are those with components of both internal and external hemorrhoids. Although there tends to be a correlation between symptoms and the grade of hemorrhoidal disease, therapeutic decisions should not be based solely on these criteria. As will be outlined later, it is important to consider the relative role of internal hemorrhoidal tissue in addition to external hemorrhoidal skin tagging when choosing a modality for complete resolution of the patient’s symptoms.(7) Clinical Evaluation Among the most common symptoms associated with hemorrhoidal disease are bleeding, protrusion, and pain. However, Mazier reported on a series of 500 patients with anorectal complaints they associated with their hemorrhoids and ultimately, only 35% of patients were found to have any significant hemorrhoidal disease at all.(14) Hemorrhoidal bleeding is characteristically painless and bright red and seen on the toilet paper or in the commode after a bowel movement. However, more vigorous bleeding can occur as the hemorrhoids enlarge, particularly in advanced stages when a portion of the complex is fixed externally, allowing the blood to drip or spurt into the commode. Generally, prompt reduction of the protruding mass will alleviate this symptom. Acute thromboses of internal or external hemorrhoids are usually associated with a palpable mass and severe pain. These patients typically present with extreme discomfort and on clinical examination the diagnosis is frequently obvious. Examination of the patient with hematochezia should be tailored by the age of the patient and include sufficient investigations to rule out a proximal source of bleeding such as inflammatory bowel disease or neoplasia. Hemorrhoidal bleeding as a cause of anemia is an uncommon occurrence with an incidence of 0.5 per 100,000 per year.(15) Consequently, hemorrhoids should not be dismissed as the cause of iron deficiency anemia. The authors examine patients in the left lateral position with the knees drawn up toward the chest as high as possible. This approach allows relative patient comfort and the ability to clearly inspect the perianal skin, perform anoscopy, and proctosigmoidoscopy. A careful digital examination of the anal canal and distal rectum should be performed with the addition of prostate examination in male patients. Examination with an anoscope is essential to adequately inspect the hemorrhoidal tissue and anal canal. Inspection of the three common locations for hemorrhoids should be performed with documentation of the size, friability, and ease of prolapse. Documentation of anal pathology should be described by anatomic position (anterior, posterior, etc.,) to avoid confusion regarding the position in which the patient was examined. Upon completion of this portion of the exam, a decision should be made regarding the need for more proximal evaluation of the colon and rectum. However, rigid proctoscopy should be the minimum in all patients. After appropriately ­grading the hemorrhoidal disease, discussion can ensue with the patient regarding the various treatment options.

Nonexcisional Options The majority of patients with hematochezia attributable to hemorrhoids can be managed conservatively without surgical intervention. Dietary and lifestyle modification, reduction of straining with defacation, sclerotherapy, infrared coagulation, and rubber band ligation are described in chapter 18. These options are ­considered before considering excisional options. Excisional Hemorrhoidectomy Approximately 5–10% of patients will require surgical management of their hemorrhoids.(16) Excisional hemorrhoidectomy should be considered in those patients with extensive symptomatic disease who have failed or are not candidates for medical and nonexcisional options. In addition to this, the customary indications for hemorrhoidectomy include frequent or persistent prolapse requiring manual reduction resulting in discomfort and anal seepage, and hemorrhoids associated with conditions such as fissure, fistula, ulceration, or extensive anal skin tags. The final indication for excisional hemorrhoidectomy, although debatable, is the development of acutely thrombosed and ­gangrenous internal hemorrhoids. It is apparent however that similar full excisional hemorrhoidectomy can be performed using standard closed hemorrhoidectomy techniques without undue complications. Specifically, the risk of stenosis appears unwarranted if careful technique is used and the maximum amount of anoderm is preserved with skin bridges between excision sites. In the case of limited external hemorrhoidal thromboses, surgical excision may also be warranted for more rapid pain relief and avoidance of a residual skin tag. (17–20) Limited external thromboses can be easily managed in the office setting with local anesthesia and complete excision with or without skin closure.(Figure 17.2) Options for excisional hemorrhoidectomy include the following techniques: Milligan-Morgan hemorrhoidectomy; Ferguson Closed hemorrhoidectomy; Whitehead hemorrhoidectomy; stapled hemorrhoidectomy; and variations of the Milligan-Morgan and Ferguson techniques using alternative energy devices. The use of lasers for excisional hemorrhoidectomy offers no advantage and in fact causes delayed healing, increased pain, and increased cost.(21) The procedures are usually performed in the operating room after minimal preoperative bowel preparation. The choice of anesthetic is typically left to the anesthesiologist and patient, however local anesthesia supplemented by the administration of intravenous narcotics and propofol is very effective and short acting. The use of spinal anesthesia, although effective, may increase the risk of postoperative urinary retention do to a higher intraoperative administration of intravenous fluids. The Milligan-Morgan hemorrhoidectomy (Figure 17.3), which is widely practiced in Europe, was originally described in 1937 and its efficacy has subsequently been documented in many series.(22–24) This technique involves resection of the internal and external hemorrhoid complex, ligation of the arterial pedicle, and preservation of the intervening anoderm.(22) The distal anoderm and external skin are left open to heal by secondary intention to minimize the risk of infection. This technique has been proven to be a safe and effective means for managing advanced hemorrhoidal disease.(22) However, the open wounds typically

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improved outcomes in colon and rectal surgery

Figure 17.2  Excision of thrombosed external hemorrhoid.

take 4–8 weeks to heal and can be a cause of considerable discomfort and prolonged morbidity after this procedure. The closed Ferguson hemorrhoidectomy (Figure 17.4) was proposed as an alternative to the Milligan-Morgan technique and enjoys a similar large body of evidence regarding its safety and efficacy.(17–20) This technique utilizes an hourglass-shaped excision of the entire internal and external hemorrhoidal complex (centered at the midportion of the anoderm), preservation of the internal and external anal sphincters, and primary closure of the entire wound. Occasionally, it is necessary to undermine flaps of anoderm and perianal skin to allow excision of intermediate hemorrhoidal tissue, while preserving the bridges of anoderm between pedicles. This technical adjustment will avoid postoperative strictures. The Whitehead hemorrhoidectomy (Figure 17.5), described in 1882, involves a circular incision at the level of the dentate line with subsequent circumferential excision of the hemorrhoidal tissue and relocation of the dentate line which is often a component of prolapsing hemorrhoids.(25) Although this technique had a long period of widespread use in the United Kingdom, it was subsequently largely abandoned because of the high rates of mucosal ectropion and anal stricture.(26–29) However, using a modification of the original technique it has enjoyed renewed support by some surgeons in the United States with minimal stricture rates and no occurrences of mucosal ectropion.(30–31) Despite these promising reports, the Whitehead procedure is technically demanding because of the need to accurately identify the dentate line and relocate it to its proper location. Stapled hemorrhoidopexy is a relatively novel technique with growing acceptance as an alternative to excisional hemorrhoidectomy for the treatment of grade III and grade IV hemorrhoids. The technique, as described in 1998 by Antonio Longo (32), involves circumferential excision of the mucosa and submucosa above the hemorrhoids using a circular stapler resulting in relocation and fixation of the internal hemorrhoids. Briefly, a circular



anoscope is inserted into the anal canal to reduce the prolapsing tissue and allow placement of a circumferential purse-string suture 4 cm proximal to the dentate line into the mucosa and submucosa. A 33 mm hemorrhoidal circular stapler (EthiconEndo-Surgery; PPH03) with the anvil fully extended is then advanced proximal to the purse-string which is then gently tightened around the shaft of the stapler. The free ends of the suture are then threaded through the lateral channels of the stapler housing to provide traction on the purse-string as the stapler is closed and advanced into the anal canal. Once in position the stapler is closed and fired. The staple line should be inspected for hemostasis and bleeding controlled with an absorbable suture.(Figure 17.6) Numerous randomized controlled trials comparing stapled hemorrhoidopexy to conventional hemorrhoidectomy have substantiated the benefits of stapled hemorrhoidectomy, namely reduced operating room time, less pain and analgesic use, and earlier return to work with similar symptom control.(33–36) In a prospective, randomized, controlled multicenter trial comparing stapled hemorrhoidopexy and closed hemorrhoidectomy Senagore et al. reported less pain, less pain at first bowel movement, less analgesic use and similar symptom control using stapled hemorrhoidopexy in which 88% of patients were treated as outpatients.(36) As demonstrated in a recent systematic review of 25 randomized, controlled trials comparing stapled hemorrhoidopexy to conventional hemorrhoidectomy, stapled hemorrhoidopexy is a safe and effective procedure for the treatment symptomatic hemorrhoids with superior short-term outcomes. (37) This review indicates that the incidence of recurrent hemorrhoids is significantly higher at one or more years after stapled hemorrhoidopexy (5.7% vs. 1%), however, the overall recurrence or persistence of hemorrhoidal symptoms was similar between the groups (SH vs. conventional: 25.3% vs. 18.7%, p = 0.07).(37) In a retrospective review of 291 patients submitted to stapled hemorrhoidopexy with grade III and grade IV hemorrhoids, the overall recurrence rate after a minimum follow-up of 5 years was 18.2%. (38) They showed a tendency for higher recurrence in grade IV

hemorrhoidal surgery (A)

(B)

(D)

(C)

(E)

(F)

Figure 17.3  Open (Milligan-Morgan) hemorrhoidectomy. (A) External hemorrhoids grasped with forceps and retracted outward. (B) Internal hemorrhoids grasped with forceps and retracted outward with external hemorrhoids. (C) External skin and hemorrhoid excised with scissors. (D) Suture placed through proximal internal hemorrhoid and vascular bundle. (E) Ligature tied. (F) Tissue distal to ligature is excised. Insert depicts completed three bundle hemorrhoidectomy.

(A)

(B)

(C)

(D)

Figure 17.4  Modified Ferguson excisional hemorrhoidectomy. (A) Double ellipitical incision made in mucosa and anoderm around hemorrhoidal bundle with a scalpel. (B) The hemorrhoid dissection is carefully continued cephalad by dissecting the sphincter away from the hemorrhoid. (C) After dissection of the hemorrhoid to its pedicle, it is either clamped, secured, or excised. The pedicle is suture ligated. (D) The wound is closed with a running stitch. Excessive traction on the suture is avoided to prevent forming dog ears or displacing the anoderm caudally.



improved outcomes in colon and rectal surgery (A)

(B)

(C)

(D)

(E)

Figure 17.5  Whitehead hemorrhoidectomy. (A) Suture placed through proximal internal hemorrhoid for orientation. Excision started at dentate line and continued to proximal bundle. (B) Internal hemorrhoidal tissue excised above ligated bundle. (C) Vascular tissue excised from underside of elevated anoderm. (D) End of anoderm reaproximated with sutures to original location of dentate line. (E) Completed procedure.

hemorrhoids with a significantly higher reoperation rate.(38) In some instances this was thought to be related to inappropriate patient selection. In a large series reported by Jongen et al. stapled hemorrhoidopexy with good patient selection was associated with a low rate (3.4%) of reoperation for persistent or recurrent hemorrhoidal prolapse.(39) The data clearly indicate that stapled hemorrhoidopexy is a safe and effective option to treat symptomatic hemorrhoids with superior short-term outcomes. Although a higher rate of late recurrence is reported with this technique in the current literature, an appropriately designed randomized trial with adequate power and longer follow-up is needed to ultimately define the durability of stapled hemorrhoidopexy. Patient selection for ­stapled hemorrhoidopexy may also play an important role in short and long term outcome analysis. Improper technique with PPH has led to significant complications. Placement of the purse-string suture too high (cranial) or too deep has led to a full thickness excision and occasional anastomotic leaks with subsequent sepsis and some deaths. Placement of the purse-string suture too low may lead to impaired continence (inclusion of sphincter muscle in staples) or pain. Chronic pain following PPH may respond to anti-inflammatory agents or time. Some success in refractory patients has been obtained with removal of residual staples (usually done under anesthesia) or injection of long duration steroids. In the quest to provide patients with the benefit of less postoperative pain, alternative devices such as the Harmonic Scalpel® and LigaSure™ have recently been used to perform excisional hemorrhoidectomy. There have been four randomized, controlled trials published in an attempt to assess the efficacy of Harmonic Scalpel® hemorrhoidectomy.(40–43) Although all studies indicate that the harmonic scalpel is an effective alternative with a similar complication profile to more conventional methods, there is inconsistency regarding the short term benefits such as postoperative pain across these studies. Multiple randomized, controlled trials evaluating LigaSure™ hemorrhoidectomy to conventional techniques have been performed; (44–50) Most of these studies demonstrate a reduction in postoperative pain and operating time when using the LigaSure™. A multicenter, prospective, randomized study by Altomare et al. showed significantly less pain



12 hours after defacation, lower analgesic requirements, and faster return to work and normal activity with no difference in early or late complications.(48) Both instruments have been shown to be a safe and effective alternative to conventional hemorrhoidectomy. However, the added cost, conflicting short term outcomes, and lack of long term follow-up prelude recommendations for their routine use. At the present time, conventional methods of excisional hemorrhoidectomy remain the “gold standard”. Postoperative Complications Regardless of the excisional technique used for treatment of advanced hemorrhoidal disease, the key to effective patient management is avoidance of postoperative complications. Pain The anoderm has a rich supply of sensory nerves and pain arises from involvement of the anoderm below the dentate line. Posthemorrhoidectomy pain is associated with reflex spasm of the urethral and anal sphincter muscles. Spasm of these muscles leads to difficulty voiding and urinary retention and difficulty with evacuation and constipation. Both of which are covered later. From the patient’s perspective, pain is the most feared element of the procedure. A variety of analgesic regimens have been recommended, usually consisting of a combination of oral and parenteral narcotics.(51–55) Local anesthetic agents such as 0.5% bupivacaine solution may provide analgesia for up to 6–8 hours after surgery. The use of ketorolac has demonstrated considerable efficacy in managing posthemorrhoidectomy pain.(51) Alternative administration routes for narcotics either by patch or subcutaneous pump have been successful in controlling pain, however due to the risk of narcotic respiratory depression, administration by these routes can be risky in the outpatient setting.(53–55) The most appropriate regimen following outpatient hemorrhoidectomy appears to be intraoperative use of ketorolac, sufficient doses of oral narcotic analgesics for home administration, and supplementation of the narcotics by an oral nonsteroidal medication. Urinary Retention Urinary retention is a frequent postoperative complication following hemorrhoidectomy with an incidence from 1–52%.(16, 56–58)

hemorrhoidal surgery

(a)

(b)

(c)

(d)

(e)

(f)

Figure 17.6  Stapled anoplasty (procedure for prolapse and hemorrhoids [PPH]). (A) Retracting anoscope and dilator inserted. (B) Monofilament pursestring suture (eight bites) placed using operating anoscope approximately 3–4 cm above anal verge. (C) Stapler inserted through pursestring. Pursestring suture tied and ends of suture manipulated through stapler. (D) Retracting on suture pulls anorectal mucosa into stapler. (E) Stapler closed and fired. (F) Completed procedure.

A variety of strategies have been used to treat this problem including parasympathomimetics, alpha-adrenergic blocking agents, and sitz baths.(59, 60) However, prevention seems to be the best strategy by limiting perioperative fluid administration to 250 ml, avoiding the use of spinal anesthesia and anal packing, and prescribing an aggressive oral analgesic regimen.(56) Elderly men with obstructive uropathy are at increased risk for urinary retention. If catheterization becomes necessary, intermittent catherization under sterile conditions is the option of choice. Urologic consultation may be

sought for patients with persistent symptoms of bladder outflow obstruction. Hemorrhage Early postoperative bleeding (<24 hours) occurs in approximately 1% of cases and represents a technical error requiring return to the operating room for repair of the offending wound.(61) Occasionally bleeding may continue undetected, with blood ­accumulating in the capacious rectum. The first



improved outcomes in colon and rectal surgery sign of this complication may be pallor, tachycardia, and hypotension. This patient requires fluid resuscitation and a return to the operating room for suture ligation or diathermy control of the bleeding site. Bleeding from the staple line when using a PPH can be controlled by oversewing the bleeding point of the staple line. This is less common with the second generation 33 mm hemorrhoidal circular stapler (Ethicon endosurgery; PPH03) which has a shorter stapler height. Delayed hemorrhage occurs in 0.5–4% of cases of excisional hemorrhoidectomy and often occurs at 5–10 days postoperatively. (62–64) The etiology has been held to be early separation of the ligated pedicle before adequate thrombosis in the feeding artery can occur.(65) Hemorrhage in this situation is frequently significant and requires some method for control of ongoing hemorrhage. Options include return to the operating room for suture ligation, or tamponade at the beside by Foley catheter or anal packing.(66–68) The outcome after control of secondary hemorrhage is generally good with virtually no risk of recurrent bleeding. It may be helpful to irrigate out the distal colon and rectum at the time of intraoperative control of hemorrhage to avoid confusion in the postoperative period. Constipation and Fecal Impaction Fecal impaction is a distressing complication of excisional hemo­ rrhoidectomies. Postoperative pain, the patient’s fear of pain associated with defecation, and the constipating effects of narcotics are contributing factors. Hence, providing adequate analgesia and patient reassurance are important. Patients should be instructed on the importance of adequate hydration. Many surgeons also recommend bulking agents and/or laxatives (e.g., polyethylene glycol solution), and topical anesthetics before a bowel movement to facilitate evacuation.(69) When fecal impaction is identified, early, simple irrigating enemas may help clear the anorectum of impacted feces. If the impactions are soft, an oral cleansing regime (17 gm of polyethelyene glycol solution in 4 oz of water every 15–20 minutes until the impaction is cleared) may be utilized.(70) In more severe cases, manual disimpaction under conscious sedation or general anesthesia may be necessary. Infection Infection of the urinary tract may result from either stasis of urine or instrumentation of the urinary tract. A 3% incidence has been reported from one institution following hemorrhoidal surgery. (16) A urine culture should be obtained before administration of appropriate antibiotics. The anoderm harbors an abundance of potentially pathologic bacterial microorganisms. Despite this, infective complications after hemorrhoidectomy are infrequent. Bacteremia and sepsis have been documented after hemorrhoidectomy, but abscess formation is rare unless a hematoma becomes infected. Isolated liver abscesses have been reported, and this very rare complication should be considered in patients with postoperative fever. It is usually currently identified by abdominal CT scan. Another potential infectious complication is postoperative pelvic sepsis. This can occur after any anorectal procedure including rubber band ligation and excisional hemorrhoidectomy. Classic findings include anorectal pain, fever, and difficulty



with urination. A high index of suspicion is required as delay in diagnosis can have fatal consequences. As described in chapter 18, patients with suspected pelvic sepsis require resuscitation, diagnostic evaluations (pelvic CT scans and/or anoscopic evaluation), and treatment (broad spectrum antibiotics and debridement of necrotic tissue). Anal Stenosis Anal stenosis results from excessive stripping of anal mucosa, which may leave inadequate bridges of anoderm for healing to occur without stenosis.(71) Secondary hemorrhoids should be managed with either submucosal hemorrhoidectomy or conservative methods such as sclerotherapy or rubber band ligation at a subsequent visit. In mild cases, stenosis may simply be a web that disappears with graduated anal dilatation in the office. In more severe cases, surgical intervention may be required to relive stenosis. Surgical correction may be accomplished by one of several reconstructive operations including skin and subcutaneous tissue flaps. These flap techniques are discussed in chapter 20. Mucosal Ectropion (Whitehead Deformity) Mucosal ectropion with the classic “Whitehead deformity” is commonly seen after an incorrectly performed procedure described by Whitehead.(22) As described previously, the operation entails making a circumferential incision at the level of the dentate line, elevating a flap of anal mucosa, and performing a submucosal hemorrhoidal excision. Redundant mucosa is then excised, and the anal canal is reconstructed with sutures. If the reconstruction does not relocate the dentate line in the correct location in the anal canal, anal mucosal will be located in the distal anal canal or perineum. Persistent mucous discharge and perianal irritation may result. Correction requires resection of the mislocated anal mucosa and reconstruction, which usually requires flaps. Fecal Incontinence Incontinence of feces results chiefly from damage to the internal anal sphincter during hemorrhoidectomy.(72) The internal anal sphincter is a thin, whitish, smooth muscle composed of circular fibers located just beneath the anal mucosa. It is almost always absent at the anal verge because its inferior limit is a few millimeters proximal to it. During surgery, the hemorrhoidal column should be lifted off the internal anal sphincter, which must be identified before excision of hemorrhoidal tissue. It is important to document the state of continence in patients before surgery. Soiling and fecal leakage are the chief impairments of continence resulting from internal anal sphincter damage. Treatment for soiling and leakage includes bulking agents and slowing agents (e.g., loperamide) and consideration of biofeedback therapy. Attempts to surgically repair damaged internal sphincter muscle have been disappointing. Anal Fistula Fistula in ano is an uncommon complication of hemorrhoidectomy and is thought to occur more commonly after a closed procedure.(73) The fistula is usually a simple submucosal tract that may be treated by simple unroofing.

hemorrhoidal surgery Anal Tags Anal skin tags after hemorrhoidal excision are not uncommon. Usually these tags are edematous areas of anoderm that generally resolve spontaneously some weeks after surgery. Reassurance will help allay patient’s concerns. It the tags remain bothersome or are associated with symptomatic pruritis, they can be excised in the office using local anesthesia. Special Situations Postpartum Hemorrhoids Postpartum hemorrhoids that are refractory to conservative measures may require surgical management. Hemorrhoidectomy in this setting is safe, has a low prevalence of complications, and in many cases will minimize recovery time. Proper patient position (usually left lateral Sims) and good anesthetic techniques are important. As in other urgent hemorrhoidectomies, preservation of as much anoderm as possible is also critical. Anorectal Varices Unlike hemorrhoids, varices result from portal venous hypertension. Differentiation from hemorrhoids is essential because excision of varices may result in venous bleeding that may be difficult to control. A history of anal bleeding in a cirrhotic patient should arouse suspicion. Varices may be present in the rectum, anal canal, or anal verge.(74) Duplex Doppler ultrasonography of the anorectum may confirm the diagnosis. Active bleeding from varices will usually require oversewing with a continuous suture technique. Conclusion The management of symptomatic hemorrhoidal disease should be directed at the symptom complex of the patient. The majority of these patients can be effectively treated by reducing strain at defacation, correcting constipation, the use of any of a variety of anal ointments. For those patients with persistent symptoms, either injection or banding of the internal hemorrhoids offers predictably successful results. Only a minority of patients should require excisional hemorrhoidectomy by any of the described techniques. Stapled hemorrhoidopexy, Harmonic Scalpel®, and LigaSure™ all offer safe and effective alternatives to the traditional open or closed excisional hemorrhoidectomy, however more long-term data is needed to provide recommendations for their routine use. References   1. Holley CJ. History of hemorrhoidal surgery. South Med J 1946; 39: 536.   2. Madoff RD. Biblical management of anorectal disease. Presented at the Midwest Society of Colon and Rectal Surgeons’ meeting. Brechenridge, CO; 1991.   3. Dirckx JH. The Biblical plague of “hemorrhoids”. Am J Dermatopathol 1985; 7: 341–6.   4. Maimonides M, Rosner F, Munter S. trans. Treatise on Hemorrhoids. Philadelphia, JB Lippincott; 1969.   5. Rachochot JE, Petourand CH, Riovoire JO. Saint Fiacre: the healer of hemorrhoids and patron saint of proctology. Am J Proctol 1971; 22: 175.

  6. Thompson WHF. The nature of haemorrhoids. Br J Surg 1975; 62: 542–52.   7. Morgado PJ, Suarez JA, Gomez LG et al. Histoclinical basis for a new classification of hemorrhoidal disease. Dis Colon Rectum 1988; 31: 474–80.   8. Burkitt DP, Graham-Stewart CW. Hemorrhoids - postulated pathogenesis and proposed prevention. Postgrad Med J 1975; 51: 631–6.   9. Haas PA, Fox TA, Haas GP. The pathogenesis of hemorrhoids. Dis Colon Rectum 1984; 27: 442–50. 10. Hancock BD. Internal sphincter and the nature of haemorrhoids. Gut 1977; 18: 651–5. 11. Arabi Y, Alexander-Williams J, Keighley MRB. Anal pressures in hemorrhoids and anal fissure. Am J Surg 1977; 134: 608–10. 12. Arscia SD ed. Morphological and Physiological Aspects of Anal Continence and Defecation. Bruxelles. Presses Academiques Europeenes, 1969: 150–1. 13. Banov L Jr, Knoepp LF Jr, Erdman LH, Alia RT. Management of hemorrhoidal disease. J S C Med Assoc 1985; 81: 398–401. 14. Benyon J. Endorectal and Anal Sonography in Surgery of the Colon, Rectum and Anus. W.B. Saunders, Philadelphia; 1995. 15. Kluiber RM, Wolff BG. Evaluation of anemia caused by hemorrhoidal bleeding. Dis Colon Rectum 1994; 37: 1006–7. 16. Bleday R, Pena PJ, Rothenberger DA, Goldberg SM, Buls JG. Symptomatic hemorrhoids: current incidence and complications of operative therapy. Dis Colon Rectum 1992; 35: 477–81. 17. Ferguson JA, Heaton JR. Closed hemorrhoidectomy. Dis Colon Rectum 1959; 2: 176–9. 18. Muldoon JP. The Completely Closed Hemorrhoidectomy: a reliable and trusted friend for 25 years. Dis Colon Rectum 1981; 24: 211–4. 19. Mc Connell JC, Khubchandani IT. Long-term Follow-Up of Closed Hemorrhoidectomy. Dis Colon Rectum 1983; 26: 797–9. 20. Ganchrow MJ, Mazier WP, Friend WG, Ferguson JA. Hemo­ rrhoidectomy revisited: a computer analysis of 2,038 cases. Dis Colon Rectum 1971; 14: 128–33. 21. Senagore A, Mazier WP, Luchtefeld MA et al. The treatment of advanced hemorrhoidal disease: a prospective randomized comparison of cold scalpel vs. contact Nd:YAG laser. Dis Colon Rectum 1993; 6: 1042–9. 22. Milligan ET, Morgan CN, Lond LE. Surgical anatomy of the anal canal, and the operative treatment of hemorrhoids. Lancet 1937; 2: 1119–24. 23. Duhamel J, Romand-Heuer Y. The technique of the Milligan and Morgan hemorrhoidectomy. Coloproctology 1980; 4: 265–6. 24. Tajana A. Hemorrhoidectomy according to MilliganMorgan: ligature and excision technique. Int Surg 1989; 74: 158–61. 25. Whitehead W. The surgical treatment of hemorrhoids. Br Med J (Clin Res) 1882; 1: 148–50. 26. Andrews E. Disastrous results following Whitehead’s operation and the so-called American operation. Columbus Med J 1895; 15: 97–106.

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improved outcomes in colon and rectal surgery 27. Andrews E. Some of the evils caused by Whitehead’s operation and by its modification, the American operation. Trans Ill Med Soc 1895: 433–46. 28. Khubchandani M. Results of Whitehead operation. Dis Colon Rectum 1984; 27: 730–2. 29. Rand AA. The sliding skin-flap graft operation for hemorrhoids: a modification of the Whitehead procedure. Dis Colon Rectum 1969; 12: 265–76. 30. Wolff BG, Culp CE. The whitehead hemorrhoidectomy. Dis Colon Rectum 1988; 31: 587–90. 31. Bonello JC. Who’s afraid of the dentate line? The whitehead hemorrhoidectomy. Am J Surg 1988; 156: 182–6. 32. Longo A. Treatment of hemorrhoidal disease by reduction of mucosa and hemorrhoidal prolapse with a circular suturing device: a new procedure. Proceeding of the 6th world congress of endoscopic surgery, Rome, 1998: 777–84. 33. Shalaby R, Desoky A. Randomized clinical trial of stapled versus Milligan-Morgan haemorrhoidectomy. Br J Surg 2001; 8: 1049–53. 34. Pavlidis T, Papaziogas B, Souparis A et al. Modern stapled Longo procedure vs. conventional Milligan-Morgan hemorrhoidectomy: a randomized controlled trial. Int J Colorectal Dis 2002; 17: 50–3. 35. Palimento D, Picchio M, Attanasio U et al. Stapled and open hemorrhoidectomy: randomized controlled trial of early results. World J Surg 2003; 27: 203–7. 36. Senagore AJ,Singer M,Abcarian H et al.A prospective, ­randomized, controlled multicenter trial comparing stapled hemorrhoidopexy and Ferguson hemorrhoidectomy: perioperative and one-year results. Dis Colon Rectum 2004; 47: 1824–36. 37. Tjandra JJ, Chan MK. Systematic review on the procedure for prolapse and hemorrhoids (stapled hemorrhoidopexy). Dis Colon Rectum 2007; 50: 878–92. 38. Ceci F, Picchio M, Palimento D et al. Long-term outcome of stapled hemorrhoidopexy for Grade III and Grade IV hemorrhoids. Dis Colon Rectum 2008; 51: 1107–12. 39. Jongen J, Bock JU, Peleikis HG, Eberstein A, Pfister K. Complications and reoperations in stapled anopexy: learning by doing. Int J Colorectal Dis 2006; 21: 166–71. 40. Chung CC, Ha JP, Tai YP, Tsang WW, Li MK. Double-blind, randomized trial comparing Harmonic Scalpel hemorrhoidectomy, bipolar scissors hemorrhoidectomy, and scissors excision: ligation technique. Dis Colon Rectum 2002; 45: 789–94. 41. Khan S, Pawlak SE, Eggenberger JC et al. Surgical treatment of hemorrhoids: prospective, randomized trial comparing closed excisional hemorrhoidectomy and the Harmonic Scalpel technique of excisional hemorrhoidectomy. Dis Colon Rectum 2001; 44: 845–9. 42. Armstrong DN, Ambroze WL, Schertzer ME, Orangio GR. Harmonic Scalpel vs. electrocautery hemorrhoidectomy: a prospective evaluation. Dis Colon Rectum 2001; 44: 558–64. 43. Tan JJ, Seow-Choen F. Prospective, randomized trial comparing diathermy and Harmonic Scalpel hemorrhoidectomy. Dis Colon Rectum 2001; 44: 677–9. 44. Bessa SS. Ligasure vs. conventional diathermy in excisional hemorrhoidectomy: a prospective, randomized study. Dis Colon Rectum 2008; 51: 940–4.

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45. Wang JY, Lu CY, Tsai HL et al. Randomized controlled trial of LigaSure with submucosal dissection versus Ferguson hemorrhoidectomy for prolapsed hemorrhoids. World J Surg 2006; 30: 462–6. 46. Chung YC, Wu HJ. Clinical experience of sutureless closed hemorrhoidectomy with LigaSure. Dis Colon Rectum 2003; 46: 87–92. 47. Franklin EJ, Seetharam S, Lowney J, Horgan PG. Randomized, clinical trial of Ligasure vs conventional diathermy in hemorrhoidectomy. Dis Colon Rectum 2003; 46: 1380–3. 48. Altomare DF, Milito G, Andreoli R et al. Ligasure Precise vs. conventional diathermy for Milligan-Morgan hemorrhoidectomy: a prospective, randomized, multicenter trial. Dis Colon Rectum 2008; 51: 514–9. 49. Palazzo FF, Francis DL, Clifton MA. Randomized clinical trial of Ligasure versus open haemorrhoidectomy. Br J Surg 2002; 89: 154–7. 50. Jayne DG, Botterill I, Ambrose NS et al. Randomized clinical trial of Ligasure versus conventional diathermy for day-case haemorrhoidectomy. Br J Surg 2002; 89: 428–32. 51. O’Donovan S, Ferrara A, Larach S, Williamson P. Intraoperative use of Toradol® Facilitates Outpatient Hemorrhoidectomy. Dis Colon Rectum 1994; 37: 793–9. 52. Kuo RJ. Epidural Morphine for Post-hemorrhoidectomy Analgesia. Dis Colon Rectum 1984; 27: 529–30. 53. Kilbride MJ, Senagore AJ, Morse M. Improving patient safety with transdermal fentanyl for post-hemorrhoidectomy pain. Dis Colon Rectum 1994. [Letter to the Editor, p. 104]. 54. Kilbride MJ, Morse M, Senagore AJ. Transdermal Fentanyl Improves Management of Postoperative Hemorrhoidectomy Pain. Dis Colon Rectum 1994; 37: 1070–2. 55. Goldstein ET, Williamson PR, Larach SW. Subcutaneous morphine pump for postoperative hemorrhoidectomy pain management. Dis Colon Rectum 1993; 36: 439–46. 56. Hoff SD, Bailey HR, Butts DR et al. Ambulatory surgical hemorrhoidectomy - a solution to postoperative urinary retension? Dis Colon Rectum 1994; 37: 1242–4. 57. Petros JG, Bradley TM. Factors influencing postoperative urinary retention in patients undergoing surgery for benign anorectal disease. Am J Surg 1990; 159: 374–6. 58. Tammela T, Kontturi M. Lukkarinen O. ������������������ Postoperative urinary retention. I. Incidence and predisposing factors. Scand J Urol Nephrol 1986; 20: 197–201. 59. Leventhal A, Pfau A. Pharmacologic management of postoperative over-distension of the bladder. Surg Gynecol Obstet 1976; 146: 347–8. 60. Shafik A. Role of warm water bath in inducing micturition in postoperative urinary retention after anorectal operations. Urol Int 1993; 50: 213–7. 61. Corman ML. Complications of hemorrhoid and fissure surgery. In: Ferrari BT, Ray JE, Gathright JB, eds. Complications of colon and rectal surgery - prevention and management. Philadelphia: WB Saunders, 1985: 91–100. 62. Kilbourne NJ. Internal hemorrhoids: comparative value of treatment by operative and by injection methods - a survey of 62,910 cases. Ann Surg 1934; 99: 600–8.

hemorrhoidal surgery 63. Salvati EP, Eisenstat TE. Hemorrhoidal disease. In: Zuidema GD, Condon RE, eds. Shackelford’s surgery of the alimentary tract. 3rd Ed. Philadelphia: WB Saunders 1991: 294–307. 64. Milsom JW. Hemorrhoidal disease. In: Wexner SD, Beck DE, eds. Fundamentals of anorectal surgery. New York: McGraw Hill, 1992: 192–214. 65. Gabriel WB. Haemorrhoids. In: The principles and practice of rectal surgery, 5th ed. Springfield, Illinois: Charles C. Thomas, 1963: 110–64. 66. Rosen L, Sipe P, Stasik JJ, Riether RD, Trimpi HD. Outcome of delayed hemorrhage following surgical hemorrhoidectomy. Dis Colon Rectum 1993; 36: 743–6. 67. Cirocco WC, Golub RW. Local epinephrine injection as treatment for delayed hemorrhage after hemorrhoidectomy. Surgery 1995; 117: 235–7.

68. Basso L, Pescatori M. Outcome of delayed hemorrhage following surgical hemorrhoidectomy. [Letter to the Editor]. Dis Colon Rectum 1994; 37: 288–9. 69. Corman ML. management of postoperative constipation in anorectal surgery. Dis Colon Rectum 1979; 22: 149. 70. Araghizadeb F. Fecal impaction. Clin Colorectal Surg 2005; 18: 116–9. 71. Parks AG. The surgical treatment of Haemorrhoids. Br J Surg 1956; 43: 337–51. 72. Anal continence after haemorrhoidectomy. Lancet 1982; 11: 696. 73. Corman ML. Complications of hemorrhoidal and fissure surgery. In Ferrari BT, Ray JE, Gathright JB, eds. Complications of Colon and Rectal Surgery. Philadelphia: WB Saunders, 1985: 91–100.

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18

Nonoperative therapy for hemorrhoid disease Kerry Hammond and Charles B Whitlow

Challenging Case A 50-year-old male, otherwise healthy, presents to your office and after evaluation is diagnosed with grade 3 internal hemorrhoids. Rubber band ligation is performed and is well-tolerated. Fortyeight hours later he develops urinary retention and worsening anal pain. Case Management The patient’s symptoms are suggestive of pelvic or postbanding sepsis. The patient should be examined urgently, admitted, started on broad-spectrum intravenous antibiotics, and intravenous fluids. A foley catheter should be placed and blood work (CBC, metabolic profile, etc) obtained. A CT scan of the abdomen and pelvis should be considered. If the initial exam (including anoscopy) is not adequate or demonstrated necrotic perianal tissue, the patient should receive an exam under anesthesia and debridement of any necrotic tissue. Introduction “Hemorrhoids” are among the most frequent presenting complaints of patients evaluated in the outpatient setting by colon and rectal surgeons. In a 1990 review of data from the National Center for Health Statistics, Johanson and Sonnenberg determined a 4.4% prevalence of symptomatic hemorrhoids in the U.S. population.(1) In a subsequent study of data collected by the National Hospital Discharge Survey, the same authors found that the annual number of surgical hemorrhoidectomies performed in the United States had decreased from a peak of 117 per 100,000 patients in 1974 to a nadir of 37 per 100,000 in 1987.(2) This decrease in operative procedures is likely the result of improvements in nonoperative therapies for symptomatic internal hemorrhoids. Anatomy and Pathophysiology Hemorrhoids are cushions of vascular and connective tissue located in the subepithelial space lining the anal canal. Arteriovenous sinusoids between the terminal branches of the superior rectal arteries and the superior, middle and inferior rectal veins are encompassed by these cushions. These sinusoids lack a muscular wall, predisposing them to bleeding.(3–5) Hemorrhoidal prolapse develops as the supportive connective tissue matrix is compromised by age and trauma.(6, 7) A simple grading system has been widely adopted for the clinical assessment of symptomatic internal hemorrhoids. This 4-part grading system can be used by clinicians to describe the extent of a patient’s pathology and to differentiate which treatment options are appropriate (Table 18.1). (4–12) Clinical Evaluation It is not uncommon for patients to attribute any anorectal discomfort to hemorrhoids. Therefore, a careful history and physical

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Table 18.1  Grading system for internal haemorrhoids. Grade

Physical Characteristics

I

Prominent hemorrhoidal vessels without prolapse

II

Prolapse with valsalva; reduce spontaneously

III

Prolapse with valsalva; manual reduction needed

IV

Prolapsed hemorrhoids that cannot be reduced

examination is necessary to differentiate hemorrhoidal disease from other pathological processes. Bleeding is the most common symptom associated with internal hemorrhoidal disease. Patients who have bled secondary to hemorrhoids typically describe painless bleeding which is bright red in color. This usually occurs with defecation, and may be ­limited to the appearance of blood on toilet tissue.(8) More severe bleeding may result in dripping of blood or even pulsatile bleeding into the commode. Hemorrhoidal prolapse can cause a sensation of incomplete emptying or mucous discharge. Patients with a significant degree of prolapse often complain of pruritis and difficulty maintaining anal hygiene. Physical examination should include a thorough visual and digital inspection of the perianal soft tissue and anorectum to rule out conditions such as fissure, abscess, and neoplasm. Anoscopy can be performed in the office setting and is useful to determine the extent of hemorrhoidal enlargement. Colonoscopy should be considered for evaluation of bleeding if indicated by age, family history of colorectal cancer, or other risk factors for colorectal cancer.(7, 8, 10) Treatment Conservative Management The goal of medical management is to provide symptomatic relief by reducing straining during defecation and thereby eliminating the repetitive trauma that contributes to hemorrhoidal congestion and prolapse. Dietary modification is the cornerstone of conservative management for symptomatic hemorrhoids. A diet high in fiber (20–30 g/ day) promotes the formation of soft, formed stool that requires less straining to eliminate. In a 2006 meta-analysis, Alonso-Coello et al. evaluated the impact of supplemental fiber on symptoms related to hemorrhoids.(13) This analysis included 7 studies in which 378 total patients had been randomized to fiber or nonfiber controls. Pooled analysis for overall improvement in symptoms demonstrated a 47% risk reduction of persistence of symptoms for patients randomized to fiber supplementation. Four studies that addressed bleeding as an individual outcome showed a combined 50% relative risk reduction in the fiber treatment arm. (14–17) No significant difference between treatment and placebo

nonoperative therapy for hemorrhoid disease arms was found in three studies that addressed hemorrhoidal prolapse.(14, 15, 17) Supplemental fiber can be delivered in several forms. Resistant starches, found in legumes and grains, are polysaccharides that are resistant to a-amylase digestion. Fermentation by colonic bacteria with consequent increases in colonic gas production can produce abdominal bloating and flatulence. Soluble fiber dissolves in water and produces a viscous solution in the gastrointestinal tract. Sources of purified soluble fiber include psyllium (Metamucil®, Konsyl®), inulin (FiberChoice®), pectins, and Methylcellulose (Citrucel®) a semisynthetic soluble fiber that is not fermented by colonic bacteria. Insoluble fiber passes largely unaltered through the gastrointestinal tract with minimal fermentation in the colon. Natural sources of insoluble fiber include foods such as dark leafy vegetables and whole wheat products. Calcium polycarbophil (Fibercon®) is a synthetic bulking agent with properties similar to those of insoluble fiber.(18, 19) While allergic reactions to the active or inactive ingredients in dietary fiber supplements are rare, patients may experience variable levels of adverse effects such as abdominal bloating and flatulence after incorporating these products into their daily diet regimen. A period of gradual dosage increase or trial-and-error with different formulations may be necessary to identify the ideal supplement in order to maximize compliance. There is a paucity of data on the utility of stool softeners and laxatives in the treatment of symptomatic hemorrhoids. These agents may be a useful adjunct for patients with severe chronic constipation who do not experience optimal relief with bulking agents alone. Warm sitz baths and topical agents are frequently prescribed components of a conservative treatment regimen. Dodi et al. demonstrated a significant reduction in anal canal pressure after patients with anorectal disorders soaked in water at 40ºC.(20) Numerous topical agents are available for treatment of the acute symptoms of hemorrhoids. Most of these agents provide a local anesthetic effect which suppresses the burning and itching sensations associated with hemorrhoidal prolapse. While there is no compelling data to support the use of these compounds, the risk of side effects is relatively low and patients typically report some symptomatic relief with their use. Patients should be advised to limit the duration of use of topical steroids, as prolonged usage has the potential to cause chronic perianal dermatitis.(21) Sclerotherapy Injection sclerotherapy, first described in 1869 by John Morgan of Dublin, is the oldest form of nonsurgical hemorrhoid treatment still in use today. This technique was originally described using iron persulphate to inject external hemorrhoids.(12) The aim of sclerotherapy is to obliterate the vascular component of the hemorrhoid and induce scarring to prevent further prolapse. Sclerosants in current clinical use include 5% phenol in oil, 5% quinine, and urea and 1–3% sodium tetradecyl sulfate. The sclerosant solution is injected by 25 gauge needle into the apex of each hemorrhoidal bundle above the dentate line.(6–12) Sclerotherapy is contraindicated in patients with inflammatory bowel disease, portal hypertension, immunocompromised states, active anorectal infection, and prolapsed thrombosed hemorrhoids.(7)

Sclerotherapy is most effective for treatment of grade 1 or 2 internal hemorrhoids. Variable success rates have been reported for this mode of therapy. In a 1988 survey, Mann et al. reported that 88% of patients felt that their symptoms had improved at 4 weeks posttreatment.(22) In contrast, Senapati and Nicholls demonstrated no significant difference in bleeding symptoms in a randomized, controlled trial (n = 43). (23) Complications associated with injection sclerotherapy are rare, and typically result from deep placement of the injection. Urinary retention, prostatitis, prostatic abscess, and mucosal sloughing have been reported.(7–9) Rubber Band Ligation In medieval times, hemorrhoid ligation was performed by encircling the entire prolapsed hemorrhoid with thread.(8) This concept was modernized by Blaisdell in 1958 (24) and was further refined by Barron in 1963 (25) with his description of hemorrhoid ligation using small rubber bands. Using specialized instruments, rubber band ligation is performed by grasping excess tissue at the hemorrhoid apex and deploying a rubber band to constrict the hemorrhoidal blood supply. The encircled tissue sloughs after 5–7 days, creating a scar that fixes the remaining tissue to the rectal wall and consequently reduces the degree of prolapse. Rubber band ligation can be performed using a Barron or McGivney hemorrhoid ligator coupled with a modified Allis clamp, or with a McGown type suction ligator. (Figure 18.1) The authors prefer the suction ligator, which is designed for singleoperator use. Rubber bands must be placed at least 2 cm above the dentate line to avoid severe pain. If the patient expresses discomfort during the tissue grasping/suction phase of the procedure, the procedure should be abandoned. Severe pain immediately following rubber ligation may necessitate band removal, which can be performed using a hooked probe.(7) Alternatively, injection of bupivacaine into the hemorrhoid above and below the level of the rubber band provides several hours of relief and subsequent pain is adequately treated with narcotics. While up to three hemorrhoids can be banded in a single session (26, 27), the authors typically limit treatment to one or two columns to minimize patient discomfort related to excessive banded tissue within the anal canal. In a review of 39 published studies (8,060 patients), Wechter found pain to be the most common complication (5.8%) following hemorrhoid banding. Other potential complications include hemorrhage (1.7%), incontinence (0.9%), thrombosis (0.6%) and infection (0.04%).(28) Patients may on occasion experience vasovagal symptoms immediately after band placement, including diaphoresis, bradycardia, nausea, and hypotension.(12) This usually spontaneously resolves after allowing the patient to lie down for 10 to 15 minutes. Postbanding hemorrhage typically occurs 4 to 7 days after the procedure. It is related to the band falling off after necrosis of tissue is complete and is most commonly self-limited. More severe bleeding may require operative ligation. Although rare, several cases of postbanding sepsis have been reported.(28–30) In a 2006 review, McCloud et al. examined 10 case reports of sepsis following rubber-band ligation of



improved outcomes in colon and rectal surgery (A)

(B)

(C)

(c)

Figure 18.1  Banding an internal hemorrhoid. The internal hemorrhoid is teased into the barrel of the ligating gun with (A) a suction (McGown) ligator or (B) a McGivney ligator. (C) The apex of the banded hemorrhoid is well above the dentate line to minimize pain.

hemorrhoids (17 total cases, 6 fatal). The majority of these 17 patients developed local or retroperitoneal abscesses within the first week following banding. Common presenting symptoms included perineal induration and pain, urinary difficulties, and fever.(31) Patients with these or similar symptoms following rubber band ligation of hemorrhoids should undergo a thorough clinical evaluation including appropriate imaging studies (CT Scan) and physical examination, with initiation of broadspectrum antibiotics, and surgical drainage or debridement if indicated.

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Reported success rates for hemorrhoid banding vary according to length of follow-up and grade of hemorrhoids treated. In 2004, Iyer et al. reported a series of 701 patients who underwent rubber band hemorrhoid ligation, with an overall success rate of 70.5%. The median follow-up time was 1,205 days. Although there was not a statistically significant difference in success between the 4 grades of hemorrhoids treated, patients with grade 1 and 2 hemorrhoids demonstrated the most improvement (72.4% and 73.1% respectively).(32) A 1998 survey of 92 patients by Savioz et al. found 77% and 68% of patients to be free of symptoms at 5 and 10 years postbanding.(33)

nonoperative therapy for hemorrhoid disease

Figure 18.2  The infrared photocoagulator creates a small thermal injury. Thus several applications are required for each hemorrhoidal column.

Treatments

1st degree

2nd degree

3rd degree

4th degree

Acute prolapse with

Dietary

X

X

X

X

X

Banding

X

X

X

Sclerotherapy

X

X

X

Infrared coagulation

X

X

X

Excisional hemorrhoidectomy

X

X

X

Emergent

Stapled hemorrhoidopexy

X

X

X (?)

Multiple thrombectomies and multiple bandings

X

Figure 18-3  Management of Hemorrhoids by Classification.

Infrared Photocoagulation Infrared photocoagulation (IRC) utilizes infrared radiation to induce protein necrosis at the base of the hemorrhoidal pedicle. The depth of tissue penetration can be controlled by altering the optical wavelength of the coagulator and the contact time.(9) Using a slotted anoscope to visualize the hemorrhoid, the procedure is performed by placing the tip of the photocoagulator at the base of the hemorrhoid and delivering a 1–1.5 second pulse of energy (Figure 18.2). Three or four applications to each hemorrhoid are recommended for optimal results. This creates a 3–4 mm2 area of coagulation which ulcerates and forms a scar within 2 weeks.(12) Most authors advocate treatment of 1–3 hemorrhoids per session. Additional treatments can be performed as indicated at 3–4 week intervals.(7, 12)

Complications associated with IRC are infrequent. As with rubber band ligation, pain can occur if the light is applied distal to the dentate line but is typically of shorter duration and lesser severity. Excessive applications can result in bleeding. Rarely, ulceration can progress to fissure formation.(12) Comparison of Techniques Numerous randomized trials have been published comparing the available nonsurgical techniques for treatment of symptomatic hemorrhoids. In a 1995 meta-analysis, MacRae et al. evaluated the results of 18 of these studies. They found that patients treated with rubber band ligation were less likely to require further therapy than those treated with sclerotherapy (p = 0.031) or IRC (p = 0.0014). However, the incidence of postprocedure pain was significantly



improved outcomes in colon and rectal surgery higher in patients who underwent rubber band ligation than the sclerotherapy (p = 0.03) and IRC (p < 0.0001) cohorts.(34) Summary Most patients with symptomatic hemorrhoids can be successfully treated with conservative management and nonsurgical techniques performed in the office setting. The authors and editors generally favor a conservative approach, beginning with a trial of supplemental fiber with sitz baths and topical preparations for symptomatic relief. If no improvement in symptoms results after 4–6 weeks, we proceed with rubber band ligation or IRC, repeating these techniques if necessary at 4–6 week intervals. Symptomatic prolapse may be an indication for rubber band ligation at the initial evaluation since conservative treatment alone is unlikely to result in complete resolution. Surgical hemorrhoidectomy (discussed in chapter 17) may be necessary in cases of failure of nonsurgical management, large grade 3 or 4 hemorrhoids or acutely thrombosed hemorrhoids. In all cases, a careful history and physical examination is necessary to rule out other causes of anorectal pathology. Management options for various classes of hemorrhoids are summarized in Figure 18.3. References   1. Johanson JF, Sonnenberg A. The prevalence of hemorrhoids and chronic constipation. An epidemiologic study. Gastroenterology 1990; 98: 380–6.   2. Johanson JF, Sonnenberg A. Temporal changes in the occurrence of hemorrhoids in the United States and England. Dis Colon Rectum 1991; 34: 585–93.   3. Thompson WHF. The nature of hemorrhoids. Br J Surg 1975; 62: 542–52.   4. Nivatvongs S. Hemorrhoids. In Gordon PH, Nivatvongs S, eds. Principles and Practice of Surgery for the Colon, Rectum, and Anus. 3rd ed. New York: Informa Healthcare USA, Inc, 2007: 143–66.   5. Margolin DA, Hammond KL. Hemorrhoids, Anal Fissure, Perianal Abscess, and Fistula in Ano. In Rakel RE, Bope ET, eds. Conn’s Current Therapy 2007. Philadelphia: Saunders/ Elsevier. 2007: 614–8.   6. Madoff RD, Fleshman JW. American Gastroenterological association technical review on the diagnosis and treatment of hemorrhoids. Gastroenterology 2004; 126: 1463–73.   7. Beck DE. Hemorrhoidal Disease. In Beck DE, Wexner SD, eds. Fundamentals of Anorectal Surgery (2nd ed). W. B. Saunders Company Ltd. 1998: 237–53.   8. Dennison AR, Whiston RJ, Rooney S, Morris DL. The management of hemorrhoids. Am J Gastroenterol 1989; 84(5): 475–81.   9. Hardy A, Chan CLH, Cohen CRG. The surgical management of haemorrhoids: a review. Dig Surg 2005; 22: 26–33. 10. Cataldo P, NealEllis C, Gregorcyk S et al. Practice parameters for the management of hemorrhoids (revised). Dis Colon Rectum 2005; 48: 189–94. 11. Salvati EP. Nonoperative management of hemorrhoids: ­evolution of the office management of hemorrhoids. Dis Colon Rectum 1999; 42(8): 989–93. 12. Larach S, Cataldo TE, Beck DE. Nonoperative treatment of hemorrhoidal disease. In: Hicks TC, Beck DE, Opelka FG, Timmcke AE. Complications of Colon and Rectal Surgery. Baltimore: Williams & Wilkins 1997: 173–80.

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13. Alonso-Coello P, Mills E, Heels-Ansdell D et al. Fiber for the treatment of hemorrhoids complications: a systematic review and meta-analysis. Am J Gastroenterol 2006; 101: 181–8. 14. Moesgaard F, Nielsen ML, Hansen JB, Knudsen JT. Highfiber diet reduces bleeding and pain in patients with haemorrhoids: a double-blind trial of Vi-Siblin. Dis Colon Rectum 1982; 25: 454–6. 15. Webster DJ, Gough DC, Craven JL. The use of bulk evacuant in patients with haemorrhoids. Br J Surg 1978; 65: 291–2. 16. Hunt PS, Korman MG. Fybogel in haemorrhoid treatment. Med J Aust 1981; 2: 256–8. 17. Broader JH, Gunn IF, Alexander-Williams J. Evaluation of a bulk-forming evacuant in the management of haemorrhoids. Br J Surg 1974; 61: 142–4. 18. Tan KY, Seow-Choen F. Fiber and colorectal diseases: separating fact from fiction. World J Gastroenterol 2007; 13(31): 4161–7. 19. Bennett WG, Cerda JJ. Benefits of dietary fiber: Myth or medicine?. Postgraduate Medicine 1996; 99(2): 153–6, 166– 8, 171–2 passim. 20. Dodi G, Bogoni F, Infantino A et al. Hot or cold in anal pain? A study of the changes in internal sphincter pressure profiles. Dis Colon Rectum 1986; 29: 248–51. 21. Johanson JF. Nonsurgical treatment of hemorrhoids. J Gastro­ intest Surg 2002; 6(3): 290–4. 22. Mann CV, Motson R, Clifton M. The immediate response to injection therapy for first-degree hemorrhoids. J R Soc Med 1988; 81: 146–8. 23. Senapati A, Nicholls RJ. A randomised trial to compare the results of injection sclerotherapy with a bulk laxative alone in the treatment of bleeding haemorrhoids. Int J Colorectal Dis 1988; 3: 124–6. 24. Blaisdell PC. Prevention of massive hemorrhage secondary to hemorrhoidectomy. Surg Gynecol Obstet 1958; 106: 485–8. 25. Barron J. Office ligation treatment of hemorrhoids. Dis Colon Rectum 1963; 6: 109–13. 26. Lee HH, Spencer RJ, Beart RW Jr. Multiple hemorrhoidal bandings in a single session. Dis Colon Rectum 1994; 37: 37–41. 27. Lau WY, Chow HP, Poon GP, Wong SH. Rubber band ligation of three primary hemorrhoids in a single session: a safe and effective procedure. Dis Colon Rectum 1982; 25: 336–9. 28. Wechter D, Luna G. An unusual complication of rubber band ligation of hemorrhoids. Dis Colon Rectum 1987; 30: 137–40. 29. O’Hara VS. Fatal clostridial infection following hemorrhoidal banding. Dis Colon Rectum 1985; 28: 291–3. 30. Russel TR, Donohue JH. Hemorrhoidal banding: a warning. Dis Colon Rectum 1985; 28: 291–3. 31. McCloud JM, Jameson JS, Scott AND. Life-threatening sepsis following treatment for haemorrhoids: a systematic review. Colerectal Disease 2006; 8: 748–55. 32. Iyer VS, Shrier I, Gordon PH. Long-term outcome of rubber band ligation for symptomatic primary and recurrent internal hemorrhoids. Dis Colon Rectum 2004; 47: 1364–70. 33. Savioz D, Roche B, Glauser T et al. Rubber band ligation of hemorrhoids: relapse as a function of time. Int J Colorect Dis 1998; 13: 154–6. 34. MacRae HM, McLeod RS. Comparison of hemorrhoidal treatment modalities: a meta-analysis. Dis Colon Rectum 1995; 38: 687–94.

19

Surgery and nonoperative therapy of perirectal abscesses and anal fistulas Brian R Kann and Charles B Whitlow

Challenging Case A 40-year-old male with poorly controlled HIV infection develops severe anorectal pain with associated fever. On physical examination, an obvious perirectal abscess is present 2 cm from the anal verge, just to the right of the posterior midline. Appropriate incision and drainage is performed and the patient is treated with a short course of oral antibiotics, with resolution of the acute event. Several months later, he presents with purulent discharge from the drainage site as well as a second area in the posterior midline, 4 cm from the anal verge. Exam under anesthesia demonstrates a single primary fistula opening anal canal, in the posterior midline 3 cm proximal to the dentate line, which communicate with both secondary openings. Draining setons are placed, and biopsies from the fistula tracts show no evidence of Crohn’s disease or malignancy. Six weeks later, he presents in septic shock due to worsening perineal infection requiring a diverting colostomy.

abscesses and fistula-in ano. Abscesses are classified according to their location in relation to the potential anorectal spaces (perianal, ischiorectal, intersphincteric, and supralevator) (Figure 19.1). Pus can spread circumferentially through the intersphincteric, supralevator, and ischiorectal spaces. Circumferential spread though contralateral ischiorectal spaces can occur via the deep postanal space, resulting in formation of a horseshoe abscess. Anal fistulas are classified according to their relationship to the anal sphincter complex (intersphincteric, transsphincteric, suprasphincteric, and extrasphincteric), as described by Parks (Figure 19.2).(2) The diagnosis of most anorectal abscesses is typically straightforward. Patients usually complain of pain and swelling at the site, and fever is not uncommon. Examination will demonstrate (A)

Case Management The patient is initially managed with additional drainage and a diverting colostomy. After recovering, he is initiated on highly active anti-retroviral therapy (HAART) with an excellent response in his CD4 count and his viral load become undetectable. After an MRI of the pelvis demonstrates no further infection in the pelvis, an anal fistula plug is placed to attempt to close the fistula; within a week, the plug has dislodged. An attempt at closing the fistula with an endorectal advancement flap several weeks later also fails. Further biopsies again show no evidence of Crohn’s disease or malignancy, and a second attempt at endorectal advancement flap closure performed 12 weeks later also fails. The patient has decided not to pursue further surgery for the fistula and remains diverted via a colostomy with draining setons in place. INTRODUCTION Anorectal abscesses and fistulae-in-ano can be incredibly frustrating, both for the patient and the managing physician. Meaningful outcomes data with large, prospective randomized trials regarding the management of these entities is extremely limited. This chapter addresses the surgical as well as nonoperative management of these common problems, focusing on means of improving clinical outcomes. Etiology and Diagnosis The vast majority of anorectal abscess are cryptoglandular, resulting from obstruction of the anal ducts and glands, resulting in stasis, infection, and abscess formation.(1) Less common causes include inflammatory bowel disease, tuberculous infection, trauma, malignancy, and radiation. Most anal fistulas are the long-term manifestations of anorectal abscesses; persistent epithelium in the tract between the infected duct and external opening created by surgical or spontaneous drainage leads to fistula formation. An intricate understanding of anorectal anatomy is essential to the diagnosis and subsequent management of anorectal

(B)

Figure 19.1  Anorectal spaces. (A) Coronal section. (B) Sagital section.



improved outcomes in colon and rectal surgery (A)

(B)

(C)

(D)

Figure 19.2  Classification of fistula-in-ano. (A) Inttersphincteric. (B) Trans-sphincteric. (C) Suprasphincteric. (D) Extrasphincteric.

Figure 19.3  Goodsall’s rule.

erythema, swelling, and possibly fluctuance at the site of the abscess. Severe rectal pain associated with defecation and a paucity of physical findings should raise one’s suspicion for an intersphincteric abscess. Confirmation generally requires exam under anesthesia with palpation of a fluctuance within the wall of the anal canal or needle aspiration of purulent material from the intersphincteric space. Severe gluteal pain in the absence of significant findings on exam may be suggestive of a supralevator abscess. Supralevator abscesses may develop as an upward extension of an ischiorectal or intersphincteric abscess, or they may develop as a downward extension of a pelvic abscess. Exam under anesthesia and/or computed tomography (CT) imaging is generally required for diagnosis. The initial diagnosis of fistula-in-ano is also fairly straightforward, though classifying the type of fistula and defining the anatomy can be much more difficult. The patient will usually give an antecedent history of an abscess that has either drained spontaneously or required surgical drainage. Examination may demonstrate an external (secondary) opening seen as an elevation of granulation tissue with a discharge of pus, sometimes



elicited on rectal examination. Identification of the internal (primary) opening by anoscopy is usually difficult, and exam under anesthesia is often required. Goodsall’s rule Figure 19.3 is useful, though its reliability has been questioned, especially when dealing with anterior fistulas; Cirocco and Reilly demonstrated that in patients with anterior secondary fistula openings, 71% tracked to an anterior midline primary opening, and in women with anterior secondary fistula openings, only 31% tracked radially inward to the nearest crypt.(3) Because of the difficulties in defining fistula anatomy, preoperative imaging has, in many cases, become common practice. Available imaging modalities include CT scan, fistulography, endoanal ultrasonography, and magnetic resonance imaging (MRI). CT scanning is really useful only in defining abscesses related to fistulas.(4) CT attenuation of the anal sphincter and pelvic floor is similar to that of the fistula itself; therefore, the fistula itself is difficult to see unless it is filled with air or contrast.(5) Fistulography as an initial diagnostic measure has several limitations.(6) Smaller extensions from the primary tract may not fill with contrast if they are plugged with debris. Also, there is no visualization of the sphincter complex or levator ani in relation to the location of the fistula. Besides creating the potential for spread of sepsis, accuracy rates are poor, ranging from 16–48%, with a false positive rate of 12%. (6, 7) The place of fistulography may be in evaluating recurrent fistulas, patients with Crohn’s disease, and patients who have had multiple prior anorectal procedures with altered anatomy (7), though with more readily available endoanal ultrasound and anal MRI, its use will likely continue to decline. The use of anorectal endosonography in the diagnosis of anorectal fistulas has gained considerable attention in recent years. It helps to identify the anatomy of the fistula in relation to the sphincter and may also be used to aid in delineation of complex fistulae and occult suppuration.(8, 9) The technique is relatively simple, inexpensive, readily performed in an office ­setting, and well tolerated by the patient. Lengyel et al. reported that endorectal ultrasound correctly predicted surgical findings in 124 of 151 (82%) patients with anal fistulas.(10) Some concerns have arisen regarding the sensitivity of endoanal ultrasound. Seow-Choen prospectively demonstrated poor sensitivity in detecting primary extrasphincteric and suprasphincteric tracts and secondary supralevator or infralevator tracts.(11) The use of hydrogen peroxide injected into the fistula tract can improve the sensitivity of endorectal ultrasound for evaluation of anorectal fistulas. Cheong demonstrated a 24% increase in locating fistula tracts and a 28% increase in the demonstration

surgery and nonoperative therapy of perirectal abscesses and anal fistulas of primary fistula openings with the addition of hydrogen peroxide.(12) Other studies have confirmed the increased sensitivity of hydrogen peroxide-enhanced endorectal ultrasound, with some studies reporting concordance rates as high as 95%.(13–16) The use of three-dimensional endoluminal ultrasound (3D-EUS) has greatly increased the sensitivity of identifying and defining fistula anatomy.(17) A study by Giordano et al. comparing 3D-EUS to conventional (two-dimensional) EUS found that 3D-EUS was significantly more accurate in assessing the fistula tract and site of primary opening.(18) As with conventional EUS, the sensitivity of 3D-EUS is increased even further with the injection of hydrogen peroxide into the fistula tract.(19) In a comparison with endoanal MRI, hydrogen peroxide-enhanced 3D-EUS was found to be superior for detection of secondary fistula tracts, fluid collections, and determining the location of primary ­fistula openings.(20, 21) The authors suggested hydrogen peroxide enhanced 3D-EUS as a less expensive, yet equally sensitive, alternative to endoanal MRI. Anorectal MRI has emerged as a valuable tool in assessing ­complex anorectal fistulas. The best spatial resolution is achieved by using a dedicated endoanal coil, combined with a surface coil to increase the field of view.(5) The precise location of the ­primary opening can be identified and information regarding the ­relation of the fistula to the sphincter, sphincter integrity, secondary tracts, and supralevator extension can be obtained. However, the disadvantages include expense and expert interpretation which may not be readily available in all centers. In a study of 104 patients comparing clinical examination, endoanal ultrasonography, and MRI, accurate classification of fistula anatomy by MRI was 97%, compared with 81% by ultrasound, and 61% by clinical examination.(22) Barker reported concordance rates for MRI diagnosis of 86% for primary fistula tracts, 91% for secondary extensions, 97% for the presence of horseshoe abscess, and 80% for the position of the primary opening.(23) In this study, failure of healing in 9% of patients was due to pathology missed at the time of surgery that was seen on preoperative MRI. Beckingham demonstrated a sensitivity and specificity of MRI for detecting anorectal fistulas of 100% and 97%, respectively.(24) In this study, MRI missed only one fistula with a complex transsphincteric tract. Phased array (PA) MRI can provide even more precise information regarding fistula anatomy when compared with body coil MRI. Beets-Tan et al. (25) reported a study in which PA-MRI was performed in 56 patients who then underwent fistula surgery. The surgeons were initially blinded to the MRI findings until they felt that they had determined the course of the fistula intraoperatively, at which point the PA-MRI findings were revealed. In 12 (21%) patients, PA-MRI imaging added additional information regarding fistula tract anatomy not found by the surgeon on initial exploration. The highest benefit was in patients with Crohn’s disease (40%) and recurrent fistula-in-ano (24%). An emerging technique in the imaging of anal fistulas is highresolution MR fistulography, in which images are obtained before and after the intravenous injection of gadolinium, following which images are subtracted that show only enhancing tissues, i.e., the wall of the fistula tract.(5) Schaefer et al. (26) performed a study of 36 patients who underwent preoperative MR fistulography, then underwent fistula surgery with the surgeon blinded to the MRI results. When operative findings were compared with

MRI findings, 89% agreement was seen. In all four patients in which there was discordance between operative findings and MR findings, multiple complex fistulas and abscesses in a setting of Crohn’s disease were present. In terms of improving the outcomes of patients who will require surgery for anal fistulas, it is well established that clear identification of the anatomy is essential. Regardless of the modality used, it seems prudent, with the technology available today, that preoperative imaging of anything more than a simple intersphincteric or low transsphincteric fistula be performed to minimize the potentially significant morbidity associated with anal fistula surgery. Surgical Management Incision and Drainage The mainstay of treatment of anorectal abscesses is incision and drainage. There is no role for treatment with antibiotics alone without drainage. Most perianal and superficial ischiorectal abscesses can be drained in the office or emergency room setting after infiltration of local anesthetic. A cruciate incision should be made over the area of fluctuance, taking care to stay as close to the anal verge as practical in the event that a fistula develops later. The skin edges should be excised to allow for adequate drainage without the need for continued packing. Alternatively, catheter drainage may be employed, as described by Beck (27), making a small incision over the area of fluctuance and placing a small (10–16 French) mushroom-tipped catheter in the abscess cavity. The catheter is typically removed when the drainage has decreased and the abscess cavity has closed down around the drain (usually 5–10 days later). Care should be taken not to cut the catheter too short to prevent it from retracting completely into the abscess cavity. Larger ischiorectal abscesses may require sedation, regional anesthesia, or general anesthesia for sufficient drainage. Adequate patient comfort is essential, as attempts to drain an abscess in an inadequately anesthetized patient lead to unnecessary patient distress, and will almost assuredly result in incomplete exploration and drainage of the abscess. Intersphincteric abscesses should be drained via division of the internal sphincter along the length of the abscess, followed by marsupialization of the wound. Drainage of a supralevator abscess depends on the etiology of the abscess. If it arises from an intersphincteric abscess, drainage should be performed transrectally by division of the internal sphincter, as external drainage would result in the development of a suprasphincteric fistula. If the origin is an ischiorectal abscess, drainage should be performed externally, through the perianal skin. If the abscess originates from an infectious process in the pelvis, drainage may be performed through the rectum, ischiorectal fossa, or abdominal wall by percutaneous drainage, ensuring that the primary infectious process is addressed. Management of horseshoe abscesses and fistulas can be especially problematic. Adequate treatment of horseshoe abscesses typically requires drainage of the deep postanal space via a midline incision between the coccyx and anus, spreading the fibers of the superficial external sphincter. An open internal sphincterotomy is performed in the posterior midline and counter-incisions are made over each ischiorectal fossa to allow for drainage of the anterolateral extensions of the abscess, as initially described by Hanley.(28) Rosen et al.



improved outcomes in colon and rectal surgery (29) reported that patients with horseshoe abscess/fistula required a median of 4 (range 1–9) operations; at a mean follow-up of 49.3 months, 60.7% of patients had either healed perineal disease or were asymptomatic with controlled disease. Those who underwent posterior midline sphincterotomy as part of their surgical ­management were more likely to be asymptomatic postoperatively (p = 0.047). There is little role for antibiotics after adequate surgical drainage of an anorectal abscess. Those for whom treatment with antibiotics should be considered postdrainage include patients with valvular heart disease or prosthetic valves, extensive soft tissue cellulitis or induration, prosthetic devices, joint replacements, diabetes, and those who are immunocompromised or immunosuppressed.(30) Fistulotomy The surgical management of anal fistulas rests on three main principles: eliminating the fistula, preventing recurrence, and preserving sphincter function. Identification of the primary opening and division of as little sphincter muscle as possible are essential to achieving these outcomes. Methods used intraoperatively to identify the primary opening include passage of a probe, injection of a dilute solution (hydrogen peroxide, methylene blue, or milk) via the secondary opening, tracing granulation tissue present in the fistula tract, and identifying puckering of the anal crypt when traction is placed on the tract.(30) Preoperative determination of fistula anatomy may also be determined using imaging modalities, as described earlier. Most simple intersphincteric fistulas and low transsphincteric fistulas can be managed by simple “lay-open” fistulotomy with curetting of the tract and marsupialization of the wound edges. Higher transsphincteric, extrasphincteric, and suprasphincteric fistulas are generally not appropriate for simple fistulotomy, as the end result would be division of a large portion of anal sphincter, resulting in altered fecal continence. Primary fistulotomy at the time of initial abscess drainage is controversial. Some argue that in the acute phase it is easier to trace the supporative process and identify the fistula tract. This eliminates the source of infection and may decrease the rate of recurrence; in turn, this may potentially eliminate the need for further surgery and its accompanying morbidity. Fucini reported no recurrences in 51 of 58 primary fistulotomies where an internal opening could be identified and no “major” incontinence, though impaired control of flatus was seen in 17%.(31) Tang et al. showed in a prospective randomized trial of drainage alone versus drainage and fistulotomy for acute perianal abscesses that there was no statistical significance in terms of recurrence.(32) The concept of primary fistulectomy at the time of abscess drainage also is controversial. Schouten and van Vroonhoven prospectively demonstrated that fistulectomy was associated with clinically significant disturbances in anal function in 39.4% of patients treated with primary fistulectomy, compared with 21.4% of patients treated with secondary fistulectomy.(33) Seton Placement In the management of higher transsphincteric fistulas, preserving the sphincter becomes even more essential. In these instances, placement of a seton may be of benefit. A seton may be used in a cutting fashion by dividing the skin and lower portion of the anal sphincter and gradually tightening the seton over regular intervals. A seton



may also be used to allow for prolonged drainage, without gradual tightening. Indications for the use of a seton include identification and promotion of fibrosis around a complex fistula that encircles most of the sphincter, marking the site of a transsphincteric fistula in cases of severe anorectal sepsis where the normal anatomic landmarks have been distorted, in anterior high transsphincteric fistulas in women, in high transsphincteric fistulas in HIV-positive patients with poor wound healing, to promote long-term drainage in patients with Crohn’s disease, and when there is suspicion that a primary fistulotomy will result in incontinence.(34) Treatment of suprasphincteric fistulas can become extremely complex, as laying-open of the entire fistula tract would inevitably lead to incontinence. The use of a cutting seton in combination with division of the internal sphincter and the superficial ­portion of the external sphincter to the level of the secondary opening has been reported with successful healing in 63% of patients. (35) Kennedy and Zegarra (36) described a modification of this approach using internal sphincterotomy along with opening of the tracts outside the external sphincter without division of any portion of the external sphincter, which is encircled by a seton to promote fibrosis and drainage; they reported complete healing in 66% of posterior fistulas and 88% of anterior fistulas. Extrasphincteric Fistulas Surgical management of an extrasphincteric fistula depends on its etiology. If it arises as a consequence of an anal fistula, the lower portion of the internal sphincter is divided and the rectal opening is closed with a nonabsorbable suture, with or without temporary diversion. If the fistula is the result of trauma, drainage must be performed along with closure of the rectal opening and proximal diversion. If the fistula is the result of downward tracking of a ­pelvic abscess, treatment of the primary process is essential. It is prudent to have a low threshold for temporary proximal diversion, as progressive perineal sepsis can lead to ­devastating consequences. Advancement Flap In patients for whom primary fistulotomy is not appropriate, the use of an anorectal or endorectal advancement flap is a useful alternative. These patients include women with anterior fistulas, patients with inflammatory bowel disease, patients with high transsphincteric and suprasphincteric fistulas, and those with multiple previous fistula operations.(37, 38) A full-thickness flap incorporating a portion of the internal sphincter should be advanced at least a centimeter beyond the primary fistula opening and sutured into place with absorbable sutures without tension (Figure 19.4). Schouten et al. (39) reported successful fistula closure in 33 of 44 (75%) patients with anal fistulas treated with endorectal advancement flaps. In patients with no or only one attempt at repair, the healing rate was 87%, compared with 50% in those with two or more prior attempts. In a series of 107 patients with anal fistulas arising from a number of etiologies who underwent endorectal advancement flap, Kodner et al. reported successful healing in 93% of patients, though nine patients initially failed and required a second procedure.(40) In a series of 29 patients with cryptoglandular and obstetric-related fistulas, Dixon et al. (41) reported 69% (20 of 29) fistula resolution with endorectal

surgery and nonoperative therapy of perirectal abscesses and anal fistulas (A)

(B)

(C)

(D)

Figure 19.4  Anorectal advancement flap. (A) Transphincteric fistula in ano. (B) Enlargement of external opening. (C) Flap of mucosa and muscle created. (D) Flap advanced and closed after excision of distal edge containing fistula.

advancement flaps at 3 months follow-up. Additionally, of the nine patients who failed, fistula resolution was seen in 4 (44%) after a second procedure, for a total success rate of 83%. Healing rates of 63.3% to 81% have also been reported for the use of endorectal advancement flaps for the management of complex anal fistulas.(42, 43) Endoanal advancement flaps have also been utilized with varying degrees of success in the management of anal fistulas. Chew and Adams (44) reported successful fistula closure using an anal sphincter advancement flap, as opposed to an endorectal advancement flap, in six patients with a mean, follow-up of 8.1 months. Amin et al. (45) reported overall 83% healing in patients undergoing V-Y advancement flaps for fistula closure, although two patients required repeat surgery. Continence was preserved in all patients. Zimmerman et al. (46) reported only 46% healing with anocutaneous advancement flaps, with success inversely correlated with the number of previous attempts at fistula repair. Fibrin Glue The injection of fibrin glue into the tract(s) of a fistula-in-ano is a simple method used to impart closure. Advantages include easy application, preservation of sphincter integrity, minimal patient discomfort, and the opportunity to repeat applications when the initial treatment fails. Earlier trials utilized injection of autologous fibrin adhesive prepared from the patient’s own blood. Cintron et al. reported successful healing in 22 of 26 patients treated with autologous fibrin at a mean follow-up of 3.5 months.(47) The same group reported less success (17 of 25 patients) with a commercially produced sealant.(48) Less favorable results were seen at a mean follow-up of 1 year, with 54% healing in patients treated with autologous fibrin sealant and 64% healing in patients treated with commercially produced fibrin sealant.(49) Most failures occurred within the first 3 months, though failures were seen as late as 11 months postoperatively. Additional studies initially failed to show consistent results. A small randomized, controlled trial comparing fibrin glue to conventional treatment (fistulotomy or seton placement with or without later advancement flap) failed to show an advantage to fibrin glue for simple fistulas, though more complex fistulas healed with fibrin glue (69% vs. 13%, p = 0.003).(50) Sentovich (51) reported complete healing in 17 of 20 (85%) patients treated with fibrin glue at a mean follow-up of 10 months, though he later reported a less favorable healing rate of 69% in a larger series of 48 patients at

a median follow-up of 22 months, including retreatment of initial failures. Even less favorable healing rates of 14–33% have been reported in other series.(52–54) More recently, improved outcomes in larger series have been published. In prospective study of 36 patients, Maralcan et al. reported a complete healing rate of 83.3% at a mean follow-up of 54 weeks.(55) Adams et al. reported healing in 66% of patients treated with fibrin glue with a mean follow-up of 3 months, with 94% of these patients asymptomatic at 6 month follow-up.(56) Fibrin glue has also been evaluated as an adjunct to advancement flap closure of anal fistulas. Ellis and Clark (57) performed a prospective, randomized, controlled study comparing flap repair alone (n = 30) to flap repair with fistula tract obliteration using fibrin glue (n = 28). At a median follow-up of 22 months, the recurrence rate for fistulas treated with advancement flaps alone was 20%, compared with 46.4% for fistulas treated with advancement flaps with fibrin glue (p < 0.05). The authors postulated that obliteration of the fistula tract with fibrin glue may prevent effective drainage from beneath the advancement flap, leading to a higher failure rate. Van Koperen et al. (58) also showed that outcomes were worse when obliteration of the fistula tract with fibrin glue was combined with endorectal advancement flap. As a more economical alternative to fibrin glue, Jain et al. (59) proposed using cyanoacrylate glue as a means toward achieving fistula closure. They reported complete fistula closure at 6 month follow-up in 17 of 20 patients after primary injection, and complete healing in two of the three initial failures after a second injection, for a composite 95% healing rate. Proposed advantages of cyanoacrylate as opposed to fibrin include a cost reduction of approximately two-thirds, commercial preparation in premade collapsible tubes that do not require premixing, and a longer shelf-life. Barilleri et al. (60) reported similar results with complete healing at 18 month follow-up in 15 of 21 patients. Four additional patients healed with repeat applications, for a composite healing rate of 90.2%. Modifications of the fibrin adhesive technique have been attempted, also with little improvement. The addition of cefoxitin to the fibrin adhesive failed to improve healing rates in a study performed by Singer et al. nor did closure of the primary opening. (61) In fact, healing rates with both modifications were lower than their earlier published result with fibrin adhesive alone.(47, 48) Gustafsson and Graf (62) looked at the addition of a gentamycinenriched collagen adhesive beneath rectal advancement flaps and found no difference in healing rates. In a prospective study with



improved outcomes in colon and rectal surgery more favorable outcomes, Zmora et al. were able to achieve a 53% healing rate in a prospective study of 60 patients with complex cryptoglandular fistulas treated with fibrin glue with intraadhesive ceftazidime.(63) The wide variety of successful healing in studies looking at the use of fibrin glue in the treatment of fistula-in-ano is multifactorial. Differences in the trials include patient selection, use of autologous versus commercially prepared fibrin adhesive, etiology of the fistula (cryptoglandular vs. Crohn’s disease vs. other causes), complexity of the fistula, and length of follow-up. While the application of the tissue adhesive seems fairly straightforward, there are also assuredly subtle differences in the application techniques of different surgeons. The heterogeneity of the published trials makes direct comparisons very difficult. While success rates vary over a wide range, the advantages of attempting to treat high transsphincteric fistulas with fibrin glue in terms of simplicity of technique, negligible complication rate, and ease of reapplication for failed treatments make it an attractive option, at least initially. Most ­surgeons seem willing to accept a higher than expected failure rate in exchange for a low complication rate, understanding that treatment failures will need to be addressed in some other manner. Anal Fistula Plug The topic that has perhaps generated the most discussion in recent years is the use of the Surgisis® Anal Fistula Plug™ (AFP) (Cook Surgical, Inc., Bloomington, IN). The AFP is a cone shaped bioprosthetic fashioned from Surgisis®, a bioabsorbable xenograft made of lyophilized porcine intestinal submucosal. Surgisis® has been used extensively in abdominal and inguinal hernia repairs. (64–66) It is relatively resistant to infection, produces no foreign body or giant cell reaction, and becomes repopulated with host cell tissue within 3–6 months, providing mechanical integrity while acting as a scaffold to guide tissue incorporation. The AFP is inserted into the fistula tract and secured at the level of the primary opening. The principal effect is to close the primary fistula opening, though incorporation of the AFP into the tract itself can theoretically contribute to fistula closure. The advantages of this technique include negligible risk of incontinence postoperatively, relative simplicity in placement of the AFP, less postoperative patient discomfort, and the ability to repeat the procedure in cases of failure without major consequences. Johnson et al. (67) initially reported a small, nonrandomized, prospective cohort study comparing the efficacy of fibrin glue versus AFP in the treatment of high transsphincteric fistulas. At a mean follow-up of 14 weeks, in the fibrin glue cohort, healing was seen in 40% (4 of 10), whereas in the AFP cohort, 13 of 15 (87%) had healed (p < 0.05). The main advantage of the plug technique compared with fibrin glue was felt to be the ability to securely close the primary opening, which is felt to be a critical step in the successful treatment of anal fistulas. The drawback of fibrin glue is its liquid nature, and its tendency to run out of the fistula tract, even when both primary and secondary openings are sutured closed. Champagne et al. (68) went on to report an overall healing rate of 83% for cryptoglandular fistulas treated with an AFP in a series of 46 patients followed for a mean of 12 months (range 6–24 months). The same authors reported a similar 80% success rate for treatment of Crohn’s-related fistulas with an AFP in 20



patients at a median follow-up of 10 months.(69) Ellis (70) also reported success in a small group patients with transsphincteric (n = 13) and rectovaginal fistulas (n = 5) with 88% complete fistula closure at a median follow-up of 6 months. Other studies report inconsistent results. Van Koperen et al. reported a series of 17 patients treated with an AFP with only 41% success.(71) Patients with cryptoglandular disease and no history of previous fistula surgery fared better than those with a history of previous surgical intervention. In the small subsets of patients with Crohn’s disease (n = 1) and HIV infection (n = 2), 100% healing was seen, as opposed to 29% complete healing (4 of 14) in patients with cryptoglandular disease. Schwandner et al. (72) reported an overall success rate of 61%. The subset of patients with Crohn’s fistulas related to Crohn’s disease showed higher closure rates than those with fistulas of cryptoglandular origin (85.7% vs. 45.5%). More recent studies have varied widely in their results, reporting healing rates ranging from 24% to 71.4%.(73–76) One of the largest prospective studies was reported by Ky et al. (77) The authors studied 45 patients with simple (n = 24) and complex (n = 20) anorectal fistulas treated with AFP’s. An early healing rate of 84% at 3 to 8 weeks postoperatively progressively declined to 54.6% at a mean follow-up of 6.5 months. Healing rates were significantly higher in patients with simple rather than complex fistulas (70.8% vs. 35%, p < 0.02) and in patients without Crohn’s disease compared to those with Crohn’s disease (66.7% vs. 26.6%, p < 0.02). Despite a number of publications attesting to the safety and efficacy of the AFP, uniformity of opinion was lacking because of contradictory reports in the literature as well as a lack of Level I evidence showing any clear benefit. Because of this, a consensus conference involving 15 surgeons with extensive experience with the AFP was held in May 2007 to make formal recommendations regarding inclusion/exclusion criteria, pre-, intra-, and postoperative management, and definition of outcome failure.(78) Some technical notes regarding placement of the plug bear mentioning. It is essential that all sources of perineal sepsis are resolved prior to placement. The use of pre- or postoperative antibiotics and preoperative bowel cleansing has not been studied in a prospective, randomized fashion. In most of the studies described herein, a preoperative dose of intravenous antibiotic was administered, and varying regimens of postoperative antibiotics were utilized. The consensus panel did not make specific recommendations regarding preoperative bowel preparation; a single dose of preoperative systemic antibiotics was recommended without postoperative ­continuation.(78) Thorough cleansing of the fistula tract with hydrogen peroxide is generally recommended. Mechanical cleansing via curetting, debridement, or brushing is not recommended due to disruption and enlargement of the tract. The technique of fixation of the plug to the primary opening recommended by the manufacturer involves a figure of eight absorbable suture through the mucosa, submucosa, and internal anal sphincter that inverts the proximal end of the anal fistula plug beneath the mucosa, anchoring it to the tract while closing the primary opening over the plug (Figure 19.5). Earlier studies as well as the manufacturer’s recommendations suggested fixation of the distal end of the plug to the secondary fistula opening as an essential step in plug placement. Most surgeons have abandoned this step, now simply trimming the

surgery and nonoperative therapy of perirectal abscesses and anal fistulas (A)

(C)

(B)

(D)

Figure 19.5  AFP product insert.

distal end of the plug flush with the skin without fixation, as it has been suggested that external fixation creates tension on the primary fixation site with patient movement, predisposing to plug extrusion. The consensus panel also recommended not fixing the distal end of the plug to the secondary opening. The majority of AFP failures are due to plug extrusion, untreated or persistent source(s) of perineal sepsis, or postoperative infectious complications. Ligation of Intersphincteric Fistula Tract An interesting new concept in the surgical management of fistulain-ano has recently been described—ligation of the intersphincteric fistula tract (LIFT).(79) In this method, intersphincteric dissection is performed and the fistula tract is identified and ligated in this plane, leaving the sphincter muscles themselves undisturbed. The authors reported complete fistula healing in 17 of 18 patients (94.4%), with a mean healing time of 4 weeks and no disturbances in anal function. While this study was small and observational in

nature, the simplicity of the technique and its negligible impact on sphincter function certainly warrant further investigation. Additional Issues Recurrence Recurrence after incision and drainage of an anorectal abscess and anal fistula, should be considered as two entities. True recurrence after abscess drainage is typically due to inadequate drainage or inadequate postoperative care. What is more commonly seen is actually “persistent” disease as the abscess cavity matures into a fistula. Vasilevsky and Gordon reported recurrent or persistent disease in 48% of patients (11% recurrent abscess, 37% fistula-in-ano) after undergoing incision and drainage of anorectal abscesses.(80) Results similar to these have been reported by several authors, which argue against primary fistulotomy at the time of initial abscess drainage, as unnecessary fistulotomy



improved outcomes in colon and rectal surgery with potential altered fecal continence can be avoided in approximately 50% of patients. Common reasons for recurrent anorectal infection include missed infection at the time of initial drainage in adjacent anatomic planes, presence of an undiagnosed fistula at the time of initial abscess drainage, and failure to completely drain the abscess initially.(81) In a series of 500 patients undergoing anorectal abscess drainage, Onaca et al. reported that 7.6% required reoperation within 10 days of the initial procedure.(82) Factors leading to reoperation included incomplete drainage (23%), missed loculations (15%), missed abscesses (4%), and postoperative bleeding (3%). Horseshoe abscesses were associated with a 50% rate of operative failure.(82) Similarly, recurrent fistula-in-ano is often seen after surgical management due to a failure to identify a primary opening or recognize secondary extensions of a fistula. Secondary tracts accounted for early recurrences in 20% of patients studied by Sangwan. (83) Sygut et al. reported a 14.3% recurrence rate after surgical management of fistula-in-ano, though recurrence was much more common after surgery for recurrent fistulas (51.7%) than primary fistulas (5.4%).(84) In this same study, recurrence was also more common in multi-tract fistulas (32.4%) than single-tract fistulas (12%). Recurrence rates after fistulotomy range from 0–18% (Table 19.1). Premature closure of the fistulotomy wound is a clear risk factor for recurrence; this can be prevented by creating an external wound larger than the anal wound, ensuring that the internal wound will heal first. Meticulous postoperative care is essential to avoid bridging and pocketing of the wound.(99, 100) Epithelialization of the tract may also occur, leading to persistent fistula-in-ano.(101) Garcia-Aguilar et al. performed a retrospective study that reviewed the records of 624 patients undergoing surgery for fistula-in-ano in an effort to determine factors associated with recurrence and incontinence.(98) Recurrence was seen in 8% of patients; univariate and multivariate regression analysis showed that factors associated with recurrence included complex fistula type, horseshoe extension, lack of identification, or lateral location of the primary fistula opening, previous fistula surgery, and the experience of the surgeon. Recurrence rates after staged fistula repairs using setons range from 0% to 9% (34, 98, 102–109), though the largest study with a 0% recurrence rate had only 21 patients.(106) Interestingly, the success rate of fistula surgery has been shown to decrease with time. In a study by van der Hagen et al. (110), recurrence rates following fistulotomy at 12, 48, and 72 months were 7%, 26%, and 39%, respectively, with 33% of recurrences occurring in the first 24 months after surgery. A similar trend was seen following the use of endorectal advancement flaps, with recurrence rates of 22%, 63%, and 63% seen at 12, 48, and 72 months respectively; 69% of recurrences were seen within the first 24 months. Van Koperen et al. (111) demonstrated recurrence rates at 3-year follow-up of 7% for fistulotomy, and 21% for rectal advancement flaps. Mizrahi et al. (112) described features associated with fistula recurrence in a series of 106 consecutive endorectal advancement flaps performed on 94 patients. Recurrence was seen in 40.4% of patients at a mean follow-up of 40.3 months. Recurrence was not associated with prior attempt at repair, type of fistula, origin of fistula, preoperative steroid use, postoperative bowel confinement, postoperative antibiotic use, or creation of a diverting



stoma. Recurrence was significantly more common in patients with Crohn’s disease (p < 0.04). Sonada et al. reported a similar recurrence rate of 36.4% of patients undergoing endorectal advancement flap for repair of anorectal and rectovaginal fistulas in a series of 105 patients.(42) Factors that negatively impacted the healing rate were Crohn’s disease (p = 0.027) and a diagnosis of rectovaginal as opposed to anorectal fistula (0.002). Patients on oral corticosteroid therapy showed a trend towards recurrence, though this did not reach statistical significance; no patients taking more than 20 mg/day of prednisone achieved long-term healing. Cigarette smoking has been shown to negatively impact ­fistula closure after endorectal advancement flap. In a series of 105 patients undergoing endorectal advancement flap for anal ­fistulas not related to Crohn’s disease, Zimmerman et al. reported successful fistula closure in 69%.(113) In patients who did not smoke cigarettes, healing was seen in 79%, compared with 60% in smokers (p < 0.037). Furthermore, a significant correlation was seen between the healing rate and the number of cigarettes smoked per day (p = 0.003). Using intraoperative laser Doppler flowmetry, it has also been shown that median bloodflow before endorectal advancement flap in nonsmokers was 35 volts, ­compared with 18 volts in smokers (p = 0.018).(114) Thus, it seems likely that impaired wound healing due to diminished perfusion may be a contributing factor in the failure of endorectal advancement flaps in smokers. Efforts to encourage smoking cessation preoperatively should be undertaken to minimize postoperative morbidity. Incontinence Fecal incontinence after abscess drainage should be relatively infrequent and is typically the result of iatrogenic damage to the sphincter mechanism. Compromised continence may also be seen postoperatively if the external sphincter is damaged during ­incision and drainage in patient with borderline preoperative ­continence. Inadvertent injury to the puborectalis during drainage of supralevator abscesses has also been reported.(115) Prolonged packing may prevent granulation tissue formation and promote generation of excessive scar tissue.(116) Primary fistulectomy at the time of incision and drainage has also been reported to cause disturbed fecal continence.(33) On the other hand, incontinence rates following surgical management of fistula-in-ano vary widely. The incidence of incontinence is related to the complexity of the fistula and the level of the primary fistula opening, with complex fistulas and those with posterior and high openings and fistula extensions at a higher risk.(97) Posterior fistulotomy has a higher incidence of recurrence due to a more circuitous route of the tract, resulting in division of more sphincter muscle. Drainage of extensions may damage small nerves and create scar tissue around the anorectum.(97) The incidence of incontinence is also related to the patient’s preoperative sphincter function and their would-healing ability. The incidence of impaired continence also increases with age and is more common in females.(98) Fecal seepage without true sphincter compromise can occur if the edges of a fistulotomy wound do not heal completely, preventing complete closure of the anus and allowing for leakage of fecal contents, and flatus.

surgery and nonoperative therapy of perirectal abscesses and anal fistulas Table 19.1  Results of fistula surgery. Author

Year

No. Patients

Recurrence %

Incontinence %

Bennett (85)

1962



108



2.0



Hill (86)

1967



626



1.0



4.0

Lilius (87)

1968



150



5.5



13.5

Mazier (88)

1971



1000



3.9



Ani & Solanke (89)

1976



82



17.0



1.0

Marks & Ritchie (90)

1977



793



–



3, 17, 25*

Ewerth et al. (91)

1978



143



2.8



3.5

Adams & Kovalcik (92)

1981



133



3.8



0.8

Kuijpers (93)

1982



51



4.0



10.0

Sainio & Husa (94)

1985



199



11.0



Vasilevsky & Gordon (95)

1985



160



6.3



0.7, 2.0, 3.3**

Fucini (96)

1991



99



3.0



0, 0.2, 0.5***

Van Tets (97)

1994



19



–



Sangwan (83)

1994



461



6.5



2.8

Garcia-Aguilar et al. (98)

1996



293



7.0



42.0

36.0

0.001

34.0

33.0

* 3% solid stool, 17% liquid stool, 25% flatus. ** 0.7% solid stool, 2.0% liquid stool, 3.3% flatus. *** 0 solid stool, 0.2% liquid stool, 0.5% flatus.

In a large review of 844 patients undergoing surgery for anal fistulas, Rosa et al. (117) demonstrated a 6.9% incidence of altered postoperative sphincter function. Incontinence to flatus was seen in 4.0%, liquid stool in 2.6%, and solid fecal material in 0.3%. The majority of patients in this series underwent fistulotomy or a combined fistulotomy-fistulectomy method. Sygut et al. reported postoperative gas and/or stool incontinence in 10.7% of patients undergoing surgical management of anal fistulas, mainly in the form of fistulotomy and cutting setons.(84) In this study, rates of incontinence were higher following surgery for recurrent vs. primary fistulas (39.7% vs. 3.7%) and after surgery for multitract as opposed to singletract fistulas (29.4% vs. 8.3%). In a review of 624 patients undergoing anal fistula surgery, Garcia-Aguilar et al. (98) showed that 45% of patients complained of some degree of altered continence. Factors associated with postoperative incontinence included female sex, high fistula type, type of surgery, and previous fistula surgery. Incontinence after staged fistulotomy using a seton ranges from 0% to 64%.(34, 97, 98, 102–109) Again, all of the studies showing no recurrences were small, with the largest being only 20 patients.(105) In a study looking at long-term functional outcome, Van Koperen et al. (111) reported that after fistulotomy for low cryptoglandular fistulas, fecal soiling was seen in 41% of patients and fecal incontinence was seen in 2.8% of patients at 3 year follow-up. Following rectal advancement flaps, soiling was seen in 43% and incontinence was seen in 2.9% at 3 year follow-up. None of potential risk factors examined (sex, age, prior fistula surgery, smoking) were significant in both univariate and multivariate analysis. Schouten et al. (39) showed that 35% of patients had deteriorated continence postoperatively after endorectal advancement flap. The number of previous attempts at fistula repair did not adversely affect continence. Zimmerman et al. (46) reported deteriorated continence after anocutaneous advancement flap in 30% of patients. Aguilar et al.

reported disturbances in continence to flatus in 7% and liquid stool in 6% in a series of 189 patients undergoing fistulectomy with endorectal advancement flap.(118) Kodner et al. reported unchanged or improved continence in 98% of patients undergoing endorectal advancement flap for anorectal fistulas.(40) Other series have reported no alteration in postoperative continence after rectal advancement flaps.(45, 119) Toyonaga et al. performed an interesting study looking at preand postfistulotomy manometry studies.(120) They found that fistulotomy significantly decreased maximum resting pressure (85.9 to 60.2 mmHg, p < 0.0001) and length of the high pressure zone (3.92 to 3.82 cm, p = 0.035), but did not affect voluntary contraction pressure (164.7 to 160.3 mmHg, p = 0.2792). Anal sphincter dysfunction, in the form of soiling, incontinence to flatus, or incontinence to liquid stool, occurred in 20.3% of patients. Multivariate analysis showed that while fistulotomy did not affect voluntary contraction pressure, those with lower preoperative voluntary contraction pressures were more likely to suffer from altered continence postoperatively, as were those who had undergone multiple drainage procedures. Age, sex, previous fistula surgery, duration of symptoms, and location and level of the primary opening did not significantly influence continence postoperatively. The authors concluded that preoperative anal manometry may be helpful in choosing the proper surgical procedure for patients with fistula-in-ano. Manometry studies following endorectal advancement flaps performed by Uribe et al. (121) also showed significant reduction in maximum resting pressure 3 months after surgery (83.6 vs. 45.6 mmHg, p < 0.001), as well as significant reduction in maximum squeeze pressure (208.8 vs. 169.5 mmHg, p < 0.001). Disturbed anal continence was seen 21.4% of patients. None of the variables looked at (age, sex, previous fistula surgery, Crohn’s disease) were predictive of postoperative incontinence. In contrast, manometry studies following endorectal advancement

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improved outcomes in colon and rectal surgery flaps were performed by Kreis et al. (122), showing no difference in preoperative and postoperative maximum squeeze pressure (100.0 vs. 118.0 mmHg), maximum resting pressure (56.6 vs. 52.8 mmHg), rectal compliance (4.4 vs. 3.5 ml/mmHg), or any other anorectal manometry parameter. Other studies evaluating preoperative manometric parameters differ somewhat. Chan and Lin (123) examined 45 patients with intersphincteric fistulas and showed low preoperative resting pressure to be the only independent factor predicting postoperative incontinence. In a prospective study by Perez et al. (124) looking at combined fistulotomy with primary sphincter reconstruction, there were significant preoperative differences seen on manometry between continent and incontinent patients that disappeared after operation. There were neither clinical nor manometric differences between pre- and postoperative values in fully continent patients, although three patients (12.5%) reported minor alterations of continence. Crohn’s Disease The overall incidence of anorectal fistulas associated with Crohn’s disease limited to the ileocecum is 20–25%; this rises to approximately 60% when Crohn’s disease affects the rectum.(125) Disease isolated to the anorectum is seen in only 5% of patients.(126) Fistulizing anorectal Crohn’s disease can be among the most frustrating conditions surgeons are called upon to manage. Surgical treatment is fraught with the problems of poor wound healing, delayed wound healing, and sphincter injury. It is widely held that incontinence in patients with anorectal Crohn’s disease is usually the result of aggressive surgeons and not aggressive disease.(127) Thus, a conservative approach is practiced in most instances, taking extreme care to protect the sphincter. When in doubt, one cannot be faulted for simply draining the suppurative process by placing a draining seton. Any acute infectious process must be drained appropriately and medical management of the disease should be optimized before even considering surgical treatment. For low-lying posterior fistulas, fistulotomy may be considered, especially if there is not rectal disease. Anterior fistulotomies in females should be avoided because of the risk of postoperative incontinence. Endorectal advancement flaps are also a viable option, especially when there is no rectal ­disease. Joo et al. (128) described 31 endorectal advancement flaps performed in 26 patients, resulting in fistula eradication in 71% of cases. Success was more likely in the absence of concomitant small bowel Crohn’s disease than in patients with concomitant small bowel Crohn’s disease (87% vs. 25%, p < 0.05). Other series have shown that the presence of Crohn’s disease predisposes endorectal advancement flaps to failure.(42, 112) Data regarding the efficacy of the Surgisis© AFP is mixed. As mentioned earlier, O’Connor et al. reported the AFP to be effective in 80% of patients and 83% of fistula tracts in a series of 20 patients with 36 fistula tracts. Patients with single fistulas were more likely to have success and success was not correlated with antitumor necrosis factor therapy.(69) Schwander et al. actually showed better healing rates with AFP’s in patients with anal fistulas and Crohn’s disease than in patients without Crohn’s (85.7% vs. 45.5%). On the other hand, Ky et al. (77) reported complete fistula healing with an AFP in 26.6% of patients with Crohn’s disease compared to 66.7% of patients without Crohn’s (p < 0.02).

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For patients with fulminant perineal sepsis due to fistulizing perineal Crohn’s, a low threshold for a diverting stoma must be entertained, especially since a large number of these patients will go on to require proctectomy. Nonsurgical Management For the most part, there is no role for nonoperative management of anorectal abscesses. Occasionally, an early inflammatory process, marked by pain and erythema or induration without fluctuance, may be prevented from progressing to an abscess with early initiation of antibiotic therapy. However, once an abscess has formed, antibiotics alone are insufficient. Failure to appropriately drain an anorectal abscess in a timely manner subjects the patient to the risk of progressive perineal sepsis, including operative risks associated with surgery in the septic patient, technical complications associated with anorectal surgery in the face of severe inflammation (unclear anatomy, bleeding, risk of inadvertent sphincter injury), and necrotizing perineal soft tissue infection (Fournier’s gangrene) with associated mortality rates as high as 67% (129–132), as described below. Nonoperative management of anal fistulas falls into two main categories – those related to cryptoglandular disease and those related to Crohn’s disease. There is very little in the literature regarding nonoperative management of chronic cryptoglandular fistulas. Obviously, acute suppurative processes must be drained, typically with a seton. Draining setons may be left in place indefinitely, with little consequence other than patient discomfort. As discussed later, in exceedingly rare cases, invasive carcinoma may develop in the setting of a chronic fistula. Conservative (nonoperative) therapy for anal fistulas in the setting of Crohn’s disease is the standard approach typically followed. (331) Initial drainage of the acute suppurative process without division of the fistula tract is typically performed by placing draining setons. Long-term indwelling draining setons may be used as an effective management modality for complex perianal Crohn’s fistulas, without a negative impact on continence.(134) A number of medical therapies are utilized for the treatment of anal fistulas related to Crohn’s disease. Ciprofloxacin has been reported to improve symptoms in two small, uncontrolled trials. (135, 136) Metronidazole had also been studied in a number of uncontrolled trials with varying rates of symptom relief and fistula healing.(137–140) Metronidazole must be used for maintenance to be effective, as high recurrence rates are seen on discontinuation.(133) The combination of ciprofloxacin and metronidazole has also been shown to be effective in a small retrospective study at reducing symptoms and healing fistulas; most patients in this series also regressed with cessation of treatment.(141) A number of immunomodulators are also employed in the medical management of perianal Crohn’s fistulas. Azathioprine and 6-mercaptopurine have been shown to induce complete fistula closure in 31–39% of patients, with even higher rates of symptom reduction without complete closure.(142–144) Again, recurrence occurred frequently with discontinuation of treatment. Methotrexate and cyclosporine A have each been shown to be efficacious in inducing remission on patients with Crohn’s disease (145, 146), though data regarding their effect specifically on anal fistulas resulting from Crohn’s disease has been lacking.

surgery and nonoperative therapy of perirectal abscesses and anal fistulas Infliximab, a chimeric monoclonal antibody against tumor necrosis factor-alpha (TNF-α), has revolutionized the medical management of Crohn’s disease. In mucosal biopsies of patients with Crohn’s disease, enhanced secretion of TNF-α with failure to release enhanced quantities of soluble TNF-α receptors is seen. Infliximab reduces disease activity by blocking the effects of TNF-α and has been shown to be an effective maintenance therapy in patients with Crohn’s disease with fistulas (147) and without fistulas.(148) Despite a lack of convincing Level 1 data proving the efficacy of infliximab specifically in the setting of perianal Crohn’s fistulas, its use in this setting is becoming more widespread. Long-term data regarding the efficacy of infliximab in effecting perianal fistula closure is lacking. The combination of seton drainage and infliximab infusion has been shown to be effective as well, with healing rates ranging from 47–100%.(149–151) The timing of seton removal in these patients is not clear. If removed too early, the patient is at risk of developing recurrent perianal abscesses, and if they are not removed, complete fistula healing will not occur. Poritz et al. (152) reported 44% complete anal ­fistula healing when the seton(s) were removed between the ­second and third infliximab infusions. As the use of infliximab escalates, patients who have failed treatment are undergoing subsequent surgical intervention for anorectal fistulas, raising concerns over whether preoperative infliximab treatment has an adverse effect on anal fistula surgery. Gaertner et al. (153) showed that patients with Crohn’s disease and anal fistulas who were treated initially with infliximab and underwent subsequent surgical treatment showed similar healing rates compared with patients who did not undergo previous infliximab treatment (60% vs. 59%). Kraemer et al. (154) reported that 9 of 11 patients with Crohn’s disease and anal fistulas who underwent preoperative infliximab treatment followed by advancement flaps demonstrated complete healing. Thus, it seems feasible to proceed with anal fistula surgery after failed infliximab treatment, expecting to acceptable rates of wound healing. HIV-positive patients Patients with anorectal abscesses who are HIV-positive require timely incision and drainage, as presentation is often delayed. In this population, the use of adjunct antibiotics is strongly recommended. Because these patients are at increased risk if of poor wound healing (155), care should be taken to minimize the size of surgical wounds while ensuring adequate drainage. In one study (155), serious septic complications or uncommon presentations of anorectal sepsis were seen in 13% of HIV-positive patients who initially presented with anorectal suppuration. In another study (156), perianal sepsis in HIV-positive patients was frequently associated with in situ neoplasia. Interestingly, immunosuppressive disease has not been found to contribute to the need for early reoperation following initial abscess drainage.(82) In a review by Munoz-Villasmil et al. (157) of 83 immunocompromised patients with perianal sepsis, 28% were HIV-positive. In this population, 91% of surgical wounds were healed in 8 weeks. Incontinence was seen in 6% of patients postoperatively, and recurrence was seen in 7%.

Carcinoma Associated with Fistula-In-Ano In rare instances, patients with long-standing anal fistulas may go on to develop invasive carcinoma. Although this occurs more commonly in the setting of Crohn’s disease, carcinomas arising from anal fistulas have been reported in patients without Crohn’s disease.(158, 159) While Crohn’s disease is associated overall with an approximately 6-fold increase in colorectal cancer compared to the general population (160), the incidence of anal cancer arising from an anal fistula in the setting a Crohn’s disease is significantly lower. In a series of over 1000 patients with anorectal manifestations of Crohn’s disease, Ky et al. (125) reported seven patients (0.7%) who developed invasive carcinoma related to anorectal fistulas. Four patients developed squamous cell carcinoma and three developed adenocarcinoma. The average duration of Crohn’s disease before cancer diagnosis was 14 years and average age at diagnosis was 47 years. Presenting symptoms included pain (n = 5), persistent ­fistula (n = 2), persistent anal ulcer (n = 1), and rectovaginal fistula (n = 1). In four patients, the diagnosis of carcinoma was overlooked at initial examination, resulting in significant delay in diagnosis. All four patients with squamous cell carcinoma were treated with chemoradiation. Two of these were successfully treated with no evidence of residual disease. One died of carcinoma 6 months after treatment. The fourth patient required abdominoperineal resection due to persistent disease and died 1.5 years later. One of the patients treated successfully with chemoradiation developed a second primary squamous cell carcinoma 11 years later, which was successfully treated with wide local excision. All three patients with adenocarcinoma were treated with abdominoperineal resection. One received preoperative chemoradiation; this patient died 3.5 years later. Of the remaining 2 patients, one died in the early postoperative period, and the second died of unrelated causes 5 years later. A number of other case reports in the literature describe patients with carcinoma arising from chronic fistulas and unhealed wounds in a setting of Crohn’s disease.(161, 162) The take home message is that one must maintain a high degree of suspicion for carcinoma in patients with persistent or complex anal fistulas, especially in the setting of long-standing Crohn’s disease. In this setting, complex fistulas with associated anorectal strictures and/or severe anorectal pain mandate a thorough examination. In cases where anorectal examination is limited or unequivocal, exam under anesthesia with biopsy or curettage of the fistula tract is essential. Because lesions are typically diagnosed at a later stage of disease, prognosis is poor. Timely diagnosis and institution of appropriate therapy is essential to improve survival rates. References    1. Parks AG. Pathogenesis and treatment of fistula-in-ano. Br Med J 1961; 1: 463–9.    2. Parks AG, Gordon PH, Hardcastle JD. A classification of fistula-in-ano. Br J Surg 1976; 63: 1–12.    3. Cirocco WC, Reilly JC. Challenging the predictive accuracy of Goodsall’s rule for anal fistulas. Dis Colon Rectum 1992; 35: 537–42.    4. Halligan S, Stoker J. Imaging of fistula in ano. Radiology 2006; 239: 18–33.

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improved outcomes in colon and rectal surgery    5. Berman L, IsraelGM, McCarthy SM et al. Utility of magnetic resonance imaging in anorectal disease. World J Gastroenterol 2007; 13: 3153–8.    6. Kuijpers HC, Schulpen T. Fistulography for fistula-in-ano: is it useful? Dis Colon Rectum 1985; 28: 103–4.    7. Weisman RI, Orsay CP, Pearl RK, Abcarian H. The role of fistulography in fistula-in-ano. Report of five cases. Dis Colon Rectum 1991; 34: 181–4.    8. Law PJ, Talbot RW, Bartram CI, Northover JMA. Anal endosonography in the evaluation of perianal sepsis and fistula-inano. Br J Surg 1989; 76: 752–2.    9. Cataldo PA, Senagore A, Lutchtefeld MA. Intrarectal ultrasound in the evaluation of perirectal abscesses. Dis Colon Rectum 1993; 36: 554–8.   10. Lengyel AJ, Hurst NG, Williams JG. Pre-operative assessment of anal fistulas using endoanal ultrasound. Colorectal Dis 2002; 4: 436–40.   11. Seow-Choen F, Burnett S, Bartram CI, Nicholls RJ. Comparison between anal endosonography and digital examination in the evaluation of anal fistulas. Br J Surg 1991; 78: 445–7.   12. Cheong DMO, Nogueras JJ, Wexner SD, Jagelman DG. Anal endosonography for recurrent anal fistulas: image enhancement with hydrogen peroxide. Dis Colon Rectum 1993; 36: 1158–60.   13. Poen AC, Felt-Bersma RJ, Eijsbouts QA et al. Hydrogen ­peroxide-enhanced transanal ultrasound in the assessment of fistula-in-ano. Dis Colon Rectum 1998; 41: 1147–52.   14. Moscowitz I, Baig MK, Nogueras JJ et al. Accuracy of hydrogen peroxide enhanced endoanal ultrasonography in assessment of the internal opening of an anal fistula complex. Tech Coloproctol 2003; 7: 133–7.   15. Navarro-Luna A, Garcia-Domingo MI, Rius-Macias J, Marco-Molina C. Ultrasound study of anal fistulas with hydrogen peroxide enhancement. Dis Colon Rectum 2004; 47: 108–14.   16. Buchanan GN, Bartram CI, Williams AB et al. Value of hydrogen peroxide enhancement of three-dimensional endoanal ultrasound in fistula-in-ano. Dis Colon Rectum 2005; 48: 141–7.   17. Gravante G, Giordano P. The role of three-dimensional endoluminal ultrasound imaging in the evaluation of anorectal diseases: a review. Surg Endosc 2008; 22: 1570–8.   18. Giordano P, Grondona P, Hetzer H et al. Three-dimensional endoanal ultrasonography is better than conventional anal endosonography in the assessment of fistula in ano. Dis Colon Rectum 2004; 47: 607–8.   19. Ratto C, Grillo E, Parello A et al. Endoanal ultrasoundguided surgery for anal fistula. Endoscopy 2005; 37: 722–8.   20. West RL, Dwarkasing S, Felt-Bersma RJ et al. Hydrogen ­peroxide-enhanced three-dimensional endoanal ultrasonography and endoanal magnetic resonance imaging in evaluating perianal fistulas: agreement and patient preference. Eur J Gastroenterol Hepatol 2004; 16: 1319–24.   21. West RL, Zimmerman DD, Dwarkasing S et al. Prospective comparison of hydrogen peroxide-enhanced three-dimensional endoanal ultrasonography and endoanal magnetic

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resonance imaging of perianal fistulas. Dis Colon Rectum 2003; 46: 1407–15.   22. Buchanan GN, Halligan S, Bartram CI et al. Clinical examination, endosonography, and MR imaging in preoperative assessment of fistula in ano: comparison with outcome-based reference standard. Radiology 2004; 233: 674–81.   23. Barker PG, Lunniss PJ, Armstrong P et al. Magnetic resonance imaging of fistula-in-ano: technique, interpretation, and accuracy. Clin Radiol 1994; 49: 7–13.   24. Beckingham IJ, Spencer JA, Ward J et al. Prospective evaluation of dynamic contrast enhanced magnetic resonance imaging in the evaluation of fistula in ano. Br J Surg 1996; 83: 1396–8.   25. Beets-Tan RG, Beets GL, van der Hoop AG et al. Preoperative MR imaging of anal fistulas: Does it really help the surgeon? Radiology 2001; 218: 75–84.   26. Schaefer O, Lohrmann C, Langer M. Assessment of anal fistulas with high-resolution subtraction MR-fistulography: comparison with surgical findings. J Magn Reson Imaging 2004; 19: 91–8.   27. Beck DE, Fazio VW, Lavery IC et al. Catheter drainage of ischiorectal abscesses. South Med J 1988; 81: 444–6.   28. Hanley PH, Ray JE, Pennington EE, Grablowsky OM. A ten year follow up study of horseshoe-abscess fistula-in-ano. Dis Colon Rectum 1976; 19: 507–15.   29. Rosen SA, Colquhoun P, Efron J et al. Horseshoe abscesses and fistulas: how are we doing? Surg Innov 2006; 13: 17–21.   30. Vasilevsky C. Fistula-in-ano and abscess. In: Beck DE, Wexner SD, eds. Fundamentals of Anorectal Surgery, 2nd Edition. Philadelphia: W.B. Saunders, 1998: 153–73.   31. Fucini C. One stage treatment of anal abscesses and fistulas. A clinical appraisal on the basis of two different classifications. Int J Colorectal Dis 1991; 6: 12–6.   32. Tang C-L, Chew S-P, Seow-Choen F. Prospective randomized trial of drainage alone vs drainage and fistulotomy for acute perianal abscesses with proven internal opening. Dis Colon Rectum 1996; 39: 1415–17.   33. Schouten WR, van Vroonhoven TMJV. Treatment of anorectal abscesses with or without primary fistulectomy: results of a prospective randomized trial. Dis Colon Rectum 1991; 34: 60–3.   34. Pearl RK, Andrews JR, Orsay CP et al. Role of the seton in the management of anorectal fistulas. Dis Colon Rectum 1993; 36: 573–9.   35. Parks AG, Stitz RW. The treatment of high fistula-in-ano. Dis Colon Rectum 1976; 19: 487–99.   36. Kennedy HL, Zegarra JP. Fistulotomy without external sphincter division for high anal fistulae. Br J Surg 1990; 77: 898–90.   37. Fazio VW. Complex anal fistulae. Gastroenterol Clin North Amer 1987; 16: 93–114.   38. Gordon PH. Management of anorectal abscess and fistulous disease. In Kodner IJ, Fry RD, Roe JP, eds. Colon, Rectal and Anal Surgery. St. Louis: CV Mosby, 1985: 91–107.   39. Schouten WR, Zimmerman DD, Briel JW. Transanal advancement flap repair of transsphincteric fistulas. Dis Colon Rectum 1999; 42: 1419–22.

surgery and nonoperative therapy of perirectal abscesses and anal fistulas   40. Kodner IJ, Mazor A, Shemesh EI et al. Endorectal advancement flap repair of rectovaginal and other complicated anorectal fistulas. Surgery 1993; 114: 682–9.   41. Dixon M, Root J, Grant S, Stamos MJ. Endorectal flap advancement repair is an effective treatment for selected patients with anorectal fistulas. Am Surg 2004; 70: 925–7.   42. Sonada T, Hull T, Piedmonte MR, Fazio VW. Outcomes of primary repair of anorectal and rectovaginal fistulas using the endorectal advancement flap. Dis Colon Rectum 2002; 45: 1622–8.   43. Hyman N. Endoanal advancement flap repair for complex anorectal fistulas. Am J Surg 1999; 178: 337–40.   44. Chew SSB, Adams WJ. Anal sphincter advancement flap for low transsphincteric anal fistula. Dis Colon Rectum 2007; 50: 1090–3.   45. Amin SN, Tierney GM, Lund JN, Armitage NC. V-Y advancement flap for treatment of fistula-in-ano. Dis Colon Rectum 2003; 46: 540–3.   46. Zimmerman DD, Briel JW, Gosselink MP, Schouten WR. Anocutaneous advancement flap repair of transsphincteric fistulas. Dis Colon Rectum 2001; 44: 1474–80.   47. Cintron JR, Park JJ, Orsay CP et al. Repair of fistulas-in-ano using autologous fibrin tissue adhesive. Dis Colon Rectum 1999; 42: 607–13.   48. Park JJ, Cintron JR, Orsay CP et al. Repair of chronic anorectal fistulae using commercial fibrin sealant. Arch Surg 2000; 135: 166–9.   49. Cintron JR, Park JJ, Orsay CP et al. Repair of fistulas-inano using fibrin adhesive: long-term follow-up. Dis Colon Rectum 2000; 43: 944–9.   50. Lindsey I, Smilgin-Humphreys MM, Cunningham C et al. A randomized, controlled trial of fibrin glue vs. conventional treatment for anal fistula. Dis Colon Rectum 2002; 45: 1608–15.   51. Sentovich SM. Fibrin glue for all anal fistulas. J Gastrointest Surg 2001; 5: 158–61.   52. Buchanan GN, Bartram CI, Phillips RK. Efficacy of fibrin sealant in the management of complex anal fistula. Dis Colon Rectum 2003; 46: 1167–74.   53. Loungnarath R, Dietz DW, Mutch MG et al. Fibrin glue treatment of complex anal fistulas has low success rate. Dis Colon Rectum 2004; 47: 432–6.   54. Gisbertz SS, Sosef MN, Festen S, Gerhards MF. Treatment of fistulas in ano with fibrin glue. Dig Surg 2005; 22: 91–4.   55. Maralcan G, Baskonus I, Aybasti N, Gokalp A. The use of fibrin glue in the treatment of fistula-in-ano: a prospective study. Surg Today 2006; 36: 166–70.   56. Adams T, Yang J, Kondylis LA, Kondylis PD. Long-term outlook after successful fibrin glue ablation of cryptoglandular transsphincteric fistula-in-ano. Dis Colon Rectum 2008; 51: 1488–90.   57. Ellis CN, Clark S. Fibrin glue as an adjunct to flap repair of anal fistulas: a randomized, controlled study. Dis Colon Rectum 2006; 49: 1736–40.   58. van Koperen PJ, Wind J, Bemelman WA, Slors JF. Fibrin glue and transanal rectal advancement flap for high transsphincteric

perianal fistulas: is there any advantage? Int J Colorectal Dis 2008; 23: 697–701.   59. Jain SK, Kaza RCM, Pahwa M, Bansal S. Role of cyanoacrylate in the management of low fistula in ano: a prospective study. Int J Colorectal Dis 2008; 23: 355–8.   60. Barillari P, Basso L, Larcinese A et al. Cyanoacrylate glue in the treatment of ano-rectal fistulas. Int J Colorectal Dis 2006; 21: 791–4.   61. Singer M, Cintron J, Nelson R et al. Treatment of fistulas-inano with fibrin sealant in combination with intra-adhesive antibiotics and/or surgical closure of the internal fistula opening. Dis Colon Rectum 2005; 48: 799–808.   62. Gustafsson UM, Graf W. Randomized clinical trial of local gentamycin-collagen treatment in advancement flap repair for anal fistula. Br J Surg 2006; 93: 1202–7.   63. Zmora O, Neufeld D, Ziv Y et al. Prospective, multicenter evaluation of highly concentrated fibrin blue in the treatment of complex cryptogenic perianal fistulas. Dis Colon Rectum 2005; 48: 2167–72.   64. Franklin ME Jr, Gonzalez JJ Jr, Michaelson RP et al. Preliminary experience with new bioactive prosthetic material for repair of hernias in infected fields. Hernia 2002; 6: 171–4.   65. Franklin ME Jr, Gonzalez JJ Jr, Glass JL. Use of porcine small intestine submucosa as a prosthetic device for laparoscopic repair of hernias in contaminated fields: 2-year follow-up. Hernia 2004; 8: 186–9.   66. Franklin ME Jr, Trevino JM, Portillo G et al. The use of small intestinal submucosa as a prosthetic material for laparoscopic hernia repair in infected and potentially contaminated fields: long-term follow-up. Surg Endosc 2008; 22: 1941–6.   67. Johnson EK, Gaw JU, Armstrong DN. Efficacy of anal ­fistula plug vs. fibrin glue in closure of anorectal fistulas. Dis Colon Rectum 2006; 49: 371–6.   68. Champagne BJ, O’Connor LM, Ferguson M et al. Efficacy of anal fistula plug in closure of cryptoglandular fistulas: longterm follow-up. Dis Colon Rectum 2006;4 9: 1817–21.   69. O’Connor L, Champagne BJ, Ferguson MA et al. Efficacy of anal fistula plug in closure of Crohn’s anorectal fistulas. Dis Colon Rectum 2006: 49: 1569–73.   70. Ellis CN. Bioprosthetic plugs for complex anal fistulas: an early experience. J Surg Educ 2007; 64: 36–40.   71. van Koperen PJ, D’Hoore A, Wolthuis AM et al. Anal fistula plug for closure of difficult anorectal fistula: a prospective study. Dis Colon Rectum 2007; 50: 2168–72.   72. Schwandner O, Stadler F, Dietl O et al. Initial experience on efficacy in closure of cryptoglandular and Crohn’s transsphincteric fistulas by the use of the anal fistula plug. Int J Colorectal Dis 2008; 23: 319–24.   73. Lawes DA, Efron JE, Abbas M et al. Early experience with the bioabsorbable anal fistula plug. World J Surg 2008; 32: 1157–9.   74. Christoforidis D, Etzioni DA, Goldberg SM et al. Treatment of complex anal fistulas with the collagen fistula plug. Dis Colon Rectum 2008; 51: 1482–7.   75. Thekkinkattil D, Botterill I, Ambrose S et al. Efficacy of the anal fistula plug in complex anorectal fistulae. Colorectal Dis 2008 Jul 15 [Epub ahead of print].

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improved outcomes in colon and rectal surgery   76. Garg P. To determine the efficacy of anal fistula plug in the treatment of high fistula-in-ano – an initial experience. Colorectal Dis 2008 Jul 15 [Epub ahead of print].   77. Ky AJ, Sylla P, Steinhagen R et al. Collagen fistula plug for the treatment of anal fistulas. Dis Colon Rectum 2008; 51: 838–43.   78. The Surgisis® AFP™ anal fistula plug: report of a consensus conference. Colorectal Dis 2008; 10: 17–20.   79. Rojanasakul A, Pattanaarun J, Sahakitrungruang C, Tantiphlachiva K. Total anal sphincter saving technique for fistula-in-ano: the ligation of intersphincteric fistula tract. J Med Assoc Thai 2007; 90: 581–6.   80. Vasilevsky CA, Gordon PH. The incidence of recurrent abscesses or fistula-in-ano following anorectal suppuration. Dis Colon Rectum 1984; 27: 126–30.   81. Abcarian H. Surgical management of recurrent anorectal abscess. Contemp Surg 1982; 21: 85–91.   82. Onaca N, Hirshberg A, Adar R. Early reoperation for perirectal abscess: a presentable complication. Dis Colon Rectum 2001; 44: 1469–73.   83. Sangwan YP, Rosen L, Riether RD et al. Is simple fistula-inano simple? Dis Colon Rectum 1994; 37: 885–9.   84. Sygut A, Zajdel R, Kedzia-Budziewska R et al. Late results of treatment of anal fistulas. Colorectal Dis 2007; 9: 151–8.   85. Bennet RC. A review of orthodox treatment for anal fistula. Proc R Soc Med 1962; 55: 756–7.   86. Hill JR. Fistulas and fistulous abscesses in the anorectal region: personal experience in management. Dis Colon Rectum 1967; 10: 421–34.   87. Lilius HG. Fistula-in-ano, an investigation of human foetal anal ducts and intramuscular glands and a clinical study of 150 patients. Acta Chir Scand 1968; 383(Suppl): 1–88.   88. Mazier WP. The treatment and care of anal fistulas: a study of 1000 patients. Dis Colon Rectum 1971; 14: 134–44.   89. Ani AN, Solanke TF. Anal fistula: A review of 82 cases. Dis Colon Rectum 1976; 19: 51–5.   90. Marks CG, Ritchie JK. Anal fistulas at St. Mark’s Hospital. Br J Surg 1977; 64: 84–91.   91. Ewerth S, Ahlberg J, Collste G, Holmstrom B. Fistula-inano: a six year follow-up study of 143 operated patients. Acta Chir Scand 1978; 482(suppl): 53–5.   92. Adams D, Kovalcik PJ. Fistula-in-ano. Surg Gynecol Obstet 1981; 153: 731–3.   93. Kuijpers JHC. Diagnosis and treatment of fistula-in-ano. Neth J Surg 1982; 34: 147–52.   94. Sainio P, Husa A. A prospective manometric study of the effect of anal fistula surgery on anorectal function. Acta Chir Scand 1985; 151: 279–88.   95. Vasilevsky CA, Gordon PH. Results of treatment of fistula-inano. Dis Colon Rectum 1985: 28: 225–31.   96. Fucini C. One stage treatment of anal abscesses and fistulas. A clinical appraisal on the basis of two different classificaions. Int J Colorectal Dis 1991; 6: 12–6.   97. Van Tets WF, Kuijpers HC. Continence disorders after anal fisulotomy. Dis Colon Rectum 1994; 37: 1194–7.   98. Garcia-Aguilar JC, Belmonte C, Wong WD, Goldberg SM, Madoff RD. Surgical treatment of fistula-in-ano. Factors



associated with recurrence and incontinence. Dis Colon Rectum 1996; 39: 723–9.   99. McElwain JM, Maclean D, Alexander RM et al. Anorectal problems: experience with primary fistulotomy for anorectal abscess, a report of 1000 cases. Dis Colon Rectum 1975; 27: 593–4. 100. Seow-Choen F, Phillips RKS. Insights gained from the management of problematic anal fistulae at St. Mark’s Hospital, 1984–88. Br J Surg 1991; 78: 539–41. 101. Lunniss PJ, Sheffield JP, Talbot IC et al. Persistence of ­idiopathic anal fistula may be related to epithelialization. Br J Surg 1995; 82: 32–3. 102. Williams JG, Macleod CAH, Goldberg SM. Seton treatment of high anal fistulas. Br J Surg 1991; 78: 1159–61. 103. Ramanujam PS, Prasad ML, Abcarian H. The role of seton in fistulotomy of the anus. Surg Gynecol Obstet 1983; 157: 419–22. 104. Kuijpers HC. Use of the seton in the treatment of extrasphincteric anal fistula. Dis Colon Rectum 1984; 27: 109–10. 105. Culp CE. Use of penrose drains to treat certain anal fistulas: a primary operative seton. Mayo Clin Proc 1984; 59: 613–17. 106. Christensen A, Miles J, Christiansen J. Treatment of transsphincteric anal fistulas by the seton technique. Dis Colon Rectum 1986; 29: 454–5. 107. Held D, Khubchandani I, Sheets J et al. Management of anorectal horseshoe abscess and fistula. Dis Colon Rectum 1986; 29: 793–7. 108. Fasth SB, Nordgren S, Hulten L. Clinical course and management of suprasphincteric and extrasphincteric fistula-in-ano. Acta Chir Scand 1990; 156: 397–402. 109. Graf W, Pahlman L, Egerbald S. Functional results after seton treatment of high transsphincteric anal fistulas. Eur J Surg 1995; 161: 289–91. 110. van der Hagen SJ, Baeten CG, Soeters PB, van Gemert WG. Long-term outcome following mucosal advancement flap for high perianal fistulas and fistulotomy for low perianal fistulas: recurrent perianal fistulas: failure of treatment or recurrent patient disease? Int J Colorectal Dis 2006; 21: 784–90. 111. van Koperen PJ, Wind J, Bemelman WA et al. Longterm functional outcome and risk factors for recurrence after surgical treatment for low and high perianal fistulas of cryptoglandular origin. Dis Colon Rectum 2008; 51: 1475–81. 112. Mizrahi N, Wexner SD, Zmora O et al. Endorectal advancement flap: are there predictors of failure? Dis Colon Rectum 2002; 45: 1616–21. 113. Zimmerman DD, Delamarre JB, Gosselink MP et al. Smoking affects the outcome of transanal mucosal advancement flap repair of trans-sphincteric fistulas. Br J Surg 2003; 90: 351–4. 114. Zimmerman DD, Gosselink MP, Mitalas LE et al. Smoking impairs rectal mucosal bloodflow – a pilot study: possible implications for transanal advancement flap repair. Dis Colon Rectum 2005; 48: 1228–32. 115. Seow-Choen F, Nicholls RJ. Anal fistula. Br J Surg 1992; 79: 197–205.

surgery and nonoperative therapy of perirectal abscesses and anal fistulas 116. Mazier WP. The treatment and care of anal fistulas: a study of 1000 patients. Dis Colon Rectum 1971; 14: 134–44. 117. Rosa G, Lolli P, Piccinelli D et al. Fistula-in-ano: anatomoclinical aspects, surgical therapy and results in 844 patients. Tech Coloproctol 2006; 10: 215–21. 118. Aguilar PS, Plasencia G, Hardy TJ et al. Mucosal advancement in the treatment of anal fistula. Dis Colon Rectum 1985; 28: 496–8. 119. Dixon M, Root J, Grant S, Stamos MJ. Endorectal flap advancement repair is an effective treatment for selected patients with anorectal fistulas. Am Surg 2004; 70: 925–7. 120. Toyonaga T, Matsushima M, Kiriu T et al. Factors affecting continence after fistulotomy for intersphincteric fistula-inano. Int J Colorectal Dis 2007; 22: 1071–5. 121. Uribe N, Millan M, Minguez M et al. Clinical and manometric results of endorectal advancement flaps for complex anal fistula. Int J Colorectal Dis 2007; 22: 259–64. 122. Kreis ME, Jehle EC, Ohlemann M et al. Functional results after transanal rectal advancement flap repair of transsphincteric fistula. Br J Surg 1998; 85: 240–2. 123. Chang SC, Lin LK. Change in anal continence after surgery for intersphincteral anal fistula: a functional and manometric study. Int J Colorectal Dis 2003; 18: 111–5. 124. Perez F, Arroyo A, Serrano P et al. Fistulotomy with primary sphincter reconstruction in the management of complex fistula-in-ano: prospective study of clinical and manometric results. J Am Coll Surg 2005; 200: 897–903. 125. Ky A, Sohn N, Weinstein MA, Korelitz BI. Carcinoma arising in anorectal fistulas of Crohn’s disease. Dis Colon Rectum 1998; 41: 992–6. 126. Lockhart-Mummery HE. Symposium. Crohn’s disease: anal lesions. Dis Colon Rectum 1975; 18: 200–2. 127. Alexander-Williams J, Buchmann P. Perianal Crohn’s disease. World J Surg 1980; 4: 203–8. 128. Joo JS, Weiss EG, Nogueras JJ, Wexner SD. Endorectal advancement flap in perianal Crohn’s disease. Am Surg 1998; 64: 147–50. 129. Huber P Jr, Kissack AS, Simonton ST. Necrotizing soft tissue infection from rectal abscess. Dis Colon Rectum 1983; 26: 507–11. 130. Bubrick MP, Hitchcock CR. Necrotizing anorectal and perineal infections. Surgery 1979; 86: 655–62. 131. Lauks SS. Fournier’s gangrene in anorectal surgery. Surg Clin North Am 1994; 74: 1339–52. 132. Kovalcik P, Jones J. Necrotizing perineal infections. Am Surg 1983; 49: 163–6. 133. Lichtenstein GR. Treatment of fistulizing Crohn’s disease. Gastroenterology 2000; 119: 1132–47. 134. Thornton M, Solomon MJ. Long-term indwelling seton for complex anal fistulas in Crohn’s disease. Dis Colon Rectum 2005; 48: 459–63. 135. Turunen U, Farkkila M, Seppala K. Long-term treatment of perianl or fistulous Crohn’s disease with Ciprofloxacin (suppl 148). Scand J Gastroenterol 1989; 24: 144. 136. Wolf J. Ciprofloxacin may be useful in Crohn’s disease. Gastroenterology 1990; 98: A212.

137. Bernstein LH, Frank MS, Brandt LJ, Riley SJ. Healing of perianal Crohn’s disease with metronidazole. Gastroenterology 1980; 79: 357–65. 138. Brandt L, Bernstein L, Boley S, Frank M. Metronidazole therapy for perianal Crohn’s disease: a follow-up study. Gastroenterology 1982; 83: 383–7. 139. Jakobovits J, Schuster MM. Metronidazole therapy for Crohn’s disease and associated fistulae. Am J Gastroenterol 1984; 79: 533–40. 140. Schneider MU, Laudage G, Guggenmoos-Holzman I, Riemann JF. Metronidazol in der behandlung des morbus Crohn. Dtsch Med Wochenschr 1985; 110: 1724–30. 141. Solomon M, McLeod R, O’Connor B et al. Combination ciprofloxacin and metronidazole in severe perianal Crohn’s disease. Can J Gastroenterol 1993; 7: 571–3. 142. Present DH, Korelitz BI, Wisch N et al. Treatment of Crohn’s disease with 6-mercaptopurine: a long-term randomized double blind study. N Engl J Med 1980; 302: 981–7. 143. Korelitz BI, Present DH. Favorable effect of 6-mercaptopurine on fistulae of Crohn’s disease. Dig Dis Sci 1985; 30: 58–64. 144. O’Brien JJ, Bayless TM, Bayless JA. Use of azathioprine or 6-mercaptopurine in the treatment of Crohn’s disease. Gastroenterology 1991; 101: 39–46. 145. Feegan BC, Rochon J, Fedorak RN et al. Methotrexate for the treatment of Crohn’s disease. N Eng J Med 1995; 332: 292–7. 146. Stein RB, Hanaper SB. Medical therapy for infammatory bowel disease. Gastroenterol Clin North Am 1999; 28: 297–321. 147. Sands BE, Anderson FH, Bernstein CN et al. Infliximab maintenance therapy for fistulizing Crohn’s disease. N Eng J Med 2004; 350: 876–85. 148. Hanauer SB, Feagan BG, Lichtenstein GR et al. Maintenance infliximab for Crohn’s disease: the ACCENT I randomised trial. Lancet 2002; 359: 1541–9. 149. Regueiro M, Mardini H. Treatment of perianal fistulizing Crohn’s disease with infliximab alone or as an adjunct to exam under anesthesia with seton placement. Inflamm Bowel Dis 2003: 9: 98–103. 150. Topstad DR, Panaccione R, Heine JA et al. Combined seton placement, infliximab infusion, and maintenance immunosuppressives improve healing rate in fistulizing anorectal Crohn’s disease: a single center experience. Dis Colon Rectum 2003; 46: 577–83. 151. Talbot C, Sagar PM, Johnston MJ et al. Infliximab in the surgical management of complex fistulating anal Crohn’s disease. Colorectal Dis 2005; 7: 164–8. 152. Poritz LS, Rowe WA, Koltun WA. Remicade does not abolish the need for surgery in fistulizing Crohn’s disease. Dis Colon Rectum 2002; 45: 771–5. 153. Gaertner WB, Decanini A, Mellgren A et al. Does infliximab infusion impact results of operative treatment for Crohn’s perianal fistulas? Dis Colon Rectum 2007; 50: 1754–60. 154. Kraemer M, Kirschmeier A, Marth T. Perioperative adjuvant therapy with infliximab in complicated anal Crohn’s disease. Int J Colorectal Dis 2008; 23: 965–9.

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improved outcomes in colon and rectal surgery 155. Consten CJ, Siors FJM, Noten HJ et al. Anorectal surgery in human immunodeficiency virus-infected patients. Dis Colon Rectum 1995; 38: 1169–75. 156. Miles AJG, Mellor CH, Gazzard B et al. Surgical management of anorectal disease in HIV-positive homosexuals. Br J Surg 1990; 77: 869–71. 157. Munoz-Villasmil J, Sands L, Hellinger M. Management of perianal sepsis in immunosuppressed patients. Am Surg 2001; 67: 484–6. 158. Onerheim RM. A case of perianal mucinous adenocarcinoma arising in a fistula-in-ano: a clue to the early pathologic diagnosis. Am J Clin Pathol 1988; 89: 809–12.

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159. Seya T, Tanaka N, Shinji S et al. Squamous cell carcinoma arising from recurrent anal fistula. J Nippon Med Sch 2007; 74: 319–24. 160. Korelitz BI. Carcinoma of the intestinal tract in Crohn’s disease: results of a survey conducted by the National Foundation for Ileitis and Colitis. Am J Gastroenterol 1983; 78: 44–6. 161. Smith R, Hicks D, Tomljanovich PI et al. Adenocarcinoma arising from chronic perianal Crohn’s disease: case report and review of the literature. Am Surg 2008; 74: 59–61. 162. Sarani B, Orkin BA. Squamous cell carcinoma arising in an unhealed wound in Crohn’s disease. South Med J 1997; 90: 940–2.

20 Surgery and nonoperative therapy of anal fissure Jaime L Bohl and Alan J Herline

Challenging Case A 35-year-old woman presents with a recurrent posterior anal ­fissure. She had a left lateral anal sphincterotomy 4 years ago for an unresponsive anal fissure. Her fissure healed until 6 months ago. She has had two previously vaginal deliveries. Exam reveals a posterior anal fissure with exposed sphincter muscle and a sentinel skin tag. Anal manometry revealed mildly decreased resting pressure and a hypertonic squeeze pressure. The patient’s symptoms have not responded to stool softners and topical medication. Case Management A repeat sphincterotomy is relatively contraindicated due to the decreased sphincter function. An acceptable surgical option is an advancement flap. Introduction An anal fissure is a longitudinal tear or ulcer in the anal canal from the dentate line to the anal verge. Fissures affect both genders equally, across age groups with young and middle aged adults constituting the majority of patients.(1) Although the true incidence is not known, anal fissure is common. In a survey of Italian proctology clinics, 10% of 15,000 consecutive referrals were diagnosed with anal fissure.(2) Fissures can be classified by etiology, location, and chronicity. It is hypothesized that most fissures are caused by trauma to the anal canal, usually from passage of hard stool. Anal fissures are commonly located in the posterior midline (75%), although a smaller percentage can be found in the anterior midline (13%) and an anterior and posterior location may be seen simultaneously (11%). Anterior fissures are seen more commonly in women (19%).(1) Fissures may be associated with other chronic medical conditions such as Crohn’s disease, HIV/AIDS, tuberculosis, syphilis, or anal carcinoma. Fissures in patient with these conditions typically occur off the midline and may be multiple or irregular (Figure 20.1). These fissures are best treated according to the underlying disease state. Early or acute fissures are a simple linear tear in the anoderm. Fissures that have been present for >4 weeks show signs of chronicity: the base of the fissure reveals internal sphincter fibers with indurated edges, and a sentinel pile (cranial) or hypertrophied apical papilla (distal). The chronicity of a fissure is important to discern from patient history and clinical exam as this will affect treatment recommendations. Pathphysiology The exact mechanisms leading to acute anal fissure and the ­factors that encourage fissure chronicity have been the subject of debate. However, anatomic and physiologic studies suggest an ischemic etiology to anal fissure chronicity. In 1986 Gibbons and Read confirmed that patients with anal fissures had elevated

POSTERIOR

Acute and Chronic anal fissure

Crohn’s disease Ulcerative colitis Syphilis Tuberculosis Leukemia Cancer HIV

Acute and Chronic anal fissure

Crohn’s disease Ulcerative colitis Syphilis Tuberculosis Leukemia Cancer HIV

ANTERIOR Figure 20.1  Fissure location related to etiology.

anal resting pressures and they hypothesized that elevated anal resting pressures led to tissue ischemia and ulceration within the anal canal.(3) This hypothesis was further supported by anatomic studies performed by Klosterhalfen and colleagues who showed that the posterior anal canal has a limited blood supply compared to the rest of the anal canal.(4) The decreased blood supply to the posterior anal canal was evident through the lack of inferior rectal artery branches to the posterior anal commissure in 85% of postmortem specimens, and the decreased capillary density in histologic specimens.(4) Schouten and ­colleagues put these findings together when they demonstrated an inverse relationship between anal resting pressure and anodermal blood flow.(5) Therefore, patients with anal fissure have less blood flow to their posterior midline secondary to anal hypertonia. The ischemia in the posterior midline allows persistence of anal fissures and poor healing. Treatments for anal fissure are therefore aimed at decreasing anal hypertonia and increasing anodermal blood flow. Anal fissures can be exquisitely painful despite the small size of the lesion. Patients complain of sharp, persistent pain during and after defecation, which may lead patients to avoid bowel movements. Patients may also notice blood on the toilet tissue or coating the stool with limited bleeding or perianal swelling.



improved outcomes in colon and rectal surgery Diagnosis The clinician should inquire about known risk factors for fissure including alteration in bowel habits (constipation or diarrhea), childbirth, previous anorectal surgery, or associated medical conditions. The clinician should also inquire to previous episodes of the presenting symptom complex. The natural history of anal fissure is one that waxes and wanes, sometimes with healing between recurrences. Anal fissure can be diagnosed by inspection of the anus. Patients are usually too symptomatic to allow for digital examination or anoscopy at the initial visit. If the clinician suspects another diagnosis because of an atypical location, the presence of multiple or chronic fissures, or a fissure cannot be diagnosed by inspection, then exam under anesthesia may be necessary. Suspicion of an alternative diagnosis may warrant biopsy and culture of the anal lesions. Treatment Anal fissures have been treated with a variety of medical and surgical therapies. A growing body of randomized controlled trials has helped to guide current treatment recommendations for anal fissure. Currently available treatments include conservative therapy, nitrates, calcium channel blockers, botulinum toxin, anal dilation, open or closed lateral sphincterotomy, and anal advancement flap. Conservative therapy comprises increased dietary fluid and fiber, sitz baths, and stool softeners. Nitrates may include ointments of nitroglycerin (NTG) or glyceryl trinitrate (GTN), nitroglycerin transdermal patch, or other nitrate analogs such as isosorbide dinitrate (IDN) or isosorbide mononitrate (IMN). Calcium channel blockers have been used in ointment or tablet form (diltiazem or nifedipine). Finally, botulinum toxin (BT) has been used in the treatment of anal fissure. It is sold in two commercially available preparations, Dysport (Speywood Biopharm Ltd, Wrexham, UK) and Botox (Allergan, Irvine, CA, USA). Both preparations of BT have been shown to have equal efficacy in the treatment of chronic anal fissure (6) with 100 units of Dysport toxin having the bioequivalence of 20 units of Botox. All of these medical and surgical treatments have been used in randomized controlled trials to assess the effect on fissure healing rates, anal resting pressure, pain, and fissure recurrence. Other treatment effects which are important to consider are complications such as incontinence to flatus or stool, headache, hypotension, and allergic reactions. Importantly, two recent meta-analyses of all medical and surgical treatments used for anal fissure are available.(7–10) This has lead to improved decision making regarding the treatment of anal fissure. Conservative therapy is often used as a comparison to other medical or surgical treatment. The effect of conservative therapy on healing rate for anal fissure has been 50% for acute (11) and 34% for chronic anal fissures.(7) Therefore, other medical and surgical treatments should be tested with this therapy in mind. The effect of conservative therapy on anal fissure healing rate, reduction in symptoms, and safety profile has lead to the recommendation by the American Society of Colon and Rectal Surgeons for conservative therapy to be the first line treatment of anal fissure.(12) Acute Anal Fissure Clinical experience dictates that over half of acute anal fissures will heal within several weeks. Therefore, most clinicians recommend



conservative therapy for acute anal fissure. Conservative therapy consists of fiber supplements and sitz baths with or without the use of topical anesthetics. However, few randomized controlled trials have evaluated acute anal fissure healing with conservative therapy as compared to no therapy. One trial compared warm sitz baths and 10 g of unprocessed bran to 2% lignocaine ointment or 2% hydrocortisone ointment applied in the anal canal twice per day. (13) After 3 weeks of treatment, patients treated with bran and sitz baths had significantly more healed fissures (88%) than patients treated with lignocaine ointment (60%). Unfortunately, patients with healed fissures were not followed long-term and rates of fissure recurrence were not measured. One randomized controlled trial does suggest the ability of long-term conservative therapy to prevent fissure recurrence.(14) Ninety patients with recently healed posterior anal fissures were randomized and blinded to three different treatments groups for 1 year. Patients received either 5 g unprocessed bran three times a day, 2.5 g unprocessed bran plus 2.5 g placebo, or 5 g placebo. Patients receiving 5 g of unprocessed bran over 1 year had significantly fewer recurrences of anal fissure (16%) as compared to patients who received the lower bran dose (60%) or placebo (60%). In addition, within 6 months of discontinuing treatment, the recurrence rate between the three groups was similar. Finally, one study evaluated the role of sitz baths in symptom relief and acute anal fissure healing while also providing psyllium supplementation over 4 weeks.(15) Although there was a trend toward improved pain scores after defecation and overall intensity of pain, there were no significant differences in fissure healing between groups (85%). The authors hypothesize that sitz baths provide transient pain relief via a thermosphincteric reflex which allows for decrease in sphincter tone and temporary pain relief. However, sitz baths do not lead to long-term reduction in anal tone that allows for fissure healing. Overall, these studies show that fiber therapy is more effective in preventing acute anal fissure recurrence, but only suggest that fiber therapy can improve acute fissure healing. In an effort to improve acute anal fissure healing rates and maintain healing, some investigators have added anal dilation or pharmacologic agents to conservative treatment. One study shows no additional therapeutic benefit of twice daily anal dilation in combination with stool softener and lignocaine jelly.(16) Another small randomized study that included patients with both acute and chronic fissures compared topical nitroglycerin to topical xylocaine.(17) In patients who had acute fissures, those receiving topical nitroglycerin had fissure healing rates of 92% compared to 0% of the control arm after 14 days of therapy. This treatment effect persisted, with the same number of patients in the nitroglycerin group maintaining healing at 28 days compared to 50% of patients who received xylocaine ointment. No long-term follow-up data was provided and all treatment failures were referred for lateral sphincterotomy. A larger randomized trial examined the healing rate of acute anal fissure after treatment with 0.2% nifedipine ointment twice daily compared to conservative therapy. (18) Patients who received nifedipine treatment had higher fissure healing rates compared to conservative therapy (98 vs. 60%) after 4 weeks of treatment. One novel approach to achieve acute anal fissure healing has been to compare the efficacy of gonyautoxin, a paralyzing phytotoxin, to normal saline placebo which are both

surgery and nonoperative therapy of anal fissure Table 20.1  Randomized Controlled Trials of Nitrate Therapy versus Placebo for the Treatment of Chronic Anal Fissure.

Author/Year

Number Patients

Treatment Groups (%)

Length Treatment (weeks)

Fissure Healing Rates (%)

Side Effects (%)

Follow-up (months)

Recurrence (%)

Lund 1997 (24)

  80

P vs. 0.2 GTN BID

 8

8 vs. 68 (p < 0.0001)

HA: 18 vs. 58 (p < 0.05)

 4

11.5% GTN

Kennedy 1999 (27)

  43

P vs. 0.2 GTN TID

 4

16 vs. 46 (p = 0.001)

HA: 21 vs. 29 Discontinued treatment: 13

29

NR

Altomere 2000 (26)

132

P vs. 0.2 GTN BID

 4

52 vs. 49 (p = ns)

HA: 8 vs. 34 (p = 0.001) Orthostatic hypotension: 6

 3

19% GTN

Chaudhuri 2001 (25)

  19

P vs. 0.2 GTN BID

 6

22 vs. 70 (p < 0.05)

Not reported

 3

None

Maan 2004 (28)

  64

P / 5 xylocaine / proctosedyl / 0.2 GTN BID

 6

25 vs. 94 (p < 0.0001)

HA: 0 vs. 19

None

NR

Carapeti 1999 (29)

  70

P / 0.2 / 0.2+0.1qwk GTN TID

 8

32 vs. 67 all GTN (p = 0.008)

 9

43 vs. 29 (p = 0.7)

Bailey 2002 (30)

304

P / 0.1 / 0.2 / 0.4 NTG BID or TID

 8

50- all groups (p < 0.62)

Discontinued treatment: 3.3

None

NR

Scholfield 2003 (31)

200

P / 0.1 / 0.2 / 0.4 GTN BID

 8

38 vs. 47 all GTN (p = 0.3)

HA: 13 vs. 31 all GTN (p < 0.01)

None

NR

Wierre 2001 (31)

  37

P vs. 1 IDN 5x/day

10

35 vs. 85 (p < 0.003)

HA:18 vs. 45

10

33 vs. 12

Tankova 2002 (32)

  19

P vs. 0.2 IMN BID

 3

22 vs. 80

HA: 0 vs. 20

 3

None

HA: 27 vs. 72 all GTN (p < 0.001)

Note: P = placebo; GTN = glyceryl trinitrate; BID = twice per day; HA = headache; TID = three times per day; NR = not recorded; NS = not statistically significant; NTG = nitroglycerin; IDN = isosorbide dinitrate; IMN = isosorbide 5-mononitrate.

injected into the internal anal sphincter.(19) This study included 17 patients with acute anal fissure and was eventually unblinded secondary to a large treatment effect of the toxin. Patients with acute anal fissures had a healing rate of 100% at 15 days as compared to 0% of the 3 patients who received placebo. All patients who were injected with the toxin showed a significant decrease in anal resting pressure from baseline. Complications included minor bleeding but did not result in any cases of incontinence to stool or flatus. After 14 months of follow-up this treatment effect has been maintained. In all, these studies show that the addition of a pharmacologic agent can increase the healing rates of acute anal fissure; however, larger trials are needed to replicate these results. Chronic Anal Fissure Medical Therapy Anal fissure chronicity is attributed to sphincter hypertonia and decreased anodermal blood flow in the posterior anal canal. Pharma­ cologic manipulation of the hypertonic internal anal sphincter has been sought, given the permanent changes that can occur with surgical intervention. Medical treatments that result in temporary relaxation of the internal anal sphincter or chemical sphincterotomy have been used in the treatment of chronic anal fissure. Nitrates Nitrates have been shown to have a relaxing effect on the human internal anal sphincter (IAS). Ex vivo studies on the human

IAS show that nitric oxide (NO) mediates sphincter relaxation through enteric inhibitory neurons which are found within the muscle fibers.(20) Nitrates which are NO donors are readily available pharmacologic agents. Loder et al. demonstrated that GTN ointment causes a decrease in anal resting pressure in normal and anal fissure patients which was comparable to sphincterotomy. (21) Schouten and colleagues then showed that anal resting pressure decreased and anodermal blood flow increased after chronic anal fissure patients were treated with isosorbide dinitrate.(22) They concluded that the reduction in anal sphincter pressure and increased blood would contribute to early pain relief, while fissure healing would require more time. More recent studies have shown conflicting data on the ability of nitrates to significantly decrease anal resting pressure in chronic anal fissure patients. Thornton et al. clarified these conflicting results with a regression analysis which showed that patients who were mostly likely to heal their fissure in response to nitrate therapy were those with higher pretreatment anal resting pressures and a greater percent reduction in posttreatment anal resting pressures.(23) Based on these physiologic studies, nitrates have become an obvious choice for the pharmacologic treatment of chronic anal fissure. Nitrates versus Placebo There are ten randomized controlled trials in the English literature which compare nitrate therapy to placebo or conservative therapy in adults with chronic anal fissure. (Table 20.1) There have been a variety nitrate preparations, ointment strengths,



improved outcomes in colon and rectal surgery schedules, treatment length, and instructions for nitrate administration that have been utilized in these studies. Five randomized controlled trials have measured the effect of 0.2% GTN ointment in comparison to placebo.(24–28) In these studies a total of 338 patients were instructed to apply an active versus inert ointment to their anal canal either twice or three time daily for a period of 4 to 8 weeks. Outcome measures included fissure healing, pain, mean anal resting pressure (MARP), fissure recurrence, and ointment side effects. Four of these studies were able to measure an increase in anal fissure healing rates with nitroglycerin ointment compared to placebo.(24, 25, 27, 28) However, there was a wide range of GTN treatment effect (8–52% placebo vs. 46–94% GTN). The fifth and largest study included 132 patients and did not measure a difference in healing rates between the placebo and GTN ointment (52% vs. 49%).(26) In four studies, pain was reported as a secondary outcome. In three studies pain was significantly decreased after treatment compared to pain at time of trial entry in both GTN and placebo groups.(24, 26, 27) However, only one study measured a significant difference in pain scores between GTN and placebo treatment groups.(28) All five studies measured treatment effect on MARP. Two studies measured a decrease in MARP after treatment compared to time at trial entry for both placebo and GTN groups.(25, 26) In the other three studies, only the GTN treatment group had a significant decrease in MARP.(24, 27, 28) One trial reported loss of decreased MARP 48 hours after discontinuing GTN therapy.(27) The most significant side effect of nitrate therapy was headache. In four trials, there was a higher rate of headaches in GTN patients (19–58%) compared to placebo treated patients (0–21%).(24, 25, 27, 28) There was also a difference in the severity of headache reported between these two groups.(27) Ultimately, headaches lead to subsequent decreases in dose or discontinuation of GTN for several patients in each trial. In two studies there was an attempt to follow patients long-term.(24, 26) The rate of fissure recurrence in the GTN treated group was 11.5–19% after 3–4 months of follow-up. Overall, these five trials suggest a slightly increased rate of anal fissure healing with GTN ointment compared to placebo. However, there is an increased incidence and severity of headache with GTN treatment which may require a decreased dose for continued patient compliance. Despite healing, there may be a high rate of fissure recurrence within several months of follow-up. Three additional trials have tested the effect of increasing doses of GTN ointment on anal fissure healing rate, MARP, pain scores, headache, and anal fissure recurrence.(29–31) Two trials compared placebo with 0.1%, 0.2% and 0.4% GTN ointment (B,S). The third trial compared placebo with 0.2% GTN ointment and an increasing dose of GTN ointment which started at 0.2% and was increased by 0.1% every week to a dose of 0.6% GTN.(28) All treatment was administered for 8 weeks and applied either BID or TID. In these trials there was only one that measured a difference in fissure healing rate of the GTN treatment group compared to placebo.(29) There were no differences found in fissure healing rate with changes in GTN dose. One trial reported a 21% reduction in pain when treated with 0.4% GTN compared to placebo. (30) There was no difference in pain scores between placebo and GTN or between GTN doses in the other studies.(29, 31) Across these three trials, MARP was not uniformly decreased in the nitrate



treated group compared to baseline. All three studies reported a high incidence of headache in the GTN group (31–72%) compared to placebo (13–27%). Headaches were more frequent and severe with increasing dose of GTN ointment. Follow-up was ­performed in one study. One third of anal fissures that initially healed recurred within 9 months.(29) These trials demonstrate that increasing doses of GTN do not increase the rate of fissure healing or improve fissure related pain, but do result in more severe and frequent headaches. Again, recurrence when reported, occurs in up to one-third of patients. Two additional studies have used alternative nitrate preparations for the treatment of chronic anal fissure for comparison with placebo. Wierre et al. used 1% isosorbide dinitrate ointment five times per day for 10 weeks.(32) There was a significant ­difference in fissure healing rate between placebo and active ointments (35 vs. 85%). However there was no significant change in MARP throughout the trial period. There was also a significant incidence of headache in the treatment group (45%) compared to placebo (18%) with 10% of patients in the active treatment discontinuing therapy. Thirty-three percent of patients in the active treatment arm had fissure recurrence and requested alternative therapy. Tankova et al. used 0.2% isosorbide mononitrate on chronic anal fissures compared to placebo administered BID over a 3 week treatment course.(33) Eighty percent in the active treatment arm healed their fissures compared to 20% in the placebo group. Twenty percent in the active group had headaches which were treated with mild analgesics. No recurrences were seen in 3 months of follow-up. The authors of both these studies agree that different nitrate preparations can be used to treat chronic anal fissure but that more studies are required to determine the optimal preparation, dose, and schedule of nitrate therapy. Two studies have compared 0.2% GTN ointment to a transdermal nitroglycerin patch for either 6 or 8 weeks of treatment.(34, 35) In both studies the transdermal patch was a 10 mg dose that was applied for either 12 or 24 hours. These studies found that both preparations resulted in equivalent fissure healing rates at 6 weeks (65–73%), 8 weeks (63–67%) and 12 weeks (79–81%). One trial reported a decrease in pain from baseline by 50% in both the ointment and patch patients.(35) The rate of headache was substantially lower in one study (16–19%) (34) compared to another (63–72%) (35) but both studies reported the headache to be responsive to mild analgesics and equal in occurrence between the two treatment groups. Six percent of patients in one study reported transient incontinence to flatus which had resolved by the time of trial resolution.(35) Recurrence at 3 months for one trial occurred in 9–15% (34) patients and 25% in the other.(35) In all, 0.2% GTN ointment seems equivalent to transdermal patch in the rate of anal fissure healing, pain relief, side effects, and recurrence. Overall, chronic anal fissure healing rates after treatment with nitrates (49%) may be slightly improved compared to placebo (37%).(7) Nitrate therapy may decrease pain associated with anal fissure but with a concomitant increase in headaches (27%) that can lead to noncompliance. Given the side effect profile and high recurrence rates after nitrate therapy (33%), the patient may request alternative therapeutic interventions. Nitrate therapy remains a treatment alternative for patients wanting to avoid surgery and does not exclude the patient from other therapies in the future.

surgery and nonoperative therapy of anal fissure Table 20.2  Randomized Controlled Trials of Nitrates versus Surgical Sphincterotomy for the Treatment of Chronic Anal Fissure. Author/ Year

Number Patients

Treatment Groups (% ointment)

Oettle 1997 (40)

24

NTG/ LIS TID

Richard 2000 (36)

82

Evans 2001 (37)

Length of Treatment (weeks)

Fissure Healing (%)

Overall Side-effects (%)

HA %

IC Flatus (%)

Follow-up (months)

Recurrence (%)

4

83 vs. 100 (p = NS)

NR

NR

NR

 1

NR

0.25/0.5 GTN/LIS TID

6

30 vs. 90 (p = 0.00)

84 vs. 29 (p < 0.0001)

21

None

 6

38 vs. 3

60

0.2 GTN/LIS TID

8

61 vs. 97 (p < 0.001)

NR

33



7.4

 5

45 vs. 4

Libertiny 2002 (38)

70

0.2 GTN/LIS TID

8

54 vs. 100 (p = 0.02)

NR

20



2.8

24

16 vs. 2.8

Parellada 2004 (39)

54

0.2 IDN/LIS TID

6

67 vs. 96 (p < 0.001)

30 vs. 44 (p = NR)

NR

4 4 @ 5 wk 15 @ 24 wk

24

13 vs. 0

Mishra 2005 (41)

40

0.2 GTN/LIS BID

6

90 vs. 85 (p = 0.347)

40 vs. 70 (p = NR)

15

15

 4

NR

Note: NTG = nitroglycerin; LIS = lateral internal sphincterotomy; TID = three times per day; NS = not statistically significant; NR = not recorded; GTN = glyceryl trinitrate; IDN = isosorbide dinitrate.

Nitrates versus Sphincterotomy Nitrate therapy has been compared to internal sphincterotomy for the treatment of chronic anal fissure. Six studies have compared these two treatments in a randomized controlled fashion.(36–41) (Table 20.2) Four studies found internal sphincterotomy to be superior to nitrate therapy for fissure healing after 6–8 weeks. (36–39) The two studies which showed no difference in ­fissure healing between treatment groups, were smaller and measured a larger nitrate treatment effect than is traditionally seen (83–90%). Richard and colleagues found nitrate therapy to help fissure related pain despite poor fissure healing (36). Parellada and colleagues found a posttreatment decrease in MARP from baseline in both treatment groups (30%) without a significant difference between groups.(39) Four studies found a significant rate of headaches in nitrate treated patients.(36–38, 41) These headaches caused significant problems with patient compliance and 20–30% of patients discontinued ointment application. In comparison, there were relatively few and minor side effects in patients undergoing sphincterotomy. While one study measured a high rate of postoperative incontinence to flatus (44%), this decreased to 15% after 2 years follow-up.(39) Initially, Richards et al. did not find any difference in immediate postoperative continence scores between patients treated with nitrates or sphincterotomy.(36) After 5 years, the investigators contacted 62% of the study patients. With the use of a sensitive incontinence scale, there were still no differences in continence scores between the two groups. However, 2/3 of patients reported some degree of incontinence. Finally, fissure recurrence occurred rarely in patients undergoing sphincterotomy (0–4%) compared to high rates of recurrence among patients treated with nitrates (13–45%). In all, nitrates are significantly less effective than sphincterotomy for fissure healing, acute relief of pain, fissure recurrence, and number of treatment side-effects when administered for treatment of chronic anal fissure. Calcium Channel Antagonists Given the frequency of adverse side effects with nitrate therapy, other medical treatments have been sought for patients with

chronic anal fissure. Calcium channel antagonists have been used as alternative agents for temporary chemical sphincterotomy. Calcium is necessary for tonic contraction and spontaneous activity in the IAS smooth muscle.(42) When IAS muscle is subjected to a calcium channel antagonist, nifedipine, tone and spontaneous contraction of the muscle is inhibited. Therefore, a calcium channel antagonist may reduce the IAS hypertonia that is observed in chronic anal fissure. Indeed, nifedipine has been shown to decrease anal resting pressure in normal controls and patients with anal fissure or hemorrhoids.(43) Nifedipine decreased anal resting pressure by approximately 30% in all groups. Decreased anal pressure is thought to cause increased anodermal blood flow and allow for fissure healing. Carapeti and colleagues showed that diltiazem ointment significantly reduced anal resting pressure and allowed for 67% of patients with chronic anal fissure to heal over 8 weeks. However, they were unable to measure a significant difference in anodermal blood flow using laser Doppler before and after diltiazem administration.(44) Due to the ability of calcium channel antagonists to reduce anal resting pressure, they have been used as alternatives to nitrates for chemical sphincterotomy in patients with chronic anal fissure. Calcium Channel Antagonists versus Placebo One study has compared the efficacy of a calcium channel antagonist, nifedipine to a treatment consisting of lidocaine, and hydrocortisone ointment for the treatment of chronic anal fissure.(45) (Table 20.3). One hundred and ten patients were given either 0.3% nifedipine ointment or 1.5% lidocaine plus 1.0% hydrocortisone ointment for twice daily application over 6 weeks. Patients who were given nifedipine ointment had a significant reduction in anal resting pressure (11%) from baseline after 3 weeks of treatment. In addition, 95% of these patients had a healed fissure after 6 weeks. Positive treatment effects were not seen in the placebo treatment arm with manometric studies measuring a 4.4% increase in anal resting pressure, and only 16% of patients experienced fissure healing. The patients did not report any side effects. Six percent of patients treated with nifedipine had fissure recurrence, 66% were



improved outcomes in colon and rectal surgery Table 20.3  Randomized Controlled Trials of Calcium Channel Blockers for the Treatment of Chronic Anal Fissure. Length of Treatment (weeks)

Fissure Healing (%)

Overall Side Effects (%)

6

16 vs. 95 (p < 0.001)

None



18

55 vs. 6 (p = NR)



6–8

86 vs. 77 (p = 0.21)

72 vs. 42 (p = 0.01)



3

2 vs. 0 (p = NR)

0.5 GTN vs. 2 D BID



8

86 vs. 86 (p = 0.95)

33 vs. 0 (p = NR)

None

NR

52

0.2 GTN vs. 0.2 N QID



24

58 vs. 89 (p < 0.04)

40 vs. 5 (p < 0.01)



12

31 vs. 42 (p = NR)



20

0.2 GTN vs. 20 mg PO N BID



8

70 vs. 60 (p = NS)

30 vs. 10 (p = NR)



3

0 vs. 10 (p = NR)

Shrivastava 2007 (48)



90

P vs. 0.2 GTN vs. 2 D BID



6

33 / 73 / 80 (p = <0.02)

0 / 67 / 0 (p = NR)



12

13 / 32 / 50 (p < 0.015)

Ho 2005 (51)



132

LIS vs. TS vs. 20 mg PO N BID



6

96/ 95/ 16 (p < 0.001)



4

0/ 2.4/ 57 (p = 0.003)

Katsinelos 2006 (52)



64

LIS vs. 0.5 N TID



8

100 vs. 97 (p = 0.49)

19 vs. 50 (p = NR)



20

0 vs. 7 (p = NR)

Jonas 2001 (53)



50

60 mg PO D vs. 2 D BID



8

38 vs. 65 (p = 0.09)

33 vs. 0 (p = 0.001)



6

11 vs. 7 (p = NR)

Author/ Year

Number of Patients

Treatment Groups (% ointment)

Perrotti 2002 (45)



110

1.5 lidocaine + 1.0 hydrocortisone vs. 0.3 N BID



Kocher 2002 (47)



60

0.2 GTN vs. 2 D BID

Bielecki 2003 (46)



43

Ezri 2003 (49)



Mustafa 2005 (50)

No difference in continence

Follow-up (months)

Recurrence (%)

Note: N = nifedipine; BID = two times per day; NR = not recorded; GTN = glyceryl trinitrate; D = diltiazem; QID = four times per day; NS = not statistically significant; LIS = lateral internal sphincterotomy; TS = tailored sphincterotomy; TID = three times per day.

retreated and, once again, their fissure healed. This is in comparison to 55% recurrence in the placebo arm. Of the 47 patients who did not achieve fissure healing or who suffered a recurrence after placebo treatment, 45 elected to have nifedipine treatment at the study conclusion with a 95% healing rate. While this study is promising for the use of nifedipine as an alternative to nitrate therapy for chronic anal fissure, the extent of treatment effect is questionable given the low fissure healing rate in the placebo arm. Calcium Channel antagonists versus Nitrates Five studies have compared calcium channel antagonists to nitrate therapy in patients with chronic anal fissure. (Table 20.3) Three of these studies have used 2% diltiazem ointment in comparison to 0.2% or 0.5% GTN administered over 6–8 weeks.(46–48) All three studies report no difference in anal fissure healing between the GTN or diltiazem treated groups. In all three studies, there were more overall side effects and headaches in the nitrate treated patients compared to the diltiazem treated patients. In the largest of the three studies, recurrence occurred sooner and more ­frequently among patient receiving GTN compared to diltiazem. (48) Overall, diltiazem ointment has equal efficacy to GTN ointment for anal fissure healing with fewer side effects, and possibly a lower rate and longer interval to recurrence. Two studies used nifedipine preparations for comparison with GTN for the treatment of chronic anal fissure.(49, 50) In one study, a 0.2% nifedipine ointment (49) was used while oral nifedipine was used in the other.(50) Ezri et al. found the nifedipine ointment to be superior to the GTN ointment in healing anal fissure. They also found a higher rate of overall side effects in the GTN treated group. However, both treatment arms were found to have a high recurrence rate over 12 months (31–42%). In contrast, the oral nifedipine was equivalent to GTN ointment in fissure healing,



recurrence, and side effects. These two studies demonstrate that multiple preparations of calcium channel antagonists may be used for the treatment of chronic anal ­fissure with equal healing efficacy and fewer side effects than GTN ointment. Calcium Antagonists versus Sphincterotomy Two studies have compared calcium channel blockade (oral and ointment preparations) to lateral internal sphincterotomy in the treatment of chronic anal fissure.(49, 50) (Table 20.3) While both studies measure a high rate of fissure healing in patients undergoing sphincterotomy (95–100%), there is a wide range in the fissure healing rate for patients receiving nifedipine treatment (16–97%). In one study, oral nifedipine was used.(51) The authors report a significant problem with patient compliance in this treatment arm secondary to side effects, slow fissure healing, and minimal symptomatic improvement. Overall 41% of patients in the oral nifedipine group experienced these problems, and 70% withdrew from the study. While these patients were analyzed on an intention to treat basis, the effect of oral nifedipine on fissure healing may have been substantially decreased. In contrast, Katsinelos and colleagues measured a high rate of fissure healing after treatment with nifedipine ointment (97%) that was not significantly different from fissure healing after sphincterotomy (100%, p = 0.49). (52) The increased treatment effect of nifedipine ointment may be secondary to a higher dose that was used in this study compared to others (0.5% vs. 0.2%). In addition, topical calcium channel antagonists have been proven more effective than oral preparations in fissure healing and side effect profile.(53) Overall, these studies suggest that oral calcium channel antagonists do not increase fissure healing rates but do increase side effects. However, increases in ointment concentrations may increase treatment ­efficacy without a change in adverse side effects.

surgery and nonoperative therapy of anal fissure Table 20.4  Randomized Controlled Trials of Botulinum Toxin for the Treatment of Chronic Anal Fissure. Author/ Year

Number of Patients

Treatment Groups

Fissure Healing (%)

Side Effects (%)

Follow-up (months)

Maria 1998 (57)



30

0.4 ml saline vs. 20 U B

13 vs. 73 (p = 0.003)

IC flatus: 3.3 overall



4

None

Colak 2002 (61)



62

Lidocaine BID 4 wks vs. 50 U B

21 vs. 71 (p = 0.006)

None



2

NR

Siproudis 2003 (62)



44

0.4 ml saline vs. 100 U Dysport

32 vs. 32 (p = NS)

Perianal thrombosis: 9.1 vs. 18.2 Abscess: 13.6 vs. 4.5



3

9.1 vs. 13.6 (p = NS)

Brisinda 1999 (64)



50

0.2%GTN BID 6 wks vs. 20 U Ba

60 vs. 96 (p = 0.005)

GTN: 20% HA BT: None



15

None

DeNardi 2006 (66)



30

0.2% GTN BID 8 wks vs. 20 U B

3 months: 67 vs. 47 (p = 0.51)

GTN: 20% HA BT:None



36

33 vs. 33 (p = NS)

Fruehauf 2006 (67)



50

0.2% GTN BID 2 wks vs. 30 U B

2 weeks: 52 vs. 24 (p < 0.05)

26% overall GTN: 48% HA



3

NR

Brisinda 2007 (65)

100

0.2% GTN TID 8 wks vs. 30 U Ba

70 vs. 92 (p = 0.009)

GTN: 34% HA BT: 6% IC flatus



21

20 vs. 0 (p = NR)

Mentes 2003 (71)

101

LIS vs. 0.3U/kg BT (20U or 30U) B

98 vs. 74 (p < 0.001)

IC: 8 vs. 0



12

5 vs. 11 (p = NR)

Iswariah 2005 (70)



38

LIS vs. 20 U B

6 weeks: 86 vs. 41 (p = 0.004)

IC: no difference



6

10 vs. 53 (p < 0.05)

Arroyo 2005 (69)



80

LIS vs. 25 U B

12 months: 93 vs. 45 (p < 0.001)

IC: 7.5 vs. 5 (p = NS)



36

7.5 vs. 55 (p < 0.001)

Recurrence (%)

Note: B = Botox; IC = incontinence; BID = two times per day; NR = not reported; NS = not statistically significant; GTN = Glyceryl trinitrate; HA = Headache; TID = three times per day; LIS = Lateral Internal sphincterotomy a. Crossover after 2 months treatment.

In summary, topical calcium channel antagonists may be used in the treatment of chronic anal fissure. They have similar efficacy to nitrates with a lower occurrence of side effects. Topical preparations of nifedipine or diltiazem are preferred over oral preparations due to a higher fissure healing rate and fewer side effects compared with oral administration. Sphincterotomy remains the gold standard for healing of chronic anal fissure, but given the chance for incontinence after surgery, topical calcium channel antagonists are preferred for first line therapy. Botulinum toxin Botulinum toxin (BT) is an exotoxin produced by the bacterium Clostridium botulinum. BT has been used medically in the treatment of multiple diseases in which there is muscular hypertonicity. Chronic anal fissure is characterized by internal anal sphincter (IAS) hypertonia and has been treated with BT since 1993. The exact mechanism of BT on internal anal sphincter relaxation is still unclear. In striated muscle, BT binds to presynaptic nerve terminals and prevents the release of acetylcholine, resulting in paralysis. However, in smooth muscle, BT reduces the release of excitatory neurotransmitters from sympathetic nerves and probably causes IAS relaxation through sympathetic blockade.(54) Manometric studies demonstrate a sustained decrease in mean anal resting pressure (MARP) when BT is injected into the internal anal sphincter. This sustained reduction in MARP is in contrast to the short-lived relaxation seen in response to GTN therapy. This longer period of IAS relaxation after BT injection may lead to higher rates of chronic anal fissure healing secondary to improved blood flow to the posterior commissure. Multiple studies have been performed to determine the optimal dose and method of delivery for BT to the IAS. Most studies

have been performed to determine the BT dose with the highest fissure healing rate and the least amount of complications.(55–59) All these studies show that fissure healing rates are improved with increasing BT doses. Botox doses as high as 40–50 units of have been used in a single injection. Increasing doses do not lead to higher complication rates but do lead to more significant decreases in MARP from baseline.(57) This increased efficacy is secondary to a dose dependent diffusion of the toxin through the IAS muscle. Higher BT doses have a direct effect throughout the muscle whereas smaller BT doses demonstrate a gradient of paralysis through the muscle length.(58) Other factors which may lead to variations in clinical response are differences in drug dilution volumes, number of injection sites, presence or absence of antibodies, variations in active drug, and susceptibility of target cells. Maria et al. examined the role of BT injection site on fissure healing.(60) Their hypothesis was that posterior injection of BT leads to impaired diffusion of the toxin secondary to increased fibrosis around posterior fissures. Indeed, they found that 20 units of Botox on either side of the anterior midline resulted in lower mean anal resting pressures as well as higher fissure healing rates compared to 20 units of Botox administered on either side of the posterior midline. Results from these studies show BT is safely administered in high doses (30–40 units Botox) as initial therapy and may be more effective if administered in the anterior rather than posterior midline. Botulinum Toxin versus Placebo Three randomized studies have evaluated BT efficacy in comparison to a “placebo” treatment.(61–63) (Table 20.4). In two studies, normal saline injections of a volume equal to that of the toxin used, were injected into the IAS.(62, 63) In the third



improved outcomes in colon and rectal surgery study, lidocaine ointment was applied twice daily and with bowel movements for a 4 week period.(61) In two studies, there was a significant difference in fissure healing between placebo and BT treated patients (13–21% vs. 71–73%).(61, 63) In the third, there was no measured difference in fissure healing between the two groups (32%).(62) Maria et al. also reported a 25% posttreatment decrease in MARP from baseline in the toxin group but not in the placebo group.(63) Reported side effects in these studies were minimal with incontinence to flatus in one patient, perianal thrombosis in six and perianal abscess in four of 136 total patients. The recurrence rate was not consistent among these studies with reports of no recurrence compared to a high of 13% in the BT treatment group after 4 months. The different findings in these three studies which compare BT to placebo for chronic anal fissure may be explained by methodological differences and baseline differences in the study groups at randomization. In one trial there were more men and higher maximal voluntary anal squeeze pressures in the placebo group as compared to the BT treated group.(63) This may have lead to a difference in treatment effect. Also, one trial was not able to be blinded secondary to the use of ointment in the placebo group and injection in the toxin group.(61) It is unclear whether clinicians who were grading fissure healing were blinded to randomized treatment groups. Finally, the third study was stopped early before reaching the intended sample size because of newly published studies demonstrating BT efficacy in fissure healing. Despite these methodological differences and group differences after randomization, these studies suggest that BT is superior to placebo in the healing of chronic anal fissure. Botulinum Toxin versus Nitrates Four randomized trials have compared the efficacy of BT to GTN ointment.(64–67) (Table 20.4) In each trial there were differences in the length of treatment (2–8 weeks) and application frequency (2–3 times per day) of GTN ointment. There were also differences in the dose of BT used with two studies using 20 units of Botox and the other two studies using 30 units. Two studies found a significant improvement in anal fissure healing for patients treated with BT compared to 0.2% GTN ointment (92–96% vs. 60–70%). (64, 65) A third study measured an advantage of GTN treatment administered over 2 weeks compared to BT (52% vs. 24%).(67) These findings are surprising given the previous studies which show 4–8 weeks are needed to achieve fissure healing with GTN treatment. In the fourth study, there was no difference in treatment efficacy between BT and GTN ointment administered over 8 weeks.(66) However, this is the smallest of the four studies and may not have been adequately powered to measure a difference in treatment efficacy. Patients treated with GTN ointment were more likely to suffer adverse side effects (20–34% headache) in comparison to BT treated patients (0–6% temporary incontinence to flatus). Fissure recurrence was more frequent in GTN treated patients in one study (65) but not in another.(66) In a different study, long-term fissure recurrence after BT treatment was 42% after 42 months.(68) Overall, these studies show a benefit of BT compared to GTN in terms of short term fissure healing and adverse medication effects. Frequent fissure recurrence after GTN and BT treatment has been observed.



In two studies of GTN versus BT treatment crossover was performed at 2 months.(64, 65) Patients who did not heal with their initial treatment and accepted the alternative treatment were able to achieve fissure healing with the alternative treatment In both studies, patients who failed BT and then received GTN (8 patients), experienced fissure healing within 2 months. Twenty one patients who failed GTN and then received BT achieved ­fissure healing within 2 months. These studies suggest that patients who fail initial therapy with GTN or BT, can be successfully treated with an alternative medical therapy before surgical treatment is considered. Botulinum Toxin versus Sphincterotomy There are three randomized studies which compare outcomes for patients receiving either BT or internal sphincterotomy (IS). (69–71) (Table 20.4) In these studies, IS was superior to BT for fissure healing (86–98% vs. 41–75%). While sphincterotomy is usually avoided secondary to fears of incontinence, there was no significant difference in continence scores in any of these four studies. Incontinence after fissure treatment with either BT or sphincterotomy was associated with lower mean anal resting pressures after treatment and age >50 years.(69) Fissure recurrence was also more common in BT treated patients compared to IS treated patients.(69, 70) Recurrences were seen 6–12 months after fissure healing.(69) Recurrence was associated with certain clinical and manometric risk factors. These include symptom duration greater than 12 months, presence of a sentinel pile, ­persistently elevated mean anal resting pressure and amount of time slow wave and ultra slow waves are present on manometric examination. Based on these studies, patients who are at high risk of anal fissure recurrence should undergo IS as a first line therapy. In patients who are at high risk of incontinence after IS, the first line therapy should be BT since healing can be achieved with lower complications even if repeat injection is required. Overall, BT injections can be used for the treatment of chronic anal fissure with improved fissure healing rates compared to ­placebo and GTN. Fissure healing may take longer after BT treatment when compared to fissure healing after IS, but is associated with few complications. Patients at high risk of incontinence (age> 50 yrs, previous anorectal surgery, multiparous females, diagnosis of inflammatory bowel disease) should be treated with BT before IS. Anal fissure recurrences after BT treatment are common, but can be treated with repeat BT injection without adverse effects. Surgical Therapy While surgical treatment of chronic anal fissure has been employed since the 19th century, improved pathophysiologic understanding in the middle of the 20th century, led to the reintroduction of surgical treatments. In 1964, Watts, Bennett and Goligher described stretching of the anal sphincter with finger dilation, and Eisenhammer recommended sectioning the internal anal sphincter to reduce sphincter resting pressure.(72, 73) Since their initial description, anal dilation and sphincterotomy have been used in numerous randomized controlled trials to determine the ideal ­surgical treatment for chronic anal fissure. Overall there is a clear benefit of sphincterotomy compared to anal stretch for fissure healing and postoperative incontinence. This has been confirmed in clinical trials as well as manometric evaluations. After sphincterotomy, mean

surgery and nonoperative therapy of anal fissure anal resting pressure is permanently reduced in patients with anal fissure who have been shown to have significantly elevated preoperative resting pressures compared to controls.(74) Yet, the initial surgical techniques of Watt and Eisenhammer have been revised with multiple studies comparing the efficacy of modified surgical interventions on fissure healing, recurrence, anal resting pressure, and treatment complications such as incontinence. Anal Dilatation Anal dilation has been used in three different forms for the treatment of chronic anal fissure. Gentle, graduated anal dilation has been accomplished with standardized anal dilators (20–27 mm) which are increased in size over several weeks of treatment. Anal dilation has also been achieved with a one time pneumatic ­balloon dilation of the sphincter to 1.4 atmospheres. Finally, anal dilation has been performed using anal stretch with 4–6 finger dilation of the sphincter. All these techniques have been criticized for the poorly controlled sphincter stretch that results in damage to both the internal and external sphincter. The result of uncontrolled sphincter stretch can lead to high rates of incontinence for both flatus and stool that may be permanent. In reality, each of these forms of anal dilation lead to variable degrees of control over the amount of sphincter stretch and thereby affect fissure healing, recurrence, and incontinence rates differently. The forceful anal stretch procedure has the least amount of standardization on sphincter dilation. It has been compared to the gold standard, internal anal sphincterotomy, in five randomized controlled trials.(75–79) Three of these studies found that internal sphincterotomy was superior to anal stretch secondary to higher fissure healing rates (90–97% vs. 70–71%) with significantly lower rates of incontinence (3.3–20% vs. 20–39%).(75–77) The other two studies found an advantage in fissure healing rates after anal stretch at 4 month follow-up with comparable rates of fissure recurrence and incontinence.(77, 79) However, these two studies have been criticized for high drop out rates, short followup, and question of inadequate sphincterotomy. Overall, internal sphincterotomy is superior to forceful anal stretch for the surgical treatment of chronic anal fissure. Given previous criticisms, techniques for controlled anal stretch have been developed. When graduated anal dilators are used over several weeks, the effect on fissure healing is inconsequential and not better than placebo.(80) The addition of heat to anal dilators along with nitroglycerin ointment may lead to improved fissure healing rates (94% at 12 months). (81) However, this was a small study which has not been replicated. Controlled anal stretch with increased dilation effect has been attempted with pneumatic balloon dilation. In a prospective clinical trial, Renzi and colleagues measured the effect of anal balloon dilatation to 1.4 atmospheres over six minutes. In 33 patients, 94% healed within 5 weeks of treatment, 3% recurred over 12 months and 6% of patients had transient incontinence. These treatment effects were achieved with a measureable decrease in anal resting pressure with no visible sphincter defect on endorectal ultrasound.(82) This study was followed by a randomized controlled trial of 36 patients who received either pneumatic sphincter dilatation or nitroglycerin ointment.(83) At 30 days, 95% of patient undergoing pneumatic sphincter dilation had healed fissures compared

to 40% of patients who received nitroglycerin ointment. While local wound problems such hemorrhoid thrombosis occurred in the short-term, there were no patients who complained of problems with continence after pneumatic dilation. In all, graduated anal dilation is not more effective than placebo for the treatment of chronic anal fissure, while pneumatic balloon dilation of the sphincter may result in improved fissure recurrence and incontinence rates than those seen with forceful anal dilation. Further studies of pneumatic balloon dilation are needed to see if it is in fact comparable to internal sphincterotomy. Sphincterotomy Internal sphincterotomy has also been subjected to revisions in technique. Initially, Eisenhammer described division of the external sphincter and then modified his technique to that of the internal sphincter at the posterior midline.(73) Overtime, it became apparent that fissurectomy with posterior midline sphincterotomy resulted in a “keyhole deformity” or deep furrow in the excision site which interfered with closure of the anal canal while at rest.(84) This deformity lead to increased rates of incontinence compared to lateral sphincterotomy with longer healing times. (78) Posterior sphincterotomy has subsequently been abandoned in favor of lateral internal sphincterotomy. Lateral internal sphincterotomy has also been performed in an open and closed fashion. The open technique involves a 1–2 cm skin incision over the intersphincteric groove and lateral to the anal canal.(85) The internal anal sphincter is then separated from the external sphincter and mucosa up to the dentate line so that it can be divided under direct vision. Closed internal sphincterotomy was first described by Notaras in 1969.(86) With this technique, an 11 blade scalpel is inserted through the anoderm into the intersphincteric plane. While using a finger for guidance, the surgeon rotates the blade 90 degrees and an internal sphincterotomy is ­performed upto the dentate line. Given the blind technique of closed internal sphincterotomy, surgeons have questioned the adequacy of sphincter division using this technique. In fact, closed sphincterotomy has been compared to open sphincterotomy in 4 randomized controlled trials with 299 patients.(87–90) All four studies found equivalent rates of fissure healing (90–100%), and recurrence (0–10%). Incontinence occurred infrequently (4.1– 7.5%) and improved with time. Therefore, both open and closed techniques have been shown through randomized controlled ­trials to have equal outcomes. Surgical treatment of chronic anal fissure can lead to variable rates of incontinence to gas and liquids that can be temporary or permanent. In an effort to reduce rates of incontinence after sphincterotomy, investigators have sought to determine the optimal length of sphincterotomy which allows for fissure healing but minimizes postoperative incontinence. Two randomized studies have examined the role of sphincterotomy length on fissure healing, recurrence, and incontinence. In these studies, limited sphincterotomy to the fissure apex was compared to a full sphincterotomy to the dentate line.(91–92) Fissure healing rates were similar (88–100%) in both studies. In one study there was no fissure recurrence after 24 weeks of follow-up (91), and, in the other, there was a 13.2% treatment failure rate in the limited sphincterotomy group.(92) There were also short-term differences in incontinence between

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improved outcomes in colon and rectal surgery limited versus full internal sphincterotomy. In one study, early incontinence in patients undergoing full sphincterotomy (10.9%) was increased compared to patients who underwent limited sphincterotomy (2.2%, p = 0.039). (91) However, this difference did not persist with long-term follow-up with only 2 patients who underwent full sphincterotomy reporting persistent incontinence. In the other study, there was no significant difference in posttreatment and baseline incontinence scores between the two types of sphincterotomy.(92) Overall, internal sphincterotomy up to the dentate line has been shown to produce faster healing and pain relief but is associated with increased rates of early incontinence compared to sphincterotomy to the fissure apex. Given the significant variation in incontinence rates after sphincterotomy, several investigators have sought to further characterize incontinence in patients with chronic anal fissure with respect to type, frequency, and permanence. In a study of preoperative and postoperative incontinence in 126 patients with chronic anal ­fissure, Anmari and colleagues found that 28% of patients had minor preoperative disturbances in continence that persisted postoperatively.(93) Casillas and colleagues found that patients endorsed a higher rate of incontinence in response to a questionnaire than was recorded in their medical record or was reported in a telephone survey.(94) In other studies, risk factors for incontinence were identified.(95–96) These include preexisting sphincter injuries, IAS division >50%, injury to external anal sphincter during the procedure, functional impairment with age, shorter sphincter in females, and posterior keyhole deformity. While external anal sphincter injury during anal stretch and a posterior keyhole deformity after posterior sphincterotomy clearly result in higher rates and more severe forms of incontinence, the presence of other risk factors in patients who are undergoing lateral internal sphincterotomy result in lower rates of minor incontinence which are frequently temporary. In fact, some incontinence scales are so sensitive to changes in continence, that one study identified no impairment in quality of life despite decreases in continence scores.(97) Overall, incontinence after sphincterotomy remains a real complication that must be considered in patients at higher risk (female, older age, previous anorectal surgery) with subsequent modification of the surgical procedure if necessary. Refractory fissures Several recent studies have been performed to identify characteristics associated with fissure persistence despite treatment. In one study the etiologic and manometric differences between anterior and posterior anal fissures which failed to heal with nitrate therapy were examined. When comparing patients with both anterior and posterior fissure who failed medical therapy, Jenkins and ­colleagues found that anterior fissures were more common in younger women (33 years vs. 44) and were more likely to be associated with obstetric trauma and an occult external anal sphincter defect.(98) Patients with anterior fissure were also more likely to have normal or low anal resting pressures compared to controls. This was ­significantly different from the elevated resting pressures measured in patients with posterior fissure. In addition, the maximum squeeze pressure was significantly lower than normal controls and patients with posterior fissure. Corby and colleagues also found that postpartum females have lower anal resting pressure and squeeze pressures than

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they did antepartum.(99) Thus, postpartum females who develop anal fissure (9% incidence) have reduced anal canal resting pressure and treatments to decrease internal sphincter tone can lead to incontinence. Other investigators have sought to identify medical therapy that can act as rescue treatments for patients with persistent anal fissure before a surgical treatment is undertaken. In one study 2% diltiazem ointment was used for treatment of chronic anal fissure refractory to GTN.(100) Fissure healing occurred in 49% of patients with no recurrence over 8 weeks of follow-up. Healing was not dependent on whether a full course of GTN was ­completed with fissure persistence or GTN treatment was discontinued secondary to adverse side-effects. In two other studies BT was used to treat nitrate resistant fissures (GTN and ISDN). (101, 102) Forty-three to 50% of patients with nitrate resistant fissures achieved healing with BT treatment. Patients with nitrate resistant fissures have also been randomized to another course of nitrates or nitrates plus BT.(103, 104) More patients healed their fissures with a combination of BT and nitrates (47–67%) compared to BT alone (20–27%). More studies are needed to determine the optimal treatment for refractory or persistent fissures. Alternative surgical therapies are available for chronic anal fissure associated with low anal resting pressure or for those that persistent after surgical sphincterotomy. These include island advancement flaps. Nyam and colleagues described advancement flaps in a series of patients with low anal resting pressure and maximum squeeze pressure.(105) Some patients had external sphincter defects and others had previous fissure surgery. Patients underwent fissurectomy with flap coverage by perianal skin. All 20 patients healed with one contracture at the donor site and minimal donor site discomfort. Leong et al. compared anal advancement flap to lateral internal sphincterotomy for the treatment of chronic anal fissure.(106) More patients healed with sphincterotomy (100%) compared to anal advancement flap (85%). A number of flaps, such a V-Y anoplasty, have been described for chronic anal fissure with good success (Figure 20.2). A key to reducing complications with flap closure is careful hemostasis, which reduces the risk of hematoma formation, flap loss, and infection. Design of the flap with good length-to-width ratio is important to ensure adequate vascularity and minimal tension. (107) Anal advancement flaps remain an important surgical alternative for patients with low pressure fissures and persistent fissure despite previous anorectal surgery. Complications of Surgery for Anal Stenosis Acquircd anal stenosis can be a late sequela of a variety of anorectal surgical procedures. It has been reported to occur after 5 to 10% of radical hemorrhoidectomies and after fissurectomy, radiation injury, and Moh’s chemosurgery.(108, 109) The cause of these strictures is excessive removal of the anodermal lining of the anal canal: and thus is generally preventable. In cases of severe, symptomatic anal stenosis, a variety of flaps can be used to resurface the anal canal and expand its circumference. The key to success with any of these flaps is that they be carefully designed to maintain vascularity and that subflap hematoma formation is averted to minimize the risk for infection and flap necrosis.

surgery and nonoperative therapy of anal fissure (A)

(B)

Figure 20.2  V-Y anoplasly. (A) Incisions create a V-shaped or triangular flap which is advanced to close defect. (B) Closure of skin behind “V” pushes the flap into the anal canal, and the flap is sutured in place.

(A)

(B)

(C)

Figure 20.3  Ana1 S-plasty. (A) Ectroion is excised and S-shaped incisions are created. (B) and (C) flaps are rotated lo close the defects and sutured in place.

Patients should undergo complete mechanical and antibiotic bowel preparation before surgery. After surgery, bowel activity may be restricted with a clear liquid diet for a day or two. After this period, patients are allowed a regular diet and given fiber supplements and laxatives to avert constipation One final, important point is the limitation of patient activity for several weeks so that flap motion is minimal, to allow neovascularity to occur Anal S-plasty (Figure. 20.3) was first proposed by Ferguson (110) as a method to correct Whitehead deformities in 13 patients. Later Corman et al. (111) modified the procedure for use in the management of anal stenosis. The key to the success of this approach is development of ’ large, full-thickness skin flaps with a base-to-length ratio >1.0. Ferguson recommended a base of 7 to 10 cm and maintenance of a thin layer of fat globules on the deep aspect of the flap so that adequate vascularity can be ensured. He further cautioned against overzealous hemostasis on the flap itself so as not to impair blood flow. The flaps are then rotated toward the anal canal so that the anodermal defect can be resurfaced. The flaps are sutured in place, and the remaining semilunar defect is sutured to allow its primary healing. It is wise

to use a closed suction drain beneath the flap to avert seroma or hematoma formation. For less severe anal strictures that require less skin coverage, the Y-V anoplasty, is an excellent alternative because it is simple to perform and is less traumatic for the patient. This technique was initially described by Penn (112) in 1948. Again, successfu1 healing of the flap requires a length-to-base ration <3.0. Gingola and Arvanitis (113) presented a series of 14 patients. Thirteen healed within 14 days with no episodes of infection or hematoma formation. Five patients sloughed a small portion of the flap tip but required no additional treatment. Experiences reported by other authors support the low rate (10 to 25%) of tip necrosis and the high rate (85 to 92%) of stenosis relief associated with this technique (114, 115). It must be remembered, however that Y-V advancement flaps limit how much anal resurfacing can be accomplished. Other uses for the Y-V advancement flap have been advocated. Rosen (116) used it to treat anal stcnosis and ectropion (Figure 20.4).The blood supply for this flap is based on perforating vessels in the subcutaneous fat. The Y-V advancemcnt flap is well suited for covering the lower anal canal but has limited application for stenosis above the dentate line.

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improved outcomes in colon and rectal surgery (B)

(A)

(C)

Figure 20.4  Y-V anoplasty. (A) Y shaped incision is made. (B) V-shaped flap is mobilized and advanced to the top of the defect. (C) Flap is and sutured in place.

(A)

(B)

(C)

Figure 20.5  House advancement flap. (A) House-shaped flap is created. (B) The flap is advanced into the anal canal and (C) sutured in place.

(A)

(B)

(C)

Figure 20.6  Diamond flap. (A) Diamond-shaped flap is created. (B) The flap is advanced into the anal canal to fill the defect. (lnsert demonstrates perforating subcutaneous blood supply). (C) Flap is sutured in place.

Other techniques of flap formation have been suggested. Christensen et al. (117). proposed the use of “house” advancement pedicle flaps. The editors prefer the house flap because it is easy to construct, can cover as much as 25% of the anal circumference, and permits primary closure of the donor site (Figure 20.5). If additional coverage is needed, two, three, or four flaps may be used. Caplin and Kodner (118) recommended the use of the diamond flap for many of the same reasons (Figure 20.6).

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Conclusion Chronic anal fissure is a common and painful anorectal disorder. Many treatments are available for benign idiopathic fissures. The goal of treatment is to reduce the high anal resting pressure or internal sphincter hypertonia in fissure patients. First line therapy consists of either topical nitrates or calcium channel antagonists. If topical therapies fail, a repeat treatment course can be prescribed. As second line therapy, botulinum

surgery and nonoperative therapy of anal fissure toxin injection or internal sphincterotomy can be performed. Ideally, patients who are at risk of incontinence after internal anal sphincter division should attempt medical therapy (age>50, multiparous female, previous anorectal surgery). If sphincterotomy is contemplated for high risk patients, preoperative anal manometry and ultrasound should be considered. Alternatively, fissurectomy with anal advancement flap can be performed. There is scarce data on the ideal treatment for resistant anal fissure. Patients at high risk of fissure persistence may be considered for internal sphincterotomy as first line therapy (symptom duration >12 months, presence of a sentinel pile, persistently elevated mean anal resting pressure). References    1. Oh C, Divino DM, Steinhagen RM. Anal Fissure:20 year experience. Dis Colon Rectum 1995; 38: 378–82.    2. Pescatori M, Interisano A. Annual report of the Italian coloproctology units. Tech Coloproctol 1995; 2: 29–30.    3. Gibbons CP, Read NW. Anal hypertonia in fissures:cause or effect? Br J Surg June 1986; 73(6): 443–45.    4. Klosterhalfen B, Vogel P, Rixen H, Mittermayer C. Topography of the inferior rectal artery: a possible cause of chronic, primary anal fissure. Dis Colon Rectum 1989; 32(1): 43–52.    5. Schouten WR, Briel JW, Auwerda JJ. Relationship between anal pressure and anodermal blood flow: the vascular pathogenesis of anal fissures. Dis Colon Rectum 1994; 37(7): 664–9.    6. Brisinda G, Albanese A, Cadeddu F et al. Botulinum neurotoxin to treat chronic anal fissure:results of a randomized ‘Botox vs. Dysport’ controlled trial. Aliment Pharmacol Ther 2004; 19: 695–701.    7. Nelson R. A systematic review of medical therapy for anal fissure. Dis Colon Rectum 2004; 47: 422–31.    8. Nelson R. Meta-analysis of operative techniques for fissure-inano. Dis Colon Rectum 1999; 42: 1424–31.    9. Nelson R. Nonsurgical therapy for anal fissure. Cochrane Database Syst Rev 2006; 4: CD003431.   10. Nelson R. Operative procedures for fissure in ano. Cochrane Database Syst Rev 2005; 2: CD002199.   11. Gough MJ, Lewis A. The conservative treatment of fissure-inano. Br J Surg 1983; 70: 175–6.   12. Orsay C, Rakinic J, Perry WB et al. Practice parameters for the management of anal fissures (revised). Dis Colon Rectum 2004; 47: 2003–7.   13. Jensen SL. Treatment of first episodes of acute anal ­fissure: prospective randomized study of lignocaine ointment ­versus hydrocortisone ointment or warm sitz baths plus bran. Br Med J (Clin Res Ed) 1986; 292(6529): 1167–9.   14. Jensen SL. Maintenance therapy with unprocessed bran in the prevention if acute anal fissure recurrence. J Royal Soc Med 1987; 80(5): 296–8.   15. Gupta PJ. Randomized, controlled study comparing sitz bath and no sitz bath treatments in patients with acute anal fissures. ANZ J Surg 2006; 76: 718–21.   16. McDonald P, Driscoll AM, Nicholls RJ. The anal dilator in the conservative management of acute anal fissures. Br J Surg 1983; 70: 25–6.

  17. Bacher H, Mischinger HJ, Werkgartner G et al. Local nitroglycerin for treatment of anal fissures: an alternative to lateral sphincterotomy? Dis Colon Rectum 1997: 40(7): 840–5.   18. Antropoli C, Perrotti P, Rubino M et al. Nifedipine for local use in conservative treatment of anal fissures. Dis Colon Rectum 1999; 42(8): 1011–5.   19. Garrido R, Lagos N, Lattes K et al. Gonyautoxin: New treatment for acute and chronic anal fissures. Dis Colon Rectum 2005; 48(2): 335–43.   20. O’Kelly T. Brading A, Mortensen N. Nerve mediated relaxation of the human internal anal sphincter: role of nitric oxide. Gut 1993; 34: 689–93.   21. Loder PB, Kamm MA, Nicholls RJ, Phillips RKS. ‘Reversiable chemical sphincterotomy’ by local application of glyceryl trinitrate. Br J Surg 1994; 81: 1386–9.   22. Schouten WR, Briel JW, Boerma MO et al. Pathophysiological aspects and clinical outcome of intra-anal application of isosorbide dinitrate in patients with chronic anal fissure. Gut 1996; 39: 465–9.   23. Thornton MJ, Kennedy ML, King DW. Manometric effect on topical glyceryl trinitrate and its impact on chronic anal fissure healing. Dis Colon Rectum 2005; 48: 1207–12.   24. Lund JN, Scholefield JH. A randomized, prospective, doubleblind, placebo controlled trial of glyceryl trinitrate ointment in treatment of anal fissure. Lancet 1997; 349: 11–4.   25. Chaudhuri S, Pal AK, Acharya A et al. Treatment of chronic anal fissure with topical glyceryl trinitrate: a double-blind, placebo-controlled trial. Indian J Gastroenterol 2001; 20(3): 101–2.   26. Altomare DF, Rinaldi M, Milito G et al. Glyceryl trinitrate for chronic anal fissure-healing or headache? Dis Colon Rectum 2000; 43: 174–81.   27. Kennedy ML, Sowter S, Nguyen H, Lubowski DZ. Glyceryl trinitrate ointment for the treatment of chronic anal ­fissure: results of a placebo-controlled trial and long-term ­follow-up. Dis Colon Rectum 1999; 42(8): 1000–6.   28. Maan MS, Mishra R, Thomas S, Hadka NS. Randomized, double-blind trial comparing topical nitroglycerin with xylocaine and proctosedyl in idiopathic chronic anal fissure. Indian J Gastroenterol 2004; 23: 91–3.   29. Carapeti EA, Kamm MA, McDonald PJ et al. Randomised controlled trial shows that glyceryl trinitrate heals anal ­fissures, higher doses are not more effective, and there is a high recurrence rate. Gut 1999; 44: 727–30.   30. Bailey HR, Beck DE, Billingham RP et al. A study to determine the nitroglycerin ointment dose and dosing interval that best promote the healing of chronic anal fissures. Dis Colon Rectum 2002; 45(9): 1192–9.   31. Scholefield JH, Bock JU, Marla B et al. A dose finding study with 0.1%, 0.2% and 0.4% glyceryl trinitrate ointment in patients with chronic anal fissures. Gut 2003; 52(2): 264–9.   32. Wierre AJ, Palamba HW, Spillenaar Bilgen EJ, Eggink WF. Isosorbide dinitrate in the treatment of anal fissure: a randomised, prospective, double blind, placebo-controlled trial. Eur J Surg 2001; 167: 382–5.

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improved outcomes in colon and rectal surgery   33. Tankova L, Yoncheva K, Muhtarov M, Kadyan H, Draganov V. Topical mononitrate treatment in patients with anal fissure. Aliment Pharmacol Ther 2002; 16: 101–3.   34. Colak T, Ipek T, Urkaya N, Kanik A, Dirlik M. A randomized study comparing systemic transdermal treatment and local application of glyceryl trinitrate ointment in the management of chronic anal fissure. Eur J Surg 2002; Suppl 588: 18–22.   35. Zuberi BF, Rajput MR, Abro H, Shaikh SA. A randomized trial of glyceryl trinitrate ointment and nitroglycerin patch in healing of anal fissures. Int J Colorectal Dis 2000; 15: 243–5.   36. Richard CS, Gregoire R, Plewes EA et al. Internal sphincterotomy is superior to topical nitroglycerin in the treatment of chronic anal fissure. Dis Colon Rectum 2000; 43: 1048–58.   37. Evans J, Luck A, Hewett P. Glyceryl trinitrate vs. lateral sphincterotomy for chronic anal fissure. Dis Colon Rectum 2001; 44: 93–7.   38. Libertiny G, Knight JS, Farouk R. Randomised trial of topical 0.2% glyceryl trinitrate and lateral internal sphincterotomy for the treatment of patients with chronic anal fissure: longterm follow-up. Eur J Surg 2002; 168: 418–21.   39. Parellada C. Randomized, prospective trial comparing 0.2 percent isosorbide dinitrate ointment with sphincterotomy in treatment of chronic anal fissure: a 2 year follow-up. Dis Colon Rectum 2004; 47: 437–43.   40. Oettle GJ. Glyceryl trinitrate vs. sphincterotomy for treatment of chronic fissure in ano. Dis Colon Rectum 1997; 40(11): 1318–20.   41. Mishra R, Thomas S, Maan MS, Hadke NS. Topical nitroglycerin versus lateral internal sphincterotomy for chronic anal fissure: prospective, randomized trial. ANZ J Surg 2005; 75: 1032–5.   42. Cook TA, Brading AF, McC. Mortensen NJ. Differences in contractile properties of anorectal smooth muscle and the effects of calcium channel blockade. Br J Surg 1999; 86: 70–5.   43. Chrysos E, Xynos E, Tzovaras G et al. Effect of nifedepine on rectoanal motility. Dis Colon Rectum 1996; 39: 212–6.   44. Carapeti EA, Kamm MA, Evans BK, Phillips RK. Topical diltiazem and bethanechol decrease anal sphincter pressure without side effects. Gut 1999; 45: 719–22.   45. Perotti P, Bove A, Antropoli C et al. Topical nifedipine with lidocaine ointment vs. active control for the treatment of chronic anal fissure: results of a prospective, randomized, double-blind study. Dis Colon Rectum 2002; 45: 1468–75.   46. Bielecki K, Kolodziejczak M. A prospective randomized trial of diltiazem and glyceryl trinitrate ointment in the treatment of chronic anal fissure. Colorectal Disease 2003; 5: 256–7.   47. Kocher HM, Steward M, Leather AJM, Cullen PT. Randomized clinical trl assessing the side effects of glyceryl trinitrate and diltiazem hydrochloride in the treatment of chronic anal fissure. Br J Surg 2002; 89: 413–7.   48. Shrivastava UK, Jain BK, Kumar P, Saifee Y. A comparison of the effects of diltiazem and glyceryl trinitrate ointment in the treatment of chronic anal fissure: a randomized clinical trial. Surg Today 2007; 37: 482–5.   49. Ezri T, Susmallian S. Topical nifedipine versus topical glyceryl trinitrate for treatment of chronic anal fissure. Dis Colon Rectum 2003; 46: 805–8.

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  50. Mustafa NA, Cengiz S, Turkyilmaz S, Yucel Y. Comparison of topical glyceryl trinitrate ointment and oral nifedipine in the treatment of chronic anal fissure. Acta Chir Belg 2005; 105: 55–8.   51. Ho KS, Ho YH. Randomized clinical trial comparing oral nifedipine with lateral anal sphincterotomy and tailored sphincterotomy in the treatment of chronic anal fissure. Br J Surg 2005; 92: 403–8.   52. Katsinelos P, Papaziogas B, Koutelidakis I et al. Topical 0.5% nifedipine vs. lateral internal sphincterotomy for the treatment of chronic anal fissure: long-term follow-up. Int J Colorectal Dis 2006; 21: 179–83.   53. Jonas M, Neal K, Abercrombie JF, Scholefield JH. A randomized trial of oral vs. topical diltiazem for chronic anal fissures. Dis Colon Rectum 2001; 44: 1074–8.   54. Jones OM, Brading AF, Mortensen NJ. Mechanism of action of botulinum toxin on the internal anal sphincter. Br J Surg 2004; 91(2): 224–8.   55. Fernandez LF, Conde Freire R, Rios Rios A et al. Botulinum toxin for the treatment of anal fissure. Dig Surg 1999; 16(6): 515–8.   56. Espi A, Melo F, Minguez M et al. Therapeutic use of botulinum toxin in anal fissure. Int J Colorectal Dis 1998; 12: 163.   57. Maria G, Brisinda G, Bentivoglio AR et al. Botulinum toxin injections in the internal anal sphincter for the treatment of chronic anal fissure: long-term results after two different dosing regimens. Ann Surg 1998; 228(5): 664–9.   58. Brisinda G, Maria G, Sganga G et al. Effectiveness of higher doses of botulinum toxin to induce healing in patients with chronic anal fissures. Surgery 2002; 131: 179–84.   59. Minguez M, Melo F, Espi A et al. Therapeutic effects of different doses of botulinum toxin in chronic anal fissure. Dis Colon Rectum 1999; 42: 1016–21.   60. Maria G, Brisinda G, Bentivoglio AR et al. Influence of botulinum toxin site of injections on healing rate in patient with chronic anal fissure. Am J Surg 2000; 179; 46–50.   61. Colak T, Ipek T, Kanik A, Aydin S. A randomized trial of botulinum toxin vs. lidocain pomade for chronic anal fissure. Acta Gastroenterol Belg 2002; 65(4): 187–90.   62. Siproudhis L, Sebille V, Pigot F et al. Lack of efficacy of botulinum toxin in chronic anal fissure. Aliment Pharmacol Ther 2003; 18: 515–24.   63. Maria G, Cassetta E, Gui D et al. A comparison of botulinum toxin and saline for the treatment of chronic anal fissure. N Engl J Med 1998; 338: 217–20.   64. Brisinda G, Maria G, Bentivoglio AR et al. A comparison of injections of botulinum toxin and topical nitroglycerin ointment for the treatment of chronic anal fissure. N Engl J Med 1999; 341: 65–9.   65. Brisinda G, Cadeddu F, Brandara F, Marniga G, Maria G. Randomized clinical trial comparing botulinum toxin injections with 0.2 percent nitroglycerin ointment for chronic anal fissure. Br J Surg 2007; 94: 162–7.   66. De Nardi P, Ortolano E, Radaelli G, Staudacher C. Comparison of glycerine trinitrate and botulinum toxin-a for the treatment of chronic anal fissure:long-term results. Dis Colon Rectum 2006; 49: 427–32.

surgery and nonoperative therapy of anal fissure   67. Fruehauf H, Fied M, Wegmueller B, Bauerfeind P, Thumshirn M. Efficacy and safety of botulinum toxin a injection compared with topical nitroglycerin ointment for the treatment of chronic anal fissure: a prospective randomized study. Am J Gastroenterol 2006; 101: 2107–12.   68. Minguez M, Melo F, Epsi A et al. Longterm followup of CAF after healing with BT. Gastroenterology 2002; 123: 112–7.   69. Arroyo A, Perez F, Serrano P et al. Surgical versus chemical (botulinum toxin) sphincterotomy for chronic anal fissure: long-term results of a prospective randomized clinical and manometric study. Am J Surg 2005; 189: 429–34.   70. Iswariah H, Stephens J, Rieger N, Rodda D, Hewett P. Randomized prospective controlled trial of lateral internal sphincterotomy versus injections of botulinum toxin for the treatment of idiopathic fissure in ano. ANZ J Surg 2005; 75: 553–5.   71. Mentes BB, Irkorucu O, Akin M, Leventoglu S, Tatlicioglu E.Comparison of botulinum toxin injection and lateral internal sphincterotomy for the treatment of chronic anal fissure. Dis Colon Rectum 2003; 46: 232–7.   72. Watts JM, Bennett RC, Goligher JC. Stretching of the anal sphincters in the treatment of chronic fissure-in-ano. BMJ 1965; 2: 342–3.   73. Eisenhammer S. The surgical correction of chronic anal (sphincteric) contracture. S Afr Med J 1951; 25: 486–9   74. Chowcat NL, Araujo JGC, Boulos PB. Internal sphincterotomy for chronic anal fissure: long term effects on anal pressure. Br J Surg 1986; 73: 915–6.   75. Jensen SL, Lund F, Nielson OV, Tange G. Lateral subcutaneous sphincterotomy versus anal dilatation in the treatment of fissure in ano in outpatients: a prospective randomized study. BMJ 1984; 289: 528–30.   76. Olsen J, Mortensen PE, Krogh Peterson I, Christiansen J. Anal sphincter function after treatment of fissure-in-ano by lateral subcutaneous sphincterotomy versus anal dilation. Int J Colorectal Dis 1987; 2: 155–7.   77. Marby M, Alexander-Williams J, Buchman P et al. A randomized controlled trial to compare anal dilation with lateral ­subcutaneous sphincterotomy for anal fissure. Dis Colon Rectum 1979; 22: 308–11.   78. Saad AM, Omer A. Surgical treatment of chronic anal fissure-in-ano: a propetive randomised study. East Afr Med J 1992; 69(11): 613–5.   79. Weaver RM, Ambrose NS, Alexander-Williams J, Keighley RB. Manual dilatation of the anus vs. lateral subcutaneous sphincterotomy in the treatment of chronic fissure-in-ano: results of a prospective, randomized clinical trial. Dis Colon Rectum 1987; 30: 420–3.   80. Gough MJ, Lewis A. The conservative treatment of fissure-inano. Br J Surg 1983; 70: 175–6.   81. Di Visconte MS, Di Bella R, Munegato G. Randomized, prospective trial comparing 0.25 percent glycerin trinitrate ointment and anal cryothermal dilators only with 0.25 percent glycerin trinitrate ointment and only with anal cryothermal dilators in the treatment of chronic anal fissure: a two year follow-up. Dis Colon Rectum 2006; 49: 1822–30.

  82. Renzi A, Brusciano L, Pescatori M et al. Pneumatic ballon dilation for chronic anal fissure: a prospective, clinical, endosonographic and manometric study. Dis Colon Rectum 2005; 48: 121–6.   83. Boschetto S, Giovannone M, Tosoni M, Barberani F. Hydro­ pneumatic anal dilation in conservative treatment of chronic anal fissure:clinical outcomes and randomized comparison with topical nitroglycerin. Tech Coloproctol 2004; 8: 89–93.   84. Abcarian H. Surgical Correction of chronic anal fissure: results of lateral internal sphincterotomy vs. fissurectomymidline sphincterotomy. Dis Colon Rectum 1980; 23: 31–6.   85. Parks A. The management of fissure in ano. Hosp Med 1967; 1: 737.   86. Notaras MJ. Lateral subcutaneous sphincterotomy for anal fissure- a new technique. Proc R Soc Med 1969; 62: 713.   87. Boulos PB, Araujo JGC. Adequate internal sphincterotomy for chronic anal fissure: subcutaneous or open technique? Br J Surg 1984; 71: 360–2.   88. Kortbeek JB, Langevin JM, Khoo REH, Heine JA. Chronic fissure in ano: a randomized study comparing open and subcutaneous lateral internal sphincterotomy. Dis Colon Rectum 1992; 35: 835–7.   89. Arroyo A, Perez F, Serrano P, Candela F. Open versus closed lateral sphincterotomy performed as an outpatient procedure under local anesthesia for chronic anal fissure: prospective randomized study of clinical and manometric longterm results. J Am Coll Surg 2004; 199: 361–7.   90. Wiley M, Day P, Rieger N, Stephens J, Moore J. Open vs. closed lateral internal sphincterotomy for idiopathic fissure-inano: A prospective, randomized, controlled trial. Dis Colon Rectum 2004; 47: 847–52.   91. Elsebae MMA. A study of fecal incontinence in patients with chronic anal fissure: prospective, randomized, controlled trial of the extent of internal anal sphincter division during lateral sphincterotomy. World J Surg 2007; 31: 2052–7.   92. Bulent Mentes B, Ege B, Leventoglu S, Oguz M, Karadag A. Extent of lateral internal sphincterotomy: up to the dentate line or up to the fissure apex? Dis Colon Rectum 2005; 48: 365–70.   93. Ammari FF, Bani-Hani KE. Faecal incontinence in patients with anal fissure: a consequence of internal sphincterotomy or a feature of the condition? Surgeon 2004; 2(4): 225–9.   94. Casillas S, Hull TL, Zutshi M et al. Incontinence after lateral sphincterotomy: Are we underestimating it? Dis Colon Rectum 2005; 48: 1193–9.   95. Garcia-Aguilar J, Belmonte Montes J, Perez JJ et al. Incontinence after lateral internal sphincterotomy:anatomic and functional evaluation. Dis Colon Rectum 1998; 41: 423–7.   96. Rosa G, Lolli R, Piccinelli D et al. Calibrated lateral internal sphincterotomy for chronic anal fissure. Tech Coloproctol 2005; 9: 127–32.   97. Hyman N. Incontinence after lateral internal sphincterotomy: a prospective study and quality of life assessment. Dis Colon Rectum 2004; 47: 35–8.   98. Jenkins JT, Urie A Molloy RG. Anterior anal fissures are associated with occult sphincter injury and abnormal sphincter function. Colorectal Dis 2008; 10(3): 280–5.

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improved outcomes in colon and rectal surgery   99. Corby H, Donnelly VS, O’Herlihy C, O’Connell PR. Anal canal pressures are low in postpartum anal fissure. B J Surg 1997; 84: 86–8. 100. Jonas M, Speake W, Scholfield JH. Diltiazem heals glyceryl trinitrate-resistant chronic anal fissures. Dis Colon Rectum 2002; 45: 1091–5. 101. Lindsey I, Jones OM, Cunningham C, George BD, Mortensen NJM. Botulinum toxin as second line therapy for chronic anal fissure failing 0.2 glyceryl trinitrate. Dis Colon Rectum 2003; 46: 361–6. 102. Witte ME, Klaase JM. Botulinum toxin A injection in ISDN ointment-resistant chronic anal fissures. Dig Surg 2007; 24: 197–201. 103. Lysy J, Israeli-Yatzkan Y, Sestiery-Ittah M et al. Topical nitrates potentiate the effect of botulinum toxin in the treatment of patients with refractory anal fissure. Gut 2001; 48: 221–4. 104. Jones OM, Merrie A, Cunningham C et al. Randomized clinical trial of botulinum toxin plus glyceryl trinitrate vs. botulinum toxin alone for medically resistant chronic anal fissure: overall poor healing rates. Dis Colon Rectum 2006; 49: 1574–80. 105. Nyam DCNK, Wilson RG, Stewart KJ, Farouk R, Bartolo DCC. Island advancement flaps in the management of anal fissures. B J Surg 1995; 82: 326–8. 106 Leong AF, Seow-Choen F. Lateral sphincterotomy compared with anal advancement flap for chronic anal fissures. Dis Colon Rectum 1995; 38: 69–71.

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107. Fleshman JW. Fissure in ano and anal stenosis. In: Beck DE, Wexner SD, eds. Fundamentals of Anorectal Surgery,New York: McGraw-Hill, 1992: 170–82. 108. Leong AFPK, Seow-Choen F. Lateral sphincterotomy compared with anal advancement flap for chronic anal fissure. Dis Colon Rectum 1995; 38: 69–71. 109. Oh C, Albanese C. S-plasty for various anal lesions. Am J Surg 1992; 163: 606–8. 110. Ferguson JA. Repair of “Whitehead defornllty” of the anus. Sur’g Gynecol Obstet 1959; 108: 115–6. 111. Corman ML, Veidenheimer MC, Coller JA. Anoplasty for anal stricture. Surg Clin North Am 1976; 56: 727–31. 112. Penn JA. A case of anal reconstruction by means of local skin flaps. Br J Plast Surg 1948; 1: 87–8. 113. Gingold BS, Arvanitis M. V-V anoplasty for treatment of anal stricture. Surg Gynecol Obstet 1986; 162: 241–2. 114. Angelchik PD, Harms BA, Starling JR. Repair of anal stricture and mucosal ectropion with V-V or pedicle flap anoplasty. Am J Surg 1993; 166: 55–9. 115. Ramanujan PS, Venkatesh KS, Cohen M. V-V anoplasty for severe anal stenosis. Contemp Surg 1988; 3: 62–8. 116. Rosen L. V- Y advancement for anal ectropion. Dis Colon Rectum 1986; 29: 596–8. 117. Christensen MA, Pitsch RM, Cali RL, Blatchford GJ, Thorson AG. “House” advancement pedicle flap for anal stenosis. Dis Colon Rectum 1992; 35: 201–3. 118. Caplin DA, Kodner IJ. Repair of anal stricture and mucosal ectropion by simple flap procedures. Ills Colon Rectum 1986; 29: 92.

21

Surgery for pilonidal disease and hidradenitis suppurativa Paula I Denoya and Eric G Weiss

Challenging Case A 35-year-old healthy male undergoes pilonidal cystectomy by wide local excision down to sacral fascia. Six months postoperatively his wound has failed to heal as manifest by a persistent 4 × 4 cm by 2 cm deep granulation bed. Case Management The patient has a nonhealing pilonidal wound. Options include surgical reexcision with intensive postop wound management or some type of excision and flap closure as described in this chapter. INTRODUCTION Pilonidal disease and hidradenitis suppurativa are both conditions affecting the perianal area, and therefore are often referred to the colorectal surgeon for management. The management of these diseases can be quite challenging. Both conditions may be complicated by recurrent disease and may result in significant scarring or large open wounds in the perianal or coccygeal area. Pilonidal Disease Pilonidal disease is a chronic suppurative condition which occurs most commonly in the sacrococcygeal area. It typically presents as a painless cyst or sinus opening in the gluteal cleft, as an acute or recurrent abscess, or as chronic draining sinuses. It most commonly affects Caucasian males between the ages of 15 and 30 and is essentially not seen after the age of 45. The true incidence is unknown, but pilonidal disease is responsible for the loss of ­significant healthcare resources and workhours. Historical Perspective Pilonidal disease is believed to have been first described by Mayo (1) in 1833. The term “pilonidal,” originating from the Latin words for “hair” and “nest,” was not coined until 1880 by Hodges. (2) The disease became more widely known during World War II, when the number of soldiers developing it put a burden on the military. At this point, it acquired the name of “jeep disease;” a term coined by Buie (3) based on the idea that the disease was caused by trauma to the skin of the lower back from riding in jeeps for extended periods of time under hot and sweaty conditions. Early in the documented history of this disease, the etiology was believed to be congenital. The pilonidal cysts and sinuses were thought to be embryologic remnants resulting from failed involution of the neural tube structures. This theory was supported by studies of fetuses, which identified remnants of midline structures. It was believed that these structures would normally involute before birth, but sometimes failed to do so and led to the development of pilonidal sinuses.(4) In 1946, Patey (5) introduced a theory of an acquired etiology for pilonidal disease, suggesting that hair piercing into the sacrococcygeal skin caused the sinuses and infected cysts. This acquired

Figure 21.1  Pilonidal cyst opened after excision showing hair inside cyst cavity.

theory was later supported by other studies (6–8) and is now widely accepted as the etiology of pilonidal disease. Loose hairs from the head or back fall and accumulate in the gluteal cleft. The hairs are then drilled into the skin deep in the cleft by friction from the buttocks rubbing together while walking. As the person ambulates, the hairs get pulled into the sinus, creating a cyst containing hair and debris. This can periodically get infected and drain spontaneously through lateral sinus tracts, or present acutely as an abscess. Studies of surgical specimens have found cysts containing hair and debris, but hair follicles have never been found in the cyst wall itself, supporting the theory that the hair is of external origin.(9) (Figure 21.1) Bascom studied the midline pits and believed that these are likely enlarged hair follicles which are involved in the etiology of the disease.(10) He theorized that ingrown hairs originating in these midline gluteal hair follicles were pushed into the subcutaneous fat and resulted in pilonidal abscess. Pilonidal disease has also rarely been described in other areas of the body, such as the hands of barbers (11), sheep shearers (12), and others who handle loose hairs.(13) This further supports the acquired nature of the disease. Diagnosis The diagnosis is made by physical examination in a patient who generally fits the demographics of being hirsute and in the 2nd or 3rd decade of life. Characteristic findings on exam are small midline pits at the superior aspect of the gluteal cleft, approximately 3–5 cm from the anus. (Figure 21.2) There may be only one or multiple pits present, and there may be tufts of hair or debris in them. Some patients may also have lateral fistula openings which can

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improved outcomes in colon and rectal surgery

Figure 21.2  Chronic pilonidal disease showing midline pit.

periodically drain purulent discharge. In the acute presentation, the patient may present with an abscess which is usually found just off the midline, along with the typical finding of midline pits. (Figure 21.3) The differential diagnosis includes perianal abscess or fistula, hidradenitis suppurativa, and other presacral or spinal lesions such as chordoma or ependymoma. However, pilonidal disease can usually be identified by its characteristic location in the gluteal cleft away from the anus, and by the presence of midline pits. In severe cases where there is doubt, imaging with CT scan or MRI (14) may be useful, though usually not necessary. There have been rare reports of malignancy developing in chronic pilonidal sinuses. Most commonly these are squamous cell carcinomas. These tumors are fairly aggressive, with a high recurrence rate and poor prognosis.(15, 16) Management of Acute Disease The treatment for an acute pilonidal abscess is similar to that of an abscess in any other location. Incision and drainage, leaving the wound to heal by secondary intention, is the accepted treatment modality. The patient can be positioned either in lateral decubitus or prone position, though prone is generally preferred. Incision and drainage may be performed under local, regional, or general anesthesia, and may be done in an ambulatory ­setting such as the office or emergency room. The area should be prepped in standard fashion and local anesthetic infiltrated over the area of fluctuance. A vertical incision or an ellipse of skin should be made over the fluctuant area, 1–2 cm off the midline. Purulent fluid, along with hair or other debris, may be found in the cyst cavity. This should be removed and the cavity packed. An alternate technique for patients with a large abscess cavity is to use catheter drainage, as described in Chapter 19. The patient may be discharged on antibiotics to treat the overlying cellulitis if present and instructed in wound care. In a series of 73 patients



Figure 21.3  Acute pilonidal abscess. Note midline opening with abscess slightly to the right of midline.

undergoing incision and drainage for first presentation of pilonidal abscess, 58% healed the wounds within 10 weeks, and 21% recurred during the 18 month follow-up period.(17) This recurrence rate of approximately 20% is consistent with that found throughout the literature. Management of Chronic Disease Chronic pilonidal disease may present in several forms: a nonhealing wound after initial drainage, chronically draining sinuses, or recurrent pain and infection. The goals of definitive treatment of the disease are to remove the diseased tissue in a manner that will prevent recurrence, to change the local environment of the gluteal cleft, to decrease the chance of recurrence and allow healing, and to allow the patient to resume their normal activities and return to work quickly. There is no one ideal approach to managing this disease. Nonsurgical Treatment There is very little role for purely nonsurgical management of pilonidal disease. In select patients who are found to have asymptomatic midline pits with no evidence of infection, it is possible to just observe the patients. Prophylactically, the patient may be instructed to ensure good hygiene, to keep the area of the gluteal cleft dry, and to periodically shave the area to keep hairs from accumulating. Patients who present with acute abscess will require drainage, but sometimes may be able to be managed nonoperatively afterwards.

surgery for pilonidal disease and hidradenitis suppurativa Table 21.1  Procedures for pilonidal disease: wide excision with healing by secondary intention or primary closure. Hospital Time (days)

Study

Closure

Number of Patients

Sondenaa et al. (24) (1996)

Open



Closed



60

Open



192



4

Al-Salamah et al. (27) (2007)

60

Follow-up (months)

Healing Time (days)

Infection (%)

Recurrence (%)

Outpatient



86



13



5



50

Outpatient



23



30



(-)





10



50

3.12



3



35

Closed



188



3.6



(-)



4.2



3.7



36

Fazeli et al. (45) (2006)

Open



72



1.76



41



13.9



4.2



22

Mentes et al. (25) (2006)

Closed



493



5.5



(-)



1.2



5.6



18

Tejirian et al. (26) (2007

Open



26



(-)



147



(-)



35



(-)

Marsupialization



42



(-)



42



(-)



2



(-)

Note: (-) not described.

Approximately 20% of patients who undergo abscess drainage will suffer from recurrent disease. There is little information available regarding the nonoperative treatment of these recurrences. Armstrong et al. (18) reported faster healing in 101 patients who were managed with gluteal cleft shaving and good perineal hygiene following incision and drainage, when compared with 229 patients who underwent surgical management after drainage. Following these initial findings, the authors implemented a policy of nonoperative management for their patient population. They reported only 150 hospital admissions for complications of pilonidal ­disease during the study period of 17 years, of whom only 23 patients required surgical management. They did not specifically report how many total patients were under their care during the study period. It is likely that the patients who responded well to nonoperative treatment had milder disease than the ones that required further surgery. This conservative approach can be considered in select patients with mild disease, or in patients with significant medical contraindications to surgery. Many surgeons advocate some form of depilation following surgery to aid in healing. Whether this is shaving, waxing, chemical depilation, or laser treatments can be left up to individual patient or surgeon preference.(19) Other methods that have been described with varying success are fibrin glue or phenol injections into the sinuses. Greenberg et al. reported a series of 30 patients treated with fibrin glue injection with no recurrence or infection after a follow-up of 23 months.(20) Another study of six patients who had injection of fibrin glue into the sinus after curettage of pits reported no recurrences at 1 year.(21) However, this technique has not been tested in larger case series or randomized trials. Phenol sclerotherapy has been used for treatment of pilonidal disease with varying success. Early studies showed potential benefit in uncomplicated cases. Dogru et al. reported a series of 41 patients (22) who had crystallized phenol applied to the wounds after ­limited excision of midline pits. Most patients required 2–3 applications, and 95% healed completely. There were two recurrences of disease. However, another study of 45 patients who had 1–2 mL of 80% phenol solution into the sinus reported 60% healing, and five patients developed abscess requiring operative drainage.(23)

Surgical Options for Chronic Pilonidal Disease Operations for chronic pilonidal disease involve excision of the diseased tissue. This may result in a large defect which is difficult to close in an area which is subject to significant tension and moisture. This challenge has fueled the development of many different surgical techniques in an attempt to find the ideal operation. So far, no technique has proven to be ideal. This section of the chapter will review the most common operations and give an algorithm for the surgical approach to the management of chronic disease. The operations described may be performed in prone or lateral decubitus position, under regional or general anesthesia. The jackknife prone position, with the operating table flexed at the waist approximately 30 degrees and the buttocks taped apart, provides the ideal exposure for most operations and is recommended unless contraindicated by individual patient factors. Standard perioperative antibiotics are given before incision. There is no need to continue antibiotics postoperatively unless there is overlying cellulitis from acute infection. Many of these operations may be done on an outpatient basis. The more complex flaps require the patients to remain in the hospital on bedrest for approximately 2 days. These patients may also receive postoperative antibiotics for a few days until the drains are removed. Sutures are usually removed between 7 and 10 days after surgery. Wide Local Excision The most commonly performed operation for pilonidal disease is wide local excision. An elliptical incision including all sinus tracks is made and carried down to the sacrococcygeal fascia, so that the entire cyst is removed. There is debate as to the best way to manage the large wound that results. The benefits of leaving the wound open to heal by secondary intention include less chance of infection or wound breakdown, but this is counterbalanced by the increased time required to completely heal the wound, the need for frequent dressing changes, the added discomfort of having an open wound, and the increased time lost from work. There are few randomized trials which examined this problem. (Table 21.1) A series of 120 patients (24) who were randomized to either excision left open to heal by secondary intention or excision with primary



improved outcomes in colon and rectal surgery (A)

(B)

(D)

(C)

Figure 21.4  Marsupialization. (A) The diseased tissue is excised with electocautery. (B) The cavity is debrided. (C) The edges of the wound are then sutured down to the base of the wound using absorbable suture. (D) Resulting in a small open wound.

wound closure reported less infectious complications(13% vs. 30%) and recurrences(5% vs. 10%) with the open technique, but more overall wound complications. Slightly more patients in the open group were not satisfied with the outcome of treatment(8% vs. 5%). However, a larger series of 493 patients (25) treated with midline excision and primary closure via an oblique elliptical incision which crossed the midline showed recurrence rate of 5.6% at 18 months, with very low incidence of wound infection(1.2%), hematoma(0.4%), or wound dehiscence (1%) postoperatively. The benefit of faster healing time and smaller final scar slightly outweighs the possible increase in infection or wound dehiscence. Recurrence is related more to inadequate excision of diseased ­tissue rather than to closure technique. Excision or Unroofing with Marsupialization Another option to leave a smaller wound is marsupialization. The excision of tissue is carried out as described above. Then the skin



edges are tacked down to the base of the wound using absorbable suture. This leaves a smaller and more shallow wound which is easier to pack.(Figures 21.4a–d) By not completely closing the wound, there is a theoretical decrease in wound complications, and the duration of healing is less than for a fully open wound. Simply unroofing the wound versus excision also results in a smaller wound. A study of 26 patients who underwent wide local excision and 42 who had unroofing and marsupialization reported significantly longer healing times (21 vs. 6 weeks) and wound complications requiring reoperation (35% vs. 2%) in the wide local excision group.(26) Simple unroofing without ­marsupialization has become the preferred initial operation for pilonidal disease and the editors’ institution. A more recent series of 380 patients (27) who underwent excision with either primary closure or wound left open reported similar length of stay, wound infection rate, and recurrence rate among the two groups. However, the length of time off from work

surgery for pilonidal disease and hidradenitis suppurativa (A)

(B)

Figure 21.5  Bascom operation. (A) A vertical incision is made overlying the cyst, 1 cm away from the gluteal cleft. The cyst cavity any communicating fistula tracts are debrided. The midline pits are excised, with the wounds communicating to the cavity. (B) The midline wounds are closed primarily with absorbable suture and the vertical wound is packed lightly and left to heal by secondary intention.

and healing time were significantly shorter in the group that had the wound closed primarily. Limited Excision In an attempt to minimize the morbidity of this disease, some surgeons have advocated a more limited excision of the sinuses rather than removing all the surrounding tissue. This technique is recommended for patients with limited disease, defined as four or less pits and no concurrent abscess or active infection. The technique as described by Oncel et al. (28) requires excising each individual pit along with a funnel-shaped cone of tissue around the track. Methylene blue may be injected into the pits to aid in identifying the tracks, though some authors believe that this leads to excision of more tissue than is necessary. Additionally, if two pits are found to be connected, the fistula overlying them should be unroofed. The goal is to remove all pits along with their underlying tracks and granulation tissue. The wounds are then left open to heal by secondary intention. The same group reported their medium-term follow-up of 62 patients treated with this technique.(29) They found that the patients were able to return to work in 2 days and healed completely in 43 days. They reported one recurrence after 1 year of follow-up. Mohamed et al. (30) reported a prospective randomized trial of 83 patients assigned to wide excision with ­primary closure, wide excision with wound left open, or limited excision of fistula tracks. They found that the limited excision group had shorter operative time, shorter length of stay and less postoperative pain, while the wide excision with open wound group had the longest time to complete healing. There was no difference in recurrence among the three groups and therefore recommended a limited excision approach when possible.

Bascom Operation Bascom described a different operation (10) based on his theory that treatment of pilonidal disease should center around removing the midline follicles or pits rather than excising large amounts of tissue. The goal of this operation is to excise the midline pits, drain the underlying abscess, and elevate the gluteal cleft. A vertical incision is made overlying the chronic abscess approximately 1 cm away from the gluteal cleft. The abscess cavity is then debrided, and any communicating fistula tracts are identified and undermined so that they connect to the open wound. The midline pits are excised via small incisions encompassing each one individually. These wounds are closed with nonabsorbable suture. The lateral wound is left open to heal by secondary intention and hair in the area is shaved until the wound is completely healed. (Figure 21.5) Bascom reported his experience with 149 patients (7) with 3.5 year follow-up after follicle-excision surgery and found that 16% had recurring problems, but that these were all minor and did not cause added morbidity. All his patients were able to return to work within 1 day of surgery and took approximately 3 weeks to heal the lateral wound. In a series of 218 patients (31) who underwent Bascom’s operation, 84% were performed under local anesthesia and all patients were discharged home the same day. 6% had infectious complications and 10% recurred, with complete healing in all but 1 patient, who required further surgery. Surgery for Complicated Pilonidal Disease and Nonhealing Wounds While most patients who undergo surgery for pilonidal disease heal without complication, a few return with chronic nonhealing wounds. Many of these patients are those who underwent wide excision and were left with an open wound to close secondarily or those

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improved outcomes in colon and rectal surgery Table 21.2  Advanced procedures for pilonidal disease. Technique

Study Year

Number of Patients Hospital time (days) Healing time (days) Infection (%) Recurrence (%) Follow-up (months)

Karydakis flap Karydakis flap Karydakis flap Rhomboid flap Rhomboid flap Rhomboid flap Rhomboid flap Rhomboid flap Bascom operation V-Y flap Z-plasty

Kitchen et al. (1996) Akinci et al.46 (2000) Keshava et al.35 (2007) Bozkurt et al.47 (1998) Milito et al.48 (1998) Arumugam et al.42 (2003) Topgul et al.43 (2003) Katsoulis et al.49 (2006) Senapati et al.31 (2000) Dylek et al.50 (1998) Fazeli et al.45 (2006 34

141 112   70   24   67   53 200   25 218   23   72



(–) 2.6 (–) 4.1 5.3 4 3.1 4 Outpatient 10   2.86





(–) 13.2 80 17.5 14 14 12.8 (–) 28 21 15.4





(–) 1.8 (–) 0 0 13 1.5 (–) 6 4 9.7

  4    0.9    4.2   0   0   7    2.5   4 10   0    4.2



18 28 36 27 74.4 24 60 20 12 18 22

(-) not described.

(A)

(B)

(C)

(D)

(E)

Figure 21.6  Karydakis flap. (A) Schematic of the operative field depicting a pilonidal cyst slightly to the left of midline with two midline pits. (B) An elliptical incision is made encompassing the cyst and pits. The excision is carried down to the sacrococcygeal fascia. (C) The medial edge of the wound is raised as a flap crossing the midline. (D) The tape retracting the buttocks is released so that the wound edges are able to be approximated without tension. (E) Final result showing a vertical incision closed primarily away from the midline, resulting in a flattened gluteal cleft.

whose incisions broke down. Those patients who have recurrence after initial surgery or have unacceptable scars also are included in this group. Several methods have been described to excise tissue in the gluteal cleft and close the resulting defect with a flap technique. (Table 21.2) These methods may be used as the initial treatment approach, and also for complicated recurrent disease. In 1973, Karydakis (32) described an asymmetric advancement flap technique which results in excision of the disease, a primarily closed wound, and a flatter gluteal cleft. An elliptical incision is made vertically and centered off midline to the most affected side. The incision should encompass all midline pits and skin sinuses. The incision is carried down to the sacrococcygeal fascia, removing the affected tissue. A skin flap is raised under the medial edge of the wound and across the midline.When the buttocks are released and approximated, the edges of the wound should come together easily. The incision is closed primarily off the midline, and a flatter gluteal cleft is created. (Figure 21.6) This is believed to aid in healing and lessen recurrence. External drainage is useful to prevent fluid collections under the flap, though one study found no effect on wound infections or recurrence.(33) In his



series of 6,545 patients treated with this technique (6), Karydakis reported less than 1% recurrence rate. While this excellent result has not been replicated, many smaller series have reported acceptable results. Kitchen reported a series of 141 patients treated by this technique.(34) He found a recurrence rate of 4%. 23% of his patients had recurred after previous operations for pilonidal disease, and all of them were cured after this procedure. More recent series have reported recurrence rates ranging from 0 to 4%, with 5% to 8% wound complications.(35–38) Similar results have been obtained in obese patients.(39) A modification of this technique was described by Bascom in 2002, known as the “cleft lift” or “Bascom II” procedure.(40) An important key to this operation is preoperative skin marking of the patient. With the patient standing up, the buttocks are pushed together so the line of contact between the two may be marked with a pen. When the buttocks are taped apart with the patient lying prone, the area between the pen markings delineates the limits of the flap dissection. An asymmetric ellipse is drawn off midline to include the midline pits. This ellipse is then excised, with the incision reaching to the sacrococcygeal fascia. The flap, consisting of

surgery for pilonidal disease and hidradenitis suppurativa (A)

(B)

Figure 21.7  Rhomboid Flap. (A) A rhomboid incision encompassing the pilonidal cyst and midline pits is marked on the skin, along with a lateral extension. The rhomboid is composed of 2 120º angles and 2 60º angles. Line BC is drawn at a 90º angle to Line CD. Line AB is drawn vertically down. All lines should be of equal length. The cavity is excised down to fascia and debrided. The flap is raised and mobilized to cover the defect. (B) The flap is rotated into the defect so that Point 2 meets Point E, Point 1 meets Point D, and Point A meets Point C. This results in a primarily closed wound and flattened gluteal cleft.

skin and subcutaneous fat, is then mobilized towards the affected side, breaking up the scar tissue in the subcutaneous fat. The flap should be mobilized until the plane of dissection reaches the pen mark on the contralateral buttock. When the tapes are released, the edges of the flap should come together. A drain is placed under the flap and the incision is closed, resulting in a scar off the midline and a flattened gluteal cleft. In the original article describing the technique, 27 patients who underwent the procedure after undergoing multiple failed operations were described.(40) They all healed completely, most having the sutures removed at 1 week, and none recurred after a mean follow-up period of 20 months. A series of 24 patients treated with the same technique but without drain placement reported no hematomas, seromas, or infections, and patients returned to work in 3 weeks. They had no recurrences with a follow-up of 10 months.(41) This procedure is a useful option for patients who have failed previous attempts at cure or who have chronic unhealed wounds. Other rotational flap techniques have been described for this disease, along with myocutaneous flaps and skin grafting. The rhomboid flap is another commonly used operation. Limberg or Dufourmentel flaps are some of the more common variations of this type of flap. For this flap, a rhomboid incision is made which includes the diseased tissue, with the vertical axis being along the gluteal cleft. This is carried down to the sacrococcygeal fascia. A triangle of skin and subcutaneous fat is incised lateral to this and then rotated into the defect.(Figure 21.7) A drain may be placed per surgeon preference. Patients stay in the hospital on average 4 days and sutures are removed in approximately 10 days. In a series of 53 patients with 24 month follow-up, 13% developed wound infections, 7% recurred, and all had an average healing time of 2 weeks. (42) Another study reported on the results of 200 patients who underwent Limberg rhomboid flap reconstruction. These patients had an overall recurrence rate of 2.5%, with complications including minimal flap necrosis in 3%, seroma formation in 1.5%, and wound infection in 1.5%. The average length of stay was 3.1 days and time to return to work was 12.8 days.(43) Other fasciocutaneous flaps which have been described include V-Y flaps, Z-plasty, W-flaps, and a variety of other rotational flaps. The goal of all of

them is to allow the surgeon to excise the diseased tissue as widely as necessary and close the defect primarily without tension while flattening the gluteal cleft. All these flaps have similar complication and recurrence rates, and the choice of which to utilize in each case depends on the size of the defect to be closed and the individual surgeon’s experience with each. The Nonhealing Sacral Wound Fortunately, most patients have limited disease that responds to conventional treatment. However, a few patients present with large open sacral defects, either due to complications of wide excision left to close secondarily, or as a result of failed primary closures. Several myocutaneous rotational flaps have been described for closing large wounds, which fortunately are not encountered very frequently. Flaps based on the gluteus maximus are frequently used to cover sacral wounds with good results. These techniques are beyond the scope of this book and are most often performed in conjunction with plastic surgeons. Another adjunct to sacral wound healing may be the vacuum wound closure system. Vacuum wound closure systems may be useful in patients who have defects which are not able to be closed primarily for a variety of reasons, and have been used extensively in defects due to pressure ulcers, traumatic wounds, and postsurgical perineal defects. A series of five patients with extensive complex infected pilonidal sinuses underwent excision with placement of a vacuum sponge.(44) Patients used the device for 6 weeks, after which wet-to-dry dressing changes were initiated. Complete epithelialization was observed in 12 weeks. One patient did not tolerate the device, and another required a return to the operating room for further debridement, after which the wound healed with use of the vacuum device. Pilonidal disease presents many treatment challenges, and therefore, multiple treatment approaches exist. Depending on the specifics of each case and individual surgeon experience, different approaches may be considered. An algorithm based on extent and chronicity of the disease is presented here. (Figure 21.8) Perianal Hidradenitis Suppurativa Hidradenitis suppurativa is a chronic inflammatory disease of the apocrine sweat glands. The disease was first described by Velpeau (51) in 1832, and its association to sweat glands in the skin was described by Vernuil (52) in 1864. These glands are found primarily in the groin and axilla, which are the most common sites of involvement of disease. However, they can also be found in the perineum, perianal area, scrotum, and labia. Hidradenitis suppurativa affects patients beginning in adolescence and peaks around age 40. The incidence of hidradenitis suppurativa is estimated to be 1:300. Perianal disease appears to be more common in men.(53) Pathophysiology Apocrine sweat glands are coiled tubular secretory structures which empty into the hair follicle. They are similar to eccrine sweat glands except that these empty directly to the skin. The etiology of hidradenitis suppurativa is unclear, but appears to be multifactorial. Obstruction of the apocrine gland duct is likely to be the inciting event, leading to secondary infection and rupture of the



improved outcomes in colon and rectal surgery Algorithm for management of chronic pilonidal disease Chronic Pilonidal Disease

Complicated Disease

Limited Disease

+ contraindications to surgery - Hygiene - Depilation

Midline excision ± closure or marsupialization Sinus excision Bascom operation

Karydakis flap Rhomboid flap Cleft Lift (Bascom II) V-Y flap Z-plasty

Large Wound

Myocutaneous flaps Vacuum sponge

Figure 21.8  Algorithm for management of pilonidal disease.

gland with extension into the surrounding dermis and subcutaneous fat. The infection then spreads to neighboring glands and is manifested by cellulitis and abscess. Initially, the infection resolves with simple incision and drainage, but long-term disease recurrence may lead to scarring and fistula formation. Microbiologic studies of the infected tissues have shown that skin flora is the usual pathogen for axillary disease, though enteric aerobes and anaerobes have also been isolated from perianal lesions. Many of the older studies were indeterminate as they evaluated superficial swab cultures. However, cultures of deeper tissue have shown Staphylococcus aureus and coagulase-negative staphylococcus in most of the samples.(54) Diagnosis Patients with perianal hidradenitis present with recurrent perianal abscesses which may extend to involve the perineum, labia or scrotum, buttocks, or the inguinal region. The lesions may start out as a simple abscess, but tend to evolve with time into thick scarred skin with open wounds and chronically draining sinuses. Perianal fistulae may also be present. The differential diagnosis includes perianal abscess, furuncles, carbuncles, lymphogranuloma venereum or other sexually transmitted diseases, pilonidal disease, tuberculosis, actinomycosis, cat-scratch disease, granuloma inguinale, and Crohn’s disease. One way to differentiate the etiology of perianal fistulae is that cryptoglandular fistulae usually involve the dentate line and intersphincteric plane, whereas fistulae associated with hidradenitis are found in the distal anal canal, where the apocrine glands are found. The dentate line is normal in cases of hidradenitis. It is important to examine other areas, such as the axilla and groin, as many patients with hidradenitis suppurativa will have concurrent involvement of these areas. Some factors which have been shown to be related to this disease include altered immune response, smoking, obesity, hormonal therapy, pregnancy, onset of puberty, familial factors, and Crohn’s disease.(55–57) The Lahey Clinic reported their experience with 43 patients with perianal hidradenitis suppurativa.



They found that 93% of the patients were male with a median age of 29 years. Patients were initially diagnosed with pilonidal ­disease (28%), anal fistula (37%), and perirectal abscess (16%). 72% of their patients were smokers.(58) In a series of 61 patients from The Cleveland Clinic, 24 (38%) were found to have concurrent Crohn’s disease. All had perianal hidradenitis, and 20 had disease in other sites as well.(59) Often the diagnosis of perianal hidradenitis is delayed due to the similarity of symptoms with other perianal diseases and the possibility of other concurrent disease processes. In situations where patients are being treated for a certain condition and they are not improving, hidradenitis should be considered as a possible complicating factor. ­Long-term sequelae of perianal hidradenitis include disfiguring scars, localized or systemic sepsis, and carcinoma, including squamous cell or adenocarcinoma.(60–62) Nonoperative Management The treatment of perianal hidradenitis suppurativa is mainly surgical. However, there is a role for nonoperative management, particularly in the milder forms of the disease. Maintaining good hygiene of the area is imperative to control infection. Patients should keep the affected area clean and dry, reduce moisture, avoid constricting or irritating clothing, and lose weight. Topical antibiotics are often used in conjunction with systemic antibiotics or alone to control secondary infection. Topical clindamycin was shown in one double-blind randomized trial of 30 patients to be of benefit in controlling infection.(63) Systemic antibiotics are rarely indicated, except in cases with significant cellulitis or ­bacteremia. In light of the similarities between acne and hidradenitis suppurativa, isotretinoin has been used to treat hidradenitis successfully. Brown et al. (64) reported on a patient treated with 1 gm/kg of isotretinoin daily for 20 weeks. The patient had no significant change in her condition until 8 weeks into the treatment, at which point she began to note improvement. Ultimately, she had an excellent response with no relapse at the 18 week follow- up visit. Minor

surgery for pilonidal disease and hidradenitis suppurativa side effects such as xerosis, cheilitis, and elevated serum alkaline phosphatase were reported, which resolved with completion of treatment. Targeting the hormonal response of hidradenitis has also had some success, including one retrospective study of 64 female patients demonstrating that antiandrogen therapy was superior to systemic oral antibiotics in controlling disease.(65–67) Other nonsurgical approaches have been attempted with varying degrees of success, including granulocyte-macrophage colonystimulating factor (68), infliximab (69, 70), and oral zinc.(71) Surgical Management The centerpiece of treatment of hidradenitis is surgical excision. Incision and drainage has a limited role to relieve pain and pressure in cases of acute abscess. There is no long-term benefit to the procedure, as it does not remove any of the affected tissue, but may be necessary to relieve pain. Patients should receive systemic antibiotics to treat the overlying cellulitis if present and may require packing of the wound for several days. Unroofing of fistula tracts is another procedure which may be useful in controlling local infection, though this also does not excise the disease and therefore has no benefit in preventing recurrence. Excision of the diseased skin, including skin appendages and subcutaneous fat, is required to adequately control the disease. In mild cases, limited excision left to heal by secondary intention is appropriate. Primary closure is usually not possible and is not advised, as the recurrence rate is increased. Rotational flaps or skin grafting are more successful wound closure methods. In a series of 106 patients, 70% underwent excision with primary closure and the rest had closure with skin grafts or flaps. 69% of the patients had a recurrence requiring surgery, the majority of whom were in the primary closure group.(72) A series of 8 patients with perineal hidradenitis who underwent wide excision had their wounds either covered with meshed split-thickness skin graft (5) or left open to heal by secondary intention. (3) All patients healed well and had no surgical site recurrence, though two recurred in other areas.(73) A larger series including 56 patients with gluteal or perianal disease was reported recently. (74) Twenty-one (37.6%) and 17 (30.6%) patients had gluteal and perineal disease, respectively. Squamous-cell carcinoma and Crohn’s disease were observed in one patient each. Wide excision was performed in all patients. Thirty-two patients (57.1%) were left to heal by secondary intention, and the remaining 24 patients underwent split-thickness skin grafting. Twenty-three patients received a diverting colostomy. Mean time for complete healing in the open wound group was 10 weeks and in the skin graft group was 6 weeks. Five patients (9%) required a second resection. Partial graft loss rate was 37.5% and only one patient had a recurrence. The benefits of skin grafting or rotational flaps include shorter healing times and less discomfort when compared to an open wound; however, some of the large defects that result from excision are difficult to adequately cover. When a large wound must be left open, a wound vaccum sponge or silastic foam may be of benefit. In summary, the primary approach to perianal hidradenitis suppurativa is surgical excision of all diseased tissue. The open defect that results may be left open to heal secondarily and heals

uneventfully in most cases. In certain cases where the defect is particularly large, a skin graft may be used. Fecal diversion is rarely necessary in managing this disease, and should be reserved for debilitated patients who will have difficulty keeping the open wound clean, patients with fecal incontinence, or patients with concurrent Crohn’s disease with perianal involvement. References   1. Mayo OH. Observations on injuries and diseases of the ­rectum. London: Burgess and Hill, 1833: 45–6.   2. Hodges RM. Pilonidal sinus. Boston Med Surg J 1880; 103: 485–6.   3. Buie LA. Jeep disease (pilonidal disease of mechanized ­warfare). South Med J 1944; 37: 103–9.   4. da Silva JH. Pilonidal cyst: cause and treatment.Dis Colon Rectum 2000; 43: 1146–56.   5. Patey DH, Scraff RW. Pathology of post-anal pilonidal sinus: its bearing on treatment. Lancet 1946; 2: 484–6.   6. Karydakis GE. Easy and successful treatment of pilonidal sinus after explanation of its causative process. ANZ J Surg 1992; 62: 385–9.   7. Bascom J. Pilonidal disease: long-term results of follicle removal. Dis Colon Rectum 1983; 26: 800–7.   8. Notaras MJ. A review of three popular methods of treatment of postanal (pilonidal) sinus disease. Br J Surg 1970; 57: 886–90.   9. Davage ON. the origin of sacroscoccygeal pilonidal sinuses based on an analysis of four hundred sixty-three cases. Am J Pathol 1954; 30: 1191. 10. Bascom JU. Pilonidal disease: origin from follicles of hairs and results of follicle removal as treatment. Surgery 1980; 87: 567–72. 11. Patel MR, Bassini L, Nashad R et al. Barber’s interdigital pilonidal sinus of the hand: a foreign body hair granuloma. J Hand Surg 1990; 15A: 652–5. 12. Phillips PJ. Web space sinus in a shearer. Med J Aust 1966; 2: 1152–3. 13. Mohanna PN, Al-Sam SZ, Flemming AFS. Subungual pilonidal sinus of the hand of a dog groomer. Br J Plas Surg 2001; 54: 176–8. 14. Taylor SA, Halligan S, Bartram CI. Pilonidal sinus disease: MR imaging distinction from fistula in ano. Radiology 2003; 226(3): 662–7. 15. de Bree E, Zoetmulder FA, Christodoulakis M, Aleman BM, Tsiftsis DD. Treatment of malignancy arising in pilonidal disease. Ann Surg Oncol 2001; 8(1): 60–4. 16. Malek MM, Emanuel PO, Divino CM. Malignant degeneration of pilonidal disease in an aimmunosuppressed patient: report of a case and review of the literature. Dis Colon Rectum 2007; 50(9): 1475–7. 17. Jensen SL, Harling H. Prognosis after simple incision and drainage for a first-episode acute pilonidal abscess.Br J Surg 1988; 75(1): 60–1. 18. Armstrong JH, Barcia PJ. Pilonidal sinus disease: the conservative approach. Arch Surg 1994; 129: 914–7. 19. Odili J, Gault D. Laser depilaton of the natal cleft – an aid to healing the pilonidal sinus. Ann RCS Engl 2002; 84(1): 29–32.

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improved outcomes in colon and rectal surgery 20. Greenberg R, Kashtan H, SKornik Y, Werbin N. Treatment of pilonidal sinus disease using fibrin glue as a sealant. Tech Coloproctol 2004; 8: 95–8. 21. Lund JN, Leveson SH. Fibrin glue in the treatment of pilonidal sinus: results of a pilot study. Dis Colon Rectum 2005; 48(5): 1094–6. 22. Dogru O, Camci C, Aygen E, Girgin M, Topuz O. Pilonidal sinus treated with crystallized phenol: an eight-year experience. Dis Colon Rectum 2004; 47(11): 1934–8. 23. Schneider IH, Thaler K, Kockerling F. Treatment of pilonidal sinuses by phenol injections. Int J Colorectal Dis 1994; 9(4): 200–2. 24. Sondenaa K, Nesvik I, Andersen E, Soreide JA. Recurrent pilonidal sinus after excision with closed or open treatment: final result of a randomized trial. Eur J Surg 1996; 162: 237–40. 25. Mentes O, Bagci M, Bilgin T et al. Management of pilonidal sinus disease with oblique excision and primary closure: results of 493 patients. Dis Colon Rectum 2006; 49(1): 104–8. 26. Tejirian T, Lee JJ, Abbas MA. Is wide local excision for ­pilonidal disease still justified? Am Surg 2007; 73(10): 1075–8. 27. Al-Salamah SM, Hussain MI, Mirza SM. Excision with or without primary closure. JPMA 2007; 57(8): 388–91. 28. Oncel M, Kurt N, Kement M et al. Excision and marsupialization versus sinus excision for the treatment of limited chronic pilonidal disease: a prospective, randomized trial. Tech Coloproctol 2002; 6(3): 165–9. 29. Kement M. Oncel M, Kurt N, Kaptanoglu L. Sinus excision for the treatment of limited chronic pilonidal disease: results after a medium-term follow-up. Dis Colon Rectum 2006; 49(11): 1758–62. 30. Mohamed HA, Kadry I, Adly S. Comparison between three therapeutic modalities for non-complicated pilonidal sinus disease. Surgeon 2005; 3(2): 73–7. 31. Senapati A, Cripps NP, Thompson MR. Bascom’s operation in the day-surgical management of symptomatic pilonidal sinus. Br J Surg. 2000; 87(8): 1067–70. 32. Karydakis G. New approach to the problem of pilonidal sinus. Lancet 1973; 2: 1414–15. 33. Gurer A, Gomceli I, Ozdogan M et al. Is routine cavity drainage necessary in Karydakis flap operation? A prospective randomized trial. Dis Colon Rectum 2005; 48(9): 1797–9. 34. Kitchen PR. Pilonidal sinus: experience with the Karydakis flap. Br J Surg 1996; 83(10): 1452–5. 35. Keshava A, Young CJ, Rickard MJ, Sinclair G. Karydakis flap repair for sacrococcygeal pilonidal sinus disease: how important is this technique? ANZ J Surg 2007; 77: 181–3. 36 Bessa SS. Results of the lateral advancing flap operation (Modified Karydakis procedure) for the management of pilonidal sinus disease. Dis Colon Rectum 2007; 50(11): 1935–40. 37. Kulacoglu H, Dener C, Tumer H, Aktimur R. Total subcutaneous fistulectomy combined with Karydakis flap for sacrococcygeal pilonidal disease with secondary perianal opening. Colorectal Dis 2006; 8(2): 120–3. 38. Morden P, Drongowski RA, Geiger JD, Hirschl RB, Teitelbaum DH. Comparison of Karydakis versus midline excision for

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treatment of pilonidal sinus disease. Pediatr Surg Int 2005; 21(10): 793–6. Sakr M, El-Hammadi H, Moussa M, Arafa S, Rasheed M. The effect of obesity on the results of Karydakis technique for the management of chronic pilonidal sinus. Int J Colorectal Dis 2003; 18(1): 36–9. Bascom J, Bascom T. Failed pilonidal surgery: New paradigm and new operation leading to cures. Arch Surg 2002; 137: 1146–50. Theodoropoulos GE, Vlahos K, Lazaris AC, Tahteris E, Panoussopoulos D. Modified Bascom’s asymmetric midgluteal cleft closure thechnique for recurrent pilonidal disease: Early experience in a military hospital. Dis Colon Rectum 2003; 46(9): 1286–91. Arumugam PJ, Chandrasekaran TV, Morgan AR, Beynon J, Carr ND. The rhomboid flap in pilonidal disease. Colo Colorectal Dis 2003; 5(3): 218–21. Topgul K, Oxdemir E, Kilic K, Gokbayir H, Ferahkose Z. Long-term results of Limberg flap procedure for treatment of pilonidal sinus: a report of 200 cases. Dis Col Rectum 2003; 46(11): 1545–8. Bendewald FP, Cima RR, Metcalf DR, Hassan I. Using negative pressure wound therapy following surgery for complex pilonidal disease: a case series. Ostomy Wound Management 2007; 53(5): 40–6. Fazeli MS, Adel MG, Lebaschi AH. Comparison of outcomes in Z-plasty and delayed healing by secondary intention of the wound after excision of the sacral pilonidal sinus: results of a randomized, clinical trial. Dis Colon Rectum 2006; 49(12): 1831–6. Akinci OF, Coskun A, Uzunkoy A. Simple and effective surgical treatment of pilonidal sinus: asymmetric excision and primary closure using suction drain and subcuticular skin closure. Dis Colon Rectum 2000; 43(5): 701–6. Bozkurt MK, Tezel E. Management of pilonidal sinus with the Limberg flap. Dis Colon Rectum 1998; 41(6): 775–7. Milito G, Cortese F, Casciani CU. Rhomboid flap procedure for pilonidal sinus: results from 67 cases. Int J Colorectal Dis 1998; 13(3): 113–5. Katsoulis IE, Hibberts F, Carapeti EA. Outcome of treatment of primary and recurrent pilonidal sinuses with the Limberg flap. Surgeon 2006; 4(1): 7–10. Dylek ON, Bekereciodlu M. Role of simple V-Y advancement flap in the treatment of complicated pilonidal sinus. Eur J Surg 1998; 164(12): 961–4. Velpeau A. Dictionnaire de Medicine, un Repertoire General des Sciences Medicales sous la Rapport. Therique et Pratique. Paris, Bechet Jeune; 1839. Vernuil A. De l’hidrosadenite phlegmoneuse et des absces sudoripares. Arch Gen Med Paris 1864; 114: 537–57. Rubin RJ, Chinn BT. Perianal hidradenitis suppurativa. Surg Clin North Am 1994; 74(6): 1317–25. Lapins J, Jarstrand C, Emtestam L. Coagulase-negative staphylococci are the most common bacteria found in cultures from the deep portions of hidradenitis suppurativa lesions, as obtained by carbon dioxide laser surgery. Br J Derm 1999; 140(1): 90–5.

surgery for pilonidal disease and hidradenitis suppurativa 55. Ebling FJG. Hidradenitis suppurativa: an androgen-dependent disorder. Br J Derm 1986; 115(3): 259–62 56. Fitzsimmons JS, Guilbert PR, Fitzsimmons EM. Evidence of genetic factors in hidradenitis suppurativa. Br J Derm 1985; 113(1): 1–8. 57. Der Werth JM, Williams HC, Raeburn JA. ������������������� The clinical genetics of hidradenitis suppurativa revisited. Br J Derm 2000; 142(5): 947–53. 58. Wiltz O, Schoetz DJ Jr, Murray JJ et al. Perianal Hidradenitis Suppurativa: The Lahey Clinic experience. Dis Colon Rectum 1990; 33(9): 731–4. 59. Church JM, Fazio VW, Lavery IC, Oakley JR, Milsom JW. The differential diagnosis and comorbidity of hidradenitis suppurativa and perianal Crohn’s disease. Int J Colorectal Dis 1993; 8(3): 117–9. 60. do Val IC, Almeida Filho GL, Correa A, Neto N. Chronic hidradenitis suppurativa and perianal mucinous adenocarcinoma. A case report J Rep Med 2007; 52(2): 100–2. 61. Shukla VK, Hughes LE. A case of squamous cell carcinoma complicating hidradenitis suppurativa. Eur J Surg Onc 1995; 21(1): 106–9. 62. Rosenzweig LB, Brett AS, Lefaivre JF, Vandersteenhoven JJ. Hidradenitis suppurativa complicated by squamous cell carcinoma and paraneoplastic neuropathy. Am J Med Sciences 2005; 329(3): 150–2. 63. Clemmensen OJ. Topical treatment of hidradenitis suppurativa with clindamycin. Int J Dermatol. 1983; 22(5): 325–8. 64. Brown CF, Gallup DG, Brown VM. Hidradenitis suppurativa of the anogenital region: response to isotretinoin. Am J of Ob Gyn 1988; 158(1): 12–5.

65. Camisa C, Sexton C, Friedman C. Treatment of hidradenitis suppurativa with combination hypothalamic-pituitary-ovarian and adrenal suppression. A case report. J Reprod Med 1989; 34(8): 543–6. 66. Sawers RS, Randall VA, Ebling FJ. Control of hidradenitis suppurativa in women using combined antiandrogen (cyproteroine acetate) and oestrogen therapy. Br J Dermatol 1986; 115(3): 269–74. 67. Kraft JN, Searles GE. Hidradenitis suppurativa in 64 female patients: retrospective study comparing oral antibiotics and antiandrogen therapy. J Cutan Med Surg 2007; 11(4): 125–31. 68. Sharon-Guidettin A, Ziv Y, Kummer E, Yogev R, Halevy A. Granulocyte-macrophage colony-stimulating factor for perianal hidradenitis suppurativa: report of a case. DCR 2006; 49(5): 682–4. 69. Thielen AM, Barde C, Saurat JH. Long-term infliximab for severe hidradenitis suppurativa. Br J Derm 2006; 155(5): 1105–7. 70. Pedraz ZJ, Dauden E, Perez-Gala S, Goiriz-Valdes R, Fernandez-Penas P, Garcia-Diez A. Hidradentis suppurativa. Response to treatment with infliximab. Actas Dermosifiliogr 2007; 98(5): 325–31. 71. Brocard A, Knol AC, Khammari A, Dreno B. HS and zinc: a new therapeutic approach. A pilot study. Dermatology 2007; 214(4): 325–7. 72. Mandal A, Watson J. Experience with different treatment modules in HS: a study of 106 cases. Surgeon 2005; 3(1): 23–6. 73. Endo Y, Tamura A, Ishikawa O, Miyachi Y. Perianal hidradenitis suppurativa: early surgical treatment gives good results in chronic or recurrent cases. Br J Derm 1998; 139: 906–10.

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22

Surgical treatment of fecal incontinence Ann C Lowry and Dimitrios Christoforidis

Challenging Case A 35-year-old woman presents to your office with complains of fecal incontinence. She is G3 P3, all vaginal deliveries and one child was 8 pounds. The patient reports fecal soiling for the last year with progressive uncontrolled passage of flatus and occasional identification of stool in her undergarments that she was unaware of having passed. There is additional incontinence associated with athletic activity. The incontinence severely affects the patient’s life style. Case Management A complete history identifies no additional risk factors. Physical examination reveals a thinned perineal body, decreased resting tone, weak squeeze (especially anterior), and an anterior sphincter defect. A flexible sigmoidoscopy was normal, anorectal manometry documents low resting tone and squeeze pressure. An anal ultrasound confirms an anterior sphincter defect. The patient is recommended to undergo an overlapping sphincter repair. Epidemiology Fecal incontinence (FI) is a common and underreported condition. It is embarrassing, stressful, and often leads to social isolation. Nevertheless, only a third of symptomatic patients in the USA discuss their fecal incontinence with their physician.(1) The reported prevalence of FI varies depending on the population studied and definition used. In nursing homes, it affects nearly 50% of residents.(2, 3) In a recent systematic review including 16 studies from across the world, the estimated prevalence of fecal incontinence (excluding flatus incontinence) varied from 0.4% to 18%. A community based US telephone survey found a prevalence of 2.2%.(4) A study from the UK analyzed over 10,000 questionnaires from community-dwellers using more strict criteria; Major FI, defined as soiling of underwear, outer clothing or bedding at least several times a month, was reported by 0.9 % adults aged 40–64 years and by 2.3% of adults aged 65 years and older.(5) In this and other epidemiology studies, men were found to be equally affected by FI as women. However, clinical series on FI are dominated by female patients as women seem to seek medical attention more often. The true reason for that is unknown. Beyond the psychological burden and the medical morbidity (such as urinary tract infections, skin breakdown, decubitus ulcers) FI causes significant expense. Estimating total costs is difficult because of imprecise prevalence data and frequency of coexisting medical conditions. By analogy, urinary incontinence was estimated to generate direct and indirect costs exceeding $14 billion in the year 2000 for US community dwellers.(6) In a US study of 63 women with FI secondary to obstetric injury, the average cost for evaluation and treatment of FI was 17,166 USD per patient in 1999.(7) FI is obviously a significant public health problem that deserves more attention.

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Etiology The physiology of the continence mechanism is complex. Sche­ matically, continence requires an anal sphincter and a rectal reservoir that are anatomically intact, normally innervated, and coordinated, a manageable fecal bolus and an adequate level of awareness and desire to avoid incontinence. A great number of conditions, traumatic events, diseases, or medication may affect continence at one or more of these levels at various degrees. FI is often multifactorial and causality is not always easy to establish. Therefore, it may be more appropriate to talk about risk factors rather than causes in the etiological assessment of a patient with FI. Anal sphincter In women with FI, the most prevalent risk factor is childbirth. The incidence of third or fourth degree tears identified clinically at the time of vaginal delivery is 0.6 to 9%.(8) The clinical incidence is an underestimate of the true sphincter injury rate, as demonstrated by studies employing ultrasound imaging. A metaanalysis of five large prospective studies assessing the integrity of the anal sphincter after vaginal delivery with 2-dimensional endosonography revealed a 27% incidence of anal sphincter defect in primiparous women and an 8.5% incidence of new sphincter defects in ­multiparous women.(9) Another study using improved 3-dimensional endosonography on 55 primiparous women reported evidence of trauma in 29% but only 11% had evidence of external sphincter injury.(10) Among those women with a documented third degree tear, FI will develop in one-third to two-thirds.(8, 9) In the general population the true incidence of persistent postpartum FI of solid stool is unknown but can be approximately estimated at 3%. Other than obstetric trauma, the anatomical integrity of the sphincter complex can be disrupted by iatrogenic trauma during anorectal surgery and accidental trauma or be the result of a congenital malformation such as imperforate anus. In addition to structural defects, alteration of sphincter innervation also contributes to decreased sphincter function. It is well recognized that traction injury to the pudendal nerve during pregnancy and delivery contributes to obstetric-injury-related FI.(11) Various conditions affecting the pelvic nerves, the spinal cord or the brain may also result in sphincter atrophy and loss of anal canal tone (Table 22.1). Rectum The reservoir function of the rectum may be impaired secondary to a) loss of capacity after rectal resection or space occupying lesions, b) loss of compliance secondary to inflammatory bowel disease, pelvic radiation, rectal ischemia, or collagen vascular diseases and, c) loss of innervation following surgery, trauma, or neurologic degenerative disease. Rectal mucosal prolapse or full thickness rectal prolapse may cause FI by preventing complete

surgical treatment of fecal incontinence Table 22.1  Pathophysiology classification of risk factors for FI. Brain – central awareness Dementia CVA Brain tumor, infection, trauma Psychiatric disorder Psychotropic drugs Bowel – Fecal bolus Diarrheal states (malabsorption, IBD, infectious diarrhea, short gut syndrome, radiation enteritis, laxative abuse etc.) IBS Proctitis (radiation, IBD) Gastrointestinal stimulant drugs and foods (caffeine, alcohol, aspartamine etc) Anorectum – Neurologic impairment Spinal cord trauma, surgery, hernia, neoplasm Diabetes mellitus Multiple sclerosis spina bifida (myelo)meningocele pelvic fracture Pelvic radiation prostatectomy proctectomy obstetric injury rectal prolapse chronic straining pelvic floor descent aging idiopathic Rectum – anatomic impairment Sphincter-saving operations (low anterior resection, coloanal anastomosis, restorative proctectomy procedures) Rectal neoplasm Extrinsic compression Collagen vascular disease Rectal ischemia Pelvic radiation Rectal agenesis Anal sphincter – anatomic impairment obstetric injury anorectal surgery (fistula surgery, internal sphincterotomy, anal stretch, hemorrhoid surgery) anal impalement anal intercourse imperforate anus Pseudoincontinence anorectal condition: prolapsing hemorrhoids, rectal prolapse, fistula in ano troublesome hygiene: obesity, physical disability

sphincter closure; if left untreated, these conditions may lead to sphincter and pudendal nerve damage. Fecal bolus Formed stool is easier to control than liquid stool. An accelerated intestinal transit with increased stool volume can cause urgency and soiling even in patients with normal anorectal function and will precipitate true FI in a patient with a weakened continence mechanism. Constipation on the other hand, can lead to impaction and overflow incontinence in patients with deficient rectal sensation combined with weakened sphincter muscles.

Central Nervous System Patients with dementia, some psychiatric disorders, or residual deficits from a stroke may lack awareness or interest in bowel function and become incontinent. This type of FI is more prevalent in elderly and institutionalized patients. Evaluation Assessment of severity There is no objective test that reliably correlates with patient reported frequency and type of fecal incontinence. Since the physical morbidity associated with FI is minimal and the mortality practically null, morbidity and mortality data is not useful to measure severity. However, the impact of FI on quality of life is immense. Consequently, any effort to rate FI should be based on the patient’s reported frequency and type of FI and its effect on quality of life. Baxter et al. (12) categorized the available measures of FI into a) descriptive measures (e.g., Mayo Clinic FI Questionnaire, Osterberg Assessment of FI, and constipation), b) severity scores including grading systems (e.g., Parks’ scale, Williams scale) and summary scores (e.g., FI Severity Index (FISI), Cleveland Clinic Florida FI score (CCF-FI), Vaizey score) and c) impact measures which can be disease specific (e.g., Fecal Incontinence Quality of Life (FIQL), FI-Manchester Health Questionnaire) or global (e.g., SF-36). A diary is a useful way to document the frequency and type of FI episodes; the data can be used to calculate a score or simply reported as number of FI episodes per week or days with FI per week. In clinical practice, FI is often described as minor (mostly underwear staining and/or gas incontinence without unintentional loss of true bowel movements) or major (accidental loss of partial or whole bowel movements), urge or passive incontinence. Obviously, these descriptions are insufficient to compare patients in studies or to assess treatment outcome precisely. Popular measures in research are severity summary scores. They are usually based on frequency and type of FI episode. Some systems incorporate the use of a pad or the presence of lifestyle alteration. However, few scoring systems are based upon patient’s perspective in the assignment of values. Most of these scores attribute the same importance to episodes of gas incontinence as episodes of solid stool incontinence. An exception is the FISI which was designed based on patients’ numerical ratings of severity of various frequencies of gas, mucus, liquid stool, and solid stool incontinence.(13) Nevertheless, frequency-based scores, even with a meticulous use of a FI diary to register events, will overlook the fact that patients often make dramatic lifestyle changes to avoid FI episodes. Therefore, a validated impact measure such as the FIQL (14) should be used in addition to severity summary scores. History and Physical The goals of a thorough history in a patient with FI are multiple. First, the interview should define character (seepage, passive/urge), severity, and impact on quality of FI. The character often ­suggests the underlying physiopathology. Generally, internal sphincter defects, prolapse or loss of sensation cause seepage and passive incontinence whereas external sphincter defects cause primarily urge incontinence. A deficient rectal reservoir through loss of capacity or ­compliance

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improved outcomes in colon and rectal surgery will result in urge incontinence as well with stool clustering and increased frequency. Secondly, the history should identify concomitant symptoms, such as urinary incontinence and pelvic organ prolapse since FI is frequently only part of a more general pelvic floor dysfunction. Thirdly, questions should elicit underlying risk factors, particularly those that are readily corrected (Table 22.1). Emphasis must be given to a detailed obstetric history to identify surrogate markers of a traumatic childbirth (instrumental delivery, prolonged second stage of labor, birth weight greater than 4 kg, episiotomy) (8) and to evaluate the presence of FI symptoms in the postpartum period. A careful assessment of stool consistency and defecation habits will help determine the potential benefits of a bowel regulating treatment. Finally, a detailed history of FI will guide selection of appropriate investigations. Physical examination should identify possible causes, effects and coexisting conditions of FI. Perineal scarring, diminished perineal body, or palpable sphincter defects will suggest obstetric trauma. A patulous anus is a sign of sphincter denervation. Dermatitis and excoriation result from prolonged exposure to feces and poor hygiene. Furthermore the clinician should actively look for any anorectal conditions causing “pseudo-incontinence” such as rectal prolapse or prolapsing hemorrhoids, skin tags, mucosal ectropion, or fistula in-ano. Digital rectal examination provides gross information on sphincter bulk, anal canal tone, anal stenosis, and presence of masses. A vaginal exam is essential to assess for coexisting conditions such as rectocele, enterocele, uterine or vaginal apex prolapse and cystocele. Additional studies The aim of additional studies is to identify the cause of FI and risk factors amenable to treatment. Endoscopic examination, at least a flexible sigmoidoscopy if not a full colonoscopy, should be performed to rule out conditions that may contribute to FI such as polyps, malignant lesions, or inflammatory bowel disease. A variety of anorectal physiology tests (ARP) are available to further clarify the etiology of FI. Sphincter anatomy can be assessed by endoanal ultrasound or MRI; resting and squeeze anal canal pressures can be measured by manometry; anorectal sensation and reflexes (minimal volume to elicit sensation, maximal tolerated volume, presence of rectoanal inhibitory reflex) can be estimated by balloon inflation manometry or with techniques that measure thermal change sensitivity or mucosal electrosensitivity; integrity of sphincter innervation can be evaluated by pudendal nerve terminal motor latency and electromyography; defecation dynamics can be assessed by barium cinedefecography, balloon expulsion tests, and more recently by dynamic MRI. However, the need for ARP testing outside of research centers is still debated (15–17) for several reasons. There is relative absence of standardization of test techniques and norm values established from large cohorts of healthy individuals. Few studies have shown clear correlations between baseline ARP and treatment outcome. Studies evaluating the clinical utility of ARP have all too often included only small numbers of patients and contained important design flaws. Having said that, in these studies ARP testing appeared to improve the understanding of etiology and change treatment strategy of FI in approximately 15%.(18–20) Most changes in treatment strategy were due to

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more accurate assessment of sphincter defects with endoanal ultrasound (EAUS). Since the decision between medical or surgical management (sphincter repair) of FI is largely based on the extent of sphincter injury, imaging of the sphincter makes sense. Both EAUS and MRI (with endorectal coil) appear to be highly accurate in identifying sphincter defects (21), especially of the distal part of the anal canal.(22) EAUS has the advantage of being inexpensive and readily available. Three-dimensional EAUS (Figure 22.1a and 22.1b) and transperineal ultrasound may further increase accuracy.(23, 24) MRI depicts the external

(a)

ES

IS

(b)

s

ES IS

Figures 22.1a and 22.1b  (a)EAUS image of a normal anal canal with complete internal sphincter (IS) hypoechogenic ring and external sphincter (ES) hyperechogenic ring. (b)EAUS image of anal canal with a wide internal (IS) and external sphincter (ES) defect. Note the thickening and retraction of the internal sphincter and the anterior scar (S) replacing the external sphincter.

surgical treatment of fecal incontinence sphincter clearly because of the contrast between fat and ­striated muscle and accurately visualizes external sphincter atrophy. External sphincter atrophy can also be accurately diagnosed with 3D-EAS (25); its significance is not fully understood but it may adversely affect outcome after sphincterplasty.(26) The value of sphincter imaging has also been demonstrated in men with FI. The presence of a sphincter defect –an internal sphincter defect secondary to anal surgery in the vast majority of men – was a clear predictor of failure of conservative ­management.(27) In conclusion, the assessment of a patient with FI must include a directed, detailed history and examination. After excluding cases of “pseudo-incontinence” or minor seepage additional work-up must include endoscopy and sphincter imaging, especially if treatment with sphincteroplasty is considered. Defecography is helpful to confirm suspected rectal procidentia. The utility of further ARP studies will depend on local availability and expertise. Treatment Medical therapy Initial treatment of FI should be conservative even if there is little evidence to guide clinicians in the selection of drug therapies.(28) The main targets of medical treatment of FI are intestinal transit and stool consistency. A thorough work-up is mandatory in patients with FI related to chronic diarrhea to identify and treat the underlying cause of diarrhea. Dietary changes and prescription of either fiber supplementation or fiber restriction must be individualized to each patient as the change in bowel transit can be very variable.(29) In a placebo controlled trial, psyllium and gum arabic, two natural soluble fibers, were shown to reduce by 50% the proportion of incontinent stools in 39 patients with FI of loose or liquid stools.(30) Antidiarrheal medication (loperamide, diphenoxylate plus atropine, bile-acid binders, codeine) is the next step in medical management of FI. Loperamide has been shown to be more effective than diphenoxylate plus atropine, and have fewer side effects than both diphenoxylate plus atropine and codeine.(31) In addition to its effect on intestinal motility, loperamide may improve sphincter tone and rectal sensation.(32) In an open label trial in 18 patients with idiopathic FI, amitriptyline, a tricyclic antidepressant agent, was shown to improve FI scores in 89% of patients after 4 weeks of treatment; the proposed mechanism is a decrease in ­rectal motor complexes and stool frequency.(33) Further studies are needed to evaluate the true efficacy of this drug. A different approach of medical treatment is to enhance anal sphincter function by application of topical agents, such as phenylephrine gel, an α1-adrenergic agonist. Three small double blind placebo trials from the St. Mark’s hospital in the UK showed significant improvement in sphincter tone (34) and FI symptoms in half of ileal pouch patients (35) and in one third of FI patients with anatomically intact sphincters.(36) Conversely, Park et al. (37) in a double blind trial on 35 patients with FI after low anterior resection found no improvement in FI or quality of life scores with 30% topical phenylephrine compared to placebo. Limited efficacy combined with frequent allergic reactions, limits wider acceptance of this treatment. Constipation and impaction can lead to overflow incontinence. Such patients will benefit from routine tap-water enemas or laxatives to empty the rectum regularly. Patients with postdefecation

seepage may also benefit from routine enemas as well as application of cotton wicks at the anus and barrier creams to avoid excoriation and pruritus. Anal plugs for the management of FI is a different approach that appears intuitive to many patients. A recent Cochrane review of published randomized trials suggested that anal plugs seem to be difficult to tolerate but if they are tolerated, they can be a useful tool in FI prevention either as substitute or adjuvant treatment option.(38) Anal plug models exist in a variety of forms, sizes, material, and function. Devices with intrarectal sensors alerting the patient of an imminent bowel movement with a beep have also been described.(39, 40) Biofeedback The goal of biofeedback is to improve external sphincter contraction (strength and duration) in response to rectal distention by providing the patient with feedback information on performance and progress. In general, three different protocols are used: (1) coordination training, which teaches patients to contract their external sphincter muscle in response to rectal distention counteracting the reflex internal sphincter relaxation; (2) sensory training, which teaches patients to recognize progressively smaller volumes of rectal distention enabling them to contract the sphincter in time; and (3) strength training, which teaches patients to isolate and exercise their sphincter muscle without using rectal distention. In most centers, either manometry equipment or an EMG probe is used to provide “feedback” information to patients. The three training methods are sometimes combined; the length and number of sessions varies widely. Biofeedback is widely used and often included as first line option in treatment algorithms for FI. No obvious clinical or physiologic predictors of success have been identified. Patient age, etiology of FI, duration, and severity of symptoms do not appear to predict outcome; biofeedback has been used successfully in a variety of situations including presence of external sphincter defects (41) or in patients with poor functional outcome after sphincteroplasty for obstetric injury.(42) A systematic review on biofeedback through 2000 (43) found 46 original studies, only 8 of which employed some form of control arm. All but one study (44), which included patients with neurogenic FI, reported improvement of symptoms in a range of 53–100% of patients. Overall, 617 of 861 (72%) reported to be cured or improved. The same author performed a Cochrane review (45), including only randomized or quasi randomized trials and concluded that the current literature provides no evidence that biofeedback or anal sphincter and pelvic floor exercises improve outcome compared to other conservative management methods. Training to enhance rectal discrimination of sensation seemed to be helpful in reducing FI in one short follow-up ­randomized study.(46) In absence of high level evidence, interpreting the ­literature on biofeedback is problematic. Some patients seem to benefit and there has been no morbidity reported. High motivation both from the patient’s and therapist’s side are crucial p ­ rerequisites for a successful outcome. Sphincteroplasty Anal sphincteroplasty is an appropriate therapy for patients with significant FI, unresponsive to medical therapy and a documented anal sphincter defect.



improved outcomes in colon and rectal surgery Overlapping sphincteroplasty is usually performed under general anesthesia, in the prone jack knife position after prior mechanical bowel preparation and prophylactic antibiotics. A curvilinear incision is made in the perineal skin closer to the vaginal introitus than the anus to preserve tissue on the anal side. A Lone Star® retractor is used for exposure and a needle tip electrocautery is preferred for more precise dissection with less char. The external sphincter, en bloc with the internal sphincter and anterior scar tissue is mobilized and dissected free from the skin and ischiorectal fat laterally, from the posterior vaginal wall anteriorly and from the anoderm and rectal wall posteriorly. Careful dissection, occasionally aided by inserting a finger in the vaginal or rectal side, avoids buttonholing, especially on the rectal side. Any injured venous sinuses on the posterior vaginal wall should be suture ligated to avoid delayed hemorrhage. Care must be taken with the posterolateral portions of the dissection to avoid injury to branches of the pudendal nerve. Dissection in the midline continues until soft, pliable tissue is reached on both the vaginal and rectal sides and laterally until the two ends of the external sphincter can be overlapped several centimeters without tension. If the midline tissue is entirely scar tissue, it is divided to perform an overlapping repair. If muscle is encountered in the midline it is left intact and an imbricating repair rather than overlapping repair is performed. The overlapping repair is done with absorbable 2–0 monofilament mattress sutures creating a snug anal opening without excess tension on the mobilized tissue. The wound is closed in a vertical or “T” fashion to decrease tension on the skin. The center of the incision is left open and a short ¼ inch Penrose or closed suction drain is placed through the opening to facilitate drainage. The drain is removed before the patient’s discharge. Vaginal packing may be placed to help with hemostasis and if used is typically removed the next day. If planned, anterior levatoroplasty is performed before the overlap. Proponents argue that the levatoroplasty adds essential bulk to the perineal body and lengthens the anal canal. Opponents believe that a levatoroplasty increases the incidence of postoperative dyspaurenia. Diversion of the fecal stream did not improve healing or functional results of the repair in a randomized trial.(47) As with any perineal wound, healing after overlapping sphincteroplasty is slow with frequent separation of the skin edges. Postoperative care includes the avoidance of impaction with the use of bulk agents and tap water enemas and protection of the

surrounding skin with barrier ointments. Vaginal tampons and intercourse are proscribed for 6 weeks. One variation is the approximation of the ends of the sphincter muscle rather than overlapping them. This technique is particularly appropriate when a portion of the muscle is intact. In a randomized study by Tjandra et al. (48) of 23 women with anterior sphincter defects on EAUS, no functional difference was found between patients repaired with the approximation technique and those undergoing an overlapping repair. Functional results after overlapping sphincteroplasty are good or excellent approximately in two-thirds of patients in studies with a follow-up under 4 years (Table 22.2a) and approximately in one half of patients in studies with a longer follow-up (Table 22.2b). Bravo-Gutierrez et al. reviewed functional outcome a median of 10 years after sphincteroplasty in 130 women and found that 58% reported some incontinence of solid stool compared to 36% at a 3 years follow-up.(49) Similarly, Barisic et al. found increased failure rates with time as poor results were reported by 39% at 80 months compared to 9% at 3 months.(50) Malouf et al. reviewed the results of sphincter repair in 46 patients a median (range) of 77 (60–96) months.(51) Excluding 8 immediate failures 85% of the others reported improvement at 15 months but only 50% at 77 months. Only 4 patients were completely continent of stool but the median subjective rating of satisfaction with the

Table 22.2a  Functional results of sphincteroplasty – short and midterm follow-up. Author Year n

Months Follow-up Median Excellent (range) or Good

Fair Poor

Nikiteas (106) Oliveira (107) Young (108) Gilliland (109) Karoui (110) Buie (111) Morren (112) Pinta (113) Evans (114)

38 (12–66) 29* 18 24 (2–96) 40a 43a (6–120) 40 (5–137) 22 (2–99) 45*

17% 9% — 14% — 26% 24% 38% —

1996 1996 1998 1998 2000 2001 2001 2003 2006

42 55 57 77 86 158 55 39 66

60% 71% 86% 55% 81% 62% 56% 31% 77%

23% 20% 14% 31% 19% 12% 20% 31% —

a. Mean.

Table 22.2b  Functional results of sphincteroplasty – long term follow-up. Author

Year

n included/n initial

Londono-Schimmer (115)

1994



94/128

Malouf (51)

2000



46/55

Halverson (116)

2002



Zorcolo (117)

2005

Barisic (50)

Years Follow-up Median (range)

Excellent or Good

Fair

4.9 (1–8.2)

50%

25%



25%

6.4 (5–8)

50%





41%

49/71

5.3 (2–11.8)

49%

—



51%



62/93

5.8a (2–9.3)

54%

16%



30%

2006



56/65

6.7a

48%

13%



39%

Bravo-Gutierrez (49)

2004



130/182

10 (7–16)

41%

—



57%

Maleskar (52)

2007



64/72

at 7

62%

24%



15%

Grey (118)

2007



47/85

5–12

60%

36%



4%

a. Mean.



9%

Poor

surgical treatment of fecal incontinence long term results was 8 out of 10. Other studies document more optimistic results. Maleskar et al. reported on 64 of 72 patients responding to a questionnaire after a median of 7 years.(52) The median CCF-FI score dropped from 16 preoperatively to 5 at 12 months and to 7 at a median follow-up of 7 years. Ninety five percent of patients were satisfied with the results and 62% were fully continent or incontinent to gas only. Interestingly, Vaizey et al. found no difference in incontinence scores, patient rating of improvement or satisfaction between the findings at 20 months and 60 months in a group of patients who underwent a repeat sphincter repair following a failed repair.(53) If the initial repair fails and a persistent defect is demonstrated by ultrasound, repeat sphincteroplasty can still provide satisfactory results (54, 55) even with long-term follow-up.(53) Breakdown of the wrap is not the only cause of failure. Progressive neuropathy and the aging process in general are thought to contribute to some deterioration of symptoms over time. Patients with poor results may be candidates for biofeedback, artificial bowel sphincter, or sacral nerve stimulation. The role of sphincteroplasty in patients with incontinence and sphincter defects is evolving with the addition of new modalities of therapy. Further research is necessary to determine which patients are appropriate candidates and whether adjunct therapies such as biofeedback or sacral nerve stimulation would improve the functional results. Artificial Bowel Sphincter The artificial bowel sphincter (ABS) is a treatment modality for urinary incontinence which was adapted for FI. In 1996, the manufacturing company (American Medical Systems, Minnetonka, MN, USA) adapted the original device for its use in FI as the ActiconTM Neosphincter device. Although other models have been recently developed (56, 57), this device is the most widely employed and reported in the literature. The ABS consists of three components: an inflatable cuff, placed around the deficient sphincter, a pressure-regulating balloon placed in the retropubic space, and a control pump placed in the scrotum or labia. The three components and the connecting tubing are filled with saline. In the neutral state, the fluid fills the cuff occluding the anal canal. When the patient desires to defecate, he empties the cuff by manually compressing the pump, which pushes the fluid into the pressure regulating balloon. The cuff refills spontaneously in approximately 45 seconds. The ABS is an invasive procedure with significant morbidity. Candidates include patients who have failed all medical treatment and are not candidates for a sphincter repair. Sufficient perineal tissue without excessive scarring or prior radiation and a normal rectal reservoir are required to minimize risk for late erosion and dysfunction.(58) Mundy et al. (59) performed a systematic review of the literature published through 2002 on safety and effectiveness of ABS in FI. They included 13 case series involving 1 to 112 patients with a mean follow-up time of up to 60 months. No study included a control group or reported intention to treat results preventing judgment of the true effectiveness of ABS. Approximately a third to half of patients needed surgical revision of the ABS and one quarter required explantation, most commonly because of

infection or erosion. Wound healing problems, material breakage or migration, fecal impaction, chronic pain, and dissatisfaction also occurred. In patients with successful implantation, all studies reported clinically significant improvements in FI severity and quality of life. O’Brien et al. (60) performed a randomized trial on 14 patients with severe FI comparing ABS to optimal medical therapy. In the ABS group one out of seven patients had explantation of the device after failed wound healing and two had prolonged hospitalization for repeated fecal impaction or wound healing problems. At 6 months, the Cleveland Continence Score showed a 75% improvement in the ABS group with significantly better quality of life scores. No significant changes were observed in the medical treatment group. Long term follow-up studies on ABS report higher rates of reintervention and explantation with a functional ABS (61–63) remaining in approximately 50 to 60% of patients. Patients who retained their ABS seemed to have sustained improvement of FI and quality of life over time (63) but a significant number experience evacuation difficulties.(58, 61) Michot et al. (58) found a reduction of the explantation rate from 50% to 20% when comparing their early and late experience. The authors related this improvement to better patient selection and liberal use of diverting colostomy. Parker et al. (63) found no difference in failure rates over time. A convened “best practice group” of colorectal surgeons, whose infection rate was 9% and long term functional device rate 82% have recently introduced a protocol to minimize infection.(64) ABS provides good continence in those patients who retain their device at the expense of significant surgical morbidity and possible chronic evacuation difficulties. Recent guidelines for intraoperative prevention of infection may help improve outcomes by decreasing morbidity. Dynamic graciloplasty The concept behind dynamic graciloplasty (DGP) is to create a sphincter with an autologous striated muscle wrap. The muscle is then stimulated with a constant low-frequency electric current by an implantable pulse generator with the goal of inducing the fast-twitch, readily fatigued (Type II) muscle fibers to change to slow-twitch, fatigue resistant (Type I) muscle fibers, similar to the normal external sphincter. A pedicled gracilis flap is harvested on one side, transposed, wrapped around the anus and anchored with its distal tendon to the contralateral ischial tuberosity. The electrode is implanted in the muscle or close to the obturator nerve and the stimulator is implanted in the lower abdomen, subcutaneously or beneath the rectus sheath. Increasing levels of neurostimulation are used to condition the muscle during the first 2 months. Thereafter, the patient can regulate defecation with the aid of an external magnet by turning the stimulator off to relax the muscle allowing emptying of the rectum and turning the stimulator back on to maintain continence. Similar to ABS, DGP is reserved as an alternative to colostomy for patients suffering severe FI unresponsive to simpler treatment. As opposed to the ABS, DPG involves transposition of healthy tissue and can be applied even to patients with severe loss of perineal tissue.



improved outcomes in colon and rectal surgery A systematic review of the literature through 1999 on DGP by the Australian Safety and Efficacy Register of New Interventional Procedures-Surgical found that DGP was effective at restoring continence in 42 to 85% of patients but was associated with an average risk of complications of 1.12 per patient and reoperation of 0.14 to 1.07 per patient (65); none of the included studies provided a high level of evidence. Overall DGP related mortality was 1% and the most common complications were infection (28%), hardware dysfunction, or displacement (15%) and leg pain (13%). The Dynamic Graciloplasty Therapy Study Group undertook a large international multicenter prospective trial including 115 eligible patients, 27 of whom had a preexisting functioning stoma.(66–68) The success rate, defined as 50% or more reduction in incontinent episodes, was 62% at 12 months and 56% at 24 months for nonstoma patients and 37.5% and 43% in patients with preexisting stoma at 12 and 24 months respectively. Significant improvement in quality of life subscales was noted. One patient died postoperatively and major complications requiring hospitalization or surgical intervention occurred 89 times in 61 (50%) patients; 90% resolved completely. Rongen et al. (69) from the Maastricht group reported the largest single center experience with DGP on 200 consecutive patients with a median follow-up of 5 years. The success rate (continent to solid and liquid stool) was 72%, ranging from 52% in patients with congenital FI to 82% in patients with traumatic FI. The success seemed to persist over time as complications decreased and technical success improved. Chronic evacuation problems persisted in 16% of the patients. The indications for sphincter replacement surgery either with ABS or DGP are decreasing in favor of SNS (70) given the significant difference in morbidity. DGP is not available in the USA as the producer of the stimulator (Medtronic Corporation, Minneapolis, MN) decided not to pursue FDA approval. Sacral Nerve Stimulation Sacral Nerve Stimulation (SNS) is an innovative and rapidly expanding treatment modality. It has been used for urinary incontinence since 1981 and was approved by the FDA for that indication in 1997. The observation that bowel symptoms simultaneously improved in many patients led to the first implantation of a sacral nerve stimulator to treat FI in 1994.(71) In the USA, a multicenter study completed enrollment of 120 patients in 2006 and the manufacturer (Medtronic Corporation, Minneapolis, MN) is expected to pursue FDA approval in 2008. The goal of placing a stimulating electrode into the sacral foramina was to recruit residual function of the striated pelvic floor and external sphincter muscles. Initial selection criteria for SNS stipulated reduced or absent voluntary sphincter function, intact nerve-muscle connection and an intact sphincter muscle.(72) It became apparent that the effect of SNS was not limited to an increase of voluntary squeeze pressure. Somewhat inconclusive and often contradictory, studies suggest that SNS may decrease urge thresholds, reduce spontaneous rectal motility, reduce spontaneous sphincter relaxation, and improve anal and perianal skin sensitivity.(72) Sheldon et al. (73) showed in a crossover study in 10 women with FI that SNS also affects the central nervous system; they documented a decrease in corticoanal excitability. More recently, in a cohort of patients with FI successfully treated with SNS, Gooneratne et al. (74) demonstrated



a normalization of elevated levels of rectal mucosal substance P, a substance known to play a role in contractility and afferent signaling in ­visceral sensation. While the understanding of the physiology of SNS still remains unclear, patient selection has become more pragmatic. The efficacy of SNS can be tested on an individual patient temporarily with minimal consequences and a high predictive value of permanent therapeutic effect. The screening procedure consists of a percutaneous stimulation of the S2–S4 roots on both sides. The testing is done under local or general anesthesia by insertion of a needle electrode into the dorsal sacral foramina. The site ­providing the most effective bellows-like motion of the pelvic floor along with plantar flexion of the first and second toes (typically S3 root) is selected for temporary stimulation. Continuous stimulation is applied for a minimum of 1 week. If the stimulation is well tolerated and successful (50% or greater reduction in incontinent episodes per week or days with incontinence per week), a permanent pulse generator is connected to the electrode and implanted. Surgical replacement of the battery is necessary after 7–10 years for Interstim I and 5–7 years for the newer and smaller model Interstim II. More than 75% of patients tested with temporary stimulation will have a 50% or more improvement in symptoms, which is required to justify permanent implantation (Table 22.3). The therapeutic benefit seems to persist in studies with follow-up over 2 years.(75–77) SNS has been shown not only to decrease the frequency of FI but also to improve the ability to postpone defecation (76), improve sexual activity (78) and quality of life. (72, 79) A Swiss group performed a cost analysis on a cohort of 36 patients including expenses generated by failures and complications and found that SNS is more cost efficient than colostomy or dynamic graciloplasty but obviously more expensive than ­conservative treatment alone.(80) The indications for SNS have progressively expanded. Accepted contraindications include conditions where implantation is impossible or too risky (e.g., spina bifida, pilonidal sinus, ­pyoderma gangrenosum), chronic diarrhea, irritable bowel syndrome, rectal prolapse, mental or physical inability to adhere to treatment, severe bleeding diathesis, pregnancy, and the presence of cardiac pacemaker or implantable defibrillator.(81) Earlier contraindications such as previous rectal surgery, multiple sclerosis, Parkinson’s disease, and spinal cord injury have been recently challenged. (82) The most interesting controversial issue is the use of SNS in patients with FI and sphincter defects as these patients are traditionally treated with sphincteroplasty. Initial studies did not include patients with sphincter defects except very minor ones. Dudding et al. (83) analyzed the 10 year experience with SNS at St. Mark’s hospital in the UK in an effort to identify predictive factors of success. Patients with evidence of sphincter trauma had a greater risk of failure compared to patients with intact sphincters (7/29 vs. 0/16, p=0.04). Conversely, in a retrospective study, Melenhorst et al. (84) compared a group of women with a functionally failed but anatomically intact previous sphincter repair to a group of women with an external sphincter defect of 17–30%. They found no significant difference in baseline characteristics and a similar outcome after a 2-year follow-up. In a controlled randomized study Tjandra et al. compared SNS to optimal medical treatment. Close to half of patients in the SNS arm had evidence of external

surgical treatment of fecal incontinence Table 22.3  Functional results of SNS in large studies. Temporary Stimulation (n)

Permanent Stimulation (n %)

f-up time months

Baseline FI Episodes (n)

Final FI Episodes (n)

Fully Continent (n %)

Author

Year

Study Design

Matzel (76)

2004

prosp MC



37



34 (92)

24



8.3b



0.75

Jarrett (119)

2004

prosp MC



59



46 (78)

12



7.5b



1

19 (41)

Leroi (120)

2005

RCT MC DB cross



34



27 (79)

6–8a



7b



1

  5 (26)

12 (37)

Melenhorst (77)

2006

observ SC



134

100 (75)

26



31.3c



4.4

nr

Holzer (121)

2007

observ SC



36



29 (81)

35



7c



2

nr

Hetzer (79)

2007

observ SC



44



37 (84)

13



14b



5

nr

Tjandra (85)

2008

RCT MC



60



54 (90)

12°





3.1

25 (47)

9.5b

a. timepoint of evaluation. b. median number of FI episodes per week. c. median or mean number of FI episodes per 3 weeks; all differences statistically significant. prosp MC: prospective multicenter. observ SC: observational single center. RCT: randomized controlled trial. DB cross: double blind cross over.

sphincter defect (120° or less) and more than half had a previous sphincter repair. Despite that, excellent results were achieved in the SNS arm as 66% of patients had a 75–100% reduction of incontinent episodes per week. On the contrary, patients in the medical treatment arm experienced no change in FI severity or FI-related quality of life scores. In absence of a randomized study that specifically addresses the question, there is currently no evidence to support the idea that SNS should replace sphincteroplasty as available studies are subject to important patient selection bias. Complications with SNS are rare and include wound problems (dehiscence, seroma, infection, bleeding), electrode dislodgment or fracture, pain at the site of the electrode or pulse generator, excessive tingling in the vaginal region, loss of effect, or deterioration of bowel symptoms. Complications leading to explantation of the stimulator occur in approximately 5%.(72, 85) The role of SNS in the treatment of FI is expected to grow. Further understanding of the physiology involved may improve patient selection and stimulation modes. Peripheral nerve stimulation may render the technique simpler and applicable to patients with sacral abnormalities. Transcutaneous intermittent stimulation of the posterior tibial nerve has been reported to improve urinary continence and has been tried more recently in FI with encouraging preliminary results.(86, 87) Direct stimulation of the pudendal nerve is another field of investigation. Injectable bulking agents The goal of injectable bulking agents (IBA) is to restore a normal contour of the anal canal and add bulk to provide a better seal. IBA are usually injected under local anesthesia as an office or outpatient procedure; the injections may be into the submucosa or in the intersphincteric space and in all quadrants of the anal canal or at the site of a sphincter defect. Injection under ultrasound guidance in the intersphincteric space yielded better results than digitally guided injections in a randomized study.(88) Small studies have reported the use of Polytetrafluoroethylene (Teflon®), autologous fat, glutaraldehyde cross-linked collagen (Contigen®), textured

silicon particles (Bioplastique®, renamed PTQ implantsTM), and pyrolytic carbon coated zirconium oxide beads (Durasphere®), but their true efficacy remains to be determined. The autologous materials are short lived and adipose tissue injections carry the risk of fat embolism. Cost as well as migration, ulceration, leakage, infection, pain and local, or distal inflammatory reactions are concerns with the synthetic materials. The two most popular agents are PTQ implantsTM and Durasphere®; both were shown to be safe and to attenuate severity of FI in a majority of patients. (88, 89) Quality of life improvements are less pronounced. Results after long-term follow-up are mixed and reinjection is necessary in some patients.(90, 91) An ongoing multicenter randomized placebo controlled study on Durasphere ® injection will hopefully help determine the place of IBA in the treatment of FI.(92, 93) The FDA has not yet approved any IBA for the use in FI. Antegrade colonic enema In 1990, Malone described the creation of a continent stoma using the appendix; this stoma was catheterized to perform ante grade colonic enemas (ACE) in five patients with intractable FI.(94) Modifications of the technique for patients in whom the appendix cannot be used due to previous appendectomy or fibrosis include construction of the stoma with a cecal flap or an “ileal neo-appendix”. ACE is used frequently in pediatric surgery for children with severe defecation disorders following anorectal malformations, spina bifida, sacrococcygeal teratomas and other abnormalities. Several small studies report its use in adults and even in patients undergoing abdomino-perineal resection in combination with a perineal colostomy.(95) Lefevre et al. (96) recently reported 25 adult patients with intractable FI treated with an ACE procedure. After a median follow-up of 21 months, 22 patients were available: 4 had stopped performing enemas but 17 reported perfect cleanliness. They performed enemas once every 2–3 days spending an average of 40 minutes. Stenosis of the mucocutaneous junction occurred in 20%; the majority responded to dilatation. It occurred more often in patients with native appendicostomy



improved outcomes in colon and rectal surgery than in those with an ileal neo-appendicostomy. Quality of life measures showed significant improvement for physical health but persistent low scores in ­psychological distress (96).(96) Others have reported similar success and complication rates.(97–99) As an option before an end colostomy, ACE may be appropriate in some patients with intractable FI, particularly those in whom incontinence is ­combined with constipation and who have failed other therapies. Postanal repair Sir Allan Parks developed the postanal repair in the 1970s relying on the theory that restoration of an obtuse anorectal angle would improve continence by recreating a flap valve mechanism. The procedure was designed to treat neurogenic FI in patients with intact sphincters. Through a V-shaped incision posterior to the anus, the intersphincteric space is dissected proximal to the puborectalis; each muscle layer is plicated in the midline. If an anterior levatorplasty is added, the procedure is called total pelvic floor repair. Browning and Parks (100) reported good to excellent results in over 80% but others have failed to reproduce those findings.(101) Orrom et al. (102) demonstrated that there were no significant changes in the anorectal angle in patients after postanal repair questioning the concept of the operation. Results tend to deteriorate over time (103) which is an additional reason this treatment has fallen out of favor. Colostomy The colostomy is traditionally the end-stage treatment of intractable FI. When it becomes an option, the patient has usually failed several medical and surgical treatments and experienced years of misery and socially debilitating symptoms. The patient must accept a body image change and a whole new type of personal care. Having said that, a colostomy offers undeniable advantages. The patient can remain clean and be socially active. Perineal skin irritation is cured. Special diets or transit regulatory medicine can be stopped. On the other hand, there is a well-known morbidity related to colostomy including immediate postoperative but also longer term complications such as peristomal hernia, skin irritation, and appliance problems. A systematic review compared DGP to colostomy in terms of mortality, morbidity, efficacy, and cost-effectiveness.(65) While it is intuitive that DGP resulted in better continence, mortality was similar and morbidity favored colostomy. Colostomy was more expensive than DGP in the long run provided that DGP does not fail resulting in a late colostomy. There are no good quality studies comparing the quality of life of a patient with severe FI prior and after colostomy. A cross-sectional study comparing patients with rather moderate FI to patients with a well functioning colostomy (the majority secondary to rectal cancer) found no significant difference other than better average adjusted social function scores for ostomates.(104) The two groups however were different; patients with FI were younger and more often female, adding further bias to this study. Data from rectal cancer surgery indicate that an end colostomy after abdominoperineal resection does not always equate to a lower quality of life than sphincter sparing surgery.(105) The option of colostomy should be discussed early enough and adequate counseling should be offered to the patient to allow a mature decision to be taken.



Conclusion Fecal incontinence is a common, underreported, devastating ­condition. The pathophysiology is complex and variable; the ­currently available instruments to measure the degree of dysfunction of the different components are often imprecise and not standardized. The integration of quality of life scores and diarybased results has substantially improved the reporting of severity of FI in the literature. The initial step in management of patients with FI is to diagnose and treat appropriately underlying conditions of “pseudoincontinence” such as hemorrhoids, anal fistula, mucosal prolapse, rectal prolapse and diarrheal conditions. The first line treatment for true FI is medical and aims to regulate bowel frequency and consistency. Biofeedback may provide some relief to motivated patients. Those patients who fail medical treatment and are physically fit enough for surgery should undergo pelvic floor testing with sphincter imaging. Sphincteroplasty is appropriate for patients with significant sphincter defects and low anal canal pressures. For those who are not candidates for sphincteroplasty, SNS seems to be the most promising solution. ABS, DGP, and ACE are second line therapies that should be considered before end colostomy and may lead to good functional outcomes especially in experienced centers. The surgical treatment of FI has evolved significantly over the past 2 decades. Postanal repair and anal encirclement have been practically abandoned. While sphincteroplasty remains central, indications for ABS and DGP are decreasing in favor of SNS. New treatment modalities have been proposed, some were short lived (SECCA procedure), and others are still under investigation (IBA). Despite the multitude of treatment options, the end colostomy may still be the best compromise solution for many severely incontinent patients. References    1. Johanson JF, Lafferty J. Epidemiology of fecal incontinence: the silent affliction. Am J Gastroenterol 1996; 91: 33–6.    2. Borrie MJ, Davidson HA. Incontinence in institutions: costs and contributing factors. CMAJ 1992; 147: 322–8.    3. Nelson R, Furner S, Jesudason V. Fecal incontinence in Wisconsin nursing homes: prevalence and associations. Dis Colon Rectum 1998; 41: 1226–9.    4. Nelson R, Norton N, Cautley E, Furner S. Communitybased prevalence of anal incontinence. JAMA 1995; 274: 559–61.    5. Perry S, Shaw C, McGrother C et al. Prevalence of faecal incontinence in adults aged 40 years or more living in the community. Gut 2002; 50: 480–4.    6. NIH State-of-the-Science Conference Statement on Prevention of Fecal and Urinary Incontinence in Adults. NIH Consens State Sci Statements 2007; 24.    7. Mellgren A, Jensen LL, Zetterstrom JP et al. Long-term cost of fecal incontinence secondary to obstetric injuries. Dis Colon Rectum 1999; 42: 857–65.    8. Dudding TC, Vaizey CJ, Kamm MA. Obstetric anal sphincter injury: incidence, risk factors, and management. Ann Surg 2008; 247: 224–37.    9. Oberwalder M, Connor J, Wexner SD. Meta-analysis to determine the incidence of obstetric anal sphincter damage. Br J Surg 2003; 90: 1333–7.

surgical treatment of fecal incontinence   10. Williams AB, Bartram CI, Halligan S et al. Anal sphincter damage after vaginal delivery using three-dimensional endosonography. Obstet Gynecol 2001; 97: 770–5.   11. Snooks SJ, Setchell M, Swash M, Henry MM. Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet 1984; 2: 546–50.   12. Baxter NN, Rothenberger DA, Lowry AC. Measuring fecal incontinence. Dis Colon Rectum 2003; 46: 1591–605.   13. Rockwood TH, Church JM, Fleshman JW et al. Patient and surgeon ranking of the severity of symptoms associated with fecal incontinence: the fecal incontinence severity index. Dis Colon Rectum 1999; 42: 1525–32.   14. Rockwood TH, Church JM, Fleshman JW et al. Fecal Incontinence Quality of Life Scale: quality of life instrument for patients with fecal incontinence. Dis Colon Rectum 2000; 43: 9–16.   15. Bharucha AE. Pro: anorectal testing is useful in fecal incontinence. Am J Gastroenterol 2006; 101: 2679–81.   16. Rao SS. A balancing view: Fecal incontinence: test or treat empirically--which strategy is best? Am J Gastroenterol 2006; 101: 2683–4.   17. Wald A. Con: Anorectal manometry and imaging are not necessary in patients with fecal incontinence. Am J Gastroenterol 2006; 101: 2681–3.   18. Keating JP, Stewart PJ, Eyers AA, Warner D, Bokey EL. Are special investigations of value in the management of patients with fecal incontinence? Dis Colon Rectum 1997; 40: 896–901.   19. Liberman H, Faria J, Ternent CA et al. A prospective evaluation of the value of anorectal physiology in the management of fecal incontinence. Dis Colon Rectum 2001; 44: 1567–74.   20. Vaizey CJ, Kamm MA. Prospective assessment of the clinical value of anorectal investigations. Digestion 2000; 61: 207–14.   21. Terra MP, Stoker J. The current role of imaging techniques in faecal incontinence. Eur Radiol 2006; 16: 1727–36.   22. Sentovich SM, Blatchford GJ, Rivela LJ et al. Diagnosing anal sphincter injury with transanal ultrasound and manometry. Dis Colon Rectum 1997; 40: 1430–4.   23. Gold DM, Bartram CI, Halligan S et al. Three-dimensional endoanal sonography in assessing anal canal injury. Br J Surg 1999; 86: 365–70.   24. Lee JH, Pretorius DH, Weinstein M et al. Transperineal threedimensional ultrasound in evaluating anal sphincter muscles. Ultrasound Obstet Gynecol 2007; 30: 201–9.   25. Cazemier M, Terra MP, Stoker J et al. Atrophy and defects detection of the external anal sphincter: comparison between three-dimensional anal endosonography and endoanal magnetic resonance imaging. Dis Colon Rectum 2006; 49: 20–7.   26. Briel JW, Stoker J, Rociu E et al. External anal sphincter atrophy on endoanal magnetic resonance imaging adversely affects continence after sphincteroplasty. Br J Surg 1999; 86: 1322–7.   27. Chen H, Humphreys MS, Kettlewell MG et al. Anal ultrasound predicts the response to nonoperative treatment of fecal incontinence in men. Ann Surg 1999; 229: 739–43.

  28. Cheetham M, Brazzelli M, Norton C, Glazener CM. Drug treatment for faecal incontinence in adults. Cochrane Database Syst Rev 2003: Issue 3: CD002116.   29. Lauti M, Scott D, Thompson-Fawcett MW. Fibre supplementation in addition to loperamide for faecal incontinence in adults: a randomized trial. Colorectal Dis 2008; 10(6): 553–62.   30. Bliss DZ, Jung HJ, Savik K et al. Supplementation with dietary fiber improves fecal incontinence. Nurs Res 2001; 50: 203–13.   31. Palmer KR, Corbett CL, Holdsworth CD. Double-blind crossover study comparing loperamide, codeine and diphenoxylate in the treatment of chronic diarrhea. Gastroenterology 1980; 79: 1272–5.   32. Hallgren T, Fasth S, Delbro DS et al. Loperamide improves anal sphincter function and continence after restorative proctocolectomy. Dig Dis Sci 1994; 39: 2612–8.   33. Santoro GA, Eitan BZ, Pryde A, Bartolo DC. Open study of low-dose amitriptyline in the treatment of patients with idiopathic fecal incontinence. Dis Colon Rectum 2000; 43: 1676–81.   34. Cheetham MJ, Kamm MA, Phillips RK. Topical phenylephrine increases anal canal resting pressure in patients with faecal incontinence. Gut 2001; 48: 356–9.   35. Carapeti EA, Kamm MA, Nicholls RJ, Phillips RK. Randomized, controlled trial of topical phenylephrine for fecal incontinence in patients after ileoanal pouch construction. Dis Colon Rectum 2000; 43: 1059–63.   36. Carapeti EA, Kamm MA, Phillips RK. Randomized controlled trial of topical phenylephrine in the treatment of faecal incontinence. Br J Surg 2000; 87: 38–42.   37. Park JS, Kang SB, Kim DW, Namgung HW, Kim HL. The efficacy and adverse effects of topical phenylephrine for anal incontinence after low anterior resection in patients with rectal cancer. Int J Colorectal Dis 2007; 22: 1319–24.   38. Deutekom M, Dobben A. Plugs for containing faecal incontinence. Cochrane Database Syst Rev 2005; Issue 3: CD005086.   39. Giamundo P, Altomare DF, Rinaldi M et al. The ProTect device in the treatment of severe fecal incontinence: preliminary results of a multicenter trial. Tech Coloproctol 2007; 11: 310–4.   40. Giamundo P, Welber A, Weiss EG et al. The procon incontinence device: a new nonsurgical approach to preventing episodes of fecal incontinence. Am J Gastroenterol 2002; 97: 2328–32.   41. Leroi AM, Dorival MP, Lecouturier MF et al. Pudendal neuropathy and severity of incontinence but not presence of an anal sphincter defect may determine the response to biofeedback therapy in fecal incontinence. Dis Colon Rectum 1999; 42: 762–9.   42. Jensen LL, Lowry AC. Biofeedback improves functional outcome after sphincteroplasty. Dis Colon Rectum 1997; 40: 197–200.   43. Norton C, Kamm MA. Anal sphincter biofeedback and pelvic floor exercises for faecal incontinence in adults--a systematic review. Aliment Pharmacol Ther 2001; 15: 1147–54.

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improved outcomes in colon and rectal surgery   44. van Tets WF, Kuijpers JH, Bleijenberg G. Biofeedback treatment is ineffective in neurogenic fecal incontinence. Dis Colon Rectum 1996; 39: 992–4.   45. Norton C, Cody JD, Hosker G. Biofeedback and/or sphincter exercises for the treatment of faecal incontinence in adults. Cochrane Database Syst Rev 2006; 3: CD002111.   46. Miner PB, Donnelly TC, Read NW. Investigation of mode of action of biofeedback in treatment of fecal incontinence. Dig Dis Sci 1990; 35: 1291–8.   47. Hasegawa H, Yoshioka K, Keighley MR. Randomized trial of fecal diversion for sphincter repair. Dis Colon Rectum 2000; 43: 961–4.   48. Tjandra JJ, Han WR, Goh J, Carey M, Dwyer P. Direct repair vs. overlapping sphincter repair: a randomized, controlled trial. Dis Colon Rectum 2003; 46: 937–42.   49. Bravo Gutierrez A, Madoff RD, Lowry AC et al. Long-term results of anterior sphincteroplasty. Dis Colon Rectum 2004; 47: 727–31.   50. Barisic GI, Krivokapic ZV, Markovic VA, Popovic MA. Outcome of overlapping anal sphincter repair after 3 months and after a mean of 80 months. Int J Colorectal Dis 2006; 21: 52–6.   51. Malouf AJ, Norton CS, Engel AF, Nicholls RJ, Kamm MA. Long-term results of overlapping anterior anal-sphincter repair for obstetric trauma. Lancet 2000; 355: 260–5.   52. Maslekar S, Gardiner AB, Duthie GS. Anterior anal sphincter repair for fecal incontinence: Good longterm results are possible. J Am Coll Surg 2007; 204: 40–6.   53. Vaizey CJ, Norton C, Thornton MJ, Nicholls RJ, Kamm MA. Long-term results of repeat anterior anal sphincter repair. Dis Colon Rectum 2004; 47: 858–63.   54. Giordano P, Renzi A, Efron J et al. Previous sphincter repair does not affect the outcome of repeat repair. Dis Colon Rectum 2002; 45: 635–40.   55. Pinedo G, Vaizey CJ, Nicholls RJ et al. Results of repeat anal sphincter repair. Br J Surg 1999; 86: 66–9.   56. Finlay IG, Richardson W, Hajivassiliou CA. Outcome after implantation of a novel prosthetic anal sphincter in humans. Br J Surg 2004; 91: 1485–92.   57. Schrag HJ, Padilla FF, Goldschmidtboing F et al. German artificial sphincter system: first report of a novel and highly integrated sphincter prosthesis for therapy of major fecal incontinence. Dis Colon Rectum 2004; 47: 2215–7.   58. Michot F, Costaglioli B, Leroi AM, Denis P. Artificial anal sphincter in severe fecal incontinence: outcome of prospective experience with 37 patients in one institution. Ann Surg 2003; 237: 52–6.   59. Mundy L, Merlin TL, Maddern GJ, Hiller JE. Systematic review of safety and effectiveness of an artificial bowel sphincter for faecal incontinence. Br J Surg 2004; 91: 665–72.   60. O’Brien PE, Dixon JB, Skinner S et al. A prospective, randomized, controlled clinical trial of placement of the artificial bowel sphincter (Acticon Neosphincter) for the control of fecal incontinence. Dis Colon Rectum 2004; 47: 1852–60.   61. Altomare DF, Binda GA, Dodi G et al. Disappointing longterm results of the artificial anal sphincter for faecal incontinence. Br J Surg 2004; 91: 1352–3.

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  62. Christiansen J, Rasmussen OO, Lindorff-Larsen K. Long-term results of artificial anal sphincter implantation for severe anal incontinence. Ann Surg 1999; 230: 45–8.   63. Parker SC, Spencer MP, Madoff RD et al. Artificial bowel sphincter: long-term experience at a single institution. Dis Colon Rectum 2003; 46: 722–9.   64. Gregorcyk S. The Current Status of the Acticon Neosphincter. Clin Colon Rectal Surg 2005; 18: 6.   65. Chapman AE, Geerdes B, Hewett P et al. Systematic review of dynamic graciloplasty in the treatment of faecal incontinence. Br J Surg 2002; 89: 138–53.   66. Baeten CG, Bailey HR, Bakka A et al. Safety and efficacy of dynamic graciloplasty for fecal incontinence: report of a prospective, multicenter trial. Dynamic Graciloplasty Therapy Study Group. Dis Colon Rectum 2000; 43: 743–51.   67. Matzel KE, Madoff RD, LaFontaine LJ et al. Complications of dynamic graciloplasty: incidence, management, and impact on outcome. Dis Colon Rectum 2001; 44: 1427–35.   68. Wexner SD, Baeten C, Bailey R et al. Long-term efficacy of dynamic graciloplasty for fecal incontinence. Dis Colon Rectum 2002; 45: 809–18.   69. Rongen MJ, Uludag O, El Naggar K et al. Long-term follow-up of dynamic graciloplasty for fecal incontinence. Dis Colon Rectum 2003; 46: 716–21.   70. Melenhorst J, Koch SM, van Gemert WG, Baeten CG. The artificial bowel sphincter for faecal incontinence: a single centre study. Int J Colorectal Dis 2008; 23: 107–11.   71. Matzel KE, Stadelmaier U, Hohenfellner M, Gall FP. Electrical stimulation of sacral spinal nerves for treatment of faecal incontinence. Lancet 1995; 346: 1124–7.   72. Matzel KE. Sacral nerve stimulation for fecal disorders: evolution, current status, and future directions. Acta Neurochir Suppl 2007; 97: 351–7.   73. Sheldon R, Kiff ES, Clarke A, Harris ML, Hamdy S. Sacral nerve stimulation reduces corticoanal excitability in patients with faecal incontinence. Br J Surg 2005; 92: 1423–31.   74. Gooneratne ML, Facer P, Knowles CH et al. Normalization of substance P levels in rectal mucosa of patients with faecal incontinence treated successfully by sacral nerve stimulation. Br J Surg 2008; 95: 477–83.   75. Holzer B, Rosen HR, Novi G et al. Sacral nerve stimulation for neurogenic faecal incontinence. Br J Surg 2007; 94: 749–53.   76. Matzel KE, Kamm MA, Stosser M et al. Sacral spinal nerve stimulation for faecal incontinence: multicentre study. Lancet 2004; 363: 1270–6.   77. Melenhorst J, Koch SM, Uludag O, van Gemert WG, Baeten CG. Sacral neuromodulation in patients with faecal incontinence: results of the first 100 permanent implantations. Colorectal Dis 2007; 9: 725–30.   78. Jarrett ME, Nicholls RJ, Kamm MA. Effect of sacral neuromodulation for faecal incontinence on sexual activity. Colorectal Dis 2005; 7: 523–5.   79. Hetzer FH, Hahnloser D, Clavien PA, Demartines N. Quality of life and morbidity after permanent sacral nerve stimulation for fecal incontinence. Arch Surg 2007; 142: 8–13.

surgical treatment of fecal incontinence   80. Hetzer FH, Bieler A, Hahnloser D et al. Outcome and cost analysis of sacral nerve stimulation for faecal incontinence. Br J Surg 2006; 93: 1411–7.   81. Matzel KE, Stadelmaier U, Hohenberger W. Innovations in fecal incontinence: sacral nerve stimulation. Dis Colon Rectum 2004; 47: 1720–8.   82. Matzel KE. Sacral Nerve Stimulation for Fecal Incontinence: An Update. In: European Society of Coloproctology 2nd Scientific and Annual General Meeting. Malta; 2007.   83. Dudding TC, Pares D, Vaizey CJ, Kamm MA. Predictive factors for successful sacral nerve stimulation in the treatment of faecal incontinence: a 10–year cohort analysis. Colorectal Dis 2008; 10: 249–56.   84. Melenhorst J, Koch SM, Uludag O, van Gemert WG, Baeten CG. Is a morphologically intact anal sphincter necessary for success with sacral nerve modulation in patients with faecal incontinence? Colorectal Dis 2008; 10: 257–62.   85. Tjandra JJ, Chan MK, Yeh CH, Murray-Green C. Sacral Nerve Stimulation is more Effective than Optimal Medical Therapy for Severe Fecal Incontinence: A Randomized, Controlled Study. Dis Colon Rectum 2008; 51(5): 494–502.   86. Mentes BB, Yuksel O, Aydin A et al. Posterior tibial nerve stimulation for faecal incontinence after partial spinal injury: preliminary report. Tech Coloproctol 2007; 11: 115–9.   87. Queralto M, Portier G, Cabarrot PH et al. Preliminary results of peripheral transcutaneous neuromodulation in the treatment of idiopathic fecal incontinence. Int J Colorectal Dis 2006; 21: 670–2.   88. Tjandra JJ, Lim JF, Hiscock R, Rajendra P. Injectable silicone biomaterial for fecal incontinence caused by internal anal sphincter dysfunction is effective. Dis Colon Rectum 2004; 47: 2138–46.   89. Davis K, Kumar D, Poloniecki J. Preliminary evaluation of an injectable anal sphincter bulking agent (Durasphere) in the management of faecal incontinence. Aliment Pharmacol Ther 2003; 18: 237–43.   90. Altomare DF, La Torre F, Rinaldi M, Binda GA, Pescatori M. Carbon-Coated Microbeads Anal Injection in Outpatient Treatment of Minor Fecal Incontinence. Dis Colon Rectum 2008; 51(4): 432–5.   91. Maeda Y, Vaizey CJ, Kamm MA. Long-term results of perianal silicone injection for faecal incontinence. Colorectal Dis 2007; 9: 357–61.   92. Chan MK, Tjandra JJ. Injectable silicone biomaterial (PTQ) to treat fecal incontinence after hemorrhoidectomy. Dis Colon Rectum 2006; 49: 433–9.   93. van der Hagen SJ, van Gemert WG, Baeten CG. PTQ Implants in the treatment of faecal soiling. Br J Surg 2007; 94: 222–3.   94. Malone PS, Ransley PG, Kiely EM. Preliminary report: the antegrade continence enema. Lancet 1990; 336: 1217–8.   95. Portier G, Bonhomme N, Platonoff I, Lazorthes F. Use of Malone antegrade continence enema in patients with perineal colostomy after rectal resection. Dis Colon Rectum 2005; 48: 499–503.

  96. Lefevre JH, Parc Y, Giraudo G et al. Outcome of antegrade continence enema procedures for faecal incontinence in adults. Br J Surg 2006; 93: 1265–9.   97. Gerharz EW, Vik V, Webb G et al. The value of the MACE (Malone antegrade colonic enema) procedure in adult patients. J Am Coll Surg 1997; 185: 544–7.   98. Krogh K, Laurberg S. Malone antegrade continence enema for faecal incontinence and constipation in adults. Br J Surg 1998; 85: 974–7.   99. Portier G, Ghouti L, Kirzin S, Chauffour M, Lazorthes F. Malone antegrade colonic irrigation: ileal neoappendicostomy is the preferred procedure in adults. Int J Colorectal Dis 2006; 21: 458–60. 100. Browning GG, Parks AG. Postanal repair for neuropathic faecal incontinence: correlation of clinical result and anal canal pressures. Br J Surg 1983; 70: 101–4. 101. Tan JJ, Chan M, Tjandra JJ. Evolving therapy for fecal incontinence. Dis Colon Rectum 2007; 50: 1950–67. 102. Orrom WJ, Miller R, Cornes H et al. Comparison of anterior sphincteroplasty and postanal repair in the treatment of idiopathic fecal incontinence. Dis Colon Rectum 1991; 34: 305–10. 103. Setti Carraro P, Kamm MA, Nicholls RJ. Long-term results of postanal repair for neurogenic faecal incontinence. Br J Surg 1994; 81: 140–4. 104. Colquhoun P, Kaiser R Jr, Efron J et al. Is the quality of life better in patients with colostomy than patients with fecal incontience? World J Surg 2006; 30: 1925–8. 105. Pachler J, Wille-Jorgensen P. Quality of life after rectal resection for cancer, with or without permanent colostomy. Cochrane Database Syst Rev 2005; 2: CD004323. 106. Nikiteas N, Korsgen S, Kumar D, Keighley MR. Audit of sphincter repair. Factors associated with poor outcome. Dis Colon Rectum 1996; 39: 1164–70. 107. Oliveira L, Pfeifer J, Wexner SD. Physiological and clinical outcome of anterior sphincteroplasty. Br J Surg 1996; 83: 502–5. 108. Young CJ, Mathur MN, Eyers AA, Solomon MJ. Successful overlapping anal sphincter repair: relationship to patient age, neuropathy, and colostomy formation. Dis Colon Rectum 1998; 41: 344–9. 109. Gilliland R, Altomare DF, Moreira H Jr et al. Pudendal neuropathy is predictive of failure following anterior overlapping sphincteroplasty. Dis Colon Rectum 1998; 41: 1516–22. 110. Karoui S, Leroi AM, Koning E et al. Results of sphincteroplasty in 86 patients with anal incontinence. Dis Colon Rectum 2000; 43: 813–20. 111. Buie WD, Lowry AC, Rothenberger DA, Madoff RD. Clinical rather than laboratory assessment predicts continence after anterior sphincteroplasty. Dis Colon Rectum 2001; 44: 1255–60. 112. Morren GL, Hallbook O, Nystrom PO, Baeten CG, Sjodahl R. Audit of anal-sphincter repair. Colorectal Dis 2001; 3: 17–22.

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improved outcomes in colon and rectal surgery 113. Pinta T, Kylanpaa-Back ML, Salmi T, Jarvinen HJ, Luukkonen P. Delayed sphincter repair for obstetric ruptures: analysis of failure. Colorectal Dis 2003; 5: 73–8. 114. Evans C, Davis K, Kumar D. Overlapping anal sphincter repair and anterior levatorplasty: effect of patient’s age and duration of follow-up. Int J Colorectal Dis 2006; 21: 795–801. 115. Londono-Schimmer EE, Garcia-Duperly R, Nicholls RJ et al. Overlapping anal sphincter repair for faecal incontinence due to sphincter trauma: five year follow-up functional results. Int J Colorectal Dis 1994; 9: 110–3. 116. Halverson AL, Hull TL. Long-term outcome of overlapping anal sphincter repair. Dis Colon Rectum 2002; 45: 345–8. 117. Zorcolo L, Covotta L, Bartolo DC. Outcome of anterior sphincter repair for obstetric injury: comparison of early and late results. Dis Colon Rectum 2005; 48: 524–31.

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118. Grey BR, Sheldon RR, Telford KJ, Kiff ES. Anterior anal sphincter repair can be of long term benefit: a 12-year case cohort from a single surgeon. BMC Surg 2007; 7: 1. 119. Jarrett ME, Varma JS, Duthie GS, Nicholls RJ, Kamm MA. Sacral nerve stimulation for faecal incontinence in the UK. Br J Surg 2004; 91: 755–61. 120. Leroi AM, Parc Y, Lehur PA et al. Efficacy of sacral nerve stimulation for fecal incontinence: results of a multicenter double-blind crossover study. Ann Surg 2005; 242: 662–9. 121. Holzer B, Rosen HR, Novi G et al. Sacral Nerve Stimulation in Patients with Severe Constipation. Dis Colon Rectum 2008; 51(5): 524–29.

23 Surgery for rectal prolapse Steven R Hunt

introduction Rectal prolapse (rectal procidentia) is defined as the full thickness intussusception of the rectum through the anal canal. The annual incidence of rectal prolapse is estimated to be 2.5 per 100,000 population.(1) The disorder tends to affect elderly women, psychiatric patients, and patients with neurologic disorders. Presenting symptoms are usually referable to the prolapse itself. Additional presenting complaints include constipation, straining, incontinence, and mucous soilage of the undergarments. Surgery remains the only definitive therapy for rectal prolapse. Over 100 operations have been described for the treatment of procidentia. Generally, these procedures can be divided into peritoneal and abdominal approaches. The optimal procedure for each patient should be determined by presenting symptoms and patient comorbid disease. Classification In the strictest sense, rectal prolapse refers only to full thickness, circumferential protrusion of the rectum beyond the anal canal. While it is often clinically obvious, several other anorectal disorders can imitate the condition. Circumferential prolapsed internal hemorrhoids, when large, are frequently diagnosed as prolapse, and prolapse is often diagnosed as hemorrhoids. Rectal polyps or cancer can protrude through the anus and mimic ­prolapse. It is important to differentiate between true procidentia and mucosal prolapse, as the entities may have similar presenting symptoms. Patients with mucosal prolapse frequently have a history of prior anorectal procedures or trauma and the prolapse is often asymmetric. Solitary rectal ulcers and colitis cystica profunda can present with symptoms similar to rectal prolapse. These disorders are associated with internal intussusception of the rectum, but may coexist in patients with rectal prolapse. Both solitary rectal ulcer and colitis cystica profunda are hypothesized to result from repeated mucosal trauma and ischemia at the lead point of the prolase. Significant rectal bleeding is relatively rare in patients with procidentia, although it is a common presentation in solitary rectal ulcer syndrome and ­colitis cystica profunda. Internal rectal intussusception without prolapse may be a predecessor to rectal prolapse, although this association has not been proven.(2) Rectal intussusception is frequently identified during defecography performed to evaluate obstructed defecation or constipation. It is also a common finding in asymptomatic patients. (3) While it is clear that surgery is the mainstay of treatment for complete rectal prolapse, the indications for surgical intervention in cases of internal intussusception are less clear. Some authors advocate surgical intervention in cases of symptomatic intussusception, while others are more cautious in their approach.(4, 5) In the author’s section, the initial approach to patients with rectal intussusception is dietary modification and pelvic floor retraining through biofeedback. Surgery is generally reserved for patients

with complications of internal prolapse (solitary rectal ulcers and colitis cystica profunda) who have failed conservative therapy. Patient Evaluation and Investigations As rectal prolapse is a benign disease, surgery need only be considered if the symptoms are debilitating. Frequency of the prolapse and initiating factors (defecation, straining or standing) should be documented. The presence of severe constipation or symptoms of obstructed defecation should be noted, as these patients may require further evaluation. Fecal incontinence occurs in 60–80% of patients, and a frank discussion should ensue regarding expected surgical outcomes with regard to continence. Most large series show improvement in fecal incontinence in >40% of procidentia patients after surgery, regardless of the approach.(6) Continence may continue to improve over the first 6 to 12 months postoperatively. A detailed surgical history should be obtained, with special attention to anorectal and pelvic operations, as this may influence the ultimate surgical approach. In patients with recurrent rectal prolapse, operative notes from the prior procedures should be obtained and scrutinized. Female patients may have a history of bladder or uterine prolapse, requiring consultation with a urogynecologist and a combined approach. All patients with prolapse should have a recent colonoscopy to rule out any mucosal lesions. Physical Exam The diagnosis of procidentia is made by demonstration of the prolapse in the surgeon’s office. Patients with advanced prolapse may be able to produce the prolapse on the examination table with minimal straining. If the patient cannot prolapse on the examination table, they should be examined after straining on the toilet. Once the prolapse has been achieved, the examiner should first differentiate between full thickness prolapse and hemorrhoidal or mucosal prolapse. Full thickness prolapse is characterized by concentric mucosal rings, as opposed to the radially oriented sulci seen with mucosal and hemorrhoidal prolapse. The digital rectal exam should exclude other anorectal pathology, and the sphincter tone and the squeeze pressure should be evaluated. Female patients should be evaluated for the presence of an enterocele or rectocele. Rigid proctoscopy should be performed in the office to rule out any rectal tumors, and to evaluate for solitary ulcer and colitis cystica profunda. Generally, a physical exam and demonstration of the complete prolapse in the office is sufficient evaluation before surgery. Additional studies are sometimes required in certain cases. Anal Physiology Patients with chronic severe straining at stool should be evaluated with anal physiology testing. Electromyography that demonstrates

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improved outcomes in colon and rectal surgery a nonrelaxing puborectalis should prompt initiation of biofeedback therapy as an adjunct to surgery. Postoperative continence can also be predicted on the basis of a prolonged pudendal nerve terminal motor latency (PNTML) and poor resting sphincter tone.(7, 8) We do not routinely obtain physiologic studies in the evaluation of procidentia, as they are expensive and a prolonged PNTML is not a contraindication for surgery. Additional Studies When the patient is unable to reproduce the rectal prolapse in the office, defecography may be used to evaluate for internal prolapse or other defecatory pathology. In patients with severe constipation and prolapse, a colonic transit study may be obtained. Concentration of the markers in the left and sigmoid colon on

(A)

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day 5, in the setting of severe constipation, is an indication for a resection rectopexy. Operative Repairs Although the modern operative procedures for rectal prolapse are not particularly morbid, the patients are frequently elderly, and morbidity is not trivial. Some series report mortalities as high as 7%. These patients often have significant comorbid conditions, and the operative approach (perineal, open or laparoscopic) should take these factors into account. The choice of procedure is frequently ­dictated by surgeon preference and experience; however, a one-­ size-fits-all approach may not be suitable for all patients. In addition to the morbidity of the procedure, the evaluation of the various surgical approaches to rectal prolapse must take efficacy and

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Figure 23.1   Perineal rectosigmoidectomy. (A & B) Incision of rectal wall. (C) Division of vessel adjacent to bowel wall. (D) Mesenteric vessels ligated. Stay sutures previously placed in distal edge of outer cylinder are placed in cut edge of inner cylinder. (E) Anastomosis of distal aspect of remaining colon to the short rectal stump. (From Beck DE, Whitlow CB. Rectal prolapse and intussusception. In Beck DE. Handbook of colorectal surgery. 2nd edition. Marcel Dekker: New York, 2003; 301–24. With permission.)

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surgery for rectal prolapse (A)

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Figure 23.2  Delorme’s procedure. (A) Subcutaneous infiltration of dilute epi­ nephrine solution. (B) Circumferential mucosal incision. (C) Dissection of mucosa off muscular layer. (D) Plicating stitch approximating cut edge of mucosa, muscular wall, and mucosa just proximal to dentate line. (E) Plicating stitch tied. (F) Completed anastomosis. (From Beck DE, Whitlow CB. Rectal prolapse and intussusception. In Beck DE. Handbook of colorectal surgery. 2nd edition. Marcel Dekker: New York, 2003, 301–24. With permission.)

functional outcomes into account. Some techniques have excellent results in terms of recurrence, but can predispose the patients to constipation or evacuatory difficulties, trading one problem for another. Perineal Repairs The preponderance of the historical literature suggests that the abdominal approach to rectal prolapse is superior to the perineal approach in terms of recurrence rates. While most single institution studies report better outcomes for abdominal procedures, this difference is not demonstrated in meta-analysis.(9, 10) The major advantage of the perineal approach is the ability to conduct the operation under spinal or even local, anesthetic. The avoidance of general anesthesia and an abdominal dissection makes this the preferred approach for patients with significant comorbidities. Perineal Proctosigmoidectomy (Altmeier Procedure) The technique of perineal proctosigmoidectomy involves mobilization and resection of the prolapsed rectosigmoid colon via a perineal

approach. Patients should have a complete mechanical bowel preparation. The prone-jackknife or left lateral position is preferred over lithotomy, as it allows easy access to the operative field for the surgeon and assistant. While general anesthetic provides more comfort for the patient, it is often necessary to use local or spinal anesthesia in frail patients. The buttocks should be taped apart and a Lonestar retractor is used to efface the anus and provide optimal exposure. The procedure is begun by recreating the prolapse. Once the bowel has been completely prolapsed, a circumferential incision is made in the rectum approximately 1.5–2 cm proximal to the dentate line. Using the electrocautery, this incision should be continued until the full thickness of the rectal wall has been incised circumferentially. The incised rectum is then everted and pulled downward. The vaginal wall is frequently adherent to the prolapsed segment and should be dissected away from the rectum to avoid the devastating complication of a postoperative colovaginal fistula. The peritoneal cavity is then entered by incising the peritoneum of the Pouch of Douglas anteriorly. Entrance into the peritoneal ­cavity facilitates

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improved outcomes in colon and rectal surgery (A)

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Figure 23.3  Anal encirclement (Thiersch). (A) Lateral incisions with prosthetic mesh tunneled around the anus. (B) Mesh completely encircling the anal opening. (C) Completed anal encirclement procedure. (From Beck DE, Whitlow CB. Rectal prolapse and intussusception. In Beck DE. Handbook of colorectal surgery. 2nd edition. Marcel Dekker: New York, 2003, 301–24. With permission.)

delivery of the prolapsed rectum and division of the mesorectum. The mesorectum is then divided and ligated with ligatures, or alternatively, a vessel sealing device may be used. Division of the mesorectum should be continued, advancing proximally on the bowel until tension is encountered (Figure 23.1). Once the redundant rectosigmoid has been mobilized, the anterior peritoneum should be repaired, including seromuscular bites of the anterior bowel wall, with a running absorbable suture to obliterate the pouch. A levatorplasty should be considered if a defect is present in the pelvic floor. If the levator muscles can be identified without extensive dissection, plication should be performed anteriorly and posteriorly. The redundant bowel is then divided and a hand-sewn anastomosis is fashioned using interrupted absorbable sutures. Alternatively, the anastomosis may be created using a circular stapler with acceptable results.(11, 12) Generally, patients have minimal narcotic requirements post­ operatively and ileus is exceedingly rare. Patients should be ambu­lated and their diet is advanced on postoperative day 1. Constipating regimens have no proven beneficial results. It is the author’s practice to discharge patients after the first bowel movement, but in some centers, the Altmeier procedure is performed on an outpatient basis.(11) In experienced hands, the Altmeier procedure has excellent results, rivaling the abdominal procedures for recurrence rates. Several recent large series report recurrence rates ranging from 6% to 16%.(7, 9, 11) Both incontinence and constipation are also significantly improved after perineal proctectomy.(7, 9, 13) Some authors describe significant improvement in recurrence rates if a levatorplasty is performed.(14) Fortunately, major morbidity and mortality for this procedure are rare. The anastomotic leak rates are reportedly 1–2%, with significant bleeding occurring in a similar percentage of patients.(7, 9, 14)

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Delorme’s Procedure Delorme’s procedure offers another alternative to the Altmeier repair. The technique involves a submucosal resection of the ­prolapsed rectum, with plication of the muscularis propria. The submucosal nature of the dissection in this procedure does not allow for a concomitant levatorplasty. As with the Altmeier procedure, mechanical bowel preparation should be performed and the procedure conducted in the pronejackknife or left lateral position with effacement of the anus. Again, local or spinal anesthesia may be used for infirm patients. The rectal prolapse is delivered, and the submucosal plane is infiltrated with local anesthetic containing epinephrine. A circumferential mucosal incision is made 1 cm proximal to the dentate line. The submucosal plane is identified and downward traction is applied to the mucosal tube. Dissection is carried out within this plane to the apex of the prolapsed segment of rectum. At this point, the exposed muscularis propria is plicated with multiple bites in four quadrants using an absorbable monofilament or braided suture. The redundant mucosa is then excised and the plication sutures are tied. The mucosal edges are then reapproximated using interrupted absorbable sutures (Figure 23.2). The recurrence rate in most recent large series ranges from 13–27%.(15–17) The morbidity and mortality rates are similar to those of the Altmeier repair. Improvement is reported in both continence and constipation in most series where these functional outcomes were evaluated.(16–18) Given the uniformly inferior results of Delorme’s procedure relative to the Altmeier repair, it is the author’s feeling that this approach should not be used as a first-line perineal procedure. Many advocate this procedure for the treatment of mucosal prolapse; however, other, less involved techniques exist for this disorder. Elastic rubber band ligation is frequently adequate for modest mucosal prolapse. The circular stapler technique used in

surgery for rectal prolapse (A)

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Figure 23.4  Mesh rectopexy (Ripstein). (A) Posterior fixation of sling on one side. (B) Sling brought anteriorly around mobilized rectum. (C) Sling fixed posteriorly on the opposite side. (D) Sagittal view of the completed rectopexy. (From Beck DE, Whitlow CB. Rectal prolapse and intussusception. In Beck DE. Handbook of colorectal surgery. 2nd edition. Marcel Dekker: New York, 2003, 301–24. With permission.)

the treatment of hemorrhoids is a second appealing option for more advanced mucosal prolapse. Anal Encirclement (Thiersch Repair) Anal encirclement has almost reached the status of historical interest, as it has been replaced by other procedures with more favorable results. The procedure can be performed in a short period of time with only local anesthetic. The original repair described by Thiersch used a silver wire to encircle the anal sphincter complex.

The wire encirclement has fallen out of favor as the wire can break or erode through the sphincters and anoderm. Marlex or Mersilene mesh are the preferred alternative to wire, as they are softer and less prone to breakage or erosion. The operation can be performed in the prone-jackknife or lithotomy position. After meticulous antiseptic preparation, small posterior and anterior incisions are made 1 cm outside the anal verge. A curved clamp is then tunneled through the ischiorectal fossa from the anterior incision to the posterior

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improved outcomes in colon and rectal surgery incision and one end of the mesh is then pulled through the tunnel. This is duplicated on the opposite side and the other end of the mesh is delivered. The redundant mesh is pulled through and the prosthetic is tightened around an 18F Hegar dilator. The mesh is then overlapped anteriorly and sewn to itself with a nonabsorbable suture. The small incisions are then closed with absorbable subcuticular sutures and the wounds are sealed with Dermabond, to prevent subsequent soilage of the wounds (Figure 23.3). Anal encirclement procedures do not repair the prolapse, but merely prevent external prolapse. Infectious complications are common with the synthetic mesh, occurring in up to 33% of patients.(19) Postoperatively, these patients frequently ­experience ­tenesmus and difficulty with evacuation.(20) This procedure should be reserved for patients who have significant contraindications to more formal repairs. One relative indication for this repair is the patient with ­significant hepatic ascites (not amenable to ­transjugular intrahepatic portosystemic shunt) and debilitating rectal prolapse. Open Abdominal Repairs A prerequisite to the open approach is the patient’s ability to tolerate a general anesthetic and laparotomy. A variety of abdominal repairs are described in the literature, but only a few have withstood the test of time. The common theme among these time-tested procedures is complete rectal mobilization and fixation of the rectum to the sacrum. It is suggested that the fibrosis resulting from the rectal mobilization is responsible for the long term fixation of the rectum and avoidance of recurrence.(21) All of the large series involving abdominal procedures show improvement in fecal continence. The same cannot be said for constipation, as rectopexy alone tends to worsen constipation. In cases of severe constipation preoperatively, a sigmoidectomy may be combined with rectal fixation. The repairs discussed below all involve complete rectal mobilization. In all cases, the rectal mobilization should be carried out in the avascular plane outside the mesorectal fascia. The peritoneum at the sacral promontory is incised and the plane posterior to the superior rectal artery is identified. Great care should be taken to prevent injury to the hypogastric plexus and the ureters should be identified and avoided. When rectal fixation sutures are placed, the position of the ureters should be reconfirmed to prevent inclusion in the suture. These approaches are not immune to the usual pitfalls of open laparotomy, with complications including small bowel obstruction, prolonged ileus, and wound complications. There is some controversy regarding the extent of rectal mobilization. While some authors advocate division of the lateral rectal ligaments to improve recurrence rates, there are some reports of worsening constipation if the lateral ligaments are divided.(22) In a small randomized prospective study comparing rectal mobilization with and without division of the lateral ligaments, Mollen et al. reported no difference between the two groups with regard to constipation scores or to total colonic transit time. Anterior rectal mobilization is recommended with all of these procedures, but this is generally a minimal dissection as these patients tend to have a deep Pouch of Douglas.

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Mesh Sling Repair (Ripstein Procedure) The Ripstein procedure involves the posterior mobilization of the rectum down to the pelvic floor followed by fixation of the rectum to the sacrum using a mesh sling. Before the advent of the laparoscopic approach, this procedure was one of the most commonly employed abdominal techniques for rectal prolapse. Patients should undergo a complete mechanical bowel preparation and the operation is performed in the lithotomy position. A complete rectal mobilization is carried down to the pelvic floor. A 3–4 cm wide piece of PTFE or polypropylene mesh is then fixed to the sacrum approximately 1 cm to the right of the midline using several nonabsorbable sutures. Traction is then applied to the rectum in a cephalad direction and the mesh is fixed at multiple points to the anterior rectum by seromuscular bites of nonabsorbable suture. The mesh is then secured to the left side of the sacrum approximately 1 cm off the midline, taking care to ensure that the mesh does not constrict the rectum (Figure 23.4). The results of the Ripstein repair are excellent in terms of recurrence, with recurrence rates of 0–7% reported in large recent series.(6, 23, 24) In spite of these enviable results, enthusiasm for this procedure has waned because of reports of mesh erosion into the rectum, late colovaginal fistulas, stenosis, and significant constipation following the procedure.(23) In light of these complications and the success of other alternative therapies, the Ripstein procedure’s role in the modern treatment of rectal prolapse should be limited. Posterior Mesh Fixation (Wells Operation) The technique of the Wells operation is similar to that of the Ripstein procedure, except the mesh fixation to the sacral promontory is posterior. Theoretically, this posterior mesh orientation may reduce the problems typically associated with the anterior sling. The procedure was originally described using an Ivalon (polyvinyl alcohol) sponge. In the US, experience with the Ivalon sponge is limited, as it has not been approved for implantation. Instead, many centers perform the procedure using polypropylene mesh. Full mechanical bowel prep is performed and the patient is positioned in lithotomy position. The rectum is mobilized down to the pelvic floor. Retracting the rectum anteriorly, a 5 × 8 cm piece of mesh is then anchored to the sacrum in the midline using nonabsorbable suture. The rectum is then retracted cephalad and the redundancy is eliminated. With the rectum under traction, the mesh is sutured bilaterally to the lateral rectal mesentery. The mesh wrap forms a trough around the dorsal half of the rectum and does not cover the anterior rectal wall. The peritoneum is then closed over the mesh to exclude it from the abdominal cavity (Figure 23.5). With regard to recurrence, the Wells operation has exceptional results with recurrence rates generally between 0–5% for most large open series.(25–27) While there are fewer reported mesh complications, these series uniformly show a worsening of constipation after the procedure.(25–28) Suture Rectopexy Before the laparoscopic era, suture rectopexy alone was not a common procedure. This technique involves rectal mobilization followed by suture fixation to the sacral promontory. Its appeal lies in the fact that no foreign bodies are used, thus negating

surgery for rectal prolapse (A)

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Figure 23.5  Ivalalon (polyvinyl alcohol) sponge rectopexy (Wells). (A) Polyvinyl sponge being fixed to the sacrum. (B) Sponge in place before fixation to the rectum. (C) Incomplete encirclement of the rectum anteriorly with the sponge sutured in place. (From Beck DE, Whitlow CB. Rectal prolapse and intussusception. In Beck DE. Handbook of colorectal surgery. 2nd edition. Marcel Dekker:New York, 2003, p301–324. With permission.)

the complications of mesh infection and erosion. A prospective randomized trial comparing open suture rectopexy to the Wells operation found no difference in the two procedures in terms of recurrence.(25) This procedure will be described in more detail under laparoscopy, as it has evolved primarily as a laparoscopic technique. Resection Rectopexy (Frykman-Goldberg Procedure) Constipation clearly worsens after rectopexy alone. Many authors advocate sigmoid colectomy with rectopexy to alleviate postoperative constipation. This technique, termed the Frykman-Goldberg procedure, involves full rectal mobilization, sigmoid colectomy

with colorectal anastomosis, and suture fixation of the rectum to the sacrum. Patients require a complete mechanical bowel preparation and are positioned in lithotomy. The rectum is completely mobilized to the pelvic floor posteriorly. The lateral stalks are left intact. The rectum is then retracted into the abdomen and the posterolateral mesorectum is fixed to the presacral fascia using nonabsorbable sutures. The sigmoid colon and upper rectum are then resected. Mobilization of the splenic flexure is usually not required as the redundant sigmoid colon allows for resection and subsequent anastomosis without tension. The anastomosis is created with circular stapler. The original description of this procedure involved

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improved outcomes in colon and rectal surgery fixation of the anterior rectum to the endopelvic fascia to eliminate the cul-de-sac. Most modern proponents of this operation have abandoned these anterior sutures as they have no proven benefit and can be difficult to place safely. The resection rectopexy has superior results with respect to both recurrence and constipation. Most large series report recurrence rates in the low single digits.(9, 29–31) Morbidity rates range from 0 to 35% and mortality from this procedure is low.(9, 29) This remains the only commonly employed abdominal procedure with significant improvement in postoperative constipation. One relative contraindication to resection rectopexy is severe incontinence with compromise of the anal sphincter, as sigmoidectomy can worsen incontinence in this patient population. The addition of a sigmoid resection confers a significantly increased risk of anastomotic complications when compared to rectopexy alone. Careful adherence to the usual tenets of a safe colorectal anastomosis (a good proximal and distal blood supply, a tension-free anastomosis, and air testing of the anastomosis) should allow safe practice of this procedure. Laparoscopy Over the past decade, the laparoscopic approach to colorectal diseases has become pervasive. The literature has been flooded with series reporting the successful treatment of rectal prolapse through minimally invasive techniques. Rectal prolapse lends itself extraordinarily well to the laparoscopic approach, as the procedure is isolated to one sector of the abdomen, and there is frequently no specimen removal or anastomosis required, avoiding a conventional incision altogether. Recent reports comparing open to laparoscopic treatment of rectal prolapse find that there are significant patient benefits to laparoscopy, including decreased pain, quicker resumption of diet, earlier return of bowel function, shorter length of stay, reduced hernia rates, and a lower incidence of small bowel obstruction.(32–34) Mortality rates for the laparoscopic approach are low. All of the open procedures discussed previously can be performed laparoscopically, however the Ripstein procedure has proven tedious to complete laparoscopically and is seldom performed. In general, these laparoscopic procedures require a steep Trendelenburg position to keep the small bowel and sigmoid colon out of the pelvis. The mesorectum is frequently elongated and thin in these patients. The mesorectal peritoneum is scored at the sacral promontory and the plane behind the superior rectal artery is identified with the aid of pneumoperitoneum. The hypogastric nerves should be spared and the ureters identified. The initial mesorectal mobilization should be posterior in the avascular plane. As with the open approach, division of the lateral ligaments is controversial. The author performs a circumferential mobilization to the pelvic floor, including division of the lateral ligaments. The editors prefer to leave the lateral ligaments intact. The Wells repair has proven more amenable to the laparoscopic approach than the Ripstein procedure. The laparoscopic technique is similar to the open technique. Three or four laparoscopic ports are required and the procedure is most easily accomplished with a 30° camera, to allow for visualization deep in the pelvis. This approach requires skill in laparoscopic sewing and knot tying. As with the open Wells procedure, the recurrence rate is excellent,

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with recurrence rates ranging from 0 to 4% in recent series.(35–37) Functional outcomes were also analogous to the open procedure in these series, with improvement in continence, but worsening of constipation. Morbidity and mortality are low. Laparoscopists, forever testing the premise that less is more, have trended toward more suture repairs without mesh. The laparoscopic suture rectopexy is more manageable, as it does not require challenging manipulations of mesh and involves less suturing. Again, three to four ports are required and a 30° camera is recommended. After the rectum is mobilized, it should be pulled in a cephalad direction and the lateral stalks are sutured to the sacral promontory using nonabsorbable sutures. One suture on each side of the rectum is generally sufficient. Patient’s diets may be advanced rapidly and they should be ambulated early after surgery. It has been our practice to discharge patients after their first bowel movement, however many centers perform this procedure with only a short postoperative stay. The laparoscopic suture rectopexy has been proven effective in several recently published series, with recurrence rates from 0%to 6%.(38–40) Continence is improved postoperatively, but the benefit of this simple technique may be found in improvement in postoperative constipation.(38, 40, 41) These series provide hope that the suture rectopexy alone, without mesh, may rival the mesh repair in efficacy, without the long term complication of constipation. This may obviate the need for a concomitant resection, and thus decrease the difficulty and morbidity of the repair. Some centers still favor laparoscopic resection rectopexy as the primary procedure for rectal prolapse. As with the open technique, splenic flexure mobilization is usually not required. The addition of sigmoidectomy increases the operative time relative to suture rectopexy alone by nearly 100 minutes.(41, 42) Results, as with the open technique, are excellent, with recurrence rates from 0% to 2.5%.(4, 43) Both constipation and incontinence are improved postoperatively. No comparative studies between open and laparoscopic techniques have proven a significant reduction in morbidity or mortality for the laparoscopic approach, but trends seem to favor the laparoscopic approach.(34, 44) What is clear from the literature is that the minimally invasive approach to rectal prolapse is not inferior. The clear benefits of the laparoscopic approach in terms of cost, length of stay, and decreased pain mandate consideration of this approach when it is feasible. Recurrent Prolapse Recurrent rectal prolapse occurs with every procedure, and the surgical approach to repair of the recurrence requires consideration of the initial procedure. The mean time to recurrence is between 18 and 24 months. Patients who have recurred require physiologic testing and defecography to evaluate for anismus. If anismus is identified, these patients should be referred for biofeedback before any surgical therapy. There is no clear algorithm for management of recurrent prolapse. Some authors advocate for a change in approach, performing perineal procedures if the initial approach was abdominal, and vice versa. Others promote the use of the same approach for repair of the recurrence. No definitive published data exists on the proper selection of the second procedure. The only absolute principle in the treatment of recurrent prolapse is that if a resection is planned,

surgery for rectal prolapse any prior anastomoses must be resected in order to avoid an intervening ischemic segment. Again, comorbid disease should play a role in the selection of the procedure. Patients unfit for general anesthetic should be offered a perineal approach if at all possible. The few published series on the treatment of recurrent prolapse offer little to no insight on the best approach. A series from the University of Minnesota suggests that the abdominal approach is superior to the perineal approach in terms of rerecurrence.(45) The Cleveland Clinic Florida has published one of the larger series on treatment of recurrent prolapse. Various surgical approaches were used and it is not clear how the procedures are selected. Compared to primary operations for rectal prolapse, there was no difference in terms of recurrence, morbidity, and bowel function.(46) A difficult situation arises in the patient who has had a prior abdominal resection rectopexy, but is now unfit for general anesthetic. Before undertaking a perineal proctectomy in such a patient, the surgeon must be sure he can mobilize and resect the prior anastomosis. If not, the surgeon is left with three less than desirable options. The patient may be counseled that an operation is not in their best interest. A Delorme procedure may be performed, or the patient may be offered anal encirclement. Conclusion While many procedures exist for rectal prolapse, only a few offer acceptable results in terms of recurrence, postoperative bowel function, and morbidity. Of the perineal techniques, the Altmeier procedure appears to offer superior outcomes in terms of these principles. All of the described open abdominal approaches have satisfactory recurrence rates, but only the resection rectopexy shows improvement in postoperative bowel function. Laparoscopy, with all of its inherent advantages, may be the preferred approach. Of these procedures, the laparoscopic suture rectopexy appears to offer the best hope of achieving favored status, given the relative simplicity of the procedure and its exceptional outcomes with minimal morbidity. The surgeon who treats this disease should possess the flexibility and breadth of skills to tailor the procedure to the individual patient. Surgeon preference and experience should play a role in the choice of procedure, but should not justify a single procedure for a complex disease. An algorithm used in our section is to offer laparoscopic suture rectopexy as the default technique. If a patient has severe constipation, a laparoscopic resection rectopexy is ­performed. The patient with a hostile abdomen or the patient who is too infirm to undergo an abdominal procedure is offered a perineal proctosigmoidectomy. References   1. Kairaluoma MV, Kellokumpu IH. Epidemiologic aspects of complete rectal prolapse. Scand J Surg 2005; 94(3): 207–10.   2. Mellgren A, Schultz I, Johansson C, Dolk A. Internal rectal intussusception seldom develops into total rectal prolapse. Dis Colon Rectum 1997; 40(7): 817–20.   3. Dvorkin LS, Gladman MA, Epstein J et al. Rectal intussusception in symptomatic patients is different from that in asymptomatic volunteers. Br J Surg 2005; 92(7): 866–72.   4. Ashari LH, Lumley JW, Stevenson AR, Stitz RW. Laparoscopicallyassisted resection rectopexy for rectal prolapse: ten years’ experience. Dis Colon Rectum 2005; 48(5): 982–7.

  5. Kruyt RH, Delemarre JB, Gooszen HG, Vogel HJ. Selection of patients with internal intussusception of the rectum for posterior rectopexy. Br J Surg 1990; 77(10): 1183–4.   6. Tjandra JJ, Fazio VW, Church JM et al. Ripstein procedure is an effective treatment for rectal prolapse without constipation. Dis Colon Rectum 1993; 36(5): 501–7.   7. Glasgow SC, Birnbaum EH, Kodner IJ, Fleshman JW, Dietz DW. Preoperative anal manometry predicts continence after perineal proctectomy for rectal prolapse. Dis Colon Rectum 2006; 49(7): 1052–8.   8. Birnbaum EH, Stamm L, Rafferty JF et al. Pudendal nerve terminal motor latency influences surgical outcome in treatment of rectal prolapse. Dis Colon Rectum 1996; 39(11): 1215–21.   9. Kim DS, Tsang CB, Wong WD et al. Complete rectal prolapse: evolution of management and results. Dis Colon Rectum 1999; 42(4): 460–6. 10. Bachoo P, Brazzelli M, Grant A. Surgery for complete rectal prolapse in adults. Cochrane Database Syst Rev 2000; 2: CD001758. 11. Kimmins MH, Evetts BK, Isler J, Billingham R. The Altemeier repair: outpatient treatment of rectal prolapse. Dis Colon Rectum 2001; 44(4): 565–70. 12. Boccasanta P, Venturi M, Barbieri S, Roviaro G. Impact of new technologies on the clinical and functional outcome of Altemeier’s procedure: a randomized, controlled trial. Dis Colon Rectum 2006; 49(5): 652–60. 13. Whitlow CB, Beck DE, Opelka FG et al. Perineal repair of rectal prolapse. J La State Med Soc 1997; 149(1): 22–6. 14. Chun SW, Pikarsky AJ, You SY et al. Perineal rectosigmoidectomy for rectal prolapse: role of levatorplasty. Tech Coloproctol 2004; 8(1): 3–8. 15. Marchal F, Bresler L, Ayav A et al. Long-term results of Delorme’s procedure and Orr-Loygue rectopexy to treat complete rectal prolapse. Dis Colon Rectum 2005; 48(9): 1785–90. 16. Watts AM, Thompson MR. Evaluation of Delorme’s procedure as a treatment for full-thickness rectal prolapse. Br J Surg 2000; 87(2): 218–22. 17. Tsunoda A, Yasuda N, Yokoyama N, Kamiyama G, Kusano M. Delorme’s procedure for rectal prolapse: clinical and physiological analysis. Dis Colon Rectum 2003; 46(9): 1260–5. 18. Lechaux JP, Atienza P, Goasguen N, Lechaux D, Bars I. Prosthetic rectopexy to the pelvic floor and sigmoidectomy for rectal prolapse. Am J Surg 2001; 182(5): 465–9. 19. Lomas MI, Cooperman H. Correction of rectal procidentia by use of polypropylene mesh (Marlex). Dis Colon Rectum 1972; 15(6): 416–9. 20. Corman M. Rectal Prolapse, Solitary Rectal Ulcer, Sydrome of the Descending Perineum, and Rectocele. 5th Edition ed. Philadelphia: Lippincott, Williams, and Wilkins; 2005. 21. Nelson R, Spitz J, Pearl RK, Abcarian H. What role does full rectal mobilization alone play in the treatment of rectal prolapse? Tech Coloproctol 2001; 5(1): 33–5. 22. McKee RF, Lauder JC, Poon FW, Aitchison MA, Finlay IG. A prospective randomized study of abdominal rectopexy with and without sigmoidectomy in rectal prolapse. Surg Gynecol Obstet 1992; 174(2): 145–8.

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improved outcomes in colon and rectal surgery 23. Schultz I, Mellgren A, Dolk A, Johansson C, Holmstrom B. Long-term results and functional outcome after Ripstein rectopexy. Dis Colon Rectum 2000; 43(1): 35–43. 24. Winde G, Reers B, Nottberg H et al. Clinical and functional results of abdominal rectopexy with absorbable mesh-graft for treatment of complete rectal prolapse. Eur J Surg 1993; 159(5): 301–5. 25. Novell JR, Osborne MJ, Winslet MC, Lewis AA. Prospective randomized trial of Ivalon sponge versus sutured rectopexy for full-thickness rectal prolapse. Br J Surg 1994; 81(6): 904–6. 26. Mann CV, Hoffman C. Complete rectal prolapse: the anatomical and functional results of treatment by an extended abdominal rectopexy. Br J Surg 1988; 75(1): 34–7. 27. Aitola PT, Hiltunen KM, Matikainen MJ. Functional results of operative treatment of rectal prolapse over an 11-year period: emphasis on transabdominal approach. Dis Colon Rectum 1999; 42(5): 655–60. 28. Allen-Mersh TG, Turner MJ, Mann CV. Effect of abdominal Ivalon rectopexy on bowel habit and rectal wall. Dis Colon Rectum 1990; 33(7): 550–3. 29. Watts JD, Rothenberger DA, Buls JG, Goldberg SM, Nivatvongs S. The management of procidentia. 30 years’ experience. Dis Colon Rectum 1985; 28(2): 96–102. 30. Huber FT, Stein H, Siewert JR. Functional results after treatment of rectal prolapse with rectopexy and sigmoid resection. World J Surg 1995; 19(1): 138–43. 31. Husa A, Sainio P, von Smitten K. Abdominal rectopexy and sigmoid resection (Frykman-Goldberg operation) for rectal prolapse. Acta Chir Scand 1988; 154(3): 221–4. 32. Duepree HJ, Senagore AJ, Delaney CP, Fazio VW. Does means of access affect the incidence of small bowel obstruction and ventral hernia after bowel resection? Laparoscopy versus ­laparotomy. J Am Coll Surg 2003; 197(2): 177–81. 33. Solomon MJ, Young CJ, Eyers AA, Roberts RA. Randomized clinical trial of laparoscopic versus open abdominal rectopexy for rectal prolapse. Br J Surg 2002; 89(1): 35–9. 34. Purkayastha S, Tekkis P, Athanasiou T et al. A comparison of open vs. laparoscopic abdominal rectopexy for full-thickness rectal prolapse: a meta-analysis. Dis Colon Rectum 2005; 48(10): 1930–40.

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35. Zittel TT, Manncke K, Haug S et al. Functional results after laparoscopic rectopexy for rectal prolapse. J Gastrointest Surg 2000; 4(6): 632–41. 36. Himpens J, Cadiere GB, Bruyns J, Vertruyen M. Laparoscopic rectopexy according to Wells. Surg Endosc 1999; 13(2): 139–41. 37. Dulucq JL, Wintringer P, Mahajna A. Clinical and functional outcome of laparoscopic posterior rectopexy (Wells) for fullthickness rectal prolapse. A prospective study. Surg Endosc 2007; 21(12): 2226–30. 38. Heah SM, Hartley JE, Hurley J, Duthie GS, Monson JR. Laparoscopic suture rectopexy without resection is effective treatment for full-thickness rectal prolapse. Dis Colon Rectum 2000; 43(5): 638–43. 39. Kessler H, Jerby BL, Milsom JW. Successful treatment of ­rectal prolapse by laparoscopic suture rectopexy. Surg Endosc 1999; 13(9): 858–61. 40. Bruch HP, Herold A, Schiedeck T, Schwandner O. Laparoscopic surgery for rectal prolapse and outlet obstruction. Dis Colon Rectum 1999; 42(9): 1189–94. 41. Kellokumpu IH, Vironen J, Scheinin T. Laparoscopic repair of rectal prolapse: a prospective study evaluating surgical outcome and changes in symptoms and bowel function. Surg Endosc 2000; 14(7): 634–40. 42. Baker R, Senagore AJ, Luchtefeld MA. Laparoscopic-assisted vs. open resection. Rectopexy offers excellent results. Dis Colon Rectum 1995; 38(2): 199–201. 43. Benoist S, Taffinder N, Gould S, Chang A, Darzi A. Functional results two years after laparoscopic rectopexy. Am J Surg 2001; 182(2): 168–73. 44. Kairaluoma MV, Viljakka MT, Kellokumpu IH. Open vs. laparoscopic surgery for rectal prolapse: a case-controlled study assessing short-term outcome. Dis Colon Rectum 2003; 46(3): 353–60. 45. Steele SR, Goetz LH, Minami S et al. Management of recurrent rectal prolapse: surgical approach influences outcome. Dis Colon Rectum 2006; 49(4): 440–5. 46. Pikarsky AJ, Joo JS, Wexner SD et al. ��������������������� Recurrent rectal prolapse: what is the next good option? Dis Colon Rectum 2000; 43(9): 1273–6.

24 Operative and nonoperative therapy for diverticular disease R Scott Nelson and Alan G Thorson

Unlike other diseases in this text diverticular disease is a common problem with multiple presentations. Challenging Case #1 A 52-year-old male presents to the Emergency Department with complaints of left lower quadrant (LLQ) abdominal pain for the last 16 hours. The patient describes the pain as escalating in nature, unrelieved with a bowel movement. History is unremarkable except for hypertension, which is treated with a beta-blocker. The patient denies any similar symptoms previously. Abdominal exam reveals a mildly distended abdomen, with tenderness to the left lower quadrant, but no guarding or rigidity. A basic metabolic profile is normal and complete blood count reveals a leukocytosis at 14,000. CT scan of the abdomen and pelvis with oral and rectal contrast demonstrates thickening of the sigmoid colon with mesenteric thickening but no identifiable abscess or perforation. CASE MANAGEMENT In a 52-year-old male patient with the aforementioned findings, a clinical and radiographic diagnosis of acute uncomplicated diverticulitis is confirmed. Treatment should consist of broad spectrum antibiotics, typically, Ciprofloxacin and Flagyl, IV fluids, and bowel rest. Admission to the hospital is based on physical examination, comorbidities, and CT findings. Treatment should be continued until the patient’s pain has resolved or symptomatic improvement is noted, and then oral intake may resume. Antibiotics are typically continued for 7–10 days following resolution of pain. CHALLENGING CASE #2 A 67-year-old female presents to the ED with a two day history of escalating LLQ pain and evidence of diverticulosis on colonoscopy 10 years ago. Physical exam reveals a tender LLQ without peritoneal signs, and fullness to palpation. WBC count is elevated at 17,000 and a CT scan shows a thickened inflamed sigmoid colon with a 3 cm abscess on the medial aspect of the colon. Case #2 Management Any patient diagnosed with a diverticular abscess, elevated WBC count, and pain, should be admitted to the hospital and started on intravenous fluids and antibiotics. The risk of requiring an emergent operation secondary to failure of conservative management is 0–30%. Patients with an abscess >2–3 cm should also be evaluated for percutaneous drainage. Following these measures the patient should be followed to assess clinical improvement. Resolution based on physical exam and bowel activity can dictate further conservative treatment. Elective surgery should be scheduled in the near future based on the patient’s overall health and ability to undergo an operation. Failure of conservative therapy deems that an operation be completed during that hospitalization.

CHALLENGING CASE # 3 65-year-old male admitted for acute uncomplicated diverticular disease is started on antibiotic therapy. After 3 days of I.V. antibiotic therapy and IV fluid the patient’s pain resolves. He is switched over to oral antibiotics and started on a low residue diet. The patient describes the same pain, increasing in the LLQ over the next 24 hours. He is once again made NPO and I.V. antibiotics are restarted. This time, attempts to switch the patient to oral antibiotics are successful and he is discharged home. However 10 days later he returns with LLQ pain again and CT scan continues to show uncomplicated diverticulitis. He is restarted on oral antibiotics and his pain resolves. Case #3 Management Chronic diverticulitis should be treated with an operation. There are not many studies in the literature dedicated to just chronic diverticular disease; however, it is a subject that probably does not need such study. Patients with pain that is clearly attributable to a surgical disease and that persists despite maximal medical therapy are candidates for an operation and should have the problem dealt with. CHALLENGING CASE #4 A 72-year-old female presents to her primary care physician for the 4th time in 6 months with a urinary tract infection (UTI). The patient has no known history of abdominal pain, and no previous history of frequent UTI, and now has noticed pneumaturia. The culture shows multiple organisms, including E. Coli. The last previous colonoscopy 2 years ago demonstrated diverticula, but was otherwise normal. Abdominal exam reveals no abnormal findings. What would be the best way to proceed in the diagnosis and treatment of this individual? Case #4 Management This patient should undergo confirmatory testing and CT scan. If the diagnosis is unsuccessful with barium enema, cystoscopy can also be attempted. If the patient is a candidate for surgery and the suspicion remains without confirmation, operative treatment is indicated. Laparoscopic resection has been shown to be possible in these types of cases as well. CHALLENGING CASE #5 A 34-year-old female 2 weeks after a renal transplant for polycystic kidney disease complains of anorexia and vague abdominal tenderness, more on the left side. Bowel movements which had been normal have now stopped over the last three days. A palpable kidney in the LLQ is not overly tender, and renal function does not seem abnormal for the time since operation. No changes have been made in her immunosuppressive medication.

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improved outcomes in colon and rectal surgery Case #5 Management Prophylactic colectomy for diverticulosis is not recommended before transplant. However, the incidence of diverticulitis following transplant is higher than the general population, though still relatively rare in the transplant population overall. Additionally patients receiving immunosuppressive therapy are at a higher risk for complicated diverticulitis and, more importantly, delay in diagnosis significantly increases their morbidity and mortality. Patients with polycystic kidney disease also show higher rates of diverticulosis and diverticulitis as opposed to other populations. These patients require aggressive diagnostic evaluation with CT scan and if diverticulitis is confirmed, aggressive surgical management.

Table 24.1  Ambrosetti classification of diverticulitis based on CT findings. Ambrosetti CT Classifications Uncomplicated—colonic wall thickening, pericolic fat stranding, inflammatory changes Complicated—Extracolonic air, abscess, perforation

Table 24.2  Intra-operative classification. Hinchey Classifications Type I—Diverticulitis with no or local peritonitis Type II—Diverticulitis with a small pericolic abscess Type III—Diverticulitis with local purulent or fecal peritonitis

Incidence of diverticulosis and diverticulitis It is estimated that nearly 30% of the U.S. population will have evidence of diverticulosis by age 60. That number increases to 60% by the time an individual reaches 80 years of age. (1) However, of these patients, only 10–25% will develop symptomatic diverticulitis and of those who become symptomatic only 10–20% of individuals will require hospitalization. Of patients who are hospitalized with symptomatic disease, 20–50% will require an operation. (2) Overall, <1% of patients with diverticula will ultimately require surgical management. In recent years there has been a shift in the treatment of patients with diverticulitis as more are treated as outpatients with oral antibiotics than with hospitalization. (2) Left sided diverticula predominant among the more western countries including the United States, Canada, United Kingdom, Europe and Brazil. While left-sided disease is still more common, right-sided disease is associated more with eastern countries such as Japan, China, Korea, and Singapore.(3) The male to female ratio appears to be about equal. Classification In order to determine how best to treat patients presenting with diverticular disease, classification of the severity of the disease is necessary. Diagnostic modalities have changed substantially within the last 40 years and along with it our paradigms of treatment. Park, in the late 60s and early 70s along with fellow contemporaries including Larson, and Haglund (4–6) attempted to evaluate the natural history of diverticulitis in order to classify the severity of disease. Many of the guidelines and recommendations by various societies for the treatment of diverticulitis are based on this original work. However, their diagnosis of the disease was based on barium enema, physical examination, and pathology reports. While all three methods are sufficient to make a diagnosis, the improved sensitivity and specificity of newer technology has changed the way we diagnosis, classify and treat this disease today. In recent years, criteria for the classification of diverticulitis has changed from findings on barium enema, history and physical examination and colonoscopy to findings based on computed tomography (CT) scanning. These scans now provide practical and predictive information that assist in the classification and severity of the disease process. A number of useful classification systems have been developed to assist the physician in deciding on a course of treatment.(1, 7, 8) These classification systems can be based on CT scans findings (Table 24.1 and Figures 24.1, 24.2

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Type IV—Diverticulitis with diffuse purulent or fecal peritonitis

Table 24.3  Definitions of diverticular disease. Diverticulitis Defined: I. Diverticulosis    1. Asymptomatic II. Diverticulitis    1. Noninflammatory      A. Symptoms without inflammation    2. Acute      A. Complicated      Perforation, Abscess, Phlegmon, Fistula, Bleeding      B. Uncomplicated (Simple)      Localized, thickening, fat stranding    3. Chronic      A. Recurring or persistent disease      Symptoms with systemic signs (may be intermittent)      B. Atypical      Symptoms without systemic signs    4. Complex      A. Fistula, Stricture, Obstruction    5. Malignant      A. Severe, fibrosing

and 24.3), intraoperative findings (Table 24.2), or a more global view of the disease (Table 24.3). Ambrosetti has done extensive work on CT findings of diverticular disease and developed a classification system based on the appearance of the inflamed colon. (7) His work is simple and divides patients into two groups; uncomplicated or complicated. (Table 24.1) Other studies have looked at the size of the abscess and amount of mesenteric air to determine if those are predictors of failure of nonoperative therapy.(8) Another useful method of evaluating diverticulitis was reported in 1978 by Hinchey. This is based on findings at the time of surgery and the decision for determining the correct surgical intervention was based on this classification system.(9) This simple formula divided the intraoperative findings into four categories based on the amount and type of peritonitis. (Table 24.2) However not all diverticular disease can be classified by CT scan or at the time of an operation. In a recent description of the

operative and nonoperative therapy for diverticular disease disease, Thorson and Goldberg described the disease based on the type of presentation, timing and duration of the disease, and complexity.(10) (Table 24.3) Acute Uncomplicated Diverticulitis Nonoperative Treatment Multiple reports have cited the successful treatment of uncomplicated diverticulitis in all patients, regardless of age.(11–16) However, the treatment can be quite variable as cited in a recent survey among members of the American Society of Colon and Rectal Surgeons (ASCRS). (12) This survey found that the treatment of patients with uncomplicated diverticulitis varied widely between type and number of antibiotics used, feeding schedule, and admission to the hospital. Further study into the natural history of the disease, with respect to both the short- and long-term outcomes of patients with uncomplicated diverticulitis, is overwhelmingly in favor of conservative treatment without operation. (13, 15–18) It is estimated that with conservative treatment 70–100% of patients will improve. Patients are even being treated as outpatients with oral antibiotics, sports drinks, and frequent follow-up in an effort to limit cost related to uncomplicated disease. (19) Outcome Measures Economic and morbidity models have been developed to evaluate the cost and risk/benefit ratio of early versus late operation for patients with uncomplicated diverticulitis. These studies determined that waiting, until after the 3rd or even 4th attack of documented diverticulitis, was both cost effective and less morbid on a population based model, than performing an early elective operation. (9, 20) Traditional teaching about diverticulitis suggested that patients suffering more than two episodes of uncomplicated diverticulitis should undergo an elective operation. In fact, most of the consensus data on elective resection after two documented episodes comes from literature that was published before the use of CT scanning and modern day antibiotic therapy. Because of these and other studies, the American Society of Colon and Rectal Surgeons (ASCRS) has revised its previous recommendations of resection. The 2006 revised practice parameters now read, “The decision to recommend surgery should be influenced by the age and medical condition of the patient, the frequency and severity of the attacks, and whether there are persistent symptoms after the acute episode.” (1) These new recommendations have changed the traditional perspective taken on this disease process and forces those involved in the care of patients with this disease to reevaluate the literature and possibly modify their practice. Thus today, surgeons must individualize the recommendation for operation for each patient. One must take into account the patient’s history, physical exam and diagnostic radiographic findings, response to medical therapy and other comorbidities before making recommendations for an operation. Progression of Disease One of the most feared complications of diverticular disease is the need for an emergent operation with possible fecal diversion. The increased morbidity and mortality to patients is not insignificant when an emergent operation is required. However,

the need for emergent fecal diversion most commonly occurs with a first episode of diverticulitis and is very rarely associated with recurrent disease. It has been estimated that only 1 in every 2,000 pt/years of follow-up will require an emergent resection after resolution of an episode of medically treated diverticulitis. (17) A recent meta-analysis reviewing the outcomes of medically versus surgically treated uncomplicated diverticulitis demonstrated that recurrent hospitalization was more frequent in the medically treated group than in a surgically treated one. Mortality rates for uncomplicated disease were generally low though, regardless of the treatment chosen, especially in patients less than 50 years of age. (21) In addition to the fear of an emergent operation and possible stoma, elective operation has long been recommended based on risk of recurrence. In the 1950s it was reported that morbidity and mortality were higher with recurrent attacks of acute inflammation and early interval resection was a means of avoiding those problems.(22–24) Recent studies have repeatedly shown that recommendations for prophylactic operation to prevent the need for an emergent operation are unfounded. In patients with uncomplicated diverticulitis, Chautems followed 118 patients after a first attack of uncomplicated diverticulitis for 9.5 years. Of these patients, 71% had no recurrent episodes and of those that did, none required emergent surgery.(25) In a population based study of over 20,000 patients admitted with nonoperatively managed diverticulitis only 5.5% required an emergent colectomy or colostomy. Younger patients in this study were found to be at higher risk than their older counterparts.(18) Other studies have also demonstrated that the risk of patients requiring an emergent operation from recurrent disease is much lower than previously thought. (Table 24.4) The number of patients who would benefit from prophylactic colectomy to prevent a future emergent operation consistently remains <5%. A step-wise progression of diverticular disease from diverticulosis to uncomplicated diverticulitis followed by complicated diverticulitis and finally complex disease such as fistula or obstruction is not the natural progression of this disease. Patients may present at any stage of the disease ranging from asymptomatic to colovesicular fistula without a history of previous attack. Janes reported that the idea that patients should undergo elective resection to avoid a colostomy is incorrect; such a concept can scare patients into “elective surgery.”(17) Prophylactic sigmoid resection based on the premise of preventing the possibility of future colostomy does not appear to be founded on evidence-based principles. Age Most studies define “young” patients as those <50 years of age. Younger patients have been thought to have more virulent disease, with a higher risk for recurrence and emergent operation. Recent publications have questioned whether or not this is the case.(7, 15, 29–31) Nelson et al. observed that in 234 patients >50 years of age, with a mean follow-up of 4 years after a CT scan diagnosed episode of acute uncomplicated diverticulitis, only 10 patients (4.2%) returned with a complicated episode; of these, 5 (2.1%) required an emergent colectomy and colostomy. (29) Anaya published a review of 25,058 patients hospitalized for an initial episode of diverticulitis. Of the 20,136 patients treated

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improved outcomes in colon and rectal surgery Table 24.4  Number of patients requiring urgent surgery who had a previous history of diverticular disease. Emergent Operation

Emergent Operation

Pts Who Would Have Benefited From Prophylactic Colectomy

Ref

Yr

# pts

Elective OR

All Pts

Pts with hx of diverticulosis

Pts with a hx of diverticulitis

F/U in years

Alexander (26)

1983

673

13

  80

37

(5.4%)

10

Nylamo (27)

1990

113

 3

  48

 2

(1.7%)

10

Lorimer (28)

1997

154

28

126

15

(5%)*

 8

Somasekar (2)

2002

108

 0

104

28

(2.7%)*

 5

* Patients who had been hospitalized previously with diverticulitis.

Table 24.5  Natural history studies of uncomplicated diverticular disease as reviewed by Janes.(1) 1st Admit

1st Admit

2nd Admit

2nd Admit

Year

# Pts

F/U

Diagnosis

All Operations

Emergent Operation

Recurrence

Emergent Operation

Parks (4)

1969

455

1–16 Y

BE, Path

138

Most

78

20

Larson (5)

1976

132

9Y

BE, Path

  33

NR

29

 9

Haglund (6)

1979

392

6Y

BE, Path

  97

97

73

 0

Ambrosetti (32)

1994

226

25 M

CT, CE

  66

NR

42

 8

Ambrosetti (33)

1997

423

46 M

CT, CE

112

33

27

NR

Makela (34)

1998

366

10 years

CE, path, Scope

101

55

57

19

Biondo (30)

2002

327

24–90 months

CE, CT, Path

103

78

52

 4

Ref

nonoperatively, 19% developed a recurrence, with those >50 years of age having a slightly higher recurrence rate (27% vs. 17%, p < .001). They projected that a policy of routine, elective colectomy in a younger population after an initial episode would require 13 elective operations to prevent one emergent colectomy. In this large series, 73% of young patients resolved with medical management and never suffered a recurrence. Only 7% of all patients <50 ever require an emergent operation. The risk of all patients of any age requiring an emergency operation was 5.5%.(18) These recurrence rates are significantly lower than previous estimations which were >30% for younger patients. Very few patients requiring an emergent operation had been previously diagnosed with or suffered from diverticulitis. An estimated 75% to 96% of patients presenting with peritonitis and requiring an emergent operation have never been diagnosed with the disease previously. This supports the notion that operating on patients with a history of acute diverticulitis to prevent complications of acute disease is ineffective at achieving that goal.(2, 26–28) Although it seems intuitive that patients with more years to live relative to their older counterparts are at a higher risk of recurrence, there is little evidence available to suggest that younger patients have a more virulent disease process that warrants aggressive surgical intervention. Despite the split over



recurrence, most groups recommend initial conservative treatment. As mentioned before, risk/benefit models recommend withholding resection until after three or four recurrent documented episodes. There has also been a suggestion that no surgical treatment should be offered despite the number of uncomplicated episodes.(8) Nonoperative therapy for patients with uncomplicated diverticulitis has been shown to be safe and effective in a majority of this population. The ASCRS practice parameter on diverticular disease also affirms that there is no clear consensus regarding whether younger patients treated for diverticulitis are at increased risk for complications or recurrent attacks.(1) Risk of Recurrence The risk of recurrence following an attack of uncomplicated diverticulitis is low. The range of recurrent episodes of diverticulitis after one uncomplicated attack is 1.4–18%. (13, 15, 16) Janes (17) reviewed 94 papers in an effort to review the evidence for recommendations put forth for elective resection after two attacks of diverticulitis. They concluded that there is inadequate evidence to suggest that complications are more likely to occur with each successive hospital admission, or that the likelihood of a successful response to medical treatment decreases (Table 24.5).

operative and nonoperative therapy for diverticular disease Acute Complicated Diverticulitis Outcome Measures When determining how best to treat patients presenting with acute diverticulitis two questions need to be answered. First, what category of diverticulitis is present based on history and physical examination and CT scan findings. Second, what is the feasibility and indication for operation versus medical therapy? With the advent and availability of CT scanning and its wide spread use for typical symptoms of diverticulitis we are better able to classify the disease. A patient presenting with an acute complicated episode of diverticulitis typically will have findings of abscess, phlegmon, or localized perforation on CT scan. In a recent review of patients presenting with complicated diverticulitis, 29.5% were found to have a paracolic abscess, 22.3% an acute phlegmon, 13.4% a fistula, 22.6% an obstruction or stricture and 44% a contained or free perforation.(35) Peritonitis, free intraabdominal air, or obstruction unrelieved by other methods is an indication for operation. Patients with signs of peritonitis or hemodynamic instability are not candidates for medical management and should be resuscitated and taken to the operating room. However, many patients presenting with an abscess, localized and contained perforation, or phlegmon are candidates for conservative therapy. These individuals should be evaluated for possible percutaneous drainage with radiographic guidance. Once stabilized, patients with complicated diverticulitis should have a complete colon evaluation and most should be scheduled for an elective operation. The American Society of Colon and Rectal Surgeons (ASCRS) have recommended that, “Elective colon resection should typically be advised if an episode of complicated diverticulitis is treated nonoperatively.”(1) However, there is a growing body of evidence to suggest that select patients with complicated disease may be safely managed if they respond to more conservative measures. Ambrosetti attempted a prospective trial of surgery versus observation after the 1st complicated attack of diverticulitis but abandoned the trial after 19 months as only 4 of the 52 (8%) had a recurrence.(36) Faramakis followed 120 patients from 30 centers over 5 years with complicated diverticulitis, defined as abscess, fistula, obstruction, or free perforation. Of these patients, 32% developed a severe complication and 10 patients died. However, many of these patients were treated nonoperatively because they were not felt to be surgical candidates and three times as many patients died from cardiovascular or pulmonary complications, compared to those who died from complications of diverticular disease.(37) One small study followed 28 patients after identification of complicated disease on CT scan. Ten patients were percutaneously drained and the rest were treated conservatively. Two patients ultimately required operation during their initial hospitalization and 18 patients (24%) had recurrence. They concluded that most patients could be managed without an operation or drainage. (38) However, until more evidence substantiates a clear path to follow, operative resection remains the standard for most patients presenting with complicated disease.

Risk of Recurrence—Indications for surgical treatment Patients presenting with peritonitis should undergo an urgent operation after appropriate resuscitation. Patients presenting with complicated disease without peritonitis should initially be treated conservatively with IV Fluids, NPO, antibiotics, and percutaneous drainage of any abscess. Evaluation in a recent study identified 511 patients diagnosed with complicated diverticulitis. Of these patients, 99 were diagnosed by CT scan with abscess and 16 of these underwent percutaneous drainage. Of those patients with continued nonoperative treatment, even after percutaneous drainage, a recurrence rate of 42% was noted with an increased probability of emergent procedure. Based on these findings it was recommended that all patients with complicated findings on CT scan undergo an elective operation.(8) Salem reviewed all hospitalized patients for the state of Washington. After evaluating over 25,000 patients, percutaneous drainage and medical management were found to decrease the need for emergency operative interventions.(39) Other studies have shown that complicated disease is not a result of multiple uncomplicated episodes. Salem, et.al., demonstrated that of 77 patients followed with complicated diverticulitis, only eight had two or more previous episodes. A majority of patients (79.4%) with fistula, perforation, bleeding, and abscess had no previous episodes of diverticulitis. They concluded that simple acute diverticulitis is not a good predictor for the development of further complications from diverticular disease as only a minority of patients with complications had previous episodes of diverticulitis.(13) Chapmen found that only 21% of patients presenting with free perforation and peritonitis had a previous history of disease. (40) Somasekar reviewed 108 patients admitted with complicated diverticulitis. Of these, 104 required emergent surgery but only 28 patients had a previous history of uncomplicated diverticulitis. However, only 3 (2.7%) of these 28 patients had suffered two previous episodes and would have qualified for an operation under the standard guidelines (2) Hart performed a case controlled study of patients presenting with perforated diverticulitis and found that 78% had no previous history.(41) Timing for Surgical Intervention Complicated diverticulitis is at this time an indication for operation. Circumstances may arise that would make continued observation a wiser decision based on the age and comorbidities of the patient, but until further evidence is available operation continues to be the standard of care. Pain is a valuable indicator for the patient’s recovery, and provides a marker for evaluation. Attempts at initiating PO intake and switching antibiotic therapy may be confidently made based on the patient’s symptoms or lack of resolution of those symptoms. Once the patient is pain free and has undergone an adequate preoperative evaluation, surgery can be undertaken. Before any surgical procedure patients should undergo endoscopic evaluation of the colon in order to rule out other disease processes that may need to be taken care of at the same time. Optimal timing for performing an operation after medical treatment of a complicated

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improved outcomes in colon and rectal surgery episode of diverticulitis has occurred and has never been studied. However, it seems prudent to offer an elective operation within 6 to 8 weeks to allow the inflammatory process to settle and provide an opportunity for safest operation. Laparoscopic surgery will also be easier without the inflammatory component of the acute setting. Chronic Diverticulitis Indications for Medical versus Surgical Treatment Chronic diverticulitis is typically defined as uncomplicated acute diverticular disease that resolves with antibiotic therapy only to flare again once antibiotics are discontinued. It is not a particularly common entity within the spectrum of diverticular disease. Patients initially respond well to antibiotic therapy but fail to fully resolve their symptoms, or have frequent recurrences within weeks of each other. Patients may experience multiple flares of the disease that resolve spontaneously but continue to plague the patient for weeks to months. Indications for surgical treatment Chronic diverticulitis is an indication for operation. However, the correct diagnosis of recurrent or chronic diverticulitis must be secure. Chronic abdominal pain unrelated to diverticular disease has been described and an operation for pain without confirmatory findings is doomed to failure. Barium enema may be the colon clearing test of choice in this situation as colonoscopy can be associated with an increased risk of perforation in the face of smoldering diverticular disease. Best Timing for surgical intervention Ideally, patients should be continued on their antibiotics up to the time of operation. A bowel prep should be instituted in these patients and their nutritional status be reassessed depending on the amount of time they have had a chronic smoldering infection and been unable to eat. A good starting place is to simply evaluate the amount of weight lost over the recent past. Patients may be candidates for either laparoscopic or open surgery, as both have been shown to be safe and effective in the hands of well practiced surgeons.

episodes of diverticulitis. This may be because the patient never sought medical attention despite having some symptoms, or the symptoms were mistaken for gastroenteritis, or other such ailment. Complications of diverticular disease appear to be related more to the severity of the attack at a specific location than from progression from simple to complex disease in an orderly fashion. This inflammatory process may range from uncomplicated to complex. Contrast enema has been described as one of the ways to diagnose an abnormal connection between the colon and another organ. However various reports put the success rate between 34–83%.(42, 43) Vaginography or cystoscopy are two other ways to confirm the diagnosis. If suspicions are still present with relevant symptoms, and CT scan confirms diverticulitis, operation can be offered without confirmatory testing. Whatever the source, patients with complex diverticulitis should undergo an operation to correct the problem, unless the patient is not a surgical candidate. These patients who are not surgical candidates can be managed on suppressive antibiotics. One important concept to remember is that fistulas do not represent an emergency. If the patient is appropriately draining, and does not appear to be septic, there is no emergency to the operation. Complex fistulas have been managed with a single operation successfully in as many as 90% of cases, both with open and laparoscopic techniques.(44–46) Obstruction from diverticular disease is quite different. Patients who present completely obstructed from diverticular disease will require urgent decompression. Depending on the stability of the patient, multiple options including resection and primary anastomosis with or without proximal diversion, Hartmann procedure, Turnbull colostomy, or stent placement are available for the surgeon. These patients may carry an extensive history of diverticular disease. Ruling out other sources of obstruction, specifically colon cancer, is important. If the patient has not been screened appropriately, one may choose to perform intraoperative colonoscopy depending on the patient’s condition and state of the bowel. If this is impossible during the operation, as is frequently the case, then follow up colonoscopy should be undertaken after the operation. Immunosuppressed Patients

Complex Diverticulitis Indications for surgical treatment Complex diverticulitis is defined as patients with colonic fistula, stricture or obstruction. Colovesicular fistulas are the most common fistula, but colosalpingo, colocutaneous, colo-colo, colovaginal, and coloenteric fistulas all have been reported as a complication of diverticular disease. Bleeding divertula is not typically associated with the inflammatory state of diverticulitis and thus falls outside the scope of this chapter. About 1–2% of patients with diverticulitis develop an internal fistula.(6) Symptoms of fistula depend on the location. Dysuria, fecaluria, and pneumaturia are the most common presenting signs for colovesicular fistula. At times, symptoms go unnoticed and a delay in diagnosis for a prolonged period of time is not uncommon. Rarely, some patients who present with complex diverticulitis have never formally been diagnosed with previous

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Risk of developing diverticulitis Difficulty arises in attempting to diagnosis diverticulitis in an immunocompromised patient because many fail to manifest the classical signs and symptoms of the disease. Patients who are considered to be immunosuppressed include transplant recipients, those with an immunodeficiency syndrome, or those taking immunosuppressive medications for arthritis, autoimmune diseases, or inflammatory bowel disease. Patients who are especially problematic are those that are receiving prednisone in dosages >20 mg/day. They present with fewer symptoms, have a longer time to operation, and higher mortality (85%) when compared with patients receiving lower doses (13%).(47) Thus, any patient taking higher doses of an immunosuppressive medication must be considered immunosuppressed and evaluated accordingly. These patients are much more likely to present with a free perforation than their nonimmunocompromised patients.(48–50) Correlation

operative and nonoperative therapy for diverticular disease between a delay of diagnosis and mortality has also been demonstrated in these patients. Transplant patients make up an ever growing population that requires immunosuppressive medication. The incidence of transplant diverticulitis varies by the type of transplant performed; however, all studies show a low incidence of the disease. One report reviewed 2,000 patients over a period of 30 years following renal transplants and reported a 0.5% risk of any colonic problems including diverticulitis.(51) Many studies have reported an incidence of diverticulitis among both lung and heart transplant patients that varies from 0.75% to 4%. However the hospital admission rate for diverticulitis in a “normal” population is 25–50 per 100,000 admissions (0.025–0.053%), which is much less than in a transplant population.(51–53) From 1985 to 1996, a review of six series including 986 of heart and lung transplant patients showed an incidence of 0.75%. The authors concluded that pretransplant screening of diverticulosis is not justified in the absence of symptoms.(54) Other authors have evaluated their experience with complicated diverticulitis in renal transplant patients. Of 1,211 patients, 13 patients had episodes of diverticular disease for a 1.1% incidence. They concluded that the problem is rare but the clinical presentation is atypical.(55) One of the major benefits among the transplant population was the introduction of cyclosporine because of the decreased steroid requirement. It has been demonstrated that a nearly 50% decrease in the rate of complicated diverticulitis was accomplished in patients who were treated with cyclosporine; however, this did not reach statistical significance due to small sample size.(55) Prophylactic Sigmoid Resection Most authors recommend that patients with symptomatic diverticulitis with appropriate confirmation undergo sigmoid resection before transplant. Diverticulosis without symptoms though does not require further investigation and is not an indication for prophylactic resection. However, these patients are at a slightly higher risk than the general population and should be monitored closely.(55) Postoperative mortality is high in immunocompromised patients who develop acute diverticulitis requiring operative intervention. An increased index of suspicion is necessary in treating immunocompromised patients. An approach incorporating an aggressive evaluation with medical support and early surgical exploration is generally warranted. One specific population deserves mention and those are patients with polycystic kidney disease. These patients appear to have a higher incidence of complicated diverticulitis than other transplant patients, and one study concluded that these individuals warrant more aggressive diagnostic evaluation for any symptoms. Pretransplant screening and prophylactic sigmoid resection deserve further study.(55) OPERATIVE MANAGEMENT What manner of operation is best? Three operations are typically recommended for patients requiring a sigmoid resection. Open sigmoid resection, laparoscopic

sigmoid resection, or hand assisted laparoscopic resection (HAL). Despite the recent eruption of literature and discussion about the benefits of laparoscopic colectomies, only 5–10% of all colectomies are currently performed using a laparoscopic technique.(56) However, with increased training and utilization, it is anticipated that this number will continue to increase substantially. Open colectomy is the gold standard for comparison. Laparoscopic colectomy has gained increased prominence following the successful application of this technique for other procedures. While it is still in its infancy, it is fast becoming the main choice for a growing number of patients and surgeons. Many large studies have been undertaken to assess the safety of laparoscopic colectomy as well as its economic feasibility. Reported benefits of laparoscopic colectomy include shorter hospital stay, less postoperative pain, earlier return of bowel function, and quicker return to daily activities. Other reported benefits include less wound, respiratory, gastrointestinal, and cardiopulmonary complications when compared to open surgery.(57–60) The downsides of laparoscopic surgery include surgeon specific initial higher complication rates and conversion rates associated with a steep learning curve, longer operating room time, and higher cost for operations.(58) However, a recent study looking directly at total cost for open sigmoid resection versus laparoscopic sigmoid resection by Senagore (59), revealed that overall total costs were significantly lower for laparoscopic patients, and that operating room costs were not different between the two types of surgery. They concluded that laparoscopic resection was a cost effective means of managing sigmoid diverticular disease. A key factor to keeping the costs equivalent between open and laparoscopic resection was the minimization of conversion and complication rates. A conversion rate of 6.6% was observed in this study. However, many factors go into a study like this including routine postoperative care, and surgeon and patient comfort levels with earlier discharge. Despite this, slow but steady progress in training of younger surgeons and greater familiarity with the new techniques will more than likely make laparoscopic surgery the standard of care in the future, much as laparoscopic cholecystectomy has become. Hand Assisted Laparoscopic (HAL) Colectomy has also been compared against laparoscopic resection and been found to be equivalent as far as outcome of patients.(56, 61) Benefits of HAL have been shorter operating times when compared with straight laparoscopic surgery as well as lower conversion rates. One recent study identified an advantage to using HAL colectomy with complicated diverticulitis and laparoscopic resection for uncomplicated diverticulitis.(56) The cost of utilizing a hand port was not significantly different when offset by the faster operating room time.(61) Much depends on the ability of the surgeon to complete the case without conversion. Conversion rates increase the total cost of the operation as well as the potential morbidity rates for the patient. In an article by Belizon (60) an analysis was made of patients undergoing conversion to an open operation. Postoperative morbidity was significantly higher for laparoscopic resection procedures that were converted to open after 30 minutes into the

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improved outcomes in colon and rectal surgery operation. Wound complications and greater length of stay in the hospital were the two most common findings. Obesity, adhesions, bleeding, and inflammation beyond area of operation were the most common predictors for conversion. The best operation for an individual seems to be the operation the surgeon can perform. However, with advancing minimally invasive techniques that can be implemented at a similar cost structure, it behooves all surgeons to continue to educate and modify their practices to provide the best care possible to their patients. Which Operation is Best? Three different operations have been proposed for the treatment of complicated diverticulitis with peritonitis. The first operative approach described was the three stage procedure encompassing drainage with stoma, followed by resection and anastomosis with continued diversion, and finally by restoration of continuity. The second approach involved resection and diversion or the traditional Hartmann procedure (HP). However, this approach is being challenged by the third approach of resection with primary anastomosis. Primary resection with anastomosis (PRA) can be performed with or without a covering stoma, and/or on-table lavage. The three stage procedure will not be discussed here as it is not considered standard of care and should be used only in very infrequent situations. In 1921, Hartman advocated his two stage resection which was superior and quickly became the standard of care. However early in the 1960s there were eight reports with a total of 50 patients that underwent resection and primary anastomosis for generalized peritonitis with a low mortality of 10%.(63) Not much debate is raised now with respect to patients presenting with recurrent or chronic diverticulitis. They are typically managed in an elective fashion with primary anastomosis. Patients are still traditionally given a bowel preparation before surgery, at least in the United States, and probably will for some time though there is a growing swell within the literature questioning its necessity. Patients who present with acute symptoms, typically Hinchey stages III or IV, are taken to the operating room urgently. These patients constitute approximately 3.2 per 100,000 patients.(63) These patients present a dilemma, because typically they are older, have a high number of comorbidities, and suffer a greater number of complications. In a recent review by Salem reviewing 98 articles on the outcome of complicated diverticulitis based on the type of operation performed, they identified 1,051 patients who underwent a Hartmann procedure from 54 studies, and 569 patients having undergone a primary anastomosis from 50 studies. (Tables 24.6 and 24.7) Of the patients undergoing a primary anastomosis, 16% had covering stomas and 10% had ontable lavage. The mortality rates of those in the Hartmann group (19.6%) were much higher than those undergoing a primary anastomosis (9.9%). The anastomotic leak rate in patients with a primary anastomosis ranged from 6.3% to 19.3%. If a diverting proximal stoma was performed at the time of a primary anastomosis the anastomotic dehiscence rate fall to 6.3%. Wound infections were also more frequently seen in the Hartman group (24.2%) versus the primary anastomosis group (9.6%). Again, patients with covering stomas had the lowest wound infection rate

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Table 24.6  Outcomes of primary anastomosis in patients with complicated diverticulitis—Salem et al.(61)

Primary Primary Primary Primary with Anastomosis Anastomosis Anastomosis Anastomosis Overall Alone with Stoma lavage

Mortality # of Studies # of Cases Anastomotic Leak # of Studies # of Cases Wound Infection # of Studies # of Cases

9.9% 48 548 13.9% 29 353 9.6% 17 219

8.1% 29 297 19.3% 14 145 16.4% 6 55

9.2% 17 109 6.3% 8 64 4% 3 25

9.6% 3 52 9.6% 3 52 12% 2 50

Table 24.7  Outcomes of Hartmann and Hartmann Reversal. Salem et al. (61) # of Patients Hartmann

1,051

Hartman Reversal

787

Mortality

Wound Infection

198 (18.8%) 70 (24.2%) 6 (0.8%)

7 (4.9%)

Stoma Complications

Leaks

12 (10.3%)

NA

NA

20 (4.3%)

at 4%. Patients undergoing a Hartmann procedure also required a larger second operation than those who had PRA with or without a covering stoma. Complications from a Hartmann reversal were associated with a mortality of 0.8%, a wound infection rate of 4.9% and an anastomotic leak rate of 4.3%. These patients also experienced stoma complications (10.3%) that required medical attention. The conclusion was the primary anastomosis is no worse than a Hartmann procedure and has several advantages including higher restoration of continuity rate, less hospitalization, and fewer infectious complications.(64) Multiple studies have evaluated the morbidity and mortality of the Hartmann procedure as well as the risks incumbent with takedown. Most seasoned surgeons realize that at times restoration of continuity can be more of a challenge to both patient and surgeon than the original operation. This was demonstrated in a recent multicenter prospective trial involving 415 patients with complicated diverticulitis. Two hundred forty-eight patients underwent resection with primary anastomosis. The other 167 had a Hartmann procedure. The mortality rate for those undergoing primary anastomosis was 4.0% while those with resection and diverting colostomy was 23.4%. After case adjustment, the data suggested that the Hartmann procedure was associated with a 1.8 fold increase in likelihood of death. This was not statistically significant. However a 2.1 fold increase in morbidity was found between the two groups and this was significant. In part this is due to the fact that surgeons typically reserved a Hartmann procedure for those older patients with more comorbidities and thus predisposed to a poorer outcome.(65) Risks associated with Hartmann Reversal Reversal of a Hartmann colostomy also carries with it a significant risk that must be entertained when considering this operation for patients who will desire continuity in the future. Failure

operative and nonoperative therapy for diverticular disease Table 24.8  The cr-POSSUM scoring system. Physiologic Parameters Age Cardiac Systolic BP Pulse

<61

62–70

>71

No Failure

Treatment for angina or HTN

Edema, cardiomyopathy, coumadin

Cardiomegaly, Raised JVD

110–130

131–170

>170

<90

50–80

80–100

100–120

<50 <10 or >18

Hgb

13–16

11.5–12.9

10–11.4

Urea

7.6–10

10.1–15

>15

Operative Parameters Type of Operation

Minor

Moderate

Major

Complex Major

Peritoneal Contamination

None

Cloudy

Pus

Fecal Mal + Mets

Malignancy Status Timing of OR

None, T1–2

T 3,4

Mal + Nodes

Elective

Urgent

Emergent < 2 hours

to reverse the colostomy has been reported in 20–50% (61) of patients and leak rates on reversal fall around 2–30% (61, 63) Mortality has been reported anywhere from 0–10% and wound infection rates range from 12–50%. A strong interest in primary anastomosis has been revived in the literature, with papers describing the successful outcomes of patients undergoing this type of operation. However, few papers are prospective, less are randomized, and such a trial is still needed today to definitively answer the questions of safety and efficacy. Multiple trials though have shown that the outcomes of primary anastomosis are indeed as safe as a Hartman and in many cases better. In a recent review, Constantinides et al. reviewed the outcomes of patients undergoing Hartmann (66), primary resection with anastomosis (PRA) (135 patients) and primary resection with anastomosis and diversion (126 patients). Patients undergoing a Hartmann procedure had a morbidity and mortality of 35% and 20% respectively. Primary anastomosis showed a slightly higher morbidity and mortality at 55% and 30%, while those with a primary anastomosis with diverting stoma demonstrated a morbidity and mortality rate of 40% and 25% respectively. Stomas were permanent in 27% of patients undergoing a Hartmann procedure and 8% of those having a primary anastomosis with diversion. They concluded that primary anastomosis with defunctioning stoma may be an optimal strategy for selected patients. Hartmann procedure should be reserved for patients with an extremely high risk of perioperative complications and only after consideration of long-term implications.(63) Patients undergoing on-table lavage have been analyzed as well, which showed similar outcomes to those who did not undergo on-table lavage. Regenet, described 60 patients, all Hinchey III or greater, in whom 27 underwent primary anastomosis with intraoperative lavage and 33 who had a Hartmann procedure. In this prospective observational study they found that the Hartmann procedure took much less time to perform, but that the mortality and morbidity for both groups were equal. Three patients in the intraoperative lavage group had an anastomotic leak (11%). A Hartmann reversal occurred in 69% of the patients. The reversal had its own associated morbidity of 24%, an anastomotic leak

rate of 7%, and no deaths. Postoperative stay after primary anastomosis and intraoperative lavage was 18.4 days and Hartmann Procedure was 38 days. They concluded that primary anastomosis with intraoperative lavage and a Hartmann Procedure are both adequate approaches for generalized peritonitis complicating diverticulitis.(17) Covering stomas have been recommended by most studies when primary anastomosis is performed because of the variable anastomotic leak rate. Both diverting colostomies and ileostomies have been described with equal success. Most of the poor outcomes noted are not necessarily due to the operation performed, but the comorbidities and peritonitis associated with the patient and disease. These risks play more into the outcome of patients than the type of operation performed. Complications of Operation Predictors of Morbidity and Mortality—Scoring Systems Multiple scoring systems have been evaluated in attempts to predict outcome and risk in patients undergoing both elective and emergent colon resection for diverticulitis. With an increasing interest in outcomes by doctors, patients, and payers, predictive scoring systems may be one of the many ways surgeons, hospitals, and systems are evaluated. Developed by Copeland in 1991, the Physiological and Operative Severity Score for the enumeration of Mortality and Morbidity (POSSUM) was developed as a tool to compare morbidity and mortality in a wide range of general surgical procedures. This was to facilitate surgical audit and the comparison of hospital performance. It has been further adapted for patients undergoing colon and rectal surgery and named cr-POSSUM (Table 24.8). The idea was to adjust risk of a surgical procedure based on the patient’s physiological condition and therefore allow a more accurate comparison of a unit (or individual’s) performance. Oomen has been one of the physiological and operative severity score (POSSUM) score’s biggest proponents and has done a number of studies attempting to validate the system. When

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improved outcomes in colon and rectal surgery Table 24.9  The Mannheim peritonitis index. Risk Factor

Scores

Age > 50

5

Female Sex

5

Organ Failurea

7

Malignancy

4

Preoperative duration of peritonitis >24 hours

4

Origin of sepsis not colonic

4

Diffuse generalized peritonitis

6

Exudate Clear

0

Cloudy/Purulent

6

Fecal

12

a. Kidney failure = creatinine level > 177 umol/L or urea level > 167 mmol/L or oliguria < 20 ml/hour; pulmonary Insufficiency = PO2 < 50 mmHg or PCO2 > 50 mmHg Intestinal obstruction/paralysis > 24 hours or complete Mechanical ileus, shock hypodynamic or hyperdynamic

they compared the POSSUM, cr (Colorectal)-POSSUM and p (General Surgery)-POSSUM they found that POSSUM over predicted mortality, while p-POSSUM and cr-POSSUM under predicted mortality for diverticular disease, but correctly predicted mortality for cancer. In a confirmatory study here in the US however, Senagore found that all of the POSSUM scoring systems over predicted mortality.(68, 69) Another scoring system that has been developed and used frequently in discussing outcomes and indications for the different types of operations performed is the Mannheim Peritonitis Index. Many studies have evaluated the efficacy of this scoring system. Bielecki found that patients with colonic perforation and an MPI > 25 had a 55% morbidity rate and 35% wound infection rate.(70) Another study confirmed these findings after evaluating 172 patients with peritonitis; the MPI was able to predict 12 of the 14 deaths. They also found that morbidity was related to the MPI score.(71) (Table 24.9) Complications of Procedure Anastomotic Leak Elective colectomy has been well documented to carry a very low anastomotic leak rate, of about 1–3%.(64) However, in the face of active inflammation or peritonitis, attempts at performing a primary anastomosis carry a higher risk of anastomotic dehiscence. Primary anastomosis in the setting of Hinchey stage III or IV carries a leak rate from 8–22%.(21, 64, 65, 72–74) Mortality Elective colectomy also carries with it a low mortality rate, typically >1%. A majority of deaths result from cardiovascular problems. However patients involved with complicated diverticulitis face greater risks that can be evaluated with numerous scoring systems. Mortality rates range from 0–36% in patients presenting with peritonitis and depend greatly on their comorbidities and time to operation.(74)

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Failure to Reverse Maggard looked at colostomy reversal at the population level for the state of California. Of the 1,176 patients who had a Hartmann procedure for diverticular disease, only 65% had a reversal at a mean of 143 days. Younger men were more likely to have their ostomy reversed, as opposed to older patients, and women. Patients with more comorbid risk factors also had fewer reversals. When evaluating all patients, 35% never had their ostomy reversed during the 4 year study. Complication rates following Hartmann reversal were quite high and included an overall rate of 57.4%. Infection (9.1%), aspiration pneumonia (8.7%), pulmonary edema (6%), and acute renal failure (4.9%) were all problematic.(75) Most of the literature quotes a 20–50% failure of reversal rate on patients for a number of factors including; comorbidities, age, and failed attempts at reversal.(75–78) Boland et al. found that 38% of patients suffered a major complication after their reversal. Failure to restore continuity in their population was 10.3%. Due to the morbidity of the Hartmann reversal as well as the number of patients who either are not reversed or fail an operative attempt at reversal they recommended always trying a primary anastomosis first with diversion if possible. (76) In another similar study Aydin et al. found that Hartmann reversal was associated with a higher prevalence of surgical or medical complications when compared with primary resection and anastomosis. The overall postoperative morbidity and 30 day mortality rates for Hartmann reversal were 48.5% and 1.7% respectively. Patients undergoing a primary resection with anastomosis suffered a morbidity rate of 26% and mortality rate of 0.7% Having controlled for the number of comorbid conditions, extent of diverticular disease, severity of peritoneal contamination and operative urgency, patients who underwent Hartmann reversal were 2.1 times more likely to have an adverse surgical event during their postoperative period.(77) The difficulty with these comparative studies is that despite attempting to find similar cohorts, patients who undergo a Hartmann procedure are usually older, frailer, and sicker than those that undergo a primary anastomosis. Surgeons generally wish to correct the problem as fast as possible and get the patient off of the operating room table. This creates the possibility of bias in evaluating the literature, as patients undergoing Hartmann’s versus primary anastomosis typically have a worse outcome. However, when added with the risks of a second complex and morbid operation of future stoma takedown, primary anastomosis and diversion with a loop ilesotomy appears much friendlier. If the patient is able to tolerate the extra 30 minutes required to perform a primary anastomosis one should be performed with diversion. Recurrence of diverticulitis after previous surgical resection Recurrence of diverticulitis or its symptoms following resection has been reported in 3–13% of elective cases.(79–81) Factors that have been found to contribute to the recurrence of diverticulitis after a resection include shorter resection length (79), and the leaving behind of a cuff of distal sigmoid.(80) Most recently, Thaler demonstrated that the level of the anastomosis is the only significant determinant of recurrence after laparoscopic resection.(82) The practice parameters of the ASCRS set out several

operative and nonoperative therapy for diverticular disease

Figure 24.1  CT scan of uncomplicated diverticular disease.

Figure 24.3  CT Scan demonstrating drain in abscess cavity.

Timing of Closure Timing of closure continues to be a contentious issue and has not been fully settled. Traditional teaching is to wait 3 to 4 months to allow the inflammatory process to subside and the patient to heal before performing another major operation. Mean time intervals in the literature range from 120 to 210 days. One study did compare closure at 4 and 8 months. Complication rates associated with timing of reoperation were 2.5 and 5 times higher at 4 and 8 months respectively.(77) Complications from the reversal included anastomotic leak, and rectovaginal fistulas in women. These fistulas are attributed to improper dissection of the vagina and failure to carefully mobilize the rectum.

Figure 24.2  Coronal recoinstruction of CT scan demonstrating air in mesentery.

general recommendations regarding resection of diverticular disease. For elective resection, all thickened, diseased colon, but not necessarily the entire proximal diverticula bearing colon, should be removed. It may be acceptable to retain proximal diverticular colon as long as the remaining bowel is not hypertrophied. Distally, all of the sigmoid colon should be removed to the level of the rectum.(1)

Conclusion Diverticular disease appears to be increasing in incidence in an ever widening spectrum of ages throughout the United States and other developed countries. However, with more experience with the disease process, coupled with better medical therapies and diagnostic measures, more patients are able to be managed conservatively then ever before. Uncomplicated diverticular disease may be treated medically without fear that recurrent episodes will lead to more complicated findings. Complicated disease is being managed medically more aggressively than ever before in an effort to prevent emergent operations. Primary anastomosis with diversion as opposed to the traditional two staged Hartmann procedure appears to be equally effective without the downside of a second major operation. Certainly the trends today for diverticular disease are to be less aggressive with operative management, and treat each individual case based on its own merits as opposed to the more stringent guidelines of the past.

259

improved outcomes in colon and rectal surgery References   1. Rafferty J, Shellito P, Hyman NH et al. Practice Parameters for Sigmoid Diverticulitis. Dis Colon Rectum 2006; 49: 939–44.   2. Somasekar K, Foster ME, Haray PN. The natural history of diverticular disease: is there a role for elective colectomy? J R Coll Sur Edinb 2002; 47: 481–4.   3. Morson BC. Pathology of diverticular disease of the colon. Clin Gastroenterol 1975; 4: 37–52.   4. Parks TG. Natural history of diverticular disease of the colon. A review of 521 cases. Br Med J 1969; 4: 639–42.   5. Larson DM, Masters SS, Spiro HM. Medical and surgical therapy in diverticular disease: a comparative study. Gastroenterology 1976; 71: 734–7.   6. Haglund U, Hellberg R, Johnsen C et al. Complicated diverticular disease of the sigmoid colon. An analysis of short and long term outcomes in 392 patients. Ann Chir Gyn 1979; 68: 41–6.   7. Ambrosetti P, Jenny A, Becker C, Terrier F, Morel P. Acute left colonic diverticulitis: compared performance of computed tomography and water-soluble contrast enema. Prospective evaluation of 420 patients. Dis Colon Rectum 2000; 43: 1363–7.   8. Kaiser AM, Jiang JK, Lake JP et al. The management of complicated diverticulitis and the role of computed tomography. Am J Gast 2005; 100: 910–7.   9. Hinchey EJ, Schaal PGH, Richard GK. Treatment of perforated diverticular disease of the colon. Adv Surg 1978; 12: 85–109. 10. Thorson AG, Goldberg SM. Benign Colon: diverticular disease. In: the ASCRS textbook of colon and rectal surgery, 1st edition. Springer Science + Business Media LLC, 2007: 271. 11. Salem L, Veenstra DL, S. Sullivan, D. Flum. The timing of elective colectomy in diverticulitis: a decision analysis. J Am Coll Surg 2004; 199: 904–12. 12. Schechter S, Mulvey J, Eisentat TE. Management of uncomplicated acute diverticulitis. Dis Colon Rectum 1999; 4: 470–6. 13. Salem TA, Molloy RG, O’Dwyer PJ. Prospective, five year follow-up study of patients with symptomatic uncomplicated diverticular disease. Dis Colon Rectum 2007; 50: 1460–4. 14. Koo V, Strange J, Lam CY, Epanomeritakis M. Young patients with diverticular disease: a preliminary quality of life study. Int J Surg 2007; 5: 244–9. 15. Broderick-Villa G, Burchette RJ, Collins JC et al. Hospi­ talization for acute diverticulitis does not mandate routine elective colectomy. Arch Surg 2005; 140: 576–83. 16. Shaikh, S, Krukowski AH. Outcome of a conservative policy for managing acute sigmoid diverticulitis. BJS 2007; 94: 876–9. 17. Janes S, Meagher A, Frizelle FA. Elective Surgery after Acute Diverticulitis. Br J Surg 2005; 92: 133–42. 18. Anaya DA, Flum DR. Risk of emergency colectomy and colostomy in patients with diverticular disease. Arch Surg 2005; 140: 681–5. 19. Mizuki A, Nagata H, Tatemichi M et al. The out-patient management of patients with acute mild to moderate colonic diverticulitis. Aliment Pharmoacol Ther 2005: 889–97.

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20. Richards RJ, Hammitt JK. Timing of prophylactic surgery in prevention of diverticulitis recurrence. Dig Dis Scien 2002; 47(9): 1903–8. 21. Peppas G, Bliziotis IA, Oikonomaki D, Falagas ME. Outcomes after medical and surgical treatment of diverticulitis: a systematic review of the available evidence. J Gast Hepatol 2007; 22(9): 1360–8. 22. Bartlett MK, McDermott WV. Surgical treatment of diverticulitis of the colon. N Engl J Med 1953; 248: 497–9. 23. Colcock BP. Surgical management of complicated diverticulitis. N Engl J Med 1958; 259: 570–3. 24. Welch CE, Allen AW, Donaldson GA. An appraisal of resection of the colon for diverticulitis of the sigmoid. Ann Surg 1953; 138: 332–43. 25. Chautems RC, Ambrosetti P, Ludwig A et al. Long-term follow-up after first acute episode of sigmoid diverticulitis: is surgery mandatory? A prospective study of 118. Dis Colon Rectum 2002; 45: 962–6. 26. Alexander J, Karl RC, Skinner DB. Results of changing trends in the surgical management of complications of diverticular disease. Surgery 1983; 94: 683–90. 27. Nylamo E. Diverticulitis of the colon: role of surgery in preventing complications. Ann Chir Gyn 1990; 79: 139–42. 28. Lorimer JW. Is prophylactic resection valid as an indication for elective surgery in diverticular disease. Can J Surg 1997; 40(6): 445–8. 29. Nelson RS, Velasco A, Mukesh BN. Management of diverticulitis in younger patients. Dis Colon Rectum 2006; 49(9): 1341–5. 30. Biondo S, Pares D, Rague MJ et al. Acute colonic diverticulitis in patients under 50 years of age. Br J Surg 2002; 89: 1137–41. 31. Schweitzer J, Casillas RA, Collins JC. Acute Diverticulitis in the Young Adult is not Virulent. Am Surg Dec 2002; 12: 1044–47. 32. Ambrosetti P, Robert JH, Witzig JA, Mirescu D et al. Incidence, outcome, and proposed management of isolated abscesses complicating acute left-sided colonic diverticulitis. A prospective study of 140 patients. Dis Colon Rectum 1992; 35: 1072–6. 33. Ambrosetti P, Grossholz M, Becker C, Terrier F, Morel P. Computed tomography in acute left colonic diverticulitis. Br J Surg 1997; 84: 532–4. 34. Makela J, Vuolio S, Kiviniemi H et al. Natural History of diverticular disease: when to operate? Dis Colon Rectum 1998; 41: 1523–8. 35. Rodkey GV, Welch CE. Changing patterns in the surgical treatment of diverticular disease. Ann Surg 1984; 200: 466–78. 36. Ambrosetti P, Robert J, Witzig JA et al. Prognostic factors from computed tomography in acute colonic diverticulitis. Br J Surg 1992; 79: 117–9. 37. Faramakis N, Tudor RG, Keighley MRB. The 5 year natural history of complicated diverticular disease. Br J Surg 1994; 81: 733–5. 38. Macias LH, Haukoos JS, Dixon MR et al. Diverticulitis: truly minimally invasive management. Am Surg 2004; 70: 932–5. 39. Salem TA, Molloy RG, O’Dwyer PJ. Prospective study on the management of patients with complicated diverticular disease. Colorectal disease 2005; 8: 173–6.

operative and nonoperative therapy for diverticular disease 40. Chapman J, Davies M, Wolff B et al. Complicated diverticulitis, is it time to rethink the rules? Ann Surg 242; 4: 576–83. 41. Hart AR, Kennedy JH, Stebbings WS et al. How frequently do large bowel diverticula perforate? An incidence and cross-sectional study. Eur J Gastroenterol Hepatol 2000; 12: 661–6. 42. Abcarian H, Udezue N. Coloenteric Fistulae. Dis Colon Rectum 1978; 21: 281–6. 43. Wychulis AR, Pratt JI. Sigmoidvaginal fistulae. A study of 37 cases. Arch Surg 1966; 92: 520–4. 44. Hjern F, Goldberg SM, Johansson C, Parker SC, Mellgren A. Management of diverticular fistulae to the female genital tract. Colorectal Disease 2007; 9(5): 438–42. 45. Mileski WJ, Joehl RJ, Rege RV et al. One-stage resection and anastomosis in the management of colovesicula fistula. Am J Surg 1987; 15: 75–9. 46. Balaguera JC, Segovia JC, Gamarra LP et al. Colovesical Fistula Complicating Diverticular Disease: one Stage Resection. Int Surg 2006; 91: 17–23. 47. Remine SG, McIlrath DC. Bowel perforation in steroidtreated patients. Ann Surg 1980; 192: 581–6. 48. Beck JC, Brown JSL, Johnson LG, Kennedy BJ, MacKenzie DW. Occurrence of peritonitis during ACTH administration. Can Med Assoc J 1950; 62: 423–6. 49. Canter JW, Shorb PE. Acute perforation of colonic diverticula associated with prolonged adrenocorticosteroid therapy. Am J Surg 1971; 121: 46–51. 50. Tyau ES, Prytowsky JB, Joehl RJ et al. Acute Diverticulitis: a complicated problem in the immunocompromised patient. Arch Surg 1991; 126: 855–9. 51. Soravia C, Baldi A, Kartheuser A et al. Acute colonic complications after kidney transplantation. Acta Chir Belg 1995; 95: 157–61. 52. Goldberg HJ, Hertz MI, Ricciardi R et al. Colon and Rectal Complications after Heart and Lung Transplantation. J Am Coll Surg 2006; 202(1): 55–61. 53. Maurer JR. The spectrum of colonic complications in a lung transplant population. Ann Transplant 2000; 5: 54–7. 54. Khan S, Eppstein AC, Anderson GK et al. Acute diverticulitis in heart and lung transplant patients. Tranplt Int 2001; 14: 12–5. 55. Lederman ED, Conti DJ, Lempert N et al. Complicated diverticulitis following renal transplant. Dis Colon Rectum 1998; 41: 613–8. 56. Lee SW, Yoo J, Dujovny N et al. Laparoscopic vs. handassisted laparoscopic sigmoidectomy for diverticulitis. Dis Colon Rectum 2006; 49: 464–9. 57. Salimath J, Jones MW, Hunt DL, Lane MK. Comparison of return of bowel function and length of stay in patients undergoing laparoscopic versus open colectomy. JSLS 2007; 11: 72–5. 58. Purkayastha S, Constantinides VA, Tekkis PP et al. Laparo­ scopic vs. open surgery for diverticular disease: a meta-analysis of nonrandomized studies. Dis Colon Rectum 2006; 49: 446–63. 59. Senagore AJ, Suepree HJ, Delaney CP et al. Cost structure of laparoscopic and open sigmoid colectomy for diverticular disease. Dis Colon Rectum 2002; 45: 485–90.

60. Belizon A, Sardinha CT, Sher ME. Converted laparoscopic colectomy. what are the consequences? Surg Endosc 2006; 20: 947–51. 61. Chang YJ, Marcello PW, Rusin LC et al. Hand assisted laparoscopic sigmoid colectomy. Surg Endosc 2005; 19: 656. 62. Wong WD, Wexner SD, Lowry A et al. Practice parameters for the treatment of sigmoid diverticulitis supporting documentation. The standards task force. the american society of colon and rectal surgeons. Dis Colon Rectum 2000; 43: 290–7. 63. Constantinides VA, Heriot A, Remzi F et al. Operative strategies for diverticular peritonitis. Ann Surg 2007; 245: 94–103. 64. Salem L, Flum DR. Primary anastomosis or hartmann’s procedure for patients with diverticular peritonitis? A systemic review? Dis Colon Rectum 2004; 47: 1953–64. 65. Constantinides VA, Tekkis PP, Senapati A. Prospective multicentre evaluation of adverse outcome following treatment for complicated diverticular disease. Br J Surg 2006; 93: 1503–13. 66. Wigmore SJ, Duthie GS, Young IE etal. Restoration of intestinal continuity following Hartmann’s procedure: the Lothian experience 1987; 92. Br J Surg 1995; 82: 27–30. 67. Regenet N, Pessaux P, Hennekinne S et al. Primary Anastomosis after Intraoperative colonic lavage vs. Hartmann’s procedure in generalized peritonitis complicating diverticular disease of the colon. Int J Colorectal Dis 2003; 18: 503–7. 68. Oomen JT, Cuesta MA, Engel AF. Comparison of outcome of POSSUM, p-POSSUM, and cr-POSSUM scoring after elective resection of the sigmoid colon for carcinoma or complicated diverticular disease. Scan J Gastroenterology 2007; 42: 841–7. 69. Bielecki K, Kaminski P, Klukowski. Large bowel perforation: morbidity and mortality. Tech Coloproctol 2002; 6: 177–82. 70. Makela JT, Kiviniemi H, Laitinen S. Prognostic factors of perforated sigmoid diverticulitis in the elderly. Dig Surg 2005; 22: 100–6. 71. Stumpf MJ, Vinces FY, Edwards J. Is primary anastomosis safe in the surgical management of complications of acute diverticulitis? Am Surg 2007; 73: 787–91. 72. Gooszen AW, Gooszen HG, Veerman W et al. Operative treatment of acute complications of diverticular disease: primary or secondary anastomosis after sigmoid resection. Eur J Surg 2001; 167: 35–9. 73. Richter S, Lindermann W, Kollmar O et al. One stage sigmoid colon resection for perforated sigmoid diverticulitis (Hinchey Stages III and IV) World J Surg 2006; 30: 1027–32. 74. Landen S, Nafteux P. Primary anastomosis and diverting colostomy in diffuse diverticular peritonitis. Acta Chir Belg 2002; 102: 24–9. 75. Maggard MA, Zingmond D, O’Connell JB, Ko CY. What proportion of patients with an ostomy for diverticulitis get reversed? Am Surg Oct 2004; 70: 928–31. 76. Boland E, Hsu A, Brand MI, Saclarides TJ. Hartmann’s colostomy reversal: outcome of patients undergoing surgery with the intention of eliminating fecal diversion. Am Surg 2007; 73: 664–8.

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improved outcomes in colon and rectal surgery 77. Aydin HN, Remzi FH, Tekkis PP, Fazio VW. Hartmann’s reversal is associated with high postoperative adverse events. Dis Colon Rectum 2005; 48: 2117–26. 78. Oomen JT, Cuesta MA, Engel AF. Reversal of Hartmann’s procedure after surgery for complications of diverticular disease is safe and possible in most patients. Dig Surg 2005; 22: 419–25. 79. Munson KD, Hensien MA, Jacob LN et al. Diverticulitis: a comprehensive follow-up. Dis Colon Rectum 1996; 39: 318–22.

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80. Benn PL, Wolff BG, Ilstrup DM. Level of anastomosis and recurrent colonic diverticulitis. Am J Surg 1986; 151: 269–71. 81. Leigh JE, Judd ES, Waugh JM. Diverticulitis of the colon: recurrence after apparently adequate segmental resection. Am J Surg 1962; 103: 51–4. 82. Thaler K, Baig MK, Berho M et al. Determinants of recurrence after sigmoid resection for uncomplicated diverticulitis. Dis Colon Rectum 2003; 46: 385–8.

25

Abdominal surgery for colorectal cancer Jason Hall and Rocco Ricciardi

Challenging Case A 65-year-old woman with no significant past medical history underwent a laparoscopic sigmoid colectomy for colon cancer. The patient had a persistent postoperative ileus and on day seven, a fever spike with increasing abdominal pain. Case Management A contrast enema revealed an anastomotic leak and she returned to the operating room for laparotomy, abdominal washout, and end colostomy. The anastomosis had a pinpoint defect posteriorly without evidence of tension or ischemia. She responded well to antibiotics and was discharged 16 days following her initial procedure. INTRODUCTION The need for improved quality in healthcare has reached the consciousness of policy makers, providers, payers, and patients. Following the publication of two Institute of Medicine reports: To Err Is Human: Building a Safer Health System and Crossing the Quality Chasm: A New Health System for the 21st Century, the quality of our nation’s health care has been critically examined while outcomes questioned. The increased attention to healthcare has lead to calls for better access, more equitable care, more rigorous monitoring and quality assessment, pay for reporting and potentially pay for performance. In fact, to accelerate the diffusion and pace of quality improvement efforts, the Institute of Medicine launched the Redesigning Health Insurance Performance Measures, Payment, and Performance Improvement Project. With an aim toward equitable and reliable high quality care, our nation has started down the road of more measurement in order to gain better outcomes. Quality has always been a major focus of attention for surgeons but with the advent of pay for reporting and soon, pay for performance, attempts to measure quality of care have become more hurried. At this time, the focus have been on process measures such as antibiotic prophylaxis and venous thrombosis prophylaxis but with time, it is likely that we will see assessment of morbidity and mortality and potentially quality of life and patient satisfaction. With respect to colon and rectal surgery, specific policies have been promoted to improve care, including measurement and reporting of performance data, payment incentives, and quality improvement initiatives. Oncologic measures are under active development and will likely standardize the way we manage colon and rectal cancer. It is for this reason that our chapter on improving outcomes for abdominal surgery in colorectal cancer is particularly important to readers of this textbook and in particular surgeons who perform these procedures. Procedures involving the colon and rectum are particularly prone to high rates of morbidity and mortality and thus, techniques to reduce the burden from disease of the colon and rectum are important. Surgical resection remains the standard of care for curative treatment of colorectal cancer. In order to improve outcomes, numerous surgical techniques have been proposed to reduce

complications and improve outcomes in resections for colorectal diseases. However, as with all surgical procedures, complications related to preoperative, intraoperative, and postoperative factors occur more often than we like to recognize. As the collective interest in surgical outcomes has increased, surgeons have been charged not only with improving their outcomes but also with documenting that improvements in surgical care are real and generalizable to the population served. This chapter provides a systematic overview of the major recent developments in outcomes and quality measurement in colorectal cancer. It also provides and evidence based platform for the minimization and management of common surgical complications, thereby improving outcomes. Oncologic Outcomes in Colorectal Cancer A number of factors affect prognosis after colorectal resection for cancer. Generally, oncologic outcomes for abdominal resection for colon cancers are inversely proportional to the patients’ stage of disease. Following attempted curative resection, survival parallels the TNM stage (I- well above 90%; II- 65–90%; and III- 45–75%).(1, 2) More specifically, local extent of disease, the presence of metastatic disease, nodal involvement, adequacy of regional node harvest, incomplete resection, preoperative CEA level, tumor grade, and tumor biology have all been correlated with oncologic outcomes.(3–7) Alternatively, tumor size and gross tumor configuration have not been correlated with prognosis following surgery. Despite these patient and tumor factors, the surgeon can greatly influence oncologic outcomes by performing a proper preoperative oncologic evaluation, adequate tumor resection, and satisfactory nodal harvest. Preoperative Evaluation Following the diagnosis of colorectal cancer, the surgeon should assess the patient’s surgical risk while determining local and distant extent of disease. Despite the lack of consensus for preoperative testing of colorectal cancer, we adhere to a thorough evaluation of the abdomen and chest to rule out distant disease while determining the local extent of disease, especially when planning a laparoscopic resection. Most importantly however, before completing a colorectal resection, colorectal cancer patients should have a complete assessment of the colon. Approximately 5% of patients will have a synchronous colorectal cancer and 25 to 76% patients will have a synchronous adenomatous polyp. (8) Colonoscopy is advantageous for identifying the position of the lesion while permitting tattooing for intraoperative localization with laparoscopic resections. Also, some assessed lesions are prohibitively large and thus the planned operation may require alteration in order to address all of the colonic neoplasia. Computed tomography, virtual colongraphy, and barium enema are other methods that may be applied if a colonoscopy cannot be performed for technical reasons. In addition, we have had

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improved outcomes in colon and rectal surgery excellent results with intraoperative CO2 colonoscopy following surgical extirpation thereby reducing the number of bowel preps. Thus, an adequate assessment of the patient’s colonic disease reduces the likelihood that the patient may require another procedure for a missed lesion.

Surgical Outcomes in Colorectal Cancer There are a number of complications that occur following colorectal resections for cancer. Although some are difficult to avoid, we will stress methods to reduce the frequency of these complications and improve outcomes.

Surgical Technique In addition, to an adequate preoperative assessment, adequate tumor resection is critical to ensuring a good prognosis. Appropriate surgical margins critically influence outcome after colorectal cancer resection. In addition to the proximal and distal bowel margins, the radial or circumferential margin is particularly important in the treatment of both colon and rectal cancers.(9) The consensus of a 5 cm proximal and distal bowel margin is generally adhered to for colon cancers, with data suggesting that mural tumor migration rarely occurs beyond a 2 cm margin in either the proximal or distal direction to cancer.(10) In the setting of rectal cancer, a distal margin of as little as 1–2 cm has become the rule in lower tumors, while it is important to note that survival is adversely affected by a distal margin of <0.8 cm.(11) Controversy regarding the point of ligation of the vascular pedicle has been a point of contention for years. Many surgeons argue that a high ligation of the vascular pedicle is critical to ensuring good oncologic outcomes. However, a comparison of high versus more distal ligation for left sided cancers by the French Association for Surgical Research demonstrated no difference in survival.(12) Despite the fact that advocates of proximal vascular ligation have little evidence to support improved outcomes, the net effect of high ligation may be to improve lymph node sampling. An adequate mesenteric resection to include an appropriate nodal sample importantly predicts survival.(5) Given the overwhelming data in this area, the College of American Pathologists has recommended additional techniques to enhance nodal recovery if <12 nodes are identified on initial examination. (6) Similarly, several national organizations have proposed setting benchmarks of 12 lymph nodes as a proxy of an adequate oncologic resection for colorectal cancer.(13–17) This proposed benchmark may someday serve as an important quality measure to compare surgeons and providers treating colorectal cancer. At this time however, advocates of lymph node benchmarks have no evidence that such thresholds will result in real measurable improvement in patient outcome. Surgical advances in laparoscopic technique have resulted in a rising tide of enthusiasm for laparoscopic cancer resections. These advances have resulted in some improvement in shortterm outcomes, such as postoperative pain, length of ileus, and hospital stay. Most importantly, multicenter trials of laparoscopic resection versus open resections for colon cancer reveal no compromise in oncologic outcomes.(18) Despite early reports of port site recurrences from laparoscopic oncologic resections, data support the oncologic equivalency of laparoscopic colectomy in the hands of experienced surgeons.(18, 19) Thus, oncologic outcomes are comparable for the experienced laparoscopic surgeon as compared to open surgery for colon cancer, with the proviso that population based data are unavailable at this time. In addition oncologic results for laparoscopic proctectomy for rectal cancer have been concerning.(20)

Anastomotic Complications Anastomotic complications are some of the most feared compli­ cations in colorectal surgery patients. Although rare, the dev­elop­ment of anastomotic complications results in a prolonged postoperative stay with a high cost to the patient, the healthcare system, and society. Perioperative anastomotic complications can also lead to long-term consequences including stricture, abdominal wall hernia, permanent diversion, poor functional outcome, and need for reoperative therapy. A number of variables have been linked to the development of anastomotic complications, particularly the technique employed, the conditions under which the anastomosis is constructed, and other patient characteristics.

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Anastomotic Leak One of the most devastating outcomes of a new anastomosis for colorectal cancer is anastomotic leak, occurring in 3–6% of all colorectal cases. These leaks occur more commonly with more distal resections and are reported to be as high as 15.3% for low rectal reconstructions.(21) Although the development of leak is frequently attributed to surgeon error, from technique or judgment, patient characteristics also importantly influence the development of leaks. For example, renal failure, chronic obstructive pulmonary disease, steroid use, elevated white blood count, and malnutrition have all been attributed to anastomotic leak.(22, 23) In addition, operative factors such as low rectal anastomoses, colocolonic anastomoses, intraoperative septic conditions, difficulties encountered during the anastomosis, and use of blood transfusion have been implicated.(22) Although surgical construction of the anastomosis is an important variable, there is no difference in the development of anastomotic leak whether the reconstruction is stapled, hand-sewn in one-layer, or even two-layers.(24, 25) With respect to anastomotic technique, emphasis should be placed on providing an adequate blood supply and ensuring a tension-free anastomosis. Adequate blood supply can be confirmed with multiple methods: by dividing the marginal artery of Drummond or other arcades and encountering pulsatile bleeding or by confirming bleeding at the cut edge of the colon. A tension free anastomosis is also critical and can be facilitated by high-ligation of the feeding vessel although this maneuver is not always critical. Other techniques to reduce tension and increase mobility include separation of the greater omentum from the transverse colon and adequate mobilization of the approximating ends. In the setting of low pelvic anastomoses, especially those anastomoses constructed following the use of neadjuvant therapy, a protective proximal intestinal stoma should be considered in order to reduce the lifethreatening consequences of anastomotic leak.(26) In addition to tension free methods and adequate blood flow, the local conditions under which an anastomosis is created can also doom the construction. Attention should be focused on the patient’s preoperative nutritional status. Golub et al. have demonstrated that

abdominal surgery for colorectal cancer an albumin concentration <3 g/L is associated with anastomotic leakage.(22) In a multivariate analysis these authors also demonstrated a relationship between preoperative corticosteroid use, peritonitis, bowel obstruction, chronic obstructive pulmonary disease as well as perioperative transfusion and the incidence of anastomotic leakage.(22) Other authors have identified perioperative conditions which increase the risk of anastomotic leakage and they include obesity, malnutrition, weight loss >5 kg, and use of alcohol.(27) If the patient’s nutritional status is in question or the local conditions are not favorable, it advisable not to construct an anastomosis. Once the unfavorable circumstances have been corrected the patient can undergo restoration of intestinal continuity under more favorable circumstances. Bowel preparations have traditionally been employed to clear the bowel of feces before colorectal operations. This practice was thought to decrease the likelihood of anastomotic leak by limiting the passage of stool through the newly constructed anastomosis. More recent data reveal an increase in anastomotic complications with the routine use of bowel preparations.(28) Others have similarly demonstrated more wound infections in addition to increased rates of anastomotic leak in patients receiving mechanical bowel preparations.(29) Because of the temporary starvation and electrolyte imbalance sometimes associated with mechanical bowel preparations, it is not clear that this practice represents anything more than surgical dogma. Despite the growing body of data describing an advantage to no bowel preparation, surgeons in North America seem slow to move away from this long-held practice, with many arguing the difficulty in colonic manipulation during laparoscopic surgery in an unprepped bowel. See Chapter 2 for a full discussion of this topic. Once an anastomotic leak develops, it often becomes evident within 5 to 8 days following the procedure. Yet in a more recent series of 1,223 patients with intestinal anastomoses, 36% were identified more than 30 days postoperatively.(30) The diagnosis is usually suspected by clinical factors and often confirmed by radiologic examination. Patients with early clinical evidence of anastomotic leak can present with fever, tachycardia, abdominal distention and tenderness, ileus, early diarrhea, or possibly septic shock. Depending on the patient’s clinical condition, presence of any one of these factors is indication for examination with a radiologic study. If there are obvious signs of peritonitis or hemodynamic collapse then urgent exploratory laparotomy is often preferable. Radiological investigation can be performed with either abdominopelvic computed tomography (CT) or with a soluble contrast enema. There have been conflicting reports as to the superiority of each technique (31, 32); however, CT scans have the additional benefit of demonstrating other intraabdominal pathology such as hematomas or abscesses. If an anastomotic leak is demonstrated by clinical or radiologic means, antibiotics should be administered and the patient resuscitated. Surgical exploration is then indicated to wash-out the abdominal cavity and examine the anastomosis. If conditions are favorable intraperitoneal anastomosis can be reconstructed although most anastomotic leaks generally require the construction of a stoma. Alternatively, the management of left-sided and low pelvic anastomoses is more complex. If the leak is secondary to bowel necrosis or ischemia and there is not sufficient bowel for reanastomosis, a colostomy should be created with a Hartmann’s pouch. This procedure should be performed with consideration

of the fact that the majority of these patients will be left with permanent stoma.(33) If there is sufficient bowel for reanastomosis and local conditions are favorable, revision of the anastomosis can be considered with the protection of a proximal loop ileostomy. If there is dense inflammation surrounding the anastomosis, a loop ileostomy should be constructed and a large drain placed in the perianastomotic area. A large number of anastomotic leaks associated with localized peritonitis and abscess formation can often be managed nonoperatively.(32) If there is a contained collection, the patient should be treated with intravenous antibiotics and drainage of the abscess should be considered by radiologic means.(34) Anastomotic Stricture Anastomotic stricture is a common occurrence following colorectal anastomosis, occurring in up to 30% of cases.(35) Strictures are often asymptomatic but may also present with partial or complete large bowel obstruction. The mechanism of stricture formation is not completely understood, but may be related to anastomotic leakage, pelvic sepsis, radiation injury, or local ischemia.(36, 37) Numerous nonrandomized trials and meta-analyses have demonstrated a higher rate of stenosis with end-to-end stapled anastomosis. The presence of a proximal diverting colostomy also seems to increase the risk of stricture, possibly due to the lack of dilation by the fecal stream.(38–40) However, patients who undergo proximal diverting ileostomy have generally more difficult anastomoses and often the ileostomy is formed because of the potentially higher risk for leakage. Thus, the higher risk of leakage in these patients may be confounded by local factors or patient variables that have been difficult to describe to date. Strictures typically present within the first postoperative year (41) and can be managed with a number of different modalities, depending on the anastomotic site. Many are asymptomatic and will resolve on their own as the bulk of the fecal stream slowly dilates the stenosis over the course of a few months. Before any therapeutic procedure is undertaken the operator should be confident that a new stricture does not represent a cancer recurrence. If there is uncertainty by visual inspection, the diagnosis can easily be ascertained through a formal biopsy of the anastomosis. Most colonic strictures following surgery can be managed with sequential digital manipulation, bougeinage, or hydrostatic balloon dilation. Patients often require several treatments before complete resolution and repeat dilations are more common following resections for cancer than for benign causes.(42) Newer techniques involve the use of endoscopic stents as well as endoscopic transanal resection of strictures. Small published series using these techniques report safe and satisfactory long-term outcomes.(43) Surgical revision of the anastomosis is occasionally necessary when the stricture is not accessible by endoscopic means or recurs after numerous less invasive procedures. Anastomotic Bleeding Postoperative bleeding related to intestinal anastomosis is a relatively rare but potentially serious event. The incidence in stapled colorectal anastomoses is 1.8–5%.(44, 45) The method of construction, whether stapled or hand-sewn, appears to be unrelated to the development of this complication.(46) The diagnosis of

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improved outcomes in colon and rectal surgery anastomotic bleeding is typically inductive as patients will pass variable amounts of maroon colored blood with their first bowel movement. More active bleeding commonly presents with large amounts of blood per rectum. To prevent this complication, we perform a simple examination of the staple line through the enterotomy. All visible bleeding is controlled with sutures rather than electrocautery as applying thermal energy to the staple line may increase the likelihood of a full thickness burn injury. The initial management of postoperative hemorrhage is typically nonoperative. Greater than 80% of patients will stop bleeding without intervention but nearly 50% of patients will require a transfusion.(47) Often simple techniques such as correcting the coagulopathy and halting unfractionated or low molecular weight heparin are sufficient. Alternatively, treatment for hemodynamically stable patients includes endoscopic electrocoagulation of the anastomotic line (48), or injection of the staple line with epinephrine or clips.(49) Although others have proposed that proximal colonic anastomoses should not be treated endoscopically (48), the data contraindicating this belief is minimal. If endoscopic methods fail, some patients are candidates for angiographic embolization or vasopressin treatment. Obviously, angiographic options should be exercised with care as embolization may interrupt the blood supply to the anastomosis and thus result in bowel infarction as well as anastomotic leak.(50) In addition, the use of vasopressin is also associated with myocardial and intestinal ischemia and should be employed with caution.(51, 52) Failure of the aforementioned hemostasis methods will often require exploratory laparotomy and revision of the anastomosis. Pelvic Hemorrhage Massive pelvic bleeding is a difficult complication that can occur rarely during proctectomy or retroperitoneal dissection. This bleeding usually results from inadvertent violation of the avascular presacral plane and resultant damage to the presacral veins. Presacral venous hemorrhage is difficult to control and can be a significant source of postoperative morbidity and mortality.(53) Conventional methods of hemostasis rarely are effective and usually result in increased bleeding. If encountered, bleeding should be controlled with direct pressure while the anesthesiology team appropriately resuscitates the patient. Laparotomy sponges are used to tamponade bleeding while microfibrillar collagen and absorbable gelatin can be used. If simple tamponade does not control the bleeding then sterile titanium thumbtacks can be inserted into the bleeding point on the sacrum.(54) In addition, endoscopic multifeed staplers used in laparoscopic mesh hernia repairs are available.(55) Others have described fixing a 4-cm2 piece of rectus muscle to the bleeding vessel while applying a high frequency electrical current to the muscle until it adheres to the presacral fascia.(56) Alternatively, bonewax can be used with some efficacy on the sacrum. In the most difficult circumstances, the pelvis is packed with sponges and the patient returned to the operating room in 1–2 days for laparotomy pad removal.(57) Splenic Injury Iatrogenic injury to the spleen is a potentially serious complication of colectomy with significant long-term adverse consequences. It is defined as any injury to the spleen caused by the operating team during a surgical procedure. Splenic injury occurs during 1.2 to

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8% of colorectal resections (21, 57, 58), although these figures likely underestimate the incidence of the problem as conservatively managed splenic injuries are rarely reported. Splenic injury is associated with the proximity of the lesion to the splenic flexure although traction on the peritoneal band attaching the greater omentum and spleen appears to be the most common mechanism by which the spleen is injured.(59–61) Other mechanisms of injury include retractor and direct instrumental damage.(62) Langevin reported no injuries to the spleen in 733 procedures in which the splenic flexure was not mobilized but 3.1% of patients requiring splenic flexure takedown sustained splenic injuries.(21) Mortality rates are higher in patients who sustain splenic injury after gastrointestinal surgery, particularly colorectal surgery.(63, 64) Splenic injury is associated with a higher incidence of early infections, potentially from hematoma formation and subsequent superinfection (58) or loss of splenic function. In a recent review of California Cancer Registry and California Patient Discharge Data, patients undergoing colorectal cancer resection with inadvertent splenectomy had an increased length of stay and a 40% increase in the probability of death.(65) There are few evidence-based recommendations for avoiding intraoperative splenic injury but basic surgical principles are obviously essential. To maximize exposure, the surgical incision should be appropriately elongated in order to obtain adequate, tension free, visualization of the appropriate structures in open surgery. All hand-held and self-retaining retractors should be placed with care and under direct visualization. Some authors have recommended a modified lithotomy position with the surgeon standing between the patient’s legs during flexure mobilization. This positioning permits clearer visualization of the structures in the left upper quadrant.(21) Unnecessary traction on the transverse and left colon should be avoided. Consideration should be given to dividing the lienocolic ligaments before commencing any left colonic resection.(62) If there is suspicion of tumor invasion into the spleen an en-bloc resection should be performed. There is some data to suggest the benefits of laparoscopy in mobilization of the spleen. Malek reported on iatrogenic splenectomies in 1911 laparoscopic resections and in 5,477 open colon resections. The authors reported 13 iatrogenic splenectomies, yet none following laparoscopic resection.(66) Prompt recognition at the time of surgery is the first step to the successful management of iatrogenic splenic injuries. Once an injury to the spleen is recognized, there are two options, either splenectomy or splenic preservation. Timely management allows the surgeon to manage bleeding at the first operation, while delayed recognition results in reduced chances of splenic salvage. (67) Optimally, the surgeon should attempt to salvage the spleen unless blood loss prohibits the more time intensive salvage methods. Techniques for splenic salvage are generally extrapolated from the trauma literature. Small, minimally bleeding, capsular tears generally improve with gentle tamponade whereas more active bleeders may require more intervention to achieve hemostasis. There is a long experience with various hemostatic agents such as thrombin, absorbable regenerated cellulose, and microfibrillar collagen. These are often placed on top of the bleeder and underneath a surgical pack for tamponade.(68) If these simple measures fail, bleeding can be controlled by segmental ligation

abdominal surgery for colorectal cancer of the feeding hilar vessels or splenorrhaphy. With severe splenic injury, complicated by continued hemorrhage and hemodynamic instability, the surgeon should obviously consider splenectomy. If splenectomy is performed, the patient should be administered pneumococcal, meningococcal, and H. Influenza vaccine in order to prevent overwhelming postsplenectomy sepsis.(69)

nervi erigentes at risk. We preserve Denonvilliers fascia unless the tumor is anterior or circumferential. When total mesorectal excision and autonomic nerve preservation are combined several authors have demonstrated a low frequency of bladder and sexual dysfunction.(74, 75) Both of these techniques should be considered standard when undertaking resection of the rectum.

Ureteral Injuries Due to the proximity of the ureters to the colon, injury is a common concern during colorectal operations. Although injuries to the ureters are uncommon during simple resections, when they occur, they can be devastating. The ureters are most commonly injured in colorectal procedures during one of several maneuvers; while ligating the inferior mesenteric artery or dissecting at the sacral promontory or laterally in the pelvis during division of the lateral stalks of the rectum. Unfortunately only 20 to 30% of intraoperative ureteral injuries are recognized at the time of the transgression.(70) Despite the fact that few injuries are recognized intraoperatively, ureteral injuries are best treated during the initial operation as the local conditions are likely to be the most favorable for a successful repair. Prompt diagnosis and institution of appropriate corrective surgical procedures often result in a very satisfactory outcome in about 94% of cases.(71) In order to prevent ureteral injuries, patients with difficult anatomy i.e. extensive pelvic adhesions after proctectomy, a large pelvic mass, or a phlegmon that makes identification of normal anatomy difficult, consideration should be given to preoperative stent placement. Ureteral stents permit quicker intraoperative ureter indentification but do not completely eliminate the risk of injury. In addition, ureteral stents permit quicker recognition of ureteral injuries, permitting immediate repair. Since these repairs can be technically challenging, they should be performed by a surgeon who is well versed with these repair techniques. General guidelines include debridement of necrotic tissues, ensuring excellent blood supply, and performing a tension-free anastomosis. More distal injuries of the pelvic portion of the ureter may be handled by reinplantation.(72)

Functional Outcomes Gastrointestinal function following rectal cancer resection is quite variable depending on the patient’s preoperative status, use of chemoradiation, anastomotic technique and local factors, and the development of anastomotic complications. Today, sphincter preservation procedures are being performed with increasing frequency for the management of mid-rectal and low rectal cancers. However, preservation of intestinal continuity frequently leads to continence disturbances which range from inadvertent passage of flatus to frank leakage of stool necessitating pad use. (76–82) Patients with a straight low anastomosis may also suffer from urgency, frequency, and clustering of bowel movements. Poor function after sphincter salvage largely results from a combination of four factors: damage to the sphincter complex; loss of normal anorectal sensation; a reduced rectal capacity and compliance, and a reduction in large intestine length resulting in more liquid effluent reaching the anal canal.(83) Increased effort has thus been exerted to minimize dysfunction following proctectomy with a focus toward reconstruction using a neorectum. In recent years, improved functional outcomes have been reported following anastomotic reconstruction with a colonic J-pouch or coloplasty. The most studied and accepted reconstruction option at this time is the colonic J-pouch, which is associated with improved physiological and functional outcomes as compared to the straight anastomosis.(83) Until recently, the advantages of a J-pouch were thought to be short-lived, but a recent multicentered study revealed sustained functional advantages after 2 years postoperatively compared to both the straight coloanal anastomosis and the coloplasty.(84) Another common technique is the use of a side to end Baker anastomosis, which in the shortterm has equivalent functional results to the colonic J-pouch or coloplasty.(85) Unfortunately, recent data suggest difficulty with complete evacuation of the Baker anastomosis as compared to the colonic J-pouch.(85) It is for these reasons that we recommend colonic J-pouch reconstruction for low anastomoses at 6 cm or closer to the anal verge.

Autonomic Nerves Injury Genitourinary function can be greatly altered by injury to the pelvic parasympathetic and sympathetic nerves during colorectal resections. Proper oncologic resection for rectal cancer has been associated with a significant incidence (10–69%) of urinary and sexual dysfunction.(73) Although urinary dysfunction is often limited to the first few postoperative days, sexual dysfunction may persist for months or indefinitely. Both forms of postoperative dysfunction are related to the patients’ preoperative function. Total mesorectal excision with autonomic nerve preservation has been advocated as an effective approach to the minimization of pelvic nerve injury. This technique mobilizes the mesorectum circumferentially with sharp dissection along the correct pelvic parietal planes while avoiding the pelvic nerves.(73) In addition, damage to the sympathetic plexus is often encountered during high ligation of the inferior mesenteric artery. The hypogastric nerves should be identified as they course over the sacral promontory and preserved. Anterior dissection should be avoided when unnecessary as dissecting in Denonvilliers’ fascia places the

Patient-Centered Outcomes There has been a growing interest in medical and surgical outcomes which are most important to patients rather than traditional measures of morbidity and mortality. This interest has developed from the growing concern that medical care fails to properly assess the needs of the patient. Patient-centered outcomes, such as patient satisfaction or quality of life are particularly meaningful for colorectal cancer patients. Despite the embryonic status of patient-centered outcomes in the surgical fields, there has been a growing push toward accurate measurement. Over the past 10 years, the Agency for Healthcare Research and Quality has funded and administered the Consumer Assessment of Healthcare Providers and Systems (CAHPS) program, a joint

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improved outcomes in colon and rectal surgery public and private initiative to develop standardized surveys of patients’ experiences with ambulatory and facility-level care.(86) CAHPS surveys provide information about patients’ care experiences rather than traditional clinical performance indicators, such as cured of disease or morbidity and mortality. The surgeons’ ability to measure and understand quality-oflife and other patient centered outcome would be of great value to the colorectal cancer patient undergoing surgery. In practical terms, patient expectations would be clearer. Few tested and useful patient centered metrics have been evaluated and even fewer are in use today.(87) Despite the lack of real progress in this area, insurers, patients, and others are very interested in determining what patients think of the treatments we provide them. At this time, surgeons need to work closely with others to facilitate more comprehensive and nontraditional outcomes following surgical care. Conclusion In summary, this chapter on improving outcomes for abdominal surgery in colorectal cancer provides an overview of potential complications, methods to reduce complications, methods to improve outcomes, surgical outcomes presently measured, and the future of patient-centered outcomes in colorectal cancer surgery. We have particularly emphasized the impact of the quality movement and the role of outcomes on quality measurement and assurance. The information presented in this chapter is critical as quality metrics and measurement are likely to become more and more important to the individual practitioner. Given that surgery for colorectal cancer has become increasingly more technical due to the refinement of open as well as laparoscopic techniques, outcomes measurement will become more and more important as we prove to our patients, payers, Congress, and ourselves that our outcomes are optimal. Although payers and other government groups have become the drivers of quality improvement, it is our duty to measure our own outcomes, assess the quality of care that we provide, and compare our own results with our colleagues. Internal efforts to improve quality are the most likely to bring about real meaningful changes in outcomes for colorectal cancer. References   1. Jagoditsch M, Lisborg PH, Jatzko GR et al. Long term prognosis for colon cancer related to consistent radical surgery: multivariate analysis of clinical, surgical, and pathologic variables. World J Surg 2000; 24: 1264–70.   2. Mcdermott FT, Hughes ESR, Pihl E et al. Comparative results of surgical management of single carcinomas of the colon and rectum: a series of 1,939 patients managed by one surgeon. Br J Surg 1981; 68: 850.   3. Chapuis PH, Dent OF, Fisher R et al. A multivariate analysis of clinical and pathological variables in prognosis after resection of large bowel cancer. Br J Surg 1985; 72: 698–702.   4. Tominaga T, Sakabe T, Koyama Y et al. Prognostic factors for patients with colon or rectal carcinoma treated with resection only. Five-year follow-up report. Cancer 1996; 78: 403–8.   5. Swanson RS, Compton CC, Stewart AK, Bland KI. The prognosis of T3N0 colon cancer is dependent on the number of lymph nodes examined. Ann Surg Oncol 2003; 10: 65–71.

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  6. Compton CC, Fielding LP, Burgart LJ et al. Prognostic factors in colorectal cancer. College of American Pathologists Consensus Statement 1999. Arch Pathol Lab Med 2000; 124: 979–94.   7. Wolmark N, Fisher B, Wieand HS et al. The prognostic significance of preoperative carcinoembryonic antigen levels in colorectal cancer. Results from NSABP (National Surgical Adjuvant Breast and Bowel Project) clinical trials. Ann Surg 1984; 199: 375–82.   8. Langevin JM; Nivatvongs S. The true incidence of synchronous cancer of the large bowel. A prospective study. Am J Surg 1984; 147: 330–3.   9. Nagtegaal ID, Quirke P. What is the role for the circumferential margin in the modern treatment of rectal cancer? J Clin Oncol 2008; 26: 303–12. 10. Quirke P, Dixon MF, Dundey P et al. Local recurrence of rectal adenocarcinoma due to inadequate surgical resection: histopathologic study of lateral tumor spread and surgical excision. Lancet 1986; 2: 996–8. 11. Vernava AM, Moran M, Rothenberger DA, Wong WD. A prospective evaluation of distal margins in carcinoma of the rectum. Surg Gynecol Obstet 1992; 175: 333–6. 12. Rouffet F, Hay J-M, Vacher B et al. Curative resection for left colonic carcinoma: hemicolectomy vs. segmental colectomy. A prospective, controlled, multicenter trial. Dis Colon Rectum 1994; 37: 651–9. 13. Nelson H, Petrelli N, Carlin A et al. Guidelines 2000 for colon and rectal cancer surgery. J Natl Cancer Inst 2001; 93: 583–96. 14. Otchy D, Hyman NH, Simmang C et al. Practice parameters for colon cancer. Dis Colon Rectum 2004; 47: 1269–84. 15. Hermanek P. [Oncologic surgery/pathologic-anatomic viewpoint]. Langenbecks Arch Chir Suppl Kongressbd 1991; 277–81. 16. ASCO/NCCN Quality Measures: Breast and Colorectal Cancer http://preview.asco.org/portal/site/ASCO/menuitem .5d1b4bae73a9104ce277e89a320041a0/?vgnextoid=1b08fcd 4eb46c010VgnVCM100000ed730ad1RCRD accessed May 6, 2007. 17. Compton CC. Updated protocol for the examination of specimens from patients with carcinomas of the colon and rectum, excluding carcinoid tumors, lymphomas, sarcomas, and tumors of the vermiform appendix: a basis for checklists. Cancer Committee. Arch Pathol Lab Med 2000; 124: 1016–25. 18. Bonjer HJ, Hop WC, Nelson H et al. Laparoscopically assisted vs open colectomy for colon cancer: a meta-analysis. Arch Surg 2007; 142: 298–303. 19. The Clinical Outcomes of Surgical Therapy Study Group. A comparison of laparoscopically assisted and open colectomy for colon cancer. NEJM 2004; 350: 2050–9. 20. Guillou PJ, Quirke P, Thorpe H et al. Short-term endpoints of conventional versus laparoscopic-assisted surgery in patients with colorectal cancer (MRC CLASICC trial): multicentre, randomised controlled trial. Lancet 2005; 365: 1718–26. 21. Langevin JM, Rothenberger DA, Goldberg SM et al. Accidental splenic injury during surgical treatment of the colon and rectum. Surg Gynecol Obstet 1984; 159: 139–44.

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40. Waxman BP, Ramsay AH. The effect of stapler diameter and proximal colostomy on narrowing at experimental circular stapled large bowel anastomosis. Aust N Z Surg 1986; 56: 797–801. 41. Matos DDM, Atallah A, Castro A, Silva Lustosa SA. Stapled versus handsewn methods for colorectal anastomosis surgery. Cochrane Database Syst Rev 2001; 3: CD003144. 42. Suchan KL, Muldner A, Manegold BC. Endoscopic treatment of postoperative colorectal anastomotic strictures. Surgical endoscopy 2003; 17: 1110–3. 43. Forshaw MJ, Maphosa G, Sankararajah D, Parker MC, Stewart M. Endoscopic alternatives in managing anastomotic strictures of the colon and rectum. Tech Coloproctol 2006; 10: 21–7. 44. Cirocco WC, Golub RW. Endoscopic treatment of postoperative hemorrhage from a stapled colorectal anastomosis. American Surgeon 1995; 61: 460–3. 45. Malik AH, East JE, Buchanan, Kennedy RH. Endoscopic haemostasis of staple-line hemorrhage following colorectal resection. Colorectal Dis 2008; 10(6): 616–8. 46. Choy PYG, Bissett Ip, Docherty JG, Parry BR, Merrie AEH. Stapled versus handsewn methods for ileocolic anastomoses. Cochrane Database of Syst Rev 2007; 3: CD004320. 47. Murray JJ, Schoetz DJ Jr. Stapling techniques in rectal surgery, In: Fazio VW(ed.) Current therapy in colon and rectal surgery. Philadelphia: BC Decker, 1990: 384–90. 48. Chardavoyne R, Stein TA, Ratner LE et al. Is colonoscopy safe in the early postcolectomy period? Am Surgeon 1991; 57: 734–36. 49. Chassin JL, Rifkind KM, Turner JW. Errors and pitfalls in stapling gastrointestinal tract anastomoses. Surg Clin N Am 1984; 64: 441–59. 50. Charlmers AG. Robinson PJ, Chapman AH. Embolisation in small bowel hemorrhage. Clin Radiology 1986; 37: 379–81. 51. Dubois JJ, Ostrow LB, Smith GB, Welling DR. Transcatheter embolization of small bowel anastomosis: A case report and review of the literature. Military Med 1989; 154: 505–7. 52. Atabek U, Pello MJ, Spence RK et al. Arterial vasopressin for control of bleeding from a stapled intestinal anastomosis. Report of two cases. Dis Colon Rectum 1992; 35: 1180–2. 53. Wang QY, Shi WJ, Zhou WQ, He ZR. New concepts in severe presacral hemorrhage during proctectomy. Arch Surg 1985; 120: 1013–20. 54. Khan FA, Fang DT, Nivatvongs S. Management of presacral bleeding during rectal resection. Surg Obst Gyn 1987; 165: 275–6. 55. Hill AD, Menzies-Dow N, Darzi A. Methods of controlling presacral bleeding. JACS 1994; 178: 183–4. 56. Xu J, Lin J. Control of presacral hemorrhage with electrocautery through a muscle fragment pressed on the bleeding vein. JACS 1994; 179: 351–2 57. Civelek A, Yegen C, Aktan AO. The use of bonewax to control massive presacral bleeding. Surg Today 2002; 32: 944–5. 58. Konstadoulakis MM, Kymionis GD, Leandros E et al. Long term effect of splenectomy on patients operated on for cancer of the left colon: a retrospective study. Eur J Surg 1999; 165: 583–87.

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improved outcomes in colon and rectal surgery 59. Lord MD, Gourevitch A. The peritoneal anatomy of the spleen with special reference to the operation of partial gastrectomy. Br J Surg 1965; 52: 202–4. 60. Cioffiro W, Schein CJ, Gliedman ML. Splenic injury during abdominal surgery. Arch Surg 1976; 111: 167–71. 61. Olsen W, Beaudoin D. Surgical Injury to the Spleen. Surg, Gynecol, Obstet 1970; 131: 57–62. 62. Cassar K, Munro A. Iatrogenic splenic injury. J R Coll Surg Edin 2002; 6: 731–41. 63. Fabri PJ, Metz EN, Nick WV, Zollinger RM. A quarter century with splenectomy. Changing concepts. Arch Surg 1974; 108: 569–75. 64. Rodkey GV, Welch CE. Changing patterns in the surgical treatment of diverticular disease. Ann Surg 1984; 200: 466–78. 65. McGory ML, Zingmond DS, Sekeris E, Ko CY. The significance of inadvertent splenectomy during colorectal cancer resection. Arch Surg 2007; 142: 668–74. 66. Malek MM, Greenstein AJ, Chin EH et al. Comparison of Iatrogenic Splenectomy During Open and Laparoscopic Colon Resection. Sur Laparosc Endosc Percutan Tech 2007; 17: 385–7. 67. Falsetto A, Della Corte M, De Pascale V, Surfaro G, Cennamo A. Iatrogenic splenic injuries. Ann Ital Chir 2005; 76: 175–81. 68. Scheele J, Gentsch HH, Matteson E. Splenic repair by fibrin tissue adhesive and collagen and fleece. Surgery 1984; 95: 6–13. 69. Working Party of the British Committee for Standards Clincal Hematology Task Force. Guidelines for the prevention and treatment of infection in patients with an absent of dysfunctioned spleen. Br Med J 1996; 312: 430–3. 70. Higgins CC. Ureteral injuries during surgery. A review of 87 cases. JAMA 1967; 199: 82–8. 71. Al-Awadi K, Kehinde EO, Al-Hunayan A, Al-Khayat A. Iatrogenic ureteric injuries: incidence, aetiological factors and the effect of early management on subsequent outcome. Int Urol Nephrol 2005; 37: 235–41. 72. Hamawy K, Smith JJ III, Libertino JA. Injuries of the distal ureter. Seminar Colon Rectal Surg 2000; 11: 163–79. 73. Pocard M, Zindindohoue F, Haab F et al. A prospective study of sexual and urinary function before and after total mesorectal excision with autonomic nerve preservation for rectal cancer. Surgery 2002; 131: 368–72. 74. Heald RJ, Ryall RD. Recurrence and survival after total mesorectal excision for rectal cancer. Lancet 1986; 1: 1479–82.

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75. Nesbakken A, Nygaard K, Bull-Njaa T, Carlsen E, Eri LM. Bladder and sexual dysfunction after mesorectal excision for rectal cancer. Br J Surg 2000; 87: 206–10. 76. McDonald PJ, Heald RJ. A survey of postoperative function after rectal anastomosis with circular stapling devices. Br J Surg 1983; 70: 727–9. 77. McAnena OJ, Heald RJ, Lockhart-Mummery HE. Operative and functional results of total mesorectal excision with ultralow anterior resection in the management of carcinoma of the lower one-third of the rectum. Surg Gynecol Obstet 1990; 170: 517–21. 78. Batignani G, Monaci I, Ficari F et al. What affects continence after anterior resection of the rectum? Dis Colon Rectum 1991; 34: 329–35. 79. Lewis WG, Holdsworth PJ, Stephenson BM et al. Role of the rectum in the physiological and clinical results of coloanal and colorectal anastomosis after anterior resection for rectal carcinoma. Br J Surg 1992; 79: 1082–6. 80. Karanjia ND, Schache DJ, Heald RJ. Function of the distal rectum after low anterior resection for carcinoma. Br J Surg 1992; 79: 114–6. 81. Lewis WG, Martin IG, Williamson ME et al. Why do some patients experience poor functional results after anterior resection of the rectum for carcinoma? Dis Colon Rectum 1995; 38: 259–63. 82. Miller AS, Lewis WG, Williamson ME et al. Factors that influence functional outcome after coloanal anastomosis for carcinoma of the rectum. Br J Surg 1995; 82: 1327–30. 83. Brown SR, Seow-Choen F. Preservation of rectal function after low anterior resection with formation of a neorectum. Semin Surg Oncol 2000; 19: 376–85. 84. Fazio VW, Zutshi M, Remzi FH et al. A randomized multicenter trial to compare long-term functional outcome, quality of life, and complications of surgical procedures for low rectal cancers. Ann Surg 2007; 246: 481–90. 85. Machado M, Nygren J, Goldman S, Ljungqvist O. Similar outcome after colonic pouch and side-to-end anastomosis in low anterior resection for rectal cancer: a prospective randomized trial. Ann Surg 2003; 238: 214–20. 86. Consumer Assessment of Healthcare Providers and Systems. Agency for Healthcare Research and Quality. URL: https:// www.cahps.ahrq.gov/default.asp. 87. Morris AM. Patient-centered outcomes after therapy for colorectal cancer. Surg Oncol Clin N Am 2006; 15: 195–211.

26 Transanal approaches to rectal cancer

Sachin S Kukreja and Theodore J Saclarides

Challenging Case A 67-year-old male underwent a screening colonoscopy and is referred because a 3 cm adenocarcinoma was found approximately 12 cm from the anal verge. Preoperative workup with a transrectal ultrasound and CT scan showed the lesion appeared to be a uT1N0 cancer without metastatic disease. He has multiple medical problems including a myocardial infarction 3 months prior and is not felt to be a good candidate for radical surgery. Case Management The patient is offered Transanal Endoscopic Microsurgery (TEM); a complete full-thickness excision is successfully performed. Post­ operatively, he has urinary retention. A bladder scan reveals 700 L of urine within the bladder and catheterization is performed. The retention resolves overnight and the patient is discharged the next morning. Pathologic evaluation of the specimen revealed a pT1N0 rectal cancer. INTRODUCTION There are approximately 42,000 newly diagnosed rectal cancers in the United States each year and approximately 9,500 people die from their disease. Although adjuvant therapies continue to improve outcomes, surgical management remains the cornerstone of therapy as few patients can be cured without a surgical resection. Surgical approaches are varied and are chosen based on the degree of rectal wall invasion, tumor histology, the presence or absence of lymph node metastases, involvement of the anal sphincter and nearby pelvic structures, and disease comorbidities. Either a local excision (with or without adjuvant therapy) or radical, transabdominal surgery (and possible chemoradiation) can be chosen. The surgical management for rectal cancer has been evolving significantly over the last few decades and across geographic boundaries. Rectal Cancer and Surgical Options Traditional and more commonly applied treatment with total mesorectal excision (TME) through either a low anterior (LAR) or abdominoperineal resection (APR) is the standard against which other procedures are compared. Such interventions are not without significant morbidity, including anastomotic leak, wound infection or dehiscence, colostomy malfunction, or pelvic dissection complications (including defecatory, urinary and sexual dysfunction, and fecal incontinence). Although such techniques are well-accepted treatment modalities, the search for less invasive and less morbid techniques that provide sphincter preservation and acceptable cure rates has led to the evolution of a wide variety of alternative surgical procedures. Although less-invasive procedures including transanal fulguration, endocavitary radiation, and transsphincteric or transsacral approaches have been utilized, the transanal approaches have proven to be the most popular and safest overall with less morbidity and mortality.(1)

Determining whether a patient may be a candidate for sphincter preservation (either through trans-anal or trans-abdominal means) usually begins during the patient’s initial assessment. More often than not, the patient comes to the surgeon after ­having already undergone lower endoscopy. Rectal bleeding may have prompted an evaluation or the patient may have been asymptomatic. Nonetheless, key questions related to the patient’s bowel habits are critical in the assessment. Symptoms of tenesmus often signal the presence of a large tumor which usually requires radical transabdominal surgery. Anal pain, with or without defecation may imply involvement of the anal sphincters or pelvic floor, precluding a sphincter-preserving operation. Patients with fecal incontinence should be identified in the preoperative workup since proctectomy and sphincter preservation may worsen continence, condemning them to significant fecal soilage, even if such a procedure is technically possible. Both digital rectal exam (DRE) and rigid sigmoidoscopy are required in the evaluation. Localizing the lesion to the lower, middle, or upper third of the rectum helps determine what options the patient may have. Involvement of the anal sphincter, the tumor’s spatial relationship to the anorectal ring, and fixation to the ­pelvic side walls are important physical findings that help guide the decision making process. Additionally, the patient’s overall medical status must be taken into consideration as some may not be able to tolerate a large abdominal operation due to a myriad of comorbidities. Finally, before planning surgery, a complete colonoscopy is essential to rule out synchronous lesions elsewhere in the colon. Accessible well-differentiated cancers that are <4 cm in size, lack lymphovascular invasion, occupy <40% of the bowel wall circumference, and do not invade the muscularis propria have historically been considered the most amenable to a transanal approach. Although these criteria are not necessarily strict guidelines, tumors larger than this are associated with a significantly higher incidence of lymph node metastasis. Many authors will not offer a transanal approach for lesions larger than 3 cm in diameter due to the risk of incomplete excision. Upon DRE, those masses that are immobile and fixed are likely to be transmural and hence, require a traditional TME surgery following neoadjuvant therapy. It is well established that even in the most experienced of hands, manual exam alone can differentiate T1/ T2 tumors from T3/T4 tumors only 80% of this time. Lymph node metastases can be detected digitally in only 50% of instances.(2) Rigid proctosigmoidoscopy allows the clinician to evaluate and more accurately localize the tumors beyond what is within reach of the DRE within the middle and upper rectum. Lesions that may have been labeled as being 15 cm from the anal verge with flexible endoscopy may be closer to the anus when evaluated with a rigid scope. Various imaging modalities exist and should be utilized to assess depth of invasion and the presence of lymph node involvement; these include CT scan, MRI, and transrectal ultrasound (TRUS). With its ease of use, widespread availability, and high

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improved outcomes in colon and rectal surgery overall accuracy, many clinicians rely on TRUS in their standard preoperative work-up for rectal cancer and consider it to be the best method of preoperative staging. Many series cite an accuracy rate of 90% for staging rectal wall penetration and an 80% accuracy rate for assessing the status of the perirectal lymph nodes. Factors such as peritumoral fibrosis, inflammation, increasing tumor height, and operator experience have all been shown to decrease the sensitivity of TRUS.(3) Some authors recommend the routine use of MRI with endorectal coils to maximize sensitivity.(4) Although traditionally indicated for only early (T1) lesions, trans-anal excision (TA) and TEM can be offered to patients with more advanced disease in specific clinical circumstances especially when combined with radiation and chemotherapy. Conventional TA is more commonly utilized in the United States than TEM; however, neither approach is capable of addressing nodal disease to its full extent. As a result, appropriate patient selection is critical when using either procedure with curative intent. Compared to TA, TEM is more likely to achieve negative margins and cause less specimen fragmentation. Transanal Excision A significant number of low rectal cancers (less than 5–10 cm from the anal verge) can be approached by transanal excision, particularly those that are early stage. The justification for less invasive techniques is largely established by the low rate of nodal metastases in T1 disease. In the absence of significant nodal involvement identified by CT, MRI, or TRUS, one can estimate the incidence of positive lymph nodes to be 3%—if the lesion is favorable (well to moderately differentiated, confined to the mucosa and submucosa, have no vascular invasion, and small size). By contrast, poor histological grade confers a 12% risk of nodal involvement.(5) Clearly, the issues are the ability to identify nodal involvement before surgical intervention and to remove the lesion with negative margins. Local excision (TA) is considered acceptable for T1 adenocarcinomas that carry favorable prognostic features. Such characteristics include small size (<4 cm), lack of fixation, histology that is either moderately or well-differentiated and absence of vascular, perineural, or lymphatic invasion. Reports describe cure rates as high as 90% with a recurrence rate of <10% for patients with the above characteristics. Unfortunately, there is significant variation in the data, as a recent review of 41 retrospective studies shows a 5-year local recurrence rate of 12% with a range of 0–19%.(6) As a general rule, local excision may be considered for less invasive tumors with good histological characteristics. Local excision can be considered for T1 and T2 (controversial) lesions depending on the clinical circumstance, but is considered contraindicated for T3 (particularly without adjuvant modalities) if one seeks oncologic cure. Comparable oncologic outcomes could be expected in T1 low risk rectal cancers removed with local excision without adjuvant therapy when compared with classic total mesorectal excision (TME). However, the outcomes are significantly worse for T2 lesions when adjuvant therapies were not applied. Recurrence rates in early T1 and T2 disease are clearly affected by unfavorable histological characteristics (e.g., Grade III, lymphovascular invasion). Because of this, local excision alone is considered inadequate for T2, T3 tumors; some authors, however, offer these patients neoadjuvant therapies. Although there is clearly a role for TA excision in T1 disease with favorable characteristics, many surgeons are looking at the

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feasibility of treating more advanced cancers with less invasive modalities than traditional TME. Studies that have evaluated outcomes with T2 and T3 tumors are difficult to interpret due to overall small population size and their retrospective nature; however, several clinical reports demonstrated promise for treating more advanced disease, some showed improved outcomes with adjuvant therapies before or after local excision.(7) A single multicenter trial showed that local excision could control rectal adenocarcinoma and reduce sphincter dysfunction with an overall 6-year survival of 85% and disease-free survival rate of 78% in select T1 and T2 cancers (<4 cm, <40% circumference, negative histological margins, and node-negative). It should be noted that the oncologic outcomes for T1 lesions and T2 lesions treated with adjuvant chemoradiation were roughly equivalent and ­differences between histological grade was not evaluated.(8) Locally advanced T3 rectal cancers represent an area of evolving research. Although most centers offer such patients neoadjuvant therapies followed by TME, some surgeons are attempting TA excision on these tumors with satisfactory results. In a 2002 study from the University of Florida, Dr. Schell performed TA excision on patients whose tumors had been significantly downstaged from T3 with neoadjuvant chemoradiation (15% of patients of an initial 74). There was no local recurrence or nodal metastasis after a mean follow-up of 55.2 ± 8.9 months (one patient developed distant metastasis). These patients had lesions 1–7 cm from the anal verge. Although the overall study size was limited and should not be considered the standard of care, it offers promise for those patients with advanced disease who may not be candidates for or refuse TME.(9) Similar results were demonstrated at the University of South Florida in 2001. Twenty-six patients with T2 or T3 disease (5 uT2N0, 13T3N0, 7T3N1 and 1 un-staged patient) underwent neoadjuvant therapy and subsequent local excision. Following excision, no specimens had vascular, neural, or lymphatic invasion and six contained lymph nodes in the perirectal fat without evidence of metastatic disease. Partial pathologic response was demonstrated in nine and complete response in 17 patients. Of the partial responders, all were offered but only two underwent subsequent APR. With a mean follow-up of 24 months, none of the complete responders had demonstrated recurrence.(10) Transanal excision may remove perirectal lymph nodes directly adjacent to the lesion while other nodes in the mesorectum may still harbor metastatic disease. For this reason, some authors favor adjuvant or neoadjuvant therapy (radiation with or without chemotherapy) for more advanced lesions. The majority of studies reporting recurrence rates are variable in their follow-up and ultimate outcomes making interpretation difficult, but the data does suggest a benefit for adjuvant therapies in this setting. Risk factors for recurrence are related to the depth of the primary tumor, surgical margins, histologic grade, and the status of the perirectal nodes. Overall recurrence rates are decreased when local excision is combined with radiation and chemotherapy, ranging from 0–15% for T1 and T2 lesions, and 0–20% for T3 lesions. (11–16) A review of the literature with regards to local excision and recurrence rates with and without adjuvant therapies was performed by Sengupta in 2001.(6) A summary of outcomes in these patients is summarized and demonstrates the variability in recurrence rates (Table 26.1).

transanal approaches to rectal cancer Table 26.1  Local Recurrence Rates by T-stage and Adjuvant Therapy (Sengupta, 2001, Ref. 6). Local Recurrence Rates (%) Study Follow-up Local Excision Alone Local Excision and Adjuvant Therapy T1 T2 T3 T1 T2 Mellgren et al. 2000 4.4 years 18a 47a Russell et al. 2000 6.1 years 7 (1/14) 0 (0/13) 16 (4/25) Chakravarti et al. 1999 51 month 11a 67a 0a 15a Graham et al. 1999 56 month 0 (0/4) 0 (0/2) 0 (0/9) Steele et al. 1999 48 month 5 (3/59) 13.7 (7/51) Varma et al. 1999 6 years 4.7 (1/21) 45.5 (5/11) 25 (1/4) 0 (0/3) 0 (0/9) Wagman et al. 1999 41 month 0 (0/8) 24 (6/25) Le Voyer et al. 1999 46 month 6.7 (1/15) 12.5 (2/16) Benoist et al. 1998 57 month 10 (2/19) 25 (2/8) Kim and Madoff 1998 NS 9 (4/44) 24 (6/25) 50 (1/2) Taylor et al. 1998 52 month 24 (6/25) 50 (4/8) 100 (1/1) 50 (1/2) 11 (1/9) Bleday 1997 40.5 month 9 (2/22) 0 (0/21) Valentini et al. 1996 54 month 11 (1/9) 17 (2/12) Baron et al. 1995 55.3 month 19 (8/42) 20 (7/34) Frazee et al. 1995 30 month 10 2/21 0 (0/9) 0 (0/2) Willett et al. 1994 48 month 17a 20a Ota et al. 1992 36 month 0 (0/16) 6.7 (1/15) Huber and Koella 1992 NS 22 (2/9) 23 (3/13) 33 (2/6) Cuthbertson and Simpson 1986 51 month 12.5 44 (4/9) Killingback 1985 >18 month 17.8 (5/28) 33 (2/6) Steams et al. 1984 ≥5 years 6.7 (1/15) 14 (2/14) 50 (1/2) Hager et al. 1983 33–40.5 month 8.3 (3/36) 16.7 (3/18)

T3 23 (3/13) 0 (0/5) 0 (0/6) 25 (2/8) 25 (1/4) 33 (1/3) 50 (1/2) 40 (2/5) 27 (3/11)

20 (3/15)

Note: NS = not stated. a. Five-year actuarial local recurrence rates.

Techniques of Transanal Excision Before surgery, rigid proctoscopy is done to determine the exact location of the lesion and whether or not it is accessible with conventional instrumentation. The rest of the colon is checked for synchronous neoplasms with either colonoscopy or a contrast enema. Overall fitness for general anesthesia is determined. In preparation for the operation, a bowel cleansing is performed, this will eliminate formed stool from the rectum and enhance visibility. The patient is positioned on the operating room table so that access to the lesion is provided, this usually necessitates the prone position for anterior lesions, the lithotomy position for posterior lesions, and the decubitus position for laterally based lesions. Various self-retaining retractors are available and are placed in the anus and deployed. Once the lower edge of the lesion is visualized, a clamp is placed on normal mucosa under the lesion and downward traction is applied to the clamp. Stay sutures may facilitate this process. This downward traction is an ongoing process during excision so that the entire lesion is delivered into the operative field. A rim of normal appearing mucosa is marked with cautery points around the lesion and then a full thickness excision is performed. It is important to obtain hemostasis as one proceeds since a bloodless field is vital for maintaining ­visibility. Once the lesion is excised, the wound is closed transversely so as to avoid narrowing the rectal lumen. Transanal excision using conventional instrumentation is limited to lesions located in the lower and possibly the mid rectum and for lesions which are not larger than 3 to 4 cm in diameter. More proximally located or larger lesions may be beyond the capability of these retractors, however, this is highly variable depending on the ­surgeon’s expertise, the body habitus of the patient, and the laxity of the rectal wall.

Overall the complication rate from transanal excision is considered low and is usually limited to urinary retention, urinary tract infection, bleeding, fecal impaction, and infections in the perirectal and ischiorectal space. Most series cite a mortality of virtually zero. Transanal Endoscopic Microsurgery (TEM) The introduction of Transanal Endoscopic Microsurgery (TEM) by G. Buess over two decades ago opened the door to transanal resection of lesions (both benign and malignant) beyond the reach of conventional TA instruments with increasingly favorable results through a method less invasive than radical open surgery. Additionally, appropriately sized tumors with certain specified histological characteristics could be removed with outcomes comparable to traditional surgery. With the potentially high recurrence rate of pT1 disease with TA excision and the morbidity of traditional TME, many surgeons have been investigating TEM. When compared with TA excision, the technique of TEM allows for superior visualization, access to lesions further from the anal verge within the mid and upper rectum, en-bloc resection rather than fragmentation, and possible excision of the mesorectal fat and the nodes contained within (Figure 26.1). Local recurrence rates may be lower with TEM (compared with TA) excision due to a reduced risk of implantation of viable tumor cells in the wound, less tissue fragmentation of the tumor, and a higher likelihood of obtaining negative margins.(1) The safety and outcomes for TEM in T1 lesions with favorable characteristics has been well-established. For this reason, TEM alone is only indicated for T1 tumors if one seeks oncologic cure. Multiple clinical trials have shown favorable oncologic outcomes

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improved outcomes in colon and rectal surgery

Figure 26.1  Schematic of TEM Specimen.

and low morbidity with virtually zero mortality. Winde was the first to demonstrate in a randomized prospective trial that there was no statistically significant difference in outcome between TEM (n = 24) and open radical surgery (n = 26) for pT1 tumors with a 5-year survival of 96% for both techniques. Overall, the local recurrence rate was 4.1% for TEM (0% with radical surgery). Patients who underwent TEM had decreased operative times, less blood loss, a shorter hospital stay, lower analgesic needs, and less morbidity.(17) Our personal experience from 1991–2003 (n = 53) showed low recurrence rates and acceptable oncologic results in patients with pT1 disease. In these patients, the average distance from the anal verge was 7 cm (25% of which were further than 10 cm from the anal verge) and the average tumor size was 2.4 cm with a local recurrence rate of 7.5%.(18) Using TEM to cure rectal cancer has been largely limited to “low-risk” T1 lesions while its role in T2 and T3 lesions is evolving. TEM without adjuvant therapy is inadequate for T2 and greater lesions and can be expected to have recurrence rates of 20–25%. Tumors staged to pT2 have a high risk of lymph node metastasis (16–40%).(5) Because many patients with rectal cancer are older, may be either unfit to undergo radical resection, or refuse TME due to its morbidities and the potential for an ostomy, many seek to broaden the applications of TEM. Multiple trials have taken place to evaluate the feasibility of achieving adequate oncologic results with the overall improved morbidity profile of TEM. In a study aimed to more clearly identify T2 disease as potentially amenable to TEM, Lezoche randomized 70 patients equally to either TEM or LAR following neoadjuvant therapy. These patients all had tumors <6 cm from the anal verge and were <3 cm in overall size. After a minimum 5-year follow-up (median 84 months), the local recurrence rate was 5.7% with TEM and 2.8% with LAR. Distant metastasis was observed in 2.8% with both population groups having equivalent survival of 94%.(19) Similar results were noted when TEM and radical surgery groups were compared when T1 (n = 52 and 17, respectively) and T2 (n = 22 and 83, respectively) lesions followed for 5 years after TEM excision without adjuvant therapies. Their 5-year survival was equivalent but the TEM group demonstrated a significantly increased local recurrence rate for T2 lesions at 19.5% vs. 9.4%.(20) Other studies followed the course of disease in those patients that were either upstaged after what was thought to be T1 disease

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before excision but did not receive further surgical therapy, or those who were unfit or unwilling to undergo a more radical operation for their advanced disease at time of initial presentation. Borschitz retrospectively evaluated patients who had undergone TEM excision of “low-risk” T1 lesions, but were found to be pT2 (n = 44) and did not undergo further surgery or treatment (n=14). It was determined that local excision for T2 lesions was insufficient without adjuvant therapies or radical reoperative resection. This was true despite an R0 resection, “low-risk” lesions had a 29% local recurrence rate within less than 2 years’ follow-up. If the patients were “high-risk” or had positive or unclear histological margins, the recurrence rate nearly doubled. “High-risk” lesions had poor tumor grade, lymphatic invasion, or blood vessel involvement. With immediate (within 4 weeks) reoperation, these patients had outcomes similar to conventional surgery barring the presence of lymph node metastasis. In those patients with “high-risk” characteristics, lymph node metastases were more common and occurred despite reoperation with significant local and systemic recurrence rates. These patients should receive adjuvant chemoradiation following their radical resections per standard protocols.(21) Although there are more studies analyzing outcomes of TEM with both adjuvant and neoadjuvant therapy, studies of adequate size and power are still lacking and the indications for local curative surgery for lesions more advanced than T1 remain gray. In conclusion, there are few prospective studies evaluating the benefits of adjuvant therapies and retrospective studies can be difficult to interpret. Overall, like transanal excision, recurrence rates for lesions treated with TEM combined with adjuvant therapy are lower when compared to TEM alone for T2 lesions. Preliminary results and reviews of smaller trials comparing TEM excision of T2 lesions with postoperative chemoradiation seem to be on par with the results of APR with adjuvant therapy from an oncologic perspective. As a result, the recommendation from some is to provide adjuvant therapies for all lesions that are T2 or greater; whereas TEM or TA alone are considered acceptable for T1 “low-risk” lesions given the low likelihood of lymph node involvement. Techniques of Transanal Endoscopic Microsurgery TEM resolves many of the limitations posed by conventional transanal excision techniques, namely limited access to lesions located beyond the distal rectum and poor visibility. Consequently, the applicability of minimally invasive surgery for rectal cancer is broadened. TEM employs an airtight, selfcontained system that constantly distends the rectum with carbon dioxide insufflation, this along with the magnification provided by the scope greatly improves visibility and allows for a more precise excision and wound closure. As a result, one is more likely to obtain tumor-free margins and avoid tumor fragmentation during the operation. The combined endosurgical unit regulates four functions simultaneously. In addition to gas insufflation, it allows for suction of smoke and blood, irrigation of the scope lens, and monitoring of intrarectal pressure. The stereoscopic binocular eyepiece provides four times magnification of the field, alternatively, vision may be transmitted to a video monitor. The long shafted instruments necessary for the dissection are inserted through air tight working ports on the

transanal approaches to rectal cancer facepiece of the scope which is 20 cm in length. Depending on the curvature of the sacrum, this scope may easily reach lesions located in upper rectum or even at the rectosigmoid junction. Patients are prepared for surgery in a fashion similar to conventional transanal excision. A bowel cleansing is paramount. The operation is performed under general anesthesia. Patients are positioned on the operating room table so that the lesion is located downward relative to the end of the scope. Again, for posterior lesions, patients are placed in the lithotomy position, while the prone position is chosen for anterior lesions. Once the lesion is visualized, cautery points are placed 1 cm around the lesion and a full thickness excision is performed. The specimen is then fixed to a cork board or Telfa paper in order to orient the pathologist to the deep and lateral margins. The wound is closed transversely with a monofilament suture. Most patients can be released the same day. Complications of Transanal and TEM The complication rates of TEM are significantly lower than ­traditional radical surgery. In a review of 12 studies performed by Casadesus in 2006, the morbidity of 893 patients was evaluated. (22) Complications were noted in 15.9% of the patients overall, more than half of which were related to urinary retention or transient incontinence. These complications are typically seen early in the postoperative period and very few patients required intervention other than catheterization for resolution. The rate of bleeding was also extremely low, seen in approximately 3% of cases of TEM and rarely required either transfusion or operative intervention. Postoperative fever, pelvic pain, and myocardial infarction have been reported but are also extremely rare. Throughout the literature, there is only one reported case of death directly following TEM. This patient died from septic shock 4 weeks following TEM excision of a rectal adenoma secondary to a retroperitoneal phlegmon.(23) With TEM surgery, there is always the possibility of rectal perforation, particularly with anteriorly located lesions. Major complications of perforation, wound dehiscence, and ­fistula formation have all been reported. Perforation with intraabdominal contamination is a rare complication and is clearly both operator and patient dependent and may require conversion to an open operation for control. This can be especially problematic in the older female who may have undergone prior hysterectomy. Perforation in these patients may yield fistula formation. Wound dehiscence has been described but is also a rare, but potential complication. In a large review of 334 patients, a major complication rate of 5.5% was cited. This included both intraperitoneal sepsis (n=3) and rectovaginal fistula (n=3).(24) The vast majority of TEM outcomes are reviewed in terms of oncologic results and complication rates. Remembering that one of the reasons for the promotion of less invasive procedures is sphincter preservation, some studies have analyzed continence and sphincter function postoperatively. Manometric studies of the anal sphincter have shown that the main risk for anal dysfunction after TEM is preoperative anal dysfunction. Additionally, other causes of postoperative anal dysfunction are advanced patient age, direct tumor involvement of the sphincter, postoperative internal sphincter defects, the extent and depth of tumor excision, loss of anal mucosa, and duration of the procedures. Sphincter function

is affected by rectoanal perception and coordination, and electrosensitivity of the anal mucosa—all of which are affected by TEM. Some patients also report an increase in bowel frequency which is likely related to decreased rectal compliance following reductions in the overall rectal diameter from full-thickness or circumferential excisions.(22) Despite these reports, complication rates related to altered bowel habits remains exceedingly low (less than 2%) and the majority of these changes such as decreased resting pressures are seen during physiologic testing, but are not often clinically significant.(25, 26) Transanal (TA) vs. Transanal Endoscopic Microsurgery (TEM) Few reviews directly comparing the results of TA vs. TEM excision exist. Surgeons at the University of Vermont recently reviewed 171 patients treated between 1990 and 2005 by either traditional TA excision (n = 89) or TEM (n = 82) for rectal cancers.(27) During the course of their experience, they transitioned to the TEM technique in 2001, after which only 20 TA excisions took place. Although the results of seven surgeons were reviewed, only one performed all the TEM. The two populations were similar with respect to age, gender, lesion type, stage, and size with an overall mean follow-up of 37 months (significant difference in follow-up between the two groups due to their change to primarily TEM during the time period studied). All patients with T1 lesions with adverse features or T2 lesions received postoperative adjuvant therapy. Patients with T3 lesions underwent local excision only if they were considered too high risk for radical ­surgery or if they refused traditional resection. The decision to give patients with T3 lesions postoperative chemoradiation was made on an ­individualized basis. Postoperative complications among the TA and the TEM group were roughly equivalent (15% and 17%, respectively, p = 0.69) with the most common being urinary retention (6% and 7%, respectively). The TA group had six major complications including two anovaginal fistulae, one leak requiring an operation, one bleed, one arrhythmia, and one patient who developed renal failure. The TEM group had two anovaginal fistulae and two leaks requiring operations. Overall, the difference between the two groups was not found to be significant. However, the patients who did undergo TEM enjoyed a significantly shorter hospital stay (0.6 days vs. 1.5 days). With regards to oncologic outcomes, 90% of the patients who underwent TEM had negative margins. TA patients had both a higher positive margin rate (15%) and indeterminate margin rate (15%) (p=0.001). Specimens were more likely to be removed intact rather than in a piece-meal fashion with TEM vs. TA (95% vs. 65%, p < 0.001). Lastly, local recurrence rates were dramatically improved with TEM (8% vs. 24%, p = 0.004) and such results were concordant with other retrospective reviews. Two-thirds of the local recurrences with TEM occurred after palliative resections defined as being T3 at the time of diagnosis or patients were either too ill to tolerate or refused a more radical operation. When considering only those TEM and TA cases performed with curative intent, the recurrence rate fell to 3% vs. 26% with transanal approaches (p = 0.06). No significant difference in distal recurrence was demonstrated (1% with TEM, 4% with TA). Although a criticism of the above data is the

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improved outcomes in colon and rectal surgery Table 26.2  Outcomes with Transanal (TA) vs. Transanal Endoscopic Microsurgery (TEM) for lesions up to T3 (Moore, 2008). TEM (n = 82)

TA (n = 89) n (%) or Mean ± SD P Value

Any complication (yes) 12 (15) 15 (17) Major complication 4 (33) 6 (40) Minor complication 8 (67) 9 (60) LOS (days) 0.63 ± 1 1.46 ± 3 Specimen fragmentation Whole 77 (94) 58 (65) Fragmented 5 (6) 28 (31) Unreported 0 (0) 3 (3) Margins negative 74 (90) 63 (71) Positive Recurrence 4 (5) 24 (29) All cause mortality 2 (2) 26 (29)

0.69

0.007 < 0.001

0.001 0.01 0.01

disparity in follow-up between the two groups, most feel that the vast majority of recurrences will usually occur within the first 2 years and the mean follow-up for both groups was well beyond this time frame. With this, TEM appears to offer superior outcomes to TA in patients with T1 or T2 lesions with appropriate adjuvant therapies (Table 26.2).(27) The Clear Advantages of Local Surgery Although the oncologic advantages of TA or TEM excision of rectal cancers remain controversial in many circles, few can argue the benefits of pursuing a less invasive procedure. For patients whose medical comorbidities may place them at a higher or even unacceptable operative risk, TA or TEM approaches offer a solution that may confer acceptable oncologic outcomes as well. The same is true for those patients that have advanced disease but require palliation of symptoms. Patients with unresectable distant disease, however, usually have large bulky primary tumors which are not amenable to transanal excision. Both LAR and APR are associated with significant morbidity and mortality which can be avoided with either TA or TEM excision in the appropriately selected patient. In patients who undergo traditional TA or TEM, the overall complication rates remain low and overall morbidity is minimal. A review of patients who had undergone TEM as compared with TME showed that although long-term quality of life was equal, patients who underwent TEM tended to have fewer defecation disorders, and, although not statistically significant, improved sexual function as well.(28) When Local Surgery Fails Following TA or TEM excision, aggressive surveillance is indicated to detect recurrent disease. The reason for both local and distal recurrence is not always clear, particularly in the face of what was considered early disease and in the absence of involved excisional margins. With regard to distant failure, occult disease may have been present at the time of initial presentation but not identified during the preoperative workup. In these instances, distant failure is not due to presumed inadequate local treatment, but rather is a reflection of aggressive tumor biology. Local recurrence is more frequently related to the mesorectal disease rather than at the pelvic walls.(3) Additionally, fragmentation of the specimen

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at the time of excision and the inability to remove full thickness tissue during excision can predispose to local recurrence. In the presence of recurrent rectal cancer, there is currently no role for either TA or TEM from an oncologic perspective. Factors associated with an increased risk of local recurrence include those characteristics previously described as “high risk” which include poor differentiation and lymphovascular invasion, and of course, those whose excision is incomplete. Studies of patients that had undergone TEM for T1 and T2 lesions without evidence of lymph node metastasis found that patients who lesions carried the above characteristics had a significantly elevated risk of local recurrence necessitating salvage surgery.(29) Recurrent disease requires a TME by way of either an LAR or APR. Patients that undergo salvage TME have decreased survival when compared with their counterparts that had the operation as part of the initial management. In a study that evaluated patients who had initially undergone TA excision (n=155) for lesions with adverse histological characteristics and subsequently salvage APR (n=21), the disease free survival was only 56% vs. 94% for those who undergone immediate APR.(30) Future Directions of Study Traditional TA surgery is evolving into TEM in many circles as surgeon familiarity and advanced laparoscopic skills become increasingly prevalent. Although TA is widely practiced by many, TEM confers the benefits of TA surgery with multiple clear clinical advantages. The indications for TEM will continue to increase in number as improved outcomes for more advanced disease are demonstrated throughout the literature. Sentinel lymphangiography may soon be applicable to colon and rectal cancer with potential TEM utilization. Additionally, with neoadjuvant therapies for advanced disease becoming increasingly effective in many patients, subjecting such patients to radical surgeries after their malignancies have often been reduced to a scar may prove to be unnecessarily aggressive, further opening the door to TEM and potential resection of the tissue that previously contained malignancy. Research into necessary tissue margins for TEM following such therapies is currently being undertaken. Although there will always be a role for traditional TME in the form of both LAR and APR procedures, the role of TA and TEM surgery continues to expand within the management of rectal cancer. References   1. Whiteford MH. Transanal endoscopic microsurgery (TEM) resection of rectal tumors. J Gastrointest Surg 2007; 11(2): 155–7.   2. Nicholls RJ, Mason AY, Morson BC et al. The clinical staging of rectal cancer. Br J Surg 1982; 69(7): 404–9.   3. Bretagnol F, Rullier E, George B et al. Local therapy for rectal cancer: still controversial? Dis Colon Rectum 2007; 50(4): 523–33.   4. Maslekar S, Pillinger SH, Monson JR. Transanal endoscopic microsurgery for carcinoma of the rectum. Surg Endosc 2007; 21(1): 97–102.   5. Hermanek P, Gall FP. Early (microinvasive) colorectal carcinoma. Pathology, diagnosis, surgical treatment. Int J Colorectal Dis 1986; 1(2): 79–84.

transanal approaches to rectal cancer   6. Sengupta S, Tjandra JJ. Local excision of rectal cancer: what is the evidence? Dis Colon Rectum 2001; 44(9): 1345–61.   7. Ruo L, Guillem JG, Minsky BD et al. Preoperative radiation with or without chemotherapy and full-thickness transanal excision for T2 and T3 distal rectal cancers. Int J Colorectal Dis 2002; 17(1): 54–8.   8. Steele GD Jr, Herndon JE, Bleday R et al. Sphincter-sparing treatment for distal rectal adenocarcinoma. Ann Surg Oncol 1999; 6(5): 433–41.   9. Schell SR, Zlotecki RA, Mendenhall WM et al. Transanal excision of locally advanced rectal cancers downstaged using neoadjuvant chemoradiotherapy. J Am Coll Surg 2002; 194(5): 584–90. 10. Kim CJ Yeatman TJ, Coppola D et al. Local Excision of T2 and T3 rectal cancers after downstaging chemoradiation. Ann Surg 2001; 234(3): 352–8. 11. Wong CS, Stern H, Cummings BJ. Local excision and postoperative radiation therapy for rectal carcinoma. Int J Radiat Oncol Biol Phys 1993; 25(4): 669–75. 12. Chakravarti A, Compton CC, Shellito PC et al. Long-term follow-up of patients with rectal cancer managed by local excision with and without adjuvant irradiation. Ann Surg 1999; 230(1): 49–54. 13. Paty PB, Nash GM, Baron P et al. Long-term results of local excision for rectal cancer. Ann Surg 2002; 236(4): 522–9. 14. Bailey HR, Huval WV, Max E et al. Local excision of carcinoma of the rectum for cure. Surgery 1992; 111(5): 555–61. 15. Willett CG, Compton CC, Shellito PC et al. Selection factors for local excision or abdominoperineal resection of early stage rectal cancer. Cancer 1994; 73(11): 2716–20. 16. Mendenhall WM, Morris CG, Rout WR et al. Local excision and postoperative radiation therapy for rectal adenocarcinoma. Int J Cancer 2001; 96(Suppl): 89–96. 17. Winde G, Nottberg H, Keller R et al. Surgical cure for early rectal carcinomas (T1). Transanal endoscopic microsurgery vs. anterior resection. Dis Colon Rectum 1996; 39(9): 969–76. 18. Floyd ND, Saclarides TJ. Transanal endoscopic microsurgical resection of pT1 rectal tumors. Dis Colon Rectum 2006; 49(2): 164–8.

19. Lezoche G, Baldarelli M, Guerrieri M et al. ������������������ A prospective randomized study with a 5-year minimum follow-up evaluation of transanal endoscopic microsurgery vs. laparoscopic total mesorectal excision after neoadjuvant therapy. Surg Endosc 2008; 22(2): 352–8. 20. Lee W, Lee D, Choi S et al. Transanal endoscopic microsurgery and radical surgery for T1 and T2 rectal cancer. Surg Endosc 2003; 17(8): 1283–7. 21. Borschitz T, Heintz A, Junginger T. Transanal endoscopic microsurgical excision of pT2 rectal cancer: results and possible indications. Dis Colon Rectum 2007; 50(3): 292–301. 22. Casadesus D. Transanal endoscopic microsurgery: a review. Endoscopy 2006; 38(4): 418–23. 23. Klaue HJ, Bauer E. Retroperitoneal phlegmon after transanal endoscopic microsurgical excision of rectal adenoma. Chirurg 1997; 68(1): 84–6. 24. Mentges B, Buess G, Schafer D et al. Local therapy of rectal tumors. Dis Col Rectum 1996; 39(8): 886–92. 25. Kennedy ML, Lubowski DZ, King DW. Transanal endoscopic microsurgery: is anorectal function compromised? Dis Colon Rectum 2002; 45(5): 601–4. 26. Cataldo PA, O’Brien S, Osler T. Transanal endoscopic microsurgery—a prospective evaluation of functional results. Dis Colon Rectum 2005; 48(7): 1366–71. 27. Moore JS, Cataldo PA, Osler T et al. Transanal endoscopic microsurgery is more effective than traditional transanal excision for resection of rectal masses. Dis Colon Rectum 2008; 51(7): 1026–30. 28. Doornebosch PG, Tollenaar RA, Gosselink MP et al. Quality of life after transanal endoscopic microsurgery and total mesorectal excision in early rectal cancer. Colorectal Dis 2007; 9(6): 553–8. 29. Lee WY, Lee WS, Yun SH et al. Decision for salvage treatment after transanal endoscopic microsurgery. Surg Endosc 2007; 21(6): 975–9. 30. Baron PL, Enker WE, Zakowski MF et al. Immediate vs. salvage resection after local treatment for early rectal cancer. Dis Colon Rectum 1995; 38(2): 177–81.

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27

Abdominoperineal resection W Brian Perry, Fia Yi, Clarence Clark, and Danny Kim

Challenging Case A 64-year-old woman is 7 days s/p an abdominopernneal resection for a T2N1 rectal adenocarcinoma. She had received preoperative. Her perineal wound has developed increased tenderness, is swollen, and is draining pus. Case Management The patient’s wound is opened and the patient is started on three times a day dressing changes. After 2 days the wound is clean and a vacuum assisted closure (VAC) dressing is placed. Introduction Abdominoperineal resection (APR) completely removes the distal colon, rectum, and anal sphincter complex using both anterior abdominal and perineal incisions, resulting in a permanent colostomy. Developed more than 100 years ago, it remains an important tool in the treatment of rectal cancer despite advances in sphincter-sparing procedures. We will examine a brief history of this procedure, current operative techniques and complications, expected results, (both oncologic and with regard to quality of life), and what the future may hold for this procedure. Several recent reports have noted the increase in the use of sphincter-sparing options for patients diagnosed with rectal cancer. Abraham and colleagues found a 10% decrease (60.1–49.9%) in the rate of APR from 1989 to 2001 as compared with low anterior resection (LAR) using national administrative data.(1) When controlled for several variables, including patient demographics and hospital volume, patients were 28% more likely to have an LAR later in the study period. Schoetz notes that LAR outnumbers APR three to one in the submitted case logs of recent colorectal fellows.(2) This ratio is similar to that found in the Swedish rectal cancer registry, where approximately 25% of over 12,000 patients with rectal cancer underwent APR from 1995–2002.(3) In no study or registry, however, has APR been eliminated. History Early in the twentieth century, most patients with rectal cancer underwent perineal procedures to address typically advanced, symptomatic disease. These included the transcoccygeal Kraske approach and the transsphincteric approach developed by Bevan in America, later attributed to A. York Mason. Patients were typically left with profound sphincter dysfunction or fistulae following a protracted recovery. A two-staged operation, consisting of an initial laparotomy and colostomy followed by perineal excision, was used until the 1930’s with reasonable results. The operation we now know as APR was first described by Miles in 1908, but initial reports showed a high operative mortality, up to 42%. Improvements in perioperative care that came later reduced this considerably. Refinements in technique continued through the first half of the twentieth century. Gabriel described

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the operation in one stage, with the abdominal portion done supine and the perineal portion done in the left lateral position. Lloyd-Davies’ synchronous approach to the abdomen and perineum with the patient in the lithotomy position eliminated the cumbersome and sometimes dangerous need to reposition the patient while under anesthesia.(4) Recent advances have included total mesorectal excision in patients undergoing APR and the addition of methods to enhance perineal wound healing, especially in patients who have received neoadjuvant chemoradiation. Minimally invasive techniques are also being applied to APR, with good initial results. Patient Preparation and Positioning Preparation for abdominoperineal resection starts with marking the ideal placement of the colostomy by the primary surgeon or enterostomal nurse.(5) Patients are instructed to take a mechanical bowel preparation the day before surgery consisting of sodium phosphate solution or polyethylene glycol. Placement of an epidural catheter may be considered to improve postoperative analgesia and to reduce postoperative ileus.(6) Before induction of general anesthesia, intermittent pneumatic compression devices are placed on the lower extremities to reduce the risk of venous thromboembolism.(7) Intravenous antibiotics with efficacy against enteric flora are administered 60 minutes before incision to decrease rate of ­surgical site infection.(8) The abdomen and perineum are prepped and appropriate monitoring is placed. After induction of anesthesia, a urinary catheter is inserted; ureteral stents should be considered if the patient has had prior pelvic surgery, tumor extension into the urinary tract, or prior pelvic radiation. The patient is placed in the lithotomy position using Allen stirrups with padding to prevent lower limb acute compartment syndrome.(9) Positioning also includes symmetric hip extension, knee flexion, and thigh abduction (Figure 27.1). Ultimately the legs are balanced in the stirrups, such that the weight is resting on the feet and the ankle and knee are in line with the opposite shoulder. A rectal exam is performed under anesthesia followed by irrigation with dilute betadine solution to remove any residual stool. Operative Technique The operative technique used today varies little from Ernest Miles’ description in 1908.(10) Unlike Miles’ method we prefer the twoteam approach with the patient in lithotomy position rather than lateral semi-prone position. A nonabsorbable purse-string suture is placed around the anus. The abdomen and perineum are prepared with antiseptic solution and draped with openings for the abdominal and perineal dissections. The abdomen and pelvis are accessed through a midline hypogastric incision that extends to the right of or through the umbilicus. The abdomen is explored for metastatic disease and synchronous colon lesions. After confirmation of resectability, a self-retaining retractor is placed.

abdominoperineal resection

Figure 27.1  Leg positioning for abdominoperineal resection.

The small bowel is packed into the upper abdomen with a moist towel. The sigmoid and descending colons are then mobilized at the white line of Toldt in the left lateral gutter. After confirming adequate mobilization of the descending colon for an end colostomy, the left ureter is identified and preserved. The peritoneum incision is carried anterior followed by incision of the right lateral peritoneum. The right ureter is identified and preserved and the peritoneal incisions are connected anteriorly at the base of the bladder. For convenience, the proximal sigmoid can be divided with a linear stapling device and the cut end used as a handle to aid with the dissection. A finger is passed below the inferior mesenteric vessels with the plan to leave the sigmoid branches. This helps minimize vascular compromise of the stoma. It is unnecessary to ligate the inferior mesenteric artery at its origin as this has not been shown to increase survival.(11) The superior hemorrhoidal vessels are transected. The presacral space is entered without breaching the endopelvic fascia and with

preservation of the mesorectum consistent with Heald’s description of total mesorectal excision.(12) After identifying this avascular plane, the dissection is aided by using a lighted St. Mark’s retractor to hold the mesorectum anteriorly. As the dissection continues distally, Waldeyer’s fascia is divided with electrocautery or sharply to avoid injuring the presacral venous plexus. Staying in the avascular plane posteriorly and laterally minimizes bleeding. The lateral ligaments are cauterized or suture-ligated close to the pelvic side wall to maximize the radial margins. Denonvillier’s fascia in males is dissected down to the pelvic floor anteriorly. Unless the tumor is anterior, it is not necessary to expose the seminal vesicles in males thus avoiding injury to the nervi erigentes. In females, the presence of an anteriorly based tumor may require performance of a posterior vaginectomy. When the pelvic floor is reached circumferentially around the rectum, the abdominal portion of the dissection is completed. Once the pelvic dissection is completed, the colostomy is created and the abdomen is closed.

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improved outcomes in colon and rectal surgery When the abdominal operator has determined that the lesion is resectable the perineal dissection begins simultaneously with the abdominal portion of the case. The perineal dissection begins with an elliptical incision from the perineal body in males or the posterior vaginal introitus in females to a point midway between the anus and coccyx. The incision should include the entirety of the external sphincter muscle, but does not need to extend laterally to the ischial tuberosities. Dissection is carried down to the levator ani muscles with cautery to minimize bleeding. The inferior hemorrhoidal arteries located posteriorlaterally are ligated. Using a finger on the tip of the coccyx as a guide, the posterior dissection is directed anterior to the coccyx and the anococcygeal raphe is divided. When all that remains are the anterior attachments, the specimen is drawn through the opening and used to provide traction to continue the remaining dissection. The specimen is then removed and the pelvis is irrigated. If sufficient levator muscle remains, the pelvic floor is reapproximated to reduce the risk for perineal herniation. Drains are placed and secured followed by closure of the skin with interrupted permanent or absorbable monofilament suture in a vertical mattress fashion. Preservation of Sexual and Urinary Function As described by Kyo et al. the neuroanatomy begins with the sympathetic nerve fibers that travel through the lumbar splanchnic nerves to the superior hypogastric plexus and then divide into two hypogastric nerves. Parasympathetic fibers emerge from the second, third, and fourth sacral spinal nerves as the pelvic splanchnic nerves and join the hypogastric nerves to form the inferior hypogastric (pelvic) plexus. The pelvic plexus is rectangular and its midpoint is located at the tips of the seminal vesicles on either side of the rectum (Figure 27.2). The most caudal portion of the pelvic plexus travels at the posterolateral border of the prostate, lateral to the prostatic capsular arteries and veins and reaches the hilum of the penis.(13) The rate of urinary dysfunction and impotence after rectal surgery ranges from 33% to 70% and 20% to 46%, respectively, while 20–60% of potent patients are unable to ejaculate.(14) A surprisingly large proportion of patients suffer various urinary tract problems and sexual problems due to extended lymphadenectomy involving the hypogastric nerve plexus. Therefore, preservation of the pelvic autonomic nerves lowers the incidence of sexual and urinary morbidity. With preservation of the superior hypogastric nerve plexus, ejaculation is maintained in 90% of the patients.(15) Utilizing precise dissection with preservation of autonomic nerves Kim et al. noted an erection rate of 80%, penetration ability rate of 75% with only 5.5% of patients in their study reporting complete inability for erection and intercourse. Study by Shirouzu et al. showed oncologic equivalence between previously described extensive resection pre-1984 and plexus preserving low rectal surgery post-1985 with local recurrence rates 9.1 and 3.9%, respectively and 10-year, disease-free survival rate of 77% and 81.5%, respectively. No significant difference was noted among the groups.(16) Methods of Closure The perineal wound can be packed open, partially closed, or ­com­­pletely closed. The peritoneal defect above the pelvic space

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Figure 27.2  Nerve supply to the rectum.

can also be sutured closed or left open. Adjunctive procedures such as drainage of the pelvic space, with or without continuous irrigation, and omental plugging may also be considered. Rates of primary healing after perineal wounds are closed range from 4% to 92%.(10, 17, 19) Open packing relegates all wounds to secondary healing, is inconvenient, and often painful but may result in a lower rate of chronic perineal sinus formation.(19) Closure of the pelvic peritoneum has been advocated to prevent perineal evisceration and postoperative small bowel obstruction. However, it may prevent obliteration of the pelvic cavity, leading to formation of a persistent perineal sinus.(20) Loops of small bowel may also become incarcerated in small defects in the ­peritoneal closure, resulting in postoperative bowel obstruction. Two studies compared various methods of peritoneal and perineal closure. Irvin and Goligher (19) prospectively randomized 106 patients undergoing proctectomy to one of three methods of perineal closure: open packing of the perineal wound; primary closure of the perineal wound without closure of the pelvic peritoneum with suction drainage of the pelvis; and primary closure of the peritoneal and perineal wounds. The overall complication rate was high: repeated surgery was necessary in 21% of patients in the open packing group, most often because of hemorrhage, and in 25% and 19% of the two closed groups, most commonly for drainage of abscesses. Primary healing occurred in 45% of the patients with primary closure of both the perineum and peritoneum and in 43% of patients with open peritoneal and closed perineal wounds. In a prospective study part of a multicentre trial in Germany, Meyer et al. published a standardized technique of perineal ­closure that reduced wound complication rates from 17% to 5.4%. The principle of their approach was to close the perineal wound tightly in multiple layers (specifically the muscle and ischiorectal as well as subcutaneous fat) which help to avoid the accumulation of fluid

abdominoperineal resection within the wound cavity. The residual amount of fluid is then removed by closed suction drainage. Additionally, it is thought that the addition of antibiotic carriers provides local infectious prophylaxis leading to lower rates of perineal wound infection. (21) This has also been demonstrated in two other ­prospective randomized studies and can be considered an adjunct in decreasing the overall morbidity of the perineal wound.(22, 23) Myocutaneous flaps have been increasingly utilized in the initial repair of the perineal defect, especially in patients who have had preoperative radiation therapy. Chessin et al. at Memorial Sloan Kettering reviewed their experience with rectus abdominis myocutaneous (RAM) flap closures of the perineal defect. Comparing the RAM flap group to a historical control, they found that the incidence of perineal wound complications was 15.8% in the RAM flap group compared to the 44.1% in the control.(24) Butler et al. also looked at vertical rectus abdominis myocutaneous flaps in previously irradiated patients undergoing APR. There was a significantly lower incidence of perineal abscess (9% vs. 37%), major perineal wound dehiscence (9% vs. 30%) and drainage procedures required for perineal or pelvic fluid collections (3% vs. 25%).(25) In an effort to fill the pelvic space after rectal resection, Page et al. advocates an omental plug. They describe mobilization of the omentum on the left gastroepiploic arterial pedicle, with subsequent placement in the pelvis. Advantages include increased local blood flow and lymphatic drainage, and obliteration of the pelvic space. The omental plug also has the advantage of keeping the small bowel out of the pelvis, thereby decreasing the chance of radiation enteritis in patients who require postoperative radiation therapy. The authors report primary healing in 26 of 34 patients (77%).(26) A recent publication by PJ Nilsson reviewed all available English language publications on the use of omentoplasty in APR wound closure. Primary wound healing was the primary outcome measure. Most authors reported positive results after omentoplasty and one study showed significant improvement in perineal healing rate at 6 months. Significant reduction in sinus formation and wound dehiscence also was reported.(27) Despite these promising results, there needs to be randomized trials with well-described patient categories, end points and follow up to firmly assess whether omentoplasty should be a standard part of the wound closure. Complications Abscess Abscess formation, intraperitoneal or of the perineal wound, is the most common major complication after APR.(17) Incidence of abscess formation ranges from 11% to 16% (17, 18, 28). In some small series, the incidence of perineal wound infection is 100%.(19) This can be attributed to the large dead space remaining after resection of the rectum and from fecal contamination. In a retrospective review of patients who had neoadjuvant chemoradiation followed by APR, Butler observed that there was a significant decrease of perineal abscess formation (3% vs. 37%) after the placement of a vertical rectus abdominis myocutaneous (VRAM) flap to the perineum. The well-vascularized flap eliminates the dead space in the pelvis, reducing the risk of

fluid ­collection. The use of a VRAM flap should be considered in patients who are at high risk for postoperative perineal wound complications.(25) Alternatively, an omental pedicle flap sutured to the perineal wound has been observed to decrease the rate of abscess formation.(29) Incision and drainage with local wound care is the treatment of choice for local perineal wound abscesses. There is a small increased risk of developing a perineal sinus after opening the skin of a subcutaneous abscess.(30) Thus if the incision is healing well, the abscess may be amenable to percutaneous drainage. In addition, percutaneous drainage is the preferred treatment of presacral and pelvic abscesses.(31) Intraoperative Hemorrhage Hemorrhage during surgery can usually be attributed to an error in technique, but when faced with a pelvis that had previously received radiation therapy, hemorrhage may be unavoidable. Bleeding may occur when dissection begins at the sigmoid. This is usually easily identified and controlled. In the previously irradiated pelvis, planes become distorted making it difficult to identify vital structures. It is easy to stray laterally, which may result in iliac vessel injury. These must be repaired immediately to avoid prolonged hemorrhage. In a pelvis that has not received radiation, or if there is minimal fibrosis, meticulous dissection in the proper plane down to the lateral stalks usually yields minimal bleeding. The most troublesome bleeding in the pelvis comes from the posterior dissection along the sacrum. Very rarely, there will be a prominent medial sacral artery that may be injured. More commonly, the bleeding from the sacrum will come from the venous plexus. If present, the basivertebral vein, which connects the internal vertebral venous system to the presacral system, can bleed ­profusely and be difficult to control. Ideally, by taking sharp dissection down the presacral plane, there should be little to no bleeding.(32, 33) Unfortunately this space may be nonexistent in certain patients or obliterated in an irradiated field. Bleeding from the sacrum can be controlled by packing, suture ligation, electrocautery, finger compression, or thumbtack compression. Thumbtack compression is a quick, safe, and effective method of controlling sacral bleeding. There are several commercial application devices available; however, using a clamp or forceps with ­finger applications works equally as well (Figure 27.3). Thumbtacks also prevent damage to the surround venous plexus that may occur when using the other methods of attempting hemostasis, such as direct suture ligation or excessive cauterization.(33, 34) Postoperative Hemorrhage Bleeding after the completion of the surgery is uncommon (<4%) and is most commonly associated with perineal wounds that are packed open.(35) When the perineal wound is packed open, it is hemostatic until the first dressing change when the tamponade is released. As the packing is removed, it may pull away clot from surrounding tissues that can result in more bleeding. Conservative treatment can be attempted with adequate resuscitation if needed, a reapplication of packing, and placement of the patient on strict bed rest. If the patient remains stable, the packing may be removed in 48–72 hours.(36) Occasionally, reoperation is necessary to control postoperative perineal hemorrhage.

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improved outcomes in colon and rectal surgery

Figure 27.3  Thumbtack occlusion of bleeding basivertebral vein.

Given that nearly all APR wounds are currently closed primarily, this complication is rare.(37, 38) Perineal Wound Complications When comparing abdominoperineal resection with other abdominal and pelvic procedures, the most striking difference is the perineal dissection and ensuing perineal wound. Treatment of this wound has long been the center of debate and controversy. Miles in his original description in 1908, recommended open packing, and his technique is still used by some surgeons. Over the following 75 years, many techniques to treat the perineal wound have been developed, including partial closure, primary closure, and closure with continuous irrigation or omental plugging. For purposes of discussion, perineal wound complications of abdominoperineal resection can be divided into four categories: hemorrhage, abscess, perineal sinus, and perineal hernia. Non Healing Wound and Perineal Sinus Perineal sinus is defined as a perineal wound that remains unhealed for a minimum of 6 months. Characteristics include a fixed fibrotic pelvic cavity, a long, narrow track lined with a thick unyielding peel, and a small external opening.(39) Silen and Glotzer compared the pelvic space after APR with the fixed pleural space after pneumonectomy. The pelvic space is bound posteriorly and laterally by the rigid bony pelvis, anteriorly by the relatively unyielding genitourinary structures, inferiorly by the slightly mobile perineal floor (if surgically closed), and superiorly by the peritoneal contents. Of all these borders, certainly the peritoneal structures are the most mobile. They contend that the pelvic space after APR is filled not with granulation tissue but with a combination of upward migration of the perineal soft tissues and descent of the peritoneal contents and argue that any forces (either iatrogenic, such as closure of the peritoneum or prolonged packing of the pelvis, or secondary to complications, such as pelvic abscess or hematoma) that

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produce a fixed fibrotic cavity are likely to result in a nonhealing perineal wound.(30) Artioukh et al. reviewed their series of APR non healing wounds and found several possible contributing factors, including distant metastases, excessive alcohol consumption, cigarette smoking, transfusion requirement and chemoradiation. Other studies have also observed the increased risk in perineal wound infection and nonhealing in those who have been exposed to radiotherapy. The Swedish Rectal Cancer trial showed an increase in wound infection from 10% to 20% and the Dutch Colorectal Cancer Group had a 31% perineal complication rate even in those exposed to short-course radiation.(40, 41) Silen and Glotzer recommended that the peritoneal contents be allowed to descend into the pelvis, the space be kept irrigated and well drained to prevent fluid accumulation, and any packing used in the perineal wound be removed early to prevent development of fibrotic wound edges. Despite the excellent description of perineal healing by Silen and Glotzer and the development of multiple techniques for perineal closure, nonhealing perineal wounds remain a common problem. Bacon and Nuguid noted a 40% incidence of persistent perineal sinus in 1042 patients after rectal resection.(42) In almost 500 patients who underwent APR at the Lahey and Mayo Clinics, 14–24% had unhealed perineal wounds at 6 months. Risk Factors Inflammatory bowel disease versus carcinoma. Rectal resection is most commonly performed to treat low rectal cancer or inflammatory bowel disease. Often the extent of soft tissue resection is much greater in the treatment of rectal cancer with complete removal of the levator musculature or posterior vaginectomy advocated by some versus the intersphincteric proctectomy (sparing the external anal sphincter and the levator ani) often used in surgical treatment of inflammatory bowel disease. An increase in perineal wound complications might be expected after APR to treat cancer, but Irvin and Goligher found a 9% incidence of unhealed perineal wounds in the treatment of cancer, compared with a 33% incidence in proctectomies performed for inflammatory bowel disease.(19) A more contemporary review of the risk factors for perineal wound complications undertaken by Christian et al. determined that higher rates of major wound complications occurred in patients who had APR performed for anal cancer (50%) as compared to rectal cancer (10%) or inflammatory bowel disease (8%). The reasons are unclear although the extensive tissue dissection involved in a cancer operation with larger soft tissue loss may be a possibility.(43) There is some evidence to support this in studies that have shown that tumor size can be a risk factor for poor wound healing. Radiation Therapy. Radiation therapy is often used in the treatment of rectal and anal neoplasia both preoperatively and postoperatively. Christian et al. found that preoperative radiation therapy for anal cancer patients appeared to be a risk factor for poor wound healing. Artioukh et al. also found that patients who had received preoperative radiotherapy were prone to wound complications (39% vs. 6.7% who did not have radiotherapy). Fecal Contamination. Fecal contamination during proctectomy significantly decreases primary healing and may increase the risk

abdominoperineal resection of chronic perineal sinus formation. This complication is presumably related to the development of pelvic infection with secondary development of a fixed abscess cavity that makes obliteration of the pelvic space more difficult.(30) Fecal contamination may also lead to a higher incidence of perineal wound tumor recurrence. Treatment Nonhealing perineal wounds develop in 8% to 69% of patients undergoing APR.(10, 18, 19, 28) Because of the scope of the problem, many techniques have been developed to ensure complete healing. Early efforts included operative debridement with wide drainage, including coccygectomy and even partial sacral resection. (20) These measures were designed to eliminate the rigid fibrotic space that always accompanies a nonhealing perineal wound. Often these measures resulted in eventual healing but required extensive wound care for many months. Despite this treatment, some wounds failed to heal. Alternative methods to improve healing and decrease wound care have been developed. Oomen et al. published a set of guidelines in treating persistent perineal sinuses or complex perineal wounds with an overall 80% success rate in healing. Their ­algorithm ­consisted of VAC therapy for large defects before placing muscle flaps in order to decrease the size of the defect. Depending on sinus length, they either placed a transposition of rectus abdominal muscle (for sinuses > 10 cm) or a gracilis muscle/gluteal thigh flap (sinus < 8 cm). Initially success rate was 57%, but after secondary surgery in some of the patients, their success rate increased to 80%. Ultimately, the best outcomes were in patients who received the gracilis or gluteal thigh flap.(44) The VAC® closure system has also been used more to assist in dealing with complex perineal wounds that result after extensive operative debridement’s for persistent perineal sinuses. Pemberton at the Mayo Clinic (45) published a review of their results with various techniques in dealing with perineal sinuses. In patients with difficult perineal sinuses requiring debridement and removal of the coccyx and caudal part of the sacrum, the VAC® system had complete resolution of the sinus in nearly all of their patients. While their evidence is anecdotal, there are documented reports with healing rates up to 95%.(46, 47) Omentoplasty is another technique that has been evaluated in both the primary repair of the perineal wound as well as in complex perineal sinus disease. Yamamoto et al. reported six patients with persistent perineal sinuses who underwent omentoplasty. The perineal sinus tract was completely excised and communication with the pelvis attained. The left or right gastroepiploic vessels were then ligated and the omentum brought down to the perineum where it was lightly sutured to the skin. After a 28-month follow-up period, 83% of the patients had completely healed wounds without any complications.(48) Perineal Hernia and Evisceration Perineal hernias are fortunately very rare and often troublesome to diagnose. Perineal hernia after abdominoperineal resection is defined as bulging of peritoneal contents through an intact perineal wound, and perineal evisceration describes extrusion of small or large bowel through an open perineal wound. However, other unusual contents have been described, including a leiomyoma,

an aggressive angiomyoma and a large bladder diverticulum.(49) Evisceration typically occurs immediately after surgery and necessitates repeat surgery with reduction of intestines and repeat packing. Perineal hernias are a rare complication and occur in about 1% of patients after APR. This figure increases to 3% after pelvic exenteration. Initial symptoms include perineal bulging, often associated with fullness or pain on sitting.(50, 51) Occasionally, patients complain of voiding problems if herniated bowel compressed the bladder.(52) Rarely, skin breakdown occurs, resulting in exposed bowel in the perineum. Perineal ­hernias, like parastomal and incisional hernias, do not always require repair. Indications for surgery are similar for all three postoperative hernias: patient discomfort refractory to conservative therapy, bowel obstruction, incarceration, and impending skin loss. Cosmesis alone should rarely merit surgical repair. Risk factors that predispose patients to developing perineal hernias are not entirely clear. Coccygectomy, previous hysterectomy, pelvic irradiation, excessive length of the small-bowel mesentery, the larger size of the female pelvis, and possibly the failure to close the peritoneal defect have been implicated as possible causes.(53, 54, 55) So et al. described 80% of their patients having perineal wounds that were laid open or had multiple large drains inserted through the wound which they postulate may have weaken the wound and allow hernia formation.(56) Diagnosis of perineal hernias can be difficult as traditional fluoroscopic imaging techniques often do not identify them. Other modalities have been used to include herniography, CT, and dynamic MRI. A comparative study of dynamic MRI and dynamic cystocolpoproctography showed that MRI was the only modality that identified levator ani hernias.(49) There is a paucity in large published series to describe which technique of perineal defect closure is superior. Various case reports and retrospective reviews provide much of the literature in this respect. In a review of the literature, closure techniques have ranged from the use of simple suture closure, prosthetic mesh, human dura mater allograft (57), gracilis myocutaneous flap (58), gluteus flap and retroflexion of the uterus or bladder. (59) So et al. described their experience with closures and ultimately found that recurrence rates were equal (20%) between simple and mesh closures. Their repair consisted of simple closure of the levator defect with nonabsorbable sutures. The approach to the repair was also felt to be a point of consideration in planning the operation. For the most part, a perineal approach was adequate with the abdominal approach reserved for recurrent hernias, or those in whom laparotomy is necessary for other reasons. The abdominal approach also provides good visualization when suturing the mesh to the bony pelvis. A combined AP approach is rarely necessary except under unusual circumstances. Skipworth et al. published their experience and technique of perineal hernia repair using Permacol® mesh. Using a perineal approach, they isolated and ligated the sac in the standard fashion before proceeding to close the perineal defect with 4-O PDS (polydiaxonone) suture. The mesh was then fashioned to the contours of the defect and sutured in place, tension free, with interrupted 2-O Prolene sutures. A small suction drain was then left superficial to the mesh and the thin, residual perineal fascia closed with Vicryl sutures. They reported no recurrence

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improved outcomes in colon and rectal surgery in the 18 months following the repair. There are also a growing number of case reports and prospective studies in the use of laparoscopy for perineal hernia repairs. Dulucq et al. describe their experience in a prospective study done over the course of a year with three patients that had received laparoscopic mesh repairs of their perineal hernia defects. A composite mesh was fixed laterally to the border of the levator muscle, anteriorly to the posterior face of the vagina with nonabsorbable sutures and posteriorly with tacks to the sacral periosteum. One suction drain was placed. The reported benefits include adequate visualization of pelvic anatomy, the ability to look for recurrence, and fast recovery. Long term results have yet to be published for laparoscopic perineal hernia repairs, but this may be an attractive option for patients and surgeons as it often avoids making large incisions in areas that have already been irradiated and can therefore be difficult to heal.(60) Before embarking on a repair of any postoperative perineal hernia it is imperative to exclude the possibility of cancer recurrence. References   1. Abraham NS, Davila JA, Rabeneck L, Berger DH, El-Serag HB. Increased use of low anterior resection for veterans with rectal cancer. Aliment Pharmacol Ther 2001; 21(1): 35–41.   2. Shoetz Jr DJ. Evolving practice patterns in colon and rectal surgery. J Am Coll Surg 2006; 203(3): 322–7.   3. Swedish Rectal Cancer Registry. Available at: http://www. oc.umu.se/rekti/rekti2002.pdf.   4. Ruo L, Guillem JG. Major 20th-century advancements in the management of rectal cancer. Dis Colon Rectum 1999; 42(5): 563–78.   5. American Society of Colon and Rectal Surgeons Committee Members; Wound Ostomy Continence Nurses Society Committee Members. ASCRS and WOCN joint position statement on the value of preoperative stoma marking for patients undergoing fecal ostomy surgery. J Wound Ostomy Continence Nurs 2007; 34(6): 627–8.   6. Marret E, Remy C, Bonnet F. Postoperative Pain Forum Group. Meta-analysis of epidural analgesia versus parenteral opioid analgesia after colorectal surgery. Br J Surg 2007; 94(6): 665–73.   7. Geerts WH, Bergqvist D, Pineo GF et al. American College of Chest Physicians. Prevention of venous thromboembolism: American College of chest physicians evidence-based clinical practice guidelines (8th Edition). Chest 2008; 133(6 Suppl): 381S–453S.   8. Bratzler DW, Houck PM. Antimicrobial prophylaxis for surgery: an advisory statement from the National Surgical Infection Prevention Project. Clin Infect Dis 2004; 38: 1706–15.   9. Beraldo S, Dodds SR. Lower limb acute compartment ­syndrome after colorectal surgery in prolonged lithotomy position. Dis Colon Rectum 2006; 49(11): 1772–80. 10. Miles WE. A method of performing abdominoperineal excision for carcinoma of the rectum and of the terminal portion of the pelvic colon. Lancet 1908; 2: 1812. 11. Corman ML. Carcinoma of the rectum. In: Colon and Rectal Surgery. Fifth Edition. Lippincott, Williams, and Wilkins. Philadelphia, 2005: 905–1061.

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12. Heald RJ, Husband EM, Ryall DH. The mesorectum in rectal cancer surgery – the clue to pelvic recurrence? Br J Surg 1982; 69: 613–6. 13. Kyo K, Sameshima S, Takahashi M, Furugori T, Sawada T. Impact of autonomic nerve preservation and lateral node dissection on male urogenital function after total mesorectal excision for lower rectal cancer. World J Surg 2006; 30(6): 1014–9. 14. Moriya Y. Function preservation in rectal cancer surgery. Int J Clin Oncol 2006; 11(5): 339–43. 15. Kim NK, Aahn TW, Park JK et al. Assessment of sexual and voiding function after total mesorectal excision with pelvic autonomic nerve preservation in males with rectal cancer. Dis Colon Rectum 2002; 45: 1178–85. 16. Shirouzu K, Ogata Y, Araki Y. Oncologic and functional results of total mesorectal excision and autonomic nervepreserving operation for advanced lower rectal cancer. Dis Colon Rectum 2004; 47(9): 1442–7. 17. Murrell ZA, Dixon MR, Vargas H et al. Contemporary indications for and early outcomes of abdominoperineal resection. Am Surg 2005; 71(10): 837–40. 18. Rosen L, Veidenheimer MC, Coller JA et al. Mortality, morbidity, and patterns of recurrence after abdominoperineal resection for cancer of the rectum. Dis Colon Rectum 1982; 25: 202–8. 19. Irvin IT, Goligher JC. A controlled clinical trial of three ­different methods of perineal wound management following excision of the rectum. Br J Surg 1975; 62: 287–91. 20. Silen W, Glotzer DJ. The prevention and treatment of the persistent perineal sinus. Surgery 1974; 75: 535–42. 21. Meyer L, Bereuter M, Marusch F et al. Perineal wound ­closure after abdomino-perineal excision of the rectum. Tech Coloproctol 2004; (8 suppl 1): S230–4. 22. Gruessner U, Clemens M, Pahlplatz PV et al. Septocoll Study Group. Improvement of perineal wound healing by local administration of gentamicin-impregnated collagen fleeces after abdominoperineal excision of rectal cancer. Am J Surg 2001; 182: 502–9. 23. Mendel V. Rektumexstirpation-Ergebnisse mit einem Kollagen-Gentamycin-verbund bei der abdomino-perinealen Rektumexstirpation. Forum Lokale Antibiose “Der Schwamm”, Essex Pharma GmbH, 1995; 50–1. 24. Chessin DB, Hartley J, Cohen AM et al. Rectus flap reconstruction decreases perineal wound complications after pelvic chemoradiation and surgery: a cohort study. Ann of Surg Onc 2005; 12(2): 104–10. 25. Butler CE, Gundeslioglu AO, Rodriguez-Bigas MA. Outcomes of immediate vertical rectus abdominis myocutaneous flap reconstruction for irradiated abdominoperineal resection defects. J Am Coll Surg 2008; 206(4): 694–702. 26. Page CP, Carlton PK, Becker DW. Closure of the pelvic and perineal wounds after removal of the rectum and anus. Dis Colon Rectum 1980; 23: 2–9. 27. Nilsson PJ. Omentoplasty in Abdominoperineal Resection: A review of the literature using a systematic approach. Dis Colon Rectum 2006; 49: 1354–61. 28. Pollard CW, Nivatvongs S, Rojanasakul A, Ilstrup DM. Carcinoma of the rectum. Profiles of intraoperative and early

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postoperative complications. Dis Colon Rectum 1994; 37: 866–74. Broux ED, Parc Y, Rondelli F et al. Sutured perineal omentoplasty after abdominoperineal resection for adenocarcinoma of the lower rectum. Dis Col Rect 2005; 48: 476–82. Baudot PE, Keighley MRB, Alexander-Williams J. Perineal wound healing after proctectomy for carcinoma and inflammatory disease. Br J Surg 1980; 67: 275–6. Michalson AE, Brown BP. Warnock NG, Simonson TM. Presacral abscesses: percutaneous transperineal drainage with use of bone landmarks and fluoroscopic guidance. Radiology 1994; 190: 574–5. Wang O, Shi W, Zhaw Y, Zhou W, He Z. New concepts in severe presacral hemorrhage during proctectomy. Arch Surg 1985; 120: 1013–20. Arnaud JP, Tuech JJ, Pessaux P. Management of presacral venous bleeding with the use of thumbtacks. Dig Sur 2000; 17(6): 651–2. Nivatvongs S, Fang DT. The use of thumbtacks to stop massive presacral hemorrhage. Dis Colon Rectum 1986; 29: 589–90. Rothenberger DA, Wong WD. Abdominoperineal resection for adenocarcinoma of the low rectum. World J Surg 1992; 16: 478–85. de Canniere L, RosiPre A, Michel LA. Synchronous abdominoperineal resection without transfusion. Br J Surg 1993; 80: 1194–5. Petrelli NJ, Nagel S, Rodriguez-Bigas M et al. Morbidity and mortality following abdominoperineal resection for rectal adenocarcinoma. Am Surg 1993; 59: 400–4. Tompkins RG, Warshaw AL. Improved management of the perineal wound after proctectomy. Ann Surg 1985; 202: 760–5. Anthony JP, Mathes SJ. The recalcitrant perineal wound after rectal extirpation. Arch Surg 1990; 125: 1371–7. Fasth S, Hulten L, Ojerskog B. Omission of pelvic peritoneal closure after abdominoperineal rectal excision. Ann Chir Gynaecol 1977; 66: 181–3. Scott H, Brown AC. Is routine drainage of pelvic anastomosis necessary? Am Surg 1996; 62: 452–7. Bacon HE, Nuguid TP. Problem of persistent perineal sinus following removal of the rectum for ulcerative colitis. Dis Colon Rectum 1962; 5: 370–2. Christian CK, Kwaan, MR, Betensky RA et al. Risk factors for perineal wound complications following abdominoperineal resection. Dis Colon Rectum 2005; 48(1): 43–8.

44. Oomen JW, Spauwen PH, Bleichrodt RP, vanGoor H. Guideline proposal to reconstructive surgery for complex perineal sinus or rectal fistula. Int J Colorectal Dis 2007; 22(2): 225–30. 45. Permberton JH. How to treat the persistent perineal sinus after excision. Colorectal Dis 5(5): 486–9. 46. Argenta LC, Morykwas MJ. Vacuum-assisted closure. A new method for wound control and treatment: clinical experiences. Ann Plastic Surg 38: 1997; 563–77. 47. Deva AK, Buckland GH, Fisher E et al. Topical negative pressure in wound management. Med J Australia 2000; 173: 128–31. 48. Yamamoto T, Mylonakis E, Keighley MR. Omentoplasty for persistent perineal sinus after proctectomy for Crohn’s disease. Am J Surg; 181(3): 265–7. 49. Skipworth RJ, Smith GH, Anderson DN. Secondary perineal hernia following open abdominoperineal excision of the rectum: report of a case and review of the literature. Hernia 2007; 11: 541–5. 50. McMullin ND, Johnson WR, Polglase AL, Hughes ESR. Postproctectomy perineal hernia: case report and discussion. Aust N Z J Surg 1985; 55: 69. 51. Rutledge RN, Smith JP, Wharton JT, O’Quinn AG. Pelvic exenteration: an analysis of 296 patients. Am J Obstet Gynecol 1977; 129: 881. 52. Brotschi E, Noe JM, Silen W. Perineal hernias after proctectomy. Am J Surg 1985; 149: 301–5. 53. Cattell RB, Cunningham RM. Postoperative perineal hernia following resection of rectum: report of a case. Surg Clin North Am 1944; 24: 679–83 54. Kelly AR. Surgical repair of post-operative perineal hernia. Aust N Z J Surg 1960; 29: 243–5. 55. Frydman GM, Polglase AL. Perineal approach for polypropylene mesh repair of perineal hernia. Aust N Z Surg 1989; 59: 895–7. 56. So JB, Palmer MT, Shellito PC. Postoperative perineal hernia. Dis Colon Rectum 1997; 40: 954–7. 57. Delmore JE, Turner DA, Gershenson DM et al. Perineal hernia repair using human dura. Obstet Gynecol 1987; 70: 507–8. 58. Bell JG, Weiser EB, Metz P, Hoskins WJ. Gracilis muscle repair of perineal hernia following pelvic exenteration. Obstet Gynecol 1980; 56(3): 377–80. 59. Remzi FH, Oncel M, Wu JS. Meshless repair of perineal hernia after abdominoperineal resection: case report. Tech Colo-proctol 2005; 9: 142–4. 60. Dulucq JL, Wintringer P, Mahajna A. Laparoscopic repair of postoperative perineal hernia. Surgical Endoscopy 2006; 20(3): 414–8.

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Indications and outcomes for treatment of recurrent rectal cancer and colorectal liver and lung metastasis Harry L Reynolds Jr, Christopher T Siegel, and Jason Robke

Challenging Case A 74 year old male underwent low anterior resection of the rectum one year previously after preoperative chemotherapy and radiation. Final pathology revealed a yPT2N0M0 lesion. He received post operative chemotherapy as well. In follow up he was noted to have an elevated carcinoembrionic antigen of seven. Digital exam revealed a palpable mass at the finger tip. It was one half circumferential, posteriorly based, involving the left pelvic sidewall and was fixed. Located at five cm from the verge on rigid proctoscopic exam, it was just at the top of the anorectal ring and involved the previous anastomosis. Computed Tomographic (CT) scan of the chest abdomen and pelvis revealed a posteriorly based mass adjacent to the sacrum without boney erosion. It suggested involvement of the left pelvic sidewall. There was a two cm hypodense lesion in segment three of the liver. The chest was clear. Positron Emission Tomography revealed intense uptake in the pelvis and in the hypodense area of the left lobe of the liver noted on CT. Magnetic Resonance Imaging of the pelvis confirmed extension into the pelvic sidewall but did not reveal boney involvement of the sacrum. Colonoscopy cleared the proximal colon. Biopsies confirmed a moderately well differentiated adenocarcinoma. Case Management The patient received a preoperative radiation boost to the pelvis supplemented with capecitabine. He was re-explored and underwent abdominal perineal resection. The left internal iliac artery and vein were ligated and partially excised with a portion of the left pelvic sidewall. He received an intraoperative radiation boost to the left sidewall and sacrum where the tumor was adherent. It was difficult to differentiate tumor from scarring over the sacrum, but there was no gross boney involvement. Intraoperative ultrasound of the liver revealed no other liver lesions and the left lateral segment metastasis was excised after the pelvic work was completed. He was reconstructed with an end descending colostomy. He was referred to oncology for further postoperative chemotherapy. Introduction Of the many challenges presented to the surgeon, patients ­presenting with recurrent rectal cancer can be among the most daunting. Likewise patients with metastatic disease to the liver or lung can be a technical challenge and can be difficult to sort out as to who is an appropriate operative candidate. These patients are best treated with a multidisciplinary approach with a Colorectal or General Surgeon serving as the team leader.(1) In this chapter we explore, in three separate sections, the indications and outcomes for surgical intervention in patients with: 1. Recurrent rectal cancer, 2. Liver metastasis, and 3. Lung metastasis. Contributing authors include a Colon and Rectal Surgeon, a Hepatobiliary Surgeon, and a Thoracic Surgeon.

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Recurrent Rectal Cancer Recurrent rectal cancers are among the most challenging for the Colon and Rectal Surgeon to manage. A multidisciplinary approach is truly essential in planning a comprehensive treatment plan if success is to be achieved. The surgeon that takes on these cases assumes the responsibility of organizing and leading a team of sub specialists consisting of Medical and Radiation Oncologists, Urologists, Radiologists, Pathologists, Enterostomal Therapists, and in selected cases, Plastic Surgeons, Vascular Surgeons, Gynecologic surgeons, Hepatobiliary Surgeons, Thoracic Surgeons, and Intensivists. The complexity of these patients makes it essential that they be treated at centers with the staff and resources necessary to undertake their care.(1, 2) Assessing Resectability A thorough workup of the patient first consists of a careful history and physical exam. Fitness for surgery should be assessed carefully as one can expect a significant physiologic insult in those who come to operation. Many will require extended en bloc resections of adjacent organs with the potential for blood loss and volume shifts not usually seen at initial proctectomy. Preoperative assessment by appropriate sub specialists with emphasis on cardiac and pulmonary optimization may be necessary in these frequently elderly patients. In some patients surgical risk may be deemed prohibitive and nonoperative management with combinations of chemotherapy and radiation and/or stenting or palliative diversion may be necessary. Assessing the extent of local and metastatic disease is best achieved with careful physical and proctoscopic exam supplemented with appropriate radiologic imaging. The importance of digital examination cannot be overemphasized. Determining location with respect to the sphincter complex and adjacent structures including vagina, uterus, prostate, seminal vesicles, bladder, pelvic sidewall, and sacrum can be preliminarily assessed with a careful digital rectal and vaginal exam. Bulk, mobility, and fixation to surrounding structures should be carefully considered with the digital. Pelvic recurrences are frequently extramucosal and may not be appreciated endoscopically but may be felt on digital. Rigid proctoscopic and digital exams are essential in determining relationships to the sphincter complex as even with pelvic recurrences, sphincter sparing options may be available in selected patients. Involvement of the sphincter complex typically necessitates abdominal perineal resection (APR). A full colonoscopy is performed to rule out synchronous lesions. Radiographic workup typically consists of PET CT to rule out extrapelvic metastatic disease. PET CT may identify patients with unsuspected metastatic disease, thus preventing overly aggressive surgical intervention. Watson reported a change in planned surgical intervention in 37% of patients based on PET CT imaging in patients with recurrent colorectal cancer.(3)

indications and outcomes for treatment of recurrent rectal cancer High quality spiral CT scanning of the chest abdomen and pelvis is frequently performed as well to define any questionable metastatic lesions and to better define the extent of pelvic disease. Pelvic MRI is felt by most authors to be the preferred imaging modality for establishing the extent of adjacent organ involvement for purposes of preoperative planning. MRI can provide insight as to whether pelvic sidewall, seminal vesicles, prostate, bladder, ureters, vascular structures, gynecologic structures, or sacrum are involved.(4–8) Although imaging can assist in preop planning, no radiographic study can reliably differentiate fibrosis and scarring from tumor, particularly in an irradiated pelvis. Radiation induced inflammatory changes in the pelvis can be PET positive as well, and can be confused for metastatic disease. Although imaging can assist with planning, the ultimate determination of involvement and resectability is made at operation. Reviewing previous operative notes and pathology reports can provide insight into the adequacy of initial resection and can be helpful in assessing likelihood of resectability at reoperation. Those that have had an optimal cancer operation at the first exploration with total mesorectal excision (TME) and high ligation of the inferior mesenteric artery can be expected to have a much more difficult reexploration. With TME and high ligation initially, combined with previous radiation therapy, recognizable planes are typically absent. Those with more proximal tumors, non-TME initial resections, and/or ligation of the superior rectal vs. the inferior mesenteric artery (IMA) may well have some pelvic plane preservation, making reexploration not so daunting a task. Those that have had a proper TME with a coloanal anastomosis or abdominal perineal resection can be expected to have more difficult lesions to deal with, as recurrences can be expected to be adherent to adjacent structures, outside of the proper mesorectum. These tumors recur in the sidewall, sacrum, anastomosis, perineal wound or in the gynecologic or urologic organs. Those that recur laterally in the pelvic sidewall or posteriorly on the sacrum are particularly challenging in terms of obtaining an R0 resection. An R0 resection refers to a complete resection with microscopically clear margins. R1 resection implies microscopic disease is left, and R2 implies gross disease is left behind. Those that recur at the anastomosis or anteriorly in the adjacent vagina, uterus, prostate, seminal vesicle, or bladder can frequently be completely excised with en bloc adjacent organ resection.(9) Likewise, the occasional patient who presents with an isolated nodal recurrence, high along the IMA after an initial low ligation, may be resectable as well. Pelvic sidewall recurrences can be very difficult to resect secondary to the extensive internal iliac arterial and venous branches encountered. Anatomy is distorted by tumor and scar, and the desmoplastic reaction associated with tumor and previous radiation can make dissection hazardous as venous bleeding can be significant. Likewise sacral recurrences below S1-2 typically can technically be resected, but morbidity and mortality can be significant. (10) Local, limited anastomotic recurrences post low anterior resection and perineal recurrences post APR, without lateral or sacral extension, are more likely to be amenable to R0 resection.(9) Patients with extrapelvic metastatic disease are typically not offered extended exenterative procedures. However, in selected otherwise fit patients presenting with isolated resectable liver or lung metastasis, it may be appropriate to proceed with extended resection. In those

with nonresectable metastatic extrapelvic disease, pelvic exenterative procedures are felt to be contraindicated by most. Role of Chemotherapy and Radiation Our approach to a diagnosed pelvic recurrence initially involves evaluation by medical and radiation oncology to determine if an additional radiation boost can be delivered to the pelvis. This will usually be administered with concomitant 5-FU based chemotherapy. Most patients will have received either preop or postop chemoradiotherapy with there first resection. Most will receive an additional preop boost of 30–40 Gy to the site, particularly if it is a bulky recurrence, with plans for surgical exploration ~8 weeks post radiation.(11–15) This is assuming the interval between radiation and reirradiation is >6 months and the small intestine can be excluded from the planned field.(11) This approach seems to be well tolerated by most in our institution and has been validated by others.(11–15) It is important to ensure exclusion of the small intestine from the pelvis with reirradiation. Dresen reports that if the small intestine is not excluded planned operation before irradiation may be undertaken for placement of a spacer for exclusion. The spacer could be biologic such as the omentum or a nonbiologic such as a breast prosthesis or tissue expander. The patient is typically diverted at the time of spacer placement.(11) Intraoperative radiation therapy (IORT) can be offered via a dedicated fixed intraop unit, a mobile unit or via after-loading catheters place intraoperatively. This is a particularly valuable treatment adjunct to patients with sidewall involvement, sacral involvement, or major vascular involvement, where an extended resection of involved areas cannot technically be accomplished or will not be tolerated by the patient. This can be technically delivered to areas directly involved by tumor while shielding organs particularly sensitive to radiation (i.e., ureters, small intestine, and bladder).While no randomized trial has been performed to demonstrate the value of IORT, such a trial is unlikely to be performed. Positive circumferential margins in rectal cancer have been associated with excessively high local recurrence rates as demonstrated by Quirke and others even after preop radiochemotherapy.(16, 17) It would seem illogical, and perhaps unethical, to randomize patients to a nontreatment arm with a known or suspected positive margin when a modality such as IORT, with little morbidity when applied appropriately, is available. There are multiple studies, with historical controls, demonstrating decreases in local recurrence and survival improvement, with little morbidity, when IORT is applied appropriately.(5, 18–26) We feel that IORT is an essential piece of the treatment algorithm. It is frequently very difficult to differentiate a true positive margin from the fibrosis and scarring associated with previous radiation therapy and previous pelvic surgery. Although frozen section analysis of surgical margins can be helpful if positive, if we are clinically concerned about margin status, IORT will be administered regardless of frozen section results. Local recurrence rates in our institution have been very favorable with this approach.(27) Likewise, others have demonstrated favorable results with this approach.(5, 18–26) With the addition of IORT to our armamentarium, it seems overly aggressive to perform sacrectomy in all cases with sacral adherence. Adherence to the presacral fascia is present in virtually all patients who have undergone a TME and it is very difficult to

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improved outcomes in colon and rectal surgery differentiate fibrosis from tumor. If there is suspicion clinically of involvement, we will treat with IORT. Sacrectomy is preserved for those who are fit for surgery with clear cortical destruction or marrow involvement by CT/MRI below S1-2. Our initial experience with this approach is encouraging.(27) Postoperative chemotherapy is usually recommended in our institution, but has been variably administered in the literature. Operative Approach The patient is placed in modified lithotomy position. Initial exploration is undertaken to carefully assess for extrapelvic metastatic disease. Careful attention is paid to the liver and the abdomen is assessed for carcinomatous implants. All adhesions are lysed and the ureters are identified. Ureteric catheters are typically used. The left colon is mobilized as is the splenic flexure and attention is focused on the IMA root. If it has not been taken it is mobilized. An assessment for resectablity is made and if the tumor is deemed resectable, the IMA, if not previously ligated, is taken high. The neorectum is mobilized posteriorly initially, laterally, then anteriorly. The areas free from tumor involvement are most easily mobilized and are approached first. As much easy dissection should be done, as can be done, to identify landmarks initially. If anterior structures are clinically involved they are taken en bloc with the neorectum. It is much easier to take the bladder, seminal vesicles and prostate en bloc with the neorectum than to try to separate them. If there is firm adherence to the posterior aspect of the bladder, seminal vesicles or prostate, they should be taken en bloc. If the lesion is quite low in the rectum and adherent to the prostate or vesicles alone, the posterior portion of the prostate and/or the seminal vesicles may be taken without the bladder, but this is much more challenging technically than proceeding with en bloc cystoprostatectomy. In a female en bloc posterior vaginectomy and hysterectomy should be performed with any adherence. Pelvic sidewall involvement is technically difficult to resect secondary to the associated desmoplastic reaction and loss of planes. The nervi erigentes and internal iliac arterial and venous branches can be taken. However, back bleeding from distal venous branches can be torrential and difficult to control despite proximal ligation. The dissection is completed to the pelvic floor circumferentially and a decision is made as to whether sphincter preservation is possible. It is sometimes feasible to preserve the sphincters even if cystoprostatectomy is performed and a coloanal anastomosis may be possible. A double stapled technique, transabdominal-transanal hand sewn technique, low Hartmann, or APR may be necessary. Any suspicious areas for microscopic involvement are treated with IORT after specimen removal. IORT for posteriorly based or pelvic sidewall based areas is relatively easily technically performed with appropriate positioning of a shielding cone. However, it is technically challenging to dose anteriorly unless APR is performed and the patient is moved to the prone position. This allows dose delivery via a cone placed through the perineal wound. If there is gross tumor left behind, we typically will not perform an anastomosis. However, if there is a suspicion of potential microscopic disease only, and this is treated with IORT, we will consider reanastomosis, assuming adequate sphincters and an appropriate margin. All coloanal anastomoses are covered with a proximal diverting loop ileosotomy.

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As noted above in the case of adherence only posteriorly, IORT is usually performed after the specimen is withdrawn. If the sacrum is clearly involved with tumor, sacrectomy is considered. The dissection for sacrectomy begins posteriorly, typically with internal iliac artery and vein ligation abdominally. The remainder of the dissection is completed, laterally then anteriorly. An osteotomy may be started, typically with the help of an orthopedic consultant. The ostomy is created, the abdomen closed and the stoma matured. A plastic surgeon may be involved prior to ostomy creation if a rectus abdominus myocutaneous flap for perineal defect reconstruction is considered. The remainder of the sacrectomy is performed after turning the patient to the prone position. Reconstruction is completed frequently with the aid of the plastics consultant. Other flaps such as a gluteus myocutaneous flap may be considered.(10) Expected Outcomes Local recurrence after proctectomy occurs in 2.6 to 32% of patients.(2, 28, 29) Chemotherapy and radiation offer palliation only with median survivals reported between 10 and 17 months. (2, 28, 30) It is estimated that ~50% of patients will present with local recurrence only, without distant metastasis.(2, 31–33) The concept of radical excision for potential cure of recurrent rectal cancer is not new and was reported by Dunphy in 1947.(2, 34) The literature has expanded in recent years with multiple larger series reported with 5 year survivals ranging from 14 to 44% (see table).(2, 5, 10, 11, 13, 35–44) In fact in a subset of patients with R0 resections reported by Valentini a 67% 5 year survival was noted.(15) Long-term outcome is directly related to ability to clear local tumor in the pelvis and the absence of metastatic disease. Surgical intervention alone typically does not suffice. It is clear that a multidisciplinary approach is essential in these complex patients. Case controlled data suggests IORT can decrease local recurrence and play a role in a potentially curative treatment algorithm even in the presence of a microscopically positive margin.(45–48) In the presence of gross persistent disease it does not appear as effective, but may be useful in a multidisciplinary approach with pre and/or postop chemo-radiotherapy. (27) Preop chemo-radiotherapy and postop chemotherapy are typically employed as outlined previously. Heriot et al. hypothesize that a significant number of patients that could be candidates for resection likely are not operated secondary to perceived excessive morbidity and mortality associated with these difficult cases.(2) They argue, however, that in carefully selected patients, resection is not only safe and reasonable, but indeed offers the only chance of cure. They advocate an extended radical en bloc resection of all involved or potentially involved structures in the pelvis. The extent of resection involves all involved areas of tumor/desmoplastic reaction. This radical en bloc extended resection is to include involved common or external iliac vessels with reconstruction, wide resection of the pelvic sidewall, sacrectomy, and or partial resection of the bony pelvis if clinically involved.(2) In their series IORT was utilized selectively and chemo-radiotherapy was typically employed. In this exceptional series of 160 patients, only 7 were found to be unresectable. Overall 5 year survival was 36.6% and cancer specific survival was 41.5% with a mean follow-up of 32 months. Unfavorable factors

indications and outcomes for treatment of recurrent rectal cancer Table 28.1  Site of involvement and likelihood of R0 Resection.

Table 28.2  Outcomes in Recurrent Rectal Cancer.

Anastomotic or perineal wound

R0 90%

Author

Anastomotic or perineal and anterior

R0 72%

Lateral and/or posterior component

R0 43%

Iliac vessels

R0 17%

N=119 patients with pelvic recurrence of colorectal cancer. Source: Moore et al. (9).

associated with impaired survival included a lymph node positive primary tumor, margin involvement, use of IORT (likely secondary to use only in more difficult tumors), and lateral recurrence (sidewall involvement). Perioperative mortality was 0.6% (1/160) secondary to hemorrhage, morbidity was 27%.(2) They note the need for extensive multidisciplinary involvement and planning, and comment that this surgery is not for the “occasional participant”.(2) These data and others confirm that the overriding principle of this challenging surgery is to attempt to obtain clear surgical margins.(2, 11, 49, 50) Others have pointed out that the pattern of pelvic invasion and the numbers of points of fixation have adverse prognostic implications.(9, 51, 52) Heriot et al’s data points to the difficulty in obtaining a clear margin when the pelvic sidewall is involved which was noted by Moore et al. in the Memorial Sloan Kettering experience.(2, 9) They noted that axial (anastomotic or perineal recurrences) or anterior based recurrences were more easily resected and had better prognosis than lateral recurrences. This was felt secondary to the difficulty in obtaining a clear margin with lateral recurrences secondary to the confines of the bony pelvis and the difficult vascular problems encountered with the iliac branches along the pelvic sidewall. See (Table 28.1).(9) Other factors associated with low likelihood of R0 resection include presentation with pelvic pain, radicular pain, or hydronephrosis.(5, 9) The use of additional preop radiation therapy in those already radiated has been questioned for fear of introducing excessive morbidity. Vermaas et al. note that the addition of a 50 Gy preop dose was associated with a statistically significant improvement in local control without increased morbidity in those eventually undergoing resection compared to a historical group which did not receive additional preop radiation.(53) Those that had a complete response (10%) had an improvement in survival as well. No chemotherapy was used with the preop radiation.(53) Dresen’s data also suggests that reirradiation is safe if the interval to reirradiation is >6 months and the small bowel can be excluded from the field.(11) They recommend a 30–40 Gy preop boost in combination with chemotherapy and introperative radiation if necessary. They noted an increased ability to perform an R0 resection in those reirradiated versus those who were not (64.9% vs. 29.2%, p = 0.004) and an improvement in metastasis free survival at three years (58.7 vs. 17.8%, p < 0.001). As noted previously, others have confirmed similar results.(13) It has been our practice to offer most patients a preop radiation boost combined with 5 FU based chemotherapy in those presenting with recurrent tumors as well, although our numbers do not allow meaningful outcome comparisons.(27) Table 28.2 compares outcomes reported in several larger series. The interpretation of the data from these series is difficult

N

5 year Survival

Morbidity

Mortality

Dresen (11)

147

31.5

59

4.8

Heriot (2)

160

36.6

27

0.1

Maetani (35)

36

28

–

–

Wiig (36)

47

18

38

4

Yamada (37)

64

23

50

2

Jiménez (38)

55

28

78

5

Kecmanovic (38)

28

17

43

10

Ike (40)

45

14

77

13

Lopez (41)

19

44

67

0

Kakuda (42)

22

12

68

5

Moriya (43)

57

36

58

4

Vermaas (44)

35

16

70

3

Mohiuddin (12)

34

22

–

0

Wanebo (10)

61

31

38

8

Valentín (11)

59

39

–

–

Source: Adopted from de Wilt et al.(5)

as they represent a diverse mix of presentations and treatment algorithms. Some included combinations of patients with locally advanced primary tumors as well as recurrent tumors. Some used extended exenterative resections with en bloc resection of adjacent bony and vascular structures and some did not. Some had preoperative radiation boosts, some did not. Some utilized IORT and some did not. The five year survivals in the series outlined ranged from 12 to 44%. The small numbers and mix of patients makes comparisons of different approaches to the close surgical margin impossible. It is not clear from the data whether extended en bloc resection of bony or vascular structures should be performed or IORT should be preferred in these cases. However, although morbidity (27 to 78%) and mortality (0–13%) is significant regardless of approach, the overriding theme in these series remains that a multimodality approach including surgery offers the only opportunity for cure, and that those patients having the longest survival undergo R0 resection. There is a suggestion that similar long term survivals and rates of local control can be obtained when IORT is utilized in patients with a microscopically involved or close margin.(5, 27) Treatment of Colorectal Liver Metastasis Liver resection for the treatment of metastatic colon cancer was first described by Lortat- Jacob in 1952 (54–56) and in the US by Woodington in 1963.(57) Fifteen years later, Attiyeh (58) described a series of 25 patients who had undergone liver resection for metastatic colon cancer with a 40% five year and a 28% ten year survival. Although these early series were highly selected patients, no other therapy to date provides a better therapeutic benefit than complete resection of isolated metastatic colon cancer to the liver. Historically, treatment with 5 fluorouracil and leucovorin for metastatic colon cancer resulted in 5 year survival rates of less than 5%.(59, 60) The addition of Oxaliplatin and Irinotecan based regimens have improved the median survival for patients with stage IV disease to over two years (61), however 5 year survival rates have

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improved outcomes in colon and rectal surgery remained below 10% (62). Interestingly in stage 3 disease, analysis of patient survival reveals three groups with markedly different survival rates. The difference in survival rates for the groups was found to be dependent on extent of nodal involvement with survival ranging from 44% for stage IIIc patients, that is four or more positive lymph nodes to 83% for stage IIIa, 1–3 positive lymph nodes.(63, 64) The ability to identify a subpopulation within a cancer stage which has a potential for improved survival also holds true for patients with stage IV colon cancer patients. Patients with isolated liver metastasis from their colon cancer treated with multimodality therapy including surgery have a significantly improved 5 year survival when compared to patients with isolated liver metastasis treated with chemotherapy alone (65–67) or patients with nonresectable stage IV disease.(68) Approximately, 150,000 new cases of colon cancer were diagnosed in 2007.(69, 70) It has been estimated that almost 20% will have isolated liver metastasis at time of presentation and for patients presenting with local disease, 25% will eventually develop isolated liver metastasis and be eligible for resection.(69, 71) Because of the marked improvement in survival for patients with metastatic colon cancer to the liver treated with resection, identification of patients who are candidates for surgical therapy and appropriate management is of paramount importance. Assessing Resectability Evaluation to determine whether a patient with colon cancer metastatic to the liver is a candidate for hepatic resection depends on 1) medical comorbidities of the patient, 2) anatomic extent of disease in the liver and 3) the presence or extent of extrahepatic disease. Before deciding whether a patient is a nonoperative candidate, thought should be given to downstaging with systemic or hepatic artery infusional chemotherapy (72–74), combined resection and radiofrequency ablation (75, 76), staged resection (77) and in the case of extended resections, portal vein embolization (78, 79). While prior dogma limited candidates for resection based on tumor margins, tumor number or extent of extrahepatic disease (80), the current National Comprehensive Cancer Network (NCCN) guidelines describe outcome objectives to determine if a patient may benefit from resection. The goals currently included in the current NCCN guidelines focus on these ten points: 1) resection must be feasible based on adequate liver reserve after resection and anatomic extent of disease 2) debulking is not recommended, 3) there should be no unresectable extrahepatic sites, 4) if tumors are downstaged, than all original sites must be resectable, 5) resection should be the treatment of choice, 6) ablations can be considered if all disease is treatable, 7) solitary lesions have a better prognosis than multiple lesions, 8) arterial embolizations should be performed only on a clinical trial, 9) the primary tumor must have been resected for cure, and 10) reresections are possible in selected candidates (81). Before surgical resection of liver metastasis, the patient requires a full staging evaluation and risk stratification to determine operative risk. Staging evaluations include a CT scan of the chest, abdomen, and pelvis obtained with oral and intravenous contrast if possible. If poor renal function precludes IV contrast administration for CT scanning then staging can be performed with a noncontrasted CT scan of the chest and other imaging of

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the abdomen. If the patient has mild, chronic kidney disease stage 1–3 (glomerular filtration rate > 30) than MRI scanning can be helpful to fully evaluate the extent of disease in the liver.(82, 83) Patients with advanced renal dysfunction, in which gadolinium poses a significant risk, may require hepatic evaluation with either transabdominal or laparoscopic ultrasound. While prior studies have suggested precluding patients with greater then three liver metastasis from consideration, outcomes data would suggest that overall tumor burden, vascular involvement and extrahepatic spread may be more important in the decision algorithm.(84) The addition of (18F) fluoro-2-deoxyD-glucose (FDG) PET scanning to CT or MRI staging has assisted in identifying patients with occult extrahepatic metastasis who may not benefit from surgery.(85–87) In these studies, the addition of FDG-PET was useful in identifying 12% of patients who were not surgical candidates, and altered surgical therapy in an additional 23% who underwent operation. Interestingly, the ability to detect lesions less than one centimeter in the liver was only 25% in the data by Fong et al. and the recurrence within the first year was 40% indicating even with PET scanning that a significant number of liver lesions were missed on imaging. Other investigators have demonstrated that addition of FDG-PET has increased both overall and disease free survival at 5 years with overall actuarial five year survival of 58% for patients which demonstrated no extrahepatic PET positive lesions on preoperative imaging. More recent reports have demonstrated the ability of recent chemotherapy to affect the ability of FDG-PET to identify viable tumor.(88–91) In a study by Akhurst et al. evaluating the sensitivity of FDG-PET, patients undergoing surgery for resection of metastatic colon cancer were evaluated by PET imaging. Thirteen of 42 patients had received chemotherapy within three months of surgery and 29 /42 had not. In the group which had received chemotherapy 37% of lesions were PET negative as compared to 27% of the lesions in the no chemotherapy group. Interestingly, no tumor >1.2 cm was missed in the group without chemotherapy while some tumors as large as 3.2 cm were PET negative after chemotherapy. In this study, 92% of all tumors smaller than 1 cm were undetected by PET imaging. In a study by Carnaghi et al. PET imaging sensitivity dropped to 62% after chemotherapy and was as low as 18% for lesions under 1 cm in size. Taken together, these data would support use of PET imaging prior to chemotherapy to fully stage the extent of disease and nonreliance on conversion of intrahepatic lesion to PET negative on decision making concerning hepatic resection. Extrahepatic disease remains a relative contraindication for liver resection although published studies would support resection in limited cases if all extrahepatic disease can be resected (92). Several studies have demonstrated decreased survival rates for patients resected with positive portal or hepatic artery lymph node metastasis (93, 94). Unfortunately, these studies do not comment on the use of adjuvant therapies after surgery or whether patients had chemotherapy sensitive disease prior to resection. In our practice we will offer resection to patients with extrahepatic lymph node metastasis if the disease is localized to the porta hepatis, is completely resectable at the time of surgery, and had a favorable response to medical therapy. In addition to staging studies, a medical workup would obviously include cardiac evaluations for those displaying cardiac risk factors and pulmonary

indications and outcomes for treatment of recurrent rectal cancer function testing for those with significant lung disease or smoking history. Cardiac stress echo testing can be performed for patients with significant cardiac risk factors. Because there is considerable variability between patients, decisions as to whether a patient is a candidate for resection must take into account the patients overall medical status and the type of procedure being planned. Decision making regarding operative timing can be complicated by presentation of the disease. For patients who present with synchronous asymptomatic colon and liver disease, no single treatment algorithm has been established in the field. Acceptable treatment protocols range from complete resection of the colon and liver disease at one operation (95–97) to neoadjuvant chemotherapy followed by synchronous or staged colon and liver resection (98–102). Outcomes from studies evaluating simultaneous liver and colon resections have suggested higher incidences of recurrence and lower overall 5 year survival rates in patients undergoing combined resection. Other authors have recommended a waiting period of 3 months between colon resection and liver resection in order to better select patients for surgery (103, 104). Regardless of the manner in which patients undergo resection, the efficacy of post operative chemotherapy has recently been shown to provide a small survival advantage.(105, 106) Treatment algorithms for resection of metachronous lesions have suggested resection followed by either chemotherapy or hepatic artery infusional (HAI) therapy.(81) Several studies have demonstrated a improvement in disease free and overall survival with the use of HAI (72, 74, 107–109), however, prior studies demonstrating lack of efficacy, introduction of newer chemotherapeutic regimens and high rates of mechanical problems with the pumps (110), have limited there widespread use. Patients who are candidates for liver resection and are on chemotherapy regimens including irinotecan, oxaliplatin, or bevacizumab should be evaluated for hepatic dysfunction prior to surgery.(111) Recent reports have associated the use of irintotecan-based chemotherapy regimens with hepatic steatosis and oxaliplatin based regimens with sinusoidal dilatation.(112, 113) These may occur in 20–30% of patients on therapy. There has been concern that Bevacizumab may potentially increase postoperative complications and mortality due to its effect on vascular endothelial growth factor. In a recent study evaluating 81 patients receiving chemotherapy with Bevacizumab to 44 patients receiving chemotherapy alone, no significant increase in complications were seen after liver resection (114), although increased morbidity and mortality has been reported with patients having increased steatosis at time of resection (113, 115). Preoperative preparation often is related to the extent of liver resection planned. For patients with bilobar disease treatment plans need to be formulated to determine if the tumor can be treated all in one operation or whether sequential procedures will be needed to treat the full extent of the disease.(78, 99) In cases of bilobar disease preference should be given to resection if possible. Occasionally, treatment will involve a combination of resection with the possibility of radiofrequency ablation of remaining contralobar lesions. If the tumors are located near or on the middle vein, and resection will involve removal of more than 70% of the liver, then thought should be given to preoperative portal vein embolization to allow for hypertrophy of the remaining segments prior to tumor removal. Studies have shown

decreased morbidity and mortality in patients undergoing preoperative portal embolization before major surgical resection.(79, 116–119) In order to determine the resectability of the patient, factors such as extent of disease, number and location of lesions, synchronous or metachronous presentation, and exposure to previous therapy should all be taken into account. Special consideration should be given for patients with rectal cancer with synchronous liver metastasis. Current standard of care for primary rectal cancers remains combined chemotherapy with rectal and pelvic radiation. The most common regimen would use 5-fluorouracil for radiation sensitization. The poor response rates of metastatic lesions from this chemotherapeutic regimen have led some investigators to suggest initial treatment with oxaliplatin or irinotecan containing regimens, yet local recurrence rates for rectal primaries treated with this regimen followed by resection have not been well defined. Currently there is no defined standard of care and the treatment of these patients should be individualized. Adjuvant Therapies In addition to surgical resection and systemic chemotherapy, a significant number of alternative liver directed therapies exist. Treatments including radiofrequency ablation, cryotherapy, microwave ablation, chemoembolization, yttrium-90 and stereotatic high dose radiation are alternate tools for site directed therapy. Cryotherapy has been shown to be an effective treatment for liver metastasis with or without resection.(120–124) When initially introduced, complications including liver fracture, bleeding, systemic cytokine induced lung injury, myoglobinuria and pleural effusion reduced its overall popularity and widespread use. Radiofrequency ablation was initially described in the treatment of metastatic colon cancer in 1996.(125) While a much less morbid procedure than resection or cryotherapy, limits to the size of treatable tumors and higher incidence of recurrence as well as lower overall survival when compared to resection have prevented this from replacing surgery as the gold standard for therapy.(126, 127) Microwave ablation, chemoembolization and stereotatic body radiotherapy remain investigational in the US at this time. Injection of yttium-90 labeled beads into the hepatic artery of tumor containing segments of liver has received approval by the Federal Drug administration for the treatment of unresectable colon cancer metastasis to the liver. Current trials are underway to determine the role of this therapy in downstaging liver metastasis and as primary therapy with chemotherapy in the adjuvant setting. Operative Approach Laparoscopy Patients who have single or peripherally located metastatic lesions may be candidates for laparoscopic liver resection. Anteriorly located lesions in either the right or left lobes can often be approached in the supine position. A full explanation of all the techniques and equipment available for resection are beyond the scope of this chapter but have been summarized recently in a review.(128–130) In our practice, we find the LigaSure™ Vessel Sealing System (Valley Lab, Boulder, CO) and the TissueLink Endo SH2.0™ Sealing Hook (SH) (TissueLink Medical Inc., Dover, NH). to be the most useful for laparoscopic resections. Port placement often varies significantly

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improved outcomes in colon and rectal surgery depending on the location of the lesion to be removed. Addition of the hand port has been described to assist with right lobe liver resection and may be useful depending on the body habitus of the patient, the location of the tumor and the characteristics of the liver, i.e, underlying fibrosis, steatosis, etc. In general, a 5–15 mm port is often placed in the plane of the liver dissection to facilitate stapling of the liver. The initial step of the procedure involves localization of the tumor and demarcation of the liver division plane. Laparoscopic ultrasound is needed to define the location and extent of the tumor and to map the appropriate vascular structures. The surface of the liver is marked in the division plane often with electrocautery. The margin status for resection has been a topic of considerable debate in the literature. Several studies have suggested that no significant margin is necessary as long as the capsule of the tumor has not been violated during the resection. Other studies have suggested higher local recurrence rates when tumor was present at the resection margin, regardless of the method of resection.(131, 132) Resection can be performed with or without hilar control. Vascular clamping before resection is not necessarily needed. Parenchmal dissection can be performed with various energy sources. Venous bleeding is controlled by adjusting the pressure of the pnuemoperitoneum and the central venous pressure. The portal vein and the hepatic vein are taken with a laparoscopic GIA stapler using 2.5 mm staples. The approach to posterior lesions can be more difficult. Descriptions on resection techniques utilizing anterior and lateral approaches to these lesions have been described (133, 134). Resection principles are similar. Open Resection The majority of resections are performed using an open technique. Open approaches may be more appropriate if there are multiple lesions, if the lesions involve or abut the major portal structures or if obtaining a margin on or near a hepatic vein may be difficult. For patients with bilobar disease or larger primary tumors, laparoscopy at the time of, but prior to open resection may help differentiate resectable from nonresectable patients. Laparoscopic ultrasound is an invaluable aid in determining the number and extent of hepatic metastases. Laparoscopy before laparotomy in patients at high risk to have unresectable disease is helpful to limit the patient morbidity and recovery time. The approach to open resection differs from laparoscopic in that vascular control is often mandatory in limiting operative blood loss. Exposure is obtained with either a Mercedes incision or via a Chevron approach. Use of the Bookwalter, Thompson or upper hand retractor often aids in exposure. Again, full descriptions of resection techniques are beyond the scope of this chapter (reviewed in (135–137)) but in general formal resections do not confer survival advantage. Studies which have evaluated long term survival would suggest that liver conservation during the resection of metasatic disease does not increase the overall recurrence rates and may confer a better long-term outcome.(138) Expected Outcomes Early series looking at survival of patients undergoing liver resection have demonstrated 5 year survival rates of 25–37%.(139, 140) Further screening patients with FDG - PET imaging has

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resulted in increasing the sensitivity of identifying patients with extrahepatic disease. Better patient selection has resulted in five year survival rates of almost 60%. Even with better imaging most patients will develop recurrent disease of which half will have liver only recurrence. These patients can safely undergo repeat resections with equivalent outcomes.(141– 143) Addition of adjuvant chemotherapy after resection has been recommended as part of the NCCN treatment recommendations based on improvement in survival for patients treated with 5-flourouracil or oxaliplatin based regimens.(61, 105, 106) Treatment of patients with synchronous colon and liver lesions with simultaneous liver and colon resection have demonstrated increased risk of early recurrence and lower overall disease free survival. These data were from studies conducted before treatment with current chemotherapy based adjuvant therapies. Treatment of patients with adjuvant therapy prior to liver resection has been advocated by several different authors as a way to identify favorable, chemotherapy sensitive tumors. Other authors have argued that resistance to chemotherapy is a poor prognostic sign even in resectable disease. (144) Multiple studies have demonstrated the ability to downstage metastatic tumor burden in the liver by neoadjuvant therapy either given systemically or by hepatic artery infusion. Rates of converting unresectable colorectal liver metastasis to resectable disease vary from 16% to 51%.(101, 145) One inherent problem with current studies evaluating the efficacy of various treatments for patients with stage IV disease is the ability to control for the extent of disease in the treatment group. Similar to the patients with stage III disease who can be divided into three separate categories based on extent of nodal involvement, stage IV patients represent a spectrum of disease burden requiring a more complex substaging to accurately identify and evaluate different treatment options. Unfortunately, this currently does not exist. Several authors have reported risk factors which correlate with patient outcome. In 1997, Fong et al. reported on scoring system which included points awarded for size of the tumor, disease free survival<12 months, number of tumors >1, node positive disease, and a CEA greater the 200. For patients with 0–1 point, 2–3 points, and 4–5 points, five years survival was 50%, 20% and 10% (146). Studies to evaluate the use of this and other scoring systems when applied to an independent population proved unsuccessful and have led to the development of other nomograms for predicting disease-specific survival.(147, 148) Although predicting outcome is useful, a staging system is needed to be able to evaluate treatment outcome in similarly controlled groups. One such system has been recently proposed.(149) Significant progress continues to be made in the treatment of metastatic colon cancer to the liver. An aggressive multimodal approach between surgical, medical and radiologic specialties is required for optimizing outcome. While treatment algorithms continue to evolve, there is one tenet that remains constant: patients need to be constantly reevaluated for the appropriate medical or surgical care and that aggressive intervention can significantly improve disease free and overall survival. Colorectal Lung Metastasis When colorectal cancer (CRC) is confined to the bowel, the workup and management are usually fairly straight forward. When

indications and outcomes for treatment of recurrent rectal cancer there is disease (suggested or proven) outside the bowel, the management becomes debatable. As early as the 1980s and 1990s, CRC which had spread to the liver or lung was considered unresectable at most hospitals, and therefore incurable. There are reports of metastectomies going back to the 1940’s (150), but this approach was not widely accepted. As new technologies developed, such as chemoembolization, cryotherapy, radiofrequency ablation, and safe techniques for metastectomies, aggressive medical centers began resecting or ablating metastatic foci once the primary site was controlled. These centers then began finding that in some situations metastectomy offered a chance at cure and long term cancer free survival. Those surgeons who pushed the envelope even further began finding that repeat lung resections for second and third recurrences can still offer chances at cure.(151–154) Cure rates for metastectomies were not high, and most patients eventually developed further metastatic deposits and succumbed to their disease, but a noticeable percentage maintained their disease free state and lived normal life spans. From the patient’s perspective, this was a tremendous leap. Imagine the difference between being told you have almost no chance of cure and will probably die of cancer in the next few years, to being told that with some extra surgery you may have a 25% chance of cure. Suddenly 25% sounds like a wonderful number. In a day when cancer still is a major cause of pain and suffering, we applaud those who work to give us further means of saving patients, and will review some of their work, as well as explain our approach to managing known CRC with known or suspected lung metastases. Assessing Resectability The first step is finding and working up lung nodules. Suspected lung mets can be found before or after the CRC is found. Most commonly the bowel cancer is found first. Preoperative chest x-rays may show an asymptomatic lung mass, or staging CT chest/ abdomen/pelvis +/- PET scan may show the suspected lung mass. If the lung mass is seen on preoperative chest x-ray, then CT/PET is recommended. Although biopsy and pathologic examination of tumors is the gold standard for differentiating malignant nodules from benign nodules, the radiographic characteristics can help. Primary lung cancers tend to have irregular, spiculated borders, and if >8 mm in diameter, most state-of–the-art PET scanners should start to show PET activity. There are, of course exceptions to this. Primary carcinoid tumors of the lung have smooth borders and have low to no PET activity. Luckily these tend to be slow growing, and if not biopsied right away, can be followed with serial scans until growth is confirmed. Bronchoalveolar lung cancer (a variant of adenocarcinoma) can present as a mass, but can also appear with an infiltrative pattern which is often read as pneumonia, initially. Failure to improve after a course of antibiotics, or lack of any recent or current infectious symptoms in the patient should increase your suspicion for cancer. Multiple smooth bordered nodules of varying sizes, especially in a patient with a known CRC, tend to be metastases. PET activity should start to show in colorectal metastases greater than 10 mm. Large (>10 mm) lung nodules without PET activity in the presence of a PET avid colorectal cancer are still concerning, but could very well be non-malignant processes such as rounded atelectasis, scar, or granulomatous disease. If old radiographs, especially CTs, are available, then these should be viewed. If

the suspected nodules are not new, and have been present for more than 2 years without increasing in number or size, then the likelihood of metastatic disease or primary lung cancer is extremely low. Any nodules that are new or increasing in size are suspect. Once the lung nodules are found, the next step is deciding what to do with them. Most CRC patients are middle aged to elderly and a good proportion have smoking histories. We need to be just as concerned about a second primary lung cancer as we are about metastatic disease. Once again, the radiographic characteristics can help. As stated before, multiple, smooth bordered, PET avid nodules are probably metastatic CRC, but intrapulmonary metastases from a lung cancer are still possible. A solitary PET avid lung mass several centimeters in size, without any other suspicious metastatic deposits either intra or extra-thoracic would be suspicious for a primary lung cancer. While CRC can spread to the hilar, internal mammary, and mediastinal lymph nodes, the presence of nodal enlargement >10 mm would also make us suspect lung cancer more than CRC. Differentiating lung cancer from CRC is important because the survival of the cancers is different, and knowing the patient’s prognosis may affect the aggressiveness of treatment for the other cancer. For example, let us imagine that two nodules are found in different lobes, with no other suspected sites of metastases, in a patient with proven CRC. If both of these nodules are resected and proven to be metastatic CRC, then aggressive management of the primary cancer is warranted, since long term survival may be 25–40%. On the other hand, if biopsies of the lung nodules show primary lung cancer with an interlobar metastasis, then the patient has stage IV lung cancer, and overall survival is usually measured in months to a couple of years, and less aggressive CRC management might be appropriate. If the PET scan shows suspected disease in other extra-thoracic and extra-abdominal sites, such as bone lesions, then these areas need to be biopsied before embarking on lung resections. Usually CT guided biopsies of suspected bone mets are safer and easier than lung resections. Who to operate on, and in which order to operate (bowel or lung first) can be tricky. Patient selection for lung surgery involves several factors. These include 1) exclusion of other sites of metastatic disease 2) adequate lung function for resection based on pulmonary function tests and clinical exam 3) ability to control intra abdominal disease. Excluding extra-thoracic and extra-colonic metastases is critical. Spread of CRC to sites other than the liver and lung, such as the bone, would preclude performing thoracic resections. If the only sites of disease are the bowel, liver, and lung, and the abdominal surgeons feel that curative resections can be performed on these two organs, then curative lung surgery is considered.(152, 153) In order to resect portions of the lung, the patient must have enough residual lung function not only to support life, but also allow for a quality of life acceptable to the patient. Pulmonary function tests are usually easy to obtain. We base our decision for resection on the FEV1 (forced expired volume in 1 second), the diffusion of carbon monoxide (DLCO), and the clinical exam. If after viewing the CT chest and deciding on the extent of resection, the predicted postoperative (ppo) FEV1 is > 0.8 L, then surgery is considered. If the predicted postoperative DLCO is >40% of predicted, then surgery is considered.(155) These formulas should by no means be followed blindly. Just, if not more, important is the clinical evaluation of the patient. As a general rule, if the patient can climb three flights of

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improved outcomes in colon and rectal surgery stairs without having to stop due to shortness of breath, then they should be able to tolerate a pneumonectomy or equivalent resection. I also ask if they can walk around the block without stopping. Usually the PFT numbers will support the patient’s answers on the clinical exam. Sometimes they don’t, and I tend to trust the clinical exam over the numbers. For example, we had a patient whose FEV1 and diffusion capacity were >100% of predicted. Based on those numbers a pneumonectomy should have been possible. When seen in clinic he could barely walk from the waiting room to the exam room due to dyspnea and desaturation. Conversely, one patient had a PFT FEV1 of 0.7 L, but biked 5 miles a day with her husband without oxygen. I based my decisions on the clinical evaluation, did not operate on the first patient, and successfully performed a lobectomy on the second patient. Some patients will be borderline resectable based on PFTs and clinical exam. A split perfusion V/Q scan can then be performed. With this test the nuclear medicine doctors can estimate which parts of the lungs are performing what percentage of the work. This allows for a more exact calculation of ppoFEV1. For example, if a tumor is obstructing a lobar bronchus, then the V/Q scan should show that that lobe is contributing almost nothing to the overall lung function, and resection can be performed with no decrease in PFTs. Operative Approach As mentioned above, part of the decision is how much lung needs to be taken out. Obviously, if we are aiming for cure, then all sites of pulmonary metastases need to be addressed. Metastatic disease is different than primary lung cancer. For lung cancer, anatomic resection is the gold standard (156), with lobectomy being preferred (unless pneumonectomy is required) over segmentectomy, and segmentectomy preferred over wedge resection. Metastectomies are the converse. Lung sparing is very important, especially since the chance for future metastases is high. Also, larger anatomic resections of metastases offer no survival advantage, so wedge resections with negative margins are adequate. Anatomic resections are considered when the size or position of the cancer precludes a wedge resection. Tumors on the periphery of the lung <3 cm in size can usually be excised by a wedge. Larger masses can sometimes be resected by a wedge, especially if in the inferior lingula. Large tumors, those positioned several centimeters deep to the visceral pleura, mid basilar tumors, or those near the hilum will probably require a segmentectomy, multiple segmentectomy (ex. basilar segmentectomy, lingular sparing left upper lobectomy), or lobectomy. Pneumonectomy will be described later. With this information a thoracic surgeon can estimate the percentage of overall lung to be resected, and calculate the ppoFEV1 and ppoDLCO. Once it has been decided that the patient could undergo lung surgery, the order of surgery is decided upon after discussion between the colon, hepatic, and lung surgeons. If the thoracic metastectomies can be performed with quick wedge resections with low morbidity, then I would operate first if my finding will change the other surgeons’ resections. If larger, more risky thoracic resections are needed (especially pneumonectomy), then I would prefer the abdominal surgeons to proceed and make sure that the primary tumor and intraabdominal metastases can be controlled first. If the resection pathology is favorable and the patient has recovered, then definitive lung resection is done. It is

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nice for the patient if combined surgery can be performed. For video-assisted thoracoscopic surgery (VATS) wedge resections I feel comfortable removing the thoracic disease and then letting the abdominal surgeons proceed at the same setting. The VATS approach allows for less pain and earlier mobility, and usually doesn’t hinder patient recovery from the laparotomy. If the lung surgery requires a thoracotomy, lobectomy, or pneumonectomy, I prefer not to operate at the same setting, as postoperative recovery becomes much more difficult for the patient. Video Assisted Thoracoscopic Surgery (VATS) A relatively new factor that has changed our approach to metastectomies is the VATS, or video assisted thoracoscopic surgery, technique. Traditionally lung resection required a lateral or posterolateral thoracotomy. These incisions are painful, usually involve transecting the latissimus muscle, require several days of hospital stay to recover and several weeks or months as an outpatient to recover, and frequently require epidural placement preoperatively for pain control. As the size of the thoracotomy increases, the chance for chronic pain increases as well. If the patient recurs on the ipsilateral side, then repeat thoracotomies are needed. The amount of scar tissue in the thorax increases after larger dissections, and any redo operation runs the risk of having to deal with this. Sometimes the lung is so scarred in that exposure and resection are not possible. Usually, however, the surgery just takes longer as the scar tissue is dealt with, and may require even further extension of the old incision to facilitate exposure. Just like surgery in other areas of the body, the longer and more difficult the dissection, the greater the risk of complications. With VATS, wedge resections require only three incisions 10 mm or less in length. Pain is managed more easily and discharge is usually anticipated in 1 to 2 days postop. Changing to lobectomy only needs one of those incisions to be lengthened to a 3–4 cm utility incision. The latissimus and serratus muscles are spared, and no rib notching is needed. We no longer use epidurals, and instead leave a PCA (patient controlled analgesia) for one day as well as placing a marcaine infuser catheter in the intercostal space and subcutaneous tissue of the utility incision. The marcaine pump we use will last for about three days. On post op day 1 the PCA is discontinued and oral pain meds are started. Discharge is anticipated on postop day 4–5 to home without any chest tubes. Since the amount of intercostal muscle being transected during VATS surgery is minimal, chest wall adhesions with redo operations is usually minimal, especially after wedge resections. Even multiple surgeries on the same side can be managed with only a short increase in operative time to take down adhesions, and often the same incisions can be used. Expected Outcomes Now that we know how to work up a patient for lung surgery, decide if they can tolerate lung surgery, and understand the latest approach to lung resections, we need to review our chances for helping these people survive metastatic CRC. We will review a select number of studies. The Mayo Clinic, Rochester, reported in 1992 their experience with 139 consecutive lung resections for metastatic CRC.(154) Resections were performed via wedge resection in 68, lobectomy in 53, and more extensive resections including pneumonectomy in 18. During follow up, 19 patients recurred in the lung and needed repeat resections. Median follow up was 7 years (range 1–20.4). Overall

indications and outcomes for treatment of recurrent rectal cancer 5- and 20- year survival was 30.5% and 16.2%, respectively. Five year survival for solitary metastases was 36.9% compared to 19.3% for patients with two lesions. For those who recurred and required repeat resection, 5- year survival after the second resection was just over 30%. Twenty patients had extrapulmonary metastases as well as lung lesions. Survival after resection for these patients was also 30%. Interestingly, they noted that patients with prethoracotomy CEA levels >5 ng/ml had much poorer survival at 5 years compared to lower CEA level patients (16% vs. 46.8%). This same poor prognostic indicator has been realized by others.(151, 157) Based on their experience, they supported resection of intra- and extrapulmonary metastases, even if they recur. Irshad et al. reported on a 25 year experience, from 1975 to 1999, in which 49 patients underwent curative colorectal surgery followed by curative thoracic metastectomies. Overall survivals at 5, 10, and 15 years were 55%, 40%, and 25%. Patients with solitary metastases did better, but multiple metastectomies still had a survival advantage.(158) One area of debate is how aggressive of a resection should be performed. More precisely, should a patient undergo pneumonectomy for stage IV colorectal cancer? Pneumonectomy alone carries a higher mortality than lesser resections, with an operative mortality around 7%. In centers accustomed to taking care of these patients, and surgeons who specialize in this procedure, the mortality is lower. Hendricks et al. looked at 10 cases of pneumonectomy for metastectomy and found 5 year survival of around 45%.(159) Koong et al. reviewed 133 patients who underwent pneumonectomy or completion pneumonectomy for metastases. Of those patients who underwent R0 resection, operative mortality was 3% and 5 year survival was 30%.(160) It is our practice to consider pneumonectomy for metastatic CRC if the abdomen is cleared of disease, there is no sign of extrathoracic metastases, and the surgical risk is acceptable. REFERENCES    1. Obias VR, Reynolds HL. Multidisciplinary teams in the management of rectal cancer. Clin Colon Rectal Surg 2007; 20: 143–7.    2. Heriot AG, Byne CM, P Lee, et al. Extended radical resection: the choice for locally recurrent rectal cancer. Dis Colon Rectum 2008; 51(3): 284–91.    3. Watson AJ, Lolohea S,Robertson GM, et al. The role of positron emission tomography in the management of recurrent colorectal cancer: a review. Dis Colon Rectum 2007; 50(1): 102–14.    4. Beets-Tan RG, Beets GL, Borstlap AC, et al. Preoperative assessment of local tumor extent in advanced rectal cancer: CT or high-resolution MRI? Abdom Imaging 2000; 25(5): 533–41.    5. de Wilt JHW, Vermaas M, Ferenschild FT, et al. Management of locally advanced primary and recurrent rectal cancer. Clin Colon Rectal Surg 2007; 20: 255–64.    6. Messiou C, Chalmers A, Boyle K, et al. Surgery for recurrent rectal carcinoma: The role of preoperative magnetic resonance imaging. Clin Radiol 2006; 61(3): 250–8.    7. Messiou C, Chalmers A, Boyle K, et al. Pre-operative MR assessment of recurrent rectal cancer. Br J Radiol 2008; 81(966): 468–73.    8. Wu J. Rectal cancer staging. Clin Colon Rectal Surg 2007; 20: 148–57.

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111. Bilchik AJ, Poston G, Curley S, et al. Neoadjuvant chemotherapy for metastatic colon cancer: a cautionary note. J Clin Oncol 2005; 23(36): 9073–8. 112. Pawlik TM, Choti M. Preoperative chemotherapy for colorectal liver metastases: impact on hepatic histology and postoperative outcome. J Gastrointest Surg 2007; 11(7): 860–8. 113. Vauthey JN, Pawlik TM, Ribero D, et al. Chemotherapy regimen predicts steatohepatitis and an increase in 90-day mortality after surgery for hepatic colorectal metastases. J Clin Oncol 2006; 24(13): 2065–72. 114. Kesmodel SB, Ellis LM, Lin E, et al. Preoperative bevacizumab does not significantly increase postoperative complication rates in patients undergoing hepatic surgery for colorectal cancer liver metastases. J Clin Oncol 2008 26:5245-60. Epub Oct 14, 2008. 115. Zorzi D, Laurent A, Pawlik TM, et al. Chemotherapyassociated hepatotoxicity and surgery for colorectal liver metastases. Br J Surg 2007; 94(3): 274–86. 116. Abulkhir A, Limongelli P, Healey A, et al. Preoperative portal vein embolization for major liver resection: a meta-analysis. Ann Surg 2008; 247(1): 49–57. 117. Covey AM, Brown K, Jarnagin W, et al. Combined portal vein embolization and neoadjuvant chemotherapy as a treatment strategy for resectable hepatic colorectal metastases. Ann Surg 2008; 247(3): 451–5. 118. Jaeck D, Oussoultzoglou E, Rosso E, et al. A two-stage hepatectomy procedure combined with portal vein embolization to achieve curative resection for initially unresectable multiple and bilobar colorectal liver metastases. Ann Surg 2004; 240(6): 1037–51. 119. Madoff DC , Hicks ME, Abdalla EK, et al. Portal vein embolization with polyvinyl alcohol particles and coils in preparation for major liver resection for hepatobiliary malignancy: safety and effectiveness–study in 26 patients. Radiology 2003; 227(1): 251–60. 120. Ravikumar TS, Kane R, Cady B, et al. A 5-year study of cryosurgery in the treatment of liver tumors. Arch Surg 1991; 126(12): 1520–3. 121. Ravikumar TS, Kan R, Cady B, et al. Hepatic cryosurgery with intraoperative ultrasound monitoring for metastatic colon carcinoma. Arch Surg 1987; 122(4): 403–9. 122. Ravikumar TS, Steele G, Kane R, et al. Experimental and clinical observations on hepatic cryosurgery for colorectal metastases. Cancer Res 1991; 51(23 Pt 1): 6323–7. 123. Yan TD, Padang R, Morris DL. Longterm results and prognostic indicators after cryotherapy and hepatic arterial chemotherapy with or without resection for colorectal liver metastases in 224 patients: longterm survival can be achieved in patients with multiple bilateral liver metastases. J Am Coll Surg 2006; 202(1): 100–11. 124. Yan TD, Padang R Xia H, et al. Management of involved or close resection margins in 120 patients with colorectal liver metastases: edge cryotherapy can achieve long-term survival. Am J Surg 2006; 191(6): 735–42. 125. Rossi S, Stasi M, Buscarini E, et al. Percutaneous RF interstitial thermal ablation in the treatment of hepatic cancer. AJR Am J Roentgenol 1996; 167(3): 759–68.

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143. Takahashi S, Nagai K, Saito N, et al. Multiple resections for hepatic and pulmonary metastases of colorectal carcinoma. Jpn J Clin Oncol 2007; 37(3): 186–92. 144. Adam R, Pascal G, Castaing D, et al. Tumor progression while on chemotherapy: a contraindication to liver resection for multiple colorectal metastases? Ann Surg 2004; 240(6): 1052–61. 145. Bismuth H, Adam R, Levi F, et al. Resection of nonresectable liver metastases from colorectal cancer after neoadjuvant chemotherapy. Ann Surg 1996; 224(4): 509–20. 146. Fong Y, Cohen AM, Fortner JG, et al. Liver resection for colorectal metastases. J Clin Oncol 1997; 15(3): 938–46. 147. Kattan MW, Gonen M, Jarnagin WR, et al. A nomogram for predicting disease-specific survival after hepatic resection for metastatic colorectal cancer. Ann Surg 2008; 247(2): 282–7. 148. Zakaria S, Donohue JH, Que FG, et al. Hepatic resection for colorectal metastases: value for risk scoring systems? Ann Surg 2007; 246(2): 183–91. 149. Poston GJ, Figueras J, Giuliante F, et al. Urgent need for a new staging system in advanced colorectal cancer. J Clin Oncol 2008; 26(29): 4828–33. 150. Blalock A. Recent Advances in Surgery. N Engl J Med 1944; 231: 261–7. 151. Girard P, Ducreux M, Baldeyrou P, et al. Surgery for lung metastases from colorectal cancer: analysis of prognostic factors. J Clin Oncol 1996; 14(7): 2047–53. 152. Headrick JR, Miller DL, Nagorney DM, et al. Surgical treatment of hepatic and pulmonary metastases from colon cancer. Ann Thorac Surg 2001; 71(3): 975–9. 153. Labow DM, Buell JE, Yoshida A, et al. Isolated pulmonary recurrence after resection of colorectal hepatic metastases– is resection indicated? Cancer J 2002; 8(4): 342–7. 154. McAfee MK, Allen MS, Trastek VF, et al. Colorectal lung metastases: results of surgical excision. Ann Thorac Surg 1992; 53(5): 780–5. 155. Colice GL, Shafazand S, Griffin JP, et al. Physiologic evaluation of the patient with lung cancer being considered for resectional surgery: ACCP evidenced-based clinical practice guidelines (2nd edition). Chest 2007; 132(3 Suppl): 161S–77S. 156. Ginsberg RJ, Rubinstein LV. Randomized trial of lobectomy versus limited resection for T1 N0 non-small cell lung cancer. Lung Cancer Study Group. Ann Thorac Surg 1995; 60(3): 615–22. 157. Saito Y, Omiya H, Kohno K, et al. Pulmonary metastasectomy for 165 patients with colorectal carcinoma: A prognostic assessment. J Thorac Cardiovasc Surg 2002; 124(5): 1007–13. 158. Irshad K, Ahmad F, Morin JE, et al. Pulmonary metastases from colorectal cancer: 25 years of experience. Can J Surg 2001; 44(3): 217–21. 159. Hendriks JM, van Putte B, Romjin S, et al. Pneumonectomy for lung metastases: report of ten cases. Thorac Cardiovasc Surg 2003; 51(1): 38–41. 160. Koong HN, Pastorino U, Ginsberg RJ. Is there a role for pneumonectomy in pulmonary metastases? International Registry of Lung Metastases. Ann Thorac Surg 1999; 68(6): 2039–43.

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29 Chemotherapy for colon and rectal cancer Liliana Bordeianou and Judith L Trudel

Challenging Case A 56-year-old man presented with a 5 cm rectal cancer. It was located posteriorally at 8 cm from the anal verge. The preop ultrasound suggested a T3N1 tumor. The patient received preoperative chemoradiotherapy. He had a superb clinical response with tumor shrinkage. Six weeks after completing the therapy, the patient underwent a low anterior resection with a diverting loop ileostomy. The final pathology was a T1N0 with five negative lymph nodes identified. All margins were negative. Should the patient receive postoperative chemotherapy? Case Management There is little data on which to base this clinical decision. Most practioneers lean toward recommendations for postoptherapy based on the pretreatment clinical stage if the patient receives neoadjuvant therapy. In a good risk patient, most would recommend 6 months of postoperative adjuvant chemotherapy. Introduction Colorectal cancer (CRC) is the third most common cancer diagnosed in men and women in the United States. Approximately 148,810 new cases of colon and rectal cancer were reported in 2007, with an estimated 49,960 deaths attributed to it.(1) This is higher than the number of deaths attributed to pancreatic cancer, liver and intrahepatic bile duct cancer or esophageal cancer. While surgery remains the mainstay of treatment for this common disease, it is the recent noteworthy changes in the indications for chemotherapy, the timing strategy as far as chemotherapy administration and the actual therapeutic regimens used to treat advanced colon and rectum cancers that may provide the next step toward the improvement in the survival rates of these patients. Chemotherapy Agents or Combinations Most Commonly Used Against Colorectal Cancer 5-FU with Either Leucovorin or Levamisole Since its original use in the 1950s, 5-FU remains one the oldest chemotherapeutic agents used today to target colorectal cancer. 5-FU inhibits DNA synthesis via blockage of thymidylate synthase. At first used alone, and then in combination with levamisole, 5-FU/levamisole combination was noted to significantly decrease recurrence rates and improve overall survival, particularly in Dukes’C patients.(2) This observation was subsequently confirmed in a large study of 971 patients with stage III and IV disease (intergroup 0035) which in 1990 showed that this drug combination reduced the risk of cancer recurrence by 41% and the overall death by 33 % in this group of patients.(3) Given these results, this drug combination was regarded as gold standard therapy for CRC till 1996, when an even more effective regimen using 5-FU in combination with leucovorin (folinic acid) was described.

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Leucovorin is a 5-FU biomodulator. Leucovorin and 5-FU form a stable ternary complex with thymydylate synthetase, permitting prolonged inhibition of the enzyme by 5-FU. Its applicability to stage II and stage II disease was confirmed by the IMPACT (International Multicenter Pooled Analyses of Colon Cancer Trials) study of 1,526 patients in 1995, which showed that 5-FU/leucovorin increased the 3-year disease free survival from 62% to 71% while overall survival increased from 78% to 83%.(4) The NSAPB C-03 randomized trial of 1,081 stage II and stage III patients comparing MOF (semustine, vincristine and 5-FU) to 5-FU/leucovorin had documented a similar advantage of 5-FU/leucovorin, with a 3 year disease-free survival increase from 64% to 73% and an overall survival increase from 77% to 84%.(5) The relative merits of levamisole and leucovorin as modulators of 5-FU-based adjuvant chemotherapy, and the optimal duration of treatment were documented in several studies between 1998 and 2000. The NCCTG/NCIC (National Cancer Institute of Canada) study of 915 patients compared 6 months 5-FU/leucovorin; 6 months 5-FU/ leucovorin/levamisole; 1 year 5-FU/levamisole; and 1 year 5-FU/leucovorin/levamisole.(6) Triple therapy for 6 months was as effective as 12 months; and 6-month triple therapy provided superior 5-year overall survival and disease-free survival compared to 5-FU/levamisole.(6) The Intergroup trial 0089 of 3,759 patients compared 1 year 5-FU/levamisole; 5-FU/high-dose leucovorin for 32 weeks; 5-FU/ low-dose leucovorin for 6 cycles; and 5-FU/low-dose leucovorin/ levamisole for 6 cycles.(7) There were no differences between the four treatment arms with regards to 5-year disease-free and overall survival. The NSABP CO-4 study essentially confirmed these results. (8) The QUASAR Collaborative Group study confirmed the survival advantage provided by leucovorin modulation over levamisole.(9) Based on the results of these studies, the new standard for treatment was changed to 6 months of adjuvant chemotherapy with 5-FU/ leucovorin for stage III, node-positive disease. Until recently, this course of therapy was the standard of care for patients with advanced colorectal cancer. However, with increasing understanding of the molecular basis of cancer and the development of biologic-based therapy, chemotherapy for CRC has evolved once more and a variety of new agents are now available to treat this disease. Oxaliplatin-Containing Regimens (FOLFOX, XELOX) Oxaliplatin inhibits DNA replication through creation of bulky DNA adducts. It was first introduced to treat patients with recurrent or metastatic colorectal cancer that was otherwise unresectable. A study of 795 patients enrolled by Intergroup N9741 compared FOLFOX (oxaliplatin and infused fluorouracil plus leucovorin) to either IFL (irinotecan and bolus fluorouracil plus leucovorin) or IROX (irinotecan and oxaliplatin) to show that patients treated with FOLFOX had an increased median survival of 19.5 months (compared to 15 and 17.4 months in

chemotherapy for colon and rectal cancer the control arms) and an increased time to progression: 8.7 months as compared to 6.9 and 6.5 months in the two control arms.(10) Given the improved response rates with FOLFOX in metastatic disease, the MOSAIC trial of 2,246 patients compared this regimen to the standard 5-FU leucovorin regimen in the adjuvant setting of resected colon cancer. After a median follow-up of 56.2 months, the 3 year diseasefree survival in the FOLFOX group was 76.4% (compared to 69.8% observed in 5-FU/leucovorin group).(11) On the strength of these results, FOLFOX is now the most popular first-line therapy for the adjuvant treatment of resected CRC and for metastatic CRC. In patients interested in avoiding IV infusions, the combination of capecitabine and oxaliplatin (XELOX) may be used. Capecitabine is the prodrug to 5-FU, and is administered orally. Irinotecan-Containing Regimens (FOLFIRI, IFL, IROX) Irinotecan inhibits DNA replication and transcription via topoisomeraze blockade. Irinotecan has been shown to have activity against CRC, though its effects are less pronounced than those of oxaliplatin. IFL therapy (5-FU, leucovorin and irinotecan) has been shown to be superior to 5FU/leucovorin therapy alone in patients with metastatic colorectal cancer.(12) However, the N9741 Intergroup trial described above showed that patients treated with FOLFOX had superior results to those treated with FOLFIRI (5-FU and irinotecan), or IROX(irinotecan and oxaliplatin).(10) Based on the results of this and other studies irinotecan containing combinations are now mostly used as second line therapy.(13) Bevacizumab (AVASTIN®) Bevacizumab (a monoclonal antibody that binds to the vascular endothelial growth factor (VEGF) ligand) is one of the first biologic

therapy agents shown to be effective against CRC. Bevacizumab, which blocks angiogenesis, was first found to improve efficacy of FOLFOX alone in patients with metastatic disease: the median duration of survival for the group treated with FOLFOX and bevacizumab was 12.9 months compared with 10.8 months for the group treated with FOLFOX alone.(14, 15) Additional information on the feasibility and efficacy of bevacizumab in combination with FOLFOX or other oxaliplatin combinations was gleaned in the TREE-2 trial, where the percentages of patients with progressive disease decreased substantially in all arms when bevacizumab was added.(16) Cetuximab (ERBITUX®) Cetuximab (a monoclonal antibody blocking epidermal growth factor (EGFR) is currently approved only as therapy as a single agent or in combination with irinotecan for patients with previously treated advanced colorectal cancer. A number of recently published trials suggested that patients treated with cetuximab have a longer time to disease progression, and this effect is augmented with addition of bevacizumab.(17) Indications and Timing of Chemotherapy for Colorectal Cancer Adjuvant Chemotherapy for Stage III and Stage IV Colon Cancer While surgical resection is the only curative treatment for localized colon cancer, the 5-year survival rates vary from 93% in the patients with Stage I disease to 44% in patients with Stage III disease (Table 29.1). For the patients who have undergone potentially curative resection, disease recurrence is thought to derive from clinically occult micrometastases. The goal of

Table 29.1  American Joint Committee on Cancer (AJCC) colon cancer staging versus survival (37). Stage

T Stage

N Stage

M Stage

5-year Survival

I

T1 (tumor invades submucosa) T2 (tumor invades muscularis propria)

N0 (no regional lymph nodes metastasis)

M0 (no evidence of distant metastasis)

93%

IIA

T3 (tumor invades through muscularis propria into subserosa or nonperitonealized pericolic tissues)

N0

M0

85%

IIB

T4 (tumor directly invades into other organs and/or perforates visceral peritoneum)

N0

M0

72%

IIIA

T1 T2

N1 (metastasis to 1–3 regional lymph nodes)

M0

83%

IIIB

T3 T4

N1

M0

64%

IIIC

Any T

N2 (metastasis to four or more regional lymph nodes)

M0

44%

IV

Any T

Any N

M1 (distant metastasis)

8%



improved outcomes in colon and rectal surgery postoperative (adjuvant) chemotherapy is to eradicate these micrometastases. Adjuvant chemotherapy for colon cancer has been studied for at least 40 years. Interestingly, 5-FU monotherapy did not improve 5-year survival following curative resection.(18) However, the discovery of modulators of 5-FU activity and of the effects of combination regimens on survival reignited the interest in adjuvant chemotherapy. The first large-scale trial to demonstrate a survival benefit for adjuvant chemotherapy in colon cancer, National Surgical Adjuvant Breast and Bowel project (NSABP) C-01 included 1,166 patients with Dukes’ B or C colon cancer.(19) The patients randomized to adjuvant MOF chemotherapy instead of surgery alone had significant improvement in their 5-year overall survival. These improvements became even more pronounced as advances in chemotherapy described earlier and postoperative (adjuvant) systemic therapy has become routine and standard for node positive or metastatic disease. Clinical data indicates that access to a multidrug regimen consisting of two or more of the agents discussed earlier (in addition to 5-FU therapy) has almost doubled median survival in the patients with advanced colorectal cancer from 10–12 months to more than 20 months. Adjuvant Chemotherapy for Stage II Colon Cancer In contrast to the clear benefit of adjuvant chemotherapy for patients with node-positive disease, its role in resected stage II colon cancer remains controversial. While a number of clinical trials have included stage II patients and have suggested a benefit from adjuvant therapy, none of these have reached statistical significance. Several metaanalyses have been performed to evaluate this question further. An NSABP analysis of the data pooled from the adjuvant C-01, C-02, C-03 and C-04 trials of 3,820 patients (1,556 with T3N0 disease) suggested that the relative reduction in recurrence and mortality from adjuvant therapy for patients with resected T3N0 colon cancer was comparable to that seen in patients with node-positive disease. (20) In contrast, a 2004 systematic review by the Ontario Cancer Care Program did not find a statistically significant improvement in survival in the T3N0 patients treated with at least one 5-FU chemotherapy regimen after surgery.(21) In hopes of settling this debate, a panel of the American Society of Clinical Oncology reviewed all the pertinent information in regards to this issue.(22) This panel concluded that routine use of adjuvant chemotherapy for medically fit patients with stage II colon cancer is not recommended. Parenthetically, the panel also felt that selected patients with stage II disease—such as patients with inadequately sampled nodes, T4 lesions, perforation, or poorly differentiated histology—could still be considered for adjuvant therapy.(22, 23) The identification of patients with stage II colon cancer who might benefit from adjuvant chemotherapy is an area of ongoing research. The prognostic value of additional molecular markers, such as microsatellite instability and loss of 18Q allele is being investigated. (http://cancer.gov). Neoadjuvant Chemoradiotherapy for T3 or Node-Positive Rectal Cancer The management of rectal cancer is radically different from the management of colon cancer. While recommendations for adjuvant postoperative therapy for advanced colon cancer are based



on the pathological stage revealed by the surgical specimen, rectal cancer staging determines initial management. This, after much debate, is based on conclusive evidence that has clearly shown neoadjuvant preoperative therapy to improve local control, diseasefree survival, and overall survival compared to surgery alone or to postoperative adjuvant therapy. The Swedish Rectal Cancer Trial examined whether neoadjuvant preoperative radiation therapy was of benefit to patients with advanced rectal cancer. The study randomly assigned 1,168 patients to receive or not receive radiation therapy prior to surgery. After 5 years, preoperative radiation therapy was associated with significant improvements in both local control (89% vs. 73%) and overall survival (58% vs. 48%).(24) The German Rectal Cancer Trial examined whether radiation is more beneficial before or after surgery. The study randomly assigned 823 patients with clinically staged T3/T4 or node-positive rectal cancer to either neoadjuvant or adjuvant chemoradiotherapy. With a 46 month median follow-up, preoperative chemoradiotherapy was associated with a significantly lower local recurrence rate (6% vs. 13%), though the 5-year disease-free and overall survival rates were similar.(25) These two studies made preoperative radiotherapy for advanced rectal cancer the standard of care. At least two randomized trials have directly assessed the potential benefits of concurrent chemotherapy with neoadjuvant radiotherapy. A European trial randomly assigned 762 patients with T3/4 rectal cancer within reach of the digital rectal exam to either preoperative radiotherapy alone or preoperative chemoradiotherapy. At a median 69 month follow-up, the combined modality group had lower local recurrence rates (8.1% vs. 16.5 %), but the rate of sphincter preservation surgery and 5-year overall survival rates were similar.(26) Another study, EORTC 22921 showed a similar benefit with chemoradiotherapy enhancing local control in comparison to radiotherapy alone.(27) Based on these studies, neoadjuvant chemoradiotherapy is generally considered in all patients with T3 N0 and node positive tumors of any T stage. Stage of the disease determines the need for neoadjuvant therapy. Because of this, the importance of pretreatment staging of rectal tumors becomes paramount and cannot be overemphasized. The standard of care now dictates that all patients with rectal cancer should undergo a staging endorectal ultrasound or pelvic MRI to determine initial management. Tumors penetrating into perirectal fat and/or lymph nodes should undergo neoadjuvant chemoradiotherapy. Tumors that do not penetrate through muscularis propria (T1-2, N0) are candidates for initial surgical resection. If the final pathological stage confirms the stage suspected on imaging, no further chemotherapy (and/or radiation) is indicated. However, if the final pathology reveals penetration into perirectal fat or into the lymph nodes, postoperative chemoradiotherapy is indicated. Adjuvant Chemotherapy Alone for T3 or Node-Positive Rectal Cancer The benefit of 5-FU based postoperative chemotherapy in patients undergoing chemoradiotherapy has not been studied in prospective randomized trials. However, in EORTC trial 22921, patients who had received preoperative radiotherapy with or without chemotherapy were then further randomized to postoperative

chemotherapy for colon and rectal cancer chemotherapy versus no further therapy.(27) In the entire group, there were trends favoring adjuvant chemotherapy in both 5-year progression free survival (58% vs. 52%), and overall survival (67% vs. 63%), but the trends were not statistically significant, Nevertheless, these results are frequently quoted as justification of adjuvant chemotherapy for patients treated with or without preoperative chemoradiotherapy. Further information of the benefits of postoperative chemotherapy are expected from the multicentre British CHRONICLE trial.(28) Side Effects of Chemotherapy The benefits of modern chemotherapy with regards to its ability to delay disease progression and improve survival in patients with advanced colon and rectal cancer are unquestionable. Nonetheless, these benefits should be balanced against individual patient tolerance to the side effects of chemotherapy (Table 29.2), as this may impact therapeutic effectiveness. The elderly and the medically compromised patients represent a group at particular risk. Very few elderly patients or patients with renal/hepatic failure or other major comorbidities have been enrolled in clinical trials; the choices of therapeutic regimens in these subgroups should be tailored to individual patients. 5-FU/leucovorin alone is fairly well tolerated, and the most commonly described side effects are those of diarrhea,

Table 29.2  Side Effects and Mechanism of Action of Commonly Used Chemotherapeutic Agents Chemotherapy Agent

Mechanism of Action

Common Side-Effects

5-FU

Inhibits DNA synthesis via blockage of thymidylate synthase

Heartburn, nausea, vomiting, anorexia, stomatitis, esophagitis, diarrhea, myelosuppression, cardiac toxicity

Oxaliplatin

Inhibits DNA replication through creation of bulky DNA adducts

Peripheral neuropathy, anemia, thrombocytopenia, neutropenia, nausea, diarrhea, vomiting, abdominal pain, fatigue

Irinotecan

Inhibits DNA replication and transcription via topoisomeraze blockade

Alopecia, diarrhea, nausea, emesis, severe myelosupression, colitis, gastrointestinal ulceration, gastrointestinal bleeding, ileus

Bevacizumab (Avastin®)

A monoclonal antibody that binds to the vascular endothelial growth factor (VEGF) ligand and inhibits tumor blood supply growth

Alopecia, thrombosis, bleeding, hyperkalemia, hypertension, abdominal pain, anorexia, vomiting, diarrhea, neutropenia, delayed wound healing and wound dehiscence, bowel perforation

Cetuximab (Erbitux®)

A monoclonal antibody that blocks epidermal growth factor (EGFR) and decreases tumor growth

Fatigue, confusion, pruritis, insomnia, abdominal pain, nausea, vomiting, diarrhea,weakness, lung disease, dyspepsia

stomatitis, vomiting and nasea. These side effects become much more pronounced when mutidrug chemotherapy regimens are used. For example, addition of oxaliplatin to 5-FU, which is the most common first line chemotherapy regimen currently used in the US to treat colorectal cancer (FOLFOX), leads to an increased rate of diarrhea, nausea and vomiting, as well as alopecia. In addition, the rates of significant neutropenia become relatively high. One of the clinically relevant side effect of oxaliplatin-based chemotherapy is a late-onset predominantly sensory neuropathy with may require drug discontinuation despite ongoing tumor response. Ultimately, more than 50 percent of patients receiving FOLFOX discontinue treatment for reasons other than disease progression.(29) Multidrug combinations adding irinotecan, or bevacizumab to the standard 5-FU can cause serious toxic events, mainly severe hematological toxicity, diarrhea, thrombotic events, and neurosensory disorders.(30) The 5-FU, leucovorin, irinotecan, plus bevacuzimab regimen especially, while having the highest probability of improving survival, might also lead to significant adverse effects to as many as 84.9% of patients, including a 1.5% chance of gastrointestinal perforation.(30) While these side effects are temporary in patients undergoing adjuvant treatment for nonmetastatic disease, their effect on quality of life becomes quite important when the treatments are continuous and indefinite, as is the current practice in the patients with metastatic disease. One potential way of reducing treatmentrelated side effects in this cohort is via a “chemotherapy holiday”, but the impact of a completely chemo-free interval on long term survival is of significant concern. Two European phase II trials, OPTIMOX1 (which compared continuous FOLFOX versus maintenance chemotherapy with 5-FU/leucovorin) and OPTIMOX2 (which compared maintenance chemotherapy using a nonoxaliplatin regimen versus a totally chemotherapy free interval) were designed to address some of these concerns.(31, 32) Their results unfortunately suggested that a full break in therapy resulted in a decrease in overall survival and that some form of maintenance treatment is preferable to chemotherapy-free intervals. Future Directions One of the major drawbacks of the current chemotherapy regimens for colorectal cancer is our inability to identify before treatment which patient will respond to a particular combination of chemotherapy drugs. Knowledge of tumor gene expression and other biomarkers will hopefully provide clues and inroads in this direction. Microarray profiling of gene expression in colorectal cancer patients has already been shown to stratify risk and predict lymph node involvement.(33) Just like in patients with breast cancer, patients with CRC might soon be screened in a prospective fashion to determine those with stage III disease that are unlikely to recur or those who may be resistant to a particular drug regimen. A promising area for colorectal cancer treatment is immunotherapy. The goal of cancer immmunotherapy is to stimulate the body’s immune system in order to improve host defense mechanisms against growing tumors, through either cell mediated or humoral immunity pathways. Over 25 different vaccines, virusmodified tumor cells, gene-modified tumor cells, tumor-antigen derived peptides, tumor lysates, proteins or carbohydrates have



improved outcomes in colon and rectal surgery been studied in Phase I and II studies. Three large studies looking at the immune stimulation with autologous irradiated tumor vaccine plus BCG in colorectal cancer patients suggest that this approach may have merits. For example, one study randomized 98 patients with colon or rectal cancer treated surgically to vaccination with autologous irradiated tumor plus BCG versus placebo. While the study did not find a significant difference in the outcomes between the two arms, a subset analysis of the colon cancer patients did show an improvement in disease-free survival.(34) Similarly, Eastern Cooperative Oncology Group (ECOG) randomized stage II and II colon cancer patients to surgery alone versus surgery and vaccine and found that patients with a marked delayed cutaneous hypersensitivity response had a trend toward better disease-free and overall survival.(35) Finally a study of 244 patients with colon cancer randomized to receive a postoperative vaccine showed that the overall risk for recurrence was decreased by 44% in all vaccinated patients, with a 61% reduction in stage II patients.(36)

  9.

10.

11.

12.

13. Conclusion In the past 20 years, advances in the adjuvant treatment of colon and rectal cancer have significantly increased the rates of diseasefree and overall survival, increased survival rates in metastatic disease, and decreased the rates of recurrence. Ongoing research focuses on developing more potent chemotherapeutic agents and on identifying patients who may best benefit from those advances. References   1. Jemal A, Siegel R, Ward E et al. Cancer statistics, 2008. CA Cancer J Clin 2008; 58(2): 71–96.   2. Laurie JA, Moertel CG, Fleming TR et al. Surgical adjuvant therapy of large-bowel carcinoma: an evaluation of levamisole and the combination of levamisole and fluorouracil. The North Central Cancer Treatment Group and the Mayo Clinic. J Clin Oncol 1989; 7(10): 1447–56.   3. Moertel CG, Fleming TR, Macdonald JS et al. Levamisole and fluorouracil for adjuvant therapy of resected colon carcinoma. N Engl J Med 1990; 322(6): 352–8.   4. Efficacy of adjuvant fluorouracil and folinic acid in colon cancer. International Multicentre Pooled Analysis of Colon Cancer Trials (IMPACT) investigators. Lancet 1995; 345(8955): 939–44.   5. Wolmark N, Rockette H, Fisher B et al. The benefit of leucovorin-modulated fluorouracil as postoperative adjuvant therapy for primary colon cancer: results from National Surgical Adjuvant Breast and Bowel Project protocol C-03. J Clin Oncol 1993; 11(10): 1879–87.   6. O’Connell MJ, Laurie JA, Kahn M et al. Prospectively randomized trial of postoperative adjuvant chemotherapy in patients with high-risk colon cancer. J Clin Oncol 1998; 16(1): 295–300.   7. Haller DG, Catalano PJ, Macdonald JS et al. Phase III study of fluorouracil, leucovorin, and levamisole in high-risk stage II and III colon cancer: final report of Intergroup 0089. J Clin Oncol 2005; 23(34): 8671–8.   8. Wolmark N, Rockette H, Mamounas E et al. Clinical trial to assess the relative efficacy of fluorouracil and leucovorin, fluorouracil and levamisole, and fluorouracil, leucovorin,

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chemotherapy for colon and rectal cancer 22. Benson AB 3rd, Schrag D, Somerfield MR et al. American Society of clinical oncology recommendations on adjuvant chemotherapy for stage II colon cancer. J Clin Oncol 2004; 22(16): 3408–19. 23. Andre T, Sargent D, Tabernero J et al. ����������������������� Current issues in adjuvant treatment of stage II colon cancer. Ann Surg Oncol 2006; 13(6): 887–98. 24. Improved survival with preoperative radiotherapy in resectable rectal cancer. Swedish Rectal Cancer Trial. N Engl J Med 1997; 336(14): 980–7. 25. Sauer R, Becker H, Hohenberger W et al. Preoperative versus postoperative chemoradiotherapy for rectal cancer. N Engl J Med 2004; 351(17): 1731–40. 26. Gerard JP, Conroy T, Bonnetain F et al. Preoperative radiotherapy with or without concurrent fluorouracil and leucovorin in T3-4 rectal cancers: results of FFCD 9203. J Clin Oncol 2006; 24(28): 4620–5. 27. Bosset JF, Calais G, Mineur L et al. Enhanced tumorocidal effect of chemotherapy with preoperative radiotherapy for rectal cancer: preliminary results–EORTC 22921. J Clin Oncol 2005; 23(24): 5620–7. 28. Glynne-Jones R, Meadows H, Wood W. Chemotherapy or no chemotherapy in clear margins after neoadjuvant chemoradiation in locally advanced rectal cancer: CHRONICLE. A randomised phase III trial of control vs. capecitabine plus oxaliplatin. Clin Oncol (R Coll Radiol) 2007; 19(5): 327–9. 29. Seymour MT, Maughan TS, Ledermann JA et al. Different strategies of sequential and combination chemotherapy for patients with poor prognosis advanced colorectal cancer

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(MRC FOCUS): a randomised controlled trial. Lancet 2007; 370(9582): 143–52. Hurwitz H, Fehrenbacher L, Novotny W et al. Bevacizumab plus irinotecan, fluorouracil, and leucovorin for metastatic colorectal cancer. N Engl J Med 2004; 350(23): 2335–42. Tournigand C, Cervantes A, Figer A et al. OPTIMOX1: ���������������� a randomized study of FOLFOX4 or FOLFOX7 with oxaliplatin in a stop-and-Go fashion in advanced colorectal cancer–a GERCOR study. J Clin Oncol 2006; 24(3): 394–400. Andre T, Tournigand C, Mineur L et al. Phase II study of an optimized 5-fluorouracil-oxaliplatin strategy (OPTIMOX2) with celecoxib in metastatic colorectal cancer: a GERCOR study. Ann Oncol 2007; 18(1): 77–81. Croner RS, Peters A, Brueckl WM et al. Microarray versus conventional prediction of lymph node metastasis in colorectal carcinoma. Cancer 2005; 104(2): 395–404. Hoover HC Jr, Brandhorst JS, Peters LC et al. Adjuvant active specific immunotherapy for human colorectal cancer: 6.5year median follow-up of a phase III prospectively randomized trial. J Clin Oncol 1993; 11(3): 390–9. Harris JE, Ryan L, Hoover HC Jr. et al. Adjuvant �������������������� active specific immunotherapy for stage II and III colon cancer with an autologous tumor cell vaccine: Eastern Cooperative Oncology Group Study E5283. J Clin Oncol 2000; 18(1): 148–57. Vermorken JB, Claessen AM, van Tinteren H et al. Active ����������� specific immunotherapy for stage II and stage III human colon cancer: a randomised trial. Lancet 1999; 353(9150): 345–50. O’Connell JB, Maggard MA, Ko CY. Colon cancer survival rates with the new American Joint Committee on Cancer sixth edition staging. J Natl Cancer Inst 2004; 96(19): 1420–5.



30 Radiation therapy: Acute and late toxicity Roland Hawkins

Challenging Case A 62-year-old man presents with blood per rectum. He has mild rectal discomfort with bowel movements and a feeling of incomplete evacuation. Two years previously he received external beam radiotherapy for prostate cancer. His rectal examination is normal except for some blood on the gloved finger. A flexible sigmoidoscopy demonstrates friable mucosa with neovascularity of the distal 4 cm of rectum. The mucosa is friable with telangectasia. Challenging Case Management The history and endoscopic exam is suggestive of radiation proctitis. Management includes fiber and topical therapy. The friable areas of the rectum can be treated with topical application of a large swab soaked with 10% formalin passed through an anoscope or proctoscope. Argon plasma coagulation is also effective treatment. Introduction Apart from a few exceptional circumstances, radiation treatment is used as an adjunct to surgical resection in the potentially curative treatment of adenocarcinoma of the rectum. As such, it is employed to reduce the tumor burden and eradicate deposits of cancer in pelvic lymph nodes and soft tissue not removed, or not expected to be removed, by the surgeon. In this setting, radiation treatment is administered either before or following en bloc resection of the involved length of large bowel by low anterior (LAR) or abdominal perineal resection (APR) that is intended to remove all evident disease, i.e., to be an R0 resection. Preoperative treatment is referred to as neoadjuvant or adjuvant, and postoperative treatment as adjuvant. These are usually administered to patients with locally advanced but resectable stage II or III disease (Table 30.1). Less often adjuvant radiation treatment is administered following local excision of less advanced disease. Local excision is elected in patients with small distal rectal tumors to avoid APR or LAR. Recurrence after apparently curative surgery for rectal cancer may develop in structures adjacent to the margin of resection or Table 30.1  Staging of rectal carcinoma. TNM (AJCC and UICC)

Dukes

TNM Group

A

I

T1N0M0 T2N0M0

Tumor limited to submucosa, Tumor into, not through, muscularis propria

B

II

T3N0M0 T4N0M0

Tumor through muscularis propria Tumor invades other organs or through peritoneal serosa.

C

III

N1 or N2, any T

N1 (1 to 3 nodes +), N2 (>3 nodes +)

D

IV

M1, any T or N

Distant metastasis



Description

regional nodes in the pelvis (local recurrence), or as metastasis to the peritoneal surface or distant organs (distant recurrence). Treatment with radiation and/or chemotherapy added to surgery is judged as beneficial in so far as it increases overall patient survival and reduces the incidence of local and distant recurrence. Overall survival is the most important outcome in judging benefit. It is unambiguously evaluable and reflects the balance of benefit and potentially lethal adverse effects of treatment. Local recurrence is not often salvagable. Its prevention is important, if not a requirement, for achieving cure of the disease. It may itself be life threatening and may act as a source of distant metastasis. Further, uncontrolled recurrence in the pelvis is particularly detrimental to the quality of life of patients who are not cured by the treatment by causing pain, bleeding, infection, obstruction and incontinence affecting bowel and urogenital organs. Distant recurrence is important because it is the most unsalvageable life threatening form of treatment failure. Evolution of the method of radiation treatment over the past 30 years has produced what are now two more or less standard regimens, referred to here as the short and long treatment courses. The short course has been used only for preoperative treatment. It typically consists of a dose of 25 Gy in fractions of 5 Gy each over a period of 5 to 7 days with surgery following within a week. The long course has been used for both pre and postoperative treatment. It typically consists of 45 to 54 Gy in fractions of 1.8 to 2 Gy over a period of 5 to 6 weeks. When used preoperatively the long course is usually followed by about 6 weeks rest before surgery and may include concurrent chemotherapy. There are several ways to compare the intensity of radiation treatment courses that differ in fractionation of dose and are given over different time intervals. One in current use consists of calculating a biologically equivalent dose (BED) for each treatment course using the relation: (1)   d g BED = nd 1 + - (T - Tk) a/b a Wherein n is the number of fractions, d is the dose per fraction, a/b is a ratio characteristic of cell type or tissue and ranging from about 2 to 20 or more. For meta-analysis overview of the effect of radiation in the treatment of rectal cancer a/b has been assumed to be about 10.(2, 3) The value of the g/a ratio corrects for the repopulation of cells during the length of the treatment course and has been assumed to be 0.6 Gy per day. The value of T is the time from first to last radiation fraction in days and Tk is a lag time taken to be 7 days. With these parameters the BED of the short course of 5 fractions of 5 Gy each is 37.5 Gy and that of a long course consisting of 50.4 Gy in 28 fractions of 1.8 Gy each is 40.9 Gy, implying they are roughly equivalent. The validity of equation 1 in establishing equivalency with respect to the chance

radiation therapy: acute and late toxicity of eliminating pelvic cancer or causing any specific organ injury is dependent on the appropriateness to the specific endpoint in question and of the values chosen for a/b, g/a and Tk. The physiologic death, disintegration, and disappearance of nearly all cells lethally injured by radiation takes place only after they and/or their descendents go through one or more, often aberrant, mitotic cell divisions. An exception to this is some lymphocyte subsets that die within hours of irradiation. As a result there is a time lag between irradiation and response of a cancer that is variable and dependent on the mitotic activity of the cancer cells. This lag ranges from a few days up to a year or more for the various carcinomas. A typical time to manifest the maximal response of a carcinoma to radiation is the order of a month or two. The same phenomenon is in part responsible for delay of up to a year or more in the development of some forms of radiation injury. With short course preoperative radiation there is little time for tumor response before surgery. There is evidence that at surgery after short course irradiation the average tumor size and average number of nodes with metastatic carcinoma has decreased slightly but this is not sufficient to produce a change in the distribution of tumor or nodal stage in a study population.(4) With long course preoperative irradiation more time is allowed for response of the disease and down staging to occur. This is evident in some of the trials listed in tables 30.3 and 30.4 and was demonstrated in a trial in which all patients were treated with 13 daily fractions of 3 Gy each and randomly assigned to surgery within 2 weeks after the end of radiation or surgery 6 to 8 weeks after radiation.(5) With both the long and short course, radiation treatment is directed at the pelvis with the superior border placed at about the L5S1 interspace. The inferior border is placed at least 3 to 5

cm below the most distal extent of tumor or below the obdurator foramen. For distal tumors it may include all or part of the anal canal. In earlier studies treatment was restricted to anteriorposterior directed beams.(6) More recently, laterally directed beams that exclude bowel in the anterior part of the pelvis are a standard part of treatment plans. Only the volume in which the beams overlap is exposed to the full prescribed dose. This usually includes, in addition to the rectum, small and large bowel in the posterior pelvis, the posterior part of bladder and prostate, the soft tissue in the ischiorectal fossa and presacral areas, the sacrum and the lymph nodes of the internal iliac and most distal part of the common iliac chains. If there is extension of tumor to invade urogenital organs the external iliac nodes are sometimes included. After APR, the perineal incision, which tends to be a site of recurrence, is included in the treatment volume.(7, 8) Tables 30.2, 30.3 and 30.4 summarize several trials in which randomization was between arms composed of various combinations of pre and postoperative radiation and chemotherapy.(9–26) The radiation treatment plans in each are similar to either the short or long course described above and can be gleaned from the table by noting the dose shown. When the dose is about 25 Gy it is a short course and when 40 to 60 Gy it is similar to the long course. The benefits and adverse effects of preoperative and postoperative radiation treatment reported in these studies will be examined and compared. Adjuvant treatment after local excision is also discussed. Benefit of Adjuvant and Neoadjuvant Radiation Treatment Several randomized trials of postoperative adjuvant therapy in the late 1970s and 1980s listed in Table 30.2 indicate that post­ operative radiation and chemotherapy can lead to statistically

Table 30.2  Postoperative adjuvant radiation studies. Study Open/Closed

Number of Pts.

Therapy Arms

GITSG (9)

202

S S–C S–44Gy S–44Gy-C

NCCTG (10) 794751

204

NSABP (11) R-01 11/77 to 10/86

Local (Pelvic) Recurrence % at 5 years

Overall Survival % at 5 years

Comments

24 27 20 11

46 56 52 59 (p = 0.07)

T3,T4 or N+ Semustine and 5Fu

S–50.4Gy S–50.4Gy+C

25 13 (p = 0.036)

47 57 (p = 0.02)

Semustine and 5Fu.

555

S S–46Gy S–C

25 16 (p = 0.06) 21.4

43 41 53 (p = 0.01)

Semustine, 5Fu, vincristine

Norway (12, 13)

144

S S–46Gy+C

30 12 (p = 0.01)

50 64 (p = 0.05)

Bolus 5Fu on 6 days during radiation

NSABP (14) R-02

694

S–C S–50.4Gy+C

14 8 (p = 0.02)

Retrospective Study of Trans anal excision (15) MGH/Emory

99

LE (T1) LE–xrt (T1) LE–(T2) LE–xrt (T2)

11 0.0 67 15 (p = 0.004)

RTOG 8902 (16)

65

LE (T1, fav) LE-xrt (T1,2,3)

14.3 17.6

58 58

Semustine, 5Fu, vincristine in 10 week cycles or 5Fu and leukovorin in 8 week cycles. Concurrent chemotherapy for some patients

86 72

fav = favorable features, see text.

S indicates LAR or APR, LE is local excision, C is chemotherapy. A dose in Gy indicates irradiation. The dash line shows time sequence.



improved outcomes in colon and rectal surgery Table 30.3  Preoperative neoadjuvant radiation studies. Number of Pts

Therapy Arms

Local (Pelvic) Recurrence % at 5 years

Overall Survival % at 5 years

Stockholm I (1) 1980 to 1987

849

S 25Gy–S

28 14 (p < 0.001)

36 36

Stockholm II (17) 3/87 to 5/93

557

S 25Gy–S

25 12 (p < 0.001)

Swedish Rectal (18) 3/87 to 2/90

1168

S 25Gy–S

27 11 (p < 0.001)

48 58 (p < 0.001)

Patients older than 80 excluded

Dutch TME (19) 1/96 to12/99

1861

S 25Gy–S

10.4 5.6 (p < 0.001)

64 64

Patients older than 80 included

Manchester (20) 1981 to 1989

284

S 20Gy–S

36 13 (p < 0.001)

39 46 (p = 0.03)

5Gy x 4, survival for those having curative resection:

MRC II (21)

289

S 40Gy–S

48 32 (p = 0.04)

19 26 (p = 0.09)

20x2Gy; S four weeks after xrt

Polish (22) 1999 to 2002

312

25Gy–S 50.4Gy+C–S

9 14 (p = 0.17)

67.2 66.2

EORTC (23) 4/93 to 5/03

1011

45Gy–S 45Gy+C–S 45Gy-S–C 45Gy+C–S–C

17.1 9.6 8.7 7.6

63.2 no post op C vs. 67.2 with post op C (p = 0.12)

Stage I and age over 80 excluded

FFCD 9203 (24) 1993

762

45Gy–S–C 45Gy+C–S–C

16.5 8.1 (p = 0.004)

67.2 66.2

Stage I and age over 75 excluded

Study Open/Closed

39 46 (p = 0.03) (Pts having curative surg)

Comments to L2 level no lateral beam Patients older than 80 excluded

Mostly TME T3/T4. Patients older than 75 excluded

Symbols as in Table 30.2.

Table 30.4  Pre versus postoperative and chemotherapy studies. Study Open/ Closed

Number of Pts random

Therapy Arms

Local (Pelvic) Recurrence % at 5 years

Overall Survival at % 5 years

Upsala (25) 10/80 to 12/85

471

25.5Gy–S S–60Gy

12 21 (p = 0.02)

44 39 (p = 0.43)

5.1x5Gy and 30x2Gy.

German (26) 2/95 to 9/02

823

50.4Gy+C–S–C S–50.4G+C–C

6 13 (p = 0.006)

74 76 (p = 0.80)

TME, exclude stage I    and age over 75

Comments

Symbols as in Table 30.2.

significant improvement in overall survival and the incidence of local recurrence compared to surgery alone. Based on Gastrointestinal Tumor Study Group and North Central Cancer Treatment Group studies a U.S. National Institutes of Health Consensus Development Conference in 1990 recommended that postoperative radiation and chemotherapy be standard treatment for stage II and III rectal cancer.(9, 10, 27) An advantage of postoperative treatment is that selection for adjuvant treatment can be based on pathologic staging whereas with preoperative treatment selection is based on necessarily imperfect clinical staging. The use of preoperative radiation has been extensively evaluated in Europe. From inspection of the randomized trials in Table 30.3 it is evident that preoperative radiation treatment reliably produces a clinically and statistically significant reduction in the incidence of local recurrence by about 50 to 60%. This remains true even in the Dutch Colorectal Cancer Group trial which was



designed to minimize the need for pelvic irradiation by mandating surgery to be total mesorectal excision (TME).(19) As indicated in the entries in Table 30.2 and 30.3 for the surgery only arms, TME is apparently more rigorously extirpative than the surgery of historical practice. Its use reduced the local recurrence at five years after surgery alone to 10.4% compared to the 25 to 28% found in comparable Stockholm I and II and Swedish rectal trials, that did not require TME.(1, 17, 18) About 35% of the patients in the Dutch study had disease found in pelvic nodes making them stage III. Among this subgroup, 20.6% of those who did not have radiation treatment and 10.6% of those who did suffered a local recurrence (p < 0.001). About 28% had stage II disease. Among these the local recurrence rate without radiation was 7.2% and with radiation 5.3% (p = 0.331). About 28% had stage I disease. Among these the local recurrence rate was 1.7% without radiation and 0.4% with (p = 0.091). Among 7% of patients with distant metastasis found

radiation therapy: acute and late toxicity at surgery (stage IV) there was local recurrence in 26.9% without radiation and 15.9 with (p = 0.207). Thus, for all four stages there was less local recurrence in patients who had radiation, but the differential only reached statistical significance for the node positive (stage III) subgroup and the entire randomized population. Similarly it was found that the difference reached statistical significance in the subgroup that had LAR but not in subgroups that had APR or Hartman pouch surgery and in the subgroup for which the distal tumor edge was between 5 and 10 cm from the anal verge but not those more proximal or distal. The Swedish Rectal study differs from the Dutch study in that TME was not required.(18) The proportion of patients in each stage was similar but the differential in rate of local recurrence between arms of the trial was greater and statistically significant for all stages. In the stage III subgroup of the Swedish study the local recurrence was 40% without preoperative radiation and 20% with (p < 0.001). For stage II it was 23% without and 10% with radiation (p = 0.002). For stage I it was 4% without and 2% with radiation (p = 0.02). Comparison of these two studies suggests that benefit from preoperative radiation in preventing local recurrence is maximal if given to patients likely to have node positive (stage III) disease, expected to have LAR as opposed to APR and with lowest tumor extent in the mid to distal rectum. However, some reduction in risk of local recurrence may be expected for all patients. As shown in Table 30.3, overall survival rate was not affected by the short course preoperative radiation treatment in the Dutch TME trial and in the earlier Stockholm I trial. On the other hand, in the Swedish Rectal trial the short course preoperative radiation treatment produced a statistically significant gain in overall survival. Two other short course preoperative radiation trials, Stockholm II and Manchester showed statistically significant improvement in overall survival among the subgroup that actually underwent curative resection but not in all randomized patients.(17, 20) Failure to improve overall survival even though local recurrence rate is significantly reduced can occur in two important ways. First, the dominant cause of death may be from development of distant metastatic disease to such an extent that a small incidence of local recurrence in the surgery only arm and its reduction by radiation treatment has no statistically significant, or even discernible, impact on survival. This may be the principle explanation in the TME trial. The other way the impact on survival of a local recurrence advantage may be reduced, or lost, is if excess non rectal cancer deaths are produced in the radiation treatment arm. This is likely the explanation for limitation of statistically significant survival benefit to the subgroup that had curative surgery in the Stockholm II trial.(17) At median follow-up of 8.8 years for this trial 19% of the radiation arm patients and 12% of the surgery only arm had died of non cancer causes (p = 0.1). There was cardiovascular death in 13% in the radiation arm and 7% in the surgery only arm (p = 0.07). This differential was established within the first 6 months after surgery, during which 5% of irradiated patients and 1% of the surgery only patients died from cardiovascular causes (p = 0.02). The excess cardiovascular deaths were predominantly in patients older than 68 years. It is suggested this

is due to change in the coagulation properties of blood during the several months of recovery from pelvic surgery and radiation that leads to increased thrombotic events in the irradiated patients. The only randomized study of preoperative radiation with a surgery only control arm that used a radiation treatment regimen resembling the long course described above is the MRC II trial.(21) Patients were eligible if they had a partially or totally fixed rectal tumor on physical exam. The population likely consisted mostly of T3 and T4 tumors, that is, there were likely more locally advanced cancers than in the short course trials. As shown in Table 30.2, there was a significant decrease in local recurrence in the radiation arm and a tendency to increased survival, though not statistically significant, similar to the findings in several short course trials. The Polish trial compares short-course preoperative radiation with long-course preoperative radiation plus concurrent chemotherapy.(22) Most of the surgery was with TME. Patients were clinically staged with physical exam, transrectal ultrasound and/ or MRI. Only those with evidence of T3 or T4 tumors that were palpable on digital exam and had no anal sphincter involvement were included. Patients found to have involved nodes at surgery usually received postoperative chemotherapy. More in the short course arm were node positive suggesting down staging by the long course treatment. There was no difference in survival between the two arms. There is a suggestive difference in local recurrence favoring the short course but it did not reach statistical significance. There was no statistically significant difference in the fraction that received a permanent stoma but with a tendency to favor the long course arm for sphincter preservation. The EORTC trial examined the effect of adding chemotherapy to long course preoperative radiation with the finding that if chemotherapy is given concurrently with preoperative radiation, post operatively, or both, the rate of local recurrence is reduced significantly relative to preoperative long course radiation with no chemotherapy.(23) This suggests concurrent radiochemotherapy does not contribute much if postoperative chemotherapy is given. On the other hand, the FFCD trial in which both arms got postoperative chemotherapy reports a significant decrease in local recurrence if concurrent chemotherapy is given with preoperative radiation.(24) There was no survival difference. Two randomized trials listed in Table 30.4 have directly compared pre and postoperative radiation treatment arms. In the earlier Upsala trial the preoperative arm had the short course of radiation.(25) Those randomized to the postoperative arm and found to have stage II or III disease were treated with long course to a higher dose of 60 Gy in 2 Gy fractions. In the recent German trial the surgery was mandated to be with TME and clinical staging was intended to exclude stage I patients from the study.(26) Those randomized to the preoperative arm and the subset of those randomized to the postoperative arm who were proved to have stage II or III disease at surgery received the similar regimens of chemotherapy and radiochemotherapy though in different sequence. The chemoradiotherapy consisted of 50.4 Gy in fractions of 1.8 Gy each except that an additional 5.4 Gy to a reduced volume was included in the postoperative treatment. Both these trials showed a statistically significant difference in local recurrence rate favoring the preoperative arm and no significant difference in



improved outcomes in colon and rectal surgery survival when grouped by intention to treat at randomization. It is of note that 28% of the postoperative arm of the German trial received no radiation treatment. Of these, in 18% the cause was finding pathologic stage I disease and in 10% the cause was postoperative death or complications or finding of stage IV disease at surgery. Patient selection and the treatment regimen of the preoperative arm of the German trial is now standard treatment in many institutions. In all the above trials surgery consisted of LAR or APR. For patients with evidence of a stage T1 or T2 rectal cancer distal to the peritoneal reflection i.e., usually within 10 cm from the anal verge, smaller than about 4 cm and occupying a limited fraction of the circumference of the rectal wall, local excision via trans anal, trans sphincteric (York-Mason) or posterior proctotomy (Kraske) procedure may be able to achieve en bloc full thickness excision of the tumor with negative margins. This limited surgery may be elected in lieu of APR or LAR to preserve sphincter function or to avoid major surgery in those not fit or not willing to undergo it. Comparison of local excision (LE) with APR or LAR as to the ability to remove all the carcinoma has not been established by any randomized trial. Nevertheless, it is expected that limited local excision will not as reliably prevent local recurrence as the more radical surgery, particularly TME. This is confirmed by the local recurrence rates reported in the retrospective series shown in Table 30.2, particularly for T2 disease. The decrease in local recurrence with adjuvant radiation, with or without concurrent chemotherapy, suggests that the local excision with adjuvant treatment is efficacious enough to be considered as an option under some circumstances. Bias in the retrospective series would be to select for radiation treatment those patients with unfavorable features in their pathology such as positive or close margins, lymphovascular invasion or high histologic grade. Thus, the benefit from adjuvant treatment may be more than indicated by the results shown. The RTOG protocol 89–02 study enrolled patients with tumors judged by their surgeon to be distal enough to not allow clearance by LAR and who underwent local excision via trans-anal, transsacral or trans-coccygial approach.(16) To be eligible the tumor had to be mobile, <4 cm in size and occupy <40% of the rectal circumference. Those patients with cancer found to be pathologic stage T1, with histologic grade 1 or 2, excised with at least 3 mm margins in all directions, absent any lymphatic or vascular invasion and with normal CEA received no post operative treatment. Patients lacking any one of these favorable features were treated with radiation to the pelvis with boost to the tumor site to a total dose of 50 to 56 Gy in 1.8 to 2 Gy fractions with concurrent 5Fu chemotherapy. If the margin was microscopically positive or closer than 3 mm the dose to the tumor bed was increased to give a total dose of 59.4 to 65 Gy. The local recurrence rate for T2 tumors, all of which received adjuvant treatment was 4 of 25 (16%) that for T3 tumors was 3 of 13 (23%). It is not clear what the chance of salvage for local failure with APR is, but it may be as much as 50%.(28) The results for local excision shown in Table 30.2 support the view that local excision with postoperative adjuvant treatment with radiation and chemotherapy, although not as likely to be curative as radical surgery, is an acceptable option for tumors of a size and position which permit it, when there is



sufficient reason to avoid radical surgery. The treatment of early rectal cancers has recently been reviewed.(29) Acute Adverse Effects The most common and limiting adverse effect that occurs during and/or shortly after a course of pelvic irradiation (acute effect) is diarrhea. A scale adopted by the RTOG and EORTC for reporting acute effects of irradiation of the lower GI tract is representative and in use in current trials.(30) Grade 1 is given for increased frequency or change in bowel habits not requiring medication or rectal discomfort not requiring analgesics. A score of grade 2 implies diarrhea requiring Immodium or Lomotil medication, or mucous or bloody discharge not requiring sanitary pads or rectal or abdominal pain requiring analgesic medication. A score of grade 3 is given for diarrhea requiring parenteral support, mucous or bloody discharge requiring sanitary pads or abdominal distention with distended bowel loops on radiograph. Grade 4 implies acute or subacute bowel obstruction, or fistula or perforation, or GI bleeding requiring transfusion or abdominal pain or tenesmus requiring tube decompression or bowel diversion. Grade 3 and 4 are often combined and reported as severe adverse effects. In the EORTC trial, 1011 patients were treated with preoperative irradiation to a dose of 45 Gy in 25 fractions over 5 weeks. (23) Half were randomly assigned to also have concurrent preoperative chemotherapy and half had none. Acute grade 2 toxicity was reported in 38.4% of those who received the concurrent preoperative chemotherapy and 29.7% of those who did not (p < 0.001). Grade 3 or 4 acute adverse effects are reported in 13.9% of those whose treatment included preoperative chemotherapy and 7.4% of those who had only preoperative radiation (p < 0.001). The rate of local recurrence as a first event was approximately 9% at five years in those who received chemotherapy preoperatively, postoperatively or both and 17% in those who had no chemotherapy at all (p < 0.002). There was no statistically significant difference in overall survival. This suggests the additional acute toxicity of preoperative concurrent radiation and chemotherapy over that of preoperative radiation alone may not be necessary if post operative chemotherapy is to be given. This is contradicted by the FFCF trial.(24) The incidence of severe diarrhea during postoperative radiation treatment following LAR or APR depends on the specific concurrent chemotherapy regimen. For 656 patients treated on a phase III NCCTG trial it was found to be 13% for bolus infusion of 5FU at a dose of 500 mg/m2 on each of three days of the first and fifth week. It was 23% for infusion of 5FU at the rate of 225 mg/m2 per day given continuously for the entire length of the course of radiation.(31) Improvement in survival at four years of 70% with the continuous regimen compared to 60% with bolus infusion was felt to justify the definite, though modest, increase in toxicity. The type of surgery was also a significant determinant of the risk of severe diarrhea. In those who had undergone LAR there was a 31% rate of severe diarrhea compared to 13% in those who had an APR (p < 0.001). This differential is not unexpected as there is a significant rate of diarrhea after LAR in the absence of radiation. In this regard, it is of note that the frequency of bowel movements at the time of discharge after LAR via total mesorectal

radiation therapy: acute and late toxicity excision in 81 patients who were not treated with radiation averaged about 8 per day.(32) In the trial that randomized patients to pre versus post operative long course chemoradiotheapy conducted by the German Rectal Cancer Study Group the incidence of sever diarrhea among 399 patients randomized to preoperative treatment was 12%. Among the 237 patients actually treated with postoperative radiation the rate of severe diarrhea was 18% (p = 0.04).(26) The post operative arm included some 23% who had APR. Thus among those who had an LAR, and are most comparable to patients in the pre operative arm with respect to bowel and anal function, the rate of severe diarrhea must have been >18% and the differential in favor of pre operative treatment even greater. On the other hand if the 110 patients in the post operative arm who, for one reason or another, had no radiation treatment are included in the toxicity score, there was no difference in rate of severe acute grade 3 or 4 toxicity. Other grade 3 or 4 acute side effects reported in the German study were hematologic and dermatologic. The percent grade 3 and 4 hematologic toxicity was 6% in the pre and 8% in the post operative arms (p = 0.27). Dermatologic toxicity refers to radiation dermatitis in the perineal skin or perineal crease suture line (Figure 30.1). Grade 3 or 4 radiation dermatitis is reported for 11% of pre and 15% of the post operative patients who had radiation (p = 0.09). The rate of grade 3 or 4 level acute toxicity of any kind was 27% in the pre and 40% in the post operative patients who had radiation (p = 0.001). These results from two randomized studies support the conclusion that pre operative standard fractionated 5 to 6 week radiation treatment with chemotherapy produces less diarrhea and other acute adverse effect than in comparable patients who have the same treatment after surgery. The differential is definitely present. However it is a modest difference so that, in itself, it does not provide a compelling reason for preferring preoperative neoadjuvant treatment over postoperative treatment. Further more, 28% of patients in the post operative arm of the German study were spared radiation treatment because of the finding of stage I disease (18%) or distant metastasis (10%) at surgery, and thus had zero adverse radiation effects. The short preoperative radiation treatment course of 5 fractions of 5 Gy each in one week rarely produces significant adverse effects in the 2 to 3 weeks during radiation treatment and before surgical resection. In the Dutch TME trial, grade 1 acute gastrointestinal side effects were reported in 12%, grade 2 in 2.3% and grade 3 in 1 of 605 patients.(19) Acute neurologic effects of radiation were reported as grade 1 (requiring no intervention) in 7.5%, as grade 2 (requiring narcotic pain medicine or adjustment of treatment) in 1% and grade 3 (intractable severe pain or causing treatment interruption) in 2.8%. This has been attributed to radiation induced lumbosacral plexopathy. It was first reported in patients treated with the short course in Upsala and in the Swedish Rectal trial.(33) It consists of pain in the lower extremities and gluteal area and in a minority of the patients it was associated with other lower extremity neurologic signs. In a few patients the effect persisted or recurred for months to years. Acute neurologic effects have not been reported with the lower fractional doses of the long course preoperative radiation treatment. Acute effects on

Figure 30.1  Radiation dermatitis.

the genitourinary and other systems were less frequent than those manifest in the GI and neurologic systems. Surgical Complications After Preoperative Irradiation Patients treated preoperatively with short course radiotherapy in the Stockholm I trial had surgical mortality of 8% compared with 2% in the surgery only arm (p < 0.01).(1) Among patients over 75 years in age the mortality in the preop arm was 16% and again only 2% in the surgery only arm. The dominant cause of the increase in post operative death was cardiovascular. The radiation treatment in Stockholm I was specified to be with AP and PA directed beams only and encompassed, in addition to the pelvis, the para-aortic nodes cephalad to the L2 vertebral level. With the inclusion of laterally directed beams and restriction of the radiated volume to the pelvis as well as exclusion of the elderly patients in the subsequent Stockholm II, Swedish Rectal and Dutch TME trials the surgical mortality was not statistically different between preop radiation and surgery only arms.(17–19) For instance, in the Dutch TME trial the surgical mortality was 3.5% in the preoperative radiation arm and 2.6% in the surgery only arm (p = 0.38).(34) The in-hospital death rate was 4% in the preop radiation arm and 3.3% in the surgery only arm (p = 0.49) and very strongly correlated with age in both arms. There was no exclusion for age in this trial with the oldest patient being 92. In the Dutch TME trial there was no significant difference between the two arms in operating time (median 180 minutes), or



improved outcomes in colon and rectal surgery length of hospital stay (15 or 14 days median).(34) Median blood loss in the preop radiation arm was 1,100 ml. In the surgery only arm it was 1,000 ml (p < 0.001). The percent of LAR patients with a diverting stoma increased from 60 to 67% in the 60 days following surgery. In the surgery only arm it increased from 54 to 63% (p = 0.17). A statistically significant difference in postoperative complications between the arms was found for cardiac events; 5% with preop radiation and 3% surgery only (p < 0.05), psychologic disorders; 4% with preop radiation and 1% surgery only (p < 0.01), and for any complication; 48% in preop radiation arm and 41% surgery only (p < 0.01). Complications in the APR patients occurred in 29% of irradiated patients and 18% of surgery only patients (p < 0.01). There was no significant difference in complication rate among LAR patients, 11 and 12% in respectively the radiation and surgery only arms. These results indicate that there is the potential for short course preoperative radiation to complicate the ensuing surgery and recovery particularly manifest in patients over the age of 70 and even more so in those over the age of 80. This is minimized but not eliminated by adherence to the now standard radiation treatment planning specifications noted in the introduction. The German trial required TME surgery but excluded patients over the age of 75. The radiation treatment was the long course (50.4 Gy in 28 fractions of 1.8 Gy each) with concurrent chemotherapy and was given either pre- or postoperatively.(26, 35) There was 0.8% surgical mortality in the preop arm and 1% in the post op arm indicating no increase attributable to the preop radiochemotherapy. The incidence of any postoperative complication was 34.5% in the preop arm and 34% in the postop arm. Anastomotic leak occurred in 13 and 12%, delayed wound healing in 5 and 6% of, respectively, pre and postop arms. All other complications occurred in <3% of each arm with no significant difference. The Polish trial randomized patients between preoperative short course radiation and long course radiation with chemotherapy.(22, 36) Surgery was by TME for the more distal tumors and patients over age 75 were excluded. The overall rate of complication events was 31% in the short course arm and 22% in the long course arm (p = 0.06) showing a near significant trend. The overall number of patients suffering a complication was 27% in the short and 21% in the long arm (p = 0.27). Post operative death occurred in 0.7% of the long course and 1.3% of the short course arm (p = 1.0). Re-operation was needed in 8.2% of the short and 9.5% of the long course patients (p = 0.85). No statistically significant difference, and no suggestive trend, was found to favor one or the other arm with respect to other less severe complications. In conclusion, it appears that if patients over age 75 are excluded there is little or no significant increase in the risk of surgical mortality and other complications with either the short or long preoperative courses of radiation treatment. The risk of surgical mortality and complications is likely increased by the short course of preoperative radiation in the more elderly patients. It has not been shown whether or not a similar increase in surgical risk is incurred in older patients with the long preoperative radiochemotherapy course. Chronic Late Adverse Effects of Radiation Patients enrolled in the Dutch TME preoperative short course radiation trial who were alive with no evident disease were sent a



questionnaire by mail to assess bowel, stoma and urinary function. (37) A response was obtained from 597 (84% of those mailed). Among these the median time since surgery was 5.09 years. The mean number of bowel movements during the day among the 362 patients who had no stoma was 3.69 in the irradiated patients and 3.02 in the surgery only patients (p = 0.011). The mean number of nocturnal movements was 0.48 in the irradiated patients and 0.35 in the surgery only (p = 0.207). Daytime fecal incontinence was reported in 62% of those irradiated and 38% of the surgery only patients (p < 0.001) and nocturnal incontinence in, respectively, 32 and 17% (p = 0.001). The incontinence also occurred more often and was more troublesome in the irradiated compared to surgery only patients. Pads were in use for incontinence and anal mucous and blood loss in 56% of irradiated and 33% of surgery only patients (p < 0.001). Among the 235 responding patients with a stoma there was no significant difference between irradiated and surgery only patients with respect to stoma function. A review of the patients treated on the Dutch TME trial was conducted to determine risk factors for development of fecal incontinence.(38) Potential risk factors examined included age, gender, childbirth, body mass index, cancer stage, tumor distance from anal verge, anastomosis distance from anal verge, duration of surgery, blood loss at surgery, presence of a pouch, temporary stoma and anastomotic leak. No risk factors emerged as statistically significant among the surgery only patients. Among the preoperative radiation patients only blood loss at surgery and distal tumor margin distance from the anal verge were statistically significant risk factors. Blood loss at surgery >1,400 ml had relative risk (RR) of incontinence of 3.24 (p = 0.005) compared to those with less blood loss. Relative to distance of distal tumor margin <5 cm from the anal verge, distance between 5 and 10 cm had RR of 0.21 (p = 0.016), and >10 cm had RR of 0.13 (p = 0.003). The location of the distal tumor extent determines the inferior extent of the radiation treatment port. Among those few respondents who had the perineum, and consequently the entire anal sphincter, included in the radiation field compared to those who did not, the RR for fecal incontinence at 2 years after surgery was 2.64 (p = 0.085) and at 5 years after surgery the RR was 7.45 (p = 0.059). It was also noted that the fraction of patients reporting fecal incontinence increased after reaching a minimum at 2 years postsurgery whereas that in surgery only patients it increased only slightly. This time course is consistent with a late effect of radiation on pelvic nerves and fibrosis. Urinary function was not significantly different in irradiated and surgery only patients. About 39% of patients in each group reported incontinence of urine. Back and buttock pain, hip stiffness and difficulty walking were not significantly different in the two groups suggesting absence of chronic radiation induced lumbosacral plexopathy in this trial. The rate of hospital admission was significantly increased in the irradiated patients compared with surgery only patients in the first 6 months after surgery. Admissions were for infection, endocrine, cardiovascular and gastrointestinal diagnoses. Of note, among gastrointestinal admissions, those for constipation and abdominal pain were significantly increased in irradiated patients but those for bowel obstruction were not. The rate of hospital admission more than six months after surgery was not

radiation therapy: acute and late toxicity significantly different for patients in the two groups including for myocardial infarction or stroke. A comparative study by phone interview of patients two or more years after they had undergone LAR for rectal cancer at Mayo clinic reports significantly more bowel symptoms in the 41 who had also had postoperative long course pelvic irradiation and chemotherapy than in the 59 who had only surgery.(39) The fraction having more than 5 bowel movements a day was 37% in the irradiated group and 14% in the surgery only group (p < 0.001). The fraction of patients who reported incontinence was 66% in the irradiated group and 7% in the surgery only group (p < 0.001). In the irradiated group 41% wore a pad and in the surgery only group 10% (p < 0.001). Urgency with inability to defer defecation for 15 minutes was reported in 78% of the irradiated and 19% of the surgery only patients (p < 0.001). A retrospective study of 192 patients who had LAR with coloanal anastomosis at the Mayo clinic and had preopertative (long course) radiation, postoperative radiation or no radiation reports anastomotic stricture was the most common late effect requiring surgical intervention.(40) This occurred with nearly the same frequency in all three groups; 16% no radiation, 14% preop radiation and 15% post op radiation. It was usually managed with dilation and was not a significant cause of permanent fecal diversion. Permanent fecal diversion resulted from recurrence, bowel obstruction, incontinence, fistula, stricture, abscess/leak and patient preference. The five year survival without colostomy was 92% in patients who had no radiation treatment and 72% in those did (p < 0.001). There was no significant difference between the rate in pre and post operatively irradiated patients. A scale adopted by the RTOG and EROTC for reporting late chronic effects of radiation on the bowel is as follows.(30) Grade 1 implies mild diarrhea, mild cramping, 5 movements per day, slight rectal discharge or bleeding. Grade 2 implies moderate diarrhea and colic, more than 5 movements per day, excessive mucous or intermittent bleeding. Grade 3 implies obstruction or bleeding requiring surgery. Grade 4 implies necrosis, perforation or fistula. Fecal incontinence was not explicitly included in the grading criteria. The German trial reports grade 3 and 4 long-term gastrointestinal effects, for example, diarrhea and small bowel obstruction, in 9% of the preop arm and 15% of the postop arm (p = 0.07); anastomotic stricture in 4% of the preop and 12% of the post op arms (p = 0.003).(26) Bladder dysfunction of grade 3 or 4 occurred in 2% of the preop and 4% of the postop arms (p = 0.21). Any grade 3 or 4 effect occurred in 14% of the preop and 24% of the postop patients (p = 0.01). With the long course fractionation of pelvic chemoradiotherapy for adjunctive treatment of rectal cancer, the preoperative irradiation appears significantly less likely to produce severe chronic long-term sequelae than postoperative irradiation. The Polish trial comparing short course preoperative radiation with long course preoperative radiochemotherapy at median follow up of 48 months reports the overall incidence of late toxicity as 28.3% in the short and 27% in the long course arms (p = 0.81).(22) The incidence of severe late toxicity, presumably grade 3 or 4, was 10.1% in the short and 7.1% in the long course arms (p = 0.36). Severe gastrointestinal toxicity occurred in 5.1% of the short and 1.4% of the long course patients, no p value given.

A quality of life questionnaire on anorectal function including questions on bowel function, continence and urgency reports no significant difference between the short and long course arms. (40) For instance, 39% and 41% of, respectively, the short course and long course patients reported use of pads. In answering the question, “did your health status and/or treatment cause your sexual life to decline” there also was no significant difference in the two arms. This direct comparison of long and short course preoperative treatment shows no statistically significant difference in late toxicity. The evidence from the several trials summarized here indicates that both preoperative and postoperative radiation treatment are associated with increased chance of chronic adverse effect on bowel function. The direct comparison of pre- and postoperative long course radiochemotherapy in the German trial indicates there is less likelihood of this with the preoperative treatment. The Polish trial comparing long and short course preoperative irradiation finds no clear difference and does not resolve the issue of which of these has the least chance of producing chronic adverse effects. Chronic Rectal Effects In contrast to acute radiation injury, chronic injury is an indolent process that can present three months after therapy completion or up to 30 years later.(41) In addition to the acute cellular toxicity, radiation causes a progressive, obliterative arteritis, and submucosal fibrosis. Transmural injury of the bowel wall can lead to a progressive vasculitis, thrombosis and ultimately, to varying degrees of ischemia and necrosis. This process may lead to narrowing of the bowel lumen and eventual obstruction. The effects of chronic radiation are primarily related to the total dose of radiation received as well as the total volume of tissue irradiated.(42) There is some evidence to suggest that chronic radiation proctitis is more likely to occur in those initially experiencing severe acute proctitis and this has been termed the consequential late effect. (43) However, the absence of acute complications does not protect against the development of chronic radiation induced injury. Several other factors have also been identified that may increase the likelihood of developing chronic radiation injury. This includes a history of prior abdominal or pelvic surgery, presumably secondary to adhesion formation resulting in entrapment of the bowel, and a history of vascular occlusive disease (including hypertension and diabetes).(41, 44) Of all the gastrointestinal organs, the rectum is most commonly affected by pelvic radiotherapy.(45) It has been estimated that 75% of subjects receiving pelvic radiotherapy will experience rectal symptoms during treatment and almost 20% will continue with chronic proctitis.(46) In addition, 5% may develop perirectal fistulas, strictures or incontinence. Symptoms include loose stools, urgency, bleeding, pain, and tenesmus. Endoscopy reveals friability and granularity, pallor, erythema or prominent submucosal telangiectasias (Figure 30.2).(47) Histologic findings in the chronic phase include severe vascular changes such as telangiectasia of capillaries, platelet thrombi formation and narrowing of arterioles always accompanied by lamina propria fibrosis and crypt distortion.(48) Though rectal bleeding is most often the presenting symptom of chronic proctitis in the setting of prior radiation, it should

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improved outcomes in colon and rectal surgery

Figure 30.2  Radiation Proctitis.

not be assumed that this is the sole cause. As up to one-third of patients were found to have a diagnosis unrelated to the previous radiotherapy and 12% had a significant neoplasia, endoscopic evaluation is mandatory. with new onset of hematochezia after prior radiation therapy.(49) Treatment Numerous therapeutic agents have been evaluated and/or are currently utilized against radiation-induced proctitis. In many cases, patients presenting initially with symptoms suggestive of radiation proctitis will first be offered treatment with antiinflammatory medications. This most commonly involves either oral or enema delivered steroids or various 5-Aminosalicylic acid (5-ASA) preparations. Though often utilized in both the acute and chronic settings, evidence is lacking for the use of steroid preparations in the treatment of radiation proctitis. A prospective, randomized trial compared oral sulfasalzine plus rectal steroids to rectal sucralfate and oral placebo. The sulfasalzine regimen did demonstrate a significant improvement in both clinical symptoms and endoscopic findings, however, by comparison clinically this was less effective than sucralfate.(50) Sucralfate provides a protective barrier and promote epithelial healing has allowed its use in the treatment of radiation proctitis. One randomized, controlled trial found that oral sucralfate decreased diarrhea symptoms in both the acute and chronic phases.(51) Short-Chain Fatty Acids (SCFA) act as a major fuel source for colorectal mucosa. Two small randomized, placebo controlled trials using SCFA enemas noted improvement in symptoms and endoscopic findings.(41, 52) Various endoscopic ablation therapies have been applied to the treatment of chronic proctitis related bleeding due to local telangiectasias. The two most commonly utilized approaches are the laser and the argon plasma coagulator. There are no prospective, randomized trials assessing either of these approaches, only several retrospective case series. The largest series reporting on the use of Nd:YAG laser found excellent response rates and a significant decrease in rectal bleeding.(53) Rare complications included mucous discharge, ulcers or stricture. Similar results

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were obtained using an argon plasma coagulator in three treatment sessions.(54) However, over 70% required maintenance treatment over the long term.(55) Four and ten percent formalin have been utilized for the treatment of bleeding related to chronic proctitis. Two approaches are commonly utilized, that of a rectal formalin irrigation and a dab technique utilizing topical application of formalin with swabs or soaked gauze. De Parades et al. reported a prospective case series using the formalin gauze application and noted a beneficial result in 70%.(56) However, significant rates of stricturing and incontinence were reported. Numerous other retrospective series have reported good success with formalin. Of those using a gauze or pledget mediated application, at least a 75% success rate for cessation or improvement in bleeding was reported.(57) Many required multiple treatments though complications were minimal. Due to the small volume used, 10% formalin is often used. Of those reporting use of formalin rectal irrigations, 50 cc aliquots of 4% formalin were utilized up to a total volume of 400–500 cc. Again a >75% success rate was noted with this approach, with the most common reported complication being anal or pelvic pain occurring in 25% of those treated.(58) There is low level evidence supporting the use of hyperbaric oxygen treatments for chronic radiation proctitis and a single prospective series which reported significant improvement of bleeding, diarrhea and urgency, but no change in rectal pain with oral vitamins E and C.(59, 60) Metronidazole along with antiinflammatory agents (oral mesalazine and betamethasone enema) produced a significantly lower incidence of rectal bleeding and diarrhea in chronic radiation proctitis.(61) Despite the numerous medical approaches available for the treatment of radiation proctitis, surgical therapy remains an option for refractory cases The indications for surgery are most commonly rectum or rectosigmoid stenoses and rectovaginal fistulae, while the most common presenting symptoms are rectal bleeding, diarrhea, or tenesmus.(61) The majority of patients undergo diversionary procedures (proctectomy with colostomy, with or without a Hartmann rectal stump) with resection performed less commonly. When continuity is restored, a coloanal anastomosis (with or without colonic J-pouch) with proximal covering stoma is the procedure of choice in select cases. Successful outcomes with diversion alone are reported in the range of 72–73%.(62) In refractory rectal bleeding this option has less morbidity. Overall, morbidity with surgical intervention is extremely high, ranging from 30% to 65% with mortality rates in the postoperative period reported at 6.7–25%.(62, 63) Conclusion Chemotherapy and radiation treatment to the pelvis as an adjuvant to surgical resection, either individually or when both are administered, reduces the chance of pelvic recurrence and can increase the chance of a patient’s surviving the disease. This has been demonstrated in several randomized trials for both the preand postoperative treatment sequences, as noted in the tables and in meta analyses.(2, 3, 64) However, the adjunctive treatment has the potential for significant adverse effects. It is important to select the form of adjuvant treatment likely to be most beneficial. It is also important to select for adjuvant treatment those

radiation therapy: acute and late toxicity patients most likely to benefit and exclude those most likely to suffer severe or life threatening adverse effects. That preoperative treatment with radiation can complicate the ensuing surgery and postoperative recovery is illustrated in the occurrence of additional non cancer, mostly cardiovascular, deaths among the irradiated patients in the immediate postoperative period and the first six months post surgery in the Stockholm trials. Similar adverse effect was not evident in the later Swedish and Dutch TME trials that also used the short course radiation regimen nor was it evident in the studies that used the long course preoperative treatment regimens. These later trials were with better radiation therapy technique and all but the Dutch TME trial excluded the most elderly patients. Nevertheless, the potential for serious adverse effect on the surgery is still a consideration. It is clear that this is minimized by restricting the irradiated volume to those parts of the pelvis at risk for harboring disease and that elderly patients are most at risk from adding preoperative adjunctive treatment to the surgery. Reduction in local recurrence by preoperative treatment is present even when surgery is by TME. In the Dutch TME trial the benefit was most significant in the node positive (stage III) patients. It was present but rather small and did not reach statistical significance in the other stage subgroups. This suggests that patients, particularly those older than about 75, may be better served by proceeding directly to surgery unless there is clinical evidence or reason to suspect nodal disease. Postoperative radiation and chemotherapy, if indicated by pathologic stage, is an acceptable treatment option. The German trial has provided evidence that preoperative long course chemoradiation is in balance preferable to the similar treatment postoperatively. The selection criteria and preoperative treatment arm of the German trial are standard in many treatment centers. However, given the inconclusive results of the Polish trial comparing similar preoperative chemoradiotherapy with short course preoperative radiation, another larger trial, with specification of post surgery chemotherapy, comparing these two forms of preoperative treatment may be helpful as both regimens have features to recommend them. The short course has better compliance, is more economical and has the theoretical advantage of more timely removal of all evident disease than the long course. The long course may facilitate complete surgical removal by more down staging, provide earlier exposure of the patient to systemic chemotherapy treatment and have less surgical and long-term adverse effects than the large fractional doses of the short course. References   1. Jones B, Dale RG, Deehen C et al. The role of biological effective dose (BED) in clinical oncology. Clin Oncol 2001; 13: 71–81.   2. Colorectal Cancer Colaborative Group. Adjuvant radiotherapy for rectal cancer: a systematic overview of 8507 patients from 22 randomised trials, Lancet 2001; 358: 1291–304.   3. Glimelius B, Groenberg H, Jaerhult J et al. A systematic overview of radiation therapy effects in rectal cancer. Acta Oncol 2003; 42: 476–92.   4. Marijnen CAM, Nagtegaal ID, Kranenbourg EK et al. No downstaging after short-term preoperative radiotherapy in rectal cancer patients. J Clin Oncol 2001; 19: 1976–84.

  5. Francois Y, Nemoz CJ, Baulieux J et al. Influence of the interval between preoperative radiation therapy and surgery on downstaging and on the rate of sphincter-sparing surgery for rectal cancer: The Lyon R90-01 randomized trial. J Clin Oncol 1999; 17: 2396.   6. Cedermark B, Johansson H, Rutqvist LE et al. The Stockholm I trial of preoperative short term radiotherapy in operable rectal carcinoma. A prospective randomized trial. Stockholm Colorectal Cancer Study Group. Cancer 1995; 75: 2269–75.   7. Walz BJ, Green MR, Lindstrom ER, Butcher HR. Anatomical prognostic factors after abdominal perineal resection. Int J Radiat Oncol Biol Phys 1981; 7: 477–84.   8. Rich T, Gunderson LL, Lew R. Patterns of recurrence of rectal cancer after potentially curative surgery. Cancer 1983; 52: 1317–29.   9. Gastrointestinal Tumor Study Group. Prolongation of disease free interval in surgically treated rectal carcinoma. New Engl J Med 1985; 312: 1465–72. 10. Krook JE, Moertel CG, Gunderson LL et al. Effective surgical adjuvant therapy for high-risk rectal carcinoma. N Engl J Med 1991; 324: 709–15. 11. Fisher B, Wolmark N, Rockette H et al. Postoperative adjuvant chemotherapy or radiation therapy for rectal cancer: results from NSABP R-01. J Natl Cancer Inst 1988; 80: 21–9. 12. Tveit KM, Guldvog I, Hagen S et al. Improved results in rectal cancer by postoperative radiotherapy and 5-fluorouricil. Norwegian Adjumant Rectal Cancer Project Group. Eur J Cancer 1995; 31(suppl 5): S146. 13. Tveit KM, Guldvog I, Hagen S et al. Randomized controlled trial of postoperative radiotherapy and short-term timescheduled 5-fluorouricil against surgery alone in the treatment of Dukes B and C rectal cancer. Norwegian Adjuvant Rectal Cancer Project Group. Br J Surg 1997; 84: 1130–5. 14. Wolmark N, Wieand HS, Hyams DN et al. Randomized trial of postoperative adjuvant chemotherapy with or without radiotherapy for carcinoma of the rectum: National Surgical Adjuvant Breast and Bowel Project Protocol R-02. J Natl Cancer Inst 2000; 92: 388–96. 15. Chakravarti A, Compton CC, Shellito PC et al. Long term follow up of patients with rectal cancer managed by local excision with and without adjuvant irradiation. Ann Surg 1999; 230: 49–54. 16. Russell AH, Harris J, Rosenberg PJ et al. Anal sphincter conservation for patients with adenocarcinoma of the distal rectum: Long term results of Radiation Therapy Oncology Group protocol 89-02. Int J Radiat Oncol Biol Phys 2000; 46: 313–22. 17. Martling A, Holm T, Johansson H et al. The Stockholm II trial on preoperative radiotherapy in rectal carcinoma: longterm follow-up of a population-based study. Cancer 2001; 92: 896–902. 18. Improved survival with preoperative radiotherapy in resectable rectal cancer. Swedish Rectal Cancer Trial. N Engl J Med 1997; 336: 980–7. 19. Koen CMJ, Peeters MD, Corrie AM. The TME trial after a median follow-up of 6 years: Increased local control but no survival benefit in irradiated patients with resectable rectal carcinoma, Ann Surg 2007; 246: 693–701.

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improved outcomes in colon and rectal surgery 20. Marsh PJ, James RD, Schofield PF. Adjuvant preoperative radiotherapy for locally advanced rectal carcinoma. Results of a prospective randomized trial. Dis Colon Rectum 1994; 37: 1205–14. 21. Randomised trial of surgery alone versus radiotherapy followed by surgery for potentially operable locally advanced rectal carcinoma. Medical Research Council Rectal Cancer Working Party. Lancet 1996; 348: 1605–10. 22. Bujko K, Nowacki A, Nasierowska-Guttmejer W et al. Longterm results of a randomized trial comparing preoperative shot-course radiotherapy with preoperative conventionally fractionated chemoradiation for rectal cancer. Brit J Surg 2006; 93: 1215–23. 23. Bosset J, Colette L, Calais G et al. Chemotherapy with preoperative radiotherapy in rectal cancer. New Engl J Med 2006; 355: 1114–23. 24. Gerard J, Conroy T, Bonnetain F et al. Preoperative radiotherapy with or without concurrent fluorouracil and leucovorin in T3-rectal cancers: Results of FFCD 9203. J Clin Oncol 2006; 24: 4620–5. 25. Frykholm GJ, Glimelius B and Pahlman L. Preopeterative or postoperative irradiation in adenocarcinoma of the rectum: final treatment results of a randomized trial and an evaluation of late secondary effects. Dis Colon Rectum 1993; 36: 564–72. 26. Sauer R, Becker H, Hohenberger W et al. Preoperative versus postoperative chemoradiotherapy for rectal cancer. New Engl J Med 2004; 351: 1731–40. 27. NIH Consensus Conference. Adjuvant therapy for patients with colon and rectal cancer. JAMA 1990; 264: 1444–50. 28. Sharma A, Hartley J, Monson JR. Local excision of rectal tumors. Surg Oncol 2003; 12: 51–61. 29. Tytherleigh MG, Warren BF, Mortensen NJM. Management of early rectal cancer. Brit J Surg 2008; 95: 409–23. 30. Cox JD, Stetz J, Pajak TF. Toxicity criteria of the radiation therapy oncology group (RTOG) and the European Organization for Research and Treatment of Cancer (EORTC). Int J Radiat Oncol Biol Phys 1995; 31: 1341–6. 31. Miller RC, Sargent DJ, Martenson JA et al. Acute diarrhea during adjuvant therapy for rectal cancer: A detailed analysis from a reandomized intergroup trial. Int J Radiat Oncol Biol Phys 2002; 54: 409–13. 32. McAnena OJ, Heald RJ, Lockhart-Mummery HE. Operative and functional results of total mesorectal excision with ultralow anterior resection in the management of the lower one third of the rectum. Surg Gynecol Obstet 1990; 170: 517–21. 33. Frykholm J, Sintorn K, Montelius A et al. Acute lumbosacral plexopathy during and after properative radiotherapy of rectal adenocarcinoma. Radother Oncol 1996; 38: 121–30. 34. Marijnen CAM, Kapiteijn E, van de Velde H et al. Acute side effects and complications after short-term preoperative radiotherapy combined with total mesorectal ecision in primary rectal cancer: Report of a multicenter randomized trial. J Clin Oncol 2002; 20: 817–25. 35. Sauer R, Fletkau R, Wittekind C et al. Adjuvant versus neoadjuvant radiochemotherapy for locally advanced rectal cancer: a progress report of a phase-III randomized trial (protocol CAO/ ARO/AIO-94). Strahlentherapie Onkol 2001; 177: 173–81.

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36. Bujko K, Nowacki MP, Kepka L et al. Postoperative complications in patients irradiated preoperatively for rectal cancer: report of a randomized trial comparing short-term radiotherapy vs. chemoradiation. Colorectal Dis 2005; 7: 410–6. 37. Peeters KCMJ, van de Velde CJH, Leer JWH et al. Late side effects of short-course preoperative radiotherapy combined with total mesorectal excision for rectal cancer: Increased bowel dysfunction in irradiated patients—A Dutch Colorectal Cancer Group Study. J Clin Oncol 2005; 23: 6199–206. 38. Lange MM, den Dulk M, Bossema ER et al. Risk factors for faecal incontinence after rectal cancer treatment. Brit J Surg 2007; 94: 1278–84. 39. Kollmorgen CF, Meagher AP, Wolff BG et al. The long term effect of adjuvant postoperative chemoradiotherapy for rectal carcinoma on bowel function. Annals Surg 1994; 220: 676–82. 40. Pietrzak L, Bujko K, Nowacki MP et al. Quality of life, anorectal and sexual functions after preoperative radiotherapy for rectal cancer: report of a randomized trial. Radiother Oncol 2007; 84: 217–25. 41. Kennedy GD, Heise CP. Radiation Colitis and Proctitis. Clinics Colon Rectal Surg 2007; 20: 64–72. 42. Nussbaum ML, Campana TJ, Weese JL. Radiation-induced intestinal injury. Clinics in Plastic Surgery 1993; 20: 573–80. 43. Eifel PJ, Levenback C, Wharton JT, Oswald MJ. Time course and incidence of late complications in patients treated with radiation therapy for FIGO stage IB carcinoma of the uterine cervix. [see comment]. Int J Radiat Oncol Biol Phys 1995; 32: 1289–300. 44. Dorr W, Hendry JH. Consequential late effects in normal tissues. Radiother Oncol 2001; 61: 223–31. 45. Strockbine MF, Hancock JE, Fletcher GH. Complications in 831 patients with squamous cell carcinoma of the intact uterine cervix treated with 3,000 rads or more whole pelvis irradiation. Am J Roentgenol Radium Ther Nucl Med 1970; 108: 293–304. 46. Hayne D, Vaizey CJ, Boulos PB. Anorectal injury following pelvic radiotherapy. Br J Surg 2001; 88: 1037–48. 47. Reichelderfer M, Morrissey JF. Colonoscopy in radiation colitis. Gastrointest Endosc 1980; 26: 41–3. 48. Haboubi NY, Schofield PF, Rowland PL. The light and electron microscopic features of early and late phase radiationinduced proctitis. Am J Gastroenterol 1988; 83: 1140–4. 49. Andreyev HJN, Vlavianos P, Blake P et al. Gastrointestinal symptoms after pelvic radiotherapy: role for the gastroenterologist? Int J Radiat Oncol Biol Phys 2005; 62: 1464–71. 50. Kochhar R, Patel F, Dhar A et al. Radiation-induced proctosigmoiditis. Prospective, randomized, double-blind controlled trial of oral sulfasalazine plus rectal steroids versus rectal sucralfate. Dig Dis Sci 1991; 36: 103–7. 51. Henriksson R, Franzen L, Littbrand B. Prevention and therapy of radiation-induced bowel discomfort. Scandinavian Journal of Gastroenterology - Supplement 1992; 191: 7–11. 52. Pinto A, Fidalgo P, Cravo M et al. Short chain fatty acids are effective in short-term treatment of chronic radiation proctitis: randomized, double-blind, controlled trial. Dis Colon Rectum 1999; 42: 788–95.

radiation therapy: acute and late toxicity 53. Viggiano TR, Zighelboim J, Ahlquist DA et al. Endoscopic Nd:YAG laser coagulation of bleeding from radiation proctopathy. Gastrointest Endosc 1993; 39: 513–7. 54. Tam W, Moore J, Schoeman M. Treatment of radiation proctitis with argon plasma coagulation. [see comment]. Endoscopy 2000; 32: 667–72. 55. Taylor JG, Disario JA, Buchi KN. Argon laser therapy for hemorrhagic radiation proctitis: long-term results. Gastrointest Endosc 1993; 39: 641–4. 56. de P, V, Etienney I, Bauer P et al. Formalin application in the treatment of chronic radiation-induced hemorrhagic proctitis–an effective but not risk-free procedure: a prospective study of 33 patients. Dis Colon Rectum 2005; 48: 1535–41. 57. Parikh S, Hughes C, Salvati EP et al. Treatment of hemorrhagic radiation proctitis with 4 percent formalin. Dis Colon Rectum 2003; 46: 596–600. 58. Luna-Perez P, Rodriguez-Ramirez SE. Formalin instillation for refractory radiation-induced hemorrhagic proctitis. J Surg Oncol 2002; 80: 41–4.

59. Dall’era MA, Hampson NB, Hsi RA, Madsen B, Corman JM. Hyperbaric oxygen therapy for radiation induced proctopathy in men treated for prostate cancer. J Urol 2006; 176: 87–90. 60. Kennedy M, Bruninga K, Mutlu EA et al. Successful and sustained treatment of chronic radiation proctitis with antioxidant vitamins E and C. Am J Gastroenterol 2001; 96: 1080–4. 61. Cavcic J, Turcic J, Martinac P et al. Metronidazole in the treatment of chronic radiation proctitis: clinical trial. Croat Med J 2000; 41: 314–8. 62. Pricolo VE, Shellito PC. Surgery for radiation injury to the large intestine - variables influencing outcome. Dis Colon Rectum 1994; 37: 675–84. 63. Anseline PF, Lavery IC, Fazio VW, Jagelman DG, Weakley FL. Radiation injury of the rectum: evaluation of surgical treatment. Ann Surg 1981; 194: 716–24. 64. Camma C, Giunta M, Fiorica F et al. Preopetative radiotherapy for respectable rectal cancer: A meta-analyis. JAMA 2000; 284: 1008–15.

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31

Surgery for ulcerative colitis Patricia L Roberts

Clinical Vignette Challenging Case A 35-year-old male is undergoing an ileoanal pouch procedure for ulcerative colitis. Following transection of the ileum flush with the cecum, the surgeon notes that it will be difficult for the pouch to reach the anus. Challenging Case Management Difficulties with the ileoanal pouch reaching the anus occur for two main reasons: failure to mobilize the small bowel, or patient-related factors such as obesity or a long narrow anal canal. Difficulty with reach is more common if a mucosectomy is performed rather than a double-stapled anastomosis. An S pouch may reach the anus easier than a J pouch. If the main reason for the pouch not reaching is patient obesity and a thickened mesentery, an initial total abdominal colectomy, ileostomy, and Hartmann closure of the rectum may be performed. Following weight reduction, an ileoanal pouch procedure can be performed. A series of technical maneuvers including mobilization of the small bowel up to the duodenum, scoring the peritoneum over the superior mesenteric artery, and the creation of mesenteric windows can facilitate pouch reach. If, despite these maneuvers, the pouch does not reach, the pouch can be left in the pelvis, a loop ileostomy created, and, after a period of several months, the pouch can then be joined to the anus. Additional details of these technical maneuvers are described in the text. INTRODUCTION Ulcerative colitis is an inflammatory condition involving the colon and rectum. The incidence in the United States is 8.8 cases per 100,000 person years.(1) Thus, in this country, there are approximately 26,000 new cases of ulcerative colitis diagnosed annually and 730,000 people with ulcerative colitis.(1, 2) Although many patients are treated effectively with medical therapy, approximately 23–45% of patients require colectomy. The risk of requiring colectomy is higher in patients with pancolitis than patients with left sided disease.(3, 4) This chapter concentrates on the indications for surgery, the operative options, and the outcome of surgery for ulcerative colitis. Indications for Surgery Surgery for ulcerative colitis is divided into two categories: urgent or emergency surgery, and elective surgery. Acute Colitis Urgent or emergent surgery is indicated for patients with acute unresolving colitis or life-threatening complications associated with colitis, including fulminant or toxic colitis, hemorrhage, colonic perforation, or obstruction. Severe acute colitis may occur in 5 to 15% of patients with ulcerative colitis. The classification system of Truelove and Witts is most commonly used and identifies clinical parameters by which colitis is categorized as mild,

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Table 31.1  Truelove and Witts Criteria for Evaluating the Severity of Ulcerative Colitis. Variable

Mild disease

Severe Disease

Fulminant Disease

Stools (Number/day)

<4

>6

>10

Blood in stool

Intermittent

Frequent

Continuous

Temperature (ºC)

Normal

>37.5

>37.5

Pulse (beats/min)

Normal

>90

>90

Hemoglobin

Normal

<75% of normal value

Transfusion required

Erythrocyte sedimentation rate

<30

>30

>30

Colonic features on x-ray

Air, edematous wall, thumb­ printing

Dilatation

Clinical Signs

Abdominal tenderness

Abdominal distention and tenderness

Source: After Truelove and Witts. BMJ 1955; 2: 1041–45. Reprinted with permission from Clinics in Colon and Rectal Surgery. Volume 17, Number 1, 2004, page 8.

moderate, and severe (5, 6) (Table 31.1). For patients with acute colitis, stool studies should be done to rule out superinfection with clostridium difficile, bacteria, or ova and other parasites. A flexible sigmoidoscopy without bowel preparation with minimal insufflation of air is helpful to biopsy the rectum to exclude cytomegalovirus (CMV). In one series of patients with steroid resistant acute ulcerative colitis, the incidence of associated cytomegalovirus was 36%.(7) The majority of patients diagnosed with CMV responded to administration of foscarnet or ganciclovir. After exclusion of an infectious etiology, patients are treated with intravenous steroids for 5–7 days. If there is no clinical response, cyclosporine or infliximab is considered. Patients who are reluctant to use cyclosporine or infliximab, or patients who do not respond, should undergo colectomy. While administration of steroids is associated with an increase in postoperative complications, immunosuppressives do not appear to increase the incidence of postoperative complications.(8) A small subset of patients may develop fulminant colitis. The classification system of Truelove and Witts does not define fulminant colitis, but Hanauer (9) has modified the classification system to define patients with fulminant colitis. In the classification system of Truelove and Witts, severe disease is defined as >6 stools per day, a temperature >37.5 degree Celsius, a pulse of >90 beats per minute, hemoglobin <75% of normal, an erythrocyte sedimentation rate of >30 mm/hr, the presence of air, edematous wall, or thumbprinting on x-ray and abdominal tenderness. Fulminant colitis is defined as >10 stools per day, continuous

surgery for ulcerative colitis bloody bowel movements, a temperature of >37.5 degree Celsius, a pulse of >90 beats per minute, transfusion requirement, an erythrocyte sedimentation rate of >30 mm/hr, dilatation of the colon and abdominal distention and tenderness. The term toxic megacolon has been used when the colonic distention of the transverse colon exceeds 6 cm, but relying on this finding to diagnose toxic colitis is not necessary, as some patients will have “toxicity” in the absence of colonic distention. Prompt treatment and diagnosis of toxic colitis is needed to avoid progression to perforation. Approximately 20–30% of patients with toxic colitis require emergency surgery. Perforation in the setting of toxic or fulminant colitis substantially increases the mortality rate. Patients whose condition worsens or who fail to make substantial improvement after a period of 48–96 hours should be considered for surgery to avoid this complication.(10) Massive hemorrhage in patients with ulcerative colitis is uncommon, accounting for <10% of emergency colectomies performed for ulcerative colitis, and raises the possibility of Crohn’s disease.(11) Emergency vs. Elective Procedures The surgical options for patients who require emergency surgery for acute colitis are aimed at restoring the patient back to a general state of health and preserving reconstructive options for subsequent surgery. The most common operation performed is total abdominal colectomy with ileostomy, and either Hartmann closure of the rectum or creation of a mucous fistula. Preoperative counseling and marking by an enterostomal therapist is optimal. This procedure removes the majority of the diseased bowel, avoids an intestinal anastomosis in an ill patient, and preserves the option for an ileoanal pouch procedure in the future. The colon is transected at the level of the sacral promontory avoiding the need for a pelvic dissection. If the severity of disease as demonstrated by severe ulcerations and friability of the bowel precludes safe closure of the stump, a variety of other options may be employed. The stump may be exteriorized as a mucous fistula. This requires a longer segment of bowel and is associated with bleeding and mucus from an additional stoma. Alternatively, it has been suggested that extrafascial placement compared with intraperitoneal closure of the Hartmann stump may be associated with fewer infectious complications.(12) Transanal drainage has also been suggested to decrease the incidence of infectious complications associated with the Hartmann stump.(13) Pelvic dissection and creation of a relatively short Hartmann pouch should be avoided as this makes dissection and subsequent ileoanal pouch creation more difficult. A laparoscopic or open approach may be used for performance of total abdominal colectomy and ileostomy in patients with acute colitis.(14) Elective Procedures The most common indication for elective surgery is intractability to medical management defined as failure of medical therapy. Intractability includes insufficient symptom control despite intensive medical therapy. Due to loss of time from work, school or activities in general, the patient may not have an acceptable quality of life. The risks of medical therapy may be substantial including potential complications from long-term steroid therapy or complications of the side effects of medical therapy. In

children, growth retardation can result from poorly controlled ulcerative colitis and is an indication for colectomy. Patients with longstanding ulcerative colitis are at an increased risk for the development of colorectal cancer. The exact risk is difficult to determine since many series have lacked longitudinal follow-up or have included patients seen at tertiary referral facilities. Surveillance colonoscopy with biopsy has been recommended in patients with left-sided or pan colitis (defined as microscopic disease proximal to the splenic flexure) after 8 years of disease symptoms. At least 33 biopsies are necessary to obtain a sensitivity of 90%, and four quadrant biopsies are recommended every 10 cm along the colon and in any abnormal appearing area. A recent meta-analysis has estimated the risk of the development of colorectal cancer in patients with long-standing ulcerative colitis to be 2% at 10 years, 8% at 20 years, and 18% after 30 years of disease. (15) There is no evidence to show that surveillance prolongs survival in such patients, although patients who develop cancers in a surveillance program tend to have earlier stage cancers.(16, 17) Proctocolectomy is indicated for patients with carcinoma, nonadenoma-like dysplasia associated lesion or mass (DALM), and patients with high grade dysplasia.(10) The presence of high grade dysplasia should ideally be confirmed by two independent expert pathologists. For those patients who underwent immediate colectomy, cancer was detected in 42% of patients with highgrade dysplasia and 19% with low-grade dysplasia.(18) Although patients with low-grade dysplasia should be offered colectomy, the natural history of low-grade dysplasia is not as well defined. The interobserver variation between pathologists confounds the recommendations about low-grade dysplasia. Studies are conflicting, with one study of a surveillance program showing that in patients with low-grade dysplasia the 5-year predictive value for the development of cancer or high-grade dysplasia was 54%.(19) Another study showed that only 18% of patients with low-grade dysplasia progressed to high-grade dysplasia or a dysplasia associated lesion/mass.(20) Strictures may also develop in 10–25% of patients with ulcerative colitis, and while the majority are benign up to 25% are malignant. Strictures which cause obstruction, develop in longstanding disease, and are found proximal to the splenic flexure, are most likely to be malignant and are another indication for colectomy.(21) PROCTOCOLECTOMY WITH BROOKE ILEOSTOMY Proctocolectomy with ileostomy has previously been the “gold standard” operation for ulcerative colitis against which other operations have been compared. This operation essentially cures the disease and restores patients back to health and to a relatively normal life. It is a one-stage procedure which removes the diseased mucosa and has fewer potential complications than the ileoanal pouch procedure. The main drawback is the presence of a permanent ileostomy, something which most patients wish to avoid. Indications This operation is indicated in those patients who require surgery for ulcerative colitis, but are not candidates for the ileoanal pouch procedure. These patients include those who are elderly, have fecal incontinence or an inadequate sphincter, patients with low rectal



improved outcomes in colon and rectal surgery cancers in association with ulcerative colitis who require proctectomy and possibly pelvic radiation, and those patients who opt for a permanent Brook ileostomy for personal preferences. Furthermore, patients who develop pouch failure and require pouch excision essentially have a completion proctectomy. Operative technique The preoperative period includes patient education about the procedure and the effects of an ileostomy. Preoperative consultation with an enterostomal nurse is helpful. The stoma site selected should be a flat area, away from bony prominences and creases. Proctocolectomy is performed through either an open or laparoscopic approach. Following mechanical bowel preparation the day before surgery, the patient is administered preoperative intravenous antibiotics and positioned in lithotomy position. After performance of a standard colectomy, pelvic dissection is performed. The retrorectal space is entered sharply and the pelvic dissection is undertaken with careful attention to the ureters and identification of the hypogastric nerves. The dissection is carried out to the pelvic floor. A pack is placed posterior to the rectum and the perineal dissection is performed. An intersphincteric dissection allows for a smaller wound, a relatively bloodless dissection, and presumably better healing. The perineal dissection is carried out to the level of the pelvic dissection. After excision of the colon and rectum, the wound is closed in layers and a Brooke ileostomy constructed. A foley catheter is left for several days in addition to a closed suction drain. Outcome Proctocolectomy with ileostomy is associated with fewer potential complications than ileoanal pouch procedure. In one series, the long-term complication rate in patients undergoing proctocolectomy with ileostomy compared to ileoanal pouch procedure was 26% vs. 52%.(22) The most common long-term complications include stoma related complications. From a physiologic standpoint, patients with an ileostomy are more prone to dehydration, electrolyte abnormalities, and kidney stone formation. Patients should be counseled to be aware of signs and symptoms of dehydration. Although problems have decreased substantially with modern pouching systems, preoperative stoma marking, and the expertise of enterostomal nurses, patients may experience peristomal skin irritation, parastomal hernia formation, stomal retraction, fistula, and stomal stenosis. In the long-term, up to one third of patients require operative revision.(23) Slow or delayed perineal wound healing occurs in up to 25% of patients after proctocolectomy with ileostomy. An intersphincteric dissection may decrease the size of the perineal wound and improve wound-related complications.(24) If infection or delayed wound healing occurs, local wound care with examination under anesthesia, debridement, and curettage is performed. The vacuum assisted closure device has been helpful to treat persistent perineal wounds.(25) In some cases, muscle transposition, such as gracilis muscle transposition is necessary to heal persistent wounds. As with any operation involving a pelvic dissection, sexual and urinary dysfunction may occur from injury to the sympathetic and parasympathetic nerves. The incidence of sexual dysfunction is felt to be less than that occurring in those patients who undergo proctectomy



for malignant disease. However, this may reflect the younger age of patients undergoing proctocolectomy for ulcerative colitis. Impotence occurs in 1–2% of patients and retrograde ejaculation may occur in up to 5% of patients.(26) Dysparuenia and increase in vaginal discharge occur in up to 30% of women from scarring and change in the in-axis of the vagina.(27) Women must also be counseled about the potential for infertility because of scarring pelvic adhesions. Despite the fact that patients have undergone a major surgical procedure, the quality of life remains high after proctocolectomy with ileostomy. Overall 90–93% of patients are satisfied with their quality of life.(28, 29) Despite the satisfaction, a number of difficulties exist, including restriction of social and recreational activities in up to 25%, and dietary restrictions in almost 30%. Proctocolectomy With Continent Ileostomy Another option for patients who require surgery for ulcerative colitis is a continent ileostomy, introduced by Nils Kock in 1969. (30) Despite initial enthusiasm, this operation is infrequently performed today because of the appreciable number of complications associated with the procedure, in addition to the fact that it has been largely supplanted by the ileal pouch anal anastomosis. Indications for a continent ileostomy include those patients who have undergone prior proctocolectomy with ileostomy and desire a continent stoma, selected patients who have a failed ileoanal pouch procedure, patients with ulcerative colitis and rectal cancer who could not undergo an ileal pouch anal anastomosis (IPAA) and patients with poor sphincter tone in whom the functional results would be quite poor. Advanced age and obesity are relative contraindications to performance of the procedure. As with the ileoanal pouch procedure, Crohn’s disease is a general contraindication to the procedure because of the risk of recurrent disease which could necessitate resection of the continent ileostomy. Operative Technique The operative technique involves initial performance of a proctocolectomy. The continent ileostomy is then constructed using the terminal 40–60 cm of the ileum. A three limb pouch with an intussuscepted nipple valve is used (Figure 31.1). The valve is created by intussuscepting the efferent loop. After being tested for integrity and continence, the exit conduit is brought through the abdominal wall. The site of continent ileostomy is generally determined preoperatively with an enterostomal therapist and is lower in the abdomen than a standard ileostomy. Catheter drainage is maintained for approximately 4 weeks to allow complete healing of the pouch.(31, 32) Guidelines for catheter management have been outlined by Beck.(33) A number of technical modifications have been made over the years to prevent nipple valve complications. Mesh was initially used to stabilize the valve, but the technique was abandoned because of a high incidence (42.5%) of fistula formation.(31) A recently described modification to avoid slippage of the nipple valve is the “T-pouch” in which a portion of the ileum is folded into the side of the pouch.(33, 34) Outcome In a large series of patients undergoing continent ileostomy with a median follow-up of 11 years, 16.6% of patients required Kock

surgery for ulcerative colitis (A)

(B)

(D)

(C)

(E)

Figure 31.1  Continent ileostomy (A) Three limbs of small bowel are measured and the bowel wall is sutured together. (B) After opening the bowel along the dotted lines in (A), the edges are sewn together to form a two-layered closure. (C) A valve is created intussuscepting the efferent limb into the pouch and fixing it in place with a linear noncutting stapler. (Inset: staples in place on valve.) (D) The valve is attached to the pouch side-wall with the linear noncutting stapler. A cross-section of the finished pouch is shown. (E) After closure of the last suture line, the pouch is attached to the abdominal wall and a catheter is inserted to keep the pouch decompressed during healing (Reprinted with permission).



improved outcomes in colon and rectal surgery pouch excision.(31) The number of complications associated with the procedure was high with an average of 3.7 (range 1–28) complications per patient. Some of the most significant complications are associated with nipple valve slippage which occurs because of the tendency of the intussuscepted segment to slide and evert on the mesenteric aspect. Manifestations of nipple valve slippage include difficult catheterization, incontinence, and obstructive symptoms from obstruction of the outflow tract. The incidence of nipple valve slippage is approximately 30%. A variety of technical modifications have been devised to reduce the incidence of this complication. Use of prosthetic materials to wrap the valve reduces the incidence of nipple valve slippage but is associated with abscess and fistula formation.(35) The T-pouch modification (34) has been advocated to avoid this complication, but there is currently no controlled data available. Pouchitis is a well recognized complication of the Kock pouch occurring in up to 25% of patients. It is manifested by increased bowel frequency, often associated with blood and mucus and at times, incontinence. The etiology of pouchitis is unknown, but the majority of patients are treated effectively with antibiotics and continuous pouch drainage. Other complications associated with the procedure include the development of fistula, parastomal hernia, and small bowel obstruction. Long-term results of patients with continent ilesotomies reveal a cumulative success rate of 71% at 29 years in 96 patients followed from 1972 to 2000.(36) The success rate with continent ileostomy is appreciably less than with the ileoanal pouch procedure. Total Abdominal Colectomy with Ileorectal Anastomosis Although the majority of patients with ulcerative colitis have rectal involvement, a small number of patients with rectal sparing may be treated with total abdominal colectomy and ileorectal anastomosis. Such patients may subsequently require rectal excision for diarrhea and poor functional results, ongoing proctitis, and malignant transformation. Surveillance for the development of dysplasia is recommended. Recent series have shown an average number of bowel movements of 3–6/day after the procedure with a failure rate of 11–57% (37, 38, 39). The incidence of developing cancer with long-term follow-up ranges from 0–6% (40, 41, 42). Restorative Proctocolectomy with Ileoanal Pouch Since its introduction in 1978, the ileoanal pouch procedure has become the procedure of choice for patients who require surgery for ulcerative colitis and familial adenomatous polyposis. Over the years, the operation has undergone a series of technical modifications and it can be performed with essentially no mortality and good long-term outcomes. The procedure avoids the need for a permanent stoma and removes the diseased bowel. Indications The most common indication for the ileoanal pouch procedure is failure of medical therapy for ulcerative colitis or development of complications from medical therapy which outweigh the benefit. Additional indications include the development of dysplasia and



certain extraintestinal manifestations. Colon cancer is not a contraindication to the procedure, but performance of an ileoanal pouch must not compromise the oncologic resection. IPAA is usually not advisable in a low- or mid-rectal cancer because of the need for chemoradiation therapy and the potential effects on the pouch and the anal sphincter. Although the majority of patients who undergo pouch surgery are young, age is not a contraindication to the performance of the procedure. We advise patients on a case by case basis over the age of 65. Nocturnal leakage and incontinence is more common in older patients who undergo pouch surgery and preoperative assessment should include assessment of anal sphincter function and extensive discussion about the potential functional outcome. Operative Technique Preoperatively, the risks and benefits of the procedure are discussed with the patient, and consultation with an enterostomal therapist is beneficial. An appropriate site for the intended stoma is marked in the right lower quadrant. The procedure is performance after mechanical and antibiotic bowel preparation. Although the procedure may be performed with an open or laparoscopic approach, pouch surgery is increasingly being performed by a laparoscopic approach. Retrospective case-matched comparative studies have shown a longer operative time (median 330 min vs. 230 min), but a quicker return of bowel function (2 days vs. 4 days) and a shorter hospital stay (7 days vs. 8 days) with laparoscopic pouch procedures (43). A recent meta- analysis of 10 studies with 329 patients confirmed that despite a longer operative time, patients had a lower blood loss, shorter hospital stay, and smoother recovery compared to open surgery.(44) In a review of 100 laparoscopic and 189 open ileoanal pouch procedures for ulcerative colitis, patients reported excellent body image and quality of life scores regardless of open or laparoscopic approach. (45) In the past 5 years, the majority of the ileoanal pouch procedures have been performed at our institution with a laparoscopic hand-assisted approach. The technical details of the procedure are outlined in videos (CineMed-American College of Surgeons). One of the critical maneuvers during the performance of ileoanal pouch surgery is the creation of a tension-free anastomosis between the pouch and the anus. Undue tension on the anastomosis leads to stricture formation, anastomotic leakage, potential pelvic sepsis, and poor function. To perform a tension-free anastomosis, the apex of the pouch should reach the inferior border of the symphysis pubis. Assessment of potential pouch reach to the anus is performed before pouch creation. In obese patients, it may be necessary to perform an initial total abdominal colectomy, ileostomy and Hartman closure of the rectum in anticipation of significant weight reduction and then pouch creation.(46) An S-pouch may afford an additional 2 cm of length compared to a J-pouch but it is more difficult to construct and has potential efferent limb problems.(47) A tension-free anastomosis is more difficult to achieve in male patients with a narrow pelvis, patients with a long anal canal, obese patients, and patients who undergo mucosectomy with handsewn anastomosis. To achieve adequate length on the mesentery, a series of technical maneuvers is performed, including mobilization of the posterior attachment

surgery for ulcerative colitis of the small bowel mesentery, exposing the inferior portion of the head of the pancreas, and scoring the peritoneum of the small bowel mesentery serially on the anterior and posterior surfaces. (48) Each of these relaxing incisions confers an additional 1 cm of distal reach. At least two relaxing incisions are made along the course of the superior mesenteric artery. If additional length is required, the mesentery of the small bowel is transilluminated to delineate the loop formed by the ileocolic artery and the terminal ileal branch of the superior mesenteric artery. Traction is placed on the small bowel by grasping the intended apex of the pouch, and vessels between the primary and secondary arcades that are under tension are identified and ligated. This maneuver adds 2–5 cm of additional length. The terminal branches of the superior mesenteric artery of the ileocolic artery can be divided for additional length. These vessels are clamped for 10–15 minutes before ligation to confirm adequate vascularity of the ileum before division. In selected cases, interposition vein grafts have been used to obtain adequate mesenteric length.(49) If there is inadequate length despite these maneuvers, the pouch may be left in the pelvis, and not anastomosed to the anal canal with plans to return at a subsequent date for anastomosis. The weight of the pouch and the dependent portion of it with the aid of gravity may facilitate reach to the anus at a later date. Outcome The mortality after ileoanal pouch surgery is <1%. The majority of the patients undergoing the procedure are young and otherwise in good health, with the exception of ulcerative colitis or familial adenomatous polyposis. Despite refinements in surgical technique, the operation is associated with an appreciable number of complications. A recent meta-analysis with a review of 5,215 patients who underwent ileoanal pouch surgery between 1988 through 2000 revealed a preoperative diagnosis of ulcerative colitis in 87.5%, indeterminate colitis in 2%, Crohn’s disease in 0.8%, familial adenomatous polyposis in 8.9%, and other diagnoses in 0.7%.(50) A diverting ileostomy was performed in 81.6%. Functional results (bowel, urinary, gynecologic and sexual function) At a median follow-up of 37.2 mos after ileoanal pouch surgery and ileostomy reversal, the mean defecation frequency was 5.2 during the day with a mean night-time frequency of 1.0.(50) Mild fecal incontinence during the day occurred in 17%, while 3.7% had severe fecal incontinence during the day and 7.3% had urge incontinence. Bowel function deteriorates with advancing age. (51) Prospective evaluation of long-term function reveals that especially 12 years or more after surgery, major and minor incontinence are worse. Twelve years following surgery, 27% of patients vs. 9% (<12 years) had major daytime incontinence and 33% vs. 10% reported more major night time incontinence. Furthermore, minor incontinence was seen in 48% of patients after 12 years vs. 16% of patients followed for under 12 years.(51) The reported incidence of sexual dysfunction in a meta-analysis of 21 studies including 5,112 patients was 3.6%.(50) The authors point out the risk of underestimating complications due to a positive publication bias, and thus studies with negative results may be

less likely to be submitted and published. Indeed, a more recent review has further quantified the impact of the ileoanal pouch procedure on sexual and gynecologic function in women. A systematic review of 22 in 1,852 women who underwent restorative proctocolectomy from 1980 to 2005 revealed a much more significant impact on function.(52) The incidence of infertility was 12% before restorative proctocolectomy and 26% after (n = 945 women, 7 studies). Sexual dysfunction occurred in 8% preoperatively and 25% postoperatively (n = 419 women, 7 studies). More Cesarean sections were performed after restorative proctocolectomy, although no significant differences in pouch function and no significant perineal trauma was seen after vaginal delivery, thus suggesting that the mode of delivery should be based on obstetric considerations. An increase in bowel actions was noted during the third trimester but bowel activity returned to normal within 6 months of delivery. Peritoneal inclusion cysts which are associated with pelvic sepsis and adhesions are an additional underreported consequence of the ileoanal pouch procedure.(53, 54) Complications Despite refinements in surgical technique, restorative proctocolectomy is associated with an appreciable number of complications including pelvic sepsis, fistulas, strictures, fecal incontinence, pouch failure, and sexual dysfunction. A recent meta-analysis on pooled data of observational studies has been performed on 43 studies comprising 9,317 patients detailing the results and complications.(50) Small Bowel Obstruction Small bowel obstruction is a common complication after restorative proctocolectomy ranging from 15–44% of patients, with approximately half of patients requiring operation for treatment of obstruction.(55) Small bowel obstruction occurs more commonly after restorative proctocolectomy than after Brook ileostomy, presumably because of the cumulative increase in obstruction after multiple procedures. Patients who develop early postoperative small bowel obstruction are more likely to resolve with conservative measures than those patients diagnosed in later follow-up.(56) In a series of 1,178 patients who underwent IPAA, the cumulative risk of small bowel obstruction was 9% at 30 days, 18% at 1 year, 27% at 5 years and 31% at 10 years.(57) The most common site of adhesions were pelvic adhesions (32%) and adhesions at the ileostomy closure site (21%). Recent strategies to decrease the risk of adhesions have focused on the use of a bioresorbable membrane which has reduced the incidence, extent, and severity of adhesions (58), as well as the use of laparoscopic surgery (which results in less adhesions). Postoperative Hemorrhage Intraabdominal hemorrhage may occur from failure to secure the vascular pedicles and from pelvic bleeding, in addition to bleeding of the pouch suture or staple line. Pouch ischemia may also be associated with bleeding. Pouch bleeding noted intraoperatively is best treated by eversion of the pouch to expose the mucosa and cauterization or suture ligation as needed. Postoperative bleeding may require examination under anesthesia and/or pouch endoscopy with suture or endoscopic clipping of the bleeding point. Bleeding, especially 5–7 days after operation, may be associated



improved outcomes in colon and rectal surgery (A)

(B)

Figure 31.2 Retrograde pouch study shows a presacral collection (A) confirmed on CT scan (B). Collections arising from the anastomosis are preferably drained into the pouch to avoid a complex fistula.

with anastomotic dehiscence. In a series of 1,005 patients, pouch bleeding occurred in 38 patients (3.8%) and was treated with local irrigation with saline and adrenaline in 30 patients and transanal suture ligation in 8.(59) Pelvic sepsis Pelvic sepsis is defined as pelvic abscess, anastomotic leakage or dehiscence, or any pelvic or perineal infection. Some series distinguish between pelvic sepsis and anastomotic leak; pelvic sepsis generally results from a defect in the ileoanal anastomosis, anastomotic leak, or defect of the other staple or suture lines. A meta-analysis noted the incidence of pelvic sepsis to be 9.8%.(50) Manifestations of pelvic sepsis include fever, leukocytosis, perineal pain, purulent drain output, and prolonged ileus. As pelvic sepsis is a significant cause of pouch failure and since those patients with sepsis are more likely to have compromise of pouch function, any patient suspected of having pelvic sepsis, should be evaluated and treated expeditiously. CT scan confirms the diagnosis of pelvic sepsis, and contrast in the pouch (either by instilling rectal contrast or contrast through the efferent limb of the ileostomy) is useful in assessing the integrity of the anastomosis. Alternatively, a pouchogram and examination under anesthesia may be necessary. Intraabdominal or pelvic abscess requires percutaneous or operative drainage in addition to broad spectrum antibiotics (Figure 31.2). For patients with leakage from the anastomotic suture or staple line the abscess can be drained into the pouch. This potentially avoids the development of a complex fistula. Untreated pelvic sepsis results in fibrosis, a stiff, non-compliant reservoir, and a higher incidence of ultimate pouch failure.(60) Anastomotic leak or dehiscence Anastomotic leak after the ileoanal pouch procedure occurs between 5–18% of patients. In a recent meta-analysis, the



Figure 31.3 Asymptomatic anastomotic sinus in patient before ileostomy closure often requires no further treatment. Delay in ileostomy closure and repeat pouch study generally shows healing.

incidence of anastomotic leakage from either the pouch-anal anastomosis or the pouch itself was 7.1%.(61) The incidence of anastomotic leakage was more common in patients who did not have a stoma at the time of pouch surgery. The presence of a stoma may help to ameliorate the clinical manifestations of a leak. A leak may occur at the pouch anal anastomosis or along any

surgery for ulcerative colitis

Figure 31.4 A leak from the efferent limb of the pouch may be difficult to diagnose. Such patients rarely heal with antibiotics and drainage alone and often require exploration and repair.

Figure 31.5 A pouch vaginal fistula is seen on retrograde study. Early fistulas are due to infection and leak at the anastomosis while late fistulas often herald unsuspected Crohn’s disease.

of the staple or suture lines including the top of the J-pouch, the ileoanal anastomosis, or the pouch itself. Manifestations of a leak include the development of an abscess, fistula, or symptoms of pelvic pain, diarrhea, and fever. Risk factors associated with leak include tension on the anastomosis and ischemia resulting from tension on the anastomosis. One study suggested a lower incidence of pelvic sepsis associated with a double-stapled anastomosis compared with a mucosectomy and hand sewn anastomosis. (62) Management of anastomotic leak is individualized; patients who have an asymptomatic sinus before ileostomy closure without associated sepsis can be treated by delay in ileostomy closure and in most cases, ultimate healing of the tract.(Figure 31.3) Patients with peritonitis who have undergone restorative proctocolectomy without diverting ileostomy require diversion and drainage. Leaks from the tip of the J pouch are challenging both to diagnose and treat and developed in 14 out of 1,309 patients; all required surgical repair and none healed with conservative treatment (63) (Figure 31.4). With expertise and individualized management, pouch salvage can be was achieved in 88% of patients who developed anastomotic leak.(64)

challenging to treat and pouch advancement and neoileoanal anastomosis may be necessary to treat such patients.(67)

Stricture at the ileal pouch anal anastomosis Strictures at the ileal pouch anal anastomosis occur in approximately 10% of patients, and are more common after mucosectomy and handsewn anastomosis than after double-stapled anastomosis.(65, 66) Tension on the anastomosis and ischemia are associated with stricture formation. A lumen which admits the DIP joint of the index finger is generally satisfactory for good bowel function. Soft strictures are treated with gentle finger dilation or with balloon dilators. Long fibrotic strictures are more

Pouch vaginal fistula The incidence of pouch-vaginal fistulas ranges from 3–16%.(68) Pouch-vaginal fistulas are a major potential cause of pouch failure. Fistulas which occur in the early postoperative period are most commonly a manifestation of sepsis, and can occur from anastomotic leak and necessitation through the vaginal wall, or may result from technical factors including entrapment of the perivaginal tissue in the staple line (Figure 31.5). An important part of the ileoanal pouch procedure is to ensure that the vagina is not incorporated within the stapler. Late pouch-vaginal fistulas are more commonly associated with unsuspected Crohn’s disease.(69) Pouch-vaginal fistulas may manifest as pelvic pain, fever, a “Bartholin’s abscess” which when drained has fecalent material, or passage of gas. Fistulas which occur before ileostomy takedown are treated by management of infection, delayed ileostomy closure, and local repair. A number of procedures have been described for treatment of pouch vaginal fistulas. Ultimate success may be achieved in over 50% (70) but often requires multiple procedures. For patients with Crohn’s disease, the use of infliximab and other biologics may be helpful. Pouch anal fistulas Early fistulas are generally a manifestation of sepsis and leakage at the ileoanal anastomosis. Late fistulas may be crytoglandular in origin and may also be a manifestation of Crohn’s disease. Our preference is for liberal use of draining setons and avoidance of fistulotomy.

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improved outcomes in colon and rectal surgery Pouchitis The most frequent long-term complication of the ileoanal pouch procedure is the development of pouchitis, a nonspecific inflammation of the ileal pouch mucosa. The precise etiology of pouchitis has not been elucidated but it is believed to potentially result from an overgrowth of anaerobic bacteria. It is disease specific and more commonly seen in patients with ulcerative colitis; it is rarely encountered in patients with familial adenomatous polyposis. Patients with ulcerative colitis associated with extraintestinal manifestations and patients with sclerosing cholangitis have a higher incidence of pouchitis.(71, 72) Presenting signs and symptoms of pouchitis include abdominal cramps, abdominal tenderness, fever, and increase in stool frequency, often associated with blood or mucus. The diagnosis may be made clinically, on the basis of endoscopic examination in addition to clinical findings, or on the basis of histologic examination of the pouch mucosa; the lack of uniform criteria to make such a diagnosis accounts for the variation in the incidence of pouchitis in many series. A pouchitis disease activity index has been devised which includes clinical, endoscopic, and histologic features.(73) Pouchitis is generally treated with antibiotic therapy and the most commonly used agents include metronidazole or ciprofloxacin. Some patients with pouchitis develop ongoing symptoms, and for patients with refractory pouchitis or rapidly relapsing symptoms, the use of probiotics appears to be helpful. Probiotics may suppress the resident pathogenic bacteria, stimulate mucin glyocoprotein, prevent adhesion of pathogenic strains to epithelial cells, and reduce host immune responses. Probiotics may also be helpful in preventing recurrent pouchitis. A diagnosis of Crohn’s disease should be considered in patients with chronic pouchitis. In some cases, pouchitis is a cause of pouch failure. Pouchitis has been termed by some as “the Achilles heel” of the ileoanal pouch procedure. It is a cause of significant long-term morbidity; elucidation of the cause of pouchitis would likely benefit a large number of patients. Dysplasia and Malignancy Following construction, the ileoanal pouch undergoes a number of histologic changes, and with time, the metaplastic changes result in the ileal mucosa resembling colonic mucosa. These changes may also occur because of inflammation in the pouch and raise concerns of malignant transformation and the development of dysplasia. Neoplastic changes appear to be extremely rare. The majority of ileoanal pouch patients who develop cancer had a prior cancer at the time of pouch construction. The recent ASCRS guidelines do not endorse routine surveillance of ileal pouches for dysplasia.(10) Pouch Failure Pouch failure defined as pouch excision or a nonfunctioning pouch at 12 months after the ileoanal pouch procedure occurs in 5 to 15%. While the majority of pouch failures occur within 2 years of pouch construction, late pouch failures also occur. The common cause of pouch failure include unsuspected Crohn’s disease, chronic pouchitis, poor function with incontinence, persistent fistula, and other pouch related complications such as stenosis with outlet obstruction. Reoperative pouch surgery with an attempt to salvage the pouch is challenging; pouch salvage is higher in patients with ulcerative colitis than Crohn’s disease.(74)

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Controversies Reservoir Design While the original report by Parks used an S-pouch configuration, a number of other pouch configurations have been described, including J-pouch, lateral isoperistaltic H-pouch, and quadruple-loop W pouch. S pouches were initially associated with an increased need for catheterization because of a long distal ileal conduit. Shortening of the ileal conduit helps to initially avoid this complication, however, with time, the exit conduit of the S-pouch seems to elongate and obstructive defecation can occur. An S pouch may confer additional length compared to a J-pouch and may be the preferred configuration if achieving adequate length to performed a tension-free anastomosis in selected cases. The long outlet tract associated with an H pouch has been associated with stasis, pouch distention, and pouchitis. There have been no significant differences in pouch function based on the configuration of the pouch. Due to the ease of construction and the lack of compelling data favoring a specific pouch design, J pouches are most frequently performed. Use of an S or W pouch adds about 45 minutes to the time of the operative procedure. A recent meta-analysis examined the short and long-term outcome of J-, S- and W- reservoirs in patients undergoing restorative proctocolectomy.(75) A total of 18 studies of 1,519 patients (689 J, 306 W, and 524 S pouches) were reviewed. There was no difference in the incidence of early complications among the 3 types of pouch design. The frequency of defecation favored an S- or W- pouch design over a J pouch, although in practical terms the difference of 1–1.5 stools in a 24 hour period is unlikely to be of clinical significance to the patient. Night evacuation was significantly lower for a W than a J pouch. S pouches were associated with a greater need for pouch intubation due to a long distal conduit; W pouches also required intubation more often than J pouches. Mucosectomy vs. Double-Stapled Technique The ileoanal anastomosis may be performed with a handsewn technique after mucosal stripping (mucosectomy) or with a double-stapled technique. The initial technique reported by Parks was mucosal stripping commencing at the dentate line and removing all diseased mucosa, thus eliminating the risk of recurrent proctitis or neoplastic transformation. A potential advantage of the doublestapled technique is greater technical ease, and potentially less tension on the anastomosis. Preservation of the anal transitional zone may minimize sphincter damage and improve functional results. Three prospective randomized trials have not shown an advantage for the double-stapled technique vs. the mucosectomy technique.(76, 77, 78) These trials have all been small and are underpowered to demonstrate a difference. A metaanalysis of 4,183 patients (2,699 hand-sewn vs. 1,488 stapled IPAA) found similar early postoperative outcomes; however, stapled IPAA patients had improved nocturnal continence and had higher resting and squeeze pressures on anorectal physiologic testing.(79)

surgery for ulcerative colitis Preservation of the anal transitional zone and performance of a double-stapled technique leaves a residual 1–2 cm of diseased rectal mucosa, which may be at risk for the development of dysplasia and subsequent malignant transformation. It has been suggested that patients who have had a double-stapled technique be followed in a surveillance program, with biopsies of the retained columnar mucosa at least every 2 years beginning 8 to 10 years after the onset of symptoms of disease.(80) The recommendations for biopsy are controversial and is an area where further study is needed to define the natural history of the retained 1–2 cm of columnar mucosa. Other authors have not found the development of dysplasia with long-term follow-up.(81) Omission of ileostomy Restorative proctocolectomy is most commonly performed in two stages with an initial proctocolectomy, pouch construction, and diverting ileostomy, followed by ileostomy takedown after demonstration of satisfactory pouch healing. However, construction of a loop ileostomy may be associated with excessive stoma output, dehydration, hernia, bowel obstruction, and subsequent anastomotic complications associated with ileostomy takedown; these have been cited as a reason to potentially avoid diverting ileostomy in selected patients after ileoanal pouch construction. Conversely, many feel that loop ileostomy construction will minimize the potential consequences of pelvic sepsis (and potentially reduce the chance of pouch failure). This issue has been characterized by a great deal of passion and no randomized controlled studies. A one stage procedure without loop ileostomy is associated with a more difficult initial recovery and most likely a slight increased rate of anastomotic disruption and pelvic sepsis. An alternate view of this is that with fecal diversion, some patients with minor leaks and sepsis may not be clinically detected. Loop ileostomy avoids some of the consequences of pelvic sepsis, which is a major cause of pouch failure. Despite aggressive treatment the risk of pouch failure after pelvic sepsis is 20%, 31% and 35% at 3, 5 and 10 years respectively.(61) A single stage IPAA without loop ileostomy decreases the risk of ileostomy related complications, and complications including small bowel obstruction associated with an additional operative procedure. A recent review compared 17 studies with 1,486 patients (765 without ileostomy and 721 with ileostomy).(61) While there was no significant difference in the functional outcome of the two groups, those patients without an ileostomy had a higher incidence of pouch related leak and stricture formation. Selective omission of an ileostomy may be considered when an anastomosis is intact and under no tension, the procedure is not complicated by excessive bleeding or other technical difficulties and the patient is not on high dose steroids before the procedure. (10) The patient should be adequately counseled preoperatively concerning the pros and cons of ileostomy omission. Crohn’s Disease and Indeterminate Colitis Crohn’s disease has been considered to be a contraindication to the performance of an ileoanal pouch procedure because of the risks of recurrent disease and the potential need for pouch excision with subsequent loss of substantial amounts of bowel.

However, there are some patients who undergo the procedure for ulcerative colitis and an ultimate diagnosis of Crohn’s disease is made. In general these patients are found to have a higher risk of pouch failure from 28–52% (82, 83, 84, 85) compared to patients with ulcerative colitis or familial adenomatous polyposis. In a cohort of 32 patients out of 790 patients with an ultimate diagnosis of Crohn’s disease, 93% had complications including perineal abscess/ fistula (63%), pouchitis (50%), and anal stricture (38%) (85). It is not known whether administration of agents such as infliximab to such patients will ultimately impact the incidence of pouch failure, or whether it will delay the diagnosis or pouch failure. All efforts should be made to confirm a diagnosis of ulcerative colitis and exclude a diagnosis of Crohn’s disease preoperatively. In addition to a thorough history and examination, a recent study suggested that a family history of Crohn’s disease and serology positive for antiSaccharomyces cerevisiae immunoglobulin-A were more likely to be diagnosed with Crohn’s s after IPAA (67%) than patients with either risk factor (18%) or neither risk factor (4%) (86). While techniques of restorative surgery for ulcerative colitis have shown substantial advances over the past several decades, further study focusing on improvements in complications and functional outcomes will ultimately further improve a patient’s quality of life. References   1. Loftus CG, Loftus EV, Sandborn WJ et al. Update on incidence and prevalence of Crohn’s disease (CD) and ulcerative colitis (UC) in Olmsted County, Minnesota [abstract]. Gastroenterology 2003; 124: A36.   2. Loftus EV Jr. Clinical epidemiology of inflammatory bowel disease: incidence, prevalence, and environmental influences. Gastroenterology 2004; 126: 1504–7.   3. Leijonmarck CE. Surgical treatment of ulcerative colitis in Stockholm county. Acta Chir Scand Suppl 1990; 554: 1–56.   4. Wexner SD, Rosen L, Lowry A et al. Practice parameters for the treatment of mucosal ulcerative colitis. Dis Colon Rectum 1997; 40: 1277–85.   5. Truelove SC, Witts L. Cortisone in ulcerative colitis: final report on a therapeutic trial. BMJ 1955; 2: 1041–8.   6. Mahadevan U. Medical treatment of ulcerative colitis. Clin Colon Rectal Surg 2004; 17: 7–19.   7. Cottone M, Pietrosi G, Martorana G et al. Prevalence of cytomegalovirus infection in severe refractory ulcerative and Crohn’s colitis. Am J Gastroenterol 2001; 96: 773–5.   8. Mahadevan U, Loftus EV Jr, Tremaine WJ et al. Azathioprine or 6-mercaptopurine before colectomy for ulcerative colitis is not associated with increased postoperative complications. Inflamm Bowel Dis 2002; 8: 311–6.   9. Hanauer SB. Drug therapy: inflammatory bowel disease. N Engl J Med 1996; 334: 841–8. 10. Cohen JL, Strong SA, Hyman NH et al. Practice parameters for the surgical treatment of ulcerative colitis. Dis Colon Rectum 2005; 48: 1979–2009. 11. Robert JH, Sachar DB, Aufses A et al. Management of severe hemorrhage in ulcerative colitis. Am J Surg 1990; 159: 550–5.

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improved outcomes in colon and rectal surgery 12. Carter FM, McLoed, Cohen Z. Subtotal colectomy for ulcerative colitis: complications related to the rectal remnant. Dis Colon Rectum 1991; 34: 1005–9. 13. Karch LA, Bauer JJ, Gorfine SR et al. Subtotal colectomy with Hartmann’s pouch for inflammatory bowel disease. Dis Colon Rectum 1995; 38: 635–9. 14. Boushey RP, Marcello PW, Martel G et al. Laparoscopic total colectomy: an evolutionary experience. Dis Colon Rectum 2007; 50: 1512–19. 15. Eaden JA, Abrams K, Mayberry JF. The risk of colorectal cancer in ulcerative colitis: a meta-analysis. Gut 2001; 48: 526–35. 16. Hata K, Watanabe T, Kazama S et al. Earlier surveillance colonoscopy programme improves survival in patients with ulcerative colitis associated colorectal cancer: results of a 23-year surveillance programme in the Japanese population. Br J Cancer 2003; 89: 1232–6. 17. Mpofu C, Watson AJ, Rhodes JM. Strategies for detecting colon cancer and/or dysplasia in patients with inflammatory bowel disease. Cochrane Database Syst Rev 2004; 2: CD000279. 18. Bernstein CN, Shanahan F, Weinstein WM. Are we telling patients the truth about surveillance colonoscopy in ulcerative colitis? Lancet 1994; 343: 71–4. 19. Connell WR, Lennard-Jones JE, Williams CB et al. Factors affecting the outcome of endoscopic surveillance for cancer in ulcerative colitis. Gastroenterology 1994; 107: 934–44. 20. Befrits R, Ljung T, Jaramillo E et al. Low-grade dysplasia in extensive, long-standing inflammatory bowel disease: a follow-up study. Dis Colon Rectum 2002; 45: 615–20. 21. Gumaste V, Sachar DB, Greenstein AJ. Benign and malignant strictures in ulcerative colitis. Gut 1992; 33: 938–41. 22. Camilleri-Brennan J, Munro A, Steele FJ. Does an ileostomy pouch offer a better quality of life than a permanent ileostomy for patients with ulcerative colitis. J Gastrointest Surg 2003; 7: 814–9. 23. Carlsen E, Bergan A. Technical aspects and complications of end ileostomies. World J Surg 1995; 19: 632–5. 24. Berry AR, Campos RDE, Lee ECG. Perineal and pelvic morbidity following perimuscular excision of the rectum for inflammatory bowel disease. Br J Surg 1986; 73: 675–7. 25. Rivadeneira DE, Schoetz DJ, Marcello PW et al. Vacuumassisted closure of complex wounds of the perineum; a new paradigm in perineal wound care (abstract). Dis Colon Rectum 2003; 46: A67. 26. Dozois E. Proctocolectomy and Brooke ileostomy for chronic ulcerative colitis. Clin Colon Rectal Surg 2004; 17: 65–70. 27. Wickland M, Jansson I, Asztely M et al. Gynaecological problems related to anatomical changes after conventional proctocolectomy and ileostomy. Int J Colorect Dis 1990; 5: 49–52. 28. Camillari-Brennan J, Steele RJ. Objective assessment of quality of life following panproctocolectomy and ileostomy for ulcerative colitis. Ann R Coll Surg 2001; 83(5): 321–4. 29. Pemberton JH, Phillips SF, Ready RR et al. Quality of life after Brooke ileostomy and ileal pouch-anal anastomosis for chronic ulcerataive colitis. Comparison of performance status. Ann Surg 1989; 209: 620–8.

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30. Kock NG. Intra-abdominal “reservoir” in patients with permanent ileostomy. Preliminary observations on a procedure resulting in fecal “continence” in five ileostomy patients. Arch Surg 1969; 99: 223–31. 31. Nessar G, Fazio VW, Tekkis P et al. Long-term outcome and quality of life after continent ileostomy. Dis Colon Rectum 2006; 49: 336–44. 32. Castillo E, Thomassie LM, Whitlow CB et al. Continent ileostomy: current experience. Dis Colon Rectum 2005; 48: 1263–8. 33. Beck DE. Clinical aspects of continent ileostomy. Clinics in colon and rectal surgery 2004; 17: 57–63. 34. Kaiser AM, Stein JP, Beart RW Jr. T-pouch: a new valve design for a continent ileostomy. Dis Colon Rectum 2002; 45: 411–5. 35. Fazio VS, Church JM. Complications and function of the continent ileostomy at the Cleveland Clinic. World J Surg 1988; 12: 148–54. 36. Lepisto AH, Jarvinen HJ. Durability of Kock continent ileostomy. Dis Colon Rectum 2003; 46: 925–8. 37. Pastore RLO, Wolff BG, Hodge D. Total abdominal colectomy and ileorectal anastomosis for inflammatory bowel disease. Dis Colon rectum 1997; 40: 1455–64. 38. Elton C, Makin G, Hitos K et al. Mortality, morbidity and functional outcome after ileorectal anastomosis. Br J Surg 2003; 90: 59–65. 39. Khubchandani IT, Sandfort MR, Rosen L et al. Current status of ileorectal anastomosis for inflammatory bowel disease. Dis Colon rectum 1989; 32: 400–3. 40. Lofberg R, Leijonmarck CE, Bronstrom O. Mucosal dysplasia and DNA content in ulcerative colitis patients with ileorectal anastomosis. Follow-up study in a definite patient group. Dis Colon Rectum 1991; 34: 566–71. 41. Gruner OP, FLatmark A, Naas R et al. Ileorectal anastomosis in ulcerative colitis. Results in 57 patients. Scand J Gastroenterol 1975; 10: 641–6. 42. Paoluzi OA, Dipaolo MC, Ricci F et al. Ileo-rectal anastomosis in ulcerative colitis: results of a long-term follow-up study. Ital J Gastroenertol 1994; 26: 392–7. 43. Marcello PW, Milsom JW, Wong SK et al. Laparoscopic restorative proctocolectomy: case-matched comparative study with open restorative proctocolectomy. Dis Colon Rectum 2000; 43: 604–8. 44. Tilney HS, Lovegrove RE, Heriot AG et al. Comparison of short-term outcomes of laparoscopic vs. open approaches to ileal pouch surgery. Int J Colorectal Dis 2007; 22: 531–42. 45. Larson DW, Davies MA, Dozois EJ et al. Sexual function, body image and quality of life after laparoscopic and open ileal pouch-anal anastomosis. Dis Colon Rectum 2007; 51: 392–6. 46. Browning SM, Nivatvongs S. Intraoperative abandonment of ileal pouch to anal anastomosis-the Mayo Clinic experience. J Am Coll Surg 1998; 186: 441–6. 47. Smith L, Friend WG, Medwell SJ. The superior mesenteric artery. The critical factor in the pouch pull-through procedure. Dis Colon Rectum 1984; 27: 741–4.

surgery for ulcerative colitis 48. Burnstein MJ, Schoetz DJ, Coller JA, Veidenheimer MC. Technique of mesenteric lengthening in ileal reservoir-anal anastomosis. Dis Colon Rectum 1987; 30: 863–6. 49. Metcalf DR, Nivatvongs S, Sullivan TM et al. A technique of extending small-bowel mesentery for ileal pouch-anal anastomosis: report of a case. Dis Colon Rectum 2008; 51(3): 363–4. 50. Hueting WE, Buskens E, Tweel IVD et al. Results and complications after ileal pouch anal anastomosis: a meta-analysis of 43 observational studies comprising 9,317 patients. Dig Surg 2005; 22: 69–79. 51. Bullard KM, Madoff RD, Gemlo BT. Is ileoanal pouch function stable with time/ Results of a prospective audit. Dis Colon Rectum 2002; 45(3): 299–304. 52. Cornish JA, tan E, Teare J, Teoh TG et al. The effect of restorative proctocolectomy on sexual function, urinary function, fertility, pregnancy and delivery: a systematic review. Dis Colon Rectum 2007; 50: 1128–38. 53. Counihan TC, Roberts PL, Schoetz DJ et al. Fertility and sexual and gynecological function after ileal pouch anal anastomosis. Dis Colon Rectum 1994; 37: 1126–9. 54. Marcello PW, Roberts PL. Cystic pelvic masses. Seminars in colon and rectal surgery 1997; 8; 190–7. 55. Francois Y, Dozois RR, Kelly KA et al. Small intestinal obstruction complicating ileal-pouch-anal anastomotis. Ann Surg 1989; 209: 46–50. 56. Marcello PW, Roberts PL, Schoetz JD Jr et al. Obstruction after ileal pouch-anal anastomosis: a preventable complication? Dis Colon Rectum 1994; 37: 1176–7. 57. MacLean AR, Cohen Z, MacRae HM et al. Risk of small bowel obstruction after the ileal pouch-anal anastomosis. Ann Surg 2002; 235: 200–6. 58. Becker JM, Dayton MT, Fazio VW et al. Prevention of postoperative abdominal adhesions by a sodium hyaluronate-based bioresorbable membrane: a prospective, randomized, doubleblind multicenter study. J Am Coll Surg 1996; 183: 297–306. 59. Fazio VW, Ziv Y, Church JM et al. Ileal pouch-anal anastomoses complications and function in 1005 patients. Ann Surg 1995; 222: 120–7. 60. Scott NA, Dozois RR, Beart RW et al. Postoperative intraabdominal and pelvic sepsis complicating ileal pouch anal anastomosis. Int J Colorectal Dis 1988; 3: 149–52. 61. Weston-Petrides GK, Lovegrove RE, Tilney HS et al. Comparison of outcomes after restorative proctocolectomy with or without defunctioning ileostomy. Arch Surg 2008; 143(4): 406–12. 62. Ziv Y, Fazio VW, Church JM et al. Stapled ileal pouch-anal anastomoses are safer than handsewn anastomosis in patients with ulcerative colitis. Am J Surg 1996; 171: 320–3. 63. Gorgun E, Remzi FH. Complications of ileoanal pouches. Clin Colon Rectal Surg 2004; 17: 43–55. 64. Raval MJ, Schnitzler M, O’Connor BI et al. Improved outcome due to increased experience and individualized management of leaks after ileal pouch-anal anastomosis. Ann Surg 2007; 246: 763–70. 65. Prudhome M, Dozois RR, Godlewski G et al. Anal cancal strictures after ileal pouch-anal anastomosis. Dis Colon Rectum 2003; 46: 20–3.

66. Marcello PW, Roberts PL, Schoetz DJ Jr et al. Long-term results of the ileoanal pouch procedure. Arch Surg 1993; 128: 500–4. 67. Fazio VW, Tjandra JJ. Pouch advancement and neoileoanal anastomosis for anastomotic stricture and anovaginal fistula complicating restorative proctocolectomy. Br J Surg 1992; 79: 694–6. 68. Fleshner PR, Schoetz DJ Jr. Surgical management of ulcerative colitis in the ASCRS textbook of colon and rectal surgery, 2007: 567–83. 69. Fazio VW, Ziv Y, Church JW et al. Ileal pouch-anal anastomosis complications and function in 1005 patients. Ann Surg 1995; 222: 120–7. 70. Shah NS, Remzi FH, Massman A et al. Management and treatment outcome of pouch-vaginal fistulas following restorative proctocolectomy. Dis Colon Rectum 2000; 46: 911–7. 71. Lohmuller JL, Pemberton JH, Dozois R et al. Pouchitis and extraintestinal manifestations of inflammatory bowel disease after ileal pouch-anal anastomosis. Ann Surg 1990; 211: 622–7. 72. Penna C, Dozois R, Tremaine W et al. Pouchitis after ileal pouch-anal anastomosis for ulcerative colitis occurs with increased frequency in patients with associated primary sclerosing cholangitis. Gut 1996; 38: 234–9. 73. Sanborn WJ, Tremaine WJ, Batts KP et al. Pouchitis after ileal pouch-anal anastomosis: a pouchitis disease activity index. Mayo Clin Proc 1994; 69: 409–15. 74. Fazio VW, Wu JS, Lavery IC. Repeat ileal pouch-anal anastomosis to salvage septic complications of pelvic pouches: clinical outcome and quality of life assessment. Ann Surg 1998; 228: 588–97. 75. Lovegrove RE, Herior AG, Constantinides V et al. Metaanalysis of short-term and long-term outcomes of J, W, and S ileal reservoirs for restorative proctocolectomy. Colorectal Dis 2006; 9: 310–20. 76. Seow-Choen F, Tsunoda A, Nicholls RJ. Prospective randomized trial comparing anal function after hand-sewn ileoanal anastomosis vs. stapled ileoanal anastomosis without mucosectomy in restorative proctocolectomy. Br J Surg 1991; 78: 430–4. 77. Luukkonen P, Jarvinen H. Stapled vs. hand sutured ileoanal anastomosis in restorative proctocolectomy: a prospective randomized trial. Arch Surg 1993; 128: 437–40. 78. Reilly WT, Pemberton JH, Wolff BG et al. Randomized prospective trial comparing ileal pouch-anal anastomosis performed by excising the anal mucosa to ileal pouch-anal anastomosis. Ann Surg 1997; 225: 666–76. 79. Lovegrove RE, Constantinides VA, Heriot AG et al. A comparison of hand-sewn vs. stapled ileal pouch anal anastomosis (IPAA) following proctocolectomy-a meta-analysis of 4183 patients. Ann Surg 2006; 244: 18–26. 80. O’Riordain MG, Fazio VW, Lavery IC et al. Incidence and natural history of dysplasia of the anal transitional zone after ileal pouch-anal anastomosis: results of a five-year to tenyear follow-up. Dis Colon Rectum 2000; 43: 1660–5. 81. Herline AJ, Meisinger LL, Rusin LC et al. Is routine pouch surveillance for dysplasia indicated for ileoanal pouches? Dis Colon Rectum 2003; 46: 156–9.

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improved outcomes in colon and rectal surgery 82. Hyman NH, Fazio VW, Tuckson WB, Lavery IC. Consequences of ileal pouch-anal anastomosis for Crohn’s colitis. Dis Colon Rectum 1991; 34: 653–7. 83. Sagar PM, Dozois RR, Wolff BG. Long-term results of ileal pouch-anal anastomosis in patients with Crohn’s disease. Dis Colon Rectum 1996; 39: 893–8. 84. Keighley MR. The final diagnosis in pouch patients for presumed ulcerative colitis may change to Crohn’s disease;

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patients should be warned of the consequence. Acta Chir Iugosl 2000; 47: 27–31. 85. Braveman JM, Schoetz DJ, Marcello PW et al. The fate of the ileal pouch in patients developing Crohn’s disease. Dis Colon Rectum 2004; 47: 1613–20. 86. Melmed GY, Fleshner PR, Bardakcioglu O et al. Family history and serology predict Crohn’s disease after ileal-pouch-anal anastomosis for ulcerative colitis. Dis Colon Rectum 2008; 51: 100–8.

32

Surgery for Crohn’s disease Jorge Canedo, Tolga Erim, and Steven D Wexner

Introduction Crohn’s Disease (CD) is a lifelong disorder of unknown etiology characterized by chronic focal, transmural, and granulomatosos inflammation that can affect any portion of the gastrointestinal tract. The transmural inflammation often leads to fibrosis and to obstructive clinical presentations. Crohn’s disease was first described by B. Crohn, L.Ginzburg, and G.Oppenheimer in 1932 as an inflammatory condition limited to the terminal ileum.(1) Later, Lockhart-Mummery and Morson (2) described granulomatous colitis, and the disease process was understood to potentially affect the large bowel. It can occur from the mouth through the anus. The clinical symptoms are related to the site of the disease. As it is more prevalent among the terminal ileum and right colon, the most frequently symptoms are: diarrhea, weight loss, abdominal pain, and perineal disease. But the clinical features indicate the site of the disease.(3) a) Oral: Aphthous ulceration on the background of a mucosal edema is the most common oral manifestation of CD. Additional lesions described include: granulomatous masses, chelitis, and granulomatous sialadenitis. Lesions usually coexist with an intestinal disease. b) Esophagus: Although more rare, lesions here may cause ­dysphagia or pain. c) Stomach and duodenum: Less than 5% of the patients present with gastroduodenal Crohn’s disease; the distal antrum and the duodenum are the most commonly affected areas. Both sites can present as a peptic ulcer disease. In addition, outlet gastric obstruction may occur after a healing stricture in the antrum. d) Small bowel: Some findings of extended involvement include malabsorption, protein-losing enteropathy, diarrhea, anemia, and steatorrhea. If segmental thickening or structuring develops, the patient may present with obstructive symptoms. e) Ileocecal: Symptoms of obstruction are more frequently due to inflammatory swelling or structuring. Transmural inflammation and local sepsis often result in a palpable inflammatory mass in the right lower quadrant. f) Colon: involvement often includes the symptoms of diarrhea, associated with pain. g) Perianal disease: Is common and may precede other manifestations; as a fistula, an abscess, or one or more fissures and tags. Patients may also have systemic symptoms; fatigue, weight loss, and fever are the primary systemic symptoms in Crohn’s disease. Postprandial obstructed symptoms from narrowed intestinal segments make the patient avoid eating. Weight loss may also be related to malabsorption and, in children, may be the presenting sign before any obvious intestinal manifestations of the disease.

Fever is common in patients with Crohn’s disease and may be due to other chronic inflammation or due to a perforation with associated fistula or abscess. Crohn’s disease is diagnosed most frequently among people aged 15 to 30 years, with no differences in prevalence between males and females. However, there is a ­second peak between the sixth and seventh decades of life (4) and diagnosis may also be made during early childhood. Since its discovery in the Mount Sinai Hospital in New York City almost 76 years ago, the exact cause of Crohn’s disease remains unknown. Among many theories are genetic, immunologic, bacterial, and bacterial antigens. The current theory about the pathophysiology is that the intestinal flora, in conjunction with unidentified environmental factors trigger and drives an exaggeradated immunologic response in a genetically susceptible host.(5) The result is a chronic inflammation that typically extends beyond the mucosa and throughout to the serosa. Potential risk factors to develop CD are smoking and having first degree relatives with the disease.(6) Evaluation Symptoms of CD are heterogeneous, but most of the time include diarrhea for more than 6 weeks, abdominal pain, and weight loss. In most cases, the patient will have a clinic, radiologic, endoscopic, and histological evaluation to have its diagnosis. Crohn’s disease most often involves the distal small bowel and proximal large bowel. Almost one half of all patients have disease that involves both the ileum and the colon. While another one-third have disease confined to the small bowel, primarily the terminal ileum. The clinical presentation might be divided according to the main symptoms into: 1. Intestinal Symptoms 2. Extraintestinal symptoms 3. Biliary and Liver Manifestations The patient with CD should undergo complete evaluation. In most cases, the leading symptom that precipitates evaluation is diarrhea. Eighty-five percent of patients with CD report more than 5 bowel movements (BM) per day and weight loss as part of the initial diagnosis.(7) The history and physical examination might uncover general complaints including weakness and fatigue. In addition, as mentioned above, there are the specific symptoms according to disease site. On physical examination, paleness of the mucosa could indicate anemia. Iron deficiency anemia occurs in up to 30% of the patients. (8) Typically, the abdominal examination reveals abnormal bowel sounds, detection of an abdominal mass, and pain to palpation. Inspection of the perianal regional can provide evidence of fistula, fissure, abscess, or skin tap. Rectal digital examination might detect a stenosis or blood.

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improved outcomes in colon and rectal surgery The initial complementary evaluation starts with blood tests and stool examination. Blood tests Blood tests can either provide specific or nonspecific diagnosis, as well the general health status of the patient. The introduction of biological therapies in IBD has renewed interest in inflammatory markers (especially C reactive protein (CRP)), given their potential to select responders to these treatments. Controversy exists as to whether or not CRP is a useful marker, and should be preferred in CD as it correlates well with disease activity.(9) But a more recent study showed that neither CRP nor other biological markers were associated with the endoscopic lesions. (10) Elevated leukocytes and thrombocyte time can also indicate active inflammation. Serologic response to various microbes and autoantigens can develop into CD. In addition to the well-established atypical perinuclear antineutrophil cytoplasmic antibodies (atypical P-ANCA) and anti-Saccharomyces cerevisiae mannan antibodies (ASCA), a number of new antibodies have recently been discovered and data on their clinical significance has been rapidly increasing. The combination of atypical P-ANCA and ASCA, may be of help in patients in whom distinction between CD and Ulcerative Colitis is not obvious with the classic diagnostic tools (patient history, radiologic examination, endoscopy and biopsy). Papp et.al (11) analyzed several studies, and found that these combinations had sensitivities of 30% to 64%, specificity more than 90%, and PPV from 77% to 96%. Newer markers derived from various microbial inhabitants of the gut, such as Omp, I2, and CBir1 offer new ways to stratify patients into serologic subgroups. Also, glycan markers including antilaminaribioside carbohydrate antibody (ALCA) (18–38%), antichitobioside carbohydrate antibody (ACCA) (21–36%), and antimannobioside carbohydrate antibody (AMCA) (28%) may play an important role in making a CD diagnosis or prognosis.(12) More importantly, 24–44% of the CD patients found ASCA negative in one study were positive for one or more of the antiglycan antibodies. The combination of several serological markers, such as gASCA, pANCA, and ALCA, had the best accuracy. Their increased amounts and levels of antibody responses against gASCA, ALCA, ACCA, AMCA and Omp were associated with more complicated disease behaviour (44.7% vs. 53.6% vs. 71.1% vs. 82.0%) and a higher frequency of Crohn’s disease-related abdominal surgery (38.5% vs. 48.8% vs. 60.7% vs. 75.4%).(12) Although the prevalence of antibodies is also higher in healthy relatives of IBD patients than in the control population, their role as subclinical markers is yet to be established. Stool marker One example of a stool marker is neutrophil determination. However, neutrophil determination in the stool is inefficient because of its brief lifetime. This means that the sample should be examined within a few hours of its collection. Other examples of stool markers include calprotectin and lactoferrin. They are produced in significant amounts in white blood cells. The mucosal barrier is altered in CD, allowing white cells to cross



the intestinal wall. Activated leukocytes infiltrate the mucosa and can be detected in feces. Lactoferrin is an iron-binding glycoprotein found concentrated in the secondary granules of the neutrophils. Granule proteins can be released from living cells, while cell death does not appear to increase this phenomenon. Calprotectin is a cytoplasmic antimicrobial component in granulocytes, monocytes, and macrophages. But besides its promises, D’Incà et al. (13) observed that calprotectin and lactoferrin determination appears to reflect endoscopic and histological disease activity in ulcerative colitis but not in Crohn’s disease. Images In clinical practice, imaging techniques are used at initial presentation to establish a diagnosis and to assess exact location, extent, and severity of disease at the time. These methods are also used as follow-up during and after treatment to direct treatment strategies and determine optimal choice and dose of medication. Patients with established CD typically undergo many investigations over a lifetime. Small bowel series The small bowel has been defined for many years as the “black box” of the gastrointestinal system, due to its lack of endoscopic accessibility. Therefore, the conventional radiological methods (small bowel enteroclysis (SBE) (Figure 32.1a, Figure 32.1b, Figure 32.1c) and small bowel follow through (SBFT)) were the only imaging methods that could provide information on the morphological features of the small bowel valuable in the diagnosis and management of CD. Both SBE and SBFT, when performed by experienced examiners, appear to be characterized by similar sensitivity (85– 95%) and specificity (89–94%) in detecting the radiological lesions typical of Crohn’s disease.(14) Preference for one technique or the other largely depends on institutional standards. Both procedures are able to evaluate small bowel peristalsis, including the presence of strictures and/or dilations, the distensibility of the intestinal loops, the presence of fistulae, the morphology of circular folds, and morphology of the mucosal surface. Enema For primary evaluation, endoscopy has widely replaced the barium enema (BE) as diagnostic method. However, BE can provide important additional information in the differential diagnosis of chronic inflammatory colonic diseases or if intestinal intubation is not achieved at colonoscopy. The advantage of a BE over endoscopy is a clear and reproducible demonstration of the patterns of distribution and character of the disease as well as the detection of fistulae.(15) With the advance of CT and MRI images, and wireless endoscopic capsule, barium examinations not only of the stomach but also of the colon are decreasing in frequency. The disadvantage of the enema is the same as the one for SBE: limited information about transmural and extraintestinal abnormalities. Upper endoscopy Lemberg et al. (16) concluded the need to include EGD in the evaluation of children suspected of having IBD. The current study

surgery for crohn's disease (A)

(B)

(C)

Figure 32.1  (A) Note the string like narrowing stricture at the terminal ileum (arrows) with proximal bowel obstruction. (X-ray courtesy of Department of radiology Cleveland Clinic Florida) (B-C) Multiple small bowel strictures with associated proximal obstruction. (X-ray courtesy of Department of radiology Cleveland Clinic Florida)

found that in children with CD, 57.4% had endoscopic abnormalities. These findings ranged from mild changes, such as erythema or nodularity of the stomach, to more obvious features, such as ulceration throughout the upper tract and cobblestoning of the duodenum. In total, 80.3% of patients had histologic evidence of inflammation in the upper gut; including granulomata, which

were evident in the upper gastrointestinal tract in approximately one-quarter of patients with CD. EGD may help in the differential diagnosis in patients with indeterminate colitis after a biopsy in the normal gastric mucosa (17) and may be used as therapeutic intervention specifically in case of antrual or duodenual stricture. EGD p ­ rovides good relief in symptomatic patients (17).

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improved outcomes in colon and rectal surgery Colonoscopy Approximately 50 percent of patients have ileocolitis which refers to involvement of both the ileum and colon, highlighting the fact that colonoscopy with intubation of the ileum plays a fundamental role in the diagnosis and evaluation of a patient with Crohn’s Disease. Colonoscopic findings often include segments of normal bowel interrupted by large areas of obvious disease. In CD, the severity of an attack is usually evaluated according to clinicobiological variables, like the Crohn’s Disease Activity Index. Colonoscopy has an increased risk of complication in such cases. But Nahon et al. (18) demonstrated that colonoscopy in severe colonic CD is useful for the diagnosis of CD versus UC. The benefits increase if the patient is suffering from a first attack of inflammatory bowel disease, a situation which is particularly common in cases of severe colitis, as has been reported in 2.3– 6% of CD.(19) In this study, colonoscopy with biopsies was able to diagnose CD after initial presentation in 50% of patients by showing either involvement of the ileum or intervening zones of healthy mucosa within the colon. According to Minderhound et al. (20), colonoscopy remains the gold standard for assessment of severity of mucosa inflammation compared to several score indexes, as well as serum and fecal markers. Transabdominal ultrasound (US) Parente et al. reviewed several studies that compared the accuracy of bowel US with other imaging techniques (barium X-ray and/ or endoscopy) and surgery in localizing CD lesions within the bowel.(21) But many of these studies have included small numbers of patients with CD diseases mainly confined to the small bowel. The overall sensitivity for diagnosis disease in the terminal ileum is approximately 90% with specificity of 93–97%. Bowel US has also been used to detect complications of CD. Although the presence of abscesses, fistulae, and strictures may be suspected from clinical history or specific complaints, it is usually necessary to undertake endoscopy, barium studies and computed tomography (CT) to clearly diagnose these complications. Barium studies and CT scans are still considered the methods of choice in detecting internal fistulae and abscesses in CD. Parente et al. in a previous prospective study compared the sensitivity and specificity of bowel US in detecting strictures in small bowel.(22) Computed tomography is currently considered the nonsurgical ‘gold standard’ for the diagnosis of CD-related abscesses. Both CT and barium studies are known for their accuracy in detecting fistulas, although Maconi et al. (23) demonstrated that CT or SBE alone might miss up to 30% of the fistulas, but US alone or in combination with SBE can detect almost 90% of internal fistulas. US when compared to CT, showed an overall high accuracy comparable in the detection of intraabdominal abscesses. Although CT showed a slightly greater accuracy and positive predictive value than did US. US also has a lower sensitivity in detecting deep abscesses. This finding can be explained by the well-known difficulties associated with transcutaneous US examination of anatomic structures deep in the pelvis or between the intestinal loops, especially when overlying bowel gas obscures the region of interest. The differentiation between abscess and enlarged loop can be challenging. Another feature in US is its utility in the evaluation of perianal disease. Transperineal US is a simple, noninvasive and cheap



Figure 32.2  New CT scan technology has improved and may substitute for standard SBS in the near future. Note the thickened bowel wall at the stricture (solid arrows) and dilated obstructed proximal bowel (arrows with dashed lines). Image courtesy of Toshiba America Medical systems, Inc.

technique that can be usefully employed to study the pelvis and perianal inflammatory diseases in static and dynamic evaluations. Additional advantages of US are that it does not require costly or specific diagnostic instruments and can be performed with adequate training and experience in most hospitals or offices.(24) Doppler sonography is part of the entire sonographic evaluation of intestinal diseases which is helpful in estimating disease activity, although it is not acceptable as the sole method to achieve diagnosis.(25) CT scan Conventional.  Computed Tomography (CT) has usually been utilized for the detection of extraintestinal complications of Crohn’s disease (mainly intraabdominal abscesses) but is also suitable in the evaluation of bowel wall thickness/ strictures, prestenotic dilatations and fistulas. Nonenhanced CT scan is also used in the diagnosis of postoperative complications indicating (intraperitoneal abscesses, anastomotic deiscence, extraabdominal abscesses and fistulas, incisional hernias, ascites, volvulus, etc.). Conventional CT is limited in its assessment of the small bowel because of the artifact caused by collapsed bowel loops.(26) Enteroclysis.  Because of the problems described above, CTenteroclysis has been great results. The ability of multislice CT machines to image larger volumes shown (1500 to 2000 mL or more of contrast agent delivered by the positioning of a nasojejunal tube) at a faster speed with the ability to perform reconstruction after the examination, has made CTE a more feasible extension of the conventional barium enteroclysis and CT methods of examining the small intestine (Figure 32.2). It can detect active

surgery for crohn's disease inflammatory changes (neutral enteral contrast with intravenous contrast media) and complications such as fistulae, sinus tracts, and strictures (positive enteral contrast).(27) Volumetric.  More recently, a row multidetector-computed tomography (MDCT) has been used to perform a virtual colonoscopy. Virtual colonoscopy studies were performed with singlerow helical CT scanners using slices of 4 mm thickness.(28) With the advent of MDCT technology, thinner collimation (up to 0.6 mm) is possible. It is possible now to detect flat or ulcerated lesions of the colon, the findings of which in the evaluation of IBD correlated highly with conventional colonoscopic findings.(29) The disadvantages in both CT enteroclysis and volumetric evaluation included: radiation exposure, and the need for intravenous Endoscopic Ultrasound(EUS) In the setting of IBD, EUS has been limited to detecting perianal disease. The accrual of EUS, MRI, and EUA are comparable. At 85%, 87%, and 91% respectively improved upon by employing any two methods.(30) The use in fistula disease is well described; Schwartz et al. (31) showed that EUS may identify patients with fistulae who can discontinue infliximab without the recurrence of a fistula. MRI MRI allows the accurate assessment of both inflammatory changes of the bowel wall and extramural complications of Crohn’s disease. The noninvasiveness of this technique and its lack of ionizing radiation has prompted many groups to perform systematic studies of MRI for evaluation of Crohn’s disease. Technological advances in MRI, including the use of respiration-suspended sequences, improved coils, fat suppression, and intravenous gadolinium, have extended the use of MRI in the evaluation of the gastrointestinal tract. MRI is capable of demonstrating pathology in both luminal and perianal Crohn’s disease. One advantage of MRI over other modalities is its ability to differentiate active inflammation from fibrosis in a thickened bowel segment.(32) It is also safe in pregnancy and in renal failure. Inflammatory diseases featuring intestinal wall abnormalities, exoenteric disease manifestations and complications, disease activity, and, to a lesser extent, mucosal abnormalities, can be appreciated on MRI. In addition, it has been reported that the sensitivity and specificity of MRI in assessing disease activity are 92 and 75%, respectively.(33) Despite closure of draining external orifices after infliximab therapy, fistula tracks persist in some patients with varying degrees of residual inflammation, which may cause recurrent fistulas and pelvic abscesses. MRI can detect whether complete fistula fibrosis occurs with complete resolution of inflammation in the internal fistula tracks.(34) Diasadvantages of the MRI include the high cost of the exam and the length of time to perform it. Double Balloon Enteroscopy(DBE) Endoscopic examination of the entire small bowel is technically very difficult. Push endoscopy is often possible only to the proximal jejunum. In 2001, Yamamoto and Kito developed the double balloon method as an insertion technique for the diagnosis and

treatment of small bowel disorders.(35) DBE requires bowel preparation, sedation, radiological exposure, and a 60–100 min examination time, but is able to take biopsies and perform therapeutic endoscopy such as endoscopic enteroclysis, hemostasis, and balloon dilatation. Oshitani et al. reported their initial experience in 40 patients. Deep small bowel involvement proximal to the terminal ileum was revealed in 27 patients, and 24 (88.9%) of these patients had no involvement of the terminal ileum itself.(36) Another study showed an 80% success rate of stricture dilatation.(37) This technique therefore represents a promising method for diagnosis and therapeutic intervention of small bowel strictures in CD and may be able to avoid surgery in such patients. However, DBE requires an experienced and skilled therapeutic endoscopist and can be quite confusing, and therefore costly. Wireless Endoscopic Capsule Wireless capsule endoscopy (WCE), initially developed for small bowel investigations in patients with occult bleeding, has been studied in small bowel Crohn’s disease. WCE enables a painless and radiation-free examination of much of the small bowel in an unsedated patient. Based on cost-effectiveness (US$ 20,000.00–US$ 30,000.00), funding issues, and the inability to obtain tissue samples, it is unlikely that WCE will soon become the primary imaging modality used to initiate a diagnosis of Crohn’s disease or to define its extent at relapse.(38) WCE is well-tolerated by most patients, requires no sedation, and carries few side effects. One of the complications of WCE is capsule retention. In a series of 52 patients, Park et al. (39) reported 5 retain WEC (9.6%). Two patients (3.8%) had to undergo a surgery for WEC removal. With the development of the “Given Patency Capsule (Given Imaging Ltd, Yoqneam, Israel), capsule technology might be suitable for cases of suspected intestinal strictures by SBE. This selfdissolving capsule is the same size as a capsule endoscope. The difference is found at the cellophane-walled cylinder filled with lactose, protected by a plug with a specially-sized hole that allows influx of intestinal fluid, which in turn dissolves the lactose in a predetermined amount of time. If the capsule is retained in the gastrointestinal tract, it disintegrates into small, mostly soft, fragments which can easily pass through strictures. Spada et al. propective studied 27 patients with known or suspected intestinal stricture. Twenty and two had CD. Twenty-five patients (92.6%) retrieved the “Given Patency Capsule” in the stools, including six of them which were dissolved. In 2 cases (7.4%), the Given Patency Capsule could not be retrieved in stools and expulsion was confirmed by fluoroscopy and by a Patency Scanner. One case (4.3%) required hospitalization due to intestinal occlusion. But in this case, the Given Patency capsule was retrieved. The authors concluded that WEC done with the Given Patency Capsule was a safe procedure even in the presence of stricture disease.(40) PET scan Positron emission tomography with fluorine 18–labeled fluoro2-deoxy-D-glucose (FDG-PET) is a functional imaging method used to detect abnormalities in glucose metabolism in a variety of disorders. Neurath et al (41) studied the efficacy of PET scan in detecting active chronic inflammation on inflamed small and large bowel segments in CD, and compared the results to those

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improved outcomes in colon and rectal surgery Table 32.1  Image tests for Small Bowel CD. Modality

Fistula

Abscess

Stricture

Inflammation ++

SBE

++

-

++

Colonoscopy

+

-

++

++

US

+

+

+

++ ++

CT enteroclysis

++

++

++

MRI

++

++

++

++

WEC

-

-

+

++

DBE

-

-

+

++

PET

+

+

-

++

Scintigraphy

+

-

+

++

Legends: - not useful + somewhat useful ++ very useful

obtained by hydro-MRI and immunoscintigraphy with granulocyte antibodies (GABs). The sensitivity was 85%, 87%, and 71%. The specificity was 89%, 93%, and 100%, respectively. FDG-PET appears to be a reliable tool for detecting inflamed gut segments in CD with higher sensitivity and specificity than either MRI or scintigraphy. Scintigraphy An increased number of T cells and macrophages within the gut lumen is a feature of CD. One of the main problems in the clinical management of CD is the identification of patients undergoing early relapse in order to ensure that appropriate preventive treatment is administered. Follow-up of patients in clinical remission is currently based on the calculations of clinical activity indexes, together with radiological and endoscopic studies. Scintigraphy with 99mTc-labelled interleukin-2 (99mTc-IL2) and with 99mTcHMPAO-labeled granulocytes (99mTc-WBC) has been evaluated to detect the presence and extent of bowel inflammation in patients with long-term inactive CD (>12 months). Annovazzi et al compared the extent of uptake of 99mTc-IL2 and 99mTc-WBC in patients with clinically inactive CD and, despite the absence of symptoms, 62% had either 99mTc-IL2 or 99mTc-WBC positive for inflammation.(42) Scintigraphy with labelled white blood cells (WBC) has been successfully used in CD patients to detect abscesses and to assess disease extent (particularly for the small bowel) and activity. Almer et al compared the 99mTc-WBC to intraoperative and laparotomy findings and found a sensitivity of 85% and specificity of 81% for bowel inflammation.(43) Although not used, scintigraphy can be an option as a noninvasive evaluation for young children and fragile adults who might have more difficulty with invasive imaging modalities. Table 32.1 summarizes the efficacy of the exams discussed above.(41, 44, 45) Medical therapy The etiology of Crohn’s disease (CD) is unknown, and therefore no curative treatments are available. The last few years have witnessed a significant change in its treatment. Recent debate on medical management of CD has focused on a step-up versus a step-down therapy. Step-up therapy has been the traditional treatment option where steroids and aminosalicylates are started

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first, and biologics and immunomodulators are only initiated if the patient fails to achieve remission. Step-down therapy advocates use of immunomodulators and, at times, biologic agents, in addition to or even before use of steroids and aminosalicylates, in order to achieve remission as soon as possible. These discussions have largely been inspired by the success of step-down therapy in rheumatoid arthritis, success in severely ill patients and in some part by the strong marketing efforts of the pharmaceutical industry. Selection of appropriate therapy remains a decision which must be made on an individual basis. The ideal drug for CD should induce and maintain remission quickly and with minimal side effects. There is no such drug right now. Agents such as corticosteroids which are rather good at induction of remission, are not effective in maintenance. Azathioprine and 6-mercaptopurine are the benchmark drugs for maintenance of remission, are not as useful in induction because it takes several months for them to be effective. The benefits of 5-ASA agents in the management of acute CD and the maintenance of remission are questionable.(46, 47, 48) Biologic agents such as Infliximab and Adalimumab, which both induce and maintain remission, are indicated only for patients considered to have moderate to severe disease. 5-Aminosalicylates (5-ASA) Although their benefit is at best questionable, aminosalicylates are often used for patients with mild-to-moderate colitis. The mechanism of action of aminosalicylates in CD is not fully understood. In vitro investigation has shown many antiinflammatory and immunosuppressive properties such as inhibition of prostaglandin and leukotriene synthesis, free radical scavenging, impairment of white cell adhesion and function, and inhibition of cytokine synthesis. Sulfasalazine, initially approved by the FDA in 1950 for rheumatoid arthritis, has been used for decades in the treatment of Ulcerative Colitis and CD. The drug is broken down by bacteria in the colon into its two products, 5-aminosalicylic acid (5-ASA) and sulfapyridine. These components possess antiinflammatory (5-ASA) and antibiotic (sulfapyridine) properties. 5-ASA acts directly on the colon and is not absorbed while sulfapyridine is mostly absorbed by the intestine and secreted into bile and, to a much lesser extent, into urine. Several clinical trials have shown that Sulfasalazine is more effective than placebo at inducing remission in mild to moderate disease, greatest benefit seen in those with colonic or ileocolonic disease. However, Sulfasalazine has a slower onset of action than prednisone and is considerably less effective. It is not effective as a steroid-sparing agent, and, when used as adjunctive therapy, it is not more effective than prednisolone alone. As the sulfapyridine portion of Sulfasalazine accounts for the majority of side effects, several aminosalicylate-containing medications have been created over the years that do not contain ­sulfapyridine and are thus sulfa free. The most commonly used drug in this class is mesalamine. Several formulations of mesalamine exist currently, with Asacol, Salofalk, Rowasa, and Pentasa being the most commonly used forms. They are formulated by either using different acrylic resins or by encapsulation in ethyl cellulose micro granules, resulting in delivery of the drug to the distal small bowel and colon. Other forms of mesalamine have

surgery for crohn's disease been created by the dimerization of 5-ASA to make the drug active only once it reaches the colon. Examples of these are olsalazine (Dipentum), which has two 5-ASAs linked together, and balsalazide (Colazal), which is 5-ASA linked to an inert unabsorbed molecule. The pharmacology, and thus the undesirable drug absorption rates, differ between these drugs, although the clinical importance of these characteristics is debatable.(49) In general, mesalamine compounds are better tolerated than Sulfasalazine. However, mesalamine has not been found to be an effective treatment for induction or maintenance of remission in adequately powered, randomized, placebo-controlled trials.(48) Antibiotics Metronidazole and Ciprofloxacin are the most commonly used antibiotics in treatment of CD. The mechanism of action of antibiotics in Crohn’s are theorized to include decreased bacterial concentration in the gut lumen, alteration of the microflora composition to favor beneficial bacteria, decrease in bacterial tissue infection and micro abscesses, decrease in bacterial translocation and systemic dissemination. In addition, some antibiotics act as immunomodulators.(50, 51) These agents have not been found to be efficacious in induction or maintenance of remission. The consensus view is that these agents should be used for perianal fistulas and postoperative management after ileocolic resection or fistula/abscess operation for CD.(52) However, this practice is not based on adequately powered, controlled evidence. In fistulizing Crohn’s disease, antibacterials, immunosuppressive drugs, infliximab, and surgery are often used in combination. Corticosteroids The mechanism of action for this class of drugs in CD is through antiinflammatory activity. Corticosteroid therapy is split into systemic versus nonsystemic types. Conventional systemic corticosteroids such as prednisone and 6-methylprednisolone have demonstrated efficacy in induction of clinical response and remission. It has also been well established that they are ineffective in maintenance of remission. The National Cooperative Crohn’s Disease Study achieved 60% remission, with 0.5–0.75 mg/kg/day prednisone tapered over 17 weeks, compared with 30% on placebo (NNT = 3).(53) The European Co-operative Crohn’s Disease Study achieved 83% remission with 6-methylprednisolone, 1 mg/kg/day over 18 weeks, compared with 38% on placebo (NNT = 2).(54) Nevertheless, approximately 50% of recipients will either fail to respond (steroid-resistant) or will be steroid dependent at 1 year. (55) The use of conventional systemic corticosteroids in patients with clinically quiescent CD does not appear to reduce the risk of relapse over a 24-month period of follow-up.(56) No dose response trial has been performed for prednisone. Treatment is usually started at 40–60 mg daily dose of prednisone and, once response is attained, it is tapered down 5 mg per week. The main disadvantage of systemic corticosteroid therapy is its many side effects. Corticosteroids are associated with increased risk for infections, osteoporosis, cataracts, hyperglycemia, and avascular necrosis of bones. A newer steroid therapy that is widely used for CD is budesonide. Budesonide is a corticosteroid with high affinity for glucocorticoid receptors but low systemic activity due to extensive first-pass

metabolism in the liver. It has been shown to be effective in inducing remission in terminal ileal and right-sided colonic disease with significantly less side effects than systemic corticosteroids. A meta-analysis of five published trials found that budesonide was superior to mesalamine and placebo in achieving remission. It was found to be similar in effectiveness to prednisone except for those with severe disease.(57) As for maintenance, an analysis of four double-blind placebo-controlled trials of budesonide with identical protocols revealed that budesonide 6 mg/day is effective for prolonging time to relapse and for significantly reducing rates of relapse at 3 and 6 months, but its effectiveness in maintaining remission is lost when measured at 12 months.(58) Immunomodulators The mechanism of action of these drugs in CD is not thoroughly understood. The most commonly used examples are azathioprine (AZA) and its metabolite, 6-mercaptopurine (6-MP). AZA and 6-MP have been researched and used successfully since 1971 in patients with CD. AZA is a prodrug that is converted to 6-MP and then metabolized to an active metabolite, 6-Thioguanine Nucleotide (6-TGN). 6-TGN is incorporated into ribonucleotides, thereby exerting an antiproliferative effect on mitotically active lymphocyte populations. AZA and 6-MP may also possess direct antiinflammatory properties by inhibiting cytotoxic T-cell and natural killer cell function and inducing apoptosis of T cells through Rac1 target gene modulation.(59) Treatment can be initiated with either drug at 50 mg/kg, and doses are adjusted while monitoring for toxicity to 1.5–2.5 mg/kg for AZA and 1–2 mg/kg for 6-MP. They are usually administered jointly with steroids for induction of remission due to their relatively slow onset of action; usually 3 months or more.(60) However, they have been found to be effective in maintenance of remission in corticosteroid-induced remission of mild to moderate CD, and in treatment of fistulizing disease. They are also considered to be steroid-sparing agents, an idea supported by a meta-analysis by Pearson et al.(61) The use of AZA in CD has evolved in the past few years with the support of new tests which can predict its toxicity and drug activity. Therapeutic efficacy, bone marrow suppression, and liver toxicity of AZA and 6-MP correlate with concentrations of its metabolite 6-TGN.(62) Thiopurine methyltransferase (TPMT) enzymatically converts 6-MP to 6-methyl-mercaptopurine (6-MMP), diverting metabolism away from 6-TGN. There is an inverse relationship between expression of TPMT and level of 6-TGN. Therefore, lower TPMT activity yielding higher levels of 6-TGN has been associated both with an increased likelihood of clinical response and bone marrow suppression.(59) TPMT deficiency is inherited in an autosomal recessive manner with 1 in 300 subjects having homozygous deficiency, and around 11% of the community having intermediate enzyme activities.(63) Measurement of TPMT genotype has been proposed to predict the likelihood of toxicity to 6-MP or AZA since patients with low TPMT activity are at increased risk of myelosuppression.(64) The strategy of determining TPMT activity in all patients before initiating treatment with AZA could help to minimize the risk of myelotoxicity, as patients with intermediate TPMT activity had fourfold more risk than high TPMT activity patients.(65) It is currently recommended to test all patients’ TPMT levels before treating with AZA/6-MP.



improved outcomes in colon and rectal surgery Although TPMT testing is helpful in avoiding early, profound bone marrow suppression, it should not take the place of careful monitoring of full blood counts throughout the duration of treatment on AZA/6-MP. If the patient is a slow metabolizer, clinical decision on treatment dose with consideration for lower dosing and closer follow-up must be made, while those that are deficient should not be treated due to bone marrow toxicity. Patients who are found to be nonresponders are suggested to have metabolite testing. The utility of measuring the 6-MP metabolites 6-TGN and 6-MMP has been debated in the literature and even referred to as the “metabolite controversy”. According to expert opinion, it would seem reasonable to recommend checking 6-TGN/6-MMP metabolites when patients are not achieving therapeutic efficacy despite adequate weight-based dosing to ascertain noncompliance or metabolism favoring 6-MMP.(59) Methotrexate has also been shown to be effective in CD for both treating active disease (66) and maintaining remission (67). However, like AZA/6-MP, its slow onset of action limits its use in induction therapy. Nausea is a common side effect of methotrexate, but more serious concerns over opportunistic infections, hypersensitivity pneumonitis, and hepatotoxicity add to the factors limiting its use as a first line immunomodulator in treatment of CD. Although some data have suggested a beneficial effect of highdose cyclosporine in active luminal CD (68), the benefit was not durable (69). An open-label trial of 16 patients with fistulizing disease found that cyclosporine treatment resulted in 88% response and 44% complete closure.(70) However, a comprehensive review of the literature has shown that 39 patients with fistulizing ­disease who were treated with cyclosporine had 82% relapse rate in absence of oral cyclosporine.(71) Therefore, cyclosporine is not recommended for use in luminal CD and its use in fistulizing disease with subsequent maintenance therapy on AZA/6-MP is debatable. (72) Cyclosporine has several serious side effects including renal failure, seizures, and opportunistic infections. Biologic Response Modifiers In 1998, the FDA approved use of Infliximab for use in treatment of moderate to severely active CD and patients with fistulizing Crohn’s disease, who have had inadequate response to conventional therapy. In fact, it is the first drug to gain FDA approval for treatment of CD. Prior to the late 1990s, patients who had failed response to first-line therapies or were steroid-dependent had few nonsurgical options. The mechanism of action of biologic response modifiers in CD is through the interaction of the interleukins and cytokines. Neutrophils from patients with colitis (e.g., CD, ulcerative colitis, and infectious colitis) all produce significantly more IL-1 and TNF than neutrophils from healthy controls.(73) Infliximab is a chimeric IgG-1 monoclonal antibody comprised of 75% human and 25% murine sequences, which has a high specificity for and affinity to tumor necrosis factor (TNF)-α. The pivotal trial for assessing the efficacy of Infliximab in CD in 1997 showed 33% rate of remission and 81% overall symptom improvement in patients who had been resistant to conventional treatment.(74) However, up to 40% of patients do not respond to treatment initially. The standard dose of Infliximab at 5 mg/ kg of body weight given as infusion every 8 weeks can sustain remission for up to 1 year in only 30% of initial responders. This



is likely due to a combination of loss of efficacy and intolerable side effects. Infliximab also has modest steroid-sparing efficacy where at week 54, about 3 times as many patients (29% vs 9%) on Infliximab versus placebo had discontinued treatment with corticosteroids while maintaining clinical remission.(75) The efficacy of regularly scheduled treatment versus episodic treatment with Infliximab for patients with CD was compared in a posthoc analysis of the ACCENT I trial in 2004.(76) It was shown that regularly scheduled treatment resulted in a higher proportion of patients in remission at weeks 10, 14, 22, and 46 compared with the episodic treatment group. Patients were also found to have improved mucosal healing, less likelihood of having antibodies to Infliximab, fewer Crohn’s-related hospitalizations, and fewer surgeries if on regularly scheduled treatment. Infliximab therapy causes antibody formation in up to 61% of patients and they correlate with increased risk of transfusion reactions as well as decline in efficacy.(77) Concomitant use of AZA/6-MP has been shown to reduce rate of antibodies to Infliximab (ATI), although currently there is no prospective trial comparing remission and response rates in patients concomitantly using AZA/6-MP and Infliximab.(78–80) Infliximab is also effective in closure of perianal enterocutaneous and rectovaginal fistulas and maintaining fistula closure. Two prospective, randomized, placebo-controlled trials have shown closure rate of 55% at week 4 and maintenance of closure in 39% of patients respectively.(81, 82) In February 2007, Adalimumab gained FDA approval for the treatment of moderate to severe CD. Adalimumab is a fully human recombinant immunoglobulin G1 (IgG1) monoclonal antibody that binds with high affinity and specificity to human soluble TNF. Its efficacy is similar to Infliximab except that there is currently not enough evidence to comment on its value in fistulizing disease.(83) However, certain features make it more attractive for use in clinical practice. It is thought that Adalimumab may be less immunogenic because it is a fully human antibody. Indeed, some evidence does exist for inducing remission in those who cannot tolerate Infliximab or have disease activity despite receiving Infliximab therapy.(84) Another advantage is that it is administered as a subcutaneous injection whereas Infliximab must be given as an infusion. Main side effects of Infliximab and Adalimumab include infections, infusion reactions, serum-sickness-like reactions and a possible increased risk of lymphoma. A tuberculin skin test should be done before initiating therapy, as reactivation of latent tuberculosis is a potential complication. Prevention of Postoperative Recurrence Approximately 75% of patients with CD require surgery within the first 20 years after symptom onset.(85, 86) Several studies have shown that, 1-year postresection, the endoscopic recurrence rate is near 73% with clinical relapse rate of 50% in 5 years.(87, 88) Increased risk of recurrence is associated with the following prognostic variables at the time of surgery: female gender, perianal disease, smoking, use of 5-ASA, jejunal site, ileal and ileocolonic site, and Nod2/Card15 gene variants. Severity of endoscopic recurrence at the neoterminal ileum within 1 year of surgery was found to be the most powerful predictor of symptomatic recurrence.(89)

surgery for crohn's disease Most studies of postoperative recurrence of CD have found that endoscopic findings predate clinical relapse. Management options to prevent postoperative recurrence vary and depend on the patient. The first line treatment, despite marginal efficacy, has been mesalamine. Most studies only demonstrate a modest relative risk reduction in recurrence rates when compared to placebo. A recent meta-analysis showed an absolute risk reduction of 10% in postoperative patients at 2 years. (90) The largest benefit was found in pts with ileitis and prolonged disease duration. The number needed to treat (NNT) to prevent one relapse was found to be 10 patients.(91) Whether or not this is a clinically relevant finding and the financial cost and effort spent in taking these medications merit their use is highly debatable. Azathioprine and 6-MP have both been used extensively in the postoperative patient, but data is limited and shows only modest efficacy for prevention of recurrence. The general consensus is that larger blinded controlled trials are warranted. A randomized, prospective, multicenter, placebo-controlled, double-blind, double-dummy trial done in 2004 by Hanauer showed relapse rates of 50% with 6-MP (50 mg), 58% with mesalamine (3 g), and 77% with placebo.(92) There were several shortcomings in this study, including the use of a suboptimal fixed dose of 6-MP, a high drop-out rate, higher clinical vs endoscopic relapse rate, and lack of a validated, reproducible clinical index used to judge clinical relapse. A prospective, open-label, randomized study of 142 patients who received AZA (2 mg/kg/day) or mesalamine (3 g/day) for 24 months found AZA effective in preventing relapse in those patients who had undergone previous intestinal resection.(93) Shortcomings of this study included open label bias. Currently, AZA/6-MP use is recommended for postoperative prophylaxis in those patients who are deemed to have high risk of recurrence or in those for whom recurrence would have substantially harmful effects. The use of antibiotics has been long debated in the prevention of recurrence in the postoperative Crohn’s patient. There are no large controlled trials that show clear effectiveness of the use of antibiotics in postoperative Crohn’s patients beyond 1 year. One large trial on metronidazole has shown a 4% clinical recurrence rate in the treatment group versus 25% in placebo group at 1 year, 52% endoscopic recurrence versus 75% in the placebo group at 3 months, and no significant difference in clinical recurrence rate at 2 or 3 years.(94) Another trial of Ornidazole showed an 8% clinical recurrence ­versus 38% with placebo at 1 year, but no significant difference at 2 or 3 years.(95) These agents may be considered for prevention of postoperative recurrence but their utility beyond 1 year and potential for considerable side effects in long- term use limit their clinical utility. The last group that has shown possible effectiveness in postoperative Crohn’s patients is the biologic response modifiers, but these have yet to be adequately studied in this setting. A nonrandomized, open-label, single-center experience involving 7 patients who received Infliximab with methotrexate has demonstrated no endoscopic or clinical recurrence at 2 years.(96) Adalimumab has not been studied in this respect. Multicenter, randomized, controlled studies are needed to further define the role of Anti-TNF agents in postoperative recurrence of CD. Treatments that have been shown to be ineffective in the prevention of postoperative recurrence are systemic corticosteroids, budesonide, probiotics, and interleukin-10.

Table 32.2  Indications for Surgery in Crohn’s Disease. Failure of medical management

Complications of Medical Management

Obstruction

Inflammatory mass

Sepsis

Free perforation/sepsis

Fistulae/abscess

Hemorrhage/anemia Dysplasia/carcinoma Growth retardation

Nutritional Therapy There is no proof that any food or substance is responsible for causing the initial episode or recurrence of CD.(97) The biggest challenge in patients with CD is restoration and maintenance of weight, particularly in the presence of sepsis and/or obstruction. Surgical Treatment Indication Table 32.2 summarizes the indications for surgical treatment of a CD.(98) Surgical management of CD has changed considerably during the past as a result of numerous advances in medical therapy. Regardless of these developments, patients with CD will undergo a surgical procedure in up to 80% of the cases.(99) Patients often come to the surgeons office with worsening symptoms, a complication, or as steroid-dependent. •• Failure of medical therapy or complications of medical therapy Surgery may be indicated if the medication cannot control inflammation and its symptoms, or if the medication causes significant intolerable or inducible side effects. Symptoms that can be an indication for surgery includes diarrhea, anemia, pain, weight loss, sepsis, and obstruction. Most patients are either steroid-dependent or steroid-resistent (100) by the time of surgical consultation. In addition, pancreatitis from GRMP, osteoporosis from steroids, and leucopenia from infliximab are all potential reasons for surgery to be recommended. •• Acute and chronic disease complications Although rates are decreasing, up to 20% of procedures are still performed to treat acute complications.(101) Among the indications is toxic megacolon, obstruction, hemorrhage, perforation with or without peritonitis, and abscess. Perforation According to the Viena classification, intestinal perforation is a penetrating disease. The penetrating disease behavior is defined by the occurrence of intraabdominal or perianal fistulas, inflammatory masses or abscesses, or perianal ulcers at any time in the course of disease. Neither postoperative intraabdominal complications nor perianal skintags constitute evidence of penetrating disease.(102) Penetration of the bowel wall often presents not as an acute abdomen but as an indolent process related to fistulization. Diffuse peritonitis due to perforation is a rare but recognized complication of Crohn’s disease. Perianal disease manifestations include perianal pain and drainage from large skin tags, anal

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improved outcomes in colon and rectal surgery fissures, perirectal abscesses, and anorectal fistulae. Emergency surgical therapy for a perforation behavior includes: free perforation, intraabdominal abscess or masses with sepsis, and intestinal obstruction. In Crohn’s disease, free perforation is a rare but severe complication occurring in 1% to 3% of cases.(103) Free perforation in the absence of a megacolon should alert for the suspicion of CD. It can occur anywhere in the gastro-intestinal tract, from the stomach through the colon; a distal stricture might exist and make the perforation possible. Other etiologies for perforation include the presence of malignancy, and of endoscopic procedures. Frequently, the perforations are sealed. Gastro-duodenum perforations are best treated by debridement and primary suture. For jejuno-ileal perforations, resection and primary anastomosis are best if feasible and conditions favorable. Factors associated with postoperative complications include abscess, enterocutaneous fistulae, steroid-dependence, and albumin <2 g/L. If one or more of the risk factors is present, a diversion is suggested.(104) Colonic perforation in Crohn’s colitis, often seen in the setting of toxic colitis, usually requires subtotal colectomy with rectal preservation and end ileostomy. If the etiology is not toxic colitis, a segmental resection and fecal diversion might be an option. (105) A postcolonoscopic perforation must be managed regarding the absence or presence of CD at the site of perforation and elsewhere in the colon. If the perforation occurs in a diseased segment, the segment along with the perforation is reseated to allow reconstruction with or without fecal diversion depending upon the factors mentioned above.(104) If perforation occurs during a follow-up for surveillance, resection or primary repair may be feasible. Abscess Between 10–30% of patients with CD may present with intraabdominal abscesses. Abscesses can develop because of a local sealed perforation, in association with a fistula, or postoperatively because of intraabdominal contamination or anastomotic leakage. Yamaguchi et al. found that almost 50% of the abscess were due to an anastomosis (surgical anastomosis and peristomal) (106), Preoperative percutaneous transcutaneous drainage and administration of antibiotics is preferable if possible. Otherwise, surgery with resection of the disease site is necessary. Perianal CD Perianal Crohn’s Disease (PCD) occurs in 5–25% of CD patients and can be associated with active disease in the proximal gastrointestinal tract or colon in about one-third to one-half of patients. It is often associated with colonic and rectal inflammation. Perianal manifestations include cutaneous (tag and ulcerations), anal canal lesions ­(fissures, ulcers, stenosis), and septic (abscess, fistulas) (Figure 32.3). The purpose of surgical treatment in PCD is to improve quality of life and offer effective palliation, and therefore is reserved for patients who develop perianal complications of the disease or are unresponsive to aggressive medical therapy. The surgical treatment of PCD can be divided into two main categories: urgent and emergent treatment (to control perineal sepsis); and elective (to treat sequelae such as perianal fistulas and anal strictures).(107)

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Figure 32.3  Typical perianal Crohn’s Disease with associated fistulas and scars from prior surgery (Picture taken by Badma Bashankaev, M.D., Cleveland Clinic Florida).

Prompt and definitive surgical incision and drainage is required in all patients suspected of having acute abscesses. These lesions will not spontaneously resolve and delays can lead to uncontrolled sepsis with necrotizing infections, sphincter impairment and anal stenosis. If a fistula is identified a noncutting Seton (nonabsorbable suture) is inserted through the fistula tract to ensure continuous drainage, leading to the resolution of the perianal sepsis. Primary fistulotomy should be avoided. Premature removal of the seton increases the incidence of recurrent perianal sepsis. If the abscess is superficial, the procedure may be completed under anesthesia. It is important to minimize trauma or additional injuries so that the incision must be as close as possible to the anal verge. Excision of skin edge or latex mushroom catheter placement can be utilized to obtain adequate drainage. Fistulotomy can be safely performed on simple (low) fistulas which do not include any significant portion of the external anal sphincter, in patients without active proctitis, well-controlled proximal luminal disease and adequate continence. Endorectal advancement flap is a surgical technique that repairs perineal fistulas with the preservation of anal sphincter function. The principal idea of this procedure is to surgically close the internal opening of the fistula using a flap made of rectal wall, allowing the healing of the fistula from inside out. The reported success rate of endorectal advancement flap in patients with Crohn’s perianal fistulas ranges from 25 to 100% in different series, with an average success of approximately 50–60%.(108) Elective surgery for PCD may include procedures for nonfistulous complications such as dilation of anorectal strictures. Most commonly, however, patients with PCD will require surgery to repair perianal and rectovaginal fistulas not responsive to medical therapy, which may include fistulotomy, fibrin glue injection, transanal endorectal flap advancement, and gracilis muscle interposition. Fibrin Glue is a technically simple procedure for the treatment of perianal fistulas and it is associated with low risk and early return to normal activity. Fibrin glue is a blood by-product that uses the activation of thrombin to form a fibrinclot, mechanically sealing the

surgery for crohn's disease fistula tract. Series using fibrin glue for perianal fistulas of mixed etiologies have yielded success rates of approximately 30–70%.(109) Gracilis transposition can be an option in patients after proctocolectomy or others types of CD related fistulas in whom other options may have failed before proctocolectomy.(110) Occasionally, temporary diverting colostomy or ileostomy is required to control symptoms, and in extremely severe cases resistant to both medical and surgical therapy, proctectomy or proctocolectomy may be required. The PCD score developed by Wexner et al. can be very helpful in selecting therapeutic alternatives and in prognostication.(111) The PCD Activity Index analyzes 6 features in PCD: abscess, ­fistula, fissure and/or ulcer, stenosis, and incontinence. Obstruction Gastrointestinal obstruction usually results from acute active inflammation superimposed on a stenotic segment. Mass effect from an adjacent phlegmon or abscess is not an uncommon scenario. Malignancy must be excluded in CD strictures involving the colon. Yamazaki et al. noted a 6.8% malignancy rate in 132 patients with colonic Crohn’s disease complicated by stricture.(112) Although traditionally by-pass without vagotomy was considered the best option for gastro-duodenal obstruction strictureplasty has become acceptable.(113) Complete or near-complete intestinal obstruction unresponsive to medical therapy requires surgical correction. Depending on location, this treatment involves either resection or strictureplasty. (114) If malignancy is present or suspected, a resection is obviously indicated following standard oncologic principles. Bleeding Whereas mild gastrointestinal bleeding is a common manifestation of inflammatory bowel disease, severe bleeding is a rare phenomenon. CD has been reported to be an established source of gastrointestinal hemorrhage, in 0.9% to 2.5% of patients with this disease.(115) CD bleeding is often from a localized source. This is caused by erosion of a blood vessel within multiple deep ulcerations that extend into bowel wall. The small bowel is the site of bleeding in 65% of cases, whereas the colon was involved in 12%, and in 23% the site could not be identified. It is important to exclude a gastroduodenal source before bowel resection. Angiography is often performed to identify and possibly treat the bleeding site by selective or superselective angiographic infusion of vasopressin.(116) Embolization should be the initial treatment of choice in CD in an attempt to avoid surgical resection. Cirocco et al. (115) reported that surgical resection offered excellent palliation, with low mortality (3%) and a low rebleeding rate (3.5%). Surgery is indicated in those patients who fail to show improvement of bleeding after 4 to 6 units of blood, have recurrent hemorrhage, or have other indications to resect diseased bowel.(114) A bowel preparation is contraindicated, and the aim is to remove the patient from life threatening hemorrhage. Toxic Megacolon Toxic megacolon is a potentially lethal complication which has gradually decreased in incidence because of earlier recognition and intensive management of severe colitis. A possible mechanism

is that mucosal inflammation sequentially leads to the release of inflammatory mediators and bacterial products, increased nitric oxide syntheses, generation of excessive nitric oxide, and colonic dilation. Toxic megacolon affects all ages and both genders. Signs and symptoms of acute colitis that are frequently resistant to therapy are often present for at least 1 week before the onset of acute dilatation. Severe bloody diarrhea is the most common presenting symptom, while improvement of diarrhea usually occurs because of the onset of megacolon. Other futures include malaise and abdominal pain and distention.(117) Up to 47% of patients require surgery due to failure in medical therapy. Factors affecting mortality are age (>40), gender (female), and presence of colonic perforation. The overall mortality rate is 16%.(118) Although the frequencies of performed emergency surgery have decreased, improved medical treatment has lead to higher rates of elective operations. Siassi et al. published a 33 years experience, and prospectively found that the rates of elective surgery rose from 69.5% (1970 to 1980) to 81.4% (1981–1991) and 80.9% (1992–2002) (101). This change might reflect the changes in disease location. Combined large/small bowel resections such as ileocecal resections increased from 27.5% (1970–1980) to 41.9% (1981–1991) and 67.1% (1992–2002) (101), as CD limited to this region that is unresponsive to medical management is best treated by ileocolectomy and anastomosis (119). Similar results were found by Reissman et al. with a 59% rate of ileocolectomy and anastomosis.(120) Specific considerations in surgical techniques for CD patient The philosophy behind surgical intervention in Crohn’s disease rests on the fact that Crohn’s disease is currently incurable and potentially involves the entire intestine, and that surgery relieve only the complications. Strictureplasty Over one-third of patients with CD will develop an intestinal stricture and the great majority of these will require at least one surgical procedure. The initial view was that strictureplasty should only be undertaken for recurrent disease and in patients who have had previous multiple resections. The potential benefits of any surgery include symptom relief, improved nutritional status, and reduced dependence on medication. The most obvious advantage of strictureplasty over resection is that the development of short bowel syndrome can be avoided. All jejunoileal strictures and most duodenal strictures are able to strictureplasty.(121) The procedure can also be undertaken in patients with symptomatic anastomotic strictures. Table 32.3 shows current indications for strictureplasty and contraindications.(122) There are two main types of operation used. The Heineke– Mikulicz procedure is used for strictures of up to 10 cm in length. For strictures up to 25 cm long, the Finney procedure (a side to side amastomosis) is done. Most of the others methods of strictureplasty are generally derivations of one of the above methods, or a combination of both. In 2000, Tichansky et al. published a meta-analysis that showed that Heineke-Mikulicz technique is most often used for Crohn’s strictureplasty. However, the outcome revealed that the Finney strictureplasty may reduce the reoperation rate.(123)

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improved outcomes in colon and rectal surgery Table 32.3  Current indication for strictureplasty and contraindications.

(A)

Indication Previous extensive (>100 cm) resections of small bowel Short bowel syndrome Duodenal strictures Rapid recurrence of disease with obstruction Strictures at previous anastomotic sites, particularly ileorectal or ileocolic Fibrotic strictures within diffuse involvement of the small bowel Small bowel stricture (active or nonactive disease) Contra indications Perforation of the small bowel, with or without peritonitis Serum albumin <2.0 g dl Fistula or phlegmonous inflammation at intended strictureplasty site Likelihood of tension on closure of strictureplasty Intended strictureplasty site next to segment requiring resection Presence of malignancy

(B)

Stricture biopsy The morbidity rate ranges from 10.2–13%, with fistula formation as the most frequent complication.(123) Strictureplasty has been found to be a safe and efficacious procedure for small bowel Crohn’s disease.(124) Resection The most common surgery is ileocolic resection (Figure 32.4a, 32.4b, 32.4c), usually undertaken for medical therapy failure, fistula, obstruction, mass, perforation, or malignancy. The development of malignancy increased to 4 to 20 times of the average population. As previously mentioned, strictureplasty site should be evaluated for intraoperative biopsy and resection, the only procedure which should be considered in the setting of carcinoma. Over the past two decades, laparoscopic resection has demonstrated clear superiority over laparotomy relative to postoperative recovery, cost, morbidity, cosmesis, and long-term bowel obstruction.(125–128) Regardless of the technique of resection performed, the anastomosis should be between two and of grossly normal bowel. Histologic disease free margins and further resection add no benefit and may predispose to the onset of short bowel syndrome. Bemelman et al. (129) showed that medical therapy was able to prevent surgery in one third of the cases of CD in the terminal ileum. Patients who probably will fail medical therapy are those with stenosis, extraintestinal manifestation, or known history of CD for more than 5 years. Some patients might undergo resection if the obstruction is contra-indicated to have strictureplasty. Many studies compare the outcomes between medical therapy and conventional laparoscopic procedure. A meta-analysis done in 2007 showed 14 studies with 881 patients. The operative time for laparoscopic ­surgery was longer, but morbidity was lower.(130) The Surgical treatment for large bowel Crohn’s disease has included total proctocolectomy, segmental colectomy or colectomy with ileorectal anastomosis (IRA), depending on severity and disease distribution. Conventional proctocolectomy is reserved for those patients with anorectal involvement, but in the 50% of patients with large bowel Crohn’s disease with rectal sparing,



(C)

Figure 32.4  (A)Terminal ileal strictures are the most common cause for surgery (Picture taken by Wang Hao, M.D., Cleveland Clinic Florida). (B) The best surgical option for stricturing terminal ileal disease is often an ileocolic resection (Picture taken by Wang Hao, M.D., Cleveland Clinic Florida). (C) The length of the narrowing in the small bowel varies. (Picture taken by Wang Hao, M.D., Cleveland Clinic Florida)

surgery for crohn's disease (A)

(B)

(C)

(D)

Figure 32.5  (A) After an ileocolic resection, the recurrence is most commoly at the anastomotic site (arrow) (Picture taken by Jorge Canedo, M.D., Cleveland Clinic Florida). (B) A 15 cm stricture; also note the creeping fat (Picture taken by Jorge Canedo, M.D., Cleveland Clinic Florida). (C) Small bowel resection and anastomosis. (Picture taken by Jorge Canedo, M.D., Cleveland Clinic Florida). (D) Note the thick fibrotic stricture (Picture taken by Jorge Canedo, M.D., Cleveland Clinic Florida)

segmental resection or colectomy with an ileorectal anastomosis has been used. A meta-analysis done in 2005 comparing segmental versus subtotal ⁄ total colectomy concluded that both procedures were equally effective as treatment options for colonic Crohn’s disease, however, patients in the SC group exhibited recurrence earlier than those in the IRA group.(131) The choice of operation is dependent on the extent of colonic disease. Better outcomes are expected for IRA in patients with two or more colonic segments involved. A meta-analysis done in 2007 compared the end-to-end anastomisis to other configurations (132) and found that end-to-end anastomosis after resection for Crohn’s disease may be associated with increased anastomotic leak rates. Side-to-side anastomosis may lead to fewer anastomotic leaks and overall postoperative complications, a shorter hospital stay, and a perianastomotic recurrence rate comparable to end-to-end anastomosis. Further randomized, controlled trials should be performed for confirmation Resection is contra-indicated in duodenum stricture, due the high risk of the procedure. In order to avoid short small bowel syndrome, the resection should include macroscopic intestinal disease. It is known that activity of CD necessitating intestinal

resection diminishes over time, especially from more than 20 years after the first resection.(133) Bypass Bypass surgery enjoyed popularity many decades ago, at the beginning of CD surgery, when complication rates for resection were high. However, it fell out of use due to high rates of recurrence, great metabolic changes, higher risk of malignancy, and higher rates of postoperative complications.(104) Bypass surgery is currently undertaken for duodenal stricture, although fecal diversion may have a long dysfunctional segment. Diversion without resection may be indicated in very selective situations, like severe perianal disease.(134) Postoperative recurrence after surgery Rates for recurrence after resection are up to 73% after 1 year, although only 20% of patients have symptoms. After 3 years, recurrence has been noted in 85% of patients, with symptoms present in only 34%. The site of recurrence is usually the anastomosis site.(135)

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improved outcomes in colon and rectal surgery Reoperation for recurrence rates after strictureplasty is between 24–26% after 5 years. Medical therapy may have a great value in lowering rates of recurrence. Smoking significantly increases the risk of recurrence after surgery for CD, especially in women, and it is dose-dependent. Another feature that influences recurrence after surgery is a short duration of disease before surgery. The site of the disease also affects recurrence rates, as small bowel and ileocolic disease have higher rates of recurrence (Figure 32.5a, 32.5b, 32.5c, 32.5d). Perforation is associated with a higher rate of recurrence in patients who have had a colonic resection.(136) Gender, family history of CD, blood transfusion, length of resection, presence of granuloma in the specimen, and postoperative complications do not correlate with recurrence. Quality of life after surgery: Patients who undergo surgical treatment for CD experience improvement in Health-related Quality of Life (HRQL) up to 1 year after surgery. Most of the studies focus on assessment of quality of life for ileocolic resection, the most common procedure. Controversies exist as to whether there is actually improvement or not in a long term follow-up for these patients. Thaler et al. (137) concluded that HRQL actually reduces in patients with CD in a long-term follow-up, no matter whether the surgery was open or laparoscopic compared to a normal control population. And recurrence was the most important factor adversely affecting quality of life. Casellas et al. (138) analyzed the impact of previous surgery for complicated or refractory CD on HRQOL. The results indicated that patients with active CD have a serious impairment in HRQOL and patients with a history of previous surgical bowel resection are not different from patients who have never had ­surgery, as long as those patients remain in clinical remission. References    1. Crohn BB, Ginzburg L, Oppenheimer GD. Regional ileitis. A pathological and Clinical entity. JAMA 1932; 99: 1323–9.    2. Lockhart-Mummery HE, Morson BC. Crohn’s disease (regional enteritis) of the large intestine and its distinction from ulcerative colitis. Gut 1960; 1: 87–105.    3. Vermeire S, Rutgeerts P. Chapter 54: Crohn’s Disease in the … edition of Diseases of the Gut and Liver.    4. Heresbach D, Alexandre JL, Bretagne JF. ABERMAD ((Association Bretonne d’Etude et de Recherche sur les Maladies de l’Appareil Digestif). Crohn’s disease in the over60 age group: a population based study. Eur J Gastroenterol Hepatol 2004; 16(7): 657–64.    5. Andres PG, Fridman LS. Epidemiology and the natural course of inflammatory bowel disease. Gastroenterology Clin North Am 1999; 28(2): 255–81.    6. Loftus EV Jr, Snadborn WJ. Epidemiology of inflammatory bowel disease. Gastroenterol clin North Am 2002; 31: 1–20.    7. Nikolaus S, Schreiber S. Diagnostics of inflamatory bowel disease. Gastroenterology 2007; 133(5): 1670–89.    8. Gasche C, Lomer MCE, Cavill I. Weiss, G. Iron, anaemia, and inflammatory bowel diseases. Gut 2004; 53(8): 1190–7.    9. Vermeire S, Van Assche G, Rutgeerts P. Laboratory markers in IBD: useful, magic, or unnecessary toys? Gut 2006; 55(3): 426–33.

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Ostomies Vance Y Sohn and Scott R Steele

Challenging Case A 55-year-old morbidly obese male undergoes a low anterior resection with concomitant defunctioning loop ileostomy for a T2 rectal cancer. Six weeks postoperatively, he presents to the clinic with an obvious parastomal hernia that is easily reducible. He complains of worsening pain, difficulty with application of his ostomy appliances, and symptoms of intermittent obstruction. Case Management In this patient, the optimal management includes reversal of the ostomy after ensuring that the distal anastomosis has healed. This is usually confirmed by a contrast study, often a gastrograffin enema or CT scan with rectal contrast. An ostomy reversal ameliorates and addresses all of the symptoms including the hernia, obstruction, and pain. After reversal, the skin of the ostomy can be primarily closed, however extreme vigilance of the wound is necessary secondary to an increased rate of local wound infection. Depending on the size of the fascial defect and corresponding hernia, additional mesh may be needed for hernia repair. Due to increased risk of infection of most prosthetics, biologic materials should be considered as a first option. For patients who are not candidates for ostomy reversal, various options are available and include both open and laparoscopic approaches. These options include primary fascial repair, repair with biologic or prosthetic mesh, and stoma relocation. The approach and the method of repair is dependant on the surgeon’s preference and experience. Certainly, observation for minimally symptomatic parastomal hernias is the preferred option until stomal takedown is possible. Introduction Intestinal stomas, either temporary or permanent, are the surgical exteriorization of either small or large bowel to the anterior abdominal wall. An ostomy may be placed temporarily, often when its primary purpose is to divert the fecal stream away from an area of concern such as a high-risk anastomosis in a field of prior radiation treatment, following a coloanal repair, or concern for leak after a stapled end-to-end anastomosis. Once the distal anastomosis has adequately healed, gastrointestinal continuity can be reestablished when the ostomy is reversed. A permanent stoma is created following an oncologic resection for rectal cancer that includes removal of the anorectum and associated sphincter complex. In this instance, a descending colostomy would be required to avoid perineal soiling with a coloanal anastomosis in the absence of the sphincters. While there are various types of ostomies described for a broad spectrum of disease processes such as the neo-bladder construction with an ileal conduit, this chapter will focus solely on outcomes for ostomies created with the small or large bowel for colon and rectal diseases.

Psychological Impact of Living with a Stoma Regardless of the type of ostomy, living with a stoma exacts a ­tremendous psychological burden on patients and requires adjustments to activities of daily living. In addition to the physical adjustment of caring for an ostomy, the possibility of participating in simple activities, such as dining out, often becomes disrupted in the patient’s mind. Unfortunately, this is one of the major fears of patients whether or not it is founded in reality. Yet, it is also one that is often not discussed in detail before the operation, nor able to be appropriately counseled and educated when stomas are required in the emergent setting. In 1952, Sutherland et al., (1) published the first report on the important psychological needs of patients living with stomas. Since then, multiple studies have reported the negative impact ostomies have on overall quality of life.(2–6) It is not surprising that the presence of a stoma is associated with decreased quality of life measurements in the immediate and early postoperative setting.(7) Unfortunately, it often appears that while overall quality of life, return to prior activity levels, pain and fatigue all improve with time following surgery, self-impression views such as body image and sexual function do not seem to change with time.(8) Thus, despite evidence to the contrary that a “return to normalcy” is achievable, many patients can never get past the idea of having to live with a stoma. More recently, Krouse and colleagues (9) evaluated the quality of life of 239 male patients from multiple Veterans Affairs (VA) hospitals living with stomas. Their report, which was a case-control survey study, used various previously-validated quality of life indices to compare patients with ostomies versus 272 patients who had undergone similar operations, but not requiring stoma formation. Their study highlighted multiple important psychosocial facts about patients living with ostomies. There was increased self-reported postoperative depression and suicidal ideations among respondents living with ostomies. Such feelings may have been compounded by issues of coping and social acceptance, as their fears related mostly to both others’ perceptions of patients with stomas and their own personal fears of having stoma-related accidents. As these fears became more frequent, they clinically translated into decreased social interactions and eventual isolation. The authors’ recommendation of encouraging social networking among ostomates to clarify issues and limit the trial and error approach that many patients with ostomies undergo, is a valid conclusion which should be supported by all physicians. This is not to say that all patients do poorly or are mentally burdened by living with a permanent stoma. In a large metaanalysis of 1,443 rectal cancer patients from 11 studies, there was no difference in general quality of life scores at 2 years following surgery between those patients undergoing an abdominoperineal resection from those undergoing a low anterior resection with incontinuity reconstruction.(10) These contradictory findings may



improved outcomes in colon and rectal surgery

Figure 33.1  Stomal placement. The site is selected to bring the stoma through the rectus abdominis muscle.

in part depend on the questionnaire given, the ­disease process for which the stoma was created, and the preoperative functional level of the patient. For example, factors such as patient age, (11) decreased preoperative continence, (12) and severe active perianal Crohn’s fistulizing disease (13) have all been shown to have an improved quality of life following stoma formation. Thus, while it would be inaccurate to state that placement of stoma will end up with a lowered quality of life and significant psychological problems, it also is naïve to think that stoma creation will not have a significant impact on a patient’s subsequent immediate and long-term recovery. It is well-established, that in addition to networking, a close relationship with a readily available and experienced enterostomal therapist is an invaluable aspect of the multidisciplinary approach. These expert therapists can significantly alleviate initial fears and anxieties that often plague patients living with a stoma. Furthermore, in our experience, preoperative counseling about expectations, education regarding the indication for the ostomy, and even “practicing” the wearing of an appliance before surgery all aid in lessening the psychological impact on the patient and promotes adaptation to their ostomy. Stoma Site Marking In 2007, the American Society of Colon and Rectal Surgeons (ASCRS), in collaboration with the Wound, Ostomy, and Continence Nurses (WOCN) Society developed a position statement on the value of preoperative stoma marking for patients undergoing ostomy surgery.(14) Their ultimate goal was to decrease stomal complications and improve quality of life for patients. In addition to precise step-by-step instructions on the proper siting of stomas, the statement recommended that all patients scheduled for ostomy surgery undergo preoperative stoma marking by an experienced, trained clinician. This evaluation

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includes examining the patient in the lying, sitting, and standing positions, and accounting for patient factors such as previous incisions, waist and belt lines, abdominal habitus, and hernias, to determine the optimal stoma position that is crucial to decreasing the incidence of stomal complications. One of the more important aspects of this preoperative marking evaluation is the identification of the rectus abdominus muscle, as placement of the stoma through the rectus muscle may prevent peristomal herniation or prolapse (Figure 33.1).(15) Furthermore, preoperative siting allows for patient participation and education regarding stoma care and the use of ostomy appliances. While this position statement has yet to be clinically validated, previous reports have demonstrated the importance of preoperative stomal siting. In a retrospective analysis, Bass and associates (16) reviewed a single institution’s stoma complication rate in 593 patients over an 18-year period. The study compared 292 patients who underwent preoperative marking by an enterostomal therapist to the remaining 301 remaining patients who did not undergo preoperative marking. The endpoints of their study, early and late complications, were favorable for the patients who underwent preoperative marking with a 23% versus 43% early complication rate (p < 0.03) and 9% versus 31% late complication rate (p = NS). This study, and the joint statement by ASCRS and WOCN, highlights the importance of proper preoperative stoma marking for decreasing complication rates. STOMAL TYPES End ostomies End ostomies, either permanent or temporary, are most often placed in the left lower quadrant of the abdominal wall using the left colon or in the right lower quadrant when utilizing the ileum. The indication for stoma creation is important, as this

ostomies often dictates whether gastrointestinal continuity can be reestablished. For instance, in patients undergoing an abdominoperineal resection (APR) for rectal cancer, a permanent end colostomy is the only option as the anorectum and surrounding musculature are removed. Similarly, patients who undergo a proctocolectomy, usually for inflammatory bowel disease (IBD) or Familial Adenomatous Polyposis (FAP), are candidates for an end ileostomy. For patients wanting more fecal control, a continent ileostomy may be offered. Ostomies remain permanent when the altered anatomy prohibits reestablishment of gastrointestinal continuity, the risks of undergoing another surgery are prohibitive due to comorbidities, or the functional results of a reanastomosis would adversely impact quality of life. This latter point is common with reanastomosis of the ileum with the mid- or distal rectum or anus (since the large absorptive capacity of the colon or the storage ability of the compliant rectum is lost), or when the patient has poor sphincter function. Barring the aforementioned contraindications, most ostomies can be reversed and thus, are temporary. A common temporary end ostomy performed routinely by surgeons is the Hartmann’s procedure. Initially described by Henri Hartmann in 1921 for rectal cancer, this versatile procedure is indicated for a variety of benign and malignant scenarios where primary resection of colon and reanastomosis is unsafe or not possible. As discussed later, reversal is associated with complications and the benefits of stoma reversal must be balanced with the potential risks to the surgery. Ideal candidates for reversal are young, healthy patients with preserved sphincter mechanisms. The optimal time for this colostomy reversal has been controversial. Some have found that reversals after 4 months were associated with a higher complication rate; after this time, the rectal stump was less readily accessible and therefore, led to increased complications.(17) Others have found no outcome differences between early or late reversals and considered the timing an insignificant factor.(18) The benefits of an end ileostomy with immediate maturation, initially described by Brooke in 1952, have decreased the incidence of stenosis, dysfunction, retraction, and serositis associated with an ileostomy.(19, 20) Since that time, this has become the standard technique for ileostomy and most colostomy formations. Despite increasing experience with restorative continuity procedures such as the ileal pouch-anal anastomosis (IPAA), an end ileostomy remains an important part of the surgical armamentarium. For instance, in patients with toxic megacolon undergoing total abdominal colectomy, when the principles of “damage control” surgery are paramount, an end ileostomy following abdominal colectomy remains the procedure of choice. Additionally, an end ileostomy would be preferred over an IPAA or an ileal-rectal anastomosis (IRA) for patients with poor anal sphincter mechanisms where continence is questionable. Alternatively, in young healthy patients with inflammatory bowel disease or FAP requiring proctocolectomy, IPAA should be considered, or IRA when the rectum is spared. Purported benefits of an IPAA compared to the end ileostomy revolve around the maintenance of continuity and thus, a more psychologically favorable outcome for the patient. Pemberton et al. (21) evaluated this relationship by comparing quality of life for 298 patients with IPAAs and 406

patients with end-ileostomies. Greater than 93% of patients in both groups were satisfied with their surgeries, although 39% in the end ileostomy group would have preferred an IPAA. After analysis, the authors concluded that patients who underwent an IPAA experienced significant advantages in performing daily activities with resultant improved quality of life. While the benefits of IPAA are beyond the scope of this chapter, this procedure should be considered as a viable alternative for patients considered for end ileostomy. It should be noted, however, that a significant portion of IPAA patients require a temporary stoma, with an additional ~10% developing pouch failure that requires either pouch excision with permanent stoma or permanent pouch diversion.(22) Thus even in this select cohort, education regarding stoma care and outcome is of utmost importance. Continent ileostomy Continent ileostomy, first reported by Nils Kock in 1969, is a less frequently performed procedure due to the technical expertise required, the significant complication rate associated with its nipple-valve mechanism, and the preference for creation of ileoanal pouches.(20) Occasionally, the continent ileostomy remains a useful option for patients undergoing proctocolectomy for FAP or IBD, or in those patients who develop IPAA failure. In 2006, Nessar et al. (23) reported the long-term outcomes of patients undergoing continent ileostomy at the Cleveland Clinic Foundation. Their study population included 181 patients with continent ileostomies, 69 of whom previously had an end ileostomy, and 35 patients who had an end ileostomy after excision of a continent ileostomy. With a median follow-up of 11 years, 17% of patients had their continent ileostomy excised; there was only a 7 month complicationfree interval, and a 14 month revision-free interval. Long-term complications were common, with 30% experiencing valve slippage, 26% developing pouchitis, 25% with fistula formation, and 15% with parastomal herniation. Other complications included valve prolapse, difficult intubation, stoma stricture, and pouch bleeding. Importantly, even in centers with significant experience, the complication profile remains considerable. Similarly, in a study by Kohler et al. (24) comparing outcomes in patients between end ileostomy, continent ileostomy, and ileal pouch-anal anastomosis (IPAA), those patients with IPAA had fewer restrictions in sport and sexual activities when compared to patients with continent ileostomy. Patients with end ileostomy fared the best with regards to the travel capabilities when compared to the other two. In our practice, continent ileostomies are seldom performed. Due to the aforementioned complication profile, patients are counseled for either an IPAA, IRA, or an end ileostomy. Yet, despite our reluctance to perform this procedure, select institutions well-versed in this procedure report excellent outcomes and overall high patient satisfaction.(25–27) Loop End Stomas A loop end stoma is a variation in which a section of the bowel several inches proximal to the divided end of the bowel is brought through the abdominal opening (Figure 33.2). The loop can be supported with a rod and the bowel is opened and matured in a fashion similar to a loop stoma. This type of stoma is helpful in challenging situations such as thick shortened

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improved outcomes in colon and rectal surgery

Figure 33.2  Z-Plasty repair for stenosis. A, incisions in skin and bowel. B, completed repair.

mesentery, tenuous blood supply, or friable bowel. Its advantage is that no blood vessels are divided and with a rod, the tension is on the back wall of the bowel rather than the mucocutaneous anastomosis. This type of stoma is slightly more difficult to pouch as it is slightly oval and may not have the protrusion of a well-formed end stoma. Diverting or loop ostomies The ultimate purpose when creating a diverting stoma is to prevent the fecal stream from reaching a distal segment of distal small bowel or large intestine for the purpose of either treating or preventing a leak. To that end, either a loop colostomy or ileostomy will suffice. However, an ileostomy is often preferred due to its perceived ease of closure. Proponents of a loop colostomy cite the lower risk of high stomal output leading to fluid and electrolyte abnormalities occasionally seen with a loop ileostomy. The common indications for concomitant proximal fecal diversion include protection of distal at-risk anastomosis, especially low-lying colo-anal anastomosis and ileal pouch anal-anastomosis (IPAA), complicated diverticulitis, treatment of anastomotic leaks and pelvic sepsis, large bowel obstruction, trauma, extensive perianal Crohn’s disease, and less commonly, fecal incontinence. The indication for a concomitant proximal fecal diversion for low lying anastomosis, most commonly performed for rectal cancer, has been intensely studied. Wong and Eu (28) reported the results from a prospective, comparative study of 1,078 patients undergoing elective low or ultra-low (defined as colonic anastomosis to the anal canal) anterior resections from 1994 to 2004. In the diverted group, 28% developed a clinically significant leak while of the nondiverted group, 13% had a clinically significant leak (p = 0.86). 95% of these leaks required a salvage operation, and analysis revealed no statistical difference between anastomotic leak complications between patients undergoing and not undergoing fecal diversion. These authors concluded that a defunctioning ileostomy did not influence the complication rate of a rectal anastomosis, rather it minimized the clinical sequela of leaks in high risk patients. They recommended that proximal diversion should be used on a selected basis. In another prospective study from Sweden, the Rectal Cancer

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Trial On Defunctioning Stoma (RECTODES) randomized 234 patients undergoing low rectal (<15 cm from the anal verge) anastomosis to fecal diversion versus no diversion.(29) Their primary endpoint was to assess whether there was a difference in the rate of symptomatic anastomotic leakage in patients between the two arms of the study. While there was a disproportionate number of patients (72%) not undergoing ­randomization due to various factors including intraoperative concerns requiring diversion, the total number of patients with and without diversion were similar (116 pts vs 118 pts). Patient characteristics were similar with increased operative times for those undergoing stoma placement as the only statistically significant difference between the two patient cohorts. In their analysis, patients without a defunctioning stoma had ­significantly more symptomatic leakages (28%) when compared to those without proximal diversion (10%). The group not undergoing diversion consequently constituted 75% of all urgent reoperations. Of the 28 out of 33 patients without initial fecal diversion who developed a leak, urgent reoperation was accompanied with either a loop ileostomy or permanent end colostomy. Consequently, these investigators recommended routine defunctioning loop stoma in low anterior resections for rectal cancer. Based on these and other studies, it is now generally acknowledged that a proximal defunctioning stoma does not abolish the risk of leakage, but certainly mitigates the consequences. In our practice, defunctioning stomas are almost always placed for any anastomosis within 5 cm of the anal verge, although exceptions such as the one stage IPAA occurs occasionally. Furthermore, patient factors such as previous irradiation, intraoperative hemodynamic instability, poor nutrition, and chronic steroid use lead us to liberally “protect” the distal anastomosis. When deciding to perform a proximal fecal diversion or a defunctioning stoma, the two traditional options include a transverse loop colostomy or a loop ileostomy. These two options were compared in a prospective randomized study by Williams et al. for elective protection of distal anastomoses.(30) In their analysis, nearly all complications were twice as common with transverse colostomies than ileostomies and included infection at the time of creation and at takedown, odor, leakage, and skin problems. Additionally, multiple visits to the stoma therapist were needed

ostomies in 58% of colostomy patients versus 18% of ileostomy patients. In another prospective randomized study by Edwards et al., there was no difference in operating time required to construct either stoma, and in fact, reversing the colostomy was easier due to the larger fascial opening.(31) This larger defect however, resulted in worse complications manifested as parastomal hernias, prolapse, fecal fistula, and in the follow-up period, incisional hernias. These increased rates of complications with loop colostomy and increased rate of hernia formation at the ostomy closure site, and has led to an almost universal preference of loop ileostomy for diverting stoma.(31, 32) Should one choose to perform a loop transverse colostomy, choosing a point in the colon adjacent to the flexures may decrease the risk of prolapse to a small extent. COMPLICATIONS WITH OSTOMIES The incidence of stoma complications varies in surgical literature from 10–70%, and can range from minor skin irritation to parastomal herniation requiring operation.(33–35) The wide variance in complication rates is due to the definition of complication and the length of follow-up in the studies. Furthermore, there are a multitude of factors that influence complication rates, including the type and location of the ostomy, patient factors such as gender, BMI, diagnosis, and urgency in which the procedure is performed. In a study from Cook County Hospital, the incidence of stoma complications was 34% in a review of 1,616 patients, with 28% having an early complication (<30 days from time of surgery) and 7% late complication (>30 days).(36) In a national audit, Cottam and associates identified 1,329 (34%) patients out of a cohort of 3,970 stomal patients that developed early complications (<3 weeks from times of surgery) defined as stoma retraction, necrosis, ischemia, muco-cutaneous separation, and dehiscence.(37) Statistically significant factors increasing postoperative complications were stoma height (<20 mm for ileostomy and <7 mm for colostomy), female gender, loop ileostomy, advanced BMI, younger age, malignant diagnosis, and emergent procedures. Similarly, in a prospective study of 97 patients, Arumugam et al. found elevated BMI, diabetes, and emergency surgery as significant risk factors for the development of stoma complications.(38) In yet another study evaluating risk factors for stoma complications, Saghir and colleagues identified advanced age, advanced American Society of Anesthesiologists (ASA) grade, and noncolorectal specialty-trained surgeons performing the ostomy as risk factors for stoma complications.(39) As evident in these studies, various patient and surgeon factors can increase the risk of developing complications. Thus, it is imperative for the surgeon caring for these patients to be well aware of not only the things they can do to prevent these complications, but also how do deal with any complications should they arise. In the following section, the presentation and management of common complications will be addressed. Skin Complications Skin conditions are common among patients living with stomas and are more prevalent in patients with ileostomies than colostomies. (5) Common causes include fungal or bacterial infections, irritation from the ostomy effluent, folliculitis, contact dermatitis from the appliance, a manifestation of IBD such as pyoderma gangrenosum, or simple skin excoriation from frequent appliance changing.

To a certain degree, minor skin irritation is unavoidable. However, preoperative stoma marking, precise ostomy creation, involvement of an enterostomal therapist, and diligent postoperative care may prevent some of the more severe complications. Proper location of an ostomy diminishes leaking from the appliance and entails avoiding previous incisions, scars, natural skin folds, and belt lines that prevent circumferential adhesion of the appliance. Leaking around the appliance and can lead to social embarrassment and dramatic skin irritation. These problems can occasionally be mitigated by careful appliance fitting which entails minimizing unprotected skin and sealing leaks from the caustic effluent. Various commercially produced barriers, powders, ointments, and creams are available especially for this purpose and should be applied with the help of an enterostomal therapist. If skin excoriation, maceration, and irritation persist despite these conservative measures, consideration should be given for ostomy reversal, revision or repositioning the ostomy, or if possible, converting a high output ileostomy to a lower output colostomy. Retraction Stoma retraction occurs in up to 15% of patients and is most often the result of a technical error from improper construction and/or tension.(40–42) Postoperatively, complete retraction of the stoma into the abdomen mandates immediate re-exploration and re-creation of the ostomy. Fortunately, this potentially catastrophic complication is extremely rare. Partial stoma retraction occurs more frequently and is more problematic for an ileostomy than a colostomy. In ileostomies, retraction leads to difficulties with appliance placement and subsequent skin irritation. In the thicker viscous colostomy effluent, skin irritation is less of an issue and can often be conservatively managed. In severe cases, operative stoma revision may be required. The principles of ­revision include tension free ostomy and adequate eversion emphasizing the Brooke method. Ischemia and Stenosis Ostomy necrosis, due to either arterial insufficiency or venous engorgement, presents in the early postoperative period and is first recognized by mucosal ischemia. Arterial insufficiency is a complication of overaggressive mesenteric mobilization with resultant lack of small vessel collateralization to the mucosa. It can also be seen in patients with foreshortened or thickened mesenteries, in obese patients with thick abdominal walls, or after an inadequate fascial opening. Likewise, stoma necrosis from venous engorgement as the etiology ultimately leads to the same end result. Clinically, differentiating the etiology of necrosis is not important as management is the same regardless of the cause. When both considering and managing stoma necrosis, it is imperative to identify the proximal extent of ischemia. This can be done by a simple bedside “test-tube test” in which a clear test tube is inserted into the stoma and then trans-illuminated or direct visualization is obtained via a pediatric anoscope or proctoscope. Necrosis seen below the fascia mandates re-exploration and revision while necrosis isolated above the fascia can be conservatively managed. Surgically, principles of revision include excision back to healthy, viable bowel, and recreation of the stoma. This may entail a more thorough intraabdominal mobilization to reduce

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improved outcomes in colon and rectal surgery (A)

(B)

(C)

Figure 33.3  Loop end colostomy. A, loop of bowel brought through abdominal wall opening. B, stoma rod is placed through the mesenteric opening to support the loop on the skin and the bowel is opened. C, Completed loop colostomy.

tension through the abdominal wall, revision of the fascial opening, or ensuring no kinking of the blood supply. In very difficult cases, consideration for a loop-end ostomy is advised since less mesenteric mobilization is required. Conservative management of stoma necrosis is possible when the necrosis is isolated above the level of the fascia. Simple measures, such as maintaining an adequate blood pressure for stoma perfusion and awaiting edema resolution after bowel manipulation can avoid the morbidity of a re-exploration. Even with frank necrosis, conservative measures with local wound care should be attempted. However, conservative management of stoma ischemia is a risk factor for ostomy stenosis which occurs in 2–9% of patients.(34, 40, 41) Stoma stenosis is described as narrowing of the lumen of the ostomy at the skin or fascia level and is due to luminal contraction from scar tissue formation. In addition to ischemia, stenosis can occur due to insufficient skin excision at the stoma site, peristomal abscess, or mucocutaneous separation. Stenosis, easily diagnosed by visual inspection and digital exam of the stoma, is rarely clinically significant and can be managed with a low residue diet and stool softeners. In refractory and symptomatic cases, dilation, excision of scar tissue, or stoma revision can be performed. A local type of revision involves a Z-plasty repair (Figure 33.3).(43, 44) Parastomal Hernias By definition, a stoma is a hernia in the anterior abdominal wall, thus leading Goligher to state that the true rate of parastomal hernias is 100%. As such, parastomal hernias are a well-known complication of stomal surgery, and can be a major source of morbidity (Figure 33.4).(45) The incidence of hernias ranges from 5–10% of stomal patients with colostomies more prone

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to herniate than ileostomies.(34, 46) Fortunately, most are well tolerated and manageable nonoperatively. However, approximately 30% of hernias require operative repair for symptoms that include bleeding, obstruction, abdominal masses, poor ­fitting appliances, and leakage.(47, 48) Surgical therapy has centered on stomal relocation, primary fascial repair, and prosthetic mesh—alone, or in combination. Each of these has been widely touted; however, significant morbidity and complication rates up to 88% have left surgeons searching for a better answer to this difficult problem.(49–52) Equally frustrating is the high rate of recurrence following initial repair. Rubin et al. found an initial recurrence rate of 60%, with approximately 70% having subsequent failures following additional surgery for both primary fascial repair alone and stomal relocation.(51) Although prosthetic mesh has shown improved results over stomal relocation and primary fascial repair, these reports are hindered by low patient numbers and lack of long-term follow-up to draw meaningful conclusions regarding complications and recurrences.(49–51, 53–56) A variety of surgical mesh repair techniques exist, including a circumferential onlay mesh, two separate intraperitoneal pieces placed lateral to the stoma, one large piece placed via a midline approach, and an incomplete mesh ring.(49, 53, 57, 58) Additionally, both open and laparoscopic approaches have been used.(59, 60) Yet, fear of mesh infection and erosion has led to concerns regarding mesh use, and the perceived need to avoid any contact between the bowel and mesh.(57) At our institution, one operative approach to symptomatic parastomal hernias commonly used is primary fascial repair with nonabsorbable suture and placement of mesh via a “stove-pipe” hat repair (Figure 33.5). In this technique, one piece of mesh is placed overlying the fascial repair, the stoma is then pulled through

ostomies mesh products, fear of contact between mesh and bowel with subsequent erosion and infection have allowed for increased use of these products using a similar technique. In addition, while not extensively studied, we have periodically placed mesh during the primary creation of a stoma in select cases, such as for those patients with diminished fascia, prolonged steroid use, and ­re-siting of stoma from prior failures. Future data on this practice awaits further recommendations.

Figure 33.4  Computed tomography image of a patient with a parastomal hernia. The arrowhead represents a herniated portion of small bowel adjacent to the ileostomy (arrow). Also note the large midline incisional hernia.

Figure 33.5  “Stove-pipe” hat repair: Parastomal hernia repair with mesh demonstrating the onlay piece of mesh in as well as circumferential component overlying the fascial repair. An additional piece (not shown) may be placed in the sub-fascial location as well. (Courtesy of Patrick Y. Lee, M.D.)

the center of the mesh, thus creating a 360-degree repair. An additional piece of mesh is then tacked to both the bowel circumferentially and to the onlay mesh. Once constructed, this creates the “stove-pipe hat” appearance. In selected cases, an additional piece of mesh is placed beneath the fascia to provide additional support. Drains are routinely placed at the time of surgery. In a recent review of our experience, we analyzed 58 patients that underwent parastomal hernia repair with polypropylene mesh.(64) With a mean follow-up of 50.6 + 40.1 months, the overall complication rate related to the polypropylene mesh was 36.2%, and occurred at a mean of 27.2 months. Complications encountered included recurrence (25.8%), surgical bowel obstruction (8.6%), prolapse (3.4%), wound infection (3.4%), fistula (3.4%), and mesh erosion (1.7%). No patients required extirpation of the mesh. Data analysis demonstrated that stomas placed for underlying colorectal cancer were associated with a decreased rate of complications while increased complications were significantly associated with younger age (59.6 vs. 67 years, p < 0.05). With the increased availability and use of the biologic

Prolapse Ostomy prolapse is the telescoping of the intestine through the stoma and can be a source of discomfort and anxiety for the patient. Causes include a large fascial opening in the abdominal musculature, redundancy of the intestine through the abdomen, failure to place the stoma through the rectus muscle, insufficient suturing to the abdominal wall, distended abdomen, and increased abdominal pressure. Prolapses are most commonly seen in loop stomas with the distal loop more prone to prolapse. The diagnosis is easily confirmed by inspection and the treatment depends on the severity of the prolapse. In severe prolapse, stoma obstruction and ischemia may result from excessive tension on the underlying mesentery. Ischemic changes manifested as ulceration or dusky appearance of the bowel mandates expeditious surgical intervention and restoration of blood flow. In the more chronic setting, prolapse can be managed conservatively with manual reduction and symptomatic relief of discomfort or pain. The application of the ostomy appliance is important for patients who suffer from prolapse. The skin barrier opening should be cut to accommodate the stoma at its largest size and two piece pouching systems with plastic rings should be avoided to prevent strangulation. Surgery may ultimately be necessary to resect the prolapse and revise the stoma if symptoms persist. Again, especially in the setting of loop colostomies, using a portion of bowel near the flexures where it tends to be more tethered, may aid in decreasing the incidence of prolapse. Special Consideration Morbidly Obese Patients Morbid obesity, defined as a body mass index >35 kg/m2, is a public health epidemic in the United States with the prevalence in the adult population ranging from 2.8–5.1%.(62, 63) The impact of obesity on the complication profile of patients undergoing colorectal surgeries have been well documented and include a higher incidence of wound infection, dehiscence, wound herniation, anastomotic, pulmonary, cardiovascular, thromboembolic complications, increased operative time and length of hospital stay, and overall increased morbidity and mortality.(61) Additionally, morbid obesity has been found to increase the complication rates associated with stomas. A prospective risk factor analysis of 97 patients for stoma complications found that elevated BMI was independently associated with an increased rate of ostomy retraction, early skin excoriation, and overflow.(36) Furthermore, in a retrospective review of 156 patients undergoing stoma formation, Duchesne et al. found obesity, defined as a BMI > 30 kg/m2, was significantly associated with stoma complications, most commonly, stoma necrosis, prolapse, and skin irritation.(65) Similarly, Leenan and Kuypers found that obese patients had a significantly higher percentage of overall stoma complication (47 vs 36%)

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improved outcomes in colon and rectal surgery (A)

(B)

(C) Figure 36.6  Loop ileostomy in an obese patient. It is important to consider stoma placement in the lying (A), seated (B), and standing (C) positions. Note the placement of the ostomy with relation to the pannus and mid-line incision. Improper cutting of the stoma appliance cause peristomal skin excoriations. This patient was preoperatively marked by an enterostomal therapist with good postoperative functional outcome.

(A)

(B)

Figure 33.7  Redundant abdominal wall folds of skin associated with ileostomy retraction. (A) Frontal view. (B) Sagittal section demonstrating skin and subcutaneous fat incisions.

including a higher incidence of stoma necrosis.(40) Cottam’s group, in a nationwide audit of stoma complications, found that increasing BMI, even that not meeting criteria for “morbid obesity”, was associated with more stoma problems.(37) Various reasons for a higher complication rate in the obese include a relatively shortened and fatty mesentery, thicker abdominal wall through which the stoma must traverse, poor small vessel circulation associated with comorbidities of obesity, and the physical difficulties of stoma appliance application in the redundant pannus. Ultimately, these factors predispose obese patients to undergo increased mesenteric mobilization so that the bowel reaches the skin, with the end result being arterial insufficiency to the super-fascial stoma. Additionally, an inadequate fascial opening or physical compression of the abdominal wall on the stoma as it traverses the abdominal wall may lead to constriction of venous return with resultant stoma engorgement, stenosis, or necrosis. In morbidly obese patients undergoing stoma formation in an elective setting, preoperative weight loss should be encouraged. Realistically however, sufficient weight loss to favorably impact the complication profile is unlikely. There may be a unique subset of patients who can defer abdominal surgery requiring stoma formation until after undergoing bariatric surgery. In these cases, stoma formation should be delayed until massive weight loss has stabilized as significant changes on the abdominal wall may require ostomy revision if the order of surgery is reversed. In addition to timing of surgery, the preoperative preparation of the morbidly obese patient is critical. This high risk patient population should undergo age appropriate and comorbidity appropriate risk stratification and work-up as they are at increased risk for perioperative complications.



In regards to ostomy complications, preoperative stoma marking is important in all patients undergoing stoma formation, but is arguably even more important in this patient population already at increased risk for local skin complications. Large skin creases prone to superficial fungal infections in the obese should be avoided, as well as low lying ostomies which may be difficult for the patient to adequately visualize and properly maintain (Figure 33.6). Technically, a sufficient fascial opening should be made to easily accommodate the bowel through the abdominal wall. Conservative mesenteric mobilization is encouraged, with minimal length required for the bowel to reach the skin without tension for proper maturation the ultimate goal. In patients with foreshortened mesenteries or those with significant abdominal wall thickness, a loop ostomy, or end-loop stoma in which a loop of bowel is brought through the fascia and the distal portion closed allowing a few additional centimeters of bowel length for construction, should be considered as these are less prone to complications associated with vascular insufficiency. Finally, removal of some local adipose tissue through which the stoma will traverse is reasonable, although over-aggressive “de-fatting” may lead to skin necrosis. Additional options include a modified abdominoplasty (abdominal wall countering), localized flaps with skin or fat removal, or liposuction. Although frequently successful, these techniques have potential for significant morbidity. Patients who may benefit from these techniques include those with stomal retraction (especially those who have bowel limitations [e.g., continent ileostomies, dense intraabdoninal adhesions or short gut], prolapse, large peristomal hernias, abdominal wall laxity (usually resulting from major weight loss), and peristomal skin problems such as pyodermia. In many of these patients stomal relocation may not be the best option. A modified abdominoplasty or abdominal wall contouring is similar to the technique employed by plastic surgeons.(66, 67) A low curvilinear transverse incision is made at the inferior abdominal fold or 2–3 cm above the pubis and anterior superior iliac spines and carried down to the fascia (Figure 33.7). A flap of skin and subcutaneous tissue is created by electrocautery dissection in a cranial direction, just above the fascia. Perforating vessels are identified and ligated or cauterized. As the dissection continues the stoma will be encountered. With the flap on traction, the intestine is separated from the skin and subcutaneous tissue. Care is taken to avoid injury to the bowel or its blood supply. The dissection should err on leaving additional subcutaneous fat attached to the intestine. This can be carefully resected later. A similar maneuver may be performed at the umbilicus if

ostomies (A)

(B)

(A)

(B)

(C)

Figure 33.8  Excess skin and subcutaneous fat have been excised. (A) Frontal view, (B).Sagittal section.

(A)

(B)

Figure 33.9  Ileostomy relocated through upper flap and skin incisions closed. Closed suction drains placed below flaps. (A) Frontal view, (B) Sagittal section.

the surgeon and patient prefer to preserve it in its normal location. Again care is taken to preserve the tissue’s blood supply. If the umbilicus is not to be maintained, it can be amputated at the fascial level. The flap dissection is continued cranially just above the fascia until enough laxity or length is obtained in the upper flap for the upper edge of the previous stomal opening to reach the inferior portion of the incision without excessive tension or to the costal margins. Any associated peristomal hernia can be repaired at this time with suture repair of the fascia and/or mesh (synthetic or biologic) reinforcement. As the flap is retracted inferiorly, new sites for the ostomy and, if desired, the umbilicus are selected and openings created in the flap. Excess subcutaneous fat can be carefully removed to thin the flap. Fortunately, there is usually less subcutaneous fat above the umbilicus compared to below it. The excess, distal portion of the flap is excised (Figure 33.8). The intestine and umbilicus are brought through the respective flap openings and matured with interrupted absorbable sutures (Figure 33.9). Excess bowel or umbilical tissue can be carefully excised. Closed suction drains are placed below the flap to avoid seromas and the inferior incision is closed in layers. As intraabdominal dissections are avoided with this technique, patients usually recover quickly. Morbidity is usually associated with infection, flap ischemia, or seromas. These are managed with wound care.

Figure 33.10  Medial approach. (A) Frontal view with skin incision marked, (B) Cross section demonstrating midline incision and areas of subcutaneous fat excision, (C) After removal of excess subcutaneous tissue, incision is closed, flaps attached to fascia, and stoma matured with adequate eversion.

A more localized procedure involves the use of flaps to modify the abdominal wall around the stomas. Most involve peristomal dissections and removal of skin and subcutaneous fat. This can be performed via a medial or inferolateral approach (Figure 33.10). An incision is made down to the fascia and advanced toward the stoma. The ostomy is dissected free of the skin and subcutaneous tissue as described above. After the stoma is freed, lateral or cranial dissection will provide enough laxity to advance the previous stoma site to the incision (advancement flap). As above, a new ostomy opening, in fresh skin, is created. Excess fat may be excised around the stoma and redundant midline skin is resected. If the skin flap is not redundant enough to advance the original ostomy opening to the midline, the subcutaneous fat can be excised and the stoma returned to its original skin opening through the thinned flap. Either method is performed in such a manner to leave a smooth, flat, thinned flap that provides a flat surface to site the appliance. The stoma is matured and the incision is closed. Subcutaneous closed suction drains are placed above and below the stoma. The circumstomal approach starts with an incision around the stoma at the mucocutaneous junction. With careful dissection, the bowel is separated from the subcutaneous tissue down to the fascia. The subcutaneous tissue is then separated from the fascia with electrocautery in a circumferential manner to a point 7–8 cm out from the stoma. A wedge of subcutaneous tissue is circumferentially created from the upper skin edge to meet the outer edge of the extrafascial dissection. Small closed suction drains may be placed and the ostomy is matured to the skin edges. If there was a preoperative stenosis, the skin opening may be enlarged or the bowel may be matured with a Z-plasty technique.(43, 68) If the preoperative stomal opening was too large or it becomes too large from the dissection, the diameter of the opening can be reduced with interrupted sutures (Figure 33.11). This type of closure has been referred to a “Mercedes technique”.(69) Rapid and significant weight gain in ostomy patients may produce stomal retraction. If attempts at weight loss have not been successful and stomal revision is not desirable or feasible (e.g., continent ileostomy or short gut patients), liposuction is an excellent option. This method is preferred if there is no associated stomal



improved outcomes in colon and rectal surgery (A)

(B)

(C)

Figure 33.11 Mercedes or triangular closure. A. Stoma site with fascia closed, B. Initial approximation of skin and subcutaneous fat, C. Completed closure with small area in center left open for drainage and secondary healing.

stenosis or hernia. Experienced plastic surgeons can carefully use liposuction techniques to remove subcutaneous fat around the stoma. Obviously, care must be taken to not injure the stoma ­during the procedure and to leave a flat smooth peristomal skin surface for the ostomy faceplate. Once the fatty tissue is removed, it will not be redeposited despite additional weight gain. Ostomy Reversal Reversal of temporary stomas should be undertaken as soon as physiologically feasible to reestablish gastrointestinal continuity and for psychological improvement. This of course implies that the purposes of the stoma placement has been met and the patient is capable and a candidate for another operative procedure. There are two main operative approaches to ostomy reversal, local or via a laparotomy. While both approaches are associated with inadvertent enterotomies, bleeding, wound infections, and anastomotic complications, the biggest advantages of the laparotomy approach is improved exposure and the ability to reexplore the abdomen. Certainly, the type of ostomy is important to consider when planning the operative approach as loop ileostomies are technically the least challenging to reverse and often amenable to local reversal. Although a local approach is preferred, patients with a prior Hartmann’s procedure or those in which the distal remnant is not available via a local approach are obviously forced to undergo a repeat laparotomy. Surprisingly, there is a paucity of recent data that highlights the potential perils of this seemingly benign operation. The most recent study, published in 2005, was a retrospective review of 533 patients undergoing stoma closure at the University Hospital of Vienna.(70) The majority of the patients (51%) underwent reversal of a colostomy, 44% had closure of an ileostomy, and 5% had combined reversals of both a colostomy and an ileostomy. All patients underwent a laparotomy using the intraperitoneal approach. Their 30-day mortality was 3% (15 patients) with rates similar for either ileostomy or colostomy reversal. Causes of death were multisystem organ ­failure after nonsurgical complications in nine patients, and anastomotic leakage, missed small bowel injury, and cecal perforation in the remaining six patients. Overall complications were 20%, with anastomotic leakage (5%), ileus (4%), postoperative bleeding (2%), and wound infection (2%). When analyzing patient related factors between survivor and nonsurvivors, only advanced patient age was found to be statistically ­significant. This study, which highlights the potential morbidity



of stoma reversal, also emphasizes the importance of meticulous surgical technique required in these challenging patients with reoperative abdomens. Our approach to ostomy reversal begins with a thorough preoperative evaluation which includes interrogation of the distal colon with either a barium enema and/or endoscopy. The primary reason for which sentinel procedure was performed is important to consider since it may reveal if the purposes of the ostomy has been met and potentially alter the decision on reversal. An obvious but sometimes overlooked step should also be the evaluation of the patient’s sphincter tone and ability to control fecal stream once continuity has been restored. This may require not only clinical evaluation, but formal documentation through anorectal physiology testing including manometry. Baseline poor sphincter tone or incontinence should be considered a contraindication for ostomy reversal in all but the rarest of cases. Finally, additional patient factors which can be altered, such as nutritional status, steroid use, and tobacco abuse, should be optimized before surgery. When planning the operative approach for end colostomy reversals, additional factors to consider before embarking on the operation should include the expected amount of adhesive disease likely to be encountered or previously encountered (i.e., review prior operative notes), whether there is a history of prior abdominal or pelvic radiation, concomitant pathology such as the presence of incisional hernias, and the type of ostomy. For instance, patients with multiple prior surgeries and a history of radiation will most likely benefit from a laparotomy approach that includes preoperative ureteral stent placement, while those patients with loop ostomies without any other comorbidities can be managed with a local approach. Whether a stapled or hand-sewn anastomosis is performed is up to the surgeon’s discretion. Key technical points in each method, however, is to ensure adequate mobilization and visualization of the distal colonic or rectal stump with resection of both the exteriorized bowel or end stump back to normal healthy bowel before the anastomosis. Finally, delayed primary closure is performed for the area in which the stoma was placed and drains are not routinely placed. Conclusion Beyond bringing a loop of bowel to the skin surface, there are a wide variety of issues that a surgeon needs to consider when creating a stoma. Having a thorough understanding of the indications

ostomies for stoma placement, the technical details for the various ostomies, and the physical and psychological impact of living with an ostomy will aid the surgeon in caring for these unique patients. Finally, understanding the potential complications from ostomy placement and having the knowledge to correctly deal with them is an essential tool for all providers and emphasizes the importance of a multidisciplinary team of specialists. References   1. Sutherland AM, Orbach CE. Psychological impact of cancer and cancer surgery. II. Depressive reactions associated with surgery for cancer. Cancer 1953; 6: 958–62.   2. Follick MJ, Smith TW, Turk DC. Psychosocial adjustment following ostomy. Health Psychol 1984; 3: 505–17.   3. Gerharz EW, Weingartner K, Dopatka T et al. Quality of life after cystectomy and urinary diversion: results of a retrospective interdisciplinary study. J Urol 1997; 158: 778–85.   4. Nilsson LO, Kock NG, Kylberg F et al. Sexual adjustment in ileostomy patients before and after conversion to continent ileostomy. Dis Colon Rectum 1981; 24: 287–90.   5. Nugent KP, Daniels P, Stewart B et al. Quality of life in stoma patients. Dis Colon Rectum 1999; 42: 1569–74.   6. Walsh BA, Grunert BK, Telford GL et al. Multidisciplinary management of altered body image in the patient with an ostomy. J Wound Ostomy Continence Nurs 1995; 22: 227–36.   7. Sharma A, Sharp DM, Walker LG et al. Predictors of early postoperative quality of life after elective resection for ­colorectal cancer. Ann Surg Oncol 2007; 14: 3435–42.   8. Gervaz P, Bucher P, Konrad B et al. A prospective longitudinal evaluation of quality of life after abdominoperineal resection. J Surg Oncol 2008; 97(1): 14–9.   9. Krouse RS, Grant M, Wendel CS et al. A mixed-methods evaluation of health-related quality of life for male veterans with and without intestinal stomas. Dis Colon Rectum 2007; 50(12): 2054–66. 10. Cornish JA, Tilney HS, Heriot AG et al. A meta-analysis of quality of life for abdominoperineal excision of rectum versus anterior resection for rectal cancer. Ann Surg Oncol 2007; 14: 2056–68. 11. Ma N, Harvey J, Stewart J et al. The effect of age on the quality of life of patients living with stomas: a pilot study. ANZ J Surg 2007; 77: 883–5. 12. Norton C, Burch J, Kamm MA. Patients’ views of a colostomy for fecal incontinence. Dis Colon Rectum 2005; 48: 1062–9. 13. Kasparek MS, Glatzle J, Temeltcheva T et al. Long-term quality of life in patients with Crohn’s disease and perianal fistulas: influence of fecal diversion. Dis Colon Rectum 2007; 50(12): 2067–74. 14. ASCRS and WOCN Joint Position Statement on the Value of Preoperative Stoma Marking for Patients Undergoing Fecal Ostomy Surgery. J Wound Ostomy Continence Nurs 2007; 34(6): 627–8. 15. Carne PW, Robertson GM, Frizelle FA. Parastomal hernia. Br J Surg 2003; 90: 784–93. 16. Bass EM, Del PA, Tan A et al. Does preoperative stoma marking and education by the enterostomal therapist affect outcome? Dis Colon Rectum 1997; 40: 440–2.

17. Roe AM, Prabhu S, Ali A et al. Reversal of Hartmann’s procedure: timing and operative technique. Br J Surg 1991; 78: 1167–70. 18. Keck JO, Collopy BT, Ryan PJ et al. Reversal of Hartmann’s procedure: effect of timing and technique on ease and safety. Dis Colon Rectum 1994; 37: 243–8. 19. Brooke BN. The management of an ileostomy, including its complications. Lancet 1952; 2: 102–4. 20. Kock NG, Darle N, Hulten L et al. Ileostomy. Curr Probl Surg 1977; 14: 1–52. 21. Pemberton JH, Phillips SF, Ready RR et al. Quality of life after Brooke ileostomy and ileal pouch-anal anastomosis. Comparison of performance status. Ann Surg 1989; 209: 620–6. 22. Das P, Smith JJ, Tekkis PP et al. Quality of life after indefinite diversion/pouch excision in ileal pouch failure patients. Colorectal Dis 2007; 9: 718–24. 23. Nessar G, Fazio VW, Tekkis P et al. Long-term outcome and quality of life after continent ileostomy. Dis Colon Rectum 2006; 49: 336–44. 24. Kohler LW, Pemberton JH, Zinsmeister AR et al. Quality of life after proctocolectomy. A comparison of Brooke ileostomy, Kock pouch, and ileal pouch-anal anastomosis. Gastroenterology 1991; 101: 679–84. 25. Berndtsson IE, Lindholm E, Oresland T et al. Health-related quality of life and pouch function in continent ileostomy patients: a 30-year perspective. Dis Colon Rectum 2004; 47: 2131–7. 26. Litle VR, Barbour S, Schrock TR et al. The continent ileostomy: long-term durability and patient satisfaction. J Gastrointest Surg 1999; 3: 625–32. 27. Castillo E, Thomassie LM, Whitlow CB et al. Continent ileostomy: current experience. Dis Colon Rectum 2005; 48(6): 1263–8. 28. Wong NY, Eu KW. A defunctioning ileostomy does not prevent clinical anastomotic leak after a low anterior resection: a prospective, comparative study. Dis Colon Rectum 2005; 48: 2076–9. 29. Matthiessen P, Hallbook O, Rutegard J et al. Defunctioning stoma reduces symptomatic anastomotic leakage after low anterior resection of the rectum for cancer: a randomized multicenter trial. Ann Surg 2007; 246: 207–14. 30. Williams NS, Nasmyth DG, Jones D et al. De-functioning stomas: a prospective controlled trial comparing loop ileostomy with loop transverse colostomy. Br J Surg 1986; 73: 566–70. 31. Edwards DP, Leppington-Clarke A, Sexton R et al. Stomarelated complications are more frequent after transverse colostomy than loop ileostomy: a prospective randomized clinical trial. Br J Surg 2001; 88: 360–3. 32. Gooszen AW, Geelkerken RH, Hermans J et al. Quality of life with a temporary stoma: ileostomy vs. colostomy. Dis Colon Rectum 2000; 43: 650–5. 33. Leong AP, Londono-Schimmer EE, Phillips RK. Life-table analysis of stomal complications following ileostomy. Br J Surg 1994; 81: 727–9. 34. Londono-Schimmer EE, Leong AP, Phillips RK. Life table analysis of stomal complications following colostomy. Dis Colon Rectum 1994; 37: 916–20.

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improved outcomes in colon and rectal surgery 35. Porter JA, Salvati EP, Rubin RJ et al. Complications of colostomies. Dis Colon Rectum 1989; 32: 299–303. 36. Park JJ, Del PA, Orsay CP et al. Stoma complications: the Cook County Hospital experience. Dis Colon Rectum 1999; 42: 1575–80. 37. Cottam J, Richards K, Hasted A et al. Results of a nationwide prospective audit of stoma complications within 3 weeks of surgery. Colorectal Dis 2007; 9: 834–8. 38. Arumugam PJ, Bevan L, Macdonald L et al. A prospective audit of stomas--analysis of risk factors and complications and their management. Colorectal Dis 2003; 5: 49–52. 39. Saghir JH, McKenzie FD, Leckie DM et al. Factors that ­predict complications after construction of a stoma: a retrospective study. Eur J Surg 2001; 167: 531–4. 40. Leenen LP, Kuypers JH. Some factors influencing the outcome of stoma surgery. Dis Colon Rectum 1989; 32: 500–4. 41. Pearl RK, Prasad ML, Orsay CP et al. Early local complications from intestinal stomas. Arch Surg 1985; 120: 1145–7. 42. Gorfine SR, Bauer JJ, Gelerni IM. Continent ileostomies. In: MacKeigan JM, Cataldo PA, eds. Intestinal Stomas. Principles, Techniques, and Management. St. Louis: Quality Medical Publishing, 1993; 154–87. 43. Beck DE. Abdominal wall modification for the difficult stoma. Clin Colon Rectal Surg 2008; 20: 71–5. 44. Pemberton JH. Management of conventional ileostomies. World J Surg 1988; 12: 203–10. 45. Ien-Mersh TG, Thomson JP. Surgical treatment of colostomy complications. Br J Surg 1988; 75: 416–8. 46. Williams JG, Etherington R, Hayward MW et al. Paraileostomy hernia: a clinical and radiological study. Br J Surg 1990; 77: 1355–7. 47. Burns FJ. Complications of colostomy. Dis Colon Rectum 1970; 13: 448–50. 48. Sjodahl R, Anderberg B, Bolin T. Parastomal hernia in relation to site of the abdominal stoma. Br J Surg 1988; 75: 339–41. 49. Franks ME, Hrebinko RL Jr. Technique of parastomal hernia repair using synthetic mesh. Urology 2001; 57: 551–3. 50. Kish KJ, Buinewicz BR, Morris JB. Acellular dermal matrix (AlloDerm): new material in the repair of stoma site hernias. Am Surg 2005; 71: 1047–50. 51. Rubin MS, Schoetz DJ Jr, Matthews JB. Parastomal hernia. Is stoma relocation superior to fascial repair? Arch Surg 1994; 129: 413–8. 52. Sugarbaker PH. Peritoneal approach to prosthetic mesh repair of paraostomy hernias. Ann Surg 1985; 201: 344–6. 53. Byers JM, Steinberg JB, Postier RG. Repair of parastomal hernias using polypropylene mesh. Arch Surg 1992; 127: 1246–7.

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54. Hopkins TB, Trento A. Parastomal ileal loop hernia repair with marlex mesh. J Urol 1982; 128: 811–2. 55. Morris-Stiff G, Hughes LE. The continuing challenge of parastomal hernia: failure of a novel polypropylene mesh repair. Ann R Coll Surg Engl 1998; 80: 184–7. 56. Rosin JD, Bonardi RA. Paracolostomy hernia repair with Marlex mesh: a new technique. Dis Colon Rectum 1977; 20: 299–302. 57. Kasperk R, Klinge U, Schumpelick V. The repair of large parastomal hernias using a midline approach and a prosthetic mesh in the sublay position. Am J Surg 2000; 179: 186–8. 58. Tekkis PP, Kocher HM, Payne JG. Parastomal hernia repair: modified thorlakson technique, reinforced by polypropylene mesh. Dis Colon Rectum 1999; 42: 1505–8. 59. Berger D, Bientzle M. Laparoscopic repair of parastomal ­hernias: a single surgeon‘s experience in 66 patients. Dis Colon Rectum 2007; 50: 1668–73. 60. Kozlowski PM, Wang PC, Winfield HN. Laparoscopic repair of incisional and parastomal hernias after major genitourinary or abdominal surgery. J Endourol 2001; 15: 175–9. 61. Steele SR, Lee P, Martin MJ et al. Is parastomal hernia repair with polypropylene mesh safe? Am J Surg 2003; 185: 436–40. 62. Hedley AA, Ogden CL, Johnson CL et al. Prevalence of overweight and obesity among US children, adolescents, and adults, 1999–2002. JAMA 2004; 291: 2847–50. 63. Livingston EH, Ko CY. Socioeconomic characteristics of the population eligible for obesity surgery. Surgery 2004; 135: 288–96. 64. Gendall KA, Raniga S, Kennedy R, Frizelle FA. The impact of obesity on outcome after major colorectal surgery. Dis Colon Rectum 2007; 50(12): 2223–37. 65. Duchesne JC, Wang YZ, Weintraub SL et al. Stoma complications: a multivariate analysis. Am Surg 2002; 68: 961–6. 66. Evans JP, Brown MH, Wilkes GH, Cohen Z, McLeod RS. Revising the troublesome stoma: combined abdominal wall recontouring and revision of stomas. Dis Colon Rectum 2003; 46: 122–6. 67. Beck DE. Abdominal wall modification for the difficult ostomy. Clinics Colon Rectal Surg 2008: 16. 68. Castillo E, Thomassie LM, Whitlow CW et al. Continent ileostomy: Current experience. Dis Colon Rectum 2005; 48: 1263–8. 69. Steel MCA, Wu JE. Late stomal complications. Clinics Colon Rectal Surg 2002; 15: 199–207. 70. Pokorny H, Herkner H, Jakesz R et al. Mortality and complications after stoma closure. Arch Surg 2005; 140: 956–60.

34

Operative and nonoperative therapy for chronic constipation Harry T Papaconstantinou

Challenging Case A 33-year-old women presents with constipation of 8 years duration. She goes 7–10 days between bowel movements, despite taking multiple laxatives. She tried extra dietary fiber, polyethylene glycol, and lubiprostone, all without relief. Her lack of bowel activity is significantly impacting on her life style.

Table 34.1  Rome III diagnostic criteria for constipation. Criteria must be fulfilled for the last 3 months. Symptom onset at least 6 months before diagnosis . 1) Must include 2 or more of the following. a. Straining ≥25% of defecation. b. Lumpy or hard bowel movements ≥25% of defecation.

Case Management A barium enema demonstrates normal anatomy. A colonic transit study demonstrates 20 markers evenly distributed throughout the colon on day 5. A balloon expulsion test and anal manometry were normal. A diagnosis of colonic inertia is made and the patient is offered a total abdominal colectomy with an ileorectal anastomosis. INTRODUCTION Constipation is a common medical complaint resulting in over 2.5 million physician visits in the United States each year.(1) Reports have indicated that constipation is a significant problem with its prevalence ranging from 2 to 27%, and associated medication costs of over $500 million each year.(2) Stool weight, transit time, and frequency of defecation correlate strongly with dietary fiber intake. It is estimated that the average daily consumption of fiber in the United States is <20 grams, therefore, the prevalence of constipation should be no surprise.(3, 4) Furthermore, constipation adversely affects work-related productivity, educational performance, and results in significantly lower quality of life and higher psychological distress.(5, 6) Constipation is not a specific disease, but rather a constellation of symptoms. Physicians typically define constipation in objective terms of bowel movement frequency, specifically fewer than three bowel movements per week. However, constipation has different meaning to individual patients, and may be described as the need to strain to defecate, having hard stools, the inability to defecate at will, incomplete evacuation, or the infrequent passage of stool. Regardless of the ambiguity of defining constipation, patients frequently perceive the need for treatment due to advertising portraying “regularity” as the secret to health and well-being.(7, 8) Therefore, it is important for the physicians to clarify patient’s intended meaning, and to establish a more objective definition for this subjective symptom. Recently, a consensus of parameters has been created and updated to more clearly define constipation and is known as the Rome III criteria (Table 34.1).(9) The establishment of these parameters has provided more uniform definition of constipation, and is a valuable tool to identify patients that require treatment. Successful treatment of constipation requires the accurate identification of the underlying etiology of the symptom. In most patients, constipation is the direct result of specific medical conditions (Table 34.2) or side effect of medications (Table 34.3). These

c. Sensation of incomplete evacuation ≥25% of defecation. d. Sensation of anorectal obstruction ≥25% of defecation. e. Manual maneuvers to facilitate bowel movement ≥25% of defecation. f. Fewer than 3 defecations per week. 2. Loose stools are rarely present without the use of laxatives. 3. Insufficient criteria for irritable bowel syndrome

Table 34.2  Medical conditions causing constipation. Endocrine and Metabolic

Neurogenic

Collagen Vascular and Musculoskeletal

Chronic renal failure

Autonomic neuropathy

Amyloidosis

Diabetes mellitus

Cerebrovascular disease

Dermatomyositis

Hypothyroidism

Dementia

Myotonic dystrophy

Hypercalcemia

Depression

Systemic sclerosis

Hypokalemia

Multiple sclerosis

Scleroderma

Pregnancy

Muscular dystrophy

Milk-alkali syndrome

Parkinson’s disease

Porphyria

Spinal chord lesions

Carcinomatosis

Hirschsprung’s disease Chaga’s disease

extracolonic causes can be easily identified in a careful and complete history and physical examination. Constipation for these patients is treated through medical management including alteration of their medications, prescription of laxatives, or dietary and lifestyle modifications. A small group of patients will have a functional disorder of the colon and anorectum resulting in constipation. It is within this group of patients that colon and rectal surgeons can make the greatest impact, and is the focus of this chapter. Functional constipation can be divided into three groups: 1) slow-transit constipation, 2) pelvic floor dysfunction, and 3) combined slow-transit constipation and pelvic floor dysfunction. Slow-transit constipation, also known as colonic inertia, is characterized by prolonged length of time for stool to pass through the colon.(10) Delay in stool transit is thought to be a primary dysfunction of the colonic smooth muscle (myopathy) or innervation (neuropathy). Pelvic floor dysfunction results in evacuation disorders, and is characterized by either difficulty or inability to expel stool from the anorectum.(11) Common disorders of pelvic floor dysfunction include obstructive defecation, pelvic floor dyssynergia, outlet obstruction, or anismus.(11–13)



improved outcomes in colon and rectal surgery Table 34.3  Drugs associated with constipation. Anticholinergics

Antidepressants Antipsychotics Aluminum (antacids, sucralfate)

Cation-containing agents

Bismuth Calcium (antacids, supplements) Iron supplements Opiates Antihypertensives

Neurally active agents

Ganglionic blockers Vinca alkaloids Calcium channel blockers Antihistamines

Others

Antiparkinsonian drugs Diuretics Nonsteroidal anti-inflammatory drugs

Recent advances in the analysis of colonic motility and pelvic floor physiology have allowed for the identification and classification of these two subtypes. This is important as treatment modalities are different. Surgery is indicated for patients with slow-transit constipation, while nonoperative treatment modalities, such as biofeedback therapy, are effective in patients with pelvic floor dysfunction. Patients with mixed conditions require correction of the pelvic floor abnormality before undergoing an operation for slow-transit constipation. Patient selection is critical for treatment success. EVALUATION AND DIAGNOSTIC STUDIES Initial evaluation of patients with constipation is a complex task and starts with a careful history and physical examination. Most patients are reluctant to discuss these issues, and establishing a trustworthy relationship is important to define the nature of bowel dysfunction. Constipated patients present with a constellation of symptoms that include excessive straining to defecate, passage of hard stools, the inability to defecate at will, digital disimpaction, vaginal splinting, feeling of blockage at the anal opening, incomplete evacuation, and/or the infrequent passage of stool. Details of defecatory characteristics and habits are helpful and should include stool frequency, stool consistency, stool size, and degree of straining during defecation. These patients should be asked about precipitating events and the duration and severity of the problem. A dietary history should be obtained to assess of the amount of daily fiber ingested and fluids consumed, as stool transit time and frequency of defecation correlate strongly with dietary fiber intake. (3, 4) If the patient has already been treated by a referring physician it is important to know the number and types of laxatives used, patient compliance, and whether there was any improvement in symptoms. A long history of constipation refractory to dietary measures and laxative use is suggestive of functional constipation, while a history of recent onset should alert the physician to seek and exclude an organic cause such as neoplastic disease or stricture. A complete medical history will provide evidence of extracolonic causes of constipation such as diabetes, hypothyroidism, or cerebrovascular disease (Table 34.2). Detailed review of the patient’s medication list will identify specific medications that are known to cause constipation (Table 34.3).

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A complete physical exam with specific emphasis on the abdomen and perineum are important. A normal physical exam is not uncommon. A detailed anorectal exam starts with inspection of the perianal skin. Perineal sensation and the anocutaneous reflex are assessed by gently stroking the perineal skin with a cotton-tipped applicator stick. Absence of a reflex contraction of the external anal sphincter indicates the presence of neuropathy. A digital rectal examination is performed to identify the presence of an anorectal stricture, distal rectal mass, and the presence of stool or blood within the rectal vault. Positive findings require further aggressive evaluation including colonoscopy. During digital examination, sphincter tone is assessed at rest and voluntary squeeze. It is important to ask the patient to bear down as if to defecate. This maneuver allows the examiner to determine relaxation of the external anal sphincter and the presence of perineal descent. Absence of these features is suggestive of pelvic floor dysfunction or dyssynergic defecation.(11) Vaginal and bimanual examination should be performed to rule out rectocoele as a cause of outlet obstruction constipation. Routine evaluation of the colon is performed when there is a lack of identifiable causes of constipation. This can be performed by colonoscopy, barium enema, or CT colonography. Although it has been reported that there is no increased incidence of colon or rectal neoplasia in patients with chronic constipation (14), routine anatomic evaluation of the colon is performed to exclude tumors, strictures, and large bowel disease. Endoscopic evaluation of the colon may reveal evidence of chronic laxative abuse (melanosis coli), diverticular disease with stricture, malignancy, or colitis cystica profunda (internal rectal prolapse). Further work-up and treatment is dependent on the findings. However, in the absence of anatomic causes of constipation, patients should be initially treated with dietary and lifestyle modifications with or without medications. If initial treatment of constipation fails to improve the patient’s symptoms, further investigational studies are required to differentiate between functional constipation types. It may seem intuitive that patients with slow-transit constipation would complain of infrequent bowel movements, while patients with pelvic floor dysfunction would report feelings of incomplete evacuation and excessive straining. However, recent reports show that symptoms alone do not differentiate between the subgroups of functional constipation.(6, 15, 16) In fact, up to 62% of patients with pelvic floor dysfunction report stool frequency of less than three bowel movements per week.(6) For this reason symptom assessment should be combined with objective testing to better assess the nature of a patient’s complaint. Physiologic studies of the colon (colonic transit study) and pelvic floor (anorectal manometry, balloon expulsion test, defecogram, and electromyography) are required to differentiate between slow-transit constipation, pelvic floor dysfunction, and patients with mixed features, and accurate diagnosis is critical for treatment success. Colonic Transit Studies Self-reported stool frequencies correlate poorly with colonic transit, and patient’s recall of stool habits is often inaccurate indicating that subjective complaints are not sufficient to determine diagnosis. Colonic transit studies provide objective assessment of

operative and nonoperative therapy for chronic constipation (A)

(B)

Figure 34.1 Colonic transit study using single capsule radiopaque markers. Abdominal radiographs shown were taken 5 days after capsule ingestion. The presence of >6 marks scattered throughout the colon is diagnostic for slow colonic transit (A). Retention of markers within the rectum and rectosigmoid region suggests pelvic outlet obstruction (B).

stool movement through the colon, and are critical tests to identify patients that will benefit from colectomy. Two methods are commonly used to measure colonic transit time and include radiopaque marker methods and scintigraphic techniques. Studies have shown that that these two tests correlate well to each other and are sensitive for identifying colonic transit delays in patients with slow-transit constipation.(17, 18) Objective documentation of slow-transit constipation is critical for patient selection for surgery, and has been shown to significantly improve outcomes after colectomy (90% vs. 67%).(19, 20) Radiopaque Marker Test. The most common and widely used study of colonic transit time is the radiopaque marker method. This test was first described by Hinton et al. in 1969, and since that time several modifications have been described including single and multiple capsule techniques.(21–23) This study is performed by having the patient swallow a single capsule (Stizmarks; Konsyl® Pharmaceuticles, Ft. Worth, Texas) containing 24 radiopaque markers, and then tracking the markers by abdominal radiographs at 3 days and 5 days. Patients are instructed to stop laxatives, cathartics, and enemas for 2–7 days before ingestion of the capsule, and during the test period to prevent false results. In patients with normal colonic motility, by day 5 of the test 19 (80%) or more of the markers will have passed through the colon and are either completely evacuated or found in the rectum. Patients with slow colonic transit show the presence of 6 or more markers scattered throughout the colon (Figure 34.1A). Patients with pelvic floor dysfunction such as functional obstructive or dyssynergic defecation, exhibit retention of 6 or more markers in the rectum or rectosigmoid region with a near normal transit of markers through the colon (Figure 34.1B).

Although this test has been shown to be highly reproducible, when considering total abdominal colectomy for colonic inertia, it has been shown that patients have more favorable results if two marker studies have demonstrated slow-colonic transit times to confirm the diagnosis.(24) Scintigraphic technique. Scintigraphic defecography is another modality available to study colonic transit. Delayed-release capsules containing charcoal or polystyrene pellets radiolabeled with technetium-99m or indium-111 are coated with a pH-sensitive polymer methacrylate. The coating dissolves in an alkaline pH within the terminal ileum and cecum. Colonic distribution of the radioisotope is determined on scans taken 24 and 48 hours after capsule ingestion, and is highly sensitive and specific for identifying slow colon transit.(25, 26) Colon transit measurements by radiopaque markers and scintigraphic techniques correlate well with each other, and are sensitive for identifying colonic transit delays in patients with slow transit constipation.(18) When a diagnosis of slow-transit constipation is made, the physician must be aware of specific conditions that may be associated with this functional disorder and adversely affect surgical treatment with colectomy. First, slow-colonic transit constipation may be a component of a generalized gastrointestinal disorder such as panenteric intertia. A recent review has suggested that patients with this generalized gastrointestinal motility disorder have significantly diminished long-term success rate after colectomy for slow-transit constipation.(27) This is supported by the high rate of recurrent small-bowel obstruction (70%) in patients with panenteric intertia.(28) Collectively, these data suggest that whole gut transit studies should be considered before colectomy

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improved outcomes in colon and rectal surgery for slow-transit constipation, and include gastric emptying, upper gastrointestinal small bowel follow-trough, and cholycystokinnin hepatic dimethyliminodiacetic acid (CCK-HIDA) scan. Colectomy in patients with a global gastrointestinal motility disorder is not likely to improve their symptoms and is discouraged. Second, in patients with findings suggestive of pelvic floor dysfunction, up to two-thirds will exhibit mixed pattern constipation with both slow transit and obstructive delay.(29) Further pelvic floor physiology testing and treatment of the pelvic floor dysfunction is required before colectomy to improve outcomes and avoid treatment failure. Pelvic Floor Physiology Tests Patients with functional constipation due to pelvic floor dysfunction and obstructive defecation have difficulty with evacuation of rectal contents. Normal evacuation requires the involuntary relaxation of the internal anal sphincter as well as the voluntary relaxation of the external anal sphincter and pelvic floor muscles. Failure of this coordinated effort results in outlet obstructive symptoms. Pelvic floor physiology testing can identify specific disorders such as blunting of the rectal anal inhibitory reflex (RAIR), paradoxical puborectalis contraction, and anatomic abnormalities that cause outlet obstruction. Common tests used to identify these disorders include anorectal manometry, balloon expulsion test, defecography, and electromyography. Anorectal Manometry. Anorectal manometry provides a comprehensive assessment of anal sphincter muscle tone and the anorectal sensory response to different stimuli. This test is useful in the evaluation of patients with obstructive defecation, and helps to detect abnormalities during attempted defecation such as pelvic floor dyssynergia or anismus.(30) The complete manometric evaluation of the anorectum includes determination of the resting pressure, squeeze pressure, length of the high-pressure zone, rectal compliance, RAIR, and the ability of the internal anal sphincter to relax with straining. In normal defecation, as rectal pressure rises there is a synchronized fall in the internal anal sphincter pressure. A blunted rectal sensation is a common finding in patients with functional obstructive defecation.(31) Absence of the RAIR suggests secondary causes of constipation such as Hirschsprung’s disease, Chagas disease, or previous surgery.(32–34) External sphincter muscle relaxation for the elimination of stool is a learned response that is under voluntary control. Inability to perform this coordinated movement represents the chief pathophysiologic abnormality in patients with dyssynergic defecation and anismus, and may be due to impaired rectal contraction, paradoxical puborectalis contraction, or impaired anal relaxation.(11, 35) Anorectal manometry has been shown to be inaccurate in the diagnosis of paradoxical puborectalis and dyssynergic defecation, and further testing with balloon expulsion test and electromyography should be performed to assist in diagnosis.(36) Balloon Expulsion Test. The balloon expulsion test is a functional evaluation of the patient’s ability to defecate. In this test, a latex balloon is filled with 60 ml of warm water or air within the rectum. The patient is asked to expel the balloon in a private bathroom while sitting on the toilet. The physiologic position and privacy allow this method to more closely approximate

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normal evacuation. Normal subjects can expel the balloon within 1 minute.(37) While seeming trivial, it is important that patients do not flush the balloon as it can severely damage the plumbing. Inability to expel the balloon is suggestive of functional outlet obstruction such as paradoxical puborectalis contraction and dyssynergic defecation. The balloon expulsion test is a simple and accurate test that has been shown to have a high specificity (89%) and negative predictive value (97%) for excluding pelvic floor dyssynergia as a cause of constipation.(36, 38, 39) Defecography. Defecography is the real time imaging of patient defecation, and provides dynamic characterization of the interaction between the anal sphincter complex and the rectum in an attempt to define abnormalities in the pelvic floor. It provides information on the anatomic and functional changes of the anorectum during defecation, and is effective in differentiating between anatomic and functional causes of obstructive defecation. Before the test is performed, the patient is cleansed of stool using an enema. Barium paste is placed into the rectum, and with the aid of fluoroscopy the process of defecation is video-recorded. Static and real-time dynamic radiographic images are obtained during the process of defecation. Specific measurements such as the anorectal angle, perineal descent, and puborectalis length during stages of squeeze and push are calculated.(40) Patients with paradoxical puborectalis contraction and dyssynergic defecation will exhibit failure of the anorectal angle to open, persistence of the puborectalis impression on the rectum, and poor rectal emptying of the barium paste.(41–43) It has been shown that patients with a diagnosis of paradoxical puborectalis on defecography have a high frequency of constipation symptoms. (44) Defecography is reported to be too sensitive for paradoxical puborectalis contraction and dyssynergic defecation leading to a high false-positive diagnosis, but this test does have the advantage of evaluating any coexistent pelvic floor pathology.(45) Anatomic causes of obstructive defecation are readily identifiable during defecography and include internal intussusception of the rectum, rectocoele, enterocoele, and sigmoidocoele. The physiologic importance of these findings is often unclear, and the surgeon must determine their significance to individual patient symptoms and complaints to determine need for surgical repair. Electromyography. Surface electromyography (EMG) can be performed by anal plug, intraanal sponge, or concentric needle technique to diagnose patterns of anal sphincter and pelvic floor muscle dysfunction. Electrodes are used to record action potentials derived from motor units within contracting muscles. Recordings are taken at rest, squeeze, and push. In normal patients, the act of defecation and push is accompanied by a decrease in motor unit activity signifying relaxation of the anal sphincter complex (Figure 34.2A). Patients with dyssynergic defecation and paradoxical puborectalis contraction exhibit increased motor unit activity during push indicating an increase in anal sphincter complex contraction during defecation (Figure 34.2B). Studies have shown that the negative predictive value for this test is high (91%) indicating EMG can accurately rule out paradoxical puborectalis contraction; however, the positive predictive value is quite low when compared with defecography.(46–48) This suggests the need for comprehensive physiologic testing to accurately diagnose paradoxical puborectalis contraction.

operative and nonoperative therapy for chronic constipation (A)

(B)

Figure 34.2  Electromyographic tracings in a patient with normal defecation (A) and paradoxical puborectalis contraction (B). Black arrows indicate push phase that normally corresponds with muscle relaxation and lower amplitude waves. (R rest; S strain; P push).

MEDICAL TREATMENT OF CONSTIPATION Initial treatment of functional constipation regardless of type is patient education, dietary and lifestyle modifications, and a trial of medical management. Education of the patient is critical and should include explanation of normal physiologic bowel patterns.(49) It is important to communicate to the patient that their symptoms will not be corrected overnight, and modifications of the treatment regimen may be required. In many patients a dietary and medication log can be helpful to accurately identify fiber and water consumption, and medication compliance. A daily diary to record bowel movements, stool characteristics, and associated abdominal symptoms is useful when assessing responses to treatment. Patients should be encouraged to recognize and respond to the urge to defecate. Most patients who have a normal bowel pattern usually empty stools at approximately the same time every day suggesting this is in part a conditioned reflex.(50) Ritualizing bowel habits may be useful to establish a regular pattern of bowel movement and should be coordinated with physiologic events that stimulate colonic motility (walking and postprandial gastrocolic response).(11) General measures such as adequate hydration and regular exercise has overall health benefit; however, there is no evidence to support success in the treatment of chronic constipation, except in situations of dehydration.(51, 52) Indirect evidence exists, as epidemiologic studies suggest that sedentary people are three times more likely to report constipation.(53) A diet high in fiber content increases stool weight and accelerates colonic transit time.(54) In contrast, a diet that is deficient in fiber may lead to constipation.(54, 55) Consensus exists that empiric treatment for constipation with a high-fiber diet is inexpensive and effective therapeutic intervention for addressing constipationrelated bowel dysfunction.(56, 57) There is a clear dose response between daily fiber intake and fecal output that is enhanced by increased fluid intake. Dietary supplements such as bran may cause significant amounts of abdominal bloating and discomfort, which may decrease patient compliance. Gradual increase in dose may

minimize these symptoms. Psyllium seed, methylcellulose, and calcium polycarbophil are bulk-forming laxatives that absorb water into the colonic lumen and increases fecal mass, which in turn stimulates motility and reduces colon transit time.(58) A literature review of articles dealing with 18 double-blind studies related to constipation found that dietary fiber supplements or bulk laxatives resulted in an average increase of 1.4 (95% CI, 0.6–2.2) bowel movements per week, while laxative agents other than bulk showed an increase of 1.5 (95% CI, 1.1–1.8) bowel movements per week. (59) Others have shown that fiber has limited value in patients with slow-transit constipation and pelvic floor dysfunction as patients with these conditions did not respond effectively to dietary supplementation with 30 grams of fiber per day.(56) Conversely, patients without an underlying motility disorder either improved or became asymptomatic with fiber therapy. Collectively, these data suggest that therapeutic trial of dietary fiber should be considered as initial treatment for patients with constipation, although fiber supplements administered alone are probably more effective in normal transit or fiber deficiency constipation than slow transit constipation or pelvic floor dysfunction.(27) Failure of fiber therapy requires alternative choices of laxative medications. A list of common medications used to treat constipation is shown in Table 34.4. With so many potential options available, the choice of laxative therapy is subject to patient preference, and physician opinion and consensus.(60, 61) Although there are a variety of preparations available, the laxatives that are frequently recommended include milk of magnesia, lactulose, sorbitol, senna compounds, bisacodyl, and polyethylene glycol preparations. Milk of magnesia, magnesium citrate, and sodium phosphate are saline laxatives that are poorly absorbed or nonabsorbed osmotic preparations that result in secretion of water in the intestines to maintain isotonicity with plasma.(62) Use of these agents is not recommended in patients with cardiac and renal dysfunction because excessive absorption may lead to electrolyte abnormalities and volume overload. When ingested as hypertonic

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improved outcomes in colon and rectal surgery Table 34.4  Medications commonly used for constipation. Type

Fiber

Stool Softener

Generic Name

Trade Name

Dosage

Bran



1 cup/day

Psyllium

Metamucil

1 tsp up to tid

Methylcellulose

Citrucel

1–2 tsp up to tid

Calcium polycarbophil

Fibercon

2–4 tabs qd

Docusate Sodium

Colace

100 mg bid

Ineffective for constipation

15–30 mL qd or bid

Nonabsorbable disaccharides

–

Sorbitol Osmotic agents

Suppository

Stimulants

Saline laxatives Lubricant

Enemas

Mechanism of action Increase stool bulk Decrease colonic transit Increase gastrointestinal motility

Lactulose

Chronulac

15–30 mL qd or bid

Accelerate colonic transit

Polyethylene glycol

Miralax

17 g/d

Osmotic increase in intraluminal fluid

Up to daily

Rectal stimulation

Glycerine Bisacodyl

Dulcolax

10 mg daily

Bisacodyl

Dulcolax

10 mg po up to 3x/wk

Increase intraluminal fluid

Antraquinones

Senokot

2 tabs qd to 4 tabs bid

Stimulation myenteric plexus

Peri-colace

1–2 tabs qd

Increase motility Osmotic increase fluid small bowel Stimulate CCK Decrease colon transit time

Magnesium

Milk of Magnesia

15–30 mL qd or bidn

Haley’s M-O

15–30 mL qd or bid

Magnesium citrate

1 bottle

Mineral oil

15–45 mL

Stool lubricantn

Mineral oil retention

100–250 mL qd

Stool softened and lubricated

Tap water Phosphate

500 mL Fleet

Soapsuds Secretory agents Lubiprostone

1 unit

Evacuation induced by distended colon; mechanical lavage

1500 mL Amitiza

24 mg bid

Stimulation of Chloride channels

tid = three times a day; qd = daily; bid = twice a day.

solutions, there is a rapid osmotic equilibration that occurs, and overuse may result in significant dehydration.(62) Lactulose and sorbitol are nonabsorbable disaccharides that are effective osmotic laxative agents. Lactulose is a known substrate for colonic bacterial fermentation with resultant production of hydrogen, methane, carbon dioxide, water, acid and short-chain or volatile fatty acids.(63) These products act as osmotic agents and also stimulate intestinal motility and secretion. Lactulose has been shown to increase stool frequency in chronically constipated patients (64); however, abdominal bloating, discomfort, and flatulence are common side effects of this medication and may decrease patient compliance. Sorbitol is a poorly absorbed sugar alcohol that produces similar effects. In a trial of constipated men over the age of 65, sorbitol administered as a 70% syrup (10.5 g/15 mL; 15 to 60 mL daily) was equivalent to lactulose in improving symptoms.(65) Furthermore, it was cheaper and better tolerated during a 4-week trial. High-molecular-weight polyethylene glycol (PEG) is a large polymer with substantial osmotic activity that obligates intraluminal water.(66) It is routinely used with a balanced electrolyte solution for colon cleansing as polyethylene glycol electrolyte lavage solution (PEG-ELS). These solutions are safe and effective, and are routinely used for bowel preparations for colonoscopy and bowel surgery.

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(67) Other forms have been effectively used as laxatives for the treatment of constipation. PEG 3350 (MiraLax, Braintree Laboratories, Braintree, MA) is a large chemically inert polymer that also functions as an osmotic laxative. It does not contain salts that can be absorbed, and has been shown not to change measured electrolytes, calcium, glucose, blood urea nitrogen (BUN), creatinine, or serum osmolality.(68) A recent randomized controlled multicenter trial has shown effectiveness of 17g of PEG 3350 laxative over a dextrose placebo, with greatest efficacy during the second week of the therapy.(69) An 8-week, double blind, placebo-controlled study showed that PEG 3350 administered to patients with chronic constipation increased stool frequency and accelerated left colonic transit, without inducing abdominal cramps or bloating. In a long-term multicenter study of PEG 4000, 14.6 g twice a day improved stool frequency, reduced straining effort, softened stools, and decreased the need for oral laxatives and enemas when compared with placebo (70); however, there was a high dropout rate (30% PEG 4000 and 60% placebo) which raises concerns about efficacy and tolerance. Stimulant laxatives. The stimulant laxatives have effects on mucosal electrolyte transport and gut motility. Commonly used laxatives in this category include bisacodyl and senna. Abdominal discomfort and cramping are common side effects of these agents. Bisacodyl produces defecation within 6 to 8 hours of taking the

operative and nonoperative therapy for chronic constipation tablet, or 15 to 30 minutes after the suppository. It is believed to exert its effect by inducing high amplitude propagated contractions of the bowel, and is an effective rescue medication for chronic constipation.(27) Senna is member of the anthraquinone family of laxatives that are common constituents of herbal and over-the-counter laxatives. They are metabolized in the colon by bacteria into their active forms. In a trial of elderly nursing home residents (n = 77), a senna and fiber combination was reported to be better than lactulose in improving stool frequency, stool consistency, and ease of passage.(71) Furthermore, the senna and fiber combination was 40% cheaper than lactulose therapy. Side effects of these laxatives include allergic reactions, electrolyte imbalance, melanosis coli, and “cathartic colon”. Melanosis coli is a result of chronic ingestion of anthraquinone-containing laxatives. This condition is an abnormal pigmentation of the colonic mucosa that is caused by the accumulation of apoptotic epithelial cells that are phagocytosed by macrophages.(72) “Cathartic colon” is an alteration of colon anatomy that was believed to be associated with chronic stimulant laxative use. Barium enema findings included colonic dilation, loss of haustral folds, strictures, colonic redundancy, and wide gaping of the ileocecal valve.(73) Initially, it was attributed to the destruction of myenteric plexus neurons by laxatives (74); however, more recent studies do not confirm those findings.(75) Current evidence supports the safety of currently available laxatives at recommended doses for long-term use. Finally, anthraquinones have been proposed to have mutagenic effects and produce tumors in animal models. Several cohort studies and one case-control study failed to find an association between anthraquinones and colorectal adenomas or carcinoma.(76) Other drugs. Patients with severe slow-transit constipation may not respond to medical therapies described above. Ideally, slow-transit constipation should be treated with an agent that restores normal colonic function. Medications such as secretagogues (lobiprostone, cholchicine, and misoprostol) and prokinetic agents (tegaserod, alvimopan, linaclotide) are currently under clinical trials for the treatment of constipation, and show promise for patients with slow-transit constipation. Lubiprostone is an oral bicyclic fatty acid that activates the type 2 chloride channels that are located on the intestinal epithelial cell leading to an active secretion of chloride in the intestinal lumen.(77) In healthy humans, this drug has been shown to slow gastric emptying, but accelerated small bowel and colonic transit time at 24 hours.(78) In a randomized control study with intent to treat analysis, lubiprostone significantly increased the number of spontaneous bowel movements per week, improved straining effort, improved overall satisfaction with bowel habits, and produced softer stools when compared with placebo.(79) Colchicine is a microtubule formation inhibitor that is commonly used to treat gouty arthritis. A significant side effect of colchicine is diarrhea. In an open labeled study of 7 patients with normal transit constipation, colchicine (0.6 mg orally 3 times per day) increased stool frequency and accelerated colon transit time.(80) Furthermore, patients reported reduced symptoms of abdominal pain, nausea, and bloating. However, long-term use may be associated with neuromyopathy, and its use for chronic constipation is not supported. The prostaglandin E1

analog misoprostol (1200 µg/d) has been shown to increase stool frequency and accelerate colonic transit (81); however, the drug is expensive and its beneficial effects appear to decline over time. Tegaserod is a serotonin 5-HT4 receptor partial agonist that has been shown to increase gastic emptying and colonic transit time.(82) Large randomized controlled trials in the United States and Europe have reported that tegaserod increases the number of complete spontaneous bowel movements per week, relieves constipation-related symptoms, and improves overall bowel satisfaction.(79, 83) However, recent reports of 0.01% incidence of coronary and cerebrovascular events have suspended sales of tegaserod. Another drug, alvimopan, is a peripherally acting µ-opioid receptor antagonist. This drug does not cross the bloodbrain barrier, and therefore, does not inhibit the analgesic effect of opioids. A physiologic study of alvimopan has shown that this drug reverses opioid-induced delayed colonic transit in healthy subjects.(84) These data were verified in another randomized trial of opioid-induced bowel dysfunction, and has been shown to be effective in the treatment of acute postoperative ileus.(85, 86) Further studies are necessary to determine efficacy of alvimopan on chronic constipation. BIOFEEDBACK THERAPY In patients with constipation due to pelvic floor dyssynergia, biofeedback therapy is frequently recommended after failure of conservative management described above.(87) Biofeedback therapy uses electronically amplified recordings of pelvic floor muscle contractions (EMG) or anorectal pressure tracings to teach patients how to relax pelvic floor muscles and to strain more effectively when they defecate.(12) The purpose of this therapeutic modality is to restore a normal pattern of defecation by using an instrument-based education program. The primary goals are to correct the underlying dyssynergy that affects the abdominal, rectal, and anal sphincter muscles, and to improve the rectal sensory perception. A series of training sessions are used to teach diaphragmatic breathing techniques to improve abdominal pushing effort and to synchronize this with anal relaxation. Visual or auditory feedback is used to provide the patent input regarding performance during attempted defecation maneuvers. Studies on biofeedback therapy for the treatment of pelvic floor dyssynergia have been reviewed extensively.(88, 89) These reviews suggest that two-thirds of these patients benefit from biofeedback training, with individual studies reporting a 30 to 100% success rate; however, attempts to draw definitive conclusions about the usefulness and effectiveness of biofeedback for the treatment of pelvic floor dyssynergia-type constipation are difficult due to the lack of adequately controlled trials of sufficient sample size.(87) In a recent review of biofeedback therapy for pelvic floor dyssynergia, 4 of 27 (<15%) studies in the adult population were controlled, and only one well-controlled study had a sample size that was sufficient to provide meaningful statistical conclusions.(87) Biofeedback therapy for dyssynergic-type constipation is directed at coordinating pelvic floor muscle relaxation with intraabdominal pressure to generate an effective propulsive force. Instrumentation protocols in these patients require either EMG monitoring of muscle tone or anorectal pressures for biofeedback training. To

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improved outcomes in colon and rectal surgery determine which method is superior, a recent meta-analysis of the available literature was used to compare the treatment outcome using EMG vs. pressure biofeedback.(87) EMG biofeedback was primarily used in 18 studies (442 subjects) with a mean success rate (improved symptoms) of 70%. Pressure biofeedback training was used in 13 studies (275 subjects) with a mean success rate of 78%. These results showed a significantly better outcome in patients with pressure biofeedback protocols. Further analysis compared intraanal to perianal EMG biofeedback and their results showed no significant difference between the two subgroups (69% vs. 72%, respectively). Overall, these data show success rates ranging from 69 to 78%, regardless of which protocol or what instrumentation is used; however, without controlled trials, the optimal protocol for subjects with dyssynergic-type constipation remains unclear. The role of other factors on the outcome of biofeedback therapy in patients with pelvic dyssynergy has been studied. In one study, the only predictor of successful outcome was the number of sessions attended (5 or more) and whether the therapist discharged the patient (63% success rate) rather than the patient terminating treatment prematurely (25% success rate).(90) To date, researchers have not been able to identify any physiologic (manometry and balloon expulsion test), anatomic (rectocele, intussusception, or abnormal perineal descent), or demographic (age, gender, duration of symptoms) variables that influence treatment outcome; however, many investigators do suggest that psychopathology may influence biofeedback treatment outcome. Anxiety and psychological distress are commonly associated with pelvic floor dyssynergy. One study showed that patients with pelvic floor dyssynergic-type constipation or rectal pain showed a tendency to use somatization as a defense mechanism to manage psychological distress.(91) This pattern was not seen in a comparison group of patients with fecal incontinence. Others have suggested that there may be a psychosomatic basis for chronic idiopathic constipation, including pelvic floor dyssynergy.(92, 93) Studies have reported up to 65% of constipated subjects were diagnosed with various psychological disorders (94); however, there is significant debate whether the psychopathology is a cause or a consequence of dyssynergic constipation. In a study of patients with slow-transit constipation without pelvic dyssynergy 60% of subjects had a concurrent affective disorder, with 66% reporting having a previous affective disorder.(95) Others have shown a high incidence of sexual or physical abuse in patients suffering from constipation. Given these results, it is of no surprise that psychological treatment for subjects with constipation is frequently recommended in addition to biofeedback therapy. Establishment of an effective psychotherapeutic relationship may be critical for success. Biofeedback therapy has been used for the treatment of slowtransit constipation. A single case series reported the successful treatment of 4 patients with slow-transit constipation without pelvic floor dyssynergy using biofeedback therapy (96); however, two of the four patients continued to require laxative use despite improved symptoms, and there was no objective confirmatory evidence (repeat colonic transit study) to support physiologic improvement. A recent study has compared the benefits of biofeedback therapy in patients with slow-transit constipation to those with pelvic dyssynergia-type constipation.(97) At

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6 months, the dyssynergic group had greater satisfaction (71% vs. 8%), and more frequently reported ≥ 3 bowel movements per week (76% vs. 8%) than the slow-transit group following a 5 weekly biofeedback sessions. These data indicate that pelvic floor biofeedback benefits patients with pelvic floor dyssynergia, but not patients with slow transit constipation. Biofeedback therapy has been suggested as the initial therapy for patients with outlet obstruction associated with pelvic floor dyssynergy. This concept is supported by a recent randomized, controlled trial of patients with pelvic floor dyssynergy where biofeedback was shown to be more effective than laxative therapy with PEG.(98) Further well designed prospective randomized controlled trials are necessary to establish biofeedback therapy as the primary treatment for patients with this condition. Failure of biofeedback therapy poses a significant treatment problem as most patients do not improve with surgical intervention. Division of the puborectalis muscle in the posterior midline has been reported in patients with intractable pelvic dyssynergy. However, results are disappointing with very few patients obtaining any benefit from the procedure.(99) These data suggest that this procedure has no role in the treatment of patients with this condition. Botulinum toxin injection has been proposed as an alternative therapeutic modality for these patients with refractory pelvic floor dyssynergy. Injection of the toxin is directed into the puborectalis muscle and external anal sphincter. Symptom improvement was reported in up to 75% of patients with benefit lasting from 1 to 3 months. Fecal incontinence was reported in 25% of patients, and was transient lasting only 1 to 3 months after injection.(100–101) Others have reported similar beneficial effects of botulinum toxin injection for dyssynergic-type constipation.(102) However, because the effects of the toxin wear off within 3 months of administration, repeated injections are necessary to maintain symptomatic improvement. Furthermore, given the expense of this drug, this treatment modality should be reserved for those patients with severe symptomatic pelvic dyssynergia that has failed all other therapies. SURGERY OPTIONS Surgical intervention for functional constipation is limited to patients with documented severe slow-transit constipation that is refractory to medical management. Patient selection is critical for success. Minimal evaluation requires colon transit studies to document slow-transit constipation, and pelvic floor physiology testing to rule out pelvic floor dysfunction. Operative procedures performed for the treatment of slow-transit constipation include segmental colectomy, subtotal colectomy with ileosigmoid anastamosis, and total abdominal colectomy with ileorectal anastamosis. Each procedure has its champions; however, the overwhelming body of literature indicates superiority of total abdominal colectomy with ileorectal anastamosis. Total abdominal colectomy with ileorectal anastamosis is the treatment of choice for patients with slow-transit constipation. The anastamosis is usually performed in the proximal rectum at or near the sacral promontory. At this level, the anastamosis is easier to perform, eliminates the risks associated with rectal mobilization, and bowel diameter does not limit the size of the anastomotic lumen.(103)

operative and nonoperative therapy for chronic constipation Timing of surgery is best decided by the patient, as this surgery is an irreversible step in the treatment of constipation. Most patients are accepting of surgical intervention when all conservative measures have failed to result in an acceptable quality of life. In addition to standard operative risk for colectomy, patients should be counseled that abdominal pain and bloating may persist postoperatively even after normalization of bowel frequency. This is significant as a recent report showed that persistent abdominal pain had the strongest correlation with quality of life scores following colectomy in these patients.(104) Standard bowel preparations may not be sufficient as many patients with slow-transit constipation have one bowel-movement per week and are already taking PEG products to assist with bowel function. A clear liquid diet for 48 hours along with multiple enemas and laxatives may be necessary to adequately evacuate the colon and rectum of stool. Perioperative antibiotics are given according to current standards (intravenous) and physician preference (oral) as described in Chapter 2. Overall success of total abdominal colectomy with ileorectal anastamosis for slow-transit constipation is approximately 90%, and reported rates of symptomatic improvement ranges from 50% to 100%.(104, 105) This variability may be the direct result of how success after surgery is defined.(104) Many studies use patient satisfaction as criteria for success; however, patient derived subjective assessment is an inaccurate measurement of surgical outcome and likely varies between patients and studies. In a review of the literature evaluating subtotal colectomy for slow-transit constipation, Knowles et al. found that only half of the 31 studies that documented success or satisfaction reported the method of data acquisition.(19) Furthermore, in these studies success rate was based on patient judgment in 14, on function in 6, and on a combination of both in 5. Criteria used to assess success or satisfaction was not reported in 6 studies. Patient satisfaction and gastrointestinal functional outcomes (i.e. bowel-movement frequency) do not correlate with quality of life.(104, 106) A recent report showed a significant increase in bowel-movement frequency after subtotal colectomy; however, the persistence of abdominal pain and the development of postoperative incontinence or diarrhea adversely affected quality of life scores.(104) The authors concluded that bowel movement frequency alone does not provide an accurate assessment of patient’s outcome. This has led investigators to suggest the use of standardized outcome measures such as questionnaire-based protocols that assess quality of life.(106) These instruments should be used along with postoperative complications, functional outcome measures as well as gastrointestinal function to provide more uniform outcomes measurement of operative success in these patients. Acute and long-term complications are significant and include prolonged postoperative ileus, recurrent bowel obstruction, abdominal pain and bloating, diarrhea, incontinence, and recurrent constipation, and are addressed in detail below. These factors all affect quality of life scores with incontinence having the greatest negative impact.(104) In fact, postoperative quality of life assessment after total abdominal colectomy and ileorectal anastamosis showed significantly decreased scores compared to those of the general population (107); however, 93% of patients that met selection criteria for total abdominal colectomy with ileorectal anastamosis for slow-transit constipation would undergo colectomy again given the chance.(104)

Early reports found that if the whole intraabdominal colon was not removed, symptoms often recurred.(108) In fact, results of segmental colectomy have been disappointing with small series reporting up to 100% failure rate.(19) Reports of subtotal colectomy with ileosigmoid anastamosis resulted in an increased incidence of constipation and conversion to total colectomy was necessary in 50% of cases.(109) Other authors support this concept and cite increased incidence of constipation recurrence and persistence resulting in the need to reoperate to remove the remaining colon.(107, 110) Removal of the colon with preservation of the cecum and ileocecal valve has been described; however, long-term results were poor as maintenance of the cecal reservoir resulted in dilatation and recurrence of constipation symptoms.(111) Modifications of colonic transit studies using multiple ingestible markers and scintigraphic defecography have been used to determine segmental colonic inertia.(112) Although the validity of these techniques to determine segmental motility dysfunction has been questioned (113), these tests have been used in recent studies to identify and successfully treat patients with segmental colonic inertia.(105, 114) In one study, 28 patients were treated with segmental resection with a median follow-up of 50 months.(114) Early failure with persistent or recurrent constipation occurred in 3 (11%) patients and required further surgery. Patient satisfaction was reported in 23 (82%) patients; however, outcome was reported as excellent in 10 patients, good in 7, fair in 7, poor in 4. If successful outcomes were assigned to the excellent and good category, the success rate would fall to 61%. Again, variability in method to define success may play a factor in these results. Another study evaluated 15 patients with slow-transit constipation classifying them into total colonic slow-transit (8 patients) and left slow-transit (7 patients). (105) Total abdominal colectomy or left colectomy was performed according to this classification and resulted in improvement in symptoms (increased daily evacuations) in 8 (100%) and 6 (86%) patients, respectively. The authors report that patients with left colonic slow-transit all had prolonged latency times and were treated with percutaneous nerve evaluation. None received permanent implantation of the device, but it does raise the question as to whether colon transit studies were affected in these patients. The weighted finding of prolonged latency times in patients with left colonic slow-transit is interesting as sacral nerve stimulation has been successful for the treatment of slow-transit and dyssynergic-type constipation. (115) Although segmental colectomy seems promising for the treatment of segmental colonic inertia, controlled data are lacking and further studies are needed to verify and support its use. In a small subset of patients with slow-transit constipation ileostomy may be necessary due to poor operative risk or in elderly patients with impaired continence. COMMON COMPLICATIONS Morbidity of colectomy in patients with slow-transit constipation includes several factors. First, the direct risks of colon resection are related to the anastamosis (leak, stricture), infections (wound and intraabdominal abscess), bleeding, and anesthesia. Mortality related to colectomy in this group has been <1%.(103) Long-term complications resulting from colectomy in patients with slow-transit constipation are significant, and have been shown to negatively impact

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improved outcomes in colon and rectal surgery outcomes with decreased quality of life.(104) Common complications in this group of patients include recurrent bowel obstruction, abdominal pain, diarrhea, incontinence, and recurrent constipation, and warrant further discussion. Recurrence of constipation is addressed in detail in the section to follow. In patients undergoing total abdominal colectomy with ileorectal anastamosis, the most frequently occurring complication is small bowel obstruction. The reported incidence ranges from 8 to 38% with surgical intervention required in up to 75%.(104, 110, 116) The etiology of obstruction is commonly attributed to adhesions formed from the extensive colectomy; however, others have reported findings of small bowel pseudo-obstruction due to proposed neuropathic disorder of the myenteric plexus affecting overall bowel motility.(104, 117, 118) A retrospective review examined the incidence of postoperative complications following subtotal colectomy with ileorectal anastamosis in 48 patients with colonic inertia, 30 with Crohn’s disease, and 22 with either Familial Adenomatous Polyposis, or other neoplasia.(119) Small bowel obstruction occurred in 10 to 18% of each group, with no significant difference between groups. Others have reported intestinal obstruction rates of 35% following total abdominal colectomy for slow-transit constipation. In this study, 33% of patients had evidence of a delay in small bowel transit time suggesting this disorder is not limited to the colon, but also affects the small bowel. Recent reviews have speculated that routine use of antiadhesive agents such as Seprafilm® may reduce the incidence of adhesion induced small bowel obstruction.(103) Postoperative persistence of abdominal pain and alteration in bowel function are significant issues that adversely affect quality of live. A recent retrospective review on quality of life after subtotal colectomy for slow-transit constipation showed that abdominal pain was persistent in 41% of patients, diarrhea in 52%, and incontinence in 45%.(104) Collectively, these factors had the strongest correlation with quality of life survey, and the development of incontinence had the most negative impact on the score. As mentioned above, the high rate of persistent abdominal pain after surgery warrants detailed counseling of the patients regarding expectations and outcomes. Patients must be aware that normalization of bowel frequency may not relieve them of their pain. Diarrhea following total abdominal colectomy with ileorectal anastamosis is not uncommon with reported incidence ranging from 0 to 46%.(104) This is not surprising as the colon is effective at water absorption and is responsible for desiccating the stool. Over time intestinal adaptation occurs and normalizes consistency and frequency of the stool, with more than 90% of patients having either solid or semisolid stools by 6 months.(120) During the intestinal adaptation period, diarrhea is treated with fiber, motility agents (loperamide, diphenoxylate and atropine sulfate), and binders (cholestyramine) to reduce bowel frequency. The incidence of postoperative incontinence has been reported in 0% to 52% of patients with a mean of 14%.(104) Intractable diarrhea, especially in the setting of fecal incontinence, may require conversion to a permanent ileostomy. RECURRENCE It is clear that colectomy for refractory constipation has demonstrated successful outcomes for total abdominal colectomy with

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ileorectal anastamosis in 89 to 100% after appropriate preoperative workup, including colon transit study, defecography, and anorectal physiology tests.(19) Therefore, the greatest assurance to success in the operative treatment of constipation starts with appropriate patient selection. Recurrence or persistence of constipation following colectomy has been reported to occur in up to 33% of patients.(104) Patients with combined slow-transit constipation with pelvic floor dyssynergy are less likely to result in successful outcomes after surgery. Outcomes in patients undergoing surgery for slow-transit constipation with or without pelvic floor dyssynergy have been compared.(121) The presence of pelvic floor dysfunction significantly decreased success rates from 78% to 56%. It has been shown that slow-transit constipation with associated pelvic floor dyssynergia can be treated initially with biofeedback therapy followed by surgery with similar improvement in outcomes such as median stool number per day, spontaneous stools, laxative use, and quality of life.(107) Patients with slow-transit constipation are believed to have a global neuropathic disorder of the myenteric plexus that affects colonic motility.(117) It has been proposed that this neuropathic disorder may extend proximal into the small bowel, or even the entire gastrointestinal tract resulting in a global gastrointestinal motility disorder (panenteric inertia). Failure to identify these patients may be a reason for early recurrence of constipation or even the high incidence of postoperative bowel obstruction. Preoperative evaluation of whole gastrointestinal transit should be performed in all patients undergoing surgery for slow-transit constipation. Successful identification of these patients should raise question as to whether they will benefit from colectomy. If this entity is identified after surgery, conversion to an ileostomy may be required. Finally, recurrence of constipation may be a direct result of incomplete colonic resection. Segmental colectomy, ileosigmoid anastamosis, and preservation of the cecum and ileocecal valve with cecorectal anastamosis are all associated with a higher incidence of constipation recurrence or persistence. Surgical failure in these patients frequently requires reoperation for conversion to ileorectal anastamosis. In patients with recurrent constipation after colectomy, workup is directed at the issues addressed above. First, anatomic evaluation of the remaining rectum should be performed. Flexible signoidoscopy is adequate and can be performed in the office after two Fleets enemas. Special attention is made to the anastamosis as stricture formation will result in constipation. In the absence of organic disease, pelvic floor physiology testing is repeated to determine the presence of pelvic floor dyssynergia. Presence of this condition requires biofeedback therapy to improve symptoms and outcome. Upper gastrointestinal small bowel follow trough and other tests of whole gut transit will determine whether panenteric inertia is present. In these patients, persistent constipation and pseudo-obstruction are difficult to manage and may require end ileostomy. A careful review of the original operative report will provide evidence as to whether adequate colectomy was performed. Complimentary tests such as colon transit studies (radiopaque markers or scintigraphy) and gastrografin enema (avoid barium if constipation is significant) will help determine if there is residual dysmotile colon remaining. Persistent constipation with evidence of residual colon may require completion colectomy with ileorectal anastamosis.

operative and nonoperative therapy for chronic constipation SUMMARY Constipation is a common and complex polysymptomatic clinical disorder that has multiple etiologies. Successful treatment requires careful workup and patient selection. A careful history and physical exam are the first step. Many medical conditions and medications can cause constipation, and correction of these disorders can improve symptoms. Anatomic evaluation of the colon to rule out neoplasia, stricture, and other organic disease is required. When these secondary causes of constipation are excluded, a functional chronic constipation exists. Functional constipation consists of three overlapping subtypes including slow-transit constipation, dyssynergic defecation, and mixed disorders. Initial therapy for all patients includes dietary and lifestyle modification with and without laxatives. Persistent constipation that is refractory to medical management requires further testing. The tests obtained will vary depending on the patients history, surgeons experience, and testing availability. Colonic motility is determined by colon transit studies such as radiopaque markers or scitigraphic defecography. Pelvic floor function and physiology is determined by anal manometry, balloon expulsion test, defecography, and electromyography. Isolated slow-transit constipation is successfully treated with total abdominal colectomy with ileorectostomy. Lesser operations result in poor outcome with a high incidence of reoperation. Before surgery global gastrointestinal motility should be assessed as the presence of panenteric inertia can negatively impact outcomes. Pelvic floor dyssynergia is treated with biofeedback therapy to improve pelvic muscle coordination for defecation. Surgical therapy has poor results and should be discouraged. The combination of slow-transit constipation and pelvic floor dyssynergia are more complex. Optimal outcomes require successful treatment of pelvic floor dysfunction with biofeedback therapy before surgery. REFERENCES    1. Johanson JF, Sonnenberg A, Koch TR. Clinical epidemiology of chronic constipation. J Clin Gastroenterol 1989; 11: 525–36.    2. Higgins PD, Johanson JF. Epidemiology of constipation in North America: a systematic review. Am J Gastroenterol 2004; 99: 750–9.    3. Davies GJ, Crowder M, Reid B et al. Bowel function measurements of individuals with different eating patterns. Gut 1986; 27: 164–8.    4. Rendtorff RC, Kashgarian M. Stool patterns of healthy adult males. Dis Colon Rectum 1967; 10: 222–8.    5. Chang L, Toner BB, Fukudo S et al. Gender, age, society, culture, and the patient’s perspective in the functional gastrointestinal disorders. Gastroenterology. 2006; 130: 1435–46.    6. Rao SS, Tuteja AK, Vellema T et al. Dyssynergic defecation: demographics, symptoms, stool patterns, and quality of life. J Clin Gastroenterol 2004; 38: 680–5.    7. Pietrusko RG. Use and abuse of laxatives. Am J Hosp Pharm 1977; 34: 291–300.    8. Agnew J. Man’s purgative passion. Am J Psychother 1985; 39: 236–46.    9. Longstreth GF, Thompson WG, Chey WD et al. Functional bowel disorders. Gastroenterol 2006; 130: 1480–91

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  49. Siegel JD, Di Palma JA. Medical treatment of constipation. Clin Colon Rectal Surg 2005; 18: 76–80.   50. Heaton KW, Wood N, Cripps HA et al. The call to stool and its relationship to constipation: a community study. Eur J Gast Hepatol 1994; 6: 145–9.   51. Meshkinpour H, Selod S, Movahedi H et al. Effects of regular exercise in management of chronic idiopathic constipation. Dig Dis Sci 1998; 43: 2379–83.   52. Young RJ, Beerman LE, Vanderhoff JA. Increasing oral fluids in chronic constipation in children. Gastroenterology Nurs 1998; 21: 156–61.   53. Whitehead WE, Drinkwater D, Cheskin IJ et al. Constipation in the elderly living at home: definition, prevalence, and relationship to life style and health status. J Am Geriatr Soc 1989; 37: 423–9.   54. Burkitt DP, Walker AP, Painter NS. Effect of dietary fiber on stools and the transit-times, and its role in the causation of disease. Lancet 1972; 2: 1408–12.   55. Tucker DM, Sandstead HH, Logan GM. Dietary fiber and personality factors as determinants of stool output. Gastroenterology 1981; 81: 879–83.   56. Vanderholzer WA, Schatke W, Muhldorfer BE et al. Clinic response to dietary fiber treatment of chronic constipation. Am J Gastroenterol 1997; 92: 95–8.   57. Anti M, Pignataro G, Armuzzi A et al. Water supplementation enhances the effect of high-fiber diet on stool frequency and laxative consumption in adult patients with functional constipation. Hepatogastroenterology 1998; 45: 727–32.   58. Schiller LR. Review article: the therapy of constipation. Aliment Pharmacol Ther 2001; 15: 749–63.   59. Tramonte SM, Brand MB, Mulrow CD et al. The treatment of chronic constipation in adults. A systematic review. J Gen Intern Med 1997; 12: 15–24.   60. Madoff RD, Fleshman JW. AGA technical review on the diagnosis and care of patients with anal fissure. Gastroenterology 2003; 124: 235–45.   61. Locke GR III, Pemberton JH, Phillips SF. AGA position statement: guidelines on constipation 2000; 119: 1761–78.   62. Lembo A, Camilleri M. Current concepts:chronic constipation. N Engl J Med 2003; 349: 1360–7.   63. Di Palma JA. Current treatment options for chronic constipation. Rev Gastroenterol Disord 2004; 4: S34–S42.   64. Bass P, Dennis S. The laxative effects of lactulose in normal and constipated patients. J Clin Gastroenterol 1981; 3(suppl): 23–8.   65. Lederle F, Busch D, Mattox K et al. Cost-effective treatment of constipation in the elderly: a randomized double-blind comparison of sorbitol and lactulose. Am J Med. 1990; 89: 597–601.   66. Schiller LR. Osmotic effects of polyethylene glycol. Gastroenterology 1988; 94: 933–41.   67. Toledo TK, Di Palma JA. Review article: colon cleansing preparation for gastrointestinal procedures. Aliment Pharmacol Ther 2001; 15: 605–11.   68. Di Palma JA, Smith JR, Cleveland MB. Overnight efficacy of polyethylene glycol laxative. Am J Gastroenterol 2002; 97: 1776–9.

operative and nonoperative therapy for chronic constipation   69. Di Palma JA, DeRidder PH, Orlando RC, Koltz BE, Cleveland MB. A randomized, placebo-controlled multicenter study of the safety and efficacy of a new polyethylene glycol laxative. Am J Gastroenterol 2000; 95: 446–50.   70. Corazziari E, Badiali D, Bazzocchi G et al. Long term efficacy, safety, and tolerability of low daily doses of isosmotic polyethylene glycol electrolyte balanced solution (PMF100) in the treatment of functional constipation. Gut 2000; 46: 522–6.   71. Passmore AP, Davies KW, Flanagan PG et al. A comparison of Agiolax and lactulose in elderly patients with chronic constipation. Pharmacology 1993; 47(Suppl 1): 249–52.   72. Oster JR, Materson BJ, Rogers AI. Laxative abuse syndrome. Am J Gastroenterol 1980; 74: 451–8.   73. Urso FP, Urso MJ, Lee CH. The cathartic colon: pathological findings and radiologic/pathologic correlation. Radiology 1975; 116: 557–9.   74. Smith B. Pathologic changes in the colon produced by anthraquinone purgatives. Dis Colon Rectum 1973; 16: 455–8.   75. Kiernan JA, Heinicke EA. Sennosides do not kill myenteric neurons in the colon of the rat or mouse. Neuroscience 1989; 30: 837–42.   76. Nusko G, Schneider B, Schneider I et al. Anthranoid laxative use is not a risk factor for colorectal neoplasia: results of a prospective case controlled study. Gut 2000; 46: 651–5.   77. Capoletti J, Malinowska DH, Tewari KP et al. SPI-0211 activates T84 cell chloride transport and recombinant human CIC-2 chloride currents. Am J Physiol Cell Physiol 2004; 297: C1173–83.   78. Camilleri M, Bharucha AE, Ueno R et al. Effect of a selective chloride channel activator, lubiprostone, on gastrointestinal transit, gastric sensory, and motor functions in healthy volunteers. Am J Physiol Gastrointes Liver Physiol 2006; 290: G942–7.   79. Johanson JF, Wald A, Tougas G et al. Effect of tegaserod in chronic constipation: a randomized, double-blind, controlled trial. Clin Gastroenterol Hepatol 2004; 2: 796–805.   80. Verne GN, Eaker EY, Davis RH, Sninsky CA. Colchicine is an effective treatment for patients with chronic constipation: an open-label trial. Dig Dis Sci 1997; 42: 1959–63.   81. Soffer E, Metcalf A, Launspach J. Misoprostol is effective treatment for patients with slow transit constipation. Dig Dis Sci 1994; 39: 929–33.   82. Prather CM, Camilleri M, Zinsmeister AR et al. Tegaserod accelerates orocecal transit in patients with constipationpredominant irritable bowel syndrome. Gastroenterology 2000; 118: 463–8.   83. Kamm MA, Muller-Lissner S, Talley NJ et al. Tegaserod for the treatment of chronic constipation: a randomized, double-blind, placebo-controlled multinational study. Am J Gastroenterol 2005; 100: 362–72.   84. Gonenne J, Camilleri M Ferber I, Burton D et al. Effect of alvimopan and codeine on gastrointestinal transit: a randomized controlled study.Clin Gastroenterol Hepatol 2005; 3: 784–91.

  85. Paulson DM, Kenedy DT, Donvick RA et al. Alvimopan: an oral, peripherally acting µ-opioid receptor antagonist for the treatment of opioid-induced bowel dysfunction- a 21 day treatment-randomized clinical trail. J Pain 2005; 6: 184–92.   86. Camilleri M. Alvimopan, a selective peripherally acting µ-opioid antagonist. Neurogastroenterol Motil 2005; 17: 157–65.   87. Heymen S, Jones KR, Scarlett Y, Whitehead WE. Biofeedback treatment of constipation: a critical review. Dis Colon Rectum 2003; 46: 1208–17.   88. Enck P. Biofeedback training in disordered defecation: a critical review. Dig Dis Sci 1993; 38: 1953–60.   89. Rao SS, Enck P, Loening-Baucke V. Biofeedback therapy for defecation disorders. Dig Dis Sci 1997; 15(Suppl 1): 78–92.   90. Gilliland R, Heymen S, Altomare DF et al. Outcome and predictors of success of biofeedback for constipation. Br J Surg 1997; 84; 1123–6.   91. Heymen S, Wexner SD, Gulledge AD. MMPI assessment of patients with functional bowel disorders. Dis Colon Rectum 1993; 36: 593–6.   92. Devroede G, Girard G, Bouchoucha M et al. Idiopathic constipation by colonic dysfunction. Relationship with personality and anxiety. Dig Dis Sci 1989; 34: 1428–33.   93. Kumar D, Bartolo DC, Devroede G et al. Symposium on constipation. Int J Colorectal Dis 1992; 7: 47–67.   94. Nehra V, Bruce B, Rath-Harvey DM, Pemberton JH, Camilleri M. Psychological disorders in patients with evacuation disorders and constipation in a tertiary practice. Am J Gastroenterol 2000; 95: 1755–8.   95. Dykes S, Smilgin-Humphreys S, Bass C. Chrinic idiopathic constipation: a psychological enquiry. Eur J Gastroenterol Hepatol 2001; 1: 29–44.   96. Brown SR, Donati D, Seow-Choen F, Ho YH. Biofeedback avoids surgery in patients with slow-transit constipation: report of four cases. Dis Colon Rectum 2001; 44: 737–9.   97. Chiarioni G, Salandini L, Whitehead WE. Biofeedback benefits only patients with outlet dysfunction, not patients with isolated slow transit constipation. Gastroenterology 2005; 129: 86–97.   98. Chiarioni G, Whitehead WE, Pezza V, Morelli A, Bassotti G. Biofeedback is superior to laxatives for normal transit constipation due to pelvic floor dyssynergia. Gastroenterology 2006; 130: 657–64.   99. Barnes PRH, Hawley PR, Preston DM, Lennard-Jones JE. Experience with posterior division of the puborectalis muscle in the management of chronic constipation. Br J Surg 1985; 72: 475–7. 100. Joo JS, Agachan F, Wolff B, Nogueras JJ, Wexner SD. Initial North American experience with botulinum toxin type A for the treatment of anismus. Dis Colon Rectum 1996; 39: 520–4. 101. Hallan RI, Williams NS, Melling J et al. Treatment of anismus in intractable constipation with botulinum. Lancet 1988; 2: 714–7. 102. Maria G, Brisinda G, Bentivoglio AR, Cassetta E, Albanese A. Botulinum toxin in the treatment of outlet obstruction constipation caused by puborectalis syndrome. Dis Colon Rectum 2000; 43: 376–80.

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improved outcomes in colon and rectal surgery 103. Beck DE. Surgical management of constipation. Clin Colon Rectal Surg 2005; 18: 81–4. 104. FitzHarris GP, Garcia-Aguilar J, Parker SC et al. Quality of life after subtotal colectomy for slow-transit constipation: both quality and quantity count. Dis Colon Rectum 2003; 46: 433–40. 105. Ripetti V, Caputo D, Greco S, Alloni R Copolla R. Is total colectomy the right choice in intractable slow-transit constipation? Surgery 2006; 140: 435–40. 106. Lim JF, Ho YH. Total colectomy with ileorectal anastamosis leads to appreciable loss in quality of life irrespective of primary diagnosis. Tech Coloproctol 2001; 5: 79–83. 107. Nyam DC, Pemberton JH, Ilstrup DM, Rath DM. Longterm results of surgery for chronic constipation. Dis Colon Rectum 1997; 40: 273–9. 108. Lane WA. The results of the operative treatment of chronic constipation. Br Med J 1908; 1: 126–30. 109. Kamm MA. Role of surgical treatment in patients with severe constipation. Ann Med 1990; 22: 435–42. 110. Vasilevsky C, Nemer FD, Balcos EG, Christenson CE, Goldberg SM. Is subtotal colectomy a valuable option in the management of chronic constipation? Dis Colon Rectum 1988; 31: 679–81. 111. Fasth S, Hedlund H, Svaninger T, Oresland T, Hulten L. Functional results after subtotal colectomy and cecorectal anastamosis. Acta Chir Scand 1983; 149: 623–7. 112. Arhan P, Devroede G, Jehannin B et al. Segmental colonic transit time. Dis Colon Rectum 1981; 24: 625–9.

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113. Ehrenpreis ED, Jorge JMN, Schiano TD et al. Why colonic marker studies don’t measure transit time. Gastroenterology 1997; 110A: 728. 114. Lundin E, Karlbom U, Pahlman L, Graf W. Outcome of segmental colonic resection for slow-transit constipation. Br J Surg 2002; 89: 1270–4. 115. Kenefick NJ, Nicholls RJ, Cohen RG, Kamm MA. Permanent sacral nerve stimulation for treatment of idiopathic constipation. Br J Surg 2002; 89: 882–8. 116. Ternent CA, Bastawrous AL, Morin NA et al. Practice parameters for the evaluation and management of constipation. Dis Colon Rectum 2007; 50: 2013–22. 117. Krishnamurthy S, Shuffler MD, Rohrmann CA, Pope CE II. Severe idiopathic constipation is associated with a distinctive abnormality of the colonic myenteric plexus. Gastroenterology 1985; 88: 26–34. 118. Mollen RM, Kuijpers HC, Claassen AT. Colectomy for slowtransit constipation: preoperative evaluation is important but not a guarantee for a successful outcome. Dis Colon Rectum 2001; 44: 577–80. 119. Nakamura T, Pikarsky AJ, Potenti FM et al. Are complications of subtotal colectomy with ileorectal anastamosis related to the original disease? Am Surg 2001; 67: 417–20. 120. Pikarsky AJ, Singh JJ, Weiss EGm Nogueras JJ, Wexner SD. Long-term followup of patients undergoing colectomy for colonic inertia. Dis Colon Rectum 2001; 44: 179–83. 121. Redmond JM, Smith GW, Barofsky I et al. Physiological tests to predict long-term outcome of total abdominal colectomy for intractable constipation. Am J Gastroenterol 1995; 90: 748–53.

35

Colorectal trauma S David Cho, Sharon L Wright, and Martin A Schreiber

challenging case A 23-year-old man sustained a through and through gun shot wound to the left lower abdomen. The patient was mildly hypotensive on arrival to the emergency room, but responded to administration of 2 L of normal saline. The abdominal exam reveals the bullet holes and moderate tenderness. The rectal exam was normal. Chest and abdominal radiographs were normal except for markers at the gunshot wounds, electrolytes and hemoglobin levels were normal. After administration of a second generation cephalosporin and a type and cross for blood, the patient was taken to the operating room for an abdominal exploration. The only injury found was a lateral injury to the mid sigmoid colon. There was minimal stool contamination of the lower abdomen. case management The colonic wound edges were debrided and the colon was repaired primarily with a two layer suture closure. The abdomen was copiously irrigated. The laparotomy wound was closed and the patient received one dose of antibiotics postoperatively. introduction The management of traumatic colon injury has been the subject of much debate and has evolved considerably over the past century. During World War I, primary repair was practiced for all colon injuries, with a resultant mortality in excess of 60%. (1, 2) Civilian series reported similar results, with LoCicero and colleagues reporting a 67% mortality rate from 1927–1942.(3) The mortality rate dropped to approximately 30% during World War II (2) at a time when several changes in management were introduced. Most notably, Ogilvie (4) described exteriorization of colon injuries, leading to the practice of mandatory colostomy, which reduced mortality to about 45%.(4) Mortality dropped further during the Korean and Vietnam conflicts, to about 10% (1), which many attributed to the standardization of colostomy. The thinking at that time was that diversion of the fecal stream and avoiding an anastomosis would greatly reduce infectious complications.(5) The specter of infection was particularly ominous during a time when antibiotics had just been introduced. Many combat surgeons did not have significant training in managing colon injuries, high-velocity wounds, or operating under conditions of resource constraint and combat triage, during which follow-up of an anastomosis would be difficult.(4, 6) These concepts became incorporated into civilian settings as well and became the standard for at least 30 years. Other innovations during this period included the introduction of antibiotics, and improvements in transport, surgical devices, critical care, and resuscitation (2, 5, 7, 8) that may well have been responsible for the improvements in survival. Despite these factors, colostomy remained the standard of care for the first three-quarters of the twentieth century.

This practice was first successfully challenged by the landmark work of Stone and Fabian (9) in 1979, when they published the results of their randomized trial of primary repair without diversion versus colostomy in 268 patients with colon injuries. They noted a similar wound infection rate, and a significantly lower peritoneal infection rate with primary repair (15% vs. 29%). Their overall complication rate was 1% for primary repair and 10% for colostomy. Further, they noted an increase in hospital length of stay of approximately 6 days in the colostomy group. Although the study excluded more severely injured patients, it was the first to provide evidence that colostomy was not mandatory in all cases. Based on this work, a growing body of evidence contributed to a shift toward primary repair of traumatic colon injury during the 1980s and 1990s. Currently, primary repair, defined as a single-staged operation establishing bowel continuity (either by direct suture repair or resection and anastomosis) without proximal diversion, is being increasingly used for most colon injuries in civilian settings.(10, 11) The military conflict in Iraq and Afghanistan has both reinvigorated the debate between primary repair and diversion, and has brought new perspectives to this issue. Clearly, optimal treatment depends not on the uniform application of one technique or the other, but depends on sound judgment and an understanding of the current evidence. epidemiology Colon injury occurs in 30% of abdominal gunshot wounds and 5% of stab wounds, and is the second most common intraabdominal organ injury in civilian penetrating trauma. (12) Penetrating mechanisms cause 85–95% of colon injuries in civilian practice.(6, 13–16) In contrast, in a recent review of colon injuries sustained by American soldiers in Operation Iraqi Freedom over a 2-year period, 71% of injuries were caused by improvised explosive devices (IED) and 24% were caused by gunshot wounds. Blunt injury is rare, with colon involvement in 0.2% of trauma admissions but 20–30% of blunt hollow viscus injuries.(17) Motor vehicle crashes and traffic accidents account for the majority of blunt colorectal injuries.(18, 19) Approximately 80–90% of colon injuries in civilian settings are nondestructive.(20) While mortality has dropped in recent decades to <3% (21, 22), morbidity has remained high. Colon related complications have been consistently reported in 15–30% of cases since 1979. (9, 14, 23–27) preoperative assessment The initial assessment of any trauma patient always begins with the ABCs (airway, breathing, and circulation) and adherence to Advanced Trauma Life Support (ATLS) principles including the primary and secondary surveys, rapid treatment of immediately

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improved outcomes in colon and rectal surgery

Figure 35.1a  Seat-belt sign. The patient was involved in a roll-over motor vehicle crash.

life-threatening injuries, establishment of appropriate intravenous access, and administration of fluids or blood products when appropriate. In cases of severe injury accompanied by marked physiologic derangement, most notably the ‘lethal triad’ (acidosis, hypothermia, and coagulopathy) (28) of trauma, the principles of damage control surgery are applicable. These include rapid triage, abbreviated laparotomy, and return to the intensive care unit (ICU) for rewarming and correction of acidosis and coagulopathy. Intraoperatively the abdomen is packed, massive hemorrhage is controlled, and injured bowel is stapled off and left in discontinuity if necessary. In 12 to 24 hours the patient is brought back to the operating room at least once for reexploration and definitive repair.(29) Diagnosis The diagnosis of bowel injury is notoriously difficult. Colon injuries are primarily diagnosed intraoperatively.(30) However, diagnostic techniques warrant a brief discussion. physical exam Peritoneal signs in the abdominal trauma victim are most often caused by hollow viscus injury. However, physical exam may be difficult to perform in the multisystem trauma patient. Intoxication, traumatic head injury, or distracting injuries may obviate a reliable physical exam. The “seat belt sign” has been described as a physical exam finding that predicts bowel injury. The classic finding is ecchymosis of the anterior abdominal wall secondary to the compressive force of the lap belt (Figure 35.1a). It is associated with a more than doubled (2.9%) relative risk of bowel injury.(31) Flexion distraction injuries of the thoracolumbar spine, termed “Chance fractures”, also should raise suspicion for blunt bowel injury.(32) Diagnostic peritoneal lavage Diagnostic peritoneal lavage (DPL) is a rapid and inexpensive test to evaluate the intraperitoneal contents and it remains a



diagnostic option in patients with suspected abdominal injury. Via an open or closed technique, the abdominal cavity is lavaged with 1 L of isotonic solution, then aspirated and tested for evidence of intraabdominal injury. In blunt trauma, DPL is considered positive if 10 mL of blood is aspirated before instillation of lavage fluid. Microscopic criteria for a positive DPL in blunt trauma include more than 100,000 red blood cells (RBCs)/mm3 or 500 white blood cells/ mm3. The criteria for a positive DPL in penetrating trauma are much less standardized and vary from more than 1,000 RBCs/mm3 to gross aspiration of >10 cc of blood. In both blunt and penetrating trauma, presence of bile, amylase, bacteria, or particulate matter should indicate visceral injury and need for laparotomy. The accuracy of DPL is 92% to 98%, as reported by the Eastern Association for the Surgery of Trauma guidelines.(33) Otomo et al. (34) posited new criteria specifically designed to diagnose intestinal injuries using DPL. Due to the fact that hemoperitoneum is not necessarily an indication for operation, they considered the DPL positive when there was a relative increase in the WBC count compared to the RBC indicating peritoneal irritation. They prospectively evaluated 250 patients with blunt abdominal trauma. In addition to other criteria, when the RBC count in the lavage fluid was greater than 10 × 104/mm3), then the DPL was considered positive when the WBC count exceeded the RBC count/150. They report that these criteria have a diagnostic sensitivity of 96.6% and specificity of 99.4% for intestinal injury. Advantages of DPL include rapidity, higher sensitivity, lower cost, and immediate performance and interpretation. Unlike computed tomography, performance of DPL does not require transfer to a noncritical area. The major disadvantages are a 1% to 3% risk of iatrogenic intraperitoneal injury and the high sensitivity of the test, which may lead  to nontherapeutic laparotomies.(33) The utility of DPL has significantly decreased in the era of nonoperative management of solid organ injuries and it is primarily used in unstable trauma patients with an unknown source of hemorrhage. However, DPL may diagnose hollow viscus injuries that are missed by other modalities. There are relative contraindications to the performance of a DPL which include pregnancy, obesity, and prior celiotomy. Lastly, DPL is primarily of value if the abdominal injury is intraperitoneal. If the injury is confined to the extraperitoneal colon and rectum, DPL may not identify these injuries. Ultrasound Focused abdominal sonography for trauma (FAST) is now a commonly used modality in the initial diagnostic management of abdominal trauma. FAST has been used as a screening modality for patients with blunt trauma to determine which stable patients should undergo further diagnostic imaging with CT scanning. It has also been used in hemodynamically unstable patients to rapidly determine presence of intraperitoneal fluid and the need for immediate surgery analogous to the use of gross blood on DPL. In FAST, the ultrasound probe is used to serially evaluate the pericardium, Morison’s pouch (hepatorenal space), splenorenal recess, and the pouch of Douglas (retrovesical portion of the intraperitoneal cavity) for free fluid. A small amount of physiologic fluid is occasionally seen in the pelvis, but anything more

colorectal trauma

Figure 35.1b  CT scan of a patient with colon injury who demonstrated a “seatbelt” sign. Note the presence of free fluid (arrow) consistent with blood in the abdominal cavity. Of note, this patient did not have a solid organ injury raising suspicion of a hollow viscus injury.

should be considered abnormal and should prompt either operative exploration or further investigation. FAST has a sensitivity of 42% to 63%, a specificity of 98% to 100%, a positive predictive value of 67% to 100%, negative predictive value of 93% to 98%, and an accuracy of 92% to 98%. (33–40) Its advantages include rapidity, easy repeatability, its noninvasive nature, the absence of radiation exposure, and low cost. Disadvantages to FAST are interobserver variability and the fact that hollow viscus injuries may not be associated with an adequate volume of free intraabdominal fluid to be diagnosed by FAST. Computed tomography Computed tomography (CT) scanning of the abdomen and pelvis is the procedure of choice for the evaluation of the hemodynamically stable blunt trauma patient.(33) It is recommended in patients with equivocal physical exam findings, multiple injuries, and neurologic injury. Abdominal CT has a sensitivity of 64% to 88%, specificity of 97% to 99%, and an accuracy of 82% to 99% for the diagnosis of hollow viscus injury.(41, 42) Disadvantages include high cost, radiation exposure, and the need to transport patients to the radiology suite. Signs of bowel trauma seen on CT include mesenteric stranding, free intraperitoneal fluid in the absence of solid organ injury, extraluminal air or contrast material, and bowel wall thickening. (43) Figure 35.1b demonstrates these findings. Improvements in CT technology have led to increasing sensitivity of CT in the detection of the more subtle signs of injury to the bowel. Laparoscopy Laparoscopy has been evaluated in the diagnosis of intraabdominal injury in a selected group of trauma patients as a method to evaluate penetrating injuries. Potential advantages include avoiding nontherapeutic laparotomy and diagnosing and treating blunt bowel injuries that are otherwise missed by imaging techniques. In patients with penetrating abdominal trauma, stable vital signs,

intact sensorium without evidence of raised intracranial pressure, and absence of contraindications for pneumoperitoneum, Ahmed et al. found that exploratory laparoscopy is safe and accurate in the diagnosis of penetrating abdominal injuries, and identified those injuries that necessitated open repair.(44) In their study, they report avoiding nontherapeutic exploratory laparotomy in 75% of their patients. The authors describe laparoscopy as having the advantage of identifying injuries to the peritoneum, diaphragm, mesentery and omentum. Mitsuhide et al. (45), prospectively evaluated the use of diagnostic laparoscopy in conjunction with CT scan in patients with blunt abdominal injury. Diagnostic laparoscopy was performed in hemodynamically stable patients who had either local peritoneal signs and indirect CT signs (bowel thickening or isolated intraperitoneal fluid), an increase in abdominal pain or tenderness, or intraperitoneal fluid increased on serial CT scan. A total of 25 laparotomies were performed in 399 patients, 14 based on physical exam or CT findings and another 11 after laparoscopy. In total, 17 laparoscopic examinations were completed and 10 injuries were repaired. Thus, in these 399 patients, laparoscopy detected 1 mesenteric laceration and 7 bowel injuries that were not diagnosed on CT scan. There were no nontherapeutic laparotomies, and 7 laparotomies were avoided. They concluded that laparoscopy can prevent nontherapeutic laparotomy and delayed diagnosis in patients with suspected blunt bowel injury. Risks of laparoscopy in trauma patients include tension pneumothorax upon CO2 insufflation, which can be decreased by limiting initial insufflation pressures to 8 mmHg.(45) Other risks include hypotension following insufflation secondary to intravascular volume depletion, and gas embolism in patients with intraabdominal solid viscus injury. Injury scales In the effort to standardize assessment of traumatic injuries and potentially predict outcomes, a number of scoring systems have been published. While these scales do not attempt to replace sound judgment, experience and individualization of treatment, they are useful as a common means of assessment and communication amongst surgeons caring for patients with these injuries. The three most commonly used in association with colonic injury are briefly discussed here. Flint and colleagues (16) described three grades of colonic injury (Table 35.1), derived from a series of 137 patients. Interestingly, this report appears to have been at least in part generated by the discussion begun by Stone and Fabian (9) just 2 years earlier. The aim of their study was to determine if selection of candidates for primary repair could be based on the severity of colon injury. They noted an increase in mortality from 4% to 25% between injury grades 1 and 3, and no complications for grade 1 versus a 31% complication rate for grade 3 injury. Although no statistics were reported, the authors concluded that primary repair was safe for injury grade 1, while colostomy was the procedure of choice for grades 2 and 3. Moore and co-workers proposed a Penetrating Abdominal Trauma Index (PATI) in 1981.(46) These authors cited a need for an injury severity index that specifically addressed intraabdominal injury, one that focused on morbidity rather than mortality,

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improved outcomes in colon and rectal surgery Table 35.1  Flint grades of colonic injury.

Table 35.2  AAST grades of colon and rectal injury.

Grade Mortality

a

Complications

a

1  Isolated colon injury, minimal contamination,   4%   0%    no shock, minimal delay 2  Through-and-through perforation, lacerations, 20% 20%    moderate contamination 3  Severe tissue loss, devascularization, heavy 25% 31%    contamination a. n = 137.

and that was reliable in the acute postinjury setting as opposed to other etiologies for critical illness (i.e. sepsis or major operation). Three hundred sixty patients undergoing laparotomy for penetrating trauma were the basis of this study. Each intraabdominal organ was assigned a weight in terms of potential for developing complications, and a sub-grading from 1–5 based on severity of the injury. A PATI cutoff of 25 separated a substantial increase in complication rates (17% vs. 50% for stab wounds, and 12% vs. 44% for gunshot wounds). Notably, this scale provided a basis for the development of the Organ Injury Scale of the American Association for the Surgery of Trauma (AAST). In 1987, Dr. Donald Trunkey, the president of the AAST at that time, appointed the Organ Injury Scaling Committee to derive an injury scaling system that unified several previously proposed scoring systems for the purposes of conducting higher-quality research, and to provide a common parlance amongst centers and authors (Trunkey, DD, personal communication). This committee cites the results of 2 prior studies of penetrating colon injuries (47, 48), in which scoring systems proved useful to guide management, as support for creating this scoring system for all abdominal organs. Their work utilized some of the structure of the PATI proposed by Moore, as previously discussed. The AAST Colon Injury Scale is shown in Table 35.2.(49) management of penetrating colon injury The argument for primary repair The management of penetrating colon injury has undergone significant changes during the past 50 years. Today, primary repair is considered the treatment of choice for most colon injuries. Stone and Fabian’s seminal paper set the stage for this strategy. Earlier authors recognized that a strategy mandated during wartime, under combat conditions, and practiced by surgeons with varying levels of experience may not be applicable to modern civilian conditions. As an example, Pontius, Creech, and DeBakey (50) reported their experience with 122 civilian colon injuries in 1957. They reviewed military series between WWII and the Korean conflict, noting a drop in mortality from 53% to 15%, and civilian series during the same era, noting a drop in mortality from 62% to 14%. These authors primarily repaired 83 colon injuries with 8% mortality and diverted 36 colon injuries with 25% mortality. They acknowledge that primary repair was only attempted in patients without extensive fecal contamination, complete destruction of a segment of bowel or rectal injuries. In addition, they note that, of all survivors in both groups, there was a 20% complication rate, including only 3 intraabdominal abscesses. This complication rate is similar to rates seen half a century later.



Gradea Description ICD-9b Organ injury scale: Colon I Hematoma Contusion/hematoma without    devascularization Laceration Partial thickness, no perforation II Laceration Laceration <50% circumference III Laceration Laceration ≥50% circumference IV Laceration Transection of the colon V Laceration Transection with segmental    tissue loss Vascular Devascularized segment

863.40 – .44 863.40 – .44 863.50 – .54 863.50 – .54 863.50 – .54 863.50 –.54 863.50 – .54

Organ injury scale: Rectum I Hematoma Contusion/hematoma without    devascularization Laceration Partial thickness, no perforation II Laceration Laceration <50% circumference III Laceration Laceration ≥50% circumference IV Laceration Full thickness laceration extending    into perineum V Vascular Devascularized segment

863.45 863.45 863.55 863.55 863.55 863.55

a. Advance one grade for multiple injuries to the same organ. b. .41 & .51 = Ascending; .42 & .52 = Transverse; .43 & .53 = Descending; .44 & .54 = Rectum.

The modern era of data supporting primary repair for penetrating colon injuries includes several randomized controlled trials (RCT). The next RCT examining this issue after the work of Stone and Fabian was not published until 1991 by Chappuis and colleagues.(14) Although there are several methodological limitations, this study was important in that it excluded only patients with rectal injuries and attempted to answer the question that Stone and Fabian did not address, which is whether primary repair was equivalent in more severely injured patients with a greater degree of colon injury. Stone and Fabian (9) excluded almost half of the patients with colon injuries due to preoperative shock, multiple organs injured, gross contamination, greater than 8 hours from injury to repair, blood loss >1 L, and destructive injury. Chappuis and colleagues randomized 56 patients into either a primary repair or a diversion group, with 28 patients in each group. There were similar grades of colon injury (primarily grade III), PATI (26 and 23.9), transfusion rates (43% and 39%), complication rates (32% and 35%), and numbers of intraabdominal abscess (3 and 4) in the primary repair and diversion groups respectively. However, the sample size was small, and the authors reported no statistics. Although the PATI was indicative of severe intraabdominal injury, only four patients were admitted in hemorrhagic shock (defined as a systolic blood pressure less than 80 mm Hg). Additionally, only 13 total patients (5 in the primary repair group and 8 in the diversion group) required more than 4 units of packed red blood cells (PRBC). Thus, although this series represented an unselected population, the sample size was insufficient to conclude that primary repair is equivalent to diversion in severely injured patients. Since these two reports, there have been four other RCT that support primary repair in most situations.(23, 25, 26, 51) Although Gonzalez and colleagues published the results of their first 109 patients in 1996 (24), the authors state that this study was continued in order to assess complication rates associated

colorectal trauma Table 35.3  Randomized trials investigating primary repair versus diversion in colon injury. Author(s) Year

Complication Mortality

n PR Div PR Div Exclusion Criteria d

Comment

Stone (9) 1979 139   1%a 10%a 1.5% 1.4% Preoperative BP < 80/60 PR lower total and BL > 1000 ml    infectious complication >2 organs injured    rate. Gross contamination Excluded group: More Operation >8 hr post-injury    infectious complications, Destructive injury    higher mortality. Loss of abdominal wall Chappuis (14) 1991 56 32% 35% 0% 0% Extraperitoneal rectal 1st study with broad    injury    inclusion criteria. Low N in shock (3 PR,    1 Div) but PATI scores    equivalent (26 & 24). Falcone (51) 1992 22 8/11b 10/9b 9% 0% Death < 24 hr post-injury Used intracolonic bypass. Admit > 8 hr post-injury Operation at another    institution Deemed inadmissible Sasaki (23) 1995 71 19%a 36%a NR NR Extraperitoneal rectal PR more shock, gross    injury    contamination,    transfusions, left-sided    injury (p < 0.05). PATI >25 independent    risk for complications. Div OR 1.99 for    complications vs. PR. Gonzalez (25) 2000 176 18% 21% 2% 1% Extraperitoneal rectal PATI > 25 subgroup no    injury    difference PR vs. Div Kamwendo (26) 2002 240 37% 26% 0% 1.7% Extraperitoneal rectal Equivalent complication    injury rate PR vs. Div: •   Overall •   Early vs. late (cutoff     12hr post-injury) Note: PR = Primary repair, Div = Diverted, NR = Not reported, PATI = Penetrating Abdominal Trauma Index. a. Significantly different. b. Total number of complications was reported, p = 0.516. c. Reported as significantly different but no p values reported. d. Number randomized.

with destructive injuries requiring resection and anastomosis.(25) Table 35.3 summarizes the findings from these studies, excluding the preliminary 1996 data generated by Gonzalez. Falcone et al. (51), also had stringent exclusion criteria, and had a small sample size of 22 patients. The other studies excluded only extraperitoneal rectal injury.(14, 23, 25, 26) Notably, Sasaki and colleagues (23) noted more patients in shock defined as a systolic blood pressure (SBP) <80 mm Hg (28% vs. 4%), a higher degree of gross contamination (60% moderate or heavy contamination vs. 25%), and more patients requiring more than 4 units of blood (16% vs. 4%) in the primary repair group as compared to the diversion group. The authors report that all of these comparisons were statistically significant, although p values were not reported. Despite these differences, and despite similar PATI scores of 25.5 and 23.4 for primary repair and diversion respectively, they found an increase in the likelihood of complications in the diversion group (odds ratio of 1.99, p = 0.02). Using a multivariate regression model, they analyzed the exclusion criteria of previous studies (associated organ injury, shock on admission, fecal contamination, location of colon injury, age, transfusion requirement,

delay of operation, extent of colon injury, abdominal wall loss, and mechanism of injury) as potential risk factors for complications. They found that only the PATI score was an independent predictor for complications but this was regardless of the type of repair. Gonzalez et al. (25) found no difference in complication rate, and noted that this lack of difference persisted when patients with a PATI >25 in each group were compared. Kamwendo and colleagues (26) randomized 240 patients to diversion or primary repair, and also further stratified these groups into those that underwent operation before and after 12 hours postinjury. They found no differences in overall complication rate, mortality, number of patients in shock or requiring transfusion, or septic complications between the primary repair and diversion groups. Further, they found no difference in complication rate between the early and late repair groups. Two meta-analyses have been published on this topic. Singer and Nelson (22) published a systematic review of the literature in 2002. They pooled data from five RCTs (9, 14, 23, 25, 51), totaling 467 patients. The following year, the Cochrane Collaboration (21) pooled data from six RCTs, including five



improved outcomes in colon and rectal surgery Table 35.4  Meta-analyses investigating primary repair vs. diversion in colon injury. Author

Singer 2002 (Ref)

Nelson 2003 (Ref)

Comment

N (patients) N (trials)

467 5

705 6

Patients analyzed in an intention to treat manner Nelson added 1 trial to Singer review (REF)

Injury severity by PATI for PR

28.9

28.9

Injury severity by PATI for Div

25.8

25.8

Only 4 trials (REFS) reported PATI Variance not provided, thus statistical analysis could not be performed PR included higher PATI patients

OR (CI) for mortality Intervention favored

1.7 (0.51 – 5.7) Neither

1.22 (0.4 – 3.74) Neither

Mortality low for both groups (1.7-2.9%) No heterogeneity among trials

OR (CI) for all complications Intervention favored OR (CI) for all complications (excluding heterogeneous study) Intervention favored

0.28 (0.18 – 0.42) PR 0.13 (0.08 – 0.23)

0.54 (0.39 – 0.76) PR 0.13 (0.08 – 0.23)

P value for heterogeneity < 0.01

PR

PR

OR (CI) for all infectious complications Intervention favored

0.41 (0.27 – 0.63) PR

0.44 (0.17 – 1.1) Neither*

Including intra-abdominal abscess, anastomotic leak, peristomal abscess, sepsis, wound infection, and abdominal wound dehiscence

OR (CI) for abdominal infection (including wound dehiscence) Intervention favored OR (CI) for abdominal infection (excluding wound dehiscence) Intervention favored

0.59 (0.38 – 0.94) PR 0.52 (0.31 – 0.86) PR

0.67 (0.35 – 1.3) Neither 0.69 (0.32 – 1.39) Neither

Including all of the above except sepsis. Kamwendo study contributed heterogeneity. OR values same as Singer review favoring PR when this trial excluded

OR (CI) for wound complications (including wound dehiscence) Intervention favored OR (CI) for wound complications (excluding wound dehiscence) Intervention favored

0.55 (0.34 – 0.89)

0.55 (0.34 – 0.9)

PR 0.43 (0.25 – 0.76)

PR 0.43 (0.24 – 0.77)

Including peristomal abscess, wound infection, and abdominal wound dehiscence No heterogeneity among trials

PR

PR

P value for heterogeneity = 0.16 Study by Gonzalez, et al (REF) contributed the heterogeneity to the meta-analysis

* When the heterogeneous study was excluded, the OR (CI) became 0.24 (0.14 – 0.40), favoring primary repair. PATI= Penetrating abdominal trauma index, PR= Primary repair, Div= Diversion, OR= Odds Ratio, CI= 95% confidence interval.

of the studies addressed in their prior meta-analysis (9, 14, 23, 25, 26, 51), comparing 361 patients in the primary repair group with 344 patients in the diversion group. They noted that the PATI was reported in five of the six trials, and although statistical analysis could not be performed on this data, the primary repair group had higher mean PATI scores (29 vs. 26). Their analysis revealed a lower overall complication rate in patients undergoing primary repair. The authors conducted a rigorous analysis in which data that contributed to possible heterogeneity were excluded. This resulted in a strengthening of the odds ratio favoring primary repair. When considering intraabdominal infection, there were no significant differences between the two groups, although when sensitivity analysis was performed, the remaining data generated an odds ratio (OR) that favored primary repair (0.59, CI 0.37–0.94). Thus, meta-analysis showed a decreased risk of complications, and an either equivalent or lower risk of intraabdominal infection with primary repair. Neither analysis found any differences in mortality between the two groups, with rates of <3%. A summary of these 2 meta-analyses is presented in Table 35.4. Both meta-analyses were authored by Nelson and Singer, and both were conducted in the same fashion by the authors. The Cochrane review included the report by Kamwendo (26), and noted that these were the only data from outside the United States. Although differences in resources, transport time, and patient

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population may have implications for including this data in the meta-analysis, similar findings amongst such a potentially different population support the generalizability of primary repair. In general, these analyses do not include the complication rate from subsequent ostomy takedown. Injuries requiring resection and anastomosis Current evidence clearly supports primary repair in the setting of uncomplicated colon injury defined as injuries easily repaired by direct suture, without significant devascularization or a destructive component. The summary of existing prospective, randomized data suggests that this is the method of choice even in the setting of significant hypotension, high transfusion requirement, associated injury, gross contamination, and delay to operation. The issue of performing primary repair in the subset of injuries requiring resection and anastomosis is less clear. The data still favor primary resection and anastomosis without proximal diversion in the sense that all of the RCTs classified these repairs as primary repair. A review of these studies finds only 43 cases of resection and anastomosis without diversion in 6 randomized studies, which is a potential source of type II error. The most well-documented data in a randomized setting comes from Sasaki and colleagues (23), who noted patient characteristics, complications, and outcomes in the subset of 12 patient who underwent resection and anastomosis versus

colorectal trauma 31 patients who did not require resection, all within their primary repair group. When these data were independently extracted and analyzed by chi squared analysis and Fisher’s exact test, there were no differences between number of organs injured (p = 1.0), proportion of patients in shock (p = 0.46), presence of either moderate or heavy gross contamination (p = 0.31), proportion of patients needing more than 4 units of PRBC (p = 0.38), left-sided injury (p = 0.75), proportion with PATI > 25 (p = 0.17), or number of complications (p = 0.67). As would be expected, the mean PATI was greater in the resection subgroup, although this was not statistically significant (29 vs. 24). Also as expected, the number of patients with Flint grade 3 injury was higher in the resection subgroup versus the direct repair group (92% vs. 23%, p < 0.001). In their study, the primary repair group as a whole was more ill than the diversion group. Despite this, the diversion group was twice as likely to develop complications as compared to the primary repair group. Within the primary repair group, there were no differences between the resection and nonresection groups. Thus, the analysis above supports resection and anastomosis without diversion. Two caveats to this statement are that the numbers of patients are small, and the study was not powered to make this conclusion definitively. Demetriades et al. (27), conducted a nonrandomized, multicenter prospective review of 297 patients who sustained colon injury that required resection. One-hundred ninety-seven patients underwent primary anastomosis exclusively and 100 patients underwent diversion at 19 trauma centers. The method of repair was left to the discretion of the operating surgeon. The authors identified severe gross contamination, transfusion >4 units of PRBC in the first 24 hours, and single agent antibiotic prophylaxis as independent risk factors for abdominal complications in a multivariate regression analysis. The presence of all 3 factors was associated with a complication rate of 68%, 2 factors with a rate of 17–38%, one factor with a rate of 17–21%, and none of these factors with a rate of 13%. Subsequently, two sets of analyses were then conducted comparing primary repair with diversion, the first controlling for these 3 independent risk factors, and the second adjusting for ‘traditional’ risk factors commonly found in the literature: hypotension (SBP < 90), transfusion >6 units of PRBC, severe contamination, PATI >25, and delay of operation >6 hours. The authors found similar rates of abdominal complications between the 2 groups, no difference in complication rate by location of repair (e.g. ileocolostomy, colocolostomy, ileostomy, colostomy), and no difference in hospital or ICU stay. They noted 24% and 22% overall rates of abdominal and extraabdominal complications respectively. One major limitation of this study was that the diversion group had a higher incidence of delayed operation, shock at admission, left colon injuries, PATI >25, small bowel and liver injuries, transfusion requirement, and severe fecal contamination. Further, the diversion group received antibiotics longer than the primary repair group, although the median duration is not reported. However, the authors performed a separate analysis controlling for these factors and again found no difference in abdominal complications, hospital stay, or ICU stay. They did note an increased colon-related mortality with the diversion group (4.5% vs. 0%, p = 0.03), which translated to 4 deaths in

this group. Thirteen patients in the primary repair group had an anastomotic leak, compared to one leak from a Hartmann pouch. No risk factors could be identified for leak within the primary repair group, and no patient died as a result of leak. The authors concluded that method of colon management does not influence the development of colon-related abdominal complications, and primary repair should therefore be practiced for all injuries. They also concluded that transfusion, severe contamination, and single agent antibiotic prophylaxis are independent risk factors associated with complications. On the other side of this argument, several retrospective series have been published that present a caution to the concept of uniform primary repair of all colon injuries. As an example, Stewart et al. (52), published a follow-up study based on their previous experience with 95 direct repairs with no suture line complications and an 11% incidence of abscess.(53) The authors changed their management strategy and repaired all injuries primarily, including destructive wounds requiring resection and anastomosis. Forty-three patients undergoing resection and anastomosis and 17 undergoing colostomy were analyzed. They noted no statistically significant difference in complication rate. However, when comparing the 6 anastomotic leaks to 37 primary repairs that did not leak, they noted a 12-fold risk of leak in patients that had an underlying illness (e.g. diabetes mellitus, cirrhosis, HIV infection). The need for transfusion was not significantly associated with increased risk, but the combination of transfusion >6 units of PRBC and medical illness resulted in a 14-fold increased risk of leak. The sample size was small, but the authors concluded that a 14% leak rate is excessively high. Other limitations include a shift in practice toward primary repair during the study period and inherent problems with determining underlying illness in the trauma population in general. Although these reports are retrospective reviews of a relatively small number of patients, high transfusion requirement (commonly 4 or 6 units) consistently appears as a risk factor for complications.(27, 53) Results of the randomized trials previously discussed did not identify this as a risk factor for complications. Damage Control Data concerning repair of colon injuries in the setting of damage control surgery (DCS) are scarce. There are no randomized data, and literature that specifically describes the management of colon injury in the context of damage control surgery is limited to three reports analyzing 34 patients.(54–56) Miller et al. (54) retrospectively analyzed 17 patients who underwent DCS and subsequent delayed definitive repair of colon injury. All patients had destructive colon injury, underwent abbreviated laparotomy at their initial operation, and were returned to the operating room after correction of acidosis, coagulopathy, and hypothermia in the ICU. Eleven patients underwent resection and primary anastomosis and 6 underwent diversion. The authors compared the 11 anastomosis after DCS patients to 21 controls, who were patients with traumatic colon injuries undergoing anastomosis at initial operation. There were no leaks in the DCS group and one in the initial anastomosis group (p = 0.66). The abscess and colon-related mortality were also similar. As would be expected, the ISS and overall



improved outcomes in colon and rectal surgery mortality were higher in the damage control group. The authors then compared the 11 anastomosis after DCS patients to the other 6 patients, who underwent colostomy after damage control. They found no differences in ISS, abscess rate, colon-related mortality, or overall survival. Chavarria-Aguilar et al. (55) reviewed the management of destructive bowel injury in the setting of the open abdomen. The data are heterogeneous, as patients with small bowel injuries are included in the analysis. Of 104 patients with destructive bowel injury requiring resection and anastomosis, 29 underwent temporary vacuum closure and the rest primary fascial closure. Eight patients with colon injuries underwent resection and delayed anastomosis after initial packing. Two leaks occurred, both from small bowel anastomoses. There were no differences in rate of abdominal abscess between the anastomosis and stoma groups in either the vacuum-closure group or the initial fascial closure group, with rates of 7–21%. These findings led the authors to conclude that resection and anastomosis is safe in the face of destructive injury and an open abdomen and should be considered in most patients. The retrospective nature of the study did not allow causality to be established, and the small sample size did not allow for the identification of risk factors or appropriate candidates for anastomosis versus ostomy. Finally, Johnson and colleagues (56) describe general changes in DCS over an 8-year period and comment on 7 colonic anastomoses and 2 primary repairs. They report one leak and 3 abscesses, but do not specify if this was within the colon resection group or the 13 small bowel resections performed. The authors of this chapter recently reviewed data collected on soldiers undergoing damage control laparotomy in Operation Iraqi Freedom (OIF) and Operation Enduring Freedom (OEF) during 2005–2006 (unpublished data). We found a 51% rate of concomitant colon injury, or 77 of 152 patients. This is more than twice the number of patients studied than in the existing civilian literature. The early colon-related complication rate (7 days postinjury) was 14%. These included 5 leaks, 3 abscesses, and 6 cases of ischemia on further evaluation requiring reoperation. Complications were essentially equally distributed among the ostomy and anastomosis groups (p = 0.54). Results are summarized in Table 35.5. Further, there were no differences in complications by location of injury (p = 0.58). There were no differences in ISS between colostomy and no colostomy (all primary repairs) and colostomy, direct repair, and resection and anastomosis groups. The colostomy group was more likely to have a massive transfusion, but there were no differences in the complication rate in any comparison. Although follow-up is currently limited to a mean of 7 days postinjury, data collection is ongoing. These results support the conclusion of Chavarria-Auguilar and colleagues (55), that even in combat settings with massive injury and tissue loss, primary repair is feasible. However, as discussed later in this chapter, war injuries in combat situations may require different management than civilian injuries. Practice patterns In an attempt to synthesize the diverse conclusions found in the literature, Miller and colleagues (57) developed a clinical pathway for destructive colon injuries in 1995 and compared patients



Table 35.5  Colon injuries in the setting of damage control surgery during Operation Iraqi Freedom 2005–2006.

Colostomy No colostomy (n = 44) (n = 30) p value

ISSa Massive    transfusion Complications

24.7 ± 2.2 25/44 (56.8%) 9/44 (20.5%)



Colostomy Direct repair Anastomosis (n = 44) (n = 10) (n = 20)

ISS Massive    transfusion Complications a

24.7 ± 2.2 25/44 (56.8%) 9/44 (20.5%)

24.8 ± 3.2 8/30 (26.7%) 4/31 (12.9%)

24.4 ± 3.8 3/10 (30%) 1/10 (10.0%)

0.98 0.02 0.54

24.9 ± 6.0 5/20 (25%) 3/20 (15%)

p value 1.00 0.04 0.69

a. mean ± standard error of the mean.

treated during this period with their experience before its implementation. Primary repair was undertaken in all colon injuries except patients with destructive injuries requiring >6 units of PRBC pre- or intraoperatively, or patients with significant underlying medical illness. These high-risk patients underwent diversion. Two hundred nine patients in the clinical pathway group were compared to 60 prepathway patients. The authors found no difference in abscess, anastomotic leak, or colon related mortality rates between the two time periods. They also found no difference in leak rates between anastomosis and direct repair groups after implementation of the clinical pathway, whereas there was a higher leak rate in the resection group in the prior era. Finally, they found that there was a reduction in the number of patients undergoing diversion from 31% to 9%. This translates to a relative risk reduction of 71%, an absolute risk reduction of 22%, and a number needed to treat of 4.5. That is, for every five patients treated according to the pathway, one colostomy and subsequent takedown was avoided. Further, there were no differences in complications with gross contamination, associated injury, or location of colon injury. These results suggest that the authors improved their patient selection for colostomy, and that destructive injury alone is not a contraindication to primary repair. The notable corollary to this conclusion is that there was a role for colostomy in their experience. summary The treatment of penetrating colon injury has changed markedly in the past 50 years. Level I evidence supports primary repair (without diversion) of nondestructive injuries as the method of choice in nearly all circumstances. Specifically these circumstances include hypotension, gross contamination, high transfusion requirement, associated injury, and delay from injury to operative treatment. Level I data also exists supporting primary repair for destructive injuries requiring resection and anastomosis but is more limited. Transfusion requirement, gross contamination, and high penetrating abdominal trauma index have been independently associated with infectious complications by a number of authors, but this has been regardless of the type of management (diversion or primary repair). Data regarding primary repair in the setting of damage

colorectal trauma control is even more limited, and no level I data exists. However, small series, including a recent large review of military injuries suggests that primary repair is feasible in the damage control setting. No convincing data exist supporting diversion as superior to primary repair. In severely injured patients, a reasonable strategy is to initiate damage control techniques, including leaving the bowel in discontinuity, and subsequently performing an anastomosis once normal physiology is restored. A low threshold of suspicion is the key to diagnosis in most cases. Most injuries are found intraoperatively, and most are uncomplicated. Thus, primary repair is appropriate for the majority of colon injuries. As always, sound judgment, skilled resuscitation, and attentive postoperative care are keys to good outcomes. The complication rate is high regardless of method of management, and providers should be aware of this fact. “… it cannot be emphasized too strongly that the dangers of the abdominal patient are not over when the last stitch has been put in. Recovery depends almost as much on the skill and the duration of the aftercare as on the operation itself.” (Ogilvie, 1944) (4)

Figure 35.1c  Intraoperative findings in a patient with a “seat-belt sign”. The patient sustained a hematoma in the cecal mesentery and a serosal tear in the sigmoid colon which was primarily repaired.

Blunt colon injury Colonic injury is uncommon after blunt abdominal trauma, accounting for only 1–5% of blunt traumatic injury.(58) It is notoriously difficult to diagnose, but a delay in diagnosis is associated with significant morbidity including fatal peritonitis, sepsis, and life-threatening hemorrhage.(59, 60) There are three primary proposed mechanisms in the pathogenesis of blunt colonic injury.(61) The first is crush injury between an object such as a steering wheel, seat belt, or vertebral column. Second, shear injury occurs at points of fixation, particularly the sigmoid mesentery. Third, burst injury can occur when a closed loop is formed at impact. The resultant injury pattern is characteristic and can include mural and mesenteric hematomas, partial thickness tears, full thickness perforations, and transection at fixation or contact points. Blunt colonic injury (BCI) is usually partial thickness, with rare exceptions (3%) being full-thickness colonic perforations. (62) The most common cause is motor vehicle crashes, both restrained and unrestrained.(62) The left colon is the most frequently injured, followed by the right and transverse colon.(62) The diagnosis of blunt colon injury is a diagnostic dilemma, and requires a high index of suspicion. In a retrospective multicenter 5 year review of patients with BCI, the diagnosis was made preoperatively only 5% of the time.(62) These injuries are often diagnosed upon laparotomy for other indications, and although rare, colon injury ranks 4th among injuries found at laparotomy in blunt trauma patients.(60) Physical exam findings are inconsistent or manifest late after injury and the patient may be difficult to evaluate secondary to traumatic head injury, intoxication, or distracting extraabdominal traumatic injury. The presence of a ‘seat-belt’ sign or a Chance fracture, as described previously, are predictors of hollow viscus injuries. Figure 35.1c demonstrates a blunt colonic injury. Nance et al. (63) studied solid organ injury as a predictor of hollow viscus injury in blunt trauma patients. They found that as the number of solid organ injuries increased, the likelihood that a hollow viscus injury coexisted increased, up to 34.4% in patients with three solid organ injuries.

CT scan is currently the most utilized modality for the diagnosis of blunt colonic injury.(33, 42) Findings suggestive of BCI on CT  include evidence of extraluminal air, extraluminal contrast material, bowel wall thickening, streaking of the mesentery, and free fluid in the absence of solid organ injury (Figure 35.1b). Williams et al. (60) studied trauma patients with blunt colonic injury. They evaluated the ability of physical exam, plain radiography, CT scan, FAST, and DPL to accurately detect BCI. They found that no individual or combination of diagnostic tests was able to accurately detect BCI. For example, the sensitivity of CT findings including free air, contrast extravasation, and free fluid had sensitivities ranging from 6–49% and positive predictive values between 50–72%. Ultrasound examination had a sensitivity of 58%, specificity of 44%, a positive predictive value of 61%, and a negative predictive value of 41%. Physical examination findings such as the seat-belt sign, peritoneal signs, and abdominal pain performed similarly, with sensitivity between 21 and 59% and positive predictive values between 57 and 63%. Diagnostic peritoneal lavage had a sensitivity of 97% but a specificity of 13%, a positive predictive value of 55% and a negative predictive value of 80%. Malhotra et al. (41) evaluated the accuracy of CT scan in the diagnosis of blunt bowel injury. They found the sensitivity and specificity of CT for these injuries was 88.3% and 99.4%, respectively, with an accuracy of 99.9%. The positive and negative predictive values were 53.0% and 99.9%, respectively. The most common finding they reported associated with BCI was unexplained free fluid. Yegiyants and colleagues (64) found 14 cases of blunt injury with free fluid on CT scan but no evidence of solid organ injury (0.5% of admissions in their review). Eleven of these patients (74%) required laparotomy, with hypotension (3 patients) and peritoneal signs (6 patients) being the two most common triggers. In their series, physical exam was predictive in 43% and FAST exam was positive in 50%. It is possible that the addition of laparoscopy may aid in the management of blunt colonic injuries. As previously noted, Ahmed (44) and Mitsuhide (45) report the avoidance of between 21–75% of laparotomies in blunt abdominal trauma.

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improved outcomes in colon and rectal surgery summary The management of blunt small bowel injury is relatively straightforward, requiring mainly primary repair or resection and anastomosis.(65) Blunt colonic injury is more complex. In a comprehensive review of the pathophysiology and management of blunt bowel and mesenteric injuries, Hughes and Elton (65) suggest that most blunt colonic injuries should be categorized as high grade (AAST grade V or Flint grade 3, Tables 35.1 and 35.2) and treated accordingly. A high index of suspicion, experience, and appropriate follow-up are the cornerstone to the diagnosis of this uncommon injury. Currently, physical exam, and CT scanning appear to be the most used methods of diagnosis. Laparoscopy may be a useful adjunct to diagnosis. Devascularized mesentery presents a challenging problem. The viability of the bowel should be assessed if in question and resected if indicated. In cases of severe injury a second look may be considered to assess for progressive ischemia. Once diagnosed, the treatment of blunt colonic injury should follow the guidelines for penetrating colonic injury. Outcomes of colostomy closure Only one RCT included subsequent colostomy takedown in the primary analysis. Chappuis et al. (14), reported 22 closures out of 28 patients in the diversion arm of their RCT with one complication (4.5%), an enterocutanous fistula after ileostomy reversal. The absence of good follow-up limits the conclusions that can be made from this study. It is thus debatable whether this is an appropriate analytical strategy, in that initial management is a separate issue from colostomy closure. However, the risk of subsequent colostomy reversal should be considered when the decision to proceed with diversion is made. This topic is well represented in the literature, with a wide array of heterogeneous conclusions made. Differences in conclusions are due to varied definitions of complications and infections, the inclusion or exclusion of rectal injury, varied indications for original diversion (trauma, cancer, etc), and the retrospective nature of published data.(66–70) Mortality as a consequence of colostomy reversal is sufficiently low (0–3%)(69) that most authors report infectious complications as their primary endpoint. Further, infectious complications remain the major source of morbidity after wounding of the abdominal cavity.(71) Two series reviewing stoma closures after diversion for any indication found complication rates of 20–36%.(66,69) These rates are similar despite the reports being separated by 20 years. Factors associated with increased complications range from reversal performed in less than 90 days (66), diverting versus loop colostomy (66), age >55 (69), and use of a silicone drain.(69) While the data is heterogeneous, conclusions that can be made are that colostomy reversal is associated with a high complication rate of approximately 20–30%, and that some retrospective data seem to suggest an increase in complications with diversion (68, 70) which supports at least consideration of primary repair in almost all cases and a more selective use of diversion than what has been taught in previous years. Military perspective The recent military conflicts in Iraq and Afghanistan have raised questions about the applicability of the civilian experience to

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combat settings and war injuries. In light of this conflict a brief overview of the impact that active wartime has had on trauma surgery—and colon injury specifically—is worthwhile. There is a long history of the lessons of war having a deep and lasting impact on civilian surgical management. One of the classic papers in the trauma literature is Ogilvie’s account of military surgery during World War II.(4) Although this is the paper most often cited as the impetus behind mandatory colostomy, it describes many classic precepts that were not widely recognized until much later decades. Ogilvie’s paper is remarkable both for his foresight but also the number of principles he describes. These include: the ‘trimodal’ peaks in trauma mortality, damage control, massive transfusion, ARDS, abdominal compartment syndrome, and many of the logistical issues later incorporated into both military and civilian trauma programs. Ogilvie reports a 60% mortality rate from colon injuries. Direct suture repair resulted in a 44% mortality rate as opposed to 45–65% for colostomy with and without resection. However, 2 of 2 patients who underwent resection and anastomosis died. He attributes the lower mortality with suture repair to less severe injury but nevertheless makes no recommendation about selective repair in these cases. Further, he acknowledges the beneficial effects that antibiotics, improved logistics, and liberal use of blood products had on outcomes. Despite these other factors, he strongly advocates for colostomy in all cases and states that it is “perhaps the greatest single factor in the improved results we are able to record”. It is likely that a mandate and automatic action were preferred in the face of the challenges involving resources, evacuation, and ever-changing groups of surgeons of vastly different levels of training and experience. This can be seen in his assertion that “the forward surgeon must have good hands, a stout heart, and not too much philosophy. He is called upon for decision rather than discussion, for action rather than a knowledge of what the best writers think should be done”. Perry and colleagues (2), in a comprehensive review of the military management of colon injury, describe its evolution throughout modern history. Before World War I, laparotomy was discouraged and observation afforded the wounded soldier the best chance of survival. Laparotomy and rapid evacuation during WWI saw a dramatic decrease in mortality from abdominal injuries from almost 90% to 40%. The changes wrought during WWII have been detailed previously. During the Korean War, air superiority led to improvements in evacuation. Further, the practice of exteriorization, in which the repaired colon was mobilized and brought out above the skin for observation, was largely abandoned. Finally, some leeway in the primary repair and anastomosis of right colon injuries was allowed. These factors led to a further decline in colon-related mortality from 35% to 16%. Aside from well-documented advances in resuscitation and critical care, the Vietnam War saw improvements in evacuation and antibiotics, as well as more location-specific trends in colon management. Left-sided wounds were diverted, while recommendations for right-sided wounds included resection and primary anastomosis, exteriorization, and resection, ileostomy and mucus fistula. During this time mortality dropped to around 10%. Perry and colleagues stress that the best results with primary repair

colorectal trauma are obtained by surgeons experienced in this strategy and when patients remain under the care of the same surgeon. Hudolin and Hudolin (72) reviewed their experience during the Bosnia-Herzegovina conflict in 1992–1995. Two-hundred fifty-nine patients with colonic injury were treated at a single receiving facility with no radiologic capability and a single field generator. Rapid evacuation made long-term follow-up impossible. Roughly equal numbers of patients were treated with primary repair and colostomy (47% and 53% respectively). Overall mortality was 7.7% in both treatment groups. There were no differences in associated injuries, or mechanism of injury (explosive or gunshot) between groups. Overall complication rate was similar between groups (27% for primary repair and 30% for colostomy). The authors did not perform statistical analysis on individual complications, citing low numbers, but there were more leaks in the primary repair group (8 vs. 2) and fewer wound complications (7 vs. 15). These authors also cite surgeon experience as an important factor in management with primary repair, but conclude that it is safe even with subsequent rapid evacuation if treatment is undertaken soon after injury and with administration of perioperative antibiotics. Steele and colleagues (73) reviewed the treatment of 175 patients during the 2003–04 period of OIF. Primary repair was undertaken in 53%, the leak rate was 10%, and overall mortality was 17.7%. Only 37% of patients were United States or coalition forces and the rest were local nationals. Mean ISS and AIS were similar among different regions of the colon. Stomas were more frequently performed for rectal or anal sphincter injuries than colonic injuries, and for left-sided versus right-sided or transverse injuries. Leaks after primary repair were equally distributed throughout the colon. Although the leak rate was higher in the primary repair group, there was no difference in rate of sepsis or mortality between groups on multivariate analysis. Only ISS >15 was associated with an increase in sepsis, while only rectal or transverse injuries were associated with an increase in mortality. Follow-up is not reported likely due to rapid evacuation and the high proportion of local nationals included in the study. We conducted a review of colon injuries sustained during OIF during 2005–2006 (unpublished data). One hundred thirtythree patients with colon injuries were admitted from Iraq and Afghanistan to Landstuhl Regional Medical Center (LRMC) in Landstuhl, Germany, the tertiary referral center for combat casualties in this theater. The average time spent in the three echelons of combat care facilities (battalion aid station, forward surgical team, and combat hospital) was 2 days and the average time spent at LRMC was 4.7 days, translating to about 7 days from injury to echelon V (tertiary US military hospital) care in the United States. Anatomic distribution of injury is depicted in Table 35.6. Primary repair or resection and anastomosis was the initial method of treatment in 34%, colostomy in 45%, and damage control consisting of bowel left in discontinuity in 21%. The complication rate was 12% overall and was not related to type of management (p = 0.172). Complications were linked to open abdomen (p = 0.031), increased ICU days (p = 0.015), gunshot wound (p = 0.021), and number of procedures before admission at LRMC (p = 0.008), but not LOS, ISS, mechanism, location of injury, or massive transfusion. These results are limited by the lack

Table 35.6  Anatomic distribution of colon injuries during Operation Iraqi Freedom 2005–2006. Location Numbera Ascending Transverse Descending Sigmoid Rectum

28 20 28 36 33

Percenta 21% 15% 21% 27% 25%

a. Totals exceed 100% due to multiple injuries in some patients.

of long-term follow-up. Data collection from US sites is ongoing, however, and will be the subject of future publications. summary These examples demonstrate that the use of primary repair in military series is lower than reported in the civilian literature. (27, 57) Contributing factors include varied training and personal philosophy of treating surgeons, higher number of damage control procedures performed, and higher incidence of rectal injury, which in turn results from the contribution of blast and high-energy mechanisms of injury. These differences in combat trauma contribute to the active debate on the method of choice, as is evidenced by recent publications by authors deployed to OIF calling for an expanded role for diversion.(74, 75) To date, however, the experience has been limited to small series and expert opinion. Larger series previously described currently lack long term follow-up. The bulk of the data seems to support primary repair. Antibiotic therapy As previously mentioned, infectious complications are the major source of morbidity after abdominal trauma.(71) Infection is a major contributor to the third peak in the ‘trimodal’ distribution of trauma mortality, which was recognized by Ogilvie in 1944 (4) and described by Trunkey in 1982.(76) Causes can be separated into two broad categories, those related to the patient or the disease process and those related to treatment. The latter are the modifiable factors. A number of disease-related factors have been reported to contribute to infectious complications. In a recent, comprehensive review of the literature addressing infections in penetrating abdominal trauma, Fabian (71) describes colon injury, rate of transfusion, shock (generally SBP < 90 mm Hg), and PATI >25 as well-investigated independent risk factors. Treatment related factors include careful attention to measures that contribute to improved outcomes in the trauma and critically ill population in general; aggressive efforts to achieve normothermia (77), correction of coagulopathy and acidosis, euglycemia (78), minimization of transfusions (79–81), and careful attention to nutrition. (82–85) Choice, timing, and duration of antibiotic therapy have been well studied and deserve a brief comment. The efficacy of preintervention versus posttreatment (postoperative) therapy is well established.(85, 86) In addition, the choice of antibiotic does not seem to matter as much as the adequacy of anaerobic and gramnegative coverage. The only study that appeared to have generated

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improved outcomes in colon and rectal surgery data favoring multiple agent therapy was the prospective nonrandomized study of colon injury requiring resection and anastomosis conducted by Demetriades and colleagues that was discussed previously.(27) In this report, single agent antibiotic therapy was an independent risk factor for abdominal complications, with an RR of 1.89 (p = 0.004) and an RR of 1.12 when adjusted for transfusion of 4 or more units of PRBC, severe fecal contamination, or method of colon injury management. However, the most recent guidelines published by the Surgical Infection Society in 2002 recommend 24 hours of organism-specific coverage in instances of peritoneal contamination due to traumatic bowel injury repaired within 12 hours.(87) There is sufficient class I evidence to recommend 24 hours of an appropriate antibiotic for the minimization of infectious morbidity in colon trauma.(88–90) Bozorgzadeh et al. (88) randomized 300 patients to either 24 hours or 5 days of therapy with cefoxitin after penetrating abdominal injury. There were no exclusion criteria and patients with colon injury (32%), shock on admission (31%), and multiple abdominal organ injuries (19%) were included. The overall infection rate was 25%, while deep surgical site infections occurred in 6%. There were no differences in complications or length of stay between groups. In addition, multivariate analysis found only colon injury to be independently associated with infection and increased length of stay. One limitation of this study was that the 5 day group had a higher incidence of intraoperative shock, multiple organ injury, and intraoperative blood loss. Cornwell and co-workers (89) randomized patients with fullthickness, penetrating colon injury and one risk factor consisting of PATI>25, transfusion of 6 or more units of PRBC, or greater than 4 hours from injury. Sixty three patients were randomized to either 24 hours or 5 days of cefoxitin therapy. There were no differences in severity of injury or other baseline characteristics, infectious complications, length of stay, or mortality. Overall abdominal infection rate was 29% and overall mortality was 9.5%. Although the sample size was adequate by power analysis, there were a small number of patients in each group. Kirton and colleagues (90) performed a multicenter, double blinded, placebo-controlled RCT in which 317 patients with penetrating hollow viscus injury were randomized to receive either 24 hours of ampicillin/sulbactam followed by 4 days of saline placebo, or 5 days of antibiotic therapy. The proportion of colon injuries (50%), AAST grade of colon injury, distributions of solid organ injury, ISS, PATI, and infection rates were similar in each group. The overall infection rate was 19%, with 9% surgical site infections. Mortality was 1.6% overall. On multivariate analysis only total number of PRBC transfused and PATI >25 were independent contributors to infectious complications. Both the Cornwell and Kirton studies identified gram-negative bacilli as the most common isolates. Although this topic has been well studied, the demonstrated risk of infection with colon injury may predispose some practitioners to inappropriately prolong the duration of antibiotic therapy. The rising incidence of resistant bacterial strains makes this a critical issue. Adherence to evidence-based guidelines and support on an individual, practice, hospital, and national level is essential in minimizing the incidence of multiply resistant nosocomial infections.

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Retained fragments The traditional teaching regarding retained fragments is that they should be left in place unless they traverse the colon, in which case they should be removed and the tract debrided. Data regarding this subject is scarce. For example, four reports specifically addressing infectious complications after missile injury to the colon have been published since 1990.(91–96) Sarmiento and colleagues, who report the largest experience on this subject, reference six other publications on this topic since 1892.(93) Flint et al. (95) reported a series of seven patients with gunshot wounds through the colon who developed abscesses, two of whom died (28%). They noted that abscess culture revealed E. Coli, Klebsiella, Bacteroides, and pseudomonal species in every case, leading to the conclusion that contaminated material was inoculating the wound tract, and that retained fragments should be removed. Based on a small series, Flint refuted the belief held at that time that bullets and missile tracts were sterile due to the heat and friction generated by the projectile.(91) Poret (91) reviewed 151 patients with gunshot wounds traversing the colon and found a 26% rate of septic complications when the bullet or fragment was retained and a 16% rate when there was no retained fragment (p = 0.15). Although not statistically significant the authors note clinical significance, and conclude that the retained missile is a nidus for infection. In contrast, Demetriades and Charalambides (92) reviewed their experience with 84 patients with gunshot wounds to the abdomen traversing the colon. Bullets were removed only if they were palpable. In 48% of patients the bullet was retained, while in 52% it was either removed or had exited the body. The two groups were matched in severity of injury, site of injury, number of colonic perforations, and method of repair (primary versus colostomy). The overall abdominal complication rate was 14% and the incidence of missile tract infection was 4% with no differences between groups. Antibiotics were given for 48 hours. The authors concluded that missiles should only be removed if they are easily palpable. Edwards et al. (93) studied the effects of low-velocity, small-fragment injury in a porcine model designed to simulate injury from antipersonnel devices in combat. They fired steel fragments through the unprepared colons of swine into a gelatin medium, then cultured several points along the missile tract, as well as the fragment itself. No culture reached 1 × 105 organisms and average tract size was 5 cm long by <1 mm in diameter. The authors concluded that small-fragment removal and debridement of wound tracts would not present an increased risk of infection if antibiotics were administered soon after injury. Sarmiento et al. (93) retrospectively reviewed 185 patients who sustained gunshot wounds in which the bullet had traversed the colon and extraperitoneal soft tissue only. The decision to extract the bullet was according to the discretion of the operating surgeon at the time of initial laparotomy. There was a fivefold lower incidence of infection in those in whom the bullet was extracted compared to retained (5% vs. 25%, p = 0.06). They also found no difference in risk of infection for injuries that traversed the right and transverse colon compared to the left colon and rectum. In summary, the evidence is sparse on this topic, but seems to support extraction of bullets, debridement of wound tracts and early antibiotic administration with retained fragments that traverse the

colorectal trauma Table 35.7  High-risk factors for rectal injury. Gunshot wound to pelvis, buttocks, lower back or abdomen Wound in which injury tract is directed caudad Penetrating gluteal injury Blast injury to perineal area Complex perineal laceration Pelvic fracture Lower genitourinary tract injury Sexual assault Erotic anal penetration Gross blood per rectum High-energy blunt injury to lower abdomen

colon and embed in soft tissue. This is consistent with the basic general surgical principle of not leaving foreign material in the presence of the open gastrointestinal tract. Small-fragment injury poses an additional problem, in that debridement of multiple small-diameter tracks may be a significantly morbid procedure.(94) Rectal injury The classic components of managing rectal injury include the three (or sometimes four) D’s: diversion, presacral drainage, distal rectal washout, and sometimes direct repair.(30, 96) These maneuvers were established during WWII and the Vietnam war (2), and were credited with decreasing mortality from 67% during WWI to essentially zero during the Vietnam war, and decreasing morbidity from approximately 70% to 10% during the same period.(1, 30, 96) Mortality in recent series is low. In a review of 39 civilian studies, Merlino and Reynolds (96) identified 42 deaths in 1105 patients with rectal injury, 10 of which (0.9%) were attributed to the rectal injury itself. They also report a range of 1.3 to 4.5 associated injuries per patient, making associated injury the rule rather than the exception. Genitourinary injury is the most commonly associated injury given the anatomic proximity of these organs. The rectum is protected by the bony pelvis and soft tissue, which makes injury less frequent, but exposure more difficult. It is mostly accessible from the anus but is only covered by peritoneum along its proximal one-third and anteriorly along the middle one-third, facilitating both repair and intraperitoneal contamination. Penetrating injury accounts for 85% of reported injuries, with the majority of these being gunshot wounds.(96) A rare source of rectal injury is iatrogenic perforation, which reportedly occur in approximately 0.1–0.2% of cases.(97, 98) Diagnosis Rectal injuries present a diagnostic challenge. Injuries to the bony pelvis should be rapidly diagnosed, and an unstable pelvis should be addressed first. Careful perineal and digital rectal examination is the next step and should be accompanied by a high clinical suspicion with risk factors outlined in Table 35.7. Sphincter tone and injuries to the sphincter complex should be carefully noted at this point as well. Digital rectal exam has a reported accuracy of 64–96%.(99–102) Sigmoidoscopy (blood or lesion visualized) for the diagnosis of rectal perforation has an accuracy of 89–100%.(99–101, 103, 104) Blood on digital exam is an indication to further assess the rectum either

by proctoscopy or sigmoidoscopy.(103, 104) Intraluminal hemorrhage identified by endoscopy should lead to the presumptive diagnosis of rectal injury and management should follow accordingly.(102–104) Contrast-enhanced CT scan and contrast studies are useful adjuncts in equivocal cases.(105) Diagnostic laparoscopy has been described for hemodynamically stable patients with evidence of extraperitoneal rectal injury (blood on rectal exam and proctoscopy), no peritonitis, and no intra­ peritoneal injury.(103, 106, 107) Management Traditionally, the cornerstone of rectal injury management is fecal diversion.(96) In distinction to colon injury, diversion is more often indicated for rectal injury. This is partly due to a lack of class I data confirming the safety and feasibility of primary repair alone with rectal injuries, combined with increased difficulty in dissection and exposure, as well as lack of a serosa for much of its extent.(104) Overall mortality rates are low, between 0–9% (99–104, 108–111), including six modern series published since 1996 with a <2% death rate. The infrequency of this injury makes it unlikely that an RCT with sufficient power will be performed. The safety of colostomy in rectal injuries has been documented. In a review of complications related to colostomy, Berne and colleagues (68) reported a 55% incidence of complications when colostomy was performed for colon injury versus a 13% incidence when performed for rectal injury. A number of reports have challenged the routine practice of distal irrigation and presacral drainage (101, 103, 108, 110–112), the majority of which cite the differences between civilian and military penetrating trauma as the primary indication for deviation from the classic teaching. Only one RCT exists on this topic, conducted by Gonzalez and colleagues.(110) Forty-eight patients were randomized to diversion and either presacral drainage or no drainage. Distal irrigation was not performed on any patient. There was no mortality attributable to rectal injury, and complications occurred in two patients in the drainage group and one in the nondrainage group (p > 0.05). The authors acknowledge that their study was underpowered to detect a difference in complication rates. Others have argued that with unrepaired extraperitoneal injury the risk of overwhelming pelvic sepsis developing within a closed space is high, and in this case presacral drainage is indicated.(96, 108) In the absence of convincing data, this argument represents a reasonable approach. Distal washout has largely been abandoned, as many authors have consistently failed to demonstrate any advantage to its use. Most authors cite the difference between high-energy, military rectal wounds, and lower-energy civilian injuries as the primary difference in results between the original reports from the Vietnam war and contemporary experience (96, 101–104, 108, 110). There may be a role for distal irrigation in wartime and with injuries resembling combat injuries. One useful convention is to approach rectal injury along anatomic lines. Intraperitoneal injury can be safely treated in a similar fashion to colon injury, as several authors have demonstrated the feasibility of primary repair without proximal diversion.(96, 101, 108) The exception is in the case of extensive contamination and tissue loss, for which most authors divert the fecal stream.

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improved outcomes in colon and rectal surgery Table 35.8  Traditional steps in the management of rectal injury.(20) Perineolithotomy position Management of concomitant injuries Debridement Proximal diversion Remove foreign bodies Presacral drainage Distal rectal washout Repair injury if possible Repair sphincters if possible External wound drainage Broad spectrum antibiotics Skin left open

Table 35.9  Modified steps in management of rectal injury. Perineolithotomy position Management of concomitant injuries Debridement Intraperitoneal injury Extraperitoneal injury Primary repair Diversion Selective presacral drainage Diversion if destructive injury (Loop colostomy    preferred) Repair if easily accessible Repair sphincters if possible Selective external wound drainage Broad spectrum antibiotics Skin left open

(96, 108) Given the relative ease of the procedure and subsequent reversal, a loop colostomy is recommended (100, 102, 103) if solely for the purpose of diversion in rectal injury, while an end colostomy is performed if there are other indications, such as associated colonic injury. Extraperitoneal injuries can be treated without repair, unless they are easily accessible or uncovered in the course of treating other injuries.(96, 102, 103, 108) There is some evidence to support this principle. Gonzalez et al. (111), implemented a protocol for the management of extraperitoneal rectal injury without fecal diversion, presacral drainage, or distal irrigation in patients with nondestructive penetrating injury. Although they had no mortality or infectious complications, the series included only 14 patients, making these results difficult to generalize. Interestingly, in all 14 patients a barium enema was performed and demonstrated complete healing by postinjury day 10, demonstrating the rapid healing capacity of the rectum, likely due to its rich blood supply. Abdominoperineal resection has been described in the setting of traumatic rectal injury (102), but should be regarded as an extraordinary measure under extremely rare circumstances. The steps in the classic, conservative management of rectal injury have been described by Stewart and Rosenthal (20) and are summarized in Table 35.8. A modification to these steps as suggested by modern series is presented in Table 35.9. Summary Rectal injury is uncommon and often accompanied by significant associated injury, most commonly genitourinary. Data is scarce, and is mostly limited to retrospective reviews. Diagnosis is challenging, and is most often made by clinical suspicion, digital exam,

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Figure 35.2  Foreign body requiring operative extraction. This patient sustained a full-thickness rectal injury from the foreign body placement.

and proctoscopy or sigmoidoscopy. Intraperitoneal injury can be treated with primary repair in a manner analogous to colon injury. Extensive destructive injury can be diverted with lower expected complication rates than colon injury. Extraperitoneal injury can be treated with diversion alone, although selected cases of partial or nondestructive injury can be treated with nonoperative management. Presacral drainage is sometimes recommended in these cases in order to prevent pelvic sepsis. Presacral drainage and distal rectal washout are more appropriate in high-velocity injuries similar to combat injuries but have less efficacy in civilian settings. Foreign bodies Anorectal foreign bodies are almost always inserted during sexual conduct.(113–117) The most common objects found are sexual implements such as vibrators and dildos (115, 116) (Figure 35.2). Other, less common causes are ingested material, most often bones, or iatrogenic causes such as thermometers and enema tips. (113) A case of a live eel inserted into the anus as a folk remedy for constipation has been reported, in which the eel migrated proximally and was found biting the perforated splenic flexure.(118) The patient presented with peritonitis, which led the clinicians to note “the shadow of an eel on abdominal radiograph”, confirming the diagnosis. There is a predominance of males, ranging from 93–100% in the largest series.(114–116, 119) Goals of initial assessment are to create an atmosphere that allows the patient to give a detailed history, to recognize the potential of rape or assault, and to recognize signs of perforation that require more urgent therapy. Multiple-view plain radiographs should be obtained. Plain films will help localize the object, although rubber will not be apparent on radiography. Free air or obvious perforation can be ruled out. Patients with signs and symptoms of obstruction or perforation should have basic labs drawn, intravenous fluids initiated, antibiotics started and proceed to urgent laparotomy with no further attempt at removal of the object.(117) A perforation should be treated as any traumatic rectal injury, with removal of the foreign body, which will be discussed subsequently.

colorectal trauma The majority of rectal foreign bodies can be removed at the bedside, which is successful in 60–75% of cases.(114, 115, 119) An attempt at bedside extraction is reasonable in patients without signs of peritonitis.(113–115, 119) Sedation and local anesthesia can assist with relaxation and extraction, and an awake patient can be asked to perform a valsalva maneuver. If these maneuvers are unsuccessful, a stable patient can be admitted and observed for 12 hours; during this time the object will often descend into the rectum.(114) Foreign bodies removed nonoperatively require a postprocedure sigmoidoscopy to assess the viability of the rectum and rule out perforation.(113–117, 119) Operative removal can be accomplished with local, regional, or general anesthesia. Either the lithotomy or prone position can be used, but one advantage of lithotomy is that pressure can be applied to the abdomen to move the object distally.(117) Retractors can be placed and the anus dilated. Obstetric forceps and balloon-tipped catheters are commonly employed.(113–117, 119) Balloon-tipped catheters are useful in the case of jars or containers that are positioned with the mouth facing proximally, where the suction generated can prevent removal. The passage of a Foley catheter past the object can serve to break the suction and can be used to aid in extraction.(113) Rarely, laparotomy is required (0–6% of cases).(114, 115, 119) Attempts should be made at distally displacing the object without entering the bowel. If this is unsuccessful, an enterotomy can be made through which the object can be removed.(117, 119) Even more uncommonly, a lateral sphincterotomy may be required. Lake and colleagues (119) performed a recent review of 93 retained colorectal foreign bodies in 87 patients to determine predictors of operative intervention. Two patients (2%) presented with signs of peritonitis and were taken to the operating room. Seventy five percent of attempts at bedside extraction were successful. Of 23 cases requiring operative management, 6 required laparotomy and 5 (6%) required creation of a colotomy. Size of object (greater than 10 cm) and time to presentation (greater than 48 hours) were not associated with an increase in operative intervention. Only location in the sigmoid was predictive of failure of nonoperative management (55% versus 24%, p = 0.04), with an associated OR of 2.25. Anal sphincter and perineal injury Anal sphincter injury Anal sphincter function is extremely complex, and a full discussion is outside the scope of this discussion. Anal sphincter trauma is highly unusual due to its protected anatomic location and abundant blood supply (113). The most common cause of anal sphincter injury is obstetric trauma, followed by sequelae of anorectal operations, and uncommonly by etiologies similar to those causing rectal injuries.(113, 120) Stapling procedures such as for hemorrhoidectomy have been shown to cause anal sphincter injuries as well.(113) Life-threatening injuries should be addressed first in trauma patients, particularly massive, complex perineal injury (discussed subsequently). In a comprehensive review, Hellinger (113) outlines the initial management of anal sphincter injury. As mentioned, documentation of the extent and nature of the sphincter

injury is imperative. Superficial injuries can be debrided and repaired without proximal diversion and minimal injury isolated to the internal sphincter can be left unrepaired. Destructive injury requires diversion following the same principles as rectal injury. In most cases primary repair should be undertaken, commonly in an end-to-end or overlapping fashion. Overlapping repair is accomplished by dissecting out the sphincter muscles and wrapping them anteriorly around the anus. Although overlapping repair increases the surface area of muscular apposition, this repair is difficult to achieve without tension in the acute setting, and thus end-to-end repair may be the principal option in the setting of acute trauma.(113, 120) Other techniques for repair include muscle transpositions (e.g. gracilis or gluteal) and artificial sphincters.(113,120) However, these procedures are best undertaken in the delayed setting and should be performed by surgeons with extensive experience. For example, graciloplasty for fecal incontinence has been shown in several large series to have success rates of 60–66% by various measures (121–123), but infectious complications in 34–39% of patients and donor-site morbidity (pain, paresthesias) have been reported in 22–72%.(121, 123) Artificial anal sphincters have been associated with success rates of 75–98% by various measures, but infection rates range from 13–34%, erosions from 8–21%, explants in 19–37%, and revisionary procedures in 26–45%.(124, 125) In the long-term, sphincter repairs tend to degenerate (120), with rates in the elective population ranging between 2.8–10%. (126, 127) It is important to arrange appropriate follow-up for the assessment of anal function in these patients. Physical exam, myography, manometry, and contrast studies are all routinely employed to assess sphincter function.(113) In addition, endoscopic ultrasound has been shown to be a useful adjunct to visualizing the anal sphincters and predicting defects. A sensitivity of 100% and specificity ranging from 83–100% has been reported when compared to intraoperative findings in elective operations for fecal incontinence.(128, 129) Delayed repair has been shown to have good results in approximately 70% of patients with fecal incontinence due to nonobstetric trauma.(130) Complex perineal injury Kudsk and Hanna (131) have published a complete review of complex perineal injuries, describing a 15-year experience in the comprehensive care of these patients. Figures 35.3a–3c illustrate complex perineal injury. The authors demonstrate the synthesis of the principles of ATLS, damage control, and distal rectal injury required to manage these potentially devastating injuries. Their review included only those patients with evidence of severe degloving (25 total) and the reported mortality was 24% during the first 2 hours of admission. Two additional patients died for reasons unrelated to their perineal injury, for an overall mortality of 32%. Their review of the literature revealed similar mortality rates. Roughly half of the patients were pedestrians hit by cars, one-third were involved in motor vehicle crashes, and the remainder sustained industrial accidents. The second most common cause of mortality after exsanguinating hemorrhage is pelvic sepsis. The authors’ review of the literature revealed a 21–25% death rate from this cause. For

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improved outcomes in colon and rectal surgery

Figure 35.3c  Pelvic fracture associated with complex perineal injury.

Figure 35.3b  CT scan of complex perineal injury. Note the large soft-tissue defect.

authors emphasize that in complex pelvic injuries, lower extremity central access is contraindicated in that it may contribute to further hemorrhage by delivering fluids and blood products directly into the abdominal cavity through lacerated vessels. Access above the diaphragm is recommended. Laparotomy should be performed and intraabdominal injuries addressed. Early pelvic fixation and hemorrhage control should proceed by packing, direct ligation or clamping, and angiography as necessary. The lithotomy position is essential to appropriate exposure. Associated genitourinary injuries should be addressed. Debridement should continue only in the absence of refractory hemorrhage and the patient should be returned to the ICU for further resuscitation before prolonged operative interventions. Following stabilization, fecal diversion should be undertaken early. Aggressive debridement and irrigation should be undertaken with frequent return trips to the operating room. Kudsk and Hanna report an average of 8 trips to the operating room using pulse-lavage before closure or coverage was attempted. These principles are similar to the management of Fournier’s gangrene. Enteral feeding should be initiated as early as possible. In the delayed setting, coverage can be achieved with skin grafts and muscle flaps as indicated. Using these techniques, the authors were able to discharge 17 of 19 patients (89%) to home. Feeding jejunostomies were placed in 6 patients and enteral nutrition was initiated in all 6 within 48 hours.

example, Maull et al. (132), reported a 25% mortality due to pelvic sepsis in their series. Kudsk and Hanna report a 21% pelvic sepsis rate but no mortality, which they attribute to their aggressive, multisystem approach as described. Immediate assessment of the ABCs, intravenous access, and limited radiographic imaging are the initial steps. In cases of severe injury resuscitation should occur in the operating room. The most serious and most common associated injury was severe complex pelvic fracture, which occurred 74% of the time (Figure 35.3c). The

Summary Anal sphincter and complex perineal injuries are uncommon in civilian settings. Life-threatening hemorrhage and pelvic fracture are the first concerns. Documentation of the extent of sphincter injury is imperative. Genitourinary and rectal injuries should be suspected until ruled out by careful investigation. Primary repair of sphincter injury should be undertaken if feasible. Referral is recommended for cases where complex repair is required. Follow-up is important for assessment of long-term function, as

Figure 35.3a  Complex perineal injury. The patient was run over by heavy roadrepair equipment. The patient also sustained urethral injury, sigmoid colon injury, and severe pelvic fracture.

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colorectal trauma functional deterioration is common after repair. Fecal diversion may be necessary in cases of massive injury. The primary concern initially is hemorrhage control, while infection and nutrition are more important in the next several days. In the longer-term, tissue coverage and functional issues become more important. With aggressive, comprehensive management, the majority of patients have good outcomes. References    1. Yaw PB, Smith RN, Glover JL. Eight years experience with civilian injuries of the colon. Surg Gynecol Obstet 1977; 145: 203–5.    2. Perry WB, Brooks JP, Muskat PC. The history of military colorectal trauma management. Semin Colon Rectal Surg 2002; 15: 70–9.    3. LoCicero J, Tajima T, Drapanas T. A half-century of experience in the management of colon injuries: Changing concepts. J Trauma 1975; 16: 575–9.    4. Ogilvie WH. Abdominal wounds in the Western desert. Surg Gynecol Obstet 1944; 78: 225–38.    5. Singer MA, Nelson RL. Primary repair of penetrating colon injuries: A systematic review. Dis Colon Rectum 2002; 45: 1579–87.    6. Burch JM, Brock JC, Gevirtzman L et al. The injured colon. Ann Surg 1986; 203: 701–11.    7. Steichen FM, Ravitch MM. Contemporary stapling instruments and basic mechanical suture techniques. Surg Clin N Am 1984; 64: 425–40.    8. Curran TJ, Borzotta AP. Complication of primary repair of colon injury: Literature review of 2964 cases. Am J Surg 1999; 177: 42–7.    9. Stone HH, Fabian TC. Management of perforating colon trauma: Randomization between primary closure and exteriorization. Ann Surg 1979; 190: 430–5.   10. Eshraghi N, Mullins RJ, Mayberry JC et al. Surveyed opinion of American trauma surgeons in management of colon injuries. J Trauma 1998; 44: 93–7.   11. Pezim ME, Vestrup JA. Canadian attitudes toward use of primary repair in management of colon trauma. Dis Colon Rectum 1996; 39: 40–4.   12. Demetriades D, Velmahos G, Cornwell E et al. Selective nonoperative management of gunshot wounds to the anterior abdomen. Arch Surg 1997; 132: 178–83.   13. Burch JM, Martin RR, Richardson RJ et al. Evolution of the treatment of the injured colon in the 1980s. Arch Surg 1991; 126: 979–84.   14. Chappuis CW, Frey DJ, Dietzen CD et al. Management of penetrating colon injuries: A prospective randomized trial. Ann Surg 1991; 213: 492–7.   15. Adkins RB, Zirkle PK, Waterhouse G. Penetrating colon trauma. J Trauma 1984; 24: 491–9.   16. Flint LM, Vitale GC, Richardson JD, Polk HC. The injured colon. Ann Surg 1981; 193: 619–23.   17. Watts DD, Fahkry SM. Incidence of hollow viscus injury in blunt trauma: An analysis from 2,75,557 trauma admissions form the EAST multi-institutional trial. J Trauma 2003; 54: 289–94.

  18. Ricciardi R, Paterson CA, Islam S et al. Independent predictors of morbidity and mortality in blunt colon trauma. Am Surg 2004; 70: 75–9.   19. Ross SE, Cobean RA, Hoyt DB et al. Blunt colonic injury—a multicenter review. J Trauma 1992; 33: 379–84.   20. Stewart RM, Rosenthal D. Colorectal Trauma. In: Corman, M, ed. Colon and Rectal Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 2005: 427–49.   21. Nelson R, Singer M. Primary repair for penetrating colon injuries. Cochrane Database of Syst Rev 2003; 3: CD002247   22. Singer MA, Nelson RL. Primary repair of penetrating colon injuries. Dis Colon Rectum 2002; 45: 1579–87.   23. Sasaki LS, Allaben RD, Golwala R, Mittal VK. Primary repair of colon injuries: A prospective, randomized study. J Trauma 1995; 39: 895–901.   24. Gonzalez RP, Merlotti GJ, Holevar MR. Colostomy in penetrating colon injury: Is it necessary? J Trauma 1996; 41: 271–5.   25. Gonzalez RP, Falimirski ME, Holevar MR. Further evaluation of colostomy in penetrating colon injury. Am Surg 2000; 66: 342–7.   26. Kamwendo NY, Modiba MCM, Matlala NS, Becker PJ. Randomized Clinical trial to determine if delay from time of penetrating colon injury precludes primary repair. Br J Surg 2002; 89: 993–8.   27. Demetriades D, Murray JA, Chan L et al. Penetrating colon injuries requiring resection: Diversion or primary anastomosis? An AAST prospective multicenter study. J Trauma 2001; 50: 765–75.   28. Schreiber MA. Damage control surgery. Crit Care Clin 2004; 20: 101–18.   29. Lee JC, Peitzman AB. Damage control laparotomy Curr Opin Crit Care 2006; 12: 346–50.   30. Demetriades D, Salim A. Colon and rectal trauma and rectal foreign bodies. In: Wolff BG, Fleshman JW, Beck DE, et al eds. The ASCRS Textbook of Colon and Rectal Surgery. New York, NY:Springer, 2008: 322–34.   31. Sokolove PE, Kuppermann N, Holmes JF et al. Association between the “Seat Belt Sign” and intraabdominal injury in children with blunt torso trauma. Acad Emer Med 2005; 12: 808–13.   32. LeGay DA, Petrie DP, Alexander DI et al. Flexion-distraction injuries of the lumbar spine and associated abdominal trauma.J Trauma 1990; 30(4): 436–44.   33. Hoff WS, Holevar M, Nagy KK et al. Practice Management Guidelines for the evaluation of blunt abdominal trauma, EAST Practice Management Guidelines Work Group. J Trauma 2002; 53: 602–15.   34. Otomo Y, Henmi H, Mashiko K et al. New diagnostic peritoneal lavage criteria for diagnosis of intestinal injury. J Trauma 1998; 44: 991–9.   35. Liu M, Lee CH, P’eng FK. Prospective comparison of diagnostic peritoneal lavage, computed tomographic scanning, and ultrasonography for the diagnosis of blunt abdominal trauma. J Trauma 1993; 35: 267–70.   36. Boulanger BR, Brenneman FD, McLellan BA et al. A prospective study of emergent abdominal sonography after blunt trauma. J Trauma 1995; 39: 325–30.

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  56. Johnson JW, Gracias VH, Schwab CW et al. Evolution in damage control surgery for exsanguinating penetrating abdominal injury. J Trauma 2001; 51: 261–71.   57. Miller PR, Fabian TC, Croce MA et al. Improving outcomes following penetrating colon wounds: Application of a clinical pathway. Ann Surg 2002; 235: 775–81.   58. Fahkry SM, Watts DD, Luchette FA et al. Current diagnostic approaches lack sensitivity in the diagnosis of perforated blunt small bowel injury: analysis from 275,557 trauma admissions from the EAST multi-institutional HVI trial. J Trauma 2003; 54: 295–306.   59. Fahkry SM, Brownstein M, Oller D et al. Relatively short diagnostic delays (<8 hrs) produce morbidity and mortality in blunt small bowel injury: an analysis of time to operative intervention in 198 patients from a multicenter experience. J Trauma 2000; 48: 408–15.   60. Williams MD, Watts D, Fakhry S et al. Colon Injury after Blunt Abdominal Trauma: Results of the EAST Multiinstitutional Hollow Viscus Injury Study.J trauma 2003; 55: 906–12.   61. Dauterive AH, Flancbaum L, Cox EF. Blunt intestinal trauma: A modern-day review. Ann Surg 1985; 201: 198–203.   62. Ross SE, Cobean RA, Hoyt DB et al. Blunt Colonic Injury – A Multicenter Review. J Trauma 1992; 33: 379–84.   63. Nance ML, Peden GW, Schwab CW et al. Solid viscus injury predicts major hollow viscus injury in blunt abdominal trauma. J Trauma 1997; 43: 618–23.   64. Yegiyants S, Abou-Lahoud G, Taylor E. The management of blunt abdominal trauma patients with computed tomography scan findings of free peritoneal fluid and no evidence of solid organ injury. Am Surg 2006; 72: 943–6.   65. Hughes TMD, Elton C. The pathophysiology and management of bowel and mesenteric injuries due to blunt trauma. Injury 2002; 33: 295–302.   66. Parks SE, Hastings PR. Complications of colostomy closure. Am J Surg 1985; 149: 672–5.   67. Bulger EM, McMahon K, Jurkovich GJ. The morbidity of penetrating colon injury. Injury 2003; 34: 41–6.   68. Berne JD, Velmahos GC, Chan LS, Asensio JA, Demetriades D. The high morbidity of colostomy closure after trauma: Further support for the primary repair of colon injuries. Surgery 1998; 123: 157–64.   69. PokornyH, Herkner H, Jakesz R, Herbst F. Mortality and complications after stoma closure. Arch Surg 2005; 140: 956–60.   70. Dente CJ, Tyburski J, Wilson RF et al. Ostomy as a risk factor for posttraumatic infection in penetrating colonic injuries: Univariate and multivariate analyses. J Trauma 2000; 49: 628–37.   71. Fabian TC. Infection in penetrating abdominal trauma: risk factors and preventive antibiotics. Am Surg 2002; 68: 29–35.   72. Hudolin T, Hudolin I. The role of primary repair for colonic injuries in wartime. Br J Surg 2005; 92: 643–7.   73. Steele SR, Wolcott KE, Mullenix PS et al. Colon and rectal injuries during Operation Iraqi Freedom: Are there any changing trends in management or outcome? Dis Colon Rectum 2006; 50: 870–7.

colorectal trauma   74. Welling DR, Hutton JE, Minken SL, Place RJ, Burris DG. Diversion defended—military colon trauma. J Trauma 2008; 64: 1119–22.   75. Duncan JE, Corwin CH, Sweeney WB et al. Management of colorectal injuries during Operation Iraqi Freedom: Patterns of stoma usage. J Trauma 2008; 64: 1043–7.   76. American College of Surgeons Committee on Trauma, eds. Advanced Trauma Life Support Course, 7th ed. Chicago, Ill: American College of Surgeons; 2004.   77. Kurz A, Sessler DI, Lenhardt R. Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. Study of Wound Infection and Temperature Group. N Engl J Med 1996; 9: 1209–15.   78. Van den Berghe G, Wouters P, Weekers F et al. Intensive insulin therapy in the critically ill patients. N Engl J Med. 2001; 345: 1359–67.   79. Dunne JR, Riddle MS, Danko J, Hayden R, Petersen K. Blood transfusion is associated with infection and increased resource utilization in combat casualties. Am Surg. 2006; 72: 619–25.   80. Taylor RW, Manganaro L, O’Brien J et al. Impact of allogenic packed red blood cell transfusion on nosocomial infection rates in the critically ill patient. Crit Care Med 2002; 30: 2249–54.   81. Taylor RW, O’Brien J, Trottier SJ et al. Red blood cell transfusions and nosocomial infections in critically ill patients. Crit Care Med 2006; 34: 2302–8.   82. Kudsk KA, Croce MA, Fabian TC et al. Enteral versus parenteral feeding. Effects on septic morbidity after blunt and penetrating abdominal trauma. Ann Surg 1992; 215: 503–13.   83. Moore FA, Moore EE, Jones TN, McCroskey BL, Peterson VM. TEN versus TPN following major abdominal trauma-reduced septic morbidity. J Trauma 1989; 29: 916–23.   84. Moore FA, Moore EE, Kudsk KA et al. Clinical benefits of an immune-enhancing diet for early postinjury enteral feeding. J Trauma 1994; 37: 607–15.   85. Polk HC, Lopez-Mayor JF. Postoperative wound infection: A prospective study of determinant factors and prevention. Surgery 1969; 66: 97–103.   86. Stone HH, Hooper CA, Kolb LD, Geheber CE, Dawkins EJ. Antibiotic prophylaxis in gastric, biliary and colonic surgery. Ann Surg 1976; 184: 443–52.   87. Mazuski JE, Sawyer RG, Nathens AB et al. The Surgical infection society guidelines on antimicrobial therapy for intra-abdominal infections: An executive summary. Surg Infect 2002; 3: 161–73.   88. Bozorgzadeh A, Pizzi WF, Barie PS et al. The duration of antibiotic administration in penetrating abdominal trauma. Am J Surg 1999; 177: 125–31.   89. Cornwell EE, Dougherty WR, Berne TV et al. Duration of antibiotic prophylaxis in high-risk patients with penetrating abdominal trauma: a prospective randomized trial. J Gastrointest Surg 1999; 3: 648–53.   90. Kirton OC, O’Neill PA, Kestner M, Tortella BJ. Perioperative antibiotic use in high-risk penetrating hollow viscus injury: a prospective randomized, double-blind, placebo-control trial of 24 hours versus 5 days. J Trauma 2000; 49: 822–32.

  91. Poret HA, Timothy TC, Croce MA, Bynoe RP, Kudsk KA. Analysis of septic morbidity following gunshot wounds to the colon: The missile is an adjuvant for abscess. J Trauma 1991; 31: 1088–95.   92. Demetriades D, Charalambides D. Gunshot wounds of the colon: Role of retained bullets in sepsis. Br J Surg 1993; 80: 772–3.   93. Sarmiento JM, Yugueros P, Garcia AF, Wolff BG. Bullets and their role in sepsis after colon wounds. World J Surg 1997; 21: 648–52.   94. Edwards DP, Brown D, Watkins PE. Should colon-penetrating small missiles be removed? An experimental study of retrocolic wound tracks. J Invest Surg 1999; 12: 25–9.   95. Flint LM, Voyles CR, Richardson JD, Fry DE. Missile tract infections after transcolonic gunshot wounds. Arch Surg 1978; 113: 727–8.   96. Merlino JI, Reynolds HL. Management of rectal injuries. Semin Colon Rectal Surg 2004; 15: 95–104.   97. Lüning TH, Keemers-Gels ME, Barendregt WB, Tan AC, Rosman C. Colonoscopic perforations: a review of 30,366 patients. Surg Endosc 2007; 21: 1975–7.   98. Gedebou TM, Wong RA, Rappaport WD et al. Clinical presentation and management of iatrogenic colon perforations. Am J Surg 1996; 172: 454–8.   99. Morken JJ, Kraatz JJ, Balcos EG et al. Civilian rectal trauma: A changing perspective. Surgery 1999; 126: 693–700. 100. evy RD, Strauss P, Aladgem D et al. Extraperitoneal rectal gunshot injuries. J Trauma 1995; 38: 273–7. 101. McGrath V, Fabian TC, Croce MA, Minard G, Pritchard FE. Rectal trauma: Management based on anatomic distinctions. Am Surg 1998; 64: 1136–41. 102. Burch JM, Feliciano DV, Mattox KL. Colostomy and drainage for civilian rectal injuries: Is that all? Ann Surg 1989; 209: 600–11. 103. Navsaria PH, Edu S, Nicol AJ. Civilian extraperitoneal rectal gunshot wounds: Surgical management made simpler. World J Surg 2007; 31: 1345–51. 104. Velmahos GC, Gomez H, Falabella A, Demetriades D. Operative management of civilian rectal gunshot wounds: Simpler is better. World J Surg 2000; 24: 114–8. 105. Rubesin SE, Levine MS. Radiologic diagnosis of gastrointestinal perforation. Rad Clin N Am 2003; 41: 1095–115. 106. Navsaria PH, Shaw JM, Zellweger R et al. Diagnostic laparoscopy and diverting sigmoid loop colostomy in the management of civilian extraperitoneal rectal gunshot injuries. Br J Surg 2004; 91: 460–4. 107. Navsaria PH, Graham R, Nicol A. A new approach to extraperitoneal rectal injuries: Laparoscopy and diverting sigmoid colostomy. J Trauma 2001; 51: 532–5. 108. Weinberg JA, Fabian TC, Magnotti LJ et al. Penetrating rectal trauma: Management by anatomic distinction improves outcome. J Trauma 2006; 60: 508–14. 109. Marti MC, Morel P, Rohner A. Traumatic lesions of the rectum. Int J Colorectal Dis 1986; 1: 152–4. 110. Gonzalez RP, Falimirski ME, Holevar MR. The role of presacral drainage in the management of penetrating rectal injuries. J Trauma 1998; 45: 656–61.

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improved outcomes in colon and rectal surgery 111. Gonzalez RP, Phelan H, Hassan M, Ellis N, Rodning CB. Is fecal diversion necessary for nondestructive penetrating extraperitoneal rectal injuries? J Trauma 2006; 61: 815–9. 112. Steinig JP, Boyd CR. Presacral drainage in penetrating extraperitoneal rectal injuries: is it necessary? Am Surg 1996; 62: 765. 113. Hellinger MD. Anal trauma and foreign bodies. Surg Clin N Am 2002; 82: 1253–60. 114. Barone JE, Sohn N, Nealon TF. Perforations and foreign bodies of the rectum: Report of 28 cases. Ann Surg 1976; 184: 601–4. 115. Barone JE, Yee J, Nealon TF. Management of foreign bodies and trauma of the rectum. Surg Gynecol Obstet 1983; 156: 453–7. 116. Busch DB, Starling JR. Rectal foreign bodies: case reports and a comprehensive review of the world’s literature. Surgery 1986; 110: 512–9. 117. Kann BR, Hicks TC. Anorectal foreign bodies: Evaluation and treatment. Semin colon rectal surg 2004; 15: 119–24. 118. Lo SF, Wong SH, Leung LS, Law IC, Yip AWC. Traumatic rectal perforation by an eel. Surgery 2004; 135: 110–1. 119. Lake JP, Essani R, Petrone Pet al. Management of retained colorectal foreign bodies: Predictors of operative intervention. Dis Colon Rectum 2004; 47: 1694–8. 120. Brill SA, Margolin DA. Anal sphincter trauma. Semin Colon Rectal Surg 2004; 15: 90–4. 121. Thornton MJ, Kennedy ML, Lubowski DZ, King DW. Longterm follow-up of dynamic graciloplasty for faecal incontinence. Colorectal Dis 2004; 6: 470–6. 122. Wexner SD, Baeten C, Bailey R et al. Long-term efficacy of dynamic graciloplasty for fecal incontinence. Dis Colon Rectum 2002; 45: 809–18.

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123. Madoff RD, Rosen HR, Baeten CG et al. Safety and efficacy of dynamic muscle plasty for anal incontinence: lessons from a prospective, multicenter trial. Gastroenterology. 1999; 116: 549–56. 124. Wong WD, Congliosi SM, Spencer MP et al. The safety and efficacy of the artificial bowel sphincter for fecal incontinence. Dis Colo Rectum 2002; 45: 1139–53. 125. Devesa JM, Rey A, Hervas PL et al. Artificial anal sphincter: Complications and functional results of a large personal series. Dis Colon Rectum 2002; 45: 1154–63. 126. Rotholtz NA, Bun M, Mauri MV et al. Long-term assessment of fecal incontinence after lateral internal sphincterotomy. Tech Coloproctol 2005; 9: 115–8. 127. Casillas S, Hull TL, Zutchi M et al. Incontinence after a lateral internal sphincterotomy: Are we underestimating it? Dis Colon Rectum 2005; 48: 1193–9. 128. Deen KI, Kumar D, Williams JG, Olliff J, Keighley MRB. Anal sphincter defects: Correlation between endoanal ultrasound and surgery. Ann Surg 1993; 218: 201–5. 129. Meyenberger C, Bertschinger P, Zala GF, Buchmann P. Anal sphincter defects in fecal incontinence: Correlation between endosonography and surgery. Endoscopy 1996; 28: 217–24. 130. Engel AF, Kamm MA, Hawley PR. Civilian war injuries of the perineum and anal sphincters. Br J Surg 1994; 81: 1069–73. 131. Kudsk KA, Hanna MK. Management of complex perineal injuries. World J Surg 2003; 27: 895–900. 132. Maull KI, Sachatello GR, Ernst CB. The deep perineal laceration—an injury frequently associated with open pelvic fractures: A need for aggressive surgical management. J Trauma 1977; 17: 685–96.

36

Urologic complications of colorectal surgery Scott Delacroix Jr and J Christian Winters

Challenging Case A laparoscopic left hemicolectomy was performed for an asymptomatic 2.0 cm sigmoid adenocarcinoma found on screening colonoscopy. Due to her previous three cesarean sections and abdominal hysterectomy with bilateral oopherectomy, she required extensive lysis of adhesions in order to mobilize the left colon. The procedure was uneventful and the patient was discharged home on postoperative day number three. On follow-up at 10 days, patient was doing well except for a new complaint of left “side pain” rated as a 3 out of 10. Management was expectant and patient was scheduled for a follow-up visit. She presented to the emergency room one week later with significant left flank pain and a fever of 102.1. Her WBC count was 21,000 and serum creatinine was 1.2 (preop 0.9). A CT scan of the abdomen and pelvis with and without intravenous contrast was ordered and left hydroureteronephrosis was seen down to the level of the mid-ureter. Case Management The patient was admitted and placed on intravenous antibiotics. Urology was consulted and the patient was taken to the cystoscopy suite where a cystoscopy and retrograde stent placement was attempted but unsuccessful. No contrast was seen beyond the level of the mid-ureter. The patient was taken to the interventional radiology suite where a percutaneous nephrostomy tube was placed. Patient improved clinically over the next 48 hours with IV antibiotics. An anterograde nephrostogram was performed and a 2.0 cm stenotic segment of ureter was visualized in the middle-third of the left ureter. Iatrogenic injury was presumed and treatment options were discussed with the patient. After a full treatment course of antibiotics for her pyelonephritis, the patient underwent a robotic ureteral reimplant with Psoas hitch and ureteral stent placement. Her percutaneous nephrostomy tube was removed 1 week later (as outpatient). The ureteral stent was removed at 4 weeks postoperatively and patient remained asymptomatic thereafter. At 4 months postreimplantation, her serum creatinine was 0.9 and renal ultrasound showed a normal left kidney without evidence of obstruction. urethral injuries The most common urologic injury in surgery is the traumatic foley catheter placement. It is essential to adequately lubricate the entire foley and insert the catheter past the point at which urine is returned into catheter tubing. Inserting the catheter in a male to the inflation port can help prevent urethral injury. The usual preoperative catheter is either a 16 french or 18 french catheter. It is not necessary to inflate the balloon before placement as this will increase the size and decrease the rigidity of the distal aspect of the catheter. If catheter placement is unsuccessful, a trial of passage with an 18 French coude’ tipped foley catheter is appropriate. Patient dehydration secondary to bowel preparation can make it difficult to determine proper placement if one only looks for urine return.

Placement of the entire foley catheter (to port)before inflation will aid in proper placement. If still unsure, usage of a 60 cc catheter tipped syringe to irrigate the bladder can confirm placement before inflation of the balloon. Intraoperative urologic consultation for cystoscopy and foley catheter placement should be performed if the above measures fail. If cystoscopy cannot accurately delineate urethral anatomy, a suprapubic catheter can be placed either through a percutaneous or an open technique. Artificial urinary sphincters (AUS) must be deactivated before insertion of a foley catheter. Deactivation is a different mechanism than the normal operating “on” and “off ” cycling. It is the author’s experience that most patients do not know how to deactivation their AUS beyond the normal cycling mode. This deactivation must be performed before placement of a foley catheter. Either a device representative or urologist can deactivate the sphincter preoperatively as an outpatient or on the day of surgery. A 12 French foley catheter can then be placed with lubrication and care to ensure placement in the bladder before inflation of balloon. Failure to deactivate the AUS can result in erosion of the urinary sphincter by means of pressure necrosis between the foley catheter and sphincter device. Removal of the catheter should be done in standard fashion postoperatively. If unable to obtain urologic consultation before or intraoperatively, a suprapubic catheter can be placed either by open or percutaneous methods. Care must be taken to avoid intraabdominal prosthetic components, which are normally placed below the rectus muscle suprapubically. An inflatable penile prosthesis (IPP) should not pose any additional difficulty in placing a urethral catheter if lubrication and the aforementioned guidelines are adhered. Urethral injuries are associated with extensive rectal neoplasm or any inflammatory processes that alter surgical planes including pelvic radiation. Urethral injuries are usually identified at the time of surgery secondary to identification of the indwelling foley catheter. Repair of a small urethral laceration can be performed with absorbable 3–0 or 4–0 synthetic absorbable suture (SAS) on a tapered needle. If the patient has had prior radiation or there is poor tissue composition, placement of either an omental flap or local tissue flap to support coverage of the repair is recommended. Injuries not identified at surgery can present postoperatively as urine drainage per rectum, pneumaturia, or fecaluria if fistula is present. It can also present as a delayed urethral stricture with difficult voiding and bladder outlet obstruction. A retrograde urethrogram will confirm the presence of a urethral stricture but must be done in the bilateral oblique as well as anterior-posterior views. A retrograde urethrogram (RUG) can be performed by affixing a 14-gauge angiocatheter to a 60 cc syringe filled with standard water-soluble contrast. A RUG should be performed around an indwelling catheter if already in place. If a radiographic enema is performed, watersoluble contrast is preferred as it does not form concretions in the bladder. Spontaneous closure of a urinary fistula is rare but a trial

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improved outcomes in colon and rectal surgery of conservative urinary diversion (foley catheter) for low-grade fistulas is recommended for 4–6 weeks. Urinary fistulas are staged according to location, size, and patient’s history.(1) •• Stage 1—low (<4 cm from the anal verge and non-irradiated) •• Stage 2—high (>4 cm for the anal verge and non-irradiated) •• Stage 3—small (<2 cm irradiated fistula) •• Stage 4—large (>2 cm irradiated fistula) •• Stage 5—large (ischial decubitus fistula) Enteric diversion by means of a diverting colostomy or ileostomy is recommended for Stages 3–5. The choices for repair are diverse and depend on local tissue integrity and staging. It is recommended to place a suprapubic catheter at the time of repair in addition to a foley catheter for maximal drainage.(2) Transanal rectal flap advancement can be used for Stage 1 fistulas or in combination with other techniques for higher stage fistulas.(3) Other techniques described include: •• transanal-transphincteric approach (dorsal lithotomy anterior sphincterotomy).(4) •• York Mason/transphincteric with rectal advancement flap (2, 5, 6) (jack-knife posterior sphincterotomy) •• Perineal approach (Jack knife or dorsal lithotomy).(7, 8) •• Gracillus and Rectus Abdominus Flaps.(9, 10) Surgical selection is based on fistula stage and the experience of the reconstructive surgeon. Higher stage fistulas and recurrences normally require regional flaps and possibly even urinary diversion.(11) Outcomes for surgically corrected rectourethral fistulas are overall favorable with recurrences mostly dependent on stage and appropriate choice in initial surgical treatment. Success rates vary from >90% for low-grade fistulas to 70% for higher-grade fistulas.(1–11) A retrograde urethrogram around foley catheter at 4–6 weeks postoperatively should be performed before urethral catheter removal. Bladder Injuries The location of the bladder within the pelvis and its, close proximity to the sigmoid colon and rectum predisposes the bladder to injury during surgery of the colon and rectum. Iatrogenic injuries to the bladder can be staged as:(12, 13) •• Grade 1 : contusion, intramural hematoma, or partial thickness laceration •• Grade 2: extraperitoneal bladder wall laceration <2 cm •• Grade 3: extraperitoneal >2 cm or intraperitoneal <2 cm bladder laceration •• Grade 4: intraperitoneal bladder wall laceration >2 cm •• Grade 5: intra or extra peritoneal bladder wall laceration extending into the bladder neck or trigone (near ureteral orifice) Risk factors for bladder injury include any process that distorts tissue planes and reduces surgical exposure.(14) This includes adhesions or scarring from prior surgery, radiation, malignant infiltration, chronic inflammation, or infection. Injuries can be apparent

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intraoperatively or present in a delayed fashion. Intra­operative identification of the injury allows for immediate cystorraphy usually in a two layer fashion. In open surgery, the mucosa is closed in a running fashion using a 3–0 SAS suture followed by a seromuscular running suture of 2–0 SAS. The bladder can then be irrigated to ensure a watertight closure. In the laparoscopic setting, a running one layer closure is performed using a 2–0 SAS to close all three layers of the bladder. Care must be taken to ensure closure of the mucosal layer in the laparoscopic one layer technique. Again, the bladder should be irrigated to ensure a watertight closure. Repair can also differ depending on the location of the injury. Anterior and dome injuries can be repaired primarily as above. Posterior injuries involving the trigone or near the ureteral orifices (possible Grade 5) dictate a more thorough inspection of the bladder and an assurance of ureteral integrity before closure. This is done through an anterior cystotomy in the sagittal plane extending down toward the pubic symphisis. This will allow placement of a Balfour or Bookwalter self-retaining retractor and placement of bilateral ureteral open-ended catheters. Giving the patient indigo carmine with Lasix can aid in identification of the ureteral orifices. Closure of the posterior bladder injury can then be done from the bladder lumen—closing the muscular layer first using 2–0 SAS followed by closure of the mucosal layer using 3–0 SAS. The anterior cystotomy is then closed as described above. In cases where neoadjuvant radiotherapy has been used, an interposition of omentum or perivesical fascia is prudent to decrease the risk of fistula formation. A delayed bladder injury will usually manifest in the early postoperative period, especially after removal of foley catheter. The injury can present as drainage from surgical incision; increased output from surgical drain; vaginal leakage; ileus; apparent oliguria; urinary ascites with increasing BUN and serum creatinine secondary to reabsorption of urine through parietal peritoneum—in the case of an unrecognized intraperitoneal injury; pneumaturia or fecaluria in the cases of an enterovesical or colovesical fistula. Delayed urine leaks can be diagnosed radiographically by fluoroscopic cystogram or the CT cystogram.(15) It is important when ordering a CT cystogram that passive filling of the bladder from the upper tracts is not the sole method of bladder opacification. A foley catheter should be placed and the bladder filled in a retrograde fashion with 300–400 cc’s of water-soluble contrast before the scan. The development of a colovesical or enterovesical fistula is a delayed complication of cystotomy.(16–17) Abdominal-pelvic CT scan with oral and/or rectal water-soluble contrast has a greater sensitivity than cystoscopy in diagnosing an enterovesical fistula (Figure 36.1). The most sensitive test to diagnose an enterovesical or colovesical fistula is the poppy seed test.(17) A 1.25-ounce container of poppy seed is mixed into a 12-ounce beverage o r a 6-ounce serving of yogurt and orally ingested by each patient. Urine was visually inspected during 48 hours, during which identification of poppy seed in the urine was a positive confirmatory test for gastrointestinal fistula to the urinary tract. The sensitivity and specificity was 100%.(17) This test does not provide anatomical information as in the case of the abdominalpelvic CT scan but it is a much more cost effective screening test in patients with equivocal symptoms (5 dollars vs. over 600 dollars). (17) When using Barium contrast, it is the authors recommendation to empty the bladder after a fistulae is diagnosed as there have been reports of Barium concretions within the bladder.

urologic complications of colorectal surgery

Figure 36.1  Enterovesical fistula (arrow).

URETERAL INJURIES Injury to the ureter is one of the most common intraoperative urologic injuries in colorectal surgery. The incidence of iatrogenic injury to the ureter is reportedly from 1 to 10%.(18–22) Iatrogenic ureteral injuries are of 4 types: laceration, ligation, devascularization, and thermal or energy related. Optimal treatment is early recognition and repair of any ureteral injury. Anatomy Iatrogenic ureteral injuries in colorectal surgery usually occur in three distinct locations: at the takeoff of the inferior mesenteric artery, where the infundibulopelvic ligament/uterine vessels crosses the pelvic brim, and between the lateral rectal ligaments (Figure 36.2).(23) The course of the ureter begins posterior to the renal artery and continues along the anterior edge of the psoas muscle. The gonadal vessels cross the ureter from lateral to medial in this region. The ureter next passes over the iliac vessels, generally marking the bifurcation of the common iliac into internal and external iliac arteries.(24) Of greatest importance to the surgeon is that arterial branches to the abdominal ureter approach from the medial direction whereas arterial branches to the pelvic ureter approach from the lateral direction.(24) For the abdominal ureter, these branches originate from the renal artery, gonadal artery, abdominal aorta, and common iliac artery. After entering the pelvis, additional small arterial branches may arise from the internal iliac artery or its branches, and also from the middle rectal and vaginal arteries.(24) The ureter will tend to adhere to the peritoneum during its reflection rather than staying adherent to the Psoas muscle and underlying tissue. The ureter can be identified by visualization and by its peristaltic activity. Gentle pressure applied to the ureter will frequently cause peristalsis—termed the Kelly sign. The right ureter is adjacent to the cecum, terminal ileum, and the appendix. The left ureter is related to the descending and sigmoid colon and their mesenteries.

Figure 36.2  Anatomy of the ureter.

Prevention Ureteral catheterization is used to aid in identification of the ureters and to help identify ureteral injury, but catheters do not prevent ureteral injury. The clinical value of prophylactic ureteral catheter placement before 162 laparoscopic segmental left and right colectomies was assessed by Nam et al. There were no complications from placement of ureteral catheters.(18) Postoperative urinary tract infection was not increased. Total operative time was increased by 11.3 minutes. The ureteral catheter group included more difficult cases including patients with Crohn’s disease and diverticulitis. There were no ureteral injuries in any of the one hundred sixty two patients.(18) An earlier study deemed ureteral catheterization necessary in 27.5% of patients when assessed in a standardized retrospective fashion.(22) There were 4 complications presumably due to ureteral catheterization which included renal colic, oliguria, and one case of anuria attributed to ureteral edema after removal of the ureteral catheters.(20, 25) Chahin et al. studied lighted ureteral stents/catheters placed before laparoscopic colectomy in 66 patients.(20) The most common complication was self-limiting hematuria in 98.4% of patients with an average duration of 2.5 days for unilateral stenting and 3.3 days with bilateral stenting. It is the authors’ opinion that the choice for ureteral stenting is a surgeon preference and depends on multiple variables including complexity of case, anatomy, and experience—especially with the laparoscopic approach in a hostile abdomen. With greater experience, iatrogenic injury decreases. In a study by Larach et al., the incidence of conversions due to iatrogenic injuries showed a decline from 7.3% in the early group to 1.4% in the latter experience group.(26) Once again ureteral catheters have not been shown to decrease ureteral injuries but aid in identification of the ureters and any iatrogenic ureteral injury. Ureteral catheters

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improved outcomes in colon and rectal surgery (A)

(B)

Figure 36.3  Ureteroureterostomy. (A) Spatulation of ureteral margins and placement of running locked sutures. Preferred technique. (B) Oblique anastomosis.

can be used to aid in diagnosis of ureteral injury by retrograde injection of methylene blue through the ureteral catheter. They can also be used to place a retrograde wire under fluoroscopic guidance for placement of an indwelling ureteral double-J stent after a ligation/crush injury. Types of Injury Laceration A laceration or transection of the ureter can usually be repaired with primary anastamosis (ureteroureterostomy with spatulated ends), ureteral stent, and placement of a closed suction drain in the area of the repair (Figure 36.3). Ligation If a ligation injury is apparent intraoperativly, the clamp or tie can be removed followed by ureteral stent placement for up to one month. The patient should undergo repeat imaging either with a renal ultrasound or intravenous pyelogram (IVP) at 3 months to ensure a ureteral stricture has not developed. If the injury is not identified until post operatively, a retrograde ureterogram and stent placement or percutaneous nephrostomy tube placement may be needed before surgical correction. Devascularization A devascularization injury will not be evident intraoperatively and results from the sacrifice of the segmental ureteral blood supply. Intraoperativley a devascularized ureter may appear discolored,

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lack peristalsis, and may not bleed at a transected site. The irradiated ureter is especially susceptible to this type of injury, as the normal healthy ureter has numerous collaterals and is very resistant to devascularization, even with extensive dissection. The anatomy of the blood supply to the ureter (as previously described) should be known as the surgeon is carrying his dissection over the pelvic brim. Thermal Thermal injuries will usually present in the early postoperative period with either fistula or stricture formation. These injuries are repaired in the same fashion as above depending on the location of the injury. Many laparoscopic surgeons use alternatives to monopolar dissectors because of the risk of thermal injury and delayed presentation of injuries. Even with these newer technologies, collateral tissue damage can be produced depending on the energy level and duration of exposure. In animal models, use of the ultrasonic dissector (Ethicon or USSC) at a level of 3 for <10 seconds per burst resulted in little to no collateral tissue damage.(27) When using an ultrasonic dissector at levels of 4 or 5, energy time should be reduced to <5 seconds to prevent collateral damage due to spread of thermal.(27) LOCATION DEPENDENT REPAIR OF THE IATROGENIC URETERAL INJURY Repair of the injured ureter does not necessitate open conversion if a urologist is available with advanced laparoscopic skills. The basic principles of a ureteral anastamosis: a tension free anastamosis; well-vascularized spatulated ends anastamosed over an indwelling ureteral stent ; use of an absorbable suture material 4–0 or 5–0; and placement of a closed drain near the area of the repair. Do not use nonabsorbable suture, as stone formation is inherent with these nonabsorbable materials. Proximal One Third The boundaries of the proximal one-third ureter is from the ureteropelvic junction (level of the kidney) to the pelvic brim (sacroiliac joint on KUB). Repairs of injuries to the proximal ureter depend on the length of the damaged segment. Simple spatulated ureteroureterostomy with ureteral stent placement is the preferred method of repair if there is significant length of the uninjured ureter. A nephropexy can be performed to bring the kidney caudad to allow a tension free anastamosis. In cases with long segments of damaged ureters, a bowel interposition with tapered ileum or an apendiceal interposition can be used (Figure 36.4). At specialized centers, autotransplantation with reanastamosis to the iliac vessels, and native more distal ureter can be performed. Middle One Third The preferred technique for mid-ureteral repair is ureteroureterostomy, either laparoscopically or through the open technique. Distal One Third The procedure of choice for the lower one-third ureteral injury is the ureteroneocystotomy. This may be accomplished primarily for very distal ureteral injuries or may require a Psoas hitch or Boari flap for patients with small capacity bladders and injuries near the iliac vessels.(24) Care must be taken to maintain a tension free

urologic complications of colorectal surgery

Figure 36.4  Ureteral replacement by ileum. Left colon retracted medially. Ileum brought through a hiatus in the colonic mesentary. Ileal ureter is in retroperitoneal position.

anastamosis. This can usually be accomplished with a Psoas Hitch (Figure 36.5). The bladder is mobilized by ligating the superior vesical pedicle on the contralateral side of the injury. It is prudent to locate the contralateral ureter and ensure its integrity before this maneuver. The bladder can then be opened through an anterior cystotomy and then secured to the Psoas muscle and tendon using several 0–0 SAS sutures through the seromuscular layer of the bladder. Care must be taken not to include the genitofemoral nerve which is located within the belly of the Psaos muscle. Suture should be placed in a linear fashion inline with the fascicles of the muscle to prevent underlying nerve entrapment. The ureter can then be tunneled by passing a clamp from the lumen through all layers of the bladder and then withdrawn with the distal aspect of the proximal salvaged ureter. The ureter should then be widely spatulated and interrupted mucosal stitches (4–0 SAS) should be used circumferentially to create the neo-orifice. A ureteral stent can also be placed. The anterior cystotomy is then closed as previously described. A closed suction drain and foley catheter is then left in place. The Boari flap is another effective yet more complex method for replacing an extensive loss of the distal and mid-ureter. A flap of the anterior bladder wall is raised in a rectangular fashion and affixed to the Psoas muscle in same fashion as a Psoas hitch. The

Figure 36.5  Psoas bladder hitch. Mobilized bladder being anchored to psoas muscle and the ureter is reimplanted.

ureter is tunneled through the most proximal portion of the flap and a neo-orifice is created as previously described. The bladder flap is then tabularized and closed in a two-layer fashion using running 3–0 SAS to close the mucosa followed by closure of the seromuscular layer using 2–0 SAS (Figure 36.6). The final option is the transureteroureterostomy. The surgeon tunnels the injured ureter under the posterior peritoneum overlying the great vessels. The allows a spatulated end to side anastamosis of the injured ureter to the patient’s native uninjured ureter (Figure 36.7). RENAL INJURIES Direct renal injury is a rare occurrence in colorectal surgery. McAnich et al. have reported that 90% of renal injuries can be managed without nephrectomy.(28) Though this work does not



improved outcomes in colon and rectal surgery (A)

(B)

(C)

Figure 36.6  Boari or bladder flap procedure. (A) Creation of tapered bladder flap, based posteriorly. (B) Submucosal ureteral reimplantation. (C) Closure of bladder flap.

address iatrogenic injuries, the principle of renal salvage should be applied. Every attempt to evaluate the extent of the injury as well as an assessment of the entire genitourinary tract should be done before undertaking repair. A one shot IVP can confirm contralateral renal function. This can be done by giving the patient 2 ml of contrast per kg up to a maximal of 150 ml IV. An on the table KUB is then done 10 minutes later. Simple palpation of the contralateral kidney does not ensure function. The literature is full of anomalous solitary kidneys which were removed necessitating dialysis or transplantation.(29, 30) Pelvic kidneys have an anomalous blood supply generally arising from multiple arteries along the aorta and iliac vessels. A total of 10% are solitary and may easily be taken for a pelvic mass as they are not reniform and have a discoid shape.(23) If caliceal or renal pelvis injury is suspected, intravenous methylene blue or indigo carmine can be administered. Once the injury is well defined, repair can be decided. Minor renal lacerations or penetrating injuries may be repaired primarily with absorbable sutures and retroperitonealized with perinephric fat, omentum, or hemostatic materials. Hilar control is paramount if an attempt at repair is to be performed. If the injury is to the collecting system or renal parenchyma and the ensuing blood loss is able to be managed by pressure and hemostatic agents alone, a ureteral stent and foley catheter can be placed from below and the area drained with a closed suction to prevent urinoma formation. Conservative management is optimal as renorraphy and exploration can lead to unnecessary nephrectomy. If a major vascular injury occurs and the patient’s intraoperative condition permits, every attempt should be made to reestablish vascular integrity. BLADDER DYSFUNCTION The reported incidence of difficulty in reestablishing micturation ranges from 15 to 25% after low anterior resection and up to 50% after abdominoperineal resection.(31) A thorough understanding of the neuroanatomy of the pelvis and the technique of total mesorectal excision (TME) and autonomic nerve preservation (ANP) can enable both local tumor control and preservation of autonomic nerve structures thus reducing the risk of urogenital dysfunction.(34, 35) Favorable oncologic outcomes have been



Figure 36.7  Transureteroureterostomy. Right-to-left, showing retroperitoneal tunnel anterior to the great vessels.

reported for these nerve sparing techniques.(35–39) APR, when performed in accordance with the principles of TME and ANP, ensures the greatest likelihood of resecting all regional disease

urologic complications of colorectal surgery

Figure 36.8  Innervation of lower urinary tract

while preserving both urinary and sexual function.(39) Locally advanced tumors and preoperative chemotherapy and radiation can make identification of the autonomic nerves and plexus more difficult and sometime impossible.(34) The most common sequela from autonomic nerve damage during surgery of the colon and rectum is detrusor denervation and areflexia. This normally requires clean intermittent catheterization, foley catheter placement, or suprapubic tube placement depending on the overall dexterity and functional status of the patient. Damage to the pudendal nerve or its branches from Alcocks canal can result in weakening of the striated urinary sphincter with resultant stress urinary incontinence and intrinsic sphincter deficiency. Detrusor function (bladder contractility) is predominantly mediated by the parasympathetic nervous system, namely the pelvic nerve.(33) These parasympathetic fibers originate from the spinal cord at the S2–S4 level. Pelvic nerve branches are redundant within the pelvis. The main trunks to the bladder and proximal urethra course in the visceral pelvic fascia, also called the posterior endopelvic fascia.(33) These preganglionic autonomic fibers course alongside the superior vesical vasculature to synapse with postganglionic autonomic fibers within the bladder wall. Multiple pelvic preganglionic nerves pass laterally from the pelvic floor over the rectal fascia investments en route medially to the bladder (Figure. 36.8).(33) Sympathetic innervation to the bladder arises at the level of L2–L4 with a presynaptic fiber to the sympathetic ganglion adjacent to the spinal cord. Synapse occurs in the ganglion and a long post ganglionic fibers travels through the pelvis to innervate the bladder. Through different end receptors located within the bladder, the sympathetic component of the autonomic nervous system helps to cause relaxation of the bladder body (compliance for storage) and contraction of the trigone and bladder neck at resting/storage states. Somatic motor innervation to the striated pelvic floor musculature and sphincter arises from the S2–S4 level and travels via the pudendal nerve through Alcocks canal. The perineal branches of the pudendal nerve follow the perineal artery into the superficial pouch to supply the ischiocavernosus, bulbospongiosus, and transverse perinei muscles. Some branches continue anteriorly to supply sensation to the posterior scrotum and perineum.

Additional perineal branches pass deep to the perineal membrane to supply the levator ani and striated urethral spincter.(40) In the study by Junginger on total mesorectal excision (TME), identification of the pelvic autonomic nerves was complete in 72%, partial identification in 10.7%, and not at all in 17.3% of patients.(34) Univariate analysis showed that the case number (experience), gender (males > females), and T stage (T1-2 vs. T3-4) exerted an independent influence on the achievement of complete pelvic nerve identification. In this series of 150 patients with adenocarcinoma of the rectum, identification and preservation of the autonomic nerves was achieved in a majority of patients and led to the prevention of urinary dysfunction (4.5% vs. 38.5%; p < 0.001).(34) Management of the postoperative patient with bladder dysfunction after colorectal surgery includes teaching clean intermittent catheterization (CIC) and having the patient return for full urodynamic evaluation around 2–3 months postoperatively. Urodynamics can be a combination of fluoroscopic pressure/flow studies with EMG tracings and sometimes urethral pressure profiling. It may take up to 6 months for bladder function to return to its new baseline and CIC may be a lifelong therapy. CIC is performed with a 12–14 french low friction catheter every 4–6 hours and the duration can be adjusted based on the storage pressures and bladder capacity at the time of urodynamic evaluation. There are no drugs with acceptable pharmacokinetics and side-effect profiles that have been shown to clinically increase contractility in the bladder. In a meta-analysis, Branagan et al., reviewed the colorectal surgery literature on suprapubic catheter placement followed by voiding trial versus urethral catheter placement and standard trial of voiding postoperatively.(31) They found favorable results for the suprapubic catheter in terms of incidence of urinary tract infection, and a shorter magnitude and duration of pain and discomfort. The ability to simply clamp and unclamp the suprapubic catheter makes management and voiding trials relatively simple especially in patients unable to perform CIC or those at especially high risk for postoperative bladder dysfunction. Suprapubic catheters are particularly useful if autonomic nerves have to be removed during radical pelvic surgery, because normal voiding may be difficult to reestablish and may take several months to recover. In the select patient with voiding dysfunction and delayed recovery, suprapubic catheter placement results in less morbidity and patient discomfort than urethral catheterization.(32) SEXUAL DYSFUNCTION In the urologic community, an emphasis on postoperative sexual function has arisen from studies by Walsh on the anatomic retropubic prostatectomy with preservation of the neurovascular bundles that contribute to erectile function.(41) Most recently, post operative penile rehabilitation is being performed in multiple settings with a theoretical benefit of reducing the time of neuropraxia to the penis and prevention of apoptosis induced atrophy. Although no standardization exists with these rehabilitation programs, patients are very interested and at the authors’ institution this is discussed preoperatively. Sexual dysfunction has long been associated with rectal surgery in both male and female patients. In male patients, erectile dysfunction is reported in 5 to 65% of patients and ejaculatory dysfunction is reported in

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improved outcomes in colon and rectal surgery 14 to 69%.(43) Damage to the sacral splanchnic nerve (parasympathetic) or the hypogastric nerve (sympathetic) during surgery is the propsed mechanism of injury.(43) Sexual dysfunction is a broad term that encompasses failure of arousal, erection, orgasm, ejaculation, and emission. Complaints from patients after radical pelvic surgery are usually mixed. Erection is parasympathetically mediated and is governed by impulses traveling along the nervi ergentes (S2–S4).(41) The pelvic plexus is located retroperitoneally on the lateral surface of the rectum 5–11 cm from the anal verge with its midpoint located at the tip of the seminal vesicles. The preganglionic fibers from the nervi ergentes coalesce on the pelvic wall with contributions from the sympathetic fibers and from the hypogastric plexus (T10–L4). Damage to the sympathetic plexus will result in problems with ejaculation including retrograde ejaculation or anejaculation. In a study by Henderson et al., eighty one women and 99 men that had undergone curative rectal cancer surgery were given a validated sexual function questionnaire.(42) Thirty-two percent of women and 50% of men were sexually active compared with 61% and 91% preoperatively. Twenty-nine percent of women and 49% of men reported that “surgery made their sexual lives worse”. Specific sexual problems in women were libido 41%, arousal 29%, lubrication 56%, orgasm 35%, and dyspareunia 46%. In men complaints were impotence/erectile dysfunction 84%, libido 47%, orgasm difficulty 41%, and ejaculation difficulties 43%. Patients seldom remembered discussing sexual risks preoperatively and were seldom referred or treated for symptoms postoperatively. Sexual dysfunction should be discussed with rectal cancer patients, and when appropriate, efforts to prevent and treat sexual dysfunction should be instituted.(42) In a study of patients by Nam et al., on patients undergoing TME and ANP for rectal carcinoma, factors that most affected postoperative sexual dysfunction were age older than 60 (sexual desire, p = 0.019), time period within 6 months of surgery (erectile function, p = 0.04), and lower rectal cancer (erectile function p = 0.02).(43) In the urologic literature, penile rehabilitation is started at approximately 1 month postoperatively with evidence suggesting that lack of natural erections during this period of time produces cavernosal hypoxia.(44) Prolonged periods of cavernosal hypoxia induce fibrosis, which later increases the incidence of venous leak and thus potentiates long-term or permanent erectile dysfunction In consultation with a urologist, sexual dysfunction in the man can be treated with many different modalities. For erectile dysfunction, oral phosphodiesterase inhibitors, intraurethral vasoactive suppositories, intracavernosal injections, vacuum errection devices, and implantable devices are all options. For ejaculatory dysfunction in a patient desiring pregnancy, semen may be collected from the bladder in the case of retrograde ejaculation. Sympathomimetic agents may also be used. For refractory cases, electro-vibratory ejaculation can be performed at specialized centers. It is important to discuss sexual function with the patient both pre and postoperatively as there are many therapeutic options that have been shown to be very satisfactory for both partners. ARTIFICIAL DEVICES Thousands of artificial urinary sphincters (AUS) and inflatable penile prosthesis (IPP) have been implanted worldwide for the



(A)

(B)

(C)

Figure 36.9  Artificial urinary sphincter (AVS-800); American Medical Systems Inc, Minnetonka, MN. (A) reservoir. (B) cuff. (C) pump.

treatment of stress urinary incontinence and erectile dysfunction, respectively (Figure 36.9). The IPP has one to three components, while the AUS has three components. The three component systems have a reservoir, pump, and cuff or prosthesis that is interconnected with reinforced tubing. These devices are silicone but develop a capsule around them after implantation. The reservoir is typically placed suprapubically in the space of Retzius. One should make every attempt to refrain from entering this capsule and to prevent contamination of these silicone devices. If contamination occurs, either device removal or salvage therapy with copious antibiotic irrigation is recommended, preferably the latter. The risk of device contamination, post operative infection, and damage to the tubing necessitating device removal or reoperation should be discussed with the patient preoperatively. It is the authors practice to be very conservative in patients with AUS, and we recommend all patients have their device de-activated by a urologist familiar with the AUS before placement of a urethral catheter. There are numerous reports of patients “turning off” their own AUS when in reality they only cycle them, followed by urethral catheterization at the time of surgery and the result is a device erosion through the urethra. This is a medico-legal issue that usually can be averted with a preoperative consultation with a urologist. The FDA approved sacral neuromodualtor is the Interstim device manufactured by Medtronic Corp.(45) It is approved for use in patients with refractory urgency and frequency or nonobstructive nonneurogenic urinary retention. A tined lead is placed through the S3 foramen and an implanted generator is placed in a pocket created in the gluteal area/upper hip. The manufacturer recommends against using electrocautery near the generator and to not perform a MRI on any patients with the Interstim device.

urologic complications of colorectal surgery It is the authors practice to turn off the device with a Medtronic supplied magnet before any radical pelvic operation. In small patients, appropriate padding must be applied to the area of the implanted generator. MRI is contraindicated although there has been at least one study to show deactivation of the device before MRI to be safe.(46, 47) REFERENCES   1. Rivera R, Barboglio PG, Hellinger M, Gousse AE. Staging rectourinary fistulas to guide surgical treatment. J Urol 2007; 177: 586–8.   2. Fengler SA, Abcarian H. The York Mason approach to repair of iatrogenic rectourinary fistulae. Am J Surg 1997; 173: 213–7.   3. Dreznik Z, Alper D, Vishne TH, Ramadan E. Rectal flap advancement-a simple and effective approach for the treatment of rectourethral fistula. Colorectal Dis 2003; 5: 53–5.   4. Culkin DJ, Ramsey CE. Urethrorectal fistula: transanal, transsphincteric approach with locally based pedicle interposition flaps. J Urol 2003; 169: 2181–3.   5. Mason AY. Surgical access to the rectum-a transsphincteric exposure. Proc R Soc Med 1970; 63 suppl: 91–4.   6. Crippa A, Dall’oglio MF, Nesrallah HJ et al. The YorkMason technique for recto-urethral fistulas. Clinics 2007; 62: 699–704.   7. Yousseff AH, Fath-Alla M, El-Kassaby AW. Perineal subcutaneous dartos pedicled flap as a new technique for repairing urethrorectal fistula. J Urol 1999; 161: 1498–500.   8. Visser BC, McAninch JW, Welton ML. Rectourethral fistulae: the perineal approach. JACS 2006; 195: 138–43.   9. Zmora O, tulchinsky H, Gur E et al. Gracilis muscle transposition for fistulas between the rectum and urethra or vagina. Dis Colon Rectum 2006; 49(9): 1316–21. 10. Bruce RG, El-Galley RE, Galloway NT et al. Use of rectus abdominis muscle flap for the treatment of complex and refractory urethrovaginal fistulas. J Urol 2000; 163: 1212–5. 11. Elliott SP, McAninch JW, Chi T et al. Management of severe urethral complications of prostate cancer therapy. J Urol 2006; 176; 2508–13. 12. Moore EE, Cogbill TH, Jurkovich GJ et al. Organ injury scaling III: Chest wall, abdominal vascular, ureter, bladder, and urethra. J Trauma 1992; 33: 337–9. 13. Armenakas NA, Pareek G, Fracchia JA. Iatrogenic bladder perforations: longterm followup of 65 patients. JACS 2004; 198: 78–82. 14. Van Goor H. Consequences and complications of peritoneal adhesions. Colorectal Dis 2007; 9(Suppl 2): 25–34. 15. Deck AJ, Shaves S, Talner L, Porter JR. Computerized tomography cystography for the diagnosis of traumatic bladder rupture. J Urol 2000; 164: 43–6. 16. Jarrett TW, Vaughan ED Jr. Accuracy of computerized tomography in the diagnosis of colovesical fistula secondary to diverticular disease. J Urol 1995; 153: 44–6. 17. Kwon EO, Armenakas NA, Scharf SC et al. The poppy seed test for colovesical fistula: big bang, little bucks! J Urol 2008; 179: 1425–7.

18. Nam YS, Wexner SD. Clinical value of prophylactic ureteral stent indwelling during laparoscopic colorectal surgery. J Korean Med Sci 2002; 17: 633–5. 19. Larach SW, Gallagher JT. Complications of laparoscopic surgery for rectal cancer: Avoidance and management. Semin Surg Oncol 2000; 18: 265–8. 20. Chahin F, Dwivedi AJ, Paramesh A et al. The implications of lighted ureteral stenting in laparoscopic colectomy. JSLS 2002; 6: 49–52. 21. Scala A, Huang A, Dowson HM, Rockall TA. Laparoscopic colorectal surgery - results from 200 patients. Colorectal Dis 2007; 9: 701–5. 22. Fry et al. Iatrogenic Ureteral Injury. Arch Surg 1983; 118: 454–7 23. Perlmutter AD, Retik AB, Gauer SB. Anomalies of the upper urinary tract. In Harrison JH, Gittees RF, Perlmutter AD, et al., eds. Campbell’s Urology, 4th ed. Philadelphia: WB Saunders, 1979: 1309–98. 24. Anderson, Kabalin, Cadeddu et al. Surgical anatomy of the Retroperitoneum, Adrenals, Kidneys, and Ureters. 34–37. Campbell-Walsh Urology, Elsevier Inc. 9th Edition; 2007 25. Kyzer S, Gordon PH. The prophylactic use of ureteral catheters during colorectal operations. Am Surg 1994; 60: 212–6. 26. Larach SW, Patankar SK, Ferrara A et al. Complications of laparoscopic colorectal surgery. Analysis and comparison of early vs. latter experience. Dis Colon Rectum 1997; 40: 592–6. 27. Emam TA, Cuschieri A. How safe is high-power ultrasonic dissection. Ann Surg 2003; 237: 186–91. 28. McAninch JW, Carroll PR, Klosterman PW et al. Renal reconstruction after injury. J Urol 1991; 145: 932–7. 29. Granat M, Gordon T, Issaq E, Shabtai M. Accidental puncture of a pelvic kidney: a rare complication of culdocentesis. Am J Obstet Gynecol 1980; 138: 233–5. 30. Zusmer NR Maturo V, Stern M. Pelvic kidney masquerading as adnexal mass. Rev Interam Radiol 1980; 5: 95–6. 31. Branagan GW, Moran BJ. Published evidence favors the use of suprapubic catheters in pelvic colorectal surgery. Dis Colon Rectum 2002; 45: 1104–8. 32. Chaudhri S, Maruthachalam K, Kaiser A et al. Successful voiding after trial without catheter is not synonymous with recovery of bladder function after colorectal surgery. Dis Colon Rectum 2006; 49: 1066–70. 33. Hollabaugh RS Jr, Steiner MS, Sellers KD et al. Neuroanatomy of the pelvis: implications for colonic and rectal resection. Dis Colon Rectum 2000; 43: 1390–7. 34. Junginger T, Kneist W, Heintz A. Influence of identification and preservation of pelvic autonomic nerves in rectal cancer surgery on bladder dysfunction after total mesorectal excision. Dis Colon Rectum 2003; 46: 621–8. 35. Shirouzu K, Ogata Y, Araki Y. Oncologic and functional results of total mesorectal excision and autonomic nervepreserving operation for advanced lower rectal cancer. Dis Colon Rectum 2004; 47:1442–7. 36. Saito N, Koda K, Nobuhiro K et al. Nerve-sparing surgery for advanced rectal cancer patients: special reference to Dukes C patients. World J Surg 1999; 23: 1062–8.

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improved outcomes in colon and rectal surgery 37. Yamakoshi H, Ike H, Oki S et al. Metastasis of rectal cancer to lymph nodes and tissues around the autonomic nerves spared for urinary and sexual function. Dis Colon Rectum 1997; 40: 1079–84. 38. Moriya Y, Sugihara K , Akasu T, Fujita S. Importance of extended lymphadenectomy with lateral node dissection for advanced lower rectal cancer. World J Surg 1997; 21: 728–32. 39. Enker WE, Havenga K, Polyak T et al. Abdominoperineal resection via total mesorectal excision and autonomic nerve preservation for low rectal cancer. World J Surg 1997; 21: 715–20. 40. Brooks. Anatomy for the Lower Urinary Tract and Male Genitalia. 2;p69. Campbell-Walsh Urology, 9th Edition, Elsevier Inc; 2007. 41. Walsh PC, Schlegel PN. Radical pelvic surgery with preservation of sexual function. Ann Surg 1988; 208: 391–400.

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42. Hendren SK, O’Connor BI, Liu M et al. Prevalence of male and female sexual dysfunction is high following surgery for rectal cancer. Ann Surg 2005; 242: 212–23. 43. Kim NK, Aahn TW, Park JK et al. Assessment of sexual and voiding function after total mesorectal excision with pelvic autonomic nerve preservation in males with rectal cancer. Dis Colon Rectum 2002; 45: 1178–85. 44. Raina R, Pahlajani G, Ararwal A, Zippe CD. Early penile rehabilitation following radical prostatectomy: Cleveland clinic experience. Int J Impot Res 2008; 20: 121–6. 45. Interstim Device Trademarked by Medtronic Corp. 46. Holley et al. MRI Following Interstim Therapy. Presentation at SESAUA Annual Meeting; 2007. 47. Elkelini MS, Hassouna MM. Safety of MRI at 1.5 Tesla in Patients with Implanted Sacral Nerve Neurostimulator. Eur Urol 2006; 50: 311–6.

Index

5-Aminosalicylates (5-ASA) 336–7 5-FU 300 Bevacizumab 301 Cetuximab 301 indications for 301 Irinotecan-Containing Regimens 301 with leucovorin 300 with levamisole 300 Oxaliplatin-Containing Regimens 300–1 see also chemotherapy 6-methyl-mercaptopurine (6-MMP) 337–8 6-methylprednisolone 337 6-Thioguanine Nucleotide (6-TGN) 337–8 AAST grades 378 abdominal colectomy ileorectal anastomosis with 322 abdominal CT 377 abdominal discomfort 367 abdominal radiography 97 bowel obstruction and dilatation 97–8 cecal volvulus 99 pneumoperitoneum 97 sigmoid volvulus 98–9 toxic megacolon 98 abdominal surgery 263 functional outcomes 267 oncologic outcomes 263 preoperative evaluation 263–4 surgical technique 264 patient-centered outcomes 267–8 surgical outcomes anastomotic bleeding 265–6 anastomotic complications 264 anastomotic leak 264–5 anastomotic stricture 265 autonomic nerves injury 267 pelvic hemorrhage 266 splenic injury 266–7 ureteral injuries 267 abdominal trauma colostomy closure outcomes of 384 antibiotic therapy 385–6 blunt colon injury 383 diagnosis 376 epidemiology 375 military perspective 384–5 physical exam computed tomography 377 diagnostic peritoneal lavage (DPL) 376 injury scale 377–8 laparoscopy 377 peritoneal sign 376 seat belt sign 376 ultrasound 376–7 preoperative assessment 375–6

retained fragments 386–7 World War I 375 World War II 375 abdominal wall contouring 356–7 caring 356–7 flap dissection 356, 357 abdominoperineal resection (APR) 278 closure, methods of 280–1 complications 281 abscess 281 intraoperativ hemorrhage 281 non-healing wound and perineal sinus 282 perineal wound complications 282 postoperative hemorrhage 281–2 epidemiology 278 evisceration 283 operative technique 278–80 perineal hernia 283 positioning 278 leg positioning 279 preparation 278 risk factors 282–3 carcinoma 282 fecal contamination 282–3 radiation therapy 282 sexual and urinary function 280 treatment 283 abscess 340 absorbable regenerated cellulose 266 ActiconTM Neosphincter device 231 acute anal fissure 200 calcium channel antagonists versus nitrates acute pilonidal disease 216 Adalimumab 338 adhesions 47–9 grading system for bowel 47, 47 adjuvant chemotherapy for T3 302–3 stage II and IV colon cancer 301–2 stage III colon cancer 302 Advanced Trauma Life Support principles 375 adynamic ileus 110 Agency for Healthcare Research and Quality (AHRQ) 164 aging 8 Altmeier procedure 241–2 alvimopan 367 American College of Surgeons (ACS) 3, 164 American Heart Association (AHA) 134 American Joint Committee on Cancer (AJCC) 301 American Society of Anesthesiologists (ASA) 2, 19 classification 2 American Society of Clinical Oncology (ASCO) 164, 165 American Society of Colon and Rectal Surgeons (ASCRS) 14, 15, 27, 164, 200, 251, 253 aminosalicylates 336 anal dilation 207



index anal encirclement 242, 243–4 anal fissure acute 200–1 chronic 201 classification 199 conservative therapy 200 diagnosis 200 pathophysiology 199 posterior and anterior 199 surgery therapy 206–8 see also acute anal fissure; chronic anal fissure anal fistula 174 Crohn’s disease 192 diagnosis 184–5 etiology 183–4 HIV-positive patient 193 incontinence 190–1 non-surgical management 192–3 recurrence 189–90 surgical therapy advancement flap 186–7 anal fistula plug 188–9 extrasphincteric fistulas 186 fibrin glue 187–8 fistulotomy 186 incision and drainage 185–6 seton placement 186 anal fistula plug 188–9 Anal Fistula Plug™ (AFP) 188 anal skin tags 175 anal sphincter 226–7 anal sphincter injury 389 life-threatening injuries 389 anal sphincteroplasty 229 anal stenosis 174, 208–210 anal ultrasonography 91–2 anastomosis 380 anastomotic complications, postoperative 56 bowel preparation , mechanical 58 case management 56 clinical presentation 59–60 considerations 56–7 dehiscence 56 diagnosis 60 diagnosis 64–5 management 60–2 asymptomatic 60–1 colocutaneous fistula 62 leak with associated abscess 61–2 leak without abscess 61 peritonitis 62 omental pedicle 58 operative intervention 62–3 colostomy creation 62 leaking anastomosis @4:exteriorization of 63 @4:leaving, in place 63 @4:repeat anastomosis after resection 63 @4:resection of 62 @4:short and long-term implications of 63 pelvic drains 59 proximal diversion 57–8 radiation 58–9



stricture 63–4 techniques 58 treatment 64–5 anastomotic leak 264, 324 anemia 1 anesthesia 1 awareness 23 local anesthesia 19 Monitored Anesthetic Care (MAC) 20–1 regional anesthesia 21–3 anoderm 172 anorectal foreign bodies bedside extraction 389 initial assessment 388–9 operative removal 389 sexual implements 388 anorectal manometry 117, 364 anorectal physiology tests (ARP) 228–9 limitations of 87 case management 87 anal ultrasonography 91–2 constipation 92 balloon expulsion test 94 biofeedback 94 colonic transit studies 93 defecography 93 MRI 94 small bowel transit 94 electromyography concentric needle 89–90 single fiber 90 surface 90 fecal continence 87 fecal incontinence, investigations for biofeedback 92 electomyography 91 manometry 87–8, 88 ultrasound 92 pudendal nerve terminal motor latency 90, 90 rectal capacity and sensation 89 Recto-Anal inhibitory reflex 89 sphincter pressure measurement 88–89 anorectal sexually transmitted disease 156–7 anorectal varices 175 antegrade colonic enema 233–4 anthraquinones 367 antibiotic prophylaxis 14 antibiotic therapy abdominal trauma 385–6 anti-Saccharomyces cerevisiae mannan antibodies (ASCA) 332 anti-Saccharomyces cerevisiae 327 apocrine sweat glands 221 appendicitis 117 areflexia 401 argon plasma coagulation 306 arteriovenous sinusoids 178 artificial bowel sphincter 231 artificial urinary sphincters (AUS) components 402 traumatic foley catheter placement 395 ASA Closed Claims Project 21 ASCRS see American Society of Colon and Rectal Surgery Aspirin 135

index ATLS principles see Advanced Trauma Life Support principles AUS see artificial urinary sphincters Australian Safety and Efficacy Register of New Interventional Procedures-Surgical 232 autonomic nerves injury 267 AVASTIN® 301 azathioprine (AZA) 337 Babcock clamp 140 bacteremia 22 bacterium Clostridium botulinum see botulinum toxin Bacteroides 386 balloon expulsion test 94, 364 balloon proctography 117 balsalazide 337 barium enema 112–15, 367 Crohn’s disease 114–15 diverticulitis 115 diverticulosis 115 double contrast 112–13 limitations of 113–14 lymphoma 115 single contrast 112–13 ulcerative colitis 114 Bascom II procedure 220 Bascom operation 219 bedside extraction 389 benzodiazepines 133 Bevacizumab (AVASTIN®) 301 biofeedback therapy failure of 368 for constipation 94 for fecal incontinence 92 limitations 92 pelvic floor dyssynergia dyssynergic-type constipation 368 treatment of 367–8 on slow-transit constipation 368 Bioplastique® 233 bispectral index (BIS) 23 bladder dysfunction autonomic nerve structures 400 innervations 401 oncologic outcomes 400–1 postoperative patient clean intermittent catheterization (CIC) 401 resection 400 total mesorectal excision 401 bladder flap see Boari flap bladder injury delayed bladder injury 396 iatrogenic injury stages 396 risk factor 396 two layer technique 396 bleeding complications 69 bleeding 178, 265–6 blunt colon injury (BCI) 383 Boari flap 399 body temperature and oxygenation 28 botulinum toxin (BT) 205 vs nitrates 206 vs placebo 205–6

randomized controlled trials 205 sphincterotomy 206 bowel function adhesions, grading system for 47, 47 preparation 33–4 mechanical 58 status 34 bowel obstruction and dilatation 97–8 Bridgewater 135 brooke ileostomy proctocolectomy with 319–20 budesonide 337 bupivicaine 19 calcium channel antagonists 203–5 vs nitrates 204 vs placebo 203–4 vs sphincterotomy 204 calcium polycarbophil 179 Cancer Care Outcomes Research and Surveillance Consortium” (CanCORS) 165 cardiovascular disease 3–4 functional status, assessment of 4 preoperative cardiac evaluation Goldman risk model 3 Lee index 3 care paths benefits of 80 case management 79 challenges and concerns 83–4 in colon and rectal surgery 79 development of 80–3 fast track surgery 84–5 guidelines 79 implementation of 80–3 institutional experience 83 objectives of 79 outcome measures, defining and improving 80 realistic expectations 84 cathartic colon” 367 caudal anesthetic 21 cecal volvulus 99 Centers of Medicare and Medicaid Services (CMS) 161, 162 central nervous system (CNS) 20, 227 central neuraxial blockade 21–2 caudal 21 contraindications 22 epidural 21–2 heparin 22 spinal 21 cerebrospinal fluid (CSF) 21 cerebrovascular accidents (CVA) 8 Cetuximab (ERBITUX®) 301 Chance fractures” 376 chemotherapy 287, 300, 314 with colorectal cancer 300–1 future directions 303–4 indications and timing 301–3 side effects 303 chlamydia trachomatis infections 157 chronic anal fissure 201 botulinum toxin (BT) 205 vs nitrates 206



index vs placebo 205–6 vs sphincterotomy 206 calcium channel antagonists 203–5 medical therapy 201 nitrates 201–3 randomized controlled trial botulinum toxin 205 calcium channel antagonists 204 complications of 208–10 surgical therapy 206–8 anal dilation 207 refractory fissures 208 sphincterotomy 207–8 chronic constipation see constipation chronic diverticulitis 254 surgical treatment 254 best timing 254 vs medical treatment 254 chronic pilonidal disease surgical therapy 216 see also pilonidal disease Ciprofloxacin 337 cisapride 73 Citrucel® 179 clean intermittent catheterization (CIC) 401 cleft lift procedure 220 Cleveland Clinic Florida 247 Clinical Outcomes of Surgical Therapy (COST) trial 59, 140 Clopidogel 135 Clostridium difficile 103 cocaine 19 Cochrane Database Review 28 Colazal 337 colchicine 367 colectomy 370 colocolic intussusception 115 colon cancer 322 colon injury abdominal injury 376–8 anastomosis 380 diversion 378–80 meta-analyses investigation 380 primary repair 378, 379, 380 arguments of 378 randomized trials investigation 379 resection 379–80 colonic inertia see slow-transit constipation colonic transit studies 362–3 radiopaque marker test 363 scintigraphic technique 363–4 colonic transit studies 93 colonoscopy 132 perforation rage 136 sedation 133 colorectal cancer 105–7 diverticulitis detection and differentiation 105 metastasis 106 postoperative complications 107 recurrence 106–7 staging 105–6 Colorectal Quality Measures 165 colorectal transit 117



colostomy closure outcomes of 384 colostomy 234, 375 colovesical fistula 396 Commission on Cancer (CoC) Joint Quality Measures 165 complex diverticulitis 255 complex perineal injury 389–90 computed tomography 390 pelvic fracture 390 computed tomographic colonography (CTC) 110–12 advanced adenoma 110–11 benefits 111 complications 111 limitations 111–12 optical colonoscopy 112 postoperative surgery 112 technique 111 computed tomography (CT scan) 99 appendix 108 bowel trauma 101–2 cecal volvulus 109 colitides 103–4 colorectal cancer 105–8 contrast enhanced multidector CT 100 diverticulitis 104–5 inflammatory bowel disease (IBD) 102–3 pneumatosis 100 pneumoperitoneum 100–1 sigmoid volvulus 109 small bowel obstruction CT enteroclysis 110 diagnosis and causes 109–10 ischemia 110 paralytic/adynamic ileus 110 tumors 108–9 unenhanced multidector CT 99–100 Condyloma Acuminatum 155 condyloma 155 congestive heart failure 5 conservative therapy 200 acute anal fissure 200 constipation 361 balloon expulsion test 94 biofeedback therapy 367–8 biofeedback 94 colectomy, successful outcomes 370 colonic transit studies 362–4 colonic transit studies 93 complications 370 defecography 93 limitations 93 drugs associated with 362 functional constipation 361 initial evaluation 362 medical condition 361 medical treatment 365–7 high-fiber diet 365 medications 366 stimulant laxatives 367 MRI 94 limitations 94 pelvic floor physiology tests 364 Rome III diagnostic criteria 361

index routine evaluation 362 small bowel transit 94 surgical intervention 368–70 timing 369 treatment 361 Contigen® 233 continent ileostomy 351 proctocolectomy with 320–2 Coronary Artery Revascularization Prophylaxis (CARP) 4 corticosteroids 337 cramping 367 Crohn’s disease after surgery health-related quality of life (HRQL) 344 postoperative occurrence 343 clinical features 331 computed tomography (CT scan) 102 evaluations of blood test 332 double balloon enteroscopy (DBE) 335 imaging techniques 332–5 PET scan 335–6 stool marker 332 fever 331 and indeterminate Colitis 327 medical therapy 336 5-Aminosalicylates (5-ASA) 336–7 antibiotics 337 biologic response modifiers 338 corticosteroids 337 immunomodulators 337–8 postoperative recurrence, prevention of 338–9 nutritional therapy 339 surgical intervention bypass surgery 343 resection 342–3 stricture biopsy 342 strictureplasty 341–2 surgical treatment abscess 340 bleeding 341 indications for 339 obstruction 341 perforation 339–40 perianal crohn’s disease 340–1 toxic megacolon 341 symptoms of 331 cryotherapy 155, 291 CT enteroclysis 110 cyclosporine 338 damage control surgery (DCS) 381–2 damage-control laparotomy 46–7, 47 deep venous thrombosis (DVT) 71–2 defecography 93, 117, 240, 364 in constipation, limitations of 93 scintigraphic 363–4 dehiscence 324–5 delayed bladder injury 396 delayed hemorrhage 135 Delorme’s procedure 241, 242–3 Denonvilliers’ fascia 267 Depositions 151

destructive injury 389 detrusor function 401 devascularization injury 398 diabetes 8 diagnostic laparoscopy 387 diagnostic peritoneal lavage (DPL) 376 dietary modification 178 Dipentum 337 Diprivan 133 diverticular disease immunosuppressed patients 254–5 incidence of 250 intra-operative classification 250 nonoperative therapy 250@ operative therapy 249, 255–7 complications of 257 Hartmann reversal 256–8 postoperative resection 258–9 procedures of 258–9 timing of closure 259 diverticulitis 143–4, 250 acute complicated 253 outcomes 253 recurrence, risk of 253 surgical intervention 253–4 chronic diverticulitis 254 complex diverticulitis 254 diverticulosis 250 acute uncomplicated 251 age 251–2 outcomes 251 progression, of disease 251 recurrence, risk of 252 postoperative surgery 258–9 procedures 258 diverting ostomies 352 Donabedian model 160 double balloon enteroscopy (DBE) 335 doxycycline 157 Duke Activity Status Index 4 duodenum stricture 343 Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography (DECREASE-V) 4 DVT prophylaxis 22 DVT see deep venous thrombosis (DVT) dynamic graciloplasty 231–2 dysplasia 326 E. Coli see Escherichia coli Eastern Cooperative Oncology Group (ECOG) 304 elective colectomy 258 elective colon resections 14 electomyography in fecal incontinence with limitations 91 electrocardiogram 4 preoperative baseline 4 electrolyte 15 electromyography (EMG) 364 concentric needle 89–90 rectal prolapse 239–40 single fiber 90 surface 90 Elsberg syndrome 157



index Emergency Department 249 end ileostomy 351 end ostomies 350–1 endometriosis 115 endorectal advancement flap 340 endoscopic ablation therapy 314 endoscopic ultrasound (EUS) 335 enterovesical fistula 396, 397 EORTC 310 epidural anesthetic 21–2 ERBITUX® 301 erythema 28 erythromycin 73 Escherichia coli 14, 386 evisceration 283 excisional hemorrhoidectomy 169–72 extrasphincteric fistulas 186

flexion distraction injury 376 Flint grade 378 fluoroscopy 112–17 barium enema 112–15 physiologic examinations 117 anorectal manometry 117 balloon proctography 117 colorectal transit 117 defecography 117 water-soluble contrast enema 115–17 focused abdominal sonography for trauma (FAST) 376–7 evaluation 376 FOLFIRI 301 FOLFOX 300 Frykman-Goldberg procedure 245–6 functional constipation 361 see also constipation

fecal bolus 227 fecal contamination 282–3 fecal continence 87 fecal incontinence, surgery for 87, 174 biofeedback 92 limitations 92 electromyography, limitations 91 manometry 87–8, 88 limitations 89 ultrasound, limitations 92 anorectal physiology tests (ARP) 228–9 epidemiology 226 etiology anal sphincter 226 central nervous system 227 fecal bolus 227 rectum 226–7 evaluation historical 227–8 physical 228 severity, assessment of 227 risk factors 227 treatment antegrade colonic enema 233 artificial bowel sphincter 231 biofeedback 229 dynamic graciloplasty 231–2 injectable bulking agents (IBA) 233 medical therapy 229 sacral nerve stimulation 232–3 sphincteroplasty 229–31 fentanyl 21, 133 Ferguson hemorrhoidectomy 170, 171 FFCF trial 310 FiberChoice® 179 Fibercon® 179 fibrin glue 187–8 Fibrin Glue 340 fibrinclot 340 fissures see anal fissures fistula 174, 219, 340 fistula-in-ano carcinoma associated with 193 classifications 184 fistulotomy 186, 340

gabapentin 68 gastrointestinal (GI) bleeding 122 gastrointestinal obstruction 341 gastrointestinal scintigraphy 121–2 Gastrointestinal Tumor Study Group and North Central Cancer Treatment Group 308 Gatrointestinal Stroma Tumors (GIST) 109 German Rectal Cancer Trial 302 glyceryl trinitrate (GTN) 200, 202 Goldman risk model 3 gracilis transposition 341



Hand Assisted Laparoscopic (HAL) Colectomy 255 Harmonic Scalpel® hemorrhoidectomy 172 Harmonic Scalpel® 172 Hartmann colostomy outcomes of 256 reversal 256–7 healthcare 263 Heineke–Mikulicz procedure 341 hemorrhage 134–5, 281 anastomosis 41 delayed bleeding 174 intraoperative 281 intraoperative 44–6 postoperative bleeding 173–4 postoperative 281–2 hemorrhoid anatomy and pathophysiology 178 bleeding 178 classifications 181 clinical evaluation 178 grading system 178 nonoperative therapy for 178 techniques, comparison of 181–2 treatment conservative management 178–9 infrared photocoagulation 181 rubber band ligation 179–80 sclerotherapy 179 hemorrhoidal surgery 168 anatomy/etiology 168–9 clinical evaluation 169 excisional hemorrhoidectomy 169–72 nonexcisional options 169

index postoperative complications anal fistula 174 anal stenosis 174 anal tags 175 constipation and fecal impaction 174 fecal incontinence 174 hemorrhage 173–4 infection 174 mucosal ectropion 174 pain 172 urinary retention 172–3 sagical section and anal cushion 168 special situation anorectal varices 175 postpartum hemorrhoids 175 heparin 22 hepatic artery infusional (HAI) therapy 290–1 hepatic disease 6 hepatic metastasis, chemoembolization of 123 herpes simplex virus (HSV) 156–7 hidradenitis suppurativa 215 diagnosis 222 nonoperative management 222–3 pathophysiology 221–2 surgical management excision 223 high-molecular-weight polyethylene glycol (PEG) 366–7 HIV/AIDS 7 human immunodeficiency virus 156 human papillomavirus (HPV) 155 hydrocortisone cream 155 hyperbaric local anesthetic 21 hyperbaric oxygen 314 hypercoaguable syndromes 9 hypersomolar oral saline laxative 15 hypertonic NaP 15 hypobaric local anesthetics 21 iatrogenic injury 266 iatrogenic perforation 144 iatrogenic ureteral injuries 397 distal one third 398–9 middle one third 398 proximal one third 398 idiopathic hypertrophic subaortic stenosis (IHSS) 22 IFL 301 ileal pouch-anal anastomosis (IPAA) 325, 351 ileal-rectal anastomosis (IRA) 351 ileocolic resection 342 ileocoloc intussusception 110, 115 ileonal pouch procedure abdominal colectomy 322 complications 323–326 controversies 326–7 functional result 323 proctocolectomy 319–23 ileorectal anastomosis with abdominal colectomy 322 ileostomy 352 selective omission 327 ilioinguinal and iliohypogastric nerve block 23 image-guided percutaneous biopsy 123 imaging studies 97

abdominalradiography 97–99 bowel obstruction and dilatation 97–8 cecal volvulus 99 pneumoperitoneum 97 sigmoid volvulus 98–9 toxic megacolon 98 computed tomographic colonography (CTC) 110–12 advanced adenoma 110–11 benefits 111 complications 111 limitations 111–12 optical colonoscopy 112 postoperative surgery 112 technique 111 computed tomography (CT scan) 99 appendix 108 bowel trauma 101–2 cecal volvulus 109 colitides 103–4 colorectal cancer 105–8 contrast enhanced multidector CT 100 diverticulitis 104–5 inflammatory bowel disease (IBD) 102–3 pneumatosis 100 pneumoperitoneum 100–1 sigmoid volvulus 109 small bowel obstruction 109–10 tumors 108–9 unenhanced multidector CT 99–100 fluoroscopy 112–17 barium enema 112–15 physiologic examinations 117 water-soluble contrast enema 115–17 interventional radiology 122–3 chemoembolization of hepatic metastasis 123 gastrointestinal (GI) bleeding 122 image-guided percutaneous biopsy 123 percutaneous abscess drainage (PAD) 122–3 radiofrequency ablation (RFA) 123 magnetic resonance imaging (MRI) 119–20 nuclear medicine imaging gastrointestinal scintigraphy 121–2 positron emission tomography 120–1 ultrasonography 117–19 endoluminal ultrasound’s (EUS) 119 intraoperative ultrasound 119 transabdominal ultrasound 118 imaging techniques in crohn’s disease colonoscopy 334 computed tomography scan 334–5 double balloon enteroscopy (DBE) 335 endoscopic ultrasound (EUS) 335 enema 332 magnetic resonance imaging 335 scintigraphy 336 small bowel series 332 transabdominal ultrasound (US) 334 upper edoscopy 332–3 imiquimod 156 immunocompromise 7 immunomodulators 337–8 immunosuppressed patients 254–5



index impaired sensorium 5 infections 69–70 surgical site 69–70 urinary tract infections 70 inflatable penile prosthesis (IPP) components 402 Infliximab 193, 338 infrared photocoagulation 181 injectable bulking agents 233 injection sclerotherapy 179 interventional radiology 122–3 gastrointestinal (GI) bleeding 122 hepatic metastasis, chemoembolization of 123 image-guided percutaneous biopsy 123 percutaneous abscess drainage (PAD) 122–3 radiofrequency ablation (RFA) 123 intestinal stomas 349 intraabdominal hemorrhage 323–4 intraabdominal infections 29 percutaneous drainage 29 intraoperative anastomosis 33 case management 33 challenges 40–1 adjuvants and drains 41 hemorrhage 41 inadequate anastomotic lumen 40–1 leakage 41 proximal protection 41 preanastomotic considerations bowel preparation 33–4 bowel status 34 exposure 34 obtaining adequate length 35–6 operative principles 33 preoperative discussion and planning 33 staples versus sutures 37 double staple 39 end-to-end 37–9 end-to-side 39–40 side-to-side 39–40 technique 36–7 test 40 types of 37 intraoperative challenges 44 abdominal wall closure 51 adhesive disease 47–9 biologic meshes 52 case management 44 damage control 46–7, 47 hemorrhage 44–6 lesion localization 49–50 preoperative evaluation 44 retention sutures 51 suture material 51 synthetic prostheses 51–2 technique 51 intraoperative positioning lateral decubitus 24 lithotomy 24 nerves, at risk 24 prone 23–4 supine 23 intraoperative radiation therapy (IORT) 287



intraperitoneal anastomoses 29 intrathecal blockade see spinal blockade intravenous antibiotics 15 effect of 15 inulin 179 IPAA 322 Irinotecan 303 IROX 301 ischemia 353 isobaric local anesthetics 21 isosorbide dinitrate (IDN) 200 isosorbide mononitrate (IMN) 200 Ivalalon sponge rectopexy 244, 245 jeep disease 215 Kaposi’s sarcoma 156 Karydakis flap 200 Klebsiella 386 Kock pouch 322 Konsyl® 179 laceration injury 398 lactulose 366 laparoscopic colorectal surgery 140 advantages 140–1 colonoscopic perforation 144 disadvantages 141 diverticulitis 143–4 inflammatory bowel disease ulcerative colitis 142–3 instruments 145 purported benefits 140 rectal prolapse 144 stoma 143 technical considerations 144 treatable conditions colon cancer 141–2 trocar placement 144–5 vascular control 145 laparoscopic intraperitoneal surgery 4 laparoscopic surgery 28 laparoscopy 246, 291–2, 377 lateral decubitus positioning 24 lateral fistula 216–16 Leapfrog Group 160–1 criteria 161 purchasing principles 160–1 Lee index 3 leucovorin 300 levamisole 300 lidocaine 19 life-threatening injuries 389 LigaSure™ Vessel Sealing System 291 LigaSure™ 172 Ligation of Intersphincteric Fistula Tract (LIFT) 189 linaclotide 367 liposuction 357–8 lithotomy 389 positioning 24 litigation injury 398 liver metastasis 289

index adjuvant therapy 291 assessing resectability 289–91 operative approach laparoscopy 291–2 open resection 292 outcomes 292 treatment of 289 local anesthesia 19, 389 drugs 19 perianal block 20 relative potency 19 systemic toxicity 20 loop end stomas 351–2 loop ileostomy 327 loop ostomies 352 loose hair 215 Lovenox® 135 low-molecular weight heparin (LMWH) 22 lubiprostone 367 lung metastasis 292 assessing resectability 293 operative approach 294 outcomes 294–5 treatment of 292 video assisted thoracoscopic surgery (VATS) 294 magnetic resonance imaging (MRI) 94, 119–20 in constipation, limitations of 94 malignancy 326 malnutrition 6–7 mannitol 15 manometry 87–8, 88 for incontinence value and limitations of 89 marsupialization 218 mechanical bowel preparation (MBP) 15, 16 randomized controlled trials 16–17, 28 Meckel’s diverticulum 104 medical legal issues 148 affordable liability insurance, lack of 148–9 documentation chart 150 high-risk areas 149 informed consent 149–50 malpractice suit, anatomy of initial phase 150–1 ploys 150–2 pretrial discovery 151 testing your memory 151 trials 152 physician-patient relationship 149 medical therapy chronic anal fissure 199–6 fecal incontinence 229 melanosis coli 367 meperidine 133 mepivacaine 19 mesh rectopexy 243 mesh sling repair 244 metabolic disease 7 Metamucil® 179 methotrexate 338 Methylcellulose 179

Metronidazole 337 microfibrillar collagen 266 midazolam 133 Milligan-Morgan hemorrhoidectomy 169–70, 171 misoprostol 367 modified abdominoplasty 356–7 flap dissection 356, 357 caring 356–7 Monitored Anesthetic Care (MAC) 20–1 morbid obesity 355–8 preoperative stoma marking 356 preoperative weight loss 356 mucosal ectropion 174 mucosectomy vs. double-stapled technique 326–7 multidector computed tomography (MCDT) 99–110 see also computed tomography National Healthcare Safety Network (NHSN) 27 National Cancer Institute (NCI) 165 National Comprehensive Cancer Network (NCCN) 165, 290 National Initiative on Cancer Care Quality (NICCQ) 164 National Nosocomial Infections Surveillance (NNIS) System 27 National Quality Forum (NQF) 164, 165 National Surgery Quality Improvement Project (NSQIP) 3, 162 National VA Surgical Risk Study (NVASRS) 162 nausea 72 neisseria gonorrhea 157 neoadjuvant chemoradiotherapy 302 tumors 302 nephropexy 398 neurologic system 8–9 Parkinson’s disease 8–9 neutropenic colitis 104 Nichols-Condon antibiotic 14 nifedipine ointment 204 nipple valve slippage manifestations of 322 nitrates 200, 201–3 vs calcium channel antagonists 204 sphincterotomy 203 nitroglycerin (NTG) 200 nitroglycerin transdermal patch 200 NJ 135 node-positive rectal cancer 302–3 neoadjuvant chemoradiotherapy for 302 T3 adjuvant chemotherapy alone for 302–3 nonabsorbable disaccharides 366 nonbladed trocars 145 noncutting Seton 340 nuclear medicine imaging gastrointestinal scintigraphy 121–2 positron emission tomography 120–1 obesity 7–8 olsalazine 337 omentoplasty 283 open abdominal repairs 244 oral antibiotic prophylaxis 28 Oral antibiotics 14 oral lavage 133



index oral preparations 15 polyethylene glycol (PEG) 15 sodium phosphate (NaP) 15 ostomy complications with ischemia 353 morbid obesity 355–8 parastomal hernias 354–5 prolapse 355 retraction 353 skin 353 stenosis 353–4 dissected free 357 preoperative stoma marking 350 psychological impact 349–50 reversal 358 types of 350–3 ostomy necrosis 353 outcome measures 161–5 and quality measures 165 overlapping sphincteroplasty 230 Oxaliplatin 303 pain management 67–8 paralytic ileus 110 parastomal hernias 354–5 parenteral antibiotic prophylaxis 14 Parkinson’s disease 8–9 patient-controlled epidural analgesia (PCEA) 21 pectins 179 pelvic floor dysfunction 361 biofeedback therapy 367–8 and slow-transit constipation 362 pelvic floor physiology tests anorectal manometry 364 balloon expulsion test 364 defecography 364 electromyography (EMG) 364 pelvic hemorrhage 266 pelvic kidneys 400 pelvic nerve 401 pelvic sepsis 29–30, 389–90 manifestations 324 penetrating colon injury damage control surgery (DCS) 381–2 penetrating colon injury 380–1 practice patterns 382 primary repair versus diversion arguments of 378–80 meta-analyses investigation 380 randomized trials investigation 379 penicillin G 157 percutaneous abscess drainage (PAD) 122–3 perianal crohn’s disease elective surgery 340 surgical treatment 340 perineal hernia 283 perineal proctosigmoidectomy 241–2 perineal rectosigmoidectomy 240 perineal sinus 282 perineal wound complications 282



perirectal abscesses Crohn’s disease 192 diagnosis 184–5 etiology 183–4 HIV-positive patient 193 incontinence 190–2 non-surgical management 192–3 recurrence 189–90 surgical therapy advancement flap 186–7 anal fistula plug 188–9 extrasphincteric fistulas 186 fibrin glue 187–8 fistulotomy 186 incision and drainage 185–6 seton placement 186 PET scan see positron emission tomography scan 335–6 phenol sclerotherapy 217 Physician Quality Reporting Initiative (PQRI) 161, 163–4 Physiologic and Operative Severity Score for enUmeration of Mortality and morbidity (POSSUM) 2, 257 pilonidal disease 215 acute disease 216 advanced procedures for 220 Bascom operation 219 chronic disease 216 chronic pilonidal disease 217 diagnosis 215–16 historical perspective 215 limited excision 219 marsupialization 218–19 nonhealing wounds 220 nonsurgical treatment 216–17 phenol sclerotherapy 217 procedures for 217 sacral wound 220 surgery for 219–20 wide local excision 217–18 plain films 97 Plavi® 135 Plavix 8 pneumonia 71 pneumoperitoneum 97 abdominalradiography 97 computed tomography (CT scan) 100–1 podophyllin 155–6 polyethylene glycol (PEG) 15 polyethylene glycol electrolyte lavage solution (PEG-ELS) 366 polypectomy 135 polyvinyl alcohol sponge rectopexy 244, 245 positron emission tomography (PET) scan 120–1, 335–6 positron emission tomography with fluorine 18–labeled fluoro-2deoxy-D-glucose (FDG-PET) 335–6 Post Dural Puncture Headache (PDPH) 22 posterior bladder injury 396 posterior mesh fixation 244 posthemorrhoidectomy pain 172 postoperative complications 67 atelectasis pneumonia 71 prevention 71 bleeding 69 case management 67

index deep venous thrombosis 71–2 infections surgical site 69–70 urinary tract 70 nausea and vomiting 72 pain 67–8 prolonged ileus 72–3 retained foreign bodies 73–5 time out” and sided surgery concerns 75 urinary retention 70–71 postoperative hemorrhage 323–4 postoperative ileus 140 postoperative patient pelvic sepsis 29–30 with sepsis 27 postoperative pneumonia 25 postoperative pulmonary complications (PPCs) 5 postpartum hemorrhoids 175 postpolypectomy bleeding 135 anticoagulant recommendations 135 management of 134 pouch anal fistulas 325 pouch vaginal fistulas 325 pouchitis 322, 326 prednisone 337 premenopausal females 2 preoperative bowel preparation 14 in elective colon resections 14 objectives 14 preoperative cardiac disease 3–4 ACC 4 hypertension 3 preoperative medical condition 1 aging 8 anesthesia consultation 1 cardiovascular disease 3–4 diabetes 8 documentation 3 hepatic disease 6 HIV/AIDS 7 hypercoaguable disorders 9 immuncompromise 7 malnutrition 6–7 metabolic disease 7 neurologic system 8–9 obesity 7 premenopausal females 2 prevent postoperative complications 1 pulmonary disease 5 renal disease 5–6 using scoring systems 2 preoperative risk assessment scoring systems 2 prilocaine 19 Priritis ani 154 causes of 154–5 measures 155 soilage 154 procaine 19 procedure for prolapse and hemorrhoids (PPH) 172, 173 proctectomy fecal contamination 282–3 proctitis 157

proctocolectomy with brooke ileostomy indications 319–20 operative technique 320 outcomes 320 with continent ileostomy operative technique 320 outcomes 320–2 with ileoanal pouch 322 indications 322 operative technique 322–3 outcome 323 prolapse 355 prone positioning 23–4, 389 jack-knife position 21 prophylactic antibiotics 27 prophylactic sigmoid resection 255 pseudodiverticula 114 pseudomonal species 386 Psoas hitch 399 psuedomembranous colitis 103–4 psychiatric evaluation 23 psyllium 179 PTQ implantsTM 233 pulmonary disease 5 American College of Physicians 5 risk factors 5 purse-string stitch, repair of 38–9, 38 quality measures assessment and improvement, in surgery 159 process measures 161, 162, 163–4 structural measures 160–1 definition 159 Donabedian model 160 Leapfrog Group 160–1 criteria 161 purchasing principles 160–1 and outcome measures 165 radiation therapy 306 acute adverse effects 310–11 adjuvant treatment 307–10 chronic late adverse effect 312–13 chronic rectal effects 313–14 neoadjuvant treatment 308 surgical complications 311–12 radiofrequency ablation (RFA) 123 randomized controlled trials 16 mechanical bowel preparation (MBP) 15, 16 rapid plasma regain (RPR) 157 rectal carcinoma staging 306 rectal injury classic components of 387 foreign bodies 388 high-risk factors of 387 intraperitoneal injury 387–8 management of fecal diversion 387 modified steps 388 traditional steps 388



index rectal procidentia 239 rectal prolapse abdominal fixation procedures 144 anal physiology 239–40 defecography 240 evaluation and investigations 239 operative procedures 240–1 anal encirclement 243–4 Delorme’s procedure 242–3 laparoscopic approach 246 mesh sling repair 244 open abdominal repairs 244 perineal proctosigmoidectomy 241 perineal repairs 241 posterior mesh fixation 244 resection rectopexy 245–6 suture rectopexy 244–5 physical exam 239 recurrent prolapse 246–7 surgery for Recto-Anal inhibitory reflex (RAIR) 89 recurrent rectal cancer 286 assessing resectability 286 chemotherapy and radiation 287 operative treatment 287, 289 outcomes 288 refractory fissures 208 regional anesthesia 21–3 central neuraxial blockade 21–2 ilioinguinal and iliohypogastric nerve block 23 Transversus Abdominis Plane (TAP) block 22–3 renal disease 5–6 resection 379–80 resection rectopexy 245–6 restorative proctocolectomy 327 Cesarean sections 323 with ileoanal pouch 322 indications 322 operative technique 322–3 outcomes 323 retrograde urethrogram (RUG) 395 Rhomboid flap 200 Ripstein procedure 243, 244 RTOG 310 rubber band ligation 179–80 sacral foramina 232 sacral nerve stimulation (SNS) 232 efficacy of 232 functional result 233 indications for 232–3 selection criteria 232 sacral neuromodualtor 402 sacral wound healing 221 sacrococcygeal fascia 217, 220, 221 Sanofi-Aventic 135 scintigraphy 336 sclerotherapy 179 seat belt sign” 376 secretagogues 367



sedation 389 senna 367 sepsis 27 intraabdominal infections 28 pelvic sepsis 29–30 postoperative patient 27 surgical site infection 27–8 seton placement 186 severe diarrhea postoperative radiation therapy 310 sexual dysfunction 323, 401–2 erection 402 male and female patients 401 modalities 402 short-chain fatty acids (SCFA) 314 sigmoid volvulus 98–9, 115 skin infection 27 skin 27 functions 27 wound infection 27 slow-transit constipation 361 and pelvic floor dysfunction 362 total abdominal colectomy and ileorectal anastamosis 369 small bowel crohn’s disease imaging techniques 336 small bowel obstruction small bowel transit constipation 94 sodium phosphate (NaP) 15, 133 dosages 15 soft tissue infection 27 sorbitol 366 sphincteroplasty fecal incontinence 229–30 functional result follow-up 230 sphincterotomy 207 vs botulinum toxin (BT) 206 vs calcium antagonists 204 nitrates 203 spinal blockade 21 spirochete 157 splenic injury 266 recognition 266 SSI see surgical site infection (SSI) Staphylococcus aureus 222 staple anastomosis vs suture 37 double staple 39 double staple 39 double staple 39 double staple 39 end-to-end 37–9 end-to-side 39–40 vs sutures 37 stapled anoplasty 170, 173 stenosis 354 Z-plasty repair 352 stimulant laxatives 367 side effects 367 stoma necrosis 353–4 stomal retraction 357–8

index stomas 143 living with 349–50 meshing 354 necrosis conservative management 354 site marking 350 types diverting ostomies 352 end ostomies 350–2 loop colostomy 352 stricture biopsy 342 stricture 265 strictureplasty 341–2 indication and contraindication 342 sucralfate 314 sulfasalazine 336 superficial injury 389 supine positioning 23 suprapubic catheter 401 Surgical Care Improvement Project (SCIP) 19, 161, 162 common and preventable complications 25 process and outcome measures 25 Surgical Infection Prevention Guideline Writers Workgroup (SIPGWW) 14 surgical site infection (SSI) 27–8, 69–70 laparoscopic surgery 28 prophylactic antibiotics 27 scaling 27 skin and soft tissue infection 27 surgical therapy abdominal surgery 264, 265–7 advancement flap 186–7 anal fistula plug 188–9 anal fistula 183, 186–7 chronic anal fissure 201–8 chronic diverticulitis 254 chronic pilonidal disease 216 Crohn’s disease 339–41 extrasphincteric fistulas 186 fecal incontinence 226 fibrin glue 187–8 fistulotomy 186 hidradenitis suppurativa 215 incision and drainage 185–6 perianal crohn’s disease 340 perirectal abscess 183, 185–9 pilonidal disease 217 seton placement 186 on stoma 354 Surgisis® 188 suture anastomosis vs staple 37 double staple 39 end-to-end 37–9 side-to-side 39–40 vs sutures 37 suture rectopexy 244–5 laparoscopy 246 Swedish Rectal Cancer Trial 302 syphilis 157 systemic inflammatory response syndrome (SIRS) 27

Teflon® 233 Tegaserod 367 temperature and oxygenation 28 test-tube test” 353 tetracaine 19 therapeutic heparin 22 thermal injury 398 Thiersch repair 243–4 thiopurine methyltransferase (TPMT) 337–8 thrombin 266 tissue oxygenation 28 TissueLink Endo SH2.0™ Sealing Hook (SH) 291 total abdominal colectomy with ileorectal anastamosis 369 total mesorectal excision (TME) 308, 401 toxic megacolon 98, 341 transabdominal ultrasound (US) 334 transanal approach, to rectal cancer benefits 276 complications 275 imaging techniques 271–2 local surgery disadvantages 276 oncologic advantages of 276 outcomes 276 surgical options 271–2 Transanal Endoscopic Microsurgery (TEM) 273 comparison with 275–6 complication of 275 techniques of 274–5 transanal excision 272 techniques 273 Transanal Endoscopic Microsurgery (TEM) comparision with 275, 276–6 complication of 275 benefits 276 local surgery disadvantages 276 oncologic advantages of 276 outcomes 276 and transanal 273, 275–6 techniques of 274–5 transanal endoscopy 132 colorectal preparation 132–4 hypertonic electrolyte solutions 133 infectious disease complications 134 intravenous sedation 133–4 oral lavage 133 nontechnical complications 132 postpolypectomy syndrome 136–7 proctoscopic perforations 137 technical complications hemorrhage 134–5 perforation 135–6 transanal excision 272 transanal rectal flap advancement 396 transcoccygeal Kraske approach 278 transureteroureterostomy 399 Transversus Abdominis Plane (TAP) block 22–3 Trendelenburg position 23, 246 Treponema pallidum 157 trichloroacetic acid 155



index trocar 144–5 typhilitis 104 ulcerative colitis, surgery for 103, 142–3 abdominal colectomy with ileorectal anastomosis 322 complications anastomotic leak 324–5 dysplasia and malignancy 326 ileal pouch anal anastomosis, stricture at 325 pelvic sepsis 324 postoperative hemorrhage 323–4 pouch anal fistulas 325 pouch failure 326 pouch vaginal fistula 325 pouchitis 326 small bowel obstruction 323 controversies 326–7 Crohn’s Disease and Indeterminate Colitis 327 ileostomy, omission of mucosectomy vs. double-stapled technique 326–7 reservoir design 326 functional result 323 indications acute unresolving colitis 318–19 elective procedures 319 proctocolectomy with brooke ileostomy 319–20 with continent ileostomy 320–2 with ileoanal pouch 322–3 restoration 322 ultrasonography 117–19 endoluminal ultrasound’s (EUS) 119 intraoperative ultrasound 119 transabdominal ultrasound 118 ultrasound in fecal incontinence with limitations 92 unfractionated subcutaneous heparin 67 ureteral injuries 267, 397 anatomy 397 gentle pressure 397 prevention 397–8 types 398 ureteral stents 144 ureteroneocystotomy 398 urethral injuries 395



urinary fistula spontaneous closure 395–6 enteric diversion 396 stages 396 surgical selection 396 urinary retention 70–1, 172–3 urinary tract infections 70, 174 urological complication artificial devices 402–3 bladder dysfunction 400–1 bladder injury 396 fistula 396 iatrogenic ureteral injury 398–9 renal injury 399–400 sexual dysfunction 401–2 ureteral injury 397–8 urethral injury 395–6 VAC® 283 Venereal Disease Research Laboratory (VRDL) 157 venous thromboembolism (VTE) 9 Vermont Colorectal Cancer Project 164 vertical rectus abdominis myocutaneous (VRAM) flap 281 Veteran Affairs (VA) hospitals 162 video assisted thoracoscopic surgery (VATS) 294 virtual colonoscopy 110–12 Visiport™ 47 vomiting 72 warfarin therapy 22 Warfarin 135 water-soluble contrast enema 115–17 anastomotic assessment 116 intussusception 115 postoperative complications 115–16 volvulus 115 Wells operation 244 Whitehead deformity 174 Whitehead hemorrhoidectomy 170, 172 wireless capsule endoscopy (WCE) 335 wound infection 28 risk 27 see also skin Wound-Vac (KCI) 28 XELOX 300 xylocaine toxicity 19

Improved Outcomes in Colon and Rectal Surgery About the book Written by many of the world’s leading colorectal surgeons, this evidence-based text investigates the risks and benefits of colorectal surgeries. By using clinical pathways, algorithms, and case discussions, the authors identify the best practices for patient safety and positive outcomes to ensure that physicians correctly recognize potential problems and carefully manage complications. Improved Outcomes in Colon and Rectal Surgery is an essential reference for all colorectal surgeons, fellows and residents, as well as those working in gastroenterology and the medico-legal profession.

About the editors Charles B Whitlow MD, Program Director, Colon and Rectal Surgery Fellowship Program, Ochsner Medical Center, New Orleans, Louisiana, USA. David E Beck MD, Chairman, Department of Colon and Rectal Surgery, Ochsner Medical Center, New Orleans, Louisiana, USA. He is President-Elect of the American Society of Colon and Rectal Surgeons and Editor-in-Chief of Clinics in Colon and Rectal Surgery and the Ochsner Journal. David A Margolin MD, Colon and Rectal Research Director, Ochsner Medical Center, New Orleans, Louisiana, USA. He is an Associate Editor of Diseases of the Colon and Rectum. Terry C Hicks MD, Associate Chairman, Department of Colon & Rectal Surgery, Ochsner Medical Center, New Orleans, Louisiana, USA. He is President of the American Board of Colon and Rectal Surgeons Alan E Timmcke, Staff Colon and Rectal Surgeon, Ochsner Medical Center, New Orleans, Louisiana, USA.

Also available Ambulatory Colorectal Surgery Edited by Laurence R Sands and Dana R Sands (ISBN: 9780824727925) Gastrointestinal Oncology: Evidence and Analysis Edited by Peter McCulloch, Martin S Karpeh, David J Kerr and Jaffer Ajani (ISBN: 9780849398650) Neoplasms of the Colon, Rectum, and Anus, Second Edition Authored by Philip H Gordon and Santhat Nivatvongs (ISBN: 9780824729615)

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